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Biomedical subjects

H Zhang

Publications and source records attributed to H Zhang.

At least 631 records · Page 35Linked to original sources
PubMed2000

Effect of intraarticular stainless steel implants on the health of the rabbit knee joint: an experimental study.

OBJECTIVE: This study was designed to investigate the histologic changes to the knee joints of rabbits after insertion of a metal implant in retrograde fashion. DESIGN: Eighteen rabbits had a modified stainless steel screw implanted in one knee, with the other knee serving as a sham-operated control. The animals were killed after two, six, or twelve months. OUTCOME MEASURES: The histologic status of the cartilage and synovium were graded by the Modified Mankin and Mirra criteria, respectively. RESULTS: At the time of killing, every insertion site was covered by fibrous tissue. Statistical analysis showed no significant differences in histologic scores between implanted and control knees. CONCLUSIONS: Insertion of a stable, well-fixed implant results in no deleterious effect to the knee joint.

Animals↗
PubMed2000

Burkholderia kururiensis sp. nov., a trichloroethylene (TCE)-degrading bacterium isolated from an aquifer polluted with TCE.

A trichloroethylene (TCE)-degrading bacterium was isolated from an aquifer sample collected at a TCE-polluted site in Japan by enriching with phenol as sole carbon source. The isolate, designated strain KP23T, was a Gram-negative, oval-shaped micro-organism. A phylogenetic study based on 16S rRNA gene sequences indicated that strain KP23T should be placed in the genus Burkholderia. Cellular fatty acids of the strain were mainly composed of C16:0, cyclopropanic acid C17:0 and cyclopropanic acid C19:0. Strain KP23T also contained notable amounts of C13:1 and C17:1. The G + C content of total DNA was 64.8 mol%. Strain KP23T oxidized various sugars and sugar alcohols as sole carbon source such as galactose, glucose, mannose, maltose, glycerol, inositol and mannitol. Comparisons of its phenotypic and genotypic characteristics with other known species belonging to the genus Burkholderia suggested that strain KP23T represents a new species in the genus. The name Burkholderia kururiensis is proposed for this species, with strain KP23T as the type strain (= JCM 10599T).

Bacterial Typing Techniques↗
PubMed2000

The complete sequence of hepatitis E virus genotype 4 reveals an alternative strategy for translation of open reading frames 2 and 3.

Isolates of hepatitis E virus (HEV) have recently been described from China that are distinct from Burmese, Mexican and US viruses and constitute a novel genotype (genotype 4). Here, the complete genomic sequence of a representative isolate of genotype 4 HEV, amplified directly from the stool of an acutely infected patient, is presented. Analysis of the entire sequence confirms our previous conclusion, based upon partial sequence data, that these Chinese isolates belong to a novel genotype. Typical of genetic variation in HEV, most nucleotide substitutions occur in the third base of the codon and do not affect the amino acid sequence. The genotype 4 virus is unusual in that a single nucleotide insertion in the ORF 3 region changes the initiation of ORF 3, and perhaps also ORF 2. The consequences of these changes are discussed.

Adult↗
PubMed2000

Differentially painting human chromosome arms with combined binary ratio-labeling fluorescence in situ hybridization.

Recently we developed a novel strategy for differentially painting all 24 human chromosomes. It is termed COBRA-FISH, short for combined binary ratio labeling-fluorescence in situ hybridization. COBRA-FISH is distinct from the pure combinatorial approach in that only 4 instead of 5 fluorophores are needed to achieve color discrimination of 24 targets. Furthermore, multiplicity can be increased to 48 by introduction of a fifth fluorophore. Here we show that color identification by COBRA-FISH of all of the p and q arms of human chromosomes is feasible, and we apply the technique for detecting and elucidating intra- and interchromosomal rearrangements. Compared with 24-color whole chromosome painting FISH, PQ-COBRA-FISH considerably enhances the ability to determine the composition of rearranged chromosomes as demonstrated by the identification of pericentric inversions and isochromosomes as well as the elucidation of the arm identity of chromosomal material involved in complex translocations that occur in solid tumors.

