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Biomedical subjects

R Zimlichman

Publications and source records attributed to R Zimlichman.

At least 73 records · Page 4Linked to original sources
PubMed1991

Expression of a gene coding for breast tumor-associated antigen in thyroid papillary carcinoma.

The expression of the H23 gene, previously shown to be overexpressed in breast cancer tissue, was examined in various thyroid pathologies. Thyroid papillary carcinomas demonstrate significant H23 mRNA levels, whereas benign thyroid pathologies have very low levels of expression. H23 gene expression in thyroid cancer inversely correlated with that of thyroperoxidase and thyroglobulin genes. Immunoblot assays of thyroid cancer tissues revealed overexpression of H23 gene at the protein level as well The data presented indicate that dedifferentiation of thyroid tissue to the malignant state is associated with increased H23 gene expression and suppression of some thyroidal differentiation marker genes.

Antigens, Neoplasm↗
PubMed1991

The effect of cilazapril, a new angiotensin converting enzyme inhibitor, on peak and trough blood pressure measurements in hypertensive patients.

Cilazapril (CLZ) is a new, long-acting nonsulfhydril converting enzyme inhibitor (ACE-I). Its effect on peak and trough sitting diastolic blood pressure (SDBP) was studied in a total of 85 patients with uncomplicated, essential hypertension at three centers. After 4 weeks of a single-blind placebo (PLA) run-in period, patients whose SDBP was between 100 and 115 mm Hg, were randomized into active treatment with either PLA (n = 27), CLZ 2.5 mg (n = 29), or CLZ 5 mg (n = 29) once daily in a double-blind fashion for another 8 weeks. At the end of the PLA run-in and after 4 and 8 weeks active therapy, an hourly blood pressure (BP) profile during 1-10 and 21-24 h postdose was performed. The drop in SDBP at the end of the active treatment period at peak and trough was statistically and clinically significant for both CLZ doses in comparison with the PLA group. The peak/trough ratio after subtraction of the PLA effect was 62% for CLZ 2.5 mg and 59% for CLZ 5 mg. These results indicate that the dose regimen of CLZ 2.5-5 mg once daily is adequate and effective for 24 h.

Adult↗
PubMed1991

Antihypertensive duration of action of cilazapril in patients with mild to moderate essential hypertension.

The efficacy of cilazapril monotherapy was evaluated in 2 multicentre double-blind dose-response trials. After 4 weeks of a single-blind placebo run-in period, patients with uncomplicated mild to moderate essential hypertension and a sitting diastolic blood pressure of 100 to 115 mm Hg, 24 hours after the last placebo dose (trough), were randomised to take either placebo or cilazapril 2.5 mg or 5 mg for 4 weeks (study 1, 86 patients) or 8 weeks (study 2, 78 patients). Sitting diastolic blood pressure was checked every 2 weeks at trough in both studies and at peak in study 2. The reductions in sitting diastolic blood pressure from baseline at trough, and the difference from placebo, were clinically and statistically significant for both cilazapril groups in the 2 studies. The reduction in blood pressure in both active treatment groups was similar, but the response rate with cilazapril 5 mg was greater than that with 2.5 mg. More than 50% of the peak effect was still present at trough for both cilazapril groups. It is concluded that both dosages of cilazapril are effective and reduce blood pressure compared with placebo over a 24-hour period.

Adult↗
PubMed1991

Hypocalciuria of preeclampsia is independent of parathyroid hormone level.

Hypocalciuria is a feature of preeclampsia. The roles of parathyroid hormone (PTH) and vitamin D 1,25(OH)2D3 (calcitriol) in its pathogenesis have not yet been determined. Fourteen preeclamptic women were compared with 12 women with chronic hypertension and 11 normotensives, all in the third trimester. Preeclamptics had the lowest urinary calcium excretion rate (62.1 +/- 32.8 mg/24 hours) compared with chronic hypertensive women (162.6 +/- 97.8 mg/24 hours) and normotensive controls (225.6 = 146.9 mg/24 hours) (P less than .05). Serum PTH was lowest in preeclamptics (9.8 +/- 5.5 pg/mL), in contrast to the chronic hypertensives (18.5 +/- 2.7 pg/mL) and normotensives (16.4 +/- 3.2 pg/mL) (P less than .005). Similarly, urinary cyclic adenosine monophosphate (cAMP) excretion was 2.9 +/- 1.4 mumol/24 hours in the preeclamptics, 5.1 +/- 1.7 mumol/24 hours in the chronic hypertensives, and 4.6 +/- 1.3 mumol/24 hours in the normotensive group (P less than .05). These data suggest that the mechanism of hypocalciuria in preeclampsia is independent of the PTH-calcitriol axis. Therefore, it is suggested that the hypocalciuria of preeclampsia is due to intrinsic renal tubular dysfunction.

