PubMed Health⌕ Search

Biomedical subjects

J Silbiger

Publications and source records attributed to J Silbiger.

10 recordsLinked to original sources
PubMed1993

Parainfectious optic neuritis and encephalomyelitis. A report of two cases with thalamic involvement.

Two children developed mental status alteration and bilateral profound visual loss secondary to optic neuritis. The clinical picture was consistent with parainfectious encephalomyelitis. Magnetic resonance imaging showed bilateral involvement of the thalamus in both cases. In one case the thalamic involvement was solitary and was suspected initially to represent a primary thalamic neoplasm. This was ruled out by a stereotactic biopsy of the thalamus, which showed perivascular inflammation consistent with parainfectious encephalomyelitis. The clinical and neuroimaging findings improved significantly following corticosteroid administration. Several relapses occurred upon initial attempts at corticosteroid cessation.

Child, Preschool↗
PubMed1992

Evaluation of corneal collagen shields as a drug delivery device for the treatment of experimental Pseudomonas keratitis.

PURPOSE: To clarify the role of corneal collagen shields as a drug delivery device for the treatment of bacterial keratitis, the authors studied the effectiveness of topical gentamicin treatment, with and without the use of corneal collagen shields, in a rabbit model of Pseudomonas keratitis. METHODS: Forty-eight New Zealand white rabbits were infected by injecting 500 colony-forming units (CFU) of Pseudomonas aeruginosa into the corneal stroma, and treatment was begun 24 hours later. A 13.6 mg/ml solution of gentamicin was topically administered during a 24-hour period. Collagen shields were soaked in gentamicin 13.6 mg/ml for 5 minutes before placing them on the cornea. Corneas were quantitatively cultured 1 hour after the treatment period ended. Six different groups of rabbits were tested, with the results analyzed as the mean log10 of bacterial CFU. RESULTS: An untreated control group had significantly more bacteria (7.96 +/- 0.74) than any of 5 treatment groups. No difference was found between groups given a loading dose of antibiotic drops at the beginning of treatment, either with (4.90 +/- 2.41) or without (6.25 +/- 0.54) an antibiotic-impregnated collagen shield. A group treated with a collagen shield augmented with gentamicin drops every 3 hours had fewer bacteria (1.52 +/- 1.82) than a group receiving drops alone (4.15 +/- 1.83) (P less than 0.05). However, treatment with a collagen shield supplemented with drops every 3 hours was not as effective as gentamicin drops administered every 30 minutes (no bacterial growth) (P less than 0.05). CONCLUSION: These results show that antibiotic-impregnated collagen shields should not replace traditional antibiotic drop therapy as the mainstay of treatment but may be a useful adjunct to treatment with topical antibiotics.

Animals↗
PubMed1990

Progesterone-cortisol interaction in control of renin activity but not aldosterone.

In addition to its effect of inhibiting adrenocorticotropic hormone (ACTH) secretion, cortisol (hydrocortisone) inhibits the renin-angiotensin system in both fetal and adult sheep. We have found that progesterone attenuates the inhibition of ACTH by cortisol. These studies test whether progesterone interacts with cortisol in control of the renin-angiotensin-aldosterone system. Conscious adult ewes were infused with vehicle, cortisol (4 micrograms.kg-1.min-1), progesterone (0.5 microgram.kg-1.min-1), or cortisol with progesterone for 60 min. Beginning 120 min after the start of the infusion, renin secretion was stimulated by infusing sodium nitroprusside (10 micrograms.kg-1.min-1 iv). Cortisol infusion decreased plasma K+ concentration and reduced the plasma renin activity (PRA) and aldosterone responses to nitroprusside. Progesterone alone had no effect on PRA, aldosterone, or K+. Progesterone reduced the inhibition of PRA, but not aldosterone or K+, by cortisol. The data also indicate that the suppression of renin, as well as the suppression of ACTH, involves receptors or intracellular mechanisms with which progesterone interacts, whereas the inhibition of aldosterone involves a mechanism that progesterone does not affect.

Aldosterone↗
PubMed1989

Cortisol-induced inhibition of ACTH secretion in adult sheep.

