Risk Factors for Radiological Progression Within Admissive One Week in the Hospitalized COVID-19 Omicron Variant-Infected Patients.

Purpose: Recently, the SARS-CoV-2 Omicron variant was identified as responsible for a novel wave of COVID-19 worldwide. We perform a retrospective study to identify potential risk factors contributing to radiological progression in the COVID-19 patients due to the Omicron variant infection. These findings would provide guiding information for making clinical decisions that could improve the Omicron infection prognosis and reduce disease-related death. Methods: This is a retrospective cohort study from a single center in China. According to the radiological change within admissive one week, enrolled cases were divided into two groups: the progressive (1w-PD) and the stable or improved disease (1w-non-PD). Separate analyses were performed on patients stratified into subgroups using the Mann-Whitney U-test, the Fisher exact test, or the Chi-squared test and a multivariable logistic regression analysis. Results: Both the 1w-non-PD and 1w-PD cohorts displayed comparable asymptomatic infection, have similar underlying disease, impairment in respiratory function, coagulation dysfunction, tissue injury, SARS-CoV-2 viral load, and disease severity. However, the 1w-PD cohort was more inclined to cluster in populations presented with age between 41 and 65, higher CURB-65 scores, undetectable SARS-CoV-2 IgG, and lung affection. Based on the multiple logistic regression analysis, complicated bilateral and ground-glass opacities (GGOs) like pneumonia at admission were independent risk factors to radiological progression within admissive one week. Conclusion: This study provided preliminary data regarding disease progression in Omicron-infected patients that indicated the development of pneumonia in the context of Omicron infection was worthy of potential risk factors.

Factors associated with delayed viral shedding in COVID-19 infected patients: A retrospective small-scale study.

BACKGROUND: The outbreak of COVID-19 has caused ever-increasing attention and public panic all over the world. Until now, data are limited about the risk factors to virus shedding in COVID-19 infected patients. METHODS: In this retrospective study, data were collected from 87 patients hospitalized with COVID-19 infection in Suzhou. Using Cox proportional hazards regression and Kaplan-Meier survival analysis, the risk factors to COVID-19 RNA shedding was to be established according to demographic information, clinical characteristics, epidemiological history, antiviral medicine and corticosteroid administration. RESULTS: The median duration of COVID-19 RNA shedding from admission was 13.11 ± 0.76 days. There was no significant difference in viral shedding duration in terms of gender, age, history of Hubei province stay, characteristics of chest CT on admission, lymphocytopenia and clinical severity. By Cox proportional hazards model, excessive 200 mg cumulative corticosteroid (HR, 3.425 [95% CI, 1.339-7.143]), time from illness onset to hospitalization (<5 days) (HR, 2.503 [95% CI, 1.433-4.371]) and arbidol-included therapy (HR, 2.073 [95% CI, 1.185-3.626]) were the independent risk factors to delay COVID-19 RNA shedding. Besides of excessive 200 mg of cumulative corticosteroid (HR, 2.825 [95% CI, 1.201-6.649]), admission within 5 days from illness onset (HR, 2.493 [95% CI, 1.393-4.462]) and arbidol-included therapy (HR, 2.102 [95% CI, 1.073-4.120]), lymphocytopenia (HR, 2.153 [95% CI, 1.097-4.225]) was further identified as another unfavorable factor to 10-day viral shedding. CONCLUSIONS: The potential risk factors could help clinicians to identify patients with delayed viral shedding, thereby providing the rational strategy of treatment and optimal anti-viral interventions.

Clinical characteristics and laboratory indicator analysis of 67 COVID-19 pneumonia patients in Suzhou, China.

BACKGROUND: Sudden exacerbations and respiratory failure are major causes of death in patients with severe coronavirus disease 2019(COVID-19) pneumonia, but indicators for the prediction and treatment of severe patients are still lacking. METHODS: A retrospective analysis of 67 collected cases was conducted and included approximately 67 patients with COVID-19 pneumonia who were admitted to the Suzhou Fifth People's Hospital from January 1, 2020 to February 8, 2020. The epidemiological, clinical and imaging characteristics as well as laboratory data of the 67 patients were analyzed. RESULTS: The study found that fibrinogen (FIB) was increased in 45 (65.2%) patients, and when FIB reached a critical value of 4.805 g/L, the sensitivity and specificity、DA, helping to distinguish general and severe cases, were 100 and 14%、92.9%, respectively, which were significantly better than those for lymphocyte count and myoglobin. Chest CT images indicated that the cumulative number of lung lobes with lesions in severe patients was significantly higher than that in general patients (P < 0.05), and the cumulative number of lung lobes with lesions was negatively correlated with lymphocyte count and positively correlated with myoglobin and FIB. Our study also found that there was no obvious effect of hormone therapy in patients with severe COVID-19. CONCLUSIONS: Based on the retrospective analysis, FIB was found to be increased in severe patients and was better than lymphocyte count and myoglobin in distinguishing general and severe patients. The study also suggested that hormone treatment has no significant effect on COVID-19.

Discrepant Clinical Significance of CD28+CD8- and CD4+CD25high Regulatory T Cells During the Progression of Hepatitis B Virus Infection.

