Friday, April 30, 2010
Short and Long Ter Vitamin Effects of Smoking
CiteULike: Long- and Short-term Effects of Tobacco Smoking on Circulating Concentrations of B Vitamins: "Ulvik, A., Ebbing, M., Hustad, S., Midttun, O., Nygard, O., Vollset, S. E., Bonaa, K. H., Nordrehaug, J. E., Nilsen, D. W., Schirmer, H., and Ueland, P. M. (2010). Long- and short-term effects of tobacco smoking on circulating concentrations of b vitamins. Clin Chem, 56(5):755-763."
Thursday, April 29, 2010
PGC-1a and Exercise and Impact on Muscle Function and Insulin Sensitivity
"modest (~25%) upregulation of PGC-1alpha, within physiologic limits, does improve mitochondrial biogenesis, fatty acid oxidation and insulin sensitivity in healthy and insulin resistant skeletal muscle."
PGC-1{alpha} REGULATION BY EXERCISE TRAINING AND AND ITS INFLUENCES ON MUSCLE FUNCTION AND INSULIN SENSITIVITY [Am J Physiol Endocrinol Metab. 2010] - PubMed result:
Wednesday, April 28, 2010
Scientists Discover Substance That Causes Pain
Scientists Discover Substance That Causes Pain: "a family of fatty acids called oxidized linoleic acid metabolites (OLAMs) play an important role in the biology of pain."
'Epigenetic' Concepts Offer New Approach To Degenerative Disease
'Epigenetic' Concepts Offer New Approach To Degenerative Disease: "'Epigenetic' Concepts Offer New Approach To Degenerative Disease"
Tuesday, April 27, 2010
Substance in Wine and Grapes Protects Against Endothelial Dysfunction.
CiteULike: Resveratrol confers endothelial protection via activation of the antioxidant transcription factor Nrf2.: "Resveratrol confers endothelial protection via activation of the antioxidant transcription factor Nrf2."
Monday, April 26, 2010
Proprionic Acid May Be Associated With IBS
"Propionic acid in rodents produces reversible behavior (e.g. hyperactivity, dystonia, social impairment, perseveration) and brain (e.g. innate neuroinflammation, glutathione depletion) changes reminiscent of autism.[3]"Propionic acid - Wikipedia, the free encyclopedia:
GSK-3b - Regulator of Intestinal Inflammation
Well gee, have I not been saying this for months now???? GSK-3b also promotes neuroinflammation and may be responsible for brain inflammatory responses by intestinal inflammation. "Since this protein can inhibit neuroprotective antioxidant system -- this is probably highly likely." HEIRS_Health
Read more: HEIRS Blog Tags: GSK-3b
*****HEIRS Library Tag: GSK-3b
Glycogen synthase kinase 3-[beta]: A master regulator of toll-like receptor-mediated chronic intestinal inflammation
A disturbed regulation of Toll-like receptor (TLR) signal transduction resulting in the exclusive activation of proinflammatory signaling pathways may be critical for the perpetuation of established chronic colitis. Glycogen synthase kinase 3-[beta] (GSK3-[beta]) was recently identified as an important regulator of TLR signaling mediating excessive inflammatory responses.
Read more: HEIRS Blog Tags: GSK-3b
*****HEIRS Library Tag: GSK-3b
Glycogen synthase kinase 3-[beta]: A master regulator of toll-like receptor-mediated chronic intestinal inflammation
Connections: Hearing Loss and Inflammatory Bowel Disease
CiteULike: Sensorineural Hearing Loss in Pediatric Patients with Inflammatory Bowel Disease: "Sensorineural Hearing Loss in Pediatric Patients with Inflammatory Bowel Disease"
Chronic Elevated Ammonia Contributes to Neuroinflammation, Cognitive and Motor Dysfunction.
CiteULike: Hyperammonemia Induces Neuroinflammation that Contributes to Cognitive Impairment in Rats with Hepatic Encephalopathy.: "Chronic moderate hyperammonemia or BDL activated the microglia, especially in cerebellum; increased iNOS, IL-1beta, and prostaglandin E2 levels; and impaired cognitive and motor function, compared with controls"
Chronic hyperammonemia alters the circadian rhythm... [J Neurosci Res. 2010] - PubMed result
Chronic hyperammonemia alters the circadian rhythm... [J Neurosci Res. 2010] - PubMed result: "Chronic hyperammonemia alters the circadian rhythms of corticosteroid hormone levels and of motor activity in rats."
Sunday, April 25, 2010
Environmental factors maybe key in autism boom since 1988 says EPA
Environmental factors maybe key in autism boom since 1988 says EPA: "Environmental factors maybe key in autism boom since 1988 says EPA"
Saturday, April 24, 2010
Anti-diabetic Drug May Ameliorate Inflammatory Effects on Kidney Tubules
Troglitazone ameliorates high glucose-induced EMT and dysfunction of SGLTs through PI3K/Akt, GSK-3{beta}, Snail1, and {beta}-catenin in renal proximal tubule cells -- Lee and Han 298 (5): F1263 -- AJP - Renal Physiology: "HG induces EMT through ROS, PI3K/Akt, GSK-3β, Snail, and β-catenin. Subsequently, HG-induced EMT may result in SGLT dysfunction that is restored by the PPAR agonist troglitazone in primary cultured PTCs"
Researchers Explain How Trauma Leads to Inflammatory Response - Beth Israel Deaconess Medical Center
Researchers Explain How Trauma Leads to Inflammatory Response - Beth Israel Deaconess Medical Center: "Findings show that mitochondria may be at the root of dangerous complications stemming from traumatic injury"
Vitiligo Tied to Immune System Dysfunction - Skin Diseases, Conditions, Symptoms, and Procedures on MedicineNet.com
Vitiligo Tied to Immune System Dysfunction - Skin Diseases, Conditions, Symptoms, and Procedures on MedicineNet.com: "Scientists have discovered several genes linked to vitiligo that confirm the skin condition is, indeed, an autoimmune disorder."
Friday, April 23, 2010
Thursday, April 22, 2010
Fatal ammonia toxicity in an adult due to an undiagnosed urea cycle defect: under-recognition of ornithine transcarbamylase deficiency.
