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Biomedical subjects

S Qian

Publications and source records attributed to S Qian.

At least 73 records · Page 4Linked to original sources
PubMed1998

Enhanced expression of HLA class I molecules in human hepatocellular carcinoma cells transduced with gamma-interferon gene.

OBJECTIVE: To investigate the expression of exogenous gamma-interferon gene in human hepatocellular carcinoma cells following retroviral transduction and the effect on the expression of surface HLA class I molecules. METHODS: Retroviral vector pLXSN was used to introduce human gamma-interferon (IFN-gamma) gene into four different human hepatocellular carcinoma cell lines (HCC). The G418-resistant colonies were isolated and cloned. The integration and expression of IFN-gamma gene were determined by PCR and RT-PCR analysis. A bioassay method was used to test the amount of IFN-gamma secreted by gene modified HCC cells. The expression of HLA class I molecules in HCC cells were analyzed by flow cytometry using indirect fluorescence staining. RESULTS: Four different HCC cell lines were successfully transduced with human IFN-gamma gene using retroviral vector. The integration and expression of IFN-gamma gene were shown only in the transduced cells. All four genetically modified HCC cells can secrete varied amount of IFN-gamma and demonstrate a significant up-regulation of surface HLA class I antigens. One specific HLA class I antigen, HLA-A2, has almost the same degree of increase as that of the total HLA class I molecules after transduction with IFN-gamma gene. CONCLUSIONS: Gene modification with IFN-gamma gene can significantly enhance the expression of HLA class I molecules in HCC cells and may increase its immunogenicity. These gene modified tumor vaccines can be helpful in tumor biotherapy.

Carcinoma, Hepatocellular↗
PubMed1998

[Studies on the antifertility effect of bis-trichloromethyl sulfone and its reversibility in male rats].

Bis-trichloromethyl sulfone(BTS) given p.o. to male Sprague-Dawley rats at a dose of 10 mg.kg-1.d-1, 6 days a week for 8 weeks(or 30 mg.kg-1.d-1 for 4 weeks), was found to lead to infertility. The density and, in particular, the motility of the spermatozoa in the cauda epididymidis were significantly lower than those of the controls (P < 0.001). The body weight, the sex behavior, the blood testosterone level and the histology of important organs were not significantly different from those of the control rats. Fertility started to recover 4 weeks after cessation of medication and was entirely recovered 2 more weeks later in rats having received BTS for 8 weeks at the dose of 30 mg.kg-1.d-1. In vitro study showed that BTS at a concentration of 0.31 mg.ml-1 would make rat spermatozoa immobile within 20 seconds. These results indicate that BTS has both antifertility effect in male rats and direct inhibitory effect on rat spermatozoa. We conclude that nontoxic doses of BTS can induce reversible infertility in male rats.

Animals↗
PubMed1998

[Studies on the selection of strains producing colominic acid and culture conditions].

One strain E. coli C-8, the highest yield of colominic acid, was selected from 40 E. coli strains in the medium in which glucose and ammonium sulfate were the only carbon and nitrogen resources. An optimum medium for the growth and colominic acid production of E. coli C-8 was studied. The optimum carbon resources for colominic acid production was sorbitol selected from 16 kinds of carbons, and its optimum concentration was 2.5%. The optimum inorganic and organic nitrogen resources for colominic acid production were ammonium sulfate (0.5%) and tryptone (1.5%), respectively. The optimum concentration of K2 HPO4 was 90 mmol/L. The optimum culture temperature was 37 degrees C, but no colominic acid was produced below 20 degrees C. The optimum pH range was 7.5-8.2. The strain growth in the optimum medium kept logarithmic phase in 40 h (maxim A = 22). The colominic acid secreted into medium was much lower before 20 h, but high biosynthetic rate of colominic acid was detected after 40 h, the colominic acid reached the highest level (1,200 micrograms/ml) at 65 h.

Culture Media↗
PubMed1998

[Studies on the chemical constituents of Citrus reticulata].

