الاستنتاج يبدو أن انتقال عدوى حمى الضنك يتأثر بتقلب المناخ. ويساعد توضيح دور العوامل المناخية في الإصابة بحمى الضنك على تقدير المخاطر والوقاية من الأوبئة.Universal health coverage (UHC) and the health-related Sustainable Development Goals (SGDs) cannot be achieved without the appropriate measurement and monitoring mechanisms. At the global level, extensive attention is given to mechanisms that focus on measuring and reporting the status of SDG indicators, to help in shaping global priorities, and to steer political will and leverage for action at the national level. Copyright © World Health Organization (WHO) 2019. Some rights reserved. This work is available under the CC BY-NC-SA 3.0 IGO license (https//creativecommons.org/licenses/by-nc-sa/3.0/igo).INTRODUCTION Osteoarthritis (OA) is the most common degenerative disease in middle-aged and elderly individuals that causes joint deformity and limb disability. Accumulating evidence has suggested that the pathogenesis of OA has been related to various mechanisms such as apoptosis, inflammation, oxidative stress and metabolic disorders. The aim of this study is to clarify the role of Foxo3a in the progress of OA in an in vitro model. MATERIALS AND METHODS The chondrocytes were derived from rabbit, and treated with IL-1b, which was used as an in vitro OA model. The over-expression and down-regulation of Foxo3a were achieved by transfected with overexpression vector or shRNA, respectively. The mRNA level of iNOS in chondrocytes was quantified by qPCR. Tenascin-c (Tnc) production was measured by ELISA and apoptosis-associated proteins were analyzed by Western blotting. The MTT assay was used to assess the viability of chondrocytes. RESULTS Foxo3a and iNOS expression were upregulated in IL-1b-treated chondrocytes. Foxo3a silencing decreased iNOS expression, and inhibited apoptosis of IL-1b-treated chondrocytes. The production of Tnc was significantly increased in IL-1b-treated chondrocytes and was positively regulated by Foxo3. Importantly, extracellular addition of Tnc abrogated the protective effects of Foxo3a knockdown on IL-1b = treated chondrocytes. CONCLUSION . The present study indicated that down-regulation of Foxo3a protected IL-1b-treated chondrocytes by decreasing iNOS expression and suppressing chondrocytes' apoptosis via modulating tenascin-c, which could be regarded as a potent therapeutic target for the treatment of OA.The identification of reliable biomarkers of Parkinson's disease (PD) is a pivotal step in the introduction of causal therapies. Saliva is a biofluid which may be involved in synuclein pathology in PD. We have reviewed current studies on salivary proteins and compounds in PD patients and healthy controls, and their potential application as biomarkers. A systematic literature search of the Pubmed and Scopus databases was performed. A total of 198 studies were screened, of which 20 were included in our qualitative analysis. We conclude that the oligomeric form of salivary alpha synuclein is higher in PD patients, and that this may serve as a potential biomarker of PD. Salivary DJ-1 concentrations fail to differentiate PD patients from controls. Other enzymes and substances (heme oxygenase-1, nitric oxide, acetylcholinesterase) have been assessed in single studies. Salivary cortisol levels are higher in PD than in healthy subjects. Further validation of these findings is needed. Saliva may be a promising source of biomarkers in PD.Staphylococcus aureus (S. aureus) osteomyelitis remains a major clinical problem. Anti-glucosaminidase (Gmd) antibodies (1C11) are efficacious in prophylactic and therapeutic murine models. Feasibility, safety and pharmacokinetics of 1C11 passive immunisation in sheep and endogenous anti-Gmd levels were quantified in osteomyelitis patients. 3 sheep received a 500 mg intravenous (i.v.) bolus of 1C11 and its levels in sera were determined by enzyme-linked immunosorbent assay (ELISA) over 52 d. A humanised anti-Gmd monoclonal antibody, made by grafting the antigen-binding fragment (Fab) portion of 1C11 onto the fragment crystallisable region (Fc) of human IgG1, was used to make a standard curve of mean fluorescent intensity versus concentration of anti-Gmd. Anti-Gmd serum levels were determined in 297 patients with culture-confirmed S. aureus osteomyelitis and 40 healthy controls. No complications or adverse events were associated with the sheep 1C11 i.v. infusion and the estimated circulating half-life of 1C11 was 23.7 d. Endogenous anti-Gmd antibody levels in sera of osteomyelitis patients ranged from 3 weeks. Anti-Gmd passive immunisation has potential to prevent and treat S. aureus osteomyelitis. Further clinical development is warranted.Mitochondrial turnover is required for proper cellular function. Both mitochondrial biogenesis and mitophagy are impaired in several degenerative and age-related diseases. The search for mitophagy activators recently emerged as a new therapeutical approach; however, there is a lack in suitable tools to follow mitochondrial turnover in a high-throughput manner. We demonstrate that the fluorescent protein, MitoTimer, is a reliable and robust probe to follow mitochondrial turnover. The screening of 15 000 small molecules led us to two chemically-related benzothiophenes that stimulate basal mitophagy in the beta-cell line, INS1. Enhancing basal mitophagy was associated with improved mitochondrial function, higher Complex I activity and Complex II and III expressions in INS1 cells, as well as better insulin secretion performance in mouse islets. The possibility of further enhancing mitophagy in the absence of mitochondrial stressors points to the existence of a 'basal mitophagy spare capacity'. To this end, we found two small molecules that can be used as models to better understand the physiological regulation of mitophagy.  https://www.selleckchem.com/products/levofloxacin-hydrochloride.html  © 2020 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.Vascular endothelial growth factor (VEGF) plays a critical role in ovarian folliculogenesis and normal reproductive function. So far, several studies focusing on association between VEGF gene polymorphisms and polycystic ovary syndrome (PCOS). However, above association between the VEGF gene polymorphisms and PCOS susceptibility is uncertain. Hence, we performed a timely meta-analysis containing all current publications to make clear this relationship. We searched articles from the PubMed, Embase and Chinese language (WanFang and CNKI) databases that were published up until May 10, 2019. Finally, we obtained 9 studies, containing 29 case-control studies and 11 different polymorphisms. The odds ratios (OR) and 95% confidence intervals (CI) were revealed association strengths. There were significantly decreased associations between rs2010963 (-634), +9812, +405 polymorphisms and PCOS risk. Nevertheless, there existed increased associations between rs699947 (-2578), rs833061, rs1570360 (-1154), rs3025020, rs3025039 polymorphisms and PCOS susceptibility.