Vestmeadows2249

Methanolic and ethyl acetate extracts of pine nuts were evaluated for in vitro antioxidant and inhibition of alpha-amylase activities. Pine nut extracts were orally administered to alloxan monohydrate-induced diabetes in mice at 250, 500, and 750 mg/kg. Both extracts showed a significant antioxidant and inhibition of alpha-amylase activities. Animal studies showed a decline in fasting blood glucose, hyperlipidemia, and weight loss in diabetic mice. The administration of plant extracts decreased the blood glucose level during the oral glucose tolerance test. Histopathological examination showed a decrease in alloxan-induced lesions in the pancreas, liver, and kidney of animals treated with pine nut extracts. Furthermore, pine nut extract ameliorated oxidative stress-induced hepatotoxicity in diabetic mice. The presence of quercetin, gallic acid, vanillic acid, benzoic acid, syringic acid, m-coumaric acid, and other phenolic compounds might be related to hypoglycemic, alpha-amylase inhibitory, antioxidant, and antihyperlipidemic potential of pine nut extracts. PRACTICAL APPLICATIONS Dry fruits are rich in dietary nutrients, minerals, and phytochemicals that can be used to treat and prevent lifestyle disease. Pine nuts are edible and have economic importance in addition to several traditional uses such as diuretic, antiseptic, expectorant, antibacterial, antiviral, antifungal, antihypertensive, and antineuralgic properties. This study was conducted to investigate the pine nut extracts for their antioxidant and antidiabetic potentials using in vitro methods and animal disease model. The findings of the present study suggest that the extracts of Pine nuts may be helpful in treating hyperglycemia during diabetes and prevent its complications such as hepatic damage, nephrotoxicity, weight loss, and hyperlipidemia. © 2020 Wiley Periodicals, Inc.To explore the effects of miR-21-3p on diabetic atherosclerosis. Using enzyme-linked immunosorbent assay (ELISA), we also detected the levels of soluble receptor for advanced glycation endproducts RAGE (sRAGE) in the cellular supernatant of vascular endothelial cells after transfecting them with adenovirus vector having miR-21-3p mimic or inhibitor. We found decrease in the expression levels of miR-21-3p in vascular endothelial cells (VECs) induced by high-concentration glucose. We also observed that the introduction of miR-21-3p mimic significantly increased the expression of ADAM10 in the VECs. Similarly, significantly higher levels of sRAGE were found in the cultured supernatant after administration of miR-21-3p mimic in human vein endothelial cells. The production of reactive oxygen species and expression of inflammatory cytokines in VECs induced by LPS and high-concentration glucose were significantly decreased after administration of miR-21-3p. in vivo studies revealed that intravenous injection of miR-21-3p at regular intervals would reduce the area of atherosclerotic lesion and elevate the serum levels of sRAGE in atherosclerotic diabetic mice. miR-21-3p may be beneficial in diabetic atherosclerosis by promoting the cleaved form of sRAGE and inhibition of RAGE/NADPH oxidase signalling depending on the increased expression of ADAM10. SIGNIFICANCE OF THE STUDY We identified a novel microRNA, miR-21-3p, which is characteristically at elevated levels in serum derived from diabetic patients and responsible for target degradation of ADAM10 mRNA. Further, we show that miR-21-3p aggravates the atherosclerotic lesion via dysfunction of the ectodomain shedding of molecular binding RAGE in the diabetic atherosclerotic mice. © 2020 John Wiley & Sons Ltd.Polycomb group proteins are evolutionary conserved chromatin-modifying complexes, essential for the regulation of developmental and cell-identity genes. Polycomb-mediated transcriptional regulation is provided by two multi-protein complexes known as Polycomb repressive complex 1 (PRC1) and 2 (PRC2). Recent studies positioned PRC1 as a foremost executer of Polycomb-mediated transcriptional control. Mammalian PRC1 complexes can form multiple sub-complexes that vary in their core and accessory subunit composition, leading to fascinating and diverse transcriptional regulatory mechanisms employed by PRC1 complexes. These mechanisms include PRC1-catalytic activity toward monoubiquitination of histone H2AK119, a well-established hallmark of PRC1 complexes, whose importance has been long debated. In this review, the central roles that PRC1-catalytic activity plays in transcriptional repression are emphasized and the recent evidence supporting a role for PRC1 complexes in gene activation is discussed. © 2020 WILEY Periodicals, Inc.It has been shown that overexpression of activated leukocyte cell adhesion molecule (ALCAM) is involved in development of resistance to tamoxifen therapy and promotion of cell invasion, migration and metastasis in ER+ breast cancer cells. Thus, we hypothesized that blockade of ALCAM interconnections with antibodies could be an effective approach for reversing mentioned negative events associated with ALCAM overexpression in breast cancer cells. Here, an anti-ALCAM scFv was recombinantly expressed and used throughout study for examination of the putative anticancer effects of ALCAM blockade. The anti-ALCAM scFv coding sequence was obtained from GenBank database and after addition of a 6× His-tag moiety, signal peptide and flanking sequences, the whole construct was expressed in Escherichia coli. Tamoxifen resistant MCF7 cells were then pretreat for 24 hours with purified recombinant anti-ALCAM scFv prior to administration of tamoxifen. In parallel, the cytotoxicity profile of anti-ALCAM scFv and tamoxifen co-t into a refractory more invasive one which ultimately ends in disease progression and relapse. Here, we reported expression of an anti-ALCAM scFv, capable of