Development of eczematous symptoms by the implanted breast prosthesis.

Unlabelled: A patient with an unidentified implanted breast prosthesis experienced eczematous symptoms 3 years after implantation, although prosthesis rapture and complications such as capsular contraction, hematoma, and seroma were not clinically observed. Surgical removal of the implanted prosthesis gradually improved the symptoms, suggesting that symptom development was likely due to the implanted prosthesis. Unidentified materials of the implanted breast prosthesis were investigated by chemical and medical analysis to determine how the developed eczematous symptoms were induced by the prosthesis.

Treatment of mesh skin grafted scars using a plasma skin regeneration system.

Objectives. Several modalities have been advocated to treat traumatic scars, including surgical techniques and laser resurfacing. Recently, a plasma skin regeneration (PSR) system has been investigated.

CT features of juxtapapillary duodenal diverticula with complications.

Objective: We evaluated the computed tomography (CT) features of juxtapapillary duodenal diverticula (JPDD) with complications in patients who had acute abdomen.

Materials And Methods: Nineteen JPDD were evaluated in 14 patients (mean age: 50 years), who had acute abdomen on contrast-enhanced helical CT with a diagnosis of complicated JPDD by endoscopic retrograde cholangiopancreatography (ERCP). The size, number, and contents of the JPDD, pacreticobiliary ductal dilation, biliary stones, and other associated findings were evaluated on CT scans.

Hyperglycemia, maturity-onset obesity, and insulin resistance in NONcNZO10/LtJ males, a new mouse model of type 2 diabetes.

As a new mouse model of obesity-induced diabetes generated by combining quantitative trait loci from New Zealand Obese (NZO/HlLt) and Nonobese Nondiabetic (NON/LtJ) mice, NONcNZO10/LtJ (RCS10) male mice developed type 2 diabetes characterized by maturity onset obesity, hyperglycemia, and insulin resistance. To metabolically profile the progression to diabetes in preobese and obese states, a 2-h hyperinsulinemic euglycemic clamp was performed and organ-specific changes in insulin action were assessed in awake RCS10 and NON/LtJ (control) males at 8 and 13 wk of age. Prior to development of obesity and attendant increases in hepatic lipid content, 8-wk-old RCS10 mice developed insulin resistance in liver and skeletal muscle due to significant decreases in insulin-stimulated glucose uptake and GLUT4 expression in muscle.

Overexpression of uncoupling protein 3 in skeletal muscle protects against fat-induced insulin resistance.

Insulin resistance is a major factor in the pathogenesis of type 2 diabetes and is strongly associated with obesity. Increased concentrations of intracellular fatty acid metabolites have been postulated to interfere with insulin signaling by activation of a serine kinase cascade involving PKCtheta in skeletal muscle. Uncoupling protein 3 (UCP3) has been postulated to dissipate the mitochondrial proton gradient and cause metabolic inefficiency.