Biomedical subjects

R Qiu

Publications and source records attributed to R Qiu.

At least 19 recordsLinked to original sources

PubMed2001

[Decomposition of aqueous sodium pentachlorophenolate (PCP-Na) by using TiO2 coating photocatalyst].

Titanium dioxide (TiO2) photocatalysts were coated on hollow glass beads by sodium silicate (Na2SiO3.9H2O) solution. The coated catalysts were characterized by BET, XRD. Their photoactivity were examined using photocatalytic degradation of sodium pentachlorophenolate(PCP-Na) and glucose solution. The impact of catalysts dosage, PCP-Na initial concentration, initial pH and oxygen concentration on reaction kinetics were also studied in detail. The experiments illustrated that the performance of C3-type catalysts was satisfactory. Conditions of the experiments were following: The initial concentration of PCP-Na and CODCr were 10 mg.L-1 and 400 mg.L-1, respectively, and illumination time was 2 hours and catalysts dosage was 2 g.L-1, the removal rates of CODCr and PCP-Na were above 65% and 92% respectively. Optimum dosage of C3-type catalysts was 2-2.5 g.L-1, DO was no less than 3 mg.L-1.

Catalysis↗

PubMed2001

[Trihalomethane formation potential (THMFP) of soils in Guangdong Province].

Trihalomethane formation potentials were analyzed with the lixivia of typical soil samples in Guangdong Province. The results showed that the bulk THMFP contents of soil lixivia (b-THMFP) range from 0.7 to 36.8 micrograms/g with a median value of 10.6 micrograms/g, and the THMFP contents of 0.45 micron filtered soil lixivia, representing the THMFP contents of dissolved organic matter (d-THMFP), from 0.5 to 21.2 micrograms/g with a median value of 3.9 micrograms/g. Sample 19 (Calcareous soil) had the highest b-THMFP and d-THMFP while sample 20 (Purple soil) had the lowest b-THMFP and sample 5 (Latored soil) had the lowest d-THMFP. In general, suspended organic matter had great contribution to the THMFP. The physico-chemical properties, such as organic matter contents and contents of various oxides, as well as soil genetic horizon and vegetation are main factors dominating the THMFP levels in the soil.

Soil Pollutants↗

PubMed2001

[Complexing mechanism on extraction of DHA ester using silver ion].

Ultraviolet spectra of docosahexaenoic acid (DHA) ester and its complex with silver ion were determined, and shifts of ultraviolet absorption peak before and after the complexing reaction were observed. Meanwhile, complexing bonds of DHA ester-silver ion were explained by molecular orbital theory. Thus, complex structure and complexing mechanism were discovered. The results showed that ultraviolet characteristic absorption peak of DHA ester-silver ion complex moved to lower wavelength. It pointed out that distance between energy levels for outer electron transition of complex is increased, and the energy for outer electron transition of complex is bigger than that of DHA ester.

Chelating Agents↗

PubMed2000

Synaptojanin 2, a novel Rac1 effector that regulates clathrin-mediated endocytosis.

The small GTPase Rac has been implicated in a wide range of cellular processes, including the organization of the actin cytoskeleton, transcriptional control and endocytic vesicle trafficking [1-3]. The signaling components that mediate these functions downstream of Rac largely remain to be identified. In this study, we have identified synaptojanin 2, a polyphosphoinositide phosphatase as a novel Rac1 effector. Synaptojanin 2 directly and specifically interacts with Rac1 in a GTP-dependent manner. Expression of constitutively active Rac1 caused the translocation of synaptojanin 2 from the cytoplasm to the plasma membrane. Both activated Rac1 and a membrane-targeted version of synaptojanin 2 inhibited endocytosis of the epidermal growth factor (EGF) and transferrin receptors, a process that is known to be dependent on polyphosphoinositide lipids. Endocytosis of growth factor receptors is thought to play an important role in the regulation of cell proliferation. Thus, these results suggest that synaptojanin 2 may mediate the inhibitory effect of Rac1 on endocytosis and could contribute to Rac1-mediated control of cell growth.

Actins↗

PubMed2000

Effects of xin mai tong capsule on vasoregulatory peptides in the patients of coronary heart disease.

