The study of mechanism of vascular endothelial growth factor on the prevention of restenosis after angioplasty.
Explore the source record for details and available documents.
Angioplasty, Balloon, Coronary↗
Biomedical subjects
Q Liu
Publications and source records attributed to Q Liu.
[Study on the infrared spectra of metallic clusters containing R2dtc ligand and V = O group].
This paper reports the features and regularities of the infrared spectra for two kinds of complexes containing R2dtc ligand. The cubane-like clusters containing R2dtc ligand possess weak and wide peaks at 400-500 cm-1 assigned to M-mu 3S vibration, while the peaks at 330-380 cm-1 and 1,470-1,510 cm-1 can be assigned to M-Sdtc and C-N vibrations, respectively. The nu(C-N) and nu(C = S) vibrations for Me2dtc-cubane cluster exhibit blue shift and red shift, respectively, when compared with those of other R2dtc ones. This would be attributed to the strong super-conjugation of the methyl group. The M-mu 3S vibrations for both types of complexes [V2Cu2S4(R2dtc)2(PhS)2]2- and [VCu4S4(R2dtc)n(PhS)4-n]3- (n = 0, 1, 2) occur at 480 and 465 cm-1, respectively. This small difference becomes a useful indication to distinguish the two types of clusters. Cluster complexes containing (R2dtc)2V2O2(mu-S)2 structural unit show the V = O vibration in the range of 844-970 cm-1. It is noted that (Et4N)[V3S2O3(Et2dtc)3] contains two sets of the V = O bonds corresponding to two sets of V = O vibrations at 970 and 844 cm-1. An additional coordination of the V = O bond to another metal atom obviously weakens the V = O bond to give rise to the red shift of the infrared frequency. Similar red shifts were also observed for other complexes and were discussed.
English Abstract↗
[Flotation and extraction spectrophotometric determination of trace silicate in water].
In HCl solution, silicate reacted with molybdate ammonium to produce silicomolibdic, then a yellow compound which was produced from the oxidation of TMB was simultaneously isolated to benzene phase by flotation and then isolated to dimethylsulfoxideformic acid by extraction. The compound gives a high absorption at 458 nm. The apparent molar absorptivity is 1.26 x 10(5) L.mol-1.cm-1. In the range of 0.02-1 mg.L-1 Si obeys Beer's law. The proposed method which combines with enrichment and measurement is simple, rapid, selective and convenient to determine silicate in water with satisfied results.
Benzidines↗
[Determination of trace bismuth in iron, steel and alloy by hydride generation-atomic fluorimetry].
With the aid of hydride generation-atomic fluorimetry, an analysis method by adding thiosemicarbazide-ascorbic acid and phosphoric acid to eliminate the interference of matrix has been developed for the determination of trace bismuth in iron, steel and alloy. The detection limit is Bi = 0.02 microgram.g-1 (3 sigma, n = 11, sample amount 0.2000 g). The method has been applied to determine trace arsenic in middle and low alloy steel, ferro and nickel-based superalloy, nickel-based superalloy, cobalt-based superalloy, copper alloy with satisfactory results.
English Abstract↗
[Photoacoustic spectra of the whole blood from leukemia patients].
Photoacoustic spectra of the whole bloods from the leukemia patients and the healthy persons were determined. The substantial differences were found in the spectra features of samples from the healthy persons and different leukemia patients. It is possibly of great clinical importance to the diagnosis of early stage leukemia patients and classification of the leakemia.
Acoustics↗
Identification of urotensin II as the endogenous ligand for the orphan G-protein-coupled receptor GPR14.
Urotensin II (UII) is a neuropeptide with potent cardiovascular effects. Its sequence is strongly conserved among different species and has structural similarity to somatostatin. No receptor for UII has been molecularly identified from any species so far. GPR14 was cloned as an orphan G protein-coupled receptor with similarity to members of the somatostatin/opioid receptor family. We have now demonstrated that GPR14 is a high affinity receptor for UII and designate it UII-R1a. HEK293 cells and COS-7 cells transfected with rat GPR14 showed strong, dose-dependent calcium mobilization in response to fish, frog, and human UII. Radioligand binding analysis showed high affinity binding of UII to membrane preparations isolated from HEK293 cells stably expressing rat GPR14. In situ hybridization analysis showed that GPR14 was expressed in motor neurons of the spinal cord, smooth muscle cells of the bladder, and muscle cells of the heart. The identification of the first receptor for UII will allow better understanding of the physiological and pharmacological roles of UII.
Amino Acid Sequence↗
Purification, characterization, and cDNA cloning of a new fibrinogenlytic venom protein, Agkisacutacin, from Agkistrodon acutus venom.
