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Biomedical subjects

Y Zhai

Publications and source records attributed to Y Zhai.

At least 55 records · Page 3Linked to original sources
PubMed1999

[The examination of SIgE in perennial allergic rhinitis with mast allergy test system].

OBJECTIVE: To explore the relation between serum specificity immunoglobulin E (SIgE) and skin test (intracutaneous test) as well as nasal provocation in Perennial allergy rhinitis (PAR) by Mast Allergy Test System. METHOD: Serum allergen-specific IgE (SIgE) were examined by Mast Allergy Test System in 57 case of PAR patients. RESULT: The SIgE positive rate of fannae and pteronvssinus are highest (52.6%), the sensitive rate of intracutaneous test is 88.4% and nasal provocation is 88.9%. The SIgE positive rates of cludosporium, penicillum and altemana are 26.3%, 24.6% and 21.0%, respectively. The SIgE positive rates of fannae, cockroach, shrimp, crab, egg and milk is direct proportion with intracutaneous test (P < 0.01). Pteronvssiaus and pigweek mix have no relationship with intracutaneous test (P > 0.05). In addition, the positive rate of ragweed mix SIgE is 22.8%, but there is non of this plant in South China. It is worthy of paying attention in clinic. CONCLUSION: It indicate that Mast Allergy Test System is one of the better examination for PAR allergens.

Adolescent↗
PubMed1998

Immunizing patients with metastatic melanoma using recombinant adenoviruses encoding MART-1 or gp100 melanoma antigens.

BACKGROUND: The characterization of the genes encoding melanoma-associated antigens MART-1 or gp100, recognized by T cells, has opened new possibilities for the development of immunization strategies for patients with metastatic melanoma. With the use of recombinant adenoviruses expressing either MART-1 or gp100 to immunize patients with metastatic melanoma, we evaluated the safety, immunologic, and potential therapeutic aspects of these immunizations. METHODS: In phase I studies, 54 patients received escalating doses (between 10(7) and 10(11) plaque-forming units) of recombinant adenovirus encoding either MART-1 or gp100 melanoma antigen administered either alone or followed by the administration of interleukin 2 (IL-2). The immunologic impact of these immunizations on the development of cellular and antibody reactivity was assayed. RESULTS: Recombinant adenoviruses expressing MART-1 or gp100 were safely administered. One of 16 patients with metastatic melanoma receiving the recombinant adenovirus MART-1 alone experienced a complete response. Other patients achieved objective responses, but they had received IL-2 along with an adenovirus, and their responses could be attributed to the cytokine. Immunologic assays showed no consistent immunization to the MART-1 or gp100 transgenes expressed by the recombinant adenoviruses. High levels of neutralizing antibody were found in the pretreatment sera of the patients. CONCLUSIONS: High doses of recombinant adenoviruses could be safely administered to cancer patients. High levels of neutralizing antibody present in patients' sera prior to treatment may have impaired the ability of these viruses to immunize patients against melanoma antigens.

Adenoviridae↗
PubMed1998

LIGHT, a novel ligand for lymphotoxin beta receptor and TR2/HVEM induces apoptosis and suppresses in vivo tumor formation via gene transfer.

LIGHT is a new member of tumor necrosis factor (TNF) cytokine family derived from an activated T cell cDNA library. LIGHT mRNA is highly expressed in splenocytes, activated PBL, CD8(+) tumor infiltrating lymphocytes, granulocytes, and monocytes but not in the thymus and the tumor cells examined. Introduction of LIGHT cDNA into MDA-MB-231 human breast carcinoma caused complete tumor suppression in vivo. Histological examination showed marked neutrophil infiltration and necrosis in LIGHT expressing but not in the parental or the Neo-transfected MDA-MB-231 tumors. Interferon gamma (IFNgamma) dramatically enhances LIGHT-mediated apoptosis. LIGHT protein triggers apoptosis of various tumor cells expressing both lymphotoxin beta receptor (LTbetaR) and TR2/HVEM receptors, and its cytotoxicity can be blocked specifically by addition of a LTbetaR-Fc or a TR2/HVEM-Fc fusion protein. However, LIGHT was not cytolytic to the tumor cells that express only the LTbetaR or the TR2/HVEM or hematopoietic cells examined that express only the TR2/HVEM, such as PBL, Jurkat cells, or CD8(+) TIL cells. In contrast, treatment of the activated PBL with LIGHT resulted in release of IFNgamma. Our data suggest that LIGHT triggers distinct biological responses based on the expression patterns of its receptors on the target cells. Thus, LIGHT may play a role in the immune modulation and have a potential value in cancer therapy.

