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Biomedical subjects

W Zhang

Publications and source records attributed to W Zhang.

At least 361 records · Page 20Linked to original sources
PubMed2001

[Expression of vascular endothelial growth factor and transforming growth factor-beta 1 in nasal polyps].

OBJECTIVE: To study the expression and significance of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) and transforming growth factor-beta 1(TGF-beta 1) in nasal polyps. METHODS: Expression of VEGF/VPF and TGF-beta 1 in nasal polyps from 34 patients and middle turbinates from 30 patients with deviation of nasal septum was prospectively studied with immunohistochemistry. Tissue sections were observed under optical microscope. RESULTS: (1) The VEGF/VPF positivity in vascular endothelium and in glandular cell was significantly higher in nasal polyps than in middle turbinates (P < 0.01 and P < 0.05, respectively); (2) The TGF-beta 1 positivity in extracellular matrix and in cells in the stroma was significantly higher in nasal polyps than in middle turbinates(P < 0.005); (3) The distribution and shape of TGF-beta 1 expressing cells in nasal polyps were similar to that of eosinophil, their positivities were significantly correlative; (4) The positivity of VEGF/VPF and TGF-beta 1 did not correlate with clinical type in nasal polyps (P > 0.05). CONCLUSION: (1) The VEGF/VPF may play a key role in the formation of heavy edema of nasal polyps; (2) The TGF-beta 1 may contribute to some of the pathologic changes observed in nasal polyps, such as thickening of the epithelial basement membrane and stromal fibrosis; (3) Eosinophils in nasal polyps represent a major source of TGF-beta 1.

Adolescent↗
PubMed2001

[Contralateral suppression of latency during distortion product otoacoustic emissions detection in guinea pigs].

OBJECTIVE: To investigate the cochlear micromechanics and the function of cochlear efferent system by detecting the distortion product otoacoustic emissions (DPOAE) with or without contralateral acoustic stimulation. METHODS: The DPOAE amplitude and latency of the cubic DPOAE (2f1-f2) were measured at f2 = 2, 4 and 6 kHz with or without 70 dB SPL broad-band noise contralateral stimulation in ears of 12 healthy pigmented guinea pigs, which were divided into two groups(A and B) and tested with different primary intensity level combinations. On the next day, an operation was made to open the acoustic bulla of right ear in Group A. Kainic Acid (KA, 1 microL of 60 mmol/L) was applied onto the round window membrane and wiped up carefully after three hours. The amplitude and latency of the cubic DPOAE from the left ear were measured after 6 hours of KA administration, with or without contralateral noise stimulation. RESULTS: Before the KA treatment, the amplitude of DPOAE induced by primaries of equal levels (L1 = L2) presented no significant change and the latency prolonged significantly during contralateral acoustic stimulation (Group A). But the amplitude at 2, 4 kHz of DPOAE induced by primaries of different levels (L1 > L2) decreased significantly and the latency also prolonged significantly (Group B). After KA administration in the contralateral ear of Group A, the contralateral acoustic stimulation had no significant effect on either amplitude or latency of DPOAE measured ipsilaterally. CONCLUSION: The result demonstrates that the latency is a sensitive index for the cochlear contralateral suppression. The efferent system may act as a negative feedback during the cochlear transduction.

Acoustic Stimulation↗
PubMed2001

[Effect of recombinant epidermal growth factor on corneal epithelial cells after excision of pterygium].

OBJECTIVE: To investigate the effects of recombinant epidermal growth factor on the wounded corneal healing after excision of pterygium. METHODS: Simple and unrecurrent pterygium was selected, excised and sewed up conjunctival flap under local anaesthesia and microscope. After operation two drops of EGF eyedrop were used, and five minutes later 0.3% Tarivid Eye Oint was used again, and then the operated eye was enswathed. Everyday the wound cornea was observed and the EGF eyedrop was used. RESULTS: The wound cornea healing time of control group was seven days and that of the EGF group was five days and gave a remarkable difference (P < 0.05). The same results were obtained after comparing the effective group and ineffective group, P < 0.05. CONCLUSIONS: EGF eyedrop can accelerate proliferation and recovery of wound corneal epithelial cells. In the clinical trial, every body felt well and no side-effect was observed.

Adolescent↗
PubMed2001

[Luminescence dependence upon concentration and temperature in YPO4:Pr3+].

