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Biomedical subjects

Q Ma

Publications and source records attributed to Q Ma.

At least 19 recordsLinked to original sources
PubMed2001

TCDD-inducible poly(ADP-ribose) polymerase: a novel response to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes pleotropic effects in mammalian species through modulating gene expression. Here we analyzed TCDD-induced mRNA expression by using mRNA differential display and report the cloning of a novel TCDD-inducible poly(ADP-ribose) polymerase (TiPARP). TiPARP cDNA contains an open reading frame of 657 amino acid residues; the carboxyl half shares sequence similarity to the catalytic domain of PARP, a family of enzymes that catalyze poly ADP-ribosylation of proteins. Expression of the cDNA by in vitro transcription/translation reveals a protein of approximately 75 kDa. The expressed TiPARP exhibits PARP activity toward histone. TiPARP is highly homologous to RM1 which is induced during long-term potentiation, a memory formation process, and to TIL which is induced in T cells infiltrating progressing tumors. TiPARP mRNA is expressed in a broad range of mouse tissues. Together, these data demonstrate that TiPARP is a novel target of TCDD that may contribute to multiple responses to TCDD by modulating protein function through poly ADP-ribosylation.

Amino Acid Sequence↗
PubMed2001

[Association between DLST gene polymorphism and Alzheimer's disease].

OBJECTIVE: To investigate the association between the polymorphic alleles of dihydrolipoamide succinyltransferase (DLST) gene cDNA at position A19117G in intron 13 and C19183T in exon 14 and the risk for sporandic Alzheimer's disease (SAD). METHODS: The polymorphism of DLST gene was detected using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) techniques in 105 patients with sporadic Alzheimer disease and 109 normal controls. RESULTS: The frequency of AT/AC genotype was found to be significantly higher in SAD patients (21%) than in controls (10%) with an odds ratio of 2.36 (P < 0.05). The frequencies of AC/AC, AT/AT genotypes and AC allele were slightly decreased in cases with SAD as compared with controls. While the frequencies of the GC/GC genotype and GC allele were slightly higher in SAD patients than in controls. However, these differences were not statistically significant (P > 0.05). CONCLUSION: The AT/AC genotype of DLST gene is associated with an increased risk for SAD.

Acyltransferases↗
PubMed2001

Formation of brainstem (nor)adrenergic centers and first-order relay visceral sensory neurons is dependent on homeodomain protein Rnx/Tlx3.

Brainstem visceral sensory and (nor)adrenergic neurons play crucial roles in modulating cardiovascular and respiratory functions. The origins and formation of these neurons are poorly understood. Here we show that these two classes of neurons are derived from Mash1-positive precursor cells, and can be prospectively identified by combinatorial expression of two homeobox genes, Rnx and Phox2 (Phox2a or Phox2b). It was previously shown that Rnx-deficient mice die from respiratory failure. Here we show that Rnx function is required for formation of first-order relay visceral sensory neurons in the brainstem. In addition, as in Phox2b-deficient mice, the development of most (nor)adrenergic centers is compromised in Rnx mutants. We also provide genetic evidence to show that Rnx and Phox2 proteins may function independently to specify the (nor)adrenergic phenotype. Our studies reveal a surprising ontogenetic relationship between relay visceral sensory and (nor)adrenergic neurons, and suggest that it may be a common theme in the developing nervous system that the same set of transcriptional regulators is associated with formation of multiple components within a neuronal network.

Animals↗
PubMed2001

Inhibition of tissue factor-activated platelets by low-molecular-weight heparins and glycoprotein IIb/IIIa receptor antagonist.

