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Biomedical subjects

D Rosenbaum

Publications and source records attributed to D Rosenbaum.

At least 109 records · Page 6Linked to original sources
PubMed1988

Efficacy and mechanism of action of a calcium channel blocker after global cerebral ischemia in rats.

Dihydropyridine calcium channel blockers such as nicardipine are under evaluation for treating acute cerebral ischemia because they may increase cerebral blood flow by causing vasodilation and because they may be cytoprotective in part by limiting production of arachidonic acid metabolites. We demonstrated in a previous study that nicardipine improves postischemic neuronal function, as measured by somatosensory evoked potentials, without reducing the extent of light-microscopic CA-1 hippocampal histologic damage. To characterize further the effect of nicardipine on global ischemic injury, we administered the drug beginning 24 hours before 30 minutes of four-vessel ischemia in Wistar rats. We then measured hippocampal ATP, phosphocreatine, and glucose contents immediately and 2 hours after ischemia, and measured learning ability (working and reference errors) on an eight-arm radial maze beginning 30 days after ischemia. To gain insight into the possible mechanism of action, we measured production of arachidonic acid metabolites (eicosanoids: TXB2 and 6-keto-PGF1 alpha) and hemispheric and hippocampal cerebral blood flow by the [14C]butanol indicator fractionation technique immediately and 2 hours after ischemia. Nicardipine was associated with fewer working errors (p less than 0.02) but no difference in reference errors. The drug had no effect on energy metabolites, cerebral blood flow, or eicosanoids immediately after ischemia, but ATP, phosphocreatine, and cerebral blood flow all returned to normal levels significantly more rapidly during reperfusion in treated rats. Nicardipine improves behavioral, electrophysiologic, and mitochondrial function after ischemia without preventing cellular damage and improves postischemic reperfusion. The drug's positive effect appears to occur during reperfusion.

Adenosine Triphosphate↗
PubMed1987

Giant cell arteritis causes recurrent posterior circulation transient ischemic attacks which respond to corticosteroid.

A 67-year-old man presented with recurrent clinically diverse posterior circulation transient ischemic attacks which continued despite full anticoagulation. Giant cell arteritis was suspected because of a markedly elevated erythrocyte sedimentation rate and confirmed by temporal artery biopsy. Treatment with corticosteroids resulted in a prompt and enduring resolution of clinical symptoms. Giant cell arteritis may represent a treatable cause of posterior circulation transient ischemic attacks, uniquely responsive to corticosteroids.

Aged↗
PubMed1985

Ventricular fluid somatostatin concentration decreases in childhood-onset dystonia.

Somatostatin was measured in CSF from individuals with a variety of neurologic diseases. In ventricular CSF, somatostatin concentration was significantly lower in individuals with childhood-onset dystonia than in individuals with other forms of dystonia or with other disorders. Severity of childhood dystonia correlated with somatostatin concentration, suggesting a progressive dysfunction of somatostatin-containing neurons with increasing disease severity. There were no significant differences in somatostatin concentration in lumbar CSF. Multiple forms of immunoreactive somatostatin were found in a pool of lumbar CSF from normal individuals. Labeled somatostatin administered intra-arterially to rats failed to cross the blood-brain barrier.

Adolescent↗
PubMed1985

Successful treatment of nocturnal enuresis: a practical approach.

In this article, the emphasis is on formulating a correct diagnosis when the symptom of nocturnal enuresis is present, so that an effective treatment plan can be initiated. Diagnosis may relate to structural, urodynamic, psychologic, dietary, nephrologic, or neurologic problems. The authors present the format for successful treatment of nocturnal enuresis used at the Center to Assist the Regulation of Enuresis at the Children's Memorial Hospital in Chicago.

Adolescent↗
PubMed1984

Inhibition of experimentally-induced murine metastases by recombinant alpha interferon: correlation between the modulatory effect of interferon treatment on natural killer cell activity and inhibition of metastases.

