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Biomedical subjects

G Tang

Publications and source records attributed to G Tang.

At least 19 recordsLinked to original sources

Menstrual cycle lengths and bone mineral density: a cross-sectional, population-based study in rural Chinese women ages 30-49 years.

INTRODUCTION: The menstrual cycle involves periodic fluctuations in estrogen and progesterone levels. Longer cycles have been associated with longer follicular phase, delayed estrogen peak and a lower mean oestradiol level of the entire cycle. METHODS: We hypothesized that prolonged menstrual cycle length is associated with decreased bone mineral density (BMD) in a population of pre- and perimenopausal women. This population-based cross-sectional study was conducted in rural Anhui province, China. It includes 4,771 women, aged 30 to 49 years, who did not smoke or drink alcohol, and did not use oral contraceptives or breastfeed during the previous year. Dual-energy X-ray absorptionometry (DEXA) BMD measurements were taken at four skeletal sites: whole body, total hip, femoral neck and lumbar spine. Menstrual cycle characteristics (polymenorrhea, short normal, long normal, oligomenorrhea, 90-day amenorrhea, irregular cycle) in the prior year were assessed by questionnaire. RESULTS: Prolonged menstrual cycle was consistently associated with decreased BMD at whole body, total hip, and femoral neck in both age 30-39, and age 40-49 stratum (p(trend)<0.05). Prolonged menstrual cycle was also associated with decreased lumbar spine BMD for women aged 40-49 (p(trend)<0.05). Among women with normal cycles aged 30-39, menstrual cycle length in the previous year was inversely associated with whole-body BMD (p<0.05). Women with 90-day amenorrhea had significantly lower mean total hip and femoral neck BMD relative to women with short normal cycles in the 30-39 age group; and had significantly lower whole body and total hip BMD relative to short normal cycles in the 40-49 age group. BMD in polymenorrheic women did not differ from BMD in women with short normal cycles at any of the skeletal sites. CONCLUSIONS: We conclude that prolonged menstrual cycle length is associated with decreased BMD in pre- and perimenopausal women in this population.

Adult↗

Comparison of microshear bond strengths of four self-etching bonding systems to enamel using two test methods.

BACKGROUND: Recent advances in enamel and dentine adhesive technology have resulted in the emergence of many new adhesive systems. Self-etching bonding systems do not require a separate etching step and the newest systems are the "all-in-one" systems which combine etching, priming and bonding into a single application. This study reports laboratory enamel microshear bond strengths of a self-etching priming and three all-in-one systems and also evaluates two different microshear bond test methods. METHODS: One hundred and nineteen enamel specimens were bonded (0.8 mm diameter) with either Clearfil Protect Bond (Kuraray), Xeno III (Dentsply), G Bond (GC) or One-Up Bond F (Tokuyama) using Palfique Estelite resin composite and stored in 37 degrees Celsius water for seven days. The microshear bond test method used either a blade or wire to apply the shear stress. Results were analysed with one-way ANOVA and post hoc (Tukey) multiple comparison analysis. RESULTS: Clearfil Protect Bond demonstrated higher and more consistent bond strengths than Xeno III, G Bond or One-Up Bond F. The wire method showed much greater reliability in results, with a coefficient of variation half that of the blade method. CONCLUSIONS: All-in-one adhesives seem to be less reliable than the two-step self-etching priming adhesive when bonding to enamel. Test method can significantly affect results in the microshear bond test method.

Acid Etching, Dental↗

Genotypic diversity of oral Actinomyces naeslundii genospecies 1 and 2 in caries-active preschool children.

A total of 991 isolates of Actinomyces naeslundii were obtained from sound approximal tooth sites in either caries-active (n = 35) or caries-free (n = 20) preschool children. From this group of isolates, 101 strains were chosen to study the genotypic diversity of A. naeslundii genospecies 1 (n = 30), catalase-positive (n = 30), and catalase-negative genospecies 2 (n = 41). Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), with a pair of primers targeting the 16S ribosome RNA gene (16S rDNA), and MnlI digestion together with randomly amplified polymorphic DNA (RAPD) with eight arbitrary, single 10-mer primers were performed to generate genetic profiles of selected Actinomyces isolates. The hierarchic relationships of genetic profiles were finally analyzed using computerized dendrograms. There was no significant difference in the prevalence rates and proportions of either genospecies 1 or 2 between the caries-free and caries-active groups, although a higher prevalence of genospecies 2 was noted in the total population. Dendrogram analyses of the 16S rDNA PCR-RFLP profiles revealed that all strains belonging to A. naeslundii genospecies 1 could be subgrouped into three genotypes (T7, T18, and T19), with a single predominant genotype, T18 (27/30). Catalase-positive strains for genospecies 2 fell into three subtypes (T4, T7, and T17), whereas the catalase-negative counterparts were distributed amongst 16 subtypes. No specific genotype was significantly associated with caries activity. We conclude that heterogeneous subgroups of A. naeslundii genospecies 1 and 2, particularly the latter, are the constituent flora of dental plaque in children and may contribute to the pathogenesis of childhood caries.