Four compounds were isolated from the pericarp of Citrus reticulata and three of them were identified as natsudaidai, nobiletin and 3,5,6,7,8,3',4'-heptamethoxyflavone. Natsudaidai and 3,5,6,7,8,3',4'-heptamethoxyflavone were obtained from this plant for the first time.

Citrus↗
PubMed1998

[Determination of trace Pb, Cu and Cd in environmental sample by slotted-tube atom-trapping atomic absorption spectrometry].

The optimal measuring conditions of slotted-tube atom-trapping atomic absorption spectrometry of Pb, Cu and Cd were examined in detail. The results show that the characteristic concentrations measured after trapping for 1min under definite conditions were 1.82 x 10(-3), 1.26 x 10(-3) and 6.7 x 10(-5) mg/L for Pb, Cu and Cd, respectively. Thus slotted tube atom-trapping AAS yields increase in sensitivety for Pb, Cu and Cd by 110, 39 and 150 fold, respectively, in comparison with the conventional FAAS. Trace elements Pb, Cu and Cd in earth surface water, tea and hair were determined by slotted tube atom-trapping. Satisfactory results were obtained.

English Abstract↗
PubMed1998

[Time resolved photoluminescence of PPV derivatives/C60 combination system].

We report the integrated and picosecond time-resolved photoluminescence (TRPL) measurement from two kinds of combination films: Poly(2-methoxy-5-(4-butenyloxy)phenylene vinylene) (MB-PPV)/C60 and Poly (2-methoxy-5-(4'-bromo-butoxy) phenylene vinylene) (MBB-PPV)/C60. Comparing with the pure MBB-PPV film, PL weakening and quenching of MBB-PPV were observed in the multilayer and mixed MBB-PPV/C60 films respectively. From TRPL spectra, the change of PL decay lifetime could be clearly seen, those could be attributed to the excitation transfer (ET) process between the excited MBB-PPV molecule and C60 molecule. Further measurements indicate that there is no noticeable dependence of the ET process on the temperature in the combination films.

English Abstract↗
PubMed1998

bcl-2/bax expression and p53 gene status in human bladder cancer: relationship to early recurrence with intravesical chemotherapy after resection.

PURPOSE: Studies have shown that the effects of chemotherapy depend on some biochemical mechanisms to induce apoptosis. Many genes are involved in apoptosis modulation, including p53, bcl-2 and bax. We determined the roles of p53 status and the ratio of bcl-2/bax proteins for predicting the recurrence of bladder superficial transitional cell carcinoma that had been treated with intravesical chemotherapy after resection. MATERIALS AND METHODS: We performed Western blot analysis to express bcl-2 and bax proteins, and PCR-SSCP to determine the alteration in the p53 gene in 43 patients with transitional cell carcinoma of the bladder treated with intravesical chemotherapy after tumor resection. RESULTS: The expression of bcl-2 or bax did not correlate with histological grade, clinical stage or relapse. In cases of relapse within 1 year after resection bcl-2/bax was greater than and less than 1 in 50 and 11%, respectively (p <0.01). Recurrence within 1 year after the initial operation was also more common in patients with than without p53 gene mutation (64 versus 22%, p <0.05). Furthermore, bcl-2/bax greater than and less than 1 was associated with p53 gene mutation in 38 and 11% of cases, respectively (p <0.05). CONCLUSIONS: A bcl-2/bax ratio greater than 1 and p53 gene mutation were closely associated with early relapse in patients with superficial transitional cell carcinoma of the bladder during intravesical chemotherapy after resection. This finding suggests that the relative levels of bcl-2 and bax, and p53 gene status may contribute to drug sensitivity and progression, and help to predict recurrence. Moreover, bcl-2/bax correlated with p53 status, which implies that cross talk among bcl-2, bax and p53 has a role in influencing drug induced apoptosis and regulating resistance to chemotherapy.

Carcinoma, Transitional Cell↗
PubMed1997

Blockade of the CD40-CD40 ligand pathway potentiates the capacity of donor-derived dendritic cell progenitors to induce long-term cardiac allograft survival.

