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Biomedical subjects

Q Y Wu

Publications and source records attributed to Q Y Wu.

At least 19 recordsLinked to original sources
PubMed2006

Mesenchymal stem cellular adhesion and cytotoxicity study of random biopolyester scaffolds for tissue engineering.

Mesenchymal stem cells (MSCs) were isolated from the bone marrow of rabbits and inoculated respectively on 3D scaffolds of poly(3-Hydroxybutyrate-co-3-Hydroxyvalerate) (PHBV), poly(butylenes succinate) (PBS) and different blends (100/0, 80/20, 50/50, 20/80, 0/100) (Wt%) in vitro. It was found that the (50/50) blends possessed the best performance on adhesion and cytotoxicity of MSCs. The scanning electronic microscopy (SEM) results showed that the (50/50) blends had the appropriate roughness for MSCs to attach and grow, which may be used as a suitable biomaterial to create small caliber vascular grafts.

Animals↗
PubMed2001

Anomalous origin of the pulmonary artery from the right coronary artery.

A 5-year-old boy who had an anomalous origin of a stenotic pulmonary artery from the right coronary artery with ventricular septal defect and pulmonary atresia is reported. The diagnosis was made at operation. Successful repair was achieved for the complex anomaly by using a pulmonary artery homograft as a conduit and closing the ventricular septal defect.

Blood Vessel Prosthesis Implantation↗
PubMed2001

Accumulation of poly-beta-hydroxybutyrate in cyanobacterium Synechocystis sp. PCC6803.

Accumulation of poly-beta-hydroxybutyrate (PHB) by photoautotrophic microorganisms makes it possible to reduce the production cost of PHB. The Synechocystis sp. PCC6803 cells grown in BG11 medium under balanced, nitrogen-starved or phosphorus-starved conditions were observed by transmission electron microscope. Many electron-transparent granules in the nitrogen-starved cells had a diameter up to 0.8 micron. In contrast, the number of granules in the normally cultured cells decreased obviously and only zero to three much smaller granules were in each cell. These granules were similar to those in bacteria capable of synthesizing PHB. They were proved to be PHB by gas chromatography after subjecting the cells to methanolysis. Effects of glucose as carbon source and light intensity on PHB accumulation in Synechocystis sp. PCC6803 under nitrogen-starved cultivation were further studied. Glucose and illumination promoted cell growth but did not favor PHB synthesis. After 7 days of growth under nitrogen-starved photoautotrophic conditions, the intracellular level of PHB was up to 4.1% of cellular dry weight and the PHB concentration in the culture broth was 27 mg/l.

Biotechnology↗
PubMed2001

[Qi deficiency and blood stasis and circulatory renin-angiotensin system as well as plasminogen activator inhibitor activity in rats with cardiac qi deficiency syndrome].

OBJECTIVE: To explore the relationship between cardiac Qi deficiency Syndrome and effect of circulatory renin-angiotensin system (RAS) and endogenous fibrinolytic system in rats with heart failure (HF). METHODS: Plasma RAS levels and plasminogen activator inhibitor (PAI-1) activity were measured in 2 groups of rats: the sham-operated group (Group A) and the HF with Heart Qi deficiency Syndrome model group (Group B) established by making arteriovenous fistula. Using radioimmunoassay and chromatography, plasma renin activity (PRA) and angiotensin II (Ang II) levels and PAI-I activity were determined before, immediately after and 30 days after the surgical operation respectively. RESULTS: After the operation was completed in Group B the left ventricular dysfunction revealed, left ventricular systolic pressure decreased and end diastolic pressure increased (P < 0.05), PRA and Ang II level and PAI-1 activity increased significantly, as compared with those in Group A and before modeling (P < 0.05). With cardiac function improved, the plasma PRA, Ang II level and PAI-1 activity lowered in Group B comparing with those immediately after modeling (P < 0.05). CONCLUSION: The activation of RAS is associated with the endogenous fibrinolyticim balance, and play an important role in endogenous fibrinolytic system dysfunction in HF with Heart Qi deficiency Syndrome and Qi deficiency-blood stasis, which was helpful to explain that cause of hypercoagulant state in HF patients and increase the risk of suffering from embolism-thrombotic diseases, and might be the pathogenetic basis of Heart Qi deficiency induced Qi deficiency-blood stasis.

