Home-based exercise is associated with improved cardiac functional performance in patients after acute myocardial infarction

ObjectiveTo evaluate the effects of home-based exercise and physical activity on cardiac functional performance in patients after acute myocardial infarction (MI) during the coronavirus disease 2019 (COVID-19) pandemic.MethodsThis retrospective study enrolled patients that received treatment of acute ST-segment elevation MI between and were followed-up 6 months later. The patients were divided into physically active and inactive groups based on their levels of home exercise after hospital discharge.ResultsA total of 78 patients were enrolled in the study: 32 were physically active and 46 were physically inactive. The baseline characteristics were comparable between the two groups. At the 6-month visit, left ventricular ejection fraction and six-minute walking test (6MWT) were significantly improved while the proportion of patients with a New York Heart Association (NYHA) functional III classification was decreased in the active patients, whereas these parameters were not significantly changed in the inactive patients. In addition, the 6MWT was greater while the proportion of patients with an NYHA III classification was lower in the active group than the inactive group at the 6-month visit.ConclusionMaintaining physical activity at home was associated with improved cardiac functional performance in patients after acute MI during the COVID-19 pandemic.     

Melatonin alleviates brain injury in mice subjected to cecal ligation and puncture via attenuating inflammation,apoptosis, and oxidative stress: the role of SIRT1 signaling

Sepsis is a systemic inflammatory response to infection that causes severe neurological complications. Previous studies have suggested that melatonin is protective during sepsis. Additionally, silent information regulator 1 (SIRT1) was reported to be beneficial in sepsis. However, the role of SIRT1 signaling in the protective effect of melatonin against septic encephalopathy remains unclear. This study aimed to investigate the role of SIRT1 in the protective effect of melatonin. EX527, a SIRT1 inhibitor, was used to reveal the role of SIRT1 in melatonin's action. Cecal ligation and puncture or sham operation was performed in male C57BL/6J mice. Melatonin was administrated intraperitoneally (30 mg/kg). The survival rate of mice was recorded for the 7‐day period following the sham or CLP operation. The blood–brain barrier (BBB) integrity, brain water content, levels of inflammatory cytokines (TNF‐α, IL‐1β, and HMGB1), and the level of oxidative stress (superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA)) and apoptosis were assessed. The expression of SIRT1, Ac‐FoxO1, Ac‐p53, Ac‐NF‐κB, Bcl‐2, and Bax was detected by Western blot. The results suggested that melatonin improved survival rate, attenuated brain edema and neuronal apoptosis, and preserved BBB integrity. Melatonin decreased the production of TNF‐α, IL‐1β, and HMGB1. Melatonin increased the activity of SOD and CAT and decreased the MDA production. Additionally, melatonin upregulated the expression of SIRT1 and Bcl‐2 and downregulated the expression of Ac‐FoxO1, Ac‐p53, Ac‐NF‐κB, and Bax. However, the protective effects of melatonin were abolished by EX527. In conclusion, our results demonstrate that melatonin attenuates sepsis‐induced brain injury via SIRT1 signaling activation.     

β-arrestin1 over-expression is associated with an unfavorable prognosis in lung adenocarcinomas and correlated with vascular endothelial growth factor

The aim of this study was to examine β-arrestin1 expression in patients with lung adenocarcinoma (ADC) and explore the relationship of β-arrestin1 protein with clinicopathologic factors, vascular endothelial growth factor (VEGF) and prognosis. A total of 105 surgically resected lung adenocarcinoma patients were recruited for the study. The expression of β-arrestin1 and VEGF were determined by immunohistochemistry (IHC). The score measuring the β-arrestin1 and VEGF were calculated by combining the percentage of positive cells and the intensity of staining. Kaplan-Meier method and multivariable Cox proportional hazards regression analyses were used to examine the relationship between β-arrestin1 and survival. The results demonstrated that a notably higher level of β-arrestin1 expression was found in lung ADC tissues. We also found that an elevated nuclear Β-arrestin1 correlates with higher intratumoral VEGF (P = 0.007). β-arrestin 1 over-expression indicated a poor 5-year overall survival (P = 0.016), and the Cox regression model confirmed that β-arrestin1 over-expression were independent prognostic factor for tumor progression (P = 0.027) and unfavorable overall survival (P = 0.015). We conclude that β-arrestin1 had a high expression in ADC and β-arrestin1 may be a promising biomarker to identify individuals with poor prognosis for patients with ADC.     

Melatonin prevents cell death and mitochondrial dysfunction via a SIRT1‐dependent mechanism during ischemic‐stroke in mice

Silent information regulator 1 (SIRT1), a type of histone deacetylase, is a highly effective therapeutic target for protection against ischemia reperfusion (IR) injury (IRI). Previous studies showed that melatonin preserves SIRT1 expression in neuronal cells of newborn rats after hypoxia–ischemia. However, the definite role of SIRT1 in the protective effect of melatonin against cerebral IRI in adult has not been explored. In this study, the brain of adult mice was subjected to IRI. Prior to this procedure, the mice were given intraperitoneal with or without the SIRT1 inhibitor, EX527. Melatonin conferred a cerebral‐protective effect, as shown by reduced infarct volume, lowered brain edema, and increased neurological scores. The melatonin‐induced upregulation of SIRT1 was also associated with an increase in the anti‐apoptotic factor, Bcl2, and a reduction in the pro‐apoptotic factor Bax. Moreover, melatonin resulted in a well‐preserved mitochondrial membrane potential, mitochondrial Complex I activity, and mitochondrial cytochrome c level while it reduced cytosolic cytochrome c level. However, the melatonin‐elevated mitochondrial function was reversed by EX527 treatment. In summary, our results demonstrate that melatonin treatment attenuates cerebral IRI by reducing IR‐induced mitochondrial dysfunction through the activation of SIRT1 signaling.     

双反牵引复位结合PFNA治疗股骨粗隆间骨折的初步临床应用

目的探讨双反牵引技术辅助闭合复位PFNA内固定治疗股骨粗隆间骨折的临床效果。 方法选取2015年5月至2017年5月在本院接受治疗的80例股骨粗隆间骨折患者为研究对象，其中失访者10例，根据复位方式的区别，将其分为双反牵引复位组与牵引床复位组。对比两组手术时间、术中出血量等各项指标间的差异。 结果70例患者术后获得随访，随访率87.5%，平均随访14个月。男性31例，女性39例，平均年龄（83.8±0.5）岁。双反牵引组患者手术时间、出血量及术中骨折复位时间、术中透视次数[（76±11）min，（80±90）ml，（12±3）min，（20±2）次]少于牵引床组[（85±13）min，（100±104）ml，（25±3）min，（25±3）次]，差异具有统计学意义（t=1.624，P=0.043；t=-1.773，P=0.037；t=1.362, P=0.041；t=-2.757，P=0.035），双反牵引复位组术后1、3个月患侧髋、膝功能评分明显优于牵引床复位组（P<0.05），术后6、12个月两组髋膝功能评分比较，差异无统计学意义（P>0.05）。 结论双反牵引复位股骨粗隆间骨折操作简便，复位质量高，对周围组织血运保护好、时间短、康复快，近期疗效优。