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So you start off in charge, youre an independent operator, you dont work inside the system, but then you figure out the system thinks it includes you, some moron must have slipped in that clause while you werent looking, so you go talk to him, and its a pretty congenial meeting, although he does come across like a company man, and then later on you get an engraved invitation to come to a party. The food is very good and the people seem reasonable in a sort of washed-out way, but the upshot is, you can come in out of the cold if you want to. Theyll take you in. You can sit in an office and make twice as much as you were making on your own. Thats what they tell you. The only thing is, you have to sign a piece of paper that says you were never born and youre actually a desk ornament. They assure you its just a formality and theyve signed the same paper, and look, it hasnt hurt them The Magician Awakes
When I was running for a Congressional seat in 1994, I was also in the middle of a fight to preserve access to alternative health care, against FDA attackand during that process, I was enlightened through meeting various members of the Pod People species, who had their own ideas about what health freedom meant.
Against the odds (with a 50% chance of relapse within 1-2 years, according to the Institute for Quality and Efficiency in Health Care1) and against the recommendations of my mental health team, I tapered off psychiatric medication and stayed well well, mostly. Let me put it this way: I have managed to avoid another admission to an acute psychiatric hospital ward, since my last encounter with psychiatry which was about three years ago. It hasnt exactly been a straight path, and I wouldnt encourage anyone to make a decision about discontinuing antidepressants (or any long-term medication) without consulting a health professional or without support in developing a robust alternative health and well-being plan.
Here follows a brief look into my rollercoaster journey of recovery, returning to work, having my trauma re-triggered, finding a way through, and finally living well. It no longer matters that I have not remained entirely symptom free. The fact that I have had further experiences of altered perception is no longer relevant. What does matter is that, despite having experienced distress again, I was kind enough to myself in allowing and claiming some space to heal.
Starting work again was interesting. After my first day back, last year, I did not make it home. We were being evacuated due to fires near our house. The noise from the helicopters was triggering for me. The first warning signs started with me becoming noise sensitive and feeling unsafe and monitored, like I did while being an inpatient. During that time, a helicopter had flown above the caged unit, peering down on us patients like identifying wild animals waiting to be darted, with us not knowing whether we would ever be set free. So I got scared again with these traumatic memories erupting. I was back in the cage (in my head) and I couldnt get out, the fires were getting closer, and I needed help again.
Despite the timing being right for my return to work my youngest at the time had just started school, and I felt I needed another challenge once again I found myself in a place where things were getting on top of me. I was hardly coping. What was different was that I recognised this and took steps to act. I knew what to focus on instead and continued to access people who would validate my experience. I had some clearer ideas by then of what I needed to try to do to get better and I would be able to tell others what I needed.
After a distressed phone call to Healthline, in desperation I briefly restarted the antipsychotic medication that I had left in the cupboard. I took them for two days and felt side effects that further triggered bad inpatient memories, so I decided to abandon it. My throat was extremely sore and I would do anything to mak...
I have to admit that it makes me sad to see children at athletic events toting around giant bottles of commercially made sports drinks like Powerade or Gatorade.
On top of being loaded with sugar and/or artificial sweeteners, colors and a myriad of chemicals, research has demonstrated that they are damaging to teeth.
From NPR: Children registering for school in Florida this year were asked to reveal some history about their mental health.
The new requirement is part of a law rushed through the state legislature after the February shooting at Marjory Stoneman Douglas High School in Parkland, Fla.
The states school districts now must ask whether a child has ever been referred for mental health services on registration forms for new students.
If you do say, Yes, my child has seen a counselor or a therapist or a psychologist, what does the school then do with that? asks Laura Goodhue, who has a 9-year-old son on the autism spectrum and a 10-year-old son who has seen a psychologist. I think that was my biggest flag. And I actually shared the story with a couple of mom friends of mine and said, Can you believe this is actually a thing?
Goodhue worries that if her childrens mental health history becomes part of their school records, it could be held against them.
If my child was on the playground and something happened, she says, they might think, This child has seen mental health services. This must mean something more than it really means.
Asparagus can make any meal feel a little more special, since
its considered a delicacy in the vegetable world. Its among the most nutritionally balanced
vegetables, as its low in fat, sodium and cholesterol, but packed
with a variety of vitamins and minerals.
One of the most notable health benefits of asparagus is its high B vitamin content, particularly folate, a vitamin that promotes the production of dopamine, serotonin and norepinephrine this is why asparagus is known as the feel-good vegetable. Its also an excellent source of:
For most people, the go-to method for cooking asparagus is steaming, but there are many other ways to cook this versatile vegetable it can be simmered, roasted, grilled, sauted and more. You can even eat it raw in a salad. Asparagus also complements a variety of seasonings, from simple salt and pepper to boldly flavored spicy sauces.
Mark Sisson, a former elite endurance athlete that qualified for the 1980 U.S. Olympic marathon trials, founder of the popular website Mark's Daily Apple and a leader in the paleo movement, was one of the first to help me understand the importance of burning fat for fuel.
Here after we cover some of the basic benefits of high-intensity interval training and strength training, previously discussed in "Primal Fitness Tips" we segue to the topic at hand, namely the use of collagen for soft tissue injuries and repair, along with a few other useful fitness tips.
"How I came to [learn about collagen] was how I arrived at a lot of my epiphanies I had a life crisis. I play ultimate Frisbee once a week, every week for the last 15 years now. But about five or six years ago, I started to develop severe Achilles' heel tendinosis.
Ultimate Frisbee is a very fast-paced game There's lots of running [and it] requires a lot of agility, a lot of side-to-side quick movement, as well as raw speed
I found over a couple of years, in my late 50s, that I was starting to get these real severe Achilles' problems. I couldn't sprint. My Achilles' were really tender. They were getting thick. I went to see an orthopedic surgeon [who] said, 'You have severe Achilles' tendinosis.' I go, 'What does that mean?' 'Well, you're screwed, basically. You can't play sports again'
An orthopedist in Southern California said, 'Well, here's what we're going to do. We're going to take the back of your heel, slit it open and scrape the Achilles' down to the raw meat. We're going to pack it up in a cast for three months, then you'll do nine months of rehab and you'll be 85 percent of where you were.' I'm like, 'No. That's not going to happen, Doc '
I went back to my house and said, 'You know, there's something I was doing wrong here.' I started to do the analysis and I thought, 'Here I am stressing my Achilles', which is attached to the calves, so I'm really stressing the calves, the plantar fascia and everything around it, on a regular basis. I'm not giving my body the raw materials it needs to recover from that stress. It is that simple.'"
Collagen-based tissue includes tendons, ligaments, cartilage and f...
Your bodys rectum and anus play major roles in temporarily storing and fully eliminating feces and other waste material from your body.1 Maintaining the health of these body parts is important; otherwise you may experience health problems that not only will hinder proper function, but cause pain and discomfort as well.
One such condition is hemorrhoids, which are enlarged and swollen blood vessels that develop in the lower portion of your rectum and anus.2
While health experts have not determined the exact cause of hemorrhoids, the Mayo Clinic notes that they may form because of an increased pressure in the lower rectum. Other risk factors linked to hemorrhoids include prolonged sitting, obesity, a low-fiber diet and constipation or diarrhea.3
Hemorrhoids usually affect adults aged 45 to 65 years old, but young people and children may experience them as well. Men are more prone to having hemorrhoids, but women may also develop them, especially during pregnancy.4
According to a 2016 Clinics in Colon and Rectal Surgery article, at least 10 million Americans (4.4 percent of the population) report a case of hemorrhoids annually.5 Harvard Health Publications notes that around half of people aged 50 years and above have already experienced at least one or more of the usual symptoms of hemorrhoids, or have required treatment.6
While most hemorrhoids are not life-threatening,7 they are literally a pain in the backside. However, there are pain-relieving protocols that are effective, inexpensive and can be done in the comfort of your own home. There are also surgical procedures for hemorrhoids, but these are advisable only if natural remedies havent worked.
Apart from addressing hemorrhoids once they appear, prevention is key. You can lower your risk for hemorrhoids (even if...
PMID: FASEB J. 2018 Oct 10:fj201800934RRR. Epub 2018 Oct 10. PMID: 30303745 Abstract Title: Bisphenol A exposure alters placentation and causes preeclampsia-like features in pregnant mice involved in reprogramming of DNA methylation of WNT2. Abstract: Preeclampsia leads to adverse outcomes for pregnant women. Bisphenol A (BPA) is an environmental endocrine disruptor and has been shown to be positively associated with increased risk of preeclampsia in human studies. We investigated whether BPA exposure causes preeclampsia-like features in pregnant mice and the associated underlying mechanisms. Experiments were performed in animal models and cell cultures. In pregnant mice, BPA-exposed mice exhibited preeclampsia-like features including hypertension, disruption of the circulation, and the placental angiogenesis biomarkers fms-related tyrosine kinase 1 and placenta growth factor, and glomerular atrophy; urinary protein was not affected. These preeclampsia-like features correlated with increased retention of smooth muscle cells and reduced vessel areas at the junctional zone of the placenta. In addition, there were disrupted expression of invasion-related genes including increased tissue inhibitors of metalloproteinases, decreased metalloproteinases, and Wnt family member WNT2/-catenin, which correlated with increased DNA methylation in its promoter region and upregulation of DNA methyltransferase (Dnmt)1. BPA exposure impeded the interaction between the human cytotrophoblast cell line, HTR-8/SVneo, and endothelium cells. BPA exposure down-regulated WNT2 expression, andelevated the DNA methylation of WNT2; these results were consistent with in vivo observations. Inhibition of DNMT in HTR-8/SVneo cells resulted in reduced DNA methylation and increased expression of WNT2. Taken together, these data demonstrate that BPA exposure alters trophoblast cell invasion andcauses abnormal placental vessel remodeling, both of which lead to the development of preeclampsia-like features in pregnant mice. Our results suggest that this phenomenon involves the epigenetic reprogramming and down-regulation of WNT2 mediated by DNMT1.-Ye, Y., Tang, Y., Xiong, Y., Feng, L., Li,X. Bisphenol A exposure alters placentation and causes preeclampsia-like features in pregnant mice involved in reprogramming of DNA methylation of WNT2.
PMID: Toxicol Sci. 2018 Oct 8. Epub 2018 Oct 8. PMID: 30295897 Abstract Title: Prenatal bisphenol A exposure alters epithelial cell composition in the rhesus macaque fetal oviduct. Abstract: Bisphenol A (BPA) is an endocrine disrupting compound that is a pervasive environmental contaminant. Although it has been reported to affect the development of a variety of fetal reproductive tissues, data on the effect of fetal BPA exposure on oviducts were extremely limited and were only available in mice. To determine if there are adverse effects of gestational BPA exposure on fetal oviduct, we exposed pregnant rhesus macaques with female fetuses to oral or non-oral BPA during the last trimester of gestation (day 100 to term). After the treatment, fetal oviducts were collected for morphology evaluation. BPA exposure altered the percentages of different cell types (ciliated, non-ciliated, and secretory) in the fetal oviduct and resulted in a significant high ciliated cell population in the BPA-exposed fetal oviduct. The distribution of ciliated cells on the epithelium in the BPA-exposed fetal oviduct was also altered. Gestational BPA exposure reduced the expression of mucosubstance and uteroglobin in secretory cells in the fetal oviduct. A comparison of the outcome of the fetal oviduct studies with similar outcomes previously reported in the lung from the same fetuses demonstrates that BPA exhibits opposite effects in these two organs. In conclusion, the BPA-associated alterations in the fetal oviduct could potentially affect the oviduct morphology and function later in life with a negative impact fertility. The mechanisms of action of the differential response of the oviduct and lung to BPA exposure require further investigation.
PMID: Food Chem Toxicol. 2018 Oct 9. Epub 2018 Oct 9. PMID: 30312649 Abstract Title: Bisphenol A exhibits cytotoxic or genotoxic potential via oxidative stress-associated mitochondrial apoptotic pathway in murine macrophages. Abstract: Bisphenol A (BPA) is primarily used in production of polycarbonate plastics and epoxy resins including plastic containers. BPA is an endocrine disruptor and supposes to induce asthma and cancer. However, so far only a few evidences have shown the BPA-induced toxic effect and its related mechanism in macrophages. BPA demonstrated cytotoxic effect on RAW264.7 macrophages in a concentration and time-dependent manner. BPA induces necrosis, apoptosis, and genotoxicity in a concentration-dependent manner. Phosphorylation of cytochrome C (cyto C) and p53 was due to mitochondrial disruption via BCL2 and BCL-Xdownregulation and BAX, BID, and BAD upregulation. Both caspase-dependent, including caspase-9, caspase-3, and PARP-1 cleavage, and caspase-independent, such as nuclear translocation of AIF, pathways were activated by BPA. Furthermore, generation of reactive oxygen species (ROS) and reduction of antioxidative enzyme activities were induced by BPA. Parallel trends were observed in the effect of BPA on cytotoxicity, apoptosis, genotoxicity, p53 phosphorylation, BCL2 family expression exchange, caspase-dependent and independent apoptotic pathways, and ROS generation in RAW264.7 macrophages. Finally, BPA-exhibited cytotoxicity, apoptosis, and genotoxicity could be inhibited by N-acetylcysteine. These results indicated that the toxic effect of BPA was functioning via oxidative stress-associated mitochondrial apoptotic pathway in macrophages.
PMID: Toxicology. 2018 Oct 9. Epub 2018 Oct 9. PMID: 30312744 Abstract Title: Bisphenol A exposure remodels cognition of male rats attributable to excitatory alterations in the hippocampus and visual cortex. Abstract: Bisphenol A, an environmental xenoestrogen, has been shown sex-specific adverse effects on cognitive function of rodents. However, the specific mechanisms underlying these outcomes remain elusive, limiting our understanding the differences in behavioral impairments due to BPA exposure between genders in humans. The present study chose the juvenile stage (with a stable estrogen level) as the exposure window to explore BPA effects on cognitive behaviors of male and female Sprague-Dawley (SD) rats and related mechanisms. Three dosages of BPA (0.04, 0.4 and 4mg/kg/day) were chose to make BPA-exposed models. Especially, the mid-dose for rats was close to the current reference daily limit for human exposure given by the U.S. Environmental Protection Agency. Our results showed that male but not female juvenile rats had a marked decline in spatial memoryafter 0.4mg/kg/day BPA exposure, which accompanied with downregulation of glutamate receptor (NR2) expression in their hippocampus and primary visual cortex (V1). In the high-dose BPA exposed groups (4mg/kg/day), there was not only a deficit of spatial memory, but also an anxiety-like behavior of male rats. Additionally, those rats had a significant decline in spine density of pyramidal neurons and a decreased expression of glutamate receptor subtypes (NR2 and GluR1) in the hippocampus. Importantly, such impairments in the hippocampus of male rats were associated with a decrease of glutamate receptor (NR2) expression in the V1, which could perturb the visual information inputs. To some extent, altered ER expression within their hypothalamus could contribute to the anxiety-like behavior after high-dose BPA exposure. However, the low-dose BPA exposed juvenile rats didn't present any structural and behavioral changes in our present study. Those results suggests that BPA exerts dose dependent and gender-specific effects on the cognition of juvenile animals. Our findings shed light on mechanisms underlying BPA effects on the juvenile animals.
PMID: Carbohydr Polym. 2018 Dec 15 ;202:461-469. Epub 2018 Sep 7. PMID: 30287023 Abstract Title: Chemical characteristics, antioxidant capacities and hepatoprotection of polysaccharides from pomegranate peel. Abstract: This proposed work aimed to investigate the chemical characteristic, antioxidant capacities and hepatoprotection effect of pomegranate peel polysaccharides (PPP) on CCl-induced oxidative damage in mice. PPP was identified as the acidic heteropolysaccharides by HPLC methods. In vitro test showed that PPP had excellent reducing power and scavenging effects against free radicals. Administration of PPP (50, 100 and 200mg/kgbw) in mice before the injection of CClcould observably antagonize the increased serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and hepatic malonaldehyde level in CCl-induced mice, especially administrated with 200mg/kgbw of PPP. Hepatic enzymatic activities of total superoxide dismutase, glutathione peroxidase, catalase and non-enzymatic activity of glutathione were markedly increased at high dosage of PPP, respectively. In addition, histopathological observation of liver further proved these biochemical characteristics. Therefore, it can be concluded that PPP exhibits strong protective effects against CCl-induced liver injury in mice.
Jacalyn Broze got her flu shot in 2017 like she did every other year, but this time it was different. I always get a flu shot, Broze said. Within 24 hours, I knew something wasnt right. She had extreme pain in her shoulder. The grocery pharmacy where she got the shot told her it could be normal temporary soreness. But 
The post CBS: Woman Undergoes Extensive Arm Surgery After Flu Shot (A Must Read) appeared first on Health Nut News.
PMID: Genes Genomics. 2018 06 ;40(6):561-567. Epub 2018 Feb 20. PMID: 29892950 Abstract Title: Obese rats supplemented with bitter melon display marked shifts in the expression of genes controlling inflammatory response and lipid metabolism by RNA-Seq analysis of colonic mucosa. Abstract: Obesity is known to induce pathological changes in the gut and diets rich in complex carbohydrates that resist digestion in the small bowel can alter large bowel ecology. The purposes of this study were to identify the effects of bitter melon powder (BMP) on the global gene expression pattern in the colon mucosa of obese rats. Obese rats were fed a high-fat diet and treated without or with BMP for 8 weeks. Genome-wide expression profiles of the colon mucosa were determined by RNA sequencing (RNA-Seq) analysis at the end of experiment. A total of 87 genes were identified as differentially expressed (DE) between these two groups (fold change>1.2). These results were further validated by quantitative RT-PCR, confirming the high reliability of the RNA-Seq. Interestingly, DE genes implicated in inflammation and lipid metabolism were found to be downregulated by BMP in the colon. Network between genes and the top 15 KEGG pathways showedthat PRKC (protein kinase C beta) and Pla2g2a (phospholipase A2 group IIA) strongly interacted with surrounding pathways and genes. Results revealed that BMP supplement could remodel key colon functions by altering transcriptomic profile in obese rats.
It seems that every day we see more people, some in the public eye, some not, who are speaking out about the flu shot. Today we have our own Florida local news reporter JAX 4s Nikki Kimbleton who said her own doctors believe her injury was from recent shot on her verified public Facebook page. 
The post Channel 4s Famous Broadcaster Goes Public She was Just Injured By Flu Shot appeared first on Health Nut News.
PMID: Curr Protein Pept Sci. 2018 Jun 21. Epub 2018 Jun 21. PMID: 29932035 Abstract Title: Emerging antitumor activities of the bitter melon (Momordica charantia). Abstract: Bitter melon or bitter gourd (Momordica charantia) is a common vegetable in Asia and it is distinctive for its bitter taste. As an ingredient in folk medicine, research from different laboratories in recent years supports its potential medicinal applications with anti-tumor, anti-diabetic, anti-HIV activities in both in vitro and animal studies. In this short review, we summarize herein the recent progress in the antitumor aspect of bitter melon with a focus on the underlying molecular mechanisms. Further mechanistic studies as well as clinical trials are necessary to further verify its medicinal applications.