The effect of a human recombinant hybrid alpha interferon (referred to as rHuIFN-alphaA/D) on pulmonary metastases induced by intravenous injection of B16 F10 melanoma cells in C57BL/6 mice was examined; rHuIFN-alphaA/D has been previously shown to have anti-viral, anti-proliferative and immunomodulatory activities in murine cells. Pretreatment of mice with 4 daily intraperitoneal injections of rHuIFN-alphaA/D resulted in a marked decrease in the number of pulmonary metastases. This inhibition was dose-dependent but was not seen when mice were similarly treated with rHuIFN-alphaA, a human recombinant alpha interferon subtype which is inactive on murine cells. Treatment of mice with rHuIFN-alphaA/D following B16 F10 injection resulted in no significant inhibition of pulmonary metastases. Mice given a similar treatment regimen of rHuIFN-alphaA/D had elevated natural killer (NK) cell activity as measured by in vitro cytotoxicity against YAC-I or in vivo pulmonary clearance of B16 F10 cells. Pretreatment of mice with 10 daily injections of rHuIFN-alphaA/D resulted in decreased NK activity and less inhibition of metastases. Therefore, in this model system, rHuIFN-alphaA/D inhibits metastases when given in the appropriate treatment schedule. Furthermore, the data are consistent with the hypothesis that rHuIFN-alphaA/D-induced inhibition is a consequence of the immunomodulation of NK cells, which prevent the establishment of pulmonary metastases.

Animals↗
PubMed1984

Modulation of murine natural killer cell activity in vitro and in vivo by recombinant human interferons.

The ability of two subtypes of recombinant human alpha interferons (IFN), rIFN-alpha A and rIFN-alpha D, and two intramolecular hybrids, rIFN-alpha A/D and rIFN-alpha D/A, to modulate murine natural killer (NK) cell activity in vitro and in vivo was examined. The cytotoxic activity of murine spleen cells was markedly augmented by rIFN-alpha A/D following in vitro incubation, while the other IFN had little or no effect. The augmentation observed was dose dependent and inhibited by monoclonal antibody to rIFN-alpha A/D. Mice treated by one of several routes with rIFN-alpha A/D had elevated levels of NK activity in their spleen, peritoneal cavity, and peripheral blood following one to three daily injections. Augmentation of cytotoxicity was dose dependent in vivo and was less efficient or absent following treatment with the other recombinant IFN. When treatment was extended to ten or 12 daily i.p. injections, marked differences in NK levels resulted, depending upon the location from which cells were obtained. Following prolonged administration of rIFN-alpha A/D, a significant decrease in NK activity was seen with peripheral blood lymphocytes, while peritoneal cells retained elevated levels of activity; in spleen, NK activity was less than in mice treated for 3 days with rIFN-alpha A/D but greater than in control mice. Treatment of mice in vivo with IFN can either increase or decrease NK levels dependent upon both the length of treatment and the site at which the NK activity is measured. The use of rIFN-alpha A/D with murine cells is an excellent model to study the regulation of NK activity by IFN.

Animals↗
PubMed1983

Fluoxetine in the treatment of intention myoclonus.

Some types of intention myoclonus respond to serotonin precursor therapy (e.g., L-5-hydroxytryptophan, L-5HTP). Fluoxetine, a specific serotonin (5HT) uptake blocker, was found to have no antimyoclonic effect when administered by itself to four patients with intention myoclonus. However, in two patients with intention myoclonus responsive to L-5HTP and carbidopa, fluoxetine reduced the required dose of L-5HTP to approximately one-third, with greater antimyoclonic activity, decreased side effects, and reduction in platelet 5HT and plasma 5-hydroxyindoleacetic acid and L-5HTP concentrations. These findings further support the hypothesis that some forms of intention myoclonus are caused by a deficiency of brain 5HT, and suggest that the addition of fluoxetine to L-5HTP and carbidopa may improve antimyoclonic therapy.

5-Hydroxytryptophan↗
PubMed1983

Cardioplegia does not prevent reperfusion injury induced by intracoronary platelet deposition.

We have shown that after global myocardial ischemia, reperfusion injury may be related to platelet deposition in the coronary microcirculation. The purpose of this study was to determine whether multidose hypothermic potassium cardioplegia suppresses platelet deposition during postischemic reperfusion. Platelets labeled with 111In and erythrocytes labeled with 51Cr were injected into dogs subjected to either 120 min of continuous cardiopulmonary bypass (control, n = 4), 60 min of global normothermic myocardial ischemia followed by 50 min of reperfusion (n = 6), or global ischemia with cardioplegia (n = 5). Intracoronary platelet deposition was determined by comparing the double-labeled isotope activity of myocardial biopsy specimens to peripheral blood. Reperfusion after global myocardial ischemia resulted in substantial deposition of platelets within the coronary vasculature in both the cardioplegia-treated (215 +/- 40 platelets/mg) and untreated (269 +/- 95 platelets/mg) groups. These increases were significantly greater than those measured during continuous bypass (48 +/- 2 platelets/mg; p less than .01). Cardioplegia, despite apparent washout of the microcirculation, does not alter platelet deposition. Thus other platelet-stabilizing measures must be used to prevent platelet deposition-induced reperfusion injury after surgical global ischemia.