Thrombotic disorders can lead to vascular distress and platelet activation eventually resulting in the rupture of the lesions where a sizable amount of tissue factor (TF) is generated during the pathogenesis of arterial diseases. Since low-molecular-weight heparins (LMWHs) and platelet glycoprotein (GP) IIb/IIIa inhibitors are clinically used for the management of acute coronary syndrome (ACS), studies were taken to determine the effects of these agents on TF-mediated activation of platelets. Freshly drawn native whole blood (WB) from normal healthy volunteers (n = 6) supplemented with a predetermined amount of TF was incubated with equivalent anti-Xa adjusted amounts of various LMWHs at 0.01-1.0 U/ml and tirofiban from 10 to 100 ng/ml. Platelet activation was assessed by measuring the expression of P-selectin (CD62) and the generation of platelet aggregates. At 0.01 U/ml, enoxaparin exhibited a stronger inhibition of TF-induced platelet activation compared to ardeparin and dalteparin. At 0.1 U/ml, these LMWHs produced a comparable inhibition of total P-selectin expression, and at 1.0 U/ml, a marked inhibition was noted. Since enoxaparin produced the best concentration-dependent inhibition of P-selectin expression (saline: 76 +/- 10% vs. 1.0 U/ml enoxaparin: 18 +/- 7%; P < .02) and platelet aggregate formation (saline: 63 +/- 7% vs. 1.0 U/ml enoxaparin: 35 +/- 6%, P < .035), this agent was used for additional studies. Unlike enoxaparin, tirofiban produced a weak concentration-dependent inhibition of platelet activation. At 100 ng/ml, tirofiban produced a 40% inhibition of P-selectin expression and about 60% inhibition of platelet aggregate formation. To elucidate the potential interaction between tirofiban and enoxaparin, the effect of 10 and 100 ng/ml tirofiban was studied with enoxaparin-supplemented WB in a 0.01-1.0 U/ml range. Additive effects between these two agents were noted only at lower concentrations. Thus, at therapeutic concentrations (0.8-1.2 U/ml), enoxaparin itself was capable of inhibiting TF-mediated activation of platelets to > 70%; whereas tirofiban failed to produce such concentration-dependent inhibition. This suggests that the simultaneous administration of GPIIb/IIIa receptor antagonist with LMWH may not have any added benefit in the clinical management of patients with ACS.

Blood Platelets↗
PubMed2001

Evaluation of propargyl bromide for control of barnyardgrass and Fusarium oxysporum in three soils.

With the scheduled phasing out of methyl bromide, there is an urgent need for alternatives. We evaluated the efficacy of propargyl bromide as a potential replacement for methyl bromide for the control of barnyardgrass (Echinochloa crus-galli) and Fusarium oxysporum in an Arlington sandy loam, a Carsitas loamy sand and a Florida muck soil. Soil was mixed with barnyardgrass seeds or F oxysporum colonized on millet seeds, and treated with propargyl bromide at a range of concentrations. The mortality of the fungi and weed seeds was determined after 24 h of exposure at 30 degrees C. The concentrations required to inhibit 50% barnyard seed germination (LC50) were 2.8, 2.4 and 48.5 micrograms g-1 in the sandy loam, loamy sand and muck soil, respectively. In contrast, the LC50 values for F oxysporum were 11.2, 10.8 and 182.1 micrograms g-1 in the sandy loam, loamy sand and muck soil, respectively. The low efficacy of propargyl bromide in the muck soil was a result of the rapid degradation and high adsorption of the compound in the soil. The degradation half-life (t1/2) was only 7 h in the muck soil at an initial concentration of 6.8 micrograms g-1, compared to 60 and 67 h in the sandy loam and loamy sand, respectively. The adsorption coefficients (Kd) were 0.96, 0.87 and 5.6 cm3 g-1 in the sandy loam, loamy sand and muck soil, respectively. These results suggest that registration agencies should consider site-specific properties in recommending application rates for propargyl bromide.

Adsorption↗
PubMed2001

Dependence of papanicolaou gradings of exfoliated urothelial cells upon GSTM1 and GSTT1 polymorphism in benzidine-exposed workers of the Shanghai dye industry.

