To compare 1-year outcomes of phacoemulsification alone (phaco-only) vs phacoemulsification with implantation of 2 trabecular microbypass stents (iStent or iStent inject; phaco-stent) in eyes with primary angle-closure glaucoma (PACG). Retrospective matched clinical cohort study. PACG eyes that underwent phaco-only vs phaco-stent at a single ophthalmology center. Groups were matched for baseline intraocular pressure (IOP) and medication use with a tolerance of ±2mm Hg and ±1 medication, respectively. Primary outcomes included postoperative change in the mean IOP and medications. One-year outcomes were assessed using generalized estimating equations corrected for baseline intergroup differences. One hundred fifty-eight eyes (79 per group) were included. At 1 year, IOP decreased by 13% (from 16.8 ± 3.1mm Hg preoperatively) in the phaco-only group (P < .001) and by 27% (from 17.6 ± 3.2mm Hg) in the phaco-stent group (P < .001). Medication use decreased by 11% (from 1.8 ± 1.3 medications preoperativand medication reductions and smaller incidences of IOP spikes among the phaco-stent eyes. While bariatric surgery induces remission of type 2 diabetes mellitus and reduces other microvascular complications, its impact on diabetic retinopathy (DR) is unclear. Some trials suggest early worsening of DR postsurgery because of rapid improvements in hyperglycemia. This meta-analysis sought to estimate the impact of bariatric surgery on DR for obese patients compared with medical treatment. Systematic review and meta-analysis. The Medline, Embase, and PubMed Central databases were searched to March 2020. Primary studies comparing DR in patients undergoing bariatric surgery with those undergoing medical management were included. this website Results were meta-analyzed using a random-effects model. Primary outcomes included prevalence of all DR and sight-threatening DR after surgery. Secondary outcomes included worsening of DR within and beyond 12months. Overall, 14 studies comprised of 110,300 surgical patients and 252,289 control subjects were included. Surgical patients had a statistically significantly lowear.Diabetes-induced coronary endothelial cell (CEC) dysfunction contributes to diabetic heart diseases. Angiotensin II (Ang II), a vasoactive hormone, is upregulated in diabetes, and is reported to increase oxidative stress in CECs. 4-hydroxy-2-nonenal (4HNE), a key lipid peroxidation product, causes cellular dysfunction by forming adducts with proteins. By detoxifying 4HNE, aldehyde dehydrogenase (ALDH) 2 reduces 4HNE mediated proteotoxicity and confers cytoprotection. Thus, we hypothesize that ALDH2 improves Ang II-mediated defective CEC angiogenesis by decreasing 4HNE-mediated cytotoxicity. To test our hypothesis, we treated the cultured mouse CECs (MCECs) with Ang II (0.1, 1 and 10 μM) for 2, 4 and 6 h. Next, we treated MCECs with Alda-1 (10 μM), an ALDH2 activator or disulfiram (2.5 μM)/ALDH2 siRNA (1.25 nM), the ALDH2 inhibitors, or blockers of angiotensin II type-1 and 2 receptors i.e. Losartan and PD0123319 respectively before challenging MCECs with 10 μM Ang II. We found that 10 μM Ang II decreased tubeed angiogenesis in MCECs. Additionally, enhancing ALDH2 activity with Alda 1 rescued Ang II-induced decrease in angiogenesis by increasing the levels of VEGFR1, VEGFR2 and decreasing the levels of AT2R. In summary, ALDH2 can be an important target in reducing 4HNE-induced proteotoxicity and improving angiogenesis in MCECs. Finally, we conclude ALDH2 activation can be a therapeutic strategy to improve coronary angiogenesis to ameliorate cardiometabolic diseases. Clinical data show that aneurysm rupture causes high mortality in aged men. MicroRNAs (miRNAs) were reported to regulate endothelial progenitor cells (EPCs) which play a vital role in repairing endothelial damage and maintaining vascular integrity. This study identified a novel miRNA regulator for the functions of EPCs in aneurysm repair. Abdominal aortic aneurysm (AAA) model was established on Sprague-Dawley rats which later underwent antagomiR-222 treatment. The histopathological changes of AAA rats were examined by hematoxylin-eosin staining. Flow cytometry was performed to quantify EPCs in peripheral blood and identify EPCs isolated from the rat femur. The potential target of miR-222-3p was predicted by TargetScan v7.2 and validated by Dual-luciferase reporter assay. The effects of miR-222-3p and ADIPOR1 on the migration, invasion and tube formation of EPCs were evaluated by wound healing, Transwell and tube formation assays. The expressions of miR-222-3p and ADIPOR1 in aortic aneurysm tissues and EPCs were assessed by qRT-PCR or Western blot. AAA exhibited histopathological abnormality, a decreased number of EPCs in the peripheral blood and an increased miR-222-3p expression. AntagomiR-222 injection reversed all these phenomena in AAA rats. Upregulating miR-222-3p expression inhibited the migration, invasion, and tube formation of EPCs, and the expressions of ADIPOR1 and phosphorylated-AMKP, while downregulating miR-222-3p expression exerted opposite effects in EPCs. ADIPOR1 was identified as a target gene of miR-222-3p. Overexpressing ADIPOR1 abrogated the effects of miR-222-3p upregulation on EPCs. Downregulated miR-222-3p prompted the migration, invasion and recruitment of EPCs by targeting ADIPOR1-induced AMKP activation.Downregulated miR-222-3p prompted the migration, invasion and recruitment of EPCs by targeting ADIPOR1-induced AMKP activation.Nutrition affects multiple aspects of insect physiology such as body size and fecundity, but we lack a detailed understanding of how nutrition influences the reproductive physiology of male insects such as mosquitoes. Given that female mosquitoes are vectors of many deadly diseases and can quickly proliferate, understanding how male nutrition impacts female fecundity could be of critical importance. To uncover the relationship between nutrition in adult male mosquitoes and its impacts on reproductive physiology, we reared larvae of the Northern house mosquito, Culex pipiens, on a standard lab diet and divided adult males among three different dietary treatments low (3%), moderate (10%), and high (20%) sucrose. We found that although overall body size did not differ among treatments, one-week-old males raised on the 3% sucrose diet had significantly smaller male accessory glands (MAGs) compared to males that consumed the 10% and the 20% sucrose diets. Diet affected whole-body lipid content but did not affect whole-body protein content.