BACKGROUND: Failure of costimulatory molecule-deficient donor dendritic cells (DCs) to induce indefinite allograft acceptance may be a result of the 'late" up-regulation of these molecules on the DCs after interaction with host T cells. Ligation of CD40 on antigen-presenting cells by its cognate ligand CD40L is thought to induce expression of CD80 (B7-1) and CD86 (B7-2). We examined the influence of anti-CD40L monoclonal antibody (mAb) on the capacity of donor-derived DC progenitors to induce long-term allograft survival. METHODS: High purity DC progenitors were grown from B10 (H2b) mouse bone marrow in granulocyte-macrophage colony-stimulating factor and transforming growth factor beta1 (TGFbeta1). Mature DC were propagated in granulocyte-macrophage colony-stimulating factor and interleukin-4. Their phenotype was characterized by flow cytometric analysis and their function by mixed leukocyte reactivity. Anti-donor cytotoxic T lymphocyte activity in grafts and spleens of vascularized heart allograft recipients was also assessed. RESULTS: The TGFbeta3-cultured cells were (1) DEC 205-positive, MHC class II-positive, CD80dim, CD86dim, and CD40dim, (2) poor stimulators of naive allogeneic T-cell proliferation, and (3) able to prolong significantly B10 cardiac allograft survival in C3H (H2k) recipients when given (2 x 10[6] i.v.) 7 days before organ transplantation (median survival time [MST] 26 days vs. 12 days in controls, and 5 days in interleukin-4 DC-treated animals). Their allostimulatory activity was further diminished by addition of anti-CD40L mAb at the start of the mixed leukocyte cultures. Anti-CD40L mAb alone (250 microg/mouse, i.p.; day -7) did not prolong cardiac graft survival (MST 12 days). In contrast, TGFbeta-cultured DCs + anti-CD40L mAb extended graft survival to a MST of 77 days, and inhibited substantially the anti-donor cytotoxic T lymphocyte activity of graft-infiltrating cells and host spleen cells assessed 8 days after transplant. CONCLUSIONS: The CD40-CD40L pathway appears important in regulation of allogeneic DC-T-cell functional interaction in vivo; its blockade increases markedly the potential of costimulatory molecule-deficient DCs of donor origin to induce long-lasting allograft survival.

Animals↗
PubMed1997

Augmentation of dendritic cells in murine organ donors by Flt3 ligand alters the balance between transplant tolerance and immunity.

Treatment of mice with the recently cloned hemopoietic growth factor Flt3 ligand (FL; 10 microg/day for 10 days) resulted in a large increase in myeloid lineage cells within the liver. While the number of nonparenchymal cells (NPC) harvested from liver increased about 9-fold, a 90-fold increase was observed in the proportion of CD11c+ dendritic cells (DC) recovered from NPC following overnight (18-h) culture in granulocyte-macrophage CSF. In contrast, only a 50% increase was seen in CD11c+ cells within heart single cell suspensions and in the number of DC obtained from hearts after 18-h culture. Liver NPC and heart cell suspensions freshly isolated from 10-day FL-treated animals exhibited increased T cell allostimulatory capacity compared with controls. Overnight cultured DC from livers of FL-treated animals expressed both higher levels of costimulatory molecules (CD80 and CD86) and allostimulatory activity than those from controls. Heart-derived DC also displayed enhanced stimulatory capacity. Pretreatment of organ donors with FL for either 5 or 10 days before transplant of organs to normal recipients abrogated the spontaneous liver allograft acceptance normally observed and resulted in delayed or acute graft rejection (median survival times, 40 and 12 days, respectively). Heart rejection was significantly accelerated by pretreatment of donors with FL for 5 or 10 days (median survival times, 8 and 7 days, respectively, vs 12 days in controls). These novel findings reveal the potent immunologic adjuvant properties of FL in vivo. They also show that substantial augmentation of the number of potential allostimulatory cells in donor organs before transplantation favors rejection rather than tolerance induction.

Animals↗
PubMed1997

Fas ligand (CD95L) and B7 expression on dendritic cells provide counter-regulatory signals for T cell survival and proliferation.