The distribution of the polymorphic alleles of the genes coding for glutathione S-transferases (GSTs) M1 and T1 was compared with the results of cytological grading of exfoliated urothelial cells (Pap test) in a non-diseased high-risk group of workers formerly exposed to benzidine in the Shanghai dyestuff industry (n = 317). All subjects were genotyped for GSTT1 and M1 gene polymorphism by allele-specific PCR. Individuals were stratified according to their job and duration of exposure. A subgroup of 78 individuals with cytological gradings of grade III or higher in the Pap test showed a significant under-representation of the combination of GSTT1 0/0 and M1 0/0 genotypes compared with 238 subjects with a cytological classification lower than grade III (OR 0.55, 95% CI 0.31-0.98. P=0.04). These results suggest that neither the GSTM1 0/0 or GSTT1 0/ 0 genotype alone nor their combination had a clear association with cytopathological changes in exfoliated urothelial cells from individuals previously exposed to benzidine in Shanghai. This contradicts the results of studies indicating that the GSTM1 0/0 genotype is associated with an increased risk for bladder cancer in the general population, mostly outside China.

Adult↗
PubMed2001

The study of spectrosgraphic properties and molecular recognition of cali.

The absorption spectrum and fluorescence spectrum of calix[n]arenes are studied systematically. The self-association of calix[n]arenes is proposed and the self-association constant is also obtained. The recognition properties of calix[n]arenes are studied and the inclusion constant is calculated.

Calixarenes↗
PubMed2001

Global anticoagulant effects of a novel sulfated pentomanan oligosaccharide mixture.

PI-88 is a potent antiproliferative agent, which is developed for various indications in cancer. This agent is obtained from yeast fermentation and is primarily composed of pentamannose and tetramannose oligosaccharide units. PI-88 is capable of producing anticoagulant effects, which are mediated by heparin cofactor II. The purpose of this study was to determine the anticoagulant properties of PI-88 in native whole blood, freshly drawn from human volunteers, supplemented with PI-88 at various concentrations (0-100 microg/mL). Whole blood activated clotting time (ACT) was measured using Hemochron instruments. PI-88 produced a strong anticoagulant effect at 100 microg/mL (479.0+/-59.5 sec). This anticoagulant effect was comparable to that observed in interventional cardiology and open-heart surgery. At the lower level, PI-88 produced concentration-dependent effects on ACT. Using thromboelastographic techniques (TEG), the effect of PI-88 was measured in terms of various parameters. PI-88 produced potent anticoagulant effects in the TEG studies. At the concentration of 25 microg/mL, it produced a complete anticoagulant effect in whole blood. Whole blood samples supplemented with PI-88 showed a concentration-dependent decrease in the generation of various markers of clotting activation. These results clearly suggest that PI-88 exerts an anticoagulant effect in whole blood. Because of the low-molecular-weight nature and a novel mechanism of action, this new drug may be considered for further development, particularly in cancer patients.

Anticoagulants↗
PubMed2001

Induction of CYP1A1. The AhR/DRE paradigm: transcription, receptor regulation, and expanding biological roles.

The CYP1A1 gene encodes microsomal cytochrome P4501A1 that catalyzes the metabolism of many xenobiotics, including the oxygenation of polycyclic aromatic hydrocarbons (PAH). Induction of CYP1A1 enhances the metabolism of PAHs, and therefore, represents an adaptive response to chemical exposure in mammalian cells. Mechanistic studies reveal an AhR/DRE paradigm for the induction, which involves activation of the aryl hydrocarbon receptor (AhR) by an agonist, dimerization of AhR with the Ah recceptor nuclear translocator (Arnt), followed by binding of the AhR/Arnt heterodimer to the dioxin-responsive enhancer (DRE) and transcription of the gene. The AhR mediated transcription is tightly regulated through, at least, two mechanisms: (a) the cytoplasmic AhR interacts with hsp90 and an immunophilin chaperone AIP for proper folding and receptivity, and (b) the agonist-activated, nuclear AhR is degraded through the ubiquitin-26S proteasome mediated protein turnover, such that the transcription by AhR is controlled at a physiologically adequate level. In addition to CYP1A1 induction, AhR mediates a broad range of biological responses to CYP1A1 inducers, typified by the environmental contaminant dioxin, via modulating gene expression. Thus, mechanistic studies of CYP1A1 induction have provided insights into P450 induction, PAH carcinogenesis, dioxin action, AhR function, and receptor-mediated mammalian gene expression.