Animals↗
PubMed2000

[A novel rabbit endothelin B receptor gene: cloning and sequence analysis].

Endothelin(ET) is the most potent mammalian vasoconstrictor identified to data. As a pathogenic factor, ET is involved in the genesis of many diseases. In this study, a pair of primers was designed and synthesized according to the human ETB receptor gene (hETBR) sequence. A 394 bp of DNA fragment was amplified by polymerase chain reaction(PCR) and labeled with alpha-32P-CTP using Random Primer-Labeling method. With this probe, rabbit lung cDNA library was screened by in situ hybridization and 11 positive clones were identified. Sequencing result showed that a complete reading frame of rabbit ETB receptor(rETBR) cDNA could be produced from three positive clones of eleven. By a series of subcloning, a recombinant plasmid including the 1326 bp of rETBR coding sequences, named pBlu Script-rETBR, was constructed. The deduced amino acid sequence indicated that the rETBR is 441 residues in length, with an expected molecular mass of approximately 49.44 kD. N-terminal 18 residues is the potential signal peptide (Score = 11.11) and therefore the molecular mass of mature rETBR is 47.65 kD with 423 amino acid residues. Analysis of the rETBR hydropathy profile indicates the presence of seven hydrophobic regions, putative transmembrane domains. Potential N-glycosylation sites are the 60th and the 118th. The structure exhibits a significant sequence and topographical similarity with G protein-coupled receptors.

Amino Acid Sequence↗
PubMed1998

Flanking proline residues identify the L-type Ca2+ channel binding site of calciseptine and FS2.

Calciseptine and FS2 are 60-amino acid polypeptides, isolated from venom of the black mamba (Dendroaspis polylepis polylepis), that block voltage-dependent L-type Ca2+ channels. We predicted that these polypeptides contain an identical functional site between residues 43 and 46 by searching for proline residues that mark the flanks of protein-protein interaction sites [Kini, R. M., and Evans, H. J. (1966) FEBS Lett. 385, 81-86]. The predicted Ca2+ channel binding site also occurs in closely related toxins, C10S2C2 and S4C8. Therefore, it is likely that these toxins also will block L-type Ca2+ channels. To test the proposed binding site on calciseptine and FS2, an eight-residue peptide, named L-calchin (L-type calcium channel inhibitor), was synthesized and examined for biological activity. As expected for an L-type Ca2+ channel blocker, L-calchin reduced peak systolic and developed pressure in isolated rat heart Langendorff preparations without affecting diastolic pressure or heart rate. Furthermore, L-calchin caused a voltage-independent block of L-type Ca2+ channel currents in whole-cell patch-clamped rabbit ventricular myocytes. Thus the synthetic peptide exhibits the L-type Ca2+ channel blocking properties of the parent molecules, calciseptine and FS2, but with a lower potency. These results strongly support the identification of a site in calciseptine and FS2 that is important for binding to L-type Ca2+ channels and reinforce the importance of proline brackets flanking protein-protein interaction sites.

Amino Acid Sequence↗
PubMed1998

Ryanodine-sensitive, thapsigargin-insensitive calcium uptake in rat ventricle homogenates.

Thapsigargin is a natural product that specifically inhibits all known SERCA calcium pumps with high affinity. We investigated the effects of thapsigargin on cardiac sarcoplasmic reticulum (SR) by measuring the oxalate-supported calcium uptake rate in the unfractionated homogenate and in the isolated SR fraction. The uptake rate in both the isolated SR and unfractionated homogenate are stimulated about two-fold by preincubation with high concentrations of ryanodine, which closes the SR efflux channel. Thapsigargin stoichiometrically and completely inhibited the calcium uptake rate in the isolated SR, both in the presence and absence of SR channel blockade. In contrast, thapsigargin nearly completely inhibited the homogenate calcium uptake only in the absence of SR channel blockade; in the presence of blockade, about 20% of the uptake activity was insensitive to thapsigargin. This result unmasks a thapsigargin-insensitive, ryanodine-sensitive component of calcium uptake in the heart. This activity is in an oxalate-permeable pool and is inhibited by cyclopiazonic acid, another inhibitor of the SERCA calcium pumps. There was no TG-insensitive activity in the rat EDL muscle homogenate. The absence of thapsigargin-insensitive uptake activity in the isolated SR can be attributed to its inactivation during the isolation of the SR. The oxalate permeability and ryanodine sensitivity suggest that the TG-insensitive calcium uptake activity is closely related to the classical SR. The different thapsigargin sensitivities suggests the existence of two kinds of intracellular calcium pumps in the heart.

