"Dr. Pichichero and colleagues concluded that with this latest data, it is time to recognize that the risk of exposure to thimerosol in vaccines is minimal to non-existent. “The H1N1 vaccine is safe and should be given to those at risk as recommended by the US Centers for Disease Control”, Dr. Pichichero said."
Link
Study Examines Mercury in Vaccines. Medwise. Retrieved on October 30, 2009.
Friday, October 30, 2009
Thursday, October 29, 2009
EPA Orders Chemical Testing for Hormone Effects
"U.S. Environmental Protection Agency has issued the first test orders for pesticide chemicals to be screened for their potential effects on the endocrine system...Click here.
Link Between Pain Thresholds, Inflammation And Sleep Problems In Arthritis Patients
"Recent advances in anti-inflammatory therapy, many RA patients continue to suffer from pain. A new study found that inflammation is associated with heightened pain sensitivity at joint sites, whereas increased sleep problems are associated with heightened pain sensitivity at both joint and non-joint sites." Click here.
Wednesday, October 28, 2009
Study: Exercise Protects the Brain from Future Neurotoxic Insults.
"In sedentary monkeys showed the expected decrease in these dopamine neurons on the right side of the brain after the neurotoxin was applied. But in the brains of monkeys that had run for the past three months, the neurotoxin had almost no effect. In the runners, dopamine neurons were just as plentiful on the right side of the brain as on the left."
Exercise helps brains bounce back:
Study of rhesus monkeys shows running protects dopamine neurons from death
Link
TNF-alpha-mediated reduction in PGC-1alpha may impair skeletal muscle function after cigarette smoke exposure
Summary: "this data suggest that in response to smoke exposure, TNF-alpha-mediated down-regulation of PGC-1alpha may be a key step leading to vascular and myocyte dysfunction, effects that are more evident in oxidative than glycolytic skeletal muscles."
Citation: Tang, K., Wagner, P. D., and Breen, E. C. (2009). Tnf-alpha-mediated reduction in pgc-1alpha may impair skeletal muscle function after cigarette smoke exposure. Journal of Cellular Physiology, 9999(9999):n/a+. http://www.citeulike.org/user/HEIRS/article/6018324
Citation: Tang, K., Wagner, P. D., and Breen, E. C. (2009). Tnf-alpha-mediated reduction in pgc-1alpha may impair skeletal muscle function after cigarette smoke exposure. Journal of Cellular Physiology, 9999(9999):n/a+. http://www.citeulike.org/user/HEIRS/article/6018324
Tuesday, October 27, 2009
Paraoxonase 1 (pon1) expression in hepatocytes is upregulated by pomegranate polyphenols: A role for ppar-gamma pathway
Summary: PJ polyphenols upregulated the hepatocyte PON1 expression, at least in part, via the intracellular signaling cascade PPARgamma-PKA-cAMP.
Citation: Khateeb, J., Gantman, A., Kreitenberg, A. J., Aviram, M., and Fuhrman, B. (2009). Paraoxonase 1 (pon1) expression in hepatocytes is upregulated by pomegranate polyphenols: A role for ppar-gamma pathway. Atherosclerosis. http://www.citeulike.org/user/HEIRS/article/5760999
Citation: Khateeb, J., Gantman, A., Kreitenberg, A. J., Aviram, M., and Fuhrman, B. (2009). Paraoxonase 1 (pon1) expression in hepatocytes is upregulated by pomegranate polyphenols: A role for ppar-gamma pathway. Atherosclerosis. http://www.citeulike.org/user/HEIRS/article/5760999
Pgc-1β: A regulator of mitochondrial function with subtle roles in energy metabolism
"As expected from PGC-1β’s ability to stimulate mitochondrial function, the loss of PGC-1β decreased the transcription of genes encoding many of the mitochondrial proteins that generate ATP and heat. Yet the mutant mice appeared essentially healthy under normal conditions. Still, a slight impairment of mitochondrial function might lead to some metabolic imbalance, for instance obesity, since mitochondria burn energy that would otherwise be stored as fat."
Chanut, F. (2006). Pgc-1β: A regulator of mitochondrial function with subtle roles in energy metabolism. PLoS Biol, 4(11):e402+. http://www.citeulike.org/user/HEIRS/article/6016816
Hydrogen Sulfide Increases Glutathione Production and Suppresses Oxidative Stress in Mitochondria
Title: Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria.
Summary: "H2S enhances GSH by enhancing cystine/cysteine transporters and redistributes GSH to mitochondria. H2S produced in mitochondria also may directly suppress oxidative stress. It provides a new mechanism of neuroprotection from oxidative stress by H2S."
Kimura, Y., Goto, Y.-I., and Kimura, H. (2009). Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria. Antioxidants & Redox Signaling, pages 091026040507095+. http://www.citeulike.org/user/HEIRS/article/6015103
Summary: "H2S enhances GSH by enhancing cystine/cysteine transporters and redistributes GSH to mitochondria. H2S produced in mitochondria also may directly suppress oxidative stress. It provides a new mechanism of neuroprotection from oxidative stress by H2S."
Kimura, Y., Goto, Y.-I., and Kimura, H. (2009). Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria. Antioxidants & Redox Signaling, pages 091026040507095+. http://www.citeulike.org/user/HEIRS/article/6015103
Monday, October 26, 2009
Carbon monoxide differentially inhibits tlr signaling pathways by regulating ros-induced trafficking of tlrs to lipid rafts.
HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
Nakahira, K., Kim, H. P., Geng, X. H., Nakao, A., Wang, X., Murase, N., Drain, P. F., Wang, X., Sasidhar, M., Nabel, E. G., Takahashi, T., Lukacs, N. W., Ryter, S. W., Morita, K., and Choi, A. M. K. (2006). Carbon monoxide differentially inhibits tlr signaling pathways by regulating ros-induced trafficking of tlrs to lipid rafts. J. Exp. Med., 203(10):2377-2389. http://www.citeulike.org/user/HEIRS/article/6013733
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Nakahira, K., Kim, H. P., Geng, X. H., Nakao, A., Wang, X., Murase, N., Drain, P. F., Wang, X., Sasidhar, M., Nabel, E. G., Takahashi, T., Lukacs, N. W., Ryter, S. W., Morita, K., and Choi, A. M. K. (2006). Carbon monoxide differentially inhibits tlr signaling pathways by regulating ros-induced trafficking of tlrs to lipid rafts. J. Exp. Med., 203(10):2377-2389. http://www.citeulike.org/user/HEIRS/article/6013733
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HO-1/CO Pathway Suppresses TLR4 Signaling
HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
The Heme Oxygenase-1/Carbon Monoxide Pathway Suppresses TLR4 Signaling by Regulating the Interaction of TLR4 with Caveolin-1.
Wang, X. M., Kim, H. P., Nakahira, K., Ryter, S. W., and Choi, A. M. K. (2009). The heme oxygenase-1/carbon monoxide pathway suppresses tlr4 signaling by regulating the interaction of tlr4 with caveolin-1. J Immunol, 182(6):3809-3818.
http://www.citeulike.org/user/HEIRS/article/4268076
The Heme Oxygenase-1/Carbon Monoxide Pathway Suppresses TLR4 Signaling by Regulating the Interaction of TLR4 with Caveolin-1.
Wang, X. M., Kim, H. P., Nakahira, K., Ryter, S. W., and Choi, A. M. K. (2009). The heme oxygenase-1/carbon monoxide pathway suppresses tlr4 signaling by regulating the interaction of tlr4 with caveolin-1. J Immunol, 182(6):3809-3818.
http://www.citeulike.org/user/HEIRS/article/4268076
Inhibition of liver fibrosis by solubilized coenzyme q10: Role of nrf2 activation
Title: Inhibition of liver fibrosis by solubilized coenzyme q10: Role of nrf2 activation in inhibiting transforming growth factor-beta1 expression.
Summary: "CoQ10 inhibited DMN-induced liver fibrosis through suppression of TGF-beta1 expression via Nrf2/ARE activation."
Choi, H.-K. K., Pokharel, Y. R. R., Lim, S. C. C., Han, H.-K. K., Ryu, C. S. S., Kim, S. K. K., Kwak, M. K. K., and Kang, K. W. W. (2009). Inhibition of liver fibrosis by solubilized coenzyme q10: Role of nrf2 activation in inhibiting transforming growth factor-beta1 expression. Toxicology and applied pharmacology, 240(3):377-384. http://www.citeulike.org/user/HEIRS/article/5366863
Summary: "CoQ10 inhibited DMN-induced liver fibrosis through suppression of TGF-beta1 expression via Nrf2/ARE activation."
Choi, H.-K. K., Pokharel, Y. R. R., Lim, S. C. C., Han, H.-K. K., Ryu, C. S. S., Kim, S. K. K., Kwak, M. K. K., and Kang, K. W. W. (2009). Inhibition of liver fibrosis by solubilized coenzyme q10: Role of nrf2 activation in inhibiting transforming growth factor-beta1 expression. Toxicology and applied pharmacology, 240(3):377-384. http://www.citeulike.org/user/HEIRS/article/5366863
Genetic dissection of systemic autoimmune disease in nrf2 deficient mice.
Title: Genetic dissection of systemic autoimmune disease in nrf2 deficient mice.
Summary: "SLE occurs with an prevalence as high as 1 in 2,500 people but predominantly affects women (35). SLE is especially prevalent in women during their childbearing years (9:1 female to male ratio) and during pregnancy, suggesting a role of female hormones in development of the disease. Most mouse models of SLE also exhibit an increased susceptibility of females to the disease. The sex-specific decreases in glutathione S-transferase -1 and -2 and µ-1, -2, and -3 have been shown previously in the livers of nrf2 knockout mice (10) and are in agreement with our study (Table 3). The findings from this data and other reports strongly suggest that a deficiency in detoxification and increased oxidative stress can result in the development of a systemic autoimmune disease."
Li, J., Stein, T. D., and Johnson, J. A. (2004). Genetic dissection of systemic autoimmune disease in nrf2 deficient mice. Physiological Genomics, pages 1-57. http://www.citeulike.org/user/HEIRS/article/6012655
Summary: "SLE occurs with an prevalence as high as 1 in 2,500 people but predominantly affects women (35). SLE is especially prevalent in women during their childbearing years (9:1 female to male ratio) and during pregnancy, suggesting a role of female hormones in development of the disease. Most mouse models of SLE also exhibit an increased susceptibility of females to the disease. The sex-specific decreases in glutathione S-transferase -1 and -2 and µ-1, -2, and -3 have been shown previously in the livers of nrf2 knockout mice (10) and are in agreement with our study (Table 3). The findings from this data and other reports strongly suggest that a deficiency in detoxification and increased oxidative stress can result in the development of a systemic autoimmune disease."
Li, J., Stein, T. D., and Johnson, J. A. (2004). Genetic dissection of systemic autoimmune disease in nrf2 deficient mice. Physiological Genomics, pages 1-57. http://www.citeulike.org/user/HEIRS/article/6012655
Military Research: New Studies Explore Connection between High Stress and High Exposure Jobs and GI Disorders
"In a six year study of World Trade Center workers, researchers probed the connection between the high frequencies of gastroesophageal reflux (GERD) and mental health disorders (MHD) reported among exposed workers during the post 9/11 cleanup. In a second study, researchers from the United States Navy examining functional gastrointestinal disorders (FGD) within the active military population and their connection to of infectious gastroenteritis (IGE) found not only a significant association between IGE and FGD, but also that almost 30% of those effected received care for two years after their initial diagnosis."
Quercetin can act either as an inhibitor or an inducer of the mitochondrial permeability transition pore: A demonstration of the ambivalent redox character of polyphenols.
"In swelling experiments with suspensions of mitochondria, high (20-50 microM) concentrations of quercetin, the most efficient inhibitor, promoted instead the onset of the MPT. Chelators of Fe(2+/3+) and Cu(+/2+) ions counteracted this effect. Fluorescent indicators of superoxide production confirmed that quercetin potentiates O(2)(*-) generation by isolated mitochondria and cultured cells. Since this was not affected by chelating Fe and Cu ions, the MPT-inducing effect can be ascribed to a "secondary", metal ion-catalyzed production of ROS."
