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Background Emerging evidence implicates excess weight as a potential risk factor for hearing loss. However, this association remained inconclusive. Therefore, we aimed to systematically and quantitatively review the published observational study on the association between body mass index (BMI) or waist circumference (WC) and hearing loss. Methods The odds ratios (ORs) or relative risks (RRs) with their 95% confidence intervals (CIs) were pooled under a random-effects model. Fourteen observational studies were eligible for the inclusion in the final analysis. Results In the meta-analysis of cross-sectional studies, the ORs for prevalent hearing loss were 1.10 (95% CI 0.88, 1.38) underweight, 1.14 (95% CI 0.99, 1.32) for overweight, OR 1.40 (95% CI 1.14, 1.72) for obesity, 1.14 (95% CI 1.04, 1.24) for each 5 kg/m 2 increase in BMI, and 1.22 (95% CO 0.88. 1.68) for higher WC. In the meta-analysis of longitudinal studies, the RRs were 0.96 (95% CI 0.52, 1.79) for underweight, 1.15 (95% CI 1.04, 1.27) for overweight, 1.38 (95% CI 1.07, 1.79) for obesity, 1.15 (95% CI 1.01, 1.30) for each 5 kg/m 2 increase in BMI, and 1.11 (95% CI 1.01, 1.22) for higher WC. Conclusions In summary, our findings add weight to the evidence that elevated BMI and higher WC may be positively associated with the risk of hearing loss.

Background Physical activity, grip strength, sedentary behaviors, and sleep duration were found to be associated with risk of developing stroke and dementia. However, the combined influence of these factors on stroke and dementia remains unclear. Objective To investigate the combined influence of these multiple lifestyle and functional factors on risk of stroke and dementia and their subtypes and to investigate the potential interaction between combined factors and the apolipoprotein E gene ε4 allele ( APOE ε4). Methods Data were obtained from the UK Biobank, including 474,983 participants. A score ranging from 0 to 4 was assigned based on adherence to healthy factors: meeting physical activity recommendations, grip strength above the sex-specific median, sleep duration of 7–8 h/day, and sedentary time < 6 h/day. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for incident stroke and dementia, adjusting for potential confounders. Results Over a median follow-up of 10.1 years, 4,992 incident strokes and 2,120 dementias were recorded. Compared with participants with 0–1 healthy factor, adjusted HRs (95% CIs) for total stroke were 0.85 (0.79–0.92), 0.71 (0.66–0.77), and 0.65 (0.59–0.72) for those with 2, 3, and 4 healthy factors, respectively (P-trend < 0.001). Similar inverse associations were observed for ischemic stroke and intracerebral hemorrhage but not subarachnoid hemorrhage. For dementia, HRs (95% CIs) were 0.74 (0.66–0.83), 0.64 (0.56–0.71), and 0.43 (0.39–0.51) across increasing numbers of healthy factors ( P -trend < 0.001), with consistent results for Alzheimer’s disease and vascular dementia. All four factors independently predicted lower risk of all-cause stroke and all-cause dementia. For stroke subtypes, associations varied by factor. Regular physical activity and higher grip strength were both associated with lower risk of intracerebral hemorrhage, while none of the healthy factors had associations with subarachnoid hemorrhage. For dementia subtypes, all healthy factors, except for physical activity, were associated with a lower risk of both Alzheimer’s disease and vascular dementia. In addition, the association between combined healthy factors and total stroke or all-cause dementia was independent of APOE ε 4 carrying status. Conclusions The cumulative association of multiple healthy factors with reduced risk of stroke and dementia highlights the importance of adopting a lifestyle with more elements of healthy factors for the prevention of these neurological diseases.

