Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular (CV) complications, associated with space flight (SF), are caused by microgravity, hypokinesia and radiation, particularly beyond earth orbit, with all three conducive to oxidative stress. Except for emergencies, pharmaceuticals appear to be contraindicated, because of unpredictable side effects from malabsorption (M) and potential hepatic and renal impairment. Magnesium (Mg) depletion and elevations of cytokines (interleukin 6) occur during SF, conducive to self-sustaining vascular inflammation mechanisms. There are potential endothelial injuries (EI) and reduced Cyclic GMP (a second messenger of nitric oxide: NO) and elevated urinary excretion of C-peptide (insulin resistance: IR). Recent findings that show reductions in vascular endothelial growth factor (VEGF) suggest that this may result from SF-related thrombocytopenia since platelets (P) are the major source of VEGF, and that NO might play a role. Both VEGF and Mg are vital for angiogenesis, endothelial function and reendothelialization. Insulin is necessary for VEGF expression. To prevent SF-related CV complications in the presence of IR and M and with the potential for renal insufficiency, closely monitored subcutaneous (SC) Mg should be provided. The dosage can be monitored by sublingual intracellular Mg assays. Needed is development of a SC Mg reservoir device, which can be replenished before extra-vehicular activities (EVA) and which must be reliable despite vigorous movements during EVA, that can last up to 8 hours. This could also be protective against decompression sickness and EVA-related 100% oxygen requirements before and during this activity, both of which predispost to EI.
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PMID:The case for a subcutaneous magnesium product and delivery device for space missions. 1546 57

Local inflammation in the colon has been associated with nutrient malabsorption and altered motility in the small bowel. These remote effects suggest the release of mediators which can act (or alter) the function of intestinal segments located far from the primary area of inflammation. This study describes the changes in the expression of pro-inflammatory cytokines in the colon and in various segments of the small intestine in two rat models of experimental colitis. Colitis was induced by the intracolonic administration of 100 microL of 6% iodoacetamide or 250 microL of 2, 4, 6-trinitrobenzene sulfonic acid. Levels of interleukin one beta, interleukin 6, and tumor necrosis factor alpha were measured by ELISA in tissue homogenate sampled from duodenum, jejunum, ileum and colon at different time intervals. In homogenates of strips isolated from duodenum, jejunum and ileum, tumor necrosis alpha and interleukin-6, increased significantly 3-6 h after iodoacetamide or TNBS administration and remained elevated until the colonic inflammation subsided. Interleukin one beta showed comparable but delayed increase. Similar, but more pronounced increase of the three cytokines was noticed in areas of the colon adjacent to the ulcer. Histologic examinations revealed important inflammatory changes in the colon; however, examination of sections from the small intestines did not reveal significant differences between controls and rats with colitis. In conclusion, expression of pro-inflammatory cytokines is increased in remote segments of the small intestines during colitis. The findings may provide a partial explanation or a molecular substrate for the associated small bowel dysfunction.
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PMID:Localized colonic inflammation increases cytokine levels in distant small intestinal segments in the rat. 1690 27

Bowel bacterial overgrowth syndrome (BBOS) is an important cause of gastrointestinal (GI) abnormalities. Proinflammatory cytokines (PICs) are excessively produced and accumulate because of kidney failure in dialysis patients who experience chronic infections such as BBOS. We explored the association between GL function, BBOS, and the malnutrition, inflammation, and atherosclerosis (MIA) syndrome. We studied GI malabsorption and maldigestion by analyzing fecal starch, sugar, fat, and nitrogen; intestinal protein permeability (alpha1-antitrypsin fecal clearance); and fecal chymotrypsin. We evaluated BBOS by breath hydrogen test (BHT) after a 3-day fat-and-carbohydrate-overload diet. Positive BHT was present in 10 patients, showing a high prevalence of GI macronutrient malabsorption and maldigestion, and compared with the other patients, the highest plasma levels of tumor necrosis factor alpha and interleukin 6 and lower levels of albumin and prealbumin. Those 10 patients were treated with a combination of several antibiotics, including neomycin, amoxicillin-clavulanate, and quinolones. Between 2 and 3 months later, the BHT, markers of nutrition, and PIC were re-tested. All treated patients showed an improvement in nutrition status and a lesser inflammatory pattern. The BBOS infectious process is found frequently in dialysis patients in association with GI malabsorption and maldigestion, malnutrition, and systemic inflammation. Hyperproduction of PIC because of BBOS induces MIA through a double pathway: GI disorders and deleterious systemic effects.
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PMID:Bowel bacterial overgrowth as another cause of malnutrition, inflammation, and atherosclerosis syndrome in peritoneal dialysis patients. 2134 95