Reporting quality of randomized controlled trials evaluating non-vitamin K oral anticoagulants in atrial fibrillation: a systematic review.

BACKGROUND: Randomized controlled trials (RCTs) are subject to bias if they lack methodological quality. Furthermore, optimal and transparent reporting of RCT findings aids their critical appraisal and interpretation. This study aimed to comprehensively evaluate the report quality of RCTs of non-vitamin K oral anticoagulants (NOACs) for the treatment of atrial fibrillation (AF) and to analyze the factors influencing the quality. METHODS: By searching PubMed, Embase, Web of Science, and Cochrane Library databases RCTs published from inception to 2022 evaluating the efficacy of NOACs on AF were collected. By using the 2010 Consolidated Standards for Reporting Tests (CONSORT) statement, the overall quality of each report was assessed. RESULTS: Sixty-two RCTs were retrieved in this study. The median of overall quality score in 2010 was 14 (range: 8.5-20). The extent of compliance with the Consolidated Standards of Reporting Trials reporting guideline differed substantially across items: 9 items were reported adequately (more than 90%), and 3 were reported adequately in less than 10% of trials. Multivariate linear regression analysis showed that the higher reporting scores were associated with higher journal impact factor (P = 0.01), international collaboration (P < 0.01), and Sources of trial funding (P = 0.02). CONCLUSIONS: Although a large number of randomized controlled trials of NOACs for the treatment of AF were published after the CONSORT statement in 2010, the overall quality is still not satisfactory, thus weakening their potential utility and may mislead clinical decisions. This survey provides the first hint for researchers conducting trials of NOACs for AF to improve the quality of reports and to actively apply the CONSORT statement.

Protective effects of lavender oil on sepsis-induced acute lung injury via regulation of the NF-κB pathway.

CONTEXT: Lavender oil (Lav) from Lavandula angustifolia L. (Lamiacease) exhibits antioxidative and anti-inflammatory properties against various diseases. OBJECTIVE: The study explores the effect of Lav pre-treatment on sepsis-induced acute lung injury (ALI). MATERIALS AND METHODS: Sprague-Dawley rats were assigned into Sham, caecal ligation and puncture (CLP), CLP + Lav (200, 400, and 800 mg/kg) groups. Lav was administered by gavage, once a day, for 7 days. Histological analysis was performed using haematoxylin and eosin staining. Cytokine and nitrite levels were detected by enzyme-linked immunosorbent assay kits and Griess reagent. Gene and protein expression were tested by quantitative real-time polymerase chain reaction and western blot. RESULTS: The levels of tumour necrosis factor-α (BALF: 64%, serum: 59%), interleukin (IL)-1ß (BALF: 63%, serum: 66%) and IL-6 (BALF: 54%, serum: 59%), and nitrite (40%) and inducible nitric oxide synthase (51%), and the level of myeloperoxidase (66%) and malondialdehyde (59%), and cleaved-caspase 3 (84%) and Bax expression (74%) induced by CLP were decreased when given Lav. Additionally, the level of superoxide dismutase (211%) and glutathione (139%), and the expression of Bcl-2 (980%) induced by CLP were increased when given Lav. The increased p-nuclear factor (NF)-κB/NF-κB (72%) and p-inhibitor of κBα (IκBα)/IκBα (77%) induced by CLP could be reversed by Lav. DISCUSSION AND CONCLUSIONS: Lav pre-treatment might protect rats from sepsis-induced ALI via deactivation of the NF-κB pathway. Our research demonstrated the regulatory mechanisms of Lav in sepsis-induced ALI and can provide a theoretical basis for the use of Lav in the treatment of sepsis-induced ALI.

[Effect of blood activating water relieving method on heart functions and serum levels of NT-proBNP in patients with heart failure with normal ejection fraction].

