Biomedical subjects

B Ding

Publications and source records attributed to B Ding.

At least 19 recordsLinked to original sources

PubMed2002

The single nucleotide polymorphism T1128C in the signal peptide of neuropeptide Y (NPY) was not identified in a Korean population.

OBJECTIVE: A single nucleotide polymorphism (SNP) T1128C, which causes an amino acid change from leucine(7) to proline(7) in the signal peptide of neuropeptide Y (NPY), has been found to be associated with multiple clinical parameters or disease. However, this SNP was not identified in the Japanese population. We asked if this is also true in the Korean population. METHODS: Genotyping was conducted by pyrosequencing, a newly developed real-time high-throughput SNP scoring technique. RESULTS: All 242 Korean subjects showed T1128/T1128 genotype. CONCLUSIONS: The T1128C SNP does not appear to exist in this Korean population.

Adult↗

PubMed2002

The increase in levels of interferon-inducible proteins p202a and p202b and RNA-dependent protein kinase (PKR) during myoblast differentiation is due to transactivation by MyoD: their tissue distribution in uninfected mice does not depend on interferons.

The murine 200 family proteins p202a, p202b, and p204, and also RNA-dependent protein kinase (PKR) are inducible by interferons (IFNs). p202a, p202b, and p204 modulate the activity of a large variety of transcription factors and also are involved in muscle differentiation. PKR is a multifunctional serine/threonine kinase, which is involved in antiviral defense and cell growth control and in the response to various stress signals. We reported earlier that the level of p204 increases during cultured C2C12 myoblast differentiation to myotubes in consequence of transactivation by the skeletal muscle-specific MyoD protein. The levels of p202a, p202b, and PKR also increase during the differentiation. We report here that these increased protein levels also are due to the transactivation of their genes by MyoD. This is made possible by the occurrence in each of these genes of at least six E boxes, which are recognition sites for MyoD. We also show that the distribution of the p204, p202a, p202b, and PKR proteins in five tissues of adult C129 mice is the same in wild-type mice and mice lacking the IFN-alpha, IFN-beta, and IFN-gamma receptors. This indicates that the synthesis and distribution of these proteins in uninfected adult mice are not affected by endogenous IFNs.

Animals↗

PubMed2001

Metoprolol attenuates postischemic depressed myocardial function in papillary muscles isolated from normal and postinfarction rat hearts.

The present study was designed to test the hypothesis that metoprolol treatment may enhance tolerance to ischemia in normal and postinfarction rat myocardium. Myocardial infarction was induced by permanent ligation of the left coronary artery in adult rats. Animals were divided into sham-operated and infarction groups with or without metoprolol treatment. Metoprolol treatment (60 mg/kg/day via gastric gavage) was started on the second day after surgery and continued until sacrifice at 6 weeks after myocardial infarction. Isometric force and intracellular Ca(2+) ([Ca(2+)](i)) transients were simultaneously recorded in isolated left ventricular papillary muscles. Ischemia was simulated by immersing the muscles into fluorocarbon with hypoxia. Metoprolol treatment induced a significant improvement of isometric force and ameliorated diastolic [Ca(2+)](i) overload in postinfarction rat myocardium at baseline. Metoprolol treatment also reduced diastolic [Ca(2+)](i), ameliorated the depression of developed tension during ischemia, and enhanced recovery of postischemic depressed myocardial function in sham-operated and postinfarction rat papillary muscles. Protein levels of the sarcoplasmic reticulum Ca(2+) ATPase of left ventricles and postischemic papillary muscles from metoprolol-treated rats were higher than those in placebo-treated animals. We concluded, therefore, that metoprolol treatment produced appreciable improvement of intracellular Ca(2+) handling during ischemia-reoxygenation cycles, and enhanced recovery of postischemic depressed myocardial function in both normal and postinfarction rat myocardium.

Adrenergic beta-Antagonists↗

PubMed2001

Cardiac-specific overexpression of cyclin-dependent kinase 2 increases smaller mononuclear cardiomyocytes.

