Feline Coronaviruses Identified in Feline Effusions in Suspected Cases of Feline Infectious Peritonitis.

Ninety-five effusion samples were collected from cats with suspected feline infectious peritonitis in northern Taiwan; these samples showed a 47.4% (45/95) feline coronavirus (FCoV) positivity rate on immunofluorescence staining and RT-PCR. Young cats (≤24 months old) were found to have a significantly higher risk than cats >24 months old (odds ratio (OR) = 6.19, 95% confidence interval (CI) 2.54-16.00). No significant association was found between the positive rates and sex or breed. The A/G ratio in positive cases was significantly lower than the A/G ratio in negative cases. Genotyping and sequencing of the positive cases revealed 71.9% single infection with type I strains and 28.1% coinfection with types I and II. No single infections with type II strains were noted. The type I sequences had high diversity, while the type II sequences had high internal sequence identity and were more similar to CoVs from other species, such as dogs, pigs, and various small mammals. This study demonstrates the latest analysis of FCoV infection cases in northern Taiwan.

Glucagon-Like Peptide-1 Receptor Agonist Attenuates Autophagy to Ameliorate Pulmonary Arterial Hypertension through Drp1/NOX- and Atg-5/Atg-7/Beclin-1/LC3ß Pathways.

Mitochondrial dysfunction is associated with cardiovascular diseases and diabetes. Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling, and the abnormal proliferation, apoptosis and migration of pulmonary arterial smooth muscle cells (PASMCs). The glucagon-like peptide-1 (GLP-1) receptor agonist, liraglutide, has been shown to prevent pulmonary hypertension in monocrotaline-exposed rats. The aim of this study was to investigate the effect of liraglutide on autophagy, mitochondrial stress and apoptosis induced by platelet-derived growth factor BB (PDGF-BB). PASMCs were exposed to PDGF-BB, and changes in mitochondrial morphology, fusion-associated protein markers, and reactive oxygen species (ROS) production were examined. Autophagy was assessed according to the expressions of microtubule-associated protein light chain 3 (LC3)-II, LC3 puncta and Beclin-1. Western blot analysis was used to assess apoptosis, mitochondrial stress and autophagy markers. Liraglutide significantly inhibited PDGF-BB proliferation, migration and motility in PASMCs. PDGF-BB-induced ROS production was mitigated by liraglutide. Liraglutide increased the expression of α-smooth muscle actin (α-SMA) and decreased the expression of p-Yes-associated protein (p-YAP), inhibited autophagy-related protein (Atg)-5, Atg-7, Beclin-1 and the formation of LC3-ß and mitochondrial fusion protein dynamin-related (Drp)1. Therefore, liraglutide can mitigate the proliferation of PASMCs via inhibiting cellular Drp1/nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) pathways and Atg-5/Atg-7/Beclin-1/LC3ß-dependent pathways of autophagy in PAH.

Severe Hypoglycemia as a Predictor of End-Stage Renal Disease in Type 2 Diabetes: A National Cohort Study.

Aims: This study investigated whether there is a link between severe hypoglycemia and progression into end-stage renal disease (ESRD) in patients with type 2 diabetes. Methods: Tapping into Taiwan's Health Insurance Research Database, we identified all type 2 diabetes patients between 1996 and 2013 and identified those diagnosed with a severe hypoglycemia episode during an emergency department visit and those who were not. Controls were then matched 1:1 for age, sex, index year, and medication. Results: We identified 468,421 type 2 diabetes patients diagnosed as having severe hypoglycemia in an emergency department visit. Compared with controls, these patients with SH had a higher risk of all-cause mortality (Hazard Ratio (HR), 1.76; 95% confidence interval, 1.61⁻1.94) and progressed into ESRD within a shorter period of time. Results were similar after controlling for competing risk. Conclusion: Severe hypoglycemia is significantly associated with worsening renal dysfunction in patients with type 2 diabetes and hastened progression into ESRD.