Objective To evaluate the effects of Burch-Schneider(BS) acetabular reinforcement ring applied in primary or revision total hip arthroplasties in 9 patients with combined or cavitary acetabular bone defects. Methods A retrospective follow up that averaged 3.8 years was performed with a special scoring system comprising the patients symptoms, signs and function. Results The excellent and good function were achieved in 89% of all cases. Conclusion 1)BS reinforcement ring could be effectively and reliably applied in primary or revision total hip arthroplasty or in patients with severe acetabular bone defects. 2)BS reinforcement ring shows the biological fixation feature, so as to provide good foundation for long-term satisfactory function of hip. 3)The lower ear of BS ring need not to be fixed to ischium with screws as usual, but be inserted in obturator foramen above transverse ligament, thus imparting some elastic resilience to it. 4)The upper ear should be folded through such a curve that its curvature was in compliance with that of ilium, which would be better performed in one session. 5)The appropriate amount of 0.8 cm?0.8 cm?0.8 cm morcellized allografting bone was used to snugly fill the space, which would be conducive to desirable incorporation between prosthesis and bone, and the authors propose that the patients should be allowed weight-bearing earlier.

In order to investigate the potential anti-leukemic effect of cyclosporin A(CsA), MTT method and cell viability assay in vitro were carried out in this study to observe the effect of CsA on the proliferation and cell viability of various leukemic cell lines, such as T-cell Jurkat, Molt-4, CCRF-CEM, Nalm-6, K562 and multi-drug-resistant leukemic cell line K562/AO2. The results fully showed that CsA did possess the same cytotoxic action on all the leukemic cell lines, particularly including multi-drug-resistant leukemic cell line,and could then inhibit the proliferation and cell viability of these leukemic cells, thereby indicating that CsA might be applied as one of the new, safe and effective anti-leukemic agents when used with clinically adoptable dosage in leukemias.

Objective: To investigate the mechanism of vascular endothelial growth factor(VEGF) inducing tolerogenic dendritic cells(DCs) in oral squamous cell carcinoma (OSCC). Methods: The DCs were divided into four groups: Control group (DC), VEGF group (VEGF added into DC), Co-culture group (DC co-cultured with SCC7) and Anti-VEGF group (anti-VEGF antibody added into DC co-cultured with SCC7). Flow cytometry (FCM) was used to detect DC surface markers. To detect the effect of DC on proliferation activity of T lymphocyte, the experiment included five groups: Nc group (T lymphocyte), Control group (T lymphocyte added into DC), VEGF group (T lymphocyte + DC + VEGF), Co-culture group (T lymphocyte + DC + supernatant of SCC7) and Anti-VEGF group (T lymphocyte + DC + supernatant of SCC7 + anti-VEGF antibody). Subsequently, the mixed lymphocyte reaction(MLR) was conducted. The expression levels of indole-2, 3-doxygenase(IDO)and programmed cell death 1 ligand 1(PD-L1)in DC were detected by western blot, real time PCR and FCM respectively. For the cytotoxic lymphocyte (CTL) assay, SCC7 cells and CTLs were mixed and CTL-mediated SCC7 cells cytotoxicity was tested. The experiment included four groups: Control group (T lymphocyte + DC), IDO inhibition group (T lymphocyte + DC + IDO inhibitor), Anti-PD-L1 antibody group (T lymphocyte + DC + anti-PD-L1 antibody) and Combination group (T lymphocyte + DC + IDO inhibitor + anti-PD-L1 antibody). The SCC7 tumor-bearing mice treated with IDO inhibitor and the anti-PD-L1 antibody were sacrificed and the tumor inhibition rate and the spleen index were determined. Results: Compared with Control group, exogenous VEGF or SCC7 co-culture inhibited the relative number of DC expressing CD11C, CD80, CD86, CD40 and MHC Ⅱ. The positive DCs were increased in the Anti-VEGF group compared with VEGF or Co-culture group. In VEGF or Co-culture group, the number of T cells stimulated by SCC7-pulsed DCs was decreased compared with Control group. However, the ability of Anti-VEGF group to induce T cell proliferation was significantly increased compared with VEGF or Co-culture group. Significantly increased expression of IDO and PD-L1 were observed in VEGF and Co-culture group. However, this was partially reversed by addition of anti-VEGF antibody into the co-culture system. Compared with Control group, the expressions of CD11C and CD86 in DC in both the IDO inhibition group and Anti-PD-L1 antibody group were increased, and were significantly higher in the Combination group compared with the single drug groups. The similar results were exhibited in MLR and CTL assay. In vivo, the results revealed that the tumors obtained from the mice in three experimental groups were smaller than those in the control group. Furthermore, the tumor volume of the Combination group was the smallest. The spleen index of each group was calculated and the results showed the spleen index of the three experimental groups was significantly higher than that of Control group. Conclusion VEGF in OSCC micro-environment inhibits the maturation and function of DC that are transformed into tolerogenic DC by high expression of IDO and PD-L1.