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Biomedical subjects

Q Chen

Publications and source records attributed to Q Chen.

At least 469 records · Page 26Linked to original sources
PubMed1997

Partially purified Echis carinatus venom cleaves active-site-mutated bovine prothrombin at two sites.

Partially purified snake venom of Echis carinatus (ECV) is a well-known enzyme used to generate meizothrombin from prothrombin. In this reaction, meizothrombin is slowly converted to two smaller fragments. It is not certain if this slow reaction is catalyzed by meizothrombin or by ECV. Using previously constructed active site mutant bovine prothrombin, we eliminated meizothrombin autolysis and examined ECV reactions. ECV did slowly generate two fragments during activation of the active site mutant prothrombin. This result indicates that ECV cleaved bovine prothrombin at two sites: at Arg323-Ile to expose the active site, at another bond at or near the known meizothrombin autolysis site. Because the former cleavage is faster than the latter one, ECV is still a reasonable tool to generate meizothrombin under proper conditions.

Animals↗
PubMed1997

Contractile responses of cultured bovine retinal pericytes to angiotensin II.

OBJECTIVE: To document that angiotensin (ANG) II contracts cultured bovine retinal pericytes via saralasin-sensitive receptors if the cells are prerelaxed. METHODS: Changes in the contractile tone were quantified as the changes in the summed length of wrinkles induced by pericytes cultured on the silicone surface. RESULTS: Angiotensin II (10(-5) mol/L) did not increase the contractile tone of cultured pericytes that were not prerelaxed. However, when the pericytes had been prerelaxed 41% with 10(-6)-mol/L sodium nitroprusside, ANG II at the range of 10(-7) to 10(-5) mol/L caused prompt, dose-related, significant (P<.01) contraction. It induced a maximum contraction (29.9%+/-5.2% [mean+/-SE]) at 10(-6) mol/L. This effect lasted at least 10 minutes. Angiotensin II receptor antagonist saralasin (10(-6) mol/L) abolished the contractile effect of ANG II (10(-6) mol/L), although by itself it did not affect the contractile tone. CONCLUSIONS: Angiotensin II contracts cultured pericytes through saralasin-sensitive ANG II receptors. If ANG II affects the contractile tone of pericytes in vivo, it may affect capillary caliber, resistance, and blood flow.

Angiotensin I↗
PubMed1997

Nitric oxide inhibits neutrophil beta 2 integrin function by inhibiting membrane-associated cyclic GMP synthesis.

The aim of this investigation was to identify the mechanism by which nitric oxide inhibits neutrophil beta 2 integrin dependent adherence. Isolated rat neutrophils from blood and peritoneal exudates were exposed for 2 min to nitric oxide generated by diethylamine-NO at rates between 1.6 and 138 nmol/min. Exposure to nitric oxide at rates less than 14 nmol/min had no effect on adherence. Exposure to 14 to 56 nmol nitric oxide/min inhibited beta 2 integrin dependent adherence to endothelial cells, nylon columns, and fibrinogen-coated plates, but higher concentrations had no significant effect on adherence. Adherence by beta 2 integrins could be restored by incubating cells with dithioerythritol, phorbol 12-myristate 13-acetate, or 8-bromo cyclic GMP. Elevations in cellular cyclic GMP concentration were associated with adherence, but this did not occur after cells were exposed to concentrations of nitric oxide that inhibited beta 2 integrin-dependent adherence. Elevations in cyclic GMP did occur after cells were incubated with dithioerythritol or phorbol 12-myristate 13-acetate. Concentrations of nitric oxide that inhibited beta 2 integrin-dependent adherence also inhibited catalytic activity of membrane associated guanylate cyclase and binding of atrial natriuretic peptide, but were insufficient to activate cytosolic guanylate cyclase. Nitric oxide did not inhibit neutrophil oxidative burst or degranulation, nor effect beta 2 integrin expression or adherence that did not depend on beta 2 integrins, nor cause oxidative stress identified in terms of cellular glutathione concentration or protein nitrotyrosine. The results indicate that nitric oxide inhibited beta 2 integrins in a concentration-dependent fashion by inhibiting cell-surface transduction of signals linked to the activity of membrane-bound guanylate cyclase. The inhibitory effect could be overcome by providing cells with cyclic GMP exogenously or by stimulating cytosolic guanylate cyclase.

Animals↗
PubMed1997

Interactions between macrophages and oxidized low density lipoprotein in the presence of type I collagen.