Actinomyces↗

Molecular evaluation of residual endodontic microorganisms after instrumentation, irrigation and medication with either calcium hydroxide or Septomixine.

BACKGROUND AND OBJECTIVE: The correct choice of antimicrobial agents as inter-appointment medicaments is as important as the instrumentation and irrigation to remove pathogens from infected root canals. Calcium hydroxide [Ca(OH)2] and framycetin sulfate (Septomixine) are common endodontic medicaments. Therefore, we evaluated the efficacy of either calcium hydroxide or Septomixine in eliminating residual intra-canal bacteria, particularly Actinomyces spp., during inter-appointment interval in endodontic therapy using molecular methods. METHODS: A total of 31 single-rooted teeth with primary root canal infections were studied immediately after opening the canals and subsequently after instrumentation, irrigation with sterile saline and 1-week medication with either Ca(OH)2 (n = 25) or Septomixine (n = 6). Whole bacterial genomic DNA was isolated directly from samples and PCR with universal primers performed to detect total intra-canal bacteria. The variable regions of 16S rDNA of bacteria were amplified and labeled with digoxigenin for further hybridization to detect Actinomyces spp. A total of seven oligonucleotide probes specific for A. bovis, A. gerencseriae, A. israelii, A. meyeri, catalase-negative A. naeslundii (genospecies 1 and 2), catalase-positive A. naeslundii genospecies 2 and A. odontolyticus were used to detect Actinomyces spp. in 22 of 31 medicated root canals [Ca(OH)2: n = 17; Septomixine: n = 5]. RESULTS: The PCR results showed that 25 of 31 examined canals were positively detected with residual microorganisms after instrumentation, irrigation with sterile saline and 1-week medication with either Ca(OH)2 (n = 20) or Septomixine (n = 5). Thus, only six canals [Ca(OH)2: n = 5, Septomixine: n = 1] were aseptic after treatment. Hybridization results showed higher detection frequency of both A. odontolyticus and A. gerencseriae after treatment. Significant correlation was found between exposed pulp before treatment and positive detection of Actinomyces spp., particularly A. odontolyticus on the second visit (P < 0.05). CONCLUSION: The conventional, 1-week medication of either Ca(OH)2 or Septomixine in endodontic therapy may not effectively inhibit residual bacterial growth in all root canals during inter-appointment intervals. Further investigations using, for instance quantitative real-time PCR analyses, are required to substantiate the present findings.

Actinomycosis↗

Development of novel oligonucleotide probes for seven Actinomyces species and their utility in supragingival plaque analysis.

OBJECTIVE: The traditional, biochemical and enzymatic methods of identifying Actinomyces species are frequently confounded by the similar phenotypic characteristics shared by the different members of this genus. Therefore, we developed novel species-specific oligonucleotide probes to accurately speciate seven pathogenic Actinomyces species, namely, Actinomyces bovis, A. gerencseriae, A. israelii, A. meyeri, A. naeslundii, A. odontolyticus and A. viscosus. METHODS: A pair of universal primers and seven 15- to 19-base oligonucleotide probes with a tail of 20 thymidines on the 5' end were developed. The variable regions of 16S ribosomal DNA of 36 strains of Actinomyces belonging to the above species were amplified and labeled with digoxigenin, and an oligonucleotide-DNA hybridization assay was performed to examine the specificity and sensitivity of these probes. RESULTS: All seven, newly developed probes were specific and sensitive, and accurately detected 36 reference and wild type strains belonging to Actinomyces species, without cross-reactions. The probe for A. naeslundii detected all strains belonging to the genospecies 1 (12 strains) and catalase-negative genospecies 2 (four strains); it failed to detect catalase-positive A. naeslundii genospecies 2 (previous A. viscosus serotype II) (two strains). However, the latter strains of catalase-positive A. naeslundii genospecies 2 were correctly detected by the probe developed for A. viscosus. The new probes were then field tested using supragingival plaque samples from 28 healthy preschool children. Whilst A. odontolyticus was detected in almost all samples (96.4%), A. gerencseriae, A. meyeri, catalase-negative A. naeslundii and catalase-positive A. naeslundii genospecies 2 were detected in < 50% samples. CONCLUSION: We conclude that the developed oligonucleotide probes, complementary to the variable regions of 16S rDNA, would be of potential value for differentiating Actinomyces spp. in clinical samples from the oral cavity and other ecosystems where such species may abound.

