Biomedical subjects

Y A Ding

Publications and source records attributed to Y A Ding.

At least 73 records · Page 4Linked to original sources

PubMed1998

Focal atrial tachycardia: reanalysis of the clinical and electrophysiologic characteristics and prediction of successful radiofrequency ablation.

INTRODUCTION: Reports about the clinical and electrophysiologic characteristics of focal atrial tachycardia vary widely. Furthermore, the impact of age, gender, associated cardiac diseases, mechanism, location of atrial tachycardia, and the prediction of results of radiofrequency catheter ablation was not clear. The purpose of this study was to further understand the clinical and electrophysiologic characteristics of focal atrial tachycardia and the prediction of results of radiofrequency ablation. METHODS AND RESULTS: We searched the literature published between January 1969 and July 1997 using the key word "atrial tachycardia" from the MEDLINE and National Library of Medicine systems. The items analyzed were age, sex, cardiac disease, mechanism, attack pattern, cycle length, location, number of atrial tachycardias, results of ablation, and recurrence after ablation. Multivariate analysis showed that age and paroxysmal type of tachycardia were independent predictors of nonautomatic mechanism; age and presence of other cardiac diseases were independent predictors of multiple atrial tachycardias, and age also was the independent predictor of right-sided atrial tachycardia. Atrial tachycardia located in the right atrium was the only significant predictor of successful radiofrequency catheter ablation. Other cardiac diseases and multiple atrial tachycardias were the significant predictors of recurrence after initial successful radiofrequency catheter ablation. CONCLUSION: Patient age is closely related to the clinical and electrophysiologic characteristics of atrial tachycardia based on our reanalysis, which found that patient age is an independent predictor of nonautomatic mechanism, right atrial location, existence of multiple atrial tachycardias, and recurrence of atrial tachycardia after initial successful ablation.

Age Factors↗

PubMed1998

Alterations of nitric oxide synthase expression with aging and hypertension in rats.

The activity and protein expression of endothelial nitric oxide synthase (eNOS) and inducible NOS (iNOS) were investigated during the development of hypertension in spontaneously hypertensive rats (SHR). SHR and Wistar-Kyoto rats (WKY) were studied at three different ages: 4, 14 to 17, and 63 weeks of age. After treatment with saline or lipopolysaccharide (LPS, 10 mg/kg IV) for 3 hours, the aortas were removed for measurement of NOS activity and protein expression assay by [3H]-L-citrulline formation method and Western blot analysis, respectively. Plasma levels of nitrite/nitrate (NO2-/NO3-) and tumor necrosis factor-alpha (TNF-alpha) were also determined. At 14 to 17 weeks and 63 weeks, the basal activity and protein expression of eNOS in the aortas were significantly lower in SHR than in WKY. In addition, the aged WKY exhibited lower eNOS activity than that of adult WKY, but this change was not seen in SHR. By comparison, the basal activity and protein expression of iNOS were only observed in SHR of the 14-to-17-week group and in the 63-week group; SHR still exhibited higher activities, and these differences were further exaggerated by treatment with LPS. The basal and LPS-induced NO2-/NO3- and TNF-alpha levels in the plasma were also higher in the SHR except the 4-week group. After treatment with quinapril, the basal and LPS-induced expressions of iNOS in SHR were significantly attenuated. Our results demonstrated that alterations of activity and protein expression of eNOS and iNOS occurred in SHR. In addition, aging may reduce the activity of eNOS in WKY but not in SHR. The decline of eNOS activity and/or expression may contribute to the development of hypertension, whereas the increase of iNOS expression may be a consequence of the pathological state of vessels associated with hypertension in SHR. However, the augmented expression of iNOS in SHR was attenuated by antihypertensive therapy, suggesting that the abnormal expression of iNOS is associated with hypertension.

Aging↗

PubMed1997

Idiopathic monomorphic ventricular tachycardia: clinical outcome, electrophysiologic characteristics and long-term results of catheter ablation.