Accumulating evidence demonstrates that CD8+CD28- regulatory T cells increase in chronic viral infection as well as tumorigenesis. However, it is still not clear about their characteristics in hepatitis B virus (HBV) infection. In addition, it is not understood whether this regulatory immune subset is distinct from CD4+CD25high regulatory T cells in the aspect of impact on or relationship to the progression of HBV infection. Hence, we investigated their dynamics and compared their correlations with clinical parameters in the chronic and advanced phases of HBV infection. The data showed that compared with healthy controls, the frequencies of CD28+CD8- and CD4+CD25high T cells increased in both chronic and advanced phases, while there is no significant difference between the two case groups. Interestingly, we found that in chronic phase, the frequency of CD8+CD28- subset was negatively correlated with the levels of alanine aminotransaminase (ALT) and aspartate aminotransferase (AST), respectively, and did not present association with HBV DNA load, whereas that of CD4+CD25high T cells was positively correlated with HBV DNA load and the levels of ALT and AST, respectively. Amazingly, in advanced phase, the frequency of CD4+CD25high T cells was negatively correlated with HBV DNA load and the levels of ALT, respectively, while there is no significant correlation between the frequency of CD8+CD28- subset and those clinical parameters. Thereby, our findings demonstrated that CD28+CD8- and CD4+CD25high regulatory T cells might exert distinct effect on modulating antiviral immune responses and mitigate immunomediated liver damage in different phases of HBV infection, which represent potential prognostic markers and therapeutic targets for HBV-infected patients based on further exploration of detailed mechanism.

[Spatiotemporal characteristics of urban land expansion in central area of Shanghai, China].

Using the high spatial resolution (2.5 m) color-infrared aerial photos acquired in 1989, 1994, 2000 and 2005, this paper analyzed the spatiotemporal characteristics of rapid urban expansion in central Shanghai with urban expansion intensity index and gradient analysis. Results showed that urban land use in Shanghai increased rapidly in a "pancake" style during the study period, and the anisotropic urban expansion moved the urban center 2.62 km toward southwest. The urban land use expansion intensity doubled and showed a rural-urban gradient. The most intensive urban expansion zone fell in the rural-urban transition zone, indicating the dominance of peripheral expansion as the primary urban expansion mode in Shanghai. However, the urban land use intensity decreased with time at the urban center. The primary driving forces of urban expansion included support from government policies and decision-making, enhanced economic activities, societal fixed assets investment, urban infrastructure investment, extension of transportation routes, as well as increase in urban population.

Enhanced phosphorylation of MAPKs by NE promotes TNF-α production by macrophage through α adrenergic receptor.

The aim of this study was to investigate whether norepinephrine (NE) could regulate macrophage production of tumor necrosis factor alpha (TNF-α) by influencing the phosphorylation of mitogen-activated protein kinases (MAPKs). Primary macrophages from male BALB/c mice were applied to explore the mechanism by which NE influences the the secretion of TNF-α when macrophages were activated by lipopolysaccharides (LPS). We found that NE could increase crophage production of TNF-α when macrophages were activated by LPS, and this effect could be inhibited by α adrenergic antagonist phentolamine. Also, NE could increase the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), and p38, through α receptor. Furthermore, JNK inhibitor SP600125, ERK inhibitor U0126, and p38 inhibitor SB203580 could all partially counteract NE's effect on the phosphorylation of MAPKs, as well as TNF-α production by macrophages. This study revealed that as macrophages were activated by LPS, NE promoted the secretion of inflammatory factors by increasing the phosphorylation of MAPKs through an α receptor-dependent pathway. Our results provide the evidence of a relationship between stress and diseases, as well as the mechanism by which stress induces or affects the inflammation-related diseases.

Corticosterone rapidly promotes respiratory burst of mouse peritoneal macrophages via non-genomic mechanism.

BACKGROUND: The immunomodulatory effects of glucocorticoids (GCs) have been described as bimodal. High concentration of GCs exerts immunosuppressive effects and low levels of GCs are immunopermissive. While the immunosuppressive mechanisms of GCs have been investigated intensely, the immunopermissive effects of GCs remain unclear. A lot of studies showed GCs could exert rapid non-genomic actions. We herein studied the rapid immunopromoting effects of GCs. METHODS: We observed the rapid (within 30 minutes) effects of corticosterone on respiratory burst of mouse peritoneal macrophages and studied their mechanisms. The superoxide anions were measured by cytochrome C reduction assay. Protein kinase C phosphorylation was measured by Western blotting and membrane fluidity was evaluated by fluorescence polarization measurement. RESULTS: The 10(-8) mol/L and 10(-7) mol/L corticosterone rapidly increased the superoxide anions production by macrophages, which were insensitive to GC-receptor antagonist, mifepristone, and protein-synthesis inhibitor, cycloheximide. Corticosterone coupled to bovine serum albumin was able to mimic the effects of corticosterone. The effects were independent of protein kinase C pathway and the change in membrane fluidity. CONCLUSIONS: The results indicate that corticosterone rapidly promote the superoxide anions production by mouse peritoneal macrophages may through non-genomic mechanisms. This study may contribute to understanding the effects of GCs under stress condition and the physiological significance of nongenomic effects of GCs.