5' Flanking Region↗

Linkage studies between attention-deficit hyperactivity disorder and the monoamine oxidase genes.

Attention-deficit hyperactivity disorder (ADHD) is a prevalent behavioral disorder in children and the etiology of this disorder is not clear. Molecular genetic and pharmacological studies suggest the involvement of dopaminergic and noradrenergic neurotransmitter systems in ADHD, e.g., several reports have found association between ADHD and the dopamine receptor gene DRD-4, the dopamine transporter gene DAT1, and the catecholamine clearance enzyme catechol-O-methyltransferase. Monoamine oxidase (MAO) A and B genes encode enzymes that participate in the metabolism of neurotransmitters of the dopaminergic and noradrenergic systems. MAO inhibitors have been shown to be effective in the treatment of ADHD. Our previous studies showed an association between ADHD and the DXS7 locus, which is located in close vicinity to the MAO genes on chromosome X. These findings suggest that there might be linkage between ADHD and MAO genes. To test this hypothesis, we used the transmission/disequilibrium test (TDT) to test for linkage between a VNTR polymorphism at the MAOA(CA)(n) or MAOB(GT)(n) locus and DSM-III-R-diagnosed ADHD in 82 nuclear families of the Chinese population. The TDT analysis revealed linkage between ADHD and the MAOA(CA)(n) locus (chi-square = 15.25, df = 7, P < 0.05), but not the MAOB(GT)(n) locus (chi-square = 11.18, df = 7, P > 0.05). The data showed that ADHD was in linkage with the MAOA gene and suggested that MAOA might be a susceptibility factor for ADHD.

Alleles↗

Inhibition of JNK activation through NF-kappaB target genes.

The proinflammatory cytokine tumour necrosis factor-alpha (TNF-alpha) regulates immune responses, inflammation and programmed cell death (apoptosis). The ultimate fate of a cell exposed to TNF-alpha is determined by signal integration between its different effectors, including IkappaB kinase (IKK), c-Jun N-terminal protein kinase (JNK) and caspases. Activation of caspases is required for apoptotic cell death, whereas IKK activation inhibits apoptosis through the transcription factor NF-kappaB, whose target genes include caspase inhibitors. JNK activates the transcription factor c-Jun/AP-1, as well as other targets. However, the role of JNK activation in apoptosis induced by TNF-alpha is less clear. It is unknown whether any crosstalk occurs between IKK and JNK, and, if so, how it affects TNF-alpha-induced apoptosis. We investigated this using murine embryonic fibroblasts that are deficient in either the IKKbeta catalytic subunit of the IKK complex or the RelA/p65 subunit of NF-kappaB. Here we show that in addition to inhibiting caspases, the IKK/NF-kappaB pathway negatively modulates TNF-alpha-mediated JNK activation, partly through NF-kappaB-induced X-chromosome-linked inhibitor of apoptosis (XIAP). This negative crosstalk, which is specific to TNF-alpha signalling and does not affect JNK activation by interleukin-1 (IL-1), contributes to inhibition of apoptosis.

Animals↗

Lack of association between the tryptophan hydroxylase gene A218C polymorphism and attention-deficit hyperactivity disorder in Chinese Han population.

Previous studies have suggested that the serotonergic (5-HT) system might be involved in the development of Attention-deficit hyperactivity disorder (ADHD). ADHD is frequently characterized by aggressive and impulsive behavior, a major symptom associated with reduction in serotonergic function. The tryptophan hydroxylase (TPH) gene is a reasonable candidate for ADHD because it encodes the rate-limiting enzyme in the process of 5-HT biosynthesis. In this study, we examined the relationship between the A218C polymorphism in TPH gene and ADHD. Sixty-nine ADHD patients and their biological parents were investigated. The A218C polymorphism in intron 7 of TPH gene was detected by PCR-RFLP method. No allele or genotype concerned with this A218C polymorphism was found to be associated with ADHD when analyzed with the haplotype relative risk method. Therefore, our data indicate that the TPH gene A218C polymorphism may not be a susceptibility factor of ADHD in the Chinese Han population.

Alleles↗

Activation of NF-kappa B is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes.