Ventricular tachycardia (VT) without structural heart disease or any identifiable predisposing causes for arrhythmia is an uncommon but well-recognized clinical entity. The purpose of this study is to assess the results of catheter ablation therapy and the long-term outcome of patients with idiopathic monomorphic VT in a large patient group. Sixty-one consecutive patients (male/female=40/21; mean age 38+/-16 years) with idiopathic VT underwent electrophysiologic study and an attempt of catheter ablation therapy. The 'left VT' group included 31 patients with QRS morphology of right bundle branch block during VT suggestive of the VT originating from the left ventricle (LV), and the 'right VT' group consisted of 30 patients with QRS morphology of left bundle branch block with normal or right frontal axis deviation suggestive of VT arising from right ventricular outflow tract (RVOT). Idiopathic left VT has sustained VT during the clinical attacks, baseline electrophysiologic study or after isoproterenol infusion; it can be entrained by overdrive ventricular pacing, terminated by verapamil, but not by adenosine (except one case with VT focus at left ventricular free wall). Catheter ablation was successful in 22 (84%) of 26 patients, with recurrence rate of 9%. The successful ablation sites were located at LV inferior-apical septum (16 patients), mid-septum (three patients), high septum (two patients) and high anterior wall (one patient). In the right VT group, 20 (67%) of 30 patients presented clinically repetitive monomorphic VT. Most of the idiopathic right VT (22/30) required isoproterenol to facilitate induction of VT, and were sensitive to both verapamil and adenosine. Successful catheter ablation was achieved in 21 (84%) of 25 patients, with recurrence rate 19%. The successful ablation sites were located at RVOT-septum in 18 patients, and RVOT-free wall in three patients. During a mean follow-up period of 29.2+/-21.7 months (range 1-76 months) after hospital discharge, all patients were alive but one left VT case died of non-cardiovascular cause. We concluded that idiopathic left side and right side VTs have their distinct clinical, electrophysiologic and electropharmacological characteristics suggestive of different underlying mechanisms, and both have a benign prognosis. Furthermore, catheter ablation can be effective in eliminating idiopathic VT originating from the right ventricular outflow tract and left ventricle.

Adult↗

PubMed1997

Ketamine inhibits nitric oxide synthase in lipopolysaccharide-treated rat alveolar macrophages.

PURPOSE: To evaluate the effects of ketamine on the activity and protein expression of inducible nitric oxide synthase (iNOS) induced by lipopolysaccharide (LPS) in rat alveolar macrophages. METHODS: Pulmonary alveolar macrophages isolated from Wistar-Kyoto rats were used. After incubation of macrophages with ketamine (1, 10, or 100 microM) and LPS (1 microgram.ml-1) for 24 hr, the cell-free medium was removed for measuring the nitrite and tumour necrosis factor-alpha (TNF-alpha) levels by Griess reaction and ELISA kit, respectively. The harvested macrophages were also used to determine the activity of iNOS by using the conversion of [3H]-L-arginine to [3H]-L-citrulline method. In addition, the protein expression of iNOS was detected by Western blot analysis. RESULTS: In rat alveolar macrophages, (i) ketamine (1 to 100 microM) caused a dose-dependent suppression of the production of nitrite and TNF-alpha induced by LPS and (ii) ketamine (100 microM) inhibited the activity (46.5 +/- 4.8%, P < 0.05) and protein expression (35 +/- 11%, P < 0.05) of iNOS in response to LPS. CONCLUSION: These results show that ketamine inhibits the activity and expression of iNOS in LPS-activated alveolar macrophages, which may be associated with the reduction of the release of TNF-alpha following LPS treatment.

Analysis of Variance↗

PubMed1997

Losartan attenuates myocardial ischemia-induced ventricular arrythmias and reperfusion injury in spontaneously hypertensive rats.