Chromosome Painting↗
PubMed2000

Cooperativity and resonances in periodically driven spin-boson systems.

We present an analytical recursive formulation for the quantum transport in symmetric two-level systems under the influence of both dissipation and periodic driving. The rate-matching condition for quantum stochastic resonance despite its different appearance is found to be physically the same as that in the classical case. Analyzed are also the Rabi resonance and its implication to quantum stochastic resonance. We demonstrate that no matter how weak the driving field is, transport can involve about 70% population in the vicinities of the third-harmonic as well as the fundamental-harmonic Rabi resonance. Recovered is also an adiabatic passage condition in which the transport carries a nearly 100% population in the low frequency and strong driving limit.

Journal Article↗
PubMed2000

Rationale for Bcl-xL/Bad peptide complex formation from structure, mutagenesis, and biophysical studies.

The three-dimensional structure of the anti-apoptotic protein Bcl-xL complexed to a 25-residue peptide from the death promoting region of Bad was determined using NMR spectroscopy. Although the overall structure is similar to Bcl-xL bound to a 16-residue peptide from the Bak protein (Sattler et al., 1997), the Bad peptide forms additional interactions with Bcl-xL. However, based upon site-directed mutagenesis experiments, these additional contacts do not account for the increased affinity of the Bad 25-mer for Bcl-xL compared to the Bad 16-mer. Rather, the increased helix propensity of the Bad 25-mer is primarily responsible for its greater affinity for Bcl-xL. Based on this observation, a pair of 16-residue peptides were designed and synthesized that were predicted to have a high helix propensity while maintaining the interactions important for complexation with Bcl-xL. Both peptides showed an increase in helix propensity compared to the wild-type and exhibited an enhanced affinity for Bcl-xL.

Amino Acid Sequence↗
PubMed2000

A frailty model of segregation analysis: understanding the familial transmission of alcoholism.

Coupled with environmental factors, genes contribute to numerous human diseases and traits. While there are many epidemiological methods to assess the familial clustering of traits, few are flexible enough to accommodate interactions between covariates and familial factors. In this paper, we propose and develop a frailty model that establishes an integrated framework to evaluate familial transmission of a disease by controlling for covariate effects and conveniently testing the interactions between covariates and familial factors. We also present a peeling algorithm that dramatically reduces the computational burden. This frailty model is employed to examine the familial transmission of major subtypes of alcoholism, namely, alcohol abuse and dependence. We conclude that alcohol dependence is strongly familial whereas alcohol abuse expresses a marginally significant pattern of familial transmission. Moreover, females manifest alcoholism at a lower threshold, and there is no sex-specific familial transmission of alcoholism after adjustment for the threshold effect.

Alcoholism↗
PubMed2000

Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats.

BACKGROUND: Galectins are characterized by specific affinity for beta-galactoside sugars, and they play a role in diverse biological processes, including cell adhesion, cell proliferation, and apoptosis. Galectin-1, -3, and -9 have been implicated in modulating the immune response. METHODS: Nephrotoxic serum nephritis, which is characterized by crescent formation and glomerular influx of CD8+ cells into glomerular capillaries, was induced in Wistar Kyoto (WKY) rats by injecting rabbit antiglomerular basement membrane serum. Following induction, the rats were treated either with phosphate-buffered saline or dexamethasone, galectin-1, galectin-3, or galectin-9 on alternate days and were sacrificed at day 14. At day 8, splenic lymphocytes were isolated and employed for terminal deoxytransferase-mediated uridine triphosphate nick end-labeling (TUNEL) assay to assess the degree of apoptosis, and the kidneys were utilized to determine the extent of influx of CD4(+) and CD8(+) cells and glomerular damage. RESULTS: Dexamethasone induced a marked apoptosis of splenic CD4(+) and CD8(+) cells, and it inhibited the production of anti-rabbit IgG and the influx of CD8+ cells and macrophages into the renal glomeruli. Crescent formation and excretion of urinary proteins were also reduced. Galectin-9 failed to induce apoptosis in the CD4(+) cells; however, it induced apoptosis in the CD8(+) cells and inhibited the infiltration of CD8(+) cells. Although galectin-1 and -3 did not induce the apoptosis in the T cells, they inhibited the accumulation of macrophages in the renal glomeruli. Like dexamethasone, the galectins also reduced the crescentic formation, proliferation of glomerular cells, and excretion of urinary proteins. CONCLUSIONS: Galectin-9 selectively induces apoptosis of the activated CD8(+) cells, while the macrophage influx into the kidney is modulated by all three galectins. This finding raises an interesting possibility for the utility of galectins in the modulation of macrophages that are involved in immune-mediated glomerular diseases.

