Search PubMed⌕ Search

Biomedical subjects

B S Hsieh

Publications and source records attributed to B S Hsieh.

At least 19 recordsLinked to original sources
PubMed1998

Integrated medical informatics with small group teaching in medical education.

National Taiwan University College of Medicine (NTUCM) introduced small groups of teaching and basic-clinical integrated courses for medical students in 1992. By using computer network and multimedia techniques, this study tried to overcome barriers to learning in small group teaching. The Department of Medical Informatics of NTUCM established campus networking and computer classrooms and provided Internet and intranet network services including mail, netnews, bulletin board systems (BBS), world wide web (WWW), gopher, ftp and local file servers. To implement an interactive learning environment, the authors first tried mail lists, newsgroups and BBS. Next an integrated learning system prototype on the WWW was developed to provide functions including online syllabus, discussion boards simulated to BBS, online talk, interactive case studies, virtual classroom with video on demand (VOD) and Internet medical resources. The results showed that after the medical students completed the required course of medical informatics and had good network access using a network to communicate with each other became a daily practice. In the future, the system will extend to the tutoring of clinical practice and continuing medical education. The authors expect a national medical education network and more international cooperation and exchange.

Curriculum↗
PubMed1998

Pharmacologic agents inhibit rat mesangial cell proliferation and collagen synthesis.

Prevention of the development of end-stage renal disease is one of the most promising areas of research in nephrology. Because mesangial cell proliferation and extracellular matrix accumulation have been regarded as antecedents of glomerulosclerosis, agents that can inhibit mesangial cell proliferation may have a potential to retard the progression of renal diseases. Therefore, we investigated several clinically available agents that might affect mesangial cell proliferation and collagen synthesis in male Sprague-Dawley rats. Cell proliferation was measured by the tetrazolium dye uptake method. Collagen synthesis was measured by 3H-proline incorporation into pepsin-resistant, salt-precipitated collagen. Intracellular cAMP levels were measured by enzyme immunoassay. Our results showed that hydralazine (82% inhibition at 10 micrograms/mL), ticlopidine (61% inhibition at 30 micrograms/mL), aminophylline (66% inhibition at 200 micrograms/mL), and nicametate (91% inhibition at 1 mg/mL) inhibited serum-stimulated rat mesangial cell (RMC) growth in a dose-dependent manner. Ticlopidine (43% inhibition at 30 mg/mL), aminophylline (52% inhibition at 200 mg/mL), and nicametate (35% inhibition at 1 mg/mL) inhibited collagen synthesis in confluent RMCs. Aminophylline may act through increasing intracellular cAMP levels (9.7 +/- 0.7 pmol/mg protein at 200 micrograms/mL of aminophylline vs 4.2 +/- 0.6 pmol/mg protein at control). These data suggest that aminophylline, ticlopidine, hydralazine, and nicametate can inhibit RMC proliferation and collagen synthesis.

Aminophylline↗
PubMed1998

Urinary endothelin-1 in patients with renal disease.

The purpose of this study was to investigate the usefulness of urinary endothelin-1 (ET-1) as a marker of renal disease. We measured urinary excretion of ET-1 in 28 patients with glomerulonephritis (GN), 22 patients with chronic renal failure (CRF), 40 patients with end-stage renal disease (ESRD), and 17 healthy volunteers. There was no significant difference in 24-hour urinary ET-1 excretion among the four groups (mean +/- SEM, 0.49 +/- 0.22 ng in controls, 0.79 +/- 0.37 ng in GN patients, 0.39 +/- 0.18 ng in CRF patients, and 0.28 +/- 0.11 ng in ESRD patients). The 24-hour urinary excretion of ET-1 in patients with GN or CRF showed significant correlation with the urinary excretion of sodium (r = 0.27, p < 0.05). The 24-hour urinary beta 2-microglobulin (beta 2M) excretion in patients with CRF (18.4 +/- 2.6 mg) or ESRD (9.7 +/- 1.1 mg) was significantly higher than in normal control subjects (0.23 +/- 0.11 mg). Serum creatinine concentration was positively correlated with the 24-hour urinary excretion of beta 2M in patients with GN or CRF (r = 0.50, p < 0.001). These findings indicate that urinary ET-1 is not as good a marker of renal disease as urinary beta 2M. However, it may be responsible for urinary sodium excretion in patients with GN or CRF.