Cyclin-dependent kinase 2 (cdk2) plays a critical role in the G1- to S-phase checkpoint of the cell cycle. Adult cardiomyocytes are believed to withdraw from the cell cycle. To determine whether forced overexpression of cdk2 results in altered cell-cycle regulation in the adult heart, we generated transgenic mice specifically overexpressing cdk2 in hearts. Transgenic hearts expressed high levels of both cdk2 mRNA and catalytically active cdk2 proteins. Cdk2 overexpression significantly increased the levels of cdk4 and cyclins A, D3, and E. There was an increase in both DNA synthesis and proliferating cell nuclear antigen levels in the adult transgenic hearts. The ratio of heart weight to body weight in cdk2 transgenic mice was significantly increased in neonatal day 2 but not in adults compared with that of wild-type mice. Analysis of dispersed individual adult cardiomyocytes showed a 5.6-fold increase in the proportion of smaller mononuclear cardiomyocytes in the transgenic mice. Echocardiography revealed that transgenic heart was functionally normal. However, adult transgenic ventricles expressed beta-myosin heavy chain and atrial natriuretic factor. Surgically induced pressure overload caused an exaggerated maladaptive hypertrophic response in transgenic mice but did not change the proportion of mononuclear cardiomyocytes. The data suggest that overexpression of cdk2 promotes smaller, less-differentiated mononuclear cardiomyocytes in adult hearts that respond in an exaggerated manner to pressure overload.

Animals↗

PubMed2001

Cellular basis of potato spindle tuber viroid systemic movement.

Viroids are small, nontranslatable pathogenic RNAs that replicate autonomously and traffic systemically in their host plants. We have used in situ hybridization to analyze the trafficking pattern of Potato spindle tuber viroid (PSTVd) in tomato and Nicotiana benthamiana. When PSTVd was inoculated onto the stem of a plant, it replicated and trafficked to sink, but not source, leaves. PSTVd was absent from shoot apical meristems. In the flowers of infected plants, PSTVd was present in the sepals, but was absent in the petals, stamens, and ovary. The replicative form of PSTVd was detected in the phloem. Our data demonstrate that (i) PSTVd traffics long distance in the phloem and this trafficking is likely sustained by replication of the viroid in the phloem, and (ii) PSTVd trafficking is governed by plant developmental and cellular factors. The dependency of PSTVd and other viroids on cellular mechanisms for RNA trafficking makes them excellent tools to study such mechanisms.

In Situ Hybridization↗

PubMed2001

Potato spindle tuber viroid as inducer of RNA silencing in infected tomato.

Potato spindle tuber viroid (PSTVd), an RNA plant pathogen encoding no known proteins, induces systemic symptoms on tomato plants. We report detection of small RNAs of approximately 25 nucleotides with sequence specificity to PSTVd in infected plants: an indication of the presence of RNA silencing. RNA silencing, however, did not appear to be responsible for the differing symptoms induced by a mild and a severe strain of PSTVd. The unique structural and biological features of viroids make them attractive experimental tools to investigate mechanisms of RNA silencing and pathogen counterdefense.

Gene Silencing↗

PubMed2001

Possible involvement of the phloem lectin in long-distance viroid movement.

Incubation with cucumber phloem exudate in vitro results in a dramatic decrease in the electrophoretic mobility of Hop stunt viroid. UV cross-linking and a combination of size exclusion and ion exchange chromatography indicate that this phenomenon reflects a previously unsuspected ability of phloem protein 2, a dimeric lectin and the most abundant component of phloem exudate, to interact with RNA. In light of its demonstrated ability to move from cell to cell via plasmodesmata as well as long distances in the phloem, our results suggest that phloem protein 2 may facilitate the systemic movement of viroids and, possibly, other RNAs in vivo.

Cucumis sativus↗

PubMed2001

Identification of Sarcocystis hominis-like (Protozoa: Sarcocystidae) cyst in water buffalo (Bubalus bubalis) based on 18S rRNA gene sequences.

DNA templates were extracted from isolates of Sarcocystis hominis-like cysts collected from cattle and water buffalo, as well as from Sarcocystis fusiformis cysts and Sarcocystis suihominis cysts. The 18S rRNA genes were amplified using DNA from a single cyst as the templates. Approximately 1,367-1,440 bp sequences were obtained. The sequence difference in isolates of Sarcocystis hominis-like cysts from water buffaloes, and isolates of S. hominis cysts from cattle were very low, only about 0.1%, much lower than the lowest value (1.7%) among different species. Combined with their morphological structure, these sequence data indicate that the 4 isolates from cattle and water buffalo might be the same species, i.e., S. hominis, suggesting that both cattle and water buffalo may serve as the intermediate hosts for this parasite. Apparently, this is the first report using a single cyst to do such work and is a useful way to distinguish the Sarcocystis cyst in an intermediate host that may be simultaneously infected by several different Sarcocystis species.

Animals↗

PubMed2000

Left ventricular hypertrophy in ascending aortic stenosis mice: anoikis and the progression to early failure.