Previous results from this laboratory have demonstrated that in preterm fetal sheep (117-131 days gestation), stimulated ACTH secretion is highly sensitive and that in term fetal sheep (129-143 days), stimulated ACTH secretion is insensitive to the negative feedback effects of cortisol. The purpose of this study was to quantitate cortisol negative feedback inhibition of stimulated ACTH secretion in adult sheep. Adult, conscious, nonpregnant ewes, chronically prepared with carotid arterial loops, were infused intravenously with vehicle or cortisol at 4 different rates (denoted Groups I, II, III, and IV) for 5 hours. These infusions increased total and unbound plasma cortisol concentrations within the range observed after stimulation of the hypothalamus-pituitary-adrenal axis. One hour after termination of the cortisol or vehicle infusions, ACTH secretion was stimulated by intravenous infusion of sodium nitroprusside for 10 min at a rate of 20 micrograms/kg.min. Cortisol infusions suppressed ACTH responses to nitroprusside in a dose-related manner. After vehicle infusion, nitroprusside increased plasma ACTH to 735 +/- 229 pg/ml. After cortisol infusions, nitroprusside increased plasma ACTH to 292 +/- 63, 101 +/- 30, 73 +/- 12, and 67 +/- 24 in Groups I, II, III, and IV, respectively. Overall, there was a significant negative exponential relationship between plateau plasma cortisol concentration during the cortisol or vehicle infusion and the peak plasma ACTH concentration during the response to nitroprusside infusion (r = -0.81). The highest rate of cortisol infusion increased total and unbound plasma cortisol concentrations to 40.1 +/- 5.7 and 19.5 +/- 5.9 ng/ml and completely suppressed the subsequent ACTH response to nitroprusside.

Adrenocorticotropic Hormone↗
PubMed1988

Does cortisol inhibit vasopressin secretion in sheep?

Glucocorticoids inhibit the plasma vasopressin responses to hemorrhage and hypoxia in dogs. Attempts to demonstrate glucocorticoid inhibition of vasopressin secretion in fetal sheep have been unsuccessful, suggesting the possibility that there is an influence of development on the expression of this interaction, or that the interaction cannot be demonstrated in all mammalian species. This study was designed to investigate these two possibilities. Adult ewes chronically prepared with carotid arterial loops, were subjected to 5 hr infusions of cortisol at a rate of 6 ug/kg min or vehicle (5% ethanol in saline). The infusion of cortisol increased plasma cortisol concentration from 26 +/- 3 to 46 +/- 8 ng/ml, while vehicle infusion was associated with a decrease in plasma cortisol concentration from 23 +/- 4 to 15 +/- 3 ng/ml. One hr after the end of the cortisol or vehicle infusions, vasopressin secretion was stimulated by arterial hypotension produced by 10 min infusions of sodium nitroprusside (20 ug/kg min). Nitroprusside decreased arterial blood pressure equally in both groups. Plasma vasopressin concentrations were increased to peak concentrations of 92 +/- 33 and 116 +/- 20 pg/ml in the vehicle- and cortisol-infused groups, responses which were not significantly different as tested by ANOVA. We conclude that increases in plasma cortisol concentration, equal to those observed during responses to stressors, do not inhibit vasopressin secretion in this species.

Animals↗
PubMed1988

Progesterone attenuates the inhibition of adrenocorticotropin responses by cortisol in nonpregnant ewes.

This study was designed to test whether increases in plasma progesterone (P) reduce the efficacy of plasma cortisol (F) in inhibition of ACTH responses to stimuli. Five nonpregnant ewes were each infused with ethanol-saline vehicle, F (4 micrograms/kg.min), P (0.5 or 2.0 microgram/kg.min), or P and F for 60 min. One hour after the end of the vehicle or steroid infusions, nitroprusside (20 micrograms/kg.min) was infused for 10 min to induce hypotension-stimulated ACTH secretion. Nitroprusside produced similar decreases in arterial blood pressure in all groups. Infusion of F alone inhibited plasma ACTH responses to hypotension. Whereas infusion of P without F did not significantly change plasma ACTH responses to hypotension, infusion of P with F caused greater ACTH responses to hypotension than did infusion of F alone. The results indicate that P can interfere with the delayed feedback effect of F in vivo.