Adjuvants, Immunologic↗
PubMed2000

Suppression of sodium current by arachidonic acid in atrial myocytes from patients with coronary heart disease.

This study was designed to examine the effects of arachidonic acid (AA) on atrial myocytes from patients with coronary heart disease. The patch clamp technique was used to record sodium current in human atrial myocytes, before and after administration of intracellular AA. The suppression of sodium current induced by AA was voltage- and dose-dependent, with an IC50 of 10.3 microM. The activation curves of relative conductance in absence versus presence of AA, 10 microM, nearly overlapped. The 50% channel activation was at 40.8 +/- 2.7 mV in the control state versus 42.5 +/- 3.1 mV in presence of AA (n = 10, P > 0.05). AA at 10 microM shifted the steady-state inactivation relationship significantly, from 94.5 +/- 3.4 mV to 116.6 +/- 4.1 mV (n = 11, P < 0.01) at the 50% channel inactivation point. The 50% recovery time from the inactivation state was significantly longer in the presence of 10 microM AA (27.3 +/- 1.7 ms), than in the control state (5.9 +/- 0.4 ms n = 8, P < 0.01). In conclusion, AA suppressed the sodium current and prolonged the duration of recovery from inactivation in atrial myocytes from patients with coronary heart disease.

Aged↗
PubMed2000

Caspase-3 activation and apoptosis induction coupled with the retrograde transport of shiga toxin: inhibition by brefeldin A.

Caspase proteolytic activities, such as caspase-3, -2 and -6, of THP-1 human monocytic cells were markedly increased in a time- and dose-dependent manner by treatment with purified Shiga toxin 1 (Stx1) or Stx2. Caspase-3 activation was strictly correlated with internucleosomal DNA fragmentation and chromatin condensation of the cells. In addition, the specific caspase-3 inhibitor, Ac-DEVD-CHO, decreased the percentage of apoptotic cells. The purified B-subunit of Stx1 did not induce apoptosis in THP-1 cells. Caspase-3 activation, DNA fragmentation and chromatin condensation caused by Stx were completely blocked by pretreatment of cells with brefeldin A, an inhibitor of Golgi functions. The findings suggest that Stx1 as well as Stx2 activate caspase-3, which plays a critical role in apoptosis, and that the apoptotic signals rise after Stx is transported to the Golgi apparatus.

Apoptosis↗
PubMed2000

In-plane elastic property characterization in composite plates

This article presents a method to deduce the in-plane elastic properties of multilayered composite plates. Drawing on a synthetic-aperture technique developed for the elucidation of materials properties in air-coupled ultrasonics, this new method exploits the high elastic anisotropy of composite materials to permit an accurate measurement of directional in-plane stiffness. It is found that comparisons of experimental measurements with plate stiffnesses calculated on the basis of lamination theory agree to within several percent for uniaxial and biaxial laminates and to within 10 percent for quasi-isotropic laminates. It is further shown that the method is largely insensitive to transducer deployment angle within a range related to the transducer beamwidth.

Journal Article↗
PubMed2000

In vitro antimicrobial properties of recombinant ASABF, an antimicrobial peptide isolated from the nematode Ascaris suum.

