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Biomedical subjects

X Yin

Publications and source records attributed to X Yin.

At least 37 records · Page 2Linked to original sources
PubMed2001

[Cloning of cNDAs involved in malignant transformation induced by glycidyl methacrylate].

The malignant transformation of human embryonic lung fibroblasts (HELF) induced by glycidyl methacrylate (GMA) in vitro was used as a model for comparing gene expression between the transformed cells and controls. Using mRNA differential display PCR(DD-PCR) technique, the three cDNA fragments up-regulated in the transformed cells were identified and highly homologous to human breast cancer transcription factor(ZABC1), Tbx3 and mouse ubiquitin conjugating enzyme(E2) gene. These results suggest that activation or inactivation of genes including ZABC1, Tbx3 and E2 may be involved in GMA-induced transformation.

Air Pollutants, Occupational↗
PubMed2001

[The role of exogenous hRAR beta gene on the growth inhibition and differentiation induction of HL-60R Cells].

OBJECTIVE: To investigate the role of hRAR beta gene in HL-60R cells and in their response to retinoids. METHODS: By electroporation, the recombinant pcDNA3-hRAR beta plasmid was transfected into the hRNA beta gene not expressed human myleocytic leukemic cell line HL-60R. In the presence of RAR-selected agonist Ch55, the effect of RAR beta gene on HL-60R was studied by the efficiency of colony formation in soft agar, cell morphology NBT reduction assay and flow cytometry. RESULTS: The HL60R-hRAR beta cells with stable hRAR beta gene expression were obtained. The growth and colony formation in soft agar of HL60R-hRAR beta cells were remarkably reduced as compared with that of their parent cells, and the cells were induced into granulocytic differentiation by Ch55 treatment at 10(-7). CONCLUSION: The expression of exogenous hRAR beta gene in HL-60R cells could resume their sensitivity to retionoids in inhibiting cell proliferation and inducing granulocytic differentiation.

Cell Differentiation↗
PubMed2001

Urinary excretion of aquaporin-2 water channel protein in chronic heart failure rats.

OBJECTIVE: To study the urinary excretion of aquaporin-2 (AQP2) water channel protein, and the relationship between urine AQP2 concentration and renal AQP2 gene expression in chronic heart failure (CHF) rats. METHODS: Male Sprague-Dawley rats (200 g-250 g) underwent either a left coronary artery ligation, a model of CHF, or a sham-operation. Nine weeks after surgery, urinary AQP2 concentrations and renal AQP2 protein levels were measured by Western blot. RESULTS: The urinary concentration of AQP2 water channel protein increased significantly in CHF rats as compared with sham-operated rats (365.6% +/- 102.9% vs 98.5% +/- 47.6%, P < 0.01). There was positive correlation between urinary AQP2 concentration and renal AQP2 protein expression (r = 0.89, P < 0.01). CONCLUSION: The urinary concentration of AQP2 water channel protein increases significantly in chronic heart failure rats.

Animals↗
PubMed2001

[Clinical study on treatment of middle-advanced stage liver cancer by combined treatment of hepatic artery chemoembolization with gan'ai no. I and no. II].

OBJECTIVE: To observe the clinical effect of combined treatment of hepatic artery chemoembolization (HACE) and Chinese herbal medicine (CHM) in treating middle-advanced stage liver cancer. METHODS: Sixty patients with middle-advanced stage liver cancer were randomly divided into two groups. The 30 patients in Group A were treated with combined HACE and Chinese herbal medicine (Gan'ai No. I and No. II) and the other 30 in Group B were treated with HACE alone. All patients were followed up for over 3 years. RESULTS: The 0.5-, 1- and 2-year survival rate in Group A was 76.7%, 56.7% and 30.0% respectively, and those in Group B was 50.0%, 33.3% and 16.7% respectively. The 1- and 2-year recurrence rate in Group A was 43.3%, 66.7% and that in Group B was 66.7%, 90.0% respectively. Moreover, Group A was significantly superior to Group B in tumor shrinking, AFP decreasing and blood leucocyte reducing (P < 0.01), as well as in improving clinical symptoms. CONCLUSION: The combined treatment has obvious effect in treating middle-advanced stage liver cancer.