Activation of T cells is induced efficiently by dendritic cells (DC), but little is known about the role of DC in the regulation of T cell death. In this study, highly purified DC (DEC-205+, MHC class II(high), B7-1+ [CD80+], B7-2high [CD86high], CD40+, CD11c+) grown from normal mouse bone marrow in granulocyte-macrophage CSF + IL-4 were found to express FasL (CD95L) mRNA by reverse transcriptase PCR and to uniformly express FasL by both flow cytometric and immunocytochemical analyses. These cells, but not DC propagated from FasL-deficient (B6.gld) mice, induced dose-dependent increases in DNA fragmentation in Fas+ Jurkat T cells over 18 h coculture. Addition of mouse Fas-Fc fusion protein at the start of the cultures diminished this effect. Even at high relative concentrations, however, B7-2high DC induced only low levels of DNA fragmentation in Con A or alloactivated splenic T cells, as determined by radio- or spectrofluorometric assays and by in situ nick-end labeling. However, in the presence of CTLA4Ig, a molecule that blocks the B7-CD28 costimulatory pathway, DC that failed to stimulate in primary MLR induced markedly augmented levels of apoptosis in alloactivated T cells. CTLA4Ig treatment also increased the level of DNA fragmentation induced by FasL-deficient DC, indicating the existence of additional potential (Fas-independent) pathways of DC-induced T cell death. These findings suggest that the costimulatory (B7-CD28) and T cell death-inducing pathways may play important counter-regulatory roles in dictating the outcome of (allogeneic) DC-T cell interactions.

Animals↗
PubMed1997

Apoptosis within spontaneously accepted mouse liver allografts: evidence for deletion of cytotoxic T cells and implications for tolerance induction.

MHC-mismatched liver grafts are accepted spontaneously between many mouse strains. The underlying mechanism(s) is unclear. In the B10 (H2(b)) to C3H (H2(k)) strain combination used in this study, donor T cells within the liver were rapidly replaced within 2 to 4 days of transplantation with those of the recipient. Freshly isolated liver graft-infiltrating cells harvested on days 4 and 7 exhibited strong CTL responses against donor alloantigens. CTL activity was reduced substantially, however, by day 14, although levels of CTL precursors in the spleen and liver remained high. Examination of the liver allografts by in situ terminal deoxynucleotidyltransferase-catalyzed dUTP-digoxigenin nick end labeling on days 4, 7, and 14 after transplantation revealed prominent apoptotic cells dispersed throughout the nonparenchymal cell population. When acute liver allograft rejection was induced by administration of IL-2 from days 0 to 4 post-transplant (median survival time, 5 days), apoptotic activity (day 4) was reduced substantially, whereas CTL activity was enhanced. Nonparenchymal cells isolated from allografts of unmodified recipients 4, 7, and 14 days after transplantation exhibited significantly higher DNA fragmentation after 18-h culture than cells from liver isografts. Moreover, the level was 4 to 5 times higher than that of cells from IL-2-treated mice (on day 4). These observations suggest that T cell deletion, not regulation, may be responsible for spontaneous liver allograft acceptance. The molecular recognition events that cause apoptosis of infiltrating T cells and why this occurs within liver grafts, but not heart or skin grafts, remain to be elucidated.

Animals↗
PubMed1997

Interleukin-2 and interleukin-12 mediate distinct effector mechanisms of liver allograft rejection.

