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Biomedical subjects

G Zhao

Publications and source records attributed to G Zhao.

At least 19 recordsLinked to original sources
PubMed1997

Association of angiotensin I-converting enzyme gene polymorphism with myocardial ischemia and patency of infarct-related artery in patients with acute myocardial infarction.

OBJECTIVES: We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism on the extent of myocardial ischemia in patients with acute myocardial infarction. BACKGROUND: The I/D polymorphism, which in part controls plasma and tissue expression of ACE, has been implicated in predisposition to myocardial infarction and ventricular remodeling. METHODS: I/D genotyping, predischarge adenosine-thallium-201 perfusion tomography and radionuclide angiography were performed in 113 patients (72 men, 41 women) with a diagnosis of acute myocardial infarction. A subgroup of 96 patients also underwent coronary angiography. RESULTS: Genotypes DD, ID and II were present in 27, 56 and 30 patients, respectively. There was no significant difference in the baseline characteristics of patients, total creatine kinase, peak MB fraction, Killip class, mean ejection fraction or the number of diseased vessels in patients with the DD, ID or II genotype. However, the size of the total and the reversible perfusion defects was greater in those with DD than in those with ID or II genotype (total defect size [mean +/- SD] 33.7 +/- 22.5%, 29.5 +/- 19.2% and 22.2 +/- 16.0%, respectively [p = 0.022]; reversible defect size 18.0 +/- 16.0%, 12.1 +/- 11.6% and 8.2 +/- 7.8%, respectively [p = 0.006]). Occlusion of the infarct-related artery was also more common in patients with DD genotype (odds ratio 3.9, 95% confidence interval 1.4 to 11.0). Multivariate analysis showed that the I/D genotype was an independent predictor of perfusion defect size and patency of the infarct-related artery (p = 0.001). CONCLUSIONS: DD genotype was associated with a larger ischemic defect and occlusion of the infarct-related artery. Patients with DD genotype, having a larger ischemic defect, are expected to be at a greater risk for subsequent cardiovascular events.

Adenosine↗
PubMed1997

A preliminary morphometric study on the endometrium from patients treated with indomethacin-releasing copper intrauterine device.

The intrauterine device (IUD) is an effective method of birth control. However, IUD-induced uterine bleeding is a major side-effect and always causes inconvenience, sometimes even anaemia. It has been reported that oral administration of indomethacin could can reduce IUD-induced uterine bleeding. In the present study, we investigated whether indomethacin-releasing copper IUD (IR-Cu-IUD) can prevent insertion-induced uterine bleeding and its mechanism. Nine healthy volunteers of reproductive age were selected for the study. Endometrial tissues were collected at same menstrual stage prior to and 3-6 months after IR-Cu-IUD insertion. Endometrial morphology, cell proliferation/differentiation, morphometry and activity of complement Factor VIII were examined. No significant difference was found in any of the parameters examined in the same patients, both prior to and after IR-Cu-IUD insertion. By comparison with data previously obtained from the patients who had Cu-IUD insertions, it is clear that IR-Cu-IUD markedly reduced IUD-induced uterine bleeding and this reduction is primarily contributed by the anti-inflammatory action of indomethacin.

Adult↗
PubMed1997

Identification, sequencing, and enzymatic activity of the erythrose-4-phosphate dehydrogenase gene of Vibrio cholerae.

We have identified a gene in Vibrio cholerae (epd) which encodes an erythrose-4-phosphate dehydrogenase activity and is located immediately downstream of an iron-regulated virulence gene, irgA, and immediately upstream of a gene encoding phosphoglycerate kinase (pgk). Expression of epd in V. cholerae is not regulated by iron, nor is it required for virulence in an infant mouse model.

Aldehyde Oxidoreductases↗
PubMed1997

Biochemical characterization of penicillin-resistant and -sensitive penicillin-binding protein 2x transpeptidase activities of Streptococcus pneumoniae and mechanistic implications in bacterial resistance to beta-lactam antibiotics.

