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Biomedical subjects

X Wang

Publications and source records attributed to X Wang.

At least 217 records · Page 12Linked to original sources
PubMed2003

Characterization of two novel KRAB-domain-containing zinc finger genes, ZNF460 and ZNF461, on human chromosome 19q13.1-->q13.4.

This study reports the cloning and characterization of two novel human zinc finger protein cDNAs (ZNF460 and ZNF461) from a fetal brain cDNA library. The ZNF460 cDNA is 3,135 bp in length encoding a 562-amino-acid polypeptide and the ZNF461 cDNA is 2,548 bp encoding a 563-amino-acid protein. Both of the proteins contain a KRAB A+B box and eleven C2H2 type zinc finger motifs. ZNF461 shows high similarity with the rat GIOT-1 gene (GIOT1). The ZNF460 gene mapped to 19q13.4 with 3 exons, and ZNF461 mapped to 19q13.1 with 6 exons. Both of the two genes are ubiquitously expressed in normal human tissues and the abundance of the ZNF460 mRNA is relatively low.

Amino Acid Sequence↗
PubMed2003

Involvement of SAPK/JNK in basic fibroblast growth factor-induced vascular endothelial growth factor release in osteoblasts.

We previously reported that basic fibroblast growth factor (FGF-2) activates p44/p42 mitogen-activated protein (MAP) kinase resulting in the stimulation of vascular endothelial growth factor (VEGF) release in osteoblast-like MC3T3-E1 cells and that FGF-2-activated p38 MAP kinase negatively regulates VEGF release. In the present study, we investigated the involvement of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) in FGF-2-induced VEGF release in these cells. FGF-2 markedly induced the phosphorylation of SAPK/JNK. SP600125, an inhibitor of SAPK/JNK, markedly reduced the FGF-2-induced VEGF release. SP600125 suppressed the FGF-2-induced phosphorylation of SAPK/JNK without affecting the phosphorylation of p44/p42 MAP kinase or p38 MAP kinase induced by FGF-2. PD98059, an inhibitor of upstream kinase of p44/p42 MAP kinase, or SB203580, an inhibitor of p38 MAP kinase, failed to affect the FGF-2-induced phosphorylation of SAPK/JNK. A combination of SP600125 and SB203580 suppressed the FGF-2-stimulated VEGF release in an additive manner. These results strongly suggest that FGF-2 activates SAPK/JNK in osteoblasts, and that SAPK/JNK plays a part in FGF-2-induced VEGF release.

Animals↗
PubMed2003

Caveolin-1 redistribution in human endothelial cells induced by laminar flow and cytokine.

Caveolin-1 is a principal component of caveolae and is involved in signaling transduction in a number of cells. A hypothesis was proposed in this work that mechanical forces due to flow induce caveolin-1 translocation. So the changes of caveolin-1 expression and distribution in cultured endothelial cells (HUVECs) exposed to a steady laminar flow were studied. For comparing with the influence of cytokine, caveolin-1 in the cells stimulated by TNF-alpha was also investigated. Indirect immunofluorescence and double fluorescence labeling showed that in control cells, caveolin-1 was primarily localized on the cell surface, which corresponded to the peripheral distribution of F-actin, and presented some local concentrations. In the cells exposed to a laminar flow (1.0 Pa), caveolin-1 distribution showed a time-dependent variation. After 24 h of shear, the local concentration of caveolin-1 was found, in the most cells, at upstream side of cell body. Also more caveolin-1 molecules were observed in the cells. In contrast, TNF-alpha induced a decrease of caveolin-1 in cells. The redistribution of caveolin-1 seems to be correlated to F-actin organization.

Actins↗
PubMed2003

The pathogenesis of Schmorl's nodes.

We examined the pathogenesis of Schmorl's nodes, correlating the histological findings from 12 lumbar vertebrae with the corresponding conventional radiographs, tomographs, MR images and CT scans. The last revealed round, often multiple cystic lesions with indistinct sclerotic margins beneath the cartilaginous endplate. The appearances are similar to the typical CT changes of osteonecrosis. Histological examination of en-bloc slices through Schmorl's nodes gave clear evidence of subchondral osteonecrosis. Beneath the cartilage endplate, we found fibrosis within the marrow cavities with the disappearance of fat cells. Osteocytes within bone trabeculae were either dead or had disappeared. We suggest that Schmorl's nodes are the end result of ischaemic necrosis beneath the cartilaginous endplate and that herniation into the body of the vertebra is secondary.