De Marchi, U., Biasutto, L., Garbisa, S., Toninello, A., and Zoratti, M. (2009). Quercetin can act either as an inhibitor or an inducer of the mitochondrial permeability transition pore: A demonstration of the ambivalent redox character of polyphenols. Biochimica et biophysica acta, 1787(12):1425-1432. http://www.citeulike.org/user/HEIRS/article/5369424
De Marchi, U., Biasutto, L., Garbisa, S., Toninello, A., and Zoratti, M. (2009). Quercetin can act either as an inhibitor or an inducer of the mitochondrial permeability transition pore: A demonstration of the ambivalent redox character of polyphenols. Biochimica et biophysica acta, 1787(12):1425-1432. http://www.citeulike.org/user/HEIRS/article/5369424
Microbial induction of IBD Through Protein Expression By TLR Signaling
HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
Summary: A number of gram negative, gram positive and other anaerobes stimulate protein that contributes to IBD. This process is dependant on TLR signaling and can be inhibited by blocking the P38 pathway. In an earlier study showed that the levels of TL1A and number of cells that expressed it correlated with the level of inflammation, especially in Crohn's disease.
Title:Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells.
Shih, D. Q., Kwan, L. Y., Chavez, V., Cohavy, O., Gonsky, R., Chang, E. Y., Chang, C., Elson, C. O., and Targan, S. R. (2009). Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells. European Journal of Immunology, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/6009014
Bamias, G., Martin, C., Marini, M., Hoang, S., Mishina, M., Ross, W. G., Sachedina, M. A., Friel, C. M., Mize, J., Bickston, S. J., Pizarro, T. T., Wei, P., and Cominelli, F. (2003). Expression, localization, and functional activity of tl1a, a novel th1-polarizing cytokine in inflammatory bowel disease. Journal of immunology (Baltimore, Md. : 1950), 171(9):4868-4874. http://www.citeulike.org/user/HEIRS/article/6009138
Summary: A number of gram negative, gram positive and other anaerobes stimulate protein that contributes to IBD. This process is dependant on TLR signaling and can be inhibited by blocking the P38 pathway. In an earlier study showed that the levels of TL1A and number of cells that expressed it correlated with the level of inflammation, especially in Crohn's disease.
Title:Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells.
Shih, D. Q., Kwan, L. Y., Chavez, V., Cohavy, O., Gonsky, R., Chang, E. Y., Chang, C., Elson, C. O., and Targan, S. R. (2009). Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells. European Journal of Immunology, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/6009014
Bamias, G., Martin, C., Marini, M., Hoang, S., Mishina, M., Ross, W. G., Sachedina, M. A., Friel, C. M., Mize, J., Bickston, S. J., Pizarro, T. T., Wei, P., and Cominelli, F. (2003). Expression, localization, and functional activity of tl1a, a novel th1-polarizing cytokine in inflammatory bowel disease. Journal of immunology (Baltimore, Md. : 1950), 171(9):4868-4874. http://www.citeulike.org/user/HEIRS/article/6009138
Sunday, October 25, 2009
Endotoxins from Cyanobacteria and Gram-negative Bacteria as the Cause of an Acute Influenza-like Reaction after Inhalation of Aerosols
HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
Title: Endotoxins from Cyanobacteria and Gram-negative Bacteria as the Cause of an Acute Influenza-like Reaction after Inhalation of Aerosols.
Summary: "The syndrome with fever, malaise, muscle pains, tightness of the chest and respiratory-tract symptoms, also known as toxic pneumonitis, occurred 1.5–6 hours after taking a bath or shower. The outbreaks were associated with mass developments of cyanobacteria in the drinking water reservoirs. "
Citation: Annadotter, H., Cronberg, G., Nystrand, R., and Rylander, R. (2005). Endotoxins from cyanobacteria and gram-negative bacteria as the cause of an acute influenza-like reaction after inhalation of aerosols. EcoHealth, 2(3):209-221. http://www.citeulike.org/user/HEIRS/article/6007949
Title: Endotoxins from Cyanobacteria and Gram-negative Bacteria as the Cause of an Acute Influenza-like Reaction after Inhalation of Aerosols.
Summary: "The syndrome with fever, malaise, muscle pains, tightness of the chest and respiratory-tract symptoms, also known as toxic pneumonitis, occurred 1.5–6 hours after taking a bath or shower. The outbreaks were associated with mass developments of cyanobacteria in the drinking water reservoirs. "
Citation: Annadotter, H., Cronberg, G., Nystrand, R., and Rylander, R. (2005). Endotoxins from cyanobacteria and gram-negative bacteria as the cause of an acute influenza-like reaction after inhalation of aerosols. EcoHealth, 2(3):209-221. http://www.citeulike.org/user/HEIRS/article/6007949
Blunting the response to endotoxin in healthy subjects: effects of various doses of intravenous fish oil. Intensive care medicine.
HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
Pittet, Y. K., Berger, M. M., Pluess, T.-T. T., Voirol, P., Revelly, J.-P. P., Tappy, L., and Chioléro, R. L. (2009). Blunting the response to endotoxin in healthy subjects: effects of various doses of intravenous fish oil. Intensive care medicine. http://www.citeulike.org/user/HEIRS/article/6007905
Pittet, Y. K., Berger, M. M., Pluess, T.-T. T., Voirol, P., Revelly, J.-P. P., Tappy, L., and Chioléro, R. L. (2009). Blunting the response to endotoxin in healthy subjects: effects of various doses of intravenous fish oil. Intensive care medicine. http://www.citeulike.org/user/HEIRS/article/6007905
A conjugated linoleic acid-enriched beef diet attenuates lipopolysaccharide-induced inflammation in mice in part through ppargamma-mediated suppression of toll-like receptor 4
HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
Inflammatory mediators can reduce the expression of PPAR-gamma!
Reynolds, C. M., Draper, E., Keogh, B., Rahman, A., Moloney, A. P., Mills, K. H., Loscher, C. E., and Roche, H. M. (2009). A conjugated linoleic acid-enriched beef diet attenuates lipopolysaccharide-induced inflammation in mice in part through ppargamma-mediated suppression of toll-like receptor 4. The Journal of nutrition. http://www.citeulike.org/user/HEIRS/article/6007864
Inflammatory mediators can reduce the expression of PPAR-gamma!
Reynolds, C. M., Draper, E., Keogh, B., Rahman, A., Moloney, A. P., Mills, K. H., Loscher, C. E., and Roche, H. M. (2009). A conjugated linoleic acid-enriched beef diet attenuates lipopolysaccharide-induced inflammation in mice in part through ppargamma-mediated suppression of toll-like receptor 4. The Journal of nutrition. http://www.citeulike.org/user/HEIRS/article/6007864
Study: Potentiation of methamphetamine neurotoxicity by intrastriatal lipopolysaccharide administration
Title: Potentiation of methamphetamine neurotoxicity by intrastriatal lipopolysaccharide administration.
Summary: "neuroinflammation, oxidative stress, and pro-apoptotic changes in the striatum were more accentuated with combined treatment of LPS and MA compared to either treatment alone. In addition, it is important that cytoplasmic accumulation of alpha-synuclein was observed in the substantia nigra of mice treated with LPS plus MA, and that L-Dopa treatment significantly attenuated behavioral changes and dopaminergic deficits induced by LPS plus MA."
Jung, B. D. D., Shin, E.-J. J., Nguyen, X.-K. T. K., Jin, C.-H. H., Bach, J.-H. H., Park, S. J. J., Nah, S.-Y. Y., Wie, M.-B. B., Bing, G., and Kim, H.-C. C. (2009). Potentiation of methamphetamine neurotoxicity by intrastriatal lipopolysaccharide administration. Neurochemistry international. http://www.citeulike.org/user/HEIRS/article/6003313
Summary: "neuroinflammation, oxidative stress, and pro-apoptotic changes in the striatum were more accentuated with combined treatment of LPS and MA compared to either treatment alone. In addition, it is important that cytoplasmic accumulation of alpha-synuclein was observed in the substantia nigra of mice treated with LPS plus MA, and that L-Dopa treatment significantly attenuated behavioral changes and dopaminergic deficits induced by LPS plus MA."
Jung, B. D. D., Shin, E.-J. J., Nguyen, X.-K. T. K., Jin, C.-H. H., Bach, J.-H. H., Park, S. J. J., Nah, S.-Y. Y., Wie, M.-B. B., Bing, G., and Kim, H.-C. C. (2009). Potentiation of methamphetamine neurotoxicity by intrastriatal lipopolysaccharide administration. Neurochemistry international. http://www.citeulike.org/user/HEIRS/article/6003313
Saturday, October 24, 2009
Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
Toll-like receptors: are a class of proteins that play a key role in the innate immune system. (Wipedia)
Background: Binding to toll-like receptors may initiate inflammatory responses including the production of chemokines. They mainly signal through NF-kappaB and increase transcription of inflammatory proteins Il-1b, Tnf-a, CCL2 (MCP-1) etc. (Devaraj) These are receptors that are highly expressed and are considered to be a link between diet and metabolism and are implicated as important factors in a number of health conditions including lupus, atherosclerosis and diabetes. (Dasu) We have noted in other blogs that they may play an important role in conditions that are most often considered "environmental illnesses" including chronic fatigue syndrome and/or contribute to symptoms of chemical sensitivity. To put it simply, toll-like receptors are considered signal transducers that initiate inflammatory processes and two common ligands are LPS endotoxin (which has been implicated in CFS) and saturated fatty acids. The ligands that bind TLR contain a "molecular pattern" the TLR recognizes and may be present in microbial and non-microbial agents or may be responsive to signals generated at the site of inflammation or from endogenously-produced proteins like heat shock proteins. Thus, their activites become a concern when ever pathogenic exposure or inflammation may be present.
The distribution of the toll-like receptors is different in different tissues but include epithelia and endothelia in the intestinal tract, the respiratory tract, the blood-brain barrier, etc. It is now believed that there is a commensal relationship that exists between the gut microbiota and TLR to maintain gut integrity (Hopkins) and may involve epigenetic influences and down-regulation of TLR gene transcription. (Takahashi) It has been determined that TLR2 and TLR4 bind to gram positive and negative bacteria respectively. However, the production of one type of TL receptor may induce the induction of the other. Devaraj demonstrated that type-1 diabetes and increased levels of IL-1b and TNF-a is correlated with expression of TLR and also endotoxin "contribute to the inflammatory burden by activating TLR receptors" and suggests their instrumental in diabetes pathology. In addition, it has also been determined that high glucose levels can stimulate the expression of these receptors in monocytes. While toll-like cells are involved in cytokine production and cell activation, the inflammatory responses initiated by activation of receptors may last long after the initial stimulus is gone or may potentiate the inflammatory responses of other insults. It may seem beneficial to blunt the responses of TLR, but it may be more harmful by making the organism more susceptible to infection.(Hopkins) On the other hand, aberrant signaling from TLR can lead to autoimmune-type conditions as we noted above.
Other studies demonstrate that the expression of TLR are widespread are can activate microglia and astocytes and play a role in neuroinflammatory responses. Microglia are sensory-type cells that are the main source of inflammatory mediators in the nervous system. Some studies show that TLR activation of microglia leads to an increase in NO, superoxide and other cytokines and that TLR-deficient microglia demonstrated a significant reduction in several types of inflammatory responses. Obata confirmed TLR3 has an important role in the development of tactile allodynia after nerve injury and blocking these receptors may provide effective treatment for neuropathic pain which has been linked to fibromyalgia. Recent findings are suggestive of the notion that fibromyalgia is a "disorder of central processing with neuroregulation/
transmission dysfunction" (NFA) and TLR4 may initiate an inflammatory profile through NF-kappaB at least in a subset of fibromyalgia patients. In one model of neuropathic pain, tactile allodynia was "abrogated" in CCR2 mice which is the receptor for CCL2 (MCP-1), the inflammatory cytokines activated by NF-kappaB and has been suggested as a possible marker for fibromyalgia. It also plays a very important role in the development of neuroinflammation via the TNF-a/CCL2/CCR2 pathway. From this, it has been suggested that activation of immune cells and microglia peripherally and in neurons may contribute to inflammatory and neuropathic pain states and (Abbadie) importantly, it is now understood that TLR agonists modulates CCR2 expression and CCL2 responsiveness. (Souto, Parker) Jo et al explains peripheral injuries that lead to neuropathic states causes pathology not only in the damaged nerves but also causes changes in the central processing of sensory information and glial activation may facilitate "noxious signal transduction" even after the initial injury has healed. Therefore, TLR may not only initiate neuropathic pain but also maintain it. Experts believe nociceptive behavior may influence symptoms of MCS (Pall) and it has been demonstrated pain caused by bacterial infection may be generated through activation of nociceptors via the TLR in neurons. (Wabachi) In addition, TLR responses play a role in viral and parasitic infections, multiple sclerosis, exacerbate injury in ischemia (Kielian) and chronic activation of TLR is associated with anxiety, avoidance and sickness behavior (Hudson) and increased sensitivity to other toxicants (Pestka).
