Biomedical subjects

Y Xie

Publications and source records attributed to Y Xie.

At least 55 records · Page 3Linked to original sources

PubMed2001

Surface-enhanced Raman scattering on uniform platinum-group overlayers: preparation by redox replacement of underpotential-deposited metals on gold.

The preparation of Pt-group metal films on roughened gold electrodes by utilizing spontaneous redox replacement of an underpotential-deposited (upd) copper or lead monolayer with a Pt-group metal cation solute is described. The resulting films display intense surface-enhanced Raman scattering (SERS) for adsorbates bound to the overlayer and free from substrate interferences. This strategy provides a useful alternative, at least for platinum, to the constant-current electrodeposition method commonly utilized to prepare SERS-active Pt-group metal films (Zou, S.; Weaver, M. J. Anal. Chem. 1988, 70. 2387). Similarly to related earlier studies, the film uniformity (specifically, the absence or otherwise of residual Au "pinhole" sites) was tested by employing carbon monoxide, and also ethylene, as "probe" chemisorbates, since they yield vibrational frequencies on Au that are blue-shifted from the corresponding bands for adsorbate bound to Pt-group metal sites. While a single redox replacement of upd Cu with Pt(IV) yielded incomplete surface coverage, as expected, the use of multiple (up to eight) replacement cycles produced Pt films displaying remarkably intense CO vibrational bands as well as apparently "pinhole-free" properties, although such imperfections were detected with the ethylene probe. A single upd Cu replacement with Pt(II), however, yielded a remarkably uniform Pt layer, as indicated by pinhole-free characteristics using both the CO and ethylene probes along with the voltammetric behavior. The use of additional redox replacement cycles yielded marked progressive attenuation in the SERS signals. Comparable, although less optimal, SERS behavior was obtained for Pd films prepared similarly from Pd(II). The value of the strategy for exploring catalytic as well as equilibrium adsorptive chemistry on Pt surfaces is also illustrated.

Journal Article↗

PubMed2001

Cloning, expression and characterization of a novel human REPS1 gene.

Ral is a member of the small GTPase-binding protein (G protein) family, and plays an important role in the Ras-RalGDS signal transduction pathway. A series of recent findings reveal several important downstream target proteins of Ral, such as RalBP1, Reps1, and others. Here we report another binding partner for RalBP1, which we have isolated from the human fetal brain library. The human REPS1 protein shares 83% amino acid identity with the mouse Reps1 protein. Northern blot analysis shows that the REPS1 is expressed in a variety of tissues, with the strongest expression in the heart and testis.

Adult↗

PubMed2001

Selenazolidines as novel organoselenium delivery agents.

Two new classes of selenazolidine-4(R)-carboxylic acids (2-oxo and 2-methyl-SCAs) were synthesized and characterized. Both were designed as latent forms of selenocysteine, intended to provide a chemically superior delivery form for selenium. The prodrugs may be clinically useful when selenium supplementation at supranutritional levels is indicated, such as in cancer chemoprevention.

Organoselenium Compounds↗

PubMed2001

Polymer-assisted formation of giant polyoxomolybdate structures.

A highly ordered, porous nanoscale network structure of polyoxomolybdate was prepared from the slow decomposition of an unstable precursor compound MoO(2)(OH)(OOH) in the presence of PEO-containing triblock copolymer gels or semidilute/concentrated poly(ethylene oxide) (PEO) homopolymer solutions. Small-angle X-ray scattering (SAXS) and wide-angle X-ray diffraction (WAXD) measurements of the 1-microm size crystals revealed an extremely ordered primitive cubic (pc) structure made of polyoxomolybdates. Scanning electron microscopy (SEM) measurements showed that the overall size of these single crystals was close to 1 microm, in agreement with estimates from the scattering peak widths. Evidence from both scattering measurements and transmission electron microscope (TEM) measurements suggested that the system formed a highly porous primitive cubic network similar to that of certain zeolite structures. However, the observed lattice constant of 5 nm was much larger. The function of the PEO-containing polymer network was found to be very subtle and complex. Presumably, PEO acted simultaneously as a weak reducing agent and as a viscous matrix to ensure sufficient time for the formation of long-range ordered structures, resulting in the growth of extremely uniform but probably hollow "nanospheres". We suggest that this new material may find unique applications as a high-efficiency absorbent or catalyst. Furthermore, the current synthetic method may open up new pathways to prepare similar functional nanomaterials.