To assess the efficacy of losartan (2-n-butyl-4-chloro-5-hydroxymethyl-1-[(2'-(1H-tetrazol-5-yl)biphe nyl-4-yl)methyl]imidazole, potassium salt), an angiotensin II receptor antagonist, on acute myocardial ischemia, 36 four-month-old spontaneously hypertensive rats were used. The animals underwent 45 min of left coronary artery occlusion and 1 h of reperfusion and were randomly assigned to control and losartan-treated groups (2, 5, and 10 mg/kg, intravenously). Losartan was administered 15 min before ischemia. Electrocardiograms (lead II) were monitored continuously throughout the experiment. To assess the anti-infarct effect of losartan, the area at risk was determined by methylene blue dye and the infarct size was determined by nitroblue tetrazolium chloride staining. The areas of risk and infarct were measured by computerized planimetry. Results demonstrated that the low and intermediate doses (2 and 5 mg/kg) of losartan significantly decreased the incidence of ventricular fibrillation and mortality during the ischemic period induced by left coronary artery occlusion. However, a significant reduction in infarct size, calculated as a percentage of the area at risk, was noted in all three losartan-treated groups (control: 41.5% +/- 5.2%, losartan, 2 mg/kg: 11.2% +/- 5.8%, 5 mg/kg: 8.5% +/- 2.7% and 10 mg/kg: 13.7% +/- 1.6%). The results suggest that losartan may be useful in the treatment of ventricular arrhythmias induced by acute myocardial infarction and attenuation of reperfusion injury in hypertension.

Acute Disease↗

PubMed1997

Interleukin-1 in ischemia-reperfusion acute lung injury.

Interleukin-1 (IL-1) is a proinflammatory cytokine produced by blood-borne and resident inflammatory lung tissue involved in the thrombotic occlusion of the pulmonary microcirculation and the increase of the vascular permeability following a wide variety of injuries and sepsis. The locally accentuated, organ-related activation of this cytokine seems to be responsible for the development of acute lung injury. The present study was conducted to determine if IL-1beta was produced in an ischemia-reperfusion (I/R) rat model subjected to lung injury. We measured sequential perfusate levels of IL-1beta by ELISA and we measured IL-1 gene expression in the rat lung tissue by a reverse-transcriptase polymerase chain reaction method. Little IL-1beta gene expression was observed in normal rat lung tissue. Perfusate IL-1beta slightly increased 2 h after induced ischemia and 3 h after reperfusion. IL-1beta gene expression rapidly increased as early as 30 min after ischemia and continued to increase for up to 120 min. IL-1beta gene expression was dramatically upregulated during reperfusion after cessation of ischemia, reached a peak at 1 h, and then gradually decreased (2 to 3 h) to near baseline levels. During ischemia, the increased IL-1 gene expression was not significantly different between the ventral and dorsal sites of the lung. However, IL-1 gene expression markedly increased on the dorsal part (the dependent site for a rat in a supine position) after reperfusion. From these results, it appears that IL-1 may have an important role in I/R lung injury.

Acute Disease↗

PubMed1996

Evidence for inducible nitric oxide synthase in spontaneously hypertensive rats.

This study investigates the mechanism of the production of nitric oxide (NO) caused by lipopolysaccharide (LPS) in spontaneously hypertensive rats (SHR) or Wistar-Kyoto (WKY) rats. The injection of LPS (5 mg/ kg, i.v.) caused a mild hypotension in WKY rats, while it induced a more severe hypotensive effect in SHR. The basal level of plasma nitrite was slightly higher in SHR than in WKY rats. At 3 h after injection of LPS, the increment in plasma nitrite was more significant in SHR. Prior to the treatment of rats with LPS, the plasma level of tumor necrosis factor-alpha (TNF alpha) was also higher in SHR than in WKY rats, and LPS induced a more significant increase of TNF alpha level (at 1 h) in SHR. In rats treated with LPS, acetylcholine-induced relaxation was significantly impaired in thoracic aortic rings obtained from WKY rats, but not in those from SHR. By contrast, L-arginine (1 mM) did not cause any relaxations in rings without the endothelium obtained from WKY rats while it slightly relaxed those from SHR, and this difference was further augmented by treatment of rats with LPS for 3 h. In addition, the basal cGMP level was higher in SHR, which was inhibited by aminoguanidine (AG, 1 mM). The treatment of rats with LPS further increased the formation of cGMP in both strains and this increment was greater in SHR than in WKY rats, which was also attenuated by AG to a similar level between both strains. Interestingly, an expression of inducible NO synthase (NOS II) protein was only observed in SHR, and further enhanced by treated rats with LPS. We conclude that an increased production of NO in SHR, which was further enhanced by LPS, is attributed to a basal expression of NOS II.

1-Methyl-3-isobutylxanthine↗

PubMed1996

The inhibitory effect of 2-thienyl 2'-hydroxyphenyl ketone (C85) on platelet thromboxane formation.