BACKGROUND: To determine potential mechanisms of the transition from hypertrophy to very early failure, we examined apoptosis in a model of ascending aortic stenosis (AS) in male FVB/n mice. METHODS AND RESULTS: Compared with age-matched controls, 4-week and 7-week AS animals (n=12 to 16 per group) had increased ratios of left ventricular weight to body weight (4.7+/-0.7 versus 3.1+/-0.2 and 5. 7+/-0.4 versus 2.7+/-0.1 mg/g, respectively, P<0.05) with similar body weights. Myocyte width was also increased in 4-week and 7-week AS mice compared with controls (19.0+/-0.8 and 25.2+/-1.8 versus 14. 1+/-0.5 microm, respectively, P<0.01). By 7 weeks, AS myocytes displayed branching with distinct differences in intercalated disk size and staining for beta(1)-integrin on both cell surface and adjacent extracellular matrix. In vivo left ventricular systolic developed pressure per gram as well as endocardial fractional shortening were similar in 4-week AS and controls but depressed in 7-week AS mice. Myocyte apoptosis estimated by in situ nick end-labeling (TUNEL) was extremely rare in 4-week AS and control mice; however, a low prevalence of TUNEL-positive myocytes and DNA laddering were detected in 7-week AS mice. The specificity of TUNEL labeling was confirmed by in situ ligation of hairpin oligonucleotides. CONCLUSIONS: Our findings indicate that myocyte apoptosis develops during the transition from hypertrophy to early failure in mice with chronic biomechanical stress and support the hypothesis that the disruption of normal myocyte anchorage to adjacent extracellular matrix and cells, a process called anoikis, may signal apoptosis.

Animals↗

PubMed2000

Molecular basis of albinism in the rhesus monkey.

Sequence analysis of the tyrosinase (TYR) coding region from one albino rhesus monkey (Macaca mulatta) family revealed that the two monkeys with phenotype similar to human TYR-negative oculocutaneous albinism (OCA) were homozygous for a missense mutation (S184TER) in exon 1 at codon 184. The offspring of one of the albino monkey ("Kangkang") are all heterozygous for the S184TER mutation, but the S184TER mutation was not observed in 93 control individuals. We conclude that the point mutation is responsible and sufficient to generate the albino rhesus monkey phenotype. The rough age of the S184TER nonsense mutation may be about 0.8 million years using a rate of 0.16% per million years.

Albinism, Oculocutaneous↗

PubMed2000

Cell-to-cell movement of the 25K protein of potato virus X is regulated by three other viral proteins.

The 25K, 12K, and 8K proteins and coat protein (CP) of Potato virus X (PVX) are required for virus cell-to-cell movement. In this study, experiments were conducted to determine whether the PVX 25K protein moves cell to cell and to explore potential interactions between the PVX 25K, 12K, and 8K proteins and CP. The PVX 25K gene was fused to the green fluorescent protein (GFP) gene and inserted into plasmids adjacent to the cauliflower mosaic virus 35S promoter. These plasmids were introduced by biolistic bombardment to transgenic tobacco expressing the PVX 12K, 8K, and CP genes. The GFP:25K fused proteins moved cell to cell on nontransgenic tobacco and tobacco expressing either the 12K or 8K proteins. However, the GFP:25K proteins did not move on transgenic tobacco expressing the combined 12K/8K genes or the CP gene. Thus, movement of the PVX 25K protein through plasmodesmata may be regulated by interactions with other PVX proteins.

Biological Transport↗

PubMed2000

Effect of PKC-zeta mediating Ang II-stimulated activation of CCDPK on rat cardiac fibroblast proliferation.

AIM: To investigate whether the effect of angiotensin (Ang) II or epidermal growth factor (EGF) on cardiac fibroblast proliferation involved in activation of extracellular signal-regulated kinase (ERK) 1/2 or Ca(2+)-calmodulin dependent protein kinase(CCDPK) mediated by protein kinase C (PKC)-zeta. METHODS: Relative activity of CCDPK was measured by Western blotting. DNA synthesis was assayed by [3H]thymidine incorporation. RESULTS: PDBU caused no decrease in Ang II- and 10% FCS-stimulated CCDPK activity and DNA synthesis. In contrary, 65% or 75% EGF- or tetradecanoylphorbol acetate (TDPA, formally called PMA)--stimulated CCDPK activity and 38% or 42% [3H]thymidine incorporation treated by PDBU were inhibited, respectively. Meanwhile 70% and 72% CCDPK activities induced by Ang II and EGF were inhibited by PD 98059, respectively. CONCLUSION: PKC-zeta mediated Ang II-induced activation of CCDPK and cardiac fibroblast proliferation.

