RAGE Mediates Accelerated Diabetic Vein Graft Atherosclerosis Induced by Combined Mechanical Stress and AGEs via Synergistic ERK Activation

Aims/Hypothesis: Diabetes with hypertension rapidly accelerates vascular disease, but the underlying mechanism remains unclear. We evaluated the hypothesis that the receptor of advanced glycation end products (RAGE) might mediate combined signals initiated by diabetes-related AGEs and hypertension-induced mechanical stress as a common molecular sensor. Methods: In vivo surgical vein grafts created by grafting vena cava segments from C57BL/6J mice into the common carotid arteries of streptozotocin (STZ)-treated and untreated isogenic mice for 4 and 8 weeks were analyzed using morphometric and immunohistochemical techniques. In vitro quiescent mouse vascular smooth muscle cells (VSMCs) with either knockdown or overexpression of RAGE were subjected to cyclic stretching with or without AGEs. Extracellular signalregulated kinase (ERK) phosphorylation and Ki-67 expression were investigated. Results: Significant increases in neointimal formation, AGE deposition, Ki-67 expression, and RAGE were observed in the vein grafts of STZ-induced diabetic mice. The highest levels of ERK phosphorylation and Ki-67 expression in VSMCs were induced by simultaneous stretch stress and AGE exposure. The synergistic activation of ERKs and Ki-67 in VSMCs was significantly inhibited by siRNA-RAGE treatment and enhanced by over-expression of RAGE. Conclusion: RAGE may mediate synergistically increased ERK activation and VSMC proliferation induced by mechanica

PARTIAL-PURIFICATION OF WESTERN EQUINE ENCEPHALITIS-VIRUS BY FRACTIONATION PROCEDURES

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EFFECT OF TEMPERATURE, PH AND SODIUM-CHLORIDE CONCENTRATIONS ON PRODUCTION OF STAPHYLOCOCCAL ENTEROTOXIN-A AND ENTEROTOXIN-B

45141306130

PRODUCTION OF STAPHYLOCOCCAL ENTEROTOXIN-D IN FOODS BY LOW-ENTEROTOXIN-PRODUCING STAPHYLOCOCCI

The goal of this investigation was to determine whether staphylococcal strains producing enterotoxins at nanogram levels per milliliter in laboratory medium, not detectable by gel diffusion methods, could produce sufficient enterotoxin in foods to result in food poisoning. Three low-enterotoxin D (SED)-producing strains were selected for this research b,cause this enterotoxin is produced in smaller amounts than the other enterotoxins. The foods used were cream pie and cooked ham, divided into two portions, sterile and non-sterile. Each portion was inoculated with known concentrations of the staphylococcal strains under study and incubated for 48 h at 25, 30, and 37-degrees-C. Samples were taken after 24 and 48 h. Enterotoxin was detectable in both sterilized and unsterilized cream and ham after 24 h at 37-degrees-C with an inoculum of 10(3)/g. Some strains produced detectable amounts of enterotoxin in the sterilized foods after 24 h at 30-degrees-C and some produced detectable amounts of enterotoxin in the sterilized foods after 24 h at 25-degrees-C with inocula of 10(4)/g. It can be concluded that staphylococcal strains producing enterotoxin at ng/ml levels in laboratory medium, not detectable by gel diffusion methods, can produce sufficient enterotoxin (ng/g) in foods to cause food poisoning.141192

EPIDEMIOLOGICAL AND MICROBIOLOGICAL STUDIES OF AN OUTBREAK OF FOODBORNE INTOXICATION

131263