Under selective excitation 3P0 state of Pr3+ ion in YPO4, the emission spectra and fluorescence decay curves are measured at different concentrations and temperatures. The origin of the spectral line located at 613.2 nm has been discussed and assigned to be the 1D2 (gamma 3)-->3H4 (gamma 5) transition. The different concentration dependence of emission intensities of levels 3P0 and 1D2 has been studied. Using static model, the fluorescence decay curve of 1D2 level is fitted, and the result shows that the cross-relaxation caused by the interaction of dipole-quadrupole between adjacent Pr3+ ions results in the concentration quenching.

Attention↗
PubMed2001

[Spectra of Ce3+, Tb3+ and Gd3+ Ions in Ln(BO3,PO4) [Ln = La, Y]].

Emission and excitation spectra of Ce3+, Tb3+ and Gd3+ in lanthanum borophosphate and yttrium borophosphate are studied. The results show that Ce3+ emission weakens and Tb3+ emission enhances in La(BO3, PO4):Ce, Tb in the presence of Gd, and in Y(BO3, PO4):Ce, Tb, the Ce3+ and Tb3+ emissions are all enhanced, and the former increases more than the latter. In a whole, Gd3+ acts as intermediate of energy transfer from Ce3+ to Tb3+ and sensitizer in La(BO3, PO4):Ce, Tb, Gd; while in Y(BO3, PO4):Ce, Tb, Gd, Gd3+ acts only as sensitizer, and prevents energy transfer from Ce3+ to Tb3+. Compared with Y(BO3, PO4):Ce, Tb, Gd, La(BO3, PO4):Ce, Tb, Gd, phosphor absorbs ultraviolet radiation easily, and emits green light with higher purity and intensity under 254 nm excitation, so it is more suitable for green-emitting phosphor in fluorescent lamp.

Cerium↗
PubMed2001

[Spectral characterization of amorphous fluorinated carbon film with a low dielectric constant].

Amorphous fluorinated carbon films have been prepared from the gaseous mixture of CH4 and C4F8 by plasma enhanced chemical vapor deposition (PECVD) method. The dielectric constant of the deposited film under the experimental conditions is 2.3. Fourier transform infrared spectrum (FTIR) indicates that the film contains minor unsaturated double bonds such as C=O, C=C, etc in addition to CFn (n = 1-3) configurations. However, no sign reveals the existence of C-H and O-H in the film. Further, X-ray photoelectron spectrum (XPS) verifies that carbon in the deposited film has six chemical states, which are CF3 (8%), CF2(19%), CF (26.7%), C-CFn (42.5%), C-C(3.3%) and C=O (0.5%). It indicates that about 54% of carbon atoms in the film bond with fluorine atoms, and around 43% bond with carbon atoms of CFn configurations instead of bonding directly with fluorine atoms. The adjacent carbon atoms without bonding with fluorine are very less.

English Abstract↗
PubMed2000

Munc-18 associates with syntaxin and serves as a negative regulator of exocytosis in the pancreatic beta -cell.

The Munc-18 protein (mammalian homologue of the unc-18 gene; also called nSec1 or rbSec1) has been identified as an essential component of the synaptic vesicle fusion protein complex. The cellular and subcellular localization and functional role of Munc-18 protein in pancreatic beta-cells was investigated. Subcellular fractionation of insulin-secreting HIT-T15 cells revealed a 67-kDa protein in both cytosol and membrane fractions. Immunohistochemistry showed punctate Munc-18 immunoreactivity in the cytoplasm of rat pancreatic islet cells. Direct double-labeling immunofluorescence histochemistry combined with confocal laser microscopy revealed the presence of Munc-18 immunoreactivity in insulin-, glucagon-, pancreatic polypeptide-, and somatostatin-containing cells. Syntaxin 1 immunoreactivity was detected in extracts of HIT-T15 cells, which were immunoprecipitated using Munc-18 antiserum, suggesting an intimate association of Munc-18 with syntaxin 1. Administration of Munc-18 peptide or Munc-18 antiserum to streptolysin O-permeabilized HIT-T15 cells resulted in significantly increased insulin release, but did not have any significant effect on voltage-gated Ca(2+) channel activity. The findings taken together show that the Munc-18 protein is present in insulin-secreting beta-cells and implicate Munc-18 as a negative regulator of the insulin secretory machinery via a mechanism that does not involve syntaxin-associated Ca(2+) channels.

Animals↗
PubMed2000

Identification and characterization of a novel gene KE04 differentially expressed by activated human dendritic cells.

