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Biomedical subjects

Q Zhang

Publications and source records attributed to Q Zhang.

At least 829 records · Page 46Linked to original sources
PubMed1994

Epstein-Barr virus (EBV) latent membrane protein 1 increases HLA class II expression in an EBV-negative B cell line.

Transformation of normal resting B cells by the Epstein-Barr virus (EBV) leads to the establishment of permanent lymphoblastoid cell lines (LCL) which express high levels of HLA antigens and which are highly efficient in antigen presentation. Certain features of the LCL phenotype can be reproduced by transfecting EBV-negative B lymphoma (BL) cell lines with individual EBV latent genes under heterologous promoters. In this work we have analyzed a series of subclones derived from the EBV-negative cell line Louckes, stably transfected with constructs encoding EBV latent genes for their expression of HLA class II molecules. Louckes parental cells and control transfectants expressed detectable levels of HLA-DR, DQ and DP antigens on the cellular surface by cytofluorometry, but these levels were significantly increased in transfectants expressing the virus-coded latent membrane protein 1 (LMP-1). Northern blotting for the individual alpha and beta chain mRNA at each of the three HLA class II loci indicated correspondingly increased levels of HLA class II transcripts in the LMP-1 transfectants. Transfectants expressing the virus-coded nuclear antigens EBNA-1, EBNA-2 or EBNA-LP showed no significant changes in these parameters. These observations indicate that up-regulation of HLA-class II molecules can be a part of the changes induced by LMP-1 in B cells.

Antigens, Viral↗
PubMed1994

Absence of transforming growth factor-beta responsiveness in the tamoxifen growth-inhibited human breast cancer cell line CAMA-1.

Tamoxifen has been an effective antiestrogen in suppressing breast cancer growth which is estrogen-responsive or dependent. Early studies have provided circumstantial evidence that transforming growth factor-beta (TGF-beta) may be an autocrine mediator of tamoxifen action. Therefore, it is both fundamentally important and clinically relevant to investigate the relationship between tamoxifen and TGF-beta. In this study, we demonstrated that CAMA-1 cells, which are sensitive to tamoxifen inhibition, did not respond to TGF-beta growth inhibition. The type I and II TGF-beta receptors were undetectable by the radio-ligand affinity labeling technique. Despite the presence of a normal TGF-beta type II receptor gene, the mRNA transcript of the gene was undetectable by the extremely sensitive Intron-differential RNA/PCR method. The possibility that the lack of TGF-beta receptors might be intimately linked to the absence of normal retinoblastoma (Rb) gene products, as suggested by previous studies of retinoblastoma cells, was further investigated. The lack of TGF-beta receptor expression was found due to reasons other than the absence, deletion or abnormality of the Rb gene because a normal Rb gene and its hyper- and hypo-phosphorylated protein products were detected in CAMA-1 cells. In conclusion, our results suggest that the TGF-beta system is not obligatory for antiestrogen growth inhibition of CAMA-1 cells.

Base Sequence↗
PubMed1994

Study on lymphocyte activation and proliferation induced by anti-CD3 McAb.

T cell activation and proliferation via CD3-TCR complex were investigated by lymphocyte DNA synthesis in vitro. Several interfering factors were also discussed. The result indicated that lymphocyte activation and proliferation are calcium-dependent. A rise of cytoplasmic free Ca2+ quickly following activation with CD3 McAb is mainly due to intracellular mobilization of Ca2+, while lymphocyte proliferation needs both intracellular mobilization of Ca2+ as well as influx of extracellular Ca2+. It was confirmed that CTX sensitive G protein plays a role in regulating T cell proliferation by pretreatment with CTX suppressing lymphocyte H-TdR incorporation obviously. PLC and PKC inhibitor neomycin and P. S. S could also decrease T cell proliferation.

Antibodies, Monoclonal↗
PubMed1994

Modulation of cell surface fibronectin assembly sites by lysophosphatidic acid.