Adolescent↗
PubMed2003

Complete nucleotide sequence of a potyvirus causing maize dwarf mosaic disease in central China.

The full-length nucleotide sequence of a potyvirus causing the maize dwarf mosaic (MDM) disease in Henan province, central China, was obtained by reverse transcription-polymerase chain reaction (RT-PCR) and rapid amplification of the cDNA 5'-end (5'-RACE). The viral genome comprised of 9596 nucleotides except the polyA tail and encoded a putative polyprotein of 3603 amino acids. The entire genomic sequence of this isolate shared identities of 94.2% and 98.3% with Sugarcane mosaic virus (SCMV) HZ isolate at the nucleotide and deduced amino acid levels, respectively, but only a 69.1% identity with MDM virus (MDMV) Bulgarian isolate (MDMV-Bg) at the nucleotide level. Phylogenetical tree analysis of the complete nucleotide sequences indicated that the Henan isolate of a potyvirus causing MDM disease is in fact a Henan strain of SCMV (SCMV-HN).

Base Sequence↗
PubMed2002

TNF-related apoptosis-inducing ligand death pathway-mediated human beta-cell destruction.

AIMS/HYPOTHESIS: The aim of this study is to investigate whether apoptosis in human beta cells can be related to the induction of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) pathway. METHODS: We examined the expression of TRAIL and TRAIL receptors in two human pancreatic beta-cell lines and in human primary islet cells using RT-PCR assays and flow cytometric analyses and tested TRAIL-mediated beta-cell destruction in (51)Cr release cytotoxicity assays, Annexin-V and APO-DIREC assays. RESULTS: Most of the human beta cells express TRAIL receptors-R1, -R2, -R3, -R4 and/or TRAIL. TRAIL induced much stronger cytotoxicity and apoptosis to beta-cell lines CM and HP62 than did FasL, TNF-alpha, LTalpha1beta2, LTalpha2beta1, LIGHT, and IFN-gamma. The cytotoxicity and apoptosis induced by TRAIL to beta-cell lines CM were inhibited competitively by soluble TRAIL receptors, R1, R2, R3 or R4. Treatment of these beta cells with antibodies against TRAIL receptors was able to block the cytotoxicity of TRAIL to these cells. Beta-cell antigen-specific CTL (CD4(+) and CD8(+)) clones express TRAIL, suggesting that these cells are potential sources of TRAIL-inducing beta-cell destruction. Normal primary islet cells from most donors are resistant to the cytotoxicity mediated by TRAIL. However, treatment with an inhibitor of protein synthesis (cycloheximide) or with an enzyme (PI-PLC) that can remove TRAIL-R3 from the islet-cell membrane was able to increase the susceptibility of TRAIL-resistant primary islet cells to the TRAIL death pathway. CONCLUSION/INTERPRETATION: The TRAIL death pathway is present and can function in human islet beta cells, but unidentified inhibitors of the TRAIL death pathway are present in normal islet cells.

Apoptosis↗
PubMed2002

Columnar organization of mechanoreceptive neurons in the cortical taste area in the rat.