PMID: Food Nutr Res. 2018 ;62. Epub 2018 Mar 22. PMID: 30026676 Abstract Title: Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver. Abstract: Background: Bitter melon (BM) improves glucose level, lipid homeostasis, and insulin resistance. However, the preventive mechanism of BM in nonalcoholic fatty liver disease (NAFLD) has not been elucidated yet.Aim & Design: To determine the protective mechanism of bitter melon extract (BME), we performed experimentsand. BME were treated palmitate (PA)-administrated HepG2 cells. C57BL/6J mice were divided into two groups: high-fat/high-fructose (HF/HFr) without or with BME supplementation (100 mg/kg body weight). Endoplasmic reticulum (ER) stress, apoptosis, and biochemical markers were then examined by western blot and real-time PCR analyses.Results: BME significantly decreased expression levels of ER-stress markers (including phospho-eIF2, CHOP, and phospho-JNK [Jun N-terminal kinases]) in PA-treated HepG2 cells. BME also significantly decreased the activity of cleaved caspase-3 (a well known apoptotic-induced molecule) and DNA fragmentation. The effect of BME on ER stress-mediated apoptosiswas similarly observed in HF/HFr-fed mice. BME significantly reduced HF/HFr-induced hepatic triglyceride (TG) and serum alanine aminotransferase (ALT) as markers of hepatic damage in mice. In addition, BME ameliorated HF/HFr-induced serum TG and serum-free fatty acids.Conclusion: These data indicate that BME has protective effects against ER stress mediated apoptosis in HepG2 cells as well as in HF/HFr-induced fatty liver of mouse. Therefore, BME might be useful for preventing and treating NAFLD.
PMID: Complement Ther Clin Pract. 2018 Aug ;32:181-186. Epub 2018 Jun 28. PMID: 30057048 Abstract Title: The effects of Momordica charantia (bitter melon) supplementation in patients with primary knee osteoarthritis: A single-blinded, randomized controlled trial. Abstract: BACKGROUND: Osteoarthritis is a common problem affecting the joints in the elderly, caused disability and consequently decrease the quality of life. The conservative treatment includes the usage of analgesia, but the use of herbal medicine is growing. Momordica charantia or bitter melon has been widely described to have anti-diabetic and anti-inflammatory effects. However, its effect on reducing pain in primary knee osteoarthritis is not well studied. We aim to determine the effects of Momordica charantia in reducing pain among primary knee osteoarthritis patients.MATERIALS AND METHODS: Thirty-eight and thirty-seven primary knee osteoarthritis patients underwent 3 months of Momordica charantia and placebo supplementation respectively. Three 500mg per capsule of Momordica charantia were taken thrice daily. Rescue analgesia was allowed as needed. Pain and symptoms throughout the Momordica charantia supplementation period were assessed using Knee Injury and Osteoarthritis Outcome Score and EQ-5D-3L Health questionnaire, while rescue analgesia intake throughout the period of supplementation was measured using analgesic score.RESULTS: After 3 months supplementation period, body weight, body mass index, and fasting blood glucose reduced significantly in the Momordica charantia group. There were also significant improvements in Knee Injury and Osteoarthritis Outcome Score subscales and EQ-5D-3L dimension score, and reduction in analgesic score. The placebo group had also shown significant improvements in certain Knee Injury and Osteoarthritis Outcome Score subscales and EQ-5D-3L dimension score, but with increased of the analgesic score.CONCLUSION: Momordica charantia supplementation offers a safe alternative to reducing pain and improving symptoms among the primary knee osteoarthritis patients while reducing the need for analgesia consumption. These beneficial effects can be seen as early as 3 months of supplementation.
PMID: Pak J Pharm Sci. 2018 Sep ;31(5):1837-1843. PMID: 30150178 Abstract Title: Hypolipidemic and antioxidant potential of bitter gourd (Momordica charantia L.) leaf in mice fed on a high-fat diet. Abstract: The purpose of this study was to investigate the antioxidant and hypolipidemic potential of bitter gourd (BG) leaf ethanol extract (LE) in mice fed a high-fat diet (HFD). Fifty mice were randomly separated into five groups with 10 animals of each group. The animals received normal diet (NC), HFD diet (HF), 200mg/kg/day LE with HFD (LLE), 400 mg/kg/day LE with HFD (MLE), 800mg/kg/day LE with HFD (HLE), respectively. After six weeks, HF group showed meaningfully (P
PMID: Food Chem Toxicol. 2018 Sep 3 ;121:203-213. Epub 2018 Sep 3. PMID: 30189316 Abstract Title: Protective effects of Manuka honey on LPS-treated RAW 264.7 macrophages. Part 1: Enhancement of cellular viability, regulation of cellular apoptosis and improvement of mitochondrial functionality. Abstract: Manuka honey (MH) is a monofloral honey from Australia and New Zealand, well-known for its healthy properties, such as antioxidant, antimicrobial and wound healing capacities. The aim of this work was to assess the phenolic composition and the total antioxidant capacity (TAC) of MH, as well as its effects on cellular viability, proliferation, apoptosis and metabolism in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages, highlighting the molecular mechanisms involved. Up to 18 compounds were identified in MH, with gallic acid and quercetin as the major ones; MH showed also remarkable TAC. In addition, MH was able to enhance cellular viability, decrease apoptosis, promote wound healing and attenuate inflammation in a dose-dependent manner, by reducing the expression of caspase 3, p-p38 and p-Erk1/2 proteins, in macrophages stressed with LPS. In addition, it improved mitochondrial respiration and glycolytic activities, stimulating the expression of p-AMPK, SIRT1 and PGC1, counteracting in this way the deleterious effects of LPS treatment. In conclusion, one of the possible mechanisms by which MH exerts its beneficial effects could be to its capacity to improve cellular viability, promote proliferation and enhance energetic metabolism, by modulating the expressionof several proteins involved in apoptosis, inflammation, metabolism and mitochondrial biogenesis.
PMID: Minerva Cardioangiol. 2018 Aug ;66(4):386-390. PMID: 29975020 Abstract Title: Behet syndrome: effects of Pycnogenol supplementation during regression phases. Abstract: BACKGROUND: The aim of this comparative registry study was to evaluate the supplementation with Pycnogenol in subjects with Behet syndrome (BS) with symptoms impairing their quality of life despite being in a remitting phase of the disease.METHODS: Thirty-four patients with a confirmed diagnosis of BS were divided into the control group (without supplement) or the active group, in this specific case using Pycnogenol (Horphag Research LTD) supplement at the daily dose of 150 mg (50 mg tid) for 4 weeks.RESULTS: All subjects receiving Pycnogenol reported a significant decrease in symptoms, such as burning/pain due to dryness and ulcerations (P
PMID: IUBMB Life. 2018 Oct 11. Epub 2018 Oct 11. PMID: 30308112 Abstract Title: Anticancer activity of thymol: A literature-based review and docking study emphasized on its anticancer mechanisms. Abstract: This review aims to summarize the anticancer effects of the natural monoterpene phenol derivative of cymenethymol and its derivatives as well as further molecular docking study to correlate the interaction of thymol and biomacromolecules that involved in cancer cell growth. For this, an up-to-date (till July 2018) literature study were made through using PubMed, Science Direct, Web of Science, Scopus, The American Chemical Society, Clinicaltrials.gov, and Google Scholar databases. Literature study demonstrated that thymol, melasolv (3,4,5-Trimethoxycinnamate thymol ester), and Mannich bases of thymol have potential anticancer effects in various test systems, including mice, rats and cultured cancer cells through various anticancer pathways such as antioxidant/oxidative stress induction, apoptosis, anti-inflammatory/immunomodulatory, anti-genotoxicity, chemo-, and radiopreventive ways. A few earlier scientific evidences showed that thymol is less toxic to mammalian systems. In silico study of thymol and its derivatives against 17 essential proteins revealed that 6BVH (PARP-1) and 5LIH (protein kinase C) are the most efficient receptor protein for interaction and binding of thymol and melaslov for the cancer prevention and initiation. On the basis of the summary of this review and docking study, it is evident that thymol may be one of promising plant-derived cancer chemotherapeutic agents. 2018 IUBMB Life, 2018.
PMID: Prev Nutr Food Sci. 2018 Jun ;23(2):134-143. Epub 2018 Jun 30. PMID: 30018892 Abstract Title: Evaluation ofAntioxidant Activity of the Water Extract Obtained from Dried Pine Needle (). Abstract: Antioxidant activities of water extracts obtained from dried pine needle () were measured at 0, 4, 20, 100, 500, 1,000, and 1,200 ppm and compared with those of phenolic compounds of butylated hydroxyanisole, butylated hydroxytoluene,-butylhydroquinone, ferulic acid, and-tocopherol. The activity was determined as the ability to scavenge 1,1-diphenyl-2-picrylhydrazyl radical and hydrogen peroxide, reductive power, and inhibition of lipid peroxidation in a linoleic acid system using the ferric thiocyanate method and thiobarbituric acid method, respectively. Pine needle water extract (PNWE) exhibited antioxidant activity in a concentration-dependent mode at the same parameters mentioned above, and a significant difference (
PMID: Rejuvenation Res. 2018 Sep 14. Epub 2018 Sep 14. PMID: 30215292 Abstract Title: Pleiotropic effects of French maritime pine bark extract (Pycnogenol) to promote healthy aging. Abstract: Extension of the healthy life span is of primary importance for the aging society. Among exercise, healthy nutrition and mental training, food supplements are widely used as preventive measures to postpone the diverse symptoms of aging. The extract from the bark of the French maritime pine, Pycnogenol, rich on flavonoids, has anti-inflammatory and anti-oxidative activity, proven in in-vivo studies. The extract reduces oxidative stress and improves endothelial health. Its anti-thrombotic properties are based on inhibition of platelet aggregation. In double-blind, placebo-controlled clinical studies Pycnogenol shows diverse positive effects. In respect to cardiovascular symptoms, the extract has an antihypertensive effect, slows down the progression of atherosclerosis and prevents venous thrombosis. As reported in studies in China and the US, diabetes type 2 as well as diabetic retinopathy is improved with Pycnogenol . The extract restores mobility of seniors in case of patients suffering from osteoarthritis, Pycnogenol reduces pain and stiffness and use of analgesics. Furthermore, cognitive functions of elderlies, especially spatial memory, are significantly ameliorated. Climacteric symptoms are significantly alleviated by the pine bark extract. Urinary symptoms of benign prostatic hyperplasia are reduced by Pycnogenol. In combination with L-arginine, Pycnogenol restores erectile function in men with erectile dysfunction. The sum of these positive effects on relevant symptoms of aging suggest to use Pycnogenol for a more extended period of healthy aging.
PMID: Iran J Public Health. 2018 Jun ;47(6):779-787. PMID: 30087862 Abstract Title: Effect of Pycnogenol Supplementation on Blood Pressure: A Systematic Review and Meta-analysis. Abstract: Background: Pycnogenol exhibits many biological activities, including control of blood pressure (BP). However, the reported results are inconsistent because of varied characteristics of participants and quality of studies. Thus, a meta-analysis was conducted to examine the effect of Pycnogenol supplementation on BP.Methods: This literature search of PubMed, the Web of Science and the Cochrane library was performed in May 2016 to identify eligible studies. Reference lists of the retrieved articles were also reviewed. Either a fixed-effects or, in the presence of heterogeneity, a random-effects model was used to calculate the effect of combined treatment.Results: We identified nine trials involving 549 participants who received Pycnogenol supplementation ranging from 150 mg/d to 200 mg/d. Compared with the control, the pooled estimate of change in systolic and diastolic BPs were -3.22 mmHg (95% CI: -6.20, -0.24) and -3.11 mmHg (95% CI: -4.60, -1.62), respectively. Subgroup analyses showed higher BP reduction among hypertensive participants or those who received intervention for more than 12 wk. However, this significant reduction was not observed in well-designed trials.Conclusion: This meta-analysis with nine trials provides better evidence that Pycnogenol exerts beneficial effects on BP.
PMID: Lab Anim Res. 2018 Sep ;34(3):111-117. Epub 2018 Sep 27. PMID: 30310407 Abstract Title: Inhibitory effects of Pycnogenol, a pine bark extract, in a rat model of testosterone propionate-induced benign prostatic hyperplasia. Abstract: Benign prostate hyperplasia (BPH) is a male reproductive disease that has gained increasing importance in recent years. The present study investigated whether Pycnogenol (PYC), a standardized French maritime pine bark extract, could prevent BPH induced by testosterone propionate (TP) in rats. Male Sprague-Dawley rats were randomly divided into five groups of six rats. One group was used as a normal control rats and the other groups received subcutaneous injections of TP for 4 weeks to induce BPH. In the two treatment groups, PYC (20 or 40 mg/kg) was administered daily for 4 weeks by oral gavage concurrently with the induction of TP. All rats were sacrificed at the scheduled termination time, the prostates were weighed, and histopathologic examinations wereconducted. Dihydrotestosterone (DHT) levels in serum and the prostate were measured, and the expression of proliferating cell nuclear antigen (PCNA) and Ki-67 proteins was investigated. BPH-treated animals showed increases in the relative weight of the prostate, higher concentrations of DHT in serumand the prostate, and higher expression of PCNA and Ki-67 in the prostate; in contrast, PYC-treated animals had significant reductions in these factors compared with the BPH animals. These findings indicated that PYC inhibited the development of BPH and that this was closely associated with a reduction in DHT concentration.
Dane Wigington GeoengineeringWatch.org How much of what we believe is actually nothing more than societal programming from the constant parade of propaganda? How many crimes and injustices does society accept because of being trained to never question the experts? Belief systems will not alter reality or the immense challenges that are closing in from every direction. The latest
PMID: J Cell Biochem. 2018 Sep 1. Epub 2018 Sep 1. PMID: 30171725 Abstract Title: Niacin deficiency modulates genes involved in cancer: Are smokers at higher risk? Abstract: The role of niacin's metabolite, nicotinamide adenine dinucleotide (NAD), in DNA repair via base-excision repair pathway is well documented. We evaluated if niacin deficiency results in genetic instability in normal human fetal lung fibroblasts (MRC-5), and further, does it leads to enhanced accumulation of cigarette smoke-induced genetic damage? MRC-5 cells were grown discretely in niacin-proficient/deficient media, and exposed to nicotine-derived nitrosamine ketone (NNK, a cigarette smoke carcinogen). Niacin deficiency abated the NAD polymerization, augmented the spontaneous induction of micronuclei (MN) and chromosomal aberrations (CA) and raised the expression of 10 genes and suppressed 12 genes involved in different biological functions. NNK exposure resulted in genetic damage as measured by the induction of MN and CA in cells grown in niacin-proficient medium, but the damage became practically marked when niacin-deficient cells were exposed to NNK. NNK exposure raised the expression of 16 genes and suppressed the expression of 56 genes in cells grown in niacin-proficient medium. NNK exposure to niacin-deficient cells raised the expression of eight genes including genes crucial in promoting cancer such as FGFR3 and DUSP1 and suppressed the expression of 33 genes, including genes crucial in preventing the onset and progression of cancer like RASSF2, JUP, and IL24, in comparison with the cells grown in niacin-proficient medium. Overall, niacin deficiency interferes with the DNA damage repair process induced by chemical carcinogens like NNK, and niacin-deficient population are at the higher risk of genetic instability caused by cigarette smoke carcinogen NNK.
If I didnt have the authentic YouTube video of vaccine-pushing-authority, Dr. Paul Offit, MD, to share with my readers below, you probably would think Ive gone off my rocker, especially if I only quoted him and did not have the physical, visual and audio proof of his admitting numerous suppressed deprecating facts about vaccinations, thereby further empowering parents valid reasons for NOT vaccinating their beloved children.
Here are some acknowledgements Dr. Offit finally admits to about vaccinations:
Paul Offit Says Vaccination is a Violent
Parents probably remember it was Dr. O...
Note from Fluoride Action Network: This regulation is currently in effect
Louisiana SIP [State Implementation Plan]: LAC 33:III Ch 23 Subchap C, 2305Phosphate Fertilizer Plants, 2305 Fluoride Emission Standards for Phosphate Fertilizer Plants; SIP effective 1989-05-08 (LAc49)
Louisiana Administrative Code, Title 33 ENVIRONMENTAL QUALITY, Part III Air (LAC 33:III)
Chapter 23. Control of Emissions for Specific Industries
Subchapter C. Phosphate Fertilizer Plants
Section 2305. Fluoride Emission Standards for Phosphate
Fertilizer Plants. LAc49
Approved by EPA 03/08/89 (54 FR 09795) at 52.970(c)(49) effective 05/08/89.
A. Purpose. The purpose of this Subchapter shall be to limit the quantity of atmospheric fluoride emissions from phosphate fertilizer plants.
B. Scope. This Subchapter applies to those phosphate fertilizer plants which were constructed, or under construction or modification, prior to August 6, 1975.
C. Definitions. Terms defined in Chapter 31 herein, shall have the same meaning when used herein.
D. Emission Limitations. On and after the date which each affected facility is required to be compliance, no owner or operator subject to this regulation shall cause to be discharged into the atmosphere from any affected facility any gases which contain total fluorides in excess of the quantities listed below for each facility.
1. Wet-Process Phosphoric Acid Plants 0.10 pounds of total fluorides per ton (50.0 grams/metric ton) of equivalent P2O5 feed.
2. Superphosphoric Acid Plants. 1.10 pounds of total fluorides per ton (550 grams/metric ton) of equivalent P2O5 feed.
3. Diammonium Phosphate Plants. 0.18 pounds of total fluorides per ton (90.0 grams/metric ton) of equivalent P2O5 feed.
E. Test Methods and Procedures. Test methods and procedures for determining compliance with this regulation shall be identical to those specified in 40 CFR 60 for corresponding types of plants or equivalent test methods and procedures approved by the administrative authority.
AUTHORITY NOTE: Promulgated in accordance with R.S.
HISTORICAL NOTE: Promulgated by the Department of Environmental Quality, Office of air Quality and Nuclear Energy, Air Quality Division in LR 13:741 (December 1987).
*Online as of October 13, 2018, at...
Research indicates that you don't need drugs to control blood sugar. Food, herbs, and spices are the future of medicine.
Before we present this weeks Weekend Reads, a question: Do you enjoy our weekly roundup? If so, we could really use your help. Would you consider a tax-deductible donation to support Weekend Reads, and our daily work? Thanks in advance. The week at Retraction Watch featured more than a dozen corrections at Sloan Kettering, three retractions Continue reading Weekend reads: Fired for challenging authorship?; homeopathy paper earns a flag; sentenced to playing piano for embezzling research funds
The past of our ancestors lives on through us: Groundbreaking research illustrates how parental experience is not only epigenetically imprinted onto offspring, but onto an unprecedented number of future generations. Rather than occurring over the elongated time scale of millions of years, genetic change can transpire in real biological time through nanoparticles known as exosomes.
