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M Goldstein

Publications and source records attributed to M Goldstein.

At least 217 records · Page 12Linked to original sources
PubMed1992

Electrophysiological correlates of dyslexic subtypes.

The construct validity of Boder's typology of dyslexia was investigated using quantified EEG. Thirty-nine children, ranging in age from 7-0 to 10-11, were recorded during a contextual reading task and at rest. During reading, children with dyslexia were expected to show increased theta and beta amplitude compared to nondisabled readers. These differences were expected in regions of presumed strength for each subtype as a sign of overengagement in task. Children with phonological deficits (dysphonetic dyslexia) were expected to adopt visuospatial processing strategies (right occipital-parietal activation), those with orthographic deficits (dyseidetic dyslexia) to emphasize phonetic strategies (left temporal-parietal activation). Results supported beta frequency differences in anticipated regions by subtype during the reading task. However, the direction of difference hypothesis was not supported. Decreased amplitudes in both groups with dyslexia compared to normally achieving readers suggest reconceptualization of the theoretical base for the Boder subtyping system.

Brain Mapping↗
PubMed1992

Modulation of noradrenergic transmission by neuropeptide Y and presynaptic alpha 2-adrenergic receptors in the hypothalamus of spontaneously hypertensive rats.

Neuropeptide Y (NPY) has a wide and specific distribution in the central nervous system, and is colocalized with catecholamines in specific neuronal systems. In this study, in order to investigate the regulatory mechanisms of NPY and presynaptic alpha 2-adrenergic receptors on central noradrenergic transmission in hypertension, we have examined the effects of NPY and the alpha 2-agonist, UK 14,304, on (3H)-noradrenaline (NA) release from hypothalamic slices of spontaneously hypertensive rats (SHR). Electrical stimulation (1 Hz)-evoked (3H)-NA release was significantly greater in the hypothalamic slices of SHR than in those of Wistar Kyoto rats (WKY). NPY and the alpha 2-agonist, UK 14,304, inhibited the stimulation-evoked (3H)-NA release in a dose-related manner. The inhibitory effects of NPY and UK 14,304 on NA release were significantly attenuated in SHR compared with WKY. These results suggest that NPY and alpha 2-adrenoceptors might be involved in the regulation of central sympathetic nervous activity in hypertension.

Adrenergic alpha-Agonists↗
PubMed1992

Clusterin production in the obstructed rabbit kidney: correlations with loss of renal function.

Clusterin, a protein associated with cell death, has been suggested as a marker of renal injury. Correlation of clusterin gene expression with changes in renal function and quantitative measurement of clusterin protein levels after ureteral obstruction have not been previously reported. With unilateral ureteral obstruction in rabbits as the experimental model, the time course of alterations in renal function, clusterin mRNA accumulation, and concentrations of clusterin protein in serum, urine, and renal tissue were investigated. RBF, GFR, and renal concentrating ability (percent sodium reabsorption and urine osmolarity) all decreased (P < 0.05) in the obstructed kidney from control values within 1 day of ureteral obstruction. Clusterin mRNA levels started to rise in the ipsilateral kidney within 12 h of ureteral obstruction and increased up to 10-fold above control levels after 3 days of obstruction. Hybridization histochemistry showed that clusterin mRNA was initially detectable in collecting ducts and distal tubules within 12 h of ureteral obstruction. After 7 days of obstruction, increased accumulation of clusterin mRNA was also detectable in proximal tubular epithelial cells. Clusterin gene expression remained elevated in collecting ducts after 60 days of obstruction. Clusterin expression in the contralateral kidney was increased twofold over control values after 12 h of obstruction. No increase in clusterin mRNA accumulation was detectable after 24 h in the contralateral kidney. Total clusterin protein in the obstructed kidney increased from 0.59 +/- 0.66 (mean +/- 1 SD) to 2.5 +/- 1.3 micrograms after 7 days of ureteral obstruction (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Measurement of urinary clusterin as an index of nephrotoxicity.

