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Biomedical subjects

J X Gao

Publications and source records attributed to J X Gao.

At least 19 recordsLinked to original sources
PubMed2005

Energy transmission in a mechanically-linked double-wall structure coupled to an acoustic enclosure.

The energy transmission in a mechanically linked double-wall structure into an acoustic enclosure is studied in this paper. Based on a fully coupled vibro-acoustic formulation, focus is put on investigating the effect of the air gap and mechanical links between the two panels on the energy transmission and noise insulation properties of such structures. An approximate formula reflecting the gap effect on the lower-order coupled frequencies of the system is proposed. A criterion, based on the ratio between the aerostatic stiffness of the gap cavity and the stiffness of the link, is proposed to predict the dominant transmitting path, with a view to provide guidelines for the design of appropriate control strategies. Numerical results reveal the existence of three distinct zones, within which energy transmission takes place following different mechanisms and transmitting paths. Corresponding effects on noise insulation properties of the double-wall structure are also investigated.

Acoustics↗
PubMed2001

B7H costimulates clonal expansion of, and cognate destruction of tumor cells by, CD8(+) T lymphocytes in vivo.

B7H/B7RP (hereby called B7H) is a new member of the B7 family of costimulatory molecules and interacts with inducible costimulatory molecule (ICOS). Its function for CD8 T cells has not been reported. We report here that expression of B7H on the tumor cells reduced tumorigenicity and induced immunity to subsequent challenge with parental tumor cells. The immune protection correlates with an enhanced cytotoxic T lymphocyte (CTL) response against P1A, the major tumor antigen expressed in the J558 tumor. To understand the mechanism of immune protection, we adoptively transferred transgenic T cells specific for tumor antigen P1A into mice that bore P1A-expressing tumors. We found that while the transgenic T cells divided faster in mice bearing the B7H(+) tumors, optimal B7H-induced clonal expansion of P1CTL required costimulation by B7-1 and B7-2 on the endogenous host antigen-presenting cells (APCs). Interestingly, when B7H(+) and B7H(-) tumors were coinjected, P1CTL selectively eliminated the B7H(+) tumor cells. Moreover, B7H expressed on the tumor cells made them highly susceptible to destruction by CTL in vivo, even if the CTL was administrated into mice with large tumor burdens. Tumors that recurred in the P1CTL-treated mice lost transfected B7H and/or H-2L(d), the class I molecule that presents the P1A peptide. Taken together, our results reveal that B7H costimulates clonal expansion of, and cognate destruction by CD8(+) T lymphocytes in vivo.

Animals↗
PubMed2001

On the site and mode of antigen presentation for the initiation of clonal expansion of CD8 T cells specific for a natural tumor antigen.

Because of the low frequency of antigen-specific T cells, early events in the activation of tumor-specific T cells in vivo have not been well characterized. There is still no direct documentation on where the clonal expansion begins and how tumor antigens are presented to the host CD8 T cells to initiate it. Here we used transgenic T cells specific for a natural tumor antigen P1A to evaluate the kinetics, location, and modes of antigen presentation for initiating CTL response in vivo. Our results demonstrate that the initial activation of P1A-specific T cells takes place in the lymphoid organs. The activated T cells then migrate into tumors, where they undergo accelerated division and acquire distinct activation markers. The site of initiation cannot be altered by either local expression of costimulatory molecules or by intratumor injection of naïve T cells. Moreover, using genetic models that allow only one mode of antigen presentation, we show here that both cross-presentation of P1A by the host antigen-presenting cells, and direct antigen presentation and costimulation by the tumor cells are sufficient to initiate rapid T cell-clonal expansion in the lymphoid organ. These results provide direct evidence for two fundamental assumptions on the mechanisms of T-cell activation in vivo.

Animals↗
PubMed2000

Preferential proliferation and differentiation of double-positive thymocytes into CD8(+) single-positive thymocytes in a novel cell culture medium.

The identification of factors that regulate the proliferation and differentiation of double-positive (DP) into CD4(+) and CD8(+) single-positive (SP) thymocytes has proven difficult due to the inability of DP thymocytes to proliferate, expand, and differentiate into SP thymocytes in available cell culture media. Here we report on the ability of DP thymocytes to differentiate in a novel conditioned medium, termed XLCM, derived from the supernatant of mitogen activated human cord blood mononuclear cells. During a 5-day culture in XLCM in the absence of thymic stromal cells, DP thymocytes from normal mice and MHC double knockout mice (lack SP thymocytes) proliferate, expand, and differentiate into several (alphabetaTCR(+), NK1.1(+)alphabetaTCR(+), and gammadeltaTCR(+)) subsets of CD4(+) and predominantly CD8(+) SP thymocytes. These studies suggest that the use of XLCM may aid in the characterization of factors that regulate the differentiation of DP thymocytes into CD8(+) SP thymocytes.