Interleukin-2 (IL-2), interleukin-12 (IL-12) or interleukin-4 (IL-4) were administered postoperatively to otherwise spontaneously accepting mouse liver allograft recipients (C57BL/10-->C3H) to test whether TH1 cytokines are critical mediators of rejection in this model. The induction of rejection at days 5 to 7 by exogenously administered IL-2 and IL-12, but not IL-4, suggests that mouse liver allograft rejection can be induced by TH1 cytokines; however, there appeared to be differences in the mechanism by which these cytokines induce liver rejection. IL-2 administration was accompanied by an increased intragraft infiltration of CD4+ and CD8+ cells and an up-regulation of natural killer (NK), lymphokine-activated killer (LAK), allospecific cytotoxic killer (CTL) activity and perforin mRNA when compared with media-treated controls. In contrast, exogenous IL-12 treatment was associated with a suppression of CTL, NK, and LAK activity compared with controls but an enhanced infiltration of F4/80+ macrophages as determined by immunohistochemistry. Determination of cytokine mRNA profiles by semi-quantitative reverse transcription polymerase chain reaction showed the up-regulation of interferon (IFN)-gamma, IL-4, IL-6, and IL-10 mRNA with IL-2 treatment when compared with media-treated controls. Interestingly, IL-2 mRNA was down-regulated in these animals, suggesting a negative feedback mechanism in IL-2 regulation. IL-12 treatment resulted in the up-regulation of IFN-gamma, IL-6, and IL-10 mRNA, but not IL-2 or IL-4 mRNA. Higher complement-directed cytotoxic antibody titers were seen in IL-12-treated recipients compared with controls, whereas IL-2 treatment showed no apparent differences in antibody titers compared with media treatment. These in vivo observations were mimicked in a mixed leukocyte reaction by supplementing the reaction with IL-2, IL-12, or media. These results suggest that rejection of mouse liver allografts may involve more than one distinct cellular immunological effector mechanism. One is mediated by IL-2 and appears to favor alloreactive CTL, whereas the other pathway is mediated by IL-12/IFN-gamma and involves macrophages and cytotoxic antibodies largely resembling a delayed-type hypersensitivity reaction.

Animals↗
PubMed1997

Functional expression of Drosophila para sodium channels. Modulation by the membrane protein TipE and toxin pharmacology.

The Drosophila para sodium channel alpha subunit was expressed in Xenopus oocytes alone and in combination with tipE, a putative Drosophila sodium channel accessory subunit. Coexpression of tipE with para results in elevated levels of sodium currents and accelerated current decay. Para/TipE sodium channels have biophysical and pharmacological properties similar to those of native channels. However, the pharmacology of these channels differs from that of vertebrate sodium channels: (a) toxin II from Anemonia sulcata, which slows inactivation, binds to Para and some mammalian sodium channels with similar affinity (Kd congruent with 10 nM), but this toxin causes a 100-fold greater decrease in the rate of inactivation of Para/TipE than of mammalian channels; (b) Para sodium channels are >10-fold more sensitive to block by tetrodotoxin; and (c) modification by the pyrethroid insecticide permethrin is >100-fold more potent for Para than for rat brain type IIA sodium channels. Our results suggest that the selective toxicity of pyrethroid insecticides is due at least in part to the greater affinity of pyrethroids for insect sodium channels than for mammalian sodium channels.

Animals↗
PubMed1997

[Video image analysis of AgNORs distribution in the testicular tumor].

For the purpose of exploring the relationship between AgNORs and the biological behaviour of the testicular tumor, the value of enumeration and image analysis of AgNORs has been investigated in 10 normal testicular tissues and 49 cases of testicular tumors. The major findings were: AgNORs value for number, area, mean area, large partical number (LPN) and roundness in normal, benign and malignant tumors had significant difference (P < 0.01). The former four parameters turned larger when the tumor became more malignant, and they were significantly higher in the good prognosis group than in the bad one. LPN was higher in stage III than in stage I and II (P < 0.05), no difference was found between stage I and II. Other parameters had no significant difference in each stage. These results indicate that AgNORs is helpfull in differentiating the benign and malignant testicular tumors, in determining the degree of malignancy and offering an additional prognostic indicator in testicular tumors. Partical numbers, area and LPN were more helpfull. It had no important value in differenciating each stage.

Endodermal Sinus Tumor↗
PubMed1997

[Clinical observation on Doula delivery].

OBJECTIVE: To improve the obstetricare quality during labour and delivery, our hospital carried out Doula delivery which is an appropriate technology in promoting natural delivery reported by Dr M Klaus, USA. METHODS: Mothers were accompanied by senior experienced midwife who afforded continuous physical, psychological and emotional support during the whole course of labour. From April to August 1996, 46 cases of primigravida were selected as study group. Another 336 primigravida given birth in the same period were taken as controls, who were accompanied by their family member during their active phase of labour. RESULTS: The results showed that the cesarean section rate was 6.5% in Doula group while 20.8% in the control group. The difference was significant (P < 0.05). The duration of labour and volume of postpartum bleeding both declined obviously in the study group (P < 0. 05). CONCLUSION: Doula delivery offered better quality of health care during labour and decreased cesarean section rate duration of labour and postpartum bleeding.

