In order to provide substantial scientific information for exploring the mechanism of porcine liver injury caused by Taenia asiatica (T.asiatica),the expression of Cysteine aspartyl proteinase 3 (Caspase-3) from liver tissues of porkets that were experimentally infected by T.asiatica was examined.The T.asiatica adults were collected from the taeniasis patients in Duyun,Guizhou Province and identified biologically.The eggs were harvested from gravid proglottids and prepared by repeated washing and centrifugation.Twelve 20-days old Yorkshire and Seghers hybrid porkets were randomly divided into experimental and control groups as six pigs per group.The experimental group was orally administrated with 1.5 × 106 eggs per porket at day 0 post-infection.The porkets of both groups were sacrificed on the day 15 and day 75 post-infection (three pigs per time point) respectively,and liver samples were collected for further experiments.Quantitative real-time polymerase chain reaction method was employed to detect the mRNA levels of Caspase-3,and western blotting and immunohistochemistry methods were performed to detect the level of Caspase-3 expression in both groups.At the day 15 post-infection,the mRNA level and expression level of Caspase-3 of the experimental group were significantly decreased,comparison with the control group (P =0.011,P=0.008 and P=0.004 respectively).It was positive with Caspase-3 when yellow or brown signal appeared in the cytoplasm of liver cells by immunohistochemistry.However,at the day 75 post-infection,the mRNA level and expression level of Caspase-3 of the experimental group were dramatically similar to the control group.Furthermore,in the experimental group,the mRNA level and expression level of Caspase-3 were significantly increased at day 75 post-infection than day 15 post-infection (P--0.018,P=0.003 and P=0.002 respectively).These results suggested that Caspase-3 might be involved into the regulation of the damage of porcine liver induced by T.asiatica challenge at the early infection stage and have on effect to the hepatic injury because of the dramatic recovery of Caspase-3 at the consequent infection stage.

Purpose To investigate the effect of silencing of CD98hc on proliferation,migration and invasion of MDA-MB-231 breast cancer cells.Methods RNA interfere technology was used to silence CD98hc in MDA-MB-231 cells.MDA-MB-231 cells (CD98hc-shRNA) with stable low expression of CD98hc and Vector control was obtained.Western blot and qRT-PCR were used to verify the down-regulation of CD98hc.MTT assay was used to test the cell proliferation.Transwell migration and invasion experiment were used to assay cell migration and invasion.Results The expression levels of CD98hc was down-regulated by CD98hc-shRNA in the MDA-MB-231 breast cancer cells.Compared to that of blank cells (0.706 ± 0.013),vector control (0.724 ± 0.018),the cell proliferation potency of CD98hc-shRNA cells (0.580-0.035) was significantly inhibited (P ＜ 0.05),and the cell migration and invasion potency also were inhibited (P ＜ 0.05),there is on significant different between blank cells and vector control (P ＜ 0.05).Conclusion CD98hc might be involved in the regulation of breast cancer cell biological behaviors.

Objective: To investigate the clinicopathological features, special morphologic variants and potential diagnostic traps of classical follicular dendritic cell sarcoma (FDCS). Methods: A total of 25 cases of classical FDCS diagnosed in the First Hospital Affiliated to Army Medical University from 2006 to 2018 were examined by hematoxylin-eosin staining, immunohistochemistry and in situ hybridization for Epstein-Barr virus-encoded mRNA (EBER). Meanwhile, the types and characteristics of the special variants of FDCS were summarized along with those reported in the literature. Results: The age of patients ranged from 23 to 77 years (mean 52 years), the male to female ratio was 1.5, and the maximum diameter of tumor was 1.5 to 20 cm (mean 7.4 cm). Twelve cases (48%) were misdiagnosed at the initial evaluation. Follow-up information was available for 17 patients, and the follow-up time was 5 to 96 months. The propotion of patients having recurrence, metastasis and mortality was 3/17, 5/17 and 2/17, respectively. Microscopically, besides the typical morphology, 10 cases of FDCS showed special histomorphologies and/or structures, including those mimicking lymphoepithelioma-like carcinoma, desmoplastic infiltrating carcinoma, classical Hodgkin′s lymphoma (CHL), anaplastic large cell lymphoma (ALCL) and hemangiopericytoma. These morphologic variants were potential diagnostic pitfalls and warranted attention. Immunohistochemistry showed that more than two markers of follicular dendritic cells (such as CD21, CD23, CD35, etc.) were expressed in cases showing typical morphology and the special variants. All 25 cases were all negative for EBER by in situ hybridization. Conclusions Classical FDCS is rare, besides the typical morphologic features, there are many special variants. In particular, these may be confused with lymphoepithelioma-like carcinoma in the nasopharynx, CHL or ALCL in the mediastinum/lymph node. Awareness of these variants is essential for accurate diagnosis.