The transcription factor NF-kappaB regulates expression of genes that are involved in inflammation, immune response, viral infection, cell survival, and division. However, the role of NF-kappaB in hypertrophic growth of terminally differentiated cardiomyocytes is unknown. Here we report that NF-kappaB activation is required for hypertrophic growth of cardiomyocytes. In cultured rat primary neonatal ventricular cardiomyocytes, the nuclear translocation of NF-kappaB and its transcriptional activity were stimulated by several hypertrophic agonists, including phenylephrine, endothelin-1, and angiotensin II. The activation of NF-kappaB was inhibited by expression of a "supersuppressor" IkappaBalpha mutant that is resistant to stimulation-induced degradation and a dominant negative IkappaB kinase (IKKbeta) mutant that can no longer be activated by phosphorylation. Furthermore, treatment with phenylephrine induced IkappaBalpha degradation in an IKK-dependent manner, suggesting that NF-kappaB is a downstream target of the hypertrophic agonists. Importantly, expression of the supersuppressor IkappaBalpha mutant or the dominant negative IKKbeta mutant blocked the hypertrophic agonist-induced expression of the embryonic gene atrial natriuretic factor and enlargement of cardiomyocytes. Conversely, overexpression of NF-kappaB itself induced atrial natriuretic factor expression and cardiomyocyte enlargement. These findings suggest that NF-kappaB plays a critical role in the hypertrophic growth of cardiomyocytes and may serve as a potential target for the intervention of heart disease.

Angiotensin II↗

Modulation of voltage-dependent K+ channel current in vascular smooth muscle cells from rat mesenteric arteries.

Voltage-dependent K+ (Kv) channels were studied in smooth muscle cells (SMCs) freshly isolated from rat mesenteric arteries. A delayed outward rectifier Kv current (IK) with a weak voltage dependence was identified. The amplitude of IK, but not its inactivation kinetics, was inhibited by 4-aminopyridine (4-AP) (IC50, 5.1 +/- 0.9 mM). The inhibitory effect of 4-AP was not use-dependent, and the unbinding of 4-AP from IK channels was complete in the absence of depolarization stimuli, suggesting the binding of 4-AP to the closed state of Kv channels. There was no change in the steady-state inactivation, but the steady-state activation curve of IK was shifted in the presence of 4-AP by +6 mV. Including 4-AP in pipette solution instantly inhibited IK upon the rupture of cell membrane, indicating that 4-AP bound to the inner mouth of Kv channel pores. Several Kv channel proteins encoding the native IK-type Kv channels, but not the transient outward A-type Kv channels, were identified. Among the identified IK-encoding gene transcripts, the expression of Kv1.5 was the most abundant. Our results elucidate the modulating mechanisms for the 4-AP-induced IK inhibition in rat mesenteric artery SMCs and suggest that the unique properties of Kv channels in these cells might be related to the heteromeric expression of the IK-encoding genes with Kv1.5 subunit playing an important role.

4-Aminopyridine↗

Effect of long-range interactions on the scaling of the noisy Kuramoto-Sivashinsky equation.

The effects of long-range interactions on the scaling properties of the noisy Kuramoto-Sivashinsky (KS) equation are studied by the dynamic renormalization-group technique. It is found that the presence of long-range nonlinearity in the KS equation can produce new stable fixed points with varying critical exponents that depend on both the long-range interaction parameter rho and the substrate dimension d.

Journal Article↗

Differential expression of KV and KCa channels in vascular smooth muscle cells during 1-day culture.

Voltage-dependent delayed rectifier K+ (KV) channels and Ca(2+)-activated K+ (KCa) channels both play important roles in the regulation of the membrane potential and contractility of vascular smooth muscle cells (SMCs). The expression and function of these K+ channels in cultured vascular SMCs have been extensively studied. The long-term in vitro cell culture would change the properties of K+ channels in SMCs. However, whether the short-term culture could differentially affect the expression and function of KV and KCa channels was not clear. In the present study, both KV and KCa channel currents were identified in freshly dissociated SMCs and in 1-day-cultured SMCs from rat tail arteries. KCa currents were inhibited by iberiotoxin or tetraethylammonium (TEA), and amplified by the calcium ionophore A-23187. Kv currents were inhibited by 4-aminopyridine or beta-dendrotoxin. By using different pharmacological agents and manipulating the calcium concentrations in the recording solutions, it was revealed that in freshly dissociated SMCs the predominant component of total outward K+ currents is KCa current, and KV current a minor component. In contrast, KV current was found to be the predominant component of total outward K+ currents in SMCs primarily cultured with 10% fetal bovine serum at 37 degrees C for 24 h. Differential expression of KV and KCa channels in 1-day-cultured SMCs was thus demonstrated under our experimental conditions. Our results are important for interpreting the electrophysiological properties of vascular SMCs under different cell culture conditions and for understanding the relative contributions of KV and KCa channels to different cellular functions.