Biomarkers↗
PubMed1996

Hydralazine inhibits human peritoneal mesothelial cell proliferation and collagen synthesis.

The integrity of the mesothelial layer is essential for both defence and solute transport in continuous ambulatory peritoneal dialysis (CAPD). The human peritoneal mesothelial cell (HPMC) culture has been shown to be a very useful tool to study the peritoneal mesothelial stem cell behaviour. We investigated whether hydralazine, an antihypertensive agent frequently used, might affect HPMC growth and collagen synthesis. HPMCs were cultured from specimens of human omentum by enzymatic disaggregation of omentum. HPMC growth was evaluated by modified methyltetrazolium (MTT) assay. Cell viability was confirmed by trypan blue exclusion and lactate dehydrogenase assay. Collagen synthesis was measured by 3H-proline incorporation into pepsin-resistant, salt-precipitated collagen. Intracellular cAMP levels were measured by enzyme immunoassay. The procollagen alpha 1 (I) mRNA expression was evaluated by Northern blot analysis. Hydralazine inhibited serum-stimulated HPMC growth in a dose-dependent manner. The maximal inhibition was 93% at a concentration of 100 micrograms/ml. Hydralazine inhibited collagen synthesis in confluent mesothelial cells (47% inhibition at a concentration of 100 micrograms/ml). The procollagen alpha 1 (I) mRNA expression was also decreased by hydralazine (about 50% decrease at 100 micrograms/ml). These effects may be due to the phosphodiesterase inhibition property of hydralazine to increase intracellular cAMP levels. These data suggest that the use of hydralazine in CAPD patients may affect peritoneal membrane function and integrity.

Antihypertensive Agents↗
PubMed1995

Quantitative analysis of messenger ribonucleic acid encoding natriuretic peptide receptors in aldosterone-producing adenoma.

There exist conflicting data regarding the inhibitory effect of atrial natriuretic peptide on aldosterone production from aldosterone-producing adenoma (APA). Natriuretic peptides mediate their actions through natriuretic peptide receptors (NPRs). Whether or not NPRs are present in the tumors remains controversial. To elucidate this paradox, gene expression of NPRs was examined by Northern blot analysis and competitive polymerase chain reaction in tumorous and non-tumorous portions of APA, and in normal adrenal gland from patients with renal cell carcinoma. The results of Northern blot analysis showed the presence of messenger ribonucleic acid (mRNA) of three NPRs in all adrenal tissues, including APA. The proportional expression of NPR gene transcripts in APA was type A (0.6%), type B (18.7%), and type C (80.7%). The levels, but not the proportions, of type C and possibly type B NPR mRNAs were lower in tumorous and non-tumorous portions of APA compared to those in normal adrenal gland (type C 190.2 +/- 24.5 [means +/- SEM, normal adrenal gland] > 168.1 +/- 20.8 [non-tumorous portion] > 112.2 +/- 15.5 [tumorous portion] pg/10 micrograms total RNA, F = 3.82, P < 0.05; type B 45.2 +/- 8.5 [normal adrenal gland] > 30.0 +/- 5.2 [non-tumorous portion] > 25.1 +/- 4.1 [tumorous portion] pg/10 micrograms total RNA, F = 3.03, P = 0.065). The mRNA levels of type C, rather than type A or type B, NPR were correlated with the percentage of zona fasciculata-like cells in APA (r = 0.90, P < 0.05). In conclusion we have demonstrated the presence of mRNA encoding the three NPRs in APA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1995

Zona fasciculata-like cells determine the response of plasma aldosterone to metoclopramide and aldosterone synthase messenger ribonucleic acid level in aldosterone-producing adenoma.