CiteULike: Fatal ammonia toxicity in an adult due to an undiagnosed urea cycle defect: under-recognition of ornithine transcarbamylase deficiency.: "Thurlow, V. R., Asafu-Adjaye, M., Agalou, S., and Rahman, Y. (2010). Fatal ammonia toxicity in an adult due to an undiagnosed urea cycle defect: under-recognition of ornithine transcarbamylase deficiency. Annals of clinical biochemistry."
Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival — Cardiovasc Res
Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival — Cardiovasc Res: "Nrf2-HO-1 signaling cascade as a crucial modulator of vascular cell survival during periods of nitrosative stress."
Reduced endothelial NO-cGMP vascular relaxation pathway during TNF-alpha -induced hypertension in pregnant rats
CiteULike: Reduced endothelial NO-cGMP vascular relaxation pathway during TNF-alpha -induced hypertension in pregnant rats: "Davis, J. R., Giardina, J. B., Green, G. M., Alexander, B. T., Granger, J. P., and Khalil, R. A. (2002). Reduced endothelial no-cgmp vascular relaxation pathway during tnf-alpha -induced hypertension in pregnant rats. Am J Physiol Regul Integr Comp Physiol, 282(2):R390-399."
Wednesday, April 21, 2010
Natural taurine promotes apoptosis of human hepatic stellate cells in proteomics analysis.
CiteULike: Natural taurine promotes apoptosis of human hepatic stellate cells in proteomics analysis.: "Deng, X., Liang, J., Lin, Z.-X. X., Wu, F.-S. S., Zhang, Y.-P. P., and Zhang, Z.-W. W. (2010). Natural taurine promotes apoptosis of human hepatic stellate cells in proteomics analysis. World journal of gastroenterology : WJG, 16(15):1916-1923."
Monday, April 19, 2010
Reducation of Pathogenic Activation with Mechanisms That Influence Tregs Production
CiteULike: Commensal-Induced Regulatory T Cells Mediate Protection against Pathogen-Stimulated NF-κB Activation: "O'Mahony, C., Scully, P., O'Mahony, D., Murphy, S., O'Brien, F., Lyons, A., Sherlock, G., MacSharry, J., Kiely, B., Shanahan, F., and O'Mahony, L. (2008). Commensal-induced regulatory t cells mediate protection against pathogen-stimulated nf-κb activation. PLoS Pathog, 4(8):e1000112+."
Sunday, April 18, 2010
Study Suggest Pain Involvement in Alterations in NO-cGMP Pathway
Nguelefack, T. B., Dutra, R. C., Paszcuk, A. F., Andrade, E. L., Tapondjou, L. A., and Calixto, J. B. (2010). Antinociceptive activities of the methanol extract of the bulbs of dioscorea bulbifera l. var sativa in mice is dependent of no-cgmp-atp-sensitive-k(+) channel activation. Journal of ethnopharmacology, 128(3):567-574.
http://www.citeulike.org/user/HEIRS/article/6664177
HEIRS Environmental Illness Research Blog: Dysfunction of Methylation and Nrf2 in Environmental Illness - A Better Explanation than NO/ONOO- ?
http://www.citeulike.org/user/HEIRS/article/6664177
HEIRS Environmental Illness Research Blog: Dysfunction of Methylation and Nrf2 in Environmental Illness - A Better Explanation than NO/ONOO- ?
Skeletal Muscle Target For Bacterial Metabolic Changes Seen in Diabetes and Obesity
"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."Toll-like receptor 4 modulates skeletal muscle sub... [Am J Physiol Endocrinol Metab. 2010] - PubMed result:
Saturday, April 17, 2010
NO-cGMP and Mitochondrial Biogenesis -- Mediator of PGC-1a
As we have noted, hyperammonia may impair the NO-cGMP pathway. Nisoli explains, "nitric oxide-cGMP-dependent pathway controls mitochondrial biogenesis and body energy balance."Nisoli, E., Clementi, E., Paolucci, C., Cozzi, V., Tonello, C., Sciorati, C., Bracale, R., Valerio, A., Francolini, M., Moncada, S., and Carruba, M. O. (2003). Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide. Science (New York, N.Y.), 299(5608):896-899. http://www.citeulike.org/user/HEIRS/article/7030900
HEIRS Environmental Illness Research Blog: Dysfunction of Methylation and Nrf2 in Environmental Illness - A Better Explanation than NO/ONOO- ?
Wnt/beta-Catenin Signaling Activates and Determines Hepatic Zonal Expression of Glutathione S-Transferases in Mouse Liver
CiteULike: Wnt/beta-Catenin Signaling Activates and Determines Hepatic Zonal Expression of Glutathione S-Transferases in Mouse Liver: "Giera, S., Braeuning, A., Kohle, C., Bursch, W., Metzger, U., Buchmann, A., and Schwarz, M. (2010). Wnt/beta-catenin signaling activates and determines hepatic zonal expression of glutathione s-transferases in mouse liver. Toxicol. Sci., 115(1):22-33."
Friday, April 16, 2010
Thursday, April 15, 2010
Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis
CiteULike: Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis: "Shawcross, D. (2004). Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis. Journal of Hepatology, 40(2):247-254."
Hyperammonemia increases sensitivity to LPS.
CiteULike: Hyperammonemia increases sensitivity to LPS.: "Marini, J. C. and Broussard, S. R. (2006). Hyperammonemia increases sensitivity to lps. Molecular genetics and metabolism, 88(2):131-137."
CiteULike: Ornithine restores ureagenesis capacity and mitigates hyperammonemia in Otc(spf-ash) mice.
CiteULike: Ornithine restores ureagenesis capacity and mitigates hyperammonemia in Otc(spf-ash) mice.: "Marini, J. C., Lee, B., and Garlick, P. J. (2006). Ornithine restores ureagenesis capacity and mitigates hyperammonemia in otc(spf-ash) mice. The Journal of nutrition, 136(7):1834-1838."
Nrf2 Inhibits Liposaccharide-Induced-Il-6 in RAW Macrophage Cell Line
CiteULike: Nrf2 Inhibits Liposaccharide-Induced-Il-6 in RAW Macrophage Cell Line: "Rangasemy, T., Chauhan, A., Singh, A., Stewart, J., Frampton, M., Yamamoto, M., Biswal, S., and Georas, S. (2009). Nrf2 inhibits liposaccharide-induced-il-6 in raw macrophage cell line. American Journal of Respiratory Critical Care Medicine, 179(A4184)."
