Oxidative stress induced by chronic hyperglycemia in type 2 diabetes plays a crucial role in progressive loss of β-cell mass through β-cell apoptosis. Glucagon like peptide-1 (GLP-1) has effects on preservation of β-cell mass and its insulin secretory function. GLP-1 possibly increases islet cell mass through stimulated proliferation from β-cell and differentiation to β-cell from progenitor cells. Also, it probably has an antiapoptotic effect on β-cell, but detailed mechanisms are not proven. Therefore, we examined the protective mechanism of GLP-1 in β-cell after induction of oxidative stress. The cell apoptosis decreased to ~50% when cells were treated with 100 µM H2O2 for up to 2 hr. After pretreatment of Ex-4, GLP-1 receptor agonist, flow cytometric analysis shows 41.7% reduction of β-cell apoptosis. This data suggested that pretreatment of Ex-4 protect from oxidative stress-induced apoptosis. Also, Ex-4 treatment decreased GSK3β activation, JNK phosphorylation and caspase-9, -3 activation and recovered the expression of insulin2 mRNA in β-cell lines and secretion of insulin in human islet. These results suggest that Ex-4 may protect β-cell apoptosis by blocking the JNK and GSK3β mediated apoptotic pathway.

Our study showed that the benefits obtained from the SES, which reduce neointimal proliferation, are not probably mediated by the attenuation of the systemic inflammatory markers hs-CRP or IL-6.

There are limited data on the optimal antithrombotic therapy for patients with atrial fibrillation (AF) who undergoing coronary stenting. We reviewed 203 patients (62.6 % men, mean age 68.3 ± 10.1 years) between 2003 and 2012, and recorded clinical and demographic characteristics of the patients. Clinical follow-up included major adverse cardiac and cerebrovascular events (MACCE) (cardiac death, myocardial infarction, target lesion revascularization, and stroke), stent thrombosis, and bleeding. The most commonly associated comorbidities were hypertension (70.4 %), diabetes mellitus (35.5 %), and congestive heart failure (26.6 %). Sixty-three percent of patients had stroke risk higher than CHADS2 score 2. At discharge, dual-antiplatelet therapy (aspirin, clopidogrel) was used in 166 patients (81.8 %; Group I), whereas 37 patients (18.2 %) were discharged with triple therapy (aspirin, clopidogrel, warfarin; Group II). The mean follow-up period was 42.0 ± 29.0 months. The mean international normalized ratio (INR) in group II was 1.83 ± 0.41. The total MACCE was 16.3 %, with stroke in 3.4 %. Compared with the group II, the incidence of MACCE (2.7 % vs 19.3 %, P = 0.012) and cardiac death (0 % vs 11.4 %, P = 0.028) were higher in the group I. Major and any bleeding, however, did not differ between the two groups. In multivariate analysis, no warfarin therapy (odds ratio 7.8, 95 % confidence interval 1.02-59.35; P = 0.048) was an independent predictor of MACCE. By Kaplan-Meier survival analysis, warfarin therapy was associated with a lower risk of MACCE (P = 0.024). In patients with AF undergoing coronary artery stenting, MACCE were reduced by warfarin therapy without increased bleeding, which might be related to tighter control with a lower INR value.

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Background and ObjectivesThe purpose of the current study was to assess left atrial (LA) physiology in relation to associations between LA volume change and regional tissue velocities and strains, and to extend this information to patients with mitral stenosis (MS) or mitral regurgitation (MR).Subjects and MethodsTwenty-two healthy persons, 22 patients with moderate-to-severe MS, and 22 patients with moderate-to-severe MR were studied. Tissue velocities, strains, and time-volume curves of the LA were acquired using tissue Doppler imaging and 3-dimensional echocardiography.ResultsIn healthy controls, the maximal LA volume was negatively correlated with the posterior wall longitudinal systolic strain (r=-0.45, p=0.03). The time-to-maximal LA volume was positively correlated with the time-to-posterior wall longitudinal peak strain (r=0.46, p=0.03) and the time-to-circumferential peak strain (r=0.59, p=0.004). The LA active emptying fraction (LAactEF) was positively correlated with the posterior wall longitudinal peak systolic and late diastolic tissue velocities. In patients with MS, the maximal LA volume was negatively correlated with the posterior wall radial peak systolic velocity and the longitudinal late diastolic velocity. In patients with MS, the LAactEF had an additional positive correlation with the anterior wall longitudinal and circumferential systolic velocities, whereas the patients with MR had an additional positive correlation between the LAactEF and the lateral wall longitudinal peak strain as compared with the healthy cantrols.ConclusionLA longitudinal and circumferential deformations are more related than radial deformation to determining LA volume and function. The LA of patients with MS revealed a greater pathologic physiology than those of patients with MR.