Mechanoreceptive neurons with or without taste responsiveness were recorded in the cortical taste area (CTA) of rats every 50 or 100 micro m along an electrode track made as perpendicular to the surface as possible. Three groups of mechanoreceptive neurons were recognized based on the adequate stimulus, i.e., low-threshold mechanoreceptive ( n=16), nociceptive-specific ( n=48), and wide-dynamic range neurons ( n=392). Except for nine neurons, almost all had receptive fields (RFs) in the oral cavity ( n=447). They were categorized into three RF types: those with RFs only in the oral cavity (OC type; n=23), those with RFs both in the oral cavity and on the lip (OL type; n=44) and those with RFs in the oral cavity and on the external surface of the body (WB type; n=380), e.g., tail. Neurons with inhibitory RFs were often located in the infragranular layers. Several neurons with the same receptive features were sequentially recorded along the track, suggesting the presence of columnar organization. The diameter of the possible functional column was the largest (mean 113.85 micro m) for WB type neurons, but smaller in the other two types (mean 85 micro m for the OC type and 62.5 micro m for the OL type). Neurons were segregated according to the adequate stimulus within the column for WB type neurons. Taste-responsive mechanoreceptive neurons ( n=33) were recorded at 15 tracks, and two taste neurons were sequentially recorded in five cases, in three of which two successive neurons sharing the best stimulus were recorded. Taste neurons are possibly arranged in a column with a very small diameter within the large column of mechanoreceptive neurons.

Animals↗
PubMed2002

Phonon spectrum in a plasma crystal.

The Fourier spectra of longitudinal and transverse waves corresponding to random particle motion were measured in a two-dimensional plasma crystal. The crystal was composed of negatively charged microspheres immersed in a plasma at a low gas pressure. The phonons were found to obey a dispersion relation that assumes a Yukawa interparticle potential. The crystal was in a nonthermal equilibrium, nevertheless phonon energies were almost equally distributed with respect to wave number over the entire first Brillouin zone.

Journal Article↗
PubMed2002

Dispersion relations of longitudinal and transverse waves in two-dimensional screened Coulomb crystals.

Dispersion relations of longitudinal and transverse waves in two-dimensional (2D) screened-Coulomb crystals were investigated. The waves were excited in 2D crystals made from complex plasmas, i.e., dusty plasmas, by applying radiation pressure of laser light. The dependencies of the dispersion relation on the shielding parameter, the damping rate, and the wave propagation direction were experimentally measured. The measured dispersion relations agree reasonably with a recently developed theory, and the comparison yields the shielding parameter and the charge on particles.

Journal Article↗
PubMed2002

Effects of collagen unwinding and cleavage on the mechanical integrity of the collagen network in bone.

The objective of this study was to investigate how molecular level changes in the collagen network affect its mechanical integrity. Our hypothesis is that the cleavage and unwinding of triple helices of collagen molecules significantly reduce the mechanical integrity of the collagen network in bone, whereas collagen crosslinks play a major role in sustaining the structural integrity of the collagen network. To test this hypothesis, the collagen molecular structure was altered in demineralized human cadaveric bone samples in the following two ways: heat induced unwinding and pancreas elastase induced cleavage of collagen molecules. Along with control specimens, the treated specimens were mechanically tested in tension to determine their strength, elastic modulus, toughness, and strain to failure. Also, the percentage of denatured collagen molecules and amounts of two major collagen crosslinks (hydroxylysylpyridinoline and lysylpyridinoline) were determined using high-performance liquid chromatography techniques. It was found that unwinding of collagen molecules may cause more reduction in stiffness (E) but less strain to failure (ef) than cleavage. Both collagen denaturation types cause similar changes in the strength (ss) and work to fracture (Wf) of the collagen network with no significant changes in hydroxylysylpyridinoline and lysylpyridinoline crosslinks. The results of this study indicate that the integrity of collagen molecules significantly affect the mechanical properties of the collagen network in bone, and that collagen crosslinks may play an important role in maintaining the mechanical integrity of the collagen network after collagen denaturation occurs.

Adult↗
PubMed2002

Alternating dose-dense chemotherapy in patients with high volume disseminated non-seminomatous germ cell tumours.