Adult↗
PubMed1990

1,25-Dihydroxyvitamin D3 enhances cytosolic free calcium in HL-60 cells.

1,25-Dihydroxyvitamin D3 (1,25[OH]2D3) caused a rise in the concentration of intracellular free calcium ions ([Ca2+]i) in HL-60 cells. This effect of 1,25(OH)2D3 parallels its suppression of cell proliferation and its induction of cell differentiation into monocyte-like cells. The changes in [Ca2+]i are dose and time dependent. The concentration of 1,25(OH)2D3 (10(-7) M) that induced maximal differentiation also caused the maximal increase in intracellular Ca2+. The rise in cytoplasmic free Ca2+ concentration was not immediate and reached statistical significance only after 24 h. The [Ca2+]i reached its peak at 48 h (134 +/- 4 nM vs 101 +/- 3 nM in controls) and remained stable at this level. The increase in intracellular Ca2+ was found to be related to new protein synthesis, because it was inhibited in the presence of specific RNA and protein synthesis inhibitors. The rise in [Ca2+]i was not observed during incubation of HL-60 cells with 24,25-dihydroxyvitamin D3 (24,25[OH]2D3), a vitamin D metabolite that does not induce the differentiation of HL-60 cells. In contrast, 25-hydroxyvitamin D3 (25-OH-D3) and phorbol 12-myristate 13-acetate (TPA), both of which induce differentiation in this cell line, also increase [Ca2+]i. In conclusion, the present study emphasizes that a significant increase in intracellular free Ca2+ occurs in the effect of 1,25(OH)2D3 on HL-60 cells.

Calcitriol↗
PubMed1989

Assessment of hemodynamic changes in the early phase of uncomplicated acute myocardial infarction.

The purpose of our study was to evaluate the early phase hemodynamic changes in patients with clinically uncomplicated acute myocardial infarction. Detailed sequential hemodynamic evaluation is hardly available in the early phase of acute myocardial infarction in this group of patients as opposed to patients with complicated acute myocardial infarction. We evaluated sequentially the hemodynamics of 17 patients with uncomplicated acute myocardial infarction (Kilip class I). Cardiac output and ventricular ejection period were determined by impedance cardiography. All patients had an uneventful recovery, without clinical evidence of derangement of myocardial function as assessed by physical examination, chest X-ray and blood gases. Despite the uniformly uncomplicated convalescence, different hemodynamic patterns were found. Based on the hemodynamic data, patients were divided into two groups. In 10 patients no significant change in hemodynamic parameters was observed, while in 7 patients a significant decrease in cardiac output was found during the early post myocardial infarction period. Total peripheral resistance was significantly elevated in the group with decreased cardiac output. No relationship was found among location of infarction, creatine phosphokinase levels and hemodynamic outcome. A considerable proportion of patients with asymptomatic and uneventful convalescence after acute myocardial infarction have a decrease in cardiac output and a significant increase in total peripheral resistance which is not detected by routine clinical evaluation.

Adult↗
PubMed1989

[Gammaglobulin for idiopathic thrombocytopenia in pregnancy].

The association of idiopathic thrombocytopenic purpura (ITP) and pregnancy is of special therapeutic significance because it increases the risk to mother and infant during labor. The specific antiplatelet immunoglobulin G (IgG) crosses the placenta and induces thrombocytopenia in the fetus. Intravenous IgG is a new treatment associated with a relatively rapid increase in platelet count. Although this increase is transient, usually lasting only several weeks, the treatment can be repeated a number of times during pregnancy. Knowing the kinetics of platelet response to treatment in the specific patient, it is usually possible to treat so as to maintain a safe platelet count during labor.

Adult↗
PubMed1988

Derivation of urinary dopamine from plasma dopa.