Journal Article↗

PubMed2001

Binuclear homoleptic copper carbonyls Cu(2)(CO)(x) (x = 1-6): remarkable structures contrasting metal-metal multiple bonding with low-dimensional copper bonding manifolds.

Binuclear homoleptic copper carbonyls Cu(2)(CO)(x) (x = 1-6) have been studied using four different density functional theory methods (DFT) in conjunction with a basis set of extended double-zeta plus polarization quality, labeled as DZP. For each homoleptic binuclear copper carbonyl compound, several stationary point structures are presented, and these structures are characterized in terms of their geometries, thermochemistry, and vibrational frequencies. The optimal unsaturated Cu(2)(CO)(x) (x = 1-6) structures are generated by joining 18-electron tetrahedral, 16-electron trigonal, 14-electron linear copper carbonyl building blocks, and/or bare copper atoms with copper-copper single bonds rather than by joining 18-electron copper carbonyl units with multiple copper-copper bonds. For Cu(2)(CO)(6) the eclipsed and staggered ethane-like structure are virtually degenerate and lie significantly lower in energy than other possible structures. The eclipsed Cu-Cu single bond distance is predicted to be 2.61 A, while that for the staggered structure is 2.65 A. The lowest energy structure for Cu(2)(CO)(5) is the eclipsed ethyl radical-like structure, with r(e)(Cu-Cu) = 2.51 A. The staggered ethyl radical-like structure lies only 0.1 kcal/mol higher in energy, with a Cu-Cu distance shorter by only approximately 0.001 A. For Cu(2)(CO)(4) a methylcarbene-like structure is predicted to lie lowest, with Cu-Cu distance 2.40 A. However, twisted and planar ethylene-like structure lie only 3-5 kcal/mol higher. For Cu(2)(CO)(3) a surprising methylcarbyne-like structure with r(e)(Cu-Cu) = 2.38 A is predicted to lie lowest with all four DFT methods. However, a classical vinyl radical-like lies only 2-4 kcal/mol higher. For Cu(2)(CO)(2) theory predicts a vinylidene-like structure with r(e)(Cu-Cu) = 2.34 A to be essentially degenerate with cis and trans bent acetylene structures with copper-copper distances 2.33 A. Finally, and consistent with earlier theoretical studies, the linear end on Cu-Cu-CO structure with r(e)(Cu-Cu) = 2.27 A is the predicted global minimum for Cu(2)(CO).

Journal Article↗

PubMed2001

Signal transduction in neuronal migration: roles of GTPase activating proteins and the small GTPase Cdc42 in the Slit-Robo pathway.

The Slit protein guides neuronal and leukocyte migration through the transmembrane receptor Roundabout (Robo). We report here that the intracellular domain of Robo interacts with a novel family of Rho GTPase activating proteins (GAPs). Two of the Slit-Robo GAPs (srGAPs) are expressed in regions responsive to Slit. Slit increased srGAP1-Robo1 interaction and inactivated Cdc42. A dominant negative srGAP1 blocked Slit inactivation of Cdc42 and Slit repulsion of migratory cells from the anterior subventricular zone (SVZa) of the forebrain. A constitutively active Cdc42 blocked the repulsive effect of Slit. These results have demonstrated important roles for GAPs and Cdc42 in neuronal migration. We propose a signal transduction pathway from the extracellular guidance cue to intracellular actin polymerization.

Actins↗

PubMed2001

Further evidence for the involvement of inhibition of cell proliferation and development in thymic and splenic atrophy induced by the peroxisome proliferator perfluoroctanoic acid in mice.

