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Biomedical subjects

X L Qi

Publications and source records attributed to X L Qi.

15 recordsLinked to original sources

Myocardial contractile responsiveness to endothelin-1 in the post-infarction rat model of heart failure: effects of chronic quinapril.

Cardiac endothelin-1 (ET-1) levels and ET receptor expression are increased in congestive heart failure (CHF). In order to determine whether this results in increased responsiveness of ET-A or ET-B receptors to ET-1, we evaluated the contractile effects of ET-1 in isolated papillary muscles isolated from hearts of control rats and from rats 4 weeks post myocardial infarction (MI) having received no therapy or chronic quinapril therapy. The ET-1 dose-response was biphasic in normal muscles. The use of the selective ET-A receptor antagonist BQ123 and the selective ET-B receptor antagonist BQ788 revealed that the initial decrease in tension was the result of ET-B receptor stimulation. Blockade of nitric oxide (NO) production with L-NAME abolished the initial decrease in tension. MI resulted in CHF that was partially reversed by quinapril. In MI, the positive inotropic effects of ET-1 were enhanced due to the loss of the initial ET-B receptor mediated decrease in tension, as well as an increase in the positive inotropic effects of ET-A receptors. This was associated with an increase in ET-A and ET-B receptor mRNA and a decrease in cardiac ecNOS protein. Four weeks of therapy with quinapril attenuated the positive inotropic effects of ET-1 and prevented the increase in ET-A receptor mRNA. Although quinapril did not restore the effects of ET-B receptor stimulation or prevent the increase in ET-B mRNA, it did restore cardiac ecNOS protein expression. Thus, the inotropic response to ET-1 is biphasic due to an overall positive inotropic effect of ET-A receptor stimulation and an ET-B receptor mediated decrease in contractility at low ET-1 concentrations which appears to be mediated by cardiac ecNOS (NO). In post-MI CHF, responsiveness to ET-A receptors increases and the ET-B mediated negative inotropic response is lost despite an increase in both receptor subtypes. Quinapril therapy attenuates these effects and normalises cardiac ecNOS protein.

Angiotensin-Converting Enzyme Inhibitors↗

Improvement of endocardial and vascular endothelial function on myocardial performance by captopril treatment in postinfarct rat hearts.

Background-Endocardial (EE) and myocardial capillary vascular endothelial (myocap VE) cells have been shown to modulate the contractile characteristics of myocardium in a calcium-dependent manner. We evaluated the endothelial-myocardial interaction in the rat postinfarction myocardial infarction (MI) model and the effects of captopril. Methods and Results-Wistar rats were divided into 4 groups treated for 4 weeks: (1) control; (2) infarcted controls (left anterior coronary artery ligation); (3) infarcted+captopril 2 g/L in drinking water; and (4) infarct+captopril+triton intracoronary injection. Coronary VE function was evaluated by infusion of serotonin in Langendorff preparations (n=31), and the myocardial contractile characteristics were investigated by use of isolated papillary muscles (n=44). Cardiac mRNA for endothelial constitutive nitric oxide synthase (ecNOS) was measured, and its cellular location was evaluated by immunohistochemistry. Serotonin-induced increase in coronary flow was decreased in infarct controls compared with controls (4.6% versus 53.4%, P<0.01) but not in the 2 infarct+captopril groups. Intracoronary triton injection decreased serotonin-induced coronary flow in the infarct+captopril+triton group. All MI groups had decreased total tension in isolated papillary muscles. EE removal by triton immersion decreased total tension in all groups except for infarct controls (3.3 versus 3.2 g/mm(2)). Cardiac ecNOS mRNA decreased in the control infarct group but remained normal in the infarct+captopril group. Conclusions-Chronic postinfarction endothelium-induced coronary vasodilatation is impaired, and both EE and myocap VE dysfunction contribute to myocardial depression. Captopril use prevents these abnormalities and the reduction of cardiac ecNOS mRNA.