Gram (+) Bacterial Component Strongly Enhances Inflammatory Response in Rheum Arthritis...
CiteULike: Lipoteichoic acid enhances IL-6 production in human synovial fibroblasts via TLR2 receptor, PKCdelta and c-Src dependent pathways.: "Tang, C.-H. H., Hsu, C.-J. J., Yang, W.-H. H., and Fong, Y.-C. C. (2010). Lipoteichoic acid enhances il-6 production in human synovial fibroblasts via tlr2 receptor, pkcdelta and c-src dependent pathways. Biochemical pharmacology, 79(11):1648-1657."
Downregulation of the Ornithine Decarboxylase/polyamine System Inhibits Angiotensin-induced Hypertrophy of Cardiomyocytes Through the NO/cGMP-dependent Protein Kinase Type-I Pathway
CiteULike: Downregulation of the Ornithine Decarboxylase/polyamine System Inhibits Angiotensin-induced Hypertrophy of Cardiomyocytes Through the NO/cGMP-dependent Protein Kinase Type-I Pathway: "Lin, Y., Liu, J.-C., Zhang, X.-J., Li, G.-W., Wang, L.-N., Xi, Y.-H., Li, H.-Z., Zhao, Y.-J., and Xu, C.-Q. (2010). Downregulation of the ornithine decarboxylase/polyamine system inhibits angiotensin-induced hypertrophy of cardiomyocytes through the no/cgmp-dependent protein kinase type-i pathway. Cellular Physiology and Biochemistry, 25(4-5)."
Downregulation of the Ornithine System, the Heart and NO-cGMP!
Hypertrophy of cardiomyocytes was induced by AngII, this caused an increase in putrescine, spermidine and total polyamine pool in association with a decreased level of NO. Expressions of eNOS and PKG-I were down-regulated, [Ca2+]i was increased, and expressions of c-Fos and c-Myc upregulated. DFMO reversed these changes induced by AngII.Lin, Y., Liu, J.-C., Zhang, X.-J., Li, G.-W., Wang, L.-N., Xi, Y.-H., Li, H.-Z., Zhao, Y.-J., and Xu, C.-Q. (2010). Downregulation of the ornithine decarboxylase/polyamine system inhibits angiotensin-induced hypertrophy of cardiomyocytes through the no/cgmp-dependent protein kinase type-i pathway. Cellular Physiology and Biochemistry, 25(4-5).
HEIRS Environmental Illness Research Blog: Dysfunction of Methylation and Nrf2 in Environmental Illness - A Better Explanation than NO/ONOO- ?
Wednesday, April 14, 2010
Lithium Chloride and NO-cGMP Pathway
Our findings demonstrated that nitric oxide-cyclic GMP pathway could be involved in the anticonvulsant properties of the lithium chloride. In addition, the role of constitutive NOS versus inducible NOS is prominent in this phenomenon.
Bahremand, A., Nasrabady, S. E., Ziai, P., Rahimian, R., Hedayat, T., Payandemehr, B., and Dehpour, A. R. (2010). Involvement of nitric oxide-cgmp pathway in the anticonvulsant effects of lithium chloride on ptz-induced seizure in mice. Epilepsy Research, pages 295-302.
http://www.citeulike.org/user/HEIRS/article/7020649
HEIRS Environmental Illness Research Blog: Dysfunction of Methylation and Nrf2 in Environmental Illness - A Better Explanation than NO/ONOO- ?
Suppression of Inflammatory Mediators by Cruciferous Vegetable-Derived Indole-3-Carbinol and Phenylethyl Isothiocyanate in Lipopolysaccharide-Activated Macrophages
I3C and PEITC both found in leafy green vegetables possess antiinflammatory effects by inhibiting the productions of NO, TNF-, and IL-10 in LPS-stimulated macrophages. NO’s inhibitory effect on I3C, in addition to decreasing the expression of iNOS, may at least partly be through interfering with iNOS enzyme activity as well as direct NO clearance activity, whereas PEITC may act through its direct NO clearance activity but not interfere with iNOS enzyme activity.CiteULike: Suppression of Inflammatory Mediators by Cruciferous Vegetable-Derived Indole-3-Carbinol and Phenylethyl Isothiocyanate in Lipopolysaccharide-Activated Macrophages: "Tsai, J.-T., Liu, H.-C., and Chen, Y.-H. (2010). Suppression of inflammatory mediators by cruciferous vegetable-derived indole-3-carbinol and phenylethyl isothiocyanate in lipopolysaccharide-activated macrophages. Mediators of Inflammation."
CFS Differences to Serotonin Suggest Different Condition Than FM
Mary Ann Liebert, Inc. - Journal of Women's Health - 0(0):: "Sex Differences in Plasma Prolactin Response to Tryptophan in Chronic Fatigue Syndrome Patients With and Without Comorbid Fibromyalgia"
Gene that changes the brain’s response to stress identified
You may recall I have written about the potential of the influence of this hormone on a number of illnesses....
HEIRS Research Tag: BDNF
Gene that changes the brain’s response to stress identified
HEIRS Research Tag: BDNF
Gene that changes the brain’s response to stress identified
Tuesday, April 13, 2010
CD154-CD40 T-cell pathway hepatic ischemia/reperfusion injury,blockade depends on HO-1
CiteULike: CD154-CD40 T-cell costimulation pathway is required in the mechanism of hepatic ischemia/reperfusion injury, and its blockade facilitates and depends on heme oxygenase-1 mediated cytoprotection.: "Shen, X.-D. D., Ke, B., Zhai, Y., Amersi, F., Gao, F., Anselmo, D. M., Busuttil, R. W., and Kupiec-Weglinski, J. W. (2002). Cd154-cd40 t-cell costimulation pathway is required in the mechanism of hepatic ischemia/reperfusion injury, and its blockade facilitates and depends on heme oxygenase-1 mediated cytoprotection. Transplantation, 74(3):315-319."
