Saturday, May 29, 2010
Immune System Troubles Could Spark Behavior Woes - Mental Health Disorders on MedicineNet.com
Immune System Troubles Could Spark Behavior Woes - Mental Health Disorders on MedicineNet.com: "-- In the first scientific illustration of exactly how some psychiatric illnesses might be linked to an immune system gone awry, researchers report they cured mice of an obsessive-compulsive condition known as 'hair-pulling disorder' by tweaking the rodents' immune systems."
Wine Compound Reduces Oxidative and Inflammatory Response via Nrf2 Upon Exposure To Nitrosamines!
CiteULike: Resveratrol Suppresses Oxidative Stress and Inflammatory Response in Diethylnitrosamine-Initiated Rat Hepatocarcinogenesis.: "Results of the present investigation provide evidence that attenuation of oxidative stress and suppression of inflammatory response mediated by Nrf2 could be implicated, at least in part, in the chemopreventive effects of this dietary agent against chemically induced hepatic tumorigenesis in rats."
Friday, May 28, 2010
Critical role of NO signaling in GMP in the Nrf2 antioxidant adaptive response.
This is the first to show a substantial corroboration of the biological significance of cellular 8-nitro-cGMP formation and potential roles of 8-nitro-cGMP in the Nrf2-dependent antioxidant response.
CiteULike: The critical role of nitric oxide signaling, via protein S-guanylation and nitrated cyclic GMP, in the antioxidant adaptive response.: "Fujii, S., Sawa, T., Ihara, H., Tong, K. I., Ida, T., Okamoto, T., Ahtesham, A. K. K., Ishima, Y., Motohashi, H., Yamamoto, M., and Akaike, T. (2010). The critical role of nitric oxide signaling, via protein s-guanylation and nitrated cyclic gmp, in the antioxidant adaptive response. The Journal of biological chemistry."
Acute stress modulates genotype effects on amygdala processing in humans
"genetic effects on brain operations can be state dependent, such that they only become apparent under specific, often environmentally controlled, conditions."
CiteULike: Acute stress modulates genotype effects on amygdala processing in humans:
CiteULike: Acute stress modulates genotype effects on amygdala processing in humans:
Postive Effects of Exercise on Memory from BDNF Resistance to Corticosterone.
Corticosterone is a main glucocorticoid involved in regulation of fuel, immune reactions, and stress responses. (Corticosterone: Wipedia)"This study suggests that the resistance of the hippocampal BDNF expression to suppression by corticosterone, as seen after water maze training, may contribute to an optimal memory performance." (Schaff)
Comment: It has been suggested that exercise exerts its influence by increasing a number of different hormones and cellular activators including BDNF and enhances memory and learning by activating the antioxidant system. (Ayoub) BDNF has been implicated as a factor in a number of mood disorders and altered levels in conditions including PTSD, fibromyagia and CFS and proteins such as GSK-3b may alter BDNF's downstream regulators. (Mai)
For more: HEIRS Library Tag: BDNF
Related Blogs: BDNF
Recommended:
CiteULike: Corticosterone effects on BDNF expression in the hippocampus. Implications for memory formation.: "suggest that the resistance of the hippocampal BDNF expression to suppression by corticosterone, as seen after water maze training, may contribute to an optimal memory performance."
Schaaf, M. J., De Kloet, E. R., and Vreugdenhil, E. (2000). Corticosterone effects on bdnf expression in the hippocampus. implications for memory formation. Stress (Amsterdam, Netherlands), 3(3):201-208. http://www.citeulike.org/user/HEIRS/article/7224956
Other Sources:
Ayoub, R. S. (2009). Effect of exercise on spatial learning and memory in male diabetic rats. 18(3). http://www.citeulike.org/user/HEIRS/article/7224997
Mai, L., Jope, R. S., and Li, X. (2002). Bdnf-mediated signal transduction is modulated by gsk3β and mood stabilizing agents. Journal of Neurochemistry, 82(1):75-83. http://www.citeulike.org/user/HEIRS/article/6621876
HEIRS Health & Home
All rights reserved.
Wednesday, May 26, 2010
Aryl hydrocarbon receptor reduced immune reactions during influenza infection.
Aryl hydrocarbon receptor activation reduces dendritic cell function during influenza virus infection -- Jin et al., 10.1093/toxsci/kfq153 -- Toxicological Sciences: "AhR activation by chemicals from our environment impacts DC function to stimulate naïve CD8+ T cells, and that immunoregulatory genes within DCs are critical targets of AhR. Moreover, our results reinforce the idea that environmental signals and AhR ligands may contribute to differential susceptibilities and responses to respiratory infection."
Study Links Heptachlor, PCBs and Form of Vitamin E to Diabetes
"An analysis of 266 potential environmental contributors to type 2 diabetes published May 20, 2010 in the online edition of the journal PLoS ONE, links the disease to individuals who have higher levels of polychlorinated biphenyls (PCBs) and the pesticide heptachlor, as well a form of vitamin E found at high levels in soybean and corn oil, in their bodies compared to the general population. PCB was banned in 1979 and most uses of heptachlor were canceled between 1978 and 1989 (except for limited control of fire ants, which continues), but the compounds persist in the environment, especially near former industrial sites or contaminated soil"
Beyond Pesticides Daily News Blog » Blog Archive » Study Links Heptachlor, PCBs and Form of Vitamin E to Diabetes:
Tuesday, May 25, 2010
SNP in Gene Associated W/ Autism Present in CFS, Study Says!
DISC1 Ser704Cys might be a functional variant that affects one of the mechanisms implicated in the biology of CFS.
"Fukuda, S., Hashimoto, R., Ohi, K., Yamaguti, K., Nakatomi, Y., Yasuda, Y., Kamino, K., Takeda, M., Tajima, S., Kuratsune, H., Nishizawa, Y., and Watanabe, Y. (2010). A functional polymorphism in the disrupted-in schizophrenia 1 gene is associated with chronic fatigue syndrome. Life sciences."
CiteULike: A functional polymorphism in the Disrupted-in schizophrenia 1 gene is associated with chronic fatigue syndrome.:
Astroglial Amino Acid Shuttle Involved in Nociceptive Pain Sensitization!
"This study has demonstrated that the central sensitization induced in functionally identified nociceptive neurons in trigeminal subnucleus caudalis (the medullary dorsal horn) by application of an inflammatory irritant to the rat's tooth pulp can be significantly attenuated by continuous intrathecal superfusion of methionine sulfoximine, an inhibitor of the astroglial enzyme glutamine synthetase that is involved in the glutamate–glutamine shuttle......Further, the lack of any observed significant effects of MSO alone, in contrast to our findings that it significantly attenuates MO-induced central sensitization, suggests that its action on astroglial GS is not evident in basal conditions but is apparent in hyperexcitable states, consistent with findings by ourselves and others that glia may not affect basal nociceptive processing but rather participate in exaggerated pain states. It is also noteworthy that an excess of glutamine in the CNS is involved in ammonia neurotoxicity possibly through its detrimental effects on mitochondrial function."
CiteULike: Astroglial Glutamate Glutamine Shuttle Is Involved in Central Sensitization of Nociceptive Neurons in Rat Medullary Dorsal Horn: "Chiang, C.-Y., Wang, J., Xie, Y.-F., Zhang, S., Hu, J. W., Dostrovsky, J. O., and Sessle, B. J. (2007). Astroglial glutamate glutamine shuttle is involved in central sensitization of nociceptive neurons in rat medullary dorsal horn. J. Neurosci., 27(34):9068-9076."
You might also like:
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http://www.citeulike.org/user/HEIRS/article/6962057
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Chen, P.-C., Vargas, M. R., Pani, A. K., Smeyne, R. J., Johnson, D. A., Kan, Y. W., and Johnson, J. A. (2009). Nrf2-mediated neuroprotection in the mptp mouse model of parkinson's disease: Critical role for the astrocyte. Proceedings of the National Academy of Sciences, 106(8):2933-2938. http://www.citeulike.org/user/HEIRS/article/6551224?show_msg=already_posted
More Support for Brain Changes in Fibromyalgia, Says Study!
"fibromyalgia is associated with deficits in intracortical modulation involving both GABAergic and glutamatergic mechanisms, possibly related to certain aspects of the pathophysiology of this chronic pain syndrome"
CiteULike: Alteration of cortical excitability in patients with fibromyalgia.:
New Study Says Prevalence for CFS Higher Than Previously Thought!
"The prevalence of CF in the general population appears to be much higher than previously indicated. Even with strict criteria for CFS, it is estimated that approximately 1% of the adult population experiences this condition."
CiteULike: Fatigue and chronic fatigue syndrome-like complaints in the general population.:
CiteULike: Fatigue and chronic fatigue syndrome-like complaints in the general population.:
C-Reactive Protein Alters Protein Interactions W/ eNOS.
"negative protein-protein interactions of eNOS were able to partly explain the CRP-induced decreases in the activity of this critical enzyme, which caused endothelial dysfunction."
CiteULike: C-Reactive Protein Adversely Alters the Protein-Protein Interaction of the Endothelial Isoform of Nitric Oxide Synthase.:
Renal protection by a soy diet associated with restoration of NO generation.
"renal protective effect of soy protein appears to be mediated by improvement of NO generation and pointed out to caveolin-1 overexpression as a potential pathophysiological mechanism in renal disease"
CiteULike: Renal protection by a soy diet in obese Zucker rats is associated with restoration of nitric oxide generation.:
CiteULike: Renal protection by a soy diet in obese Zucker rats is associated with restoration of nitric oxide generation.:
PTSD may raise diabetes risk in service members
It's possible that the stress response associated with PTSD could contribute to widespread inflammation in the body and lower sensitivity to the blood-sugar-regulating hormone insulin, which could lead to diabetes, researchers say.