Lysophosphatidic acid is a product of activated platelets and has diverse actions on cells. We have characterized the effect of lysophosphatidic acid on cell-mediated binding and assembly of fibronectin, an extracellular matrix protein. Serum made from whole blood, but neither platelet-poor plasma nor serum made from platelet-poor plasma, caused enhanced binding of fibronectin to cultured fibroblastic cells. The ability of whole blood serum to enhance binding of fibronectin was abolished by phospholipase B. These results indicate that lysophosphatidic acid derived from platelets is the principal component in whole blood serum that is active in the fibronectin binding assay. 1-oleoyl lysophosphatidic acid, 20-200 nM, was as active as 0.1-0.2% whole blood serum. The stimulatory effect of lysophosphatidic acid on the binding of fibronectin or the amino-terminal 70-kD fragment of fibronectin was rapid, sustained, and lost upon removal of lysophosphatidic acid. The stimulatory effect on binding could not be duplicated by bradykinin, platelet-activating factor, bombesin, or a peptide agonist of the thrombin receptor. Enhanced binding of the 70-kD fragment was due to increases in both the number and affinity of binding sites. Enhanced binding and assembly of fibronectin correlated with changes in cell shape and actin-containing cytoskeleton. The binding sites for fibronectin on lysophosphatidic acid-stimulated cells, as assessed by fluorescence, video, and scanning electron microscopy, were on areas of cell membrane containing numerous filopodia that extended between cells or between cells and substratum. These observations suggest that lysophosphatidic acid functions as a powerful and specific modulator of cell shape and early matrix assembly during wound healing.

Actin Cytoskeleton↗
PubMed1994

Glycolipid receptors for attachment of Mycoplasma hyopneumoniae to porcine respiratory ciliated cells.

Glycolipid receptors for Mycoplasma hyopneumoniae attachment were analyzed by using a thin-layer chromatography (TLC) overlay assay. M. hyopneumoniae bound specifically to sulfatide, globoside, and monosialoganglioside GM3. No binding to sphingomyelin, cerebroside, lactosyl ceramide, ceramide trihexoside, monosialogangliosides GM1 and GM2, disialogangliosides (GD1a, GD1b, and GD3), trisialoganglioside (GT1b), cholesterol, cholesterol sulfate, palmitic acid, tripalmitin, or cholesteryl palmitate was detected. Total lipids extracted from cilia of the swine respiratory epithelium, the natural targets of M. hyopneumoniae infection, were also separated on TLC plates and overlaid with mycoplasmas. M. hyopneumoniae bound specifically to three ciliary glycolipids identified as La, Lb, and Lc. Binding to Lc was stronger than to La and Lb. All three lipids were believed to be sulfated glycolipids, as determined by laminin binding and staining with azure A. Lc was identified as a putative sulfatide because it has a mobility similar to that of authentic sulfatide and comigrated with sulfatide on TLC plates. Laminin bound to La, Lb, and Lc and produced dose-dependent inhibition of adherence of the mycoplasma to the three ciliary receptors. Binding of the mycoplasma to sulfatide, La, Lb, and Lc was partially inhibited by dextran sulfate, heparin, fucoidan, mucin, and chondroitin sulfate B. These substances blocked the adherence of M. hyopneumoniae to cilia and ciliated cells as shown in a previous study (Q. Zhang, T. F. Young, and R. F. Ross, Infect. Immun. 62:1616-1622, 1994). These results indicate that La, Lb, and Lc are the major native receptors for M. hyopneumoniae adherence to ciliated cells.

Animals↗
PubMed1994

Microtiter plate adherence assay and receptor analogs for Mycoplasma hyopneumoniae.