Animals↗
PubMed2001

Gas exchange by pods and subtending leaves and internal recycling of CO(2) by pods of chickpea (Cicer arietinum L.) subjected to water deficits.

Terminal drought markedly reduces leaf photosynthesis of chickpea (Cicer arietinum L.) during seed filling. A study was initiated to determine whether photosynthesis and internal recycling of CO(2) by the pods can compensate for the low rate of photosynthesis in leaves under water deficits. The influence of water deficits on the rates of photosynthesis and transpiration of pods and subtending leaves in chickpea (cv. Sona) was investigated in two naturally-lit, temperature-controlled glasshouses. At values of photosynthetically active radiation (PAR) of 900 micromol m(-2) s(-1) and higher, the rate of net photosynthesis of subtending leaves of 10-d-old pods was 24 and 6 micromol m(-2) s(-1) in the well-watered (WW) and water-stressed (WS) plants when the covered-leaf water potential (Psi) was -0.6 and -1.4 MPa, respectively. Leaf photosynthesis further decreased to 4.5 and 0.5 micromol m(-2) s(-1) as Psi decreased to -2.3 and -3.3 MPa, respectively. At 900--1500 micromol m(-2) s(-1) PAR, the net photosynthetic rate of 10-d-old pods was 0.9-1.0 micromol m(-2) s(-1) in the WW plants and was -0.1 to -0.8 micromol m(-2) s(-1) in the WS plants. The photosynthetic rates of both pods and subtending leaves decreased with age, but the rate of transpiration of the pods increased with age. The rates of respiration and net photosynthesis inside the pods were estimated by measuring the changes in the internal concentration of CO(2) of covered and uncovered pods during the day. Both the WW and WS pods had similar values of internal net photosynthesis, but the WS pods showed significantly higher rates of respiration suggesting that the WS pods had higher gross photosynthetic rates than the WW pods, particularly in the late afternoon. When (13)CO(2) was injected into the gas space inside the pod, nearly 80% of the labelled carbon 24 h after injection was observed in the pod wall in both the WW and WS plants. After 144 h the proportion of (13)C in the seed had increased from 19% to 32% in both treatments. The results suggest that internal recycling of CO(2) inside the pod may assist in maintaining seed filling in water-stressed chickpea.

Carbon Dioxide↗
PubMed2001

Alterations in the adhesion behavior of osteoblasts by titanium particle loading: inhibition of cell function and gene expression.

Total joint replacement prostheses are required to withstand corrosive environments and sustain millions of loading and articulation cycles during their term of implantation. Wear debris generation has been implicated as one of the primary causes of periprosthetic osteolysis and subsequent implant loosening in total joint replacements. Particulate debris consisting of metals, polyethylene, ceramics, and bone cement have each been shown to provoke a biological response in joint tissues. The major cell types within the interfacial granulomatous fibrous tissues consist of fibroblasts, macrophages, lymphocytes, and foreign-body giant cells. Osteoblasts are one of the principal cell types in the bone tissue adjacent to prostheses, maintaining physiologic bone remodeling through the balanced coordination of bone formation and resorption in concert with osteoclasts. To date the phenomenon of osteoblast phagocytosis of titanium particles has been suggested, but has not been sufficiently studied or confirmed. This study seeks to clarify the influence of titanium particles on osteoblast adhesion, deformability, proliferation, and gene expression profile. These studies were accomplished by performing biorheological testing, Northern blot analysis and RNase protection assay. The uptake of metallic particles by the osteoblast resulted in a particle-filament complex formation, which induced a series of variations in cell function. Understanding these variations is critical to expanding our knowledge of implant loosening and elucidating the nature of prosthetic joint failure. This study suggests that the impact of titanium particles on osteoblast function and subsequent implant loosening may have been previously underestimated.