PMID: Drug Chem Toxicol. 2018 Sep 7:1-7. Epub 2018 Sep 7. PMID: 30192646 Abstract Title: Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury. Abstract: Humans and animals can be exposed to different chemical forms of mercury (Hg) in the environment. For example, methylmercury (MeHg)-contaminated fish is part of the basic diet of the riparian population in the Brazilian Amazon Basin, which leads to high total blood and plasma Hg levels in people living therein. Hg induces toxic effects mainly through oxidative stress. Different compounds have been used to prevent the damage caused by MeHg-induced reactive oxygen species (ROS). This study aims to investigate the in vivo effects of sub-chronic exposure to low MeHg levels on the mitochondrial oxidative status and to evaluate the niacin protective effect against MeHg-induced oxidative stress. For this purpose, Male Wistar rats were divided into four groups: control group, treated with drinking water on a daily basis; group exposed to MeHg at a dose of 100g/kg/day; group that received niacin at a dose of 50mg/kg/day in drinking water, with drinking water being administered by gavage; group that received niacin at a dose of 50mg/kg/day in drinking water as well as MeHg at a dose of 100g/kg/day. After 12weeks, the rats, which weighed500-550g, were sacrificed, and their liver mitochondria were isolated by standard differential centrifugation. Sub-chronic exposure to MeHg (100g/kg/day for 12weeks) led to mitochondrial swelling (p
PMID: J Med Food. 2017 Dec ;20(12):1240-1249. Epub 2017 Sep 28. PMID: 28956702 Abstract Title: The Effect of Anthocyanin-Rich Purple Vegetable Diets on Metabolic Syndrome in Obese Zucker Rats. Abstract: Consumption of highly colored fruits and vegetables rich in anthocyanins has been associated with numerous health benefits. Purple carrots (PC) and purple potatoes (PP) have higher anthocyanin concentrations and higher biological activities compared with less pigmented cultivars. We hypothesized that substitution of the majority of carbohydrate in a high fat diet with PP or PC, for 8 weeks, would improve insulin resistance and hypertension, major components of metabolic syndrome, compared with orange carrots (OC), white potatoes (WP) or a control, high fat, sucrose-rich diet (HFD) in obese Zucker rats. After 8 weeks of feeding, intraperitoneal glucose tolerance test, intraperitoneal insulin tolerance test (ipITT), and invasive hemodynamic tests were performed. The PP group had better glucose tolerance compared with the WP and the HFD groups and higher insulin sensitivity as measured by the ipITT and homeostatic model assessment of insulin resistance (P=.018) compared with the HFD without having any effect on blood pressure. The PC reduced left ventricular pressure compared with both the HFD (P=.01) and the OC (P=.049) groups and reduced systolic and diastolic blood pressures compared with the HFD group (P=.01 and
PMID: BMC Complement Altern Med. 2018 Jul 13 ;18(1):216. Epub 2018 Jul 13. PMID: 30005651 Abstract Title: Ipomoea batatas L. Lam. ameliorates acute and chronic inflammations by suppressing inflammatory mediators, a comprehensive exploration using in vitro and in vivo models. Abstract: BACKGROUND: Ipomoea batatas L. Lam. is a functional food and belongs to family Convolvulaceae. It is used as an antiinflammatory, aphrodisiac, antiasthmatic, anticonvalescent, antitumor, antanemic and antidiabetic agent by local communities. This study has been planned to evaluate its antiinflammatory and antiarthritic potentials.METHODS: Dry powder of I. batatas tuber and roots were extracted with ethyl acetate (IPT-EA, IPR-EA) and methanol (IPT-M, IPR-M), respectively. These extracts were tested for total phenolic and flavonoid contents (TPC and TFC), HPLC finger printing, multidimensional in vitro and in vivo antioxidant potential and albumin denaturation inhibition. Carrageenan-induced paw edema, croton oil-induced ear and anal edema inhibition and Complete Freund's Adjuvant (CFA)-induced antiarthritic assays were executed at a dose of 300 mg/kg body weight on Sprague-Dawley rats. Serum levels of interleukins IL-1 and IL-6 and nitric oxide (NO) were assessed to measure the inhibition of inflammation.RESULTS: Maximal TPC (319.8114.20 g GAE/mg dry extract) and TFC (208.779.09 g QE/mg DE) were estimated in IPR-EA extract. IPT-EA and IPR-EA yielded the maximum amounts of rutin (7.31.12 and 4.50.55), caffeic acid (1.600.25 and 2.170.26) and myricetin (2.70.14 and 1.010.08 g/mg DE), respectively in HPLC-DAD analysis. All extracts showed dose dependent response in in vitro antioxidant assays. Best inhibition (76.923.07%) of albumin denaturation was shown by IPT-EA in comparison to ibuprofen (79.484.71%). IPR-EA exhibited highest edemainhibition in models of carrageenan-induced paw edema (79.115.47%) and croton oil-induced ear and anal edema (72.017.80% and 70.804.94%, respectively). Significant inhibition of CFA-induced arthritic edema and arthritic score were observed by IPR-EA as compared to ibuprofen.Suppression of pro-inflammatory cytokines (IL-1, IL-6) and NO levels was shown by IPR-EA and IPT-EA, respectively.CONCLUSION: These results depict that richness of polyphenols and phytoconstituents in I. batatas ameliorates oxidative stress and inflammation of acute and chronic nature. Dose dependent antioxidant potential and inhibition of inflammatory edema, pro-inflammatory cytokines and hematological, biochemical and histological changes prove I. batatas therapeutic potential as an antiinflammatory and antiarthritic agent.
PMID: Pak J Pharm Sci. 2018 Jul ;31(4(Supplementary)):1539-1548. PMID: 30058546 Abstract Title: Anti-diabetic activity of aqueous extract of Ipomoea batatas L. in alloxan induced diabetic Wistar rats and its effects on biochemical parameters in diabetic rats. Abstract: Diabetes is a condition where the fasting blood glucose level elevated above the normal range (80-120mg/dL). This increase in blood glucose level may be due to the insulin deficiency i.e. insulin dependent diabetes mellitus (IDDM or type I) or due to insulin resistance i.e. non-insulin dependent diabetes mellitus (NIDDM or type II). Diabetes leads to severe complications in the body even life treating complications e.g. nephropathy, retinopathy, neuropathy increased vascular permeability and delayed wound healing if left untreated. Different drugs are used for the treatment of diabetes mellitus, but synthetic drugs are costly and possess severe side effects. So, more emphasis is being placed on the use of traditional medicines because these sources have fewer side effects than the synthetics drugs and are economical. So the white skinned sweet potato (Ipomoea batatas L.) peel-off was selected for its anti-diabetic effect as well as to see its effects on biochemical parameters. Both young (3-4 months) and old (up to 1 year) Wistar rats were selected for current study. It was found that the aqueous extract of WSSP peel-off had shown beneficial effects. In addition to the decrease in blood glucose level it also decreased protein glycation level total cholesterol, triglycerides, and LDL-cholesterol. Increase in HDL-cholesterol was also observed after treating the rats with aqueous extract of Ipomoea batatas. Additionally, WSSP peel-off had also shown positive results on total protein concentration, albumin, globulin, and plasma enzymes (SGOT and SGPT). Further research would be needed in order to purify the anti-diabetic components and it should be available in compact dose form for all diabetic patients.
PMID: J Med Food. 2018 Jul ;21(7):689-700. Epub 2018 Jun 4. PMID: 29862890 Abstract Title: The Effects of Curcuma longa L., Purple Sweet Potato, and Mixtures of the Two on Immunomodulation in C57BL/6J Mice Infected with LP-BM5 Murine Leukemia Retrovirus. Abstract: The immune response is stimulated to protect the body from external antigens and is controlled by several types of immune cells. In the present study, the immunomodulatory effects of Curcuma longa L., purple sweet potato, and mixtures of the two (CPM) were investigated in C57BL/6 mice infected with LP-BM5 murine leukemia virus (MuLV). Mice were divided into seven groups as follows: normal control, infected control (LP-BM5 MuLV infection), positive control (LP-BM5 MuLV infection+dietary supplement of red ginseng 300mg/kg body weight), the original powder of C. longa L. (C; LP-BM5 MuLV infection+dietary supplement of C 189mg/kg body weight), the original powder of purple sweet potato (P; LP-BM5 MuLV infection+dietary supplement of P 1811mg/kg body weight), CPM Low (CPL; LP-BM5 MuLV infection+CPM 2g/kg body weight), and CPM High (CPH; LP-BM5 MuLV infection+CPM 5g/kg body weight). Dietary supplementation lasted for 12 weeks. Dietary supplementation of CPM inhibited LP-BM5 MuLV-induced lymphadenopathy and splenomegaly and inhibited reduction of messenger RNA (mRNA) expression of major histocompatibility complex (MHC) I and II. Moreover, CPM reduced the decrease in T- and B cell proliferation, reduced the population of CD4(+)/CD8(+) T cells, and remedied the unbalanced production of T helper-1 (Th1)/T helper-2 (Th2) cytokines in LP-BM5 MuLV-infected mice. In addition, CPM inhibited reduction of phagocytosis in peritoneal macrophages and decreased serum levels of immunoglobulin A (IgA), immunoglobulin E (IgE), and immunoglobulin G (IgG). These results suggest that CPM had a positive effect on immunomodulation in C57BL/6 mice induced by LP-BM5 leukemia retrovirus infection.
PMID: Wei Sheng Yan Jiu. 2018 Jul ;47(4):517-524. PMID: 30081974 Abstract Title: [Purple sweet potato anthocyanins attenuates steatohepatitis induced by high fat diet combined with carbon tetrachloride in rats]. Abstract: OBJECTIVE: To explore the mechanism of purple sweet potato anthocyanins through NF-B pathway in attenuating steatohepatitis induced by high fat diet combined with carbon tetrachloride in rats.METHODS: Seventy male rats were randomly divided into control group( n = 10) and high-fat diet group( n = 60), models were prepared by highfat diet and intraperitoneal injection of carbon tetrachloride and olive oil( 50 : 50) 2 mL/kg, two times a week. After 10 weeks of feeding, the weight variations of all rats were tested before and after modeling. The colorimetric technique was used to test the concentration of serum ALT, AST, TG, and TC. A total of 58 rats were succeeded in modeling, the random choice of 50 rats were divided into model group, purple sweet potato anthocyanin low dose group( 60 mg/kg), middle dose group( 120 mg/kg), high dose group( 240 mg/kg), positive drug group( 150 mg/kg), 10 rats in each group. After 8 weeks of continuous administration, the method of colorimetric technique was used to test the concentration of ALT, AST, TG, TC, HDL and LDL. The method of ELISA kit was used to test the levels of the pro-inflammatory factors TNF-, IL-1 and the levels of the anti-inflammatory IL-4, IL-13. The Real-time PCR was used to test the expression of TNF-, IL-1, IL-4, IL-13, PPAR- and HMGB-1 mRNA of rats liver. The western blotting method was adopted to test the level of IB phosphorylation in liver tissues as well as the PPAR- and HMGB-1 protein expression.RESULTS: After modeling, the body weight of rats increased( P
From YES! Magazine: As I was reading the current series of YES! articles on the mental health crisis, I received an email from Darcia Narvaez, professor of psychology at University of Notre Dame. She was sending me articles being prepared for an anthology she is co-editing with the working title Sustainable Vision. The articles present lessons from indigenous culture that underscore why community is the solution to so much of what currently ails humanity.
Both these collections underscore why so much of what currently ails us can be traced to the ongoing global process of commodification, monetization, corporatization, and the increasing trend of machines, robots, and artificial intelligence replacing people in jobs ranging from manufacturing to customer service. All this is separating us from one another and from nature so that billionaires can grow their fortunes. The consequencesincluding environmental, social, and political collapseare dramatic, devastating, and unnecessary.
PMID: Molecules. 2018 Aug 17 ;23(8). Epub 2018 Aug 17. PMID: 30126082 Abstract Title: Aqueous-Methanol Extracts of Orange-Fleshed Sweet Potato () Ameliorate Oxidative Stress and Modulate Type 2 Diabetes Associated Genes in Insulin Resistant C2C12 Cells. Abstract: Edible plants such as sweet potato are sources of natural antioxidants that can be exploited in the management and treatment of insulin resistance. This present study investigated the effects of the extracts of an orange-fleshed sweet potato on oxidative stress biomarkers (glutathione status and lipid peroxidation) and activities of antioxidant enzymes (catalase, CAT and glutathione peroxidase, GPx) in palmitate-induced insulin resistant C2C12 cells. The intracellular antioxidant status of the cells was also measured using Ferric reducing antioxidant power (FRAP) and Trolox equivalent antioxidant capacity (TEAC) assays. Furthermore, this study determined the effect of the extracts on the regulation of some type 2 diabetes associated genes; glucose transporter 4 (), Nuclear respiratory factor 1 (), Myocyte enhanced factor 2A (), Carnitine palmitoyltransferase 1 () and Acetyl-CoA carboxylase 2 (). The results showed a significant (
PMID: Iran J Basic Med Sci. 2018 May ;21(5):508-516. PMID: 29922432 Abstract Title: Cyclooxygenase inhibitors combined with deuterium-enriched water augment cytotoxicity in A549 lung cancer cell line via activation of apoptosis and MAPK pathways. Abstract: Objectives: Combination chemotherapy is a rational strategy to increase patient response and tolerability and to decrease adverse effects and drug resistance. Recently, the use of non-steroidal anti-inflammatory drugs (NSAIDs) has been reported to be associated with reduction in occurrence of a variety of cancers including lung cancer. On the other hand, growing evidences suggest that deuterium-enriched water (DEW, D2O) and deuterium-depleted water (DDW) play a role both in treatment and prevention of cancers. In the present study, we examined the effects of DEW and DDW in combination with two NSAIDs, celecoxib and indomethacin, on A549 human non-small lung cancer cell to identify novel treatment options.Materials and Methods: The cytotoxicity of celecoxib or indomethacin, alone and in combination with DDW and DEW was determined. The COX-2, MAPK pathway proteins, the anti-apoptotic Bcl2 and pro-apoptotic Bax proteins and caspase-3 activity were studied for cytotoxic combinations.Results: Co-administration of selective and non-selective COX-2 inhibitors with DEW led to a remarkable increase in cytotoxicity and apoptosis of A549 cells. These events were associated with activation of p38 and JNK MAPKs and decreasing pro-survival proteins Bcl-2, COX-2 and ERK1/2. Furthermore, the combination therapy activated caspase-3, and the apoptosis mediator, and disabled poly ADP-ribose polymerase (PARP), the key DNA repair enzyme, by cleaving it.Conclusion: The combination of DEW with NSAIDs might be effective against lung cancer cells by influence on principal cell signalling pathways, and this has a potential to become a candidate for chemotherapy.
PMID: Exp Ther Med. 2018 Aug ;16(2):1241-1249. Epub 2018 Jun 19. PMID: 30116375 Abstract Title: Premature senescence activation in DLD-1 colorectal cancer cells through adjuvant therapy to induce a miRNA profile modulating cellular death. Abstract: Cancer, and particularly colon cancer, is associated with an increasing number of cases resistant to chemotherapy. One approach to overcome this, and to improve the prognosis and outcome of patients, is the use of adjuvant therapy alongside the standard chemotherapy regiment. In the present study, the effect of deuterium-depleted water (DDW) as a potential modulator of adjuvant therapy on DLD-1 colorectal cancer models was assessed. A number of functionality assays were performed, including MTT, apoptosis and autophagy, and mitochondrial activity and senescence assays, in addition to assessing the capacity to modify the pattern of released miRNA via microarray technology. No significant effect on cell viability was identified, but an increase in mitochondrial activity and a weak pro-apoptotic effect were observed in the treated DLD-1 cells cultured in DDW-prepared medium compared with those grown in standard conditions (SC). Furthermore, the findings revealed the capacity of DDW medium to promote senescence to a higher degree compared with SC. The exosome-released miRNA pattern was significantly modified for the cells maintained in DDW compared with those maintained in SC. These findings suggest that DDW may serve as an adjuvant treatment; however, a better understanding of the underlying molecular mechanism of action will be useful for developing novel and efficient therapeutic strategies, in which the transcriptomic pattern serves an important role.
PMID: Basic Clin Pharmacol Toxicol. 2017 Jun ;120(6):560-570. Epub 2017 Mar 7. PMID: 28032440 Abstract Title: Magnolol Attenuates Concanavalin A-induced Hepatic Fibrosis, Inhibits CD4T Helper 17 (Th17) Cell Differentiation and Suppresses Hepatic Stellate Cell Activation: Blockade of Smad3/Smad4 Signalling. Abstract: Magnolol is a pharmacological biphenolic compound extracted from Chinese herb Magnolia officinalis, which displays anti-inflammatory and antioxidant effects. This study was aimed at exploring the potential effect of magnolol on immune-related liver fibrosis. Herein, BALB/c mice were injected with concanavalin A (ConA, 8 mg/kg/week) up to 6 weeks to establish hepatic fibrosis, and magnolol (10, 20, 30 mg/kg/day) was given to these mice orally throughout the whole experiment. We found that magnolol preserved liver function and attenuated liver fibrotic injury in vivo. In response to ConA stimulation, the CD4T cells preferred to polarizing towards CD4T helper 17 (Th17) cells in liver. Magnolol was observed to inhibit Th17 cell differentiation in ConA-treated liver in addition to suppressing interleukin (IL)-17A generation. Hepatic stellate cells were activated in fibrotic liver as demonstrated by increased alpha smooth muscle actin (-SMA) and desmin. More transforming growth factor (TGF)-1 and activin A were secreted into the serum. Magnolol suppressed this abnormal HSC activation. Furthermore, the phosphorylation of Smad3 in its linker area (Thr179, Ser 204/208/213) was inhibited by magnolol. In vitro, the recombinant IL-17A plus TGF-1 or activin A induced activation of human LX2 HSCs and promoted their collagen production. Smad3/Smad4 signalling pathway was activated in LX2 cells exposed to the fibrotic stimuli, as illustrated by the up-regulated phospho-Smad3 and the enhanced interaction between Smad3 and Smad4.These alterations were suppressed by magnolol. Collectively, our study reveals a novel antifibrotic effect of magnolol on Th17 cell-mediated fibrosis.
PMID: Drug Des Devel Ther. 2017 ;11:2653-2661. Epub 2017 Sep 6. PMID: 28919715 Abstract Title: In vitro inhibitory activities of magnolol againstspp. Abstract: spp. cause various infections involving the skin, mucosa, deep tissues, and even life-threatening candidemia. They are regarded as an important pathogen of nosocomial bloodstream infection, with a high mortality rate. As a result of prolonged exposure to azoles, the therapeutic failure associated with azoles resistance has become a serious challenge in clinical situations. Therefore, novel, alternative antifungals are required urgently. In the present study, the CLSI M-27A broth microdilution method and the 2,3-Bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) reduction assay were used to evaluate the antifungal effects of magnolol against various standardstrains in planktonic mode and biofilm formation, respectively. The antifungal activity of magnolol was demonstrated in planktonicand non-albicansspecies, especially fluconazole-resistant, with the minimum inhibitory concentrations ranging from 10 to 40g/mL. The BMIC(minimum concentration with 90%biofilm inhibited) values of magnolol ranged from 20 to 160g/mL, whereas the BMICvalues of fluconazole were more than 128g/mL. As an alternative and broad-spectrum antifungal agent, magnolol might be of benefit to the treatment of refractoryinfection.
PMID: Am J Chin Med. 2017 ;45(7):1421-1439. Epub 2017 Sep 25. PMID: 28946769 Abstract Title: Magnolol Reduces Renal Ischemia and Reperfusion Injury via Inhibition of Apoptosis. Abstract: Magnolol, a constituent of the bark of Magnolia officinalis, has been reported to decrease myocardial stunning and infarct size. In this study, we investigated whether magnolol can reduce renal ischemia and reperfusion (I/R) injury. Renal I/R, induced by a 60-min occlusion of bilateral renal arteries and a 24-h reperfusion, significantly increased blood urea nitrogen (BUN) and creatinine levels, and caused histological damage to the kidneys of rats. Apoptosis, as evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and caspase-3 activation, was significantly increased in the kidneys. Furthermore, serum levels of tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1 (IL-1), and interleukin-6 (IL-6) were significantly elevated, while the interleukin-10 (IL-10) level was suppressed. However, intravenous pretreatment with magnolol at doses of 0.003[Formula: see text]mg/kg and 0.006[Formula: see text]mg/kg 10[Formula: see text]min before renal I/R significantly limited the increases of BUN, creatinine, the histological damage, and apoptosis in the kidneys. The increases in TNF-[Formula: see text], IL-1, and IL-6, and the decrease in IL-10 were also significantly inhibited. Additionally, magnolol increased Bcl-2 and decreased Bax in the kidneys. Phosphorylation of the prosurvival kinases, including Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2), was elevated, while phosphorylation of the pro-apoptotic mitogen-activated protein kinases, including p38 and c-Jun N-terminal kinase (JNK), was suppressed. In conclusion, magnolol reducesrenal I/R injury. The underlying mechanisms for this effect might be related to the prevention of apoptosis, possibly via the inhibition of both extrinsic and intrinsic apoptotic pathways, including the reduction of TNF-[Formula: see text] production and the modulation of pro- and anti-apoptotic signaling elements.
