BackgroundThe prognostic nutritional index (PNI) is calculated based on the serum albumin concentration and the total lymphocyte count. The aim of this study was to investigate the prognostic ability of the PNI for postoperative complications after liver resection to treat hepatocellular carcinoma (HCC) within the Milan criteria.ResultsPostoperative complications were observed in 166 (44.6%) patients. The optimal cutoff value of the PNI was set at 45.6 for postoperative complications. Patients in the PNI-low (PNI < 45.6) group were more likely to have postoperative complications, more blood loss, a longer surgery time and a longer hospital stay than patients in the PNI-high group (PNI > 45.6). Our regression analysis demonstrated that the preoperative PNI and albumin-bilirubin (ALBI) score were significantly associated with postoperative complications (Pearson correlation coefficient, -0.865, p < 0.001). The multivariate analysis revealed that the PNI was an independent predictor of postoperative complications.Materials and MethodsThree-hundred and seventy-two patients who underwent partial hepatectomy for HCC from 2003 to 2014 were identified. The cutoff value of the PNI was determined by a receiver operating characteristic (ROC) curve analysis. Univariate and multivariate analyses were performed to identify clinicopathological features associated with postoperative complications.ConclusionThe PNI may be a significant prognostic factor for evaluating short-term outcomes of patients with HCC after partial hepatectomy.
Nonalcoholic fatty liver disease (NAFLD) has become a major risk factor for hepatocellular carcinoma (HCC) worldwide. However, the underlying mechanism remains insufficiently elucidated. The expression of Collagen I, an important component of extracellular matrix (ECM), was increased during the progression from simple steatosis to NASH. The purpose of this study was to investigate the role of Collagen I in NAFLD-related HCC. To study this, the decellularized liver matrix, which preserves the pathological changes of ECM, was prepared from the human fatty liver (FLM) and human normal liver (NLM). HepG2 cells cultured in FLM had a higher proliferation rate than those in NLM. SMMC-7721 and HepG2 cells cultured on Collagen I-coated plates grew faster than those on either Collagen IV- or fibronectin-coated plates. This effect was dose-dependent and associated with elevated integrin β1 expression and activation of downstream phospho-FAK. Knocking down the expression of integrin β1 significantly decreased the proliferation of HCC cells. Additionally, an orthotopic tumor model was established in NAFLD mice at different stages. The over-expressed Collagen I in the mice liver increased the expression of integrin β1 and downstream phospho-FAK, resulting in the proliferation of HCC cells. This proliferation could be inhibited by blocking the integrin β1/FAK pathway. In summary, our study demonstrated that Collagen I promoted HCC cell proliferation by regulating the integrin β1/FAK pathway. Decellularized liver matrix can be used as a platform to three-dimensionally culture HCC cells and reproduce the impact of changed ECM on the progression of NAFLD-related HCC.
Parainfluenza viruses are significant respiratory-tract pathogens that are notorious for infecting children. However, there are no clinical drugs to control the infection caused by these viruses. Sendai virus (SeV) belongs to the family Paramyxoviridae and causes fatal pneumonia in mice, its natural host. Baicalein is a flavonoid derived from the root of Scutellaria baicalensis, which is a traditional Chinese medicine that has been used for hundreds of years and has demonstrated a variety of biological activities. Our findings reveal that oral administration of baicalein to mice infected with Sendai virus results in a significant reduction in virus titers in the lungs and protection from death. The in vivo inhibitory effects of baicalein on Sendai virus are determined by baicalin in the serum. The mean IC(50) of baicalin was 0.71 μg/ml in an HA inhibition assay and 3.22 μg/ml in an NA inhibition assay. The mean IC(50) of baicalin in a CPE assay was measured to be 0.70 μg/ml, and significant inhibition was observed in a plaque assay at a concentration of 1.6 μg/ml baicalin in overlay medium, which suggests that baicalein is a potential anti-parainfluenzaviral agent in vivo.
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