PTSD may raise diabetes risk in service members Reuters: "PTSD may raise diabetes risk in service members"
Folates Benefits on CNS Injury Mediates Through Methylation!
"New study implicates an epigenetic mechanism in CNS repair. Folic acid and possibly other nontoxic dietary methyl donors may therefore be useful in clinical interventions to promote brain and spinal cord healing. If indeed the benefit of folate is mediated by epigenetic mechanisms that promote endogenous axonal regeneration, this provides possible avenues for new pharmacologic approaches to treating CNS injuries."
CiteULike: Folate regulation of axonal regeneration in the rodent central nervous system through DNA methylation.: "Iskandar, B. J., Rizk, E., Meier, B., Hariharan, N., Bottiglieri, T., Finnell, R. H., Jarrard, D. F., Banerjee, R. V., Skene, P. H., Nelson, A., Patel, N., Gherasim, C., Simon, K., Cook, T. D., and Hogan, K. J. (2010). Folate regulation of axonal regeneration in the rodent central nervous system through dna methylation. The Journal of clinical investigation, 120(5):1603-1616."
Green Tea Activates Reexpression of Glutathione Via Methylation Mechanisms.
New study demonstrates that green tea polyphenols (GTP) has dual potential to alter DNA methylation and chromatin modeling and reexpression of glutathione transferase, the 2 global epigenetic mechanisms of gene regulation and their lack of toxicity makes them excellent candidates for the chemoprevention of prostate cancer.
CiteULike: Promoter demethylation and chromatin remodeling by green tea polyphenols leads to re-expression of GSTP1 in human prostate cancer cells.: "Pandey, M., Shukla, S., and Gupta, S. (2010). Promoter demethylation and chromatin remodeling by green tea polyphenols leads to re-expression of gstp1 in human prostate cancer cells. International journal of cancer. Journal international du cancer, 126(11):2520-2533."
Berry Compounds Reduce DNA Damage By Increasing DNA Repair!
Dietary berries and ellagic Acid prevent oxidative... [Int J Mol Sci. 2008] - PubMed result: "red raspberry and ellagic acid reduce endogenous oxidative DNA damage by mechanisms which may involve increase in DNA repair."
Monday, May 24, 2010
Green Tea Compounds Reduce Blood Brain Barrier Permeability in Brain Injury!
CiteULike: Effects of green tea polyphenols on caveolin-1 of microvessel fragments in rats with cerebral ischemia.: "Zhang, S., Liu, Y., Zhao, Z., and Xue, Y. (2010). Effects of green tea polyphenols on caveolin-1 of microvessel fragments in rats with cerebral ischemia. Neurological research."
Hormone Modulates Immune Cell Activation after Cigarette Smoke Exposure in Mice.
Recent study says leptin may modulate the immune responses from cigarette smoke. Other studies demonstrate that leptin and Il-6 may be involved with sickness syndrome and may include modulation of hormones that regulate behavior such as orexins and may contribute to inflammation-induced insulin resistance.
Notes: Recent study also demonstrates that cigarette smoke induced epigenetic changes in epithelial cells in vitro that may contribute to cancer growth.
CiteULike: Leptin Modulates Innate and Adaptive Immune Cell Recruitment after Cigarette Smoke Exposure in Mice.: "Vernooy, J. H., Bracke, K. R., Drummen, N. E., Pauwels, N. S., Zabeau, L., van Suylen, R. J. J., Tavernier, J., Joos, G. F., Wouters, E. F., and Brusselle, G. G. (2010). Leptin modulates innate and adaptive immune cell recruitment after cigarette smoke exposure in mice. Journal of immunology (Baltimore, Md. : 1950)."
HEIRS H&H
Harden, L. M., du Plessis, I., Poole, S., and Laburn, H. P. (2006). Interleukin-6 and leptin mediate lipopolysaccharide-induced fever and sickness behavior. Physiology & behavior, 89(2):146-155.
http://www.citeulike.org/user/HEIRS/article/4745011
Liu, F., Killian, J. K., Yang, M., Walker, R. L., Hong, J. A., Zhang, M., Davis, S., Zhang, Y., Hussain, M., Xi, S., Rao, M., Meltzer, P. A., and Schrump, D. S. (2010). Epigenomic alterations and gene expression profiles in respiratory epithelia exposed to cigarette smoke condensate. Oncogene, aop(current).
http://www.citeulike.org/user/HEIRS/article/7154109
Notes: Recent study also demonstrates that cigarette smoke induced epigenetic changes in epithelial cells in vitro that may contribute to cancer growth.
CiteULike: Leptin Modulates Innate and Adaptive Immune Cell Recruitment after Cigarette Smoke Exposure in Mice.: "Vernooy, J. H., Bracke, K. R., Drummen, N. E., Pauwels, N. S., Zabeau, L., van Suylen, R. J. J., Tavernier, J., Joos, G. F., Wouters, E. F., and Brusselle, G. G. (2010). Leptin modulates innate and adaptive immune cell recruitment after cigarette smoke exposure in mice. Journal of immunology (Baltimore, Md. : 1950)."
HEIRS H&H
Harden, L. M., du Plessis, I., Poole, S., and Laburn, H. P. (2006). Interleukin-6 and leptin mediate lipopolysaccharide-induced fever and sickness behavior. Physiology & behavior, 89(2):146-155.
http://www.citeulike.org/user/HEIRS/article/4745011
Liu, F., Killian, J. K., Yang, M., Walker, R. L., Hong, J. A., Zhang, M., Davis, S., Zhang, Y., Hussain, M., Xi, S., Rao, M., Meltzer, P. A., and Schrump, D. S. (2010). Epigenomic alterations and gene expression profiles in respiratory epithelia exposed to cigarette smoke condensate. Oncogene, aop(current).
http://www.citeulike.org/user/HEIRS/article/7154109
Altered Metabolism, Toxicity, Glutamate Dehydrogenase and NRF-1 and Its Activator PGC-1
Altered Metabolism, Toxicity, Glutamate Dehydrogenase and NRF-1 and Its Activator PGC-1 - PFOS alters genes for glutamate ammonioa ligase
Hurricanes - How To Prepare for Them!
Hurricanes: "A hurricane is a severe tropical storm that forms in the North Atlantic Ocean, the Northeast Pacific Ocean or the South Pacific Ocean. Hurricanes need warm tropical oceans, moisture, and light winds above them. If the right conditions last long enough, a hurricane can produce violent winds, large waves, torrential rains, and floods."
Sunday, May 23, 2010
Fear potentiation is associated with hypothalamic–pituitary–adrenal axis function in PTSD
Fear potentiation is associated with hypothalamic–pituitary–adrenal axis function in PTSD: "impaired fear inhibition and associated alterations in HPA feedback may reflect amygdala hyperactivity in subjects with PTSD"
Gulf War and Health: Links to Fibromalgia, PTSD, IBS
IOM determines that Gulf War service causes post-traumatic stress disorder (PTSD) and that service is associated with multisymptom illness; gastrointestinal disorders such as irritable bowel syndrome; alcohol and other substance abuse; and anxiety disorders and other psychiatric disorders. To ensure that our veterans receive the best possible care, now and in the future, the government should continue to monitor their health and conduct research to identify the best treatments to assist Gulf War veterans still suffering from persistent, unexplained illnesses. The report also says there is some limited evidence of a link to fibromyalgia and ALS but the connection is less clear. Read more.
Increased levels of homocysteine in patients with ... [World J Gastroenterol. 2010] - PubMed result
Increased levels of homocysteine in patients with ... [World J Gastroenterol. 2010] - PubMed result: "Increased levels of homocysteine in patients with ulcerative colitis."
Glutamine Synthetase, PFOS and Neurotransmission
PFC are chemicals that are ubiquitous in the environmental and can or could be found in products including building materials, fabrics, packaging, clothing, protective gear etc. Recent studies show that these chemicals have the capacity to regulate or impair gene expression including those that regulate the excretion of toxic waste products that may result in alterations of neurotransmission and contribute to their toxicity. In addition, genetic problems may aggravate this inhibition and augment the physical consequences of exposure. Glutamine synthetase is one enzyme that is important for regulation of toxins such as ammonia in the brain as well as production of glutathione. In addition, certain conditions, such as in endotoxemia and implicated as a causal factor is CFS, the activity of this enzyme is further reduced. Nrf2 is protective against PFOS through the generation of HO-1 and reductions in its production may augment oxidative stress damage from PFOS.
Yang, X., Wang, L., Sun, W., and Xue, Z. (2009). [effects of perfluorooctane sulfonate on amino acid neurotransmitters and glutamine synthetase in rats]. Wei sheng yan jiu = Journal of hygiene research, 38(1):19-21. http://www.citeulike.org/user/HEIRS/article/6999108
Häussinger, D. and Schliess, F. (2007). Glutamine metabolism and signaling in the liver. Frontiers in Bioscience, 12:371-391.
http://www.citeulike.org/user/HEIRS/article/7208003
Shi, X. and Zhou, B. (2010). The role of nrf2 and mapk pathways in pfos-induced oxidative stress in zebrafish embryos. Toxicol. Sci., 115(2):391-400.
http://www.citeulike.org/user/HEIRS/article/6761678
Yang, X., Wang, L., Sun, W., and Xue, Z. (2009). [effects of perfluorooctane sulfonate on amino acid neurotransmitters and glutamine synthetase in rats]. Wei sheng yan jiu = Journal of hygiene research, 38(1):19-21. http://www.citeulike.org/user/HEIRS/article/6999108
Häussinger, D. and Schliess, F. (2007). Glutamine metabolism and signaling in the liver. Frontiers in Bioscience, 12:371-391.
http://www.citeulike.org/user/HEIRS/article/7208003
Shi, X. and Zhou, B. (2010). The role of nrf2 and mapk pathways in pfos-induced oxidative stress in zebrafish embryos. Toxicol. Sci., 115(2):391-400.
http://www.citeulike.org/user/HEIRS/article/6761678
PGC-1a Improves Lipid Use, Insulin Signalling and Glucose Transport in Muscle.