Animals↗
PubMed2000

Regulation of fas ligand expression during activation-induced cell death in T cells by p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase.

Activation-induced cell death (AICD) is a mechanism of peripheral T cell tolerance that depends upon an interaction between Fas and Fas ligand (FasL). Although c-Jun NH2-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) may be involved in apoptosis in various cell types, the mode of regulation of FasL expression during AICD in T cells by these two MAPKs is incompletely understood. To investigate the regulatory roles of these two MAPKs, we analyzed the kinetics of TCR-induced p38 MAPK and JNK activity and their regulation of FasL expression and AICD. We report that both JNK and p38 MAPK regulate AICD in T cells. Our data suggest a novel model of T cell AICD in which p38 MAPK acts early to initiate FasL expression and the Fas-mediated activation of caspases. Subsequently, caspases stimulate JNK to further upregulate FasL expression. Thus, p38 MAPK and downstream JNK converge to regulate FasL expression at different times after T cell receptor stimulation to elicit maximum AICD.

Animals↗
PubMed2000

New chiral catalysts for reduction of ketones.

The condensation of o-(diphenylphosphino)benzaldehyde and various chiral diamine gives a series of diimino-diphosphine tetradentate ligands, which are reduced with excess NaBH4 in refluxing ethanol to afford the corresponding diaminodiphosphine ligands in good yield. The reactivity of these ligands toward trans-RuCl2(DMSO)4 and [Rh(COD)Cl]2 had been investigated and a number of chiral Ru(II) and Rh(I) complexes with the PNNP-type ligands were synthesized and characterized by microanalysis and IR, NMR spectroscopic methods. The chiral Ru(II) and Rh(I) complexes have proved to be excellent catalyst precursors for the asymmetric transfer hydrogenation of aromatic ketones, leading to optically active alcohols in up to 97% ee.

Chemistry↗
PubMed1999

p38 mitogen-activated protein kinase mediates signal integration of TCR/CD28 costimulation in primary murine T cells.

Optimal T cell activation requires two signals, one generated by TCR and another by the CD28 costimulatory receptor. In this study, we investigated the regulation of costimulation-induced mitogen-activated protein kinase (MAPK) activation in primary mouse T cells. In contrast to that reported for human Jurkat T cells, we found that p38 MAPK, but not Jun NH2-terminal kinase (JNK), is weakly activated upon stimulation with either anti-CD3 or anti-CD28 in murine thymocytes and splenic T cells. However, p38 MAPK is activated strongly and synergistically by either CD3/CD28 coligation or PMA/Ca2+ ionophore stimulation, which mimics TCR-CD3/CD28-mediated signaling. Activation of p38 MAPK correlates closely with the stimulation of T cell proliferation. In contrast, PMA-induced JNK activation is inhibited by Ca2+ ionophore. T cell proliferation and production of IL-2, IL-4, and IFN-gamma induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580. Our findings demonstrate that p38 MAPK 1) plays an important role in signal integration during costimulation of primary mouse T cells, 2) may be involved in the induction of c-Jun activation and augmentation of AP-1 transcriptional activity, and 3) regulates whether T cells enter a state of functional unresponsiveness.

Activating Transcription Factor 2↗
PubMed1999

CD40-deficient dendritic cells producing interleukin-10, but not interleukin-12, induce T-cell hyporesponsiveness in vitro and prevent acute allograft rejection.