Tumor Necrosis Factor alpha and CD40 Ligand Antagonize the Inhibitory Effects of Interleukin 10 on T-Cell Stimulatory Capacity of Dendritic Cells
CiteULike: Tumor Necrosis Factor alpha and CD40 Ligand Antagonize the Inhibitory Effects of Interleukin 10 on T-Cell Stimulatory Capacity of Dendritic Cells: "Brossart, P., Zobywalski, A., Grunebach, F., Behnke, L., Stuhler, G., Reichardt, V. L., Kanz, L., and Brugger, W. (2000). Tumor necrosis factor alpha and cd40 ligand antagonize the inhibitory effects of interleukin 10 on t-cell stimulatory capacity of dendritic cells. Cancer Res, 60(16):4485-4492."
Immunosuppressive Effects of Vitamin D
Potent Inhibition of Dendritic Cell Differentiation and Maturation by Vitamin D Analogs: "Griffin, M. (2000). Potent inhibition of dendritic cell differentiation and maturation by vitamin d analogs. Biochemical and Biophysical Research Communications, 270(3):701-708."
Probiotic-Type Substances Act By Inducing HO-1
CiteULike: Oligosaccharides from Agar Inhibit Pro-Inflammatory Mediator Release by Inducing Heme Oxygenase 1.: "Enoki, T., Okuda, S., Kudo, Y., Takashima, F., Sagawa, H., and Kato, I. (2010). Oligosaccharides from agar inhibit pro-inflammatory mediator release by inducing heme oxygenase 1. Bioscience, biotechnology, and biochemistry."
Sunday, April 11, 2010
Dysfunction of Methylation and Nrf2 in Environmental Illness - Is This A Better Explanation than NO/ONOO- ?
One of the most important themes of my research is that accumulation of ammonia may play a causal role in including in conditions such MCS and autism through alterations in the methionine and glutamine synthetase pathway and elevations of ammonia in general which may change the expression of a variety of genes that regulate cell function. Of course, this has been suggested by a number of experts. Further, I also have proposed that the dysfunction in Nrf2 and related genes contribute to the severity and elicits autoimmune-type responses and chemicals such as PFOS may influence it or "trigger" it in addition to other chemicals that are more commonly considered as more toxic. In support, in support it has been suggested that hyperammonemia may alter that nitric-oxide-cGMP pathway (Hermenegildo) and as a result this could alter NO funtioning and contribute to conditions such as fibrosis in some tissuesand endothelial dysfunction. Alterations in the ornithine pathway may contribute to this but it is worth mentioning that NO may alter this pathway on it own. (Bauer) Interestingly, recently it has been reported that one of the benefits of fish oil may be mediated through the eNOS-cGMP pathway. (Lopez) Nrf2 also has an important role in regulating NO and CO through its interaction with the antioxidant HO-1 and plays a substantial neuroprotective role against diseases such as Parkinson's disease. The deficiency or lack of Nrf2 expression offers one explanation of why individuals with MCS are so sensitive to carbon monoxide, nitrous oxide and other greenhouse gases. Mainly, because of the dysregulation of their regulator HO-1 by Nrf2. Tinnitus is common with MCS and can be associated with over-exposure to nitrous oxide which may also indicate problems associated with vitamin B and methylation. (Wipedia) Genetic polymorphisms in HO-1 and metal toxicity may also contribute to this problem. (You can see how lead, mercury and aluminum alter function in different steps in the cycle....here but you have to look closely.) Other Nrf2 interactions include modulation of Il-6 which is elevated in neuroinflammatory responses in the brain and Il-10 which is an anti-inflammatory that modulates sickness syndrome. According to a new report, sickness syndrome may be implicated in causing some of the symptoms of Gulf War Syndrome.
In addition, conditions such as elevations of ammonia activate the CRF pathway in animals that display hyperanxious behavior and recently this pathway has been shown to regulate both anxiety and depression as a consequence of stress. (Biomedicine) Interestingly, the glutamine pathway is also altered during depression and as a result, one may suggest this pathway may be dysregulated from exposure to chemicals such as PFOS and cause mood changes such as depression and anxiety and endogenous elevations of ammonia may induce mood changes even more. In addition, dysfunction of Nrf2 may lead to neurotoxicity and other consequences including augmenting ammonia accumulation. Chemical sensitivity has been implied as important in autism and ammonia may contribute to this which is produced endogenously and exogenously and many therapies used for MCS have also been used to reduce ammonia levels in autism. An interesting suggestion is that in some form through the dysfunction of Nrf2, deficits in the ornithine pathway contribute to the cellular toxicity experienced in MCS and autism. Of course, there are a number of other genetic defects that may alter the urea-cycle, including minor ones that may not appear until adulthood or later because of compensation from other pathways lost with ageing. Ammonia production is higher correlated with inflammatory markers in liver injury and has a profound effect on the permeability of the blood-brain-barrier, providing access of more toxic agents to brain tissue. (Jalan)
Alterations in the methionine pathway have also been suggested to play an important role in autism and we suggest here, MCS and relies on the notion of abherrant methylation "tagging" that potentiate the problems or vice versa. Q10 and vitamin B12 has been used as a therapy for MCS but is also used to assist mitochondrial function and support the methionine cycle and reduce ammonia, respectively. In methyl cycle disfunction, BH4 is drained in ammonia detoxification (Yasko ?) in addition in contrast to its role for NOS production and peroxynitrite which is part of the NO/ONOO- hypothesis. (Pall) Here we see the dichotomy between the Methyl Pathway and the NO/ONOO- hypothesis where BH4 is concerned. In one BH4-dependant process, NOS is converted to nitric oxide and on the other hand it assists in ammonia detoxification in the methylation cycle. If you put alterations in Nrf2 function, which is activated by ONOO- into the mix it can alter expression of genes important for these processes. ONOO- is not the only pro-oxidant that activates the Nrf2, it has been suggested that H2O2 is a much stronger activator and numerous other conditions normally upregulate Nrf2 in normal circumstances. Marzec recently demonstrated that SNPs that exist in the Nrf2 may make on more or less susceptible to oxidative stress and therefore cellular injury and disfunction. The inheritability hypothesis of epigenetics also relies on methylation and helps to explain why environmental illnesses largely run in families and the relationships between gene expression help to explain why gender plays an important role too! Unfortunately, alterations in methylation and consequently, alteration of function has been demonstrated in Nrf2 and several other genes implicated in environmental illness including autism. (To get an idea of how complicated genetics in environmental illness is --click here. ) In addition, alterations in Nrf2 and PGC-1a may contribute to diabetes and insulin resistance and are associated with POP exposures. In addition, GSK-3b involvement from reduced expression of PGC-1a, elevations in dopamine and exposures to bacteria (endotoxin) are a few additional factors that may hamper Nrf2 detoxification system which can lead to more elevations of neuroinflammatory processes, mood changes and significantly increase the likelihood of more neurodegeneration; all associated with environmental illness. GSK-3b signalling also may involve alterations in dopamine-regulated behaviors such as twitching (Tourette's) and ADHD that are often co-morbid with environmental illnesses after exposure injury. Incidentally, a number of behavioral responses to drugs (ie cocaine) can be reduced by GSK-3b inhibitors.
