Objective To explore the clinical therapeutic efficacy and value of endovascular embolization treatment for Hunt-Hess poor-grade intracranial aneurysms. Methods Eighty-seven patients with Hunt-Hess grade Ⅳ - Ⅴ intracranial aneurysrns were treated with endovascular embolization from May 2001 to February 2010,77 patients were grade Ⅳ and 10 patients were grade Ⅴ. Outcomes were assessed by using the Glasgow outcome scale (GOS). Results Follow-up time was from 3 months to 9 years. The therapeutic efficacy was as following according to GOS: 25 patients were grade Ⅰ , 5 patients were grade Ⅱ , 9 patients were grade Ⅲ , 12 patients were grade Ⅳ ,and 36 patients were grade Ⅴ. There were 55.17%(48/87) favorable outcome rate and 28.74% (25/87) mortality rate in all patients. There were 61.70%(29/47) favorable outcome rate and 25.53%(12/47) mortality rate in early stage treatment patients (diseased within 3 d), otherwise there were 47.50% (19/40) favorable outcome rate and 32.50%(13/40) mortality rate in medium and late stage treatment patients (diseased 3 d or later). There were no statistically significance in favorable outcome rate and mortality rate between them (P > 0.05). All the patients were embolized successfully ,technical complications occurred in 8 patients, 10 patients were found angiographic evidence of vasospasm. Conclusions Endovascular embolization is an effective method for treating Hunt-Hess poorgrade intracranial aneurysms. Early stage treatment is a feasible option because it can improve prognosis by reducing rebleeding and vasospasm.

Background::Pancreatic adenocarcinoma (PAAD) is an extremely lethal malignancy. Identification of the functional genes and genetic variants related to PAAD prognosis is important and challenging. Previously identified prognostic genes from several expression profile analyses were inconsistent. The regulatory genetic variants that affect PAAD prognosis were largely unknown.Methods::Firstly, a meta-analysis was performed with seven published datasets to systematically explore the candidate prognostic genes for PAAD. Next, to identify the regulatory variants for those candidate genes, expression quantitative trait loci analysis was implemented with PAAD data resources from The Cancer Genome Atlas. Then, a two-stage association study in a total of 893 PAAD patients was conducted to interrogate the regulatory variants and find the prognostic locus. Finally, a series of biochemical experiments and phenotype assays were carried out to demonstrate the biological function of variation and genes in PAAD progression process.Results::A total of 128 genes were identified associated with the PAAD prognosis in the meta-analysis. Fourteen regulatory loci in 12 of the 128 genes were discovered, among which, only rs4887783, the functional variant in the promoter of Ring Finger and WD Repeat Domain 3 ( RFWD3), presented significant association with PAAD prognosis in both stages of the population study. Dual-luciferase reporter and electrophoretic mobility shift assays demonstrated that rs4887783-G allele, which predicts the worse prognosis, enhanced the binding of transcript factor REST, thus elevating RFWD3 expression. Further phenotypic assays revealed that excess expression of RFWD3 promoted tumor cell migration without affecting their proliferation rate. RFWD3 was highly expressed in PAAD and might orchestrate the genes in the DNA repair process. Conclusions::RFWD3 and its regulatory variant are novel genetic factors for PAAD prognosis.

The Coronavirus disease 2019 (COVID-19) has spread globally. Although mixed liver impairment has been reported in COVID-19 patients, the association of liver injury caused by specific subtype especially chronic hepatitis B (CHB) with COVID-19 has not been elucidated. In this multi-center, retrospective, and observational cohort study, 109 CHB and 327 non-CHB patients with COVID-19 were propensity score matched at an approximate ratio of 3:1 on the basis of age, sex, and comorbidities. Demographic characteristics, laboratory examinations, disease severity, and clinical outcomes were compared. Furthermore, univariable and multivariable logistic and Cox regression models were used to explore the risk factors for disease severity and mortality, respectively. A higher proportion of CHB patients (30 of 109 (27.52%)) developed into severe status than non-CHB patients (17 of 327 (5.20%)). In addition to previously reported liver impairment markers, such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and total bilirubin, we identified several novel risk factors including elevated lactate dehydrogenase (⩾ 245 U/L, hazard ratio (HR) = 8.639, 95% confidence interval (CI) = 2.528-29.523; P < 0.001) and coagulation-related biomarker D-dimer (⩾ 0.5 µg/mL, HR = 4.321, 95% CI = 1.443-12.939; P = 0.009) and decreased albumin (< 35 g/L, HR = 0.131, 95% CI = 0.048-0.361; P < 0.001) and albumin/globulin ratio (< 1.5, HR = 0.123, 95% CI = 0.017-0.918; P = 0.041). In conclusion, COVID-19 patients with CHB were more likely to develop into severe illness and die. The risk factors that we identified may be helpful for early clinical surveillance of critical progression.
COVID-19 ; Cohort Studies ; Hepatitis B, Chronic/epidemiology* ; Humans ; Retrospective Studies ; Risk Factors