Adiponectin is an independent determinant of insulin resistance in women with polycystic ovary syndrome.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is frequently associated with insulin resistance and a consequent increased risk of metabolic diseases. The aim of the present study was to investigate the role of adiponectin in insulin resistance in PCOS women. MATERIALS AND METHODS: Forty-seven patients with PCOS and 23 control subjects, matched for age and body mass index (BMI), were enrolled in the study. Clinical, metabolic and hormonal parameters and adiponectin levels were measured, and HOMA-IR score (homeostasis model assessment-insulin resistance index) was calculated for each subject. RESULTS: There was no difference in adiponectin levels between PCOS patients and the control group. However, adiponectin levels were negatively correlated with obesity-associated parameters and HOMA-IR score in PCOS patients and controls. As adiponectin is modulated by BMI we adjusted for BMI among the PCOS patients, and found a negative correlation between adiponectin levels and HOMA-IR score (r = -0.51, p < 0.001). Adiponectin and BMI were independent determinants of insulin resistance in PCOS patients (adjusted R2 = 0.66, p < 0.001). CONCLUSION: Adiponectin did not seem to be actively involved in the pathogenesis of PCOS. However, adiponectin levels were independently associated with insulin resistance in PCOS patients, suggesting that adiponectin might play a role in the complicated metabolic abnormalities of PCOS.     

Identifying and Predicting Distinct Patterns of Implementation in a School-Wide Behavior Support Framework

The purpose of this study was to examine the extent to which distinct patterns of fidelity of implementation emerged for 5331 schools over a 5-year course of implementing school-wide positive behavioral interventions and supports (SWPBIS). We used latent class analysis to classify schools based on their likelihood of implementing SWPBIS with fidelity each year, then assessed school and district predictors of classifications. A four-class solution fit the model well, with two patterns of sustained implementation (Sustainers and Slow Starters) and two patterns of practice abandonment (Late Abandoners and Rapid Abandoners). Significant predictors of group membership included grade levels served, enrollment, proportion of schools implementing SWPBIS in the district (“critical mass”), and size of the implementation cohort (“community of practice”). Elementary schools, larger schools, schools in districts with more schools already implementing SWPBIS, and those starting within a larger initial district cohort were more likely to be in the sustaining classes. Results are discussed in terms of understanding patterns of implementation in schools to enhance sustained implementation of school practices.     

The role of angiotensin converting enzyme genotype in coronary artery ectasia

Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.     

Pharmacological approach to acute pancreatitis

The aim of the present review is to summarize the current knowledge regarding pharmacological prevention and treatment of acute pancreatitis （AP） based on experimental animal models and clinical trials. Somatostatin （SS） and octreotide inhibit the exocrine production of pancreatic enzymes and may be useful as prophylaxis against Post Endoscopic retrograde cholangiopancreatography Pancreatitis （PEP）. The protease inhibitor Gabexate mesilate （GM） is used routinely as treatment to AP in some countries, but randomized clinical trials and a meta-analysis do not support this practice. Nitroglycerin （NGL） is a nitrogen oxide （NO） donor, which relaxes the sphincter of Oddi. Studies show conflicting results when applied prior to ERCP and a large multicenter randomized study is warranted. Steroids administered as prophylaxis against PEP has been validated without effect in several randomized trials. The non-steroidal anti-inflammatory drugs （NSAID） indomethacin and diclofenac have in randomized studies showed potential as prophylaxis against PEP. Interleukin 10 （IL-10） is a cytokine with anti-inflammatory properties but two trials testing IL-10 as prophylaxis to PEP have returned conflicting results. Antibodies against tumor necrosis factor-alpha （TNF-α） have a potential as rescue therapy but no clinical trials are currently being conducted. The antibiotics beta- lactams and quinolones reduce mortality when necrosis is present in pancreas and may also reduce incidence of infected necrosis. Evidence based pharmacological treatment of AP is limited and studies on the effect of potent anti-inflammatory drugs are warranted.