Sex-Specific Association of Blood Pressure Categories With All-Cause Mortality: The Rural Chinese Cohort Study.

INTRODUCTION: The relationship between blood pressure categories and all-cause mortality has not been fully addressed in cohort studies, especially in the general Chinese population. Our study aimed to assess the sex-specific association of systolic blood pressure (SBP), diastolic blood pressure (DBP), and 2017 United States hypertension guidelines with all-cause mortality in China. METHODS: We conducted a prospective study of 13,760 rural Chinese adults aged 18 or older (41.1% men). Mean age overall was 49.4, 51.0 for men, and 48.3 for women. We analyzed the blood pressure-mortality relationship by using restricted cubic splines and Cox proportional-hazards regression analysis, estimating hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: During a mean follow-up of 5.95 years, 710 people died (60.3% men) from any cause. We found a U-shaped SBP-mortality or DBP-mortality relationship for both sexes. Mortality risk was increased for men with SBP 120-139 mm Hg (adjusted HR [aHR], 1.42; 95% CI, 1.10-1.82) or ≥140 mm Hg (aHR, 2.05; 95% CI, 1.54-2.72), and for DBP ≥90 mm Hg (aHR, 1.53; 95% CI, 1.10-2.13) as compared with SBP 100-119 mm Hg or DBP 70-79 mm Hg. Mortality risk also was increased for men with blood pressure status defined according to 2017 US hypertension guidelines as elevated, SBP 120-129 and DBP >80 mm Hg (aHR 1.48; 95% CI,1.11-1.98); stage 1 hypertension, SBP/DBP 130-139/80-89 mm Hg (aHR 1.53; CI, 1.19-1.97); and stage 2 hypertension, SBP/DBP ≥140/90 mm Hg (aHR 1.83; CI, 1.33-2.51). No significant relationship was observed for women. CONCLUSION: Elevated blood pressure and stages 1 and 2 hypertension were positively associated with all-cause mortality for men but not women in rural China.

Chemoprophylaxis, diagnosis, treatments, and discharge management of COVID-19: An evidence-based clinical practice guideline (updated version).

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of a rapidly spreading illness, coronavirus disease 2019 (COVID-19), affecting more than seventeen million people around the world. Diagnosis and treatment guidelines for clinicians caring for patients are needed. In the early stage, we have issued "A rapid advice guideline for the diagnosis and treatment of 2019 novel coronavirus (2019-nCoV) infected pneumonia (standard version)"; now there are many direct evidences emerged and may change some of previous recommendations and it is ripe for develop an evidence-based guideline. We formed a working group of clinical experts and methodologists. The steering group members proposed 29 questions that are relevant to the management of COVID-19 covering the following areas: chemoprophylaxis, diagnosis, treatments, and discharge management. We searched the literature for direct evidence on the management of COVID-19, and assessed its certainty generated recommendations using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) approach. Recommendations were either strong or weak, or in the form of ungraded consensus-based statement. Finally, we issued 34 statements. Among them, 6 were strong recommendations for, 14 were weak recommendations for, 3 were weak recommendations against and 11 were ungraded consensus-based statement. They covered topics of chemoprophylaxis (including agents and Traditional Chinese Medicine (TCM) agents), diagnosis (including clinical manifestations, reverse transcription-polymerase chain reaction (RT-PCR), respiratory tract specimens, IgM and IgG antibody tests, chest computed tomography, chest x-ray, and CT features of asymptomatic infections), treatments (including lopinavir-ritonavir, umifenovir, favipiravir, interferon, remdesivir, combination of antiviral drugs, hydroxychloroquine/chloroquine, interleukin-6 inhibitors, interleukin-1 inhibitors, glucocorticoid, qingfei paidu decoction, lianhua qingwen granules/capsules, convalescent plasma, lung transplantation, invasive or noninvasive ventilation, and extracorporeal membrane oxygenation (ECMO)), and discharge management (including discharge criteria and management plan in patients whose RT-PCR retesting shows SARS-CoV-2 positive after discharge). We also created two figures of these recommendations for the implementation purpose. We hope these recommendations can help support healthcare workers caring for COVID-19 patients.