1. We estimated the extent to which circulating dopa (3,4-dihydroxyphenylalanine) is the source of urinary dopamine (DA; 3,4-dihydroxyphenethylamine). Tritiated dopa ([3H]dopa) was infused for 90 min into the left renal artery of seven anaesthetized foxhounds, and levels of labelled and unlabelled dopa and DA were measured in the ureteral urine and in the femoral arterial and left renal venous plasma. 2. Only a small percentage of [3H]dopa delivered to the kidneys was excreted as [3H]DA (0.59% from the left kidney, 0.68% from the right); however, the arterial concentration of endogenous dopa (1220 pg/ml) and the renal plasma flows (144 and 141 ml/min by p-aminohippurate clearances) were such that all of the urinary excretion of endogenous DA (about 1 ng/min from each kidney) could be accounted for by uptake and decarboxylation of circulating endogenous dopa. 3. Plasma dopa is the main source of urinary DA.

Animals↗
PubMed1988

Metabolic and hemodynamic effects of antihypertensive treatment with ketanserin.

Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 hours), blood pressures measured 12 hours after dosing were not significantly different from those obtained after placebo. However, 2 hours after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (P less than 0.01) and 6 +/- 5 mm Hg (P less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. Except for a slight decline in serum prolactin levels 12 hours after dosing with ketanserin, no changes were observed in pituitary hormone levels, serum testosterone, plasma catecholamines, plasma renin activity, aldosterone, or lipoproteins. Stroke volume, measured 2 hours after dosing, increased with ketanserin therapy, but cardiac output, systemic resistance, and heart rate were unchanged. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24 hours of antihypertensive activity.

Adult↗
PubMed1988

Antihypertensive therapy with ketanserin: metabolic and hemodynamic effects.

Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 h), blood pressures measured 12 h after dosing were not significantly different from those obtained during the placebo period. However, 2 h after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (p less than 0.01) and 6 +/- 5 mm Hg (p less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. At the time of peak antihypertensive activity, plasma renin activity, aldosterone, growth hormone, and prolactin levels were unchanged. Prolactin levels decreased slightly (4.1 +/- 3.0 vs. 3.7 +/- 2.9 ng/ml, p less than 0.05) during ketanserin therapy when measured 12 h after dosing. Other pituitary hormones, serum testosterone, plasma catecholamines, and plasma lipids showed no changes. Heart rate was also unchanged. Stroke volume, measured 2 h after dosing, increased (70 +/- 22 vs. 85 +/- 31 ml, p less than 0.05) with ketanserin therapy, but cardiac output did not change significantly. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24-h antihypertensive activity.

Adult↗
PubMed1988

Complete atrioventricular block induced by methyldopa.

We present two patients who developed complete heart block due to treatment with methyldopa. After discontinuing methyldopa, conduction disturbances completely disappeared and recurred upon rechallenge with the medication. It is assumed that methyldopa can impair the myocardial conduction system by its central sympatholytic effect. Conduction anomalies should be excluded prior to treatment with methyldopa, and during treatment with the medication, the patients should be routinely screened for the presence of conduction anomalies.

Aged↗
PubMed1987

Dietary salt intake and the clonidine suppression test.

We studied the effects of one week of dietary salt restriction and one week of salt loading on hemodynamic and plasma catecholamine responses to clonidine. Among 11 outpatients with essential hypertension, urinary sodium excretion averaged 29 mEq/d during salt restriction and 322 mEq/d during salt loading. Among eight inpatient normotensive subjects, urinary sodium excretion averaged 11 mEq/d during salt restriction and 300 mEq/d during salt loading. Three hours after administration of oral clonidine 300 micrograms, the hypertensive patients had an average (+/- one standard deviation) decrease in mean arterial pressure of 20 +/- 6% while receiving the low salt diet and 19 +/- 9% while taking the high salt diet, with decreases in venous plasma norepinephrine (NE) of 61 +/- 15% and 61 +/- 16%, respectively. The normotensive subjects had a decrease in mean arterial pressure of 16 +/- 8% with the low salt diet and 15 +/- 9% with the high salt diet, with decreases in venous plasma NE of 64 +/- 10% and 66 +/- 8%. Thus, in neither group were the percent decreases in plasma NE or in mean arterial pressure after clonidine affected by diet. Short-term, large-magnitude changes in dietary intake of sodium do not affect the sympathetic contribution to blood pressure as indicated by percent responses of plasma NE or of mean arterial pressure to clonidine administration.

Adult↗