A new synthetic compound, 2-thienyl 2'-hydroxyphenyl ketone (C85), was demonstrated as an antiplatelet agent. In rabbit washed platelets, C85 dose-dependently inhibited arachidonic acid(AA), collagen and platelet activating factor(PAF)-induced platelet aggregation and ATP release with IC50 values of 0.6 +/- 0.2, 20.5 +/- 8.3 and 145.6 +/- 28.6 microM respectively. In human platelet rich plasma(PRP), C85 selectively inhibited the second phase of platelet aggregation and ATP release induced by epinephrine. The formation of platelet thromboxane B2 (TXB2) caused by AA, collagen and thrombin was completely inhibited by C85(10 microM). C85 could significantly reduce cyclooxygenase activity as reflected by attenuation of prostaglandin E2(PGE2) formation. C85 also possess weakly inhibitory effect on thromboxane synthase as reflected by slightly inhibition of prostaglandin H2 (PGH2)-induced TXB2 formation. In Fura-2/AM loaded platelets, the rise of intracellular calcium level challenged by AA, collagen and thrombin were inhibited by C85. The C85(10 microM) also significantly suppressed the phosphoinositide breakdown induced by AA and collagen. In vivo, C85(50 micrograms/Kg i.p.) produced a marked prolongation of tail bleeding time than that treated by indomethacin in mice. In summary, the antiplatelet mechanism of C85 is mainly inhibition of platelet cyclooxygenase activity and partly inhibition of thromboxane synthase activity and lead to diminution of TXA2 formation.

Adenosine Triphosphate↗

PubMed1996

Thrombogenic and lipid risk factors in hypertension and coronary artery disease.

Hypertension is not solely a phenomenon of elevation of systemic blood pressure. It frequently occurs in association with a great deal of metabolic derangement's and should never be regarded as coincidental only. Furthermore, a knowledge of these metabolic derangements may provide a clue to unveil the underlying mechanisms how essential hypertension and its associated complications arise. Therefore we devoted our attention to platelet dysfunction and dyslipidemia which are closely associated with atherosclerosis-the commonest complication of hypertension. We found there exists enhanced platelet aggregation in essential hypertension and a variety of its associated atherosclerotic diseases. Such an aberration in platelet function may be modified after administration of antihypertensive medications such as angiotensin converting enzyme (ACE) inhibitors, calcium channel blockades, beta blockades and dietary manipulation. We also demonstrated the close association between hypertension and its associated atherosclerotic complications and abnormal lipids profile. Hypertriglyceridemia which was initially regarded unimportant in the pathogenesis of atherosclerosis is found to be closely related to hypertension. In an intensive review, we found that people in Taiwan has experienced a huge increase in dietary calories and total fat consumption. In order to solve this emerging problem, a national guideline for diagnosis and management of lipid disorders in Taiwan was developed and announced. Through these efforts, we hope we can reduce the cardiovascular morbidity and mortality in Taiwan and even extend our experience to other countries.

Arteriosclerosis↗

PubMed1996

Relationship between smoking status and cardiovascular disease risk factors in young adult males in Taiwan.

BACKGROUND: To evaluate smoking status and cardiovascular risk factors in young male adults in Taiwan. METHODS: After cluster sampling, we performed a cross-sectional survey to assess smoking status, duration, and number of cigarettes smoked in 781 young adult males (mean age 20 years, range 18-24). Cardiovascular disease risk factors, including anthropometric factors, blood pressure, lipoproteins and apolipoprotein levels were also measured. RESULTS: In total 211 subjects (27.0%) had never smoked, 38 subjects (4.9%) were ex-smokers, and 532 (68.1%) still smoked cigarettes. The prevalence of smoking was higher than in 1989 and 1990 (54.8 and 59.4%, respectively). Current smokers had significantly higher serum triglyceride and lower high-density lipoprotein-cholesterol levels than subjects who had never smoked (56.2 versus 46.9 and 55.6 versus 59.0 mg/dl, respectively; P < 0.05 for both). No difference was found in other cardiovascular risk actors among subjects in the different smoking groups or among current smokers who had smoked for different periods of time or who smoked different numbers of cigarettes. CONCLUSION: These data suggest that the prevalence of smoking in young adult males in Taiwan has increased progressively. No differences were found in anthropometric factors or blood pressure among subjects of different smoking status. Abnormal lipoprotein levels (higher triglyceride and lower high-density lipoprotein cholesterol) were found in current smokers compared with non-smokers. A longer follow-up study will be needed to confirm whether the smoking status of these young adults can be correlated with the risk of cardiovascular disease.