Currently, the NO/ONOO- cycle hypothesis which implicates elevation in ONOO as an important cause for responses in the conditions and proposed by Martin Pall, PhD is one of the most commonly accepted hypothesis to explain many of the symptoms in many environmental illnesses including MCS, chronic fatigue syndrome, fibromyalgia and PTSD. While this hypothesis is an important one, I can not say that it accurately describes the multi-inflammatory processes that occur in all of these illnesses and fails to adequately describe the metabolic processes that lead to these conditions. For one, obesity and insulin resistance and diabetes are important in environmental disease and the complications of ageing augment most of these and others as well. Recent evidence is highly suggestive these conditions may influence the development of the more commonly accept EI conditions and for this reason, I have to include them under that umbrella as well. In addition, there is no mention of methylation or how dysregulation of the antioxidant system Nrf2 negatively impacts the expression of NO, CO, HO-1, Il-10 as well as, modulates inflammatory cytokine expression. HO-1 (again with interaction from Nrf2) and vitamin D are involved in the suppressive function of regulatory Tcells. Their absence has been implicated in autoimmune disease that provides an explanation for why environmental illnesses like CFS and GWS and others including diabetes have autoimmune-type behavior. A recent study has presented the hypothesis that exposure to environmental pollutants and high ammonia levels directly alters Treg behavior. In would suggest the inability of oxidants including peroxynitrite and H2O2 to activate Nrf2 is one explanation for failure of the Nrf2 antioxidant system in addition to impairments in activation and regulation of Keap1 and genetic expression of the many genes that regulate the system in different ways. Not only does Nrf2 regulate NO but so does SIRT1 through AMPK, all of which are indirectly or directly involved in activating PGC-1a upregulated by exercise which prevents activation of GSK-3b that turns off the antioxidant system which provide upregulation of nuclear factors including NRF1. In further support, pharmaceutical therapies such as those that elevate PGC-1a and reduce ammonia levels, electroacupuncture, food therapies that elevate Nrf2 through sauna or Waon therapy and nutrition and antioxidant support to reduce mitochondrial dysfunction may be a valuable "tool kit" for the treatment of MCS, autism, provide some relief in CFS and PTSD and help prevent endothelial damage that may be instrumental in causing a number of conditions in many of them.
HEIRS Tags: ammonia, hyperammonemia, homocitrulline, diabetes, insulin resistance, GSK-3b, HO-1, Nrf2, PGC-1a, SIRT1, AMPK, NO/ONOO-, H2O2, dopamine, DAR, cocaine, encephelopathy, Il-6, neuropathy, B12, methionine
HEIRS Tags: ammonia, hyperammonemia, homocitrulline, diabetes, insulin resistance, GSK-3b, HO-1, Nrf2, PGC-1a, SIRT1, AMPK, NO/ONOO-, H2O2,
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Original Article and Citations:
In addition, conditions such as elevations of ammonia activate the CRF pathway in animals that display hyperanxious behavior and recently this pathway has been shown to regulate both anxiety and depression as a consequence of stress. (Biomedicine) Interestingly, the glutamine pathway is also altered during depression and as a result, one may suggest this pathway may be dysregulated from exposure to chemicals such as PFOS and cause mood changes such as depression and anxiety and endogenous elevations of ammonia may induce mood changes even more. In addition, dysfunction of Nrf2 may lead to neurotoxicity and other consequences including augmenting ammonia accumulation. Chemical sensitivity has been implied as important in autism and ammonia may contribute to this which is produced endogenously and exogenously and many therapies used for MCS have also been used to reduce ammonia levels in autism. An interesting suggestion is that in some form through the dysfunction of Nrf2, deficits in the ornithine pathway contribute to the cellular toxicity experienced in MCS and autism. Of course, there are a number of other genetic defects that may alter the urea-cycle, including minor ones that may not appear until adulthood or later because of compensation from other pathways lost with ageing. Ammonia production is higher correlated with inflammatory markers in liver injury and has a profound effect on the permeability of the blood-brain-barrier, providing access of more toxic agents to brain tissue. (Jalan)
Alterations in the methionine pathway have also been suggested to play an important role in autism and we suggest here, MCS and relies on the notion of abherrant methylation "tagging" that potentiate the problems or vice versa. Q10 and vitamin B12 has been used as a therapy for MCS but is also used to assist mitochondrial function and support the methionine cycle and reduce ammonia, respectively. In methyl cycle disfunction, BH4 is drained in ammonia detoxification (Yasko ?) in addition in contrast to its role for NOS production and peroxynitrite which is part of the NO/ONOO- hypothesis. (Pall) Here we see the dichotomy between the Methyl Pathway and the NO/ONOO- hypothesis where BH4 is concerned. In one BH4-dependant process, NOS is converted to nitric oxide and on the other hand it assists in ammonia detoxification in the methylation cycle. If you put alterations in Nrf2 function, which is activated by ONOO- into the mix it can alter expression of genes important for these processes. ONOO- is not the only pro-oxidant that activates the Nrf2, it has been suggested that H2O2 is a much stronger activator and numerous other conditions normally upregulate Nrf2 in normal circumstances. Marzec recently demonstrated that SNPs that exist in the Nrf2 may make on more or less susceptible to oxidative stress and therefore cellular injury and disfunction. The inheritability hypothesis of epigenetics also relies on methylation and helps to explain why environmental illnesses largely run in families and the relationships between gene expression help to explain why gender plays an important role too! Unfortunately, alterations in methylation and consequently, alteration of function has been demonstrated in Nrf2 and several other genes implicated in environmental illness including autism. (To get an idea of how complicated genetics in environmental illness is --click here. ) In addition, alterations in Nrf2 and PGC-1a may contribute to diabetes and insulin resistance and are associated with POP exposures. In addition, GSK-3b involvement from reduced expression of PGC-1a, elevations in dopamine and exposures to bacteria (endotoxin) are a few additional factors that may hamper Nrf2 detoxification system which can lead to more elevations of neuroinflammatory processes, mood changes and significantly increase the likelihood of more neurodegeneration; all associated with environmental illness. GSK-3b signalling also may involve alterations in dopamine-regulated behaviors such as twitching (Tourette's) and ADHD that are often co-morbid with environmental illnesses after exposure injury. Incidentally, a number of behavioral responses to drugs (ie cocaine) can be reduced by GSK-3b inhibitors.