The induction of an immune response or tolerance is mediated by corresponding subsets of dendritic cells (DC). However, the property of tolerogenic DC is not clear. Recently, we have characterized a population of CD11c+ splenic DC derived from long-term mixed leucocyte culture (LT-MLC), which are able to proliferate upon stimulation and have a strong primary mixed leucocyte reaction (MLR)-stimulating activity in conventional MLR. In this study, we show that, in contrast to the irradiated ones, non-irradiated LT-MLC-derived DC induce polyclonal antigen-specific T-cell hyporesponsiveness when cocultured with allogeneic splenocytes for 3-11 days. The degree of the hyporesponsiveness increased with the length of coculture. Although these DC expressed major histocompatibility complex class II and B7 costimulatory molecules, which are down-regulated during coculture, they expressed very low or undetectable CD40 before and after coculture, respectively. The CD40-deficient DC spontaneously produce interleukin-10 (IL-10), but not IL-12. The skewed balance between IL-10 and IL-12 is associated with their capability to induce T-cell hyporesponsiveness, because a neutralizing antibody to IL-10, exogenous recombinant IL-12 or lipopolysaccharide (LPS) significantly blocked the hyporesponsiveness. Accordingly, infusion of a small number of non-irradiated LT-MLC-derived DC (5x105) significantly prolonged the survival of a vascularized heterotopic murine heart transplant, whereas irradiated DC accelerated graft rejection. These data suggest that CD40-deficient DC producing IL-10, but not IL-12 can induce T-cell hyporesponsiveness in vitro and in vivo.

Adoptive Transfer↗
PubMed1998

Structure and expression of the mouse AhR nuclear translocator (mArnt) gene.

Aryl hydrocarbon receptor (AhR) nuclear translocator (Arnt) gene has been isolated and characterized from a mouse genomic DNA library. The gene is about 60 kilobases long and split into 22 exons. An unusual exon/intron junctional sequence was found in the 11th intron of the gene that begins with GC at its 5'-end. The exon/intron arrangement of mArnt gene differs greatly from those of the other members of the same basic-helix-loop-helix/PAS family. The gene is TATA-less and has several transcription start sites. The promoter region of the mArnt gene is GC-rich and contains a number of putative regulatory DNA sequences such as two GC-boxes, a cAMP-responsive element, E-box, AP-1 site, and CAAT-box. Deletion experiments revealed that all these DNA elements made substantial contributions to a high level of expression of the gene, except for the cAMP-responsive element. Of all, two GC-boxes displayed the most dominant enhancing effects. It was demonstrated that there exist specific factors binding to these DNA elements in the nuclear extracts of HeLa cells. Among them, Sp1 and Sp3, and CAAT-box binding factor-A were identified to bind the GC-boxes and CAAT-box, respectively. Expression of MyoD in HeLa cells stimulated the Arnt promoter activity by binding to the E-box.

Amino Acid Sequence↗
PubMed1998

TCR alpha beta chains associate with the plasma membrane independently of CD3 and TCR zeta chains in murine primary T cells.

The TCR is a multisubunit complex composed of the clonotypic alpha/beta disulfide-linked heterodimer and noncovalently linked invariant CD3 gamma epsilon and CD3 delta epsilon and TCR zeta chains. Recent studies demonstrate that the surface expression of CD3 components can occur independently of the clonotypic TCR complexes in both thymocytes and splenic T cells. In this study, we report that free noncovalently associated TCR alpha beta heterodimers that exist independently of CD3 and TCR zeta chains are expressed on the cell surface of immature thymocytes and peripheral T cells, but not of T cell lines and T cell hybridomas. This suggests that the regulation of surface expression of TCR alpha beta heterodimers differs between primary T cells and T cell lines or T cell hybridomas. The isolation and biochemical characterization of surface clonotype-independent CD3 complexes and free membrane-associated TCR alpha beta complexes may provide a structural basis for the quantitative difference in amount of T cell proliferation stimulated by anti-CD3 epsilon and anti-TCR beta.

Animals↗
PubMed1997

Generation of dendritic cell-like antigen-presenting cells in long-term mixed leucocyte culture: phenotypic and functional studies.

The mechanisms contributing to the proliferation and differentiation of antigen-presenting cell (APC) precursors upon antigen stimulation or tissue injury are poorly understood. Herein, we report the induction of a population of dendritic cell-like cells (DLC) with potent antigen-presentation function from unfractionated spleen cells by means of repetitive allostimulation in long-term mixed leucocyte cultures (LT-MLC). Initially, only a few adherent DLC were observed. By 4-6 weeks, however, there were large numbers of DLC which survived persistently. Features of these DLC are closely related to dendritic cells (DC), including (1) dendritic, veiled or spiny-processed morphology; (2) expression of a wide array of leucocyte surface markers including DC-associated or restricted antigens: 33D1, NLDC-145, CD11c (N418), heat-stable antigen (HSA), CD44, B7-1 and B7-2; (3) ability to migrate to draining lymph nodes and white pulp area of spleen; (4) expression of high level of major histocompatability complex (MHC) class II molecules and (5) more potent mixed leucocyte reaction (MLR)-stimulating capacity than peritoneal macrophages and APC-enriched spleen cells. DLC-stimulated MLR was inhibited by monoclonal antibodies (mAbs) to B7-1, B7-2, intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), leucocyte-function associated antigen-1 (LFA-1) or very-late activation antigen-4 (VLA-4) by 30-55%. When maintained for more than 2 months, the DLC did not lose their MLR-stimulating activity, but many surface markers were down-regulated except for Mac-2 and VCAM-1, which remained stable or were up-regulated, respectively. In short-term culture, the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin (IL)-2 enhanced proliferation of DLC, while tumour necrosis factor-alpha (TNF-alpha) and IL-4 did not. IL-4 suppressed not only 'spontaneous', but also GM-CSF-enhanced proliferation, suggesting that cytokines play a differential role in DLC proliferation. These results confirm that professional APC can proliferate in response to repetitive antigen stimulation, and their proliferation is differentially regulated by cytokines. A comparison study of DLC with typical DC is being carried out in our laboratory.