Animals↗
PubMed1998

[GABA mediated inhibitory effect of amygdala on the activity of medial geniculate body neurons].

On 10 New Zealand white rabbits immobilized with Flaxedil, the inhibitory effect of amygdaloid stimulation on the responses of medial geniculate body (MGB) neurons to tone bursts and the involved neurotransmitter mechanism were investigated with microiontophoresis technique. The results showed that application of GABA could cause a suppression of spontaneous activity of MGB neurons while GABAA antagonist bicuculline had an opposite effect. Iontophoretic injection of GABA gave an inhibitory effect on MGB neurons similar to that caused by stimulating the amygdala or the auditory cortex behind the rhinal sulcus (ACBRS), and in particular, the GABA induced suppression could be completely antagonized by application of bicuculline. Taken together, these data suggested that GABA mediated the amygdaloid inhibitory effect. It seemed unlikely that glycine was involved in the effect, since strychnine, a glycine antagonist, could not affect the descending inhibition from ACBRS area.

Amygdala↗
PubMed1997

Effect of ischemia on the fraction of ryanodine-sensitive cardiac sarcoplasmic reticulum.

The effect of 15 min of global, normothermic ischemia on cardiac sarcoplasmic reticulum (SR) was investigated using the Ca2+ uptake rate and 3H-ryanodine binding of ventricular homogenates and isolated SR vesicles. Ischemia did not affect ryanodine binding in the homogenate, while it increased it in the isolated SR vesicles. Although ischemia decreased the homogenate oxalate-supported Ca2+ uptake rate, measured in the presence of high ryanodine to close the ryanodine-sensitive efflux pathway (+RY), its decrease of the Ca2+ uptake rate, measured in the absence of ryanodine (-RY), was more marked. This finding was also observed in the isolated SR. Although inhibition of the Ca-ATPase and its coupled Ca2+ uptake by thapsigargin proportionately decreased SR Ca2+ uptake -RY and +RY, ischemia decreased the Ca2+ uptake -RY proportionately more. This result suggested that there was a greater fraction of Ca2+ uptake activity in ryanodine-sensitive vesicles after ischemia. However, ischemia also reduced the yield of SR activity in the isolated SR fraction and the results could potentially be due to differential selection of ryanodine-sensitive and ryanodine-insensitive SR in the isolation procedure. We directly tested the hypothesis that ischemia changes the fraction of Ca2+ uptake activity in the ryanodine-sensitive vesicles by estimating the Ca-oxalate capacity measured +RY and -RY. Ischemia decreased the capacity -RY much more than +RY in the homogenate, indicating that more of the SR volume and Ca2+ uptake activity was in the ryanodine-sensitive vesicles after ischemia.

Animals↗
PubMed1996

Ryanodine perfusion decreases cardiac mechanical function without affecting homogenate sarcoplasmic reticulum Ca2+ uptake: comparison with the stunned heart.

This study tested the hypothesis that perfusion with low concentrations of ryanodine, which opens the sarcoplasmic reticulum (SR) Ca2+ channel in a sub-conducting state, could mimic the effects of stunning on both mechanical and SR activity. Perfusion of isolated rat hearts with 10-160 nM ryanodine progressively decreased left ventricular developed pressure (LVDP) and increased end-diastolic pressure (EDP), but LVDP decreased more and EDP increased less than in the stunned heart. The effect of ryanodine perfusion on LVDP and EDP is consistent with the opening of the SR Ca2+ channel by high-affinity ryanodine binding, reducing SR Ca2+ content and interfering with mechanical function. In contrast to stunning, ryanodine perfusion did not affect the homogenate Ca2+ uptake rates measured in the presence or absence of high [ryanodine]. Perfusion with 80 nM 3H-ryanodine resulted in a large decline in LVDP, but only a small degree of ryanodine binding. Thus, prolonged opening of only a few channels affects the SR in situ, whereas this is undetectable in the homogenate. Higher levels of ryanodine binding (0.3 pmol/mg) to the in vitro homogenate also did not affect the homogenate Ca(2+)-uptake rate in the presence or absence of high [ryanodine], whereas it reduced the stimulation of Ca2+ uptake by ruthenium red. High-affinity ryanodine binding to the SR Ca2+ channel, either by perfusion or by binding after homogenisation, did not duplicate the increased Ca2+ efflux observed in the stunned heart, suggesting that the SR defect in the stunned heart is not a prolonged opening of a sub-conducting state of the SR Ca2+ channel.