Currently, the NO/ONOO- cycle hypothesis which implicates elevation in ONOO as an important cause for responses in the conditions and proposed by Martin Pall, PhD is one of the most commonly accepted hypothesis to explain many of the symptoms in many environmental illnesses including MCS, chronic fatigue syndrome, fibromyalgia and PTSD. While this hypothesis is an important one, I can not say that it accurately describes the multi-inflammatory processes that occur in all of these illnesses and fails to adequately describe the metabolic processes that lead to these conditions. For one, obesity and insulin resistance and diabetes are important in environmental disease and the complications of ageing augment most of these and others as well. Recent evidence is highly suggestive these conditions may influence the development of the more commonly accept EI conditions and for this reason, I have to include them under that umbrella as well. In addition, there is no mention of methylation or how dysregulation of the antioxidant system Nrf2 negatively impacts the expression of NO, CO, HO-1, Il-10 as well as, modulates inflammatory cytokine expression. HO-1 (again with interaction from Nrf2) and vitamin D are involved in the suppressive function of regulatory Tcells. Their absence has been implicated in autoimmune disease that provides an explanation for why environmental illnesses like CFS and GWS and others including diabetes have autoimmune-type behavior. A recent study has presented the hypothesis that exposure to environmental pollutants and high ammonia levels directly alters Treg behavior. In would suggest the inability of oxidants including peroxynitrite and H2O2 to activate Nrf2 is one explanation for failure of the Nrf2 antioxidant system in addition to impairments in activation and regulation of Keap1 and genetic expression of the many genes that regulate the system in different ways. Not only does Nrf2 regulate NO but so does SIRT1 through AMPK, all of which are indirectly or directly involved in activating PGC-1a upregulated by exercise which prevents activation of GSK-3b that turns off the antioxidant system which provide upregulation of nuclear factors including NRF1. In further support, pharmaceutical therapies such as those that elevate PGC-1a and reduce ammonia levels, electroacupuncture, food therapies that elevate Nrf2 through sauna or Waon therapy and nutrition and antioxidant support to reduce mitochondrial dysfunction may be a valuable "tool kit" for the treatment of MCS, autism, provide some relief in CFS and PTSD and help prevent endothelial damage that may be instrumental in causing a number of conditions in many of them.
HEIRS Tags: ammonia, hyperammonemia, homocitrulline, diabetes, insulin resistance, GSK-3b, HO-1, Nrf2, PGC-1a, SIRT1, AMPK, NO/ONOO-, H2O2, dopamine, DAR, cocaine, encephelopathy, Il-6, neuropathy, B12, methionine
HEIRS Tags: ammonia, hyperammonemia, homocitrulline, diabetes, insulin resistance, GSK-3b, HO-1, Nrf2, PGC-1a, SIRT1, AMPK, NO/ONOO-, H2O2,
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Original Article and Citations:
CiteULike: Responses of Nitric Oxide-cGMP Release in Acupuncture Point to Electroacupuncture in Human Skin In Vivo Using Dermal Microdialysis
CiteULike: Responses of Nitric Oxide-cGMP Release in Acupuncture Point to Electroacupuncture in Human Skin In Vivo Using Dermal Microdialysis: "Jou, N.-T. and Ma, S.-X. (2009). Responses of nitric oxide-cgmp release in acupuncture point to electroacupuncture in human skin in vivo using dermal microdialysis. Microcirculation, 16(5):434-443."
Nrf2 is critical in defense against high glucose-induced oxidative damage in cardiomyocytes.
Nrf2 is critical in defense against high glucose-induced oxidative damage in cardiomyocytes.: "Glucose at high concentrations induced ROS production in both primary neonatal and adult cardiomyocytes from the Nrf2 wild type (WT) mouse heart, whereas, in Nrf2 knockout (KO) cells, ROS was significantly higher under basal conditions and high glucose markedly further increased ROS production in concentration and time-dependent manners. Concomitantly, high glucose induced significantly higher levels of apoptosis at lower concentrations and in shorter time in Nrf2 KO cells than in WT cells."
Chemicals in Textiles May Exert Toxicity By Altering Amino Acid Synthesis
CiteULike: [Effects of perfluorooctane sulfonate on amino acid neurotransmitters and glutamine synthetase in rats]: "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."
Saturday, April 10, 2010
Toll-Like Receptor-4 Mediates Intestinal Barrier Breakdown after Thermal Injury
CiteULike: Toll-Like Receptor-4 Mediates Intestinal Barrier Breakdown after Thermal Injury: "Peterson, C. Y., Costantini, T. W., Loomis, W. H., Putnam, J. G., Wolf, P., Bansal, V., Eliceiri, B. P., Baird, A., and Coimbra, R. (2010). Toll-like receptor-4 mediates intestinal barrier breakdown after thermal injury. Surgical Infections, 11(2):137-144."
Dietary fiber alleviates intestinal barrier dysfunction in post-trauma rats.
CiteULike: Dietary fiber alleviates intestinal barrier dysfunction in post-trauma rats.: "Hou, H., Ping, X., Zhu, Y., Zhao, Z., Li, Y., and Li, J. (2010). Dietary fiber alleviates intestinal barrier dysfunction in post-trauma rats. Clinical and investigative medicine. Médecine clinique et experimentale, 33(2)."
