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Biomedical subjects

X Zhu

Publications and source records attributed to X Zhu.

At least 721 records · Page 40Linked to original sources
PubMed1993

Percutaneous transseptal balloon valvuloplasty for dilating mitral valve stenosis (report of 200 cases).

Two hundred cases with mitral valve stenosis were treated by percutaneous single balloon (Inoue balloon) valvuloplasty at our institute from May 1988 to July 1992. The subjects included 137 females and 63 males with a mean age of 36.5 +/- 8.8 years (15-58 years). Hemodynamic and left ventriculographic findings were evaluated immediately before and after the procedure, and the results showed that the mean left atrial pressure was reduced from 25.08 +/- 9.13 mmHg to 10.64 +/- 4.10 mmHg (P < 0.001), the pressure gradient across the mitral valve was reduced from 25.49 +/- 10.22 mmHg to 6.71 +/- 4.87 mmHg (P < 0.001), and systolic pulmonary pressure was reduced from 52.78 +/- 21.42 mmHg to 38.56 +/- 16.47 mmHg (P < 0.001). At the same time, cardiac output and mitral orifice area were increased from 3.84 +/- 0.11 L/min to 4.66 +/- 0.28 L/min (P < 0.001) and from 1.08 +/- 0.28 cm2 to 2.20 +/- 0.47 cm2 (P < 0.001) respectively. Follow-up of 6-48 months (median 24 months) in 50 nonselective patients showed a symptomatic improvement rate of 100%. Percutaneous transseptal balloon mitral valvuloplasty (PBMV) proved to be a highly effective and safe nonsurgical method that can yield very good results in relieving symptomatic rheumatic mitral stenosis, with minimal morbidity and no mortality in this group. PBMV works by splitting the adhered mitral commissures toward the mitral annulus.

Adolescent↗
PubMed1993

Chloroquine inhibits macrophage tumour necrosis factor-alpha mRNA transcription.

Although chloroquine administration in vivo following haemorrhage in mice decreases tumour necrosis factor-alpha (TNF-alpha) release by macrophage (M phi), the mechanism remains unknown. To study this, peritoneal M phi (pM phi) from unmanipulated, sham-operated and post-haemorrhage mice were isolated, treated with 0.13 mg/ml chloroquine for 2 hr, and then stimulated with lipopolysaccharide (LPS) for 48 hr. Pretreatment of pM phi from various groups of mice with chloroquine resulted in 75-90% inhibition of TNF-alpha release, determined by bioassay. Total RNA was isolated from pM phi and murine M phi-derived cell lines (P388D1 and RAW 264.7), stimulated with LPS for 0.5 or 1 hr, respectively, and Northern blot analysis for TNF-alpha mRNA performed. Chloroquine inhibited TNF-alpha mRNA expression without interfering with mRNA stability, suggesting that this agent reduces M phi TNF-alpha release by disrupting TNF-alpha gene transcription.

Animals↗
PubMed1993

The dosimetry of iodine-123-labeled TISCH: a SPECT imaging agent for the D1 dopamine receptor.

TISCH is an iodinated D1 specific dopamine receptor antagonist that may be useful as a SPECT imaging agent. This report documents its pharmacological safety in animals and its radiation dosimetry in humans. The dose of radiation that 123I-TISCH delivered to seven healthy subjects was estimated with the absorbed fraction technique. Conjugate images of the body were serially acquired for up to 24 hr after the administration of a known amount of activity. The count rates in the organs that could be visualized were measured on each image. These count rates were corrected for attenuation with 123I transmission scans. The doses to the other organs that did not take up enough activity to be visualized on the images were estimated with established models. The dosimetry was calculated for each subject individually before the results were averaged. Rapid biological washout minimizes the radiation exposure to most organs. The dose to the large bowel is limiting in healthy volunteers. The proximal colon receives about 0.67 rad/mCi (180 microGy/MBq) or about 5 rads for every 7.5 mCi of TISCH injected. This low radiation burden should make it feasible to study the D1 dopamine receptor in patients who have neuropsychiatric disorders before and after treatment.

Adult↗
PubMed1993

Loss of telomeric DNA during aging of normal and trisomy 21 human lymphocytes.

The telomere hypothesis of cellular aging proposes that loss of telomeric DNA (TTAGGG) from human chromosomes may ultimately cause cell-cycle exit during replicative senescence. Since lymphocytes have a limited replicative capacity and since blood cells were previously shown to lose telomeric DNA during aging in vivo, we wished to determine: (a) whether accelerated telomere loss is associated with the premature immunosenescence of lymphocytes in individuals with Down syndrome (DS) and (b) whether telomeric DNA is also lost during aging of lymphocytes in vitro. To investigate the effects of aging and trisomy 21 on telomere loss in vivo, genomic DNA was isolated from peripheral blood lymphocytes of 140 individuals (age 0-107 years), including 21 DS patients (age 0-45 years). Digestion with restriction enzymes HinfI and RsaI generated terminal restriction fragments (TRFs), which were detected by Southern analysis using a telomere-specific probe (32P-(C3TA2)3). The rate of telomere loss was calculated from the decrease in mean TRF length, as a function of donor age. DS patients showed a significantly higher rate of telomere loss with donor age (133 +/- 15 bp/year) compared with age-matched controls (41 +/- 7.7 bp/year) (P < .0005), suggesting that accelerated telomere loss is a biomarker of premature immunosenescence of DS patients and that it may play a role in this process. Telomere loss during aging in vitro was calculated for lymphocytes from four normal individuals, grown in culture for 10-30 population doublings. The rate of telomere loss was approximately 120 bp/cell doubling, comparable to that seen in other somatic cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Cross-linking of surface immunoglobulin activates src-related tyrosine kinases in WEHI 231 cells.