In order to inquire into the therapeutic effects of Xin Mai Tong Capsule ([symbol: see text]) on coronary heart disease with myocardial ischemia, 40 patients were randomly divided into two groups (Xin Mai Tong group and the control group). The plasma endothelin (ET) levels in the two groups of patients were markedly higher than that of the healthy people (P < 0.001), and the calcitonin gene related peptide (CGRP) was similar to that of the healthy people (P > 0.05). After treatment, ET and symptomatic scores in the two groups decreased markedly (P < 0.01), and their S-T segments were elevated obviously (P < 0.01). But the decrease of ET and symptomatic scores and elevation of S-T segment in Xin Mai Tong group were superior to those of the control group (P < 0.05-0.01). The CGRP level in the control group did not vary obviously post-treatment, but it increased markedly (P < 0.01) with the addition of Xin Mai Tong Capsule in Xin Mai Tong group.

Aged↗

PubMed2000

[Effect of xinmaitong capsule on total ischemia burden in coronary heart disease patients with myocardial ischemia and analysis of its therapeutical mechanism].

OBJECTIVE: To assess the effect of Xinmaitong (XMT) capsule in treating ischemical cardiac disease. METHODS: Sixty coronary heart disease (CHD) patients with myocardial ischemia were divided randomly into two groups. XMT group (30 cases) was treated with XMT plus western medicine, and control group (30 cases) with western medicine alone. The changes of the scores for clinical symptoms, the total ischemia burden (TIB), the plasma endothelin (ET), the nitric oxide (NO), the superoxide dismutase (SOD), and the malonyldialdeyde (MDA) levels were observed before and after treatment. RESULTS: After treatment with XMT the scores of clinical symptoms, TIB, ET and MDA levels were significantly decreased (P < 0.01), the levels of NO and SOD were significantly increased (P < 0.01) in the XMT group, comparing with the control group these changes were statistically different (P < 0.01). CONCLUSIONS: XMT capsule can act against myocardial ischemia effectively, one of the mechanisms of which is protecting the function of vascular endothelium and resisting lipid peroxidation injury. The effects of adding XMT capsule on conventional treatment of western medicine were better than those of using western medicine alone.

Aged↗

PubMed1999

Physical and biological properties of cationic triesters of phosphatidylcholine.

The properties of a new class of phospholipids, alkyl phosphocholine triesters, are described. These compounds were prepared from phosphatidylcholines through substitution of the phosphate oxygen by reaction with alkyl trifluoromethylsulfonates. Their unusual behavior is ascribed to their net positive charge and absence of intermolecular hydrogen bonding. The O-ethyl, unsaturated derivatives hydrated to generate large, unilamellar liposomes. The phase transition temperature of the saturated derivatives is very similar to that of the precursor phosphatidylcholine and quite insensitive to ionic strength. The dissociation of single molecules from bilayers is unusually facile, as revealed by the surface activity of aqueous liposome dispersions. Vesicles of cationic phospholipids fused with vesicles of anionic lipids. Liquid crystalline cationic phospholipids such as 1, 2-dioleoyl-sn-glycero-3-ethylphosphocholine triflate formed normal lipid bilayers in aqueous phases that interacted with short, linear DNA and supercoiled plasmid DNA to form a sandwich-structured complex in which bilayers were separated by strands of DNA. DNA in a 1:1 (mol) complex with cationic lipid was shielded from the aqueous phase, but was released by neutralizing the cationic charge with anionic lipid. DNA-lipid complexes transfected DNA into cells very effectively. Transfection efficiency depended upon the form of the lipid dispersion used to generate DNA-lipid complexes; in the case of the O-ethyl derivative described here, large vesicle preparations in the liquid crystalline phase were most effective.

3T3 Cells↗

PubMed1999

Molecular cloning and expression of Galbeta1,3GalNAc alpha2, 3-sialyltransferase from human fetal liver.

Based on the sequences of the highly conserved segments in the previously cloned sialyltransferases, a cDNA encoding Galbeta1, 3GalNAc alpha2,3-sialyltransferase (SIATFL) has been isolated from human fetal liver. Expression analysis of the gene has been performed with various carcinoma cell lines, fetal tissues, fetal and adult liver and both hepatoma and the surrounding tissue from the same liver. The SIATFL gene was expressed poorly in fetal liver and in adult liver, slightly in hepatoma and highly in the surrounding tissue of hepatoma. The cDNA encoding the putative active domain was expressed in COS-1, Escherichia coli, and Pichia pastoris. The recombinant protein expressed in COS-1 could catalyse the transfer of NeuAc from CMP-NeuAc to asialo-fetuin. No enzyme activity was detected with a 32-kDa protein in E. coli and both 32-kDa and 41-kDa proteins in P. pastoris. These results suggested that correct glycosylation of the enzyme might play a key role in its folding that may be directly related to the enzymatic activity.

