PubMed Health⌕ Search

Biomedical subjects

Yu Jiang

Publications and source records attributed to Yu Jiang.

51 records · Page 3Linked to original sources

[The mechanism of anti-tumor immune response against mouse melanoma to xenogeneic vaccination].

OBJECTIVE: To investigate the immunological mechanism for inhibiting melanoma growth in mouse by vaccination with xenogeneic melanocytes. METHODS: Xenogeneic vaccine was prepared from pig eye melanocytes. By means of indirect ELISA the antibodies against pig melanocytes and B16 melanoma cells in immunized mice sera were detected and the immunoglobulin subclass were analyzed. Then after purification, the immunoglobulins were used for the inhibition of cell proliferation in vitro. Analyses of cross-reactive antigen in both pig melanocytes and B16 melanoma cells were performed by Western blot. Xenogeneic vaccine was used before B16 melanoma challenge in C57 BL/c mice and then the growth of tumor was monitored. Meanwhile, other mice immunized with xenogeneic vaccine were depleted of NK cells or CD4+ or CD8+ T lymphocytes. RESULTS: The antibodies against pig melanocytes and B16 melanoma cells in mice sera were not detected by indirect ELISA until 2 weeks after first xenogeneic vaccination, and after the first finding, the antibody titers increased with the time of immunization. The anti-tumor activity and production of autoantibodies, conspicuously those of the elevated IgG, could be abrogated by the depletion of CD4+ T lymphocytes. The cross-reactive antigen with 180 kda protein in both pig melanocytes and B16 melanoma cells was confirmed. Xenogeneic vaccination resulted in inhibition of tumor growth in 90% of the immunized mice. The protective immune response elicited in this fashion was dispelled in the mice depleted of CD4+ T lymphocytes. However this response was found in 70% of the mice depleted of CD8+ T lymphocytes, and the depletion NK cells did not influence the anti-tumor effect of the vaccine. CONCLUSION: The anti-tumor immune response is capable of inhibiting melanoma growth; both humoral immunity and cellular immunity could be induced by xenogeneic melanocytes vaccination. This immune response is mainly mediated by CD4+ T lymphocytes.

Animals↗

[Effect of quercetin on the signal pathway of TGFbeta1 in activated hepatic stellate cells].

OBJECTIVE: To investigate the effect of quercetin on the expression of connective tissue growth factor (CTGF) and fibronectin (FN) in hepatic stellate cells (HSCs) stimulated with transforming growth factor (TGF)beta1. METHODS: HSCs of rat were isolated by in situ perfusion and gradients centrifugation; the activated HSCs were incubated with quercetin (10(-9)-10(-5) mol/L) for 24, 48 and 72 h. TGFbeta1 was detected by flow cytometry. The expression of CTGF was detected by reverse transcription-polymerase chain reaction (RT-PCR), and then FN was detected by immunohistochemistry. RESULTS: Quercetin (10(-8) to 10(-5) mol/L) inhibited the expression of TGFbeta1 in HSCs. TGFbeta1 expression decreased after the HSCs being incubated with quercetin (10(-7) mol/L) for 48 h (mean fluorescence: 13.33+/-2.44 and 18.08+/-2.54, t=16.52, P<0.01). TGFbeta1 increased the expression of CTGF mRNA in HSCs, but this effect was abrogated by quercetin (10(-7) mol/L) within 72 h. Quercetin (10(-7) mol/L) significantly inhibited the expression of FN in HSCs. CONCLUSION: Quercetin may have an inhibitory effect on the signal pathways of TGFbeta1, including the expression of TGFbeta1, FN and CTGF.

Animals↗

[Clinical analysis of nosocomial pulmonary fungal infection in patients with cancer].