We recently demonstrated that severe thymic and splenic atrophy occur upon dietary treatment of mice with potent peroxisome proliferators (PPs), e.g. perfluorooctanoic acid (PFOA), WY-14,643, nafenopin, and di(2-ethylhexyl)phthalate (DEHP). In the present study, we investigated this phenomenon further employing a relative inert PP, PFOA. Comparison of the dose-dependencies and time-courses indicated that the peroxisome proliferative effect occurred prior to atrophy of both the thymus and spleen. However, following withdrawal of PFOA from the diet, the weight of the thymus and spleen rapidly returned to normal within 10 and 5 days, respectively, in contrast to the more persistent peroxisome proliferation. Furthermore, the changes in thymus and spleen weight upon PFOA treatment and the following withdrawal from diet paralleled the changes in total thymocyte and splenocyte counts, respectively. It was found previously that the decreases in the thymocyte populations present in the S and G2/M phases, as well as in the number of CD4+CD8+ cells upon PFOA treatment, were the most dramatic, perhaps reflecting inhibition of thymocyte proliferation in connection with thymocyte development. Here, the recovery of thymocytes began with increases in the populations in these same phases of the cell cycle, with CD4+CD8+ cells recovering most rapidly, lending further support to our previous hypothesis. The possible relationship of these immunotoxic effects of PPs to the changes they cause in fatty acid metabolism is discussed.

Animals↗

PubMed2001

Positive allosteric modulation by ultraviolet irradiation on GABA(A), but not GABA(C), receptors expressed in Xenopus oocytes.

1. Recombinant rat GABA(A) (alpha1beta2, alpha1beta2gamma2, beta2gamma2) and human GABA(C) (rho1) receptors were expressed in Xenopus oocytes to examine the effect of ultraviolet (UV) light on receptor function. 2. GABA-induced currents in individual oocytes expressing GABA receptors were tested by two-electrode voltage clamp before, and immediately after, 312 nm UV irradiation. 3. UV irradiation significantly potentiated 10 microM GABA-induced currents in alpha1beta2gamma2 GABA receptors. The modulation was irradiation dose dependent, with a maximum potentiation of more than 3-fold. 4. The potentiation was partially reversible and decayed exponentially with a time constant of 8.2 +/- 1.2 min toward a steady-state level which was still significantly elevated (2.7 +/- 0.3-fold) compared to the control level. 5. The effect of UV irradiation on GABA(A) receptors varied with receptor subunit composition. UV irradiation decreased the EC50 of the alpha1beta2, alpha1beta2gamma2 and beta2gamma2 GABA(A) receptors, but exhibited no significant effect on the rho1 GABA(C) receptor. 6. UV irradiation also significantly increased the maximum current 2-fold in alpha1beta2 GABA(A) receptors with little effect on the maximum of alpha1beta2gamma2 (1.1-fold) or beta2gamma2 (1.1-fold) GABA(A) receptors. 7. The effect of UV irradiation on GABA(A) receptors did not overlap the effect of the GABA receptor- allosteric modulator, diazepam. 8. The UV effect on GABA(A) receptors was not prevented by the treatment of the oocytes before and during UV irradiation with one of the following free-radical scavengers: 40 mM D-mannitol, 40 mM imidazole or 40 mM sodium azide. In addition, the effect was not mimicked by the free-radical generator, H2O2. 9. Potential significance and mechanism(s) of the UV effect on GABA receptors are discussed.

Allosteric Regulation↗

PubMed2001

A new phenomenon in the induction period of the methane dehydroaromatization reaction.

The induction period of dehydroaromatization of methane to benzene over Mo/HZSM-5 had been investigated in real-time by the resonant-enhanced two-photon ionization (RE2PI) technique; it is remarkable that there is a small amount of benzene formed in the early stage of the induction period; we suggest that the trace amount of benzene was caused by the reduction of the original Mo6+ ion during the induction period and the Mo6+ species has a slight catalytic activity for methane-benzene conversion.

Journal Article↗

PubMed2001

Identification of dopamine responsive mRNAs in glial cells by suppression subtractive hybridization.