Angiotensin-Converting Enzyme Inhibitors↗

Stereo capture: local rematching driven by binocularly attended 3-D configuration rather than retinal images.

Previous explanations for stereo capture were mainly based on the low-level perceptual processing of binocular stereopsis which usually shows that one pair of retinal images corresponds to only one 3-D perceptual configuration. Stereo capture, however, may encounter multiple perceptual configurations due to the matching ambiguity of wallpaper elements that may not be solved merely by bottom-up processing of the retinal stimuli. The present study suggests that binocular attention plays an important role in stereo capture by way of selecting and enhancing a perceptual configuration that is often ambiguous without attention involved. Stereo capture results from wallpaper's local rematching driven by binocularly attended 3-D configuration rather than retinal images.

Attention↗

Vascular endothelial dysfunction contributes to myocardial depression in ischemia-reperfusion in the rat.

Endocardial and vascular myocardial capillary endothelium has been shown to modulate the contractile characteristics of myocardium by altering myofibrillar affinity for calcium. Although the release of endothelial-derived substances that modify myocardial contractility has been shown to be altered in certain physiologic and pathologic situations, until now no study has evaluated whether the direct modulatory effects of endothelium on its subjacent myocardium were altered in pathologic situations and contributed to loss of contractile function. This study was designed to evaluate whether the direct contractile modulatory effects of endocardial and (or) vascular endothelium were altered and whether these alterations contributed to contractile dysfunction in a model of ischemia-reperfusion. Sixty-two perfused rat hearts as Langendorff preparations were randomized to no intervention, intracoronary Triton X100 injection (to render vascular endothelium dysfunctional), ischemia (30 min)-reperfusion (20 min), and ischemia-reperfusion followed by intracoronary Triton X100 injection. Coronary endothelial-dependent vascular reactivity and vascular smooth muscle reactivity were assessed by serotonin and sodium nitroprusside, respectively. Myocardial damage was assessed by coronary effluent creatine phosphokinase and by morphologic studies. Papillary muscles were then excised and contractile characteristics evaluated at varying extracellular calcium concentration prior to and after endocardial endothelial removal with Triton X100. All three interventions eliminated all coronary vascular response to serotonin but did not modify response to nitroprusside. Creatine phosphokinase values rose only in hearts with ischemia-reperfusion, and only minor morphologic changes occurred, mostly in hearts with ischemia-reperfusion. Papillary muscles from hearts with intracoronary Triton X100 injection had lower contractile indices compared with normal controls (total tension 4.0 vs. 4.6 g/mm2, p < 0.01) and an abbreviation of contraction duration. Increasing extracellular calcium concentration from to 0.7 to 3.25 mM eliminated these differences. Similar but more marked decreases in contractile indices and twitch duration were noted in the two ischemia-reperfusion groups, but consistent with some myocardial damage being present, increasing extracellular calcium concentration to 3.25 or 7 mM did not fully eliminate these differences. In both ischemia-reperfusion groups and the intracoronary Triton X100 group, the relative increase in total tension with increasing extracellular calcium concentrations was similar (35 to 38%) and greater than that of the control group (25%), consistent with dysfunction of vascular endothelium contributing to myocardial dysfunction in the three intervention groups. Endocardial endothelial removal had a similar effect in all four groups, suggesting that dysfunction of endocardial endothelium does not play a role in this model. We conclude that vascular but not endocardial endothelial dysfunction contributes to the myocardial dysfunction that occurs during ischemia-reperfusion injury.

Animals↗

Effect of temperature on the secondary structure of beta-lactoglobulin at pH 6.7, as determined by CD and IR spectroscopy: a test of the molten globule hypothesis.