In order to investigate the influence of collagen on the interactions between macrophages and oxidatively modified low density lipoprotein (ox-LDL), type I collagen was isolated from rat tail tendon and prepared as a gel. The binding of 125I-ox-LDL, 125I-malondialdehyde (MDA)-LDL and 125I-acetyl-LDL to collagen was higher but the binding of 125I-4-hydroxynonenal (HNE)-LDL was lower than that of native 125I-LDL. When mouse peritoneal macrophages were cultivated on this collagen gel, most of the modified LDL was bound to the collagen gel rather than taken up by macrophages. The amount of modified 125I-LDL degraded by the macrophages decreased in the presence of the collagen gel. In the absence of gel a similar degree of reduction in degradation of modified 125I-LDL by macrophages was obtained when the cells were treated with cytochalasin D, an inhibitor of non-specific phagocytosis. However, the treatment of the macrophages cultivated on the collagen gel with cytochalasin D did not influence the degradation of 125I-ox-LDL and 125I-HNE-LDL. These results suggest that the uptake of ox-LDL by macrophages grown on collagen gel is primarily mediated via the scavenger receptors pathway, whereas in the absence of collagen also other mechanisms of uptake are operating.

Animals↗
PubMed1997

Co-expression and regulation of Met and Ron proto-oncogenes in human hepatocellular carcinoma tissues and cell lines.

Met and ron proto-oncogenes encode the cell surface receptors for hepatocyte growth factor (HGF) and hepatocyte growth factor-like (HLP) protein, respectively, and induce mitogenesis, motogenesis, morphogenesis, and metastatic activity in various cell types. Overexpression of met in human carcinoma has been reported by several groups including ours; however, the mechanisms that control met gene expression are thus far unclear. The present study focuses on the expression and regulation of the Met and Ron receptors in human hepatocellular carcinoma (HCC). We report here that abnormal expression of met and ron proteins occurs in some cases of human HCC. Using several HCC cell lines as a model system, we show that HGF, as well as other cytokines, such as epidermal growth factor (EGF), interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha), induce met and ron expression. Using several chimeric constructs consisting of various lengths of the met promoter region fused to the reporter gene of chloramphenicol acetyl transferase (CAT), and by performing transient transfection of these constructs into HepG2 cells, we show that induction of met gene expression by HGF and other cytokines is, at least in part, through up-regulation of met gene promoter activity. The DNA region conferring responsiveness to cytokine induction was located within 0.2 kb of the met core promoter. Interestingly, EGF did not stimulate met promoter activity in any of the met-CAT chimeric constructs. These results provide evidence that met and ron are modulated in the liver by a similar cytokine network. In the case of met expression, the 0.2-kb region in the met gene promoter may play an important role in mediating its gene induction in response to HGF and other cytokines. Our results also suggest that unregulated expression of met and ron may be associated with pathological conditions, such as HCC, in the liver.

Animals↗
PubMed1997

STAR-HASTE: perfusion imaging without magnetic susceptibility artifact.

A novel magnetic resonance imaging technique (STAR-HASTE) based on pulsed arterial spin labeling using a single shot acquisition method is described for perfusion imaging. The method is similar to EPISTAR in using STAR (Signal Targeting with Alternating Radiofrequency) technique for pulsed radiofrequency labeling of inflowing blood, but uses a half-Fourier single shot turbo spin-echo (HASTE) sequence for data acquisition instead of echo-planar imaging (EPI). Our preliminary studies show that STAR-HASTE permits perfusion imaging to be performed without many of the artifacts encountered with other imaging methods based on EPI acquisition. The novel method not only provides similar perfusion information to that obtained by EPISTAR, as demonstrated in the functional brain imaging study, but also eliminates magnetic susceptibility artifacts and image distortion commonly observed in EPI images. Furthermore, this technique can be readily implemented in MR systems without EPI capability.

Artifacts↗
PubMed1997

Half-Fourier BURST imaging on a clinical scanner.

A modified BURST imaging technique with a nearly twofold reduction in acquisition time, improved signal-to-noise ratio and clear improvement of the image quality is introduced. The method applies half-Fourier reconstruction and can be implemented on a standard clinical scanner. This approach allows the collection of single-shot magnetization prepared images of the human brain with a matrix size of 112 x 128 within 86-250 ms. The signal-to-noise properties of the pulse sequence are analyzed and compared with a standard BURST experiment.

Brain↗
PubMed1997

Age-dependent differences in survival of striatal somatostatin-NPY-NADPH-diaphorase-containing interneurons versus striatal projection neurons after intrastriatal injection of quinolinic acid in rats.

