No abstract

Limited data are available for clinical characteristics of patients with coronavirus disease 2019 (COVID-19) outside Wuhan. This study aimed to describe the clinical characteristics of COVID-19 and identify the risk factors for severe illness of COVID-19 in Jiangsu province, China. Clinical data of hospitalized COVID-19 patients were retrospectively collected in 8 hospitals from 8 cities of Jiangsu province, China. Clinical findings of COVID-19 patients were described and risk factors for severe illness of COVID-19 were analyzed. By Feb 10, 2020, 202 hospitalized patients with COVID-19 were enrolled. The median age of patients was 44.0 years (interquartile range, 33.0-54.0). 55 (27.2%) patients had comorbidities. At the onset of illness, the common symptoms were fever (156 [77.2%]) and cough (120 [59.4%]). 66 (32.7%) patients had lymphopenia. 193 (95.5%) patients had abnormal radiological findings. 11 (5.4%) patients were admitted to the intensive care unit and none of the patients died. 23 (11.4%) patients had severe illness. Severe illness of COVID-19 was independently associated with body mass index (BMI) � 28 kg/m 2 (odds ratio [OR], 9.219; 95% confidence interval [CI], 2.731 to 31.126; P<0.001) and a known history of type 2 diabetes PLOS NEGLECTED TROPICAL DISEASES PLOS Neglected Tropical Diseases | https://doi.org/10.1371/journal.pntd.

BackgroundCigarette smoking is a known risk factor for cardiovascular disease (CVD), but the association between smoking and blood pressure is unclear. Thus, the current study examined the association between cigarette smoking and blood pressure in men.MethodsSystolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP) were examined using digital blood pressure measuring device, and smoking status was determined with China National Health Survey.ResultsThe ANCOVA showed that the adjusted DBP and MAP were lower in current smokers versus nonsmokers and the adjusted SBP was lower in current smokers versus former smokers (P < 0.05). Additionally, the adjusted PP tend to be decreased steadily as the pack·years increased in current smokers. In a fully adjusted logistic regression model, former smokers had increased ORs (95% CI) of 1.48 (1.01, 2.18) of hypertension and current smokers had not increased ORs (95% CI) of 0.83 (0.61, 1.12), compared with never smokers.ConclusionsThe findings revealed that the adjusted blood pressure were lower in current smokers versus nonsmokers and former smokers. No significant dose-dependent effect of current smoking on blood pressure indices except PP was observed. Smoking cessation was significantly associated with an increased risk of hypertension. However, current smoking was not a risk factor of hypertension.

Background and Aims Previous studies reported that coronavirus disease 2019 (COVID‐19) was likely to result in liver injury. However, few studies investigated liver injury in COVID‐19 patients with chronic liver diseases. We described the clinical features in COVID‐19 patients with non‐alcoholic fatty liver disease (NAFLD). Methods Confirmed COVID‐19 patients from hospitals in 10 cities of Jiangsu province, China were retrospectively included between January 18, 2020, and February 26, 2020. Hepatic Steatosis Index (HSI) was used to defined NAFLD. Results A total of 280 COVID‐19 patients were enrolled. Eighty‐six (30.7%) of 280 COVID‐19 patients were diagnosed as NAFLD by HSI. 100 (35.7%) patients presented abnormal liver function on admission. The median ALT levels (34.5 U/L vs. 23.0 U/L, P<0.001) and the proportion of elevated ALT (>40 U/L) (40.7% vs. 10.8%, P<0.001) were significantly higher in patients with NAFLD than in patients without NAFLD on admission. The proportion of elevated ALT in patients with NAFLD was also significantly higher than patients without NAFLD (65.1% vs. 38.7%, P<0.001) during hospitalization. Multivariate analysis showed that age over 50 years (odds ratio [OR] 2.077, 95% confidence interval [CI] 1.183‐3.648, P=0.011), and concurrent NAFLD (OR 2.956, 95% CI 1.526‐5.726, P=0.001) were independent risk factors of ALT elevation in COVID‐19 patients, while the atomized inhalation of interferon α‐2b (OR 0.402, 95%CI 0.236‐0.683, P=0.001) was associated with the reduced risk of ALT elevation during hospitalization. No patient developed liver failure or death during hospitalization. The complications and clinical outcomes were comparable between COVID‐19 patients with and without NAFLD. Conclusions NAFLD patients are more likely to develop liver injury when infected by COVID‐19. However, no patient developed severe liver‐related complications during hospitalization.

No abstract

No abstract

Clopidogrel plus aspirin is superior to aspirin alone for reducing END and RIS within 30 days and improves outcomes in certain subgroups at 6 months.

Lung adenocarcinoma (LUAD) is the most common form of malignant tumor and closely correlated with high risk of death worldwide. Accumulating researches have manifested that long noncoding RNAs (lncRNAs) are deeply involved in the progression of multiple cancers. LncRNA LOXL1 antisense RNA 1 (LOXL1‐AS1) was identified as an oncogene in several cancers, nonetheless, its biological effect and regulatory mechanism have not been explained in LUAD. Our present study suggested that LOXL1‐AS1 expression was considerably increased in LUAD tissues and cells. Moreover, LOXL1‐AS1 deficiency notably hampered cell proliferation and migration as well as dramatically facilitated cell apoptosis. Through molecular mechanism assays, LOXL1‐AS1 was identified as a cytoplasmic RNA and acted as a sponge of miR‐423‐5p. Furthermore, MYBL2 was targeted and negatively modified by miR‐423‐5p. Rescue experiments revealed that MYBL2 knockdown could counteract miR‐423‐5p repression‐mediated enhancement on the progression of LOXL1‐AS1 downregulated LUAD cells. More importantly, MYBL2 was discovered to interact with LOXL1‐AS1 promoter, indicating a positive feedback loop of LOXL1‐AS1/miR‐423‐5p/MYBL2 in LUAD. These findings manifested the carcinogenic role of LOXL1‐AS1 and LOXL1‐AS1/miR‐423‐5p/MYBL2 feedback loop in LUAD, which could be helpful to explore effective therapeutic strategy for LUAD patients.