To better understand the molecular mechanisms of dendritic cells (DC) function, we isolated differentially expressed genes in Ag-activated DC by a PCR-based subtractive hybridization technique. A novel full-length cDNA, KE04, was thus isolated from KLH-activated human PBMC-derived DC. KE04 cDNA encoded a 346-aa protein devoid of functionally indicative motifs. KE04 protein showed 64% identity with a Caenorhabditis elegans protein and 83% identity with a human putative protein. Distant relationship was also found with other prokaryotic and eukaryotic proteins. Differential expression of KE04 in activated DC other than nonactivated DC was confirmed at both mRNA and protein levels. KE04 mRNA expression was detectable in various human tissues and cell lines by Northern blot and RT-PCR. Western blot and confocal microscopy analysis indicated that its cytolocalization was intracellular. Our data suggest the potential involvement of KE04 in DC activation and will facilitate the research of molecular mechanism of DC function.

Amino Acid Sequence↗
PubMed2000

The delayed induction of c-jun in apoptotic human leukemic lymphoblasts is primarily transcriptional.

Because of their ability to induce lymphoid cell apoptosis, glucocorticoids have been used for decades to treat certain human leukemias and lymphomas. Studies presented in this paper complement our previous work demonstrating that sustained induction of the proto-oncogene c-jun plays a crucial role in the glucocorticoid-induced apoptotic pathway in CEM cells, human leukemic lymphoblasts. Results from measurements of c-jun mRNA half-life with RNase protection assays and of transcription by nuclear run-on assays indicate that, in the dexamethasone-sensitive cloned CEM-C7 cells, c-jun is induced at the transcriptional level. Consideration of time-course, however, suggested that this might be a secondary or possibly a delayed primary response. Use of cycloheximide to block protein synthesis strongly induced c-jun mRNA, suggesting that there had been relief from a labile protein repressor of transcription. Comparing the level of induction by cycloheximide with that of dexamethasone indicated that the two did not induce by an identical mechanism. The high induction by cycloheximide obscured simple interpretation of elevated c-jun mRNA levels after concomitant administration of cycloheximide and dexamethasone. This was resolved by nuclear run-on experiments, which showed that the dexamethasone induction of c-jun mRNA in this system does require protein synthesis.

Apoptosis↗
PubMed2000

Synergistic cooperation between Sp1 and Smad3/Smad4 mediates transforming growth factor beta1 stimulation of alpha 2(I)-collagen (COL1A2) transcription.

Transforming growth factor-beta1 (TGFbeta) is a strong activator of extracellular matrix accumulation. TGFbeta stimulates the gene coding for human alpha2(I)-collagen (COL1A2) by inducing binding of an Sp1-containing complex to an upstream promoter element (TGFbeta responsive element or TbRE) that contains a CAGA box. Here we report that the CAGA box of the TbRE is the binding site of the Smad3/Smad4 complex, and that the binding of the complex is required for TGFbeta-induced COL1A2 up-regulation. Recombinant Smad3 and Smad4 bind in vitro to the CAGA box of COL1A2; TGFbeta treatment of cultured fibroblasts induces Smad3/Smad4 binding to the TbRE; transient overexpression of Smad3 and Smad4 in fibroblasts transactivates TbRE-driven transcription; and COL1A2 gene up-regulation by TGFbeta is abolished in cells stably transfected with plasmids that express dominant negative forms of Smad3 or Smad4. In Sp1-deficient Drosophila Schneider cells, there was cooperative synergy between Smad3/Smad4 and Sp1 at the TbRE site. The analysis also emphasized the requirement of both Sp1- and Smad-binding sites for optimal promoter transactivation. In cells stably transfected with a plasmid expressing a dominant negative form of Sp1, the synergy was shown to be promoter-specific and dependent on the binding of Sp1 to the TbRE. Interestingly, overexpression of dominant negative Sp1 was found to block the antagonistic signal of tumor necrosis factor-alpha on COL1A2 transcription, as well. These results provide the first linkage between the Smad3 and Smad4 proteins and TGFbeta stimulation of type I collagen biosynthesis.

3T3 Cells↗
PubMed2000

DNA damage-induced phosphorylation of p53 at serine 20 correlates with p21 and Mdm-2 induction in vivo.

We investigated the induction and physiological role of Ser20 phosphorylation of p53 in response to DNA damage caused by ionizing radiation (IR) or ultraviolet radiation (UV). A polyclonal antibody that specifically recognizes a p53 peptide containing phosphorylated Ser20 was generated and used to detect p53 phosphorylation at Ser20. Western blot analyses of p53 in four cell lines with this antibody revealed that the p53 protein was phosphorylated at Ser20 to a different extent after treatment with IR or UV. The phosphorylation of Ser20 of wild-type p53 correlated with enhanced induction of the p53 downstream target genes p21WAF1/Cip1 (p21) and mdm-2. These results suggest that DNA damage-induced phosphorylation of p53 at Ser20 enhances the transactivation function of p53 for p21 and mdm-2 in vivo.