A microtiter plate adherence assay for Mycoplasma hyopneumoniae was established by use of purified swine tracheal cilia which contained receptors for the mycoplasmas. M. hyopneumoniae bound specifically to plates coated with solubilized cilia. The binding was dependent on both the concentration of cilia and the number of mycoplasmas. Dextran sulfate, heparin, chondroitin sulfate, laminin, mucin, and fucoidan significantly inhibited the binding of the mycoplasmas. The six inhibitors also disrupted the adherence of the mycoplasmas to intact ciliated cells. Preincubation with either mycoplasmas or cilia indicated that heparin, mucin, fucoidan, and chondroitin sulfate interacted with the adhesive molecules on the surface of the mycoplasmas, while laminin blocked the receptors in cilia. The basis for the inhibition induced by dextran sulfate was unknown. Treatment of cilia with neuraminidase appeared to promote adherence of the mycoplasmas, whereas treatment of cilia with sodium metaperiodate decreased binding. These results indicate that receptors for M. hyopneumoniae in the ciliated epithelium of the respiratory tract of pigs are glycoconjugate in nature.

Animals↗
PubMed1994

Functional and physical interaction between p53 and BZLF1: implications for Epstein-Barr virus latency.

The p53 tumor suppressor protein, which is commonly mutated in human cancers, has been shown to interact directly with virally encoded from papillomavirus, adenovirus, and simian virus 40. The disruption of p53 function may be required for efficient replication of certain viruses and may also play a role in the development of virally induced malignancies. Infection with Epstein-Barr virus (EBV) has been associated with the development of B-cell lymphomas and nasopharyngeal carcinoma. Here we show that the EBV immediate-early protein, BZLF1 (Z), which is responsible for initiating the switch from latent to lytic infection, can interact directly in vitro and in vivo with the tumor suppressor protein, p53. This interaction requires the coiled-coil dimerization domain of the Z protein and the carboxy-terminal portion of p53. Overexpression of wild-type p53 inhibits the ability of Z to disrupt viral latency. Likewise, Z inhibits p53-dependent transactivation in lymphoid cells. The direct interaction between Z and p53 may play a role in regulating the switch from latent to lytic viral infection.

Cells, Cultured↗
PubMed1994

The bZIP transactivator of Epstein-Barr virus, BZLF1, functionally and physically interacts with the p65 subunit of NF-kappa B.

The Epstein-Barr virus (EBV) BZLF1 (Z) immediate-early transactivator initiates the switch between latent and productive infection in B cells. The Z protein, which has homology to the basic leucine zipper protein c-Fos, transactivates the promoters of several replicative cycle proteins. Transactivation efficiency of the EBV BMRF1 promoter by Z is cell type dependent. In B cells, in which EBV typically exists in a latent form, Z activates the BMRF1 promoter inefficiently. We have discovered that the p65 component of the cellular factor NF-kappa B inhibits transactivation of several EBV promoters by Z. Furthermore, the inhibitor of NF-kappa B, I kappa B alpha, can augment Z-induced transactivation in the B-cell line Raji. Using glutathione S-transferase fusion proteins and coimmunoprecipitation studies, we demonstrate a direct interaction between Z and p65. This physical interaction, which requires the dimerization domain of Z and the Rel homology domain of p65, can be demonstrated both in vitro and in vivo. Inhibition of Z transactivation function by NF-kappa B p65, or possibly by other Rel family proteins, may contribute to the inefficiency of Z transactivator function in B cells and may be a mechanism of maintaining B-cell-specific viral latency.

Cell Line↗
PubMed1994

BCL3 encodes a nuclear protein which can alter the subcellular location of NF-kappa B proteins.

BCL3 is a candidate proto-oncogene involved in the recurring translocation t(14;19) found in some patients with chronic lymphocytic leukemia. BCL3 protein acts as an I kappa B in that it can specifically inhibit the DNA binding of NF-kappa B factors. Here, we demonstrate that BCL3 is predominantly a nuclear protein and provide evidence that its N terminus is necessary to direct the protein into the nucleus. In contrast to I kappa B alpha (MAD3), BCL3 does not cause NF-kappa B p50 to be retained in the cytoplasm; instead, in cotransfection assays, it alters the subnuclear localization of p50. The two proteins colocalize, suggesting that they interact in vivo. Further immunofluorescence experiments showed that a mutant p50, lacking a nuclear localization signal and restricted to the cytoplasm, is brought into the nucleus in the presence of BCL3. Correspondingly, a wild-type p50 directs into the nucleus a truncated BCL3, which, when transfected alone, is found in the cytoplasm. We tested whether BCL3 could overcome the cytoplasmic retention of p50 by I kappa B alpha. Results from triple cotransfection experiments with BCL3, I kappa B alpha, and p50 implied that BCL3 can successfully compete with I kappa B alpha and bring p50 into the nucleus; thus, localization of NF-kappa B factors may be affected by differential expression of I kappa B proteins. These novel properties of BCL3 protein further establish BCL3 as a distinctive member of the I kappa B family.

