The neutrophil-to-lymphocyte ratio (NLR) reflects the systematic inflammatory status, and the aspartate aminotransferase-to-alanine aminotransferase ratio (AAR) is a biomarker of liver fibrosis and cirrhosis. These values can be conveniently obtained from routine blood tests; however, their combined clinical utility has not been extensively studied in patients with hepatocellular carcinoma (HCC) undergoing transarterial chemoembolization (TACE). This study aimed to investigate the prognostic value of NLR-AAR in patients with unresectable HCC undergoing TACE. Data for 760 patients with newly diagnosed HCC were retrospectively evaluated. The NLR-AAR was calculated as follows: patients in whom both the NLR and AAR were elevated according to the receiver operating characteristic (ROC) curve analysis were assigned a score of 2; patients showing an elevation in one or neither of these indicators were assigned a score of 1 or 0, respectively. Univariate and multivariate analyses were performed to identify the clinicopathological variables associated with overall survival. An ROC curve was also generated and the area under the curve (AUC) was calculated to evaluate the discriminatory ability of each index at 1, 3, and 5 years of follow-up, as well as overall. The NLR-AAR consistently had a greater AUC value at 1 year (0.669), 3 years (0.667), and 5 years (0.671) post-TACE compared with either NLR or AAR alone. The median survival times of patients with a NLR-AAR of 0, 1, and 2 were 31.0 (95% confidence interval [CI] 24.0–38.0), 15.0 (95% CI 11.2–18.8), and 5.0 (95% CI 4.0–5.9) months, respectively (P < .001). Multivariate analysis showed that the NLR-AAR, elevated total bilirubin level, and vascular invasion were independently associated with overall survival. NLR and AAR, when combined to produce an inflammation-based index and fibrosis score, is an independent marker of poor prognosis in patients with HCC receiving TACE.

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BackgroundLipopolysaccharide (LPS) is generally associated with sepsis, which causes multiple system injuries and systemic inflammatory response. Mitochondrial DNA (mtDNA) is of great importance in mediation of inflammation. The aim of this study was to investigate the protective profiles of Cyclosporine-A (CsA) in LPS-induced acute lung injury (ALI) and systemic inflammation by the inhibition of mtDNA and Toll-like receptor.Material/MethodsTwenty-four C57BL/6 mice were randomly assigned to 4 groups: a sham group (n=6); an experiment group (ALI induced through intraperitoneal injection of 10 mg/ml LPS, n=6); a low-CsA group (injection of 2.5 mg/kg of CsA 15 min after injection of LPS, n=6); and a high-CsA group (injection of 25 mg/kg of CsA 15 min after injection of LPS, n=6). Lung tissue, bronchoalveolar lavage fluid (BALF), and blood samples were collected at 6 h for further analyses.ResultsCsA treatment significantly attenuated LPS-induced lung histopathological changes (P<.05), myeloperoxidase (MPO) activity (P<.05) and lung wet-to-dry weight ratio (P<.05). In addition, injection of CsA decreased total cells (P<.05), neutrophils (P<.05), and total protein (P<.05) in BALF and inflammatory mediators, including tumor necrosis factor-α (TNF-α, P<.05) and interleukin-6 (IL-6, P<.05) in a dose-dependent manner. A significant decrease in mtDNA was observed in the CsA group when compared with controls (P<.05). Furthermore, we demonstrated that there was a significant difference between the high-CsA group and low-CsA group in lung injury score (P<.05), mtDNA (P<.05), and MPO (P<.05).ConclusionsThe evidence from this study suggests that CsA attenuated lung inflammation after LPS injection, and the protective mechanism may at least in part involve decreasing the release of inflammatory cytokines and mtDNA.

Primary intraventricular hemorrhage (PIVH) is a rare type of hemorrhagic stroke that is poorly understood. We aimed to explore the features of this disease in Chinese population via an institutional prospective study. Adult patients diagnosed with PIVH from January 2013 to January 2016 were enrolled in this study. Data, including clinical variables, radiological features, and yield of angiography, were collected to evaluate the clinical features, etiological causes, and prognostic factors of this disease. A total of 67 patients (73.6%) were diagnosed with PIVH which constituted 3.2% of contemporary patients with hemorrhagic stroke in our hospital. Thirty-four patients (52.3%) were diagnosed with vascular structural abnormality (VSA)-related PIVH, and the etiologies included Moyamoya disease (22.4%), arteriovenous malformations (17.9%), aneurysms (7.5%), bilateral internal carotid artery dissection (1.5%), and tumor (1.5%). Idiopathic PIVH was diagnosed in 31 patients (47.7%), including coagulopathy in 3 (4.5%). Patients with VSA-related PIVH were younger than idiopathic PIVH patients, with a mean age of 37.1 ± 14.6 years, and idiopathic PIVH patients were more commonly hypertensive. The overall mortality rate was 11.9%, and 21 patients (31.3%) had a poor outcome at the 6-month follow-up. Patients with younger age, lower Graeb score, and a known etiology of arteriovenous malformation might be associated with a favorable outcome. We recommended routine thin-slice computed tomography (CT) scan, computed tomographic angiography (CTA), and digital subtraction angiography (DSA) for patients with PIVH. The etiological causes and prognostic factors of PIVH in Chinese patients were associated with distinctive features.

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