Antibodies↗
PubMed2000

A tyrosine hydroxylase-neurofilament chimeric promoter enhances long-term expression in rat forebrain neurons from helper virus-free HSV-1 vectors.

Helper virus-free herpes simplex virus (HSV-1) plasmid vectors are attractive for neural gene transfer, but a promoter that supports neuronal-specific, long-term expression is required. Although expression from many promoters is unstable, a 6.8-kb, but not a 766-bp, fragment of the tyrosine hydroxylase (TH) promoter supports long-term expression. Thus, 5' upstream sequences in this promoter may enhance expression. In this study, we evaluated expression from vectors that contain 5' upstream sequences from this promoter (-0.5 to -6.8 kb) inserted at the 5' end of either a neurofilament heavy subunit (NF-H) promoter or the cytomegalovirus (CMV) immediate early promoter. The TH-NFH promoter supported expression for 6 months in the striatum, 2 months in the hippocampus, and for 1 month in both perirhinal and postrhinal cortex (the longest time points examined). Expression was targeted to neurons. The enhanced expression may require specific sequences in the TH promoter fragment because replacing this fragment with a similar sized fragment of bacteriophage lambda DNA did not enhance expression. The reverse orientation of the TH promoter fragment also enhanced expression. Insertion of insulators from the chicken beta-globin locus between the TH-NFHlac transcription unit and the vector backbone may support a modest additional enhancement in expression. Other eucaryotic sequences may also enhance expression; a S. cerevisiae (40-kb fragment)-NFH promoter enhanced expression. In contrast, the TH-CMV promoter did not enhance expression. Thus, the TH-NFH promoter may support some physiological studies that require long-term expression in forebrain neurons.

Animals↗
PubMed2000

Multisite mutagenesis of interleukin 5 differentiates sites for receptor recognition and receptor activation.

Multisite mutagenesis of single-chain and monomeric forms of human interleukin 5 (IL-5) was performed to investigate mechanistic features of receptor activation and the possibility of differentiating sites of activation from those for receptor interaction. The normally dimeric human IL-5 contains two domains, each containing a four-helix bundle. IL-5 has previously been re-engineered into the monomeric, one-domain GM1 form by introducing an eight-residue linker between the third and fourth helices. In this study, we tested a combination of mutations in a single-chain IL-5 (scIL-5) construct, [(89)SLRGG(92),W(110)/(89)AAAAA(92), A(110)]scIL-5. This mutein was found to retain substantial IL-5 receptor alpha-chain binding but with selectively suppressed proliferation of the IL-5-dependent cell line TF-1.28. This result confirms recent findings that IL-5 receptor alpha-chain recognition can be supported by the (89)SLRGG(92) epitope and that, in contrast, Glu110 is important in receptor activation. On the basis of this result, two mutants of GM1 were constructed with the intent to retain receptor alpha-chain binding while modifying receptor activation epitopes. In the first, [(88)SLRGG(92),W(110)]GM1, the wild-type CD-loop sequence (89)EERRR(92) was converted to the mimotope (89)SLRGG(92), and Glu110 to Trp. In the second, [A(13), A(110)]GM1, wild-type Glu13, and Glu110 were both mutated to Ala. GM1 and mutants were expressed in high yield in Escherichia coli, purified under denaturing conditions from inclusion bodies, and refolded. Monomers were screened for binding to shIL-5Ralpha-Fc using optical biosensor and ELISA and for bioactivity by proliferation of TF-1.28 cells. Both [(88)SLRGG(92),W(110)]GM1 and [A(13),A(110)]GM1 were found to interact with the shIL-5Ralpha-Fc, with affinities of 69-585 nM, 2-15-fold weaker than that of the original GM1. The mutants also were able to compete with IL-5 for binding to shIL-5Ralpha in an ELISA. In contrast, both mutants exhibited a disproportionately decreased capacity to stimulate TF-1. 28 cell proliferation. [A(13),A(110)]GM1 bioactivity was 160-fold lower than that of GM1, while that for the [(88)SLRGG(92),W(110)]GM1 mutant was 2600-fold lower. The largely retained IL-5 receptor alpha-chain binding affinities versus relatively suppressed bioactivities of [A(13),A(110)]GM1 and [(88)SLRGG(92),W(110)]GM1 variants, in particular the latter, point to the existence of separable IL-5 epitopes for receptor binding and activation and establish the potential to design smaller IL-5 mimetic antagonists.

