Biomedical subjects
J Quan
Publications and source records attributed to J Quan.
Rate at which glutamine enters TCA cycle influences carbon atom fate in intestinal epithelial cells.
Glutamine carbon entry into the tricarboxylic acid (TCA) cycle was assessed in small intestinal epithelial cells by measuring CO2 production from [1-14C]glutamine, and these data together with [U-14C]glutamine data were used to calculate fractional oxidation rates for glutamine. CO2 production from either [1-14C]glutamine or [U-14C]glutamine showed saturation kinetics, and the concentration needed to achieve the half-maximal rate of CO2 production was 0.7 and 0.4 mmol/l, respectively. Maximal rate for [1-14C]glutamine was twice that for [U-14C]glutamine. Increasing glutamine concentration did not cause proportional increases in glutamine entry into the TCA cycle and glutamine oxidation. Consequently, fractional oxidation of glutamine decreased with increasing glutamine concentration. Fractional oxidation could be predicted from the rate at which glutamine carbon entered the TCA cycle. (Aminooxy)acetic acid, an aminotransferase inhibitor, reduced entry of glutamine into the TCA cycle and increased fractional oxidation of glutamine. Glutamate carbon entered the TCA cycle at about one-half the rate of glutamine-derived glutamate carbon and had a higher fractional oxidation rate when provided at equivalent concentrations to glutamine. These differences in the rate of entry predictably account for the differences in the metabolic fate of glutamine vs. glutamate carbon.
[Protective effect of Astragalus membranaceus (Fisch.) Bge. and Hedysarum polybotrys Hand.-Mazz. on experimental model of cerebral ischemia in rats].
The experimental model of middle cerebral artery embolism in rats was made by inserting nylon thread. It was discovered that Astragalus membranaceus decoction(both 4.26 g.kg-1 and 7.1 g.kg-1) could reduce the capillary hyperpermeability and alleviate the dyskinesia caused by cerebral ischemia in rats. Purified Hedysarum polybotrys decoction (waste substances removed with alcohol after decocting with water) (12.5 g.kg-1) could reduce the water content in brain caused by occlusion of bilateral carotids in rats. Purified Hedysarum polybotrys decoction showed a tendency to reduce the water content in brain, but without statistical significance.
Fluctuations in GAD65 antibodies after clinical diagnosis of IDDM in young children.
OBJECTIVE: To investigate whether the presence of GAD antibodies at onset of IDDM correlates to a more aggressive rate of beta-cell destruction after clinical onset. RESEARCH DESIGN AND METHODS: We studied GAD antibodies at onset of disease, after 1 year, and after 6 years in 33 consecutively referred children (mean age 8.08, range 1.7-16.3). In a subset of 11 patients, GAD antibodies were studied very frequently. The correlation between GAD antibodies and clinical parameters, including glycosylated hemoglobin, residual insulin secretion, and insulin dosage, was evaluated. RESULTS: GAD antibody titers were highly variable. Four patients became GAD antibody positive weeks to years after clinical onset. Other patients switched between testing positive and negative for GAD antibodies shortly after clinical onset. No correlation was found between the presence of GAD antibodies and the rate of beta-cell destruction, but patients with high GAD antibody indexes at onset had significantly higher glycosylated hemoglobin levels. CONCLUSIONS: GAD antibodies at clinical onset do not predict the rate of beta-cell destruction in young children with newly diagnosed IDDM. The highly variable GAD antibody levels suggest variation of the autoimmune process.
Activation of T Cells by Autoantigen Immobilized by Specific Antibodies
A convenient microtiter-plate assay that uses immobilized antibody to capture specific antigens for presentation to T cells has been developed. Initial experiments used KLH as the antigen, immune antisera and draining lymph node cells from immunized NOD mice as the source of antibody and T cells, and spleen cells from naive NOD mice as the source of antigen-presenting cells (APCs). The resulting proliferation of the T cells was shown to be antibody- and antigen-specific, suggesting that the APCs had internalized and processed the captured antigen, presenting it to the T cells in the form of peptide/MHC complexes. The approach was also tested for an autoimmune disease as part of an effort to identify autoantigens responsible for the proliferation of T cells in the synovial fluid of rheumatoid arthritis patients. When immunoglobulin from autologous synovial fluid was captured on plates coated with anti-human immunoglobulin antibodies, the addition of HLA-DR4 peripheral blood mononuclear cells as APCs and synovial fluid-reactive HLA-DR4-restricted T-cell clones resulted in significant proliferation, indicating that the specific antigen in the crude synovial fluid was human immunoglobulin. This response was also shown to be antigen-specific and HLA-DR4-restricted. This assay format should permit the definition of autoantigens by capturing with antibodies to crude autoantigen extracts, followed by the addition of the appropriate APC and T-cell populations.
Validity of three clinical performance assessments of internal medicine clerks.
PURPOSE: To analyze the construct validity of three methods to assess the clinical performances of internal medicine clerks. METHOD: A multitrait-multimethod (MTMM) study was conducted at the Case Western Reserve University School of Medicine to determine the convergent and divergent validity of a clinical evaluation form (CEF) completed by faculty and residents, an objective structured clinical examination (OSCE), and the medicine subject test of the National Board of Medical Examiners. Three traits were involved in the analysis: clinical skills, knowledge, and personal characteristics. A correlation matrix was computed for 410 third-year students who completed the clerkship between August 1988 and July 1991. RESULTS: There was a significant (p < .01) convergence of the four correlations that assessed the same traits by using different methods. However, the four convergent correlations were of moderate magnitude (ranging from .29 to .47). Divergent validity was assessed by comparing the magnitudes of the convergence correlations with the magnitudes of correlations among unrelated assessments (i.e., different traits by different methods). Seven of nine possible coefficients were smaller than the convergent coefficients, suggesting evidence of divergent validity. A significant CEF method effect was identified. CONCLUSION: There was convergent validity and some evidence of divergent validity with a significant method effect. The findings were similar for correlations corrected for attenuation. Four conclusions were reached: (1) the reliability of the OSCE must be improved, (2) the CEF ratings must be redesigned to further discriminate among the specific traits assessed, (3) additional methods to assess personal characteristics must be instituted, and (4) several assessment methods should be used to evaluate individual student performances.