Adolescent↗

PubMed1996

Analysis of 109 cases of infective endocarditis in a tertiary care hospital.

BACKGROUND: Early diagnosis and treatment can benefit the outcome of patients with infective endocarditis. The older diagnostic criteria (von Reyn criteria) relied upon tissue pathology and blood culture results, but the sensitivity was low. A newly proposed criteria, Duke criteria which apply echocardiographic findings as a major factor in diagnosis, have shown a better sensitivity in the diagnosis of infective endocarditis. METHODS: From 1984 to 1994, 120 episodes of endocarditis in 119 patients were reviewed retrospectively. One hundred and nine episodes fulfilling the Duke criteria were enrolled. The demographic data, antecedent disease, predisposing factors for infective endocarditis including systemic disease, prosthetic valve, intravenous drug abuse, dental or surgical manipulation, culture results, echocardiographic findings, complications and outcome were recorded and analyzed. RESULTS: Sixty-six percent (72/109) was definite endocarditis, and 34% (37/109) was possible endocarditis, as categorized by Duke criteria. Eleven percent (12/109) of the patients were rejected by von Reyn criteria. The common possible predisposing factors were rheumatic heart disease, congenital heart disease, mitral valve prolapse, dental manipulation and intravenous drug abuse. Both patients with positive blood culture and negative blood culture results had one-fourth mortality rate. A notably higher mortality rate was found in patients with S. aureus endocarditis as compared with those of endocarditis caused by viridans streptococci(44% vs. 8%, p < 0.05). Patients with echocardiographic vegetations had a higher mortality rate (32% vs. 11%, p < 0.05) and more peripheral or organ embolic events (26% vs. 6%, p < 0.05) than those without vegetation. CONCLUSIONS: The Duke criteria are more sensitive than the von Reyn criteria for diagnosis of infective endocarditis. S. aureus endocarditis carried a higher mortality rate than viridans streptococci endocarditis. The present study also indicated that patients with discernible valvular vegetation on echocardiogram had a high mortality rate and occurrence of peripheral or organ embolic events. However, there was no statistical significance in the development of congestive heart failure and CNS complications between the patients with and without vegetation.

Adolescent↗

PubMed1996

Acute myocarditis as an initial manifestation of systemic lupus erythematosus: a case report.

A rare case of systemic lupus erythematosus with initial manifestation of myocarditis is reported here, found in a 24-year-old female who presented first with an episode of exertional dyspnea, later developing life-threatening arrhythmia, and left ventricular dysfunction. There were no classical clinical manifestations of SLE such as arthragia or malar rashes as initial symptoms. Subsequently, the only clue was traced with positive ANA screening test. Central nervous system manifestations were found and proteinuria was detected. We ordered intravenous "pulses" of methylprednisolone, followed by maintenance of daily glucocorticoid because the criteria of SLE seemed applicable. The patient responded well and rapidly. This initial manifestation for SLE is so rare and unusual that it has not previously been described.

Acute Disease↗

PubMed1995

Antiplatelet actions of 2-(4-[1-(2-chlorophenyl) piperazinyl]) methyl-2,3-dihydroimidazo[1,2-c]quinazolin-5(6H)-one compound.

The new quinazolinone derivative, 2-(4-[1-(2-chlorophenyl)piperazinyl]) methyl-2,3-dihydroimidazo[1,2-c]quinazolin-5(6H)-one(CK53 ), inhibited platelet aggregation and ATP release induced by arachidonic acid, collagen, PAF and U46619 in washed rabbit platelets. In human platelet-rich plasma CK53 also significantly suppressed the platelet aggregation and ATP release challenged by epinephrine and ADP. The thromboxane B2 formation of rabbit washed platelets caused by collagen and thrombin was reduced by CK53 but that induced by arachidonic acid. CK53 inhibited the intracellular calcium increase stimulated by collagen and thrombin in quin-2/AM-loaded rabbit platelets. Phosphoinositides breakdown caused by collagen, U46619, PAF and thrombin was inhibited by CK53. CK53 also suppressed the aggregation of elastase-treated human platelets induced by fibrinogen but no alteration in platelet cyclic-AMP level. In conclusion, these data indicate that antiplatelet effect of CK53 may be mainly due to the direct inhibition of phosphoinositides breakdown.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1995

Chronic exercise enhances endothelium-mediated dilation in spontaneously hypertensive rats.

