In this prospective study, AHRF had high possibilities to develop ARDS and death risk, as impacted by ventilation settings and fluid intake in the early treatment, as well as socioeconomic factors, which should be considered for implementation of standard of care in respiratory therapy.

Silymarin is a potent antioxidant medicine and has been widely used for the treatment of liver diseases over 30 years. Recent studies suggest that silymarin may benefit patients with glucose intolerance. However, the mechanism underlying the action of silymarin is not clarified. The aim of this work was to assess the impact of silymarin on glucose intolerance in high-fat diet (HFD)-fed mice, and explore the potential therapeutic mechanisms. C57BL/6 mice were fed with HFD for 12 weeks, randomized, and treated orally with vehicle saline or silymarin (30 mg/kg) daily for 30 days. We found that silymarin significantly improved HFD-induced body weight gain, glucose intolerance, and insulin resistance in mice. Silymarin treatment reduced HFD-increased oxidative stress indicators (reactive oxygen species, lipid peroxidation, protein oxidation) and restored HFD-down-regulated activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) in the plasma and/or liver of the HFD-fed mice. Furthermore, silymarin decreased HFD-up-regulated hepatic NADPH oxidase expression and NF-κB activation in mice. Additionally, silymarin treatment mitigated HFD-increased plasma IL-1β, TNF-α levels, and HFD-enhanced hepatic NO, TLR4, and iNOS expression in mice. These novel data indicate that silymarin has potent anti-diabetic actions through alleviating oxidative stress and inflammatory response, partially by inhibiting hepatic NADPH oxidase expression and the NF-κB signaling.

medRxiv preprint critical condition, and 54 patients were transferred to ICU with aggravated condition.Over fifty six percent (56.4%) of patients were laboratory confirmed by RT-PCR, and 43.6% were consistent with clinical diagnostic criteria.Among them, 64 were males and 37 were females, with average age of 65.46 years (SD 9.74). Interestingly, all deaths shwed significant difference in blood type distribution, with 44.44% of type A , 29.29% of type B , 8.08% of type AB, and 18.19% of type O.The clinical manifestations of the novel coronavirus pneumonia are non-specific,the common symptoms included fever (91,,90.10%), cough (69,68.32%) and dyspnea (75,74.26%). Neutrophils, procalcitonin(PCT),C-reactive protein(CRP),and interleukin-6(IL-6), D-dimer gradually increased with progress of the disease. Myocardial enzymes were abnormal in most patients at admission, myocardial damage indicators were significantly increased. Sixty one (60.40%) patients were given antiviral drugs, 59(58.42%),received glucocorticoids, 63.37% were given intravenous immunoglobulins, and 44.55% were treated with thymosin preparations. All patients received antibiotic treatment, 63(62.38%) were given restricted antibiotics, 23(22.78%) were administrated to antifungal drugs. Non-invasive ventilator or high-flow oxygen therapy were given in 84(83.17%) patients , and invasive mechanical ventilation was used in 76.24%

We aimed to describe the clinical features in coronavirus disease 2019 (COVID-19) cases. We studied 134 critically ill COVID-19 cases from 30 December 2019 to 20 February 2020 in an intensive care unit (ICU) at Wuhan Jinyintan Hospital. Demographics, underlying diseases, therapy strategies and test results were collected and analysed from patients on admission, admission to the ICU and 48 h before death. The non-survivors were older (65.46 (s.d. 9.74) vs. 46.45 (s.d. 11.09)) and were more likely to have underlying diseases. The blood group distribution of the COVID-19 cases differed from that of the Han population in Wuhan, with type A being 43.85%; type B, 26.92%; type AB, 10% and type O, 19.23%. Non-survivors tend to develop more severe lymphopaenia, with higher C-reactive protein, interleukin-6, procalcitonin, D-dimer levels and gradually increased with time. The clinical manifestations were non-specific. Compared with survivors, non-survivors more likely to have organ function injury, and to receive mechanical ventilation, either invasively or noninvasively. Multiple organ failure and secondary bacterial infection in the later period is worthy of attention.

To describe the clinical features of coronavirus disease 2019 . Methods: We recruited 73 patients with COVID-19 [49 men and 24 women; average age: 58.36 years (SD: 14.31)] admitted to the intensive care unit of Wuhan Jinyintan Hospital from December 30, 2019 to February 16, 2020. Demographics, underlying diseases, and laboratory test results on admission were collected and analyzed. Data were compared between survivors and non-survivors. Results: The non-survivors were older (65.46 [SD 9.74]vs 46.23 [12.01]) and were more likely to have chronic medical illnesses. Non-survivors tend to develop more severe lymphopenia, with higher Creactive protein, interleukin-6, D-dimer, and hs-Troponin I(hs-TnI) levels. Patients with elevated hs-TnI levels on admission had shorter duration from symptom onset to death. Increased hs-TnI level was related to dismal prognosis. Death risk increased by 20.8% when the hs-TnI level increased by one unit. After adjusting for inflammatory or coagulation index, the independent predictive relationship between hs-TnI and death disappeared. Conclusions: Cardiac injury may occur at the early stage of COVID-19, which is associated with high mortality. Inflammatory factor cascade and coagulation abnormality may be the potential mechanisms of COVID-19 combined with cardiac injury.