Only about half of patients with a poor-prognosis non-seminomatous germ-cell tumours can achieve a cure. The aim of this phase II study was to assess the efficacy and toxicity of a dose-dense alternating chemotherapy regimen in this subset of patients. High volume non-seminomatous germ-cell tumours was defined as follows: at least two sites of non pulmonary metastases, an extragonadal primary tumour, a serum human chorionic gonadotropin level higher than 10 000 mIU x ml(-1), or a alpha-foetoprotein level higher than 2000 mIU ml(-1). Patients who fulfilled these criteria were treated with the so-called BOP-CISCA-POMB-ACE regimen (bleomycin, vincristine, and cisplatin; cisplatin, cyclophosphamide, and doxorubicin; cisplatin, vincristine, methotrexate, and bleomycin; etoposide, dactinomycin, and cyclophosphamide) plus granulocyte colony-stimulating factor. A total of 58 patients were enrolled. Patients were retrospectively classified according to the International Germ-Cell Cancer Consensus Group classification; 38 patients (66%) had poor-prognosis disease and 19 patients (33%) had intermediate-prognosis. Patients received a median of 2.5 courses (range 0.25 to five courses) of the BOP-CISCA-POMB-ACE regimen. Forty-two patients (72.4%) had a complete response to therapy. With a median follow-up time of 31 months, the 3-year progression-free survival rate was 71% (95% confidence interval, 60 to 84%) and the 3-year overall survival rate was 73% (95% confidence interval: 62 to 86%). The 3-year PFS rates were 83% (95% confidence interval: 68 to 100%) in the intermediate-prognosis group and 65% (95% confidence interval: 51 to 82%) in the poor-prognosis group. Early side effects included mainly grade 4 haematologic toxicity (neutropaenia in 79% of patients, thrombocytopaenia in 69%, anaemia in 22%), grade 4 stomatitis (19%), and four early deaths (7% of patients), at least partially related to toxicity. The dose-dense BOP-CISCA-POMB-ACE regimen is highly active in patients with non-seminomatous germ-cell tumours classified as intermediate-prognosis or poor-prognosis according to the International Germ-Cell Cancer Consensus Group. Because outcomes with this regimen compare favourably with outcome after standard therapy, dose-dense chemotherapy should be further investigated in this subset of patients.

Adolescent↗
PubMed2002

Down-regulation of Id-1 expression is associated with TGF beta 1-induced growth arrest in prostate epithelial cells.

Transforming growth factor beta1 (TGF beta 1) plays important roles in the regulation of cell growth and differentiation in both normal and malignant prostate epithelial cells. Although certain pathways have been suggested, the mechanisms responsible for the action of TGF beta 1 are not well understood. In the present study, using a human papilloma virus 16 E6/E7 immortalized prostate epithelial cell line, HPr-1, we report that TGF beta 1 was able to suppress the expression of Id-1, a helix-loop-helix (HLH) protein, which plays important roles in the inhibition of cell differentiation and growth arrest. In addition, a decrease at both Id-1 mRNA and protein expression levels was associated with TGF beta 1-induced growth arrest and differentiation, indicating that Id-1 may be involved in TGF beta 1 signaling pathway. The fact that up-regulation of p21(WAF1), one of the downstream effectors of Id-1, was observed after exposure to TGF beta 1 further indicates the involvement of Id-1 in the TGF beta 1-induced growth arrest in HPr-1 cells. However, increased expression of p27(KIP1) was also observed in the TGF beta 1-treated cells, suggesting that in addition to down-regulation of Id-1, other factors may be involved in the TGF beta 1-induced cell growth arrest and differentiation in prostate epithelial cells. Our results provide evidence for the first time that TGF beta 1 may be one of the upstream regulators of Id-1.

Blotting, Western↗
PubMed2002

Tamoxifen decreases fibroblast function and downregulates TGF(beta2) in dupuytren's affected palmar fascia.