BACKGROUND & OBJECTIVE: Nosocomial fungal infection is an important complication of cancer patients. Among them, pulmonary fungal infection is over 20%. This study was designed to analyze and evaluate risk factors, and clinical features of nosocomial pulmonary fungal infection in patients with cancer. METHODS: In 1 229 patients with malignant tumor, clinical records of 78 patients with nosocomial pulmonary fungal infection were retrospectively analyzed. RESULTS: Pulmonary fungal infection rate was 6.35% (78/1 229). The major fungus was Candida albicans (68.18%). The main risk factors were age of > or =50 years (P< 0.005), primary site (lung cancer, P< 0.001), cancer stage (stage IV, P< 0.005), pulmonary radiotherapy (P< 0.001), chemotherapy (P< 0.001), and long-term hospitalization ( >2 weeks, P< 0.005). CONCLUSION: The effective methods to reduce nosocomial pulmonary fungal infection in patients with cancer are reducing risk factors, early diagnosis, and timely treatment.

Adult↗

Synchronization and symmetry-breaking bifurcations in constructive networks of coupled chaotic oscillators.

The spatiotemporal dynamics of networks based on a ring of coupled oscillators with regular shortcuts beyond the nearest-neighbor couplings is studied by using master stability equations and numerical simulations. The generic criterion for dynamic synchronization has been extended to arbitrary network topologies with zero row-sum. The symmetry-breaking oscillation patterns that resulted from the Hopf bifurcation from synchronous states are analyzed by the symmetry group theory.

Journal Article↗

Interaction with Tap42 is required for the essential function of Sit4 and type 2A phosphatases.

In Saccharomyces cerevisiae, Pph21 and Pph22 are the two catalytic subunits of type 2A phosphatase (PP2Ac), and Sit4 is a major form of 2A-like phosphatase. The function of these phosphatases requires their association with different regulatory subunits. In addition to the conventional regulatory subunits, namely, the A and B subunits for Pph21/22 and the Sap proteins for Sit4, these phosphatases have been found to associate with a protein termed Tap42. In this study, we demonstrated that Sit4 and PP2Ac interact with Tap42 via an N-terminal domain that is conserved in all type 2A and 2A-like phosphatases. We found that the Sit4 phosphatase in the sit4-102 strain contains a reverse-of-charge amino acid substitution within its Tap42 binding domain and is defective for formation of the Tap42-Sit4 complex. Our results suggest that the interaction with Tap42 is required for the activity as well as for the essential function of Sit4 and PP2Ac. In addition, we showed that Tap42 is able to interact with two other 2A-like phosphatases, Pph3 and Ppg1.

Adaptor Proteins, Signal Transducing↗

Immunotherapy of tumors with vaccine based on quail homologous vascular endothelial growth factor receptor-2.

The breaking of immune tolerance of "self-antigens" associated with angiogenesis is an attractive approach to cancer therapy by active immunity. We used vascular endothelial growth factor receptor-2 (VEGFR-2) as a model antigen to explore the feasibility of the immunotherapy with a vaccine based on a xenogeneic homologous protein. To test this concept, we prepared a quail homologous VEGFR-2 protein vaccine (qVEGFR) based on quail VEGFR-2. At the same time, a protein vaccine based on the corresponding ligand-binding domain of mouse self-VEGFR-2 (mVEGFR) was also prepared and used as a control. We found that immunotherapy with qVEGFR was effective at protective and therapeutic antitumor immunity in several solid and hematopoietic tumor models in mice. Autoantibodies against mouse VEGFR-2 (Flk-1) were identified by Western blot analysis and enzyme-linked immunosorbent assay (ELISA). Anti-VEGFR antibody-producing B cells were detectable by ELISPOT. Endothelial deposition of immunoglobulins developed within tumor. VEGF-mediated endothelial cell proliferation was inhibited in vitro by immunoglobulins from qVEGFR-immunized mice. Antitumor activity was caused by the adoptive transfer of the purified immunoglobulins. Antitumor activity and production of autoantibodies against Flk-1 could be abrogated by the depletion of CD4+ T lymphocytes. Angiogenesis was apparently inhibited within the tumors, and the vascularization of alginate beads was also reduced. No marked toxicity was found in the immunized mice. The observations may provide a vaccine strategy for cancer therapy through the induction of autoimmunity against the growth factor receptor associated with angiogenesis in a cross-reaction with single xenogeneic homologous protein.