Animals↗
PubMed1994

Airway and tissue mechanics during physiological breathing and bronchoconstriction in dogs.

In five open-chest dogs and with four to five alveolar capsules we used an optimal ventilator waveform (OVW) to follow frequency and tidal volume (VT) dependence of lung, airway, and tissue resistance (R) and elastance (E) before and during constant infusion of histamine (16 micrograms.kg-1.min-1). OVW contains sufficient flow energy between 0.234 and 4.7 Hz, avoids nonlinear harmonic interactions, and simultaneously ventilates with physiological VT. Each OVW breath permits a smooth estimate of frequency dependence of R and E for the whole lung. A constant-phase model analysis provided estimates of purely viscous resistance (Rvis), which represents the sum of airway resistance (Raw) and any purely newtonian component of tissue resistance (Rti), and parameters G and H, which govern frequency dependence of Rti and tissue elastance (Eti), respectively. Tissue structural damping (eta) is calculated as G/H. This model was applied to the whole lung and tissue impedance as estimated from each capsule. We found a small but inconsequential purely newtonian component of Rti, even during constriction. Four dogs showed a peak response at approximately 4 min in lung Rvis coupled (in time) to initial increases in G, H, eta, and airway inhomogeneities. In two of these dogs the response was severe. Tissue properties estimated from whole lung impedance (G, H, and eta) were nearly identical to values estimated from unobstructed capsules throughout infusion. By using a technique independent of alveolar capsules, our results indicate that a major if not dominant response to a constrictive agonist occurs in lung tissues, resulting in a large increase in Rti and Eti. With severe constriction, significant increases occur in Raw and airway inhomogeneities as well. Finally, separation of airway and tissue properties using input impedance estimated from the frequency-rich OVW avoids use of alveolar capsules and may prove an effective tool for partitioning airway and tissue properties in humans.

Airway Resistance↗
PubMed1994

[Hair cell regeneration and recovery following gentamicin induced damage in the chick cochlea].

Two-day old chicks were given gentamicin (GM) and kanamycin (KM) for 10 days and then the cochleas were processed for both scanning electron microscopy and light microscopy on the same day and in 1, 2, 3, and 4 weeks following the last injection to examine hair cells regeneration and recovery. The result showed that hair cell loss was up to 40% in the base of the basilar papilla following GM and KM administration. One week after injection, however, most of the damaged region was replaced with regenerated hair cells. Three to four weeks later, the regenerated hair cells were developed into normal sensory hair cells. This experiment demonstrated that the hair cells in the chick cochlea were able to regenerate and recover following GM and KM induced damage.

Animals↗
PubMed1994

[Changes in lymphocyte membrane fluidity after burn and its significance].

In the present experiment, the change in lymphocyte membrane fluidity after burn was observed by measurement of fluorescent depolarization with DPH as a probe. 11%-12% TBSA of full-thickness skin burn was made in Balb/c mice. Six days later the animals were killed and their spleen were obtained. Then membrane fluidity and IL-2 production of splenic lymphocytes were measured, and lipid peroxide level of the spleen was assayed. The results showed that the fluidity decreased significantly with suppression of lymphocyte proliferation and IL-2 production, and that the lipid peroxide level increased. There was a negative correlation between the decrease in membrane fluidity and the suppression of lymphocyte functions. The same correlation also existed between the changes in membrane fluidity and the lipid peroxide level. The data indicated that the decreased membrane fluidity might be one of the causes for lymphocyte dysfunction and related to the enhancement of lipid peroxidation after burn.

Animals↗
PubMed1994

Preliminary report of molecular detection of retinoblastoma gene mutations.

