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BackgroundExisting studies investigating the impact of serum calcium (Ca), phosphate (P), 25 hydroxyvitamin D (25[OH]D), and parathyroid hormone (PTH) levels on kidney function have produced inconsistent results. Further research is needed to establish the direct causal relationship between these factors and kidney function.MethodsThe study used genome-wide association study datasets for exposure and outcome, mainly derived from the UK Biobank and CKDGen Consortium, with sample sizes ranging from 3,310 to 480,699 individuals of European ancestry. Heritability and genetic correlations among these phenotypes were assessed using linkage disequilibrium score regression (LDSC) and phenotypes with a heritability z-score

Abstract Background Muscle dysfunction is prevalent in dialysis patients. Gait speed and handgrip strength are simple and reliable methods of assessing muscle function. Numerous observational studies have linked 25-hydroxy vitamin D[25(OH)D] status with gait speed and handgrip strength in populations without kidney diseases. This study aimed to evaluate the potential associations of 25(OH)D status with gait speed and handgrip strength in patients on hemodialysis. Methods In this observational cross-sectional study, demographic data, biological data, and dialysis parameters were collected. Gait speed and handgrip strength were measured. Multiple linear regression and logistic regression analysis were used to investigate the relationship of 25(OH)D status with gait speed and handgrip strength after adjusting for potential confounders. Results Overall, a total of 118 participants undergoing hemodialysis were included. Seventy-one (60.2%) participants were male. The median 25(OH)D status in participants was 11.58 (interquartile range: 8.51 to 15.41) ng/ml. When controlling for age, gender, dialysis vintage, and other confounders with a p-value

Introduction Primary membranous nephropathy (PMN) is a major cause of nephrotic syndrome in adults. Rituximab has been recommended in the treatment of PMN by the updated Kidney Disease Improved Outcome guideline. However, the optimal dosing regimen of rituximab for the initial treatment of patients with PMN is unclear.Methods and analysis A comprehensive screening will be performed by searching PubMed, Embase and the CENTRAL (Cochrane Central Register of Controlled Trials) without language restriction. Studies evaluating the efficacy of rituximab monotherapy using the following types of dosing regimens will be included: high-dose regimen; standard regimen and low-dose regimen. Studies with less than 10 participants will be excluded. The primary outcome is the remission rate at 12 months. The secondary outcomes are remission rate at 6 and 24 months, complete remission rate at 6, 12 and 24 months, relapse at 6, 12 and 24 months, and side effects. Risk of Bias In Non-randomised Studies of Interventions tool will be used to assess the risk of bias for non-randomised studies and the Cochrane risk of bias assessment tool will be used for randomised controlled trials. The pooled remission rate, complete remission rate, relapse rate and side effects will be estimated using the metaprop command. All analyses will be calculated using Stata software (V.15.0; StataCorp).Ethics and dissemination Ethics approval is not required. The results of our study will be submitted to a peer-review journal.PROSPERO registration number CRD42022319401

Introduction During the COVID-19 pandemic, approximately 10%–35% of COVID-19 infected patients experience post-COVID sequela. Among these sequelae, pain symptoms should not be neglected. In addition, the sequelae of COVID-19 also decrease the quality of life of these populations. However, meta-analyses that systematically evaluated post-COVID pain are sparse.Methods and analysis A comprehensive screening will be performed by searching MEDLINE and Embase without language restriction from inception to August 2021. Cohort studies, case–control studies, cross-sectional studies and case series will be included. Case report and interventional studies will be excluded. Studies with less than 20 participants will be also excluded. We aim to investigate the prevalence of pain-related symptoms in patients after the acute phase of COVID-19. The impact of COVID-19 on the quality of life and pain symptoms among these populations in the post-acute phase will also be evaluated. ROBINS-I tool will be used to assess the risk of bias of cohort studies. The risk of bias tool developed by Hoy et al will be used to assess the risk of bias of prevalence studies. Metaprop command in Stata will be used to estimate the pooled prevalence of pain symptoms. DerSimonian and Laird random-effects models will be used to calculate the pooled relative risks. All analyses will be calculated using Stata software (V.15.0; StataCorp)Ethics and dissemination Ethics approval is not required. Results of our study will be submitted to a peer-review journal.PROSPERO registration number CRD42021272800.