Measurements of tissue immunoassayable clusterin, a protein associated with programmed cell death and tissue reorganization, were performed in rats treated with nephrotoxic doses of gentamicin sulfate. Adult Lewis rats were treated with 100 mg/kg/day of gentamicin sulfate for 12 days. Urine, serum, and tissue levels of clusterin protein were measured, as were urinary N-acetyl beta-glucosaminidase (NAG) and serum creatinine levels. Induction of renal injury by gentamicin was detectable within 4 days by increased levels of urinary N-acetyl beta-glucosaminidase (from 280 +/- 66 (mean +/- SD) to 910 +/- 210 nmol/mg creatinine), and within 9 days of initiating gentamicin treatment by increased serum creatinine (from 0.5 +/- 0.1 to 1.2 +/- 0.4 mg/dl). Paralleling these changes, renal, urinary, and serum levels of clusterin increased 10-, 116-, and 3-fold (P less than 0.05). Treatment with gentamicin sulfate did not increase clusterin levels in the seminal vesicle, ventral prostate, testis, or epididymis. The measurement of urinary or serum clusterin may play a role in the early detection of renal injury.

Acetylglucosaminidase↗
PubMed1992

Urinary incontinence. Why people do not seek help.

Some of the most frequently cited reasons for not seeking treatment for urinary incontinence are a belief that incontinence is a normal part of aging; a belief that incontinence is a normal sequelae of childbirth; and a lack of knowledge about existing treatment. There is often a lack of knowledge concerning urinary incontinence and its treatment on the part of health-care providers. Some of the methods available to treat urinary incontinence are pelvic floor muscle exercises, medications, and biofeedback. To overcome the barriers to seeking treatment for incontinence, healthcare providers should ask direct questions about urinary incontinence as part of the routine history and physical examination.

Aged↗
PubMed1992

Dopaminergic mechanisms in the pathogenesis of schizophrenia.

The dopamine hypothesis of schizophrenia has been the dominant theoretical construction guiding research and treatment of the schizophrenic disorders over the past generation. This hypothesis, in its simplest guise, posits the presence of a functional alteration in central dopaminergic systems in the brains of schizophrenic patients. Recent findings have resulted in a greater understanding of the complexity of the central dopaminergic systems and have led to revisions of the hypothesis of a simple functional hyperactivity of central dopaminergic systems. These recent data suggest that there may be regionally restricted changes in the function of the mesotelencephalic dopamine system, and that these changes may be in opposite directions. Such changes may be associated with dysfunctions of interactions between distinct dopaminergic terminal field regions, and may be subserved by functional derangements in other transmitter systems or reflect regionally restricted changes in expression or function of distinct dopamine receptors or catecholamine synthetic enzymes. A recent FASEB symposium reviewed new advances in molecular biology, biochemistry, pharmacology, anatomy, and systems neuroscience as they relate to schizophrenia, and discussed the implications of these data for guiding future research and treatment strategies.

Animals↗
PubMed1992

The role of the regulatory enzymes of catecholamine synthesis in Parkinson's disease.

The major neuropathology of Parkinson's disease (PD) is the degeneration of nigrostriatal dopamine (DA), resulting in a deficiency of DA, and of the enzyme tyrosine hydroxylase (TH), which catalyzes the synthesis of L-dopa. The symptomatic treatment of PD consists of replenishing DA by administering L-dopa, which is enzymatically converted to DA in the striatum. The increase of TH activity by modification of the enzyme leads to an increased synthesis of striatal L-dopa, and thereby replenishes the missing DA more efficiently. The activity of TH is increased by protein kinase-dependent phosphorylation of the enzyme or by inhibition of dephosphorylation with specific phosphatase inhibitors. Thus, modification of TH results in an activated form of the enzyme, which might provide a basis for developing new strategies in the treatment of PD. The extraneuronal enzyme, catechol-O-methyl transferase (COMT), inactivates catecholamines by O-methylation, and its inhibition leads to increased levels of striatal DA. The availability of selective and nontoxic COMT inhibitors makes it possible to assess their therapeutic role in treatment of PD. The intraneuronal enzymes, monoamine oxidase (MAO)-A and MAO-B, inactivate catecholamines and other biogenic amines, such as serotonin, by deamination. Inhibition of these enzyme activities leads to increased levels of striatal DA. The irreversible MAO-B inhibitor selegiline was shown to exert antiparkinsonian activity, especially in the early stages of parkinsonism. Selegiline also prevents the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism in MPTP-treated mice and monkeys. Its role in the prevention of the disease is under investigation in several clinical centers.

Catechol O-Methyltransferase↗
PubMed1992

Neuropeptides and classical transmitters. Localization and interaction.

The present article briefly reviews some aspects on the localization and possible functional roles of neuropeptides. It is emphasized that a large number of peptides can be found in the nervous system and that they in many instances occur together with classical transmitters such as acetylcholine and catecholamines in the same neurons. In agreement, functional studies have revealed that they interact in different ways, both synergistically and antagonistically, with the transmitters. In some instances peptides may also have trophic effects. The recent cloning of neuronal peptide receptors has further substantiated a physiological role for these compounds in the nervous system. Moreover, the recent development of peptide antagonists, which pass the blood brain barrier, now opens up new possibilities to elucidate the functional role of neuropeptides and thus of the coexistence phenomenon.