This study investigated the effect of physical training on endothelial function in spontaneously hypertensive rats (SHR). After 3 months, in conscious trained- and untrained-SHR body weight, systolic blood pressure and heart rate were 220 +/- 6 g vs 271 +/- 9 g, 172 +/- 7 mmHg vs 210 +/- 8 mmHg and 314 +/- 10 vs. 348 +/- 12 beats/min, respectively. In vitro, the dose-response curves of norepinephrine in isolated intact aortic and mesenteric rings form the exercise trained-SHR were significantly lower than those from the untrained-SHR. With denuded preparations, norepinephrine concentration-response curves were shifted to the left both in the trained- and untrained-SHR. This shift in the trained-SHR exceeded that in the untrained-SHR. The vasodilator response to acetylcholine in the trained-SHR was significantly greater than that in the untrained-SHR. Either N omega-nitro-L-arginine (100 mumol/l) or methylene blue (10 mumol/l) inhibited acetylcholine-induced vasodilator effect in aorta of trained- and untrained-SHR, but not in mesenteric artery of trained-SHR. Tetraethylammonium (10 mmol/l) inhibited significantly the N omega-nitro-L-arginine and methylene blue-resistant relaxation in mesenteric artery of trained-SHR, but not only by indomethacin (10 mumol/l). Collectively, these data demonstrate that chronic exercise increases EDRF/EDHF production (presumably by increasing endothelial shear stress), and may contribute to the enhanced effects of post-exercise hypotension.

Acetylcholine↗

PubMed1995

Cilazapril reverses endothelium-dependent vasodilator response to acetylcholine in mesenteric artery from spontaneously hypertensive rats.

This study was designed to evaluate the effect of chronic treatment with cilazapril on vascular reactivity of aorta and mesenteric artery from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Cilazapril (5 mg/kg), an angiotensin converting enzyme inhibitor, was injected intraperitoneally twice a day for 4 weeks. Results demonstrated that acetylcholine (ACh)-induced relaxation in aorta and mesenteric artery from SHR was significantly less than that from WKY, cilazapril-treated WKY, and SHR. The impairment of ACh-induced relaxation in SHR was significantly reversed after cilazapril treatment and there were no significant differences among WKY, cilazapril-treated WKY, and SHR. Meanwhile, both N omega-nitro-L-arginine (LNNA; 10(-4) mol/L) and methylene blue (MB; 10(-5) mol/L) completely blocked the vasodilator response to ACh in aorta but only partly inhibited in mesenteric artery from WKY, cilazapril-treated WKY, and SHR. These LNNA- and MB-resistant vasodilator responses to ACh in mesenteric artery were only slightly inhibited by TEA (10(-3) mol/L) but not by indomethacin (5 x 10(-6) mol/L). These findings suggest that there may be an unidentified endothelium-dependent relaxing factor(s) (EDRF), which exists in the endothelium and may participate in the modulation of blood pressure in SHR. Results further demonstrate that the antihypertensive effect of cilazapril may be partly mediated by the reversing function of endothelium to release EDRF and LNNA-resistant, unidentified relaxing factor(s).

Acetylcholine↗

PubMed1995

2-Heteroaryl 2-substituted phenylketone derivatives and their inhibitory activity on platelet aggregation.

R 68070 and CV-4151 are two compounds possessing both thromboxane synthetase inhibitory activity and thromboxane receptor antagonist properties. 2-Heteroaryl 2-substituted phenylketone derivatives with a partial structural similarity to R 68070 and CV-4151, i.e. possessing a phenyl and a heteroaryl moiety, have been prepared and found to have antiplatelet activity. The compound 2-thienyl 2'-hydroxyphenyl ketone (4) was shown to completely inhibit platelet aggregation induced by arachidonic acid at a concentration of 5.0 microM. Structure-activity analysis indicated that the presence of a ketone group is an important requirement for this inhibitory activity. An o-hydroxyl substitution on the phenyl ring, and a 2-thienyl of heteroaryl ring might increase inhibitory activity.