Some authors have reported greater sparing of neurons containing somatostatin (SS)-neuropeptide Y (NPY)-NADPH-diaphorase (NADPHd) than projection neurons after intrastriatal injection of quinolinic acid (QA), an excitotoxin acting at NMDA receptors. Such findings have been used to support the NMDA receptor excitotoxin hypothesis of Huntington's disease (HD) and to claim that intrastriatal QA produces an animal model of HD. Other studies have, however, reported that SS/NPY/NADPHd interneurons are highly vulnerable to QA. We examined the influence of animal age (young versus mature), QA concentration (225 mM versus 50 mM), and injection speed (3 min versus 15 min) on the relative SS/NPY/NADPHd neuron survival in eight groups of rats that varied along these parameters to determine the basis of such prior discrepancies. Two weeks after QA injection, we analyzed the relative survival of neurons labeled by NADPHd histochemistry, SS/NPY immunohistochemistry, or cresyl violet staining (which stains all striatal neurons, the majority of which are projection neurons) in the so-called lesion transition zone (i.e., the zone of 40-60% neuronal survival). We found that age, and to a lesser extent injection speed, had a significant effect on relative SS/NPY/NADPHd interneuron survival. The NADPHd- and SS/NPY-labeled neurons typically survived better than projection neurons in young rats and more poorly in mature rats. This trend was greatly accentuated with fast QA injection. Age-related differences may be attributable to declines in projection neuron sensitivity to QA with age. Since rapid QA injections result in excitotoxin efflux, we interpret the effect of injection speed to suggest that brief exposure to a large dose of QA (with fast injection) may better accentuate the differential vulnerabilities of NADPHd/SS/NPY interneurons and projection neurons than does exposure to the same total amount of QA delivered more gradually (slow injection). These findings reconcile the discordant results found by previous authors and suggest that QA injected into rat striatum does reproduce the neurochemical traits of HD under some circumstances. These findings are consistent with a role of excitotoxicity in HD pathogenesis, and they also have implications for the basis of the more pernicious nature of striatal neuron loss in juvenile onset HD.

Aging↗
PubMed1997

Effect of oxygen on relaxation of retinal pericytes by sodium nitroprusside.

BACKGROUND: This study addresses whether oxygen modulates the relaxation induced in retinal pericytes by sodium nitroprusside (SNP), a nitric oxide (NO) donor that stimulates the NO/guanylate cyclase pathway. METHODS: Bovine retinal pericytes were cultured on silicone. On the silicone surface, basal pericyte contractile tone induces wrinkles. Drug-induced changes in pericyte contractile tone were assessed by changes in the number of wrinkles. The effects of 100% nitrogen (hypoxia) and 100% oxygen (hyperoxia) were studied on: (a) the basal tone of quiescent pericytes, (b) the relaxation to 3 and 10 microM SNP or 1 microM forskolin, and (c) the recontraction that followed the washout of 3 microM SNP or 1 microM forskolin. RESULTS: Neither hypoxia nor hyperoxia had any apparent influence on pericyte basal tone, on forskolin-induced relaxation, or on pericyte recontraction after a forskolin-induced relaxation. In hypoxia, relaxations to SNP 3 microM (P < 0.05) and 10 microM (P < 0.01) were significantly more pronounced than in hyperoxia. Hypoxia also reduced the recontraction after an SNP-induced relaxation (P < 0.001). CONCLUSION: Oxygen modulates the relaxation of bovine retinal pericytes evoked by SNP (guanylate cyclase-mediated), but not the relaxation induced by forskolin (adenylate cyclase-mediated). These results suggest that in the retinal capillary circulation an interaction between oxygen and the NO/guanylate cyclase pathway modulates pericyte tone, and thus potentially blood flow.

Animals↗
PubMed1997

Determination of bromine and iodine in normal tissues from Beijing healthy adults.

The contents of bromine and iodine in samples of heart, liver, spleen, lung, muscle, and hair from healthy adults living in Beijing, China, were determined using epithermal neutron activation analysis. The results indicate that the contents of bromine in lung and iodine in liver are higher than those in other tissues, except human hair. The bromine contents in Beijing human tissues are significantly lower than those in other countries. The contents of iodine are slightly lower than those in other countries, but the difference is not significant. Three biological standard reference materials were simultaneously determined with the samples, and our results agree well with the certified values.

Adult↗
PubMed1997

Parametric imaging of patient pharmacokinetics.