Other reports show in epithelial cells, TLR mediate immune cells production from exposure to particulate matter and contribute to airway hypersensitivity from exposure to ozone. (Williams) More recently, it has been shown that the aryl hydrocarbon receptor (AhR), which plays a role in the detoxification of polyaromatic hydrocarbons and halogenated hydrocarbons, negatively regulates TLR signaling. Animals that are deficient in the AhR exhibit exaggerated inflammatory responses including significant elevations in TNF-a and IL-6 and are highly susceptible to septic shock. (Ogawa, Kimura) We have expressed the belief that the abnormal functioning of the AhR may contribute to environmental illnesses including multiple chemical sensitivity because of its role in detoxification and its relationship to the antioxidant system regulator Nrf2. The Nrf2 protects neurons and other cells against oxidative and environmental insults in primary and secondary injury. TLR activates NF-kappaB through the universale adaptor protein MyD88 and it has been shown that Nrf2 has a "global influence" on MyD88-dependant and independant signaling. Deficiency of Nrf2 dysregulated expression of genes that encode molecular components of innate immunity (e.g., peptidoglycan-recognition proteins, proinflammatory cytokines, chemokines, and adhesion molecules and receptors." (Thimmulappa)
Study Highlight: Pestka provides evidence that the preexposure of a TLR agonist such as LPS endotoxin increases the inflammatory response of DON, a mycotoxin. This response which included production of IL-1b, Il-6, and TNF-a was at levels higher than either produced alone. During the study, preexposure to other TLR agonists, also increased the pro-inflammatory responses of DON in a similar manner as LPS. In addition, similar heightened responses occured from LPS preexposure of TLR and subsequent effects of microbial and non-microbial "agents" including satratoxin, Shiga toxin, zearalenone and toxicants such as nickel chloride, triphenyltin, dinitrochlorobenzene (a known irritant) and dioxin. It has been concluded from this study that prior exposure to TLR agonists (ie endotoxin, saturated fat and others) "might render macrophages highly sensitive to subsequent induction of proinflammatory gene expression by xenobiotics with diverse mechanisms of action." (Pestka)
Notes:
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Original document and citations can be accessed here.
Background: Binding to toll-like receptors may initiate inflammatory responses including the production of chemokines. They mainly signal through NF-kappaB and increase transcription of inflammatory proteins Il-1b, Tnf-a, CCL2 (MCP-1) etc. (Devaraj) These are receptors that are highly expressed and are considered to be a link between diet and metabolism and are implicated as important factors in a number of health conditions including lupus, atherosclerosis and diabetes. (Dasu) We have noted in other blogs that they may play an important role in conditions that are most often considered "environmental illnesses" including chronic fatigue syndrome and/or contribute to symptoms of chemical sensitivity. To put it simply, toll-like receptors are considered signal transducers that initiate inflammatory processes and two common ligands are LPS endotoxin (which has been implicated in CFS) and saturated fatty acids. The ligands that bind TLR contain a "molecular pattern" the TLR recognizes and may be present in microbial and non-microbial agents or may be responsive to signals generated at the site of inflammation or from endogenously-produced proteins like heat shock proteins. Thus, their activites become a concern when ever pathogenic exposure or inflammation may be present.
The distribution of the toll-like receptors is different in different tissues but include epithelia and endothelia in the intestinal tract, the respiratory tract, the blood-brain barrier, etc. It is now believed that there is a commensal relationship that exists between the gut microbiota and TLR to maintain gut integrity (Hopkins) and may involve epigenetic influences and down-regulation of TLR gene transcription. (Takahashi) It has been determined that TLR2 and TLR4 bind to gram positive and negative bacteria respectively. However, the production of one type of TL receptor may induce the induction of the other. Devaraj demonstrated that type-1 diabetes and increased levels of IL-1b and TNF-a is correlated with expression of TLR and also endotoxin "contribute to the inflammatory burden by activating TLR receptors" and suggests their instrumental in diabetes pathology. In addition, it has also been determined that high glucose levels can stimulate the expression of these receptors in monocytes. While toll-like cells are involved in cytokine production and cell activation, the inflammatory responses initiated by activation of receptors may last long after the initial stimulus is gone or may potentiate the inflammatory responses of other insults. It may seem beneficial to blunt the responses of TLR, but it may be more harmful by making the organism more susceptible to infection.(Hopkins) On the other hand, aberrant signaling from TLR can lead to autoimmune-type conditions as we noted above.
Other studies demonstrate that the expression of TLR are widespread are can activate microglia and astocytes and play a role in neuroinflammatory responses. Microglia are sensory-type cells that are the main source of inflammatory mediators in the nervous system. Some studies show that TLR activation of microglia leads to an increase in NO, superoxide and other cytokines and that TLR-deficient microglia demonstrated a significant reduction in several types of inflammatory responses. Obata confirmed TLR3 has an important role in the development of tactile allodynia after nerve injury and blocking these receptors may provide effective treatment for neuropathic pain which has been linked to fibromyalgia. Recent findings are suggestive of the notion that fibromyalgia is a "disorder of central processing with neuroregulation/
transmission dysfunction" (NFA) and TLR4 may initiate an inflammatory profile through NF-kappaB at least in a subset of fibromyalgia patients. In one model of neuropathic pain, tactile allodynia was "abrogated" in CCR2 mice which is the receptor for CCL2 (MCP-1), the inflammatory cytokines activated by NF-kappaB and has been suggested as a possible marker for fibromyalgia. It also plays a very important role in the development of neuroinflammation via the TNF-a/CCL2/CCR2 pathway. From this, it has been suggested that activation of immune cells and microglia peripherally and in neurons may contribute to inflammatory and neuropathic pain states and (Abbadie) importantly, it is now understood that TLR agonists modulates CCR2 expression and CCL2 responsiveness. (Souto, Parker) Jo et al explains peripheral injuries that lead to neuropathic states causes pathology not only in the damaged nerves but also causes changes in the central processing of sensory information and glial activation may facilitate "noxious signal transduction" even after the initial injury has healed. Therefore, TLR may not only initiate neuropathic pain but also maintain it. Experts believe nociceptive behavior may influence symptoms of MCS (Pall) and it has been demonstrated pain caused by bacterial infection may be generated through activation of nociceptors via the TLR in neurons. (Wabachi) In addition, TLR responses play a role in viral and parasitic infections, multiple sclerosis, exacerbate injury in ischemia (Kielian) and chronic activation of TLR is associated with anxiety, avoidance and sickness behavior (Hudson) and increased sensitivity to other toxicants (Pestka).
Other reports show in epithelial cells, TLR mediate immune cells production from exposure to particulate matter and contribute to airway hypersensitivity from exposure to ozone. (Williams) More recently, it has been shown that the aryl hydrocarbon receptor (AhR), which plays a role in the detoxification of polyaromatic hydrocarbons and halogenated hydrocarbons, negatively regulates TLR signaling. Animals that are deficient in the AhR exhibit exaggerated inflammatory responses including significant elevations in TNF-a and IL-6 and are highly susceptible to septic shock. (Ogawa, Kimura) We have expressed the belief that the abnormal functioning of the AhR may contribute to environmental illnesses including multiple chemical sensitivity because of its role in detoxification and its relationship to the antioxidant system regulator Nrf2. The Nrf2 protects neurons and other cells against oxidative and environmental insults in primary and secondary injury. TLR activates NF-kappaB through the universale adaptor protein MyD88 and it has been shown that Nrf2 has a "global influence" on MyD88-dependant and independant signaling. Deficiency of Nrf2 dysregulated expression of genes that encode molecular components of innate immunity (e.g., peptidoglycan-recognition proteins, proinflammatory cytokines, chemokines, and adhesion molecules and receptors." (Thimmulappa)
Study Highlight: Pestka provides evidence that the preexposure of a TLR agonist such as LPS endotoxin increases the inflammatory response of DON, a mycotoxin. This response which included production of IL-1b, Il-6, and TNF-a was at levels higher than either produced alone. During the study, preexposure to other TLR agonists, also increased the pro-inflammatory responses of DON in a similar manner as LPS. In addition, similar heightened responses occured from LPS preexposure of TLR and subsequent effects of microbial and non-microbial "agents" including satratoxin, Shiga toxin, zearalenone and toxicants such as nickel chloride, triphenyltin, dinitrochlorobenzene (a known irritant) and dioxin. It has been concluded from this study that prior exposure to TLR agonists (ie endotoxin, saturated fat and others) "might render macrophages highly sensitive to subsequent induction of proinflammatory gene expression by xenobiotics with diverse mechanisms of action." (Pestka)
Notes:
- An important source of bacterial and endotoxin contamination is from our drinking water. Find out more about the importance of healthy water with a clip from the Dr. Oz Show. Other main sources include from the air we breath.
- IRAK-1 is necessary for LPS-mediated suppression of PPARalpha and PGC-1alpha, nuclear factors essential for the expression of anti-oxidative enzymes such as GPX3 and catalase (Maitra) "ROS trafficking(NADPH oxidase) mediates LPS/TLR signals in neutraphils and downstream targets including IRAK-1. Deficiency of Nrf2 predisposes neutraphils to greater responsiveness to LPS which is mediated by increased ROS generation. (Thimmulappa)
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Stable COPD patients with hypersensitive cough reflex at risk for exacerbations
Stable chronic obstructive pulmonary disease patients with a hypersensitive cough reflex in response to inhaled capsaicin have increased serum C-reactive protein levels and an increased frequency of subsequent exacerbations, research shows. Click here.
Boys with urogenital birth defects are 33 percent more common in villages sprayed with DDT
Women who lived in villages sprayed with DDT to reduce malaria gave birth to 33% more baby boys born with urogenital defects between 2004 and 2006....click here to read more.
Asthma and genes encoding components of the vitamin D pathway
Genetic variants at the vitamin D receptor (VDR) locus are associated with asthma and atopy. We hypothesized that polymorphisms in other genes of the vitamin D pathway are associated with asthma or atopy.
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Scientists link fat hormone to death from potentially deadly blood infection
Scientists link fat hormone to death from potentially deadly blood infection
A new Canadian study has found that lower-than-normal levels of a naturally-occurring fat hormone may increase the risk of death from sepsis—an overwhelming infection of the blood which claims thousands of lives each year.
A new Canadian study has found that lower-than-normal levels of a naturally-occurring fat hormone may increase the risk of death from sepsis—an overwhelming infection of the blood which claims thousands of lives each year.
Friday, October 23, 2009
PON-1 dysregulation in obesity linked to reduced cellular repair, protection
Title: PON-1 dysregulation in obesity linked to reduced cellular repair, protection.
Summary: "evaluation of PON1 activity in obesity and in other diseases associated with alterations of lipid metabolism could therefore represent a useful approach to study the effect of drugs used in the therapy and to determine whether weight reduction, diet, and nutritional approaches affect endogenous antioxidant capabilities."
Citation: Lyford, J. (2009). Pon-1 dysregulation in obesity linked to reduced cellular repair, protection. http://www.citeulike.org/user/HEIRS/article/5998953
Summary: "evaluation of PON1 activity in obesity and in other diseases associated with alterations of lipid metabolism could therefore represent a useful approach to study the effect of drugs used in the therapy and to determine whether weight reduction, diet, and nutritional approaches affect endogenous antioxidant capabilities."
Citation: Lyford, J. (2009). Pon-1 dysregulation in obesity linked to reduced cellular repair, protection. http://www.citeulike.org/user/HEIRS/article/5998953
Inflammation and Alterations in Fat Cells By Pesticide Alterations of Anti-inflammatory Protein Genes!
