Preparation of Core-Shell Silver Nanoparticles@Mesoporous Silica Nanospheres with Catalytic Activities.

Core-shell silver nanoparticles@mesoporous silica spherical nanoparticles (Ag NPs@MSNs) were prepared by a two-step method. First, Ag NPs were synthesized by chemical reduction using silver nitrate (AgNO₃) as the precursor, cetyl trimethyl ammonium bromide (CTAB) as the stabilizer, and sodium borohydride (NaBH₄) as the reductant. Then, MSNs were obtained by employing CTABstabilized Ag NPs as the template and hydrolyzing tetraethoxysilane (TEOS) precursor in the presence of the alkaline precipitant, triethanolamine (TEOA).

Fentanyl inhibits the invasion and migration of colorectal cancer cells via inhibiting the negative regulation of Ets-1 on BANCR.

Background: Recent studies have shown the potential anti-tumor effect of fentanyl on colorectal cancer (CRC). However, its underling mechanism is still unclear. Since studies indicates the abnormal expression of transcription factor Ets-1 and BRAF-activated lncRNA (BANCR) in CRC progress, the relationship between Ets-1 and BANCR was investigated here to illustrate the fentanyl-induced mechanism on CRC in vitro.

Study on blocking the leukemia immune escape after BMT by Fas-Fas ligand pathway.

Background: To investigate if bone marrow transplantation (BMT) with bone marrow mononuclear cells (BMMCs) transducted with murine soluble Fas gene (sFas) using adenovirus vector could block the immune escape of leukemia cells eliminate the residual leukemia cells and reduce their relapse.

Methods: The recombinant adenovirus vector with murine sFas, adsFas, and the control vector adEGFP were constructed using homologous recombination between two plasmids in Escherichia coli. BMT was carried out after the BMMCs were infected with Adenoviruses.

[Study on blocking the tumor immune escape by Fas ligand pathway].

The expression of Fas ligand (FasL) on the membrane of many kinds of leukemia or solid tumor cells played an important role in the immune escape of tumor cells. This study was aimed to know if the soluble Fas (sFas), expressed by adenovirus, could block the immune escape of tumor cells by FasL pathway. The two recombinant adenoviral vectors, AdsFas with murine soluble Fas gene and AdEGFP with enhanced GFP protein gene, were constructed by homologous recombination between two plasmids in Escherichia coli with the AdEasy adenovirus vector system.

[Experimental study on blocking immune escape of leukemia cells in the recipient after bone marrow transplantation].

Objective: To investigate whether murine soluble Fas gene transfected marrow graft could block the immune escape of leukemia cells, so as to eliminate the residual leukemia cells and reduce relapse after bone marrow transplantation (BMT).

Methods: The murine leukemia/lymphoma models were established by inoculating female C57BL/6 mice (H-2b) with 10(5) EL4 cells/mouse through caudal vein. Donors of BM grafts were C57BL/6 male mice.

[FasL-cDNA transfected into mouse bone marrow cells ex vivo to prevent graft versus host disease].

To explore the new approach to prevent graft versus host disease (GVHD) by purging ex vivo T lymphocytes of bone marrow graft through Fas-FasL way, FasL-cDNA was transfected into BALB/c mouse bon e marrow cells by liposome ex vivo. The transfected cells were cultured together with BAC (BALB/c x C57BL/6) mouse bone marrow graft. The mixing bone marrow graft was infused into BALB/c mouse recipients after 60Co-gamma irradiation.

[Retroviral vector-mediated in vitro expression of human soluble fas].

Leukemic cells from patients expressed high level FasL cause apoptosis of autologous activated T cells via the Fas/FasL pathway. To investigate the role of soluble Fas (sFas) in reversing this process, a retroviral-mediated expression vector pLXIN-sFas was established. A retroviral-mediated expression system of human sFas was established in vitro and the biological activity of the expression product sFas was observed.

[Study on expression and function of fas ligand in human myeloid leukemia cells].

To determine whether the Fas receptor-Fas ligand (FasR-FasL) system, which triggers apoptosis in sensitive cells, is an important mechanism of cytotoxicity in myeloid leukemia. FasL expression was investigated in myeloid leukemia cells and its upregulation by a combination of IL-2 and INF-gamma, +/- as well as its function of inducing Jurkat cells to apoptosis mainly by flow cytometry (FCM). Results showed that leukemia cells expressed more FasL (3.