Animals↗

PubMed1995

Anthropometry and lipoproteins-related characteristics of young adult males in Taiwan.

OBJECTIVES: To investigate the prevalence of obesity and the lipoprotein-related characteristics among young male adults in the Taiwan area. DESIGN AND SUBJECTS: After cluster sampling, a cross-sectional survey with a total of 936 males (mean age 20, 18-24) were enrolled. MAIN OUTCOME MEASURES: The distribution of anthropometric and lipoprotein-related variables and their correlations in young male adults were measured. The prevalence of obesity by different criterion and the lipoprotein characteristics of obese and non-obese were analyzed separately. RESULTS: The prevalence of obesity was 9.6% by the criterion of body weight greater than 20% of ideal body weight, or 12.6% by the criterion of body mass index (BMI) greater than 25. The obese subjects had significantly higher serum total cholesterol (CHOL), triglyceride (TG) and apo-lipoprotein B (apo B) and lower higher density lipoprotein-cholesterol (HDL-C) levels than the non-obese. The apo A1 levels were 141.3 and 141.9 mg/dl and the lipoprotein [a] (Lp[a]) were 17.4 and 17.1 mg/dl in obese and non-obese respectively, the difference being not statistically significant. Pearson correlation coefficients of body weight, body height, BMI, waist circumference, hip circumference and waist-hip ratio (WHR) to lipoprotein variables showed that both BMI and WHR are positively correlated with CHOL, TG and apo B, but negatively correlated with HDL-C. Furthermore the lipoprotein variables were better correlated with BMI than WHR in lean subjects (BMI < 25). However, this phenomenon was quite different in obese (BMI > 25) subjects, where the WHR was more highly correlated with lipoprotein variables than with BMI. CONCLUSION: The prevalence of obesity is slightly higher than reported in previous studies in Taiwan. The obese subjects had various abnormal lipoprotein metabolic characteristics, such as higher CHOL, TG, and apo B and lower HDL-C levels than non-obese subjects. The BMI was more highly correlated with lipoprotein variables than was WHR in lean subjects, but the WHR was more highly correlated with lipoprotein variables than was BMI in obese subjects.

Adolescent↗

PubMed1995

Comparison of amlodipine and quinapril on ambulatory blood pressure and platelet function in hypertension.

The effect of calcium channel blocker (CCB), amlodipine (5-10 mg/day) and angiotensin-converting enzyme (ACE) inhibitor, quinapril (10-40 mg/day) on ambulatory blood pressure (ABP), rheological and platelet function in hypertension were compared in this randomised double-blind placebo-controlled cross-over study. This study was preceded by 4 weeks placebo run-in period and the total duration of the study was 28 weeks. Casual and 24 h ABP, plasma renin activity (PRA) and plasma aldosterone (PA) concentration as well as metabolic and platelet function were determined before and at the end of each drug therapy. A total of 27 patients completed this study. Casual BP was significantly reduced after amlodipine or quinapril treatment, but there was no change in heart rate. Regarding the 24 h ABP, amlodipine produced a fall from 145 +/- 8/94 +/- 7 to 130 +/- 13/85 +/- 10 mm Hg (P < 0.001 for both SBP and DBP). Quinapril also caused a reduction from 144 +/- 10/94 +/- 7 to 134 +/- 12/88 +/- 8 mm Hg (P < 0.001 for both SBP and DBP). Neither amlodipine nor quinapril produce any significant change in heart rate. The level of 6-keto-prostaglandin Fl alpha (6-Keto-PGFl alpha) was increased from 36.8 +/- 4.4 to 45.1 +/- 2.5 pg/ml (P < 0.05) and no significant change of thromboxane B2(TXB2) was noted after amlodipine treatment. PRA was increased from 1.24 +/- 0.31 to 1.62 +/- 0.41 ng/ml/h (P < 0.05) after quinapril treatment. Other biochemical parameters were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