To develop gene diagnosis for retinoblastoma predisposition, it is necessary to disclose the retinoblastoma gene mutations or deletions in detail. Genomic DNA from tumor and peripheral white blood cells in 33 patients with retinoblastoma was detected with 3.8kb probe derived from 3' end of retinoblastoma gene cDNA. The gene abnormalities, including deletion, partial deletion and rearrangement, were found in 18 patients. Further research will be aimed at microdeletions or mutations for those patients without detectable variations in Southern hybridization.

Blotting, Southern↗
PubMed1994

[Site-directed mutagenesis at Ser177 of penicillin G acylase gene].

Site-directed mutagenesis was performed at Ser177 of Penicillin G Acylase (PGA) gene of E. coli by gap duplex method. Screened by 2-nitro-5-phenylacetaminobenzoic acid (NIPAB) test paper assay and confirmed by DNA sequencing, the mutants Cys177, Gly177, Arg177 and Asn177 were obtained. They have no activity of PGA. The mutant enzyme was expressed and detected by PAGE. It is suggested that Ser177 is at the substrate binding center of PGA and can not be replaced.

Base Sequence↗
PubMed1994

Mutation analysis of the Fanconi anemia gene FACC.

Fanconi anemia (FA) is a genetically heterogeneous autosomal recessive disorder characterized by a unique hypersensitivity of cells to DNA cross-linking agents; a gene for complementation group C (FACC) has recently been cloned. We have amplified FACC exons with their flanking intron sequences from genomic DNA from 174 racially and ethnically diverse families in the International Fanconi Anemia Registry and have screened for mutations by using SSCP analysis. We identified eight different variants in 32 families; three were detected in exon 1, one in exon 4, one in intron 4, two in exon 6, and one in exon 14. Two of the eight variants, in seven families, did not segregate with the disease allele in multiplex families, suggesting that these variants represented benign polymorphisms. Disease-associated mutations in FACC were detected in a total of 25 (14.4%) of 174 families screened. The most frequent mutations were IVS4 + 4 A-->T (intron 4; 12 families) and 322delG (exon 1; 9 families). Other, less common mutations include Q13X in exon 1, R185X and D195V in exon 6, and L554P in exon 14. The polymorphisms were S26F in exon 1 and G139E in exon 4. All patients in our study with 322delG, Q13X, R185X, and D195V are of northern or eastern European or southern Italian ancestry, and 18 of 19 have a mild form of the disease, while the 2 patients with L554P, both from the same family, have a severe phenotype. All 19 patients with IVS4 + 4 A-->T have Jewish ancestry and have a severe phenotype.

Base Sequence↗
PubMed1993

Gender-specific impairment on Morris water maze task after entorhinal cortex lesion.

After unilateral entorhinal cortex lesion, deficits on a working spatial memory Morris water maze task were examined in male and female rats to determine if gender differences exist in response to hippocampal deafferentation. Brain-damaged males showed a persistent water maze deficit that persisted throughout the 10 days of testing. Brain-damaged females did not. The performance of the injured females was only slightly impaired relative to sham males and females, and was significantly better than males with EC damage. This lack of a water maze deficit in lesion females is hypothesized to be due either to gender differences in sprouting responses or to a more flexible use of multiple cues by females relative to males.

Animals↗
PubMed1993

CACC box and enhancer response of the human embryonic epsilon globin promoter.

The functional interaction between the human epsilon globin promoter and an erythroid-specific transcription enhancer, 5' HS-2, has been analyzed by transient expression assay. While stepwise deletion of DNA sequences between -852 and -122 had only small effects, removal of the CACC box at position -111 greatly decreased epsilon-globin promoter activity, as well as its response to the enhancer function of 5' HS-2 in erythroid cells. Our data demonstrated that the three ubiquitous promoter elements, the CACC, CCAAT, and TATA boxes, of the epsilon-globin-encoding gene together form a minimal promoter that would interact efficiently with 5' HS-2, and that at least the CACC box is an essential functional component of this enhancer-promoter interaction.

Base Sequence↗