Background: Some experts believe that changes in gene expression may be a consequence of certain chemical exposures. Researchers are now focusing a lot of attention on the effects of these exposures on adipocytes which can produce inflammatory chemokines which may generate inflammation. It has been observed that some types of exposures are associated with obesity which is a risk factor for diabetes while, others can lead to weight reduction. Arsenescu demonstrated toxic exposures can stimulate and increase expansion of adipose tissue and other studies show alterations in the process of differentiation of preadipoctyes into adipocytes. In 2008, a preliminary study suggested endothelial dysfunction contributes to fat cell development because adipose stromal cells are in close contact with endothelial cells of capillaries and small blood vessels. (ScienceDaily) Long-term high serum levels of dioxin has been shown to contribute to endothelial dysfunction which provides a possible mechanism for the association of certain exposures to endothelial dysfunction, obesity and a higher risk for diabetes. (Peclova)
In the past, obesity has been characterized by differentiation of preadipocytes to adipocytes and involves the coordinated responses of a number of proteins with fatty acids that leads to increases of the size of fat cells.(Uto-Kondo) However, a recent study suggests that in in the case of abdominal obesity which may have more severe long-term health effects, there is impairment of the ability for preadipocytes to differentiate into adipocytes. Irakson says that "inhibition of this type can lead to a proinflammatory state and macrophage-like phenotype and as Hou explains "elevated levels of TNF-a or Il-1b in inflammatory tissues prolongs the survival of these immune cells and lengthens the durations they remain in an inflammatory state."
In one study, eldrin causes inhibition of a binding protein and interfered with expression of the anti-inflammatory protein PPAR-gamma and altered the expression of NF-kappaB which usually decreases as adipocytes differentiate. (Moreno-Aliego) We have suggested that the aberrant signaling from the AhR, which normally is important for cellular homeostasis and contributes to detoxification of PAHs and HAHS, may be an important factor in MCS. Hanlon et el notes that activation of the AhR by dioxin blocks hormone-induced adipocyte differentiation through the suppression of PPAR-gamma. The presence of inflammatory mediators are also associated with insulin resistance which can further impair normal cell function and reductions in the expression of Nrf2 may further complicate it. Chronic inflammation have been suggested as a causal factor in environmental illnesses including obesity and diabetes. One study shows proteins associated with cell death are less efficient in diffentiated adipocytes than in undifferentiated cells when introduced to a reactive species stimulus. Kojima confirmed an increase in antioxidants including MnSOD, catalase, Cu/ZnSOD as well as, FOXO with the the progression of adipocyte differentiation. From this study, it has been concluded that ROS-generated apoptosis is associated with the expression of FOXO3a in undifferentiated adipocytes and FOXO expression suppresses ROS-apoptosis through activation of scavenging enzymes in differentiated ones. With this study in mind and considering that uncontrolled production of ROS contribute to cellular processes that cause inflammation, preventing differentiation of adipocytes may have negative consequences in certain cases.
Kojima, T., Norose, T., Tsuchiya, K., and Sakamoto, K. Mouse 3t3-l1 cells acquire resistance against oxidative stress as the adipocytes differentiate via the transcription factor foxo. Apoptosis. http://www.citeulike.org/user/HEIRS/article/5998696
Isakson, P., Hammarstedt, A., Gustafson, B., and Smith, U. (2009). Impaired preadipocyte differentiation in human abdominal obesity. Diabetes, 58(7):1550-1557. http://www.citeulike.org/user/HEIRS/article/5017576
Hou, F. F., Boyce, J., Zhang, Y., and Owen, W. F. (2000). Phenotypic and functional characteristics of macrophage-like cells differentiated in pro-inflammatory cytokine-containing cultures. Immunology and cell biology, 78(3):205-213. http://www.citeulike.org/user/HEIRS/article/5998701
Hanlon, P. (2003). Ahr- and erk-dependent pathways function synergistically to mediate 2,3,7,8-tetrachlorodibenzo-p-dioxin suppression of peroxisome proliferator-activated receptor-γ1 expression and subsequent adipocyte differentiation. Toxicology and Applied Pharmacology, 189(1):11-27. http://www.citeulike.org/user/HEIRS/article/5778106
Moreno-Aliaga, M. J. and Matsumura, F. (1999). Endrin inhibits adipocyte differentiation by selectively altering expression pattern of ccaat/enhancer binding protein-alpha in 3t3-l1 cells. Mol Pharmacol, 56(1):91-101. http://www.citeulike.org/user/HEIRS/article/5998840
Uto-Kondo, H., Ohmori, R., Kiyose, C., Kishimoto, Y., Saito, H., Igarashi, O., and Kondo, K. (2009). Tocotrienol suppresses adipocyte differentiation and akt phosphorylation in 3t3-l1 preadipocytes. J. Nutr., 139(1):51-57. http://www.citeulike.org/user/HEIRS/article/5998926
Healthy Blood Vessels May Prevent Fat Growth. ScienceDaily. September 23, 2008.
Pelclová, D., Prázny, M., Skrha, J., Fenclová, Z., Kalousová, M., Urban, P., Navrátil, T., Senholdová, Z., and Smerhovsky, Z. (2007). 2,3,7,8-tcdd exposure, endothelial dysfunction and impaired microvascular reactivity. Human & experimental toxicology, 26(9):705-713. http://www.citeulike.org/group/7254/article/6000451
In the past, obesity has been characterized by differentiation of preadipocytes to adipocytes and involves the coordinated responses of a number of proteins with fatty acids that leads to increases of the size of fat cells.(Uto-Kondo) However, a recent study suggests that in in the case of abdominal obesity which may have more severe long-term health effects, there is impairment of the ability for preadipocytes to differentiate into adipocytes. Irakson says that "inhibition of this type can lead to a proinflammatory state and macrophage-like phenotype and as Hou explains "elevated levels of TNF-a or Il-1b in inflammatory tissues prolongs the survival of these immune cells and lengthens the durations they remain in an inflammatory state."
In one study, eldrin causes inhibition of a binding protein and interfered with expression of the anti-inflammatory protein PPAR-gamma and altered the expression of NF-kappaB which usually decreases as adipocytes differentiate. (Moreno-Aliego) We have suggested that the aberrant signaling from the AhR, which normally is important for cellular homeostasis and contributes to detoxification of PAHs and HAHS, may be an important factor in MCS. Hanlon et el notes that activation of the AhR by dioxin blocks hormone-induced adipocyte differentiation through the suppression of PPAR-gamma. The presence of inflammatory mediators are also associated with insulin resistance which can further impair normal cell function and reductions in the expression of Nrf2 may further complicate it. Chronic inflammation have been suggested as a causal factor in environmental illnesses including obesity and diabetes. One study shows proteins associated with cell death are less efficient in diffentiated adipocytes than in undifferentiated cells when introduced to a reactive species stimulus. Kojima confirmed an increase in antioxidants including MnSOD, catalase, Cu/ZnSOD as well as, FOXO with the the progression of adipocyte differentiation. From this study, it has been concluded that ROS-generated apoptosis is associated with the expression of FOXO3a in undifferentiated adipocytes and FOXO expression suppresses ROS-apoptosis through activation of scavenging enzymes in differentiated ones. With this study in mind and considering that uncontrolled production of ROS contribute to cellular processes that cause inflammation, preventing differentiation of adipocytes may have negative consequences in certain cases.
Kojima, T., Norose, T., Tsuchiya, K., and Sakamoto, K. Mouse 3t3-l1 cells acquire resistance against oxidative stress as the adipocytes differentiate via the transcription factor foxo. Apoptosis. http://www.citeulike.org/user/HEIRS/article/5998696
Isakson, P., Hammarstedt, A., Gustafson, B., and Smith, U. (2009). Impaired preadipocyte differentiation in human abdominal obesity. Diabetes, 58(7):1550-1557. http://www.citeulike.org/user/HEIRS/article/5017576
Hou, F. F., Boyce, J., Zhang, Y., and Owen, W. F. (2000). Phenotypic and functional characteristics of macrophage-like cells differentiated in pro-inflammatory cytokine-containing cultures. Immunology and cell biology, 78(3):205-213. http://www.citeulike.org/user/HEIRS/article/5998701
Hanlon, P. (2003). Ahr- and erk-dependent pathways function synergistically to mediate 2,3,7,8-tetrachlorodibenzo-p-dioxin suppression of peroxisome proliferator-activated receptor-γ1 expression and subsequent adipocyte differentiation. Toxicology and Applied Pharmacology, 189(1):11-27. http://www.citeulike.org/user/HEIRS/article/5778106
Moreno-Aliaga, M. J. and Matsumura, F. (1999). Endrin inhibits adipocyte differentiation by selectively altering expression pattern of ccaat/enhancer binding protein-alpha in 3t3-l1 cells. Mol Pharmacol, 56(1):91-101. http://www.citeulike.org/user/HEIRS/article/5998840
Uto-Kondo, H., Ohmori, R., Kiyose, C., Kishimoto, Y., Saito, H., Igarashi, O., and Kondo, K. (2009). Tocotrienol suppresses adipocyte differentiation and akt phosphorylation in 3t3-l1 preadipocytes. J. Nutr., 139(1):51-57. http://www.citeulike.org/user/HEIRS/article/5998926
Healthy Blood Vessels May Prevent Fat Growth. ScienceDaily. September 23, 2008.
Pelclová, D., Prázny, M., Skrha, J., Fenclová, Z., Kalousová, M., Urban, P., Navrátil, T., Senholdová, Z., and Smerhovsky, Z. (2007). 2,3,7,8-tcdd exposure, endothelial dysfunction and impaired microvascular reactivity. Human & experimental toxicology, 26(9):705-713. http://www.citeulike.org/group/7254/article/6000451
Dura Coat Products, Inc., Joins EPA’s National Partnership for Environmental Priorities
Company commits to reducing lead chromate and polycyclic aromatic compounds from paint formulations. Click here.
Fibromyalgia pain severity not linked to psychological symptoms
"A new study finds that the pain of fibromyalgia is linked to reduced activity in the areas of the brain that inhibit sensation and dispells the myth that the illness and severity of pain reported is linked to psychological causes." According to researcher, "we've made careful measurements and have found no correlation at all between pain sensitivity in fibromyalgia patients and the degree of anxiety or depression they show." Click here to read more.
Thursday, October 22, 2009
Phytochemicals Help To Reduce Oxidative Stress, Inflammation,Obesity and Diabetes
"The cheeseburger and French fries might look tempting, but eating a serving of broccoli or leafy greens first could help people battle metabolic processes that lead to obesity and heart disease, a new University of Florida study shows." Click here.
Pesticides exposure linked to suicidal thoughts
A new study in China has found that people with higher levels of pesticide exposure are more likely to have suicidal thoughts. The study was carried out by Dr. Robert Stewart from the Institute of Psychiatry at King's College London together with scientists from Tongde Hospital Zhejiang Province.
Pesticides exposure linked to suicidal thoughts. Click here.
Pesticides exposure linked to suicidal thoughts. Click here.
Manipulating brain inflammation may help clear brain of amyloid plaques, Mayo Clinic researchers say
"In a surprising reversal of long-standing scientific belief, researchers at the Mayo Clinic campus in Florida have discovered that inflammation in the brain is not the trigger that leads to buildup of amyloid deposits and development of Alzheimer's disease."
Manipulating brain inflammation may help clear brain of amyloid plaques, Mayo Clinic researchers say
Manipulating brain inflammation may help clear brain of amyloid plaques, Mayo Clinic researchers say
Caffeine Activates AMPK and Increases Glucose Transport in Skeletal Muscle
Title: Caffeine acutely activates 5′adenosine monophosphate–activated protein kinase and increases insulin-independent glucose transport in rat skeletal muscles.
Summary: These results suggest that caffeine has similar actions to exercise by acutely stimulating skeletal muscle AMPK activity and insulin-independent glucose transport with a reduction of the intracellular energy status.
Agawaa, T., Hamadab, T., Kamedac, N., Karaikea, K., Maa, X., Masudaa, S., Iwanakaa, N., and Hayash, T. (2009). Caffeine acutely activates 5′adenosine monophosphate–activated protein kinase and increases insulin-independent glucose transport in rat skeletal muscles. Metabolism Clinical and Experimental, 58(11):1609-1617. http://www.citeulike.org/user/HEIRS/article/5989180
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Wednesday, October 21, 2009
Tuesday, October 20, 2009
Mercury Levels In Children With Autism And Those Developing Typically Are The Same, Study Finds
Mercury Levels In Children With Autism And Those Developing Typically Are The Same, Study Finds
ScienceDaily (2009-10-20) -- In a large population-based study, researchers report that after adjusting for a number of factors, typically developing children and children with autism have similar levels of mercury in their blood streams. ... > read full article
Monday, October 19, 2009
Hypersensitivity of ahr-deficient mice to lps-induced septic shock
Background: Recent studies suggest endotoxin may be a pathway to chronic fatigue syndrome and the associated inflammtory processes associated with it may contribute to a number of other acute, chronic and environmental diseases as well.
