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Biomedical subjects

Y Gao

Publications and source records attributed to Y Gao.

At least 127 records · Page 7Linked to original sources
PubMed2001

Preliminary study of three-tone paradigm auditory P300 on aging dementia.

OBJECTIVE: To explore the changes of three-tone paradigm P300 and observe the improvement of the diagnostic sensitivity of P300 in aging dementia. METHODS: Thirty-four patients of aging dementia underwent traditional P300 (2t-P300) and three-tone paradigm auditory P300 (3t-P300). The results of these two methods were compared. RESULTS: Abnormal P300 was found in 18 of 34 dementia cases (52.9%) by 2t-P300, and in 26 of 30 patients who finished the 3t-P300 tests (86.7%). In 2t-P300, 9 of 24 mild cases, 7 of 8 moderate cases and 2 severe cases showed abnormal results. In 3t-P300, 20 of 24 mild cases and all 6 moderate cases showed abnormal results. Abnormal 3t-P300 was found in 13 of 16 cases which showed normal 2t-P300. Besides prolonged and bad-shaped P300, no certain response of P300 to rare non-target stimulus (r-nT) was found in 10 mild cases by 3t-P300. CONCLUSION: Three-tone paradigm auditory P300 had higher sensitivity in early diagnosis of aging dementia than traditional auditory P300. No P300 response to r-nT in 3t-P300 is an important index in early diagnosis of mild dementia.

Aged↗
PubMed2001

[Gene clone of autoantigen hnRNP A2/B1 and research on expression in synovium].

OBJECTIVE: To investigate hnRNPA2/B1's role in rheumatoid synovitis by obtaining its cDNA sequence and analyzing its expression in synovium. METHODS: Total RNA was isolated from peripheral blood mononuclear cells (PBMC) and the RT-PCR was performed. The fragment was cloned into PUC-T1 plasmids and further sequenced. We detected it's expression in synovium with monoclonal antibodies and specific cDNA probes by immunohistochemistry and in situ hybridization. RESULTS: The fragment was identified by DNA sequencing. The expression in rheumatoid synovium was higher than that from osteoarthritis and the normal controls (P < 0.05). CONCLUSION: hnRNP A2/B1 cDNA has been cloned successfully and hnRNP A2/B1 might play an important role in rheumatoid synovitis.

Adult↗
PubMed2001

[The role of neuroimmunoregulation mobilized by enhancing immunologic function via hou hai acupoint antigen injection].

OBJECTIVE: To study the mechanism of neuroimmunoregulation which is triggered by enhancing immunologic function via Hou Hai acupoint antigen injection. METHODS: Immunohistochemical method, immunofluorometric method and RT-PCR were used to examine the different distribution of cytokine immunopositive cells in the brain and expression of cytokines in the spleen of the human IgG sensitized rats received acupoint, subcutaneous and normal rats antigen injections. RESULTS: In the areas of lateral hypothalamic nucleus (LH) and amygdaloid nuclear complex (AA), the distribution of cytokines immunopositive cells with acupoint injection group was significantly increased more than that in the subcutaneous injection group. But the expression of cytokines immunopositive cells both by the acupoint injection and the subcutaneous injection groups reached their peak value in similar time. Double-labelling results showed that the cytokine immunopositive cells were neurons. In the spleens, the expressions of cytokines, IL-2 and IFN, were significantly increased by acupoint injection more than subcutaneous injection. CONCLUSIONS: The time course of neuroimmunoregulation is similar in the immunized rats via both acupoint injection and subcutaneous injection of antigens. But the activity of neuroimmunoregulation is not the same in acupoint and subcutaneous injection groups. Neurons of the LH and AA are the main source of the neuroimmunomodulators. The effect of enhancing immunologic function via Hou Hai acupoint injection is may be more efficient to mobilize the activity of neuroimmunoregulation of immune-associated brain region than modulation of the immune system.

Acupuncture Points↗
PubMed2001

[Study on the correlation of the cytokine secreted by the endometrium focus and the microenvironment of the fleument fluid].