"Increases in PGC-1α levels, similar to those that can be induced by physiological stimuli, altered intramuscular lipids and improved fatty acid oxidation, insulin signalling and insulin-stimulated glucose transport, albeit to different extents in lean and insulin-resistant muscle."
CiteULike: Increased levels of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α) improve lipid utilisation, insulin signalling and glucose transport in skeletal muscle of lean and insulin-resistant obese Zucker rats:
CiteULike: Increased levels of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α) improve lipid utilisation, insulin signalling and glucose transport in skeletal muscle of lean and insulin-resistant obese Zucker rats:
CiteULike: Insulin Reduces Plasma Arginase Activity in Type 2 Diabetic Patients
NO availability, critical for vascular tone and normal function, is reduced in insulin resistance, including diabetes. Diabetes has been associated with exposures and bioaccumulation of persistant organic pollutants.
CiteULike: Insulin Reduces Plasma Arginase Activity in Type 2 Diabetic Patients: "Kashyap, S. R., Lara, A., Zhang, R., Park, Y. M., and DeFronzo, R. A. (2008). Insulin reduces plasma arginase activity in type 2 diabetic patients. Diabetes Care, 31(1):134-139."
Health Notes, Insulin
Health Notes, Insulin: "pH of the blood affects the function of insulin. If the extra-cellular fluids are not alkaline enough, glucose cannot enter the cell. The result is fatigue (Allergies Diseases ...Bateson-Koch, p. 76)."
Ornithines Role in Muscle Building
Health Notes, Insulin: "Ornithine stimulates insulin secretion and helps insulin work as an anabolic (muscle building) hormone. (Mindell's Vitamin Bible, p. 112)"
Pathology in Hepatocerebral Disorders Include Ammonia Toxicity from Metals!
CiteULike: Metal Toxicity, Liver Disease and Neurodegeneration.: "Pathophysiologic mechanisms responsible for cerebral dysfunction and neuronal cell death in hepatocerebral disorders include ammonia toxicity and neurotoxic effects of metals such as copper, manganese, and iron"
Ammonia and Urea in Acidosis
"Ammonia is excreted only as a defense against an acidosis condition because the neutralization of acid by ammonia has the effect of conserving bases in the blood."
Urea Cycle:
Urea Cycle:
Lactic acidosis from Heavy Metal Poisoning.
"Heavy metal toxicity, including poisoning with arsenic, can raise lactate levels and lead to generalized metabolic acidosis"
Lactic acidosis - Wikipedia, the free encyclopedia:
Lactic acidosis - Wikipedia, the free encyclopedia:
Il-6 Modulates CRF in the Hypothalamus in Response to Different Signals.
Module: 5/22/2010
Background: CRF can regulate signaling in response to different odors. In those cases, it can lead to an anxiolytic or elevation and other responses typical of the stress response including pain generation, immune regulation, itch, rash and other changes such as gastric function alterations. Of course, these are symptoms characteristic of chemical sensitivity and also some symptoms characteristic of other environmentally influenced conditions such as CFS and sickness syndrome.
A major regulator of sickness syndrome is Il-6 which can be functionally modulated through Il-10 and ultimately most probably HO-1 which has been shown in other studies to increase during exercise. Interestingly, one can identify similarities in cancer-related fatigue to some chronic symptoms of CFS and sickness syndrome including the exhausting fatigue and cachexia that is exhibited in the latter, in animals and humans. Preliminary studies suggest cytokine Il-6/Il-8 may modulate the severity of cancer-related fatigue and others show cancer-related fatigue is common with serotonin dysregulation. Coincidentally, in the trout corticotrophin activation by ammonia is associated with alterations in neurotransmitter levels including dopamine and serotonin. So here again, we see potential especially with periods of aberrant corticotrophin signalling, where symptoms of environmental illness such as anxiety, depression, weakeness and fatigue may present itself. These findings supports past studies that suggest that fatigue in CFS may be in part due to serotonin dysregulation and elevations in Il-6.(Ryan)
CiteULike: Transcriptional regulation of hypothalamic corticotropin-releasing factor gene.: "Glucocorticoid-dependent repression of cAMP-stimulated CRF promoter activity is mediated by both nGRE and SRE in hypothalamic cells. Interleukin (IL)-6 produced in the hypothalamus stimulates the CRF gene. Suppressor of cytokine signaling-3, which is induced by a cAMP stimulant and IL-6, is involved in the negative regulation of CRF gene expression in hypothalamic cells. Such complex mechanisms would contribute to stress responses and homeostasis in the hypothalamus."
Related: Hummel, M., Cummons, T., Lu, P., Mark, L., Harrison, J. E., Kennedy, J. D., and Whiteside, G. T. (2010). Pain is a salient ßtressor" that is mediated by corticotropin- releasing factor-1 receptors. Neuropharmacology.
http://www.citeulike.org/user/HEIRS/article/7177466
Coric, V., Feldman, H. H., Oren, D. A., Shekhar, A., Pultz, J., Dockens, R. C., Wu, X., Gentile, K. A., Huang, S.-P. P., Emison, E., Delmonte, T., D'Souza, B. B., Zimbroff, D. L., Grebb, J. A., Goddard, A. W., and Stock, E. G. (2010). Multicenter, randomized, double-blind, active comparator and placebo-controlled trial of a corticotropin-releasing factor receptor-1 antagonist in generalized anxiety disorder. Depression and anxiety, 27(5):417-425.
http://www.citeulike.org/user/HEIRS/article/7193107
Theoharides, T. C., Singh, Boucher, W., Pang, X., Letourneau, R., Webster, E., and Chrousos, G. (1998). Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects. Endocrinology, 139(1):403-413.
http://www.citeulike.org/user/HEIRS/article/7207688
Mustian, K. M., Fisher, S., Adams, J., Janelsins, M., Palesh, O., Darling, T., Peppone, L., Heckler, C., Williams, J., and Morrow, G. (2009). Cytokine-mediated changes associated with improvements in cancer-related fatigue induced by exercise: Results from a randomized pilot study of cancer patients receiving radiotherapy. Journal of Clinical Oncology, 27(15s).
http://www.citeulike.org/user/HEIRS/article/7207720
Ryan, J. L., Carroll, J. K., Ryan, E. P., Mustian, K. M., Fiscell, K., and Morrow, G. R. (2007). Mechanisms of cancer-related fatigue. The Oncologist, 12(1 supp):22-34.
http://www.citeulike.org/user/HEIRS/article/7207823
Background: CRF can regulate signaling in response to different odors. In those cases, it can lead to an anxiolytic or elevation and other responses typical of the stress response including pain generation, immune regulation, itch, rash and other changes such as gastric function alterations. Of course, these are symptoms characteristic of chemical sensitivity and also some symptoms characteristic of other environmentally influenced conditions such as CFS and sickness syndrome.
A major regulator of sickness syndrome is Il-6 which can be functionally modulated through Il-10 and ultimately most probably HO-1 which has been shown in other studies to increase during exercise. Interestingly, one can identify similarities in cancer-related fatigue to some chronic symptoms of CFS and sickness syndrome including the exhausting fatigue and cachexia that is exhibited in the latter, in animals and humans. Preliminary studies suggest cytokine Il-6/Il-8 may modulate the severity of cancer-related fatigue and others show cancer-related fatigue is common with serotonin dysregulation. Coincidentally, in the trout corticotrophin activation by ammonia is associated with alterations in neurotransmitter levels including dopamine and serotonin. So here again, we see potential especially with periods of aberrant corticotrophin signalling, where symptoms of environmental illness such as anxiety, depression, weakeness and fatigue may present itself. These findings supports past studies that suggest that fatigue in CFS may be in part due to serotonin dysregulation and elevations in Il-6.(Ryan)
CiteULike: Transcriptional regulation of hypothalamic corticotropin-releasing factor gene.: "Glucocorticoid-dependent repression of cAMP-stimulated CRF promoter activity is mediated by both nGRE and SRE in hypothalamic cells. Interleukin (IL)-6 produced in the hypothalamus stimulates the CRF gene. Suppressor of cytokine signaling-3, which is induced by a cAMP stimulant and IL-6, is involved in the negative regulation of CRF gene expression in hypothalamic cells. Such complex mechanisms would contribute to stress responses and homeostasis in the hypothalamus."