Administration, Cutaneous↗
PubMed2000

Cloning and characterization of PHIP, a novel insulin receptor substrate-1 pleckstrin homology domain interacting protein.

Insulin receptor substrate-1 (IRS-1) protein is a major substrate of the insulin receptor tyrosine kinase and is essential for transducing many of the biological effects of insulin including mitogenesis, gene expression, and glucose transport. The N terminus of IRS-1 contains a pleckstrin homology (PH) domain that is critical for recognition and subsequent phosphorylation of IRS-1 by the activated insulin receptor. Here we report the isolation of a novel protein, PHIP (PH-interacting protein), which selectively binds to the PH domain of IRS-1 in vitro and stably associates with IRS-1 in vivo. Importantly, mutants of the IRS-1 PH domain that disrupt the PH fold fail to bind to PHIP. Anti-phosphotyrosine immunoblots of PHIP revealed no discernible insulin receptor-regulated phosphorylation, suggesting that PHIP is not itself a substrate of the insulin receptor. In contrast to full-length PHIP, overexpression of the PH-binding region of PHIP has a pronounced inhibitory effect on insulin-induced IRS-1 tyrosine phosphorylation levels. Furthermore, expression of this dominant-negative PHIP mutant leads to a marked attenuation of insulin-stimulated mitogen-activated protein kinase activity. We conclude that PHIP represents a novel protein ligand of the IRS-1 PH domain that may serve to link IRS-1 to the insulin receptor.

Amino Acid Sequence↗
PubMed2000

A mouse homologue of the Drosophila tumor suppressor l(2)tid gene defines a novel Ras GTPase-activating protein (RasGAP)-binding protein.

p120 GTPase-activating protein (GAP) down-regulates Ras by stimulating GTP hydrolysis of active Ras. In addition to its association with Ras, GAP has been shown to bind to several tyrosine-phosphorylated proteins in cells stimulated by growth factors or expressing transforming tyrosine kinase variants. Here we report the cloning and characterization of a novel GAP-binding protein, mTid-1, a DnaJ chaperone protein that represents the murine homolog of the Drosophila tumor suppressor l(2)tid gene. Three alternatively spliced variants of mTid-1 were isolated, two of which correspond to the recently identified hTid-1(L) and hTid-1(S) forms of the human TID1 gene that exhibit opposing effects on apoptosis. We demonstrate that both cytoplasmic precursor and mitochondrial mature forms of mTid-1 associate with GAP in vivo. Interestingly, although mTid-1 is found tyrosine-phosphorylated in v-src-transformed fibroblast cells, GAP selectively binds to the unphosphorylated form of mTid-1. In immunofluorescence experiments, GAP and Tid-1 were shown to colocalize at perinuclear mitochondrial membranes in response to epidermal growth factor stimulation. These findings raise the possibility that Tid chaperone proteins may play a role in governing the conformation, activity, and/or subcellular distribution of GAP, thereby influencing its biochemical and biological activity within cells.

3T3 Cells↗
PubMed2000

Depletion of a gamma delta T cell subset can increase host resistance to a bacterial infection.

Gammadelta T lymphocytes have been shown to regulate immune responses in diverse experimental systems. Because distinct gammadelta T cell subsets, as defined by the usage of certain TCR V genes, preferentially respond in various diseases and disease models, we have hypothesized that the various gammadelta T cell subsets carry out different functions. To test this, we compared one particular gammadelta T cell subset, the Vgamma1(+) subset, which represents a major gammadelta T cell type in the lymphoid organs and blood of mice, to other subsets and to gammadelta T cells as a whole. Using Listeria monocytogenes infection as an infectious disease model, we found that bacterial containment improves in mice depleted of Vgamma1(+) gammadelta T cells, albeit mice lacking all gammadelta T cells are instead impaired in their ability to control Listeria expansion. Our findings indicate that Vgamma1(+) gammadelta T cells reduce the ability of the innate immune system to destroy Listeria, even though other gammadelta T cells as a whole promote clearance of this pathogen.