Background and objectives Epidemiological trends indicate a concerning rise in early-onset cases of myocardial infarction (MI). We aimed to assess and compare the ability of plasma proteomics, conventional risk factors, and polygenic risk score (PRS) for the risk prediction of early-onset myocardial infarction (EOMI). Methods Included were 13,097 participants aged 50 or younger, without prevalent cardiovascular diseases. The participants were randomly divided into training and validation sets. EOMI was defined as MI diagnosed before age 55. In the training set, 2,093 plasma proteins were assessed for the associations with incident EOMI using Cox proportional hazards regression models. Important proteins were selected by the least absolute shrinkage and selection operator (LASSO) regression to develop protein-based models. The predictive performance of protein-based models, conventional risk factors, and PRS, either alone or as combinations, was assessed in the validation set. Results Two protein-based models were constructed using 22 key proteins selected by LASSO. Each standard-deviation increment of a weighted protein score was associated with a 2.57-fold higher risk of EOMI. Incorporating this protein score (ΔC-index = 0.125; 95% CI: 0.040, 0.213), a protein panel (ΔC-index = 0.189; 95% CI: 0.065, 0.276), or other conventional risk factors (ΔC-index = 0.158; 95% CI: 0.039, 0.239) each significantly improved the predictive performance over a basic model including age, sex, and race/ethnicity, whereas adding PRS did not. The combination of the protein panel and conventional risk factors demonstrated the best discrimination ability (C-index = 0.875; 95% CI: 0.814, 0.935). Conclusions Plasma proteomics enhanced the risk prediction for EOMI beyond conventional risk factors and PRS. These findings may have implications for risk stratification and personalized prevention which prevent or delay the onset of myocardial infarction among relatively younger population.

【摘要】 背景 通过不同生物标志物估计的肾小球滤过率(eGFRs)是否与死亡率不同相关，或者这种相关性是否因糖尿病状态而不同仍然不清楚，特别是在中国人群中。 方法 本研究纳入了6 995名非糖尿病患者(平均年龄60.4岁)和1 543例糖尿病患者(平均年龄61.8岁)。每项eGFR测量分为正常[≥90 mL/min ‐1 ·(1.73 m 2 ) ‐1 ]、中度下降[ 60~90 mL/min ‐1 ·(1.73 m 2 ) ‐1 ]和慢性肾病(CKD) [ <60 mL/min ‐1 ·(1.73 m 2 ) ‐1 ]组。 Cox 比例风险模型用于估计与每种eGFR相关的全因死亡率的风险比( HR )。 结果 在7年的随访中，非糖尿病患者有677人死亡，糖尿病患者有215人死亡。在非糖尿病的患者中，eGFR轻度下降的所有指标都与死亡率无关，而由eGFRcys和eGFRcr‐cys定义的CKD( HR 分别为1.71和1.55)，而不是由eGFRcr定义的CKD与较高的死亡风险相关。在糖尿病患者中，所有适度下降的eGFR(分别为eGFRcr、eGFRcys和eGFRcr‐cys的 HR 1.53、1.56和2.09)和CKD(分别为eGFRcr、eGFRcys和eGFRcr‐cys的 HR 2.57、2.99和3.92)与较高的死亡风险相关。无论糖尿病状态如何，在传统的危险因素中加入eGFRcys或eGFRcr‐cys，比加入eGFRcr，在预测全因死亡风险方面有更大的改善。 结论 在中国老年人群中，eGFR与死亡风险的关系似乎因其测量方法和糖尿病状况而异，这需要在临床实践中加以考虑。

摘要 【摘要】 背景 通过不同生物标志物估计的肾小球滤过率(eGFRs)是否与死亡率不同相关，或者这种相关性是否因糖尿病状态而不同仍然不清楚，特别是在中国人群中。方法 本研究纳入了6 995名非糖尿病患者(平均年龄60.4岁)和1 543例糖尿病患者(平均年龄61.8岁)。每项eGFR测量分为正常[≥90 mL/min‐1·(1.73 m2)‐1]、中度下降[ 60~90 mL/min‐1·(1.73 m2)‐1]和慢性肾病(CKD) [ <60 mL/min‐1·(1.73 m2)‐1]组。Cox比例风险模型用于估计与每种eGFR相关的全因死亡率的风险比(HR)。结果 在7年的随访中，非糖尿病患者有677人死亡，糖尿病患者有215人死亡。在非糖尿病的患者中，eGFR轻度下降的所有指标都与死亡率无关，而由eGFRcys和eGFRcr‐cys定义的CKD(HR分别为1.71和1.55)，而不是由eGFRcr定义的CKD与较高的死亡风险相关。在糖尿病患者中，所有适度下降的eGFR(分别为eGFRcr、eGFRcys和eGFRcr‐cys的HR 1.53、1.56和2.09)和CKD(分别为eGFRcr、eGFRcys和eGFRcr‐cys的HR 2.57、2.99和3.92)与较高的死亡风险相关。无论糖尿病状态如何，在传统的危险因素中加入eGFRcys或eGFRcr‐cys，比加入eGFRcr，在预测全因死亡风险方面有更大的改善。结论 在中国老年人群中，eGFR与死亡风险的关系似乎因其测量方法和糖尿病状况而异，这需要在临床实践中加以考虑。

