"Modulation of AhR signaling pathway via the diet, cessation of smoking, or administration of AhR antagonists could be viable strategies for the treatment of IBD."
Arsenescu, R., Arsenescu, V., Zhong, J., Nasser, M., Melinte, R., Dingle, C. W., Swanson, H., and de Villiers, W. J. (2010). Role of the xenobiotic receptor in inflammatory bowel disease. Inflammatory bowel diseases.
http://www.citeulike.org/user/HEIRS/article/7950224
Explores the mental, physical, cellular and biochemical aspects of environmental illnesses such as obesity, diabetes, chronic fatigue syndrome, PTSD, fibromyalgia, chemical sensitivities, neurological disorders and numerous others. We advocate for better access to medical care, healthier lifestyles, resource conservation and the use of assistance animals for the disabled to promote a better quality of life.
Showing posts with label inflammatory bowel disease. Show all posts
Showing posts with label inflammatory bowel disease. Show all posts
Tuesday, October 5, 2010
Saturday, August 28, 2010
AMPK agonist downregulates innate and adaptive immune responses in TNBS-induced murine acute and relapsing colitis.
"AICAR-initiated AMPK activation may act as a central downregulator in ongoing innate and adaptive immune responses of murine colitis, providing a novel therapeutic approach in the treatment of IBD."
Read more: CiteULike: AMPK agonist downregulates innate and adaptive immune responses in TNBS-induced murine acute and relapsing colitis.:
For further reading: AMPK
Sunday, August 15, 2010
Gut Inflammation and Changes in Intestinal Function From Loss of NO Neurons~!
In a recent study the author writes "enteric neurons are supported by glial cells, the ENS counterparts of astrocytes of the CNS, that can modulate enteric neuron function. Enteric neurons are known to control virtually all GI functions, including motility, secretion, blood flow, mucosal growth and aspects of the local immune system. Consequently, permanent or even transient structural alterations in the ENS, as occur in IBD, disrupt normal GI function. Structural changes in the ENS are predictive of disease evolution suggesting that neuroprotection would decrease disease severity and may play a role in recurrence in CD." Further he continues that under conditions of experimental trichinosis infection in the murine "that in this animal model of colitis, there was a significant loss of nitric oxide synthase- (NOS-) immunoreactive neurons in the myenteric plexus of infected rats. Moreover, the selective loss of NOS-positive neurons appears to underlie changes in motility." (Lakhan) Recent reports also suggest that hormones such as serotonin influences gut regulation and may activate inflammatory cytokines in the intestine leading to alterations in gut function. (Khan) Inflammatory activity such as Tnf-a in the periphery such as the gut may influence production of cytokines and changes in gene expression in the brain that change behavior and have other unexpected health effects.
Khan, W. I. and Ghia, J. E. (2010). Gut hormones: emerging role in immune activation and inflammation. Clinical and experimental immunology, 161(1):19-27.
http://www.citeulike.org/user/HEIRS/article/7323747
Lakhan, S. E. and Kirchgessner, A. (2010). Neuroinflammation in inflammatory bowel disease. Journal of neuroinflammation, 7:37+.
http://www.citeulike.org/user/HEIRS/article/7471133
Khan, W. I. and Ghia, J. E. (2010). Gut hormones: emerging role in immune activation and inflammation. Clinical and experimental immunology, 161(1):19-27.
http://www.citeulike.org/user/HEIRS/article/7323747
Lakhan, S. E. and Kirchgessner, A. (2010). Neuroinflammation in inflammatory bowel disease. Journal of neuroinflammation, 7:37+.
http://www.citeulike.org/user/HEIRS/article/7471133
Thursday, July 1, 2010
Plant Extract May be Effective Against Inflammatory Bowel Disease
"Newswise — A South Dakota State University scientist’s research shows an extract made from a food plant in the Brassica family was effective in alleviating signs of ulcerative colitis, an inflammatory bowel condition, in mice......The ongoing study by associate professor Moul Dey in SDSU’s Department of Health and Nutritional Sciences — funded by the National Institutes of Health — moves on now to examine the potential use of the plant extract against colon cancer."
Read more:Plant Extract May be Effective Against Inflammatory Bowel Disease:
Monday, April 26, 2010
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"
Sunday, February 21, 2010
Researchers Find Gut Protein that Protects Against Infection
A signaling protein that is key in orchestrating the body’s overall immune response has an important localized role in fighting bacterial infection and inflammation in the intestinal tract, according to a study by UC San Diego School of Medicine investigators, published in the journal Cell Host and Microbe. Further the author says, "diminished levels may be potentially an underlying factor in the severe illness caused by pathogens such as E. coli, and inflammation of the intestine by diseases such as Crohn’s disease
Researchers Find Protein that Protects Gut from Infection: "Researchers Find Protein that Protects Gut from Infection"
Thursday, December 31, 2009
Inflammatory mediator NF-KappaB regulates diarrhea in inflammatory bowel disease
Inflammatory mediator regulates diarrhea in inflammatory bowel disease
ScienceDaily (2009-12-30) -- Researchers have discovered that activation of NK-kappa B, an inflammatory mediator, results in diarrhea in inflammatory bowel disease (IBD). ... > read full article
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Tuesday, December 15, 2009
Asthma linked to increased risk for IBD in children
Asthma linked to increased risk for IBD in children: "URL: Asthma linked to increased risk for IBD in children
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Friday, December 11, 2009
Potential role of Th17 cells in the pathogenesis of inflammatory bowel disease.