Apgar Score↗
PubMed1996

Systemic administration of cellular interleukin-10 can exacerbate cardiac allograft rejection in mice.

Cellular interleukin-10 (cIL-10) has been shown to inhibit cytokine production by T helper type 1 (Th1) cells by blocking antigen presenting cell function. This activity has suggested that IL-10 might be useful in the treatment of transplant rejection. Stimulatory effects of IL-10 however, have also been observed both on T and B cell differentiation. In this study, we examined the influence of recombinant (r) mouse (m) IL-10 on heterotopic vascularized heart allograft survival in the B10(H2b)-->C3H(H2k) strain combination that crosses both major histocompatibility complex (MHC) and non-MHC-histocompatibility antigen (non-MHC-HA) barriers. The influence of IL-10 was also examined in the B10.BR (H2k)--> C3H combination with disparity at only non-MHC-HA loci. Postoperative intraperitoneal administration of IL-10 (100 microg/d, days 0-6) significantly accelerated heart graft rejection both in the B10-->C3H (mean survival time [MST] 7.8+/-0.2 days; control MST 10.6+/-0.6 days; P<0.05) and the B10.BR-->C3H combination (MST 14.3+/-0.5 days; control MST 77.7+/-14.4 days). Ex vivo IL-10 perfusion of donor hearts for either 15 min or 2 hr did not affect subsequent graft survival. Immunologic monitoring of transplanted mice revealed that IL-10 treatment (100 microg/d, i.p., days 0-6) increased both the circulating complement-dependent cytotoxic (CDC) antibody titer and splenic anti-donor cytotoxic T lymphocyte (CTL) activity measured up to 3 weeks posttransplant. These findings indicate that post transplant systemic administration of cIL-10 can promote vascularized allograft rejection, and that this may reflect stimulation both of B and T cell alloimmune responses.

Animals↗
PubMed1996

Costimulatory molecule-deficient dendritic cell progenitors (MHC class II+, CD80dim, CD86-) prolong cardiac allograft survival in nonimmunosuppressed recipients.

We have shown previously that granulocyte-macrophage colony-stimulating factor-stimulated mouse bone marrow-derived MHC class II+ dendritic cell (DC) progenitors that are deficient in cell surface expression of the costimulatory molecules B7-1 (CD80) and B7-2 (CD86) can induce alloantigen-specific T-cell anergy in vitro. To test the in vivo relevance of these findings, 2 x 10(6) B10 (H2b) mouse bone marrow-derived DC progenitors (NLDC 145+, MHC class II+, B7-1dim, B7-2-/dim) that induced T-cell hyporesponsiveness in vitro were injected systemically into normal C3H (H2k) recipients. Seven days later, the mice received heterotopic heart transplants from B10 donors. No immunosuppressive treatment was given. Median graft survival time was prolonged significantly from 9.5 to 22 days. Median graft survival time was also increased, although to a lesser extent (16.5 days), in mice that received third-party (BALB/c; H2d) DC progenitors. Ex vivo analysis of host T-cell responses to donor and third-party alloantigens 7 days after the injection of DC progenitors (the time of heart transplant) revealed minimal anti-donor mixed leukocyte reaction and cytotoxic T lymphocyte reactivity. These responses were reduced substantially compared with those of spleen cells from animals pretreated with "mature" granulocyte-macrophage colony-stimulating factor + interleukin-4-stimulated DC (MHC class IIbright, B7-1+, B7-2bright), many of which rejected their heart grafts in an accelerated fashion. Among the injected donor MHC class II+ DC progenitors that migrated to recipient secondary lymphoid tissue were cells that appeared to have up-regulated cell surface B7-1 and B7-2 molecule expression. This observation may explain, at least in part, the temporary or unstable nature of the hyporesponsiveness induced by the DC progenitors in nonimmunosuppressed recipients.

Animals↗