PMID: Mol Med Rep. 2018 Mar ;17(3):3455-3464. Epub 2017 Dec 20. PMID: 29286109 Abstract Title: The protective effects of magnolol on acute trinitrobenzene sulfonic acidinduced colitis in rats. Abstract: The present study aimed to investigate the protective effects of magnolol on acute 2,4,6-trinitrobenzene sulfonic acid (TNBS)induced colitis, and its underlying mechanisms. Experimental colitis was induced by intracolonic administration of TNBS/ethanol into rats. The model rats were randomly assigned into groups: TNBS, magnolol (high, medium and low doses), and salazosulfapyridine (positive control). All intervention regimens were administered by oral gavage, once a day for 7 consecutive days, 24 h after colitis induction. Histological and biochemical changes in colonic inflammation were evaluated by hematoxylin and eosin and immunohistochemistry, respectively. Rats treated with all doses of magnolol exhibiteddecreased colonic myeloperoxidase activity (P
A San Francisco judge said Wednesday she is considering tossing out the lions share of the $289 million judgment against agribusiness giant Monsanto and ordering a new trial over whether the companys weed-killer caused a groundskeepers cancer. San Francisco Superior Court Judge Suzanne Bolanos didnt formally rule on any issues after a two-hour hearing to consider Monsantos 
PMID: Int J Mol Med. 2018 Apr ;41(4):2252-2262. Epub 2018 Jan 15. PMID: 29336466 Abstract Title: Magnolol protects against ischemic-reperfusion brain damage following oxygen-glucose deprivation and transient focal cerebral ischemia. Abstract: In the present study, the neuroprotective potential of magnolol against ischemia-reperfusion brain injury was examined via in vivo and in vitro experiments. Magnolol exhibited strong radical scavenging and antioxidant activity, and significantly inhibited the production of interleukin6, tumor necrosis factora and nitrite/nitrate (NOX) in lipopolysaccharide-stimulated BV2 and RAW 264.7 cells when applied at concentrations of 10 and 50 M, respectively. Magnolol (100 M) also significantly attenuated oxygenglucose deprivationinduced damage in neonatal rat hippocampal slice cultures, when administered up to 4 h following the insult. In a rat model of stable ischemia, compared with a vehicletreated ischemic control, pretreatment with magnolol (0.011 mg/kg, intravenously) significantly reduced brain infarction following ischemic stroke, and posttreatment with magnolol (1 mg/kg) remained effective and significantly reduced infarction when administered 2 h following the onset of ischemia. Additionally, magnolol (0.3 and 1 mg/kg) significantly reduced the accumulation of superoxide anions at the border zones of infarction and reduced oxidative damage in the ischemic brain. This was assessed by measuring the levels of NOX, malondialdehyde and myeloperoxidase, the ratio of glutathione/oxidized glutathione and the immunoreactions of 8hydroxy2'deoxyguanosine and 4hydroxynonenal. Thus, magnolol was revealed to protect against ischemiareperfusion brain damage. This may be partly attributed to its antioxidant, radical scavenging and antiinflammatory effects.
PMID: Life Sci. 2018 Mar 1 ;196:69-76. Epub 2018 Feb 2. PMID: 29355546 Abstract Title: Magnolol treatment attenuates dextran sulphate sodium-induced murine experimental colitis by regulating inflammation and mucosal damage. Abstract: Magnolol, the main and active ingredient of the Magnolia officinalis, has been widely used in traditional prescription to the human disorders. Magnolol has been proved to have several pharmacological properties including anti-bacterial, anti-oxidant and anti-inflammatory activities. However, the effects of magnolol on ulcerative colitis (UC) have not been reported. The aim of this study was to investigate the protective effects and mechanisms of magnolol on dextran sulphate sodium (DSS)-induced colitis in mice. The results showed that magnolol significantly alleviated DSS-induced body weight loss, disease activities index (DAI), colon length shortening and colonic pathological damage. In addition, magnolol restrained the expression of TNF-, IL-1 and IL-12 via the regulation of nuclear factor-B (NF-B) and Peroxisome proliferator-activated receptor- (PPAR-) pathways. Magnolol also enhanced the expression of ZO-1 and occludin in DSS-induced mice colonic tissues. These results showed that magnolol played protective effects onDSS-induced colitis and may be an alternative therapeutic reagent for colitis treatment.
PMID: Front Immunol. 2018 ;9:147. Epub 2018 Feb 5. PMID: 29467759 Abstract Title: Magnolol Alleviates Inflammatory Responses and Lipid Accumulation by AMP-Activated Protein Kinase-Dependent Peroxisome Proliferator-Activated Receptor Activation. Abstract: Magnolol (MG) is a kind of lignin isolated from, which serves several different biological functions, such as antifungal, anticancer, antioxidant, and hepatoprotective functions. This study aimed to evaluate the protective effect of MG against oleic acid (OA)-induced hepatic steatosis and inflammatory damage in HepG2 cells and in a tyloxapol (Ty)-induced hyperlipidemia mouse model. Our findings indicated that MG can effectively inhibit OA-stimulated tumor necrosis factor (TNF-) secretion, reactive oxygen species generation, and triglyceride (TG) accumulation. Further study manifested that MG significantly suppressed OA-activated mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-B) signaling pathways and that these inflammatory responses can be negated by pretreatment with inhibitors of extracellular regulated protein kinase and c-Jun N-terminal kinase (U0126 and SP600125, respectively). In addition, MG dramatically upregulated peroxisome proliferator-activated receptor (PPAR) translocation and reduced sterol regulatory element-binding protein 1c (SREBP-1c) protein synthesis and excretion, both of which are dependent upon the phosphorylation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), acetyl-CoA carboxylase, and AKT kinase (AKT). However, MG suspended the activation of PPAR expression and was thus blocked by pretreatment with LY294002 and compound c (specific inhibitors of AKT and AMPK). Furthermore, MG clearly alleviated serum TG and total cholesterol release; upregulated AKT, AMPK, and PPAR expression; suppressed SREBP-1c generation; and alleviated hepatic steatosis and dyslipidemia in Ty-induced hyperlipidemia mice. Taken together, these results suggest that MG exerts protective effects against steatosis, hyperlipidemia, and the underlying mechanism, which may be closely associated with AKT/AMPK/PPAR activation and MAPK/NF-B/SREBP-1c inhibition.
PMID: Steroids. 2018 Jul ;135:73-78. Epub 2018 Mar 17. PMID: 29555480 Abstract Title: Antidepressant effects of magnolol in a mouse model of depression induced by chronic corticosterone injection. Abstract: Evidence showed that the stress hormone corticosterone (CORT) injection resulted in dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis implicated in major depressive disorder. Magnolol, main constituent identified in the barks of Magnolia officinalis, exerted antidepressant effects in a rat model of depression induced by chronic unpredictable mild stress in previous studies. However, its antidepressant-like effects and mechanisms have never been studied in depression model induced by CORT administration in rodents. This study aimed to investigate the antidepressant-like effects and possible mechanisms of magnolol in CORT-treated mice by utilizing a combination of behavioral and biochemical analysis. The depressive model was developed by subcutaneous injection of CORT for 21days at a dose of 20mg/kg. CORT administration formed depressive-like behaviors in mice, as indicated by increased immobility time in the forced swim test (FST) and tail suspension test (TST), as well as decreased sucrose intake in sucrose preference test (SPT). Moreover, we also found that CORT levels in serum were significantly increased, along with the decrease of brain-derived neurotrophic factor (BDNF) mRNA, BDNF protein, 5-hydroxytryptamine (5-HT) and norepinephrine (NE) levels in the hippocampus. Treatment with magnolol alleviated depressive-like behaviors, reduced the levels of CORT, and improved the levels of BDNF protein, 5-HT, and NE compared with those in CORT-treated mice. These findings indicated that magnolol possessed antidepressant effects in mice exposed to CORT, which might be partially related to modulate HPA axis, up-regulate BDNF expression and increase neurotransmitters levels in the hippocampus.
PMID: Pol J Vet Sci. 2018 Mar ;21(1):111-118. PMID: 29624001 Abstract Title: Magnolol inhibits Streptococcus suis-induced inflammation and ROS formation via TLR2/MAPK/NF-B signaling in RAW264.7 cells. Abstract: Our previous studies have shown that Magnolol (Mag) improves the symptoms and decreases the levels of cytokines during infection induced by Streptococcus suis (S. suis) in mice. Although some reports show that Mag inhibits lipopolysaccharide-induced inflammatory responses via downregulating mitogen-activated protein kinases (MAPK) and nuclear factor-B (NF-B) signaling pathways, the molecular mechanisms underlying Mag-mediated inhibition of S. suis-induced inflammatory responses are poorly understood. Here, RAW264.7 cells were stimulated with S. suis in the presence or absence of Mag. Cell viability and bactericidal effects were examined, and the concentrations of tumor necrosis factor-a (TNF-), IL-1 (interleukin-1), IL-6 (interleukin-6), and IL-8 (interleukin- 8) were determined by ELISA. The change in ROS (reactive oxygen species) was determined by fluorescence microscopy and ELISA. The levels of Toll-like receptor 2 (TLR2) andMAPK family proteins and NF-B signaling were determined by Western blot analysis. S. suis induced massive RAW264.7 cell death, a decline in bactericidal activity, the release of inflammatory cytokines, increased oxidative stress, and activation of TLR2/MAPK/NF-B signaling pathways. Mag treatment significantly suppressed macrophage cell death and caused a decline in bactericidal activity. Furthermore, Mag decreased inflammatory cytokines production and ROS generation. It also prevented p38, extracellular regulated protein kinases (ERK), c-Jun N-terminal kinase (JNK), inhibitor of NF-B (IB), and NF-B phosphorylation induced by S. suis in a dose-dependent manner. Our results indicate that Mag exerts anti-inflammatory and cell-protective effects and mediates the activation of MAPK and NF-B signaling by downregulating the expression of TLR2 upregulated by S. suis.
PMID: Int Immunopharmacol. 2018 Jun ;59:61-67. Epub 2018 Apr 5. PMID: 29627576 Abstract Title: Magnolol abrogates chronic mild stress-induced depressive-like behaviors by inhibiting neuroinflammation and oxidative stress in the prefrontal cortex of mice. Abstract: Magnolol, the main constituent of Magnolia officinalis, has been shown to produce antidepressant-like effect in rodents. Growing evidence shows that neuroinflammation, oxidative stress and neuroendocrine contribute to the pathogenesis of major depression. Here, the aim of this present study was to determine whether magnolol affected these systems in mice exposed to chronic mild stress (CMS). The ameliorative effect of magnolol on depressive-like symptoms was investigated through behavioral tests, including the classical sucrose preference and forced swimming tests. The behavioral evaluation showed that magnolol reversed the depressive-like deficits both in sucrose preference test and forced swimming test. The elevation of prefrontal cortex pro-inflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor- (TNF-) was decreased by magnolol. Consistently, the microglia activation by CMS was also alleviated by magnolol. In addition, the hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis induced by CMS was attenuated by magnolol.Moreover, the increased lipid peroxidation such as malonaldehyde (MDA) and decreased antioxidant defense enzymes including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) induced by CMS were also reversed by magnolol. These findings suggest that administration of magnolol could alleviate depressive-like behaviors in CMS mice that are mediated by suppressing neuroinflammation and oxidative stress in the prefrontal cortex.
PMID: Int J Mol Sci. 2018 08 10 ;19(8). Epub 2018 Aug 10. PMID: 30103472 Abstract Title: Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer. Abstract: The past few decades have witnessed widespread research to challenge carcinogenesis; however, it remains one of the most important health concerns with the worst prognosis and diagnosis. Increasing lines of evidence clearly show that the rate of cancer incidence will increase in future and will create global havoc, designating it as an epidemic. Conventional chemotherapeutics and treatment with synthetic disciplines are often associated with adverse side effects and development of chemoresistance. Thus, discovering novel economic and patient friendly drugs that are safe and efficacious is warranted. Several natural compounds have proved their potential against this dreadful disease so far. Magnolol is a hydroxylated biphenyl isolated from the root and stem bark of Magnolia tree. Magnolol can efficiently prevent or inhibit the growth of various cancers originating from different organs such as brain, breast, cervical, colon, liver, lung, prostate, skin, etc. Considering these perspectives, the current review primarily focuses on the fascinating role of magnolol against various types of cancers, and the source and chemistry of magnolol and the molecular mechanism underlying the targets of magnolol are discussed. This review proposes magnolol as a suitable candidate that can be appropriately designed and established into a potent anti-cancer drug.
PMID: Front Pharmacol. 2018 ;9:357. Epub 2018 Apr 24. PMID: 29755347 Abstract Title: Honokiol, a Polyphenol Natural Compound, Attenuates Cisplatin-Induced Acute Cytotoxicity in Renal Epithelial Cells Through Cellular Oxidative Stress and Cytoskeleton Modulations. Abstract: Cisplatin is a potent anti-cancer drug that has been widely used in the treatment of various cancers; however, cisplatin administration results in severe nephrotoxicity and impedes its clinical applications. In this study, we showed that honokiol, a polyphenol constituent extracted fromexhibited a short-term protective effect against cisplatin-induced damages in renal epithelial cells. The protective effects of honokiol were resulted from the combination of (1) reduced cellular oxidative stress ranging from 53 to 32% reduction during a 24-h incubation, (2) the maintenance of cellular antioxidant capacity and (3) the stabilization of cytoskeletal structure of the kidney epithelial cells. By promoting the polymerization of actin (1.6-fold increase) and tubulin (1.8-fold increase) cytoskeleton, honokiol not only maintained epithelial cell morphology, but also stabilized cellular localizations of tight junction protein Occludin and adhesion junction protein E-Cadherin. With stabilized junction protein complexes and structural polymerized cytoskeleton network, honokiol preserved epithelial cell polarity and morphology and thus reduced cisplatin-induced cell disruption and damages. Our data demonstrated for the first time that honokiol could counteract with cisplatin-induced damages in renal epithelial cells, futurestudies would further validate the potential clinical application of honokiol in cisplatin-based cancer treatments with reduced nephrotoxicity.
PMID: Life Sci. 2018 Aug 15 ;207:184-204. Epub 2018 Jun 5. PMID: 29883720 Abstract Title: Proteomic analysis of honokiol-induced cytotoxicity in thyroid cancer cells. Abstract: AIMS: Honokiol is a natural product extracted from herbal plants such as the Magnolia species which have been shown to exhibit anti-tumor and anti-metastatic properties. However, the effects of honokiol on thyroid cancers are largely unknown.MATERIALS AND METHODS: To determine whether honokiol might be useful for the treatment of thyroid cancer and to elucidate the mechanism of toxicity of honokiol, we analyzed the impact of honokiol treatment on differential protein expression in human thyroid cancer cell line ARO using lysine-labeling two-dimensional difference gel electrophoresis (2D-DIGE) combined with mass spectrometry (MS).KEY FINDINGS: This study revealed 178 proteins that showed a significant change in expression levels and also revealed that honokiol-induced cytotoxicity in thyroid cancer cells involves dysregulation of cytoskeleton, protein folding, transcription control and glycolysis.SIGNIFICANCE: Our work shows that combined proteomic strategy provides a rapid method to study the molecular mechanisms of honokiol-induced cytotoxicity in thyroid cancer cells. The identified targets may be useful for further evaluation as potential targets in thyroid cancer therapy.
PMID: ACS Chem Neurosci. 2018 Jul 19. Epub 2018 Jul 19. PMID: 29989791 Abstract Title: Honokiol Alleviates Oxidative Stress-Induced Neurotoxicity via Activation of Nrf2. Abstract: Honokiol (Hon), a polyphenol and main active ingredient from the bark of Magnolia officinalis, has been documented as having multiple pharmacological functions, including neuroprotection. However, the mechanisms underlying its neuroprotective effects are not well-defined. In this study, we reported that Hon attenuates the HO- or 6-hydroxydopamine (6-OHDA)-induced apoptosis of PC12 cells by increasing the glutathione level and upregulating a multitude of cytoprotective proteins, including heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, thioredoxin 1, and thioredoxin reductase 1. Further studies reveal that Hon promotes transcription factor Nrf2 nuclear translocation and activation. Moreover, the cytoprotection of Hon was antagonized by silence of Nrf2 expression, highlighting the fact that Nrf2 is critically engaged in the cellular functions of Hon. Taken together, our study identified that Hon is an effective agonist of Nrf2 in the neuronal system and displays potent neuroprotection against oxidative stress-mediated PC12 cell damage. These findings indicate that Hon is promising for further development as a therapeutic drug against oxidative stress-related neurodegenerative disorders.
PMID: J Pharmacol Exp Ther. 2018 Sep ;366(3):470-478. Epub 2018 Jul 10. PMID: 29991481 Abstract Title: Honokiol Ameliorates Amyloidosis and Neuroinflammation and Improves Cognitive Impairment in Alzheimer's Disease Transgenic Mice. Abstract: The present study examined the effects of honokiol on amyloid-(A)-induced cognitive impairment and the underlying mechanisms in APPswe/PS1dE9 transgenic mice. The results showed that honokiol administration (20 mg/kg per day, intraperitoneally) for 6 weeks effectively improved spatial memory deficits in APPswe/PS1dE9 transgenic mice. Honokiol significantly lowered Aproduction and senile plaque deposition by downregulating-site amyloid precursor protein cleavage enzyme 1 and enhancing Aphagocytosis by microglia. Honokiol reduced glial cell activation and the production of proinflammatory cytokines (TNF-, IL-1, and IL-6). Honokiol increased the transcriptional activity and protein levels of peroxisome proliferator-activated receptor-(PPARHowever, all of the beneficial effects of honokiol on pathologic changes, including biochemistry and cognitive function, could be blocked by GW9662, a specific PPARinhibitor. These findings suggested that honokiol may be a natural PPARagonist, acting to attenuate Ageneration and neuroinflammation. Therefore, honokiol may be a potential therapeutic approach for Alzheimer's disease.
By Dr. Mercola
The question posed in the headline is a common one heard by doctors everywhere: "How long does it take to have an empty stomach?" It's an important question for anyone taking prescription drugs because what you eat and drink, as well as the timing of your meals, can affect the way certain medications work.
Beyond that, there is value in becoming aware of the health benefits associated with regularly emptying your stomach. If your first thought, when you hear the words "empty stomach," is a negative one, it's time to update your thinking. Not only can you survive on an empty stomach, you can also thrive.
In my experience, emptying your stomach as a daily habit through intermittent fasting or another safe type of fasting can boost your health and well-being. The effects can be so radical that you actually may be able to reduce (or potentially eliminate) your use of prescription drugs as your health improves.
"Ask Well," a medical question and answer feature presented in The New York Times,1 recently fielded this inquiry: "Many medications should be taken on an empty stomach. How do you know when your stomach is empty?"
Dr. Richard Klasco, assistant professor of emergency medicine at the University of Colorado School of Medicine, who provided the answer, wrote, "Two hours after eating is a crude rule of thumb. A more accurate answer depends on the drugs you are taking and your medical conditions."2
Klasco goes on to note that research on gastric emptying the length of time it takes for your stomach to return to empty after a meal has been going on since the 1940s.
Over the years, the experiments have changed based on scientific and medical advances. Since 1966, nuclear medicine, which involves the use of a small amount of radioactive material to emit photon energy, has remained as the established standard for measuring gastric emptying. Says Klasco:3
"Standards for such testing have been set by the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine. They state that a normal stomach should be 90 percent empty after four hours.4
The difference between this standard and the earlier study probably reflects differences in foods. Solids take longer to digest than liquids; fats take longer to digest than protein or ca...
Moringa oleifera may have been unfamiliar to some Americans until recently, but it's actually been used as a traditional herbal medicine for centuries. In fact, it's been mentioned in the Annals of Ayurvedic Medicine, one of the world's oldest medical systems, as a cure for over 300 diseases.1
One of the ways to harness the benefits of Moringa is by steeping its leaves in hot water to create an energizing tea that provides a wide array of nutrients. Continue reading this article to learn more about the benefits of Moringa tea, its nutritional profile and the ways you can make it at home.
