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Diverse Influences of Androgen-Disrupting Chemi... [Inflammation. 2013] - PubMed - NCBI - 0 views

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    Study proposed immune dysfunction as a result of EDC like BPA. Bisphenol A induced cell apoptosis as well as a reduction of nitric oxide.
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Maternal Cypermethrin Exposure during the Perinatal... [PLoS One. 2014] - PubMed - NCBI - 0 views

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    another study points to the negative development effects of EDCs.  In this animal study, Cypermethrin exposure in the Perinatal period, disrupts testes development which resulted in decreased Testosterone production in adults.
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Cadmium - a metallohormone? - 0 views

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    Great review article on the endocrine disrupting role of Cadmium.  Cadmium binds to the ER-alpha inducing an estrogen signal.  Cadmium also binds to the androgen receptor as well.  This study proposes a similar activation of ER-alpha and AR by Cadmium.
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Effects of maternal dietary exposure to cadmium during pregnancy on mammary cancer risk... - 0 views

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    Animal study finds that Cadmium is estrogenic.  This study found that not only was Cadmium an endocrine disruptor for the pregnant animals, but was also estrogenic in the mammary glands of the offspring.
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New aspects of cadmium as endocrine disruptor. [Environ Sci. 2006] - PubMed - NCBI - 0 views

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    Cadmium is an endocrine disruptor: binds to estrogen receptors and the androgen receptor. 
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http://apps.who.int/iris/bitstream/10665/78102/1/WHO_HSE_PHE_IHE_2013.1_eng.pdf - 0 views

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    2012 WHO review on EDCs
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Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correl... - 0 views

  • low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
  • supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier
  • oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
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  • malnutrition progressing to cachexia is another common manifestation of cirrhosis
  • Malnutrition can be mitigated with BCAA supplementation
  • Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease
  • Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
  • BCAAs metabolites inhibit proteolysis
  • Patients with cirrhosis have both insulin deficiency and insulin resistance
  • BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization
  • Coadministration of BCAAs and glucose has been found to be particularly useful
  • BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
  • Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
  • another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
  • BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves
  • BCAA administration has also been shown to have a positive effect on liver regeneration
  • A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells
  • BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
  • Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
  • long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding
  • The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation
  • Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
  • patients taking BCAA supplementation report improved quality of life
  • BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
  • BCAAs make up 20-25% of the protein content of most foods
  • Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran
  • In addition to BCAAs from diet, oral supplements of BCAAs can be used
  • Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy
  • Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
  • Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
  • the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
  • A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs
  • Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
  • hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia
  • BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver
  • patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
  • Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
  • the serum BCAA concentration is strongly correlated with the serum albumin level
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    great review of cirrhosis and BCCA supplementation.
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Environmental Health Perspectives: Environmental Chemicals in Pregnant Women in the US:... - 0 views

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    100% of expecting mothers found to be toxic
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UEPI - PPERC - Find a greener cleaner near you! - 0 views

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    find a green cleaner near you
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Developmental exposure to endocrine disruptors and... [Reprod Toxicol. 2007 Apr-May] - ... - 0 views

  • e review the literature that proposes an association of exposure to environmental endocrine disrupting chemicals with the development of obesity
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    exposure to toxins perinatally likely playing a significant role in the run-away-train obesity epidemic over last 3 decades
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Arch Intern Med -- Abstract: Human Chorionic Gonadotropin (HCG) Treatment of Obesity, F... - 0 views

  • hese results indicate that HCG has no effects on chemical and hormonal parameters measured and offers no advantage over calorie restriction in promoting weight loss.
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    HCG injections appear to have no effect on weight loss over those following 500 cal diets
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ScienceDirect - Food and Chemical Toxicology : Neuroprotective effect of ginger on anti... - 0 views

  • A marked decrease in anti-oxidant marker enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced glutathione (GSH) and increase in malondialdehyde (MDA) was observed in the diabetic rats
  • inger may be used as therapeutic agent in preventing complications in diabetic patients.
  • These results suggest that ginger exhibit a neuroprotective effect by accelerating brain anti-oxidant defense mechanisms and down regulating the MDA levels to the normal levels in the diabetic rats
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    Ginger reduces oxidative stress in diabetic rat model
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Determination of bisphenol A concentrations in hum... [Hum Reprod. 2002] - PubMed result - 0 views

  • he potential for human exposure to endocrine-disrupting chemicals
  • suggest accumulation of BPA in early fetuses and significant exposure during the prenatal period
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    BPA is found in significant levels in the prenatal period
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Exposure to Bisphenol A Prenatally or in Adulthood Promotes TH2 Cytokine Production Ass... - 0 views