Recent studies have established that glial cells are important targets of the neurotransmitter dopamine (DA), but the regulatory effects of DA on glial cells have not been extensively studied. In the present study, we have investigated the influence of DA on gene transcription in glial cells. Two-directional (forward and backward) suppression subtraction hybridization (SSH) was performed on astrocytes cultured from rat cerebral tissues in standard media or in culture media treated with DA. PCR-select differential screening was used to further verify the differentially expressed cDNA clones, positive clones were sequenced, and the mRNAs were re-examined on Northern blots. Fourteen sequences were identified of which eleven are homologous to known genes, three are homologous to expressed sequence tags (ESTs). Three novel full-length cDNAs were isolated using the EST fragments as probes to screen a cDNA library constructed from human brain. Analysis of these sequences suggested that complex intracellular signaling pathways, involving crosstalk with growth factor pathways, steroid hormone pathways, and an interferon-regulated 2-5 A pathway, are responsive to DA in astrocytes. The responsive proteins downstream from the signaling pathways were found to fall into at least three groups, including a series of metabolic enzymes, stress proteins, transfer proteins, etc. In addition, several of them have established their relationships with specific neurodegenerative diseases, showing that there is overlap in the pathogenic mechanisms of different diseases. Our results have provided a foundation for better understanding of the molecular basis of glial cell functions in dopaminergic transmission and an approach to find possible medication for the related disorders.

Animals↗

PubMed2001

Evidence that Gal11 protein is a target of the Gal4 activation domain in the mediator.

The mediator is an approximately 20 protein complex that is essential for the transcription of most genes in yeast. It is contacted by a number of gene-specific activators, but the details of these interactions are not well understood in most cases. Here, evidence is presented that the mediator component Gal11 represents at least one target of the Gal4 activation domain (AD). Deletion of Gal11 is shown to decrease the affinity of the Gal4 AD for the mediator, and direct binding of an N-terminal domain of Gal11 with the Gal4 AD is demonstrated. Quantitative studies, however, indicate that the K(D) of the 1:1 Gal4 AD--Gal11 complex is modest. Combined with in vivo data showing that Delta gal11 cells exhibit reduced, but still significant, Gal4-mediated gene expression, these results suggest that the dimeric activator might also contact another protein in the mediator in addition to Gal11.

Binding, Competitive↗

PubMed2001

[Expression of vascular endothelial growth factor in primary esophageal squamous cell carcinoma and its significance in angiogenesis and prognosis of the tumor].

OBJECTIVE: To study the expression of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in primary esophageal squamous cell carcinoma and to clarify the association of VEGF expression with the angiogenesis and prognosis of this tumor. METHODS: VEGF expression and MVD in 82 specimens of primary esophageal squamous cell carcinoma, resected from Jan 1981 through May 1994, were examined by immunohistochemistry staining (SP method), using anti-VEGF polyclonal antibody and anti-factor VIII monoclonal antibody. The relationship between VEGF expression and MVD and postoperative survival of patient was analyzed. RESULTS: Fifty-two out of the eighty-two specimens of esophageal squamous cell carcinoma (63.4%) showed positive expression of VEGF. The median of MVD in tumor was 37/mm2 (9-150/mm2). There was a close correlation between MVD and VEGF expression (P = 0.001). The survival rate of patients with high MVD in the tumor was significantly lower than that of patients with low MVD (P = 0.017). The higher the level of expression of VEGF in tumor, the poorer prognosis for the patients (P = 0.000). CONCLUSION: In primary esophageal squamous cell carcinoma, angiogenesis is mediated mainly by VEGF. VEGF is associated with tumor progression and may increase the malignancy via angiogenesis. It may be used as an independent indicator for prognosis of esophageal squamous cell carcinoma.

Adult↗

PubMed2001

The leukocyte common antigen-related protein tyrosine phosphatase receptor regulates regenerative neurite outgrowth in vivo.

Drosophila and leech models of nervous system development demonstrate that protein tyrosine phosphatase (PTP) receptors regulate developmental neurite outgrowth. Whether PTP receptors regulate neurite outgrowth in adult systems or in regenerative states remains unknown. The leukocyte common antigen-related (LAR) receptor is known to be present in rodent dorsal root ganglion (DRG) neurons; therefore, the well established model of postcrush sciatic nerve regeneration was used to test the hypothesis that LAR is required for neurite outgrowth in the adult mammalian nervous system. In uninjured sciatic nerves, no differences in nerve morphology and sensory function were detected between wild-type and LAR-deficient littermate transgenic mice. Sciatic nerve crush resulted in increased LAR protein expression in DRG neurons. In addition, nerve injury led to an increase in the proportion of LAR protein isoforms known to have increased binding affinity to neurite-promoting laminin-nidogen complexes. Two weeks after nerve crush, morphological analysis of distal nerve segments in LAR-deficient transgenic mice demonstrated significantly decreased densities of myelinated fibers, decreased axonal areas, and increased myelin/axon area ratios compared with littermate controls. Electron microscopy analysis revealed a significant twofold reduction in the density of regenerating unmyelinated fibers in LAR-/- nerves distal to the crush site. Sensory testing at the 2 week time point revealed a corresponding 3 mm lag in the proximal-to-distal progression of functioning sensory fibers along the distal nerve segment. These studies introduce PTP receptors as a major new gene family regulating regenerative neurite outgrowth in vivo in the adult mammalian system.