Moringa tea comes from the leaves of Moringa oleifera, a tree that's native to the sub-Himalayan regions of India, Pakistan, Bangladesh and Afghanistan, but is now commonly grown in various tropical and subtropical areas around the world.2
Also known as "horseradish tree" and "drumstick tree," Moringa has been dubbed as a "miracle tree" because of its potential medicinal properties. It also earned the superfood status, thanks to its extensive nutritional content, which you may still obtain even after brewing its leaves into tea. Some of these nutrients include:3
Flavonoids (such as quercetin and kaempferol)
To make Moringa tea, the freshly harvested leaves are dried at room temperature to retain their valuable nutrients before they're crushed, powdered or shredded into loose pieces.4 These loose Moringa leaves may be steeped as is or placed into tea bags. In terms of flavor, pure Moringa leaf tea is said to have a slightly "green" or earthy taste, though it lacks the bitterness of kale or spiciness of arugula.5,6
The health benefits of Moringa oleifera tea are attributed to its rich nutritional profile. A lot of these benefits are not just backed by traditional beliefs, but also are supported by scientific research....
Can vaccines trigger autism? This is the topic of the film "Vaxxed: From Cover-Up to Catastrophe,"1 directed by Andrew Wakefield and produced by Del Bigtree, an Emmy Award-winning producer of "The Doctors" talk show.
The film became the center of controversy when it was pulled from the Tribeca Film Festival lineup in 2016 by Robert De Niro and Jane Rosenthal, the two founders of the well-known film festival. According to Rosenthal, other filmmakers had threatened to withdraw their films from the festival if "Vaxxed" was shown.
While De Niro admitted feeling pressured to pull the film, he urged people to see it, saying there are many issues relating to the way the U.S. Centers for Disease Control and Prevention (CDC) evaluates and monitors the safety of vaccines that are not being openly spoken about, and really should be addressed.
The official stance repeated by most mainstream media is that vaccines have been thoroughly researched, that "hundreds" of studies have proven their safety, and that no link between vaccines and health problems, such as autism, have ever been found.
Again and again, you hear that the autism-vaccine link was based on a single study published in 1998 by a now-discredited doctor (Wakefield), and the hypothetical association between vaccines and autism has since been thoroughly and repeatedly debunked. It sounds definitive enough, and is often repeated as established fact. Yet it's far from the whole truth.
Importantly, the vaccine industry has long shied away from evaluating vaccinated versus unvaccinated populations to determine potential differences in general health outcomes. The few independent scientists who have attempted such an investigation have little comfort to give to those who believe vaccines are essential for health, and mandatory use of vaccines by all children is the only way to protect society from disease.
One such study,2 published just last year, examined health outcomes among infants 3 to 5 months old following the introduction of diphtheria-tetanus-pertussis (DTP) and oral polio vaccine in Guinea-Bissau, which took place in the early 1980s. This population offered the rare opportunity to compare vaccinated and...
PMID: Pak J Pharm Sci. 2018 Jul ;31(4):1279-1284. PMID: 30033411 Abstract Title: Oral administration of honokiol attenuates airway inflammation in asthmatic mouse model. Abstract: Allergic asthma is a disease that pathologically characterized by eosinophilia infiltration, airway inflammation and hyper responsiveness. In this study, we evaluated the anti-inflammatory and anti-allergy possibilities of honokiol, a bi-phenolic compound obtained from species of the genus Magnolia, which has long been involved in traditional Chinese prescriptions for asthma-related lung diseases, in an ovalbumin-induced mouse model of allergic asthma. We found honokiol significantly inhibited the eosinophilia infiltration, reduced the airway inflammation and suppressed the production of inflammatory cytokines) as well as the IgE in serum. Moreover, MMP-9 and? (IL-4 and IFN- NF-B were found to be involved in the honokiol induced biological process. These results suggested that honokiol may be a possible candidate in the treatment of lung asthma related diseases.
PMID: Artif Cells Nanomed Biotechnol. 2018 Jul 25:1-16. Epub 2018 Jul 25. PMID: 30043652 Abstract Title: Functional paclitaxel plus honokiol micelles destroying tumour metastasis in treatment of non-small-cell lung cancer. Abstract: Treatment effect of chemotherapy for aggressive non-small-cell lung cancer (NSCLC) is usually unsatisfactory for non-selective distributions of anticancer drugs, generation of vasculogenic mimicry (VM) channels, high metastasis and recurrence rate. Therefore, we developed a kind of dequalinium (DQA) modified paclitaxel plus honokiol micelles in this study to destroy VM channels and inhibit tumour metastasis. In vitro assays indicated that the targeting paclitaxel micelles with ideal physicochemical characteristics could exhibit not only the powerful cytotoxicity on Lewis lung tumour (LLT) cells but also the effective suppression on VM channels and tumour metastasis. Action mechanism studies manifested that DQA modified paclitaxel plus honokiol micelles could activate apoptotic enzymes caspase-3 and caspase-9 as well as down-regulate FAK, PI3K, MMP-2 and MMP-9. In vivo assays indicated that polymeric micelles could increase selective accumulation of chemotherapeutic drugs at tumour sites and showed a conspicuous antitumour efficacy. Hence, the DQA modified paclitaxel plus honokiol micelles prepared in this study provided a potential treatment strategy for NSCLC.
PMID: Environ Toxicol. 2018 Aug 4. Epub 2018 Aug 4. PMID: 30076764 Abstract Title: Chemosensitizing effect of honokiol in oral carcinoma stem cells via regulation of IL-6/Stat3 signaling. Abstract: Oral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide with poor prognosis. Numerous studies have attempted to explore alternative regimens aimed at reducing cancer stem cells (CSCs) without compromising the efficacy of conventional chemoradiotherapy. The present study sought to assess the effect of a natural compound honokiol on the reduction of elevated cancer stemness, metastatic capacity, and chemoresistance of oral carcinoma stem cells (OCSCs). Our results demonstrated that honokiol attenuated the cell survival and self-renewal of OCSCs in a dose-dependent manner. Moreover, honokiol downregulated the expression of 2 selective markers of OCSCs, ALDH1, and CD44, as well as the migration and invasion abilities, indicating its potential to suppress cancer stemness. We showed that honokiol reduced the secretion of IL-6 and phosphorylation of STAT3, and the honokiol-inhibited self-renewal, invasion and colony formation were reversed by administration of IL-6. Most importantly, our data demonstrated that honokiol was able to potentiate the effect of Cisplatin, leading to a lower proportion of OCSCs and the decreased cancer stemness features. Taken together, this study demonstrated the benefits of utilizing honokiol as an adjunct therapy for OSCC treatment.
PMID: Exp Ther Med. 2018 Aug ;16(2):1278-1284. Epub 2018 Jun 14. PMID: 30116378 Abstract Title: Protective effects of honokiol against oxidative stress-induced apoptotic signaling in mouse podocytes treated with H2O2. Abstract: Honokiol (HNK), an important bioactive compound purified from, has been demonstrated to have manifold beneficial anti-oxidative, anti-inflammatory, anti-bacterial and antitumor pharmacological effects. In the present study, the association of HNK in the signaling mechanism associated with hydrogen peroxide (HO)-induced apoptosis of cultured mouse podocytes was investigated. HNK did not cause significant changes in podocyte viability when its concentration remained below 20M. MTS assay and flow cytometry confirmed that HOsignificantly enhanced the rates of apoptosis while produce significant reduction in viability of podocytes. Following 24 h of pre-treatment with different concentrations of HNK, the viability of adherent podocytes increased and apoptosis significantly decreased in a dose-dependent manner below 20M. Reverse transcription-polymerase chain reaction and western blot results indicated that HNK significantly decreased the expression of mRNA and cleaved protein of caspase-3 and caspase-9 in podocytes pre-treated with HO. Furthermore, phosphorylation of the signaling molecules protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) 1/2 appeared to increase following HNK treatment. In conclusion, HNK largely eliminated the role of promoting podocyte apoptosis in an oxidative stress environment, which was a protective factor on podocytes cultured with HO. The anti-oxidative stress mechanisms of HNK are partly due to suppressing the expression of caspase-3 and caspase-9 and upregulating phosphorylated-Akt and -Erk 1/2.
PMID: Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2018 Jul 28 ;43(7):718-724. PMID: 30124206 Abstract Title: [Effects of honokiol on particulate matter 2.5-induced lung injury in asthmatic mice and its mechanisms]. Abstract: To explore the therapeutic effect of honokiol on particulate matter 2.5 (PM2.5)-induced lung injury in asthmatic mice and the possible mechanisms. Methods: A total of 32 BALB/C mice were randomly divided into four groups: a normal saline group, a model group, a PM2.5 group and a honokiol group (n=8 in each group). The asthma mouse model was established by ovalbumin treatment. The mice were treated with physiological saline, ovalbumin, PM2.5 and honokiol, respectively. Lung tissues and serum were collected. The pathological changes of lung tissues were evaluated. The levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum were measured and the expressions of Toll like receptor 4 (TLR4), nuclear factor kappa B(NF-B), retinoid-related orphan receptor gamma-t (RORt) and forkhead box protein 3 (Foxp3) in lung tissues were detected. Results: 1) The lung tissues of mice in the asthma group showed obvious pathological changes and inflammatory state, suggesting that the asthma model was established successfully. PM2.5 could aggravate the pathological condition of inflammatory injury in lung tissues in asthmatic mice. 2) Compared to the PM2.5 group, the pathological symptoms in the lung tissues were alleviated in the honokiol group and the percentage of inflammatory cells in BALF and the levels ofinflammatory cytokines in BALF and serum were significantly reduced (all P
PMID: Life Sci. 2018 Oct 1 ;210:86-95. Epub 2018 Aug 29. PMID: 30171880 Abstract Title: Honokiol protects pulmonary microvascular endothelial barrier against lipopolysaccharide-induced ARDS partially via the Sirt3/AMPK signaling axis. Abstract: AIMS: Acute respiratory distress syndrome (ARDS) is characterized by acute hypoxemia with diffuse alveolar damage and increased pulmonary microvascular permeability. Honokiol (HKL), the principal active ingredient of Chinese herb magnolia officinalis, protected the lung of experimental ARDS models via attenuation of inflammation and oxidative stress. However, whether HKL has protective effects against the dysfunction of pulmonary microvascular endothelial barrier and the potential mechanisms remain unclear.MAIN METHODS: In the present study, we examined the levels of plasma Angiopoietin-2 (Ang-2) in ARDS patients, explored the effects of HKL on the vascular endothelial barrier at the ARDS animal and cell levels.KEY FINDINGS: Our data showed that compared with the healthy controls, circulating Ang-2 level was higher in the patients with ARDS, and were usually supposed to be positively related to the severity of ARDS. Moreover, HKL effectively inhibited lung inflammatory injury and microvascular leakage, and improved ARDS mice survival. HKL also inhibited the expression of Ang-2, ICAM-1 and VCAM-1, and restored the expression of Sirt3,-Catenin and VE-Cadherin. Furthermore, HKL improved ECs survival and inhibited the apoptosis of ECs. The inhibition of Ang-2 expression in vitro by HKL is accompanied by the upregulation of Sirt3 and AMPK phosphorylation.SIGNIFICANCE: Our data demonstrated that HKL protected pulmonary microvascular endothelial barrier against LPS-induced ARDS at least in part through activating the Sirt3/AMPK signaling and inhibiting the Ang-2 expression. Thus, our findings show that the activation of Sirt3 signaling is a potential mechanism for the protective effects of HKL on vascular barrier.
PMID: J Neuroimmunol. 2018 Oct 15 ;323:78-86. Epub 2018 Jul 25. PMID: 30196838 Abstract Title: Anti-inflammatory properties of Honokiol in activated primary microglia and astrocytes. Abstract: Honokiol has been used in traditional medicine for the treatment of inflammatory diseases. Activation of glial cells plays an essential role in neurodegenerative disorders. In this study, we show that Honokiol reduces the inflammatory response to LPS of primary cultures of microglia and astrocytes through the inhibition of pro-inflammatory mediators (iNOS, IL-6, IL-1 and TNF-) and the simultaneous stimulation of anti-inflammatory cytokines (IL-10). Expression of KLF4 was induced in microglia and astrocytes after treatment with LPS and this response was mitigated by Honokiol. These findings extend our understanding of the anti-inflammatory properties of Honokiol on central glial cells and support its use as a therapeutic compound in neuroinflammatory disorders.
PMID: Phytomedicine. 2018 Oct 1 ;49:41-51. Epub 2018 Aug 8. PMID: 30217261 Abstract Title: Honokiol enhances temozolomide-induced apoptotic insults to malignant glioma cells via an intrinsic mitochondrion-dependent pathway. Abstract: BACKGROUND: Temozolomide (TMZ) is a first-line chemotherapeutic drug for malignant gliomas. Nonetheless, TMZ-induced side effects and drug resistance remain challenges. Our previous study showed the suppressive effects of honokiol on growth of gliomas.PURPOSE: This study was further aimed to evaluate if honokiol could enhance TMZ-induced insults toward malignant glioma cells and its possible mechanisms.METHODS: Human U87 MG glioma cells were exposed to TMZ, honokiol, and a combination of TMZ and honokiol. Cell survival, apoptosis, necrosis, and proliferation were successively assayed. Fluorometric substrate assays were conducted to determine activities of caspase-3, -6, -8, and -9. Levels of Fas ligand, Bax, and cytochrome c were immunodetected. Translocation of Bax to mitochondria were examined using confocal microscopy. Mitochondrial function was evaluated by assaying the mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and complex I enzyme activity. Caspase-6 activity was suppressed using specific peptide inhibitors. The honokiol-induced effects were further confirmed using human U373 MG and murine GL261 cells.RESULTS: Exposure of human U87 MG glioma cells to honokiol significantly increased TMZ-induced DNA fragmentation and cell apoptosis. Interestingly, honokiol enhanced intrinsic caspase-9 activity without affecting extrinsic Fas ligand levels and caspase-8 activity. Sequentially, TMZ-induced changes in Bax translocation, the MMP, mitochondrial complex I enzyme activity, intracellular ROS levels, and cytochrome c release were enhanced by honokiol. Consequently, honokiol amplified TMZ-induced activation of caspases-3 and -6 in human U87 MG cells. Fascinatingly, suppressing caspase-6 activity concurrently decreased honokiol-induced DNA fragmentation and cell apoptosis. The honokiol-involved improvement in TMZ-induced intrinsic apoptosis was also confirmed in human U373 MG and murine GL261 glioma cells.CONCLUSIONS: This study showed that honokiol can enhance TMZ-induced apoptotic insults to glioma cells via an intrinsic mitochondrion-dependent mechanism. Our results suggest the therapeutic potential of honokiol to attenuate TMZ-induced side effects.
PMID: Oncol Rep. 2018 Oct 1. Epub 2018 Oct 1. PMID: 30272350 Abstract Title: Mangiferin induces radiosensitization in glioblastoma cells by inhibiting nonhomologous end joining. Abstract: Although surgery and highdose radiotherapy have been the standard treatments for glioblastoma multiforme (GBM), these therapies are palliative, due to the high risk of local relapse. Emerging evidence has demonstrated that DNA doublestrand break (DSB) repair serves a critical role in resistance to radiotherapy. Previous studies have revealed that mangiferin possesses antineoplastic effects on human lung adenocarcinoma and ovarian cancer. The present study aimed to investigate the role of mangiferin in radiosensitivity inhuman GBM. Through in vitro experiments, decreased proliferation and increased DNA damage were observed in cells pretreated with mangiferin following radiation. Further study of the repair pathway indicated that mangiferin inhibits the nonhomologous endjoining (NHEJ) DSB repair pathway. Furthermore, studies on key proteins in the NHEJ DSB repair pathway revealed that mangiferininhibited the phosphorylation of serineprotein kinase ATM, TP53binding protein 1 and histone H2AX (H2AX). In addition, observations on the average percentages of H2AXpositive cells and the average number of H2AX foci per cell suggested that treatment with mangiferin decreased the number of H2AX foci in GBM cells following radiation. However, mangiferin selectively inhibited DSB repair in GBM cells, and was not able to trigger DSB repair inhibition in normal neuronal Schwann cells. Through in vivo tumorbearing mouse experiments, a smaller tumor volume, decreased tumor weight and prolonged life span were observed in mice treated with mangiferin following radiation. Therefore, xenograft GBM models clearly demonstrated that treatment with mangiferin treatment may increase tumor sensitivity to radiotherapy. Taken together, as demonstrated by in vivo and in vitro data, mangiferin may be a potential novel therapeutic drug for improving the radiation sensitivity of glioblastoma.
PMID: Mol Med Rep. 2018 Oct 2. Epub 2018 Oct 2. PMID: 30280187 Abstract Title: Mangiferin: An effective therapeutic agent against several disorders (Review). Abstract: Mangiferin (1,3,6,7tetrahydroxyxanthoneC2Dglucoside) is a bioactive ingredient predominantly isolated from the mango tree, with potent antioxidant activity and multifactorial pharmacological effects, including antidiabetic, antitumor, lipometabolism regulating, cardioprotective, antihyperuricemic,neuroprotective, antioxidant, antiinflammatory, antipyretic, analgesic, antibacterial, antiviral and immunomodulatory effects. Therefore, it possesses several healthendorsing properties and is a promising candidate for further research and development. However, low solubility, mucosal permeability and bioavailability restrict the development of mangiferin as a clinical therapeutic, and chemical and physical modification is required to expand its application. This review comprehensively analyzed and collectively summarized the primary pharmacological actions of mangiferin that have been demonstrated in the literature, to support the potential future development of mangiferin as a novel therapeutic drug.
PMID: Cancer Res. 2018 Sep 25. Epub 2018 Sep 25. PMID: 30254147 Abstract Title: Pharmacological ascorbate reduces radiation-induced normal tissue toxicity and enhances tumor radiosensitization in pancreatic cancer. Abstract: Chemoradiation therapy is the mainstay for treatment of locally advanced, borderline resectable pancreatic cancer. Pharmacological ascorbate (P-AscH-, i.e., intravenous infusions of ascorbic acid, vitamin C), but not oral ascorbate, produces high plasma concentrations capable of selective cytotoxicity to tumor cells. In doses achievable in humans, P-AscH- decreases the viability and proliferative capacity of pancreatic cancer via a hydrogen peroxide (H2O2)-mediated mechanism. In this study, we demonstrate that P-AscH- radiosensitizes pancreatic cancer cells but inhibits radiation-induced damage to normal cells. Specifically, radiation-induced decreases in clonogenic survival and double-stranded DNA breaks in tumor cells, but not in normal cells, were enhanced by P-AscH-, while radiation-induced intestinal damage, collagen deposition, and oxidative stress were also reduced with P-AscH- in normal tissue. We also report on our first-in-human phase 1 trial that infused P-AscH- during the radiation therapy 'beam on.' Specifically, treatment with P-AscH- increased median overall survival compared to our institutional average (21.7 vs. 12.7 mo, p = 0.08) and the E4201 trial (21.7 vs. 11.1 mo). Progression-free survival in P-AscH--treated subjects was also greater than our institutional average (13.7 vs. 4.6 mo, p
PMID: Biochem Soc Trans. 2018 Oct 8. Epub 2018 Oct 8. PMID: 30301842 Abstract Title: Vitamin C and immune cell function in inflammation and cancer. Abstract: Vitamin C (ascorbate) is maintained at high levels in most immune cells and can affect many aspects of the immune response. Intracellular levels generally respond to variations in plasma ascorbate availability, and a combination of inadequate intake and increased turnover during severe stress can result in low plasma ascorbate status. Intracellular ascorbate supports essential functions and, in particular, acts as an enzyme cofactor for Fe- or Cu-containing oxygenases. Newly discovered enzymes in this family regulate cell metabolism and epigenetics, and dysregulation of their activity can affect cell phenotype, growth and survival pathways, and stem cell phenotype. This brief overview details some of the recent advances in our understanding of how ascorbate availability can affect the hydroxylases controlling the hypoxic response and the DNA and histone demethylases. These processes play important roles in the regulation of the immune system, altering cell survival pathways, metabolism and functions.