Animals↗

Inhibition of tumor growth with a vaccine based on xenogeneic homologous fibroblast growth factor receptor-1 in mice.

Angiogenesis is important for the growth of solid tumors. The breaking of the immune tolerance against the molecule associated with angiogenesis should be a useful approach for cancer therapy. However, the immunity to self-molecules is difficult to elicit by a vaccine based on autologous or syngeneic molecules due to immune tolerance. Basic fibroblast growth factor (bFGF) is a specific and potent angiogenic factor implicated in tumor growth. The biological activity of bFGF is mediated through interaction with its high-affinity receptor, fibroblast growth factor receptor-1 (FGFR-1). In this study, we selected Xenopus FGFR-1 as a model antigen by the breaking of immune tolerance to explore the feasibility of cancer therapy in murine tumor models. We show here that vaccination with Xenopus FGFR-1 (pxFR1) is effective at antitumor immunity in three murine models. FGFR-1-specific autoantibodies in sera of pxFR1-immunized mice could be found in Western blotting analysis. The purified immunoglobulins were effective at the inhibition of endothelial cell proliferation in vitro and at the antitumor activity in vivo. The antitumor activity and production of FGFR-1-specific autoantibodies could be abrogated by depletion of CD4+ T lymphocytes. Histological examination revealed that the autoantibody was deposited on the endothelial cells within tumor tissues from pxFR1-immunized mice, and intratumoral angiogenesis was significantly suppressed. Furthermore, the inhibition of angiogenesis could also be found in alginate-encapsulate tumor cell assay. These observations may provide a new vaccine strategy for cancer therapy through the induction of autoimmunity against FGFR-1 associated with angiogenesis in a cross-reaction.

Alginates↗

Immunogene therapy of tumors with vaccine based on xenogeneic epidermal growth factor receptor.

The breaking of immune tolerance against self epidermal growth factor receptor (EGFr) should be a useful approach for the treatment of receptor-positive tumors with active immunization. To test this concept, we constructed a plasmid DNA encoding extracellular domain of xenogeneic (human) EGFr (hEe-p) or corresponding control mouse EGFr (mEe-p) and empty vector (c-p). Mice immunized with hEe-p showed both protective and therapeutic antitumor activity against EGFr-positive tumor. Sera isolated from the hEe-p-immunized mice exhibited positive staining for EGFr-positive tumor cells in flow cytometric analysis and recognized a single 170-kDa band in Western blot analysis. Ig subclasses responded to rEGFr proteins were elevated in IgG1, Ig2a, and Ig2b. There was the deposition of IgG on the tumor cells. Adoptive transfer of the purified Igs showed the antitumor activity. The increased killing activity of CTL against EGFr-positive tumor cells could be blocked by anti-CD8 or anti-MHC class I mAb. In vivo depletion of CD4(+) T lymphocytes could completely abrogate the antitumor activity, whereas the depletion of CD8(+) cells showed partial abrogation. The adoptive transfer of CD4-depleted (CD8(+)) or CD8-depleted (CD4(+)) T lymphocytes isolated from mice immunized with hEe-p vaccine showed the antitumor activity. In addition, the increase in level of both IFN-gamma and IL-4 was found. Taken together, these findings may provide a new vaccine strategy for the treatment of EGFr-positive tumors through the induction of the autoimmune response against EGFr in a cross-reaction between the xenogeneic homologous and self EGFr.

Adoptive Transfer↗

The Tap42-protein phosphatase type 2A catalytic subunit complex is required for cell cycle-dependent distribution of actin in yeast.