Animals↗

PubMed2001

[Expression and significance of tissue inhibitors of metallproteinases-1 and -2 in serum and liver tissue of patients with liver cirrhosis].

OBJECTIVE: To investigate the expression and location of tissue inhibitors of metallproteinases-1 and -2 (TIMP-1 and TIMP-2) in liver tissue of patients with cirrhosis and to investigate the correlation between TIMPs in liver and those in serum. METHODS: TIMP-1 and TIMP-2 in the serum of 106 patients with liver cirrhosis were detected by solid-phase absorption to sensitized erythrocytes (SPASE). The expression of TIMP-1 and TIMP-2 related antigens in liver biopsy specimens from 30 patients with liver cirrrhosis was detected by immunohistochemical method with specific monoclonal antibody (McAb), and the results thus obtained were compared with the results of the seral TIMPs from the same patients. 10 normal livers were used as controls. RESULTS: The positive rates of TIMP-1 and TIMP-2 in the 106 serum samples of patients with cirrhosis were 73.58% and 61.32% respectively. TIMP-1 and TIMP-2 related antigens were detected in all of the 30 liver tissues from patients with liver cirrhosis and the expression of TIMP-1 was higher than that of TIMP-2 (P < 0.01). The staining signal of TIMP-1 and TIMP-2 related antigen was mainly located in the cytoplasm of liver cells. There was no signal in nuclear of liver cells. None of the normal liver tissues was positive in expression of TIMP-related antigen. The positive rate was 100% for serum TIMP-1 and 77% for serum TIMP-2. CONCLUSION: Expression of TIMPs at different degrees can be found in liver tissue with cirrhosis. TIMPs are located in cytoplasm of liver cells of patients with cirrhosis. There is a significant correlation between serum TIMPs level and liver TIMPs level. Serum TIMP-1 and TIMP-2 can be used as diagnostic indexes for liver fibrosis in chronic liver diseases.

Adult↗

PubMed2001

An Abd-B class HOX.PBX recognition sequence is required for expression from the mouse Ren-1c gene.

Expression from the mouse Ren-1(c) gene in As4.1 cells is dependent on a proximal promoter element (PPE) located at approximately -60 and a 241-base pair enhancer region located at -2625 relative to the transcription start site. The PPE (TAATAAATCAA) is identical to a consensus HOX.PBX binding sequence. Further, PBX1b has been shown to be a component of a PPE-specific binding complex present in nuclear extracts from As4.1 cells. The binding affinities of different paralog HOX members to the PPE were examined in the absence or presence of PBX1b. HOXB6, -B7, and -C8 failed to bind the PPE alone but showed weak affinity in the presence of PBX1b. In contrast, HOXD10 and to a lesser degree HOXB9 bound the PPE with high affinities regardless of whether PBX1b was present. Abd-B HOX members, including HOXD10, -A10, -A9, -B9, and -C9, are expressed in As4.1 cells. The ability of HOX and PBX1b to form a ternary complex with PREP1 on the PPE is also demonstrated both in vivo and in vitro. Point mutations in either the HOX or PBX half-site of the PPE disrupted the formation of the HOX.PBX complex and dramatically decreased transcriptional activity of the Ren-1(c) gene demonstrating that both the HOX and PBX half-sites are critical for mouse renin gene expression. These results strongly implicate Abd-B class Hox genes and their cofactors as major determinants of the sites of renin expression.

Animals↗

PubMed2001

Kinetic modulation of Kv4-mediated A-current by arachidonic acid is dependent on potassium channel interacting proteins.