Animals↗
PubMed1997

The beta 1 integrin, very late activation antigen-4 on human neutrophils can contribute to neutrophil migration through connective tissue fibroblast barriers.

Polymorphonuclear leucocyte (PMNL) accumulation in extravascular tissues and inflammatory exudates is dependent on their migration through blood vessel endothelium and then through connective tissue. Previously we utilized a barrier of human synovial and dermal fibroblasts (HSF or HDF) grown on microporous filters, as a model of PMNL migration through connective tissue. Those studies showed that beta 2 (CD18) and the beta 1 integrins, very late activation antigen-5 (VLA-5) and VLA-6, in part mediate this PMNL migration. Here we report that VLA-4, which can also be expressed at low levels on activated PMNL, is also involved in PMNL migration induced by C5a through fibroblast (HSF and HDF) barriers, because monoclonal antibody (mAb) to VLA-4 significantly inhibited (by 20-30%) PMNL migration. Blocking the function of CD18, VLA-5 or VLA-6 was not required for detection of the VLA-4-mediated migration. Combination treatment with mAb to VLA-4 and with mAb to VLA-5 or to VLA-6 further inhibited PMNL migration, irrespective of whether CD11/CD18 mechanisms were blocked with anti-CD18 mAb or not. Treatment of PMNL with a peptide based on the VLA-4-binding domain in the CS-1 fragment of fibronectin, but not a control peptide, inhibited PMNL migration to a comparable extent to treatment with mAb to VLA-4. A low level of VLA-4 was expressed on C5a-activated PMNL, detected by immunofluorescence flow cytometry. These results suggest that VLA-4 can be mobilized by human peripheral blood PMNL and can, in addition to VLA-5, VLA-6 and CD11/CD18 integrins, mediate PMNL migration through connective tissue. This is in marked contrast to PMNL transendothelial migration, where beta 1 integrins appear to play no significant role.

CD18 Antigens↗
PubMed1997

[Measurement of the three dimensional shape about crown with the digital speckle correlation method]

It is the first step that the data about relative teeth's shape are catched for CAD/CAM system in dental rehabilitation.That is how to measure the teeth's shape.The digtal speckle correlation method are introduced to measure the teeth's shape in the article.For one posterior tooth,we measured the five surfaces that the occlusal surface and the four axial surfaces.According to some special marks,we changed the five group's local data into one coordinate and reconstructed the three dimensional shape of the tooth.At last we drew the graph with the computer.In this paper the author also discussed some factors about the measure system's sensitive and precise and the extent scale.etc.

Journal Article↗
PubMed1997

Schistosomiasis: the cleanup continues.

During the past 40 years immense progress has been made in the control of schistosomiasis in China. The authors consider how the 100 million people in the country who are still at risk from the disease can be protected.

China↗
PubMed1996

Mac-1 (CD11b/CD18) is the predominant beta 2 (CD18) integrin mediating human neutrophil migration through synovial and dermal fibroblast barriers.