Serum biomarkers may play a reliable role in predicting the outcomes of patients with aneurysmal subarachnoid hemorrhage. This study retrospectively analyzed the relationship between serum biomarkers on admission and outcomes in patients with aneurysmal subarachnoid hemorrhage. We recruited 146 patients with aneurysmal subarachnoid hemorrhage who were treated in Renmin Hospital of Wuhan University of China between 1 May 2014 and 30 March 2016. There were 57 males and 89 females included and average age of included patients was 57.03 years old. Serum samples were taken immediately on admission（within 48 hours after initial hemorrhage） and the levels of serum biomarkers were detected. Baseline information, complications, and outcomes at 6 months were recorded. Univariate and multivariate logistic regression analyses were used to explore the relationship between biomarkers and clinical outcomes. Receiver operating characteristic curves were obtained to investigate the possibility of the biomarkers predicting prognosis. Of the 146 patients, 102 patients achieved good outcomes and 44 patients had poor outcomes. Univariate and multivariate analyses showed that high World Federation of Neurosurgical Societies grade, high serum D-dimer levels, and high neurological complications were significantly associated with poor outcomes. Receiver operating characteristic curves verified that D-dimer levels were associated with poor outcomes. D-dimer levels strongly correlated with neurological complications. In conclusion, we suggest that D-dimer levels are a good independent prognostic factor for poor outcomes in patients with aneurysmal subarachnoid hemorrhage.

Background： Current risk stratification of idiopathic dilated cardiomyopathy （IDC） lacks sufficient sensitivity and specificity. The objective of this study was to investigate the predictive role of frontal QRS-T angles in IDC. Methods： A prospective study with 509 IDC patients was performed from February 2008 to December 2013 in the Affiliated Drum Tower Hospital, Nanjing University School of Medicine. Baseline values and changes in QRS-T angles were recorded. Follow-up was conducted every 6 months. Analyses by Cox Proportional Hazards model were performed to evaluate the association between QRS-T angle and outcomes. The primary outcome of interest was all-cause mortality. Results： During a median follow-up of 34 months, 90 of 316 patients with QRS-T angles 〉90° died compared to 31 of 193 patients with QRS-T angles ≤90° （hazard ratio [HR] 2.4, P 〈 0.001）. Cardiac death was more prevalent in patients with a wide QRS-T angle （HR 2.4, P 〈 0.001）, similar to heart failure rehospitalization （HR = 2.5, P 〈 0.001）. After adjustment for potential prognostic factors, the QRS-T angle was independently associated with all-cause mortality （HR - 2.5, P 〈 0.05）, cardiac mortality （HR = 1.9, P 〈 0. 05）, and heart failure rehospitalization （HR = 2.3, P 〈 0.01）. Optimized therapy significantly narrowed the frontal QRS-T angle （100.9 ±53.4° vs. 107.2 ± 54.4°, P 〈 0.001 ）. The frontal QRS-T angle correlated well with established risk factors, such as left ventricular ejection fraction, brain natriuretic peptide, and New York Heart Association functional class. Conclusions; The frontal QRS-T angle is a powerful predictor of all-cause mortality, cardiac mortality, and worsening heart failure in IDC patients, independent of well-established prognostic factors. Optimized therapy significantly narrows the QRS-T angle, which might be an indicator of medication compliance, but this requires further investigation.

Aim： The dried tuber root of Ophiopogonjaponicus has been used in the traditional Chinese medicine for treatment of myocardial ischemia and thrombosis. In this study we investigated the effects of methylophiopogonanone A （MO-A）, a major homoisoflavonoid in Ophiopogonjaponicus, on myocardial ischemia/reperfusion （I/R）injury. Methods： Mice were pretreated with MO-A （10 mg.kg-l.d1, po） for 2 weeks and then subjected to transient occlusion of the left anterior descending coronary artery. Cardiac function was evaluated, and the infarct size and apoptosis index were assessed. The mechanisms underlying the cardio-protection of MO-A were analyzed in H9C2 rat cardiomyocytes subjected to hypoxia/reoxygenation （H/R）. The cell viability and apoptosis were evaluated; apoptotic and relevant signaling proteins were analyzed. NO levels in the culture medium were assessed. Results： In I/R mice, pretreatment with MO-A significantly reduced the infarct size （by 60.7%） and myocardial apoptosis （by 56.8%）, and improved cardiac function. In H9C2 cells subjected to H/R, pretreatment with MO-A （10 pmol/L） significantly decreased apoptosis and cleaved caspase-3 expression, elevated the Bcl-2/Bax ratio and restored NO production. Furthermore, pretreatment with MO-A markedly increased the activation of PI3K/Akt/eNOS pathway in H9C2 cells subjected to H/R, and the protective effects of MO-A were abolished in the presence of the PI3K inhibitor wortmannin （100 nmol/L）. Conclusion： MO-A attenuates I/R-induced myocardial apoptosis in mice via activating the PI3K/Akt/eNOS signaling pathway.

