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Biomedical subjects

Q Huang

Publications and source records attributed to Q Huang.

At least 217 records · Page 12Linked to original sources
PubMed1997

[Renal involvement in primary Sjögren's syndrome: a clinicopathological study of 26 cases].

Previous study suggested that renal involvement in primary sjögren's syndrome (SS) was rare and renal damage in SS cases has not been reported in Chinese literature. In this study the clinical and pathological features in 26 primary SS patients (23 female and 3 male, with an average age of 40.9 years) were analyzed. The spectrum of renal disorders in these patients was as follows: renal tubular acidosis (20/26), hypokelemia (18/26), hypocalcemia (14/26), mild proteinuria (less than 1.5 g/d, 12/26), massive proteinuria (more than 1.5 g/d, 9/26, including 5 nephrotic syndrome), and renal insufficiency (5/26). Light microscopy (LM) might show acute or chronic interstitial nephritis (IN, 10/26), or IN accompanied with focal glomerulonephritis (FGN, 4/26), focal segmental glomerulosclerosis (FSGS, 4/26), membranous nephropathy (MN, 3/26), diffuse mesangial proliferative glomerulonephritis (MePGN, 1/26) and membranoproliferative glomerunephritis (MPGN, 1/26) in these SS patients. A variable degree of interstitial lesion was also noted in all patients with glomerular damage. Immunofluorescent examination revealed deposits of IgG (9/24), IgA (8/24), IgM (7/24), C3 (10/24) and C1q (2/24) in granular distribution on the glomerular basement membrane (GBM) or focal masangium and focal deposits of IgG and C3 (7/24) on the tubular basement membrane (TBM). These results suggested that renal tubular acidosis is the most common finding in Chinese SS patients with renal involvement, but glomerular damage is not uncommon. Although IN was the major pathological manifestation in SS patients, FGN, FSGS, MN, MePGN and MPGN might also be found. The exact incidence of secondary glomerular disease in primary SS needs to be studied further.

Adult↗
PubMed1996

Substrate recognition by tissue factor-factor VIIa. Evidence for interaction of residues Lys165 and Lys166 of tissue factor with the 4-carboxyglutamate-rich domain of factor X.

Tissue factor (TF) is the protein cofactor for factor VIIa (FVIIa), the first serine protease of the clotting cascade. Previous studies using alanine mutagenesis have identified TF residues Lys165 and Lys166 as important for factor X (FX) activation, hypothesizing either that these residues interact with phospholipid head groups or that they directly or indirectly promote macromolecular substrate binding. In the recently reported x-ray crystal structure of the isolated extracellular domain of TF, both Lys165 and Lys166 are solvent-exposed and predicted to be near the phospholipid surface in intact TF. We hypothesized that these residues may in fact be ideally positioned to interact with the 4-carboxyglutamate-rich domain (Gla domain) of FX. We therefore predicted that mutations at Lys165 and Lys166 should have no effect on the activation of Gla domainless FX. To test this hypothesis, we mutated both residues Lys165 and Lys166 of TF to Ala, Glu, or Gln and examined the ability of these double mutants to support FVIIa-mediated activation of FX, Gla domainless FX, and factor IX (FIX). Each TF mutant was equivalent to wild-type TF in both FVIIa binding and promotion of FVIIa amidolytic activity. However, all three mutants were markedly deficient in supporting FIX and FX activation, with FX activation rates decreased more than FIX activation rates. In both reactions, the TF mutants exhibited different extents of activity: Gln165-Gln166 > Ala165-Ala166 > Glu165-Glu166. In sharp contrast, all three TF mutants were equivalent to wild-type TF in supporting activation of Gla domainless FX by FVIIa. Interestingly, the deficiency of the mutants in FX activation was less pronounced when Gla domainless FVIIa was used in place of native FVIIa. Together, these findings suggest that TF residues Lys165 and Lys166 contribute to a binding site for the Gla domain of FX (and perhaps other substrates) and that this interaction may be facilitated by the presence of the Gla domain of FVIIa.