Crosslinking of sIgM on the B cell line WEHI 231 with anti-sIgM antibody induces protein tyrosine phosphorylation, implicating protein tyrosine kinases (PTKs) in sIg-mediated signal transduction. We have analyzed this cell line for members of the src family of PTKs and have evaluated whether these PTKs might be involved in the process of sIgM-mediated signaling. Our results show that Blk, Lyn, Lck, and Hck are detectable in WEHI 231 cells. Addition of antibodies to sIgM were found to variably stimulate the activities of Blk, Lyn, Lck, and Hck as measured by immune-complex protein kinase assays. Autophosphorylation of these src PTKs, as assessed by reaction with anti-phosphotyrosine antibodies, increased over the time course of sIgM-mediated activation. Co-immunoprecipitation studies to investigate the potential physical interaction of src PTKs with the sIgM receptor complex revealed that, under digitonin and Brij 96 lysis conditions Lyn, Lck, Hck, but not Blk associated with sIgM.

Animals↗
PubMed1992

Activation of resting peripheral blood lymphocytes through the T cell receptor induces rapid phosphorylation of Op18.

Op18 is a highly conserved major cytosolic phosphoprotein that has been implicated in signal transduction in a wide variety of cell types. Freshly isolated peripheral blood lymphocytes (PBL) constitutively express low levels of mostly unphosphorylated Op18. After mitogenic stimulation of PBL, Op18 synthesis is induced at a time when cells are entering S-phase. In this study, we have examined the phosphorylation of Op18 in freshly isolated PBL after activation of the T cell receptor by OKT3. Quantitative analysis of Op18 phosphorylation was undertaken by metabolic labeling with 32Pi and PhosphorImager analysis of two-dimensional gels. After 10 or 15 min of activation by OKT3, one of the three major phosphorylated forms of Op18, designated Op18c, increased approximately 10-fold, which represented a most pronounced change among a large number of phosphoproteins analyzed. In time course experiments, increased Op18 phosphorylation to yield Op18c was observed as early as 2 min. Continued OKT3-induced activation for 20 to 72 h resulted in a further increase in phosphorylated Op18 forms, which paralleled new Op18 synthesis and occurred at a time when cells were entering S-phase, as determined by [3H]-thymidine incorporation. Inhibitors of lymphoid proliferation, cyclosporin A and RPM, had no effect on early (less than 15 min) phosphorylation. Addition of calphostin C, a specific inhibitor of protein kinase C, 1 min prior to stimulation of resting T cells with OKT3 completely inhibited further phosphorylation of Op18. Incubation of PBL with calphostin C for 75 min decreased constitutive levels of phosphorylated Op18. In contrast, inhibition of cyclic nucleotide-dependent protein kinases with HA1004 had no effect on Op18 phosphorylation. Activation of cAMP-dependent protein kinase with Forskolin or 8Br-cAMP did not increase Op18 phosphorylation. Our results suggest that Op18 phosphorylation is mediated by protein kinase C activation as an early event in T cell activation through the T cell receptor.

Cells, Cultured↗
PubMed1992

Evidence that the hamster tunicamycin resistance gene encodes UDP-GlcNAc:dolichol phosphate N-acetylglucosamine-1-phosphate transferase.

A cDNA clone isolated from Chinese hamster ovary cells conferred elevated GlcNAc-1-P-transferase (GPT) activity and resistance to tunicamycin in transfected cells (Zhu, X., and Lehrman, M. A. (1990) J. Biol. Chem. 265, 14250-14255). It had been assumed that this cDNA, termed TRG for tunicamycin resistance gene, encoded GPT enzyme. However, other functions were not ruled out. Thus, by one of several mechanisms, the TRG protein could have instead functioned by activation of the transfected host's endogenous GPT enzyme. To analyze the biochemical function of the TRG protein, hamster TRG cDNA was stably expressed at high levels in Chinese hamster ovary cells. In addition, several antipeptide polyclonal antibodies directed against the predicted TRG protein were obtained. With these tools in hand, experiments were performed to test the hypothesis that the TRG encodes GPT enzyme, as well as to rule out other possible functions for the TRG protein. These experiments included examination of the effects of solubilization of membranes on TRG-dependent GPT activity, the apparent binding of tunicamycin to the TRG protein, and the immunoadsorption of GPT activity with TRG protein-specific antibodies. From these results, we conclude that the hamster TRG most likely encodes GPT enzyme.

Animals↗