Isoflurane, a widely used volatile anesthetic, induces neuronal apoptosis and memory impairments in various animal models. However, the potential mechanisms and effective pharmacologic agents are still not fully understood. The p38MAPK/ATF-2 pathway has been proved to regulate neuronal cell survival and inflammation. Besides, atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, exerts neuroprotective effects. Thus, this study aimed to explore the influence of atorvastatin on isoflurane-induced neurodegeneration and underlying mechanisms. Aged C57BL/6 mice (20 months old) were exposed to isoflurane (1.5%) anesthesia for 6 h. Atorvastatin (5, 10, or 20 mg/kg body weight) was administered to the mice for 7 days. Atorvastatin attenuated the isoflurane-induced generation of ROS and apoptosis. Western blotting revealed a decrease in cleaved caspase-9 and caspase-3 expression in line with ROS levels. Furthermore, atorvastatin ameliorated the isoflurane-induced activation of p38MAPK/ATF-2 signaling. In a cellular study, we proved that isoflurane could induce oxidative stress and inflammation by activating the p38MAPK/ATF-2 pathway in BV-2 microglia cells. In addition, SB203580, a selected p38MAPK inhibitor, inhibited the isoflurane-induced inflammation, oxidative stress, and apoptosis. The results implied that p38MAPK/ATF-2 was a potential target for the treatment of postoperative cognitive dysfunction.

Introduction Endothelial and cardiac dysfunction are highly prevalent and are associated with cardiovascular morbidity and mortality among patients undergoing dialysis. For patients undergoing dialysis, no study has explored the effect of supplementation of coenzyme Q10 (CoQ10) on endothelial function. To our best of knowledge, only two small sample studies focused on the efficacy of supplementation of CoQ10 on cardiac function. However, the effect of CoQ10 supplementation on cardiac function remains uncertain in patients who undergo haemodialysis. The aim of this study is to explore whether CoQ10 supplementation can improve endothelial and cardiac function in patients undergoing haemodialysis.Methods and analysis This is a pilot randomised controlled study. Eligible patients undergoing haemodialysis in our haemodialysis centre will be randomly allocated to the CoQ10 and control groups. The follow-up time is 12 months. The primary outcome is to assess the change of brachial artery endothelial-dependent flow-mediated dilation, left ventricular systolic function, diastolic function and Myocardial Performance Index at 12 months from baseline. Secondary outcomes are death or hospitalisation due to cardiovascular events, all-cause mortality, change of CoQ10 concentration, the ratio of ubiquinol to ubiquinone, the change of oxidative stress markers (including malondialdehyde and 8-hydroxy-deoxyguanosine) and Left Ventricular Mass Index.Ethics and dissemination Risks associated with CoQ10 are minor, even at doses as high as 1800 mg according to previous studies. The trial has received ethics approval from the Medical Ethics Committee for Clinical Trials of Drugs, the 306th Hospital of Chinese PLA. The results of the study are expected to be published in a peer-reviewed journal and presented at academic conferences.Trial registration number ChiCTR1900022258.

