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Biomedical subjects

M Tang

Publications and source records attributed to M Tang.

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

The -590C/T and -34C/T interleukin-4 promoter polymorphisms are not associated with atopic eczema in childhood.

Susceptibility to the development of asthma and other atopic diseases is known to have a genetic component. To date, several studies have linked chromosome 5q31 to asthma and atopy in human beings. This region harbors a cluster of cytokine and growth factor genes, IL-4 presenting as a prime atopy candidate gene, inasmuch as it plays a pivotal role in the atopy pathway. Our approach was to identify polymorphisms within the promoter regions of IL-4 and test their association with atopic eczema. Polymorphisms were typed in a cohort of 76 small nuclear families and 25 triads with childhood atopic eczema. The genotypes were used to test for linkage in the presence of association with atopic eczema. A new polymorphism, -34C/T, was identified and studied with a known polymorphism, -590C/T. On its own, each polymorphism showed no association with atopic eczema. The 2 polymorphisms were used to generate haplotypes, and a significant result was found for the -590C/-34C haplotype. However, after Bonferroni correction for multiple testing, the association became nonsignificant. Neither polymorphism predisposes to early-onset atopic eczema by itself, but suggestive linkage was found for the -590C/-34C haplotype in this study.

Child↗
PubMed2001

Preliminary results from an EIT breast imaging simulation system.

An electrical impedance tomography (EIT) simulation system for breast imaging has been developed using impedance data from a previous study and a finite-element model (FEM). This system has the functionality to construct various models of the breast, image the boundary voltages developed from any injection schema and provide parametric Cole-Cole modelling. Simulations indicate that breast carcinoma can be imaged and multi-frequency Cole-Cole dispersion data can be extracted. This is intended as the first stage towards providing an artificial intelligence based system capable of producing clinically relevant analytical data.

Algorithms↗
PubMed2001

Clinical outcome and client satisfaction of an anger management group program.

This retrospective quasi-experimental study evaluated the effectiveness of an anger management group program for clients with mental health problems. The program, based on the cognitive-behavioral approach, was offered by outpatient mental health occupational therapy services of a community general hospital. Sixty-four clients, about 59% diagnosed with depressive disorder, enrolled in the program and participated in the study. The pre-treatment and post-treatment scores of the participants on the Anger Control Inventory and the State-Trait Anger Expression Inventory were compared. The results indicated significant reduction in the overall experience of intense anger, improvement in cognitive and behavioural coping mechanisms, and significant improvement in anger control after treatment. Most respondents (90%) found the program definitely helpful. The pace of the program and the variety of learning activities were identified as areas for improvement. The results showed the program had positive impact on anger management. Useful suggestions were identified for continuous quality improvements of the program.

Adaptation, Psychological↗
PubMed2001

LMP1 activates NF-kappa B via degradation of I kappa B alpha in nasopharyngeal carcinoma cells.

OBJECTIVE: To elucidate the mechanisms by which Epstein-Barr virus-encoded latent membrane protein 1 activates NF-kappa B in nasopharyngeal carcinoma cells. METHODS: A tetracycline-regulated LMP1-expressing nasopharyngeal carcinoma cell line, Tet-on-LMP1-HNE2, was used as the cell model. The kinetics of the expression of proteins, including LMP1, I kappa B alpha and I kappa B beta, was analyzed by Western blotting. The subcellular localization of NF-kappa B (p65) was detected by indirect immunofluorescence assay. The NF-kappa B transactivity was studied by transient transfection and reporter gene assay. RESULTS: I kappa B alpha was phosphorylated and degraded after the inducible expression of LMP1, although the total protein levels remained stable. The steady-state level of total I kappa B beta protein may have resulted from the initiation of an autoregulation loop after the activation of NF-kappa B. No change in the I kappa B beta level was detected. NF-kappa B (p65) was translocated from the cytoplasm to the nucleus following degradation of I kappa B alpha. After the introduction of the dominant-negative mutant of I kappa B alpha (Del 71) into Tet-on-LMP1-HNE2 cells, both nuclear translocation and transactivation of NF-kappa B induced by LMP1 was significantly inhibited. CONCLUSIONS: The results indicated that in nasopharyngeal carcinoma cells, LMP1 activated NF-kappa B via phosphorylation and degradation of I kappa B alpha, but not I kappa B beta. The dominant-negative mutant of I kappa B alpha (Del 71) could completely inhibit both the nuclear translocation and transactivation of NF-kappa B induced by LMP1.

