Lykkegaardgonzalez3597

EC apoptosis was significantly increased in diabetic EC (isolated from HFD animal aorta) or high glucose high lipid (HGHL) cultured HUVECs. These pathological alterations were further potentiated by gCTRP5 and attenuated by CTRP5Ab. Pathway specific discovery-driven approach revealed that Nox1 expression was one of the signaling molecules commonly activated by HFD, HGHL, and gCTRP5. Treatment with CTRP5Ab reversed HFD-induced Nox1 upregulation. Finally, Nox1siRNA was used to determine the causative role of Nox1 in gCTRP5 induced EC apoptosis in diabetes. Results showed that gCTRP5 activated the mitochondrial apoptotic signal of EC in diabetes, which was blocked by the silencing Nox1 gene. CONCLUSION We demonstrated for the first time that gCTRP5 is a novel molecule contributing to diabetic vascular EC dysfunction through Nox1-mediated mitochondrial apoptosis, suggesting that interventions blocking gCTRP5 may protect diabetic EC function, ultimately attenuate diabetic cardiovascular complications. OBJECTIVE To determine clinicopathological features, risk of lymph node metastasis (LNM) and survival outcome in synchronous multiple early gastric cancer (MEGC) patients. METHODS A total of 338 solitary early gastric cancer (SEGC) and 26 MEGC patients who underwent surgical resection were retrospectively reviewed. The clinicopathological features and predictive factors for MEGC patients were evaluated. Also, we analyzed risk factors for LNM and compared survival difference between SEGC and MEGC patients. RESULTS The frequency of multiple synchronous lesions was 7.1% in early gastric cancer (EGC) patients. The main and minor lesions were mostly confined to the same third of the stomach (84.6%, 22/26), and the most common location was the lower third of the stomach. With regard to the number of coexisting lesions, most of the patients had two lesions and more than three lesions were not common. Tumor size≤2cm (OR2.684, 95%CI1.131-6.368, P less then 0.05) and the presence of atrophic gastritis (OR2.418, 95%CI1.052-5.555, P less then 0.05) were independent risk factors for synchronous MEGC. There was no significant statistical difference between SEGC and MEGC for LNM (17.5% vs 23.1%, P=0.311). The number of coexisting lesions was not associated with the risk of LNM in EGC. In addition, the survival outcome of MEGC patients was similar to that of SEGC (5-year RFS rate, 96.0% vs 93.7%, P=0.329;5-year OS rate, 96.0% vs 88.3%, P=0.479). CONCLUSION Meticulous endoscopic examination at the initial diagnosis of MEGC was very important, especially for those with precancerous lesions such as atrophic gastritis. In terms of treatment methods, endoscopic resection may be equally suitable for synchronous MEGC if the lesions fulfilled its indication criteria. AIMS The purpose of this study was to investigate the impact of diabetic neuropathy (dNP) on lower limb endurance, explosive and maximal muscle strength in patients with Type 2 Diabetes Mellitus (T2DM). METHODS Fifty-four participants, aged between 55 and 85, were enrolled in this observational comparative study. The patients with T2DM had an average HbA1c of 7.4% (±1.03) and diabetes duration of 13 years. Participants were classified by means of electroneuromyography as T2DM without dNP (dNP-; n = 8), T2DM with sensory dNP (dNPs; n = 13), T2DM with sensorimotor dNP (dNPsm; n = 14), and healthy controls without neuropathy (C; n = 19). Maximal muscle strength and muscle endurance of the dominant knee and ankle were measured by dynamometry, while explosive muscle strength was evaluated by mechanography. RESULTS Muscle endurance "total work" in knee extension and ankle plantar flexion was higher in the healthy controls compared to dNP-, dNPs and dNPsm, in knee flexion compared to dNPs and dNPsm, and in ankle dorsiflexion compared to dNPsm only (p less then 0.05). Furthermore, relative explosive muscle strength "total power/body weight" and relative maximal muscle strength "peak torque/lean body mass of the dominant leg" considering knee flexion, ankle plantar flexion and dorsiflexion, were higher in healthy controls compared to the dNPsm group, and for maximal muscle strength ankle dorsiflexion even between dNP- and dNPsm (p  less then  0.05). CONCLUSIONS Muscle endurance is impaired in patients with T2DM, independent of the presence of dNP. Explosive and maximal muscle strength are more likely affected by the presence and severity of dNP. BACKGROUND AND PURPOSE Although diabetes is associated with multiple ocular complications, there are limited data on the incidence and predictors of visual acuity (VA) loss in type 2 diabetes. The aim of this study was to determine the 4-year cumulative incidence of visual impairment and blindness, and the predictors of vision loss, in a representative community-based cohort. METHODS The longitudinal Fremantle Diabetes Study Phase II recruited 1551 participants with type 2 diabetes between 2008 and 2011. CNQX cell line Participants attended biennial face-to-face assessments including VA measurement. Multivariable logistic regression was used to determine the predictors of vision loss (defined as a decrease in VA by >10 letters at the Year 4 assessment), excluding those with visual impairment (VA >6/19 and ≤6/48) and blindness (VA >6/48) at baseline. RESULTS 882 participants with normal/near normal vision at baseline had VA data at Year 4 available. During a median [interquartile range] 4.1 [4.0-4.4] years of follow-up, the cumulative incidences of visual impairment and vision loss were 0.9% (n = 8) and 2.9% (n = 26), respectively. No participants developed blindness and 1.9% (n = 17) improved their VA. Multivariable logistic regression showed baseline smoking (OR 3.17 (95% CI 1.15-8.76)), prior severe hypoglycemia (5.59 (1.32-23.61)) and urinary albumincreatinine ratio (uACR) (1.42 (1.09-1.84) for an increase of 1 in ln(uACR)) had higher odds of vision loss during follow-up. CONCLUSIONS Smoking cessation and management strategies that avoid severe hypoglycemia and preserve kidney function may potentially prevent vision loss in people with type 2 diabetes.