To understand the biochemical basis of resistance of bacteria to beta-lactam antibiotics, we purified a penicillin-resistant penicillin-binding protein 2x (R-PBP2x) and a penicillin-sensitive PBP2x (S-PBP2x) enzyme of Streptococcus pneumoniae and characterized their transpeptidase activities, using a thioester analog of stem peptides as a substrate. A comparison of the k(cat)/Km values for the two purified enzymes (3,400 M(-1) s(-1) for S-PBP2x and 11.2 M(-1) s(-1) for R-PBP2x) suggests that they are significantly different kinetically. Implications of this finding are discussed. We also found that the two purified enzymes did not possess a detectable level of beta-lactam hydrolytic activity. Finally, we show that the expression levels of both PBP2x enzymes were similar during different growth phases.

Anti-Bacterial Agents↗
PubMed1997

Short-term exercise training enhances reflex cholinergic nitric oxide-dependent coronary vasodilation in conscious dogs.

The effects of exercise training on the coronary vasodilation following activation of the Bezold-Jarisch reflex were examined in conscious dogs. Mongrel dogs were chronically instrumented using sterile techniques for measurements of systemic hemodynamics and left circumflex coronary blood flow (CBF). With the heart rate controlled (150 bpm), veratrine (0.5 to 20 micrograms/kg) caused dose-dependent increases in CBF; eg, 5 micrograms/kg of veratrine increased CBF by 61 +/- 6% from 31 +/- 1.3 mL/min (P < .05). After exercise training, the dose-response curve of CBF in response to veratrine was shifted to the left; eg, 5 micrograms/kg of veratrine increased CBF by 101 +/- 12% (P < .05 compared with control) from 34 +/- 2.3 mL/min. The enhanced coronary vasodilation was blunted by nitro-L-arginine (NLA, 35 mg/kg). In anesthetized dogs after exercise training, electrical stimulation of the left vagus nerve caused greater increases in CBF, and NLA inhibited increases in CBF. Acetylcholine, norepinephrine, angiotensin II, and bradykinin caused greater increases in NO2- production in coronary microvessels from exercise-trained dogs compared with those from normal dogs. Our results indicate that the coronary vasodilation following activation of the Bezold-Jarisch reflex is enhanced in conscious dogs after exercise training. Since electrical stimulation of the vagus nerve caused greater coronary vasodilation and since the agonists resulted in greater increases in NO production in coronary microvessels from exercise-trained dogs, the mechanism responsible for the enhanced coronary vasodilation following activation of the Bezold-Jarisch reflex is most likely due to the increased release of NO from the endothelial cells.

Acetylcholine↗
PubMed1997

Expression of a mutant (Arg92Gln) human cardiac troponin T, known to cause hypertrophic cardiomyopathy, impairs adult cardiac myocyte contractility.

The mechanism(s) by which mutations in sarcomeric proteins cause hypertrophic cardiomyopathy (HCM) remains unknown. A leading hypothesis proposes that mutant sarcomeric proteins impair cardiac myocyte contractility, providing an impetus for compensatory hypertrophy. To test this hypothesis, we determined the impact of expression of a mutant (Arg92Gln) human cardiac troponin T (cTnT), known to cause HCM in humans, on adult cardiac myocyte contractility. A full-length human cTnT cDNA was cloned, and the Arg92Gln mutation was induced. Recombinant adenoviruses Ad5/CMV/cTnT-N and Ad5/CMV/cTnT-Arg92Gln were generated through homologous recombination. Adult feline cardiac myocytes were infected with recombinant adenoviruses or a control viral vector (Ad5 delta E1) at a multiplicity of infection of 100. Expression levels of the full-length normal and mutant cTnT proteins were equal on Western blots. Expression of the exogenous cTnT proteins in cardiac myocytes was also shown by immunocytochemistry and immunofluorescence, and their incorporation into myofibrils was confirmed by Western blotting on myofibrillar extracts. Electron microscopy showed intact sarcomere structure in rod-shaped cardiac myocytes in all groups. Cell fractional shortening and the peak velocity of shortening were not significantly different among the groups 24 hours after transduction. However, 48 hours after transduction, both fractional shortening and the peak velocity of shortening were significantly reduced (24% [P < .001] and 26% [P < .001], respectively) in cardiac myocytes in the Ad5/CMV/cTnT-Arg92Gln compared with the Ad5/CMV/cTnT-N groups. The magnitude of the reductions was greater at 72 hours after transduction (45% and 39%, respectively; P < .001). Our results indicated that expression of the mutant (Arg92Gln) cTnT, known to cause HCM in humans, impaired intact adult cardiac myocyte contractility. Our data also show that both normal and mutant cTnT were incorporated into myofibrils. These results provide a potential mechanism by which mutations in sarcomeric proteins cause HCM.