Previous CD measurements of changes in the conformation of beta-lactoglobulin at neutral pH as a function of temperature indicated the formation of a molten globule state above approx. 70 degrees C. New CD measurements are reported at temperatures up to 80 degrees C with an instrument on the Daresbury synchrotron radiation source which gives spectra of good signal-to-noise ratio down to 170 nm. IR spectra were recorded up to 94.8 degrees C with a ZnSe circle cell and a single simplified model of the substructure of the amide I' band was used to give the fractional contents of beta-sheet structure unambiguously and independently of the CD spectroscopy. The results of both techniques, however, were in agreement in showing a progressive loss of beta-sheet structure with increasing temperature, beginning below the denaturation temperature. Nevertheless, the CD spectroscopy showed a fairly abrupt loss of virtually all the helical conformation at approx. 65 degrees C. Comparison of the present results with other studies on the molten globule formed at acid pH in the lipocalin family suggests that above 65 degrees C a partly unfolded state is formed, possibly by destabilization of the intermolecular beta-strand I and the loss of the main helix, but it is not a classical molten globule transition.

Animals↗

Age-dependent changes in the effects of endocardial endothelium on the contractile characteristics of its adjacent myocardium in rats.

Cardiac contractility and the ability of myocardium to respond to various stimuli have been shown to be age-related. Endocardial endothelium has been shown to modulate the performance of its adjacent myocardium, and it has been proven that these changes are reversible by increasing extracellular calcium. This study was designed to evaluate whether the effects of endocardial endothelium and their modifications with changing extracellular calcium were age-dependent. Experiments were carried out on left ventricular papillary muscles isolated from male Wistar rats belonging to three different age groups 7 weeks, 4 months, and 9 months old. Extracellular calcium concentration (0.7 to 5 mM) curves were conducted in papillary muscles with intact endocardial endothelium (+ EE) and after its removal (- EE) with Triton X-100. At a low extracellular calcium concentration (0.7 mM), total tension (TT), maximum rate of tension development (+ dT/dt), time to peak tension (TTPT), and time to half tension decline from maximum tension (RT1/2) increased with increasing age (P < 0.01). Increasing extracellular calcium concentration eliminated age-related differences in TT and RT1/2 did not affect TTPT and caused + dT/dt to increase to greater levels in 7-week-old as compared to 4-month-old myocardium. Endocardial endothelial removal (-EE) had a greater effect on contractile indices in younger rats. Increasing extracellular calcium concentration eliminated EE-mediated changes in contractile indices regardless of age. Thus, increasing extracellular calcium concentration had a greater effect in younger rats and after -EE. Increasing extracellular calcium from 0.7 to 2.5 mM increased total tension in 7-week-olds, between 56% +EE and 131% -EE (P < 0.01): in 4-month-olds, from 29% +EE to 57% -EE (P < 0.01): and in 9-month-olds. from 13% +EE to 23% -EE (P = 0.08). These results indicate that the contractile effects of endocardial endothelium are both age- and calcium-dependent, with responsiveness to endocardial endothelium decreasing with age. Myocardial contractile characteristics also vary with age and these differences are only partially reversible with increasing extracellular calcium concentration.

Age Factors↗

Thermal denaturation of beta-lactoglobulin: effect of protein concentration at pH 6.75 and 8.05.

Previous work on the thermal denaturation of beta-lactoglobulin at about neutral pH and concentrations generally above 50 mg/ml has shown that the temperature of the maximum in the thermogram increases only slightly with concentration. Likewise, there is little if any concentration dependence at acid pH over a wide concentration range. However, so far as we are aware, no work has been described on the thermal denaturation of beta-lactoglobulin in the physiological range of protein concentration and pH appropriate to milk. We report measurements at pH 6.75 and 8.05 in the concentration range 2-120 mg/ml and show that below about 50 mg/ml the position of the maximum becomes strongly dependent on concentration, passing through a minimum near 25 mg/ml and increasing towards the lowest concentrations where measurements were practicable. Moreover, the narrow, well defined and nearly symmetrical thermal transition observed at high protein concentrations contrasts with a broader and more asymmetric curve at lower concentrations. An explanation for the behaviour seen at the lower protein concentrations is suggested, based on the temperature- and concentration-dependent dissociation of the beta-lactoglobulin dimer and an associated conformational transition. The position of the maximum in the thermogram has a marked dependence on the rate of heating down to the lowest rate investigated of 10 degrees C per hour, showing the importance of slow kinetic effects in the denaturation of this protein.