Title: Hypersensitivity of ahr-deficient mice to lps-induced septic shock.
Summary: This study suggests that absence of AhR expression results in increased expression of Il-1b and are hypersensitive to shock after exposure to LPS endotoxin.
Citation: Sekine, H., Mimura, J., Oshima, M., Okawa, H., Kanno, J., Igarashi, K., Gonzalez, F. J., Ikuta, T., Kawajiri, K., and Fujii-Kuriyama, Y. (2009). Hypersensitivity of ahr-deficient mice to lps-induced septic shock. Molecular and cellular biology. http://www.citeulike.org/user/HEIRS/article/5971045
Title: Hypersensitivity of ahr-deficient mice to lps-induced septic shock.
Summary: This study suggests that absence of AhR expression results in increased expression of Il-1b and are hypersensitive to shock after exposure to LPS endotoxin.
Citation: Sekine, H., Mimura, J., Oshima, M., Okawa, H., Kanno, J., Igarashi, K., Gonzalez, F. J., Ikuta, T., Kawajiri, K., and Fujii-Kuriyama, Y. (2009). Hypersensitivity of ahr-deficient mice to lps-induced septic shock. Molecular and cellular biology. http://www.citeulike.org/user/HEIRS/article/5971045
Sunday, October 18, 2009
New study identifies cellular mechanism that causes lupuslike symptoms in mice
New study identifies cellular mechanism that causes lupuslike symptoms in mice
Macrophages, the scavenger cells of the body's immune system, are responsible for disposing of dying cells. Stanford University School of Medicine researchers have identified one pathway in this important process in mice that, if disrupted, causes a lupuslike autoimmune disease.
Saturday, October 17, 2009
MDA, NO and endotoxin associated with circulatory changes in cirrhotic livers
Title: Increased plasma malondialdehyde in patients with viral cirrhosis and its relationships to plasma nitric oxide, endotoxin, and portal pressure.
Summary: "strongest factors to predict HVPG, WHVP, and HSR are plasma levels of NOx, MDA, and endotoxin, respectively. Conclusion "
Citation: Lee, K.-C., Yang, Y.-Y., Wang, Y.-W., Lee, F.-Y., Loong, C.-C., Hou, M.-C., Lin, H.-C., and Lee, S.-D. Increased plasma malondialdehyde in patients with viral cirrhosis and its relationships to plasma nitric oxide, endotoxin, and portal pressure. Digestive Diseases and Sciences.
Summary: "strongest factors to predict HVPG, WHVP, and HSR are plasma levels of NOx, MDA, and endotoxin, respectively. Conclusion "
Citation: Lee, K.-C., Yang, Y.-Y., Wang, Y.-W., Lee, F.-Y., Loong, C.-C., Hou, M.-C., Lin, H.-C., and Lee, S.-D. Increased plasma malondialdehyde in patients with viral cirrhosis and its relationships to plasma nitric oxide, endotoxin, and portal pressure. Digestive Diseases and Sciences.
Friday, October 16, 2009
Estrogen May Make Women Prone To Autoimmune-type Il-1b Inflammatory Conditions
Title: Alternatively activated macrophages in infection and autoimmunity.
Summary: "Women may be at an increased risk of M2-mediated infection and autoimmunity due to estrogen's ability to increase Th2 responses."
Citation: Fairweather, D. and Cihakova, D. (2009). Alternatively activated macrophages in infection and autoimmunity. Journal of autoimmunity. http://www.citeulike.org/user/HEIRS/article/5948117
Summary: "Women may be at an increased risk of M2-mediated infection and autoimmunity due to estrogen's ability to increase Th2 responses."
Citation: Fairweather, D. and Cihakova, D. (2009). Alternatively activated macrophages in infection and autoimmunity. Journal of autoimmunity. http://www.citeulike.org/user/HEIRS/article/5948117
Title: Association of variation in the interleukin-1 gene family with diabetes and glucose homeostasis. The Journal of clinical endocrinology and metabolism.
Summary: Specific haplotypes of Il-1b are associated with higher glucose, higher insulin resistance. higher insulin and increased prevalence of diabetes.
Citation: Luotola, K., Pääkkönen, R., Alanne, M., Lanki, T., Moilanen, L., Surakka, I., Pietilä, A., Kähönen, M., Nieminen, M. S., Kesäniemi, Y. A., Peters, A., Jula, A., Perola, M., Salomaa, V., and for the Health 2000 and AIRGENE Study Groups (2009). Association of variation in the interleukin-1 gene family with diabetes and glucose homeostasis. The Journal of clinical endocrinology and metabolism. http://www.citeulike.org/user/HEIRS/article/5938589
Summary: Specific haplotypes of Il-1b are associated with higher glucose, higher insulin resistance. higher insulin and increased prevalence of diabetes.
Citation: Luotola, K., Pääkkönen, R., Alanne, M., Lanki, T., Moilanen, L., Surakka, I., Pietilä, A., Kähönen, M., Nieminen, M. S., Kesäniemi, Y. A., Peters, A., Jula, A., Perola, M., Salomaa, V., and for the Health 2000 and AIRGENE Study Groups (2009). Association of variation in the interleukin-1 gene family with diabetes and glucose homeostasis. The Journal of clinical endocrinology and metabolism. http://www.citeulike.org/user/HEIRS/article/5938589
Nuerotoxicity, Noradrenaline and Il-1
Title:
Summary: "In parallel with its ability to increase IL-1ra and IL-1RII, noradrenaline prevented neurotoxicity in cortical primary neurons induced by conditioned medium from IL-1beta treated mixed glial cells. These data indicate that noradrenaline negatively regulates IL-1 system in glial cells and has neuroprotective properties in situations where IL-1 contributes to pathology."
Citation: McNamee, E. N., Ryan, K. M., Kilroy, D., and Connor, T. J. (2009). Noradrenaline induces il-1ra and il-1 type ii receptor expressions in primary glial cells and protects against il-1beta-induced neurotoxicity. European journal of pharmacology. http://www.citeulike.org/user/HEIRS/article/5923308
Summary: "In parallel with its ability to increase IL-1ra and IL-1RII, noradrenaline prevented neurotoxicity in cortical primary neurons induced by conditioned medium from IL-1beta treated mixed glial cells. These data indicate that noradrenaline negatively regulates IL-1 system in glial cells and has neuroprotective properties in situations where IL-1 contributes to pathology."
Citation: McNamee, E. N., Ryan, K. M., Kilroy, D., and Connor, T. J. (2009). Noradrenaline induces il-1ra and il-1 type ii receptor expressions in primary glial cells and protects against il-1beta-induced neurotoxicity. European journal of pharmacology. http://www.citeulike.org/user/HEIRS/article/5923308
Fats Interact With Immune Complex to Activate Inflammation -May Aggravate Autoimmune and Pathogen Infection
HEIRS Environmental Illness Research Blog: Infection/Endotoxin in Chronic Fatigue, Fibromyalgia and Multiple Chemical Sensitivity.
The interaction between toll-like receptors and fatty acids "engage" the immune complex Il-1b and its receptor to activate other inflammatory processes in the pancreas.
Böni-Schnetzler, M., Boller, S., Debray, S., Bouzakri, K., Meier, D. T., Prazak, R., Kerr-Conte, J., Pattou, F., Ehses, J. A., Schuit, F. C., and Donath, M. Y. (2009). Free fatty acids induce a proinflammatory response in islets via the abundantly expressed interleukin-1 receptor i. Endocrinology, pages en.2009-0543+. http://www.citeulike.org/user/HEIRS/article/5922922
The interaction between toll-like receptors and fatty acids "engage" the immune complex Il-1b and its receptor to activate other inflammatory processes in the pancreas.
Böni-Schnetzler, M., Boller, S., Debray, S., Bouzakri, K., Meier, D. T., Prazak, R., Kerr-Conte, J., Pattou, F., Ehses, J. A., Schuit, F. C., and Donath, M. Y. (2009). Free fatty acids induce a proinflammatory response in islets via the abundantly expressed interleukin-1 receptor i. Endocrinology, pages en.2009-0543+. http://www.citeulike.org/user/HEIRS/article/5922922
Copper and Magnetic Bracelets 'Useless' in Pain and Stiffness of Arthritis
Copper bracelets and magnetic wrist straps are useless for relieving pain in people with arthritis, say University of York researchers. Click here...
Study: What Makes Patients With Fibromyalgia Feel Better?
Title: What makes patients with fibromyalgia feel better? correlations between patient global impression of improvement and changes in clinical symptoms and function: A pooled analysis of 4 randomized placebo-controlled trials of duloxetine.
Summary: Factors that may make a patient with fibromyalgia feel better determined by the results of this study include reductions in pain, reduced fatigue, physical functioning, better mood and improved quality of life.
Citation: Hudson, J. I., Arnold, L. M., Bradley, L. A., Choy, E. H. S., Mease, P. J., Wang, F., Ahl, J., and Wohlreich, M. M. (2009). What makes patients with fibromyalgia feel better? correlations between patient global impression of improvement and changes in clinical symptoms and function: A pooled analysis of 4 randomized placebo-controlled trials of duloxetine. The Journal of Rheumatology, 36(10). http://www.citeulike.org/user/HEIRS/article/5952226
Summary: Factors that may make a patient with fibromyalgia feel better determined by the results of this study include reductions in pain, reduced fatigue, physical functioning, better mood and improved quality of life.
Citation: Hudson, J. I., Arnold, L. M., Bradley, L. A., Choy, E. H. S., Mease, P. J., Wang, F., Ahl, J., and Wohlreich, M. M. (2009). What makes patients with fibromyalgia feel better? correlations between patient global impression of improvement and changes in clinical symptoms and function: A pooled analysis of 4 randomized placebo-controlled trials of duloxetine. The Journal of Rheumatology, 36(10). http://www.citeulike.org/user/HEIRS/article/5952226
Low waking and Secretion of Cortisol Associated with the Presence and Genesis of Fatigue.
New study shows that low salivary waking cortisol and flat slope of diurnal secretion associated with fatigue. Cortisol is associated with future fatigue and cortisol secretion occurs early in the genesis of fatigue.
Kumaria, M., Badrick, E., Chandola, T., Adam, E. K., Stafford, M., Marmot, M. G., Kirschbaum, C., and Kivimaki, M. (2009). Cortisol secretion and fatigue: Associations in a community based cohort. Psychoneuroendocrinology, 34(10):1476-1485. http://www.citeulike.org/user/HEIRS/article/5951174
Kumaria, M., Badrick, E., Chandola, T., Adam, E. K., Stafford, M., Marmot, M. G., Kirschbaum, C., and Kivimaki, M. (2009). Cortisol secretion and fatigue: Associations in a community based cohort. Psychoneuroendocrinology, 34(10):1476-1485. http://www.citeulike.org/user/HEIRS/article/5951174
CAMKII Regulator of Dopamine Receptor in Limbic System.
Liu, X.-Y., Mao, L.-M., Zhang, G.-C., Papasian, C. J., Fibuch, E. E., Lan, H.-X., Zhou, H.-F., Xu, M., and Wang, J. Q. (2009). Activity-dependent modulation of limbic dopamine d3 receptors by camkii. 61(3):425-438. http://www.citeulike.org/user/HEIRS/article/5951122
Oxidative Stress from Low Dose Ozone Causes Neurodegeneration in the Brain
Oxidative Stress Caused by Ozone Exposure Induces Loss of Brain Repair in The Hippocampus of Adult Rats
Summary: "oxidative stress caused by low doses of ozone causes dysregulation of inflammatory processes, progressive neurodegeneration, chronic loss of brain repair in the hippocampus causing impaired memory, and brain plasticity changes in the rat analogous to those seen in Alzheimer's disease."
Rivas-Arancibia, S., Guevara-Guzman, R., Lopez-Vidal, Y., Rodriguez-Martinez, E., Gomes, M. Z., Angoa-Perez, M., and Raisman-Vozari, R. (2009). Oxidative stress caused by ozone exposure induces loss of brain repair in the hippocampus of adult rats. Toxicol. Sci., pages kfp252+.
Link
Note: ozone is ozone -- does not matter if it produced mechanically or from chemical components in air.
Summary: "oxidative stress caused by low doses of ozone causes dysregulation of inflammatory processes, progressive neurodegeneration, chronic loss of brain repair in the hippocampus causing impaired memory, and brain plasticity changes in the rat analogous to those seen in Alzheimer's disease."