The Kv4 subfamily of voltage-gated potassium channels is responsible for the transient A-type potassium current that operates at subthreshold membrane potentials to control membrane excitability. Arachidonic acid was shown recently to modulate both the peak amplitude and kinetics of the hippocampal A-current. However, in Xenopus oocytes, arachidonic acid only inhibited the peak amplitude of Kv4 current without modifying its kinetics. These results suggest the existence of Kv4 auxiliary subunit(s) in native cells. We report here a K-channel interacting protein (KChIP)-dependent kinetic modulation of Kv4.2 current in Chinese hamster ovary cells and Kv4.2 and Kv4.3 currents in Xenopus oocytes by arachidonic acid at physiological concentrations. This concentration-dependent effect of arachidonic acid resembled that observed in cerebellar granule neurons and was fully reversible. Other fatty acids, including a nonhydrolyzable inhibitor of both lipooxygenase and cyclooxygenase, 5,8,11,14-eicosatetraynoic acid (ETYA), also mimicked arachidonic acid in modulating Kv4.3 and Kv4.3/KChIP1 currents. Compared with another transient potassium current formed by Kv1.1/Kvbeta1, Kv4.3/KChIP1 current was much more sensitive to arachidonic acid. Association between KChIP1 and Kv4.2 or Kv4.3 was not altered in the presence of 10 microm ETYA as measured by immunoprecipitation and association-dependent growth in yeast. Our data suggest that the KChIP proteins represent a molecular entity for the observed difference between arachidonic acid effects on A-current kinetics in heterologous cells and in native cells and are consistent with the notion that KChIP proteins modulate the subthreshold A-current in neurons.

5,8,11,14-Eicosatetraynoic Acid↗

PubMed2001

A humanized monoclonal antibody constructed from intronless expression vectors targets human hepatocellular carcinoma cells.

An anti-human hepatocellular carcinoma (HCC) monoclonal antibody, hHP-1, was genetically humanized from a murine monoclonal antibody. In this study, a concept of positional template approach was applied to design the amino acid sequence of hHP-1's variable region, and synthetic DNA fragments for protein expression were produced through overlapping PCR from single strand oligonucleotides. Synthetic DNA fragments and human antibody constant region cDNA were used to construct two CMV promotor-based expression vectors for the antibody light and heavy chains, in which the variable region was connected directly to the constant region without an intron sequence. Completely assembled humanized antibody was successfully expressed in mammalian cells as IgG1 kappa molecules and purified using protein A affinity column. The immunogenicity of the hHP1 was estimated by the amino acid sequence and determined through a HAMA (human anti-murine antibody) serum reaction assay. Results indicated that the immunogenicity of hHP-1 was significantly reduced. In vitro binding activity assay showed that the hHP-1 had retained its binding function to a human HCC SMMC-7721 cell-line, without cross binding to other human normal tissues. Immunofluorescence staining showed that hHP-1 had a strong binding activity to SMMC cells. A competitive binding assay showed that the relative binding activity of hHP-1 was approximately 25% binding activity of the original murine antibody. Our results indicate that a humanized antibody could be produced using intronless vectors and expressed as a complete IgG1 kappa antibody. Hence we believe that hHP-1 could be a potential candidate for HCC treatment.

Amino Acid Sequence↗

PubMed2001

Triptolide induced cytotoxic effects on human promyelocytic leukemia, T cell lymphoma and human hepatocellular carcinoma cell lines.

Triptolide, a traditional Chinese medicine, has been reported to be effective in the treatment of auto-immune diseases, and it can also induce anti-neoplastic activity on several human tumor cell lines. This study investigates the cytotoxic function and the functional mechanism of triptolide on tumor cells. Promyelocytic leukemia, (HL-60), T cell lymphoma (Jurkat), and human hepatocelluar carcinoma (SMMC-7721) cells were subjected to triptolide treatment, and cell growth inhibition was examined by XTT cell viability assay. Cell death mechanism (apoptosis) was confirmed through DNA fragmentation and DAPI staining. Triptolide inhibited 50% of cell growth (IC(50)) on HL-60 cells at 7.5 nM, Jurkat cells at 27.5 nM and SMMC cells at 32 nM. Characteristic apoptotic features including internucleosomal DNA fragmentation and chromatin condensation were observed in triptolide treated cells. Data from the study indicates that triptolide could induce apoptosis in human tumor cell lines and it may be applicable as a potential chemotherapeutic agent for cancer treatment.

Antineoplastic Agents, Alkylating↗