The purpose of this study was to investigate whether taurine ameliorate the diabetic retinopathy, and to further explore the underlying mechanisms. The Sprague-Dawley rats were injected with streptozotocin to establish experimental diabetic model, then fed without or with 1.2% taurine for additional 4-12 weeks. After that, the protective effects of dietary taurine supplementation on diabetic retinopathy were estimated. Our results showed that chronic taurine supplement effectively improved diabetic retinopathy as changes of histopathology and ultrastructure. The supplementation could not lower plasma glucose concentration (P > 0.05), but caused an elevation in taurine content and a decline in levels of glutamate and gamma-aminobutyric acid (GABA) in diabetic retina (P < 0.05). Moreover, chronic taurine supplementation increased glutamate transporter (GLAST) expression (P < 0.05), decreased intermediate filament glial fibrillary acidic protein (GFAP) and N-methyl-D: -aspartate receptor subunit 1 (NR1) expression in diabetic retina (P < 0.05). These results demonstrated that chronic taurine supplementation ameliorates diabetic retinopathy via anti-excitotoxicity of glutamate in rats.

Considerable evidence demonstrates that phenotypic switching of vascular smooth muscle cells (VSMCs) is influenced by aging and hypertension. During phenotypic switching, VSMCs undergo a switch to a proliferative and migratory phenotype, with this switch being a common pathology in cardiovascular diseases. The aim of this study was to explore the joint influence of age and hypertension on thoracic aortic smooth muscle phenotypic switching and the balance of Akt and mitogen-activated protein kinase (MAPK) signaling during this switch. Different ages of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were used to establish hypertension and aging models. The phenotypic state was determined by detecting the marker proteins α-SM-actin, calponin, and osteopontin (OPN) via immunohistochemical staining and Western blot. Signaling proteins associated with the Akt and MAPK pathways were detected in rat thoracic aorta using Western blot. Both aging and hypertension caused a decrease in contractile (differentiated) phenotype markers (α-SM-actin and calponin), while the synthetic (proliferative or de-differentiated) phenotype maker was elevated (OPN). When combining hypertension and aging, this effect was enhanced, with Akt signaling decreased, while MAPK signaling was increased. These results suggested that VSMCs phenotype switching is modulated by a balance between Akt and MAPK signaling in the process of aging and hypertension.

Background: Regular exercise is a lifestyle intervention for controlling hypertension and has an improving effect on vascular function. Voltage-gated L-type Ca2+ (LTCC) and large-conductance Ca2+-activated K+ (BKCa) channels are two principal mediators of vascular smooth muscle cell contractility and arterial tone. The present study tested the hypothesis that DNA methylation dynamics plays a key role in exercise-induced reprogramming and downregulation of LTCC and BKCa channel in mesenteric arteries from spontaneously hypertensive rats (SHRs). Methods: SHRs and Wistar–Kyoto (WKY) rats were subjected to exercise training or kept sedentary, and vascular molecular and functional properties were evaluated. Results: Exercise inhibited hypertension-induced upregulation of LTCC and BKCa channel function in mesenteric arteries by repressing LTCC α1c and BKCa β1 subunit expression. In accordance, exercise triggered hypermethylation of α1c and β1 gene in SHR, with concomitant decreasing TET1, increasing DNMT1 and DNMT3b expression in mesenteric arteries, as well as altering peripheral α-KG and S-adenosylmethionine/ S-adenosylhomocysteine ratio. Acting synergistically, these exercise-induced functional and molecular amelioration could allow for attenuating hypertension-induced elevation in arterial blood pressure. Conclusion: Our results indicate that exercise suppresses LTCC and BKCa channel function via hypermethylation of α1c and β1 subunits, which contributes to the restoration of mesenteric arterial function and vasodilation during hypertension.

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Background Candida auris is a pathogen first found in external ear canal, becoming a major threat to global health. Here, we describe a candidemia case caused by a novel drug-resistant Candida auris strain. Case Presentation An 80-year-old patient, with multiple serious medical conditions, was suffered from candidemia caused by Candida auris , died 9 days after admission in our hospital. Phylogenetic analysis indicates that this C. auris isolate (designated BJCA003) belongs to the South Asian clade, carries the Y132F mutation in the protein Erg11. And antibiotic susceptibility test indicated that BJCA003 is resistant to fluconazole and amphotericin B, not susceptible to caspofungin. In addition, this strain has multiple colony and cellular morphologies under different culture conditions. Conclusion Strain BJCA003 is a novel drug resistant C. auris strain in mainland China, the Y132F mutation in Erg11 may attribute to fluconazole-resistance, alarming that we still face more challenges about C. auris.