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Background The outbreak of COVID-19 has led to international concern. We aimed to establish an effective screening strategy in Shanghai, China, to aid early identification of patients with COVID-19. MethodsWe did a multicentre, observational cohort study in fever clinics of 25 hospitals in 16 districts of Shanghai. All patients visiting the clinics within the study period were included. A strategy for COVID-19 screening was presented and then suspected cases were monitored and analysed until they were confirmed as cases or excluded. Logistic regression was used to determine the risk factors of COVID-19. Findings We enrolled patients visiting fever clinics fromJan 17 to Feb 16, 2020. Among 53 617 patients visiting fever clinics, 1004 (1•9%) were considered as suspected cases, with 188 (0•4% of all patients, 18•7% of suspected cases) eventually diagnosed as confirmed cases. 154 patients with missing data were excluded from the analysis. Exposure history (odds ratio [OR] 4•16, 95% CI 2•74-6•33; p<0•0001), fatigue (OR 1•56, 1•01-2•41; p=0•043), white blood cell count less than 4 × 10⁹ per L (OR 2•44, 1•28-4•64; p=0•0066), lymphocyte count less than 0•8 × 10⁹ per L (OR 1•82, 1•00-3•31; p=0•049), ground glass opacity (OR 1•95, 1•32-2•89; p=0•0009), and having both lungs affected (OR 1•54, 1•04-2•28; p=0•032) were independent risk factors for confirmed COVID-19.Interpretation The screening strategy was effective for confirming or excluding COVID-19 during the spread of this contagious disease. Relevant independent risk factors identified in this study might be helpful for early recognition of the disease.

BackgroundEpidemiological studies to date have evaluated the association between genetic variants and the susceptibility to obstructive sleep apnea (OSA). However, the results of these studies have been inconclusive. In this current study we performed meta-analysis of genetic association studies (GAS) to pool OSA-susceptible genes in Chinese population, to perform a more precise evaluation of the association.MethodsVarious databases (i.e., PubMed, EMBASE, HuGE Navigator, Wanfang and CNKI) were searched to identify all eligible GAS-related variants associated with susceptibility to OSA. The generalized odds ratio metric (ORG) and the odds ratio (OR) of the allele contrast were used to quantify the impact of genetic variants on the risk of OSA. Cumulative and recursive cumulative meta-analyses (CMA) were also performed to investigate the trend and stability of effect sizes as evidence was accumulated.ResultsThirty-two GAS evaluating 13 polymorphisms in 10 genes were included in our meta-analysis. Significant associations were derived for four polymorphisms either for the allele contrast or for the ORG. The variants TNF-α-308G/A, 5-HTTLPR, 5-HTTVNTR, and APOE showed marginal significance for ORG (95% confidence interval [CI]): 2.01(1.31–3.07); 1.31(1.09–1.58); 1.85(1.16–2.95); 1.79(1.10–2.92); and 1.79(1.10–2.92) respectively. In addition, the TNF-α-308G/A, 5-HTTLPR, and 5-HTTVNTR variants showed significance for the allele contrast: 2.15(1.39–3.31); 2.26(1.58–3.24); 1.32(1.12–1.55); and 1.86(1.12–3.08) respectively. CMA showed a trend towards an association, and recursive CMA indicated that more evidence was needed to determine whether this was significant.ConclusionsTNF-α, 5-HTT, and APOE genes can all be proposed as OSA-susceptibility genes in Chinese population. Genome-wide association studies (GWAS) are therefore urgently needed to confirm our findings within a larger sample of OSA patients in China.

INTRODUCTIONChronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and concurrent progressive airflow limitation [1][2][3]. Patients may experience episodes of exacerbated respiratory symptoms, and the frequency of exacerbations requiring hospitalization increases, resulting in significant social and economic burden and one of the major causes of morbidity and mortality worldwide [4,5]. The pathogenesis of COPD and exacerbations may be associated with inflammatory cells, including macrophages, neutrophils, and T lymphocytes [6,7]. These cells are crucial in parenchymal destruction and development of airflow limitation in patients with COPD [8,9]. Chemokines and their receptors regulate leukocyte adhesion and homing, and these receptors play a critical role in trafficking of leukocytes to sites of injury and www.aging-us.com