Livin is a new member of the inhibitor of apoptosis proteins family of proteins that interacts with downstream caspases, such as caspase-3, caspase-7, and caspase-9, however, its role in human ampullary carcinoma has not been clearly defined. Immunohistochemistry was used to evaluate tissue samples from patients with ampullary carcinomas (n=71) using antibodies against livin, Ki-67 (a proliferation marker), and caspase-3. Livin was detected in 33/71 cases (in the cytoplasm of all and in the nucleus of only 2 cases). High livin expression correlated with cell differentiation, tumor-node-metastasis stage, and lymph node metastasis (P=0.001, P<0.001, and P=0.028, respectively). Caspase-3 and Ki-67 expression were significantly associated with differentiation (P<0.001, P=0.008, respectively). There was a significant negative correlation between livin and caspase-3 (r=-0.575, P<0.001), and a positive correlation between livin and Ki-67 (r=0.308, P=0.009). Survival of patients with high livin expression was shorter compared with that of patients with low livin expression (P=0.001). Expression of caspase-3 was not associated with overall survival in this cohort (P=0.335). Livin expression was an independent prognostic factor (hazard ratio 2.693, P=0.017), as was lymph node metastasis (hazard ratio 4.959; P<0.001). In this study livin expression significantly correlated with the proliferation marker Ki-67, but was negatively correlated with caspase-3 expression. These data suggest that livin may be a valuable prognostic factor for human ampullary carcinoma.

Chronic infection with hepatitis B virus (HBV) is one of most important risk factors for the development of hepatocellular carcinoma (HCC). Several long non-coding RNAs (lncRNAs) have been shown to be involved in the etiology of HBV-related HCC. AX800134 is one recently identified lncRNA associated with HCC. In this study, we validated the upregulated expression of AX800134 in HBV-positive HCC compared with HBV-negative HCC. Furthermore, we found that HBV X protein (HBx) directly triggered AX800134 expression in human hepatoma HepG2 cells. Pro-inflammatory cytokine TNFα also induced AX800134 upregulation in HBx-expressing HepG2 cells, which could be reversed by reactive oxygen species (ROS) scavenger pyrrolidine dithiocarbamate (PDTC). Additionally, silencing AX800134 with siRNA interference remarkably inhibited the growth and invasion of HBx-expressing HepG2 cells. AX800134 antagonism also enhanced spontaneous apoptosis of HepG2 cells under serum deprivation condition. Therefore, our results indicate that highly expressed AX800134 acts as an oncogenic factor in HCC, and its upregulation is related with the viral product HBx and chronic inflammation.

Circularly polarized luminescence with high dissymmetry factors can be realized by introducing fluorescent materials into intrinsic chiral nematic mesostructure of cellulose nanocrystals. In particular, semiconductor quantum nanocrystals with optical activity...

BackgroundHistone deacetylase inhibitors are promising drugs for the future application in cancer therapy. Trichostatin A (TSA), a histone deacetylase inhibitor, exhibits effective antitumor effects in various cancers. However, the effects and underlying mechanisms of TSA on multiple myeloma (MM) are not fully investigated.MethodsIn the present study, RPMI8226 and MM.1S cells treated with TSA were used for cell proliferation, cell cycle, and survival examinations, then the localization and post transcriptional modification of GLI1 protein as well as the target gene P21 were analyzed using immunofluorescence, immunoprecipitation, western blots and qPCR, respectively.ResultsTSA exerted a time and dose-dependent cytotoxicity on MM cell lines, and suppressed the proliferation of MM cells and induced an upregulation of p21 protein accompanied by a decreased expression of cyclin D1. TSA treatment led to a downregulation of GLI1, and the nuclear accumulation of GLI1 was also inhibited. As a result of hedgehog inhibition, the expression of MYC and SURVIVIN was greatly weakened after TSA treatment. Furthermore, TSA accelerated GLI1 degradation in a proteasome-dependent manner. Additionally, p21 induction also contributed to GLI1 downregulation via reducing the transcription of GLI in mRNA level. Rescue experiments verified that exogenous expression of GLI1 alleviated MM cell apoptosis induced by TSA.ConclusionThese results indicated that TSA represses MM cell growth and induces cell apoptosis. The inhibition of hedgehog signaling is an important mechanism accounting for the cytotoxic effects of TSA.

Objective: To investigate the clinical efficacy of zoledronic acid in the treatment of senile osteoporosis. Methods: One hundred and six cases of senile osteoporosis who visited to our hospital from August 2017 to December 2018 for treatment were selected and randomly divided into a control group and an observation group. The control group was treated with conventional therapy, while the observation group was treated with zoledronic acid in addition to the treatment of the control group. Bone mineral density, pain degree, therapeutic effect and adverse reactions of the two groups were compared. Results: The total effective rate of the observation group was 96.67%, higher than 80.00% of the control group (P<0.05); the bone mineral density of lumbar vertebrae, femoral neck and Ward’ area in the two groups increased after 6 months of treatment, and the bone mineral density of the observation group increased more than that of the control group (P<0.05); the pain degree of the observation group was lower than that of the control group after 6 months of treatment, and the difference was significant (P<0.05). There was no significant difference in the occurrence of adverse reactions between the two groups (P>0.05). Conclusion: Zoledronic acid is helpful to alleviate clinical symptoms, reduce the degree of bone pain, and promote the increase of bone mass, and has high safety in the treatment of senile osteoporosis, which is worth promotion. doi: https://doi.org/10.12669/pjms.36.7.1964 How to cite this:Kong L, Zuo K, Ma L. Clinical effect of Zoledronic Acid in the treatment of Senile Osteoporosis. Pak J Med Sci. 2020;36(7):1703-1707.   doi: https://doi.org/10.12669/pjms.36.7.1964 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.