OBJECTIVE: To investigate the correlation of endometriotic focus and peritoneal fluid as well as its effect on reproduction. METHODS: Forty-three women with surgical treatment or laproscope with infertility are divided into endometriosis group (24 cases) and normal pelvic group (control group 19 cases) . The pathophysiology of patient' s peritoneal fluid, celiac macrophages and endometriotic cells are analyzed by chemotactic test on monocytes, dot blot hybridize, enzyme linked immunoadsorbent assay and the level of cytoplasmic [Ca2+]i respectively. Meanwhile, the influence of peritoneal fluid and endometriotic cells to sperm motivity as well as the effects to rat embryo cleavage are evaluated. RESULTS: The monocyte moving distance induced by peritoneal fluid in endometriosis group vs. control is (87.2 +/- 9.4) m vs. (51.9 +/- 3.7) microm (P < 0.01). The count of celiac macrophages (1.47 +/- 0.87) x 10(6)/ml vs. (0.67 +/- 0.73) x 10(6)/ml (P < 0.01), The basic expression level of monocyte chamotactic protein-1 (MCP-1) in endometriotic cells is (18.34 +/- 3.95) A. After exposured to IL-1beta and tumor necrosis factor-alpha, the OD of MCP-lmRNA is 56.84 +/- 3.21 A and 41.58 +/- 2.48 A respectively (P < 0.01 ). CONCLUSION: With the influence between endometriotic focus and microenvironment of peritoneal fluid, the level of cytokines expressed by celiac macrophages and endometriotic focus are enhanced, and it can interfere some process in reproduction.

Animals↗
PubMed2000

Oligomerization of Rac1 gtpase mediated by the carboxyl-terminal polybasic domain.

The Rho family GTPase Rac1 mediates a variety of signal transduction processes leading to activation of NADPH oxidase, actin cytoskeleton reorganization, transcription activation, and stimulation of DNA synthesis. In this study, Rac1 was found to form a reversible monomer and oligomer in both the GDP- and GTP-bound states in vitro and in cells. Mutational analysis and peptide competition experiments showed that the unique C-terminal domain of Rac1 consisting of six consecutive basic residues (amino acids 183-188) is required for the homophilic interaction. Oligomerization of Rac1-GTP led to a self-stimulatory GTPase-activating protein (GAP) activity, resulting in a significantly enhanced intrinsic GTP hydrolysis rate of Rac1-GTP. Deletion or mutation of the polybasic residues drastically decreased its intrinsic GTPase activity and resulted in a loss of the self-stimulatory GAP activity. In the oligomeric state, Rac1 became insensitive to the RhoGAP stimulation, albeit maintaining the responsiveness to the guanine nucleotide exchange factor. The ability of the Rac1 C-terminal mutants to activate the effector p21(cdc42/rac)-activated kinase-1 correlated with their oligomerization states, suggesting that oligomer formation potentiates effector activation. Furthermore, the oligomer-to-monomer transition of Rac1-GDP could be driven effectively by interaction with the Rho guanine nucleotide dissociation inhibitor. Building on previous characterizations of Rac1 interaction with regulatory proteins and effectors, these results suggest that Rac1 may employ yet another means of regulation by cycling between the monomeric and oligomeric states to effectively generate a transient and augmented signal.

Amino Acid Sequence↗
PubMed2000

Streptozotocin-induced beta-cell death is independent of its inhibition of O-GlcNAcase in pancreatic Min6 cells.

Streptozotocin (STZ) injection into experimental animals selectively causes massive beta-cell death. The mechanism of this specific toxicity is not fully understood. Recently, it has been discovered that O-linked N-acetylglucosamine (O-GlcNAc) is enriched in the beta-cells. It has been proposed that STZ toxicity may be due to its inhibition of neutral O-GlcNAcase activity, the enzyme that removes O-GlcNAc from cytosolic proteins (K. Liu et al., 2000, Proc. Natl. Acad. Sci. USA 97, 2820-2825). To further ascertain the role of O-GlcNAcase in beta-cell death, we have used PUGNAc, a potent and specific O-GlcNAcase inhibitor, together with STZ in pancreatic Min6 cells. Both STZ and PUGNAc increased O-GlcNAc to similar levels on intracellular proteins. STZ, but not PUGNAc, decreased cellular protein synthesis by 66.0% within 8 h, killed 80.9% of the cells within 18 h, and decreased insulin secretion. STZ, but not PUGNAc, also caused genomic DNA fragmentation, suggesting that some of the cells were undergoing apoptosis. Prolonged treatment with PUGNAc (72 h) maintained high intracellular O-GlcNAc levels, but did not result in any apparent cell damage. Furthermore, the toxicity of STZ can be largely reversed by 3-aminobenzamide, a poly(ADP-ribose) polymerase inhibitor. These data strongly indicate that STZ-induced beta-cell death is not caused by elevated intracellular O-GlcNAc levels, but instead likely involves poly(ADP-ribose) polymerase in the mechanism.