Potential role of Th17 cells in the pathogenesis of inflammatory bowel disease.: "URL: Potential role of Th17 cells in the pathogenesis of inflammatory bowel disease.
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Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items HEIRS Health & Home online.
Tuesday, December 8, 2009
Researchers Unveil Two Genetic Mutations Associated with Early-onset Inflammatory Bowel Disease
Researchers Unveil Two Genetic Mutations Associated with Early-onset Inflammatory Bowel Disease: "URL: Researchers Unveil Two Genetic Mutations Associated with Early-onset Inflammatory Bowel Disease
HEIRS Health & Home
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heirshealth@gmail.com
Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items in the HEIRS Store at HEIRS Health & Home.

"
HEIRS Health & Home
www.heirs-online.com
heirshealth@gmail.com
Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items in the HEIRS Store at HEIRS Health & Home.
Monday, November 2, 2009
Nitric Oxide Production by the Human Intestinal Microbiota by Dissimilatory Nitrate Reduction to Ammonium
Summary: "the human fecal microbiota were shown to produce NO from trace levels of nitrate under gastrointestinal conditions. Moreover, our data indicate that NO was produced by DNRA and not by denitrification or the L-arginine pathway. Studying the interaction between bacterially produced NO and the host epithelial cells might be pivotal in the etiology of inflammatory diseases of the gastrointestinal tract."
Vermeiren, J., Van de Wiele, T., Verstraete, W., Boeckx, P., and Boon, N. (2009). Nitric oxide production by the human intestinal microbiota by dissimilatory nitrate reduction to ammonium. Journal of Biomedicine and Biotechnology.http://www.citeulike.org/user/HEIRS/article/6056766
Vermeiren, J., Van de Wiele, T., Verstraete, W., Boeckx, P., and Boon, N. (2009). Nitric oxide production by the human intestinal microbiota by dissimilatory nitrate reduction to ammonium. Journal of Biomedicine and Biotechnology.http://www.citeulike.org/user/HEIRS/article/6056766
Monday, October 26, 2009
Microbial induction of IBD Through Protein Expression By TLR Signaling
HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!
Summary: A number of gram negative, gram positive and other anaerobes stimulate protein that contributes to IBD. This process is dependant on TLR signaling and can be inhibited by blocking the P38 pathway. In an earlier study showed that the levels of TL1A and number of cells that expressed it correlated with the level of inflammation, especially in Crohn's disease.
Title:Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells.
Shih, D. Q., Kwan, L. Y., Chavez, V., Cohavy, O., Gonsky, R., Chang, E. Y., Chang, C., Elson, C. O., and Targan, S. R. (2009). Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells. European Journal of Immunology, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/6009014
Bamias, G., Martin, C., Marini, M., Hoang, S., Mishina, M., Ross, W. G., Sachedina, M. A., Friel, C. M., Mize, J., Bickston, S. J., Pizarro, T. T., Wei, P., and Cominelli, F. (2003). Expression, localization, and functional activity of tl1a, a novel th1-polarizing cytokine in inflammatory bowel disease. Journal of immunology (Baltimore, Md. : 1950), 171(9):4868-4874. http://www.citeulike.org/user/HEIRS/article/6009138
Summary: A number of gram negative, gram positive and other anaerobes stimulate protein that contributes to IBD. This process is dependant on TLR signaling and can be inhibited by blocking the P38 pathway. In an earlier study showed that the levels of TL1A and number of cells that expressed it correlated with the level of inflammation, especially in Crohn's disease.
Title:Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells.
Shih, D. Q., Kwan, L. Y., Chavez, V., Cohavy, O., Gonsky, R., Chang, E. Y., Chang, C., Elson, C. O., and Targan, S. R. (2009). Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells. European Journal of Immunology, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/6009014
Bamias, G., Martin, C., Marini, M., Hoang, S., Mishina, M., Ross, W. G., Sachedina, M. A., Friel, C. M., Mize, J., Bickston, S. J., Pizarro, T. T., Wei, P., and Cominelli, F. (2003). Expression, localization, and functional activity of tl1a, a novel th1-polarizing cytokine in inflammatory bowel disease. Journal of immunology (Baltimore, Md. : 1950), 171(9):4868-4874. http://www.citeulike.org/user/HEIRS/article/6009138
Wednesday, October 7, 2009
Saturday, September 19, 2009
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