This paper presents an approach to extracting patient pharmacokinetic information from a set of longitudinal scintigraphic images and representing the kinetic information in parametric image form. In this approach, three or four pairs of simultaneously acquired anterior and posterior images, for internal dosimetry with iodine-131, are obtained at 24-h intervals. Each pair of anterior and posterior images is converted to a "conjugate-view" image. The sequential conjugate-view images are then spatially registered to each other using a symmetric phase-only matched filter technique. With the registered images, the value at each pixel location, over time, is fitted to a monoexponential function. The resulting decay constant and intercept parameters are then represented as "decay-constant" and "intercept" images. Further analytical integration of the exponential function results in a "cumulated-activity" image. Phantom studies demonstrated that the proposed method is accurate and reliable in the registration and kinetic data extraction of the longitudinal images. Clinical application of the approach to patients with thyroid carcinoma showed that regions of rapid uptake or clearance that would not otherwise be highlighted were easily identified and some regions with unexpected kinetics were observed. It is concluded that decay-constant, intercept, and cumulated-activity images provide a rapid and comprehensive visual assessment of patient pharmacokinetics. The technique may have a greater impact on the care of patients with extensive and distributed disease.

Algorithms↗
PubMed1997

Gallbladder relaxation in patients with pigment and cholesterol stones.

BACKGROUND & AIMS: Gallbladders with cholesterol stones show a defective contraction in response to agonists. The aim of this study was to investigate the muscle relaxation of human gallbladders with cholesterol or black pigment gallstones. METHODS: Gallbladder relaxation was measured in vitro using muscle strips and single muscle cells. Relaxation was expressed as percent inhibition of either basal active tension in strips or maximal cell contraction induced by diacylglycerol. The production of cyclic nucleotides was determined using a 125I-labeled radioimmunoassay kit. RESULTS: Frequency-dependent relaxation evoked by electrical field stimulation was significantly lower in gallbladders with cholesterol stones than in gallbladders with pigment stones. Relaxation and adenosine 3',5'-cyclic monophosphate (cAMP) production induced by isoproterenol, vasoactive intestinal peptide, and forskolin were also significantly decreased in gallbladders with cholesterol stones. However, the relaxation in response to 8-bromo-cAMP, nitric oxide (NO), and the NO donor S-nitroso-N-acetylpenicillamine (SNAP), which circumvent plasma membrane receptors and directly activate intracellular mechanisms, was similar in gallbladders with cholesterol and pigment stones. Guanosine 3',5'-cyclic monophosphate production induced by NO and SNAP was also similar. CONCLUSIONS: Human gallbladder muscle from specimens with cholesterol stones show an impaired relaxation and lower cAMP production compared with specimens with pigment stones. The muscle defect(s) responsible for this impairment seem to be in the plasma membranes.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Localization of V1a vasopressin receptor mRNA expression in cultured neurons, astroglia, and oligodendroglia of rat cerebral cortex.

Previous studies suggested the existence of V1a vasopressin receptors (V1aR) in the cerebral cortex. Here, we investigated the cellular and regional localization of V1aR in the E18 rat cerebral cortex using RT-PCR and Southern blot analysis of V1aR mRNA derived from enriched cultures of neurons, astroglia, and oligodendroglia from four cortical regions (rostral, caudal, dorsal and ventral). V1aR mRNA was detected in each of the cell types within each of the regions studied. These data indicate that V1aR is broadly distributed throughout the cerebral cortex and suggest that vasopressin plays an important role in cortical functions.

Animals↗
PubMed1997

A comparison of the kinetics of low-density lipoprotein oxidation initiated by copper or by azobis (2-amidinopropane).

This article describes the kinetics of low density lipoprotein (LDL) oxidation catalyzed by azobis (2-amidinopropane) dihydrochloride, ABAP, or by copper. The LDLs were isolated from nonhuman primates fed diets enriched in one of three types of fatty acids: saturated fatty acids, monounsaturated fatty acids, predominantly, oleic acid, or polyunsaturated fatty acids, predominantly linoleic acid. Oxidation was followed by monitoring the formation of conjugated diene hydroperoxides from polyunsaturated fatty acids (PUFA). For both copper and ABAP-initiated oxidation, the rate of LDL oxidation depended on the concentrations of initiator, PUFA, and LDL. Except for the dependence on PUFA concentration the rate of LDL oxidation was not directly influenced by the fatty acid composition of the LDL particle. The two initiators had very different dependence on initiator concentration. Because LDL particles are essentially small, lipid-rich droplets, the kinetic descriptions of LDL oxidation assumed: (1), that there was only one chain per particle, and (2) that the radical chain was terminated when a second radical either entered or was formed in the particle. When two LDL samples having very different lag times were mixed, the oxidation profile was bimodal. This finding demonstrated that the oxidation of native LDL particles was independent of the oxidation state of the other native LDL particles in solution, i.e., LDL particles do not rapidly exchange radicals, for example, hydroperoxyl radicals. Oxidation initiated by ABAP was proportional to [ABAP]0.5, suggesting that hydroperoxyl radical recombination between the lipid hydroperoxyl radical and the ABAP-hydroperoxyl radical was the chain-terminating step. The reciprocal of the rate of copper oxidation was linearly related to the reciprocal copper concentration, demonstrating that the binding of copper to LDL was necessary to initiate oxidation. This binding constant showed considerable variability among LDL samples. The kinetic descriptions of LDL oxidation reflect the differences in the mechanisms of initiation and termination.