Binding, Competitive↗
PubMed2000

Synthesis of alpha-Gal epitope derivatives with a galactosyltransferase-epimerase fusion enzyme.

Alpha-Gal epitopes are carbohydrate structures bearing an alpha-D-Galp-(1-->3)-beta-D-Galp terminus and are the main cause of antibody-mediated hyperacute rejection in xenotransplantation. Nine monosaccharides and ten disaccharides were evaluated as substrates for a fusion protein, which contains both alpha-(1-->3)-galactosyltransferase and uridine-5'-diphosphogalactose 4-epimerase. Four disaccharide and six trisaccharide alpha-Gal epitope derivatives were synthesized utilizing this novel fusion enzyme.

Animals↗
PubMed2000

PSGR, a novel prostate-specific gene with homology to a G protein-coupled receptor, is overexpressed in prostate cancer.

PSGR, a new prostate tissue-specific gene with homology to the G protein-coupled odorant receptor gene family, has been identified. Here we report the characteristics of the predicted protein sequence of PSGR and its prostate tissue specificity and expression profile in human prostate cancer and matched normal tissues. Using multiple tissue Northern blots from over 50 different tissues, PSGR expression was restricted to human prostate tissues. Paired normal and tumor specimens from 52 primary prostate cancers, obtained by laser capture microdissection or manual microdissection, were analyzed for PSGR expression by semiquantitative and real-time PCR assays. The differential expression of PSGR between normal and tumor tissues was highly significant (P < 0.001), and 32 of 52 (62%) matched prostate specimens exhibited tumor-associated overexpression of PSGR. Of note, there was very little or no expression of PSGR in many normal specimens in comparison with the generally high expression of PSGR seen in matched tumor specimens. In situ hybridization assays showed restricted PSGR expression in the epithelial cells of the normal and tumor tissue sections. Restricted expression of PSGR in prostatic epithelial cells, overexpression of the PSGR in a significant percentage of prostate cancers, and the predicted protein sequence of PSGR with seven transmembrane domains provide a foundation for future studies evaluating the potential of PSGR as a prostate cancer gene expression marker and the utility of PSGR protein as a novel target for developing immunotherapeutic strategies for prostate cancer.

Amino Acid Sequence↗
PubMed2000

Modulation of tumor angiogenesis by stem cell factor.

Mast cells accumulate within solid tumors and can release many angiogenic factors, suggesting that they may modulate vascularization of tumors. Stem cell factor (SCF) stimulates mast cell migration, proliferation, and degranulation and therefore may influence mast cell behavior within tumors. We investigated the contribution of SCF to tumor angiogenesis by manipulating its level in mammary tumors. Sense or antisense cDNA fragments of rat SCF were ligated into an episomal expression vector. Ethylnitrosourea-induced rat mammary tumor cell lines were transfected with vector containing either control (no insert, C-P), sense (S-P), or antisense (AS-P) SCF DNA. The functional nature of the transfectants was confirmed by measuring SCF in cell lysates and conditioned media. Immunohistochemical analysis of the tumors induced in Berlin-Druckrey rats by these transfected cells demonstrated that mast cell number and microvascular density were significantly higher in S-P tumors and significantly lower in AS-P tumors, compared with C-P tumors. The expression of von Willebrand factor, an endothelial cell marker, showed a similar pattern. AS-P tumors were significantly smaller than either C-P or S-P tumors. These data suggest that SCF modulates tumor growth and angiogenesis via the involvement of mast cells.

Animals↗
PubMed2000

Effect of the lipid phase transition on the lactose permease from Escherichia coli.

The temperature dependence of lactose active transport, efflux down a concentration gradient, and equilibrium exchange were analyzed in right-side-out membrane vesicles from Escherichia coli containing wild-type lactose permease and mutant Glu325 --> Ala. With respect to uphill transport and efflux down a concentration gradient, both of which involve H(+) symport, Arrhenius plots with wild-type permease exhibit a discontinuity at 18-19 degrees C with a 7-8-fold decrease in activation energy above the phase transition. For equilibrium exchange, which does not involve H(+) symport, the change in activation energy is much less pronounced (2-3-fold) than that observed for active transport or efflux. Strikingly, mutant Glu325 --> Ala, which catalyzes equilibrium exchange as well as wild-type permease but is defective in all translocation reactions that involve net H(+) translocation, exhibits no change whatsoever in activation energy. The findings are consistent with the conclusion that the primary effect of the lipid phase transition is to alter coupling between substrate and H(+) translocation rather than the conformational change(s) responsible for translocation across the membrane.

Alanine↗