OBJECTIVE: To study the effect of blood activating water relieving method (BAWRM) on heart functions and serum levels of NT-proBNP in patients with heart failure with normal ejection fraction (HFNEF). METHODS: Sixty-four HFNEF patients were admitted to our hospital during January 2011 to June 2012. They were randomly assigned to the treatment group (32 cases) and the control group (32 cases). Patients in the control group received routine Western medical treatment, while those in the treatment group additionally took Chinese medical recipes for activating blood circulation and relieving water retention. Changes of Chinese medical syndromes, E/E', serum NT-proBNP contents were observed between the two groups. RESULTS: Compared with before treatment, their Chinese medical syndromes and E/E' were significantly improved, and serum NT-proBNP contents decreased in the two groups (P < 0.05). Compared with the control group, Chinese medical syndromes, E/E', serum NT-proBNP contents obviously decreased in the treatment group, showing statistical difference (P < 0.05). CONCLUSION: BAWRM was an effective way to improve the diastolic function of HFNEF patients and lower the serum level of NT-proBNP with confirmative efficacy.

Quality reporting of randomized controlled trials on SGLT2 inhibitors for heart failure: a comprehensive assessment.

Randomised controlled trials (RCTs) provide clinicians with the best evidence of the effectiveness of an intervention, and complete and transparent trial reports help to critically assess and use trial results. The objective of our study was to assess the quality of reporting in RCTs of sodium-glucose co-transporter protein 2 (SGLT2) inhibitors for heart failure (HF) and identify factors associated with improved reporting quality. Two researchers conducted a comprehensive search in four databases (PubMed, Web of Science, EMBASE, and Cochrane). The quality of each report was assessed using a 25-point Overall Quality Score (OQS) based on the guidelines provided in the 2010 Consolidated Standards for Reporting of Trials (CONSORT) statement. We included a total of 58 relevant RCTs. The median OQS in the 2010 CONSORT statement was 15 (range 7.5-24). The missing items were primarily found in the 'Methods' and 'Results' sections of the 2010 CONSORT statement. Multivariate regression modeling revealed that a more recent publication year, high impact factor, and large sample size were significant predictors of OQS improvement. The findings suggest that the overall quality of reported RCTs of SGLT2 inhibitors in HF is unsatisfactory, which reduces their potential usefulness.

Deep Multiview Clustering by Pseudo-Label Guided Contrastive Learning and Dual Correlation Learning.

Deep multiview clustering (MVC) is to learn and utilize the rich relations across different views to enhance the clustering performance under a human-designed deep network. However, most existing deep MVCs meet two challenges. First, most current deep contrastive MVCs usually select the same instance across views as positive pairs and the remaining instances as negative pairs, which always leads to inaccurate contrastive learning (CL). Second, most deep MVCs only consider learning feature or cluster correlations across views, failing to explore the dual correlations. To tackle the above challenges, in this article, we propose a novel deep MVC framework by pseudo-label guided CL and dual correlation learning. Specifically, a novel pseudo-label guided CL mechanism is designed by using the pseudo-labels in each iteration to help removing false negative sample pairs, so that the CL for the feature distribution alignment can be more accurate, thus benefiting the discriminative feature learning. Different from most deep MVCs learning only one kind of correlation, we investigate both the feature and cluster correlations among views to discover the rich and comprehensive relations. Experiments on various datasets demonstrate the superiority of our method over many state-of-the-art compared deep MVCs. The source implementation code will be provided at https://github.com/ShizheHu/Deep-MVC-PGCL-DCL.

Mets-IR as a predictor of cardiovascular events in the middle-aged and elderly population and mediator role of blood lipids.