Base Sequence↗
PubMed1996

E2F1 inhibition of transcription activation by myogenic basic helix-loop-helix regulators.

Cellular transcription factor E2F1 is thought to regulate the expression of genes important for cell cycle progression and cell proliferation. Deregulated E2F1 expression induces S-phase entry in quiescent cells and inhibits myogenic differentiation. We show here that E2F1 inhibits the activation of gene transcription by myogenic basic helix-loop-helix proteins myoD and myogenin. Transfection assay using different deletion constructs indicates that both the DNA binding and the transactivation domains of E2F1 are required for its inhibition of myoD transcription activation. However, the retinoblastoma protein (RB) binding domain is not required. Furthermore, co-transfection with the RB, which inhibits the transcription activity of E2F1, can also repress E2F1 inhibition of myoD transactivation. These results suggest an essential role of E2F1-mediated transcription in its inhibition of myogenesis.

Animals↗
PubMed1996

Identification of a peroxisome proliferator-responsive element upstream of the human peroxisomal fatty acyl coenzyme A oxidase gene.

Peroxisome proliferators cause a rapid and coordinated transcriptional activation of genes encoding the enzymes of the peroxisomal beta-oxidation pathway in rats and mice. Cis-acting peroxisome proliferator responsive elements (PPREs) have been identified in the 5'-flanking region of H202-producing rat acyl-CoA oxidase (ACOX) gene and in other genes inducible by peroxisome proliferators. To gain more insight into the purported nonresponsiveness of human liver cells to peroxisome volume density and in the activity of the beta-oxidation enzyme system, we have previously cloned the human ACOX gene, the first and rate-limiting enzyme of the peroxisomal beta-oxidation system. We now present information on a regulatory element for the peroxidase proliferator-activated receptor (PPAR)/retinoid X receptor (RXR) heterodimers. The PPRE, consists of AGGTCA C TGGTCA, which is a direct repeat of hexamer half-sites interspaced by a single nucleotide (DR1 motif). It is located at -1918 to -1906 base pairs upstream of the transcription initiation site of this human ACOX gene. This PPRE specifically binds to baculovirus-expressed recombinant rat PPAR alpha/RXR alpha heterodimers. In transient transfection experiments, the maximum induction of luciferase expression by ciprofibrate and/or 9-cis-retinoic acid is dependent upon cotransfection of expression plasmids for PPAR alpha and RXR alpha. The functionally of this human ACOX promoter was further demonstrated by linking it to a beta-galactosidase reporter gene or to a rat urate oxidase cDNA and establishing stably transfected African green monkey kidney (CV1) cell lines expressing reporter protein. The human ACOX promoter has been found to be responsive to peroxisome proliferators in CV1 cells stably expressing PPAR alpha, whereas only a basal level of promoter activity is detected in stably transfected cells lacking PPAR alpha. The presence of a PPRE in the promoter of this human peroxisomal ACOX gene and its responsiveness to peroxisome proliferators suggests that factors other than the PPRE in the 5'-flanking sequence of the human ACOX gene may account for differences, if any, in the pleiotropic responses of humans to peroxisome proliferators.

Acyl-CoA Oxidase↗
PubMed1996

A large-scale population-based study of the association of vitamin D receptor gene polymorphisms with bone mineral density.

Conflicting results have been reported on the association between restriction fragment length polymorphisms (RFLPs) at the vitamin D receptor (VDR) gene locus (i.e., for BsmI, ApaI, and TaqI) and bone mineral density (BMD). We analyzed this association in a large population-based sample (n = 1782) of men and women aged 55-80 years using a novel direct haplotyping polymerase chain reaction (PCR) test to monitor the three polymorphic sites simultaneously. The direct haplotyping test we developed demonstrated a larger degree of genetic polymorphism at the VDR gene locus than described until now. None of the individual RFLPs were associated with BMD at the proximal femur. By analyzing allele dose effects, we identified a VDR haplotype allele weakly associated with low BMD. This allele, as one representative of the group of b alleles, is different from the BsmI allele previously reported by other groups to be associated with low BMD. This suggests allelic heterogeneity at the VDR locus in relation to BMD. Our results indicate at most a small effect of the VDR genotype on BMD in this elderly population. Since anonymous polymorphisms were analyzed, alternative explanations for our results include linkage to another nearby bone-metabolism related gene.