Animals↗
PubMed2000

Oncogenic base substitution mutations in circulating leukocytes of normal individuals.

The background frequency of mutations in human tissues is an important issue in cancer susceptibility and genotoxic exposure determinations. Here we report the detection of rare mutant leukocytes containing oncogenic base substitutions of the Harvey-ras, N-ras, and p53 genes by the Needle-in-a-Haystack mutation assay with a sensitivity of one cell in a million. Altogether, we detected and identified 17 independent mutations of 66 separate base site analyses of peripheral blood specimens obtained from 19 apparently normal individuals. Two individuals harbored a substantially increased frequency of mutant cells, representing 9 of the 17 independent mutations found. These results suggest that up to 1 in 10 normal individuals may harbor a significant frequency of oncogenic mutations in circulating leukocytes.

Base Sequence↗
PubMed2000

[Effects of glycidyl methacrylate on gap junctional intercellular communication].

In order to probe into the mechanism of glycidyl methacrylate (GMA)-induced cell transformation, the effects of GMA on gap junctional intercellular communication (GJIC) in human lung, embryonic fibroblasts(HLEF) were studied by using scrape-loading and dye transfer(SLDT) technique. HLEF cells were treated with GMA at concentrations of 0.5, 2.5 and 5.0 mg/L for 12 hours and Lucifer Yellow was introduced by scrape-loading after exposure. The GJIC in exposed cells and that of control were determined directly as the diffusion extent of fluorescent dye into adjacent cells. The results indicated that GMA could inhibit the GJIC in exposed cells in a dose-dependent manner. Significantly decreased GJIC was found in 2.5 and 5.0 mg/L dose groups. It was suggested that the inhibition of GJIC might be one of the mechanisms responsible for GMA-induced cell transformation.

Cell Communication↗
PubMed2000

Casein kinase II phosphorylates lens connexin 45.6 and is involved in its degradation.

Connexin (Cx) 45.6, an avian counterpart of rodent Cx50, is phosphorylated in vivo, but the sites and function of the phosphorylation have not been elucidated. Our peptide mapping experiments showed that the Ser(363) site in the carboxyl (COOH) terminus of Cx45.6 was phosphorylated and that this site is within casein kinase (CK) II consensus sequence, although showing some similarity to CKI sequence. The peptide containing Ser(363) could be phosphorylated in vitro by CKII, but not by CKI. Furthermore, CKII phosphorylated Cx45.6 in embryonic lens membrane and the fusion protein containing the COOH terminus of Cx45.6. Two-dimensional peptide mapping experiments showed that one of the Cx45.6 peptides phosphorylated in vivo migrated to the same spot as one of those phosphorylated by CKII in vitro. Furthermore, CKII activity could be detected in lens lysates. To assess the function of this phosphorylation event, exogenous wild type and mutant Cx45.6 (Ser(363) --> Ala) were expressed in lens primary cultures by retroviral infection. The mutant Cx45.6 was shown to be more stable having a longer half-life compared with wild type Cx45.6. Together, the evidence suggests that CKII is likely a kinase responsible for the Ser(363) phosphorylation, leading to the destablization and degradation of Cx45.6. The connexin degradation induced by phosphorylation has a broad functional significance in the regulation of gap junctions in vivo.

Amino Acid Sequence↗
PubMed2000

Schwann cell myelination requires timely and precise targeting of P(0) protein.

