Intracerebral hemorrhage (ICH) is associated with the highest mortality and morbidity despite only constituting approximately 10–15% of all strokes. Complex underlying mechanisms consisting of cytotoxic, excitotoxic, and inflammatory effects of intraparenchymal blood are responsible for its highly damaging effects. Oxidative stress (OS) also plays an important role in brain injury after ICH but attracts less attention than other factors. Increasing evidence has demonstrated that the metabolite axis of hemoglobin-heme-iron is the key contributor to oxidative brain damage after ICH, although other factors, such as neuroinflammation and prooxidases, are involved. This review will discuss the sources, possible molecular mechanisms, and potential therapeutic targets of OS in ICH.

NLR and PLR as novel inflammatory biomarkers are independent predictors of DCI development and functional outcome after acute aSAH. When combined together, they may help to identify high-risk patients more powerfully.

Recently, hepatitis B core-related antigen (HBcrAg) has been suggested as an additional marker of hepatitis B virus (HBV) infection. This study aimed to investigate whether serum quantitative HBcrAg (qHBcrAg) was a satisfactory surrogate marker of intrahepatic covalently closed circular DNA (cccDNA). A total of 139 patients with liver biopsy were enrolled, consisting of 59 patients in immune tolerance (IT) phase, 52 patients in immune clearance (IC) phase, 18 patients in low-replication (LR) phase, and 10 patients in reactivation phase. All patients in IC phase have received entecavir (ETV) therapy, and 32 of them undergone a second liver biopsy at 24 months. Among those patients, qHBcrAg was strongly correlated with intrahepatic cccDNA, which is superior to that of qHBsAg and HBV DNA. And similar findings were also observed in patients in IT, IC, LR and reactivation phases. Among the 32 ETV-treated patients with a second liver biopsy in IC phase, the decline of intrahepatic cccDNA was accompanied by changes in both qHBcrAg and qHBsAg. However, as compared to qHBsAg, the change of qHBcrAg was more strongly associated with intrahepatic cccDNA-decline. In summary, serum qHBcrAg should be a satisfactory surrogate of intrahepatic HBV cccDNA in CHB patients.

Elevated levels of AWC, ANC and NLR were independently related to poor 90-day outcome after ICH. NLR may be a novel inflammatory biomarker following ICH.

BackgroundAs the fifth most common cancer worldwide, Hepatocellular carcinoma (HCC) is also the third most common cause of cancer-related death in China. Several lncRNAs have been demonstrated to be associated with occurrence and prognosis of HCC. However, identification of prognostic lncRNA signature for HCC with expression profiling data has not been conducted yet.MethodsWith the reuse of public available TCGA data, expression profiles of lncRNA for 371 patients with HCC were obtained and analyzed to find the independent prognostic lncRNA. Based on the expression of lncRNA, we developed a risk score model, which was evaluated by survival analysis and ROC (receiver operating characteristic) curve. Enrichment analysis was performed to predict the possible role of the identified lncRNA in HCC prognosis.ResultsFour lncRNAs (RP11-322E11.5, RP11-150O12.3, AC093609.1, CTC-297N7.9) were found to be significantly and independently associated with survival of HCC patients. We used these four lncRNAs to construct a risk score model, which exhibited a strong ability to distinguish patients with significantly different prognosis (HR = 2.718, 95% CI [2.103–3.514], p = 2.32e−14). Similar results were observed in the subsequent stratification survival analysis for HBV infection status and pathological stage. The ROC curve also implied our risk score as a good indicator for 5-year survival prediction. Furthermore, enrichment analysis revealed that the four signature lncRNAs may be involved in multiple pathways related to tumorigenesis and prognosis.DiscussionOur study recognized four lncRNAs to be significantly associated with prognosis of liver cancer, and could provide novel insights into the potential mechanisms of HCC progression. Additionally, CTC-297N7.9 may influence the downstream TMEM220 gene expression through cis-regualtion. Nevertheless, further well-designed experimental studies are needed to validate our findings.