We reexamine the branching ratios, CP -asymmetries, and other observables in a large number of B q → V V (q = u, d, s) decays in the perturbative QCD (PQCD) approach, where V denotes a light vector meson (ρ, K * , ω, φ). The essential difference between this work and the earlier similar works is of parametric origin and in the estimates of the power corrections related to the ratio) (m V and m B denote the masses of the vector and B meson, respectively). In particular, we use up-to-date distribution amplitudes for the final state mesons and keep the terms proportional to the ratio r 2 i in our calculations. Our updated calculations are in agreement with the experimental data, except for a limited number of decays which we discuss. We emphasize that the penguin annihilation and the hard-scattering emission contributions are essential to understand the polarization anomaly, such as in the B → φK * and B s → φφ decay modes. We also compare our results with those obtained in the QCD factorization (QCDF) approach and comment on the similarities and differences, which can be used to discriminate between these approaches in future experiments.

We make a systematic investigation on the two-body nonleptonic decays B c → J=Ψðη c Þ; M by employing the perturbative QCD approach based on k T factorization, where M is a light pseudoscalar or vector or a heavy charmed meson. We predict the branching ratios and direct CP asymmetries of these B c decays and also the transverse polarization fractions of B c → J=ΨV; J=ψD Ã ðsÞ decays. It is found that these decays have a large branching ratios of the order of 10 −4 − 10 −2 and could be measured by the future LHCb experiment. Our predictions for the ratios of branching fractions c →J=Ψπ þ Þ are in good agreement with the data. A large transverse polarization fraction which can reach 48% is predicted in B þ c → J=ΨD Ãþ s decay, which is consistent with the data. We find a possible direct CP violation in B c → J=ψD Ã decays, which are helpful to test the CP violating effects in B c decays.

Although a technically demanding and time-consuming procedure, LGD2 may be safe and effective, and offer some advantages over OGD2 for treatment of locally AGC.

The non-SMC condensin I complex subunit G (NCAPG) that organizes the coiling topology of individual chromatids, represents an overexpressed antigen in various types of cancer, and also contributes to restructuring chromatin into rod-shaped mitotic chromosomes and ensuring the segregation of sister chromatid during cell division. In this study, we investigated the association between NCAPG expression and the biological behavior of hepatocellular carcinoma (HCC) to further explore the potential of NCAPG as a therapeutic target. The expression of NCAPG was detected in human HCC cell lines and tumor samples. The effects of NCAPG on the cell cycle, apoptosis and metastasis were investigated by various assays. NCAPG was found to be overexpressed in HCC compared with the adjacent normal tissue (P<0.001), and high levels of NCAPG expression were found to significantly correlate with recurrence, the time of recurrence, metastasis, differentiation and TNM stage. Furthermore, an elevated expression of NCAPG was associated with a poor overall survival (P<0.05). In addition, in vitro experiments further confirmed the ex vivo data; i.e., the knockdown of NCAPG expression reduced HCC cell viability, but induced apoptosis and arrested the cells at the S phase of the cell cycle. The knockdown of NCAPG expression also inhibited tumor cell migration and the cell invasive capacity in vitro. At the protein level, the knockdown of NCAPG expression upregulated Bax, cleaved caspase-3 and E-cadherin, but downregulated cyclin A1, CDK2, Bcl-2, N-cadherin and HOXB9 expression, suggesting that the knockdown of NCAPG expression suppressed tumor cell epithelial-mesenchymal transition. On the whole, this study demonstrates that NCAPG plays an important role in the development and progression of HCC, and that it may be a novel therapeutic target for patients with HCC.

The targeting protein for Xenopus kinesin-like protein 2 (TPX2) is a putative oncogene in different human cancers. This study assessed TPX2 expression in gastric cancer tissue samples and then determined the effects of TPX2 knockdown on the regulation of gastric cancer cell malignant behaviors in vitro. Tissue samples from 115 gastric cancer patients were analyzed for TPX2 expression. The effects of TPX2 siRNA on gastric cancer cells were assessed in vitro, including cell viability, cell cycle distribution, apoptosis, migration, and invasion. The data showed that TPX2 was overexpressed in gastric cancer tissues compared to that in the adjacent normal epithelia. Moreover, TPX2 overexpression was associated with a poor overall survival and was an independent prognostic predictor of gastric cancer. In addition, the in vitro study further confirmed the ex vivo data, i.e., knockdown of TPX2 expression reduced gastric cancer cell viability but induced apoptosis and arrested cells at the G2/M phase of the cell cycle. Knockdown of TPX2 expression also inhibited the tumor cell migration and invasion capacity in vitro. At the gene level, knockdown of TPX2 expression upregulated the levels of cyclin B1, cdk4, p53, Bax, caspase-3, and E-cadherin, but downregulated the levels of cyclin D1, cdk2, N-cadherin, slug, matrix metalloprotease (MMP)-2, and MMP-9, suggesting that knockdown of TPX2 expression suppressed tumor cell epithelial-mesenchymal transition (EMT). This study demonstrated that detection of TPX2 overexpression could serve as a prognostic marker and therapeutic target for gastric cancer.