Related: Hummel, M., Cummons, T., Lu, P., Mark, L., Harrison, J. E., Kennedy, J. D., and Whiteside, G. T. (2010). Pain is a salient ßtressor" that is mediated by corticotropin- releasing factor-1 receptors. Neuropharmacology.
http://www.citeulike.org/user/HEIRS/article/7177466
Coric, V., Feldman, H. H., Oren, D. A., Shekhar, A., Pultz, J., Dockens, R. C., Wu, X., Gentile, K. A., Huang, S.-P. P., Emison, E., Delmonte, T., D'Souza, B. B., Zimbroff, D. L., Grebb, J. A., Goddard, A. W., and Stock, E. G. (2010). Multicenter, randomized, double-blind, active comparator and placebo-controlled trial of a corticotropin-releasing factor receptor-1 antagonist in generalized anxiety disorder. Depression and anxiety, 27(5):417-425.
http://www.citeulike.org/user/HEIRS/article/7193107
Theoharides, T. C., Singh, Boucher, W., Pang, X., Letourneau, R., Webster, E., and Chrousos, G. (1998). Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects. Endocrinology, 139(1):403-413.
http://www.citeulike.org/user/HEIRS/article/7207688
Mustian, K. M., Fisher, S., Adams, J., Janelsins, M., Palesh, O., Darling, T., Peppone, L., Heckler, C., Williams, J., and Morrow, G. (2009). Cytokine-mediated changes associated with improvements in cancer-related fatigue induced by exercise: Results from a randomized pilot study of cancer patients receiving radiotherapy. Journal of Clinical Oncology, 27(15s).
http://www.citeulike.org/user/HEIRS/article/7207720
Ryan, J. L., Carroll, J. K., Ryan, E. P., Mustian, K. M., Fiscell, K., and Morrow, G. R. (2007). Mechanisms of cancer-related fatigue. The Oncologist, 12(1 supp):22-34.
http://www.citeulike.org/user/HEIRS/article/7207823
Saturday, May 22, 2010
Toll-like receptor 4 modulates skeletal muscle substrate metabolism.
"skeletal muscle is a target for circulating endotoxin and may provide critical insight into the link between a proinflammatory state and dysregulated metabolism as observed with obesity, type 2 diabetes, and metabolic syndrome."
CiteULike: Toll-like receptor 4 modulates skeletal muscle substrate metabolism.:
CiteULike: Toll-like receptor 4 modulates skeletal muscle substrate metabolism.:
Tetrahydrobiopterin (BH4) and the MTHFR gene
"With certain combinations of the MTHFR gene, some people have a limited supply of BH4."
Detox Puzzle: Tetrahydrobiopterin (BH4):
Detox Puzzle: Tetrahydrobiopterin (BH4):
Friday, May 21, 2010
CiteULike: S-Glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide
CiteULike: S-Glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide: "irreversible oxidation of key thiol(s) in disease impairs NO-induced relaxation by preventing reversible S-glutathiolation and activation of SERCA by NO/ONOO−."
Thursday, May 20, 2010
Acute and chronic exposure to shear stress have opposite effects on endothelial permeability to macromolecules
We conclude that chronic application of shear stress reduces endothelial permeability to macromolecules by a PI3K-NO-cGMP-dependent mechanism. Since atherosclerosis can be triggered by excessive entry of plasma macromolecules into the arterial wall, the phenomenon may help explain the atheroprotective effects of shear and NO.
CiteULike: Acute and chronic exposure to shear stress have opposite effects on endothelial permeability to macromolecules: "Warboys, C. M., Eric Berson, R., Mann, G. E., Pearson, J. D., and Weinberg, P. D. (2010). Acute and chronic exposure to shear stress have opposite effects on endothelial permeability to macromolecules. Am J Physiol Heart Circ Physiol, 298(6):H1850-1856."
Wednesday, May 19, 2010
Dark Chocolate for Fibromyalgia & Chronic Fatigue Syndrome
Dark Chocolate for Fibromyalgia & Chronic Fatigue Syndrome: "Dark Chocolate for Fibromyalgia & Chronic Fatigue Syndrome"
Resveratrol confers endothelial protection via act... [Am J Physiol Heart Circ Physiol. 2010] - PubMed result
Resveratrol confers endothelial protection via act... [Am J Physiol Heart Circ Physiol. 2010] - PubMed result: "Resveratrol confers endothelial protection via activation of the antioxidant transcription factor Nrf2"
Overexpression of Nrf2 Protects Striatal Neurons from Mitochondrial Dysfunction.
"these results to show that multiple methods of astrocyte-specific Nrf2 overexpression provide protection from neurotoxicity in vivo."
CiteULike: Astrocyte-Specific Overexpression of Nrf2 Protects Striatal Neurons from Mitochondrial Complex II Inhibition:
The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos
"knockdown of Nrf2 reduced PFOS-induced HO-1 gene expression"
CiteULike: The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos:
Altered expression of genes involved in inflammation and apoptosis in frontal cortex in major depression
CiteULike: Altered expression of genes involved in inflammation and apoptosis in frontal cortex in major depression: "Shelton, R. C., Claiborne, J., Sidoryk-Wegrzynowicz, M., Reddy, R., Aschner, M., Lewis, D. A., and Mirnics, K. (2010). Altered expression of genes involved in inflammation and apoptosis in frontal cortex in major depression. Molecular Psychiatry."
Tuesday, May 18, 2010
Spicing the Meat Also Cuts the Cancer Risk
Spicing the Meat Also Cuts the Cancer Risk: "Newswise — Spices will do more than just enhance the taste of ground beef. They’ll also cut down on the risk of compounds that can cause cancer."
Rise in HO-1 is Associated With Rise in cGMP!
Our data show that it is possible to transduce rat endothelial cells with hHO-1 gene and to achieve selective hHO-1 expression to levels significantly higher than those of endogenous rat HO-1 expression. The overexpression of hHO-1 in rat endothelial cells was associated with an elevation in cGMP. Our data also reveal that augmentation of hHO-1 activity in transduced cells conferred substantial protection against cellular toxicity produced by H2O2 and heme.
CiteULike: Retrovirus-mediated HO gene transfer into endothelial cells protects against oxidant-induced injury: "Yang, L., Quan, S., and Abraham, N. G. (1999). Retrovirus-mediated ho gene transfer into endothelial cells protects against oxidant-induced injury. Am J Physiol Lung Cell Mol Physiol, 277(1):L127-133."
CiteULike: NO Says Yes to Mitochondria
Small amounts of NO stimulate mitochondrial biogenesis and boost the supply of oxygen and respiratory substrates to mitochondria. In contrast, high amounts of NO produced by iNOS block mitochondrial respiration, and can be cytotoxic. Cold exposure results in noradrenaline release by sympathetic nerves, which elevates intracellular calcium ions and cAMP (via b3-adrenergic receptors) in brown fat adipocytes. This increase induces NO production by eNOS, which activates cGMP production from soluble guanylate cyclase. Expression of the transcriptional coactivator PGC-1 is enhanced by cGMP, resulting in increased production of NRF-1 and mtTFA, which stimulate mitochondrial biogenesis. Vasodilation of blood vessels (due to the action of NO on vascular smooth muscle) results in an increased supply of oxygen and respiratory substrates to mitochondria. Inflammation enhances iNOS expression, resulting in elevated production of NO, which directly blocks mitochondrial respiration and energy production.
CiteULike: NO Says Yes to Mitochondria: "Brown, G. C. (2003). No says yes to mitochondria. Science, 299(5608)."
Reductions in Anxiety with Increased cGMP
CiteULike: Anxiolytic Effects of Phosphodiesterase-2 Inhibitors Associated with Increased cGMP Signaling: "Masood, A., Huang, Y., Hajjhussein, H., Xiao, L., Li, H., Wang, W., Hamza, A., Zhan, C.-G., and O'Donnell, J. M. (2009). Anxiolytic effects of phosphodiesterase-2 inhibitors associated with increased cgmp signaling. Journal of Pharmacology and Experimental Therapeutics, 331(2):690-699."
Memory and NO/cGMP
CiteULike: Critical Time-Window for NO-cGMP-Dependent Long-Term Memory Formation after One-Trial Appetitive Conditioning: "Kemenes, I., Kemenes, G., Andrew, R. J., Benjamin, P. R., and O'Shea, M. (2002). Critical time-window for no-cgmp-dependent long-term memory formation after one-trial appetitive conditioning. J. Neurosci., 22(4):1414-1425."
Monday, May 17, 2010
Melatonin attenuates methamphetamine-induced overexpression of pro-inflammatory cytokines in microglial cell lines.
In highly aggressively proliferating immortalized (HAPI) cells, a rat microglial cell line, METH reduced cell viability in a concentration- and time-dependent manner and initiated the expression of interleukin 1beta (IL-1beta), interleukin 6 (IL-6) and tumor necrosis factor alpha. METH also induced the production of both ROS and RNS in microglial cells. Pretreatment with melatonin, a major secretory product of the pineal gland, abolished METH-induced toxicity, suppressed ROS and RNS formation and also had an inhibitory effect on cytotoxic factor gene expression
CiteULike: Melatonin attenuates methamphetamine-induced overexpression of pro-inflammatory cytokines in microglial cell lines.: "Tocharus, J., Khonthun, C., Chongthammakun, S., and Govitrapong, P. (2010). Melatonin attenuates methamphetamine-induced overexpression of pro-inflammatory cytokines in microglial cell lines. Journal of pineal research, 48(4):347-352."
Heating and Ventilation Can Redistribute Meth Lab Contaminants
bulk contaminants and remove obvious pseudoephedrine or methamphetamine-contaminated surfaces prior to heating, ventilation or sealing of a clandestine laboratory to avoid redistribution of material around the site.
CiteULike: Recoveries of trace pseudoephedrine and methamphetamine residues from impermeable household surfaces: implications for sampling methods used during remediation of clandestine methamphetamine laboratories.: "Abdullah, L. F. and Miskelly, G. M. (2010). Recoveries of trace pseudoephedrine and methamphetamine residues from impermeable household surfaces: implications for sampling methods used during remediation of clandestine methamphetamine laboratories. Talanta, 81(1-2):455-461."
The impact of IL-1 modulation on the development of lipopolysaccharide-induced cognitive dysfunction
"blocking IL-1 signaling, the inflammatory cascade to LPS is attenuated, thereby reducing microglial activation and preventing the behavioral abnormality."
CiteULike: The impact of IL-1 modulation on the development of lipopolysaccharide-induced cognitive dysfunction: "Terrando, N., Fidalgo, A. R., Vizcaychipi, M., Cibelli, M., Ma, D., Monaco, C., Feldmann, M., and Maze, M. (2010). The impact of il-1 modulation on the development of lipopolysaccharide-induced cognitive dysfunction. Critical Care, 14(3):R88+."