Introduction COVID-19 has spread rapidly in China and around the world. Published studies have revealed that some patients with COVID-19 had abnormal liver function in laboratory tests. However, the results were inconsistent and the analysis of epidemiological data stratified by the severity of COVID-19 was not available in previous meta-analyses. Furthermore, these meta-analyses were suspected of overestimating the incidence of liver injury in patients with COVID-19 because some studies considered transaminase elevation as liver injury, which might partially result from cardiac and muscle injury. This systematic review aims to enrol published literatures related to COVID-19 without language restriction, analyse the data based on the severity of the COVID-19 and explore the impact of varied definitions of liver injury on the incidence of liver injury.Methods and analysis We have conducted a preliminary search on PubMed and Excerpta Medica Database on 13 April 2020, for the studies published after December 2019 on the prevalence of acute liver injury and hypertransaminemia in patients with COVID-19. Two reviewers will independently screen studies, extract data and assess the risk of bias. We will estimate the pooled incidence of hypertransaminemia and acute liver injury in patients with COVID-19 by using the random-effects model. The I² test will be used to identify the extent of heterogeneity. Publication bias will be assessed by funnel plot and performing the Begg’s and Egger’s test if adequate studies are available. We will perform a risk of bias assessment using the Joanna Briggs Institute’s critical appraisal checklist.Ethics and dissemination Since this study will be based on the published data, it does not require ethical approval. The final results of this study will be published in a peer-reviewed journal.PROSPERO registration number CRD42020179462.

This paper uses unique data on the shareholdings of both institutional and individual investors to directly investigate whether institutional investors have better stock selection ability than individual investors in China. Controlling for other factors, we find that institutional investors increase (decrease) their shareholdings in stocks that subsequently exhibit positive (negative) short- and long-term cumulative abnormal returns. In contrast, individual investors decrease (increase) their shareholdings in stocks that subsequently exhibit positive (negative) short- and long-term cumulative abnormal returns. These findings indicate that institutional investors have superior stock selection ability in China.

Introduction COVID-19 has spread rapidly in China and around the world. Published studies have revealed that some patients with COVID-19 had abnormal liver function in laboratory tests. However, the results were inconsistent and the analysis of epidemiological data stratified by the severity of COVID-19 was not available in previous meta-analyses. Furthermore, these meta-analyses were suspected of overestimating the incidence of liver injury in patients with COVID-19 because some studies considered transaminase elevation as liver injury, which might partially result from cardiac and muscle injury. This systematic review aims to enrol published literatures related to COVID-19 without language restriction, analyse the data based on the severity of the COVID-19 and explore the impact of varied definitions of liver injury on the incidence of liver injury. Methods and analysis We have conducted a preliminary search on PubMed and Excerpta Medica Database on 13 April 2020, for the studies published after December 2019 on the prevalence of acute liver injury and hypertransaminemia in patients with COVID-19. Two reviewers will independently screen studies, extract data and assess the risk of bias. We will estimate the pooled incidence of hypertransaminemia and acute liver injury in patients with COVID-19 by using the random-effects model. The I² test will be used to identify the extent of heterogeneity. Publication bias will be assessed by funnel plot and performing the Begg’s and Egger’s test if adequate studies are available. We will perform a risk of bias assessment using the Joanna Briggs Institute’s critical appraisal checklist. Ethics and dissemination Since this study will be based on the published data, it does not require ethical approval. The final results of this study will be published in a peer-reviewed journal. [ABSTRACT FROM AUTHOR]

Introduction Coenzyme Q10 (CoQ10) is a fat-soluble vitamin-like quinone that exerts antioxidative functions and is also an important factor in mitochondrial metabolism. Plasma concentrations of CoQ10 are depressed in patients with chronic kidney disease (CKD). CoQ10 supplement can reduce adverse cardiovascular events, improve mitochondrial function and decrease oxidative stress in patients with non-dialysis CKD and dialysis CKD. We performed this study as a systematic review to comprehensively assess the effect of CoQ10 supplement on patients with CKD. Methods and analysis The present systematic review protocol is reported in accordance with the Preferred Reporting Items for Systematic Reviews and Metaanalysis Protocols guidelines. The MEDLINE, EMBASE and Cochrane library databases will be searched without language restrictions in December 2018. Two reviewers will independently screen the references in two stages: screening of the title/abstract and then of the full-text, to identify references meeting the inclusion criteria. A descriptive overview and tabular and/or graphical summaries will be generated, and directed content analysis will be carried out on the extracted data. Ethics and dissemination This systematic review will evaluate the efficacy and safety of CoQ10 in patients with CKD. Ethical approval is not required for this study. The results of this systematic review will be presented in relevant conferences and published in a peer-review journal. [ABSTRACT FROM AUTHOR]