The primary objective was to determine superiority of dulaglutide 1.5 mg versus placebo in HbA(1c) change at 26 weeks. RESEARCH DESIGN AND METHODS This 52-week, multicenter, parallel-arm study (primary end point: 26 weeks) randomized patients (2: 2: 2: 1) to dulaglutide 1.5 mg,

dulaglutide 0.75 mg, exenatide 10 mg, or placebo (placebo-controlled period: 26 weeks). Patients were treated with metformin (1,500-3,000 mg) and pioglitazone (30-45 mg). Mean baseline HbA(1c) was 8.1% (65 mmol/mol). RESULTS Least squares mean 6 SE HbA(1c) change from baseline to the primary end point was -1.51 +/- CH5183284 molecular weight 0.06% (-16.5 +/- 0.7 mmol/mol) for dulaglutide 1.5 mg, -1.30 +/- 0.06% (-14.2 +/- 0.7 mmol/mol) for dulaglutide 0.75 mg, -0.99 +/- 0.06% (-10.8 +/- 0.7 mmol/mol) for exenatide, and -0.46 +/- 0.08% (-5.0 +/- 0.9 mmol/mol) for placebo. Both dulaglutide doses were superior to placebo at 26 weeks (both adjusted one-sided P smaller than 0.001) and exenatide at 26 and 52 weeks (both adjusted one-sided P smaller than 0.001). Greater percentages of patients reached HbA(1c) targets with dulaglutide 1.5 mg and 0.75 mg than with placebo and exenatide (all P smaller than 0.001). At 26 and 52 selleck inhibitor weeks, total hypoglycemia incidence was lower in patients receiving dulaglutide 1.5 mg than in those receiving exenatide; no dulaglutide-treated patients reported severe hypoglycemia.

The most common gastrointestinal 4 adverse events for dulaglutide were nausea, vomiting, and diarrhea. Events were mostly mild to moderate and transient. CONCLUSIONS Both once-weekly dulaglutide doses demonstrated superior glycemic control versus placebo and exenatide with an acceptable tolerability and safety profile.”
“Background: Hyperechogenicity of the substantia nigra (SN) measured by transcranial sonography (TCS) is a characteristic feature observed in patients with Parkinson’s disease (PD). To our knowledge, no SN hyperechogenicity

data are available for Polish population. Moreover most of studies come from few centres, which used the one type of ultrasound find more device. The main aim of the study was to investigate the association between PD and SN hyperechogenicity measured by sonographic machine, not assessed so far. Materials and methods: In this study cross-sectional study SN hyperechogenicity was evaluated in 102 PD patients and 95 control subjects. Midbrain was visualised by Aloka Prosound 7 ultrasound device. SN area measurement, the relation to the clinical features of PD, inter- and intra-observer reliability were evaluated. Results: We confirmed that SN echogenicity is significantly increased in PD patients compared to control subjects (p smaller than 0.001). The area under curve for PD patients vs. controls was 0.93. Receiver operating characteristic analysis indicated a cut-offs for SN echogenicity at 0.19 cm(2) with accuracy equal to 90%, specificity – 86% and sensitivity – 93.7%. The SN hyperechogenicity was not related to PD clinical findings.