Acetylglucosamine↗
PubMed2000

Reversal of angiogenesis in vitro, induction of apoptosis, and inhibition of AKT phosphorylation in endothelial cells by thromboxane A(2).

Thromboxane A(2) (TxA(2)) causes platelet aggregation, vasoconstriction, and inhibition of endothelial cell (EC) migration and prevents vascular tube formation via its specific receptors (TP), of which there are two isoforms (TPalpha and TPbeta), both expressed in human ECs. In this study, we demonstrate that the TxA(2) mimetic IBOP increases apoptosis of human ECs and inhibits the phosphorylation of Akt kinase, an intracellular mediator required for cell survival. Treatment with IBOP destroyed EC networks formed on a basement membrane matrix in vitro. To distinguish the role of the TP isoforms, each isoform was expressed in TP-null ECs to create TPalpha and TPbeta ECs. IBOP induced apoptosis and inhibited phosphorylation of Akt kinase in both TPalpha and TPbeta. IBOP increased cAMP levels in TPalpha but not in TPbeta. Apoptosis induced by IBOP in TPalpha was not affected by either the adenylyl cyclase activator forskolin or the protein kinase A inhibitor 14-22 amide or H-89, whereas that in TPbeta was suppressed by forskolin and enhanced by the protein kinase A inhibitor 14-22 amide or H-89, suggesting that the TP isoforms differ in their signal pathways in mediating apoptosis. In conclusion, apoptosis may be the mechanism by which TxA(2)-mediated destruction of vascular structures in ECs occurs; although both TP isoforms induce apoptosis, possibly via inhibiting Akt phosphorylation, the signaling differs in each isoform, in that activation of the adenylyl cyclase pathway prevents apoptosis caused by TPbeta, but not by TPalpha, stimulation.

Adenylyl Cyclase Inhibitors↗
PubMed2000

Acylation of myelin Po protein is required for adhesion.

The extracellular domains of myelin Po protein interact homophilically and hence hold myelin compact at the intraperiod line. The cytoplasmic domain of Po, however, can also affect the interactions of its extracellular sequences. Po is acylated, mostly with palmitic acid, at Cys 153, just at the transmembrane:cytoplasmic domain interface. Here we show that Po mutated at Cys 153 to alanine (C153A), is not acylated and is not adhesive. Like wild-type Po, C153A Po clusters within the membrane and seems to interact with the cytoskeleton. On the other hand, the rate of turnover of C153A Po in transfected Chinese hamster ovary cells is almost 4 times faster than wild-type Po. The increased instability of C153A Po compared to wild-type Po may account for its loss of adhesion.

Acylation↗
PubMed2000

Functional interactions between Drosophila bHLH/PAS, Sox, and POU transcription factors regulate CNS midline expression of the slit gene.

During Drosophila embryogenesis the CNS midline cells have organizing activities that are required for proper elaboration of the axon scaffold and differentiation of neighboring neuroectodermal and mesodermal cells. CNS midline development is dependent on Single-minded (Sim), a basic-helix-loop-helix (bHLH)-PAS transcription factor. We show here that Fish-hook (Fish), a Sox HMG domain protein, and Drifter (Dfr), a POU domain protein, act in concert with Single-minded to control midline gene expression. single-minded, fish-hook, and drifter are all expressed in developing midline cells, and both loss- and gain-of-function assays revealed genetic interactions between these genes. The corresponding proteins bind to DNA sites present in a 1 kb midline enhancer from the slit gene and regulate the activity of this enhancer in cultured Drosophila Schneider line 2 cells. Fish-hook directly associates with the PAS domain of Single-minded and the POU domain of Drifter; the three proteins can together form a ternary complex in yeast. In addition, Fish can form homodimers and also associates with other bHLH-PAS and POU proteins. These results indicate that midline gene regulation involves the coordinate functions of three distinct types of transcription factors. Functional interactions between members of these protein families may be important for numerous developmental and physiological processes.