Agkisacutacin is a new fibrinogenlytic protein from Agkistrodon acutus venom. It consists of two heterologous subunits linked by an intersubunit disulfide bond. The cDNAs encoding the two chains of Agkisacutacin were cloned from a lambdagt11 cDNA library of the snake venom gland and sequenced, including the leader peptides (23/23 amino acid residues) and mature subunits (129/123 amino acid residues). It is structurally related to the family of IX/X-binding protein (IX/X-bp)-like proteins and shows high similarity (alpha-70%/beta-64%) to habu IX/X-bp from Trimeresurus flavoridis, but displays distinct biological activity with direct action on fibrinogen.
Agkistrodon↗
Cell type-specific activation of neuronal nicotinic acetylcholine receptor subunit genes by Sox10.
The regulatory factor Sox10 is expressed in neural crest derivatives during development as well as in the adult CNS and peripheral nervous system. Mutations of the human Sox10 gene have been identified in patients with Waardenburg-Hirschsprung syndrome that is characterized by defects in neural crest development. Previous studies suggested that Sox10 might function as an important transcriptional regulator of neural crest development. No natural target genes of Sox10 have yet been identified. Although human Sox10 activates a synthetic promoter consisting of a TATA box and multiple Sox consensus sequences, no transcriptional activity of the rat Sox10 homolog has been detected. Here we report that the neuronal nicotinic acetylcholine receptor beta4 and alpha3 subunit gene promoters are transactivated by rat Sox10 in a cell type-specific manner. The alpha3 and beta4 subunits, in combination with the alpha5 subunit, make up the predominant nicotinic receptor subtype expressed in the peripheral nervous system. Transfections using Sox10 mutants indicate that the C-terminal region is dispensable for its ability to activate the beta4 and alpha3 promoters. Rat Sox10 was originally identified as an accessory protein of the POU domain protein Tst-1/Oct6/SCIP in glial cells. Tst-1/Oct6/SCIP was shown previously to activate the alpha3 promoter. We now demonstrate that it can transactivate the beta4 promoter as well. However, we were unable to detect any synergistic effects of Sox10 and Tst-1/Oct6/SCIP on beta4 or alpha3 promoter activity. Finally, we present data suggesting that recombinant Sox10 protein can directly interact with a previously characterized regulatory region of the beta4 gene.
3T3 Cells↗
Preparative isolation and purification of hydroxyanthraquinones from Rheum officinale Baill by high-speed counter-current chromatography using pH-modulated stepwise elution.
Analytical and preparative high-speed counter-current chromatography was successfully used for the isolation and purification of hydroxyanthraquinones from Rheum officinale Baill (Dahuang) using pH-modulated stepwise elution. Four major components including chrysophanol, emodin, physcion and aloe-emodin were isolated each at over 98% purity.
Anthraquinones↗
A new mechanism of neurodegeneration: a proinflammatory cytokine inhibits receptor signaling by a survival peptide.
Heightened expression of both a proinflammatory cytokine, tumor necrosis factor alpha (TNF-alpha), and a survival peptide, insulin-like growth factor I (IGF-I), occurs in diverse diseases of the central nervous system, including Alzheimer's disease, multiple sclerosis, the AIDS-dementia complex, and cerebral ischemia. Conventional roles for these two proteins are neuroprotection by IGF-I and neurotoxicity by TNF-alpha. Although the mechanisms of action for IGF-I and TNF-alpha in the central nervous system originally were established as disparate and unrelated, we hypothesized that the signaling pathways of these two cytokines may interact during neurodegeneration. Here we show that concentrations of TNF-alpha as low as 10 pg/ml markedly reduce the capacity of IGF-I to promote survival of primary murine cerebellar granule neurons. TNF-alpha suppresses IGF-I-induced tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2) and inhibits IRS-2-precipitable phosphatidylinositol 3'-kinase activity. These experiments indicate that TNF-alpha promotes IGF-I receptor resistance in neurons and inhibits the ability of the IGF-I receptor to tyrosine-phosphorylate the IRS-2 docking molecule and to subsequently activate the critical downstream enzyme phosphatidylinositol 3'-kinase. This intracellular crosstalk between discrete cytokine receptors reveals a novel pathway that leads to neuronal degeneration whereby a proinflammatory cytokine inhibits receptor signaling by a survival peptide.
Animals↗
The polyoma virus enhancer cannot substitute for DNase I core hypersensitive sites 2-4 in the human beta-globin LCR.