PMID: Crit Care. 2018 Oct 11 ;22(1):258. Epub 2018 Oct 11. PMID: 30305111 Abstract Title: Evidence is stronger than you think: a meta-analysis of vitamin C use in patients with sepsis. Abstract: Two recent publications by Sheikh and Horner and Teng et al. reviewed studies on incorporating vitamin C to treat septic patients; however, a meta-analysis was not offered in either report. This commentary extends both reviews by integrating a meta-analysis and sharing aggregated results. Pooled analyses demonstrated a marked reduction in mortality and duration of vasopressor administration in the group with the use of vitamin C.
PMID: Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2005 Jun ;23(3):163-6. PMID: 16124885 Abstract Title: [Influence of 1.8 GHz microwave on DNA damage induced by 4 chemical mutagens]. Abstract: OBJECTIVE: To observe the influence of 1.8 GHz microwave (MW) specific absorption rate (SAR, 3 W/kg) on human lymphocytes DNA damage induced by 4 chemical mutagens [mitomycin C (MMC), bleomycin (BLM), methyl methanesulfonate (MMS), and 4-nitroquinoline 1-oxide (4NQO)].METHODS: Comet assay in vitro was used to detect human lymphocyte DNA damage induced by 1.8 GHz MW, 4 chemical mutagens, and MW plus 4 chemicals 0 h and 21 h respectively after exposure. The time exposed to MW or mutagens was 2 h or 3 h respectively. The results were showed by tail length (TL) and tail moment (TM).RESULTS: The difference of DNA damage between MW group and control group was not statistically significant (P>0.05). DNA damages in MW plus MMC groups and MW plus 4NQO groups were significantly greater than those in the corresponding concentrations of MMC groups and 4NQO groups (P
PMID: Cell Biochem Biophys. 2010 ;56(1):39-47. PMID: 19851891 Abstract Title: The influence of 1800 MHz GSM-like signals on hepatic oxidative DNA and lipid damage in nonpregnant, pregnant, and newly born rabbits. Abstract: The aim of our study is to evaluate the possible biological effects of whole-body 1800 MHz GSM-like radiofrequency (RF) radiation exposure on liver oxidative DNA damage and lipid peroxidation levels in nonpregnant, pregnant New Zealand White rabbits, and in their newly borns. Eighteen nonpregnant and pregnant rabbits were used and randomly divided into four groups which were composed of nine rabbits: (i) Group I (nonpregnant control), (ii) Group II (nonpregnant-RF exposed), (iii) Group III (pregnant control), (iv) Group IV (pregnant-RF exposed). Newborns of the pregnant rabbits were also divided into two groups: (v) Group V (newborns of Group III) and (vi) Group VI (newborns of Group III). 1800 MHz GSM-like RF radiation whole-body exposure (15 min/day for a week) was applied to Group II and Group IV. No significant differences were found in liver 8 OHdG/10(6) dG levels of exposure groups (Group II and Group IV) compared to controls (Group I and Group III). However, in Group II and Group IV malondialdehyde (MDA) and ferrous oxidation in xylenol orange (FOX) levels were increased compared to Group I (P0.05, Mann-Whitney) while liver FOX levels were found significantly increased in Group VI with respect to Group V (P
PMID: Medicine (Baltimore). 2018 Aug ;97(34):e11918. PMID: 30142802 Abstract Title: Whole-body vibration training and bone health in postmenopausal women: A systematic review and meta-analysis. Abstract: BACKGROUND: The aims of the present systematic review and meta-analysis were to evaluate published, randomized controlled trials that investigate the effects on whole-body vibration (WBV) training on total, femoral neck, and lumbar spine bone mineral density (BMD) in postmenopausal women, and identify the potential moderating factors explaining the adaptations to such training.METHODS: From a search of electronic databases (PubMed, Web of Science, and Cochrane) up until September 2017, a total 10 studies with 14 WBV groups met the inclusion criteria. Three different authors tabulated, independently, the selected indices in identical predetermined forms. The methodological quality of all studies was evaluated according to the modified PEDro scale. For each trial, differences within arms were calculated as mean differences (MDs) and their 95% confidence intervals between pre- and postintervention values. The effects on bone mass between exercise and control groups were also expressed as MDs. Both analyses were performed in the total sample and in a specific class of postmenopausal women younger than 65 years of age (excluding older women).RESULTS: The BMD of 462 postmenopausal women who performed WBV or control protocol was evaluated. Significant pre-post improvements in BMD of the lumbar spine were identified following WBV protocols (P=.03). Significant differences in femoral neck BMD (P=.03) were also found between intervention and control groups when analyzing studies that included postmenopausal women younger than 65 years.CONCLUSIONS: WBV is an effective method to improve lumbar spine BMD in postmenopausal and older women and to enhance femoral neck BMD in postmenopausal women younger than 65 years.
PMID: Int J Mol Sci. 2018 Sep 13 ;19(9). Epub 2018 Sep 13. PMID: 30217051 Abstract Title: Whole Body Vibration Therapy after Ischemia Reduces Brain Damage in Reproductively Senescent Female Rats. Abstract: A risk of ischemic stroke increases exponentially after menopause. Even a mild-ischemic stroke can result in increased frailty. Frailty is a state of increased vulnerability to adverse outcomes, which subsequently increases risk of cerebrovascular events and severe cognitive decline, particularly after menopause. Several interventions to reduce frailty and subsequent risk of stroke and cognitive decline have been proposed in laboratory animals and patients. One of them is whole body vibration (WBV). WBV improves cerebral function and cognitive ability that deteriorates with increased frailty. The goal of the current study is to test the efficacy of WBV in reducing post-ischemic stroke frailty and brain damage in reproductively senescent female rats. Reproductively senescent Sprague-Dawley female rats were exposed to transient middle cerebral artery occlusion (tMCAO) and were randomly assigned to either WBV or no-WBV groups. Animals placed in the WBV group underwent 30 days of WBV (40 Hz) treatment performed twice daily for 15 min each session, 5 days each week. The motor functions of animals belonging to both groups were tested intermittently and at the end of the treatment period. Brains were then harvested for inflammatory markers and histopathological analysis. The results demonstrate a significant reduction in inflammatory markers and infarct volume with significant increases in brain-derived neurotrophic factor and improvement in functional activity after tMCAO in middle-aged female rats that were treated with WBV as compared to the no-WBV group. Our results may facilitate a faster translation of the WBV intervention for improved outcome after stroke, particularly among frail women.
By Zack Perdue
When most people smoke cannabis, its effects are felt a few minutes later thanks to the psychoactive ingredient, THC. Yet, to feel the non-psychoactive substance in cannabis, specifically cannabidiol or CBD, a person may need to take several doses. Therefore, you may be wondering: what is the most effective and quickest way to reap the natural benefits of CBD oil?
Before answering this question, it is important to recognize that each person is different. Everyones biology is different, making it difficult to pinpoint exactly how each person can get CBD oil to work quickly. How you take CBD oil, your age, health, genetic makeup, metabolism, and tolerance can all have an influence on how quickly your body responds to CBD oil.
However, science has found several ways that CBD oil typically works faster in most people. Check them out below.
The fastest way to feel the effects of CBD oil is to get it into your bloodstream. When CBD oil enters the bloodstream, it begins working with the endocannabinoid system nearly immediately. This is the simplest explanation for getting CBD oil to work faster. However, it is important to understand the different ways to administer CBD oil so it efficiently ent...
PMID: J Cosmet Laser Ther. 2018 Oct 9:1-8. Epub 2018 Oct 9. PMID: 30300017 Abstract Title: Whole-body vibration in the reduction of the cellulite. Abstract: OBJECTIVE: Evaluate the effects of the whole body vibration in improving of cellulite in the women's gluteal region.METHODS: Controlled clinical trial performed with 42 women, with cellulite in the gluteal region, detected by means of clinical examination. After evaluation, the women were divided into two groups: Whole-Body Vibration (WBV_G) and control (C_G). The evaluations were performed at the beginning and the end of 10 sessions and superficial skin temperature, perimetry in the gluteal region, analysis of body contouring, analysis of improvement by blind reviewers and instrument of satisfaction, by numeric scale were investigated.RESULTS: In the thermographic analysis, the WBV_G obtained significant increase of superficial skin temperature on the right (p = 0.02) and left (p = 0.02) gluteal region. There was no difference in intra- and intergroups in perimetry and the analysis of body contour. The WBV_G obtained a higher percentage of improvement by assessment of the blind reviewers (p = 0.003) and greater aesthetics satisfaction (p = 0.006), when compared to C_G.CONCLUSION: WBV provided an improvement in the aspect of the cellulite when assessed by blind reviewers and greater participants' satisfaction, providing a significant increase in the superficial skin temperature in the gluteal region.
By Carey Wedler
California state lawmakers recently passed a bill forcing restaurants to offer specific beverages to children. Governor Jerry Brown signed the legislation, which passed easily in both the Senate and Assembly, at the end of September.
Though SB 1192 allows customers to order other drinks upon request, the Golden State is now mandating that only unflavored milk and water be listed as default beverages on menus (a provision also allows for non-dairy fluid milk substitutes containing under 130 calories).
According to the new law, violations of the rule will be punishable by fines up to $500:
[The] first violation shall result in a notice of violation. A second violation within a five-year period from the notice of violation shall be punishable by a fine of not more than two hundred fifty dollars ($250). For a third or subsequent violation within a five-year period, the fine shall be not more than five hundred dollars ($500).
As with most government policies that restrict individual and economic freedom, lawmakers appealed to the pu...
PMID: Biomed Environ Sci. 2010 Jun ;23(3):199-207. PMID: 20708499 Abstract Title: Effects of exposure to GSM mobile phone base station signals on salivary cortisol, alpha-amylase, and immunoglobulin A. Abstract: OBJECTIVE: The present study aimed to test whether exposure to radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phone base stations may have effects on salivary alpha-amylase, immunoglobulin A (IgA), and cortisol levels.METHODS: Fifty seven participants were randomly allocated to one of three different experimental scenarios (22 participants to scenario 1, 26 to scenario 2, and 9 to scenario 3). Each participant went through five 50-minute exposure sessions. The main RF-EMF source was a GSM-900-MHz antenna located at the outer wall of the building. In scenarios 1 and 2, the first, third, and fifth sessions were"low"(median power flux density 5.2 microW/m(2)) exposure. The second session was"high"(2126.8 microW/m(2)), and the fourth session was"medium"(153.6 microW/m(2)) in scenario 1, and vice versa in scenario 2. Scenario 3 had four"low"exposure conditions, followed by a"high"exposure condition. Biomedical parameters were collected by saliva samples three times a session. Exposure levels were created by shielding curtains.RESULTS: In scenario 3 from session 4 to session 5 (from"low"to"high"exposure), an increase of cortisol was detected, while in scenarios 1 and 2, a higher concentration of alpha-amylase related to the baseline was identified as compared to that in scenario 3. IgA concentration was not significantly related to the exposure.CONCLUSIONS: RF-EMF in considerably lower field densities than ICNIRP-guidelines may influence certain psychobiological stress markers.
PMID: Cell Biochem Biophys. 2013 Nov ;67(2):743-51. PMID: 23526187 Abstract Title: Effects of prenatal and postnatal exposure to GSM-like radiofrequency on blood chemistry and oxidative stress in infant rabbits, an experimental study. Abstract: We aimed to investigate the potential hazardous effects of prenatal and/or postnatal exposure to 1800 MHz GSM-like radiofrequency radiation (RFR) on the blood chemistry and lipid peroxidation levels of infant rabbits. A total of 72 New Zealand female and male white rabbits aged 1-month were used. Thirty-six female and 36 male were divided into four groups which were composed of nine infants: (i) Group 1 were the sham exposure (control), (ii) Group 2 were exposed to RFR, 15 min daily for 7 days in the prenatal period (between 15th and 22nd days of the gestational period) (prenatal exposure group). (iii) Group 3 were exposed to RFR 15 min/day (14 days for male, whereas 7 days for female)after they reached 1-month of age (postnatal exposure group). (iv) Group 4 were exposed to RFR for 15 min daily during 7 days in the prenatal period (between 15th and 22nd days of the gestational period) and 15 min/day (14 days for male, whereas 7 days for female) after they reached 1-month ofage (prenatal and postnatal exposure group). Results showed that serum lipid peroxidation level in both female and male rabbits changed due to the RFR exposure. However, different parameters of the blood biochemistry were affected by exposure in male and female infants. Consequently, the whole-body1800 MHz GSM-like RFR exposure may lead to oxidative stress and changes on some blood chemistry parameters. Studies on RFR exposure during prenatal and postnatal periods will help to establish international standards for the protection of pregnants and newborns from environmental RFR.
PMID: Electromagn Biol Med. 2014 Sep ;33(3):216-22. Epub 2013 Jun 19. PMID: 23781998 Abstract Title: Long-term effects of 900MHz radiofrequency radiation emitted from mobile phone on testicular tissue and epididymal semen quality. Abstract: The purpose of this study is to bridge this gap by investigating effects of long term 900MHz mobile phone exposure on reproductive organs of male rats. The study was carried out on 14 adult Wistar Albino rats by dividing them randomly into two groups (n: 7) as sham group and exposure group. Rats were exposed to 900MHz radiofrequency (RF) radiation emitted from a GSM signal generator. Point, 1g and 10g specific absorption rate (SAR) levels of testis and prostate were found as 0.0623W/kg, 0.0445W/kg and 0.0373W/kg, respectively. The rats in the exposure group were subject to RF radiation 3h per day (7d a week) for one year. For the sham group, the same procedure was applied, except the generator was turned off. At the end of the study, epididymal sperm concentration, progressive sperm motility, abnormal sperm rate, all-genital organs weights and testis histopathology were evaluated. Any differences were not observed in sperm motility and concentration (p>0.05). However, the morphologically normal spermatozoa rates were found higher in the exposure group (p
PMID: J Biomed Phys Eng. 2015 Sep ;5(3):105-14. Epub 2015 Sep 1. PMID: 26396966 Abstract Title: Effect of 900 MHz Electromagnetic Radiation on the Induction of ROS in Human Peripheral Blood Mononuclear Cells. Abstract: BACKGROUND: Despite numerous studies over a decade, it still remains controversial about the biological effects of RF EMF emitted by mobile phone telephony.OBJECTIVE: Here we investigated the effect of 900 MHz GSM on the induction of oxidative stress and the level of intracellular reactive oxygen species (ROS) in human mononuclear cells, monocytes and lymphocytes as defence system cells.METHOD: 6 ml Peripheral Blood samples were obtained from 13 healthy volunteers (21-30 year-old). Each sample was devided into 2 groups: one was exposed RF radiation emitted from a mobile phone simulator for 2 hour and the other used as control group which was not exposed to any fields. After that, mononuclear cells were isolated from peripheral blood by density gradient centrifugation in Ficoll-Paque. The intracellular ROS content in monocytes and lymphocytes was measured by the CM-H2DCFDA fluorescence probe using flowcytometry technique.RESULTS: Our results showed significant increase in ROS production after exposure in population rich in monocytes. This effect was not significant in population rich in lymphocytes in comparison with non exposed cells.CONCLUSION: The results obtained in this study clearly showed the oxidative stress induction capability of RF electromagnetic field in the portion of PBMCs mostly in monocytes, like the case of exposure to micro organisms, although the advantages or disadvantages of this effect should be evaluated.
PMID: Int J Radiat Biol. 2016 ;92(1):1-10. Epub 2015 Dec 2. PMID: 26630175 Abstract Title: Activity and expression of acetylcholinesterase in PC12 cells exposed to intermittent 1.8 GHz 217-GSM mobile phone signal. Abstract: PURPOSE: Due to its role in learning, memory and in many neurodegenerative diseases, acetylcholinesterase (AChE) represents an interesting endpoint to assess possible targets of exposure to radiofrequency electromagnetic fields (RF-EMF) generated by mobile phones. We investigated possible alterations of enzymatic activity, gene and protein expression of AChE in neuronal-like cells exposed to a 1.8 GHz Global System for Mobile Communication (GSM) modulated signal (217-GSM).MATERIALS AND METHODS: Rat PC12 cells were exposed for 24 h to 1.8 GHz 217-GSM signal. Specific adsorption rate (SAR) was 2 W/kg. AChE enzyme activity was assessed spectrophotometrically by Ellman's method, mRNA expression level was evaluated by real time polymerase chain reaction, and protein expression was assessed by Western blotting.RESULTS: AChE enzymatic activity increased of 1.4-fold in PC12 cells exposed to 217-GSM signal for 24 h, whilst AChE transcriptional or translational pathways were not affected.CONCLUSION: Our results provide the first evidence of effects on AChE activity after in vitro exposure of mammalian cells to the RF-EMF generated by GSM mobile phones, at the SAR value 2 W/kg. The obtained evidence promotes further investigations on AChE as a possible target of RF-EMF and confirm the ability of 1.8 GHz 217-GSM signal to induce biological effects in different mammalian cells.
PMID: Ecotoxicol Environ Saf. 2016 Jul ;129:137-44. Epub 2016 Mar 24. PMID: 27017260 Abstract Title: Effects of GSM-like radiofrequency irradiation during the oogenesis and spermiogenesis of Xenopus laevis. Abstract: We aimed to evaluate the effect of GSM-like radiofrequency electromagnetic radiation (RF-EMR) on the oogenesis, and spermiogenesis of Xenopus laevis, and so the development of the embryos obtained from Normal Females+Normal Males (i.e."N(F)+N(M)"); Normal Females+RF-exposed Males (i.e."N(F)+RF(M)"); RF-exposed Female+Normal Male (i.e."RF(F)+N(M)"); and RF-exposed Female+RF-exposed Male (i.e."RF(F)+RF(M)". Various, assessments were performed to determine potential teratogenic effects and mortality, body growth and behavior on first generation embryos. After exposing adults frogs of both sexes to 900MHz RF-EMR (at 1.0W/kg) for 8h a day over a 5-week period, the embryos' specific energy absorption rate (SAR) was calculated. In our present study (control group; 2.2% abnormal, 0.0% dead); with the N(F)+RF(M) combination, the long-term exposure of adult males to GSM-like radiation at 900MHz (RF: 2W) for 5 week/8h/day resulted in normal, abnormal and dead embryo ratios of 88.3%, 3.3% and 8.3%, respectively (p
PMID: Bratisl Lek Listy. 2016 ;117(11):672-676. PMID: 28125894 Abstract Title: GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant rabbits. Abstract: BACKGROUND: There have been several Radio Frequency (RF) field researches on various populations and groups of different ages in recent years. However, the most important group for research has been declared as the pregnant women and their babies.OBJECTIVE: The aim of the study was to analyse the effect on apoptotic factors of RF fields on newborn rabbit liver tissues.MATERIALS AND METHODS: Cytochrome c and AIF (Apoptosis Inducing Factor) levels were measured by western blot and caspase 1, 3 and 9 activities were measured by colorimetric method.RESULTS: Cytochrome c and AIF levels were not altered, but all caspase activities were increased in female infant rabbits that exposed to 1800 MHz GSM-like RF signals when they reached 1 month of age and caspase 1 and caspase 3 levels were decreased in male infant rabbits that exposed to 1800 MHz GSM-like RF signals between 15th and 22nd days of the gestational period. Results showed that 1800 MHz GSM-like RF exposure might lead to apoptosis in infant rabbit's liver tissues.CONCLUSION: According to the results, we suggest that postnatal RF exposure causes caspase dependent apoptosis in female infant rabbits liver tissues (Tab. 1, Fig. 2, Ref. 27).