increasing the sensitivity of tamoxifen resistant ER+ MCF-7 cells to tamoxifen therapy following a 24-hour pretreatment period. In addition, we demonstrated that the anti-ALCAM scFv monotherapy was also capable of suppressing invasion and migration of MDA-MB-231 cells in Boyden chamber assays. © 2020 John Wiley & Sons Ltd.In the fragment molecular orbital (FMO) method, a given molecular system is usually fragmented at sp3 carbon atoms. However, fragmentation at different sites sometimes becomes necessary. Hence, we propose fragmentation at sp2 carbon atoms in the FMO method. Projection operators are constructed using sp2 local orbitals. To maintain practical accuracy, it is essential to consider the three-body effect. In order to suppress the corresponding increase of computational cost, we propose approximate models considering local trimers. Numerical verification shows that the present models are as accurate as or better than the standard FMO2 method in total energy with fragmentation at sp3 carbon atoms. © 2020 Wiley Periodicals, Inc.Nocardia seriolae, a Gram-positive bacterium, is the main pathogen of fish nocardiosis. Protein NlpC/P60 is a cell-wall peptidase and a potential virulence factor of N. seriolae. Subcellular localization research revealed that both NlpC/P60-GFP and NlpC/P60Δsig-GFP fusion proteins were evenly distributed in the whole cell of fathead minnow (FHM) cells. Furthermore, typical apoptotic features, such as nuclear pyrosis and apoptotic bodies, were observed in the transfected FHM cells and grouper spleen cells by the overexpression of protein NlpC/P60. Then, quantitative assays of mitochondrial membrane potential (ΔΨm) value, caspase-3 activity and apoptosis-related gene (Bax, BNIP3, TNF1 and TNF6) mRNA expression were conducted. The results showed that ΔΨm was decreased, caspase-3 was significantly activated, and the mRNA expression of pro-apoptotic genes (Bax and BNIP3) and tumour necrosis factors (TNF1 and TNF6) was up-regulated in NlpC/P60-overexpressed cells. Taken together, the results indicated that the protein NlpC/P60 of N. seriolae might involve in apoptosis regulation. This study may lay the foundation for further study on the function of N. seriolae NlpC/P60 and promote the understanding of the virulence factors and pathogenic mechanism of N. seriolae. © 2020 John Wiley & Sons Ltd.BACKGROUND Utilization of catheter ablation of Ventricular Tachycardia (VT) has steadily increased in recent years. Exploring short term outcomes is vital in health care planning and resource allocation. METHODS The Nationwide Readmission Database from 2010 to 2014 was queried using the ICD-9 codes for VT (427.1) and catheter ablation (37.34) to identify study population. Incidence, causes of 30-day readmission, in-hospital complications as well as predictors of 30-day readmissions, complications, and cost of care were analyzed. RESULTS Among 11725 patients who survived to discharge after index admission for VT ablation,1911 (16.3%) were readmitted within 30 days. Paroxysmal VT was the most common cause of 30-day readmission (39.51%). Dyslipidemia, chronic kidney disease (CKD), previous CABG, congestive heart failure (CHF), chronic pulmonary disease and anemia predicted increased risk of 30-day readmissions. The overall in-hospital complication rate was 8.2% with vascular and cardiac complications being the most common. Coexisting CKD and CHF and the need for mechanical circulatory support (MCS) predicted higher complication rates. Similarly increasing age, CKD, CHF, anemia, in-hospital use of MCS or left heart catheterization, teaching hospital and disposition to nursing facilities predicted higher cost. CONCLUSION Approximately 1 in 6 patients were readmitted after VT ablation, with paroxysmal VT being the most common cause of the readmission. A complication rate of 8.2% was noted. We also identified a predictive model for increased risk of readmission, complication, and factors influencing the cost of care which can be utilized to improve the outcomes related to VT ablation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.In evidence-based healthcare, randomized clinical trials provide the most accurate and reliable information on the effectiveness of an intervention. This project aimed to develop reporting guidelines, exclusively for randomized clinical trials in the dental specialty of Endodontology, using a well-documented, validated consensus-based methodology. The guidelines have been named Preferred Reporting Items for RAndomized Trials in Endodontics (PRIRATE) 2020. A total of eight individuals (PD, VN, HD, LB, TK, JJ, EP, SP), including the project leaders (PD, VN) formed a steering committee. The committee developed a checklist based on the items in the Consolidated Standards for Reporting Trials (CONSORT) guidelines and Clinical and Laboratory Images in Publications (CLIP) principles. A PRIRATE Delphi Group (PDG) and PRIRATE Face-to-Face Meeting group (PFMG) were also formed. Thirty PDG members participated in the online Delphi process and achieved consensus on the checklist items and flowchart that make up the PRIRATE guidelines. The guidelines were discussed at a meeting of the PFMG at the 19th European Society of Endodontology (ESE) Biennial congress, held on 13th September 2019 in Vienna, Austria. A total of 21 individuals from across the globe and four steering committee members (PD, VN, HD, LB) attended the meeting. As a consequence of the discussions, the guidelines were modified and then piloted by several authors whilst writing a manuscript. The PRIRATE 2020 guidelines contain a checklist consisting of 11 sections and 58 individual items as well as a flowchart, considered essential for authors to include when writing manuscripts for randomized clinical trials in Endodontics. This article is protected by copyright. All rights reserved.