Adult↗
PubMed1997

Role of iron in ischemia-reperfusion oxidative injury of rat lungs.

We have previously shown that isolated, oxygen-ventilated rat lungs generate reactive oxygen species during ischemia and reperfusion. To evaluate the role of free iron in lung ischemia/reperfusion injury, we measured desferrioxamine-chelatable iron (DC-Fe), protein carbonyls, and thiobarbituric acid reactive substances (TBARS) in lungs subjected to global ischemia and reperfusion. There were no changes in DC-Fe, TBARS, or protein carbonyls during 2 h of control perfusion. There was a 2.3-fold increase in DC-Fe during 1 h ischemia and a further doubling during reperfusion. Results were similar when lungs were ventilated with O2 or N2. Lung TBARS increased 214% during ischemia/reperfusion with oxygen ventilation; unlike DC-Fe release, this change was blocked by N2 ventilation. Protein carbonyl content of the lung also increased significantly (113%) with ischemia/reperfusion. Ferric 8-hydroxyquinoline added to the perfusate before ischemia increased DC-Fe in lung tissue and significantly enhanced the lipid and protein oxidation of ischemic/reperfused lungs. The added perfusate iron had no effect on control lungs. Proteins isolated from the iron-supplemented ischemic/reperfused lungs were resistant to further in vitro oxidation induced by hydrogen peroxide (30 microM) whereas proteins from control perfused lungs were oxidized under these conditions. These results indicate that DC-Fe plays an important role in lung oxidative injury with ischemia/reperfusion. DC-Fe is released from iron-storage sites during ischemia and promotes tissue oxidation when oxygenation is maintained during ischemia or restored during reperfusion.

Animals↗
PubMed1996

Microemulsion Formation and Phase Behavior of Anionic and Cationic Surfactants with Sodium Dodecyl Sulfate and Cetyltrimethylammonium Bromide

The phase behavior and solubilization of multiphase microemulsions in mixed anionic-cationic surfactant systems were studied for fixed ratios of water-to-oil and surfactant-to-alcohol. In the mixed surfactants (sodium dodecyl sulfate + cetyltrimethylammonium bromide)/heptane/alcohol/water systems, microemulsion and birefringent phases are formed by adjusting the surfactant ratio epsilon and the cationic weight fraction delta. The bicontinuous (or w/o microemulsion) --> birefringent o/w microemulsion transition takes place and microemulsion domain enlarges with increasing epsilon. The optimum surfactant concentration gamma increases and the corresponding optimum delta decreases with increasing epsilon and both of them decrease with increasing the alcohol chain length from butanol to hexanol. The birefringent region shrinks rapidly with increasing alcohol and/or CTAB weight fractions in total surfactant concentration. Conductivity measurements have been performed in the single-phase region of the system containing mixed surfactants and alcohols at 25&deg;C. The conductivity results indicate where a transition takes place and which of these different types of phase structures may be in the single-phase of the system containing anionic-cationic mixed surfactants.

Journal Article↗
PubMed1996

Identification of the pdxK gene that encodes pyridoxine (vitamin B6) kinase in Escherichia coli K-12.

