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Biomedical subjects

N Stern

Publications and source records attributed to N Stern.

At least 127 records · Page 7Linked to original sources
PubMed1985

The tilted posterior tooth. Part III: Abutment for a fixed partial denture.

The problem of achieving a common path of insertion for a fixed partial denture when a tilted posterior abutment is involved can usually be solved by well planned tooth preparation in conjunction at times with intentional endodontic therapy. When tooth preparation alone cannot solve the problem, the mechanical solutions of the locked attachment and the telescopic retainer are available and must be considered. Other problems involved with the tilted abutment, adjacent tilted teeth, space reduction, supraversion of the antagonist, and the problem of a long-span fixed partial denture were discussed.

Bicuspid↗
PubMed1984

Altered dopaminergic modulation of sympathetic nervous system activity in idiopathic edema.

Hormonal and mean arterial pressure responses to posture and isometric handgrip exercise were examined in 6 women with idiopathic edema and 10 age- and weight-matched normal women before and after 5-7 days of administration of the dopamine agonist, bromocriptine (2.5 mg three times a day). Edema patients demonstrated greater orthostatic weight gain, greater upright epinephrine values, and greater supine and upright norepinephrine values than did the control group. However, supine and upright plasma dopamine levels were similar in the two groups. In edema patients there was a greater supine and posture related norepinephrine and epinephrine to dopamine ratio than in normal controls. These abnormalities were not corrected by treatment with bromocriptine. Supine and upright plasma norepinephrine and epinephrine levels were decreased following bromocriptine treatment in normal subjects but not in edema patients. These data are consistent with the concept that there is decreased dopaminergic regulation of sympathetic nervous activity in patients with idiopathic edema.

Adult↗
PubMed1984

Repairing a crown-sleeve coping prosthesis. Part II.

A crown-and-sleeve coping prosthesis and its retainer have been defined and reasons for the failure of an abutment tooth have been discussed. A detailed procedure for repairing a CSC prosthesis when extraction of one abutment tooth is necessary has been presented. A technique for restoration of a carious abutment tooth that supports a CSC prosthesis will be described in a future article.

Crowns↗
PubMed1984

Repairing a crown-sleeve coping prosthesis. Part III.

The problem of an abutment tooth that has become carious and an inadequate support for a CSC prosthesis has been presented. The advantages and disadvantages of the various routine restorative techniques have been discussed. A detailed procedure for restoring a carious abutment tooth that also requires periodontal surgery was described.

Crowns↗
PubMed1984

The role of corticosteroids in the regulation of myocardial Na, K-ATPase in normotensive and spontaneously hypertensive rats.

Sodium, potassium-dependent adenosine triphosphatase (ATPase) of the renal tubule is known to be dependent on both gluco- and mineralocorticoids. Recent evidence suggests that corticosteroids may modulate ATPase activity at extrarenal sites. The myocardium contains glucocorticoid receptors to which mineralocorticoids can also bind. Thus, the possibility that myocardial ATPase is corticosteroid dependent was examined in the Wistar-Kyoto (WKY) normotensive rat and also in the spontaneously hypertensive (SH) rat, a strain previously shown to exhibit reduced myocardial ATPase activity. WKY and SH rats (in groups of 10) were either sham operated or adrenalectomized and placed on 1% NaCl solution as drinking water. Adrenalectomized rats subsequently received daily intraperitoneal injections of either vehicle (1% NaCl, 0.5 ml), aldosterone (30 micrograms/kg) or dexamethasone (60 micrograms/kg). Renal cortical and myocardial ATPase activities were determined 21 days later in all groups. Adrenalectomized WKY rats had reduced myocardial ATPase activity (5.15 +/- 0.88 vs 8.18 +/- 0.93 mumol of phosphate h-1 mg-1 of protein in controls; P less than 0.01). This observed decrease in ATPase in adrenalectomized rats could be at least partly prevented by selective aldosterone or dexamethasone replacement. Parallel changes were observed with renal cortical ATPase. SH rat myocardial ATPase was lower than in WKY rats (P less than 0.05, 5.88 +/- 0.99 mumol of phosphate h-1 mg-1 of protein) and was unaffected by adrenalectomy (5.47 +/- 0.68 mumol of phosphate h-1 mg-1 of protein) whether accompanied by aldosterone (6.08 +/- 0.68 mumol of phosphate h-1 mg-1 of protein) or dexamethasone (6.47 +/- 0.84 mumol of phosphate h-1 mg-1 of protein) therapy or not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗
PubMed1984

Enhanced response of plasma aldosterone to metoclopramide in essential hypertension.