Recently we reported that polymorphonuclear leucocyte (PMNL) migration in vitro through a barrier of human synovial fibroblasts (HSF) involves both beta 2 (CD18) and beta 1 (CD29) integrins on the PMNL. Here we investigated the role of the beta 2 integrin family members, lymphocyte function-associated (LFA)-1 (alpha L beta 2 or CD11a/CD18) and Mac-1 ( alpha M beta 2 or CD11b/CD18), in PMNL migration through HSF and human dermal fibroblast (HDF) monolayers. Treatment of PMNL with monoclonal antibody (mAb) to LFA-1 (anti-alpha L) did not inhibit PMNL migration through either monolayer in response to C5a. In contrast, mAb to Mac-1 (Cd11b) inhibited (by 30-40%) PMNL migration, and by virtually the same extent as mAb to the beta 1 integrin chain (CD18) (40% inhibition). Addition of mAb to LFA-1 to mAb to Mac-1 did not result in greater inhibition. This was in contrast to PMNL migration through human umbilical vein endothelium (HUVE) monolayers, where mAb to LFA-1 or to Mac-1 each partially inhibited PMNL transendothelial migration, and when these mAbs were combined, synergistic inhibition of migration was observed, reaching 90-95% inhibition. Intercellular adhesion molecule 1 (ICAM-1) was not required for Mac-1 mediated migration through HSF or HDF, because treatment of the fibroblasts with mAb R6.5 (F(ab)2) to ICAM-1, which blocks the Mac-1 binding site on ICAM-1, did not inhibit PMNL migration. An LFA-1-ICAM-1 mechanism of PMNL migration through HSF and HDF monolayers could be detected after treatment (4 hr) of the monolayers with TNF-alpha plus IFN-gamma, which upregulated ICAM-1 on the fibroblasts. The results demonstrate the beta 2 integrin dependent PMNL migration in connective tissue may involve primarily Mac-1, with little involvement of LFA-1 or ICAM-1, a situation in marked contrast to PMNL migration across endothelium. However, in inflammatory conditions in which TNF-alpha and/or IFN-gamma may be generated, a role for LFA-1-ICAM-1 may be induced.

CD18 Antigens↗
PubMed1996

Expression of VCAM-1 and VLA-4 dependent T-lymphocyte adhesion to dermal fibroblasts stimulated with proinflammatory cytokines.

In chronic inflammatory conditions, mononuclear cells infiltrate the involved connective tissue and may persist, perhaps because of binding to adhesion molecules on connective tissue cells, as well as extracellular matrix. Here we investigated whether vascular cell adhesion molecule-1 (VCAM-1) may be induced on human dermal fibroblasts by proinflammatory cytokines. Expression of VCAM-1 was determined by Northern blotting, cell enzyme-linked immunosorbent assay (ELISA) and flow cytometry. Only trace amounts of VCAM-1 mRNA or protein were constitutively expressed on dermal fibroblasts but both were rapidly (within 4 hr) upregulated by tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) and somewhat slower (20 hr) by interferon-gamma (IFN-gamma). The combination of TNF-alpha and IFN-gamma had at least an additive effect. The adhesion function of the expressed VCAM-1 was examined by studying the adhesion of the Jurkat T lymphocytes to fibroblasts. Adhesion of Jurkat cells to dermal fibroblasts was markedly increased by stimulation of fibroblasts with TNF-alpha and IFN-gamma (22% of cells adhered versus 9% on unstimulated fibroblasts). The increased adhesion was inhibited to that on unstimulated fibroblasts by monoclonal antibody (mAb) to domain 1 of VCAM-1, but not by mAb to domain 4. MAb to very late antigen-4 (VLA-4), the integrin counter-receptor on lymphocytes for VCAM-1, completely inhibited the increase in Jurkat cell adhesion to activated fibroblasts and partly also inhibited basal adhesion to unstimulated fibroblasts. These results suggest that VCAM-1 expression by dermal fibroblasts is inducible at the mRNA, protein and functional levels by proinflammatory cytokines. The VLA-4/VCAM-1 pathway maybe involved in adhesive interactions between T lymphocytes and activated fibroblasts in the skin during chronic dermal inflammatory conditions.

Blotting, Northern↗
PubMed1996

Patellofemoral joint study via image processing.

Plain Merchant-view X-rays of patellofemoral joints are used to study the geometry and kinematics of the patellofemoral joint. A method for calculating the kinematic parameters: sulcus angle (SA), patellofemoral congruence angle (PFC), lateral patellar angle (LPA), patellar rotation angle (PR) and lateral patellar displacement (LPD) is presented. Using digitized X-ray images of patellofemoral joints, contours of the patella and the femur can be acquired by boundary detection and morphological thinning. A radiograph is converted to a line drawing and the data points required for calculation of the parameters are chosen automatically without human intervention. Parameter measurements were demonstrated for 5 X-rays of 3 patients. Comparisons between computer calculated and hand calculated parameters were made. This technique is inexpensive but will provide the necessary information, and is practical, especially during the evaluation of patients with patellofemoral abnormalities.

Femur↗