  • BPA promotes the development of TH2 cells in adulthood and both TH1 and TH2 cells in prenatal stages by reducing the number of regulatory T cells.
  • Bisphenol A (BPA), an estrogenic endocrine-disrupting chemical (EDC
  • BPA is one of the most widespread EDCs.
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  • BPA antagonizes the actions of thyroid hormone
  • Prenatal exposure to BPA has been shown to alter a variety of reproductive endocrine parameters, such as testosterone and luteinizing hormone levels
  • arly onset of sexual maturation of female mice
  • imbalanced T-helper (TH)1/TH2 immune responses have been demonstrated on exposure to BPA
  • indicating that BPA exerted its effects by reducing the number of Treg cells.
  • Exposure to BPA by subcutaneous injection in adulthood significantly promoted antigen-stimulated production of IL-4, IL-10, and IL-13 in TH2-skewed
  • BPA can leak from the placenta and accumulate in the fetus
  • We showed that prenatal exposure to BPA increased the production of a TH1 cytokine, IFN-γ, and a TH2 cytokine, IL-4, after the offspring developed, suggesting that prenatal exposure to BPA can induce persistent immunologic effects lasting into adulthood.
  • These results are consistent with a previous report that fetal exposure to BPA augmented TH1 and TH2 immune responses
  • our results clearly demonstrate that the production of TH2 cytokines is promoted by BPA in adult mice and in offspring during developmental exposure.
  • The decrease of Treg cells would predispose to immune dysfunction in aged individuals, explaining their higher risk of immune-mediated diseases, cancer, and infections.
  • BPA might cause these diseases. Thus, avoiding exposure to or promoting the excretion of BPA and other EDCs would help in preventing diseases and adverse health effects.
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    BPA as endocrine disruptor and as immune disruptor
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Urinary Phthalate Metabolites Are Associated With Decreased Serum Testosterone in Men, ... - 0 views

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    Phthalate exposure is a cause of low Testosterone in men, women, and children.   In boys 6-12, exposure was associated with a 24-34% reduction in Testosterone.
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Saccharomyces boulardii decreases inflammation and intestinal colonization by Candida a... - 0 views

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    Saccharomyces boulardii decreased TNF-alpha and INF-gamma as well as decreased candida colonization.
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The current state and future perspectives of cannabinoids in cancer biology - 0 views

  • The activation of each of them leads to an inhibition of adenylyl cyclase via G proteins (Gi/o), which in turn activates many metabolic pathways such as mitogen‐activated protein kinase pathway (MAPK), phosphoinositide 3‐kinase pathway (PI3K), cyclooxygenase‐2 pathway (COX‐2), accumulation of ceramide, modulation of protein kinase B (Akt), and ion channels
  • phytocannabinoids, endocannabinoids, and synthetic cannabinoids
  • Action of THC in human organism relies on mimicking endogenous agonists of CB receptors—endocannabinoids
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  • The upregulated expression of CB receptors and the elevated levels of endocannabinoids have been observed in a variety of cancer cells (skin, prostate, and colon cancer, hepatocellular carcinoma, endometrial sarcoma, glioblastoma multiforme, meningioma and pituitary adenoma, Hodgkin lymphoma, chemically induced hepatocarcinoma, mantel cell lymphoma)
  • concentration of endocannabinoids, expression level of their receptors, and the enzymes involved in their metabolism frequently are associated with an aggressiveness of cancer
  • CB2 receptor contributes to human epidermal growth factor receptor (HER2) pro‐oncogenic signaling and an overexpression of CB2 increases susceptibility for leukemia development after leukemia viral infection
  • endocannabinoid‐degrading enzymes are upregulated in cancer cell lines and in human tumors
  • Many cannabinoids, ranging from phytocannabinoids (THC, CBD), endocannabinoids (2‐arachidonoylglycerol, anandamide), to synthetic cannabinoids (JWH‐133, WIN‐55,212‐2), have shown ability to inhibit proliferation, metastasis, and angiogenesis in a variety of models of cancer
  • Despite some inconsistent data, the main effect of cannabinoids in a tumor is the inhibition of cancer cells’ proliferation and induction of cancer cell death by apoptosis
  • CB1 and CB2 receptor agonists stimulate apoptotic cell death in glioma cells by induction of de novo synthesis of ceramide, sphingolipid with proapoptotic activity
  • process of autophagy is upstream of apoptosis in mechanism of cell death induced by cannabinoids
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The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic... - 0 views

  • orally active competitive opioid receptor antagonist
  • 4.5 mg, though the dosage can vary a few milligrams below or above that common value
  • At the low dosage level, naltrexone exhibits paradoxical properties, including analgesia and anti-inflammatory actions
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  • LDN may be an effective treatment for FM
  • In addition to the antagonist effect on mu-opioid and other opioid receptors, naltrexone simultaneously has an antagonist effect on non-opioid receptors (Toll-like receptor 4 or TLR4) that are found on macrophages such as microglia
  • It is via the non-opioid antagonist path that LDN is thought to exert its anti-inflammatory effects
  • Once activated, microglia produce inflammatory and excitatory factors that can cause sickness behaviors such as pain sensitivity, fatigue, cognitive disruption, sleep disorders, mood disorders, and general malaise
  • The neuroprotective action appears to result when microglia activation in the brain and spinal cord is inhibited
  • By suppressing microglia activation, naloxone reduces the production of reactive oxygen species and other potentially neuroexcitatory and neurotoxic chemicals
  • suppressed TNF-alpha, IL-6, MCP-1, and other inflammatory agents in peripheral macrophages
  • individuals with greater ESR at baseline experienced a greater drop in pain when taking LDN
  • LDN has been reported to reduce not only self-reported pain in that condition but also objective markers of inflammation and disease severity
  • Naltrexone has also shown some promise in improving disease severity in multiple sclerosis
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    LDN maybe useful in treating chronic pain via anti-inflammatory effects on microglia.
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