Quantitative analyses of neuroepithelial cell shapes during bending of the mouse neural plate.
Despite a wealth of information about cell behaviors contributing to neurulation in chick embryos, similar behaviors in mouse embryos have yet to be well characterized. This study examines cell behaviors occurring during bending of the mouse neural plate, in particular, qualitative and quantitative changes in neuroepithelial cell shape. Our current results demonstrate that in mouse embryos 1) the median hinge point (MHP), a localized region of neural plate that becomes anchored to the underlying prechordal plate mesoderm or notochord/notochordal plate and forms a midline longitudinal furrow around which folding of the remaining neural plate (i.e., the part of the neural plate not involved in MHP formation) occurs, develops during stages of neural fold elevation; 2) the MHP is enriched with wedge-shaped neuroepithelial cells but has significantly fewer spindle-shaped, inverted wedge-shaped, and globular neuroepithelial cells than do the adjacent paired lateral areas of the neuroepithelium (L); and 3) each L is enriched with spindle-shaped, inverted wedge-shaped, and globular neuroepithelial cells but has significantly fewer wedge-shaped neuroepithelial cells than does the MHP. Thus wedging of neuroepithelial cells occurs during bending of the mouse neural plate and is localized to the MHP during neural fold elevation. Similarly, previous studies in the chick have shown that neuroepithelial cells become wedge shaped during bending of the neural plate and that such cell wedging is localized to the MHP during neural fold elevation. Such studies also have shed light on the roles of MHP formation and localized wedging of neuroepithelial cells within the MHP in the chick; however, such roles have yet to be elucidated in the mouse.(ABSTRACT TRUNCATED AT 250 WORDS)
Joint-derived T cells in rheumatoid arthritis react with self-immunoglobulin heavy chains or immunoglobulin-binding proteins that copurify with immunoglobulin.
Rheumatoid arthritis patients were found to have CD4+ T cells that proliferate in response to autologous synovial fluid and plasma. T cell clones and polyclonal T cell lines were found to respond to antigen(s) eluted from protein A Sepharose and anti-human immunoglobulin (Ig) antibody Sepharose. The antigen(s) was further resolved to fractions that contained intact Ig or Ig heavy chain since the T cells responded to > 100 kDa and 40-60 kDa polypeptides derived from purified Ig under nonreducing and reducing conditions, respectively. These results indicated that the antigen(s) is either Ig heavy chain or Ig-binding proteins that copurify with Ig and Ig subunits. Pepsin and papain digestion of the antigenic fractions eluted from protein A destroyed the T cell reactivity. Since most Fab regions are resistant to these enzymes, further analyses are required to localize the antigenic epitope(s). The presence of Ig- or Ig-antigen complex-reactive T cells in arthritic joints implies that B cells expressing anti-Ig antibody (i.e. rheumatoid factor) may play an important role in antigen presentation to autoreactive T cells.
The influence of LFA 1 on human T cells stimulated by solid-phase immobilized HLA class II-peptide complexes.
Purified HLA class II-peptide complexes immobilized to a solid support induce proliferation of human T-cell clones, indicating that human T-cell clones can proliferate in the absence of secondary signals from accessory cells. We hypothesized that T cells can provide co-stimulatory signals to T cells. LFA-1 molecules play an important role in homotypic interactions of T cells and murine monoclonal antibodies reactive with LFA 1 can inhibit T cell-T cell interactions. LFA-1 reactive monoclonal antibodies inhibited cytolysis of peptide-pulsed T cells by T cells and partially inhibited T-cell proliferation. To study the direct effect of the LFA 1 molecule on T-cell activation, we co-immobilized HLA-class II-peptide complexes with LFA-1 reactive MoAbs. Co-immobilization resulted in an enhanced proliferative response of the T-cell clones. This could indicate that the LFA 1 molecule on T cells is not a passive adhesion molecule, but is capable of transducing a signal that synergizes with the stimulatory signal via the T-cell receptor.
The glutamate decarboxylase and 38KD autoantigens in type 1 diabetes: aspects of structure and epitope recognition.
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[The factors potentially conditioning the food habits of older Guatemalans from a suburban area].
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Hemorrhagic fever with renal syndrome imported to Hawaii from West Germany.
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Enhanced cell-mediated protection against fatal Escherichia coli septicemia induced by treatment with recombinant IL-2.
Administration of rIL-2 to BALB/c mice induces a rapid, cell-mediated response that is sufficient to protect mice from a lethal i.p. dose of Escherichia coli. Mice were protected from septic death if IL-2 was administered i.p. within 1 h after the bacterial challenge. Optimal protection was provided by treating the lethally challenged mice with rIL-2 at 1 and 5 h or 1, 5, and 10 h after the bacterial challenge and was dose-dependent (greater than or equal to 5.0 x 10(5) U/kg). Furthermore, treatment of mice with anti-IL-2R antibody abolished the protective effect induced by rIL-2 administration. These data suggest that the rIL-2-induced protection against septic death in mice is mediated by a cell type expressing a functional IL-2R. One potentially important therapeutic application of rIL-2 may be to modulate the course of sepsis once the host has been exposed to potentially lethal microbial pathogens.
Legionellosis in cardiac transplant recipients: results of a nationwide survey.
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Relapse and non-relapse in alcoholic patients.
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