Animals↗
PubMed1977

Long-term therapy of myoclonus and other neurologic disorders with L-5-hydroxytryptophan and carbidopa.

We evaluated the therapeutic effect of L-5-hydroxytryptophan (L-5HTP), the precursor of serotonin (5-hydroxytryptamine), combined with carbidopa, a peripheral decarboxylase inhibitor, in patients with intention myoclonus and examined the serotonin metabolites in spinal fluid, blood and urine before and during therapy. In 18 patients with intention myoclonus due to anoxia or other brain damage, 11 derived more than 50% overall improvement during treatment with L-5HTP and carbidopa. Spinal-fluid 5-hydroxyindoleacetic acid was 35% lower in patients with intention myoclonus than in controls (P less than 0.05). Therapy with L-5HTP and carbidopa increased the concentration of serotonin metabolites in urine and spinal fluid. We postulate that a deficiency of brain serotonin is causally related to intention myoclonus and that the therapeutic effect of L-5HTP and carbidopa may be due to the repletion of serotonin in regions of the brain where serotoninergic neurons have degenerated.

5-Hydroxytryptophan↗
PubMed1976

Gilles de la Tourette's syndrome: biochemical approaches.

Haloperidol, a dopamine receptor blocking agent, is the most effective therapy for Tourette's syndrome. In five patients with Tourette's syndrome, we found in the CSF an elevated probenecid-induced accumulation of HVA, the major metabolite of dopamine. This supports the hypothesis that Tourette symptoms are related to an increased firing of dopaminergic neurons in the central nervous system; haloperidol relieves these symptoms by blocking dopamine receptors. Some similarities of Tourette's syndrome to Lesch-Nyhan's syndrome prompted us to compare these two disorders, obtaining data from a large number of Tourette patients. In a questionnaire completed by 114 patients with Tourette's syndrome, the incidence of self-destructive behavior was 43%, a family history of gout or hyperuricemia was present in 27%, and 11% had a family history of Tourette's syndrome or tics. We propose that Tourette's syndrome could be a genetic disorder of purine metabolism which may result in neurotransmitter abnormalities such as an increased brain dopamine turnover.

Haloperidol↗
PubMed1976

Serotonin and myoclonus.

Biochemical studies of serotonin metabolism and a therapeutic trial of L-5-hydroxytryptophan (L-5-HTP) in combination with carbidopa were carried out in 19 patients with myoclonus. In 6 patients with intention myoclonus, the cerebrospinal fluid concentration of 5-hydroxyindoleacetic acid, a metabolite of serotonin was found to be significantly decreased. L-5-HTP with carbidopa dramatically decreased the frequency and intensity of myoclonus, particularly in those patients with a diagnosis of postanoxic intention myoclonus. The major side effects have been anorexia, nausea, vomiting, diarrhea and mental stimulation. We suggest that a deficiency of brain serotonin is causally related to myoclonic muscle movements and the therapeutic efficacy of L-5-HTP plus carbidopa may be due to the repletion of serotonin in regions of the brain where serotoninergic neurons have degenerated.

5-Hydroxytryptophan↗
PubMed1975

Practical kinetics I: Quantitation of barbiturate stability by TLC.

The purpose of this work was the application of established techniques to the quantitation of stability investigations of liquid formulations as well as in solution kinetic studies. The process consists of streaking aliquots of reaction solution on TLC plates, development, elution, and analysis of the substances in the eluate. Several barbiturates were investigated regarding their decomposition at elevated temperatures. Reasonable correlation is noted between obtained rate constants and literature data. This technique represents a utilitarian approach to stability screening of compounds in solution, aqueous or otherwise, where chromatographic separation and analytical methodology for the pure compound are available.

Amobarbital↗