4-Aminopyridine↗

Blocking caspase-3-mediated proteolysis of IKKbeta suppresses TNF-alpha-induced apoptosis.

The transcription factor NF-kappaB is essential for survival of many cell types. However, cells can undergo apoptosis despite the concurrent NF-kappaB activation. It is unknown how the protection conveyed by NF-kappaB is overridden during apoptosis. We report here that IkappaB kinase (IKK) beta was specifically proteolyzed by Caspase-3-related caspases at aspartic acid residues 78, 242, 373, and 546 during tumor necrosis factor (TNF)-alpha-induced apoptosis. Proteolysis of IKKbeta eliminated its enzymatic activity, interfered with IKK activation, and promoted TNF-alpha killing. Point mutations that abrogate IKKbeta proteolysis generated a caspase-resistant IKKbeta mutant, which suppressed TNF-alpha-induced apoptosis. Thus, our study demonstrates that TNF-alpha-induced apoptosis requires caspase-mediated proteolysis of IKKbeta.

Amino Acid Chloromethyl Ketones↗

Lysine catabolism: a stress and development super-regulated metabolic pathway.

Lysine is a nutritionally important essential amino acid whose level in plants is largely regulated by the rate of its synthesis. In some plant tissues and under some stress conditions, however, lysine is also efficiently catabolized into glutamate and several other stress-related metabolites by novel mechanisms of metabolic regulation. Lysine catabolism is important for mammalian brain function; it is possible that the generation of glutamate regulates nerve transmission signals via glutamate receptors. Plants also possess homologues of animal glutamate receptors. It is thus likely that lysine catabolism also regulates various plant processes via these receptors.

Animals↗

A T-DNA insertion knockout of the bifunctional lysine-ketoglutarate reductase/saccharopine dehydrogenase gene elevates lysine levels in Arabidopsis seeds.

Plants possess both anabolic and catabolic pathways for the essential amino acid lysine (Lys). However, although the biosynthetic pathway was clearly shown to regulate Lys accumulation in plants, the functional significance of Lys catabolism has not been experimentally elucidated. To address this issue, we have isolated an Arabidopsis knockout mutant with a T-DNA inserted into exon 13 of the gene encoding Lys ketoglutarate reductase/saccharopine dehydrogenase. This bifunctional enzyme controls the first two steps of Lys catabolism. The phenotype of the LKR/SDH knockout was indistinguishable from wild-type plants under normal growth conditions, suggesting that Lys catabolism is not an essential pathway under standard growth conditions. However, mature seeds of the knockout mutant over-accumulated Lys compared with wild-type plants. This report provides the first direct evidence for the functional significance of Lys catabolism in regulating Lys accumulation in seeds. Such a knockout mutant may also provide new perspectives to improve the level of the essential amino acid Lys in plant seeds.

Arabidopsis↗

[The normalization creep functions of C5.6,T6.7,L4.5 interverbral discs of human vertebral column].

In this paper are reported the creep experimental studies on 9 fresh C5.6 intervertebral discs,9 fresh T6.7 intervertebral discs and 10 L4.5 intervertebral discs that were taken from the bodies of ten men(aged 19-35 years) who had died of head injury 1-4 h before. By simulating the temperature of human body (36.5 degrees C +/- 0.5 degree C) and putting 300 N load on the discs, we measured the intervertebral creep effects and obtained the strain-time curves.

Adult↗

[Study of susceptibility loci located within Xp11 in attention deficit hyperactivity disorder].

OBJECTIVE: To detect the genetic relationship between monoamine oxidase(MAO) A type gene and attention deficit hyperactivity disorder(ADHD) in Chinese. METHODS: The haplotype-based haplotype relative risk(HHRR) and the transmission disequilibrium test(TDT) methods were used to analyze the genetic association and linkage in 60 ADHD children and their parents. RESULTS: In this sample were found significant association (chi(2)=4.90, P<0.05) and linkage (chi(2)=4.84, P<0.05) between the MAOCA 114bp allele and DSM-III-R-diagnosed ADHD in trios composed of father, mother and affected offspring. CONCLUSION: The above results suggested that ADHD was associated and in linkage with MAO A gene, and the susceptibility loci might reside in chromosome Xp11 for ADHD.

Attention Deficit Disorder with Hyperactivity↗