Absorptiometry, Photon↗
PubMed1996

Preclinical evaluation of SPECT imaging with 131I-labeled monoclonal antibody SZ39 in nude mice bearing human glioma xenografts.

The imaging characteristics of monoclonal antibody SZ39 against glioma were evaluated in glioma-bearing nude mice. Monoclonal antibody SZ39 is a murine IgG2a that reacts with a glycoprotein epitope (molecular weight 180,000), a human glioma-associated membrane antigen. Monoclonal antibody SZ39 was labeled with 131I using a modified chloramine T method. Each glioma-bearing nude mouse was given 50 microCi/40 micrograms of the experimental agent, 131I-labeled monoclonal antibody, or 50 microCi/46 micrograms of a control agent, 131I-labeled monoclonal antibody C50, an antibody against colon cancer. Single-photon emission computed tomography (SPECT) was performed every 24 hours in the first week after administration. Glioma-bearing nude mice were killed in groups of 3 at 24 hours and daily up to 72 hours. The ratio of radioactivity uptake in glioma to normal organs was calculated. After administration of the labeled SZ39, glioma was visualized with SPECT on days 1 to 7, particularly at 72 hours. There was no accumulation of radioactivity in glioma with the labeled C50 antibody. All glioma-organ ratios increased with time. At 72 hours, the ratio of glioma to brain was 22.46 and of the other organs was 2.64 on average. SZ39 had a relatively low endocytosis rate and was favorable for 131I labeling. These characteristics were helpful to reduce free 131I in the blood and reduce the uptake by other organs. The results suggest that 131I-labeled SZ39 selectively accumulates in glioma, representing a potential strategy for SPECT imaging of these lesions.

Adult↗
PubMed1996

Dot-immunogold filtration assay as a screening test for syphilis.

A dot-immunogold filtration assay (DIGFA) for the rapid detection of reaginic antibody in the serum of syphilitic patients was developed. The assay was simple, rapid, and reproducible. The test completion time was 2 min, and the assay required no equipment. The positive dot was very obvious, and the results could easily be determined with the naked eye. A total of 350 serum samples were examined by DIGFA, the rapid plasma reagin test, and the fluorescent treponemal antibody-absorption test. The levels of agreement between DIGFA and the rapid reagin test and between DIGFA and the fluorescent treponemal antibody-absorption test were 100 and 98%, respectively. The results of clinical application indicated that DIGFA could be used as a routine screening test for syphilis.

Antibodies, Bacterial↗
PubMed1996

Synergistic interactions between overlapping binding sites for the serum response factor and ELK-1 proteins mediate both basal enhancement and phorbol ester responsiveness of primate cytomegalovirus major immediate-early promoters in monocyte and T-lymphocyte cell types.