Animals↗

Determinants of arterial stiffness in Chinese migrants to Australia.

The determinants of arterial properties in Chinese migrants to Australia were evaluated. Fifty-eight migrants had recently arrived while 25 were long term residents. All were apparently free of cardiovascular disease. In addition to ultrasound determination of the stiffness of the thoracic aorta, measurements were also made of pulse wave velocities in the trunk and limbs. Factors investigated as potential determinants of arterial properties included age, sex, blood pressure, plasma lipids, urinary electrolyte excretion and duration of residence in Australia. Aortic PWV (PWVAF), PWV from the femoral to dorsalis pedis artery (PWVFD) and the aortic elastic modulus Ep were all dependent on age and mean arterial pressure. Ep was additionally dependent on sodium excretion (negatively), PWVAF on LDL cholesterol (negatively) and migrant status and PWVFD on sex and potassium excretion (negatively). PWV in the arm (PWVBR) was only dependent on sex. Regional aortic stiffness Ep and PWVAF were significantly higher in the established compared with the recent migrants. Dietary differences were evident between the two migration groups, with recent migrants eating significantly more rice meals, but there were no differences in plasma total or HDL cholesterol or triglyceride concentrations. Determinants of the stiffness of the arterial circulation in disease free Chinese subjects change considerably from proximal to distal sites, with age, blood pressure and cholesterol effects being most pronounced proximally and sex and urinary potassium excretion distally. Increasing duration of Australian residence appears to be accompanied by an increase in proximal arterial stiffness.

Adult↗

Molecular cloning, characterization, subcellular localization and dynamics of p23, the mammalian KDEL receptor.

We have isolated a cDNA clone (mERD2) for the mammalian (bovine) homologue of the yeast ERD2 gene, which codes for the yeast HDEL receptor. The deduced amino acid sequence bears extensive homology to its yeast counterpart and is almost identical to a previously described human sequence. The sequence predicts a very hydrophobic protein with multiple membrane spanning domains, as confirmed by analysis of the in vitro translation product. The protein encoded by mERD2 (p23) has widespread occurrence, being present in all the cell types examined. p23 was localized to the cis-side of the Golgi apparatus and to a spotty intermediate compartment which mediates ER to Golgi transport. A majority of the intracellular staining could be accumulated in the intermediate compartment by a low temperature (15 degrees C) or brefeldin A. During recovery from these treatments, the spotty intermediate compartment staining of p23 was shifted to the perinuclear staining of the Golgi apparatus and tubular structures marked by p23 were observed. These tubular structures may serve to mediate transport between the intermediate compartment and the Golgi apparatus.

Amino Acid Sequence↗

Neural wave representation in early vision.

The neural wave representation which describes spatiotemporal information in early vision is proposed in terms of extended Gabor functions in this paper. Its reasonability, completeness and uncertainty in spatiotemporal domains and their frequency domains were investigated. The ranges of these parameters in this representation were estimated on electrophysiological and psychophysical data. We derived the partial differential equations which the neural wave satisfied. The general significance of 3D neural wave representation has been explored.

Animals↗

Formation of glucoside conjugate of acetaminophen by fungi separated from soil.