Apoptosis↗
PubMed1998

TRANK, a novel cytokine that activates NF-kappa B and c-Jun N-terminal kinase.

We searched the expressed sequence tag database using sequence homology and identified a novel cytokine, which we have named TRANK (thioredoxin peroxidase-related activator of NF-kappa B and c-Jun N-terminal kinase). The predicted amino acid sequence of TRANK was highly homologous to that of the thiol-specific antioxidant proteins. Unlike these proteins, however, TRANK had a putative secretory signal polypeptide and was found to be secreted by cells. TRANK was expressed in most tissues and cell lines, and the gene that encodes it was mapped to chromosome Xp21-22.1. TRANK activated NF-kappa B and induced the degradation of the inhibitory subunit of NF-kappa B. In addition, TRANK up-regulated the expression of NF-kappa B-dependent gene products, ICAM-1, and inducible nitric oxide synthase. TRANK also activated c-Jun N-terminal kinase and induced the proliferation of normal human foreskin fibroblasts. Its homology with antioxidant proteins, wide distribution in tissues, and ability to activate NF-kappa B and c-Jun N-terminal kinase suggest that TRANK plays an important role in inflammation.

Amino Acid Sequence↗
PubMed1998

Recombinant adenovirus encoding gp100 modulates experimental melanin-protein induced uveitis (EMIU).

Experimental melanin-protein induced uveitis (EMIU) is a T-cell mediated autoimmune uveitis induced by immunization with bovine uveal melanin protein. Gp100, a melanocyte lineage-specific protein, is identified as a human melanoma antigen. A recombinant adenovirus construct encoding gp100 (Ad2CMV-gp100) has been used as a vaccine for cancer therapy. This study examines the effect of Ad2CMV-gp100 on EMIU. To induce EMIU, rats were injected intraperitoneally on day 7 before immunization with ad2CMV-gp100, control adenovirus encoding LacZ (Ad2CMV-LacZ), or no virus. On day 21 after immunization, the right eye was processed for histology and the left eye was analysed for cytokines by quantitative reverse transcriptase-polymerase chain reaction. Western blot analysis showed that uveal melanin-protein contains gp100. In three independent experiments, ocular inflammation was significantly suppressed, and expression of ocular IL-12p40 mRNA was much lower in the rats which received Ad2CMV-gp100 before immunization than in those that received Ad2CMV-LacZ or no virus. No abnormalities developed in rats which received Ad2CMV-gp100 or Ad2CMV-LacZ alone. Therefore, Ad2CMV-gp100 injection prevents the development of EMIU, at least in part, through cytokine regulation.

Adenoviridae↗
PubMed1998

Two distinct forms of soluble MHC class I molecules synthesized by different mechanisms in normal rat cells in vitro.

Rat soluble MHC class I synthesis was studied at both RNA and protein levels to determine whether multiple forms of soluble MHC class I molecules are produced by different mechanisms. RT-PCR and sequencing of MHC class I transcripts identified an alternatively spliced nonclassical MHC class I gene product, lacking both exon 5 and 6, in both spleen and liver. Immunoprecipitation and SDS-PAGE identified two distinct soluble MHC class I proteins in both splenocyte- and hepatocyte-culture supernatants. The 36Kd classical soluble MHC class I protein (RT1.Aa) was precipitated by both allele-specific (MN4.91.6, R3/13, R2/15S) and pan-reactive (OX18) mAbs. The 39Kd non-RT1.A soluble MHC class I protein was precipitated only by OX18. The production of soluble RT1.Aa was inhibited by a metalloproteinase inhibitor, but not by serine/thiol protease inhibitors. None of these protease inhibitors interfered with the soluble non-RT1.A production, suggesting that it might be derived from an alternatively spliced MHC class I transcript. The soluble non-RT1.A was always associated with beta2m. However, soluble RT1.Aa molecule was cleaved in beta2m-free form and was reassociated with beta2m in culture supernatants. Thus two soluble MHC class I molecules, classical (36Kd RT1.Aa) and nonclassical (the alternatively spliced transcript), were produced from rat cells. Alternative splicing led to the nonclassical soluble MHC class I synthesis. Proteolytic cleavage by metalloproteinase led to the classical soluble MHC class I synthesis.

Alleles↗
PubMed1998

Modulation of alloimmunity to major histocompatibility complex class I by cotransfer of cytokine genes in vivo.

