BACKGROUND Acute exacerbation (AE) of chronic obstructive pulmonary disease (COPD) may be accompanied by the deterioration of cardiovascular comorbidities, as evidenced by the increased incidence of acute cardiovascular events. RESEARCH QUESTION Whether preceding AE might be associated with mortality of cardiovascular events remains unknown. STUDY DESIGN AND METHODS Using a health insurance research database in Taiwan, we identified patients with COPD who experienced first-time acute myocardial infarction (AMI; n=26,442), ischemic stroke (n=54,959) and intracranial hemorrhage (ICH; n=14,893) over a 13-year period. In each cohort, 4,356, 6,655 and 1,727 patients, respectively, had been hospitalized for AE within the previous year before the index cardiovascular events, and COPD patients without hospitalized AE constituted the controls. Odds ratios (ORs) of 90-day mortality and hazard ratios (HRs) of overall mortality during follow-up in relation to hospitalized AE and the frequency of hospitalized AEs (i.e., 1 and ≥2 hospitalized AEs) were estimated with adjustment for potential confounders. RESULTS Hospitalized AE was independently associated with 90-day mortality of AMI (OR=1.33, 95% confidence interval [CI] 1.24-1.43), ischemic stroke (OR=1.46, 95% CI 1.36-1.56) and ICH (OR=1.19, 95% CI 1.06-1.32). Hospitalized AE was associated with overall mortality of AMI (HR=1.23, 95% CI 1.19-1.27), ischemic stroke (HR=1.29, 95% CI 1.26-1.33) and ICH (HR=1.19, 95% CI 1.13-1.26). In addition, compared with controls, patients with more frequent hospitalized AEs exhibited significant trends at higher risk of 90-day and overall mortality of AMI, ischemic stroke and ICH. Finally, these results were consistent with propensity score matching-based estimates. INTERPRETATION Preceding hospitalized AE is associated with 90-day and overall mortality of cardiovascular events in COPD. AIM The aim of the present study was to identify the affected gene in a French family with maturity-onset diabetes of the young (MODY) using whole-exome sequencing (WES). METHODS WES was performed in one patient with MODY, and candidate variants were confirmed in members of the immediate family by Sanger sequencing. RESULTS In the proband, a new heterozygous missense mutation (c.340A>C) was identified in the NEUROD1 gene by WES analysis and confirmed by Sanger sequencing. Additional Sanger sequencing of the proband's sister and mother revealed the same heterozygous mutation. The proband and his sister displayed typical clinical characteristics of MODY, while their mother had the same typical MODY features except for later onset. When clinical and biological profiles were established for all three patients, the severity of diabetes-related complications varied substantially from one family member to another. CONCLUSION A novel missense mutation found in NEUROD1 was associated with MODY 6 features in a single French family. BACKGROUND Urinary neutrophil gelatinase-associated lipocalin is an established biomarker of acute kidney injury, however, the levels are affected by the number of white blood cells in the urine. As we suspected the portion of the urinary stream sampled could also have a significant influence on the urinary NGAL levels in female subjects, we investigated the influence of the urine sampling procedure on the urinary NGAL levels. METHODS We collected 25-mL urinary specimens from each of initial-stream and midstream urinary specimens, including 28 healthy adult female volunteers without kidney diseases or UTI. Then we compared the WBC count, NGAL level, and creatinine level between these specimens. RESULTS We observed that the urinary NGAL levels were significantly higher in the specimens obtained from initial-stream urinary samples than in midstream specimens, and that they were strongly correlated with the leukocyte esterase activity and WBC count. Moreover, the differences in the urinary NGAL levels between the initial- and midstream urine samples were greater for initial-stream samples with higher leukocyte esterase activities, with a significant difference even for the initial-stream samples with no detectable leukocyte esterase activity. CONCLUSION Therefore, midstream urine sampling is strongly recommended for accurate measurement of the urinary NGAL levels. https://www.selleckchem.com/products/(-)-Epigallocatechin-gallate.html Nasal polyposis is a recurring research topic, as it affects 2 to 4% of the population. The aim of this historical note is to delve back into the original texts written by Hippocrates and discuss their relevance to the term "polyp", meaning "many feet", like an octopus. Various severe ocular diseases are associated with an elevated intravitreal expression of VEGF-A which increases the permeability of retinal endothelial cells (REC) or retinal pigment epithelial (RPE) cells in vivo and in vitro. Inhibition of VEGF receptor 2 (VEGFR2) is sufficient to completely prevent VEGF-A165-induced dysfunctions of barriers formed by long-term cultivated, immortal human ARPE-19 cells or immortalized bovine retinal endothelial cells (iBREC). Extended exposure to VEGF-A could result in additional activation of other growth factor receptors, potentially promoting synergistic effects of corresponding factors on various cellular processes including angiogenesis. Based on these observations, we investigated whether blocking of VEGFR2 is also sufficient to revert VEGF-A-induced changes of the barriers consisting of iBREC (i.e. inner blood-retina barrier) or ARPE-19 cells (i.e. outer blood-retina barrier) in vitro. Alterations of confluent monolayers' properties induced by treatment with VEGF-A16ich was also accompanied by a significant loss of the then strongly plasma membrane-expressed TJ-protein ZO-1. These alterations were completely reverted within one day by 10 nM nintedanib of which higher concentrations were not superior. None of the inhibitors tested diminished the strong barrier properties of iBREC or long-term cultivated ARPE-19 cells. Taken together, inhibition of VEGFR2 efficiently reverts VEGF-A165-induced barrier disturbances of both cell types forming and regulating the inner and outer blood-retina barrier. As synergistic actions of growth factors seem to play only a minor role in inducing a barrier dysfunction, specific inhibition of VEGFR2 could be an interesting option to treat VEGF-A-induced macular edema without obvious effects on vitality and functions of REC and RPE cells.