Angiotensin II↗

PubMed2000

Antisense Ca(2+)-calmodulin dependent protein kinase oligonucleotide inhibits bFGF-induced proliferation of rat vascular smooth muscle cells.

AIM: To investigate the role of Ca(2+)-calmodulin dependent protein kinase (CCDPK) on basic fibroblast growth factor (bFGF)-induced vascular smooth muscle cell (VSMC) proliferation and the inhibitory effect of antisense CCDPK oligonucleotides (ODN). METHODS: Before being exposed to bFGF, cultured rat VSMC CCDPK activity was inhibited by pretreatment with either a phosphorothioate-protected 17-mer antisense CCDPK ODN-directed against the initiation of translation sites of the p42 and p44 CCDPK isoform or with CCDPK kinase inhibitor PD98059. All ODN were introduced into cells by liposomal transfection. DNA synthesis was measured by [3H]thymidine incorporation. P44- and p42-CCDPK protein expression and phosphorylation were measured by Western blot. RESULTS: PD98059 inhibited bFGF-induced phosphorylation of CCDPK and DNA synthesis. Antisense CCDPK ODN 0.2-0.8 mumol.L-1 reduced both p44- and p42-CCDPK expression and phosphorylation of CCDPK in a concentration-dependent manner and DNA synthesis induced by bFGF. Lipofectin alone or sense and random CCDPK ODN did not affect p44- and p42-CCDPK protein expression or bFGF-induced phosphorylation of CCDPK or DNA synthesis. CONCLUSION: bFGF-stimulated rat VSMC proliferation is mediated by CCDPK. The antisense CCDPK ODN can inhibit bFGF-induced VSMC proliferation through down-regulating p44- and p42-CCDPK level.

Animals↗

PubMed2000

Prevention of intima hyperplasia by mitogen-activated protein kinase antisense oligodeoxynucleotide.

AIM: To investigate the preventive effect of Ca(2+)-calmodulin dependent kinase (CCDPK) (formerly: mitogen-activated protein kinase or MAPK) antisense phosphorothioate oligodeoxynucleotide (ODN) on vascular smooth muscle cell (VSMC) proliferation in vitro and on intima hyperplasia after injury in vivo. METHODS: Liposomal transfection was used to introduce phosphorothioate-protected 17-mer antisense CCDPK ODN directed against the initiation of translation sites of the p42 and p44 CCDPK isoforms into cultured rat VSMC to deplete CCDPK and DNA synthesis induced by endothelin-1 (ET) or platelet derived growth factor (PDGF). A 17-mer sense and a random sequence CCDPK ODN were used as controls. CCDPK protein p44 and p42 levels were measured by Western blot. DNA synthesis was measured by [3H]thymidine incorporation. In in vivo study, rat balloon angioplasty was performed by a 2F Fogarty catheter. The antisense CCDPK ODN 200 micrograms was administered to the adventitial surface of the injured carotid artery by pluronic gel 30% (w/v) solution. Two weeks after vascular injury, carotid arteries were removed and cross sections were made and stained with hematoxylin/eosin for patho-histological examination. Fluorecein isothiocynate (FITC)-labeled and phosphorothioate-protected ODN was used to detect the uptake of ODN in vitro and in vivo. RESULTS: CCDPK antisense ODN (0.4 mumol.L-1) reduced p42/p44 protein expression and inhibited VSMC [3H]thymidine incorporation stimulated by ET and PDGF. Antisense CCDPK ODN treatment at 2 wk after injury resulted in a significant inhibition of intima hyperplasia, compared with untreated vessels. CONCLUSION: The p42/p44-CCDPK antisense ODN inhibits in vitro stimulated rat VSMC proliferation and in vivo injured arterial intima hyperplasia.

Animals↗

PubMed2000

[Comparison of susceptibility testing results of M. tuberculosis by different methods].

OBJECTIVE: To compare the susceptibility testing results of M. tuberculosis detected with different standards and methods. METHOD: 158 strains of M. tuberculosis isolated from clinical patients were detected for the drug sensitivity by Chinese standard and method (absolute concentration method), 1% resistance ratio and absolute concentration method of WHO/IUATLD standard. RESULTS: The drug-resistant rate detected by the standard of WHO/IUATLD was 53.8%(85/158), while by the Chinese standard 50.0%(79/158). The drug-resistant rates to INH, SM, EMB and RFP by WHO/IUATLD standard were 41.8%(66/158), 34.2%(54/158), 22.1%(35/158) and 27.8%(44/158) respectively, whereas by the Chinese standard 34.2%(54/158), 30.4% (48/158), 18.4%(29/158) and 27.2%(43/158) respectively. There was no significant difference between the results detected with WHO/IUATLD and Chinese standard, except for the results of INH. There was no significant difference between the results detected with WHO/IUATLD standard by 1% resistant ratio and absolute concentration methods. CONCLUSION: The results of drug-sensitivity were interfered by the detected standards but not by the tested methods.