PMID: J Biomed Phys Eng. 2016 Dec ;6(4):243-252. Epub 2016 Dec 1. PMID: 28144594 Abstract Title: Effects of RF-EMF Exposure from GSM Mobile Phones on Proliferation Rate of Human Adipose-derived Stem Cells: An In-vitro Study. Abstract: BACKGROUND: As the use of mobile phones is increasing, public concern about the harmful effects of radiation emitted by these devices is also growing. In addition, protection questions and biological effects are among growing concerns which have remained largely unanswered. Stem cells are useful models to assess the effects of radiofrequency electromagnetic fields (RF-EMF) on other cell lines. Stem cells are undifferentiated biological cells that can differentiate into specialized cells. Adipose tissue represents an abundant and accessible source of adult stem cells. The aim of this study is to investigate the effects of GSM 900 MHz on growth and proliferation of mesenchymal stem cells derived from adipose tissue within the specific distance and intensity.MATERIALS AND METHODS: ADSCs were exposed to GSM mobile phones 900 MHz with intensity of 354.6W/cmsquare waves (217 Hz pulse frequency, 50% duty cycle), during different exposure times ranging from 6 to 21 min/day for 5 days at 20 cm distance from the antenna. MTT assay was used to determine the growth and metabolism of cells and trypan blue test was also done for cell viability. Statistical analyses were carried out using analysis of one way ANOVA. P
PMID: Neurotox Res. 2017 Oct ;32(3):444-459. Epub 2017 Jun 3. PMID: 28578480 Abstract Title: Acute Neuroinflammation Promotes Cell Responses to 1800 MHz GSM Electromagnetic Fields in the Rat Cerebral Cortex. Abstract: Mobile phone communications are conveyed by radiofrequency (RF) electromagnetic fields, including pulse-modulated global system for mobile communications (GSM)-1800 MHz, whose effects on the CNS affected by pathological states remain to be specified. Here, we investigated whether a 2-h head-only exposure to GSM-1800 MHz could impact on a neuroinflammatory reaction triggered by lipopolysaccharide (LPS) in 2-week-old or adult rats. We focused on the cerebral cortex in which the specific absorption rate (SAR) of RF averaged 2.9 W/kg. In developing rats, 24 h after GSM exposure, the levels of cortical interleukin-1 (IL1) or NOX2 NADPH oxidase transcripts were reduced by 50 to 60%, in comparison with sham-exposed animals (SAR = 0), as assessed by RT-qPCR. Adult rats exposed to GSM also showed a 50% reduction in the level of IL1 mRNA, but they differed from developing rats by the lack of NOX2 gene suppression and by displaying a significant growth response of microglial cell processes imaged in anti-Iba1-stained cortical sections. As neuroinflammation is often associated with changes in excitatory neurotransmission, we evaluated changes in expression and phosphorylation of -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the adult cerebral cortex by Western blot analyses. We found that GSM exposure decreased phosphorylation at two residues on the GluA1 AMPAR subunit (serine 831 and 845). The GSM-induced changes in gene expressions, microglia, and GluA1 phosphorylation did not persist 72 h after RF exposure and were not observed in the absence of LPS pretreatment. Together, our data provide evidence that GSM-1800 MHz can modulate CNS cell responses triggered by an acute neuroinflammatory state.
PMID: J Neurophysiol. 2018 Aug 22. Epub 2018 Aug 22. PMID: 30133383 Abstract Title: DECREASED SPONTANEOUS ELECTRICAL ACTIVITY IN NEURONAL NETWORKS EXPOSED TO RADIOFREQUENCY 1800 MHZ SIGNALS. Abstract: So far, the only identified biological effects of radiofrequency fields (RF) are known to be caused by heating but the issue of potential nonthermal biological effects, especially on the central nervous system (CNS), remains open. We previously reported a decrease in the firing and bursting rates of neuronal cultures exposed to a Global System for Mobile (GSM) RF field at 1800 MHz for 3 min (Moretti et al. 2013). The aim of the present work was to assess the dose-response relationship for this effect, and also identify a potential differential response elicited by pulse-modulated GSM and continuous-wave (CW) RF fields. Spontaneous bursting activity of neuronal cultures from rat embryonic cortices was recorded using 60-electrode Multi Electrode Arrays (MEAs). At 17-28 days in vitro, the neuronal cultures were subjected to 15-min RF exposures, at SARs (Specific Absorption Rates) ranging from 0.01 to 9.2 W/kg. Both GSM and CW signals elicited a clear decrease in bursting rate during the RF exposure phase. This effect became more marked with increasing SAR and lasted even beyond the end of exposure for the highest SAR levels. Moreover, the amplitude of the effect was greater with the GSM signal. Altogether, our experimental findings provide evidence for dose-dependent effects of RF signals on the bursting rate of neuronal cultures and suggest that part of the mechanism is nonthermal.
PMID: Brain Res. 2010 Jan 22 ;1311:189-96. Epub 2009 Oct 30. PMID: 19879861 Abstract Title: Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial DNA in primary cultured neurons. Abstract: Increasing evidence indicates that oxidative stress may be involved in the adverse effects of radiofrequency (RF) radiation on the brain. Because mitochondrial DNA (mtDNA) defects are closely associated with various nervous system diseases and mtDNA is particularly susceptible to oxidative stress, the purpose of this study was to determine whether radiofrequency radiation can cause oxidative damage to mtDNA. In this study, we exposed primary cultured cortical neurons to pulsed RF electromagnetic fields at a frequency of 1800 MHz modulated by 217 Hz at an average special absorption rate (SAR) of 2 W/kg. At 24 h after exposure, we found that RF radiation induced a significant increase in the levels of 8-hydroxyguanine (8-OHdG), a common biomarker of DNA oxidative damage, in the mitochondria of neurons. Concomitant with this finding, the copy number of mtDNA and the levels of mitochondrial RNA (mtRNA) transcripts showed an obvious reduction after RF exposure. Each of these mtDNA disturbances could be reversed by pretreatment with melatonin, which is known to be an efficient antioxidant in the brain. Together, these results suggested that 1800 MHz RF radiation could cause oxidative damage to mtDNA in primary cultured neurons. Oxidative damage to mtDNA may account for the neurotoxicity of RF radiation in the brain.
PMID: Int J Radiat Biol. 2018 Sep 27:1-8. Epub 2018 Sep 27. PMID: 30028652 Abstract Title: What is adverse effect of wireless local area network, using 2.45GHz, on the reproductive system? Abstract: AIM: To investigate the inflammatory effect and testicular damage on rats exposed to low level of electromagnetic fields (EMF) at 2.45GHz microwave radiation.METHODS: Twenty two Wistar rats were divided into two groups. Group 1 was the control group and not exposed to EMF. Group 2 was exposed to low level EMF (average E-field 3.680.36 V/m, whole body average SAR, 0.0233 W/kg, in 10g tissue) at 2.45GHz for 1hour/day for 30 consecutive days. At the end of the study, interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-32 (IL-32), C-reactive protein (CRP) were measured in rat serum and IL-6, IL-10, IL-32were measured in rat testis tissue. Furthermore, testicular tissues were evaluated histopathologically in terms of spermatogenesis and coagulation necrosis.RESULTS: Serum IL-6 and CRP levels were found to be significantly different in the study group compared to the control group (p.05). On the other hand, histopathological evaluation of testicular tissue revealed a significant difference in necrosis and spermatogenesis when compared with the control group (p
On Wednesday, we reported that a month after media reports of undisclosed conflicts of interest by top brass at Memorial Sloan Kettering Cancer Center, a researcher there had corrected two papers to include financial conflicts of interest. Today, The New York Times and ProPublica which had broken the original story about former chief medical Continue reading More than a dozen papers by Sloan Kettering researchers have now been updated with financial disclosures
by Paul Fassa
Health Impact News
Many of us are aware of the endocrine disrupting potential of BPA (bisphenol-A) used in many plastic containers and inner linings of cans that the food processors label BPA Free as a marketing device.
Unfortunately, the replacement chemical, BPS (biphenol-S) has been discovered with, at least, the same endocrine mimicking dangers or perhaps even worse effects on hormonal health than BPA.
This leads to conscientious consumers being duped into exposure from biphenol endocrine disruptors from containers labeled BPA Free if other bisphenols such as BPS are used. Those who arent duped have to deal with concerns about labels and do more research.
But theres one ubiquitous item that openly contains BPA in order for it to function, and that is ink-less printing paper. Thermal paper is used by almost all cash registers, ATMs, medical equipment, and other machines that offer printouts.
There have been concerns about skin exposure with BPA thermal paper and its consequences, and there are studies now confirming that handling these receipts are exposing our bodies to BPA toxicity even more than consuming food in BPA packaging.
A 2017 study discovered that skin contact with thermal paper is a pathway that leads to BPA in the body at higher levels and with longer residual effects than oral consumption of foods or beverages packaged in BPA plastic containers.
This study, Prolonged Exposure to Bisphenol A from Single Dermal Contact Events was published online by the journal Environmental Science and Technology on July 31, 2017.
Knowing that thermal paper is coated with BPA, the researchers were curious about the...
PMID: J Chem Neuroanat. 2016 09 ;75(Pt B):85-93. Epub 2015 Sep 12. PMID: 26371078 Abstract Title: The link between radiofrequencies emitted from wireless technologies and oxidative stress. Abstract: Wireless communication such as cellular telephones and other types of handheld phones working with frequencies of 900MHz, 1800MHz, 2100MHz, 2450MHz have been increasing rapidly. Therefore, public opinion concern about the potential human health hazards of short and long-term effect of exposure to radiofrequency (RF) radiation. Oxidative stress is a biochemical condition, which is defined by the imbalance between reactive oxygen species (ROS) and the anti-oxidative defense. In this review, we evaluated available in vitro and in vivo studies carried out on the relation between RF emitted from mobile phones and oxidative stress. The results of the studies we reviewed here indicated that mobile phones and similar equipment or radars can be thought as a factor, which cause oxidative stress. Even some of them claimed that oxidative stress originated from radiofrequencies can be resulted with DNA damage. For this reason one of the points to think on is relation between mobile phones and oxidative stress. However, more performance is necessary especially on human exposure studies.
PMID: Reproduction. 2016 12 ;152(6):R263-R276. Epub 2016 Sep 6. PMID: 27601711 Abstract Title: The effects of radiofrequency electromagnetic radiation on sperm function. Abstract: Mobile phone usage has become an integral part of our lives. However, the effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted by these devices on biological systems and specifically the reproductive systems are currently under active debate. A fundamental hindrance to the current debate is that there is no clear mechanism of how such non-ionising radiation influences biological systems. Therefore, we explored the documented impacts of RF-EMR on the male reproductive system and considered any common observations that could provide insights on a potential mechanism. Among a total of 27 studies investigating the effects of RF-EMR on the male reproductive system, negative consequences of exposure were reported in 21. Within these 21 studies, 11 of the 15 that investigated sperm motility reported significant declines, 7 of 7 that measured the production of reactive oxygen species (ROS) documented elevated levels and 4 of 5 studies that probed for DNA damage highlighted increased damage due to RF-EMR exposure. Associated with this, RF-EMR treatment reduced the antioxidant levels in 6 of 6 studies that discussed this phenomenon, whereas consequences of RF-EMR were successfully ameliorated with the supplementation of antioxidants in all 3 studies that carried out these experiments. In light of this, we envisage a two-step mechanism whereby RF-EMR is able to induce mitochondrial dysfunction leading to elevated ROS production. A continued focus on research, which aims to shed light on the biological effects of RF-EMR will allow us to test and assess this proposed mechanism in a variety of cell types.
PMID: J Environ Sci Health A Tox Hazard Subst Environ Eng. 2018 Jan 28 ;53(2):132-138. Epub 2017 Nov 17. PMID: 29148897 Abstract Title: Oxidative stress response in SH-SY5Y cells exposed to short-term 1800 MHz radiofrequency radiation. Abstract: The exact mechanism that could explain the effects of radiofrequency (RF) radiation exposure at non-thermal level is still unknown. Increasing evidence suggests a possible involvement of reactive oxygen species (ROS) and development of oxidative stress. To test the proposed hypothesis, human neuroblastoma cells (SH-SY5Y) were exposed to 1800 MHz short-term RF exposure for 10, 30 and 60 minutes. Electric field strength within Gigahertz Transverse Electromagnetic cell (GTEM) was 30 V mand specific absorption rate (SAR) was calculated to be 1.6 W kg. Cellular viability was measured by MTT assay and level of ROS was determined by fluorescent probe 2',7'-dichlorofluorescin diacetate. Concentrations of malondialdehyde and protein carbonyls were used to assess lipid and protein oxidative damage and antioxidant activity was evaluated by measuring concentrations of total glutathione (GSH). After radiation exposure, viability of irradiated cells remained within normal physiological values. Significantly higher ROS level was observed for every radiation exposure time. After 60 min of exposure, the applied radiation caused significant lipid and protein damage. The highest GSH concentration was detected after 10 minute-exposure. The results of our study showed enhanced susceptibility of SH-SY5Y cells for development of oxidative stress even after short-term RF exposure.
PMID: Anat Histol Embryol. 2018 Jun ;47(3):222-230. Epub 2018 Mar 5. PMID: 29504145 Abstract Title: Effect of a 1800 MHz electromagnetic field emitted during embryogenesis on chick development and hatchability. Abstract: The level of artificial electromagnetic field (EMF) has steadily increased with the development of human civilization. The developing chicken embryo has been considered a good model to study the effects of EMF on living organisms. The aim of the study was to determine the effect of a 1800 MHz electromagnetic field during embryogenesis on the frequency of chick embryo malformations, morphometric parameters of the heart and liver and concentration of corticosterone in blood plasma, lipid and glycogen content in the liver of newly hatched chicks. A 1800 MHz EMF was found to shorten the duration of embryogenesis (earlier pipping and hatching of chicks) while having no effect on the quantity and quality of chicks and on increasing the incidence of embryo malformations. Exposure of chick embryos to EMF caused decreases in relative heart weight and right ventricle wall thickness. The pipping and hatching of chicks can be accelerated by stressful impact of EMF, which is confirmed by a significant increase in plasma corticosterone concentrations and decrease in fat and glycogen in the liver of chicks exposed during embryogenesis on the electromagnetic field with a frequency of1800 MHz.
PMID: Electromagn Biol Med. 2015 Mar ;34(1):85-92. Epub 2014 Mar 25. PMID: 24665905 Abstract Title: Oxidative changes and apoptosis induced by 1800-MHz electromagnetic radiation in NIH/3T3 cells. Abstract: To investigate the potential adverse effects of mobile phone radiation, we studied reactive oxygen species (ROS), DNA damage and apoptosis in mouse embryonic fibroblasts (NIH/3T3) after intermittent exposure (5min on/10min off, for various durations from 0.5 to 8h) to an 1800-MHz GSM-talk mode electromagnetic radiation (EMR) at an average specific absorption rate of 2W/kg. A 2',7'-dichlorofluorescin diacetate fluorescence probe was used to detect intracellular ROS levels, immunofluorescence was used to detect H2AX foci as a marker for DNA damage, and flow cytometry was used to measure apoptosis. Our results showed a significant increase in intracellular ROS levels after EMR exposure and it reached the highest level at an exposure time of 1h (p
What does not, or at least should not happen, is that an agent of the government, charged with the task of safeguarding the welfare of children, would completely fabricate contact with a family in order to mask non-compliance with the agencys policy. Providing false testimony of any kind is an unfathomable violation of the trust that the people in the State of Iowa place in their public servants and cast a dark and permanent shadow upon all of us. Judge Adam Sauer
Commentary by Terri
Health Impact News
An Iowa judge recently reprimanded the Department of Human Services (DHS) after a social worker was found to have repeatedly lied...
PMID: J Biosci. 2018 Jun ;43(2):263-276. PMID: 29872015 Abstract Title: Electromagnetic radiation 2450 MHz exposure causes cognition deficit with mitochondrial dysfunction and activation of intrinsic pathway of apoptosis in rats. Abstract: Electromagnetic radiation (EMR) can induce or modulate several neurobehavioral disorders. Duration and frequency of exposure of EMR is critical to develop cognitive disorders. Even though EMR-2450 is widely used, its effects on cognition in relation to mitochondrial function and apoptosis would provide better understanding of its pathophysiological effects. Therefore, a comparative study of different frequencies of EMR exposure would give valuable information on effects of discrete frequencies of EMR on cognition. Male rats were exposed to EMR (900, 1800 and 2450 MHz) every day for 1 h for 28 consecutive days. The cognitive behavior in terms of novel arm entries in Y-maze paradigm was evaluated every week after 1 h to last EMR exposure. Animals exposed to EMR-2450 MHz exhibited significant cognitive deficits. EMR- 2450 MHz caused loss of mitochondrial function and integrity, an increase in amyloid beta expression. There was release of cytochrome-c and activation of apoptotic factors such as caspase-9 and -3 in the hippocampus. Further, there was decrease in levels of acetylcholine, and increase in activity of acetyl cholinesterase, indicating impairment of cholinergic system. Therefore, exposure of EMR-2450 in rats caused cognitive deficit with related pathophysiological changes in mitochondrial and cholinergic function, and amyloidogenesis.
PMID: Reprod Health. 2015 Aug 4 ;12:65. Epub 2015 Aug 4. PMID: 26239320 Abstract Title: Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3 signaling pathways in rats. Abstract: BACKGROUND: The decreased reproductive capacity of men is an important factor contributing to infertility. Accumulating evidence has shown that Electromagnetic radiation potentially has negative effects on human health. However, whether radio frequency electromagnetic radiation (RF-EMR) affects the human reproductive system still requires further investigation. Therefore, The present study investigates whether RF-EMR at a frequency of 900 MHz can trigger sperm cell apoptosis and affect semen morphology, concentration, and microstructure.METHODS: Twenty four rats were exposed to 900 MHz electromagnetic radiation with a special absorption rate of 0.660.01 W/kg for 2 h/d. After 50d, the sperm count, morphology, apoptosis, reactive oxygen species (ROS), and total antioxidant capacity (TAC), representing the sum of enzymatic and nonenzymatic antioxidants, were investigated. Western blotting and reverse transcriptase PCR were used to determine the expression levels of apoptosis-related proteins and genes, including bcl-2, bax, cytochrome c, and capase-3.RESULTS: In the present study, the percentage of apoptotic sperm cells in the exposure group was significantly increased by 91.42% compared with the control group. Moreover, the ROS concentration in exposure group was increased by 46.21%, while the TAC was decreased by 28.01%. Radiation also dramatically decreased the protein and mRNA expression of bcl-2 and increased that of bax, cytochrome c, and capase-3.CONCLUSION: RF-EMR increases the ROS level and decreases TAC in rat sperm. Excessive oxidative stress alters the expression levels of apoptosis-related genes and triggers sperm apoptosis through bcl-2, bax, cytochrome c and caspase-3 signaling pathways.
PMID: Toxicol Ind Health. 2007 Aug ;23(7):411-20. PMID: 18536493 Abstract Title: 900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat endometrium: protection by vitamins E and C. Abstract: There are numerous reports on the effects of electromagnetic radiation (EMR) in various cellular systems. Mechanisms of adverse effects of EMR indicate that reactive oxygen species (ROS) may play a role in the biological effects of this radiation. The aims of this study were to examine 900 MHz mobile phone-induced oxidative stress that promotes production of ROS and to investigate the role of vitamins E and C, which have antioxidant properties, on endometrial tissue against possible 900 MHz mobile phone-induced endometrial impairment in rats. The animals were randomly grouped (eight each) as follows: 1) Control group (without stress and EMR, Group I), 2) sham-operated rats stayed without exposure to EMR (exposure device off, Group II), 3) rats exposed to 900 MHz EMR (EMR group, Group III) and 4) a 900 MHz EMR exposed + vitamin-treated group (EMR + Vit group, Group IV). A 900 MHz EMR was applied to EMR and EMR + Vit group 30 min/day, for 30 days using an experimental exposure device. Endometrial levels of nitric oxide (NO, an oxidant product) and malondialdehyde (MDA, an index of lipid peroxidation), increased in EMR exposed rats while the combined vitamins E and C caused a significant reduction in the levels of NO and MDA. Likewise, endometrial superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities decreased in EMR exposed animals while vitamins E and C caused a significant increase in the activities of these antioxidant enzymes. In the EMR group histopathologic changes in endometrium, diffuse and severe apoptosis was present in the endometrial surface epithelial and glandular cells and the stromal cells. Diffuse eosinophilic leucocyte and lymphocyte infiltration were observed in the endometrial stroma whereas the combination of vitamins E and C caused a significant decrease in these effects of EMR. It is concluded that oxidative endometrial damage plays an important role in the 900 MHz mobile phone-induced endometrial impairment and the modulation of oxidative stress with vitamins E and C reduces the 900 MHz mobile phone-induced endometrial damage both at biochemical and histological levels.