The different responses of plasma aldosterone to ACTH and angiotensin II in aldosterone-producing adenoma (APA) is thought to be due to the various cellular compositions of the tumors. To investigate whether the dopaminergic regulation of aldosterone in APA is also dependent on the cellular types, we studied the effects of metoclopramide on plasma aldosterone in six patients with APA. The messenger RNA (mRNA) levels of aldosterone synthase (P450aldo), 11 beta-hydroxylase (P450(11) beta), and 17 alpha-hydroxylase (P450(17) alpha) of APA and normal adrenal glands were determined by competitive polymerase chain reaction. After administration of metoclopramide (an antagonist of dopamine-2 receptor), the increment of plasma aldosterone correlated inversely with the percentage of zona fasciculata cells of APA. The mRNA level of P450aldo in the tumorous portion was much higher, whereas the levels of P450(11) beta and P450(17) alpha mRNAs were lower, than those of the nontumorous portion and normal adrenals. There was a correlation of the percentage of zona fasciculata cells in APA with the levels of P450aldo and P450(11) beta mRNAs, but not with P450(17) alpha mRNA. These results suggest that differential responsiveness of plasma aldosterone to metoclopramide may be due to various proportions of different cell types in APA that may have different expression of dopamine-2 receptor. In addition, this histologically dependent expression was present at the transcriptional level of the gene responsible for aldosterone biosynthesis.

Adenoma↗
PubMed1994

Blood pressure, circulating atrial natriuretic peptide and sodium excretion responses during acute saline infusion in patients with essential hypertension.

In order to examine whether changes in circulating atrial natriuretic peptide (ANP) and sodium excretion during saline infusion in patients with essential hypertension (EH) could be modulated by the severity of resting arterial blood pressure (BP), 30 subjects with EH and nine normotensive subjects were given 2 L of isotonic saline infusion at a rate of 500 mL/hour. Plasma ANP concentrations in EH increased significantly from 64.9 +/- 5.1 (mean +/- SEM) to 92.5 +/- 12.8 pg/mL at the first hour and peaked at the second hour. In normotensives, the increase of plasma ANP was not significant until the fourth hour of infusion. Hypertensive subjects sustained a greater percentage increment of mean BP (MBP) than normotensives at the end of infusion. Those with pre-saline MBP exceeding 107 mmHg (group A) exhibited a faster and greater rise in plasma ANP after saline loading than those having less than or equal to 107 mmHg (group B). The post-saline four-hour natriuresis was appreciably higher in group A than group B, while the percentage increment of MBP at the fourth hour was significantly greater in the latter as compared to normal controls. These results indicate that patients with higher basal arterial pressure attain a faster and greater ANP response following saline infusion than those with lower BP. This phenomenon may be responsible for the maintenance of short-term fluid-volume and BP homeostasis during acute sodium loading in established EH.

Adult↗
PubMed1993

The acute effect of nicardipine on the renin-angiotensin-aldosterone system in salt-sensitive essential hypertension.

To determine the role of the renin-angiotensin-aldosterone (RAA) system in the acute effect of calcium channel blockers, we examined the acute effect of 40 mg nicardipine in 21 essential hypertensive patients. Nine patients whose mean blood pressure (MBP) decreased more than 5% at 2 hours after 20 mg furosemide i.v. were classified as salt-sensitive (SS); the remainder as salt-resistant (SR). The percentage decrease of MBP with nicardipine was not different between the two subgroups (12.4 +/- 2.5% for SS, and 17.7 +/- 4.1% for SR). The percentage decrease of MBP correlated with the pretreatment MBP (r = 0.67, p < 0.001), but not with the basal plasma renin activity (PRA), plasma aldosterone concentration (PAC), or natriuretic response. A significant increase of heart rate was noted in SR (31.2%) but not in SS (6.5%), and was associated with a higher increase of PRA in SR (90.7%) than in SS (25.5%). A correlation between the increase of PRA and the percentage increase of heart rate was noted (r = 0.77 p < 0.001). Decrease of PAC was observed in SS but not in SR until the third hour. The 3-hour sodium excretion was slightly greater in SR than in SS (59.9 +/- 9.1 vs. 35.1 +/- 3.0 mEq; p < 0.05). In summary, the acute hypotensive effect of nicardipine is dependent upon the vascular tone regardless of the status of the RAA system. An increase in PRA by nicardipine resulting from a baroreflex mechanism may counteract the inhibitory effect of aldosterone secretion by nicardipine. The unchanged PRA in SS is due to their blunted baroreflex control of heart rate. Mechanisms other than the change in the RAA system by nicardipine may account for the acute natriuretic effect.