Animals↗
PubMed1992

No-scalpel vasectomy.

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Ambulatory Surgical Procedures↗
PubMed1991

Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human.

The distribution of acidic (aFGF) and basic (bFGF) fibroblast growth factor mRNA and protein were examined in mesencephalon by immunohistochemistry, immunoblot analysis, in situ hybridization histochemistry, and RNA analysis. Coexistence of aFGF or bFGF with tyrosine hydroxylase protein in nigral cells was observed with immunohistochemistry. Both aFGF and bFGF mRNAs were found in the substantia nigra. Unilateral 6-hydroxydopamine lesions of nigrostriatal neurons resulted in a loss of aFGF and tyrosine hydroxylase [L-tyrosine, tetrahydropteridine: oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] mRNA-positive neurons on the lesioned side. The distribution of aFGF mRNA in monkey brain was similar to that seen in the rat. RNA and immunoblot analysis confirmed the presence of both aFGF and bFGF mRNAs and proteins in the substantia nigra of rat, monkey, and human.

Animals↗
PubMed1991

Effects of Bay K 8644, a Ca2+ channel agonist, on [3H]norepinephrine release in hypothalamus of spontaneously hypertensive rats.

We describe the effects of Bay K 8644, a dihydropyridine-sensitive Ca2+ channel agonist, on [3H]norepinephrine (NE) release from the hypothalamus of spontaneously hypertensive rats (SHR). The electrical stimulation-evoked [3H]NE release was greater in hypothalamic slice of SHR than in those of Wistar Kyoto (WKY) rats. Bay K 8644 (10(-6) M) significantly increased the stimulation-evoked [3H]NE release in SHR. However, the agonist showed no significant effects in normotensive WKY rats. The results suggest that the dihydropyridine-sensitive Ca2+ channels might participate actively in the regulation of the central sympathetic tone of hypertension.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Hypertrophy of dopamine neurons in the primate following ventromedial mesencephalic tegmentum lesion.

Morphological changes in ventral mesencephalic dopamine (DA) neurons of a monkey sustaining a unilateral electrolytic lesion of the ventromedial mesencephalic tegmentum four years earlier were examined. Substantia nigra (A9) DA neurons lateral to the lesion underwent hypertrophic changes. The mean area of these neurons was enlarged by approximately 30% relative to corresponding neurons in the contralateral substantia nigra. Semi-quantitative immunohistochemical measurements of the intensity of tyrosine hydroxylase-like immunoreactivity (TH-li) indicated an increase in the amount of TH-li protein per cell in the hypertrophied neurons. Hypertrophic changes were also observed in ipsilateral A11 DA neurons of the caudal hypothalamus, suggesting that the increase in size was related to transection of the axons of DA neurons as they pass through the midbrain in their projections to target sites. The lesion did not overtly change the density or pattern of the substance P innervation of the substantia nigra, indicating that the striato- and pallido-nigral projections were spared by the lesion. These data suggest that hypertrophy may be a compensatory mechanism of dopaminergic neurons in response to partial lesions of the nigrostriatal system, and thus represent a morphological counterpart to the compensatory biochemical processes effected in response to partial lesions of the striatal dopaminergic innervation.

Animals↗
PubMed1991

Changes in striatal dopamine neurohistochemistry and biochemistry after incomplete transient cerebral ischemia in the rat.