Amino Acid Sequence↗

PubMed1999

Cloning and sequencing of sialyltransferase gene from human fetal liver.

Based on sequences of the highly conserved segments in the previously cloned sialyltransferases, 150 bp fragments were amplified and sequenced using human fetal liver mRNA as template. One of them (s38) showed 57%-97% identities with the active domains of previously cloned sialyltransferases. Based on the sequence of s38, an oligonucleotide was synthesized and labeled to screen human fetal liver cDNA library. A cDNA encoding alpha 2, 3-sialyltransferase has been isolated. The cDNA sequence included an open reading frame coding for 340 amino acid residues, and the deduced amino acid sequence showed 100% identity with that of human submaxillary gland Gal beta 1, 3GalNAc alpha 2, 3-sialyltransferase, 83.2% identity with that of pig submaxillary gland alpha 2, 3-sialyltransferase. These results suggested that the protein encoded by the cDNA from human fetal liver cDNA library was a Gal beta 1, 3GalNAc alpha 2, 3-sialyltransferase.

Base Sequence↗

PubMed1998

A role for guanyl nucleotide-binding regulatory protein beta- and gamma-subunits in the expression of the adrenocorticotropin receptor.

Mutant Y1 mouse adrenocortical tumor cells, isolated on the basis of their resistance to the growth-inhibitory effects of forskolin, arise from single mutational events. These mutants present complex phenotypes in which the activity of Gbeta/gamma is impaired, ACTH receptor gene expression is markedly diminished, and ACTH-responsive adenylyl cyclase activity is lost. In this study, we have tested the hypothesis that the impairment in Gbeta/gamma activity is responsible for the loss of ACTH receptor gene expression and ACTH-responsive adenylyl cyclase activity. Transfection of one of the mutant clones with expression vectors encoding either Gbeta1 or Gbeta2 together with Ggamma2 increased ACTH receptor expression and restored ACTH-responsive adenylyl cyclase activity. Interestingly, either Gbeta2 or Ggamma2 alone was effective. These results thus support the hypothesis that the impairment in Gbeta/gamma activity is responsible for the loss of ACTH receptor expression. A luciferase reporter plasmid driven by the proximal promoter region of the mouse ACTH receptor gene was expressed poorly in the mutants compared with parental Y1 cells, suggesting that the Gbeta/gamma defect compromised transcriptional activity at the proximal promoter region of the ACTH receptor gene.

Adenylyl Cyclases↗

PubMed1998

[Clinical study on protective effect of xinmaitong capsule on damage of vascular endothelial cells].

OBJECTIVE: To assess the effect of Xinmaitong (XMT) capsule in treating coronary heart disease (CHD). METHODS: Thirty-eight patients of coronary heart disease with myocardial ischemia were divided randomly into XMT group (20 cases) and control group (18 cases). Conventional western medical therapy was given to both groups and the XMT group received additional XMT treatment. The changes of endothelin (ET) and calcitonin gene-related peptide (CGRP) levels, ST segment of ECG and clinical symptoms after treatment in all the patients were observed. Data of 14 healthy persons were taken as normal control. RESULTS: The ET level of all patients was significantly higher than that of the normal control (P < 0.001), and level of CGRP in patients was not different from normal control significantly (P > 0.05). After treatment, results showed that: (1) The ET levels and the scores of clinical symptoms of both groups decreased significantly (P < 0.01), and ST segment elevated markedly (P < 0.01) as compared with before treatment, and the changes revealed more evident in XMT group in comparison with those of the control group (P < 0.05-P < 0.01). (2) The level of CGRP was significantly increased in XMT group (P < 0.01) while unchanged in the control group (P > 0.05). CONCLUSIONS: There is severe damage of vascular endothelial cells in CHD patients. XMT could not only reduce significantly the plasma ET content, but also enhance markedly the production and release of CGRP, so it has a good anti-ischemic effect, which may be closely related with its action on improving the function of vascular endothelial cells and regulating metabolism of ET and CGRP.

Aged↗

PubMed1997

[Distribution of 70kDa heat shock protein in rabbit brains after heat stress and heat stroke].