Major histocompatibility complex (MHC) class I antigen is a potent stimulus for alloimmune responses and is the principal immunologic target mediating acute cellular rejection of allografts. Using a method of direct in vivo gene transfer of cDNA encoding donor type MHC class I, we showed in a rat model that recipient muscle could express the transferred MHC class I cDNA, resulting in alloimmunization of the recipient. This was most graphically demonstrated by accelerated rejection of cardiac allografts expressing the same MHC class I as encoded by the immunizing cDNA. We now report the use of the particle-mediated gene transfer via a gene gun (Geneva, Middleton, WI, USA) to transfer MHC class I, as well as cytokine gene expression vectors, into rat skin. Compared to intramuscular injection, gene gun transfer to skin resulted in more efficient immunization. Donor-specific cytotoxic T lymphocyte (CTL) responsiveness and antibody levels increased. Furthermore, coexpression of certain cytokine genes with the MHC class I cDNA modulated the immune response. Specifically, coimmunization with IL-10 cDNA abrogated immunity to allo-MHC class I, while coimmunization with GM-CSF cDNA enhanced it. The influence of expression of these genes in skin was demonstrated by alteration of donor cardiac allograft survival. This model is useful for induction and modulation of alloimmune responses and may be used to develop gene therapy strategies to modify them.

Animals↗
PubMed1998

High resolution analysis of DNA copy number variation using comparative genomic hybridization to microarrays.

Gene dosage variations occur in many diseases. In cancer, deletions and copy number increases contribute to alterations in the expression of tumour-suppressor genes and oncogenes, respectively. Developmental abnormalities, such as Down, Prader Willi, Angelman and Cri du Chat syndromes, result from gain or loss of one copy of a chromosome or chromosomal region. Thus, detection and mapping of copy number abnormalities provide an approach for associating aberrations with disease phenotype and for localizing critical genes. Comparative genomic hybridization (CGH) was developed for genome-wide analysis of DNA sequence copy number in a single experiment. In CGH, differentially labelled total genomic DNA from a 'test' and a 'reference' cell population are cohybridized to normal metaphase chromosomes, using blocking DNA to suppress signals from repetitive sequences. The resulting ratio of the fluorescence intensities at a location on the 'cytogenetic map', provided by the chromosomes, is approximately proportional to the ratio of the copy numbers of the corresponding DNA sequences in the test and reference genomes. CGH has been broadly applied to human and mouse malignancies. The use of metaphase chromosomes, however, limits detection of events involving small regions (of less than 20 Mb) of the genome, resolution of closely spaced aberrations and linking ratio changes to genomic/genetic markers. Therefore, more laborious locus-by-locus techniques have been required for higher resolution studies. Hybridization to an array of mapped sequences instead of metaphase chromosomes could overcome the limitations of conventional CGH (ref. 6) if adequate performance could be achieved. Copy number would be related to the test/reference fluorescence ratio on the array targets, and genomic resolution could be determined by the map distance between the targets, or by the length of the cloned DNA segments. We describe here our implementation of array CGH. We demonstrate its ability to measure copy number with high precision in the human genome, and to analyse clinical specimens by obtaining new information on chromosome 20 aberrations in breast cancer.

Animals↗
PubMed1998

[A study on EEG-Encephalofluctuographic characteristics in alpha frequency band in pilots].

The frequency-fluctuation characteristics in alpha frequency band were studied by EEG-Encephalofluctuographic Technology (EEG-ET) in 261 pilots. The electrical activity was recorded from 12 scalp monopolar leads of the international 10-20 system using linked ear lobes as reference. The components of the competitive frequency-fluctuation structure in alpha frequency band was analysed. The results showed that the predominant frequency component of the competitive structure was 9 Hz in the 261 normal healthy pilots. The second was 10 Hz. And the third was 7 Hz. The other competitive frequency components were inhibited. The relative entropy value (percentage) of the competivity structure was calculated for each EEG derivation of each pilot. We also analysed the spectra of the EEG-Encephalofluctuograph. We found that there was a dominant power peak at 21.39mHz in 57 pilots who complained in-flight blackout sometimes during acceleration.

Acceleration↗
PubMed1998

[Ergonomical study on Chinese speech warning].