PMID: J Androl. 2012 May-Jun;33(3):350-6. Epub 2011 Jul 28. PMID: 21799142 Abstract Title: Effects of the exposure to mobile phones on male reproduction: a review of the literature. Abstract: The use of mobile phones is now widespread. A great debate exists about the possible damage that the radiofrequency electromagnetic radiation (RF-EMR) emitted by mobile phones exerts on different organs and apparatuses. The aim of this article was to review the existing literature exploring the effects of RF-EMR on the male reproductive function in experimental animals and humans. Studies have been conducted in rats, mice, and rabbits using a similar design based upon mobile phone RF exposure for variable lengths of time. Together, the results of these studies have shown that RF-EMR decreases sperm count and motility and increases oxidative stress. In humans, 2 different experimental approaches have been followed: one has explored the effects of RF-EMR directly on spermatozoa and the other has evaluated the sperm parameters in men using or not using mobile phones. The results showed that human spermatozoa exposed to RF-EMR have decreased motility, morphometric abnormalities, and increased oxidative stress, whereas men using mobile phones have decreased sperm concentration, decreased motility (particularly rapid progressive motility), normal morphology, and decreased viability. These abnormalities seem to be directly related to the duration of mobile phone use.
What does not, or at least should not happen, is that an agent of the government, charged with the task of safeguarding the welfare of children, would completely fabricate contact with a family in order to mask non-compliance with the agencys policy. Providing false testimony of any kind is an unfathomable violation of the trust that the people in the State of Iowa place in their public servants and cast a dark and permanent shadow upon all of us. Judge Adam Sauer
Commentary by Terri
Health Impact News
An Iowa judge recently reprimanded the Department of Human Services (DHS) after a social worker was found to have repeatedly lied to...
PMID: J Clin Endocrinol Metab. 2018 Sep 27. Epub 2018 Sep 27. PMID: 30265356 Abstract Title: Role of Selenium Intake for Risk and Development of Hyperthyroidism. Abstract: Purpose: To investigate the importance of dietary Se supply for hyperthyroidism.Methods: We performed a more in-depth analysis of a large cross-sectional study of 6152 participants from two counties within the Shaanxi Province, China, which are characterized by different habitual Se intakes, and investigated the effects of different dietary Se supply (0.02, 0.18, 0.6 or 2.0 ppm Se) on disease development in a mouse model of GD.Results: The cross-sectional study revealed a comparable prevalence of hyperthyroidism irrespective of Se intake in both counties. However, an unexpected sex-specific difference was noted, and Se deficiency may constitute risk factor for hyperthyroidism particularly in males. In the mouse model, pathological thyroid morphology was affected, and higher Se intakes exerted some protecting effects on the pathological distortion. Circulating thyroid hormone levels, malondialdehyde concentrations, total antioxidant capacity or the titer of GD-causing TSH receptor autoantibodies (TRAb) were not affected by Se. Expression analysis of transcripts in spleen indicated regulatory effects on genes implicated in the immune response, erythropoiesis and oxygen status. However, the humoral immune response including the ratio of CD4/CD8 or Th1/Th2 cells, and the concentration of Treg cells were similar between the experimental groups, despite their varying Se intakes.Conclusions: Our data highlight a novel sexual dimorphism for the interaction of Se and thyroid disease risk in humans, and indicate local protective effects of Se on thyroid gland integrity which appear not to be reflected in the circulating biomarkers tested.
PMID: Biometals. 2018 Oct 4. Epub 2018 Oct 4. PMID: 30288658 Abstract Title: Selenium-Rich Yeast protects against aluminum-induced peroxidation of lipide and inflammation in mice liver. Abstract: To investigate the effect of Selenium Rich Yeast (SeY) on hepatotoxicity of Aluminium (Al), SeY (0.1 mg/kg) was orally administrated to aluminium-exposed mice (10 mg/kg) for 28 days. The risk of oxidative stress was assessed by detecting the total antioxidant capacity (T-AOC), catalase activity, HOcontent, and mRNA levels of the Keap1/Nrf-2/HO-1 pathway. Inflammatory reactions were assessed by detecting the mRNA levels of inflammatory biomarkers. Our results showed that SeY protected against the liver histological changes induce by Al. The body weight gain of mice treated with SeY+ Al restore to normal compare with mice exposed to Al alone. Al treatment significantly decreased the activities of antioxidant enzymes, reduced T-AOC levels, and up-regulated the mRNA level of Nrf2 and HO-1, thereby ultimately leading to peroxidation. SeY shown a significant protective effectagainst oxidative stress caused by Al. In addition, Al exposure induced inflammatory responses in rat liver by promoting the release of inflammatory cytokines (TNF-a, NF-kB, TNF-R1, IL-1, IL-6, and COX-2). SeY protected against changes in liver by regulating the mRNA expression levels of inflammatory factors. These results suggested that Se protected the liver from the Al-induced hepatotoxicity by regulating the mRNA level of Keap1/Nrf2/HO-1, and inhibited inflammatory responses by down-regulating the expression level of inflammatory cytokine.
By Sara Tipton
The end of the summer garden is always bittersweet for me. I miss my daily fresh cut lettuce but I also love the falling leaves and bright reds and oranges of autumn. Luckily, those fallen leaves are more than just pleasing to look at. In this helpful guide, well walk you through a few easy ways to use your fallen autumn leaves as zero waste and cheaper options around your place.
One of the best sustainable and organic ways to help prepare your garden is to add a mulch, and the beautiful fallen leaves of autumn are a great way to this. According to Ready Nutrition, in the gardening community, leaves are huge. When they are composted they become known as black gold, a nutrient-rich material that can be used in a multitude of ways in the garden.
The life cycle of a leaf begins when a tree makes its leaves in the spring. The tree concentrates all of its energy and nutrients into making the leaves because the more leaves there are, the more photosynthesis can occur. When the leaves drop in autumn, they create a ground cover for the trees to conserve moisture. As the leaves decompose, they provide the tree with nutrients and resupply the depleted soil with microbes. The roots of trees can then absorb the nutrients and minerals via the soil in order to create even more leaves the next spring. Its a unique life cycle that can be taken advantage of.
By Elizabeth Millard
Robust gut health isnt just about digestionalthough it plays a major role. The way your digestion system functions has been linked to an array of physiological processes, including hormone regulation, toxin elimination, defense against bacteria and viruses, cell regeneration, and more.
Theres so much control happening throughout your GI tract, that its been called the second brain, and when disease, stress, pollutants, or poor nutrition negatively affects that brain, it can have a profound impact on how you operate. Thats why a substance like CBD oilwhich has effects throughout the digestive systemshows such promise for gut health.
There are cannabinoid receptors in the GI tract that are there to help maintain homeostasis within the body, says Michelle Weiner, DO, MPH, of the Spine and Wellness Centers of America. When your gut is out of whack, it can have a ripple effect throughout every system, affecting everything from your immune response to your emotional health. CBD can help get you back on track by addressing and correcting imbalances in the gut.
When it comes to the mechanisms...
PMID: Int J Radiat Biol. 2012 Nov ;88(11):799-805. Epub 2012 Aug 8. PMID: 22788526 Abstract Title: Oxidative stress induced by 1.8 GHz radio frequency electromagnetic radiation and effects of garlic extract in rats. Abstract: PURPOSE: We aimed to study the oxidative damage induced by radiofrequency electromagnetic radiation (RF-EMR) emitted by mobile telephones and the protective effect of garlic extract used as an anti-oxidant against this damage.MATERIALS AND METHODS: A total of 66 albino Wistar rats were divided into three groups. The first group of rats was given 1.8 GHz, 0.4 W/kg specific absorption rate (SAR) for 1 h a day for three weeks. The second group was given 500 mg/kg garlic extract in addition to RF-EMR. The third group of rats was used as the control group. At the end of the study, blood and brain tissue samples were collected from the rats.RESULTS: After the RF-EMR exposed, the advanced oxidation protein product (AOPP) levels of brain tissue increased compared with the control group (p0.05). We did not detect any PON levels in the brain tissue.CONCLUSIONS: The exposure of RF-EMR similar to 1.8 GHz Global system for mobile communication (GSM) leads to protein oxidation in brain tissue and an increase in serum NO. We observed that garlic administration reduced protein oxidation in brain tissue and that it did not have any effects on serum NO levels.
PMID: Mol Vis. 2008 May 19 ;14:964-9. Epub 2008 May 19. PMID: 18509546 Abstract Title: Electromagnetic noise inhibits radiofrequency radiation-induced DNA damage and reactive oxygen species increase in human lens epithelial cells. Abstract: PURPOSE: The goal of this study was to investigate whether superposing of electromagnetic noise could block or attenuate DNA damage and intracellular reactive oxygen species (ROS) increase of cultured human lens epithelial cells (HLECs) induced by acute exposure to 1.8 GHz radiofrequency field (RF) of the Global System for Mobile Communications (GSM).METHODS: An sXc-1800 RF exposure system was used to produce a GSM signal at 1.8 GHz (217 Hz amplitude-modulated) with the specific absorption rate (SAR) of 1, 2, 3, and 4 W/kg. After 2 h of intermittent exposure, the ROS level was assessed by the fluorescent probe, 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA). DNA damage to HLECs was examined by alkaline comet assay and the phosphorylated form of histone variant H2AX (gammaH2AX) foci formation assay.RESULTS: After exposure to 1.8 GHz RF for 2 h, HLECs exhibited significant intracellular ROS increase in the 2, 3, and 4 W/kg groups. RF radiation at the SAR of 3 W/kg and 4 W/kg could induce significant DNA damage, examined by alkaline comet assay, which was used to detect mainly single strand breaks (SSBs), while no statistical difference in double strand breaks (DSBs), evaluated by gammaH2AX foci, was found between RF exposure (SAR: 3 and 4 W/kg) and sham exposure groups. When RF was superposed with 2 muT electromagnetic noise could block RF-induced ROS increase and DNA damage.CONCLUSIONS: DNA damage induced by 1.8 GHz radiofrequency field for 2 h, which was mainly SSBs, may be associated with the increased ROS production. Electromagnetic noise could block RF-induced ROS formation and DNA damage.
PMID: Toxicol Lett. 2013 Mar 27 ;218(1):2-9. Epub 2013 Jan 18. PMID: 23333639 Abstract Title: Exposure to 1800 MHz radiofrequency electromagnetic radiation induces oxidative DNA base damage in a mouse spermatocyte-derived cell line. Abstract: Whether exposure to radiofrequency electromagnetic radiation (RF-EMR) emitted from mobile phones can induce DNA damage in male germ cells remains unclear. In this study, we conducted a 24h intermittent exposure (5 min on and 10 min off) of a mouse spermatocyte-derived GC-2 cell line to 1800 MHz Global System for Mobile Communication (GSM) signals in GSM-Talk mode at specific absorption rates (SAR) of 1 W/kg, 2 W/kg or 4 W/kg. Subsequently, through the use of formamidopyrimidine DNA glycosylase (FPG) in a modified comet assay, we determined that the extent of DNA migration was significantly increased at a SAR of 4 W/kg. Flow cytometry analysis demonstrated that levels of the DNA adduct 8-oxoguanine (8-oxoG) were also increased at a SAR of 4 W/kg. These increases were concomitant with similar increases in the generation of reactive oxygen species (ROS); these phenomena were mitigated by co-treatment with the antioxidant-tocopherol. However, no detectable DNA strand breakage was observed by the alkaline comet assay. Taking together, these findings may imply the novel possibility that RF-EMR with insufficient energy for the direct induction of DNA strand breaks may produce genotoxicity through oxidative DNA base damage in male germ cells.
John C. Dvorak from the No Agenda Show podcast wrote for PC Magazine for THIRTY YEARS. However, while he wrote extensively for the magazine, in August of this year he wrote a less than PC (pun intended!) article about the dangers of 5G (read it here) entitled, The Problem With 5G. Unhappy with what he wrote, 
A few months ago I was surprised to receive a request from an obscure journal of consciousness studies to review a paper. I was surprised because, although it was not immediately obvious from the title, the paper contained the first reports of the primary outcome measure of the massive and notorious STAR-D study, 14 years after the study was finished.
What in the world were the main findings of the worlds largest ever antidepressant trial doing being presented now in a little known journal? The answer may lie in the fact that they show how miserably poor the results of standard medical treatment for depression really are!
With 4041 participants, the STAR-D study is by far the largest and most expensive study of antidepressants ever conducted. The intention of the study was to see how antidepressant treatment combined with high quality care performed in usual clinical conditions. It did not involve a placebo or any sort of control. All treatment was provided free for the duration of the study to maximise engagement.
The paper I was asked to review, which is now published in Psychology of Consciousness: Theory, Research and Practice, is written by a group led by Irving Kirsch and based on the original data obtained through the NIMH.1 Shannon Peters describes its findings in detail.
Kirschs group point out that the paper that describes the design of the STAR-D trial clearly identifies the Hamilton Rating Scale for Depression (HRSD) as the primary outcome.2 This makes sense since the HRSD is one of the most commonly used rating scales in trials of treatment of depression, especially trials of antidepressants. As the STAR-D authors note in the study protocol the HAM-D17 (HRSD), the primary outcome, allows comparison to the vast RCT literature (cited in (1)).
Yet the outcome that was presented in almost all the study papers was the QIDS (Quick Inventory of Depressive Symptomatology), a measure made up especially for the STAR-D study, with no prior or subsequent credentials. In fact, as the authors of the present paper point out, this measure was devised not as an outcome measure, but as a way of tracking symptoms during th...
So much of what we are is based on what we eat. Plain and simple. Eat good, whole foods and youll nourish your body. Put junk in it and youll feel it. And with prolonged bad eating habits, there might even be serious consequences. RELATED STORY: The filthiest food you can eat, yet most think 
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A recent report in the Lok Sabha secretariat revealed that groundwater in a number of districts in Delhi contains a high level of fluoride, arsenic, and nitrate affecting the health of Delhiites. With one-third of groundwater in Delhi and the NCR containing an excessive concentration of fluoride, an increasing number of people are getting afflicted with arthritis and osteoarthritis, a rheumatic condition that affects joints and worsens with growing age.
In India, the most common cause of fluorosis is high-fluoride well water derived from borewells dug deep into the earth. High concentration of fluoride in groundwater beyond the permissible limit of 1.5 mg/L is a major health problem in India. Nearly 90 per cent of the rural population of the country uses groundwater for drinking and domestic purposes and due to excess fluoride in groundwater, a huge chunk of the rural population is threatened with health hazards triggered by fluorosis, said Dr Raju Vaishya, President, Indian Cartilage Society and Arthritis Care.
According to medical studies, skeletal fluorosis occurs when the fluoride concentration in water exceeds one part per million (ppm). Radiologically detectable skeletal fluorosis occurs in populations with typical exposures of 8 mg/day.
Fluoride can cause chronic joint pain prior to causing x-ray-detectable fluorosis. Thus, for some individuals, the doses that can cause arthritic pain will be less than the 6 to 8 mg/day that causes radiologically detectable bone changes. While the advanced stages produce extreme, visibly crippling, effects on the skeleton, the earlier stages are less obvious, and extremely difficult to diagnose. There are three forms of fluoride poisoning or fluorosis. These are dental fluorosis, non-skeletal fluorosis, and skeletal fluorosis. Among individuals with skeletal fluorosis, the fluoride-induced changes to the bone, joints, and spine can cause widespread joint pain, arthritis and osteoarthritis, said Vaishya.
A common finding among researchers investigating fluorosis is that the early stages are marked by symptoms (stiff and painful joints) which are frequently difficult to differentiate from various types of arthritis.
Dear Retraction Watch readers: Have you seen our database of retractions? While were still putting finishing touches on it before an official launch, with more than 18,000 retractions, its already the most comprehensive collection of retractions anywhere. We have learned a great deal as weve gathered those retractions, which we look forward to sharing quite soon, Continue reading Retraction Watch readers, we need your help to be able to continue our work
Legalizing marijuana in the United States is a consistent debate. Its recently seen an interesting development with a 2018 Gallup poll, however, in which it was revealed that 64% of American citizens support the legalizations. If you happen to be interested in the debate on cannabis use, try reading about these women who have dedicated... View Article
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I read the Oct. 5 opinion letter by a group of local doctors trying to convince Parry Sounders to vote in favour of fluoridation in the upcoming plebiscite.
As one of the persons derogatorily labeled as a so-called expert, Id like to offer some corrections and facts in response based on science, not politics or endorsements.
Claim1: As health professionals we serve as first-hand witnesses to the impact that poor dental hygiene has on the overall health of the community.
This is an odd statement, since physicians do not practice dentistry and are not familiar with dental science.
Fact: poor dietary choices (frequent sugar intake) cause cavities. Poor dental hygiene is a not a major factor in the prevalence and severity of dental decay.
Claim 2. Cavities cost Canadians over a billion dollars a year.
Sounds impressive, but thats only $27/person/yr.
Fact: Other dental costs, including cosmetic dentistry to treat the dental fluorosis side effects of fluoridation, are 12 times higher.
Claim 3. The truth is, fluoride in drinking water has been scientifically studied for over 70 years without ever finding evidence that the low levels recommended in municipal drinking water have any negative health effects
Fact: While fluoridation has been in place for 70 years, studies have not been conducted to show safety. Our expert review panel (the National Academies of Sciences Committee on Fluoride in Drinking Water) reviewed over hundreds of studies on fluoride toxicity. See https://www.nap.edu/catalog/11571/fluoride-in-drinking-water-a-scientific-review-of-epas-standards We found several problems with fluoride in drinking water because fluoride accumulates in the body, primarily the skeletal system.
Our own study (Chachra et al, 2010) published after our NAS Review of 2006 comparing the bones of fluoridated Torontonians with the bones of the non-fluoridated Montrealers showed that the people in Toronto had more fluoride in their bones and the physical properties of their bones had changed. Fluoride accumulation in bones weakens them.
But if you dont look for problems you wont find them.
There has never been a randomized, double-blinded clinical trial to see if fluoridation actually works. This kind of study is required for every drug that seeks approval from Health Canada or the US FDA.
Claim 4. In recent years, when communities have voted to remove fluoride from drinking water, cavity rates have risen.
Fact. This is incorrect. Nearly all studies, including in Canada, showed that where fluoridation was halted, dental decay continued to d...
Pack your bags ladies, were relocating into nature! Our prayers for finding the fountain of youth have been answered! Ok, well maybe not entirely the fountain of youth, BUT, hear me out. Recent studies have confirmed that women who surround themselves in or live within nature, live longer! Research has shown that stress reduction, as... View Article
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The world is a large and mysterious place. So many mysteries surround nature and were only just barely beginning to understand what anything really means. Scientists are constantly making new discoveries about the oceans, the deserts, and even the plant life on our home, Earth. There is so much to learn that at times it... View Article
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Confession time: I hate spiders. I am terrified of them. While logically I understand that regular little spiders in my home or out in nature are fine, there is something creepy and scary about them. I am terrified of them, and it is only getting worse as I get older. Why Killing Spiders Is A... View Article
The post Should I Kill Spiders In My Home? An Entomologist Explains Why Not To appeared first on Healthy Holistic Living.
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