To evaluate the development of striatal ischemic cell damage in relation to alterations in dopamine (DA) transmission, one year old male Wistar rats underwent a 15 min incomplete cerebral ischemia (ICI) induced by occlusion of the common carotid arteries and by hypovolemic hypotension. The animals were divided into the following experimental groups: sham operated rats, rats with ICI without reperfusion, and rats with ICI followed by 60 min, 24 h, 72 h and 144 h of recirculation. The ischemia induced striatal lesions were investigated in serial coronal brain sections, stained with cresylviolet or immunostained for dopamine and cAMP regulated phosphoprotein (DARPP-32), for tyrosine hydroxylase (TH) and for glial fibrillary acidic protein (GFAP) immunoreactivities (IR). Measurements of striatal dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels were made on analogous experimental groups using HPLC methods. Signs of degeneration in small to medium sized neurons were already seen after 60 min of postischemic reperfusion together with slight decreases of DARPP-32 IR and increases of GFAP IR. The damage continued to increase up to 144 h, and after 24 h of recirculation there were clearly defined areas of reduced DARPP-32 IR, overlapping with increased TH IR and increased GFAP IR. The levels of DA, DOPAC and HVA increased sharply after 60 min (151%, 462% and 201%, respectively) remained high after 24 h and normalized after 72 h of recirculation. The DA metabolism was high after 60 min and had already normalized after 24 h of recirculation. The increased DA metabolism in striatal nerve terminals in response to ischemic injury may reflect an early degenerative change in the DA terminals. The long-lasting increase in TH IR may to some extent represent an adaptive change in response to the disappearance of DA receptor-containing nerve cells. Based on the present findings it is possible that an increased D1 transmission in neostriatum immediately following the ischemic injury may contribute to striatal nerve cell degeneration in which an enhancement of NMDA receptor transduction may be implicated.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Distribution of opioidergic, sympathetic and neuropeptide Y-positive nerves in the sphincter of Oddi and biliary tree of the monkey, Macaca fascicularis.

The opioidergic, sympathetic and neuropeptide Y-positive innervation of the sphincter of Oddi (common bile duct sphincter and pancreatic duct sphincter), as well as other segments of the extrahepatic biliary tree was studied in the monkey by use of immunohistochemistry. Methionine-enkephalin-positive nerves were seen to innervate the smooth muscle of all portions of the sphincter of Oddi and also local ganglion cells. No methionine-enkephalin-positive nerves could be detected in the common bile duct, pancreatic duct or gallbladder. Tyrosine hydroxylase-positive nerves occurred between smooth muscle bundles and also ran to local ganglion cells as well as along the common bile duct. Neuropeptide Y-positive nerves were observed within smooth muscle of the sphincter of Oddi (all portions), common bile duct, pancreatic duct and gallbladder. No evidence of any differential innervation of the pancreatic duct and common bile duct sphincters could be detected with these markers.

Animals↗
PubMed1991

Hemodynamic evaluation of bisoprolol after coronary artery surgery in patients with altered left ventricular function.

Bisoprolol is a new cardioselective beta1 adrenergic blocking agent without intrinsic sympathomimetic activity but with minimal effects on myocardial contractility. Bisoprolol was compared to propranolol in 24 patients after cardiac surgery for coronary artery bypass graft (CABG). Each patient had been treated preoperatively with beta-blocking agents and had a cineangiographic left ventricular ejection fraction between 35% and 55%. Patients were randomized to receive orally either 10 mg of propranolol three times a day or 5 mg of bisoprolol once a day. Both drugs resulted in a significant and similar decrease in heart rate. This was associated with significant decreases in cardiac index, stroke index, and thermodilution right ventricular ejection fraction 6 hours after administration of propranolol, but not after bisoprolol. Systolic function measured by Doppler techniques significantly increased in the 10 postoperative days in patients under bisoprolol but not significantly after propranolol. Each drug was well tolerated during the 10 postoperative days, and the recovery was uneventful in each patient. These results indicate that in patients with altered systolic function after CABG, bisoprolol is susceptible to reduce heart rate with less cardiovascular alteration than propranolol.

Adrenergic beta-Antagonists↗
PubMed1991

Dopamine- and adenosine-3',5'-monophosphate (cAMP)-regulated phosphoprotein of 32 kDa (DARPP-32) in the adrenal gland: immunohistochemical localization.

The cellular localization of a dopamine- and adenosine-3',5'-monophosphate (cAMP)-regulated phosphoprotein of an apparent molecular weight of 32,000 (DARPP-32) was investigated in mouse, rat, rabbit, guinea pig, cat, monkey (Macaca fascicularis and Marmoset) and human adrenal gland by means of indirect immunofluorescence histochemistry. DARPP-32-like immunoreactivity (-LI) was demonstrated in chromaffin cells in the adrenal medulla of rabbit, guinea-pig, cat, monkey and human, but not in mouse or rat. In the Marmoset monkey, DARPP-32-LI was also observed in the zona glomerulosa of the adrenal cortex. It has been shown that dopamine and dopaminergic agonists inhibit catecholamine release from chromaffin cells and aldosterone secretion from cells in the adrenal cortex. The present results suggest that DARPP-32, an intracellular third messenger for dopamine, may be part of the signal transduction mechanism for dopamine acting on the adrenal gland.

Adrenal Glands↗