Adult↗
PubMed1993

Atrial natriuretic peptide and blood pressure responses during acute sodium loading in patients with essential hypertension.

Atrial natriuretic peptide (ANP) response during acute saline loading and its relationship to changes in blood pressure (BP) and sodium excretion were studied in 21 patients with essential hypertension (EH) and nine normotensive volunteers. Following 2 liters of isotonic saline infusion at a rate of 500 mL/hour, plasma ANP concentrations in patients with EH increased significantly from 69.9 +/- 6.0 (mean +/- SEM) to 103.6 +/- 17.1 pg/mL (p < 0.05) in the first hour and peaked at the second hour. In normal subjects, the increase in plasma ANP was not significant until the third hour of infusion (64.6 +/- 6.2 to 82.0 +/- 7.5 pg/mL, p < 0.05). Mean BP (MBP) remained stable and the natriuretic responses were similar in the two groups. However, hypertensive patients with a prompt rise in ANP during the initial two hours of infusion (fast responders) maintained a BP balance more efficiently than those with a delayed rise in ANP (slow responders), as the latter displayed a significant increase in MBP two hours after saline loading (126 +/- 5 to 133 +/- 5 mmHg, p < 0.05). Fast responders also had a greater percent of suppression of plasma aldosterone (-49.7 +/- 9.2 vs 15.9 +/- 42.0%, p = 0.05) one hour after saline loading, and a higher increment of natriuresis (263.9 +/- 43.8 vs 97.5 +/- 27.4%, p < 0.025) in the second hour of infusion than slow responders. Our results indicate that during acute saline loading, patients with EH have a faster and greater rise in plasma ANP than normotensives.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Heterogeneous blood pressure response to furosemide and captopril in primary aldosteronism.

The hypertension associated with primary aldosteronism (PA) is often regarded as volume dependent/salt-sensitive. However, not all patients sustain an increase in blood pressure upon sodium loading. In order to examine the sodium sensitivity in PA, 21 patients with aldosteronoma were tested for acute hypotensive response to intravenous furosemide and oral captopril. Ten patients having a decrease in mean blood pressure (MBP) exceeding 5% at the second hour after a 20 mg furosemide injection were defined as diuretic-responders (DR), while the remainder were defined as diuretic-non-responders (DN). The DR group had a higher baseline MBP (135 +/- 6 [mean +/- SE] vs 121 +/- 4 mmHg, p < 0.05) and serum sodium concentration (145.7 +/- 1.4 vs 143.0 +/- 0.7 mmol/L, p < 0.05) than the DN group. The extent of natriuresis induced by furosemide was not different between the two subgroups. Following 100 mg of captopril administered orally, the DR group had a smaller change in MBP (%) than the DN group (3.08 +/- 5.14 vs -7.78 +/- 3.37, p < 0.05). According to the different BP responses to furosemide and captopril, we conclude that PA patients may be further divided into DR and DN. The DR group had a good response to diuretics whereas the DN group responded better to converting enzyme inhibitors. This classification of PA in terms of blood pressure response to furosemide may have therapeutic implications.

Adult↗
PubMed1993

Correlation between renin responsiveness to furosemide and antihypertensive effect of captopril in patients with normal-renin essential hypertension.