We isolated a miniTn10(Cmr) insertion mutant lacking pyridoxine (PN) kinase and cloned the structural gene, designated pdxK, by complementation. P1 transduction and PCR mapping and DNA sequence analysis showed that pdxK was adjacent to the crr sugar transport gene (53.95 min). Growth properties of pdxK::miniTn10 mutants supported the hypotheses that PN kinase, which also phosphorylates pyridoxal (PL) and pyridoxamine (PM) in vitro, functions solely in the B6-vitamer salvage pathway and that E. coli contains an additional PL kinase. The amino acid sequence of PdxK has signature motifs of the PfkB superfamily of carbohydrate kinases, which includes phosphofructokinases and ribokinases, and suggests that three unidentified ORFs of Salmonella typhimurium, Haemophilus influenzae, and Saccharomyces cerevisiae correspond to PN/PL/PM kinases.

Amino Acid Sequence↗
PubMed1996

The homogenetic estimate for the variance of survival rate.

The homogenetic estimate for the variance of survival rate is proposed based on generalization and reduction between the complement of the empirical distribution function and the Kaplan--Meier or Berkson--Gage estimate. It reduces to the binomial variance estimate when there is no censoring. A Monte Carlo simulation study was carried out under various sample sizes, survival and censoring configurations, number of tied observations, and confidence levels with 2000 replications. It verifies that the commonly employed Greenwood estimate understimates, and the Simon and Lee expression for the Peto estimate strictly overestimates, the variance of survival rate to an extent dependent on the censoring distributions. The conclusions are identical with those of Peto et al. (1977) and Slud et al. (1984). The bias of the homogenetic estimate is less than that of both the Greenwood estimate and the Simon and Lee expression for the Peto estimate. The homogenetic estimate slightly overestimates when there are no ties and becomes unbiased and then slightly underestimates as the number of tied observations increases.

Analysis of Variance↗
PubMed1996

4-Phospho-hydroxy-L-threonine is an obligatory intermediate in pyridoxal 5'-phosphate coenzyme biosynthesis in Escherichia coli K-12.

We show that thrB-encoded homoserine kinase is required for growth of Escherichia coli K-12 pdxB mutants on minimal glucose medium supplemented with 4-hydroxy-L-threonine (synonym, 3-hydroxyhomoserine) or D-glycolaldehyde. This result is consistent with a model in which 4-phospho-hydroxy-L-threonine (synonym, 3-hydroxyhomoserine phosphate), rather than 4-hydroxy-L-threonine, is an obligatory intermediate in pyridoxal 5'-phosphate biosynthesis. Ring closure using 4-phospho-hydroxy-L-threonine as a substrate would lead to formation of pyridoxine 5'-phosphate, and not pyridoxine, as the first B6-vitamer synthesized de novo. These considerations suggest that E. coli pyridoxal/pyridoxamine/pyridoxine kinase is not required for the main de novo pathway of pyridoxal 5'-phosphate biosynthesis, and instead plays a role only in the B6-vitamer salvage pathway.

Acetaldehyde↗
PubMed1996

Dual-electrode detection for capillary electrophoresis/electrochemistry.

The extremely low sample volumes required for capillary electrophoresis and the high sensitivity and selectivity of electrochemical detection make capillary electrophoresis/electrochemistry (CEEC) a very useful method for bioanalysis. In this paper, two types of dual-electrode detectors for CEEC are described. The first employs a ring-disk microelectrode placed in a wall-jet configuration and is used for the selective detection of substances undergoing chemically reversible oxidations. Collection efficiencies obtained for catecholamines with this configuration were between 25 and 35%. The second electrode design consists of two adjacent carbon fibers embedded in an epoxy matrix and is analogous to the parallel dual-electrode configuration used in liquid chromatography/electrochemistry. This configuration can be used to confirm peak identity and purity by operating the electrodes at two different potentials. Alternatively, it is possible to perform simultaneous oxidative and reductive electrochemical detection.