Biological Transport↗
PubMed2001

[EBV latent membrane protein 1 induces p53 expression via NF-kappa B in nasopharyngeal carcinoma].

OBJECTIVE: To ascertain if EBV-encoded latent membrane protein 1 (LMP1) induces p53 expression via NF-kappa B signaling. METHODS: A nasopharyngeal carcinoma cell line, Tet-on-LMP1 HNE2, transfected with LMP1, the expression of which was regulated by tetracycline, was used in this study. Functional activity of NF-kappa B was determined by luciferase reporter assay and expression of p53 and bcl-2 was detected by Western blot. RESULTS: LMP1 induced p53 expression via NF-kappa B signaling pathway. Induction of p53 expression could be blocked by phosphorothiate analogs of antisense oligonucleotides to NF-kappa B p65 and LMP1, but not by NF-kappa B p50. However, it seemed that LMP1 had no influence on bcl-2 expression in nasopharyngeal carcinoma. CONCLUSION: Induction expression of p53 by EBV-encoded LMP1 implies that p53 may act as a mediator in apoptosis triggered by LMP1, which brings about a complex balance in nasopharyngeal carcinogenesis.

Herpesvirus 4, Human↗
PubMed2001

[Positive immunoglobulin A expression in human epithelial carcinoma cell lines].

OBJECTIVE: In the present study, we try to further elucidate which class of immunoglobulin is expressed in epithelial carcinoma cell lines. METHODS: Three assays, immunohistochemistry, Western blot and enzyme-linked immunosorbent assay (ELISA) were used to detect the cellular protein extracts and the cultivated supernatant. RESULTS: Seven human epithelial carcinoma cell lines, MCF-7 (human breast carcinoma cell line), SW480 (human colon carcinoma cell line), MGC (human gastric carcinoma cell line), HeLa (human cervical carcinoma cell line), HNE2, CNE1-LMP1 and Tet-on-LMP1-HNE2 (three human nasopharyngeal carcinoma cells) expressed IgA protein in their cellular extracts and cultivated supernatants. CONCLUSION: Immunoglobulin is expressed in epithelium-derived carcinoma cell lines, which is in conflict with the traditional immunoglobulin theory. Our findings imply that the immunoglobulin expressed in epithelial carcinoma cells might play a role in the carcinogenesis of epithelium-derived carcinoma. Understanding the mechanism of immunoglobulin expression by cancer cells may possibly further facilitate the improvement techniques in cancer diagnosis, therapy or the mechanism of carcinogenesis.

Culture Media↗
PubMed2001

[Antibacterial activities of seven commonly used antibiotics to 106 isolated strains of porphyromonas gingivalis in vitro].

OBJECTIVE: Porphyromonas gingivalis (Pg) is one of the main putative pathogens of periodontal disease, especially of adult periodontitis. This in vitro study was aimed at observing the inhibitory activities of 7 commonly used antimicrobical drugs on 106 stains of Pg which isolated from subgingival plaques of sites with adult periodontits. METHODS: Kirby-Bauer paper disk method was used in this study. RESULTS: Pg was highly susceptible to Clindamycin, Sulfamzthoxazole timethoprin, Tetracycline and Cefazolin, the susceptibility rates were 93.4%, 78.3%, 60.4% and 56.6% respectively. CONCLUSION: Majority of the strains of Pg was moderately susceptible to cefalexin and acetylspiramycin, while no strains of Pg was susceptible to Penicillin G. The concentrations of Pg solutions (10(5) CFU/ml, 10(6) CFU/ml and 10(8) CFU/ml) had not influence on the results. This data is helpful for clinically antibiotic selection of periodontal treatment.

