Background: The novel severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has spread worldwide.Hypothesis: The possible risk factors that lead to death in critical inpatients with coronavirus disease 2019 (COVID‐19) are not yet fully understood.Methods: In this single‐center, retrospective study, we enrolled 113 critical patients with COVID‐19 from Renmin Hospital of Wuhan University between February 1, 2020 and March 15, 2020. Patients who survived or died were compared.Results: A total of 113 critical patients with COVID‐19 were recruited; 50 (44.3%) died, and 63 (55.7%) recovered. The proportion of patients with ventricular arrhythmia was higher in the death group than in the recovery group (P = .021) and was higher among patients with myocardial damage than patients without myocardial damage (P = .013). Multivariate analysis confirmed independent predictors of mortality from COVID‐19: age > 70 years (HR 1.84, 95% CI 1.03‐3.28), initial neutrophil count over 6.5 × 10⁹/L (HR 3.43, 95% CI 1.84‐6.40), C‐reactive protein greater than 100 mg/L (HR 1.93, 95% CI 1.04‐3.59), and lactate dehydrogenase over 300 U/L (HR 2.90, 95% CI 1.26‐6.67). Immunoglobulin treatment (HR 0.39, 95% CI 0.21‐0.73) can reduce the risk of death. Sinus tachycardia (HR 2.94, 95% CI 1.16‐7.46) and ventricular arrhythmia (HR 2.79, 95% CI 1.11‐7.04) were independent ECG risk factors for mortality from COVID‐19.Conclusions: Old age (>70 years), neutrophilia, C‐reactive protein greater than 100 mg/L and lactate dehydrogenase over 300 U/L are high‐risk factors for mortality in critical patients with COVID‐19. Sinus tachycardia and ventricular arrhythmia are independent ECG risk factors for mortality from COVID‐19.

Activation of brown adipose tissue (BAT) contributes to energy dissipation and metabolic health. Although mineralocorticoid receptor (MR) antagonists have been demonstrated to improve metabolism under obesity, the underlying mechanisms remain incompletely understood. We aimed to evaluate the role of BAT MR in metabolic regulation. After 8 weeks of high-fat diet (HFD) feeding, BAT MR KO (BMRKO) mice manifested significantly increased bodyweight, fat mass, serum fasting glucose, and impaired glucose homeostasis compared with littermate control (LC) mice, although insulin resistance and fasting serum insulin were not significantly changed. Metabolic cage experiments showed no change in O₂ consumption, CO₂ production, or energy expenditure in obese BMRKO mice. RNA sequencing analysis revealed downregulation of genes related to fatty acid metabolism in BAT of BMRKO-HFD mice compared with LC-HFD mice. Moreover, H&E and immunohistochemical staining demonstrated that BMRKO exacerbated HFD-induced macrophage infiltration and proinflammatory genes in epididymal white adipose tissue (eWAT). BMRKO-HFD mice also manifested significantly increased liver weights and hepatic lipid accumulation, an increasing trend of genes related to lipogenesis and lipid uptake, and significantly decreased genes related to lipolytic and fatty acid oxidation in the liver. Finally, the level of insulin-induced AKT phosphorylation was substantially blunted in eWAT but not liver or skeletal muscle of BMRKO-HFD mice compared with LC-HFD mice. These data suggest that BAT MR is required to maintain metabolic homeostasis, likely through its regulation of fatty acid metabolism in BAT and impacts on eWAT and liver.

Hepatitis B virus (HBV) infection remains a significant global health burden, primarily due to its chronic complications, including acute exacerbation, cirrhosis, hepatocellular carcinoma (HCC), and related sequelae. Acute exacerbation of chronic hepatitis B (CHB-AE) is common and often represents the earliest clinical manifestation. The Hepatitis B virus X protein (HBx) (17-kDa) is not only essential for viral replication but also plays a role in the development of HCC. To investigate the role of HBx mutation in CHB-AE progression, we enrolled 33 hospitalized CHB-AE patients and 31 patients with HBV-related liver failure (controls) from mainland China between January 2017 and June 2018. Single mutation 36 of HBx was significantly more prevalent in CHB-AE patients (p < 0.05), whereas Joint Mutation 1 was more frequent in HBV-related liver failure patients (p < 0.05). HBx mutations, including Single mutation 36 and Joint Mutations 2 and 3, were significantly associated with high HBV DNA levels (p < 0.05), while Joint mutation 1 predominated in the low HBV DNA group (p < 0.01). Age-stratified analysis showed that Single mutation 36 and Joint Mutation 2 were more common in younger patients (<35 years old) (p < 0.05), whereas Joint mutation 1 was more frequent in older age (≥35 years old) (p < 0.05). Moreover, antiviral therapy markedly reduced the prevalence of Joint mutation 1 from 82.98% in treatment-naïve patients to 29.41% in treatment-experienced patients (p < 0.0001). These findings suggest that specific HBx mutations are associated with viral replication levels, disease progression, and patient demographics. Such mutations may serve as molecular markers for disease severity and potential therapeutic targets in both CHB-AE and HBV-related liver failure.