Aldosterone responses to posture and the dopamine antagonist, metoclopramide, were studied in seven normotensive controls and 12 patients with essential hypertension. Both groups had similar basal supine plasma renin activity and aldosterone levels. Aldosterone levels of the hypertensive patients were greater than those of the controls 10 min after assuming an upright posture but indistinguishable at 120 min. Metoclopramide induced a peak fourfold increase above basal aldosterone levels in the hypertensive group as compared to a peak twofold increase observed in the normotensive controls. Mean 120-min integrated aldosterone response area for the hypertensives (237 +/- 44 10(-10) mol min/l) was greater (P less than 0.05) than that for normotensive subjects (106 +/- 32 10(-10) mol min/l). Simultaneous cortisol, plasma renin activity, and serum potassium levels were unaffected by metoclopramide. It is concluded that dopaminergic modulation of aldosterone secretion may be altered in essential hypertension.

Adult↗
PubMed1984

Sodium-potassium ATPase in deoxycorticosterone-salt hypertension: opposing effects of sodium load and mineralocorticoids.

Previous studies of the sodium-potassium pump in the deoxycorticosterone (DOC)-salt (DS) model of hypertension yielded contrasting results, some investigators reporting increased and others finding decreased pump activity. To test the possibility that the net pump activity in the DS rats results from separate effects of sodium overload and mineralocorticoid activity, we compared the Na+-K+-ATPase pump in DS rats with that in other experimental models in which these potential determinants do not coincide. Renocortical and myocardial ATPase activities were measured in control rats; adrenalectomized-saline-repleted rats; adrenalectomized aldosterone- or dexamethasone-repleted rats; uninephrectomized, saline-drinking rats; and uninephrectomized, saline-drinking, DOC- and salt-treated rats. DOC- and salt-treated rats had higher (P less than 0.001) blood pressures and lower (P less than 0.05) serum potassium levels than control rats. Renocortical and myocardial ATPase activities were considerably (P less than 0.01) decreased in adrenalectomized, saline-repleted rats, but could be at least partially restituted by either aldosterone or dexamethasone therapy. Uninephrectomized, saline-drinking rats had reduced (P less than 0.01) renocortical and myocardial ATPase activities compared with control rats. In uninephrectomized, saline-drinking rats treated with DOC, renocortical and myocardial ATPase activities were not different from control values. The results of this study suggest that the Na+-K+-ATPase pump in DOC- and salt-treated rats is modulated by the opposing effects of sodium overload-associated suppression and DOC-mediated stimulation.

Adrenalectomy↗
PubMed1983

Glucocorticoid suppression enhances the 18-hydroxycorticosterone and aldosterone response to metoclopramide in man.

18-Hydroxycorticosterone (18-OHB) is a precursor of aldosterone and is the only corticosteroid, other than aldosterone, that is synthesized predominantly in the zona glomerulosa. Administration of the dopamine antagonist, metoclopramide results in parallel rises in plasma 18-OHB and aldosterone levels without affecting the plasma levels of other aldosterone precursors. However, 18-OHB is a product of the zona fasciculata as well as the glomerulosa. Thus, it is possible that metoclopramide may stimulate zona fasciculata secretion of 18-OHB. In order to more selectively examine dopaminergic regulation of zona glomerulosa secretion of 18-OHB we have examined the effect of glucocorticoid suppression of the fasciculata on the 18-OHB and aldosterone responses to metoclopramide, 10 mg iv in 6 normal volunteers. Dexamethasone, 2 mg every 6 hours for 5 days, suppressed basal levels of cortisol, corticosterone, 18-OHB and aldosterone. Dexamethasone treatment had no effect on basal levels of PRA or PRA responses to metoclopramide. The 18-OHB and aldosterone responses to metoclopramide were enhanced (p less than .05) by dexamethasone suppression. The results suggest that dopaminergic mechanisms selectively suppress glomerulosa production of 18-OHB. Endogenous ACTH may inhibit zona glomerulosa production of 18-OHB and aldosterone in response to the dopamine antagonist, metoclopramide.

18-Hydroxycorticosterone↗
PubMed1983

Effects of chlorocyclizine on pulmonary lipid metabolism in rats.

Pulmonary lipidosis was induced in rats by including 0.36 and 0.54% chlorocyclizine in their diet. Chemical analyses of the lung tissue revealed a very marked increase in phosphatidylcholine concentration. Phosphatidylglycerol and phosphatidylinositol concentrations were also markedly increased. An increase in the phosphatidylcholine content was also observed in lavage fluid and macrophages. Microscopic examination of the cell fraction showed that almost all the cells of the lavage fluid were macrophages and that histochemically demonstrable acid esterase activity was mostly inversely related to storage of lipids in the cells. Sonication of macrophages isolated from normal or chlorocyclizine-treated rats yielded a soluble acid phospholipase (pH optimum, 4.0) and a neutral (pH optimum, 8.2) membrane-bound, CaCl2-dependent enzyme. An inhibitory effect of chlorocyclizine in vitro on the activity of the soluble phospholipase was shown.

Animals↗
PubMed1983

Effect of aldosterone on the human erythrocyte sodium--potassium pump in vitro.