Rivas-Arancibia, S., Guevara-Guzman, R., Lopez-Vidal, Y., Rodriguez-Martinez, E., Gomes, M. Z., Angoa-Perez, M., and Raisman-Vozari, R. (2009). Oxidative stress caused by ozone exposure induces loss of brain repair in the hippocampus of adult rats. Toxicol. Sci., pages kfp252+.
Link
Note: ozone is ozone -- does not matter if it produced mechanically or from chemical components in air.
COX-1 - One way endotoxin may influence the HPA axis.
Background: Some health experts believe that endotoxin may involve a pathway to chronic fatigue syndrome and alterations in HPA function has been suggested as an important factor in the condtion.
Cox-1 may modulate HPA axis responses to pro-inflammatory responses in endothelial and vascular cells. Cox enzymes work inside cells responsible for inflammation but have other functions as well. (mednet.com) Link
References:
COX-1.Mednet.com. Retrieved on October 16, 2009.
Cox-1 may modulate HPA axis responses to pro-inflammatory responses in endothelial and vascular cells. Cox enzymes work inside cells responsible for inflammation but have other functions as well. (mednet.com) Link
References:
COX-1.Mednet.com. Retrieved on October 16, 2009.
Thursday, October 15, 2009
Central administration of resveratrol improves diet-induced diabetes.
Ramadori, G., Gautron, L., Fujikawa, T., Vianna, C. R., Elmquist, J. K., and Coppari, R. (2009). Central administration of resveratrol improves diet-induced diabetes. Endocrinology. http://www.citeulike.org/user/HEIRS/article/5947822
Melatonin Metabolite Levels Associated with Migraine
Title: Urinary 6-sulphatoxymelatonin levels are depressed in chronic migraine and several comorbidities
Summary: This study suggest a relationship between urinary melatonin and migraine. An inverse correlation of melatonin to anxiety, depression and fatigue that points to a hypothalamic function in migraine.
Citation: Masruha, M. R., Lin, J., de Souza Vieira, D. S., Minett, T. S., Cipolla-Neto, J., Zukerman, E., Vilanova, L. C., and Peres, M. F. (2009). Urinary 6-sulphatoxymelatonin levels are depressed in chronic migraine and several comorbidities. Headache. http://www.citeulike.org/user/HEIRS/article/5947791
Summary: This study suggest a relationship between urinary melatonin and migraine. An inverse correlation of melatonin to anxiety, depression and fatigue that points to a hypothalamic function in migraine.
Citation: Masruha, M. R., Lin, J., de Souza Vieira, D. S., Minett, T. S., Cipolla-Neto, J., Zukerman, E., Vilanova, L. C., and Peres, M. F. (2009). Urinary 6-sulphatoxymelatonin levels are depressed in chronic migraine and several comorbidities. Headache. http://www.citeulike.org/user/HEIRS/article/5947791
Mitochondria has Role in Vitamin E Metabolism
Title: alpha-tocopherol beta-oxidation localized to rat liver mitochondria
Summary: "unexpected finding was that alpha-CEHC, the end product of alpha-tocopherol metabolism, was found almost exclusively in mitochondria. These data are the first to indicate a mitochondrial role in alpha-tocopherol metabolism."
Mustacich, D. J., Leonard, S. W., Patel, N. K., and Traber, M. G. (2009). alpha-tocopherol beta-oxidation localized to rat liver mitochondria. Free radical biology & medicine.http://www.citeulike.org/user/HEIRS/article/5931429
Summary: "unexpected finding was that alpha-CEHC, the end product of alpha-tocopherol metabolism, was found almost exclusively in mitochondria. These data are the first to indicate a mitochondrial role in alpha-tocopherol metabolism."
Mustacich, D. J., Leonard, S. W., Patel, N. K., and Traber, M. G. (2009). alpha-tocopherol beta-oxidation localized to rat liver mitochondria. Free radical biology & medicine.http://www.citeulike.org/user/HEIRS/article/5931429
Wednesday, October 14, 2009
Oxidative Stress, T3 and Other Markers May Be Beneficial to Monitor Liver Disease
Title: Oxidative stress and thyroid hormones in patients with liver diseases
Summary: The measurement of the total T(3), NO, MDA, GSH reduced and GSHPx as biomarkers for liver diseases might be a beneficial tool, helping in monitoring the state of liver disease patients.
Citation: Moustafa, A. H. H., Ali, E. M., Mohamed, T. M., and Abdou, H. I. (2009). Oxidative stress and thyroid hormones in patients with liver diseases. European journal of internal medicine, 20(7):703-708. http://www.citeulike.org/user/HEIRS/article/5787830
Summary: The measurement of the total T(3), NO, MDA, GSH reduced and GSHPx as biomarkers for liver diseases might be a beneficial tool, helping in monitoring the state of liver disease patients.
Citation: Moustafa, A. H. H., Ali, E. M., Mohamed, T. M., and Abdou, H. I. (2009). Oxidative stress and thyroid hormones in patients with liver diseases. European journal of internal medicine, 20(7):703-708. http://www.citeulike.org/user/HEIRS/article/5787830
Tuesday, October 13, 2009
Surgeons Discover a Visceral Fat Hormone That Could Protect Against Life-threatening Sepsis
"A study exhibited at the conference showed that low levels of the hormone adiponectin placed animals at a profoundly high risk of death from a septic insult." Click here to read more.....
Humidifiers -- Not Just for Children Anymore --Find Out More About New Humidifiers
An author from Biomedicine writes about the recent advances in humidifiers....."In an era of going green and saving money, people are turning to unexpected sources for natural remedies and ways to conserve. Humidifiers, unexpectedly, serve both purposes by offering relief from dry air, making the air feel warmer, and relieving symptoms of colds and the flu through proper humidification. Click here for more is pleased to announce its all new warm mist humidifiers offering."
Source: Humidifiers -- Not Just for Children Anymore -- AchooAllergy.com Announces All New Humidifiers Offering. Biomedicine. Retrieved on October 13, 2009. http://www.bio-medicine.org/medicine-news-1/Humidifiers----Not-Just-for-Children-Anymore----AchooAllergy-com-Announces-All-New-Humidifiers-Offering-59335-2/
| Warm Mist Humidifiers Warm Mist Humidifiers protect against the risk of spreading pathogens. |
Source: Humidifiers -- Not Just for Children Anymore -- AchooAllergy.com Announces All New Humidifiers Offering. Biomedicine. Retrieved on October 13, 2009. http://www.bio-medicine.org/medicine-news-1/Humidifiers----Not-Just-for-Children-Anymore----AchooAllergy-com-Announces-All-New-Humidifiers-Offering-59335-2/
Thyrotropin Secretion Profiles Not Different In Men and Women
HEIRS Environmental Illness Research Blog: Infection/Endotoxin in Chronic Fatigue, Fibromyalgia and Multiple Chemical Sensitivity.
Roelfsema, F., Pereira, A. M., Veldhuis, J. D., Adriaanse, R., Endert, E., Fliers, E., and Romijn, J. A. (2009). Thyrotropin secretion profiles are not different in men and women. J Clin Endocrinol Metab, pages jc.2009-1155+. http://www.citeulike.org/user/HEIRS/article/5930318
Roelfsema, F., Pereira, A. M., Veldhuis, J. D., Adriaanse, R., Endert, E., Fliers, E., and Romijn, J. A. (2009). Thyrotropin secretion profiles are not different in men and women. J Clin Endocrinol Metab, pages jc.2009-1155+. http://www.citeulike.org/user/HEIRS/article/5930318
Monday, October 12, 2009
Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome p450 enzymes in rat liver ßtem-like" cells
Title: Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome p450 enzymes in rat liver ßtem-like" cells.
Summary: "This is the first evidence that capsaicin-sensitive afferents exert a protective role in endotoxin-induced airway inflammation, but contribute to increased bronchoconstriction."
Umannova, L., Zatloukalova, J., Machala, M., Krcmar, P., Majkova, Z., Hennig, B., Kozubik, A., and Vondracek, J. (2007). Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome p450 enzymes in rat liver ßtem-like" cells. Toxicol. Sci., 99(1):79-89.
Summary: "This is the first evidence that capsaicin-sensitive afferents exert a protective role in endotoxin-induced airway inflammation, but contribute to increased bronchoconstriction."
Umannova, L., Zatloukalova, J., Machala, M., Krcmar, P., Majkova, Z., Hennig, B., Kozubik, A., and Vondracek, J. (2007). Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome p450 enzymes in rat liver ßtem-like" cells. Toxicol. Sci., 99(1):79-89.
Vegetable Neutraceutical Protects Against Prooxidant Such as Dopamine and Acrolein in Cigarettes.
Background: Past studies have demonstrated that D3T a potent enzyme inducer has a positive effect on upregulating the Nrf2 antioxidant system. (Kwak)
Title: Cruciferous nutraceutical 3h-1,2-dithiole-3-thione protects human primary astrocytes against neurocytotoxicity elicited by mptp, mpp(+), 6-ohda, hne and acrolein.
Summary: This is one of the first studies that in "human astrocytes cruciferous nutraceutical D3T potently induces the cellular GSH system and the phase 2 enzyme NQO1, which is accompanied by dramatically increased resistance of these cells to the damage induced by various neurotoxicants. The results of this study may have important implications for the development of novel neuroprotective strategies.
Citation: Jia, Z., Zhu, H., Li, Y., and Misra, H. P. (2009). Cruciferous nutraceutical 3h-1,2-dithiole-3-thione protects human primary astrocytes against neurocytotoxicity elicited by mptp, mpp(+), 6-ohda, hne and acrolein. Neurochemical research, 34(11):1924-1934. http://www.citeulike.org/user/HEIRS/article/4483340
Other References: Kwak, M.-K., Itoh, K., Yamamoto, M., and Kensler, T. W. (2002). Enhanced expression of the transcription factor nrf2 by cancer chemopreventive agents: Role of antioxidant response element-like sequences in the nrf2 promoter. Mol. Cell. Biol., 22(9):2883-2892. http://www.citeulike.org/user/HEIRS/article/883878
Title: Cruciferous nutraceutical 3h-1,2-dithiole-3-thione protects human primary astrocytes against neurocytotoxicity elicited by mptp, mpp(+), 6-ohda, hne and acrolein.
Summary: This is one of the first studies that in "human astrocytes cruciferous nutraceutical D3T potently induces the cellular GSH system and the phase 2 enzyme NQO1, which is accompanied by dramatically increased resistance of these cells to the damage induced by various neurotoxicants. The results of this study may have important implications for the development of novel neuroprotective strategies.
Citation: Jia, Z., Zhu, H., Li, Y., and Misra, H. P. (2009). Cruciferous nutraceutical 3h-1,2-dithiole-3-thione protects human primary astrocytes against neurocytotoxicity elicited by mptp, mpp(+), 6-ohda, hne and acrolein. Neurochemical research, 34(11):1924-1934. http://www.citeulike.org/user/HEIRS/article/4483340
Other References: Kwak, M.-K., Itoh, K., Yamamoto, M., and Kensler, T. W. (2002). Enhanced expression of the transcription factor nrf2 by cancer chemopreventive agents: Role of antioxidant response element-like sequences in the nrf2 promoter. Mol. Cell. Biol., 22(9):2883-2892. http://www.citeulike.org/user/HEIRS/article/883878
High Fat Diet Alters Testosterone and Cortisol Levels in Healthy Volunteers.
Title: Effect of meal fat content on salivary testosterone and cortisol levels in healthy female volunteers.
Summary: "indicate that the amount of fat consumed in a meal, can influence postprandial levels of salivary testosterone and cortisol and their circadian rhythm profile. Such an effect on steroid hormones might have an impact on the person’s daily activities and general health and wellbeing."
Citations: Al-Dujaili, E. A. S. and Bryant, M. L. (2005). Effect of meal fat content on salivary testosterone and cortisol levels in healthy female volunteers. http://www.citeulike.org/user/HEIRS/article/5927406
Summary: "indicate that the amount of fat consumed in a meal, can influence postprandial levels of salivary testosterone and cortisol and their circadian rhythm profile. Such an effect on steroid hormones might have an impact on the person’s daily activities and general health and wellbeing."
Citations: Al-Dujaili, E. A. S. and Bryant, M. L. (2005). Effect of meal fat content on salivary testosterone and cortisol levels in healthy female volunteers. http://www.citeulike.org/user/HEIRS/article/5927406
Acidophilus Reduces Cholesterol Absorption Says New Study
Title: The probiotic lactobacillus acidophilus reduces cholesterol absorption through the down-regulation of niemann-pick c1-like 1 in caco-2 cells.