Ergonomical experiments on speech warning under noise background were carried out in 40 healthy males, aged 20-33. Through the determination of auditory reaction time to the Chinese speech warning under dual-tasks and the subjective evalution of the suitable time length of main warning voice by the subject, the optimum parameters of Chinese speech warning in accordance with space ergonomics were determined. It was found that: suitable time length of main warning voice is 0.35-0.55s, main interval is 0.15-0.35s, speech speed is 4-6 word/s, and sentence interval is 0.2-0.4s. Meanwhile, the analysis of heart rate (HR) and heart rate variability (HRV) demonstrated that the speech warning using aforementioned parameters didn't increase the operator's work load. The results can serve as the objective ergonomical basis and the evaluation criterion for design of speech warning in manned space vehicle.

Adult↗
PubMed1998

[Psychological study of parameter selection for Chinese speech warning].

To study the effects of the parameters of Chinese speech warning on cognitive property, and to obtain the optimal parameters in accordance with cognitive property, experiments of cognitive property for Chinese speech warning was carried out in 20 healthy males. Combining our study on the sensation-reaction time, the optimal parameters in accordance with space ergonomics [correction of ergonormics] and cognitive property were determined: suitable time length of prewarning sound is 0.35 approximately 0.55 s; prewarning interval is 0.3-0.4 s; interval between sentences is 0.3-0.4 s; word number of warning sentence < or = 7. The result can serve as the objective ergonomical basis for the design of Chinese speech warning system in manned space vehicle, and as the evaluation criterion.

Adult↗
PubMed1998

Agonist interactions with chimeric and mutant beta1- and beta3-adrenergic receptors: involvement of the seventh transmembrane region in conferring subtype specificity.

beta1- and beta3-adrenergic receptors (AR) are the predominant beta-AR subtypes in adipocytes, and analysis of native and recombinant beta-AR has revealed several pharmacological and biochemical differences between these subtypes. This study used chimeric and mutated rat beta-AR expressed in Chinese hamster ovary cells to examine the basis of certain characteristic differences in the agonist properties of catecholamines and prototypic beta3-AR agonists. The exchange of sequence beyond transmembrane (TM) region 6 between the beta-AR subtypes had dramatic and reciprocal effects on the affinity and efficacy of the prototypic beta3-AR agonists BRL 37,344 and CL 316,243, without affecting the interactions with catecholamines. Mutation of Phe350 and Phe351 in TM7 of the beta1-AR to Ala and Leu found in the beta3-AR was sufficient to allow activation by prototypic beta3-AR agonists. Interestingly, this mutation did not affect catecholamine action and it did not impair the ability of propranolol to block the actions of isoproterenol or the selective beta3-AR agonists. beta1-AR containing beta3-AR sequence from predicted TM5 through TM6 exhibited reduced affinity for catecholamines without altering agonist potency, suggesting enhanced coupling efficiency. Inclusion of the homologous beta1-AR sequence in the beta3-AR, however, did not produce reciprocal effects. These results are the first to define a major determinant of beta3-AR subtype-selective agonism in TM7 and demonstrate that the determinants of selective phenethanolamines, catecholamines, and propranolol action are distinct.

Adrenergic beta-Agonists↗
PubMed1998

Reduced expression of calponin h1 in leiomyosarcoma of the uterus.

To determine the genetic differences between various smooth muscle tumors of the uterus, the expression of calponin h1 (cytoskeletal protein) was examined in normal myometrium and in smooth muscle tumors of the uterus (leiomyosarcoma, smooth muscle tumors of uncertain malignant potential, cellular leiomyoma, bizarre leiomyoma, and ordinary leiomyoma) using immunohistochemistry and Western blotting. Analysis of calponin h1 transcripts using the reverse-transcription-PCR was also performed. Immunohistochemically, calponin h1 was expressed in normal myometrium and in all leiomyomas; however, its expression was markedly weaker in leiomyosarcoma. The results of both Western blotting and the analysis of calponin h1 transcripts were compatible with the immunohistochemical results. It is suggested that reduced expression of calponin h1 is associated with leiomyosarcoma of the uterus, and that calponin h1 expression may serve as a valuable molecular maker in the differential diagnosis of smooth muscle tumors of the uterus.

Adult↗
PubMed1998

Molecular characterization of human and rat RGS 9L, a novel splice variant enriched in dopamine target regions, and chromosomal localization of the RGS 9 gene.

