Aims Sacubitril-valsartan has been shown to have superior effects over angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in patients with heart failure (HF) and hypertension. The efficacy and safety of sacubitril-valsartan in patients with HF are controversial. We performed a meta-analysis of randomized controlled trials to assess and compare the effect and adverse events of sacubitril-valsartan, valsartan, and enalapril in patients with HF. Methods and results We conducted a systematic search using PubMed, Embase, the Cochrane Library, and ClinicalTrials.gov. Randomized controlled trials involving the use of sacubitril-valsartan in patients with HF were included. We assessed the pooled odds ratio (OR) of all-cause mortality, cardiovascular mortality, and hospitalization for HF in fixed-effects models and the pooled risk ratio (RR) of symptomatic hypotension, worsening renal function, and hyperkalaemia in fixed-effects models. Of the 315 identified records, six studies involving 14 959 patients were eligible for inclusion. Sacubitril-valsartan reduced the endpoints of all-cause mortality and cardiovascular mortality in patients with HF with reduced ejection fraction (HFrEF) in three trials with pooled ORs of 0.83 (P = 0.0006) and 0.78 (P < 0.0001), respectively. Regarding the composite outcome of hospitalization for HF in five trials, the pooled OR was 0.79 (P < 0.00001). Compared with enalapril or valsartan, sacubitril-valsartan was associated with a high risk of symptomatic hypotension (RR 1.47, P < 0.00001), low risk of worsening renal function (RR 0.81, P = 0.005), and low rate of serious hyperkalaemia (≥6.0 mmol/L) (RR 0.76, P = 0.0007) in all six trials. Conclusions Compared with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, sacubitril-valsartan significantly decreased the risk of death from all causes or cardiovascular causes in HFrEF and hospitalization for HF in both patients with HFrEF and HF with preserved ejection fraction. Sacubitril-valsartan reduced the risk of renal dysfunction and serious hyperkalaemia but was associated with more symptomatic hypotension.

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The intensive use of antibiotics as growth-promoting agents in animal production has resulted in the spread of animal antibiotic resistance and possibly human antibiotic resistance. Based on this premise, it is significant to explore an alternative approach to preventing infectious diseases and promoting animal growth and health. Yeast as the main natural growth promoter in livestock nutrition has been extensively studied for decades. Numerous yeasts and yeast-containing products are produced, marketed, and used in animal feed as providers of nutrient sources, probiotics, and nutrients or serve distinct nutritional functions. A large amount of scientific research suggests that yeasts and their derivatives may be good for animal growth performance and health, especially when animals are housed in poor sanitation or are suffering from disease. However, when yeasts are used as a surrogate for livestock antibiotics, the results vary according to several factors, including yeast species, yeast product components, feed ingredients, animal category, type of symptoms, and differences in the rearing environment. In this review, the effects of different yeasts on different animals will be reviewed. The types of widely used yeast products, their functional characteristics, and application effects will be discussed in order to provide a reference for the development and application of yeast feed products.

Myocardial infarction (MI) is believed to be one of the most common cardiovascular diseases, and it is seriously threatening the health of people in the world. The extracellular vesicles (EVs) isolated from mesenchymal stem cells and zinc finger antisense 1 (ZFAS1) have been believed to be involved in the regulation of MI, but the mechanism has not been fully clarified. Left anterior descending artery ligation was used to establish MI animal model, hypoxia treatment was applied to establish MI cell model. CCK8, transwell, and wound healing methods were applied to measure cell proliferation, invasion, and migration. Overexpression of ZFAS1 was established via transfecting pcDNA-ZFAS1. Overexpression of ZFAS1 significantly reversed the influence of EVs on cell migration, invasion, and apoptosis. Similar effect of EVs and ZFAS1 on morphological changes of MI rat heart tissues were also observed. The activation of Akt/Nrf2/HO-1 pathway by EVs was remarkably suppressed by pcDNA-ZFAS1. Inhibitor of Akt/Nrf2/HO-1 pathway remarkably reversed the impact of EVs on the cell viability. EVs might improve MI through inhibiting ZFAS1 and promoting Akt/Nrf2/HO-1 pathway. This study might provide a new thought for the prevention and treatment of MI damage through regulating ZFAS1 or Akt/Nrf2/HO-1 pathway.

To investigate the efficacy and safety of cilostazol for atherosclerosis. PubMed, Embase, and the Cochrane Central Register of Controlled Trials from inception to May 29, 2021, were searched for randomized clinical trials (RCTs). Ten trials with 1577 patients were included. Treatment with cilostazol significantly reduced carotid intima-media thickness [mean difference (MD), 20.12 mm; 95% confidence interval (CI), 20.17 to 20.06].According to the difference in intervening measures, the cilostazol group was superior to the control group in inhibiting the progression of carotid intima-media thickness: cilostazol versus placebo (MD, 20.04 mm; 95% CI, 20.06 to 20.02; P , 0.00001), cilostazol versus no antiplatelet drug (MD, 20.14 mm; 95% CI, 20.26 to 20.03; P = 0.02), cilostazol versus aspirin (MD, 20.17 mm; 95% CI, 20.32 to 20.02; P = 0.02), cilostazol + aspirin versus aspirin (MD, 20.08 mm; 95% CI, 20.14 to 20.02; P = 0.007), cilostazol + aspirin versus clopidogrel + aspirin (MD, 20.07 mm; 95% CI, 20.14 to 20.00; P = 0.04), and cilostazol + clopidogrel + aspirin versus clopidogrel + aspirin (MD, 20.16 mm; 95% CI, 20.30 to 20.02; P = 0.03). Cilostazol treatment considerably decreased triglyceride (MD, 220.18 mg/dL; 95% CI, 239.03 to 21.34) and improved high-density lipoprotein cholesterol (MD, 4.35 mg/dL; 95% CI, 2.61-6.10). Cilostazol therapy significantly increased the risk of adverse events of headache (odds ratio, 12.91; 95% CI 5.33-31.29). Our research has revealed that cilostazol has potent antiatherosclerotic effects and can reverse atherosclerosis progress even in high-risk patients, such as those with type 2 diabetes mellitus, and does not increase the risk of bleeding.