Adult↗
PubMed2001

[Observation of the biological characterizations of nasopharyngeal epithelial cells by EB virus infection in early phase of immortalization].

The multi-stage cell model of the nasopharyngeal carcinoma development in vitro by Epstein-Barr virus transformation is beneficial for the elucidation of the mechanism of nasopharyngeal cancer. To observe the biological changes of primary human nasopharyngeal epithelial cells in early phase of immortalization, in this study, we have detected the morphological changes and the expression profile of senescence-associated beta-galactosidase (SA-beta-Gal) in primary culture. In addition, the expression of EB virus latent membrane protein 1 (LMP1) and the growth curve of primary cells were also detected. Our results showed a low percentage of cells infected with EB virus expressing SA-beta-Gal activity at the late primary culture. In morphology, the cells also formed multilayer foci, and the cell population doubling time was showed. These results demonstrated that the nasopharyngeal epithelial cells by EB virus infection have passed through the senescence and entered the early phase of immortalization. These cells have some of the transformed characteristics. Our results provided the data for further study on the mechanism of immortalization and the establishment of human nasopharyngeal epithelial cell line.

Cell Transformation, Viral↗
PubMed2000

The trio guanine nucleotide exchange factor is a RhoA target. Binding of RhoA to the trio immunoglobulin-like domain.

Trio is a complex protein containing two guanine nucleotide exchange factor domains each with associated pleckstrin homology domains, a serine/threonine kinase domain, two SH3 domains, an immunoglobulin-like domain, and spectrin-like repeats. Trio was originally identified as a LAR tyrosine phosphatase-binding protein and is involved in actin remodeling, cell migration, and cell growth. Herein we provide evidence that Trio not only activates RhoA but is also a RhoA target. The RhoA-binding site was mapped to the Trio immunoglobulin-like domain. RhoA isoprenylation is necessary for the RhoA-Trio interaction, because mutation of the RhoA carboxyl-terminal cysteine residue blocked binding. The existence of an intramolecular functional link between RhoA activation and RhoA binding is suggested by the finding that Trio exchange activity enhanced RhoA binding to Trio. Furthermore, immunofluorescence studies of HeLa cells showed that although ectopically expressed Trio was evenly distributed within the cell, co-expression of Trio with RhoA resulted in relocalization of Trio into punctate structures. Relocalization was not observed with Trio constructs lacking the immunoglobulin-like domain, indicating that RhoA acts to regulate Trio localization via binding to the immunoglobulin-like domain. We propose that Trio-mediated RhoA activation and subsequent RhoA-mediated relocalization of Trio functions to modulate and coordinate Trio signaling.

Animals↗
PubMed2000

Genetic susceptibility to breast cancer: HLA DQB*03032 and HLA DRB1*11 may represent protective alleles.

Tumors are believed to emerge only when immune surveillance fails. We wished to ascertain whether the failure to inherit putative protective alleles of HLA class II genes is linked to the development of breast cancer. We molecularly typed HLA DPB1, DQB1, DRB1, and DRB3 alleles in 176 Caucasian women diagnosed with early-onset breast cancer and in 215 ethnically matched controls. HLA DQB*03032 was identified in 7% of controls but in no patients with early-onset breast cancer (P = 0.0001). HLA DRB1*11 alleles were also significantly overrepresented (P < 0.0001) in controls (16. 3%) as compared with patients with early-onset breast cancer (3.5%). HLA DQB*03032 and HLA DRB1*11 alleles may have a protective role in human breast cancer.

Adult↗
PubMed2000

Reversible electromechanical characteristics of carbon nanotubes under local-probe manipulation

The effects of mechanical deformation on the electrical properties of carbon nanotubes are of interest given the practical potential of nanotubes in electromechanical devices, and they have been studied using both theoretical and experimental approaches. One recent experiment used the tip of an atomic force microscope (AFM) to manipulate multi-walled nanotubes, revealing that changes in the sample resistance were small unless the nanotubes fractured or the metal-tube contacts were perturbed. But it remains unclear how mechanical deformation affects the intrinsic electrical properties of nanotubes. Here we report an experimental and theoretical elucidation of the electromechanical characteristics of individual single-walled carbon nanotubes (SWNTs) under local-probe manipulation. We use AFM tips to deflect suspended SWNTs reversibly, without changing the contact resistance; in situ electrical measurements reveal that the conductance of an SWNT sample can be reduced by two orders of magnitude when deformed by an AFM tip. Our tight-binding simulations indicate that this effect is owing to the formation of local sp3 bonds caused by the mechanical pushing action of the tip.