In Saccharomyces cerevisiae, the Tor proteins mediate a wide spectrum of growth-related cellular processes in response to nutrients. The pleiotropic role of the Tor proteins is mediated, at least in part, by type 2A protein phosphatases (PP2A) and 2A-like protein phosphatases. Tor-mediated signaling activity promotes the interaction of phosphatase-interacting protein Tap42 with PP2A and 2A-like protein phosphatases. The distinct complexes formed between Tap42 and different phosphatases mediate various cellular events and modulate phosphorylation levels of many downstream factors in the Tor pathway in a Tor-dependent and rapamycin-sensitive manner. In this study, we demonstrate that the interaction between Tap42 and the catalytic subunits of PP2A (PP2Ac) is required for cell cycle-dependent distribution of actin. We show that mutations in PP2Ac and Tap42 that perturb the interaction cause random distribution of actin during the cell cycle and that overexpression of the Rho2 GTPase suppresses the actin defects associated with the mutants. Our findings suggest that the Tap42-PP2Ac complex regulates the actin cytoskeleton via a Rho GTPase-dependent mechanism. In addition, we provide evidence that PP2A activity plays a negative role in controlling the actin cytoskeleton and, possibly, in regulation of the G(2)/M transition of the cell cycle.

Actins↗

Color Doppler ultrasonographic assessment of the risk of injury to major branch of the middle hepatic vein during laparoscopic cholecystectomy.

OBJECTIVE: To investigate the causes of hemorrhage from the gallbladder bed during laparoscopic cholecystectomy. METHODS: 617 patients who had received laparoscopic cholecystectomy from September, 2000 to March, 2001 at this hospital were reviewed retrospectively. Ninety-one of these patients were selected randomly for prospective observation. Color Doppler ultrasound was used to examine the cause of venous hemorrhage from the gallbladder bed during laparoscopic cholecystectomy and to examine the anatomic relationship between the gallbladder bed and the branches of the middle hepatic vein in 91 patients preoperatively. RESULTS: A large branch of the middle hepatic vein extended closely behind the gallbladder bed in all 91 patients. The mean distance between the closest point (C point) of this branch to the gallbladder bed was 5.0+/-4.6 mm. The branch of the middle hepatic vein was completely adherent to the gallbladder bed in 14 (15.38%) of the 91 patients. The distance between this branch and the gallbladder bed was within 1 mm in 10 (10.99%) of the 91 patients. The inside diameter at C point of this branch was 3.2+/-1.1 mm. The C point was found on the left side of the longitudinal axis of the gallbladder in 31 (34.66%) of the 91 patients, on the right side in 39 patients (42.86%), just on the axis in 21 patients (23.08%). The venous blood flow rate at the C point was 9.9+/-3.3 cm/s. CONCLUSIONS: A large branch of the middle hepatic vein passes behind the gallbladder. The inside diameter of this branch is relatively larger. The bleeding of this branch during operation can only be stopped by transfixion. The closest point of this vein to the gallbladder is mostly situated on the right side of the longitudinal axis of the gallbladder. Patients with large branches of the middle hepatic vein close to the gallbladder bed are at risk of hemorrhage during laparoscopic cholecystectomy and should be identified preoperatively with ultrasound.

Blood Loss, Surgical↗

[Synthesis of prodrugs of tacrine hydrochloride and evaluation of the stability and biodistribution in mice].

AIM: To synthesize acylated prodrug of tacrine hydrochloride (THA) to improve the infiltration ability across the blood brain barrier (BBB). METHODS: A series of prodrugs were prepared by acylation of the 7-amino group of THA. The degradation of prodrugs was investigated under different conditions. Biodistribution studies of N-butyramide-THA (BTHA) in mice were carried out to evaluate the function of brain targeting. RESULTS: The structures of prodrugs were confirmed by IR, 1HNMR and MS. All prodrugs were stable in different medium. Octanol-water partition coefficients indicated increased lipophlicity for various prodrugs compared to the THA. In vivo distribution studies showed that BTHA was mainly distributed in brain, blood and liver (the maximum concentrations were 17.5725, 13.1400 and 22.8279 mg.L-1, respectively), while the THA concentration were very low in lung and heart (the maximum concentrations were 4.9475 and 4.4925 mg.L-1, respectively). The BTHA concentration (2.4159 mg.L-1) was relatively high even 12 h after administration, showing that BTHA degraded more slowly in brain than in other tissues. CONCLUSION: The infiltration ability of THA across BBB was increased in the form of N-acylate-THA prodrug, indicating that this kind of prodrug is a promising brain-targeting delivery system.

