Objective To develop a automatic infusion alarm device. Methods The automatic infusion alarm device was subtly reformed according to the principal of the character of the spring that the different gravity caused its length to be different. It consisted of two parts: springs and alarm circuit controller box. Results Clinical test was undertaken. Conclusions The automatic infusion alarm device is simply manufactured, reliable and cheap. It is valuable to advocate clinically.

AIM: To explore the characteristics of T cell activation and regulatory T cells derived from murine Peyer's patches through comparative studies on Peyer's patches, mesenteric lymph nodes and inguinal lymph nodes. METHODS: Signal cell suspendsions were prepared from murine mesenteric lymph nodes (MLNs), the Peyer's patches (PPs) and inguinal lymph nodes (ILNs), respectively. The percentage of cell subpopulations such as CD3+ T cells, CD3+CD4+ helper T cells and regulatory T cells (Treg, CD4+CD25+) were analyzed. Lymphocytes were activated by polyclonal stimulators such as concanavalin (Con A), phorbol 12, 13-dibutyrate (PDB) only, and PDB plus ionomycin (Ion). The expression of CD69 (the early marker of CD3+ T cell activation) was measured by FACS. RESULTS: A lower ratio of CD3+ T cells was seen in PPs than those in MLNs and ILNs. The ratios of CD3+ CD4+ T cells to CD3+ T cells in PPs, MLNs and ILNs were almost the same. A higher rate of Treg was seen in CD4+ T cells from the PPs as compared with those from MLNs and ILNs. A higher percentage of activated CD3+ T cells derived from the PPs cultured without polyclonal stimulators were detected as compared to MLNs and ILNs, while lower responsiveness of CD3+ T cells from the PPs stimulated by Con A was seen as compared with those from MLNs and ILNs. CONCLUSIONS: The lower rate of CD3+ T cells as well as higher rate of Treg in PPs was due to its desensitization. The higher rate of basic activated state in CD3+ T cells from the PPs indicated that the T cells were activated by enteric antigens in physiological conditions. The lower responsiveness of activation to some polyclonal stimulators probably reveals that the T cells are in a state of anergy. All the characteristics mentioned above contribute to prevent pathological inflammations and maintain tolerance to enteric antigens such as food proteins and commensal bacteria but simultaneously retain proper immune responses to pathogenic microbes.

AIM:To study the changes of mitochondria during apoptosis in Jurkat cells induced by arsenic oxide(As2O3).METHODS:By treated with 4?10-6 mol/L As2O3,apoptosis and necrosis of Jurkat cells were assessed by annexin V-FITC/PI double staining flowcytometry.Mitochondrial mass and its membrane potential(△?m)was measured by NAO/PI and DiOC6(3)/PI staining,respectively.Free radical formation was detected by DCFDA staining.RESULTS:After 48 h of As2O3 treatment,the rates of early apoptotic Jurkat cells in As2O3 and control groups were(18.98?1.40)% and(5.17?0.80)%,respectively(P

AIM: To study the effect of natural killer(NK)-cells on graft-versus-host disease(GVHD), graft rejection, engraftment and reconstituting of hematopoiesis in mouse allogeneic bone marrow transplantation. METHODS: Lethally irradiated BALB/c(H-2 d) mice were transplanted with C57/6j(H-2 b) bone marrow containing donor peripheral T cells and/or NK cells. Recipients CD 34 + cell counts and the expression of H-2K b+ cell were detected by flow cytometry, peripheral white blood cell(WBC) was detected by auto-cytometry, and the recipients survival rates, GVHD, engraftment and hematopoiesis recovery were then observed. RESULTS: In the group of transplanted with NK cells infusion, the incidence of GVHD was evidently lessened, the survival rates, WBC and CD 34 + cell counts and the expression of H-2K b+ cell were significantly high than that without NK cells infusion. CONCLUSION: In mouse allogeneic bone marrow transplantation, alloreactivity NK cells prevent GVHD, reduce graft rejection, and promote engraftment and reconstituting of hematopoiesis. [

AIM: To study mitochondrial mass and structural protein changes in dexamethasone (DEX)-mediated mouse thymocyte apoptosis process. METHODS: DEX-induced mouse thymocyte apoptosis model was established. Annexin V-FITC/PI double staining was used to identify apoptotic and necrotic cells by flowcytometry, JC-1 staining was adopted to test mitochondrial membrane potential (△?_m), and cellular structural protein changes were studied with CFDA-SE staining. RESULTS: By 1?10~(-6) mol/L DEX stimulation, the apoptotic rate was 51.25%?5.51% and had significantly difference from control group (12.03%?2.00%); the necrotic rate in DEX group was 30.25%?3.67% and also had significantly difference from control group (10.11%?1.11%, P

Objective To investigate the T cell cytotoxicity induced by recombinant adenovirus carrying HIV-1 vpr gene.Methods C8166 cells infected with rAd-vpr or negative control rAd-vector,were analyzed for cell cycle distribution and cell death by flow cytometry.The discrimination of living cells,apoptotic and necrotic cells were differentiated with Hoechst-PI double staining under the confocal microscopy.Changes of mitochondrial membrane potential(△ψm)were monitored by JC-1 staining method.Results Annexin V-PI and Hoechst-PI staining indicated the death effects of HIV-1 Vpr on C8166 cells.PI flow cytometric analysis showed that cell cycle arrested in G2 phase.C8166 cell△ψm collapse mediated by Vpr was detected by JC-1 fluorescent staining.Conclusion The ability of recombinant adenovirus carrying HIV-1 vpr gene to induce mitochondria dysfunction,cell cycle G2 phase arrest and cell death was confirmed in C8166 cells.

