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Background: Short or long sleep duration is proposed as a potential risk factor for all-cause mortality in the older people, yet the results of published studies are not often reproducible. Methods: Literature retrieval, study selection and data extraction were completed independently and in duplicate. Only prospective cohort studies were included. Effect-size estimates are expressed as hazard ratio (HR) and 95% confidence interval (CI). Results: Summary data from 28 articles, involving a total of 95,259 older people, were meta-analyzed. Overall analyses revealed a remarkably significant association between long sleep duration and all-cause mortality (adjusted HR = 1.24, 95% CI: 1.16-1.33, P < .001), whereas only marginal significance was observed for short sleep duration (adjusted HR = 1.04; 95% CI: 1.00-1.09; P = .033). Funnel plots suggested no publication bias for short sleep duration (P = .392). The probability of publication bias was high for long sleep duration (P = .020), yet the trim-and-fill method strengthened its significance in predicting all-cause mortality. In subgroup analyses, the association of long sleep duration with all-cause mortality was statistically significant in both women (HR = 1.48; 95% CI: 1.18-1.86; P = .001) and men (HR = 1.31; 95% CI: 1.10-1.58; P = .003). By contrast, with regard to short sleep duration, statistical significance was observed in men (HR = 1.13; 95% CI: 1.04-1.24; P = .007), but not in women (HR = 1.00; 95% CI: 0.85-1.18; P = .999) (Two-sample Z test P = .099). Besides gender, geographic region, sleep survey method, baseline age and follow-up interval were identified as possible causes of between-study heterogeneity in subgroup analyses. Further dose-response regression analyses revealed that trend estimation was more obvious for long sleep duration (regression coefficient: 0.13; P < .001) than for short sleep duration (regression coefficient: 0.02; P = .046). Conclusions: Our findings indicate a significantly increased risk of all-cause mortality associated with long sleep duration, especially in women, as well as with short sleep duration in men only.

Background: This study aimed to diagnose and treat a patient with anti-Ro52-positive antisynthetase syndrome (ASS), investigate the association between anti-Ro52 antibodies and ASS, and determine its clinical significance. The objective of this clinical report is to highlight this unusual syndrome to avoid incorrect diagnosis.Case Description: A middle-aged woman presenting with obvious lung symptoms was admitted to our hospital. A physical examination revealed swollen joints in both hands, mechanic's hands, and normal muscle strength and muscle tone in all 4 extremities. A myositis-specific antibody panel, lung computed tomographic (CT) imaging, electromyography, and muscle biopsy were performed as auxiliary examinations, and appropriate treatment was administered after the confirmed diagnosis. The myositis-specific antibody panel yielded strongly positive results for anti-Jo-1 and anti-Ro52 antibodies, lung CT imaging revealed interstitial lung disease, electromyography revealed myogenic damage, and muscle magnetic resonance imaging revealed multiple inflammatory exudates. A definitive diagnosis of ASS was made, and glucocorticoid and immunosuppressant therapy were administered. After treatment, the patient's symptoms were alleviated, creatine kinase activity was reduced, and signs of disease activity and secondary tumors were not observed on a subsequent follow-up evaluation.Conclusions: Anti-Ro52 antibodies, being myositis-associated antibodies, can lead to an atypical clinical presentation in ASS patients and are potentially associated with a poor prognosis. Therefore, thorough follow-up evaluation is required for such cases.

This study explored circulating pneumoproteins in the diagnosis, severity, and prognosis of COVID-19 by meta-analysis. We searched six English databases until December 16, 2021. Standardised mean difference (SMD) and 95% confidence interval (CI) were the overall outcomes. RevMan 5.3, Stata 16, and Meta-DiSc 1.4 were utilised for pooled analyses. Totally, 2902 subjects from 29 studies were included. COVID-19 patients had higher circulating KL-6, SP-D, and SP-A levels (SMD=1.34, 95% CI [0.60, 2.08]; SMD=1.74, 95% CI [0.64, 2.84]; SMD=3.42, 95% CI [1.31, 5.53], respectively) than healthy individuals. Circulating KL-6 levels were lower in survivors than in non-survivors (SMD=-1.09, 95% CI [-1.63, -0.55]). Circulating KL-6, SP-D, and RAGEs levels in mild to moderate patients were significantly lower (SMD=-0.93, 95% CI [-1.22, -0.65]; SMD=-1.67, 95% CI [-2.82, -0.52]; SMD=-1.17, 95% CI [-2.06, -0.28], respectively) than severe patients. Subgroup analysis and meta-regression suggested that age may be responsible for the heterogeneity (P=0.071) when analysing KL-6 in mild to moderate vs. severe patients. The meta-analysis of diagnostic accuracy including KL-6 for severity and mortality, and SP-D for severity demonstrated that they all had limited diagnostic values. Therefore, circulating pneumoproteins (KL-6, SP-D, and RAGEs) may reflect the diagnosis, severity, and prognosis of COVID-19 to some extent.