Background: Cardiovascular disease (CVD) is a global health concern, with a significant impact on morbidity and mortality rates. Using fasting glucose, fasting triglycerides, body mass index (BMI), and high-density lipoprotein cholesterol (HDL-C), the metabolic score of insulin resistance (Mets-IR), a novel index created by Mexican researchers to assess insulin sensitivity, is a more precise way to measure insulin sensitivity. This study aimes to explore the association between Mets-IR and CVD, as well as investigate the potential mediating role of of low-density lipoprotein cholesterol (LDL-C). Methods: The study's data came from the 2011 and 2018 China Health and Retirement Longitudinal Studies (CHARLS). We used three logistic regression models to account for the potential effects of ten factors on cardiovascular disease/stroke/heart disease. Moreover, We performed mediation analyses to evaluate the role of LDL-C in the association between Mets-IR and incident CVD. Results: This study comprised 4,540 participants, of whom 494 (10.88%) were found to develop disease (CVD). Each interquartile range (IQR) increased in Mets-IR raised the risk of developing CVD by 38% (OR=1.38; 95% CI, 1.21-1.56) and there was a linear dose-response relationship between Mets-IR and the risk of new-onset cardiovascular disease, stroke, and heart disease (P overall<0.05, P non-linear>0.05). Approximately 5% (indirect effect/total effect) of the significant association of Mets-IR with stroke was mediated by LDL-C, respectively. With the addition of Mets-IR to the base model, the continuous net reclassification improvement and integrated discrimination improvement for predicting cardiovascular disease increased by 0.175 (P <0.001) and 0.006 (P <0.001), respectively. Conclusion: ets-IR is associated with an increased risk of cardiovascular disease/stroke/cardiac issues, with LDL-C mediating these relationships. Improving insulin sensitivity and lipid regulation may be essential and effective preventive measures for cardiovascular events.

Hesperidin prevents hyperglycemia in diabetic rats by activating the insulin receptor pathway.

Diabetes, a disease with high prevalence in China, is a major risk factor of cardiovascular disease. Hesperidin is a flavanone glycoside with anti-hyperglycemic and anti-hyperlipidemic activities. Therefore, the present study aimed to investigate the potential preventive effect of hesperidin against type 2 diabetes mellitus (T2DM) using a rat model of alloxan and high fat diet (HFD)-induced insulin resistance. Male Sprague Dawley rats were orally administered with 100 mg/kg hesperidin or vehicle (sodium carboxy methyl cellulose) for 35 days. Insulin resistance was induced by feeding animals a HFD for 3 weeks (from day 7) and then with an alloxan injection on day 28. Results from the in vivo study demonstrated that hesperidin improved fasting serum glucose (from 19.8 to 10.6 mmol/l) without changing the fasting insulin level, suggesting that hesperidin prevented the development of insulin resistance and diabetes by improving insulin sensitivity. In the oral glucose tolerance test, the development of impaired glucose tolerance was also prevented by hesperidin treatment. Hesperidin was found to regulate glycolysis and gluconeogenesis by enhancing the activity of glucokinase, inducing the phosphorylation of insulin receptor (IR) and phosphoinositide-dependent kinase 1 (PDK1), while decreasing the activity of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase in the liver. In a cell-based assay, hesperidin increased glucose uptake in primary rat adipocytes. Collectively, the present study identified the potent preventive effect of hesperidin against HFD-induced insulin resistance by activating the IR/PDK1 pathway. The current results may provide a potential strategy lacking sides effects to improve metabolic health and reduce risks.

The influence of dehydroepiandrosterone (DHEA) on fasting plasma glucose, insulin levels and insulin resistance (HOMA-IR) index: A systematic review and dose response meta-analysis of randomized controlled trials.

AIMS: The effect of DHEA supplementation on fasting plasma glucose (FPG), insulin levels (IN) and the homeostasis model assessment-estimated insulin resistance (HOMA-IR) index in humans has not been assessed so far. Thus, we aimed to conduct a systematic review and meta-analysis of the randomized controlled trials (RCT) which assessed the effects of DHEA supplementation on FPG, IN and the HOMA-IR index in humans. METHODS: An extensive search was performed in Scopus, PubMed/MEDLINE, and Web of Science from inception to June 2020. Data was combined using the random effects model. RESULTS: 14 publications were included in this study. Overall results demonstrated that FPG was significantly altered after DHEA consumption (WMD: -2.185 mg/dl, P = 0.029). DHEA administration did not result in any significant changes in IN (WMD: 0.057 µU/mL, P = 0.067), and the HOMA - IR index (WMD: 0.174, P = 0.060). In the subgroup analyses, FPG significantly decreased in the subgroup who received DHEA supplementation in dosages of ≤50 mg/day (WMD: -2.29 mg/dl), when the treatment duration was <12 weeks (WMD: -5.25 mg/dl), and in subjects aged ≥60 years (WMD: -2.94 mg/dl). CONCLUSION: This systematic review evaluated the association between FPG and DHEA, revealing that the administration of DHEA reduces FPG levels. However, we found no association between DHEA administration and IN levels or insulin resistance.