Summary: According to this researcher, this study underscores that probiotics may be useful in controlling cholesterol.
Citation: Huang, Y. and Zheng, Y. (2009). The probiotic lactobacillus acidophilus reduces cholesterol absorption through the down-regulation of niemann-pick c1-like 1 in caco-2 cells. The British journal of nutrition, pages 1-6. http://www.citeulike.org/user/HEIRS/article/5926674
Summary: According to this researcher, this study underscores that probiotics may be useful in controlling cholesterol.
Citation: Huang, Y. and Zheng, Y. (2009). The probiotic lactobacillus acidophilus reduces cholesterol absorption through the down-regulation of niemann-pick c1-like 1 in caco-2 cells. The British journal of nutrition, pages 1-6. http://www.citeulike.org/user/HEIRS/article/5926674
HPA Dysregulation Negatively Influences Cognitive Function in the Elderly.
Title: HPA Dysregulation Negatively Influences Cognitive Function in the Elderly.
Summary: HPA axis dysregulation seems to be associated with low cognitive performance in the elderly. Slower cortisol elimination rates could predict cognitive decline affecting principally non-verbal functioning in men and verbal functioning in women. Interventions blocking this pathway may provide new therapies for blocking cognitive decline.
Citation: Beluche, I., Carrière, I., Ritchie, K., and Ancelin, M. L. (2009). A prospective study of diurnal cortisol and cognitive function in community-dwelling elderly people. Psychological medicine, pages 1-11. http://www.citeulike.org/user/HEIRS/article/5926636
Summary: HPA axis dysregulation seems to be associated with low cognitive performance in the elderly. Slower cortisol elimination rates could predict cognitive decline affecting principally non-verbal functioning in men and verbal functioning in women. Interventions blocking this pathway may provide new therapies for blocking cognitive decline.
Citation: Beluche, I., Carrière, I., Ritchie, K., and Ancelin, M. L. (2009). A prospective study of diurnal cortisol and cognitive function in community-dwelling elderly people. Psychological medicine, pages 1-11. http://www.citeulike.org/user/HEIRS/article/5926636
Sunday, October 11, 2009
Infection/Endotoxin in Chronic Fatigue, Fibromyalgia and Multiple Chemical Sensitivity.
Definition: Endotoxin: a toxic component of bacteria not excreted by live bacteria but induces the inflammatory cascade and production of NO. (Endotoxin)
An increasing number of scientific publications support the hypothesis that endotoxin infection and sickness syndrome may be important factors in environmental illnesses including fibromyalgia, chronic fatigue syndrome and quite possibly MCS. In fact, sickness syndrome would be a reasonable and holistic approach for explaining many of the behavioral, physical and emotional complications that are common in environmental illness. Sickness syndrome is described as the presence of a variety of symptoms including malaise, fatigue, sleep disturbances, appetite changes, brain inflammation, mood changes such as anxiety and depression and a host of other symptoms that occur as a reponse to injury or infection. These responses occur both in humans and animals and some propose it is in part, adapative responses that are generated to alter the responses of the host and their social network. Over the past several years, there has been an significant amount of research on sickness syndrome. The occurence of which can be attributed to inflammatory cytokines that alter neurotransmission and genetic expression. There have been studies that show altered gene expression in environmental illnesses; the consequences of which can be quite severe and unexpected. Il-10 is an anti-inflammatory cytokine that has been shown to modulate the severity of sickness syndrome through interaction with HO-1. HO-1 is also a cytokine that is induced by activation of Nrf2, although there are other pathways that can induce this antioxidant. Recently, it has been demonstrated that the protective effect of an endogenous peptide thryotropin, against the damaging effect on the dopamine system from paraquat, is due to the chemicals ability to activate Nrf2 to reduce reactive species and increase the antioxidant glutathione. Other studies have demonstrated that thyrotropin is able to reverse hyperglycemia by increasing beta cell function and reducing programmed cell death. (Luo) Insulin resistance and diabetes are suspected to be important consequences of the sustained presence of inflammation and inflammatory cyokines that are characteristic of environmental illnesses.
A recent published study showed that there is brain disfunction in multiple chemical sensitivity (Orriols) and last week I suggested that some of the cognitive effects could be from an altered expression of BDNF. Of course, there are any number of factors such as malnutrition and inflammation that can influence cognitive function. Neurotransmitter regulate and can alter cognition and are modulated by factors that produce "sickness syndrome". According to the author of the recent MCS study, SPECT scans showed alterations in the regions of the brain including the cingulus, striatum and the hippocampus in addition to others. Pekary et al explains that a common environmental toxin LPS has the potential to alter the expression of thyrotropin which may have an impact on LPS toxicity. The study showed elevations of cytokines and corticosterone after LPS with a transient drop in T3. Other results showed a decrease in thyrotropin-releasing hormone in certain areas of the brain while increasing it in others. Thyrotropin has been shown to improve recovery after neurological dysfunctions such as brain trauma and epilepsy in humans and animals and be neuroprotective against NMDA neurotoxicity. (Pizzi) These regions the author noted are areas that are associated with the neuroimmunomodulatory effects of sickness and injury and danger and appear to be similar to those effected in MCS SPECT scans. Also, a sustained elevation in TRH was present in b-cells accompanied by LPS-impaired insulin secretion. From these findings, the author concluded that thyrotropins can mediate and moderate the behavioral and toxic effects of LPS. In addition, LPS elevates inflammatory cytokines including Tnf-a, Il-6 and Il-1b and also increases expression of TLR receptors 2 and 4 and causes a prolonged sickness behavior in aged animals. Taking these findings into account and the fact that thryotropin mediate their positive effects through Nrf2, then one can assume that alterations in the antioxidant system may exacerbate the toxic effects generated by LPS endotoxin It is also important to mention that Nrf2 levels drop as a consequence of the aging process(Godbout). This could lead one to propose that Nrf2 alterations from aging and other impairments and LPS may at least in part, mediate the effects in MCS. There has been evidence that hyperglycemia (which can be reversed with thyrotropin) sensitizes TRPV1 receptors which is implicated in MCS (Pall) and diabetes complications and TRPV1 may have direct or indirect effect on the release of neurotransmitters. (Pabbidi) Neuropeptides releases from capsaicin-sensitive efferents provide a protective mechanism against LPS but also increase bronchoconstriction which can increase airway hyperresponse. (Elekes) From these results and other studies, I have suggested that insulin resistance and hyperglycemia from chemical exposures may contribute to some of the inflammatory responses in MCS.
Endotoxin or LPS has been implicated as a possible pathway to the development of chronic fatigue syndrome. Above we noted that LPS increases the expression of toll-like receptors 2 and 4. Toll receptors recognize certain components on bacteria and transduces bacterial invasion through this recognition and has important relevance in preventing infection (Light) and expressed on a variety of cells including dendritic cells, B cells, neutraphils and macrophages. Defects in TLR expression can lead to an increase in susceptibility to infection from a number of pathogens while aberrant signaling of TLR such as from LPS are implicated in causing sepsis or even inflammatory or autoimmune-type conditions. (Harding) Activation of TLRs can lead to initiation of the the inflammatory pathway NF-kappaB and LPS endotoxins are ligand of TL4. Interestingly, saturated fats (bad fat) can induce inflammatory markers through TLR4 and therefore, saturated fats can alter gene expression through TLR4 interaction. For instance, the main component of coconut oil, lauric acid, has been demonstrated to potentiate the inflammatory effects of LPS COX-2. (Lee) The just published Light study on chronic fatigue syndrome shows an increase in TLR4 after exercise and Light suggests this is due to "lesser fitness" in CFS patients. Light goes on to further explain that Il-10 is upregulated in CFS patients after exercise and one of its roles is to inhibit the production of Tnf-a which is also consistent with recent reports of an anti-inflammatory profile in FM. This and other studies of CFS revealed symptom flares may be related to cytokine activity postexercise. Notably, Tnf-a was elevated in muscle and Light explains that fatigue and muscle pain in CFS might be from the enhanced activation of "fatigue" and "nociceptive" afferents supplying muscle. Other supporting evidence of muscle involvement included elevations of ASIC3 channels that are often increased by muscle and joint inflammation. The elevation of Il-10 in the Light study was correlated to those patients with prolonged fatigue and pain but who also had elevations in pro-inflammatory cytokines and evidence of overall enhanced immune response. LPS has been shown to have a close relationship with sensory nerves and TLR4 receptors have been found on sensory nerves. The interaction between LPS and TLR4 may enhance the complications of TRPV1 activation. (Clark) In addition, Suter demonstrated that TLR2 and TLR4 are necessary for nerve-induced microglia activation and pain sensitization. (Suter)The presence of nociceptors on trigeminal nerves that suggests they recognize bacterial products and contribute to pain during infection. (Ball)
HIF-1 May Provide Protection in Parkinson's and Metal-Induced Oxidative Stress Disorders
Title: Inhibition of prolyl hydroxylase protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity.
Summary: "protection against MPTP neurotoxicity may be mediated by alterations in iron homeostasis and defense against oxidative stress and mitochondrial dysfunction brought about by cellular HIF-1α induction. This study provides novel data extending the possible therapeutic utility of HIF induction to a Parkinson disease model of neurodegeneration, which may prove beneficial not only in this disorder itself but also in other diseases associated with metal-induced oxidative stress."
Lee, D. W., Rajagopalan, S., Siddiq, A., Gwiazda, R., Yang, L., Beal, M. F., Ratan, R. R., and Andersen, J. K. (2009). Inhibition of prolyl hydroxylase protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity. Journal of Biological Chemistry, 284(42):29065-29076.
Summary: "protection against MPTP neurotoxicity may be mediated by alterations in iron homeostasis and defense against oxidative stress and mitochondrial dysfunction brought about by cellular HIF-1α induction. This study provides novel data extending the possible therapeutic utility of HIF induction to a Parkinson disease model of neurodegeneration, which may prove beneficial not only in this disorder itself but also in other diseases associated with metal-induced oxidative stress."
Lee, D. W., Rajagopalan, S., Siddiq, A., Gwiazda, R., Yang, L., Beal, M. F., Ratan, R. R., and Andersen, J. K. (2009). Inhibition of prolyl hydroxylase protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity. Journal of Biological Chemistry, 284(42):29065-29076.
Saturday, October 10, 2009
How Activation of Antioxidant System Nrf2 Reverses Endothelial Dysfunction in Vascular Disease and Environmental Illness!
Background: Vascular disease is an important consequence of diabetes and is associated with endothelial dysfunction from hyperglycemia. Other conditions can contribute to endothelial dysfunction and a decrease in NO in endothelial tissue or loss of NO bioavailability. Certain agents and the loss of heat shock proteins which is important for sustained coupled activity contributes to the uncoupling of eNOS and endothelial dysfunction . Uncoupling of eNOS elevates the production of superoxide causing oxidative stress.Both eNOS uncoupling and oxidative stress have been implicated as factors in environmental illness.(Pall)
Heiss recently demonstrated that Nrf2 increases the bioavailability of NO while reducing reactive species and assists in the maintenance of coupling of eNOS. Kim explains that loss of Nrf2 results in increased susceptibility to oxidative and electrophilic stress but also enhances tissue injury because of an impairment in the "adaptive response". Impairments of the Nrf2 system have been associated with a number of diseases such as asthma, atherosclerosis, colitis and COPD. Incidentally, heat shock proteins are included in a class of genes whose expression may be Nrf2-dependant.
Studies have shown that inflammation, endothelial dysfunction, and endothelial damage mediators are upregulated upon exposure to particulate matter (PM) and therefore, environmental pollutants can compromise overall vascular health. Particulate matter is of concern because it is small enough to be carried deep into the lungs where it promotes the production of inflammatory cytokines. In a study published in 2008, TNF and inflammatory cytokines was associated with ultra-fine particulate matter PM2.5 while a 7-day exposure of PM2.5 was negatively associated with the number of white blood cells in exposed children. In addition, these children had increased levels of endothelin-1 and subclinical inflammation. This study suggest that children exposed to PM may be at risk for cardiovascular disease, stroke and other diseases later in life. (Calderón-Garcidueñas) These findings support others that showed higher hospitilizations for children and higher mortality rates in the elderly over 75 years of age exposed to PM2.5. (Jimenez and Linares)
Recent Research:
Title: Activation of Nrf2 reverses biochemical dysfunction of endothelial cells induced by hyperglycemia linked to vascular disease.