Catecholamines↗
PubMed1996

Neural regulation of coronary vascular resistance: role of nitric oxide in reflex cholinergic coronary vasodilation in normal and pathophysiologic states.

A number of reflexes participate in the control of coronary vascular resistance through activation of the sympathetic or parasympathetic nervous system. Classically, activation of vagal efferent fibers to the heart results in vasodilation due to the release of acetylcholine and activation of muscarinic receptors. Recently, we have found that activation of a number of reflexes in conscious dogs, the Bezold-Jarisch reflex and the carotid chemoreflex in particular, results in cholinergic coronary vasodilation which is blocked by an inhibitor of nitric oxide synthesis, nitro-L-arginine. After the development of pacing-induced heart failure, the cholinergic dilation subsequent to activation of the Bezold-Jarisch or carotid chemoreflex is essentially abolished, since coronary blood vessels no longer produce nitric oxide. In contrast, after brief exercise training, there is a potentiation of Bezold-Jarisch reflex-induced coronary vasodilation since exercise upregulates nitric oxide production by coronary blood vessels. Since the Bezold-Jarisch reflex may be important as a compensatory mechanism during acute myocardial infarction, and the carotid chemoreflex is the acute mechanisms responsible for ameliorating systemic hypoxemia, the role of nitric oxide in reflex cholinergic coronary vasodilation may be essential in the compensatory vascular adjustments evoked by these and other reflexes.

Animals↗
PubMed1996

Experimental study on the early efficacy of excimer laser with adjunctive balloon angioplasty in dog's femoral artery.

The effect of domestically-manufactured excimer laser with adjunctive balloon angioplasty in achieving revascularization and reduction of residual stenosis was assessed. 20 femoral arteries with thrombosis and occlusion from 12 dogs were subject to angiography. At first excimer laser angioplasty was done followed by balloon angioplasty. The diameter and residual stenosis of revascularized vessel were measured. The result showed that 17 out of 20 vessels (85%) were revascularized. The diameter of revascularized vessel by excimer laser were 1.22 +/- 0.14 mm, while residual stenoses were 54% +/- 5%. After adjunctive balloon angioplasty the diameter and residual stenoses were 2.04 +/- 0.16 mm and 20% +/- 7% respectively (P < 0.05 and P < 0.01). Complication in form of vasoperforation occurred in 3/20 vessels (15%). It is concluded that China- manufactured excimer laser angioplasty is effective when used for revascularization. While the reduction of narrowing and residual stenoses was enhanced after adjunction of balloon angioplasty. This method can be employed in treating peripheral occlusive disease effectively and safely.

Angioplasty, Balloon, Laser-Assisted↗
PubMed1996

Free and complexed prostate-specific antigen serum ratios to predict probability of primary prostate cancer and benign prostatic hyperplasia.

OBJECTIVES: Ratios of free to total prostate-specific antigen (f/t PSA ratio) improved differentiation of benign prostatic hyperplasia (BPH) from prostate cancer (CaP). Using sera obtained at least 1 month prior to biopsy-confirmed diagnosis and logistic regression adjusted for disease prevalence, probability curves are constructed to predict the presence of CaP. METHODS: The patient population included 122 (44%) BPH sera and 155 (56%) prostate carcinoma sera collected prior to any therapy. The total PSA range = 2.0-20.0 ng/mL; median age = 69 years. External reference standards for both free and total PSA assays were used to standardize the assays and correct the ratio. Probability curves and tables for cancer incidence were formulated for a subset of the total test population (total PSA range = 2.0-10.0 ng/mL; 98 BPH, 118 CaP patients) by using logistic regression and prior cancer prevalence statistics derived from a published patient screening study. RESULTS: Median f/t PSA ratios were 0.18 and 0.12 in the overall sample and 0.19 and 0.12 in the subset for BPH and CaP, respectively (P = 0.0001). The median total PSA concentrations for BPH and CaP were 5.8 and 6.7 ng/mL when total PSA range = 2.0-20.0 ng/mL and were 4.9 and 5.9 ng/mL when total PSA range = 2.0-10.0, respectively. CONCLUSIONS: Cancer probability curves were constructed to help guide decisions concerning biopsy and other aspects of prostate cancer disease management. Further validation of this approach in another series of patients is necessary and is planned.