Actin Cytoskeleton↗
PubMed2001

[Correlation between enhanced anoxic tolerance induced by hypoxic preconditioning and the stability of mitochondrial membrane potential in cultured hypothalamic cells].

The relationship between enhanced anoxic tolerance induced by hypoxic preconditioning and mitochondrial membrane potential (MMP) was studied in cultured hypothalamic cells. Dynamic changes in MMP were monitored by confocal laser scanning microscopy and expression of B-cell lymphoma/leukemia-2 (bcl-2) was examined by flowcytometry. Hypoxic preconditioning increased the cell survival rate and decreased the lactate dehydrogenase leakage under acute anoxia, in addition to maintaining MMP at a relatively higher level and inducing bcl-2 overexpression during anoxia. The results suggest that hypoxic preconditioning can enhance the tolerance of hypothalamic cells to anoxia, and the underlying mechanism may be related to increased stability of MMP. Overexpression of bcl-2 induced by hypoxic preconditioning may play a role in sustaining the stability of MMP.

Animals↗
PubMed2001

[Suppression of glutamate neurotoxicity by 5-HT in hippocampal neurons].

The effects of excess glutamate on the survival rate of cultured hippocampal neurons, the population spike (PS) of CA1 area of hippocampal slices and the Ca(2+) current of hippocampal neurons were observed in rats. Decreased survival rate of hippocampal neurons in the presence of excess glutamate was partially reversed by 5-HT, which was in association with a less decrease of PS magnitudes. The Ca(2+) inward current induced by glutamate was significantly diminished in the presence of 5-HT. It is suggested that 5-HT can inhibit excess glutamate-induced neurotoxicity by suppressing the glutamate triggered calcium influx.

Animals↗
PubMed2001

[Construction of plasmid gene bank of V. cholerae O139 and detection of O-antigen genes].

Because O-antigen biosynthesis genes are a tandem gene cluster. Gnomic fragments of 4-20 kilobases (kb) were obtained by digesting genomic DNA of V. cholerae O139 with restriction endonuclease EcoRI, then plasmid gene bank was constructed. Recombinant colony, E. coli DH5 alpha (pMG320), expressing O-antigen of V. cholerae O139 was detected from the bank by immunological agglutinative reaction. The futher analysis showed O-antigen expressed by recombinant colony had both immunogenicity and reactogenicity, and the size of O-antigen biosynthesis genes was about 4.6 kb.

DNA, Bacterial↗
PubMed2000

Superinduction of CYP1A1 gene expression. Regulation of 2,3,7, 8-tetrachlorodibenzo-p-dioxin-induced degradation of Ah receptor by cycloheximide.

Cycloheximide superinduces the transcription of CYP1A1 in the presence of an agonist for the Ah receptor (AhR). To investigate the molecular target for "superinduction," we analyzed the agonist-induced degradation of AhR. Whereas 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent agonist of AhR, induces a rapid reduction of the AhR protein, cycloheximide blocks the down-regulation of steady state AhR. Analyses of the turnover of AhR reveal that cycloheximide blocks the shortening of the half-life of AhR by TCDD. Blocking of the TCDD-induced AhR degradation requires inhibition of protein synthesis, because (a) cycloheximide inhibits protein synthesis at the concentration at which it causes superinduction and inhibition of AhR degradation; and (b) puromycin, an inhibitor of protein synthesis by mimicking aminoacyl-tRNA, also blocks the TCDD-induced AhR degradation. The blocking of the TCDD-induced AhR degradation correlates with the superinduction of CYP1A1 gene expression in a time- and dose-dependent manner. Furthermore, cycloheximide is shown to increase the accumulation of the TCDD-activated AhR and the functional AhR x Arnt complex in nucleus. Collectively, our results reveal a mechanism of superinduction by cycloheximide by enhancing the stability of agonist-activated AhR. The finding that inhibition of protein synthesis blocks the TCDD-induced AhR turnover implicates a cycloheximide-sensitive, labile factor (designated as AhR degradation promoting factor, or ADPF) in controlling the removal of agonist-activated AhR in nucleus.