According to this author "nrf2 by the dietary activator sulforaphane, limited to concentration ranges found in plasma after consumption of broccoli, increased the expression of protective enzymes under ARE-linked transcriptional control and prevented metabolic dysfunction in endothelial cells induced by hyperglycemia.........decreasing the expression of nrf2 exacerbated ROS production in both normoglycemic and hyperglycemic cultures which provides evidence that ROS generation can be reduced by Nrf2 and that sulforaphane acts through Nrf2 to achieve reductions and prevent endothelial cell damage."
Summary: These findings provide the biochemical basis for the link of a vegetable-rich diet with decreased endothelial dysfunction, including that part of the Mediterranean diet, suggesting that dietary exposure to nrf2 activators derived from cruciferous vegetables may have be involved.
Notes:
Citation: Xue, M., Qian, Q., Adaikalakoteswari, A., Rabbani, N., Babaei-Jadidi, R., and Thornalley, P. J. (2008). Activation of nf-e2–related factor-2 reverses biochemical dysfunction of endothelial cells induced by hyperglycemia linked to vascular disease. Diabetes, 57(10):2809-2817. http://www.citeulike.org/user/HEIRS/article/3438451
Cheng, J., Ou, J.-S., Singh, H., Falck, J. R., Narsimhaswamy, D., Pritchard, K. A., and Schwartzman, M. L. (2008). 20-hydroxyeicosatetraenoic acid causes endothelial dysfunction via enos uncoupling. Am J Physiol Heart Circ Physiol, 294(2):H1018-1026. http://www.citeulike.org/user/HEIRS/article/5919352
Kim, J., Cha, Y.-N. N., and Surh, Y.-J. J. (2009). A protective role of nuclear erythroid 2-related factor-2 (nrf2) in inflammatory disorders. Mutation research. http://www.citeulike.org/user/HEIRS/article/5884341
Pall, Martin. (2007) Explaining "Unexplained Illness". Harrinton Park Press. Pg 34-35.
Kwak, M.-K., Wakabayashi, N., Itoh, K., Motohashi, H., Yamamoto, M., and Kensler, T. W. (2003). Modulation of gene expression by cancer chemopreventive dithiolethiones through the keap1-nrf2 pathway. Journal of Biological Chemistry, 278(10):8135-8145. http://www.citeulike.org/user/HEIRS/article/883885
Calderón-Garcidueñas, L., Villarreal-Calderon, R., Valencia-Salazar, G., Henríquez-Roldán, C., Gutiérrez-Castrellón, P., Torres-Jardón, R., Osnaya-Brizuela, N., Romero, L., Torres-Jardón, R., Solt, A., and Reed, W. (2008). Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants. Inhalation toxicology, 20(5):499-506. http://www.citeulike.org/user/HEIRS/article/5919414
Heiss, E. H., Schachner, D., Werner, E. R., and Dirsch, V. M. (2009). Active nf-e2-related factor (nrf2) contributes to keep endothelial no synthase (enos) in the coupled state: the role of reactive oxygen species (ros)-, enos- and heme oxygenase (ho-1) levels. The Journal of biological chemistry. http://www.citeulike.org/user/HEIRS/article/5886348
Jiménez, E., Linares, C., Rodríguez, L. F., Bleda, M. J., and Díaz, J. (2009). Short-term impact of particulate matter (pm2.5) on daily mortality among the over-75 age group in madrid (spain). The Science of the total environment, 407(21):5486-5492. http://www.citeulike.org/user/HEIRS/article/5395518
Linares, C. and Díaz, J. (2009). [impact of particulate matter with diameter of less than 2.5 microns [pm2.5] on daily hospital admissions in 0-10-year-olds in madrid. spain [2003-2005]]. Gaceta sanitaria / S.E.S.P.A.S, 23(3):192-197. http://www.citeulike.org/user/HEIRS/article/5919502
Soylemez, S., Sepici, A., and Akar, F. Resveratrol supplementation gender independently improves endothelial reactivity and suppresses superoxide production in healthy rats. Cardiovascular Drugs and Therapy. http://www.citeulike.org/user/HEIRS/article/5919555
Heiss recently demonstrated that Nrf2 increases the bioavailability of NO while reducing reactive species and assists in the maintenance of coupling of eNOS. Kim explains that loss of Nrf2 results in increased susceptibility to oxidative and electrophilic stress but also enhances tissue injury because of an impairment in the "adaptive response". Impairments of the Nrf2 system have been associated with a number of diseases such as asthma, atherosclerosis, colitis and COPD. Incidentally, heat shock proteins are included in a class of genes whose expression may be Nrf2-dependant.
Studies have shown that inflammation, endothelial dysfunction, and endothelial damage mediators are upregulated upon exposure to particulate matter (PM) and therefore, environmental pollutants can compromise overall vascular health. Particulate matter is of concern because it is small enough to be carried deep into the lungs where it promotes the production of inflammatory cytokines. In a study published in 2008, TNF and inflammatory cytokines was associated with ultra-fine particulate matter PM2.5 while a 7-day exposure of PM2.5 was negatively associated with the number of white blood cells in exposed children. In addition, these children had increased levels of endothelin-1 and subclinical inflammation. This study suggest that children exposed to PM may be at risk for cardiovascular disease, stroke and other diseases later in life. (Calderón-Garcidueñas) These findings support others that showed higher hospitilizations for children and higher mortality rates in the elderly over 75 years of age exposed to PM2.5. (Jimenez and Linares)
Recent Research:
Title: Activation of Nrf2 reverses biochemical dysfunction of endothelial cells induced by hyperglycemia linked to vascular disease.
According to this author "nrf2 by the dietary activator sulforaphane, limited to concentration ranges found in plasma after consumption of broccoli, increased the expression of protective enzymes under ARE-linked transcriptional control and prevented metabolic dysfunction in endothelial cells induced by hyperglycemia.........decreasing the expression of nrf2 exacerbated ROS production in both normoglycemic and hyperglycemic cultures which provides evidence that ROS generation can be reduced by Nrf2 and that sulforaphane acts through Nrf2 to achieve reductions and prevent endothelial cell damage."
Summary: These findings provide the biochemical basis for the link of a vegetable-rich diet with decreased endothelial dysfunction, including that part of the Mediterranean diet, suggesting that dietary exposure to nrf2 activators derived from cruciferous vegetables may have be involved.
Notes:
- Resveratrol has been demonstrated to improve endothelial function and suppress oxidative stress such as superoxide from NADPH. (Soylemez) In the blog, A Small Book on the Benefits of Resveratrol we explained how other studies have shown some of its activities are regulated through SIRT1 and elevates a number of antioxidants and increases the expression of GCH1 which prevents the elevations in superoxide and (HEIRS Nutrition) alters eNOS expression.
Citation: Xue, M., Qian, Q., Adaikalakoteswari, A., Rabbani, N., Babaei-Jadidi, R., and Thornalley, P. J. (2008). Activation of nf-e2–related factor-2 reverses biochemical dysfunction of endothelial cells induced by hyperglycemia linked to vascular disease. Diabetes, 57(10):2809-2817. http://www.citeulike.org/user/HEIRS/article/3438451
Cheng, J., Ou, J.-S., Singh, H., Falck, J. R., Narsimhaswamy, D., Pritchard, K. A., and Schwartzman, M. L. (2008). 20-hydroxyeicosatetraenoic acid causes endothelial dysfunction via enos uncoupling. Am J Physiol Heart Circ Physiol, 294(2):H1018-1026. http://www.citeulike.org/user/HEIRS/article/5919352
Kim, J., Cha, Y.-N. N., and Surh, Y.-J. J. (2009). A protective role of nuclear erythroid 2-related factor-2 (nrf2) in inflammatory disorders. Mutation research. http://www.citeulike.org/user/HEIRS/article/5884341
Pall, Martin. (2007) Explaining "Unexplained Illness". Harrinton Park Press. Pg 34-35.
Kwak, M.-K., Wakabayashi, N., Itoh, K., Motohashi, H., Yamamoto, M., and Kensler, T. W. (2003). Modulation of gene expression by cancer chemopreventive dithiolethiones through the keap1-nrf2 pathway. Journal of Biological Chemistry, 278(10):8135-8145. http://www.citeulike.org/user/HEIRS/article/883885
Calderón-Garcidueñas, L., Villarreal-Calderon, R., Valencia-Salazar, G., Henríquez-Roldán, C., Gutiérrez-Castrellón, P., Torres-Jardón, R., Osnaya-Brizuela, N., Romero, L., Torres-Jardón, R., Solt, A., and Reed, W. (2008). Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants. Inhalation toxicology, 20(5):499-506. http://www.citeulike.org/user/HEIRS/article/5919414
Heiss, E. H., Schachner, D., Werner, E. R., and Dirsch, V. M. (2009). Active nf-e2-related factor (nrf2) contributes to keep endothelial no synthase (enos) in the coupled state: the role of reactive oxygen species (ros)-, enos- and heme oxygenase (ho-1) levels. The Journal of biological chemistry. http://www.citeulike.org/user/HEIRS/article/5886348
Jiménez, E., Linares, C., Rodríguez, L. F., Bleda, M. J., and Díaz, J. (2009). Short-term impact of particulate matter (pm2.5) on daily mortality among the over-75 age group in madrid (spain). The Science of the total environment, 407(21):5486-5492. http://www.citeulike.org/user/HEIRS/article/5395518
Linares, C. and Díaz, J. (2009). [impact of particulate matter with diameter of less than 2.5 microns [pm2.5] on daily hospital admissions in 0-10-year-olds in madrid. spain [2003-2005]]. Gaceta sanitaria / S.E.S.P.A.S, 23(3):192-197. http://www.citeulike.org/user/HEIRS/article/5919502
Soylemez, S., Sepici, A., and Akar, F. Resveratrol supplementation gender independently improves endothelial reactivity and suppresses superoxide production in healthy rats. Cardiovascular Drugs and Therapy. http://www.citeulike.org/user/HEIRS/article/5919555
Friday, October 9, 2009
Oxidative stress-induced necrotic cell death via mitochondira-dependent burst of reactive oxygen species.
Summary: "The inhibition of mitochondrial hyperpolarization by diphenylene iodonium or rotenone, potent inhibitors of mitochondrial respiratory chain complex I, also resulted in reduced ROS production and subsequent neuronal cell death in vitro and in vivo. The inhibition of mitochondrial hyperpolarization can protect neuronal cells from oxidative stress-induced necrotic cell death, suggesting a novel method of therapeutic intervention in oxidative stress-induced neurological disease."
Choi, K., Kim, J., Kim, G. W., and Choi, C. (2009). Oxidative stress-induced necrotic cell death via mitochondira-dependent burst of reactive oxygen species. Current neurovascular research. http://www.citeulike.org/user/HEIRS/article/5918128
Choi, K., Kim, J., Kim, G. W., and Choi, C. (2009). Oxidative stress-induced necrotic cell death via mitochondira-dependent burst of reactive oxygen species. Current neurovascular research. http://www.citeulike.org/user/HEIRS/article/5918128
Caffeic Acid in Bee Hive Propolis and Melatonin Show Benefits on Aging Brain Cells.
Background: At normal levels, numerous studies have shown that caffeic acid which is an antioxidant helps prevent acute immune and inflammatory responses and in found in honey bee hive propolis. (Wipedia)
Title: The ultrastructural and biochemical evidences of the beneficial effects of chronic caffeic acid phenethyl ester and melatonin administration on brain and cerebellum of aged rats.
Summary: Study shows benefits of "supplemental administration of caffeic acid phenethyl ester and melatonin is beneficial in delaying age-related cellular damage in nervous system."
Citation: Mukaddes Eşrefoğlu, Mehmet Gül, Burhan Ateş, İsmet Yılmaz (2009). The ultrastructural and biochemical evidences of the beneficial effects of chronic caffeic
Title: The ultrastructural and biochemical evidences of the beneficial effects of chronic caffeic acid phenethyl ester and melatonin administration on brain and cerebellum of aged rats.
Summary: Study shows benefits of "supplemental administration of caffeic acid phenethyl ester and melatonin is beneficial in delaying age-related cellular damage in nervous system."
Citation: Mukaddes Eşrefoğlu, Mehmet Gül, Burhan Ateş, İsmet Yılmaz (2009). The ultrastructural and biochemical evidences of the beneficial effects of chronic caffeic