Sunday, May 16, 2010
Molecular and Biochemical Features of the Mitochondrial Enzyme Ornithine Transcarbamylase: A Possible New Role as a Signaling Factor.
CiteULike: Molecular and Biochemical Features of the Mitochondrial Enzyme Ornithine Transcarbamylase: A Possible New Role as a Signaling Factor.: "DÃaz-Muñoz, M. and Hernández-Muñoz, R. (2010). Molecular and biochemical features of the mitochondrial enzyme ornithine transcarbamylase: A possible new role as a signaling factor. Current medicinal chemistry."
Nitric Oxide Metabolite Production During Exercise in Chronic Fatigue Syndrome: A Case-Control Study"
Mary Ann Liebert, Inc. - Journal of Women's Health - 0(0):: "Nitric Oxide Metabolite Production During Exercise in Chronic Fatigue Syndrome: A Case-Control Study"
Saturday, May 15, 2010
Research may help patients with intestinal failure, other malabsorptive disorders
Research may help patients with intestinal failure, other malabsorptive disorders: "ScienceDaily (May 15, 2010) — New treatments for intestinal failure and other intestinal absorption disorders are a step closer to the patients who need them after a discovery in Kelly Tappenden's University of Illinois laboratory."
Intestinal damage after surgery
Intestinal damage after surgery: "Dr. Joep Grootjans and colleagues at the Maastricht University Medical Center, Maastricht, the Netherlands demonstrate that intestinal ischemia/reperfusion (I/R) induces inflammation in humans. Their report can be found in the May 2010 issue of The American Journal of Pathology."
How odors activate the stress response and inflammatory mediators!
"enhanced IL-6 activity may stimulate the HPA axis at the level of the hypothalamus via a CRH-mediated mechanism For example, inhalation of citralva, a sample used during the study, may enhance the stress response or may itself act as a stress."
Effects of Odorants on the Hypothalamic-Pituitary-Adrenal Axis and Interleukin-6 (IL-6) and IL-6 Receptor mRNA Expression in Rat Hypothalamus after Restraint Stress -- Komori et al. 28 (9): 767 -- Chemical Senses: "enhanced IL-6 activity may stimulate the HPA axis at the level of the hypothalamus (Naitoh et al., 1988; Fukata et al., 1989; Navarra et al., 1991; Tominaga et al., 1991) via a CRH-mediated mechanism (Navarra et al., 1991; Lyson and McCann, 1992), i.e. inhalation of citralva may enhance the stress response or may itself act as a stress."
Effects of Odorants on the Hypothalamic-Pituitary-Adrenal Axis and Interleukin-6 (IL-6) and IL-6 Receptor mRNA Expression in Rat Hypothalamus after Restraint Stress -- Komori et al. 28 (9): 767 -- Chemical Senses: "enhanced IL-6 activity may stimulate the HPA axis at the level of the hypothalamus (Naitoh et al., 1988; Fukata et al., 1989; Navarra et al., 1991; Tominaga et al., 1991) via a CRH-mediated mechanism (Navarra et al., 1991; Lyson and McCann, 1992), i.e. inhalation of citralva may enhance the stress response or may itself act as a stress."
Pathway Impairment that Regulates Stress Response Could Lead to A Variety of Environmental Diseases
A recent study determined that caffeine can be a preventative against some of the health effects in Parkinson's disease caused by pesticides. The following pathway is a good representation of the NO/cGMP pathway that is more than likely effected by caffeine in these conditions and can account for some of the locomoter problems in PD. As one can see, expression of other proteins including BDNF rely on its activity. In other blogs, we have noted that BDNF is altered in environmental illnesses including CFS and may account for mood changes that occur with the condition. Proper signaling of the NO/cGMP pathway is important for a number of health conditions because the pathways are consistently activated by a number of different xenobiotics and environmental cues.
Alterations in the functioning of Nrf2 and other conditions like excretory defects that increase ammonia levels with negatively impact this system. While NO is an important component of this pathway - the actual dysfunction is not related to peroxynitrite, although oxidative stress to some may increase dysfunction though loss of NO signalling. Madhusoodanan explains that in this case, "nitric oxide is a short lived free radical species synthesized by NOS. The physiological role of NO depends on its local concentration as wells as the availability of downstream targets. At low levels, activation of guanalyl cyclase is the major event by NO. The resulting elevation of cGMP serves as an regulator of many events." I suggest that many environmental diseases including CFS and MCS are probably due more to the impairments of NO/cGMP which is also negatively effected by endogenous gases including ammonia and the impairment of the system results in astrocyte damage. Because Nrf2 is also neuroprotective --- alterations in Nrf2 will contribute to neural injury. Also, cGMP inhibits the protein GSK-3b which is an off/on switch for Nrf2. Studies have demonstrated that Nrf2 regulates the antioxidant complexes of HO-1/CO which modulates CRF (which can be activated by odors) and CO activates cGMP. These pathways seem to strongly suggest that Nrf2 ultimately may influence the regulation of the stress response from environmental cues. In any case, HO-1/CO does modulate the CRF system which can be activated by response cytokines such as Il-1.
Recent studies show that increasing Nrf2 may be beneficial in limiting neural injury and in this case, I would say it probably would too. The article discusses hormetic responses that we have also discussed at length and as Mattson describes "recent findings have elucidated hormetic mechanisms of action of phytochemicals (e.g., resveratrol, curcumin, sulforaphanes and catechins) using cell culture and animal models of neurological disorders. Examples of hormesis pathways activated by phytochemicals include the transcription factor Nrf-2 which activates genes controlled by the antioxidant response element, and histone deacetylases of the sirtuin family and FOXO transcription factors." This of course may act on activities involved in methylation.
Notes:
Madhusoodanan, K. and Murad, F. (2007). No-cgmp signaling and regenerative medicine involving stem cells. Neurochemical Research, 32(4):681-694.
http://www.citeulike.org/user/HEIRS/article/1245237
Chan, M.-H., Chien, T.-H., Lee, P.-Y., and Chen, H.-H. (2004). Involvement of no/cgmp pathway in toluene-induced locomotor hyperactivity in female rats. Psychopharmacology, 176(3):435-439.
http://www.citeulike.org/user/HEIRS/article/7170771
van Staveren, W. (2001). The effects of phosphodiesterase inhibition on cyclic gmp and cyclic amp accumulation in the hippocampus of the rat. Brain Research, 888(2):275-286.
http://www.citeulike.org/user/HEIRS/article/7170748
Kachroo, A., Irizarry, M. C., and Schwarzschild, M. A. (2010). Caffeine protects against combined paraquat and maneb-induced dopaminergic neuron degeneration. Experimental neurology, 223(2):657-661.
http://www.citeulike.org/user/HEIRS/article/6835294
Mattson, M. P., Son, T. G., and Camandola, S. (2007). Viewpoint: mechanisms of action and therapeutic potential of neurohormetic phytochemicals. Dose-response : a publication of International Hormesis Society, 5(3):174-186.
http://www.citeulike.org/user/HEIRS/article/3812627
Angulo, J., González-Corrochano, R., Cuevas, P., Fernández, A., Fuente, J. L. M., Rolo, F., Allona, A., and Sáenz de Tejada, I. (2009). Diabetes exacerbates the functional deficiency of no/cgmp pathway associated with erectile dysfunction in human corpus cavernosum and penile arteries. The journal of sexual medicine. http://www.citeulike.org/user/HEIRS/article/7170872
Yang, R., Wang, J., Chen, Y., Sun, Z., Wang, R., and Dai, Y. (2008). Effect of caffeine on erectile function via up-regulating cavernous cyclic guanosine monophosphate in diabetic rats. J Androl, 29(5):586-591. http://www.citeulike.org/user/HEIRS/article/7170883
Nisoli, E. and Carruba, M. O. (2006). Nitric oxide and mitochondrial biogenesis. J Cell Sci, 119(14):2855-2862.http://www.citeulike.org/user/HEIRS/article/7170901
Alterations in the functioning of Nrf2 and other conditions like excretory defects that increase ammonia levels with negatively impact this system. While NO is an important component of this pathway - the actual dysfunction is not related to peroxynitrite, although oxidative stress to some may increase dysfunction though loss of NO signalling. Madhusoodanan explains that in this case, "nitric oxide is a short lived free radical species synthesized by NOS. The physiological role of NO depends on its local concentration as wells as the availability of downstream targets. At low levels, activation of guanalyl cyclase is the major event by NO. The resulting elevation of cGMP serves as an regulator of many events." I suggest that many environmental diseases including CFS and MCS are probably due more to the impairments of NO/cGMP which is also negatively effected by endogenous gases including ammonia and the impairment of the system results in astrocyte damage. Because Nrf2 is also neuroprotective --- alterations in Nrf2 will contribute to neural injury. Also, cGMP inhibits the protein GSK-3b which is an off/on switch for Nrf2. Studies have demonstrated that Nrf2 regulates the antioxidant complexes of HO-1/CO which modulates CRF (which can be activated by odors) and CO activates cGMP. These pathways seem to strongly suggest that Nrf2 ultimately may influence the regulation of the stress response from environmental cues. In any case, HO-1/CO does modulate the CRF system which can be activated by response cytokines such as Il-1.
Recent studies show that increasing Nrf2 may be beneficial in limiting neural injury and in this case, I would say it probably would too. The article discusses hormetic responses that we have also discussed at length and as Mattson describes "recent findings have elucidated hormetic mechanisms of action of phytochemicals (e.g., resveratrol, curcumin, sulforaphanes and catechins) using cell culture and animal models of neurological disorders. Examples of hormesis pathways activated by phytochemicals include the transcription factor Nrf-2 which activates genes controlled by the antioxidant response element, and histone deacetylases of the sirtuin family and FOXO transcription factors." This of course may act on activities involved in methylation.