Animals↗
PubMed2000

2,3,7,8-tetrachlorodibenzo-p-dioxin-induced degradation of aryl hydrocarbon receptor (AhR) by the ubiquitin-proteasome pathway. Role of the transcription activaton and DNA binding of AhR.

Activation of the aryl hydrocarbon receptor (AhR) by 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent agonist of AhR, induces a marked reduction in steady state AhR. To analyze the mechanism of regulation of ligand-activated AhR, we examined the biochemical pathway and function of the down-regulation of the receptor by TCDD. Pulse-chase experiments reveal that TCDD shortens the half-life (t1/2) of AhR from 28 to 3 h in mouse hepatoma cells. Inhibitors of the 26 S proteasome, lactacystin and MG132, block the TCDD-induced turnover of AhR. The TCDD-induced degradation of AhR involves ubiquitination of the AhR protein, because (a) TCDD induces formation of high molecular weight, ubiquitinated AhR and (b) degradation of AhR is inhibited in ts20 cells, which bear a temperature-sensitive mutation in the ubiquitin-activating enzyme E1, at a nonpermissive temperature. Inhibition of proteasomal degradation of AhR increases the amount of the nuclear AhR.Arnt complex and "superinduces" the expression of endogenous CYP1A1 gene by TCDD, indicating that the proteasomal degradation of AhR serves as a mechanism for controlling the activity of the activated receptor. We also show that deletion of the transcription activation domain of AhR abolishes the degradation, whereas a mutation in the DNA-binding region of AhR or Arnt reduces the degradation; these data implicate the transcription activation domain and DNA binding in AhR degradation. Our findings provide new insights into the regulation of TCDD-activated AhR through ubiquitin-mediated protein degradation.

Animals↗
PubMed2000

Long-term fluoxetine produces behavioral anxiolytic effects without inhibiting neuroendocrine responses to conditioned stress in rats.

The aim of the present study was to investigate the anxiolytic effects of long-term treatment with fluoxetine in rats. Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, are used to treat anxiety and panic disorders, in addition to treating depression. A major concern with SSRIs is a 2-3-week delay in their therapeutic effects. SSRIs share with anxiolytic 5-HT(1A) agonists the ability to produce desensitization of post-synaptic 5-HT(1A) receptors. To investigate the anxiolytic effects of fluoxetine, rats were treated for 14 days with fluoxetine (10 mg kg(-1) day(-1), i.p. ). The rats were stressed using a conditioned stress procedure and tested one day after the last fluoxetine injection. Fluoxetine decreased stress-induced defecation (by 60%), reversed the stress-induced suppression of exploring behavior (by 59%) and shortened the duration of stress-induced freezing behavior (by 11. 5%). However, the stress-induced increase in plasma levels of ACTH, corticosterone, oxytocin, prolactin and renin were not inhibited by fluoxetine treatment. These findings suggest that neuroadaptive changes induced by sustained inhibition of serotonin (5-HT) reuptake, contribute to the mechanism of the anxiolytic effects of fluoxetine. In contrast, the neuroendocrine responses to conditioned stress are not affected by these neuroadaptive changes.

Adrenocorticotropic Hormone↗