BACKGROUND: Dupuytren's contracture is a fibroproliferative disorder that is associated with increased collagen deposition. Isoforms of transforming growth factor beta (TGF(beta)), normally TGF(beta1) and TGF(beta2), are involved in the progressive fibrosis of Dupuytren's disease. It has been suggested that downregulation of TGF(beta) may be useful in the treatment of the condition. Tamoxifen, a synthetic nonsteroidal antiestrogen, is known to modulate the production of TGF(beta). This study examined the role of tamoxifen in decreasing fibroblast function and downregulating TGF(beta2). METHODS: Primary cultures of fibroblasts were obtained from Dupuytren's affected fascia and carpal tunnel affected fascia as a control. Collagen lattices were prepared and populated with the fibroblasts. The fibroblast-populated collagen lattices (FPCL) were then measured for contraction every 24 h for 5 days. Supernatant was obtained from the culture medium following completion of the FPCL portion of the experiment and used for a TGF(beta2) immunoassay. RESULTS: Dupuytren's affected fibroblasts contracted the FPCLs significantly more than carpal tunnel control fibroblasts. Treating the fibroblasts with tamoxifen caused a decreased contraction rate in both Dupuytren's affected fibroblasts and carpal tunnel controls. There was increased TGF(beta2) expression in the Dupuytren's affected fascia group compared to the carpal tunnel control group. Tamoxifen decreased TGF(beta2) expression in Dupuytren's affected fascia group but not in the carpal tunnel control group. CONCLUSION: TGF(beta) appears to be the key cytokine in the fibrogenic nature of Dupuytren's disease. Tamoxifen treatment has been demonstrated to decrease the function of fibroblasts derived from Dupuytren's affected fascia and downregulated TGF(beta2) production in these same fibroblasts. These data suggest a method to manipulate and control Dupuytren's contracture in the clinical setting.

Carpal Tunnel Syndrome↗
PubMed2002

Multidrug-resistance-associated protein MGr1-Ag is identical to the human 37-kDa laminin receptor precursor.

We report the isolation and functional characterization of the gene encoding MGr1-Ag, a multidrug-resistance-associated protein. A lambdagt11 cDNA library derived from colorectal carcinoma SW480 cells was screened with monoclonal antibody MGr1. DNA homology analysis of 22 positive clones (designated R1-R22) suggested human 37-kDa laminin receptor precursor (37LRP, R7/R9/R15/R16/R19/R20) and a novel gene (R22) as candidate genes encoding MGr1-Ag. Western blot analysis showed that anti-R20 serum reacted with a unique protein band that was consistent with MGr1-Ag, while anti-R22 serum could not react with MGr1-Ag. The coding gene for MGr1-Ag was amplified using reverse transcription-PCR. Sequence analysis revealed that the MGr1-Ag and 37LRP genes shared the same coding sequence. An in vitro drug sensitivity assay indicated that down-regulation of 37LRP by an antisense technique could significantly enhance the cytotoxicity of anticancer drugs to gastric cancer cells. Thus we draw the conclusion that MGr1-Ag is identical to 37LRP.

Carcinoma↗
PubMed2002

Determination of toxicokinetic parameters for bioconcentration of water-soluble fraction of petroleum hydrocarbon associated with no. 0 diesel in Changjiang estuary and Jiaozhou bay: model versus mesocosm experiments.

A method is proposed for determination of toxicokinetic parameters for bioconcentration by phytoplankton of the water-soluble fraction (WSF) of petroleum hydrocarbon (PH) associated with No. 0 diesel, in which WSF-PH concentration in phytoplankton cells, C(A(d)), is estimated by subtracting concentration in water (S-bottle) containing a phytoplankton sample from that in a C-bottle without phytoplankton. It was demonstrated that C(A(d)) agrees well with the concentration found by direct ultrasonication extraction of collected cells, C(A(ind)) ( r = 0.88, p < 0.0001), and its uncertainty was about 17.6%. Mesocosms in 25-m3 ethylene vinyl acetate or 4-m3 polyethylene bags were performed at two sites in China: Changjiang Estuary in spring/summer 1998 and Jiaozhou Bay in autumn 1999 and spring/summer 2000. The experiments were designed to determine toxicokinetic parameters, including specific rates of uptake and elimination, and bioconcentration factor (BCF), for bioconcentration of WSF-PH by phytoplankton. A modified kinetic two-compartment model for bioconcentration of WSF-PH by phytoplankton was developed to estimate the toxicokinetic parameters. In the model, the influence of phytoplankton growth on bioconcentration and WSF-PH decline due to biotic and abiotic processes other than bioconcentration, such as volatilization, microbial degradation, phytolysis, and sorption expressed as an exponential-decay equation, are taken into account. Size-dependent BCF was observed in the laboratory experiment. BCFs were 1.0 x 10(4) in summer in Changjiang Estuary, 1.6 x 10(4) in summer, and 1.1 x 10(4) in autumn in Jiaozhou Bay. The difference in BCF may be interpreted by its size dependence.

Biological Availability↗