The relationship between renin responsiveness to furosemide and the antihypertensive effect of captopril in patients with normal-renin essential hypertension were studied in 23 patients including nine men (mean age, 41 years) and 14 women (mean age, 40 years). Those who had an increment of more than 50% in plasma renin activity (PRA) two hours after an intravenous injection of 20 mg furosemide were classified as group A (n = 13) and the others were classified as group B (n = 10). Baseline PRA, plasma aldosterone and mean blood pressure (MBP) were not different between the two groups. Both groups showed no significant difference in natriuresis following furosemide administration. Significant change in MBP was observed after an oral dose of 100 mg captopril within four hours in group A, but not in group B. These data suggest that renin responsiveness to a single intravenous dose of furosemide can be a useful test for predicting the therapeutic response to captopril in patients with normal-renin essential hypertension. The furosemide test had a sensitivity of 75%, a specificity of 64%, a positive predictive value of 69% and a negative predictive value of 70%.

Adult↗
PubMed1993

Blood pressure response to angiotensin converting enzyme inhibitor in essential hypertension: its relation to the renin status and natriuresis during acute sodium loading.

We examined the antihypertensive response to enalapril and its relation to the changes of the renin-angiotensin-aldosterone axis (RAA) in essential hypertensive patients. The responders, whose blood pressure reduced after enalapril administration, had significant elevation of plasma renin activity after enalapril (7.5 +/- 4.0 to 31.9 +/- 10 ng/mL/h, p < 0.05). There was no significant change in the plasma renin activity of the nonresponders (3.0 +/- 1.0 to 5.6 +/- 1.9 ng/mL/h). Natriuretic response to acute salt loading was compared between the two subgroups. The natriuresis on acute salt loading of nonresponders was better than that of the responders (82.9 +/- 13.2 vs 44.5 +/- 5.7 mmol/4h, p < 0.05). These results imply that the RAA and extracellular fluid volume both contribute in different ways to the maintenance of high blood pressure in different subgroups of essential hypertension.

Adult↗
PubMed1993

Renin suppressibility and blood pressure response during acute sodium loading in patients with essential hypertension.

Sequential changes in renin-aldosterone secretions and blood pressure (BP) response during acute sodium (Na) loading were studied in 50 patients with essential hypertension (EH) and nine normotensive volunteers. Following an infusion of 2 L of isotonic saline at a rate of 500 mL/h, plasma renin activity (PRA) and the plasma aldosterone concentration (PAC) were similarly suppressed, while sodium excretion appreciably increased in hypertensive as well as normotensive subjects. When patients were divided into two subgroups according to the extent of renin suppression, 26 were classified as adequate responders with the proportion of decrement of PRA at the end of the infusion exceeding 50% of the baseline values, while 24 were inadequate responders with a decrement of less than 50%. The extent of renin suppression was consistently greater in adequate responders than in inadequate responders throughout the course of infusion. Adequate responders also had a higher pre-saline PRA and attained a smaller post-saline natriuretic response than inadequate responders. Although the mean BP in both subgroups remained stable at all periods, inadequate responders had a minor but significantly higher percent of increment of MBP at the end of the infusion than adequate responders (3.6 +/- 2.0 vs -1.7 +/- 1.4%, p < 0.05). These results suggest that renin suppressibility during acute Na loading may be either linked with maintenance of BP homeostasis or may merely reflect the sodium-volume status of essential hypertension, with patients with greater suppression of renin being more Na-volume resistant than those with less inhibition.

Adult↗
PubMed1993

Changes in renin activity, aldosterone level and electrolytes in pregnancy-induced hypertension.

In order to observe the sequential changes in the renin-angiotensin-aldosterone system (RAAS) in hypertensive pregnancies, blood and urine samples of pregnant women were collected every four weeks from the 20th week of gestation to the fourth week after delivery in a consecutive and prospective study. Nine subjects developed pregnancy-induced hypertension in later gestation, and six of them with proteinuria were classified as having preeclampsia. The gestational ages at the onset of hypertension were the 28th week for one patient, the 32nd week for three patients and the 36th week for five patients. Plasma renin activity in most of the cases decreased to non-pregnant levels after hypertension was established, while the plasma aldosterone level did not. Marked variations in daily sodium and potassium excretion were observed at the various gestational weeks, while serum concentrations of these electrolytes changed only within a narrow range. No correlation between the changes in RAAS and electrolytes were shown in our cases.

Adult↗