In recent decades, studies on delayed system dynamics have attracted increasing attention and advances have been achieved in stability, nonlinearity, delay identification, delay elimination and application. However, most of the existing work is on the theoretical basis and little is on the experiment. This paper presents our experimental studies on delayed feedback control conducted in recent years with the focus on the discussion of a DSP-based delayed experiment system. Some phenomena in our delay experiments are discussed and a few topics of interest for further research are brought forward.

Background： Myocardial infarction （MI） is a major disease burden. Wild-type p53-induced phosphatase 1 （Wipl） has been studied extensively in the context of cancer and the regulation of different types of stem cells, but the role of Wipl in cardiac adaptation to M I is unknown. We investigated the significance of Wipl in a mouse model of MI. Methods： The study began in June 2014 and was completed in July 2016. We compared Wipl-knockout （Wipl-KO） mice and wild-type （WT） mice to deternline changes in cardiac function and survival in response to MI. The heart weight/body weight （HW/BW） ratio and cardiac function were measured before MI. Mouse MI was established by ligating the left anterior descending （LAD） coronary artery under 1.5% isoflurane anesthesia. After M1, survival of the mice was observed for 4 weeks. Cardiac function was examined by echocardiography. The HW/BW ratio was analyzed, and cardiac hypertrophy was measured by wheat germ agglutinin staining. Hematoxylin and eosin （H＆E） staining was used to determine the infarct size. Gene expression of interleukin-6 （IL-6）, turnor necrosis factor-α （TNF-α）, and interleukin-1β （IL-1β） was assessed by quantitative real-time polymerase chain reaction （qPCR）, and the levels of signal transducers and activators of transcription 3 （stat3） and phosphor-stat3 （p-stat3） were also analyzed by Western blotting. Kaplan-Meier survival analysis, log-rank test, unpaired l-test, and one-way analysis of variance （ANOVA） were used for statistical analyses. Results： Wipl-KO mice had a marginally increased HW/BW ratio and slightly impaired cardiac fiinction before LAD ligation. Alter MI, Wipl-deficient mice exhibited increased mortality （57.14% vs. 29.17%; n = 24 [WT], n - 35 [WipI-KO], P 〈 0.05）, increased cardiac hypertrophy （HW/BW ratio： 7 days： 7.25±0.36 vs. 5.84 ± 0.18, n cross-sectional area： 7 days： 311.80 ± 8.29 vs. 268.90 ± 11.15, n P 〉 0.05）, and reduced cardiac function （ejection fraction： 7 days 10, p〈 0.01, and 4 weeks： 6.05± 0.17 vs. 5.87 ±0.24, n= 10, P〉0.05; P 〈 0.05, and 4 weeks： 308.80 ± 11.26 vs. 317.00 ±13.55, n = 6 29.37± 1.38 vs. 34.72 ± 1.81, P 〈 0.05, and 4 weeks： 19.06 ± 2.07 vs 26.37 ± 2.95, P〈 0.05; fractional shortening： 7 days： 13.72 ± 0.71 vs. 16.50 ± 0.94, P〈 0.05, and 4 weeks： 8.79 ±1.00 vs. 12.48 ±1.48, P 〈 0.05; n = l0 [WT], n = 15 [Wipl-KO]）. H＆E staining revealed a larger infarct size in Wipl-KO mice than in WT mice （34.79% ± 2.44% vs. 19.55% ± 1.48%, n = 6, P 〈 0.01 ）. The expression oflL-6 and p-stat3 was downregulated in Wipl-KO mice （IL-6：1.71 ± 0.27 vs. 4.46 ± 0.79, n = 6, P 〈 0.01 ; and p-stat3/stat3：1.15 ±0.15 vs. 1.97 ± 0.23, n = 6, P 〈 0.05）. Conclusion： The results suggest that Wipl could protect the heart from MI-induced ischemic injury.