[Acute kidney injury in patients hospitalized with COVID-19 in Wuhan, China: a single-center retrospective observational study].

OBJECTIVE: To assess the predictors and outcomes of acute kidney injury (AKI) among patients with coronavirus disease 2019 (COVID-19). OBJECTIVE: This retrospective observational study was conducted among patients with a confirmed diagnosis of COVID-19 admitted to Hankou Hospital between January, 5 and March 8, 2020. We evaluated the association of AKI with the demographic and biochemical parameters and clinical outcomes of the patients using univariate regression analysis. OBJECTIVE: Atotal of 287 COVID-19 patients, including 55 with AKI and 232 without AKI, were included in the analysis. Compared with the patients without AKI, the patients with AKI were older, predominantly male, and were more likely to have hypoxia and pre-existing hypertension and cerebrovascular diseases. The patients with AKI also had higher levels of white blood cells, D-dimer, aspartate aminotransferase, total bilirubin, creatine kinase, lactate dehydrogenase, procalcitonin, C-reactive protein, a higher prevalence of hyperkalemia, lower lymphocyte counts, and higher chest computed tomographic scores. The incidence of stage 1 AKI was 14.3% and that of stage 2 or 3 AKI was 4.9%. The patients with AKI had much higher mortality rate than those without AKI. OBJECTIVE: AKI is an important complication of COVID-19. An older age, a male gender, multiple pre- existing comorbidities, lymphopenia, increased infection indicators, elevated D-dimer, and impaired heart and liver functions are all potential risk factors ofAKI. COVID- 19 patients with AKI that progresses into stages 2 or 3 AKI have a high mortality rate. Prevention of AKI and monitoring kidney function is critical in the care of COVID-19 patients.

CircRNA_103762 promotes multidrug resistance in NSCLC by targeting DNA damage inducible transcript 3 (CHOP).

BACKGROUND: CircRNAs have been found to play crucial roles in multiple tumor including non-small cell lung cancer (NSCLC). Here, we researched the correlation between circRNA_103762 and chemotherapy resistance. METHODS: RT-PCR assay was performed to detect circRNA_103762 and DNA damage inducible transcript 3 (CHOP) expression. CCK8 assay was performed to examine cell proliferation and IC50 of different drug. Migration and invasion assay was used to detect cell migration and invasion. RESULTS: In our study, circRNA_103762 expression was upregulated in NSCLC tissues and cell. Knockdown of circRNA_103762 can inhibited cell proliferation, migration and invasion in NSCLC. In addition, downregulation of circRNA_103762 promoted CHOP expression and inhibited multidrug resistance (MDR) in NSCLC. CONCLUSION: Together, we demonstrated that circRNA_103762 is upregulated in NSCLC and functions as an oncogene in NSCLC, and circRNA_103762 enhanced MDR by inhibited CHOP expression in NSCLC cells. These results will help us understand the MDR of NSCLC, providing better effective therapy strategies for patients.

Phosphorylation of low density lipoprotein receptor-related protein 6 is involved in receptor for advanced glycation end product-mediated ß-catenin stabilization in a toluene diisocyanate-induced asthma model.

BACKGROUND: We have previously demonstrated that the receptor for advanced glycation end products (RAGE)/ß-catenin axis plays a vital role in regulating airway inflammation and airway remodeling in a toluene diisocyanate (TDI)-induced murine asthma model. However, the exact mechanism of ß-catenin activation remains unclear. Given that phosphorylation of the low-density lipoprotein receptor-related protein 6 (Lrp6) is a key step in mediating ß-catenin stabilization in canonical wnt/ß-catenin signaling, we explored the possible relationship between RAGE and Lrp6 in regulating ß-catenin stabilization in TDI-induced asthma. METHODS: In this study, a TDI-induced murine asthma model was generated, and mice were treated with a specific inhibitor of RAGE. In vitro, the human bronchial epithelial cell line 16HBE was treated with TDI-human serum albumin (TDI-HSA). RAGE overexpression or knockdown cells were also constructed and assessed. RESULTS: The results showed that RAGE inhibition or RAGE knockdown decreased ß-catenin nuclear accumulation and the expression of relevant ß-catenin targeted genes (VEGF, MMP9, TGF-ß1) in the TDI-induced murine asthma model and TDI-HSA-treated 16HBE cells, respectively. Silencing of RAGE reversed the TDI-induced increase in phospho-ERK1/2 (p-ERK) and phospho-Lrp6 (p-Lrp6) in 16HBE cells. Pretreatment with the extracellular signal-regulated kinase (ERK)1/2 inhibitor U0126 suppressed TDI-induced Lrp6 phosphorylation. Furthermore, knockdown of Lrp6 in 16HBE cells decreased ß-catenin nuclear translocation and the expression of VEGF, MMP9, and TGF-ß1. CONCLUSION: These data suggested that the RAGE/ERK axis modulates Lrp6 phosphorylation, contributing to ß-catenin stabilization in a TDI-induced murine model.

Albuterol inhalation increases FeNO level in steroid-naive asthmatics but not COPD patients with reversibility.

INTRODUCTION: Fractional exhaled nitric oxide (FeNO) has been used as a marker of airway inflammation. Airway caliber is related to the level of FeNO in asthmatics. OBJECTIVES: This study aimed to investigate whether airway obstruction could interfere with real FENO levels and if different FeNO changes after albuterol inhalation could assist in distinguishing asthma from chronic obstructive pulmonary disease (COPD). METHODS: FeNO and spirometry measurements were performed before and after albuterol inhalation in the following three patient groups: 30 steroid-naive asthmatics, 25 asthmatics inhaling corticosteroids/long-acting ß(2)-adrenergic agonists for at least 1 month and 20 COPD patients. Bronchodilator test (BDT) results were positive in all patients enrolled. The correlations among FeNO levels, pulmonary function and sputum eosinophil counts were analyzed. RESULTS: FeNO increased significantly after albuterol inhalation in steroid-naive asthmatics but not in ICS-treated asthmatics or COPD patients. The FeNO levels demonstrated no significant correlation with spirometry results or sputum eosinophil counts before or after inhaling bronchodilator in all three groups. Both the levels of FeNO and changes in FENO after albuterol inhalation in steroid-naive asthma patients were higher than those in ICS-treated asthmatics and COPD patients (P < 0.001). The differences remained after proper adjustment for confounding factors (gender, age, smoking pack-years, ICS-treated and pulmonary function index). CONCLUSIONS: Our results support the role of FeNO in differentiating asthmatics from COPD patients with positive BDT. FeNO detection after albuterol inhalation should be encouraged in steroid-naive asthma patients with airway obstruction.