Notes:
- Diabetes exacerbates functional deficiency of NO/cGMP in ED
Madhusoodanan, K. and Murad, F. (2007). No-cgmp signaling and regenerative medicine involving stem cells. Neurochemical Research, 32(4):681-694.
http://www.citeulike.org/user/HEIRS/article/1245237
Chan, M.-H., Chien, T.-H., Lee, P.-Y., and Chen, H.-H. (2004). Involvement of no/cgmp pathway in toluene-induced locomotor hyperactivity in female rats. Psychopharmacology, 176(3):435-439.
http://www.citeulike.org/user/HEIRS/article/7170771
van Staveren, W. (2001). The effects of phosphodiesterase inhibition on cyclic gmp and cyclic amp accumulation in the hippocampus of the rat. Brain Research, 888(2):275-286.
http://www.citeulike.org/user/HEIRS/article/7170748
Kachroo, A., Irizarry, M. C., and Schwarzschild, M. A. (2010). Caffeine protects against combined paraquat and maneb-induced dopaminergic neuron degeneration. Experimental neurology, 223(2):657-661.
http://www.citeulike.org/user/HEIRS/article/6835294
Mattson, M. P., Son, T. G., and Camandola, S. (2007). Viewpoint: mechanisms of action and therapeutic potential of neurohormetic phytochemicals. Dose-response : a publication of International Hormesis Society, 5(3):174-186.
http://www.citeulike.org/user/HEIRS/article/3812627
Angulo, J., González-Corrochano, R., Cuevas, P., Fernández, A., Fuente, J. L. M., Rolo, F., Allona, A., and Sáenz de Tejada, I. (2009). Diabetes exacerbates the functional deficiency of no/cgmp pathway associated with erectile dysfunction in human corpus cavernosum and penile arteries. The journal of sexual medicine. http://www.citeulike.org/user/HEIRS/article/7170872
Yang, R., Wang, J., Chen, Y., Sun, Z., Wang, R., and Dai, Y. (2008). Effect of caffeine on erectile function via up-regulating cavernous cyclic guanosine monophosphate in diabetic rats. J Androl, 29(5):586-591. http://www.citeulike.org/user/HEIRS/article/7170883
Nisoli, E. and Carruba, M. O. (2006). Nitric oxide and mitochondrial biogenesis. J Cell Sci, 119(14):2855-2862.http://www.citeulike.org/user/HEIRS/article/7170901
Friday, May 14, 2010
Cognitive Impairment from Stress Improves w Plant Compound!
GTPs and EGCG modulation could improve the cognitive impairments induced by psychological stress. The related mechanisms may be involved with the changes of catecholamines, 5-hydroxytryptamine, cytokines and expressions of metallothioneins
CiteULike: Effects of epigallocatechin-3-gallate on behavioral impairments induced by psychological stress in rats.: "Chen, W.-Q. Q., Zhao, X.-L. L., Wang, D.-L. L., Li, S.-T. T., Hou, Y., Hong, Y., and Cheng, Y.-Y. Y. (2010). Effects of epigallocatechin-3-gallate on behavioral impairments induced by psychological stress in rats. Experimental biology and medicine (Maywood, N.J.), 235(5):577-583."
Neuroprotection through Stimulation of Mitochondrial Antioxidant Protein Expression.
Nrf2 system and its protection against mitochondrial bioenergetic dysfunction may therefore constitute a powerful mechanism for both pre-conditioning against neurodegeneration and for post-conditioning against neural cell death associated with acute neurologic injury.
CiteULike: Neuroprotection through Stimulation of Mitochondrial Antioxidant Protein Expression.: "Greco, T. and Fiskum, G. (2010). Neuroprotection through stimulation of mitochondrial antioxidant protein expression. Journal of Alzheimer's disease : JAD."
Ghrelin Provides Positive Metabolic Effects Through Nitric Oxide Regulation.
"ghrelin plays a significant role in the regulation of glucose homeostasis, lipid profiles and body composition. Importantly, ghrelin has antinflammatory and antiapoptotic effects both in vivo and in vitro."
CiteULike: Cardiovascular and Metabolic Effects of Ghrelin.: "Tesauro, M., Schinzari, F., Caramanti, M., Lauro, R., and Cardillo, C. (2010). Cardiovascular and metabolic effects of ghrelin. Current diabetes reviews."
Note: Some of its action is achieved through signalling via NO/cGMP. Excess production of ammonia such as those from bacteria may influence the regulation of this protein.
CiteULike: Cardiovascular and Metabolic Effects of Ghrelin.: "Tesauro, M., Schinzari, F., Caramanti, M., Lauro, R., and Cardillo, C. (2010). Cardiovascular and metabolic effects of ghrelin. Current diabetes reviews."
Thursday, May 13, 2010
Is This a Plausible Mechanism for Multiple Chemical Sensitivity Responses?
The results of this study suggest that "electrical or chemical stimulation of the dorsal periaqueductal gray matter (DPAG) evokes escape, defensive behavior that has been related to panic attacks and that serotonin signaling may influence the panic behavior."
"Considering the triggers, this seems like a very plausible explanation for the mechanism or something similar in multiple chemical sensitivity. This area seems to be influenced by stress signalling and also interacts with certain proteins including the CRH which reacts to environmental cues that leads to changes in neurotransmission. According to one source, "periaqueductal gray matter is responsible for inhibiting nociceptive activity (often leading to pain) though the release of certain proteins. Nociceptive signaling forms a platform for the "central sensitization" in fibromyalgia and other pain conditions and involves the enhancement of impulses and dysfunction in the pain system." For this reason, it very well could be an important component in the responses associated with chemical sensitivity.(Spaeth) As far as fibromyalgia, alterations in serotonin have been noted in past studies.
CiteULike: Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter.: "Miguel, T. L. B. L., Pobbe, R. L. H. L., Junior, A. S. S., and Junior, H. Z. Z. (2010). Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter. Behavioural brain research."
Sources:
The Neurochemical Response Patterns to Acute Stress. Retrieved on May 13, 2010. http://focus.psychiatryonline.org/cgi/content/full/2/3/368/T1
Spaeth, M. (2006). Fibromyalgia syndrome: The role of neurochemicals. Primary Psychiatry, 13(9):72-75.
http://www.citeulike.org/user/HEIRS/article/7167665
"Considering the triggers, this seems like a very plausible explanation for the mechanism or something similar in multiple chemical sensitivity. This area seems to be influenced by stress signalling and also interacts with certain proteins including the CRH which reacts to environmental cues that leads to changes in neurotransmission. According to one source, "periaqueductal gray matter is responsible for inhibiting nociceptive activity (often leading to pain) though the release of certain proteins. Nociceptive signaling forms a platform for the "central sensitization" in fibromyalgia and other pain conditions and involves the enhancement of impulses and dysfunction in the pain system." For this reason, it very well could be an important component in the responses associated with chemical sensitivity.(Spaeth) As far as fibromyalgia, alterations in serotonin have been noted in past studies.
CiteULike: Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter.: "Miguel, T. L. B. L., Pobbe, R. L. H. L., Junior, A. S. S., and Junior, H. Z. Z. (2010). Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter. Behavioural brain research."
Sources:
The Neurochemical Response Patterns to Acute Stress. Retrieved on May 13, 2010. http://focus.psychiatryonline.org/cgi/content/full/2/3/368/T1
Spaeth, M. (2006). Fibromyalgia syndrome: The role of neurochemicals. Primary Psychiatry, 13(9):72-75.
http://www.citeulike.org/user/HEIRS/article/7167665
Tuesday, May 11, 2010
Changes in Gene Expression From Dioxin Exposure
CiteULike: Comparative toxicogenomic analysis of the hepatotoxic effects of TCDD in Sprague Dawley rats and C57BL/6 mice.: "Boverhof, D. R., Burgoon, L. D., Tashiro, C., Sharratt, B., Chittim, B., Harkema, J. R., Mendrick, D. L., and Zacharewski, T. R. (2006). Comparative toxicogenomic analysis of the hepatotoxic effects of tcdd in sprague dawley rats and c57bl/6 mice. Toxicological sciences : an official journal of the Society of Toxicology, 94(2):398-416."
AMP-Activated Protein Kinase Mediates Activity-Dependent Regulation of PGC-1alpha and NRF-1 Expression in Rat Visual Cortical Neurons.
CiteULike: AMP-Activated Protein Kinase Mediates Activity-Dependent Regulation of PGC-1alpha and NRF-1 Expression in Rat Visual Cortical Neurons.: "Yu, L. and Yang, S. J. (2010). Amp-activated protein kinase mediates activity-dependent regulation of pgc-1alpha and nrf-1 expression in rat visual cortical neurons. Neuroscience."
Monday, May 10, 2010
Implications of the NO/cGMP system for olfaction
CiteULike: Implications of the NO/cGMP system for olfaction: "Implications of the NO/cGMP system for olfaction"
Synaptic plasticity and NO-cGMP-PKG signaling coordinately regulate ERK-driven gene expression in the lateral amygdala and in the auditory thalamus following Pavlovian fear conditioning
CiteULike: Synaptic plasticity and NO-cGMP-PKG signaling coordinately regulate ERK-driven gene expression in the lateral amygdala and in the auditory thalamus following Pavlovian fear conditioning: "Ota, K. T., Monsey, M. S., Wu, M. S., Young, G. J., and Schafe, G. E. (2010). Synaptic plasticity and no-cgmp-pkg signaling coordinately regulate erk-driven gene expression in the lateral amygdala and in the auditory thalamus following pavlovian fear conditioning. Learning & Memory, 17(4):221-235."