1. The effects of aldosterone in vitro on the Na+, K+-dependent ATPase activity of isolated human erythrocyte membranes and on rubidium (86Rb) uptake and [3H]ouabain binding of intact erythrocytes were studied. 2. ATPase activity was nearly doubled (0.061 +/- 0.006 to 0.110 +/- 0.01 mumol of Pi h-1 mg-1 of protein) by the addition of a physiological concentration of aldosterone (2.7 X 10(-10) mol/l). Higher concentrations had no greater effect. 3. Aldosterone had no significant effect on 86Rb uptake or [3H]ouabain binding. 4. Erythrocytes contain aldosterone at concentrations similar to that in plasma. The effect of aldosterone on ATPase is probably maximal.

Adult↗
PubMed1983

Plasma norepinephrine responses to posture and isometric exercise increase with age in the absence of obesity.

This study examines the effects of age on plasma norepinephrine (NE) responses to upright posture and isometric handgrip exercise in nonobese men. Increasing age was associated with increased basal levels of plasma NE as well as increased NE responses to upright posture. These results suggest that aging affects sympathetic system activity by mechanisms largely independent of the increasing adiposity generally associated with aging.

Adult↗
PubMed1983

Effects of bromocriptine on the circadian rhythm of 18-hydroxycorticosterone and cortisol secretion in essential hypertensives.

This study examines the influence of bromocriptine, a dopamine agonist, on circadian secretory patterns of plasma 18-hydroxycorticosterone (18-OHB) and cortisol in essential hypertension. Patients with sustained essential hypertension were studied after they had reached equilibrium on a constant 150 mmol sodium and 80 mmol potassium intake. Plasma 18-OHB and cortisol determinations were made at 30-min intervals over 24 h during a control and bromocriptine treatment period (bromocriptine, 2.5 mg t.i.d. for five days). Circadian patterns for plasma 18-OHB and cortisol were observed in all patients before and after bromocriptine. Although bromocriptine did not affect the circadian rhythm of 18-OHB and cortisol it did decrease mean 24-h recumbent 18-OHB from 23 +/- 42.2 to 14.3 +/- 1.4 ng/dl. These results suggest that there is a circadian rhythm of both 18-OHB and cortisol secretion in patients with essential hypertension as in normotensives. Dopaminergic mechanisms exert an effect on the quantitative secretion of 18-OHB. However, the circadian rhythm for 18-OHB and cortisol does not appear to be dependent on dopaminergic mechanisms.

18-Hydroxycorticosterone↗
PubMed1983

Altered corticosteroid control of the erythrocyte sodium-potassium pump in the spontaneously hypertensive rat.

Recent evidence suggests that corticosteroids may participate in the regulation of erythrocyte Na,K pump activity. To examine the possible role of mineral- and glucocorticoids in the physiological control of Na,K pump in vivo, 10-week-old Sprague-Dawley (SD), Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were randomly assigned to four treatment groups (n = 10 for each): (a) sham operation, (b) bilateral adrenalectomy, (c) bilateral adrenalectomy followed by daily intraperitoneal (i.p.) injection of aldosterone, 10 micrograms/kg, (d) bilateral adrenalectomy followed by daily i.p. injections of dexamethasone 60 micrograms/kg. Fourteen days later all rats were sacrificed and the erythrocyte Na,K pump activity was assessed by two different assays: ouabain sensitive ATP hydrolysis in isolated membranes (ATPase) and 86Rb uptake by intact erythrocytes. SHR exhibited reduced Na,K pump activity as measured by ATPase (compared to WKY) and by 86Rb uptake (compared to WKY and SD rats). Adrenalectomy was associated with 22-44% reduction in ATPase in all three rat species (P less than 0.05-0.01). Adrenalectomized aldosterone or dexamethasone treated SHR, WKY and SD rats exhibited ATPase activity that was indistinguishable from the corresponding control groups. Similarly, 86Rb uptake was lower in adrenalectomized SD and WKY rats. This reduction could be at least partially prevented by daily treatment with either aldosterone or dexamethasone. In SHR adrenalectomy had no effect on 86Rb uptake whether accompanied by daily treatment with aldosterone or dexamethasone or not. These results suggest that the erythrocyte sodium potassium pump is corticosteroid dependent in normotensive rats. An abnormal response of the Na,K pump to corticosteroids is observed in SHR, with a dissociation between steroid stimulated enzymatic ATP hydrolysis and actual transmembrane pumping as measured by 86Rb uptake.

Adenosine Triphosphatases↗
PubMed1983

Effects of metoclopramide on plasma corticosteroid levels in sheep.

This study investigated the role of dopaminergic mechanisms in modulation of corticosteroid secretion in sheep. Administration of the dopamine antagonist metoclopramide (200 micrograms/kg iv) in six mature sheep resulted in rapid and parallel rises in plasma cortisol, corticosterone, 18-hydroxycorticosterone, and aldosterone. Treatment of the sheep with 4 mg dexamethasone im every 6 h for 4 days abolished the response of all four corticosteroids to metoclopramide in the six sheep. These observations suggest that metoclopramide may stimulate corticosteroid secretion in sheep via nonspecific stressor effects.

18-Hydroxycorticosterone↗