Animals↗
PubMed2000

The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations.

We have used spectral karyotyping to assess potential roles of three different components of the nonhomologous DNA end-joining pathway in the maintenance of genomic stability in mouse embryonic fibroblasts (MEFs). MEFs homozygous for mutations that inactivate either DNA ligase IV (Lig4) or Ku70 display dramatic genomic instability, even in the absence of exogenous DNA damaging agents. These aberrant events range from chromosomal fragmentation to nonreciprocal translocations that can involve several chromosomes. DNA-dependent protein kinase catalytic subunit deficiency also promotes genome instability. Deficiency for the p53 cell cycle checkpoint protein has little effect on spontaneous levels of chromosomal instability in Lig4-deficient fibroblasts. However, in the context of ionizing radiation treatment, p53 deficiency allowed visualization of massive acute chromosomal destruction in Lig4-deficient MEFs, which in surviving cells manifested as frequent nonreciprocal translocations. We conclude that nonhomologous DNA end-joining plays a crucial role as a caretaker of the mammalian genome, and that an alternative repair pathway exists that often leads to nonreciprocal translocations.

Animals↗
PubMed2000

Polyglycylation of tubulin is essential and affects cell motility and division in Tetrahymena thermophila.

We analyzed the role of tubulin polyglycylation in Tetrahymena thermophila using in vivo mutagenesis and immunochemical analysis with modification-specific antibodies. Three and five polyglycylation sites were identified at glutamic acids near the COOH termini of alpha- and beta-tubulin, respectively. Mutants lacking all polyglycylation sites on alpha-tubulin have normal phenotype, whereas similar sites on beta-tubulin are essential. A viable mutant with three mutated sites in beta-tubulin showed reduced tubulin glycylation, slow growth and motility, and defects in cytokinesis. Cells in which all five polyglycylation sites on beta-tubulin were mutated were viable if they were cotransformed with an alpha-tubulin gene whose COOH terminus was replaced by the wild-type COOH terminus of beta-tubulin. In this double mutant, beta-tubulin lacked detectable polyglycylation, while the alpha-beta tubulin chimera was hyperglycylated compared with alpha-tubulin in wild-type cells. Thus, the essential function of polyglycylation of the COOH terminus of beta-tubulin can be transferred to alpha-tubulin, indicating it is the total amount of polyglycylation on both alpha- and beta-tubulin that is essential for survival.

Amino Acid Sequence↗
PubMed2000

Expression and role of p27(kip1) in neuronal differentiation of embryonal carcinoma cells.

We examined the expression and the regulation of p21(waf1) and p27(kip1) cdk inhibitors in P19 mouse embryonal carcinoma (EC) cells following treatment with all-trans retinoic acid (ATRA) to induce neuronal differentiation. The levels of p27 mRNA and protein increased within 24 h of treatment with ATRA, reaching a plateau 4-5 days later prior to neurite formation. In contrast, levels of p21 expression remained low until after neurites were extensively formed. Induction of muscle differentiation from P19 cells by treatment with dimethyl sulfoxide caused only transient increases in p27 levels. In a mutant P19 cell line, RAC65, treatment with ATRA induced neither p27 accumulation nor neuronal differentiation, but p21 mRNA expression increased markedly. In contrast, treatment of RAC65 cells with 9-cis retinoic acid induced both p27 expression and neuronal differentiation. Correlation between p27 expression and neuronal differentiation was also observed in NT2/D1 human EC cells. Luciferase reporter assays showed that p27 promoter activity increased in ATRA-treated cells, consistent with the elevation of p27 mRNA levels. Arrest of neuronal differentiation of P19 cells by okadaic acid resulted in inhibition of p27 expression, whereas p21 mRNA expression was greatly enhanced. Conversely, inhibition of p27 expression by antisense p27 oligonucleotides resulted in blockade of neuronal differentiation. Taken together, these results strongly suggest that the expression of p27 is indispensable for neuronal differentiation of EC cells.

Animals↗
PubMed2000

Examination of novel non-phosphorus-containing phosphotyrosyl mimetics against protein-tyrosine phosphatase-1B and demonstration of differential affinities toward Grb2 SH2 domains.