Cytomegalovirus (CMV) infection is nonpermissive or persistent in many lymphoid and myeloid cell types but can be activated in differentiated macrophages. We have shown elsewhere that both the major immediate-early gene (MIE) and lytic cycle infectious progeny virus expression can be induced in otherwise nonpermissive monocyte-like U-937 cell cultures infected with either human CMV (HCMV) or simian CMV (SCMV) by treatment with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). Two multicopy basal enhancer motifs within the SCMV MIE enhancer, namely, 11 copies of the 16-bp cyclic AMP response element (CRE) and 3 copies of novel 17-bp serum response factor (SRF) binding sites referred to as the SNE (SRF/NFkappaB-like element), as well as four classical NFkappaB sites within the HCMV version, contribute to TPA responsiveness in transient assays in monocyte and T-cell types. The SCMV SNE sites contain potential overlapping core recognition binding motifs for SRF, Rel/NFkappaB, ETS, and YY1 class transcription factors but fail to respond to either serum or tumor necrosis factor alpha. Therefore, to evaluate the mechanism of TPA responsiveness of the SNE motifs and of a related 16-bp SEE (SRF/ETS element) motif found in the HCMV and chimpanzee CMV MIE enhancers, we have examined the functional responses and protein binding properties of multimerized wild-type and mutant elements added upstream to the SCMV MIE or simian virus 40 minimal promoter regions in the U-937, K-562, HL-60, THP-1, and Jurkat cell lines. Unlike classical NFkappaB sites, neither the SNE nor the SEE motif responded to phosphatase inhibition by okadaic acid. However, the TPA responsiveness of both CMV elements proved to involve synergistic interactions between the core SRF binding site (CCATATATGG) and the adjacent inverted ETS binding motifs (TTCC), which correlated directly with formation of a bound tripartite complex containing both the cellular SRF and ELK-1 proteins. This protein complex was more abundant in U-937, K-562, and HeLa cell extracts than in Raji, HF, BALB/c 3T3, or HL-60 cells, but the binding activity was altered only twofold after TPA treatment. A 40-fold stimulation of chloramphenicol acetyltransferase activity mediated by four tandem repeats of the SNE could be induced within 2 h (and up to 250-fold within 6 h) after addition of TPA in DNA-transfected U-937 cells, indicating that the stimulation appeared likely to be a true protein kinase C-mediated signal transduction event rather than a differentiation response. Slight differences in the sequence of the core SRF binding site compared with that of the classical c-Fos promoter serum response element, together with differences in the spacing between the SRF and ETS motifs, appear to account for the inability of the SCMV SNEs to respond to serum induction.

3T3 Cells↗
PubMed1996

VEGF induces NO-dependent hyperpermeability in coronary venules.

The purpose of this study was to investigate the direct effect of vascular endothelial growth factor (VEGF) on microvascular permeability and its signaling mechanisms. The apparent permeability coefficient to albumin was measured in isolated coronary venules. Topical application of VEGF dose-dependently and transiently increased albumin permeability by two- to threefold. Inhibition of nitric oxide (NO) synthesis with NG-monomethyl-L-arginine abolished VEGF-induced venular hyperpermeability. Furthermore, because NO exerts vasoactive effects through stimulation of guanylate cyclase (GC) and the subsequent production of guanosine 3',5'-cyclic monophosphate (cGMP), we examined the role of GC and cGMP-dependent protein kinase (PKG) in the mediation of VEGF's action. The permeability response to VEGF was measured in the presence of the selective GC inhibitor 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one and the specific PKG inhibitor KT-5823. Both inhibitors reduced basal permeability and prevented the hyperpermeability response to VEGF. Therefore, we suggest that VEGF modulates microvascular permeability via a signaling cascade involving NO synthesis, GC stimulation, and PKG activation.

Alkaloids↗
PubMed1996

Studies on metabolites of mycoparasitic fungi. V. Ion-spray ionization mass spectrometric analysis of trichokonin-II, a peptaibol mixture obtained from the culture broth of Trichoderma koningii.

The sequence of a peptide, trichokonin-II (TK-II), obtained from the culture broth of Trichoderma koningii OUDEMANS, was examined by ion-spray ionization mass spectrometry (ISI-MS), including the collision-induced dissociation (CID) technique. TK-II was concluded to be a mixture of three peptaibols, TK-IIa, TK-IIb, and TK-IIc.

Alamethicin↗
PubMed1996

Modulation effects of hexamethylene bisacetamide on growth and differentiation of cultured human malignant glioma cells.