The polyoma virus enhancer (PyE) is capable of conferring integration position-independent expression to linked genes in stably transfected erythroid cells after joining to DNase I hypersensitive site (HS) 5 of the human beta-globin locus control region (LCR). In attempting to separate the chromatin opening activity of the LCR from its enhancer activity and to investigate contributions of the individual HS core elements to LCR function, the human beta-globin LCR HS2, HS3 and HS4 core elements were replaced with the PyE within the context of a yeast artificial chromosome (YAC) bearing the whole locus. We show here that, in contrast to its function in cultured cells, the PyE is unable to replace HS core element function in vivo. We found that the PyE substitution mutant LCR is unable to provide either chromatin opening or transcriptional potentiating activity at any erythroid developmental stage in transgenic mice. These data provide direct evidence that the human beta-globin LCR core elements specify unique functions that cannot be replaced by a ubiquitous enhancer activity.
Animals↗
Spatial correspondence between R-cadherin expression domains and retinal ganglion cell axons in developing zebrafish.
Mechanisms underlying axonal pathfinding have been investigated for decades, and numerous molecules have been shown to play roles in this process, including members of the cadherin family of cell adhesion molecules. We showed in the companion paper that a member of the cadherin family (zebrafish R-cadherin) is expressed in retinal ganglion cells, and in presumptive visual structures in zebrafish brain, during periods when the axons were actively extending toward their targets. The present study extends the earlier work by using 1,1'-dioctadecyl-3,3,3',3', tetramethylindocarbocyanine perchlorate (DiI) anterograde tracing techniques to label retinal ganglion cell axons combined with R-cadherin in situ hybridization to explicitly examine the association ofretinal axons and brain regions expressing R-cadherin message. We found that in zebrafish embryos at 46-54 hours postfertilization, DiI-labeled retinal axons were closely associated with cells expressing R-cadherin message in the hypothalamus, the pretectum, and the anterolateral optic tectum. These results demonstrate that R-cadherin is appropriately distributed to play a role in regulating development of the zebrafish visual system, and in particular, pathfinding and synaptogenesis of retinal ganglion cell axons.
Animals↗
R-cadherin expression in the developing and adult zebrafish visual system.
Cell adhesion molecules in the cadherin family have been implicated in histogenesis and maintenance of cellular structure and function in several organs. Zebrafish have emerged as an important new developmental model, but only three zebrafish cadherin molecules have been identified to date (N-cadherin, paraxial protocadherin, and VN-cadherin). We began a systematic study to identify other zebrafish cadherins by screening zebrafish cDNA libraries using an antibody raised to the cytoplasmic domain of mouse E-cadherin. Here, we report a partial cDNA with extensive sequence homology to R-cadherin. Spatial and temporal expression of this putative zebrafish R-cadherin was examined in embryos and adults by Northern analysis, RNase protection, and in situ hybridization. R-cadherin message increased during embryogenesis up to 80 hours postfertilization (hpf) and persisted in adults. In the embryonic brain, R-cadherin was first expressed in groups of cells in the diencephalon and pretectum. In adult zebrafish brain, R-cadherin continued to be expressed in several specific regions including primary visual targets. In the retina, R-cadherin was first detected at about 33 hours postfertilization in the retinal ganglion cell layer and the inner part of the inner nuclear layer. Expression levels were highest during periods of axon outgrowth and synaptogenesis. Retrograde labeling of the optic nerve with 1,1'-dioctadecyl-3,3,3',3', tetramethylindocarbocyanine perchlorate (DiI) followed by in situ hybridization confirmed that a subset of retinal ganglion cells in the embryo expressed R-cadherin message. In the adult, R-cadherin expression continued in a subpopulation of retinal ganglion cells. These results suggest that R-cadherin-mediated adhesion plays a role in development and maintenance of neuronal connections in zebrafish visual system.
Age Factors↗
Expression of wild-type and V210I mutant prion protein in human neuroblastoma cells.
The conversion of the host-encoded prion protein (PrPc) into the insoluble, protease-resistant isoform (PrPsc) is the main pathogenic mechanism of transmissible spongiform encephalopathies. They are fatal neurodegenerative disorders, which in human occur as sporadic, inherited or familial forms. These last forms are linked to insert or point mutations of PrPc which may facilitate the spontaneous conversion into PrPsc. We have established stably transfected human neuroblastoma cells (SH-SY5Y) expressing mutant V210I, or wild-type PrPc. Both proteins were expressed and attached to the cell surface. The mutation in position 210 did not alter the biochemical properties of the protein in comparison with the wild-type protein nor induced any conformational changes similar to those observed in PrPsc.
Amino Acid Substitution↗
The mannose 6-phosphate/insulin-like growth factor-II receptor is a substrate of type V transforming growth factor-beta receptor.
