Intraocular pressure and aqueous humor flow during a euglycemic-hyperinsulinemic clamp in patients with type 1 diabetes and microvascular complications

<p>Abstract</p> <p>Background</p> <p>Microvascular complications, including retinopathy and nephropathy are seen with type 1 diabetes. It is unknown whether functional changes in aqueous humor flow or intraocular pressure (IOP) develop in parallel with these complications. This study was designed to test the hypothesis that clinical markers of microvascular complications coexist with the alteration in aqueous humor flow and IOP.</p> <p>Methods</p> <p>Ten patients with type 1 diabetes and ten healthy age- and weight-matched controls were studied. Aqueous flow was measured by fluorophotometry during a hyperinsulinemic-euglycemic clamp (insulin 2 mU/kg/min). Intraocular pressure was measured by tonometry at -10, 90 and 240 minutes from the start of the clamp, and outflow facility was measured by tonography at 240 minutes.</p> <p>Results</p> <p>During conditions of identical glucose and insulin concentrations, mean aqueous flow was lower by 0.58 μl/min in the diabetes group compared to controls (2.58 ± 0.65 versus 3.16 ± 0.66 μl/min, respectively, mean ± SD, p = 0.07) but statistical significance was not reached. Before the clamp, IOP was higher in the diabetes group (22.6 ± 3.0 mm Hg) than in the control group (19.3 ± 1.8 mm Hg, p = 0.01) but at 90 minutes into the clamp, and for the remainder of the study, IOP was reduced in the diabetes group to the level of the control group. Ocular pulse amplitude and outflow facility were not different between groups. Systolic blood pressure was significantly higher in the diabetes group, but diastolic and mean arterial pressures were not different.</p> <p>Conclusions</p> <p>We conclude that compared to healthy participants, patients with type 1 diabetes having microalbuminuria and retinopathy have higher IOPs that are normalized by hyperinsulinemia. During the clamp, a reduction in aqueous flow was not statistically significant.</p

The role of anti-HCV signal/cuttoff ratio in diagnosis of HCV infection

12th Annnual Meeting of the European-Society-for=Clinical-Virology -- SEP 27-30, 2009 -- Istanbul, TURKEYWOS: 000270629000149European Soc Clin Viro

DNA insitu hybridization in the diagnosis of human papillomavirus infection

International Symposium on Recent Advances in the Diagnosis of Viral Diseases -- JUL 20-22, 1995 -- ISTANBUL, TURKEYWOS: A1996UW22400019PubMed ID: 15566883Background: Certain types of human papillomavirus (HPV) are shown to be associated with the development of genital lesions. DNA hybridization methods are used for the diagnosis of HPV infections. Objective: To use a nonradioactive DNA in situ hybridization system for the investigation of HPV infections responsible for the development of genital lesions in women. Study design: Sections from archival paraffin embedded biopsy specimens of 59 cases were screened for the presence of HPV DNA sequences by using digoxigenin labeled DNA probe which is specific for all types of HPVs and digoxigenin detection system. The study group consisted of samples diagnosed as squamous hyperplasia of the vulva (group 1), koilocytosis (group 2), condyloma acuminatum/koilocytotic atypy (group 3), cervical intraepithelial neoplasia (CIN), and epidermoid carcinoma (group 4). Results: No HPV DNA was detected in groups 1 and 2 which consisted of 3 and 13 specimens respectively. Seven of 11 (63.6%) specimens in group 3 and 7 of 32 (21.9%) in group 4 were found to be positive for in situ HPV DNA. Seven positive samples in group 3 and one positive sample in group 4 were typed as HPV 6/11. Five samples of the remaining positives in group 4 were typed as HPV 16/18. One case was found to be positive with both 16/18 and 31/33. Conclusion: Nonradioactive DNA in situ hybridization is an easy and efficient method to be performed for the diagnosis of HPV infections. Koilocytosis with atypy is directly correlated with HPV infection and it is suggested to monitor the CIN cases with HPV type 16/18 infection since the pathology can be progressive.Federat European Microbiol So

Clinical significance of basal core promoter and precore mutations in chronic hepatitis B

WOS: 000251892800030PubMed ID: 18265656Background/Aims: The mutations in the basal core promoter and precore region of hepatitis B virus genome in hepatitis B e antigen-positive and -negative chronic hepatitis B patients have been described. The reports about their prevalence and clinical significance in the Mediterranean region where D is the predominant genotype, are very limited. Methodology: The serum samples were collected from 44 naive chronic hepatitis B patients. For detection of the mutations basal core promoter and precore regions of HBV genome were amplified and sequenced. Results: All samples were determined as genotype D. Before initiation of treatment basal core promoter mutations were found as 55% (11/20) and 46% (11/24) in HBeAg-positive and -negative patients, respectively (p > 0.5). HBeAg-negative samples were associated with precore mutations (G1896(A) and G1899(A)). Three of 20 (15%) patients of HBeAg-positive and seven of 24 (29%) of HBeAg-negative populations showed sustained response to therapy at the 24th month of initiation. Conclusions: The presence of precore stop codon mutant in those with sustained response was 89%, overall at the end of therapy. At initiation of therapy basal core promoter mutations were more common in non-responders than responders (65% vs. 20%; p < 0.001). While 23% of cases totally showing sustained response, absence of mutations in the basal core promoter region of hepatitis B virus genotype D may be related to sustained response in patients with chronic hepatitis B