No abstract

No abstract

A series of binuclear ruthenium vinyl complexes [RuCl(CO)(PMe 3 ) 3 ] 2 (µ-CHdCH-Ar-CHdCH) (Ar 6l), and C 6 H 3 CF 3 (6m)) have been prepared. The respective products have been characterized by elemental analyses, NMR spectrometry, and UV/vis spectrophotometry. The structures of 6h, 6i, and 6j have been established by X-ray crystallography. Electrochemical studies have revealed that intermetallic electron communication between the two Ru centers may be fine-tuned by modification of the bridging spacers, that is, by introducing one or two substituent groups on the 1,4-diethenylphenylene bridge. Electron-releasing substituents have been found to facilitate electron communication between the two metal centers.

Objectives To determine the prognostic significance of preoperative prognostic nutritional index (PNI) in patients with primary oral squamous cell carcinoma (OSCC) after ablative surgery. Materials and Methods A total of 333 patients from two tertiary referral centers were enrolled as training and validation cohorts. The PNI was calculated as 10× serum albumin (g/dL) + 0.005 × total lymphocyte number (per mm3), and its optimal cutoff value for patient stratification was identified by X‐tile software. Cox's proportional regression analyses and receiver operating characteristic (ROC) curves were employed to identify prognostic factors and their predictive performance. Results The optimal cutoff value of PNI was 47.4. Patients with low PNI had significantly shorter overall (OS) and disease‐free survival than those with high PNI. Moreover, multivariate regression analyses indicated that PNI was an independent prognostic factor for OS in the training (hazard ratio [HR], 2.267; 95% confidence interval [CI]:1.335–3.849; p = .002) and validation (HR, 2.247; 95% CI: 1.352–3.735; p = .002) cohorts. ROC analyses revealed similar or superior predictive performance of PNI as compared to other prognostic parameters. Conclusions Our findings reveal that decreased preoperative PNI significantly associates with worse prognosis for patients with OSCC, which serves as a novel prognostic biomarker for OSCC.

HOX genes are transcription factors that control morphogenesis, organogenesis and differentiation. Increasing evidence suggests that HOX genes play a role in hepatocellular carcinoma (HCC) progression; however few studies have defined the functional roles and mechanisms of action. In the present study, we used siRNA and forced-expression in multiple cell lines to define the role of HOXA7 in the regulation of proliferation of HCC in vitro and in vivo. Knockdown of endogenous HOXA7 decreased the proliferation of HepG2 and QGY-7703 cells. These changes were not associated with significant changes in cyclin D1 and CDK4. However, downregulation of HOXA7 significantly reduced cyclin E1 and CDK2 protein levels. Conversely, overexpression of HOXA7 in QSG-7701 cells stimulated proliferation and increased cyclin E1 and CDK2 protein levels. Our results confirmed that HOXA7 promoted cell proliferation, and these changes were mediated by cyclin E1/CDK2. These observations contribute to our understanding of the important roles of HOXA7 in HCC development and progression and HOXA7 could be a promising molecular target for the development of new diagnostic and therapeutic strategies for HCC.