sodium-acetate--anhydrous has been researched along with Acute-Disease* in 2 studies
2 other study(ies) available for sodium-acetate--anhydrous and Acute-Disease
Article | Year |
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Gut Microbial Metabolites Induce Donor-Specific Tolerance of Kidney Allografts through Induction of T Regulatory Cells by Short-Chain Fatty Acids.
Short-chain fatty acids derived from gut microbial fermentation of dietary fiber have been shown to suppress autoimmunity through mechanisms that include enhanced regulation by T regulatory cells (Tregs).. Using a murine kidney transplantation model, we examined the effects on alloimmunity of a high-fiber diet or supplementation with the short-chain fatty acid acetate. Kidney transplants were performed from BALB/c(H2. Wild-type mice fed normal chow exhibited dysbiosis after receiving a kidney allograft but not an isograft, despite the avoidance of antibiotics and immunosuppression for the latter. A high-fiber diet prevented dysbiosis in allograft recipients, who demonstrated prolonged survival and reduced evidence of rejection compared with mice fed normal chow. Allograft mice receiving supplemental sodium acetate exhibited similar protection from rejection, and subsequently demonstrated donor-specific tolerance. Depletion of CD25. Manipulation of the microbiome by a high-fiber diet or supplementation with sodium acetate modified alloimmunity in a kidney transplant model, generating tolerance dependent on Tregs and GPR43. Diet-based therapy to induce changes in the gut microbiome can alter systemic alloimmunity in mice, in part through the production of short-chain fatty acids leading to Treg cell development, and merits study as a potential clinical strategy to facilitate transplant acceptance. Topics: Acute Disease; Allografts; Animals; Butyric Acid; Chronic Disease; Dietary Fiber; Dietary Supplements; Dysbiosis; Fatty Acids, Volatile; Gastrointestinal Microbiome; Graft Rejection; Graft Survival; Immune Tolerance; Kidney Transplantation; Lymphocyte Activation; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Receptors, G-Protein-Coupled; Sodium Acetate; T-Lymphocytes, Regulatory | 2020 |
Cardioplegic solution: a contamination crisis.
Eleven patients were given varying doses of cardioplegic solution contaminated with Enterobacter cloacae. Five patients died. Early bleeding, necessitating reoperation, occurred in eight patients and a total of 126 units of blood and 203 units of platelets were given (range 2 to 19 and 15 to 47 units, respectively). Mycotic aneurysms developed in four patients, rupturing between the ninth and eleventh postoperative day. Only one of these patients survived. Other complications included adult respiratory distress syndrome (three patients), renal failure (four patients), sternal infections (six patients), and organic brain syndrome (five patients). Although some factors of gram-negative septicemia were identified in retrospect, others were masked by the clinical setting in which it occurred. We recommend that each dose of cardioplegic solution be prepared on an individual basis and used immediately. We also recommend that "sternal blood" be cultured on all patients. The subtle features of "gram-negative septicemia" necessitate urgent investigation and treatment. The combination of low white cell count, high cardiac output, and low peripheral vascular resistance should be assumed to indicate septicemia until proved otherwise. A full coagulation screen including platelet function and fibrin degradation products should be performed in any and all patients with these findings. Mycotic aneurysms mandate urgent reoperation with interposition of a saphenous vein segment of these patients are to survive. Topics: Acute Disease; Aged; Aneurysm, Infected; Blood Coagulation Tests; Cardiac Tamponade; Coronary Disease; Drug Contamination; Enterobacteriaceae Infections; Gluconates; Heart Arrest, Induced; Hemodynamics; Hemorrhage; Humans; Isotonic Solutions; Magnesium Chloride; Middle Aged; Potassium; Potassium Chloride; Potassium Compounds; Sepsis; Sodium Acetate; Sodium Chloride | 1986 |