Amidines↗
PubMed1997

Accurate assessment of mitral valve area in patients with mitral stenosis by three-dimensional echocardiography.

The accuracy of measurements of mitral valve orifice area (MVA) from three-dimensional echocardiographic (3DE) image data sets obtained by a transthoracic or transesophageal rotational imaging probe was studied in 15 patients with native mitral stenosis. The smallest MVA was identified from a set of eight parallel short-axis cut planes of the mitral valve between the anulus and the tips of leaflets (paraplane echocardiography) and measured by planimetry. In addition, MVA was measured from the two-dimensional short-axis view (2DE). Values of MVA measured by 3DE and 2DE were compared with those calculated from Doppler pressure half-time (PHT) as a gold standard. Observer variabilities were studied for 3DE. MVA measured from PHT ranged between 0.55 and 3.19 cm2 (mean +/- SD 1.57 +/- 0.73 cm2), from 3DE between 0.83 and 3.23 cm2 (mean +/- SD 1.55 +/- 0.67 cm2), and from 2DE between 1.27 and 4.08 cm2 (mean +/- SD 1.9 +/- 0.7 cm2). The variability of intraobserver and interobserver measurements for 3DE measurements was not significantly different (p = 0.79 and p = 0.68, respectively); for interobserver variability, standard error of the estimate = 0.25. There was excellent correlation, close limits of agreement (mean difference +/- 2 SD), and nonsignificant differences between 3DE and PHT for MVA measurements (r = 0.98 [0.02 +/- 0.3] and p = 0.6), respectively. There was moderate correlation, wider limits of agreement, and significant difference between 2DE and PHT for MVA measurements (r = 0.89 [0.32 +/- 0.66] and p = 0.002), respectively. This may be related to the difficulties in visualization of the smallest orifice in precordial short-axis views. This study suggests that three-dimensional image data sets, by providing the possibility of "computer slicing" to generate equidistant parallel cross sections of the mitral valve independently from physically dictated ultrasonic windows, allow accurate and reproducible measurement of the MVA.

Adult↗
PubMed1997

Solid-state variable-temperature 1H MAS NMR studies on deuterated polyethylene.

Solid-state variable-temperature/magic angle spinning (VT/MAS) 1H NMR measurements were carried out on deuterated polyethylene. From these experimental results it was found that the 1H chemical shift induced by conformational and morphological changes of the polyethylene sample is within the linewidth of approximately 0.5 ppm. Furthermore, from MAS/dipolar decoupling experiments it was found that the resonance frequency of the proton varies linearly with the inverse square of the deuterium decoupling power. This experimental finding is discussed theoretically.

Deuterium↗
PubMed1997

v-Abl protein tyrosine kinase (PTK) mediated suppression of apoptosis is associated with the up-regulation of Bcl-XL.

We demonstrated previously that the activation of v-Abl protein tyrosine kinase (PTK) in IC.DP murine pre-mast cells resulted in suppression of apoptosis after withdrawal of interleukin 3 (IL-3), that protein kinase C (PKC) translocated to the nucleus 6 h after v-Abl PTK activation and that inhibition of PKC restored apoptosis after IL-3 deprivation in the presence of v-Abl PTK activity. Here we demonstrate that v-Abl PTK activation is followed by an approximately twofold increase in mRNA level of Bcl-XL by 6 h and a corresponding increase in Bcl-XL protein level by 24 h. Bcl-xL RNA and protein decreased in IL-3 deprived cells in the absence of v-Abl PTK activity. Exposure of cells with v-Abl PTK active to the PKC inhbitor calphostin C (125 ng/ml) prevented the increase in Bcl-xL protein and resulted in apoptosis. No changes in Bax or Bcl-2 protein level were noted after IL-3 withdrawal and/or activation of v-Abl PTK. Bak was barely detectable and Bad protein level decreased in cells undergoing apoptosis. The data suggest that suppression of apoptosis by v-Abl PTK in the absence of IL-3 is associated with PKC signalling and the upregulation of Bcl-xL in IC.DP cells.

Animals↗