Inhibitory potencies were compared of several mono- and dicarboxy-based pTyr mimetics in Grb2 SH2 domain versus PTP1B assays. Although in both systems pTyr residues provide critical binding elements, significant differences in the manner of recognition exist between the two. This is reflected in the current study, where marked variation in relative potencies was observed between the two systems. Of particular note was the poor potency of all monocarboxy-based pTyr mimetics against PTP1B when incorporated into a hexapeptide platform. The recently reported high PTP1B inhibitory potency of similar phenylphosphate mimicking moieties displayed in small molecule, non-peptide structures, raises questions on the limitations of using peptides as platforms for pTyr mimetics in the discovery of small molecule inhibitors.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Interplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development.

XRCC4 is a non-homologous end-joining protein employed in DNA double strand break repair and in V(D)J recombination. In mice, XRCC4-deficiency causes a pleiotropic phenotype, which includes embryonic lethality and massive neuronal apoptosis. When DNA damage is not repaired, activation of the cell cycle checkpoint protein p53 can lead to apoptosis. Here we show that p53-deficiency rescues several aspects of the XRCC4-deficient phenotype, including embryonic lethality, neuronal apoptosis, and impaired cellular proliferation. However, there was no significant rescue of impaired V(D)J recombination or lymphocyte development. Although p53-deficiency allowed postnatal survival of XRCC4-deficient mice, they routinely succumbed to pro-B-cell lymphomas which had chromosomal translocations linking amplified c-myc oncogene and IgH locus sequences. Moreover, even XRCC4-deficient embryonic fibroblasts exhibited marked genomic instability including chromosomal translocations. Our findings support a crucial role for the non-homologous end-joining pathway as a caretaker of the mammalian genome, a role required both for normal development and for suppression of tumours.

Animals↗
PubMed2000

Structure determination of the two-domain ( 1x4) anatase TiO2(001) surface

The reconstructed anatase TiO2(001) surface has been investigated by low-energy electron diffraction (LEED), x-ray photoelectron spectroscopy (XPS), and angle-resolved mass spectroscopy of recoiled ions (AR-MSRI). Prior investigations have observed or considered only a (1x1) unreconstructed termination for this surface with no detailed structural analysis. Our LEED results indicate a previously unobserved two-domain (1x4) reconstruction after sputtering and annealing the (1x1) surface. The XPS data for this reconstruction indicate the presence of only Ti4+. Simulations of the AR-MSRI experimental data indicate a best fit for a microfaceted surface, revealing both (103) and (1;03) surface planes.

Journal Article↗
PubMed2000

Expression of immunoregulatory cytokines in neurons of the lateral hypothalamic area and amygdaloid nuclear complex of rats immunized against human IgG.

Present results showed that interleukin-1 (IL-1), IL-6 and transforming growth factor-beta (TGF-beta) were constitutively expressed in the supraoptic and paraventricular nuclei of the rat hypothalamus. Immunoreactive cells were also detected, but to a lesser extent, in other parts of hypothalamus as well as in the cerebral cortex. In rats immunized with IgG, there was moderate increase in immunoreactivities of the cytokines. A notable feature, however, was the induction of the cytokine expression in the lateral hypothalamic area and the amygdaloid nuclear complex, suggesting that the neurons in these two areas are involved in possible immune regulation.

Amygdala↗
PubMed2000

Defective embryonic neurogenesis in Ku-deficient but not DNA-dependent protein kinase catalytic subunit-deficient mice.

Mammalian nonhomologous DNA end joining employs Ku70, Ku80, DNA-dependent protein kinase catalytic subunit (DNA-PKcs), XRCC4, and DNA ligase IV (Lig4). Herein, we show that Ku70 and Ku80 deficiency but not DNA-PKcs deficiency results in dramatically increased death of developing embryonic neurons in mice. The Ku-deficient phenotype is qualitatively similar to, but less severe than, that associated with XRCC4 and Lig4 deficiency. The lack of a neuronal death phenotype in DNA-PKcs-deficient embryos and the milder phenotype of Ku-deficient versus XRCC4- or Lig4-deficient embryos correlate with relative leakiness of residual end joining in these mutant backgrounds as assayed by a V(D)J recombination end joining assay. We conclude that normal development of the nervous system depends on the four evolutionarily conserved nonhomologous DNA end joining factors.

Animals↗