OBJECTIVE: Evaluation of the relationship between the induction of 70kDa heat shock protein in rabbit brains and heat stress. METHODS: HSP70 was detected using monoclonal antibody by ABC method in rabbit hypothalamus, hippocampus and cerberal cortex. RESULTS: Intense HSP70 staining was displayed in rabbit brains of the heat stroke group (rectal temperature 43 degrees C to death). Positive cells were distributed mainly in the CA1, CA2 regions of the hippocampus; granular cell layer I and pyramidal layer (II) of the cerebral cortex; and the periventricular area of hypothalamus. HSP70-psoitive substances were localized in the cytoplasm and neuronal processes, a few neurons exhibited dark staining nucle. Hosever, the rabbit brains of the general heat stress group (rectal temperature 42.0 degrees C, 30 minutes) had much weaker staining. CONCLUSION: Hyperthermia causes neuronal expression of HSP70, particularly under strong heat stress, and may be sustained till death.

Animals↗

PubMed1996

cDNA for the beta 1 subunit of guanyl nucleotide-binding regulatory proteins from mouse adrenal glands.

cDNA encoding the beta 1 subunit of guanyl nucleotide binding regulatory proteins was isolated from a mouse adrenal cDNA library. The coding region was 90% identical to human and bovine beta 1 at the cDNA level and 100% identical at the protein level. In the 5' untranslated region, two sequence variants were isolated that differed by the presence or absence of a 49 base pair insert presumed to arise from alternative splicing.

Adrenal Glands↗

PubMed1996

Delivery of membrane-impermeant fluorescent probes into living neural cell populations by lipotransfer.

Use of fluorescent probes to monitor f-actin in living cells typically relies on difficult microinjection procedures. The current work has developed cationic lipotransfer of membrane-impermeant probes as an alternative to microinjection. BODIPY FL-phallacidin, a fluorescent f-actin probe, was packaged into 40-50 nm cationic liposomes. Packaging, verified by gel filtration, enabled delivery of the probe into living nerve cells and provided an image of f-actin that was identical to that seen in fixed, permeabilized cells. Phallacidin alone did not enter living cells, nor was its uptake stimulated by the presence of empty liposomes. All predicted f-actin structures were fluorescent in living cells, indicating a high efficacy of delivery. Cationic lipotransfer of fluorescent probes was rapid, not disruptive to cells, and delivered a probe en masse to a large sample population. Lipotransfer appears to be a promising alternative to microinjection for introducing membrane-impermeant probes and reagents into living cells.

Actins↗

PubMed1996

Stabilization of helical peptides by mixed spaced salt bridges.

Whether or not surface salt bridges have a strong stabilizing effect on the native structure in proteins remains uncertain. Previous studies of model peptides have shown that salt bridges spaced at i,i +4 along the chain are more stabilizing than those spaced at i,i +3, with a preference for the order acid-base rather than base-acid from N to C terminus. An analysis of the effect of spacing the ion pairs in short helical peptides is presented, in which acidic and basic side chains spaced two or three residues apart alternate along the chain. The mixed spacing proves to be stabilizing relative to pure spacings. A control peptide in which salt bridges were spaced uniformly three residues apart proved to form a beta-sheet structure rather than alpha-helix. This is due to formation of a silk-like apolar face consisting of alanine side chains; the mesoscopic structure formed by these sheets can be imaged by scanning microscopy.

Alanine↗

PubMed1996

Mutations to forskolin resistance result in loss of adrenocorticotropin receptors and consequent reductions in levels of G protein alpha-subunits.

A family of mutants isolated from the Y1 mouse adrenal cell line on the basis of their resistance to the growth inhibitory effects of forskolin have an underlying mutation that affects the activity of adenylyl cyclase. As part of the mutant phenotype, adenylyl cyclase is partially resistant to activation by forskolin, completely insensitive to ACTH, and fully responsive to NaF; the levels of Gs alpha and G1 alpha in plasma membrane fractions are decreased; and the activity of G beta/gamma is impaired. In the present study, we examine the basis for the complex phenotype associated with forskolin resistance to better understand the factors that contribute to the regulation of adenylyl cyclase activity. We demonstrate that the resistance of these mutants to ACTH results from the failure to express ACTH receptor transcripts. Transfection of these mutants with a gene encoding the mouse beta 2-adrenergic receptor led to the recovery of transformants with normal receptor-G protein coupling and with increased levels of Gs alpha and G1 alpha that approached those in parental Y1 cells. These beta 2-adrenergic receptor transformants, nonetheless, remained resistant to forskolin and ACTH. Two spontaneous Y1 mutants, Y6 and OS3, previously characterized as ACTH-resistant clones that failed to accumulate ACTH receptor transcripts, were shown to be forskolin resistant and to contain less Gs alpha in membrane fractions, indicating that forskolin resistance, failure to express the ACTH receptor, and the consequent reduction in Gs alpha are closely linked. Expression of the human ACTH receptor in Y6 and OS3 cells restored ACTH-responsive adenylyl cyclase activity and increased the level of Gs alpha, but did not otherwise reverse the forskolin-resistant phenotype. Together, these results demonstrate that mutations to forskolin resistance have downstream consequences that result in the loss of ACTH receptor expression and the consequent reduction in levels of membrane-associated G alpha subunits. The results further suggest that G protein-coupled receptors may have a stabilizing influence on G alpha subunits associated with the cell membrane. According to current models, forskolin activates adenylyl cyclase by forming a ternary complex with adenylyl cyclase and Gs alpha. Our results suggest that this model may be incomplete and that an additional component, acting directly or indirectly, is required for optimal activation of adenylyl cyclase by forskolin.

