Predictive factors of progression to severe COVID-19.

AIM: Early diagnosis and treatment are crucial for the survival of severe Coronavirus Disease 2019 (COVID-19) patients, but data with regard to risk factors for disease progression from milder COVID-19 to severe COVID-19 remain scarce. METHODS: We conducted a retrospective analysis on 116 patients. RESULTS: Three factors were observed to be independently associated with progression to severe COVID-19 during 14 days after admission: (a) age 65 years or older (hazard ratio [HR] = 8.456; 95% CI: 2.706-26.426); (b) creatine kinase (CK) ≥ 180 U/L (HR = 3.667; 95% CI: 1.253-10.733); and (c) CD4+ T-cell counts <300 cells/µL (HR = 4.695; 95% CI: 1.483-14.856). The difference in rates of severe COVID-19 development was found to be statistically significant between patients aged 65 years or older (46.2%) and those younger than 65 years (90.2%), between patients with CK ≥ 180 U/L (55.6%) and those with CK < 180 U/L (91.5%), and between patients with CD4+ T-cell counts <300 cells/µL (53.8%) and those with CD4+ cell counts ≥300 cells/µL (83.2%). CONCLUSIONS: Age ≥ 65 years, CK ≥ 180 U/L, and CD4+ T-cell counts <300 cells/µL at admission were risk factors independently associated with disease progression to severe COVID-19 during 14 days after admission and are therefore potential markers for disease progression in patients with milder COVID-19.

Cerebral air embolism following an endoscopic variceal ligation: A case report.

BACKGROUND: Cerebral air embolism (CAE) is a rare but potentially devastating complication of endoscopic procedures. Only 3 cases, to our knowledge, have been reported. CASE PRESENTATION: A 50-year-old female patient presented with hepatitis C virus-related hepatic cirrhosis, emergency endoscopy and endoscopic variceal ligation was performed in an awakened state. CAE occurred during procedure, the patient passed away the next day in the intensive care unit. CONCLUSIONS: CAE is a rare but potentially devastating complication in endoscopic procedures. We need more preventive tools and treatments.

Hypoxia-inducible factor-1α and Wnt/ß-catenin signaling pathways promote the invasion of hypoxic gastric cancer cells.

The present study aimed to examine the association between hypoxia-inducible factor (HIF)-1α and the Wnt/ß-catenin signaling pathway in a hypoxic environment. The study also aimed to explore the possible mechanisms underlying the invasion of hypoxic gastric cancer cells in vitro and in vivo. The pcDNA™ 6.2­GW/EmGFP­miR­ß­catenin plasmid was transfected into SGC­7901 gastric cancer cells, resulting in cells with stable suppression of ß­catenin expression. The biological characteristics of the control, liposome, negative control, ß­catenin knockdown, hypoxia and hypoxia ß­catenin knockdown groups were tested using an invasion assay. The differences in the invasive capacity of the control, negative control and liposome groups were not statistically significant. However, the hypoxia group demonstrated a significantly enhanced invasive capacity, as compared with that in the control group (P<0.05). In the hypoxia ß­catenin knockdown group, reduced cell penetration and diminished invasive behavior was observed (P<0.05). In the hypoxia and double (chemical + physical) hypoxia groups, HIF­1α, ß­catenin, urokinase­type plasminogen activator (uPA) and matrix metalloproteinase (MMP­7) protein and mRNA expression levels were elevated. In response to knockdown of ß­catenin expression, HIF­1α, ß­catenin, uPA and MMP­7 protein as well as mRNA expression levels were significantly reduced in the hypoxia ß­catenin knockdown and the double hypoxia ß­catenin knockdown groups. In an in vivo experiment, the growth rate of xenograft tumors of hypoxic and control cells was high alongside increased HIF­1α, ß­catenin, uPA and MMP­7 levels according to western blot and immunohistochemical analyses, while growth and protein levels of tumors from hypoxic ß­catenin knockdown cells were significantly lower and those of ß­catenin knockdown cells were lowest. In conclusion, these results suggested that HIF­1α activation was able to regulate the Wnt/ß­catenin pathway, and that HIF­1α may be controlled by the Wnt/ß­catenin pathway. A potential mechanism underlying SGC­7901 tumorigenicity is the activation of the Wnt/ß­catenin signaling pathway, which activates uPA and MMP­7 expression and contributes to the enhanced invasion of hypoxic cancer cells.