Mortality of critically ill patients with coronavirus disease 2019 (COVID-19) was high. Aims to examine whether time from symptoms onset to intensive care unit (ICU) admission affects incidence of extra-pulmonary complications and prognosis in order to provide a new insight for reducing the mortality. A single-centered, retrospective, observational study investigated 45 critically ill patients with COVID-19 hospitalized in ICU of The Third People's Hospital of Yichang from January 17 to March 29, 2020. Patients were divided into 2 groups according to time from symptoms onset to ICU admission (>7 and ≤7 days) and into 2 groups according to prognosis (survivors and non-survivors). Epidemiological, clinical, laboratory, radiological characteristics and treatment data were studied. Compared with patients who admitted to the ICU since symptoms onset ≤7 days (55.6%), patients who admitted to the ICU since symptoms onset >7 days (44.4%) were more likely to have extra-pulmonary complications (19 [95.0%] vs 16 [64.0%], P = .034), including acute kidney injury, cardiac injury, acute heart failure, liver dysfunction, gastrointestinal hemorrhage, hyperamylasemia, and hypernatremia. The incidence rates of acute respiratory distress syndrome, pneumothorax, and hospital-acquired pneumonia had no difference between the 2 groups. Except activated partial thromboplastin and Na + concentration, the laboratory findings were worse in group of time from symptoms onset to ICU admission >7 days. There was no difference in mortality between the 2 groups. Of the 45 cases in the ICU, 19 (42.2%) were non-survivors, and 16 (35.6%) were with hospital-acquired pneumonia. Among these non-survivors, hospital-acquired pneumonia was up to 12 (63.2%) besides higher incidence of extra-pulmonary complications. However, hospital-acquired pneumonia occurred in only 4 (15.4%) survivors. Critically ill patients with COVID-19 who admitted to ICU at once might get benefit from intensive care via lower rate of extra-pulmonary complications.

Objective SSTR2 is a member of superfamily of SST receptor (SSTR), and widely expressed in the brain; however, the knowledge of its functions in area adjacent to hematoma after intracerebral hemorrhage (ICH) is still limited. Method The role of SSTR2 in the processes of ICH was explored by conducting an ICH rat model. Western blot and immunohistochemistry were employed to examine the level of SSTR2 in area adjacent to hematoma after ICH. Immunofluorescent staining was used to observe the spatial correlation of SSTR2 with cellular types adjacent to hematoma after ICH. RNA interference specific to SSTR2 was adopted in PC12 cells to clarify the causal correlation between SSTR2 and neuronal activities. Results Increased expression of SSTR2 was observed and restricted to the neurons adjacent to hematoma following ICH. Immunofluorescent staining showed that SSTR2 was significant increased in neurons, but not astrocytes or microglia. Increasing SSTR2 level was found to be accompanied by the up-regulation of activated caspase-3 and the down-expression of p-Akt in a time-dependent manner. What's more, using SSTR2 RNA interference (SSTR2-RNAi) in PC12 cells, we indicated that SSTR2 might have a pro-apoptotic role in neurons. Conclusion We speculated that SSTR2 might exert its pro-apoptotic function in neurons through inhibiting Akt activity following ICH.