, there have been 77,269 officially reported confirmed cases of 2019 novel corona virus (SARS-CoV-2) infection in China. As lung abnormalities may develop before clinical manifestations and nucleic acid detection, experts have recommended early chest computerized tomography (CT) for screening suspected patients [1]. The high contagiousness of SARS-CoV-2 and the risk of transporting unstable patients with hypoxemia and hemodynamic failure make chest CT a limited option for the patient with suspected or established COVID-19. Lung ultrasonography gives the results that are similar to chest CT and superior to standard chest radiography for evaluation of pneumonia and/ or adult respiratory distress syndrome (ARDS) with the added advantage of ease of use at point of care, repeatability, absence of radiation exposure, and low cost [2]. In this report, we summarize our early experience with lung ultrasonography for evaluation of SARS-CoV-2 infection in China with the intent of alerting frontline intensivists to the utility of lung ultrasonography for management of COVID-19. Ultrasonographic features of nCoV pneumonia We performed lung ultrasonography on 20 patients with COVID-19 using a 12-zone method [3]. Characteristic findings included the following:

Up to 24 February 2020, there have been 77,269 officially reported confirmed cases of 2019 novel coronavirus (nCoV) infection in China. Circulatory dysfunction is considered to have a late onset in severe cases of nCoV pneumonia, which is often ignored in clinical treatment. The main causes of acute respiratory failure and subsequent circulatory dysfunction include the rapid progress of lung injury, fluid overload, lung consolidation, and mechanical ventilation for hypoxemia. Most injuries are related to fluid overload, acute lung injury, and longterm hypoxia. Echocardiographic is an important part of critical ultrasonography, which helps to quickly identify the hemodynamic status. We summarized the echocardiographic features of critically ill COVID-19 patients and its clinical use in the treatment of nCoV pneumonia. The echocardiographic features of critically ill COVID-19 patientsThe echocardiographic features of COVID-19 are mainly related to the severity of disease and cardiovascular complications. Abnormal findings include (1) hyperdynamic cardiac function, presented as the increase of cardiac output (CO) and ejection faction (EF) of the left ventricular (LV), with/without the decrease of peripheral vascular resistance, which is often seen in the early stage following the systemic inflammatory response; (2) acute stress-induced (takotsubo) cardiomyopathy, characterized as LV segmental contraction abnormalities and apical ballooning [1]; (3) right ventricular (RV) enlargement and acute pulmonary hypertension, which are mainly caused by "internal factors" (including alveolar and pulmonary capillary damage caused by inflammation, hypoxia, and hypercapnia, leading to the increase of RV afterload) and "external factors" (including fluid overload, which causes the increase of RV preload, and unsuitable mechanical ventilation parameter setting, which affects the cardiac function by cardiopulmonary interaction); further, LV function will be affected because the right and left hearts are in the same pericardium; and (4) diffuse myocardial inhibition in the late stage, which is often caused by severe hypoxia, and long term of anoxia and inflammation. The echocardiographic features of nCoV pneumonia and their probable causes are shown in Table 1. The protocol of echocardiography examination in nCoV pneumoniaEchocardiography can help to quickly identify the circulatory status of nCoV pneumonia patients and guide hemodynamic management. Five basic views of echocardiography (apical four chamber view, parasternal long axis view, parasternal short axis view, subarachnoid four chamber view, subarachnoid inferior vena cava (IVC) long and short axis view) should be measured, which help to quickly understand the patient's volume status, cardiac function, and organ perfusion and help to develop hemodynamic management plans. It is suggested to measure the diameter of IVC, EF, velocity-time integral of the left ventricular outflow during continuous and dynamic evaluation of patients' volume state and fluid responsiveness, left ven...

Both diagnostic criteria cause misdiagnosis, and the sensitivity did not differ significantly. The incidence of SAE was high, and 28-day and 180-day mortality rates were significantly higher than those without SAE. Sepsis-associated encephalopathy is a risk factor for poor outcome. The overall long-term prognosis of patients with sepsis was poor, and the quality of life decreased.

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This study aimed to investigate the mechanism underlying the neuroprotective effect of hemin in oxygen-glucose deprivation (OGD)-treated neurons. OGD-treated SH-SY5Y cells (human neuroblastoma cells) were used in the study. The cellular viability of SH-SY5Y cells was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and the cell apoptosis rate was determined by flow cytometry analysis with Annexin V-fluorescein isothiocyanate and propidium iodide staining with or without hemin pretreatment. Cell viability and apoptotic activation were detected after hemin administration combined with neuroglobin (Nqb), thioredoxin-1, peroxiredoxin-2, or heme oxygenase-1 siRNA transient transfection. The release of cytochrome c from mitochondria and the interaction between Ngb and cytochrome c were examined with hemin pretreatment. Hemin had a neuroprotective effect in OGD-treated SH-SY5Y cells, which was mainly mediated by the upregulation of Ngb. Moreover, the release of cytochrome c from mitochondria was inhibited by hemin-induced Ngb expression through facilitating the interaction of Ngb with cytochrome c in mitochondria. The present findings provided new insights into the neuroprotective mechanisms of hemin. It was concluded that low-dose hemin pretreatment had a neuroprotective effect in OGD-treated SH-SY5Y cells, through inhibiting cell apoptosis. The neuroprotective effects of hemin following hypoxic-ischemic neuronal damage were mainly mediated by Ngb. One underlying mechanism was hemin-induced overexpression of mitochondrial Ngb, which inhibited endogenous apoptosis via the association with cytochrome c.