[Analysis of chest imaging features of novel coronavirus pneumonia, bacterial pneumonia and viral pneumonia].

OBJECTIVE: To investigate and summarize the chest CT imaging features of patients with novel coronavirus pneumonia (COVID-19), bacterial pneumonia and other viral pneumonia. METHODS: Chest CT data of 102 patients with pulmonary infection due to different etiologies were retrospectively analyzed, including 36 patients with COVID-19 admitted to Hainan Provincial People's Hospital and the Second Affiliated Hospital of Hainan Medical University from December 2019 to March 2020, 16 patients with other viral pneumonia admitted to Hainan Provincial People's Hospital from January 2018 to February 2020, and 50 patients with bacterial pneumonia admitted to Haikou Affiliated Hospital of Central South University Xiangya School of Medicine from April 2018 to May 2020. Two senior radiologists and two senior intensive care physicians were participated to evaluated the extent of lesions involvement and imaging features of the first chest CT after the onset of the disease. RESULTS: Bilateral pulmonary lesions were more common in patients with COVID-19 and other viral pneumonia, and the incidence was significantly higher than that of bacterial pneumonia (91.6%, 75.0% vs. 26.0%, P < 0.05). Compared with other viral pneumonia and COVID-19, bacterial pneumonia was mainly characterized by single-lung and multi-lobed lesion (62.0% vs. 18.8%, 5.6%, P < 0.05), accompanied by pleural effusion and lymph node enlargement. The proportion of ground-glass opacity in the lung tissues of patients with COVID-19 was 97.2%, that of patients with other viral pneumonia was 56.2%, and that of patients with bacterial pneumonia was only 2.0% (P < 0.05). The incidence rate of lung tissue consolidation (25.0%, 12.5%), air bronchial sign (13.9%, 6.2%) and pleural effusion (16.7%, 37.5%) in patients with COVID-19 and other viral pneumonia were significantly lower than those in patients with bacterial pneumonia (62.0%, 32.0%, 60.0%, all P < 0.05), paving stone sign (22.2%, 37.5%), fine mesh sign (38.9%, 31.2%), halo sign (11.1%, 25.0%), ground-glass opacity with interlobular septal thickening (30.6%, 37.5%), bilateral patchy pattern/rope shadow (80.6%, 50.0%) etc. were significantly higher than those of bacterial pneumonia (2.0%, 4.0%, 2.0%, 0%, 22.0%, all P < 0.05). The incidence of local patchy shadow in patients with COVID-19 was only 8.3%, significantly lower than that in patients with other viral pneumonia and bacterial pneumonia (8.3% vs. 68.8%, 50.0%, P < 0.05). There was no significant difference in the incidence of peripheral vascular shadow thickening in patients with COVID-19, other viral pneumonia and bacterial pneumonia (27.8%, 12.5%, 30.0%, P > 0.05). CONCLUSIONS: The probability of ground-glass opacity, paving stone and grid shadow in chest CT of patients with COVID-19 was significantly higher than those of bacterial pneumonia, and it was more common in the lower lungs and lateral dorsal segment. In other patients with viral pneumonia, ground-glass opacity was distributed in both upper and lower lungs. Bacterial pneumonia is usually characterized by single lung consolidation, distributed in lobules or large lobes and accompanied by pleural effusion.

Effect of different treatments on macrophage differentiation in chronic obstructive pulmonary disease and repeated pulmonary infection.

OBJECTIVE: To observe the differentiation of macrophages in lung tissue and alveolar lavage fluid of mice with severe pulmonary infection and the changes after intervention with ceftriaxone and ulinastatin, and to explore the pathogenesis of severe pulmonary infection under immunosuppressive state and the intervention effect of two drugs. METHODS: 40 male Balb/c mice are randomly divided into normal group, model group, ulinastatin group, and ceftriaxone group with 10 mice in each group. Mice models of acute lung injury with immunodeficiency are established by methylprednisolone and endotoxin, and then treated with ulinastatin and ceftriaxone. Respiratory frequencies of mice in each group are measured at 3 h and 6 h after drug use through trachea, and then the mice are anaesthetized with uratan and killed 6 h after drug use. The number of alveolar macrophages and neutrophils in alveolar lavage fluid is collected and detected, and the pathological changes are observed. The positive expression of CD163 in lung tissue is detected by IHC (immunohistochemistry), and real-time quantitative PCR (Polymerase Chain Reaction) is used to detect the expression of Ml and M2 markers in bronchoalveolar lavage fluid (BALF). RESULT: Compared with the normal group, the mice in the model group breathed shallowly and quickly, occasionally nodded breathing, respiratory distress, and respiratory rate increased. Compared with the model group, the mice in the ulinastatin group and ceftriaxone group breathed slowly, occasionally have shortness of breath, smooth breathing, and slow breathing rate, and the mice in ulinastatin group breathe more smoothly. The number of macrophages and neutrophils in BALF of model group is higher than that of normal group. The number of macrophages and neutrophils in ulinastatin group and ceftriaxone group is lower than that of model group and the difference is statistically significant, and the number of macrophages and neutrophils in ulinastatin group is relatively less than that in model group. CONCLUSION: In the early stage of severe pulmonary infection under immunosuppressive state, the organism is in the CARS (Compensatory Anti-inflammatory Response Syndrome) stage; M1 macrophages had immune paralysis and M2 macrophages are abnormally activated. Compared with ceftriaxone, ulinastatin can alleviate lung injury more effectively and protect the lung of mice with acute lung injury. The protective mechanism of ulinastatin on lung of mice infected with immunocompromised endotoxin may be through inhibiting M1 macrophages and regulating non-specific immune function.

Protective effects of combined treatment with mild hypothermia and edaravone against cerebral ischemia/reperfusion injury via oxidative stress and Nrf2 pathway regulation.

Mild hypothermia (MH) and edaravone (EDA) exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury through activation of the nuclear factor erythroid 2­related factor 2 (Nrf2) pathway. However, whether MH and EDA exert synergistic effects against cerebral I/R injury remains unknown. The aim of the present study was to investigate the effects and mechanism of action of MH in combination with EDA in cerebral I/R injury. A rat cerebral I/R injury model was constructed by middle cerebral artery occlusion (MCAO) followed by reperfusion, and the mice were treated by MH, EDA or the inhibitor of the Nrf2 signaling pathway brusatol (Bru). It was observed that mice treated by MCAO had higher neurological deficit scores and oxidative stress levels, and low spatial learning and memory capacity; moreover, the CA1 region of the hippocampi of the mice exhibited reduced neuronal density and viability, and reduced mitochondrial dysfunction. However, MH in combination with EDA reversed the effects of MCAO, which were blocked by Bru injection. The levels of glutathione (GSH), GSH peroxidase, catalase and superoxide dismutase in rat ischemic hemisphere tissues were reduced by Bru. Western blotting demonstrated that the combined treatment with MH and EDA promoted the nuclear localization of Nrf2, and increased the levels of NAD(P)H quinone oxidoreductase and heme oxygenase (HO)­1. In conclusion, MH combined with EDA exerted synergistic neuroprotective effects against cerebral I/R injury involving changes in the Nrf2/HO­1 pathway.