Adult↗
PubMed1996

Analysis of a cation-transporting ATPase of Plasmodium falciparum.

We have cloned and characterised one gene, PfATPase4 which encodes a P-type ATPase containing all the primary sequence motifs characteristic of this class of transmembrane ion transporters, and also a fragment of a second P. falciparum P-type ATPase pseudogene (PfATPase5). Analysis of conserved domains and motifs of specific ATPases reveals that PfATPase4 is most analogous to Ca2+ ATPases of the endoplasmic reticulum. The PfATPase4 gene gives rise to a transcript of 8 kb shortly after erythrocyte invasion. Although this mRNA is not detected in later stages, the protein detected immunologically at 190 kDa persists throughout and is detected in free merozoites. Immunofluorescence microscopy reveals that the PfATPase4 protein is concentrated in discrete compartments at the periphery of the parasite. Detailed sequence and structural analyses of these and the other P-type ATPases of P. falciparum described previously, reveals that they comprise an unusual family in several respects. Firstly, the large number of non-homologous genes so far characterised reflects the complexities of ionic regulation in the diverse environments encountered by the parasite. Secondly, the plasmodial P-type ATPase family may be classified both at primary sequence and structural levels into two distinct groups-those typical of P-type ATPases (including PfATPase4) and those which are much more divergent. A third complexity is illustrated by the fact that one of the other members [1] here termed PfATPase6, has an even greater similarity to the sarcoplasmic reticulum Ca2+ ATPases than does PfATPase4, which raises questions about the possible functional relationship between these two members.

Adenosine Triphosphatases↗
PubMed1996

Loss of nitric oxide production in the coronary circulation after the development of dilated cardiomyopathy: a specific defect in the neural regulation of coronary blood flow.

1. The aims of our study were to determine the role of nitric oxide (NO) in cholinergic reflex dilation of the coronary circulation in normal healthy conscious dogs and after the development of pacing-induced dilated cardiac myopathy and overt congestive heart failure. 2. Dogs were instrumented using sterile surgical techniques under general anaesthesia and allowed to fully recover. The Bezold-Jarisch reflex was stimulated by the intra-atrial injection of veratrine or the intravenous injection of PGI2, while the carotid chemoreflex was stimulated by the intracarotid injection of nicotine. Experiments were performed before and after the development of overt congestive heart failure (HF) caused by rapid left ventricular pacing for 4 weeks. 3. The release of NO, or NO-mediated vascular relaxation following administration of acetylcholine (ACh) may have little physiological significance since as ACh is released from nerve endings in vivo. Stimulation of the Bezold-Jarisch or carotid chemoreflex resulted in typical vagal cholinergic reflex coronary vasodilation, an increase in coronary blood flow and a decrease in coronary vascular resistance, which was substantially reduced following NO synthesis inhibition with nitro-L-arginine. 4. After the development of severe congestive HF, the production of NO by sieved coronary microvessels from the heart was markedly reduced accompanied by a 60-80% reduction in both the mRNA (northern blot) and protein (western blot) for endothelial NO synthase in the aorta. 5. After the development of severe pacing-induced HF, activation of the Bezold-Jarisch or carotid chemoreflex no longer resulted in coronary vasodilation due to the disappearance of NO production from the coronary circulation. 6. Therefore, cholinergic reflex coronary vasodilation is mediated by NO. Because coronary blood vessels lose the ability to produce NO after the development of HF, reflex cholinergic coronary vasodilation is markedly altered, uncovering a previously undiscovered specific defect in the integrated control of the coronary circulation in the failing heart.

Animals↗