This report investigated mechanisms responsible for failed Schwann cell myelination in mice that overexpress P(0) (P(0)(tg)), the major structural protein of PNS myelin. Quantitative ultrastructural immunocytochemistry established that P(0) protein was mistargeted to abaxonal, periaxonal, and mesaxon membranes in P(0)(tg) Schwann cells with arrested myelination. The extracellular leaflets of P(0)-containing mesaxon membranes were closely apposed with periodicities of compact myelin. The myelin-associated glycoprotein was appropriately sorted in the Golgi apparatus and targeted to periaxonal membranes. In adult mice, occasional Schwann cells myelinated axons possibly with the aid of endocytic removal of mistargeted P(0). These results indicate that P(0) gene multiplication causes P(0) mistargeting to mesaxon membranes, and through obligate P(0) homophilic adhesion, renders these dynamic membranes inert and halts myelination.

Aging↗
PubMed2000

P(0) glycoprotein overexpression causes congenital hypomyelination of peripheral nerves.

We show that normal peripheral nerve myelination depends on strict dosage of the most abundantly expressed myelin gene, myelin protein zero (Mpz). Transgenic mice containing extra copies of Mpz manifested a dose-dependent, dysmyelinating neuropathy, ranging from transient perinatal hypomyelination to arrested myelination and impaired sorting of axons by Schwann cells. Myelination was restored by breeding the transgene into the Mpz-null background, demonstrating that dysmyelination does not result from a structural alteration or Schwann cell-extrinsic effect of the transgenic P(0) glycoprotein. Mpz mRNA overexpression ranged from 30-700%, whereas an increased level of P(0) protein was detected only in nerves of low copy-number animals. Breeding experiments placed the threshold for dysmyelination between 30 and 80% Mpz overexpression. These data reveal new points in nerve development at which Schwann cells are susceptible to increased gene dosage, and suggest a novel basis for hereditary neuropathy.

Animals↗
PubMed2000

Detection of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 2(PAI-2) in gingival crevicular fluid from healthy, gingivitis and periodontitis patients.

BACKGROUND: The regulation of plasminogen activation is a key element in controlling proteolytic events in the extracellular matrix. Our previous studies had demonstrated that in inflamed gingival tissues, tissue-type plasminogen activator (t-PA) is significantly increased in the extracellular matrix of the connective tissue and that interleukin 1beta(IL-1beta) can up regulate the level of t-PA and plasminogen activator inhibitor-2 (PAI-2) synthesis by human gingival fibroblasts. METHOD: In the present study, the levels of t-PA and PAI-2 in gingival crevicular fluid (GCF) were measured from healthy, gingivitis and periodontitis sites and compared before and after periodontal treatment. Crevicular fluid from106 periodontal sites in 33 patients were collected. 24 sites from 11 periodontitis patients received periodontal treatment after the first sample collection and post-treatment samples were collected 14 days after treatment. All samples were analyzed by enzyme-linked immunosorbent assay (ELISA) for t-PA and PAI-2. RESULTS: The results showed that significantly high levels of t-PA and PAI-2 in GCF were found in the gingivitis and periodontitis sites. Periodontal treatment led to significant decreases of PAI-2, but not t-PA, after 14 days. A significant positive linear correlation was found between t-PA and PAI-2 in GCF (r=0.80, p<0.01). In the healthy group, different sites from within the same subject showed little variation of t-PA and PAI-2 in GCF. However, the gingivitis and periodontitis sites showed large variation. These results suggest a good correlation between t-PA and PAI-2 with the severity of periodontal conditions. CONCLUSION: This study indicates that t-PA and PAI-2 may play a significant rôle in the periodontal tissue destruction and tissue remodeling and that t-PA and PAI-2 in GCF may be used as clinical markers to evaluate the periodontal diseases and assess treatment.