Reduced NO-cGMP Signaling Contributes to Vascular Inflammation and Insulin Resistance Induced by High-Fat Feeding
Reduced signaling via the NO-cGMP pathway is a mediator of vascular inflammation and insulin resistance during overnutrition induced by high-fat feeding. Therefore, phosphodiesterase-5, soluble guanylyl cyclase, and other molecules in the NO-cGMP pathway (eg, protein kinase G) constitute potential targets for the treatment of vascular dysfunction in the setting of obesity.
CiteULike: Reduced NO-cGMP Signaling Contributes to Vascular Inflammation and Insulin Resistance Induced by High-Fat Feeding: "Rizzo, N. O., Maloney, E., Pham, M., Luttrell, I., Wessells, H., Tateya, S., Daum, G., Handa, P., Schwartz, M. W., and Kim, F. (2010). Reduced no-cgmp signaling contributes to vascular inflammation and insulin resistance induced by high-fat feeding. Arterioscler Thromb Vasc Biol, 30(4):758-765."
Saturday, May 8, 2010
Bacillus Anthracis Endospores Regulate Ornithine Decarboxylase and Inducible Nitric Oxide Synthase Through ERK1/2 and p38 Mitogen-Activated Protein Kinases.
CiteULike: Bacillus Anthracis Endospores Regulate Ornithine Decarboxylase and Inducible Nitric Oxide Synthase Through ERK1/2 and p38 Mitogen-Activated Protein Kinases.: "Porasuphatana, S., Cao, G.-L. L., Tsai, P., Tavakkoli, F., Huwar, T., Baillie, L., Cross, A. S., Shapiro, P., and Rosen, G. M. (2010). Bacillus anthracis endospores regulate ornithine decarboxylase and inducible nitric oxide synthase through erk1/2 and p38 mitogen-activated protein kinases. Current microbiology."
Friday, May 7, 2010
Thursday, May 6, 2010
Ammonia, Smoking,Insulin Resistance and Protein Dysfunction in MCS
Background: Manufacturers of cigarettes have admitted to adding ammonia since the 1960s to make them more addictive by boosting the absorption of nicotine significantly. This may make cigarette smoke more toxic to some including people that are more vulnerable such as young children with immature immune systems, the elderly or other individuals that have urinary impairments or genetic factors that alter excretory metabolism. Below are some examples of why adding ammonia to cigarettes may be indirectly responsible, at least in part, for the rise in cardiovascular and other diseases from smoking because of its toxic effects on genes and different tissues in the body.
In cells, chemical toxins effect metabolic pathways which may run parallel, are independant and/or interact, potentiate or possibly minimize the effects of each another. For this reason, it is difficult to predict the severity and the consequences of them on the health of an organism. Exposure to cigarette smoke is no different and has been shown to act differently in different people and on more than one molecular pathway at the same time. Through the years, hundreds of studies have demonstrated the health hazards associated with the toxic effects of smoking and one of these effects includes the dysregulation of metabolism including altering blood sugar homeostasis. Personally, I have suspected this to be the case for some time. Over the past several years, scientists have discovered smoking not only increases the risk for diabetes which includes higher glucose levels, higher insulin levels and increased blood pressure it may also contribute to episodes of hypoglycemia in diabetes. As one article state, "this may be due to an effect of smoking on insulin clearance, leading to hyperinsulinemia, increasing hypoglycemia, and worsening metabolic control. In addition, smoking has been shown to increase the secretion of hormones (i.e., growth hormone, vasopressin, and cortisol) that counteract insulin action, leading to an increased insulin requirement. Smokers have been found to require more insulin than nonsmokers to achieve the same level of glycemic control in some, but not all, studies." (Hirai)
In addition to ammonia making cigarettes more addictive, ammonia can act on the cortico-releasing factor (CRF) system which regulates behavior including feeding and increases serotonin and dopamine levels. As a consequence, it can influence mood and alter homeostasis leading the conditions like the weight loss and weight gain from smoking and cessation, respectively. Activation of this pathway, in fact, mediates psychological effects of nicotine withdrawal. (Grunberg) I recently mentioned that because ammonia activates the CRF pathway that regulates neuroendocrine, drug abuse responses and aversion one could relate MCS behaviors to a scewed form of addictive behavior. (Kreibich, Sahuque) More simply, its activation leads to changes in hormone production and alter behaviors, it is possible that abherrant signaling in this system may be responsible for some of the symptoms of MCS and similar to those from chemical withdrawal but modified into aversive response. It is also possible the addictive nature of smoking from ammonia or other volatiles on the CRF from smoke exposure could be a sensitizing factor, stimulate the immune system and also initiate a "loss of tolerance" which has been suggested as an explanation of multiple chemical sensitivity and sensitivities in autism. An interesting research study could be designed to determine wether a potential correlation of MCS sensitization and smoking could exist.
To support this idea further, researchers have demonstrated the addictive nature of smoking involves a cellular pathway called CREB that involves the relationship of reward to smoking behaviors and their association with environmental cues. Also, recent research findings show a strong association of CREB and CRF in stress-induced drug reward behavior. It is not beyond reason to suggest that alterations in signals that lead to physical and psychological symptoms of drug withdrawal may also influence physical and emotional aversive behaviors of MCS and argues against the notion of that symptoms of MCS are "psychosomatic". The high levels of cadmium may further disrupt the CREB pathway and normal cell functions. Both of these discoveries provide an important mechanism to explain activation of MCS by environmental cues and suggests that insulin resistance may play a part in some of its reactions. "Previously,it has been shown the CREB pathway keeps blood sugar in balance under certain metabolic conditions and excessive CREB activity in diabetes contributes to high blood sugar and insulin resistance. New findings show CREB encourages insulin resistance by lowering adiponectin and the insulin-sensitive glucose transporter 4 (GLUT4)." (US Health News) CREB is a mediator of inflammation and both of these findings demonstrate that overactive CREB may contribute to endothelial dysfunction and impair cognitive function by mediating inflammation and insulin resistance. (Ishiki) On the other hand, downregulation of the cGMP/NO/CREB by amyloid or hyperammonemia may contribute to neurodegenerative diseases and Alzheimer's. (Copper Mountain, CO, Puzzo) This has important implications not only for cigarette smoke but persistent organic pollutants considering they both may contribute to diabetes complications.Other environmental factors such as other exposures to heavy metals implicated in contributing to diabetes and altered methylation may also contribute to these conditions. (Pozharny)
Along those same lines, cigarette smoking also contributes to weight loss through activation of the aryl hydrocarbon and endoplasmic reticulum stress. In other blogs, I have suggested this process also is involved in MCS. A recent study agrees with findings that cigarette smoke and dioxin does lower adiponectin but also demonstrated that PPAR-gamma and c/EPB were also decreased. In another study, ornithine impairments in c/EPB knock-outs from hypoglycemia presented with significantly higher levels of ammonia. Further, it has been shown ornithine enzymes interact with C/EPB and is important for ammonia detoxification. Without it, you get impaired excretion of urea and gluconeogenesis. As one can see, metabolically cigarette smoke may cause severe alterations in metabolism. This may include alterations of ammonia which may potentially sensitize an individual towards development and contribute to multiple chemical sensitivity.
Citations and other documents available here.
In cells, chemical toxins effect metabolic pathways which may run parallel, are independant and/or interact, potentiate or possibly minimize the effects of each another. For this reason, it is difficult to predict the severity and the consequences of them on the health of an organism. Exposure to cigarette smoke is no different and has been shown to act differently in different people and on more than one molecular pathway at the same time. Through the years, hundreds of studies have demonstrated the health hazards associated with the toxic effects of smoking and one of these effects includes the dysregulation of metabolism including altering blood sugar homeostasis. Personally, I have suspected this to be the case for some time. Over the past several years, scientists have discovered smoking not only increases the risk for diabetes which includes higher glucose levels, higher insulin levels and increased blood pressure it may also contribute to episodes of hypoglycemia in diabetes. As one article state, "this may be due to an effect of smoking on insulin clearance, leading to hyperinsulinemia, increasing hypoglycemia, and worsening metabolic control. In addition, smoking has been shown to increase the secretion of hormones (i.e., growth hormone, vasopressin, and cortisol) that counteract insulin action, leading to an increased insulin requirement. Smokers have been found to require more insulin than nonsmokers to achieve the same level of glycemic control in some, but not all, studies." (Hirai)
In addition to ammonia making cigarettes more addictive, ammonia can act on the cortico-releasing factor (CRF) system which regulates behavior including feeding and increases serotonin and dopamine levels. As a consequence, it can influence mood and alter homeostasis leading the conditions like the weight loss and weight gain from smoking and cessation, respectively. Activation of this pathway, in fact, mediates psychological effects of nicotine withdrawal. (Grunberg) I recently mentioned that because ammonia activates the CRF pathway that regulates neuroendocrine, drug abuse responses and aversion one could relate MCS behaviors to a scewed form of addictive behavior. (Kreibich, Sahuque) More simply, its activation leads to changes in hormone production and alter behaviors, it is possible that abherrant signaling in this system may be responsible for some of the symptoms of MCS and similar to those from chemical withdrawal but modified into aversive response. It is also possible the addictive nature of smoking from ammonia or other volatiles on the CRF from smoke exposure could be a sensitizing factor, stimulate the immune system and also initiate a "loss of tolerance" which has been suggested as an explanation of multiple chemical sensitivity and sensitivities in autism. An interesting research study could be designed to determine wether a potential correlation of MCS sensitization and smoking could exist.