The type V transforming growth factor beta (TGF-beta) receptor (TbetaR-V) is a ligand-stimulated acidotropic Ser-specific protein kinase that recognizes a motif of SXE/S(P)/D. This motif is present in the cytoplasmic domain of the mannose 6-phosphate/insulin-like growth factor-II (Man-6-P/IGF-II) receptor. We have explored the possibility that the Man-6-P/IGF-II receptor is a substrate of TbetaR-V. Purified bovine Man-6-P/IGF-II receptor was phosphorylated by purified bovine TbetaR-V in the presence of [gamma-32P]ATP and MnCl2 with an apparent Km of 130 nM. TGF-beta stimulated the phosphorylation of the Man-6-P/IGF-II receptor at 0 degrees C in mouse L cells overexpressing the Man-6-P/IGF-II receptor and in wild-type mink lung epithelial (Mv1Lu cells) metabolically labeled with [32P]orthophosphate. The in vitro and in vivo phosphorylation of the Man-6-P/IGF-II receptor occurred at the putative phosphorylation sites as revealed by phosphopeptide mapping and amino acid sequence analysis. TGF-beta stimulated Man-6-P/IGF-II receptor-mediated uptake (approximately 2-fold after 12 h treatment) of exogenous beta-glucuronidase in Mv1Lu cells and type II TGF-beta receptor (TbetaR-II)-defective mutant cells (DR26 cells) but not in type I TGF-beta receptor (TbetaR-I)-defective mutant cells (R-1B cells) and human colorectal carcinoma cells (RII-37 cells) expressing TbetaR-I and TbetaR-II but lacking TbetaR-V. These results suggest the Man-6-P/IGF-II receptor serves as an in vitro and in vivo substrate of TbetaR-V and that both TbetaR-V and TbetaR-I may play a role in mediating the TGF-beta-stimulated uptake of exogenous beta-glucuronidase.
Amino Acid Sequence↗
Intracellular Ca2+ oscillations drive spontaneous contractions in cardiomyocytes during early development.
Activity of cardiac pacemaker cells is caused by a balanced interplay of ion channels. However, it is not known how the rhythmic beating is initiated during early stages of cardiomyogenesis, when the expression of ion channels is still incomplete. Based on the observation that early-stage embryonic stem cell-derived cardiomyocytes continuously contracted in high extracellular K+ solution, here we provide experimental evidence that the spontaneous activity of these cells is not generated by transmembrane ion currents, but by intracellular [Ca2+]i oscillations. This early activity was clearly independent of voltage dependent L-type Ca2+ channels and the interplay between these and ryanodine sensitive Ca2+ stores. We also show that intracellular Ca2+ oscillations evoke small membrane depolarizations and that these can trigger L-type Ca2+ channel driven action potentials.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Characterization of the human cysteinyl leukotriene CysLT1 receptor.
The cysteinyl leukotrienes-leukotriene C4(LTC4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators of human bronchial asthma. Pharmacological studies have determined that cysteinyl leukotrienes activate at least two receptors, designated CysLT1 and CysLT2. The CysLT1-selective antagonists, such as montelukast (Singulair), zafirlukast (Accolate) and pranlukast (Onon), are important in the treatment of asthma. Previous biochemical characterization of CysLT1 antagonists and the CysLT1 receptor has been in membrane preparations from tissues enriched for this receptor. Here we report the molecular and pharmacological characterization of the cloned human CysLT1 receptor. We describe the functional activation (calcium mobilization) of this receptor by LTD4 and LTC4, and competition for radiolabelled LTD4 binding to this receptor by the cysteinyl leukotrienes and three structurally distinct classes of CysLT1-receptor antagonists. We detected CysLT1-receptor messenger RNA in spleen, peripheral blood leukocytes and lung. In normal human lung, expression of the CysLT1-receptor mRNA was confined to smooth muscle cells and tissue macrophages. Finally, we mapped the human CysLT1-receptor gene to the X chromosome.
Amino Acid Sequence↗
The binding interface between an E2 (UBC9) and a ubiquitin homologue (UBL1).
Human UBC9 is a member of the E2 (ubiquitin conjugation enzyme) family of proteins. Instead of conjugating to ubiquitin, it conjugates with a ubiquitin homologue UBL1 (also known as SUMO-1, GMP1, SMTP3, PIC1, and sentrin). UBC9 has been shown to be involved in cell cycle regulation, DNA repair, and p53-dependent processes. The binding interfaces of the UBC9 and UBL1 complex have been determined by chemical shift perturbation using nuclear magnetic resonance spectroscopy. The binding site of UBL1 resides on the ubiquitin domain, and the binding site of UBC9 is located on a structurally conserved region of E2. Because the UBC9-UBL1 system shares many similarities with the ubiquitin system in structures and in conjugation with each other and with target proteins, the observed binding interfaces may be conserved in E2-ubiquitin interactions in general.
Humans↗