A novel splice variant of RGS 9 was isolated from a rat hypothalamus, human retina, and a human kidney (Wilm's) tumor. This variant, termed RGS 9L, differs from the retinal form (termed RGS 9S) identified previously in that it contains a 211- (rat) or 205- (human) amino acid proline-rich domain on the carboxyl terminus. The pattern of RGS 9 mRNA splicing was tissue specific, with striatum, hypothalamus- and nucleus accumbens expressing RGS 9L, whereas retina and pineal expressed RGS 9S almost exclusively. This pattern of mRNA splicing seemed to be highly conserved between human and rodents, suggesting cell-specific differences in the function of these variants. Transient expression of RGS 9L augmented basal and beta-adrenergic receptor-stimulated adenylyl cyclase activity while suppressing dopamine D2 receptor-mediated inhibition. Furthermore, RGS 9L expression greatly accelerated the decay of dopamine D2 receptor-induced GIRK current. These results indicate RGS 9L inhibits heterotrimeric Gi function in vivo, probably by acting as a GTPase-activating protein. The human RGS 9 gene was localized to chromosome 17 q23-24 by radiation hybrid and fluorescent in situ hybridization analyses. The RGS 9 gene is within a previously defined locus for retinitis pigmentosa (RP 17), a disease that has been linked to genes in the rhodopsin/transducin/cGMP signaling pathway.

Alternative Splicing↗
PubMed1997

cDNA cloning and characterization of a cis-retinol/3alpha-hydroxysterol short-chain dehydrogenase.

We report a mouse cDNA that encodes a 317-amino acid short-chain dehydrogenase which recognizes as substrates 9-cis-retinol, 11-cis-retinol, 5alpha-androstan-3alpha,17beta-diol, and 5alpha-androstan-3alpha-ol-17-one. This cis-retinol/androgen dehydrogenase (CRAD) shares closest amino acid similarity with mouse retinol dehydrogenase isozymes types 1 and 2 (86 and 91%, respectively). Recombinant CRAD uses NAD+ as its preferred cofactor and exhibits cooperative kinetics for cis-retinoids, but Michaelis-Menten kinetics for 3alpha-hydroxysterols. Unlike recombinant retinol dehydrogenase isozymes, recombinant CRAD was inhibited by 4-methylpyrazole, was not stimulated by ethanol, and did not require phosphatidylcholine for optimal activity. CRAD mRNA was expressed intensely in kidney and liver, in contrast to retinol dehydrogenase isozymes, which show strong mRNA expression only in liver. CRAD mRNA expression was widespread (relative abundance): kidney (100) > liver (92) > small intestine (9) = heart (9) > retinal pigment epithelium and sclera (4.5) > brain (2) > retina and vitreous (1.6) > spleen (0.7) > testis (0.6) > lung (0.4). CRAD may catalyze the first step in an enzymatic pathway from 9-cis-retinol to generate the retinoid X receptor ligand 9-cis-retinoic acid and/or may regenerate dihydrotestosterone from its catabolite 5alpha-androstan-3alpha,17beta-diol. These data also illustrate the multifunctional nature of short-chain dehydrogenases and provide a potential mechanism for androgen-retinoid interactions.

Alcohol Oxidoreductases↗
PubMed1997

Immunohistochemical analysis of the expression of cdk4 and p16INK4 in human endometrioid-type endometrial carcinoma.

BACKGROUND: Abnormalities in G1 cell cycle regulation have been associated with the malignant transformation of cells. To obtain further information about the role of factors regulating the G1 cell cycle in the development of endometrial carcinoma, the authors analyzed the expression of cdk4 (cyclin-dependent kinase) and p16INK4 (an inhibitor of cdk4). METHODS: Immunohistochemical staining was performed on 20 specimens of normal endometria and 41 specimens of endometrioid-type endometrial carcinoma using antibodies against cdk4 and p16INK4. RESULTS: In the glandular epithelia of the normal endometria, cytoplasmic staining of cdk4 and p16INK4 was observed only in the proliferative phase, but nuclear staining of these agents was negligible. In endometrial carcinomas, 8 (19.5%) and 14 (34.2%) were positive for cdk4 and p16INK4 in the nucleus, respectively. Topographically, the nuclear cdk4 positive tumor cells were negative for p16INK4 and the nuclear p16INK4 positive tumor cells were found in areas without nuclear cdk4 expression, suggesting an inverse correlation between the two agents. In addition, the poorly differentiated carcinomas were more frequently positive for nuclear cdk4 than were the highly differentiated carcinomas (P = 0.03). CONCLUSIONS: These data suggest that increased expression of nuclear cdk4 associated with loss of p16INK4 expression could be involved in the carcinogenesis of a subset of endometrial carcinomas.

Carcinoma, Endometrioid↗