Animals↗
PubMed1995

Effect of ischemia and ischemia--reperfusion on ryanodine binding and Ca2+ uptake of cardiac sarcoplasmic reticulum.

The effect of 15 min of global, normothermic ischemia on 3H-ryanodine binding and the oxalate-supported Ca2+ uptake of cardiac sarcoplasmic reticulum (SR) was investigated in parallel using ventricular homogenates of isolated perfused rat hearts. Ischemia increased the Ca2+ efflux under the uptake assay conditions, as demonstrated by the greater stimulation of Ca2+ uptake by high concentrations of ryanodine (+RY) to close the SR Ca2+ channel. This effect was partially reversed by reperfusion. Ischemia depressed Ca2+ uptake rate -RY at free [Ca2+] of 0.4 microM and above, while the depression + RY was significant only above 10 microM Ca2+. We tested the hypothesis that inhibition of the Ca-ATPase alone, by adding thapsigargin or cyclopiazonic acid, could reproduce the effects of ischemia on the homogenate Ca2+ uptake rate. Thapsigargin or cyclopiazonic acid proportionally depressed Ca2+ uptake rate +RY and -RY and produced distinctly different effects of ischemia. Ischemia did not change the Bmax or Kd for equilibrium 3H-ryanodine binding, or the Hill coefficient or KCa for the [Ca2+]-dependence of equilibrium 3H-ryanodine binding. The rate of ryanodine binding, measured under the uptake conditions, was increased by ischemia and further increased by reperfusion. The effect of ischemia on the rate and extent of equilibrium binding to the high-affinity ryanodine binding site were unrelated to the highly reproducible effects on SR Ca2+ uptake rates measured in the homogenate.

Animals↗
PubMed1995

[Hypoxia induced increase of MDA and echinocytes from erythrocytes in rabbit's blood with special reference to inhibition of the increase by MPEG-SOD].

When rabbits acutely exposed to hypobaric hypoxia (at imitative altitude 5,000 m, PaO2 = 6.7 kPa), the percentage of the activity of superoxide dismutase (SOD in erythrocyte; EC 1.15.1.1) decreased respectively to 86%, 76%, 81%, 84%, 55%, 81%, 84% and 95% for a period of 0.25, 0.5, 1, 2, 3, 4, 5 and 24 h hypoxia while MDA (malondialdehyde) in erythrocyte and plasma increased significantly during hypoxia periods of 1, 2, 3, 5 and 24 h (n = 5, P < 0.05, P < 0.01 vs. normoxia group). The increase of MDA in plasma could be prevented by vitamin E (V. E, i.p, 1 mg daily for 3 consecative days before hypoxia), but that in erythrocyte did not show significant change probably because the injected V.E. without vehicle cannot penetrate through the erythrocyte membrane effectively. The echinocytes from erythrocytes increased significantly after hypoxia for 24 h (n = 5, P < 0.05 vs. normoxia group). However, by injecting MPEG-SOD (monomethoxypolythlene glycol-SOD) intravenously 30 min before hypoxia, the increase of MDA (both of erythrocyte and plasma) and echinocytes (from erythrocytes) were both inhibited obviously during hypoxia for 24 h (n = 5, P < 0.05, P < 0.01 vs. hypoxia group). It is inferred that the increase of MDA and echinocytes from erythrocytes may be due to lipid peroxidation by superoxide free radicals (O2-.) generated in erythrocytes through Fenton pattern Haber-Weiss reaction during hypobaric hypoxia.