ASABF is a CSalphabeta-type antimicrobial peptide that contains four intramolecular disulfide bridges (Y. Kato and S. Komatsu, J. Biol. Chem. 271:30493-30498, 1996). In the present study, a recombinant ASABF was produced by using a yeast expression system, and its antimicrobial activity was characterized in detail. The recombinant ASABF was active against all gram-positive bacteria tested (7 of 7; minimum bactericidal concentration [MBC], 0.03 to 1 microg/ml) except Leuconostoc mesenteroides, some gram-negative bacteria (8 of 14; MBC, >0.5 microg/ml), and some yeasts (3 of 9; MBC >3 microg/ml). Slight hemolytic activity (4.2% at 100 microg/ml) against human erythrocytes was observed only under low-ionic-strength conditions. Less than 1 min of contact was enough to kill Staphylococcus aureus ATCC 6538P. The bactericidal activity against S. aureus was inhibited by salts.

Amino Acid Sequence↗
PubMed2000

Tumor necrosis factor receptor p55-deficient mice respond to acute Yersinia enterocolitica infection with less apoptosis and more effective host resistance.

Tumor necrosis factor (TNF) has generally been regarded as a protective cytokine in host defense against bacterial infections. In the present study, we evaluated the role of TNF in the acute phase of infection by Yersinia enterocolitica by using mice rendered genetically deficient in TNF receptor p55 (TNFRp55(-/-)). Unexpectedly, TNFRp55(-/-) mice showed more effective resistance to the bacteria, reflected in enhanced bacterial clearance and less tissue damage, than did control C57BL/6 mice. C57BL/6 mice showed evidence of extensive apoptosis in the spleen accompanied by a selective decrease in the CD4(+)-T-cell population of splenocytes, whereas TNFRp55(-/-) mice were spared these changes. The splenocytes from TNFRp55(-/-) mice also maintained a robust gamma interferon IFN-gamma response to mitogenic stimulation, while the comparable response in C57BL/6 mice was impaired. In addition, splenocytes harvested from infected mice demonstrated lower production of interleukin-10 IL-10 in TNFRp55(-/-) mice than in C57BL/6 mice. These findings suggest that Yersinia can induce TNFRp55-mediated apoptosis of splenocytes in the acute phase of the infection and that alteration of T-cell-generated cytokines can dramatically alter the early events in host defense against this pathogen.

Acute Disease↗
PubMed2000

Identification of the ubiD gene on the Escherichia coli chromosome.

The open reading frame at 86.7 min on the Escherichia coli chromosome, "yigC," complemented a ubiD mutant strain, AN66, indicating that yigC is the ubiD gene. The gene product, a 497-amino-acid-residue protein, showed extensive homology to the UPF 00096 family of proteins in the Swiss-Prot database.

Amino Acid Sequence↗
PubMed2000

Characterization of enterovirus isolates from patients with heart muscle disease in a selenium-deficient area of China.

An association of enterovirus infection with endemic cardiomyopathy (Keshan disease [KD]) and outbreaks of myocarditis in selenium-deficient rural areas of southwestern China has been established. Enteroviruses have been isolated from patients with KD or during outbreaks of myocarditis in last two decades. Six of these isolates grew readily in cell lines (Vero or HEp-2) and were investigated by a novel molecular typing method apart from serotyping and pathogenicity. A neutralization assay identified two isolates from KD as coxsackievirus serotype B2 (CVB2) and two isolates from myocarditis as coxsackievirus serotype B6 (CVB6) but failed to type the remaining two isolates, also from myocarditis. Direct nucleotide sequencing of reverse transcription-PCR products amplified from the 5' nontranslated region (5'NTR) of these viruses confirmed that they belong to a phylogenetic cluster consisting of coxsackie B-like viruses, including some echovirus serotypes. Sequence analysis of the coding region for viral capsid protein VP1 showed that two isolates serotyped as CVB2 have the highest amino acid sequence homology with CVB2 and that the remaining four isolates, two CVB6 and the two unknown serotypes, are most closely related to the sequence of CVB6. Sequences among these isolates varied from 82.3 to 99% in the 5'NTR and from 69 to 99% in VP1, indicating no cross contamination. The pathogenicity of these viruses in adult and suckling mice was assessed. None caused pathologic changes in the hearts of adult MF-1 or SWR mice, although pancreatitis was evident. However, the four CVB6-like viruses caused death in suckling mice, similar to a virulent coxsackievirus group B3 laboratory strain. In conclusion, the sequence data confirm that coxsackievirus group B serotypes are predominant in the region in which KD is endemic and may be the etiological agents in outbreaks of myocarditis. VP1 genotyping of enteroviruses is accurate and reliable. Animal experiments indicate that isolates may differ in pathogenicity.