Clinical Trial Registration and Reporting: Drug Therapy and Prevention of Cardiac-Related Infections.

Objective: Clinical trials are the source of evidence. ClinicalTrials.gov is valuable for analyzing current conditions. Until now, the state of drug interventions for heart infections is unknown. The purpose of this study was to comprehensively assess the characteristics of trials on cardiac-related infections and the status of drug interventions. Methods: The website ClinicalTrials.gov was used to obtain all registered clinical trials on drug interventions for cardiac-related infections as of February 16, 2019. All registration studies were collected, regardless of their recruitment status, research results, and research type. Registration information, results, and weblink-publications of those trials were analyzed. Results: A total of 45 eligible trials were evaluated and 86.7% of them began from or after 2008 while 91.1% of them adopted interventional study design. Of all trials, 35.6% were completed and 15.6% terminated. Besides, 62.2% of interventional clinical trials recruited more than 100 subjects. Meanwhile, 86.7% of the eligible trials included adult subjects only. Of intervention trials, 65.8% were in the third or fourth phase; 78.1% adopted randomized parallel assignment, containing two groups; 53.6% were masking, and 61.0% described treatment. Moreover, 41.5% of the trials were conducted in North America while 29.3% in Europe. Sponsors for 40.0% of the studies were from the industry. Furthermore, 48.9% of the trials mentioned information on monitoring committees, 24.4% have been published online, and 13.3% have uploaded their results. Drugs for treatments mainly contained antibiotics, among which glycopeptides, ß-lactams, and lipopeptides were the most commonly studied ones in experimental group, with the former ones more common. Additionally, 16.2% of the trials evaluated new antimicrobials. Conclusions: Most clinical trials on cardiac-related infections registered at ClinicalTrials.gov were interventional randomized controlled trials (RCTs) for treatment. Most drugs focused in trials were old antibiotics, and few trials reported valid results. It is necessary to strengthen supervision over improvements in results, and to combine antibacterial activity with drug delivery regimens to achieve optimal clinical outcomes.

Valsartan regulates TGF-ß/Smads and TGF-ß/p38 pathways through lncRNA CHRF to improve doxorubicin-induced heart failure.

This study investigated the interaction among valsartan (VAL), TGF-ß pathways, and long non-coding RNA (lncRNA) cardiac hypertrophy-related factor (CHRF) in doxorubicin (DOX)-induced heart failure (HF), and explored their roles in DOX-induced HF progression. HF mice models in vivo were constructed by DOX induction. The expression of CHRF and TGF-ß1 in hearts was detected, along with cardiac function, caspase-3 activity, and cell apoptosis. Primary myocardial cells were pretreated with VAL, followed by DOX induction in vitro for functional studies, including the detection of cell apoptosis with terminal deoxynucleotidyl transferase dUTP nick-end labeling and the expression of proteins associated with TGF-ß1 pathways. HF models were established in vivo and in vitro. Expression of CHRF and TGF-ß1 was up-regulated, and cell apoptosis and caspase-3 activity were increased in the hearts and cells of the HF models. VAL supplementation alleviated the cardiac dysfunction and injury in the HF process. Moreover, overexpressed CHRF up-regulated TGF-ß1, promoted myocardial cell apoptosis, and reversed VAL's cardiac protective effect, while interference of CHRF (si-CHRF) did the opposite. Down-regulation of CHRF reversed the increased expression of TGF-ß1 and the downstream proteins induced by pcDNA-TGF-ß1 in HL-1 cells, while overexpression of CHRF reversed the VAL's cardiac protective effect in vivo. In conclusion, VAL regulates TGF-ß pathways through lncRNA CHRF to improve DOX-induced HF.