To support this idea further, researchers have demonstrated the addictive nature of smoking involves a cellular pathway called CREB that involves the relationship of reward to smoking behaviors and their association with environmental cues. Also, recent research findings show a strong association of CREB and CRF in stress-induced drug reward behavior. It is not beyond reason to suggest that alterations in signals that lead to physical and psychological symptoms of drug withdrawal may also influence physical and emotional aversive behaviors of MCS and argues against the notion of that symptoms of MCS are "psychosomatic". The high levels of cadmium may further disrupt the CREB pathway and normal cell functions. Both of these discoveries provide an important mechanism to explain activation of MCS by environmental cues and suggests that insulin resistance may play a part in some of its reactions. "Previously,it has been shown the CREB pathway keeps blood sugar in balance under certain metabolic conditions and excessive CREB activity in diabetes contributes to high blood sugar and insulin resistance. New findings show CREB encourages insulin resistance by lowering adiponectin and the insulin-sensitive glucose transporter 4 (GLUT4)." (US Health News) CREB is a mediator of inflammation and both of these findings demonstrate that overactive CREB may contribute to endothelial dysfunction and impair cognitive function by mediating inflammation and insulin resistance. (Ishiki) On the other hand, downregulation of the cGMP/NO/CREB by amyloid or hyperammonemia may contribute to neurodegenerative diseases and Alzheimer's. (Copper Mountain, CO, Puzzo) This has important implications not only for cigarette smoke but persistent organic pollutants considering they both may contribute to diabetes complications.Other environmental factors such as other exposures to heavy metals implicated in contributing to diabetes and altered methylation may also contribute to these conditions. (Pozharny)
Along those same lines, cigarette smoking also contributes to weight loss through activation of the aryl hydrocarbon and endoplasmic reticulum stress. In other blogs, I have suggested this process also is involved in MCS. A recent study agrees with findings that cigarette smoke and dioxin does lower adiponectin but also demonstrated that PPAR-gamma and c/EPB were also decreased. In another study, ornithine impairments in c/EPB knock-outs from hypoglycemia presented with significantly higher levels of ammonia. Further, it has been shown ornithine enzymes interact with C/EPB and is important for ammonia detoxification. Without it, you get impaired excretion of urea and gluconeogenesis. As one can see, metabolically cigarette smoke may cause severe alterations in metabolism. This may include alterations of ammonia which may potentially sensitize an individual towards development and contribute to multiple chemical sensitivity.
Citations and other documents available here.
Alterations in cGMP/NO in liver disease
CiteULike: Alterations in soluble guanylate cyclase content and modulation by nitric oxide in liver disease: "Rodrigo, R. (2004). Alterations in soluble guanylate cyclase content and modulation by nitric oxide in liver disease. Neurochemistry International, 45(6):947-953."
Hypoxia-induced megaloblastosis in vitamin B12-deficient rats
CiteULike: Hypoxia-induced megaloblastosis in vitamin B12-deficient rats.: "Ebara, S., Adachi, S., Takenaka, S., Enomoto, T., Watanabe, F., Yamaji, R., Inui, H., and Nakano, Y. (2003). Hypoxia-induced megaloblastosis in vitamin b12-deficient rats. The British journal of nutrition, 89(4):441-444."
CiteULike: Hypoglycemia-associated Hyperammonemia Caused by Impaired Expression of Ornithine Cycle Enzyme Genes in C/EBPα Knockout Mice
CiteULike: Hypoglycemia-associated Hyperammonemia Caused by Impaired Expression of Ornithine Cycle Enzyme Genes in C/EBPα Knockout Mice: "Kimura, T., Christoffels, V. M., Chowdhury, S., Iwase, K., Matsuzaki, H., Mori, M., Lamers, W. H., Darlington, G. J., and Takiguchi, M. (1998). Hypoglycemia-associated hyperammonemia caused by impaired expression of ornithine cycle enzyme genes in c/ebpα knockout mice. Journal of Biological Chemistry, 273(42):27505-27510."
Wednesday, May 5, 2010
Curcumin Mediated Glutathione Efflux w. Nrf2 Is Neuroprotective
CiteULike: Enhanced Glutathione Efflux from Astrocytes in Culture by Low Extracellular Ca(2+) and Curcumin.: "Stridh, M. H., Correa, F., Nodin, C., Weber, S. G., Blomstrand, F., Nilsson, M., and Sandberg, M. (2010). Enhanced glutathione efflux from astrocytes in culture by low extracellular ca(2+) and curcumin. Neurochemical research."
New Culprit In Muscle Defects, Insulin Resistance That Come With Age
Type 2 diabetes is a widespread problem for many people these days, and our risk for insulin resistance and diabetes only grows as we age. Now, a new report in the May issue of Cell Metabolism, a Cell Press publication, reveals a new contributor to the problem: The muscles of elderly people and of people with type 2 diabetes contain lower concentrations of a protein known as PARL (short for "presenilin-associated rhomboid-like").
New Culprit In Muscle Defects, Insulin Resistance That Come With Age
The Not So FINE Trial Study for CFS.
A million and a half dollars, two hundred fifty patients and seven years later the UK government's best hope for locking in its twisted approach to ME/CFS permanently, fell to earth with a crash.
Chronic Fatigue Syndrome (ME/CFS) News From Phoenix Rising - FINE: "A million and a half dollars, two hundred fifty patients and seven years later the UK government's best hope for locking in its twisted approach to ME/CFS permanently, fell to earth with a crash."
Present Case Definitions Still Not Accurate for CFS Diagnosis.
CiteULike: Sensitivity and Specificity of the CDC Empirical Chronic Fatigue Syndrome Case Definition: "Jason, L. A., Evans, M., Brown, A., Brown, M., Porter, N., Hunnell, J., Anderson, V., and Lerch, A. (2010). Sensitivity and specificity of the cdc empirical chronic fatigue syndrome case definition. Psychology, pages 9-16."
Tuesday, May 4, 2010
Nova Scotia banning lawn pesticides
Nova Scotians won't be allowed to use pesticides on their lawns starting nextspring
Nova Scotia banning lawn pesticides
Down-regulation of Regulatory T Cells May Augment Autoimmune Disease.
In conclusion, inhibiting components of the adaptive immune response, like Tregs, are down-regulated during a stress-induced activation of the adaptive immune response. In situations of chronic stress, this scenario might result in an exacerbation of inflammatory conditions such as autoimmune diseases. (Source: Psychoneuroendocrinology)
Decrease of CD4+FOXP3+ T regulatory cells in the peripheral blood of human subjects undergoing a mental stressor
Trauma-induced changes to genes may lead to PTSD
A study by researchers at Columbia University's Mailman School of Public Health suggests that traumatic experiences "biologically embed" themselves in select genes, altering their functions and leading to the development of post-traumatic stress disorder (PTSD).
Trauma-induced changes to genes may lead to PTSD
Monday, May 3, 2010
Biological definition of MCS from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes.
CiteULike: Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes.: "De Luca, C., Scordo, M. G., Cesareo, E., Pastore, S., Mariani, S., Maiani, G., Stancato, A., Loreti, B., Valacchi, G., Lubrano, C., Raskovic, D., De Padova, L., Genovesi, G., and Korkina, L. G. (2010). Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes. Toxicology and applied pharmacology"
The Ammonia Hypothesis - A Science and Protocal of Spiritual Alchemy
The following ties together much of what I have written on the possible physiology of kundalini so far and is the most speculative piece in this book. I am pretty sure that convulsive/seizure/kindling can actually produce ammonia, as well as be caused by ammonia. If so this could be one of the main causes of people running into extended periods of difficulty with kundalini.
CiteULike: The Ammonia Hypothesis - A Science and Protocal of Spiritual Alchemy: "The ammonia hypothesis - a science and protocal of spiritual alchemy."
Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcal Infections | vactruth.com
Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcal Infections | vactruth.com: "Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcal Infections: Clinical Description of the First 50 Cases"
Saturday, May 1, 2010
Thought for the Day: Hyperammonemia and Environmental Illness...
Does anyone see these as being familiar symptoms? To me, they seem like some common symptoms in CFS or exposures????
HEIRS Library Tags: Hyperammonemia
Blog Tags: Hyperammonemia, ammonia
Edwards, W. ARM CRANK POWER AND HYPERAMMONEMIA IN RESPONSE TO L-ASPARTIC ACID SUPPLEMENTATION. PhD thesis, Louisiana State University.
http://www.citeulike.org/user/HEIRS/article/7111333
The symptoms and blood ammonia values of mild to moderate chronic hyperammemia (CH) are similar to those observed during physical exhaustion with ‘exercise-induced hyperammonemia’ (EIH). These include confusion, hyperventilation, and muscular dysfunction.....Treatments for lowering CH and EIH are similar, and include: 1) restriction of dietary
protein, 2) increasing carbohydrate (%) intake, 3) administration of amino acids (AA’s)that enhance ammonia clearance into (the less toxic) urea, and 4) correction of the underlying metabolic etiology
HEIRS Library Tags: Hyperammonemia
Blog Tags: Hyperammonemia, ammonia
Edwards, W. ARM CRANK POWER AND HYPERAMMONEMIA IN RESPONSE TO L-ASPARTIC ACID SUPPLEMENTATION. PhD thesis, Louisiana State University.
http://www.citeulike.org/user/HEIRS/article/7111333
Toxicology: Cells Deficient in Ornithine Decarboxylase Activity Induced by Ethyl Methane Sulfonate.
"one null mutant, which was induced with ethyl methane sulfonate and which makes ODC mRNA but no active enzyme, is nevertheless revertible with 5-azacytidine."CiteULike: Chinese hamster cells deficient in ornithine decarboxylase activity: reversion by gene amplification and by azacytidine treatment.:
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