AIM: To investigate the relationship between the intracellular expression of Th1 and Th2 type cytokines in placental lymphocytes and the pregnancy outcomes in NOD/SCID mice. METHODS: The resorption rate of embryos (RR) was compared between BALB/c and NOD/SCID mice. In addition, the expression rates of Th1 type (TNF-? and IL-2) and Th2 type (IL-10) cytokines were detected intracellularlly in placental lymphocytes by four-color flow cytometry. RESULTS: Although multiple-immunodeficiency was confirmed in the NOD/SCID, no significant difference was observed in RR between BALB/c and NOD/SCID mice. At the same time, a dramatically elevated level of CD8+IL-10+/CD8+ cell percentage was found at the feto-maternal interface in NOD/SCID?NOD/SCID, as compared with BALB/c?BALB/c mice, while no significant difference was observed for TNF-? and IL-2 expression in CD4+ and CD8+ cell subsets isolated from these mice. CONCLUSION: The spontaneous elevation of CD8+IL-10+/CD8+ cell percentage at the feto-maternal interface may be related to the roughly normal fertility in NOD/SCID mice.

AIM: To study the effect of supernatants from cord blood mononuclear cells (CBMC) and peripheral blood mononuclear cells (PBMC) on infection of HIV-1 in vitro, and develop effectively soluble factors for human acquired immunodeficiency syndrome (AIDS) treatment. METHODS: Different supernatants from CBMC and PBMC activated by PHA for 5 hours and 12 hours were added to cell culture systems between HIV-1ⅢB/H9 cells labeled by calcein-AM and MT-2 cells, then to count the fusion under a reverted fluorescent microscope after 2 hours, respectively, and different soluble factors in supernatants were detected by Luminex 100~ TM . RESULTS: These supernatants from CBMC and PBMC activated by PHA for 5 hours and 12 hours inhibited the formation of fusion, and there is no difference between supernatants collected in CBMC and PBMC at same time point. However, the supernatants collected in 5 hours were more effective to inhibit the formation of fusion than those in 12 hours (P

AIM: To study the effect of ERK inhibition on the mitochondrial potential change in dexamethasone (DEX)-induced thymocyte apoptosis. METHODS: ERK activity was inhibited by PD098059 (PD), and 4 experimental groups were set: control, PD only, DEX and PD+DEX. Annexin V-FITC/PI double staining flowcytometry was used to detect apoptotic cells at time points of 3 h, 5 h and 7 h. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (△?m) at time points of 3 h, 7 h and 11 h. RESULTS: By stimulation with 1 ?mol/L DEX, the apoptotic rates of mouse thymocytes at 3 h, 5 h and 7 h were (19.63?0.35)%, (41.84?1.67)% and (67.00?2.43)%, respectively, and had significantly difference from control group (4.98?0.39)%, (6.08?0.33)% and (9.31?0.34)% (P0.05). At 3 h, 7 h and 11 h, the rates of low △?m cells were (21.23?1.43)%, (55.34?1.78)% and (70.88?2.87)%, significantly higher than that in control group (P0.05). CONCLUSION: DEX induces mouse thymocyte apoptosis at least partly through ERK pathway, and ERK inhibition has an important biological significance during this process.

AIM: To study the effects of ultraviolet (UV) on mitochondrial functions and apoptosis in HaCaT cells.METHODS: After irradiation by UV at low dose(UVA 2 J/cm~2,UVB 10 mJ/cm~2) and high dose(UVA 6 J/cm~2,UVB(30 mJ/cm~2),) HaCaT cells were cultured for 15 hours.Flow cytometry was used to measure mitochondrial membrane potential,mitochondrial mass and apoptotic rate.Annexin V-FITC/PI staining of apoptotic cells was analyzed by laser confocal microscopy.RESULTS: After UV irradiation,cell proportion with low mitochondrial membrane potential increased with irradiation doses.The proportion of control group,low dose group and high dose group were 7.94%?1.02%,25.87%?4.55% and 39.27%?5.32%,respectively.Cells proportion with low mitochondrial mass increased with irradiation doses.The proportion of control group,low dose group and high dose group were 15.19%?1.58%,40.36%?4.41% and 68.79%?5.46%,respectively.The hypodiploid peaks of DNA content analysis represented the apoptotic rate of HaCaT cells.The apoptotic rate of control group,low dose group and high dose group were 1.82%?0.51%,30.16%?5.47% and 58.49%?5.98%,respectively.To analyze the cells apoptosis by staining with annexin V-FITC and PI,the results were consistent with those of DNA content analysis.Cells in control group showed almost no positive staining cells.Single annexin V-FITC positive cells in low dose group and double positive cells in high dose group were predominant,respectively.CONCLUSION: UV irradiation induces HaCaT cell mitochondrial depolarization,as well as mitochondrial mass loss.These changes are related to cell apoptosis.