Adenylyl Cyclases↗

PubMed1995

Neurotransmitter release evoked by nerve impulses without Ca2+ entry through Ca2+ channels in frog motor nerve endings.

1. The requirement for extracellular Ca2+ in the process of evoked acetylcholine (ACh) release by nerve impulses was tested at endplates in frog skeletal muscle. Ca(2+)-containing lipid vesicles (Ca2+ liposomes) were used to elevate cytoplasmic Ca2+ concentrations under conditions in which Ca2+ entry from the extracellular fluid was prevented. 2. In an extracellular solution containing no added Ca2+ and 1 mM Mg2+ ('Ca(2+)-free' solution), Ca2+ liposomes promoted the synchronous release of ACh quanta, reflected electrophysiologically as endplate potentials (EPPs), in response to temporally isolated nerve impulses. 3. Motor nerve stimulation generated EPPs during superfusion with Ca2+ liposomes in Ca(2+)-free solutions containing the Ca2+ channel blocker Co2+ (1 mM), and the Ca2+ chelator EGTA (2 mM). As a physiological control for Ca2+ leakage from the liposomes to the extracellular fluid, the effect of Ca2+ liposomes on asynchronous evoked ACh release mediated by Ba2+ was examined. In contrast to the effects of 0.2-0.3 mM extracellular Ca2+, which generated EPPs but antagonized Ba(2+)-mediated asynchronous ACh release, Ca2+ liposomes generated EPPs but did not reduce asynchronous release mediated by Ba2+. The effects of Ca2+ liposomes were thus not due to leakage of Ca2+ from the liposome to the extracellular fluid. 4. Morphological studies using fluorescently labelled liposomes in conjunction with a confocal microscope demonstrate that lipid is transferred from the liposomes to nerve endings and liposomal contents are delivered to the nerve terminal cytoplasm. 5. The results suggest that when intracellular Ca2+ is elevated using liposomes as a vehicle, evoked ACh release can occur in the absence of Ca2+ entry via Ca2+ channels.

Acetylcholine↗

PubMed1995

Adrenocorticotropin-resistant mutants of the Y1 adrenal cell line fail to express the adrenocorticotropin receptor.

This report examines the basis for adrenocorticotropin (ACTH) resistance in two mutant clones (Y6 and OS3) derived from the ACTH-responsive Y1 mouse adrenocortical tumor cell line. These two mutants were originally characterized by their failure to respond to ACTH with increased adenylyl cyclase activity and as a consequence were resistant to the steroidogenic effects of the hormone. We now demonstrate that ACTH resistance in the Y6 and OS3 mutants results from the failure to express the gene encoding the ACTH receptor. Whereas parental Y1 cells express ACTH receptor transcripts at low levels and are stimulated by ACTH or 8-bromo-cAMP to increase the accumulation of ACTH receptor transcripts approximately twofold, the Y6 and OS3 mutants do not express receptor transcripts either in the presence or absence of 8-bromo-cAMP. The gene encoding the ACTH receptor appears to be present in the Y6 and OS3 mutants, as determined by Southern blot hybridization analysis. Moreover, in the Y6 mutant the ACTH receptor gene appears to be silenced by a modification that is reversed following the growth of the cells as tumors in mice. Clonal isolates of Y6 cells grown as tumors recover the ability to express ACTH receptor transcripts at low but detectable levels and acquire the ability to respond to ACTH with increased adenylyl cyclase activity. Finally, Y6 and OS3 cells transformed with a gene encoding the mouse beta 2-adrenergic receptor respond to the beta-adrenergic agonist, isoproterenol, in a manner that is indistinguishable from the similarly transformed parent Y1 cell line. These latter results demonstrate the functional integrity of the adenylyl cyclase system in the ACTH-resistant mutants and indicate that the failure to express ACTH receptor transcripts limits the responsiveness of these clones.

Adenylyl Cyclases↗