Antitubercular Agents↗

PubMed2000

[A cross-sectional study on the effects of microcystin in drinking water to the health of human beings].

OBJECTIVE: To understand the effects of microcystin (MC) in drinking water on health of human beings. METHODS: In Taixing, a cross-sectional study was conducted in two middle schools with different types of drinking water, from which 111 and 92 students were randomly selected and investigated. Blood samples from all individuals were collected and tested for serum HBsAg, HBeAg, anti-HBe, anti-HBs, anti-HBc with enzyme linked immunoabsorbent assay and for serum alanine aminotransferase (ALT), gamma-glutamyltransferase (gamma-GT) and alkaline phosphatase (ALP) contents by colorimetry. These levels of enzymes in sera were compared after the students were stratified according to the status of HBV infection. RESULT: With the exclusion of the effect of HBV infection, three enzymes levels in sera between two groups of students showed significant differences (P < 0.01), much higher in exposure group than those in control group. CONCLUSION: MC was possibly harmful to human beings in drinking water and induced the contents of some enzymes from the liver of human beings to increase in sera.

Adolescent↗

PubMed1999

Pressure overload induces severe hypertrophy in mice treated with cyclosporine, an inhibitor of calcineurin.

Cardiac hypertrophy is the fundamental adaptation of the adult heart to mechanical load. Recent work has shown that inhibition of calcineurin activity with cyclosporine suppresses the development of hypertrophy in calcineurin transgenic mice and in in vitro systems of neonatal rat cardiocytes stimulated with peptide growth factors. To test the hypothesis that the calcineurin signaling pathway is critical for load-induced hypertrophy in vivo, we examined the effects of cyclosporine treatment on left ventricular hypertrophy induced by experimental ascending aortic stenosis for 4 weeks in mice. Left ventricular systolic pressure was elevated to a similar level in aortic stenosis mice that were treated with cyclosporine versus no drug. Left ventricular mass and myocyte size were similar in treated and untreated aortic stenosis animals and significantly greater than control animals, showing that cyclosporine treatment does not suppress hypertrophic growth. Both treated and untreated animals showed increased left ventricular expression of the load-sensitive gene atrial natriuretic factor. Calcineurin activity was measured in the left ventricle and the spleen from control mice and aortic stenosis mice treated with cyclosporine versus no drug. Levels of calcineurin activity were similar in the spleens of control and untreated aortic stenosis mice. However, calcineurin activity was severely depressed in left ventricular tissue of untreated aortic stenosis mice compared with control mice and was further reduced by cyclosporine treatment. Thus, pathological hypertrophy and cardiac-restricted gene expression induced by pressure overload in vivo are not suppressed by treatment with cyclosporine and do not appear to depend on the elevation of left ventricular calcineurin activity.

Animals↗

PubMed1999

Genetic diversity of Chinese native pigs inferred from protein electrophoresis.

We examined protein polymorphism of 20 native pig breeds in China and 3 introduced pig breeds. Thirty loci have been investigated, among which six loci were found to be polymorphic. Especially, the polymorphism of malate dehydrogenase (MDH), adenylate kinase (AK), and two new alleles of adenosine deaminase (ADA) had not been reported in domestic pigs and wild pigs. The percentage of polymorphic loci (P), the mean heterozygosity (H), and the mean number of alleles (A) are 0.200, 0.065, and 1.300, respectively. The degree of genetic variability of Chinese pigs as a whole was higher than that of goats, lower than that of cattle and horses, and similar to that of sheep. Using the gene frequencies of the 30 loci, Nei's genetic distance among the 20 native breeds in China and 3 introduced pig breeds was calculated by the formula of Nei. The program NEIGHBOR in PHYLIP 3.5c was chosen to construct an UPGMA tree and a NJ tree. Our results show that, of the total genetic variation found in the native pig breeds in China, 31% (0.31) is ascribable to genetic differences among breeds. About 69% of the total genetic variation is found within breeds. Most breeds are in linkage disequilibrium. The patterns of genetic similarities between the Chinese native pig breeds were not in agreement with the proposed pig type classification.

Adenosine Deaminase↗