Adrenocorticotropic Hormone↗
PubMed1987

Cortisol-induced inhibition of ovine renin and aldosterone responses to hypotension.

Previous studies from this laboratory have demonstrated that in preterm fetal sheep increases in plasma cortisol (F) concentration equal in amplitude to fetal F stress responses suppress plasma renin activity (PRA). The purpose of this study was to investigate the possibility that this negative interaction exists in adult sheep. Five conscious ewes with chronically prepared carotid arterial loops were infused intravenously with F (6 micrograms X kg-1 X min-1) or vehicle (5% ethanol in 0.9% saline) for 5 h. One hour after the end of F or vehicle infusion, renin secretion was stimulated by hypotension produced by infusion of sodium nitroprusside (20 micrograms X kg-1 X min-1, iv). F infusion increased plasma F from 26 +/- 3 to 46 +/- 8 ng/ml; during vehicle infusion plasma F did not change from 20 +/- 4 ng/ml. F infusion decreased hematocrit from 29 +/- 2 to 26 +/- 1%. Basal PRA in vehicle- and F-infused groups were 0.4 +/- 0 and 0.2 +/- 0.1 ng angiotensin I X ml-1 X h-1 and did not change. In vehicle-infused ewes, PRA increased from 0.4 +/- 0 and 0.2 +/- 0.1 ng angiotensin I X ml-1 X h-1 and did not change. In vehicle-infused ewes, PRA increased from 0.4 +/- 0 to 4.6 +/- 0.4 and plasma aldosterone from 26.0 +/- 1.0 to 173.1 +/- 21.8 pg/ml, while, in F-infused ewes, PRA increased from 0.2 +/- 1 to 3.3 +/- 0.4 ng angiotensin I X ml-1 X h-1 and aldosterone from 25.0 +/- 0 to 48.2 +/- 23.2 pg/ml, significantly smaller responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMedDate not supplied

Magnetic resonance angiography of vascular lesions causing neuro-ophthalmic deficits.

Magnetic resonance angiography (MRA) is a noninvasive, rapidly evolving technique for imaging the intra- and extracranial carotid and vertebrobasilar circulations. It may in some circumstances obviate conventional angiography and the accompanying risks associated with catheterization and contrast injection. MRA exploits the different physical properties between moving protons and stationary tissue to yield flow sensitive data in the form of anatomic images or velocity and flow measurements. Since patients with various vascular disorders may present exclusively with ophthalmologic signs and symptoms, it is expected that MRA will become more frequently utilized by ophthalmologists. The exact role of MRA in the workup of vascular disorders remains to be more precisely defined, pending the performance of additional well-controlled standardized studies. At present, MRA is utilized to complement the conventional spin-echo studies of patients with arterial and venous occlusion, vascular malformations, intracranial aneurysms, and neoplastic vascular invasion. With further refinements, it is expected that MRA will become a standard diagnostic tool for the evaluation of patients with vascular disorders.

Blood Flow Velocity↗
PubMedDate not supplied

Periodic alternating esotropia.

Periodic alternating esotropia (PAE) is a rare ocular motility disturbance observed in association with periodic alternating gaze deviation (PAG) or periodic alternating nystagmus. We examined a 9-month-old developmentally delayed girl who showed PAE occurring synchronously with PAG. The ocular motility disorder consisted of rhythmic alternating fixation with the right eye in abduction, a left face turn and esotropia of the left eye (90 seconds), a changeover phase (10 to 15 seconds) during which the eyes are straight and the head is upright, then fixation with the left eye in abduction, a right face turn, and esotropia of the left eye (90 seconds). There was no spontaneous jerk nystagmus present. These findings continued incessantly during a follow-up period of 18 months. Magnetic resonance imaging revealed pronounced cerebellar vermis hypoplasia. Only three clinically similar cases have been previously reported, but none had been studied with modern neuroimaging techniques.

Atrophy↗