Exogenous advanced glycosylation end products induce diabetes-like vascular dysfunction in normal rats: a factor in diabetic retinopathy

BACKGROUND. Diabetic retinopathy has been shown to be directly associated with the degree and duration of hyperglycemia, and advanced glycosylation end products (AGEs) have been implicated in this pathological process. The purpose of the experiments reported here was to study the effect of AGE deposition on retinal vascular damage which leads to diabetic retinopathy. METHODS. Intravenous injection of exogenous AGEs was used to treat wild-type non-diabetic Sprague-Dawley rats. One of the two retinal slides from each animal was treated using immunohistochemical staining to label retinal vascular AGE deposition, the other H&E staining for counting of capillary pericytes. The results were compared with the findings in untreated wild-type and diabetic controls and in rats treated with unmodified rat serum albumin (RSA). RESULTS. After 2 weeks of continuous treatment, AGEs were identified in the retinal vascular tissue of the AGE-RSA-injected group. The average number of retinal capillary pericytes per 10x100 microscope power field was 4.313+/-0.34 (mean +/- SD) in the AGE-RSA-injected group, compared with 5.798+/-0.481 in the control group ( P<0.01). CONCLUSION. These experiments demonstrate that AGEs, independent of other metabolic factors, can induce vascular change resembling that of diabetic retinopathy.     

Treatment of two postoperative endophthalmitis cases due to <Emphasis Type="Italic">Aspergillus flavus</Emphasis> and <Emphasis Type="Italic">Scopulariopsis</Emphasis> spp. with local and systemic antifungal therapy

Background  

Endophthalmitis is the inflammatory response to invasion of the eye with bacteria or fungi. The incidence of endophthalmitis after cataract surgery varies between 0.072–0.13 percent. Treatment of endophthalmitis with fungal etiology is difficult.     

Clinical influence of vagotomy on postoperative acute phase response

BACKGROUND: Although there is increasing evidence suggesting that the vagus nerve functions as a connector between the nervous and immune systems in animals, little is known about the role of the vagus nerve in postoperative acute phase response in humans. MATERIALS AND METHODS: The extent of fever and acute phase protein response and the production of inflammatory cytokine during the early postoperative period were compared among the patients who had undergone total gastrectomy including truncal vagotomy (n = 13), those having distal gastrectomy with division of vagal branches (n = 14), and the patients with vagal nerve preserving gastrectomy (n = 12). RESULTS: There was no significant difference in serum levels of C-reactive protein, alpha-1-antirypsin, and interleukin-6 among the three groups. Also, postoperative maximum body temperature was similar. CONCLUSIONS: Vagotomy did not influence acute phase response after gastric cancer surgery. A multipathway mechanism for acute phase response including the induction of fever is suggested.     

Reliability of movement control tests in the lumbar spine

Background  

Movement control dysfunction [MCD] reduces active control of movements. Patients with MCD might form an important subgroup among patients with non specific low back pain. The diagnosis is based on the observation of active movements. Although widely used clinically, only a few studies have been performed to determine the test reliability. The aim of this study was to determine the inter- and intra-observer reliability of movement control dysfunction tests of the lumbar spine.     

Metabolic Characterization of Nondiabetic Severely Obese Patients Undergoing Roux-en-Y Gastric Bypass: Preoperative Classification Predicts the Effects of Gastric Bypass on Insulin–Glucose Homeostasis

Introduction Obese individuals may have normal insulin–glucose homeostasis, insulin resistance, or diabetes mellitus. Whereas gastric bypass cures insulin resistance and diabetes mellitus, its effects on normal physiology have not been described. We studied insulin resistance and β-cell function for patients undergoing gastric bypass. Methods One hundred thirty-eight patients undergoing gastric bypass had fasting insulin and glucose levels drawn on days 0, 12, 40, 180, and 365. Thirty-one (22%) patients with diabetes mellitus were excluded from this analysis. Homeostatic model of assessment was used to estimate insulin resistance, insulin sensitivity, and β-cell function. Based on this model, patients were categorized as high insulin resistance if their insulin resistance was >2.3. Results Body mass index did not correlate with insulin resistance. Forty-seven (34%) patients were categorized as high insulin resistance. Correction of insulin resistance for this group occurred by 12 days postoperatively. Sixty (43%) patients were categorized as low insulin resistance. They demonstrated an increase of β-cell function by 12 days postoperatively, which returned to baseline by 6 months. At 1 year postoperatively, the low insulin resistance group had significantly higher β-cell function per degree of insulin sensitivity. Conclusions Adipose mass alone cannot explain insulin resistance. Severely obese individuals can be categorized by degree of insulin resistance, and the effect of gastric bypass depends upon this preoperative physiology.