Inhibition of lncRNA Neat1 by catalpol via suppressing transcriptional activity of NF-κB attenuates cardiomyocyte apoptosis.

Oxidative stress is considered as a major pathogenesis in myocardial damage; however, effective therapies are limited so far. The present study aimed to investigate the in vitro antioxidative mechanism of Catalpol in cardiomyocytes. The results indicated that Catalpol attenuated high glucose (HG)-induced apoptosis in mouse cardiomyocytes via significantly downregulating long noncoding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (Neat1) expression. Furthermore, Catalpol downregulated Neat1 expression and attenuated apoptosis by inhibiting production of intracellular reactive oxygen species (ROS) in HG-treated cardiomyocytes. Moreover, Catalpol also suppressed HG-induced degradation of IκBα and the nuclear localization of nulear factor-κB (NF-κB) by decreasing the intracellular ROS levels. Additionally, chromatin immunoprecipitation (ChIP) and dual-luciferase activity assays validated that NF-κB bound to Neat1 promoter to activate Neat1 expression. In summary, these results implied that Catalpol protected mouse cardiomyocytes against oxidative injury at least partly through ROS-NF-κB-Neat1 axis.

Catalpol attenuates cardiomyocyte apoptosis in diabetic cardiomyopathy via Neat1/miR-140-5p/HDAC4 axis.

The cardioprotection of catalpol and its mechanism in diabetic cardiomyopathy (DCM) remains unclear. Here, mouse cardiomyocytes were treated with high glucose (HG) to establish a model of cellular injury induced by HG. In vitro experiments were carried out and confirmed that Catalpol attenuated HG-induced long noncoding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (Neat1) expression in mouse cardiomyocytes. Mechanistically, luciferase reporter analysis indicated that Neat1 could decrease the transcription of miR-140-5p to positively regulate histone deacetylase 4 (HDAC4) expression. Notably, overexpression of miR-140-5p or silencing of HDAC4 rescued Neat1-induced cardiomyocyte apoptosis. DCM was induced in male C57BL/6 mice by intraperitoneal injection with streptozotocin (STZ) combined with a high-fat/high-sugar diet. Further in vivo experiments identified that Catalpol alleviated myocardial damage by regulating Neat1/miR-140-5p/HDAC4 axis in DCM mice. Thus, our results demonstrated that Catalpol could exert cardioprotective effect against DCM via Neat1/miR-140-5p/HDAC4 pathway.

L-arginine attenuates high glucose-accelerated senescence in human umbilical vein endothelial cells.

OBJECTIVE: Endothelial dysfunction is a key event in the onset and progression of atherosclerosis associated with diabetes. Increasing cell senescence may lead to endothelial dysfunction and contribute to vascular complications. Therefore, we aimed to elucidate the possible role and mechanism of L-arginine in preventing cell senescence induced by high glucose. METHODS: HUVECs were respectively cultured under normal control glucose (5.5mM), high glucose (33mM), co-incubation with L-arginine (800microM)and high glucose, and senescence was identified by beta-galactosidase staining, change of cell cycle and telomerase activity. Akt and eNOS activity was analyzed by western blot. RESULTS: High glucose significantly increased number of beta-galactosidase-positive stained cells, inhibited telomerase activity, increased proportion of cells in the G(0)/G(1) phase and reduced proportion in the S phase, and decreased NO synthesis. L-arginine significantly attenuated these senescent alterations. Furthermore, high glucose induced a decrease in Akt and eNOS activity, and L-arginine prevented the decrease in activity. The PI3K inhibitor LY294002 or eNOS inhibitor L-NAME attenuated anti-senescence effect of L-arginine. CONCLUSION: L-arginine may have an anti-senescence effect via the PI3K/Akt pathway in HUVECs exposed to high glucose and it might be a therapeutic agent for diabetic vascular complications.