Adult↗
PubMed2000

Promotion of growth and apoptosis in c-myc nullizygous fibroblasts by other members of the myc oncoprotein family.

c-myc nullizygous fibroblasts (KO cells) were used to compare the abilities of c-myc, N-myc and L-myc oncoproteins to accelerate growth, promote apoptosis, revert morphology, and regulate the expression of previously described c-myc target genes. All three myc oncoproteins were expressed following retroviral transduction of KO cells. The proteins all enhanced the growth rate of KO cells and significantly shortened the cell cycle transition time. They also accelerated apoptosis following serum deprivation, reverted the abnormal KO cell morphology, and modulated the expression of previously described c-myc target genes. In most cases, L-myc was equivalent to c-myc and N-myc in restoring all of the c-myc-dependent activities. These findings contrast with the previously reported weak transforming and transactivating properties of L-myc. Myc oncoproteins may thus impart both highly similar as well as dissimilar signals to the cells in which they are expressed.

Animals↗
PubMed2000

Coupling estimated effects of QTLs for physiological traits to a crop growth model: predicting yield variation among recombinant inbred lines in barley.

Advances in the use of molecular markers to elucidate the inheritance of quantitative traits enable the integration of genetic information on physiological traits into crop growth models. The objective of this study was to assess the ability of a crop growth model with QTL-based estimates of physiological input parameters to predict the yield of recombinant inbred lines (RILs) of barley. The model used predicts yield as spike biomass accumulated over the post-flowering period. We describe a two-stage procedure for predicting trait values from estimated additive and epistatic effects of QTLs. Values of physiological traits estimated by that procedure or measured in the field were used as input to the crop growth model. The output values (yield and shoot biomass) from the growth model using these two types of input values were highly correlated, indicating that QTL information can successfully replace measured input parameters. With the current crop growth model, however, both types of input values often resulted in large discrepancies between observed and predicted values. Improvement of performance may be achieved by incorporating physiological processes not yet included in the model. The prospects of using QTL-based predictions of model-input traits to identify new, high yielding barley genotypes are discussed.

Chromosome Mapping↗
PubMed2000

[The application study of mimic operation with 3D-cut in maxillofacial bone tumor].

OBJECTIVE: To study the feasibility of guiding operation planning and complication prevention. METHODS: Ten patients suffer from Maxillofacial bone tumour were examined with spiral CT. Firstly, to get three-dimensional reconstructive image of tumour and other tissues. Secondly, use 3D-cut software to cut off every layer of normal tissue and tumour mass. Lastly, to compare virtual operation with mimic operation in virtual operation process. RESULTS: Three-dimensional mimic operation clearly displays the relationship between tumor and surrounding tissues, reflect the actual operation condition. CONCLUSIONS: It is very useful designing operation program and predicting the potential complications before the actual operation.

Adult↗
PubMed2000

[A case-control study on the relationship between abnormal homocysteine metabolism and essential hypertension].

OBJECTIVE: To examine the relationship between abnormal homocysteine metabolism and essential hypertension in a Chinese population, a community-based case-control study was conducted. METHODS: 127 essential hypertensive patients aged 35 to 75 were randomly selected from a community. Another 170 control subjects with blood pressure < 140/90 mmHg were selected from the same community. Serum homocysteine was determined using HPLC. Folate and vitamin B(12) were measured by radioimmunoassay. MTHFR genotypes were identified by PCR and restriction fragment length polymorphism analysis with Hinf I digestion. RESULTS: After adjusting for age and sex, the mean homocysteine level was 10.56 micromol/L for hypertensive patients and 10.34 micromol/L for controls (F = 0.234, P = 0.63). No association between either SBP or DBP and Hcy concentration was found in subjects without anti-hypertensive medications. The prevalence of homozygousity for thermolabile MTHFR variant for this population was 13.1%, and the mutant allele frequency was 38.7%. There was no significant difference on genotype distributions and the mutant allele frequency for the two studied groups. However, the concentrations of folate and B(12) for the hypertensive subjects were generally higher than the controls. CONCLUSIONS: The present study did not discover that the elevation of Hcy levels or MTHFR mutation were independent risk factors for essential hypertension. The higher folate and B(12) in the hypertensive subjects might contribute to a lower risk.

Adult↗