Hyperammonemia caused by impaired mitochondrial ornithine transport in a patient with partial quantitative deficiency of ornithine carbamoyltransferase.
CiteULike: Hyperammonemia caused by impaired mitochondrial ornithine transport in a patient with partial quantitative deficiency of ornithine carbamoyltransferase.: "Kuno, T., Miyazaki, S., Inoue, I., and Saheki, T. (1990). Hyperammonemia caused by impaired mitochondrial ornithine transport in a patient with partial quantitative deficiency of ornithine carbamoyltransferase. Clinical biochemistry, 23(2):143-147."
PGC-1alpha REGULATION BY EXERCISE TRAINING AND ITS INFLUENCES ON MUSCLE FUNCTION AND INSULIN SENSITIVITY.
CiteULike: PGC-1alpha REGULATION BY EXERCISE TRAINING AND ITS INFLUENCES ON MUSCLE FUNCTION AND INSULIN SENSITIVITY.: "Lira, V. A., Benton, C. R., Yan, Z., and Bonen, A. (2010). Pgc-1alpha regulation by exercise training and its influences on muscle function and insulin sensitivity. American journal of physiology. Endocrinology and metabolism."
Pathophysiology and antioxidant status of patients with fibromyalgia
CiteULike: Pathophysiology and antioxidant status of patients with fibromyalgia: "Iqbal, R., Mughal, M., Arshad, N., and Arshad, M. (2010). Pathophysiology and antioxidant status of patients with fibromyalgia. Rheumatology International."
Friday, April 9, 2010
Thursday, April 8, 2010
New study of autism reveals a 'DNA tag' (methylation) amenable to treatment
New study of autism reveals a 'DNA tag' (methylation) amenable to treatment: "New study of autism reveals a 'DNA tag' (methylation) amenable to treatment"
High cortisol linked to age-related cognitive decline in older Type 2 diabetics
MedWire News - Most Popular Stories - High cortisol linked to age-related cognitive decline in older Type 2 diabetics: "High cortisol linked to age-related cognitive decline in older Type 2 diabetics"
MedWire News - Most Popular Stories - HDL levels predict sepsis risk in hospitalized patients
MedWire News - Most Popular Stories - HDL levels predict sepsis risk in hospitalized patients: "HDL levels predict sepsis risk in hospitalized patients"
Counterintuitive Cure: A Nanovaccine That Stops Autoimmune Disease by Boosting the Immune System: Scientific American
Counterintuitive Cure: A Nanovaccine That Stops Autoimmune Disease by Boosting the Immune System: Scientific American: "Counterintuitive Cure: A Nanovaccine That Stops Autoimmune Disease by Boosting the Immune System"
Tuesday, April 6, 2010
Monday, April 5, 2010
Statin reverses reduction of adiponectin receptor expression in infarcted heart and in TNF-alpha-treated cardiomyocytes in association with improved glucose uptake.
CiteULike: Statin reverses reduction of adiponectin receptor expression in infarcted heart and in TNF-alpha-treated cardiomyocytes in association with improved glucose uptake.: "Saito, Y., Fujioka, D., Kawabata, K.-i., Kobayashi, T., Yano, T., Nakamura, T., Kodama, Y., Takano, H., Kitta, Y., Obata, J.-e. E., and Kugiyama, K. (2007). Statin reverses reduction of adiponectin receptor expression in infarcted heart and in tnf-alpha-treated cardiomyocytes in association with improved glucose uptake. American journal of physiology. Heart and circulatory physiology, 293(6)."
Sunday, April 4, 2010
Toxic Chemicals In Upholstery May Increase Susceptibility to Infection.
Findings of a new study on the toxicity of PFOA chemicals in carpets, upholstery, etc. may alter the function of immune cells called lysozymes. Wipedia explains these cells are responsible for providing protection from damage from invading bacteria and are found in secretions from membranes such as tears and mucus. Infants lacking these enzymes have elevations in diarrheal disease; potentially because they fight against infection of bacteria such as Salmonella, E. coli and Pseudomonas.
Question: Why on earth do they still use this stuff?
Further Reading: PFOA alters liver gene expression.(CHEMICAL EXPOSURES): An article from: Environmental Health Perspectives
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Wu, L.-L. L., Chen, L., Song, C., Liu, X.-W. W., Deng, H.-P. P., Gao, N.-Y. Y., and Gao, H.-W. W. (2010). Potential enzyme toxicity of perfluorooctanoic acid. Amino acids, 38(1):113-120. http://www.citeulike.org/user/HEIRS/article/3746495
Functional analysis of a tomato salicylic acid methyl transferase and its role in synthesis of the flavor volatile methyl salicylate.
CiteULike: Functional analysis of a tomato salicylic acid methyl transferase and its role in synthesis of the flavor volatile methyl salicylate.: "Tieman, D., Zeigler, M., Schmelz, E., Taylor, M. G., Rushing, S., Jones, J. B., and Klee, H. J. (2010). Functional analysis of a tomato salicylic acid methyl transferase and its role in synthesis of the flavor volatile methyl salicylate. The Plant journal : for cell and molecular biology."
Researchers uncover novel genetic pathway responsible for triggering vascular growth
Researchers uncover novel genetic pathway responsible for triggering vascular growth
Most solid cancers can't grow beyond a limited size without an adequate blood supply and supporting vascular network. Because of this, cancer researchers have sought to understand how a tumor's vascular network develops—and, more importantly, how to prevent it from developing: If the vascular network never develops, the theory goes, the tumor cannot grow.
Most solid cancers can't grow beyond a limited size without an adequate blood supply and supporting vascular network. Because of this, cancer researchers have sought to understand how a tumor's vascular network develops—and, more importantly, how to prevent it from developing: If the vascular network never develops, the theory goes, the tumor cannot grow.
Toluene regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma.
Concept: Toluene is a chemical that needs to be handled correctly to prevent occupational injury.
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CiteULike: Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma.: "Kim, S.-H. H., Choi, G.-S. S., Ye, Y.-M. M., Jou, I., Park, H.-S. S., and Park, S. M. (2010). Toluene diisocyanate (tdi) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma. Clinical and experimental immunology."
New study suggests therapeutic approaches to elevate HO-1/Ferritin through the Nrf2 pathway may help alleviate symptoms from exposure to toluene.Read more about: HO-1 tag in the library and on the Blog: Tag HO-1.