The modulation effects of hexamethylene bisacetamide (HMBA), a differentiation-inducing agent, on growth and differentiation of cells from human malignant glioma cell line SHG-44 were studied. At cytostatic doses (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 15 days), HMBA exerted a marked inhibitory effect on cell proliferation. Exposure to HMBA (5 mM and 10 mM for 12 days) also resulted in an accumulation of cells in G0/G1 phase and a decrease of cells in S phase as analyzed by flow cytometry. The reversible effects of 7.5 mM HMBA and 10 mM HMBA on cell proliferation and 10 mM HMBA on disruption of cell cycle distribution were observed when HMBA was removed from culture media on Day 6 and replaced with HMBA-free media. Colony-forming efficiency (CFE) in soft agar was remarkably decreased by HMBA (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 14 days), and in 7.5 mM HMBA- and 10 nM HMBA treated cells, the CFEs were reduced to 25% and 12.5%, respectively, of that in untreated cells. Cells treated with HMBA (5 mM and 10 mM for 15 days) remained tumorigenic in athymic nude mice, but the growth rates of the xenografts were much slower than those in the control group. The effects of HMBA on cell proliferation, cell cycle distribution, CFE, and growth of xenografts were dose dependent. A more mature phenotype was confirmed by the morphological changes from spindle shape to large polygonal stellate shape and remarkably elevated expression of glial fibrillary acidic protein in cells exposed to HMBA (5 mM, 10 mM for 15 days). Our results showed that a more differentiated phenotype with marked growth arrest was induced in SHG-44 cells by HMBA.

Acetamides↗
PubMed1996

Target imaging diagnosis of human brain glioma. Clinical analysis of 40 cases.

OBJECTIVE: To establish a method for localization and qualitative diagnosis of glioma. METHODS: The monoclonal antibody SZ-39 against human glioma was labelled with 131I and injected intravenously into 40 patients with intracranial occupying lesions proved by X-CT. 72 hours after 131I-McAb-SZ39 administration, cranial bone nuclide-imaging agent 99mTc-MDP was injected intravenously, and the patients were examined by SPECT scan with dual nuclide double channel tomography and special software. On radio-immuno-image, the immunocomplex formed by specific conjugation of 131I-McAb-SZ39 with target tissue was red, while the cranial bone incorporated with 99mTc-MDP was green. The location of the immunocomplex area could be identified by the superimposition of the images. RESULTS: 21 patients with positive targeting diagnosis of glioma showed the accuracy rate checked by SPECT was 81%(17/21) and by X-CT 48% (10/21). Seven patients with negative targeting diagnosis showed the accuracy rate checked by SPECT was 86%(6/7) and by X-CT 14% (1/7). Pathologically, the sensitivity of targeting SPECT to glioma was 94.5%(17/18) and that of X-CT 55%(10/18). CONCLUSIONS: Targeting SPECT examination could be used for localization and qualitative diagnosis of glioma and make up the inadequacy of X-CT in the qualitative diagnosis of atypical incipient and recurrent glioma, meningioma, metastatic carcinoma, and inflammatory lesions of brain.

Adolescent↗
PubMed1996

[Relationship between disturbances of microcirculation and TNF during burn shock].

The changes in microcirculation and the level of plasma TNF in rat at the early stage of burn shock were measured, and the effects of Polygonum cuspidatum (PC) on above mentioned changes were observed. It was shown when the level of plasma TNF was increased, the number of adhesive leukocytes on venule wall was increased and the number of open capillaries were reduced significantly, and there were apparent aggregation of leukocytes and injury in lungs. The level of plasma TNF and the number of adhesive leukocytes were nearly normal, and the degree of aggregation of leukocytes and injury of lungs were attenuated by giving PC. The present study showed that the level of elevated plasma TNF in the early stage of burn shock was directly correlated with the adherence of leukocytes and the closing of capillaries. The administration of PC could apparently inhibit the increase of leukocytes, and at the meantime, attenuate the adherence of the neutrophils and injury of the lung. The results confirmed that the elevation of plasma TNF might be involved in the development of adherence of neutrophils and the disturbances of microcirculation in burn shock.

Animals↗