Journal Article↗
PubMed2000

Controllable reversibility of an sp(2) to sp(3) transition of a single wall nanotube under the manipulation of an AFM tip: A nanoscale electromechanical switch?

A simulation of the deflection of a single wall nanotube under the manipulation of an atomic force microscope tip revealed the key feature characterizing the deformation at relatively small bending angles to be a reversible transition from sp(2) to sp(3) bonding configurations in the bending region, leading to a 2 orders of magnitude reduction in conductance consistent with our most recent experimental observation. A local analysis elucidating the underlying physics of the findings is also discussed.

Journal Article↗
PubMed2000

Targeting of lung cancer mutational hotspots by polycyclic aromatic hydrocarbons.

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in combustion products of organic matter, including cigarette smoke. Metabolically activated diol epoxides of these compounds, including benzo[a]pyrene diol epoxide (B[a]PDE), have been suggested as causative agents in the development of lung cancer. We previously mapped the distribution of B[a]PDE adducts within the p53 tumor suppressor gene (also known as TP53), which is mutated in 60% of human lung cancers, and found that B[a]PDE adducts preferentially form at lung cancer mutational hotspots (codons 154, 157, 158, 245, 248, and 273). Other PAHs may be important in lung cancer as well. METHODS: Here we have mapped the distribution of adducts induced by diol epoxides of additional PAHs: chrysene (CDE), 5-methylchrysene (5-MCDE), 6-methylchrysene (6-MCDE), benzo[c]phenanthrene (B[c]PDE), and benzo[g]chrysene (B[g]CDE) within exons 5, 7, and 8 of the p53 gene in human bronchial epithelial cells. RESULTS: CDE exposure produced only low levels of adducts. Exposure of cells to the other activated PAHs resulted in DNA damage patterns similar to those previously observed with B[a]PDE but with some distinct differences. 5-MCDE, 6-MCDE, B[g]CDE, and B[c]PDE efficiently induced adducts at guanines within codons 154, 156, 157, 158, and 159 of exon 5, codons 237, 245 and 248 of exon 7, and codon 273 of exon 8, but the relative levels of adducts at each site varied for each compound. B[g]CDE, B[c]PDE, and 5-MCDE induced damage at codon 158 more selectively than 6-MCDE or B[a]PDE. The sites most strongly involved in PAH adduct formation were also the sites of highest mutation frequency (codons 157, 158, 245, 248, and 273). CONCLUSION: The data suggest that PAHs contribute to the mutational spectrum in human lung cancer.

Base Sequence↗
PubMed2000

Roles of E. coli DNA polymerases IV and V in lesion-targeted and untargeted SOS mutagenesis.

The expression of the Escherichia coli DNA polymerases pol V (UmuD'2C complex) and pol IV (DinB) increases in response to DNA damage. The induction of pol V is accompanied by a substantial increase in mutations targeted at DNA template lesions in a process called SOS-induced error-prone repair. Here we show that the common DNA template lesions, TT (6-4) photoproducts, TT cis-syn photodimers and abasic sites, are efficiently bypassed within 30 seconds by pol V in the presence of activated RecA protein (RecA*), single-stranded binding protein (SSB) and pol III's processivity beta,gamma-complex. There is no detectable bypass by either pol IV or pol III on this time scale. A mutagenic 'signature' for pol V is its incorporation of guanine opposite the 3'-thymine of a TT (6-4) photoproduct, in agreement with mutational spectra. In contrast, pol III and pol IV incorporate adenine almost exclusively. When copying undamaged DNA, pol V exhibits low fidelity with error rates of around 10(-3) to 10(-4), with pol IV being 5- to 10-fold more accurate. The effects of RecA protein on pol V, and beta,gamma-complex on pol IV, cause a 15,000- and 3,000-fold increase in DNA synthesis efficiency, respectively. However, both polymerases exhibit low processivity, adding 6 to 8 nucleotides before dissociating. Lesion bypass by pol V does not require beta,gamma-complex in the presence of non-hydrolysable ATPgammaS, indicating that an intact RecA filament may be required for translesion synthesis.