The phase II metabolite of acetaminophen in filamentous fungi and actinomycetes separated from soil was investigated. Fifty-four filamentous fungi and twenty-seven actinomycetes were screened to transform acetaminophen. The metabolites of acetaminophen were assayed using liquid chromatography-tandem mass spectrometry. The only metabolite was subject to enzymatic hydrolysis to confirm its structure. Acetaminophen was converted into glucoside conjugate, by filamentous fungi JX1-60, LN17-2, LN20-1 and the yield of the conjugate was 60.01%, 44.27%, 100%, respectively, and no phase I metabolites were detected. Glucoside conjugation of acetaminophen in filamentous fungi differs from the phase II metabolism of glucuronidation in humans. The fungus LN20-1 could be a suitable model to synthesize glucoside conjugate of acetaminophen.

Acetaminophen↗

Absence of detectable regression of human hypertensive left ventricular hypertrophy following drug treatment for 1 year.

1. The present study was designed to compare and contrast the effects of 1 year's treatment with angiotensin-converting enzyme inhibition (captopril 25-100 mg daily) and beta-blockade (atenolol 50-100 mg daily) on hypertensive cardiac structure and function as well as the other established cardiovascular risk factors of high blood pressure (BP), lipid profile and blood glucose. 2. This was a prospective randomized open drug trial with blinded end-point echocardiographic and cardiac Doppler assessment in 37 subjects who had primary essential hypertension and left ventricular hypertrophy of captopril (n = 20) versus atenolol (n = 17), adding hydrochlorothiazide if BP was not controlled by 1 month. Multiple time point measurements throughout the 1 year treatment period of the study were made of BP, echocardiographic parameters of cardiac structure and function, as well as lipid profile and blood glucose. 3. There were no significant between-group differences for captopril or atenolol with regard to BP (at baseline (mean +/- SD) 154.0/101.1 +/- 13.3/5.1 and 152.5/101.8 +/- 10.0/5.8 mmHg, respectively) which was normalized by 1 month (138.7/85.6 +/- 18.8/11.7 and 135.4/88.5 +/- 16.9/9.5 mmHg, respectively) in both treatment groups (both P < 0.01 vs baseline). Also, there were no between-group or within-group differences for any of the measures of left ventricular hypertrophy or systolic function throughout the 12 month treatment period; however, captopril alone significantly increased left ventricular early diastolic filling (P < 0.05 vs baseline) at most of the measured time points. Furthermore, there were no significant between- or within-group differences with regard to metabolic (lipids and glucose) profile over the 1 year treatment period of the present study. 4. Markers of cardiovascular risk, including BP, echocardiographic measures of left ventricular hypertrophy, lipid profile and blood glucose were not significantly different between therapies. Despite good BP control by 1 month, neither drug regimen regressed left ventricular hypertrophy. However, captopril significantly increased left ventricular early diastolic filling after 3 months of treatment.

Adolescent↗

An optimal synthetic aperture for circular tomosynthesis.

In circular tomosynthesis obtained from a sufficient number of radiographs with projection directions forming a single cone, object detail at a distance from the plane of interest is blurred according to the zero order Bessel function. The main lobe of this window function defines slice thickness, while its ringing side lobes are undesirable because they permit further outlying structures to "leak" through. Using the orthogonality of Bessel functions, a sampling scheme consisting of multiple, concentric projection cones was designed to synthesize by a finite Fourier-Bessel series a slice window with superior side lobe suppression. The window that concentrates the most "energy" within a finite slice, and can be realized by a limited number of sampling cones, is the zero order circular prolate spheroidal function. Its application to tomosynthesis of 3 mm thick slices with a characteristic detail size of 0.5 mm, concentrated 95% of the total series expansion to only 3 concentric circular scans, yielding a theoretical suppression of the first side lobe of -38 dB, to be compared to -8 dB achieved with the Bessel function. Experimental implementation of this optimal sampling scheme using 3, 8, and 14 projection views, distributed over cones with opening half-anges of 1.92, 4.39, and 6.88 degrees, respectively, resulted in a side-lobe attenuation of at least -20 dB. This attenuation reduced significantly artifacts arising from out-of-plane detail of high spatial frequency (e.g., edges) in tomosynthetic images of clinical interest in dentistry.

Humans↗