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CiteULike: Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma.: "Kim, S.-H. H., Choi, G.-S. S., Ye, Y.-M. M., Jou, I., Park, H.-S. S., and Park, S. M. (2010). Toluene diisocyanate (tdi) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma. Clinical and experimental immunology."
Chemical stress induces the UPR stress response in olfactory neurons.
Activity of Nrf2 is also involved with the response of chemical exposures on the nasal system which I have noted at length may be altered by a number of factors including hormone levels, ageing, nutrition,genetic factors, etc. As this article notes, the UPR response can become independant of odor-evokation and induce a loss of the enzyme CYP2A5 and REG3g. Notably, continuous activation of the UPR can alter signaling via the protein PERK through Nrf2. In 2003 Piras demonstrated that "CYP2A5 mRNA and the corresponding protein co-localized at most sites and were predominantly detected in the olfactory region." In these findings, and because changes occurred in region that are analagous to neural glia which are active in neuroinflammation, future studies may show that changes in this area also induce neuroinflammatory responses without changes in Nrf2 levels. This study also noted alteraction in the abundance of the lectin called Reg3g....Several studies show this protein serves a homeotstatic function and this becomes important because the reduction of this lectin which kills gram (+) in the intestinal tract increases susceptibility to the effects of bacteria and includes changes in TLR signaling which may alter resistance to factors that lead to environmental disease in addtion to bacterial infection. The study of Reg3g is just begining and I am sure more studies will further clarify its role in nasal epithelia. From what has been observed thus far, this protein has been shown to have anti-diabetic properties and also may be regulated through a WNT pathway. Both of which, I have mentioned previously may influence autoimmunity, ammonia metabolism and other physiological effects that impact environmental illness especially in MCS and CFS.
You can read more about the Unfolded Protein Response here:
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Piras, E., Franzen, A., Fernandez, E. L., Bergstrom, U., Raffalli-Mathieu, F., Lang, M., and Brittebo, E. B. (2003). Cell-specific expression of cyp2a5 in the mouse respiratory tract: Effects of olfactory toxicants. J. Histochem. Cytochem., 51(11):1545-1555.
http://www.citeulike.org/user/HEIRS/article/6948536
Sammeta, N. and McClintock, T. S. (2010). Chemical stress induces the unfolded protein response in olfactory sensory neurons. The Journal of comparative neurology, 518(10):1825-1836.
http://www.citeulike.org/user/HEIRS/article/6873277?show_msg=already_posted
Kinnebrew, M. A., Ubeda, C., Zenewicz, L. A., Smith, N., Flavell, R. A., and Pamer, E. G. (2010). Bacterial flagellin stimulates toll-like receptor 5-dependent defense against vancomycin-resistant enterococcus infection. The Journal of infectious diseases, 201(4):534-543.
http://www.citeulike.org/user/HEIRS/article/6533280
Castellarin, M. L., Petropavlovskaia, M., Lipsett, M. A., and Rosenberg, L. (2007). The identification and sequence analysis of a new reg3gamma and reg2 in the syrian golden hamster. Biochimica et biophysica acta, 1769(9-10):579-585 http://www.ncbi.nlm.nih.gov/pubmed/17673309 .
Bluestone, J. A. and Hebrok, M. (2008). Safer, longer-lasting regulatory t cells with β-catenin. Nature Medicine, 14(2):118-119.
http://www.citeulike.org/user/HEIRS/article/2350828
Wipedia. Unfolded Protein Response. Retrieved on April 4, 2010. http://en.wikipedia.org/wiki/Unfolded_protein_response
Cortopassi, G., Danielson, S., Alemi, M., Zhan, S. S., Tong, W., Carelli, V., Martinuzzi, A., Manzuki, S., Majamaa, K., and Wong, A. (2006). Mitochondrial disease activates transcripts of the unfolded protein response and cell cycleand inhibits vesicular secretion and oligodendrocyte-specific transcripts. Mitochondria, 6:161-175. http://www.citeulike.org/user/HEIRS/article/6948589
Saturday, April 3, 2010
Friday, April 2, 2010
Scientist to Study Inflammatory Response of Lymphocytes
"if we can understand the cytokine, or IL-6 requirements, for lymphocyte recruitment during acute inflammation it may lead to novel intervention strategies in chronic inflammatory disorders such as autoimmune diseases"
Scientist to Study Inflammatory Response of Lymphocytes
Common Test For Detecting Liver Problems In Children Is Often Interpreted Incorrectly
Common Test For Detecting Liver Problems In Children Is Often Interpreted Incorrectly: "Common Test For Detecting Liver Problems In Children Is Often Interpreted Incorrectly"
Scientists Identify Potential New Method For Treating Sleeping Sickness
Very interesting......
Scientists Identify Potential New Method For Treating Sleeping Sickness: "Scientists Identify Potential New Method For Treating Sleeping Sickness"
Scientists Identify Potential New Method For Treating Sleeping Sickness: "Scientists Identify Potential New Method For Treating Sleeping Sickness"
Ammonia, Hyperglycemia and Metabolism in Ferrets
Interesting statement: Hyperglycemia has also been reported in near-adult cats fed arginine-free diet. Hyperglycemia is usually associated with high ammonia levels and is probably due to release of glucagon by the action of ammonia.
CiteULike: Effect of Arginine-Free Diet on Ammonia Metabolism in Young and Adult Ferrets12: "Thomas, P. E. and Deshmukh, A. R. (1986). Effect of arginine-free diet on ammonia metabolism in young and adult ferrets12. The Journal of Nutrition, 116:545-551."
Investigating Inflammatory Mediators in Rheumatoid Arthritis
CiteULike: Investigation of the role of tumour necrosis factor-alpha, interleukin-1beta, interleukin-10, nitric oxide and rheumatoid factor-immunoglobulin M in a rat model of arthritis: "Khalifeh, M. S., Al-Rukibat, R., Hananeh, W., Boumezrag, A., and Okour, O. (2010). Investigation of the role of tumour necrosis factor-alpha, interleukin-1beta, interleukin-10, nitric oxide and rheumatoid factor-immunoglobulin m in a rat model of arthritis. Lab Anim, 44(2):143-149."
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