Adolescent↗
PubMed2000

Human immunodeficiency virus type 1 Vif protein is an integral component of an mRNP complex of viral RNA and could be involved in the viral RNA folding and packaging process.

Virion infectivity factor (Vif) is a protein encoded by human immunodeficiency virus types 1 and 2 (HIV-1 and -2) and simian immunodeficiency virus, plus other lentiviruses, and is essential for viral replication either in vivo or in culture for nonpermissive cells such as peripheral blood lymphoid cells, macrophages, and H9 T cells. Defects in the vif gene affect virion morphology and reverse transcription but not the expression of viral components. It has been shown that Vif colocalizes with Gag in cells and Vif binds to the NCp7 domain of Gag in vitro. However, it seems that Vif is not specifically packaged into virions. The molecular mechanism(s) for Vif remains unknown. In this report, we demonstrate that HIV-1 Vif is an RNA-binding protein and specifically binds to HIV-1 genomic RNA in vitro. Further, Vif binds to HIV-1 RNA in the cytoplasm of virus-producing cells to form a 40S mRNP complex. Coimmunoprecipitation and in vivo UV cross-linking assays indicated that Vif directly interact with HIV-1 RNA in the virus-producing cells. Vif-RNA binding could be displaced by Gag-RNA binding, suggesting that Vif protein in the mRNP complex may mediate viral RNA interaction with HIV-1 Gag precursors. Furthermore, we have demonstrated that these Vif mutants that lose the RNA binding activity in vitro do not support vif-deficient HIV-1 replication in H9 T cells, suggesting that the RNA binding capacity of Vif is important for its function. Further studies regarding Vif-RNA interaction in virus-producing cells will be important for studying the function of Vif in the HIV-1 life cycle.

Amino Acid Sequence↗
PubMed2000

Partial rescue of the Vif-negative phenotype of mutant human immunodeficiency virus type 1 strains from nonpermissive cells by intravirion reverse transcription.

Virion infectivity factor (Vif) is a protein encoded by human immunodeficiency virus type I (HIV-1) and is essential for viral replication. It appears that Vif functions in the virus-producing cells and affects viral assembly. Viruses with defects in the vif gene (vif-) generated from the "nonpermissive cells" are not able to complete reverse transcription. In previous studies, it was demonstrated that defects in the vif gene also affect endogenous reverse transcription (ERT) when mild detergents were utilized to permeabilize the viral envelope. In this report, we demonstrate that defects in the vif gene have much less of an effect on ERT if detergent is not used. When ERT was driven by addition of deoxyribonucleoside triphosphates (dNTPs) at high concentrations, certain levels of plus-strand viral DNA could also be achieved. Interestingly, if vif- viruses, generated from nonpermissive cells and harboring large quantities of viral DNA generated by ERT, were allowed to infect permissive cells, they could partially bypass the block at intracellular reverse transcription, through which vif- viruses without dNTP treatment could not pass. Consequently, viral infectivity can be partially rescued from the vif- phenotype. Based on our observations, we suggest that vif defects may cause the reverse transcription complex (RT complex) to become sensitive to mild detergent treatments within HIV-1 virions and become unstable in the target cells, such that the process of reverse transcription cannot be efficiently supported. Further dissection of RT complexes of vif- viruses may be key to uncovering the molecular mechanism(s) of Vif in HIV-1 pathogenesis.

DNA, Viral↗