DNA Damage↗
PubMed2000

C5 cytosine methylation at CpG sites enhances sequence selectivity of mitomycin C-DNA bonding.

We have established that UvrABC nuclease is equally efficient in cutting mitomycin C (MC)-DNA monoadducts formed at different sequences and that the degree of UvrABC cutting represents the extent of drug-DNA bonding. Using this method we determined the effect of C5 cytosine methylation on the DNA monoalkylation by MC and the related analogues N-methyl-7-methoxyaziridinomitosene (MS-NMA) and 10-decarbamoylmitomycin C (DC-MC). We have found that C5 cytosine methylation at CpG sites greatly enhances MC and MS-NMA DNA adduct formation at those sites while reducing adduct formation at non-CpG sequences. In contrast, although DC-MC DNA bonding at CpG sites is greatly enhanced by CpG methylation, its bonding at non-CpG sequences is not appreciably affected. These cumulative results suggest that C5 cytosine methylation at CpG sites enhances sequence selectivity of drug-DNA bonding. We propose that the methylation pattern and status (hypo- or hypermethylation) of genomic DNA may determine the cells' susceptibility to MC and its analogues, and these effects may, in turn, play a crucial role in the antitumor activities of the drugs.

Alkylating Agents↗
PubMed2000

Ligand-activated progesterone receptor isoform hPR-A is a stronger transactivator than hPR-B for the expression of IGFBP-1 (insulin-like growth factor binding protein-1) in human endometrial stromal cells.

In human endometrium, the levels of progesterone receptor (PR) isoforms hPR-A and hPR-B are differentially regulated during the reproductive cycle. Progesterone significantly increases the content of hPR-A, the predominant isoform in decidualized stromal cells (1). The purpose of this study was to determine the capacity of hPR-A and hPR-B to transactivate the progestin-dependent target gene in human endometrial stromal cells. We examined the effect of cotransfection of hPR-A or hPR-B on the expression of the human insulin-like growth factor binding protein-1 (IGFBP-1) in endometrial stromal cells. The primary culture of human endometrial stromal cells was transfected with the hPR-A or hPR-B expression vector and the IGFBP-1 promoter construct p275CAT, which contains two functional progesterone response elements (PRE1 and PRE2) in decidualized stromal cells. Medroxyprogesterone acetate (MPA) increased the promoter activities ranging from 1.2- to 27-fold in cells cotransfected with hPR-A or hPR-B in eight endometrial specimens. The promoter activity increased by the hPR-A was significantly higher than hPR-B (15 +/- 8 vs. 4 +/- 2, mean +/- SD; n = 8, P < 0.005). Site-specific mutation showed that the induced activity by hPR-A was mediated through the PRE1 and PRE2 sites. Addition of hPR-B reduced the effect of hPR-A. The high transactivation capacity of hPR-A was also activated by other ligands, progesterone, Org 2058, and norethindrone. These observations indicate that hPR-A is a stronger transactivator than hPR-B for the IGFBP-1 promoter in endometrial stromal cells. Previous studies have shown the progestin-dependent production of IGFBP-1 correlates with its mRNA levels and transcription rate. Thus, we have determined the effect of hPR-A and hPR-B on the production of IGFBP-1 in stromal cells treated with MPA. The production rate in cells uniformly infected with AdPRA (recombinant Ad5-directed PR expression system) was significantly higher (P < 0.001) than the rate in uninfected cells and in cells infected with AdPRB or AdCMV (the Ad5 viral expression vector). This result, in concert with the promoter analysis, provides evidence that hPR-A is a strong inducer for the chromosomal IGFBP-1 gene in endometrial stromal cells.

Adult↗