Altitude↗
PubMed1994

[Tricuspid valve re-replacement: analysis of 4 cases].

The patients underwent tricuspid valve replacement may occur the mechanical valve failure caused by thrombosis and so on. It is necessary to reoperate urgently otherwise the patients will die. Four patients with this complications were treated successfully with tricuspid valve re-replacement at Fuwai Hospital in Beijing, China since 1989. The experience of management, the technique of tricuspid valve re-replacement and the choice of the valves were discussed.

Adult↗
PubMed1994

[Surgical correction of mitral valve prolapse].

Thirty-five patients with mitral valve prolapse were repaired at Fu Wai Hospital in Beijing between Jan. 1988 and June, 1993. 20 males and 15 females of them aged ranging from 7 to 52 years. 9 patients was less than 14 years old in this group. The mitral prolapse were caused by degeneration, congenital heart disease, trauma and rheumatic heart disease. The mitral anterior leaflet were eroded in 7 patients, posterior leaflet in 26 patients, both anterior and posterior leaflets in 2 patients. The dilation of the mitral annulus, rupture and prolongation of chordae and defect in the leaflets were found in these patients. The reconstruction of mitral valve were performed in all patients under cardiopulmonary bypass using the resection or plication of the prolapse parts of the leaflets or reduce the diameter of mitral annulus with a carpentier ring. The results were satisfactory without mortality in hospital or in following-up period. The indication and method of the operation were discussed.

Adolescent↗
PubMed1994

[Management of nocturnal nasal mask continuous positive airway pressure in central hypoventilation in patients with respiratory diseases].

The effect of nasal mask CPAP administered during night in four central hypoventilation patients with various causes were investigated. On the basis of their histories, specific clinical manifestations, cranial CT and MRI, cerebral angiography and polysomnography. The patients (three males and one female) are diagnosed as primary alveolar hypoventilation and central hypoventilation, the later mainly caused by the compression of bulbar respiratory centre due to congenital deformity of right vertebral artery and deformity of foramen magnum. In order to assess the severity of nocturnal hypoventilation and blood oxygen level of the patients, polysomnography was taken before treatment, during 2L/min of oxygen via nasal tube and CPAP ventilation. Only oxygen administration did not ameliorate hypoventilation episodes and hypoxemia, lowest SaO2 is less than 50% on four patients, hypoventilation index is greater than 20 times/hour in three patients and 6.4 in a patient. Applying CPAP with the pressure fixed to 6-12 cm H2O can significantly improve hypoventilation index and hypoxemia with lowest SaO2 more than 70% (P < 0.001) and hypoventilation index less than 7 (P < 0.01). We conclude that nocturnal nasal mask CPAP is an effective treatment for central hypoventilation.

Adult↗
PubMed1993

Identification of a nonsense mutation at amino acid 584-arginine of platelet glycoprotein IIb in patients with type I Glanzmann thrombasthenia.

Using Southern blot, the restriction digests of genomic DNAs in 11 patients with Glanzmann thrombasthenia from 10 unrelated kindreds were probed with a full-length GPIIb cDNA. An additional 2.3 kb Taq I fragment and two 1.65 kb and 0.65 kb fragments with reduced band intensity were found in the genes of two affected siblings from a family originating from the city of Huang Yan in the Zhejiang province. The Taq I digest of the abnormal gene was further probed with three portions of GPIIb cDNA, revealing that the heterozygous mutation was present in the region around exons 15-17 of the GPIIb gene. Two primers for polymerase chain reaction (PCR) were then designed, and a 394 bp PCR product was generated and sequenced, indicating that a stop codon (TGA) was substituted for an Arg codon (CGA) at amino acid position 584 of GPIIb, and resulted in a premature termination of translation and production of a shortened protein. The Western blot analysis showed that GPIIIa at the platelet surface was apparently deficient, it may be ascribed to the rapid turn-over of GPIIIa uncomplexed with the truncated GPIIb. The abnormal 2.3 kb Taq I fragment was used as a specific genetic marker to detect the carrier status of the patient family. The abnormal allele was proved to be derived from the mother, the two affected siblings are double heterozygotes, and one clinically unaffected daughter has also inherited this defective allele, while the father carries another recessive abnormal allele unidentified.

Amino Acid Sequence↗