Animals↗

Immunogene therapy of tumors with a vaccine based on the ligand-binding domain of chicken homologous integrin beta3.

The breaking of immune tolerance against angiogenesis-associated molecules should be a useful approach for cancer therapy by active immunity. We used chicken integrin beta3 as a model antigen to explore the feasibility of immunogene therapy of the tumors with a vaccine based on a single xenogeneic homologous gene, targeting the molecules associated with angiogenesis. To test this concept we constructed a plasmid DNA encoding the ligand-binding domain of chicken integrin beta3 (P-BD-C) and control vectors. We found that immunogene therapy of tumors with a vaccine based on the ligand-binding domain of chicken integrin beta3 (P-BD-C) was effective in both protective and therapeutic anti-tumor immunity in several tumor models in mice. Autoantibodies against integrin beta3 in sera of mice immunized with the ligand-binding domain of chicken integrin beta3 could be found by Western blot analysis and ELISA assay. The purified immunoglobulins were effective in the inhibition of endothelial cell proliferation in vitro, and in anti-tumor activity as well as in the inhibition of angiogenesis by adoptive transfer in vivo. The anti-tumor activity and the production of integrin beta3-specific autoantibodies (manifested by significantly elevated Ig G1 and Ig G2b) could be abrogated by the depletion of CD4+ T lymphocytes. These observations may provide a vaccine strategy for cancer therapy through the induction of the autoimmunity against the molecules associated with tumor growth in a cross-reaction with a single xenogeneic homologous gene and may be of importance in the further exploration of the applications of other xenogeneic homologous genes identified in human and other animal genome sequence projects in cancer therapy.

Animals↗

[Color Doppler ultrasonographic assessment of the risk of injury to major branch of the middle hepatic vein during laparoscopic cholecystectomy].

OBJECTIVE: To investigate the cause of hemorrhage from the gallbladder bed during laparoscopic cholecystectomy. METHODS: Color Doppler ultrasound was used to examine the cause of venous hemorrhage from the gallbladder bed during laparoscopic cholecystectomy in 1 patient postoperatively and to examine the anatomic relationship between the gallbladder bed and branches of the middle hepatic vein in 91 patients preoperatively. RESULTS: There is a major branch of middle hepatic vein extended close to the gallbladder bed. The branch of the middle hepatic vein was completely adherent to the gallbladder bed in 14 of 91 patients (15.4%). The mean distance between the closest point of the middle hepatic vein and the gallbladder bed is 5.0 +/- 4.6 mm, the mean diameter of this point is 3.2 +/- 1.1 mm. CONCLUSIONS: Patients with large branches of the middle hepatic vein close to the gallbladder bed are at risk of hemorrhage during laparoscopic cholecystectomy and should be identified preoperatively with ultrasound.

Cholecystectomy, Laparoscopic↗

LOOH, CD, TBARS and REM Kinetic Changes during Oxidation of High Density Lipoproteins Induced by Cu(2+) in Vitro.

Oxidation of HDL can be mediated by Cu(2+) in vitro. In order to study kinetic changes of several products during HDL oxidatively modified in vitro, the kinetic changes of thiobarbituric acid reaction substance (TBARS), lipid hydroperoxide (LOOH), conjugated diene(CD) and relative electrophoretic mobility (REM) during the oxidation of HDL induced with Cu(2+) and HDL incubation 2-24 hours in vitro were observed. These results indicated that kinetic changes of LOOH and CD showed three different phases lag, propagation and decomposition phases and the kinetic changes of TBARS and REM showed two different phases lag and propagation phases, but no decomposition phase.

Journal Article↗