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L Weisberg

Publications and source records attributed to L Weisberg.

13 recordsLinked to original sources
PubMed1989

Aldosterone-induced proteins: purification and localization of GP65,70.

Aldosterone stimulates sodium transport in responsive epithelia by inducing "effector" proteins that control or modulate transcellular sodium flux. We have previously identified a group of electrophoretically microheterogeneous (pI 5.8-6.2) and polymorphic (Mr 65 and 70) glycoproteins that are specifically induced by aldosterone in toad urinary bladders (TUBs) and cultured toad kidney cells (A6 cell line). We raised a series of monoclonal antibodies (MAb) to these proteins and, using light and electron immunohistochemistry, localized the higher Mr glycoproteins (GP70) to the apical plasma membrane and subapical granules of the sodium-transporting cell of the TUB epithelium, the granular cell. GP70 appears to be discharged into the bladder lumen; this process is increased by phorbol myristate acetate, an agent known to induce granule exocytosis. These findings are consistent with the possibility that GP70 represent components or modulators of the "high-resistance" renal epithelial sodium channel. MAbs reactive against GP65 did not identify these glycoproteins within TUB epithelial cells; these lower Mr aldosterone-induced proteins may be incompletely processed forms of GP70.

Aldosterone↗
PubMed1988

Aldosterone-induced glycoproteins: electrophysiological-biochemical correlation.

Aldosterone induces the synthesis of a group of glycoproteins (GP65,70) in toad urinary bladders which are potential effectors of the natriferic action of this hormone. In the present study we have confirmed that aldosterone produces a two-phase electrophysiological response. During the early phase (less than 3 h) short-circuit current and transepithelial conductance increase in parallel, while during the late phase (greater than 3 h) short-circuit current continues to increase without any further change in conductance. By biosynthetically labeling aldosterone-treated toad bladders with [35S]methionine either during the early (h 0-2 or 1-3) or the late (h 4-6 or 7-9) phases of the natriferic response, we have demonstrated that GP65,70 is synthesized as a late effect of aldosterone. Since synthesis of GP65,70 occurs at a time when the electromotive force of the Na+ pump is increasing, and since GP65,70 biochemically resembles the beta subunit of Na+/K+-ATPase, studies were undertaken to examine whether GP65,70 is the beta subunit. Purified amphibian renal beta subunit was analyzed by two-dimensional polyacrylamide gel electrophoresis and was found to have an isoelectric point and Mr value similar to those of GP65,70. However, when nitrocellulose blots containing wheat germ agglutinin-purified proteins from aldosterone-treated bladders were stained with monospecific polyclonal antibodies developed against the beta subunit, GP65,70 was not recognized, whereas a group of slightly more acidic proteins of similar Mr were recognized. Thus, GP65,70 is not the beta subunit of Na+/Ka+-ATPase. Further studies are needed to determine the cellular function of GP65,70.

Aldosterone↗
PubMed1988

The clinical and computed tomographic features of cerebellar peduncular hemorrhage.

Three patients with medial ventral cerebellar peduncular hemorrhages presented with a characteristic syndrome. This included (1) ipsilateral ataxia, (2) lower motor neuron type facial weakness, and (3) ipsilateral gaze paresis. The gaze paresis could not be overcome with a doll's head maneuver. The findings are explained by compression of the facial colliculus, with involvement of the sixth nerve nucleus and the middle cerebellar peduncle. Two patients were hypertensive; one was normotensive, and no etiology was identified with angiography. Of 40 patients with cerebellar hemorrhage seen at our institution, only those with medial cerebellar peduncular hematomas demonstrated this clinical triad, and we have not seen this clinical triad in other pathologic conditions. The diagnosis of a small medial cerebellar peduncular hemorrhage was established by CT. In two patients, repeat CT showed complete hematoma resolution. The patients shared a favorable prognosis.

Adult↗
PubMed1986

Subdural empyema. Clinical and computed tomographic correlations.

The clinical and computed tomographic (CT) findings in 15 patients with subdural empyema (SDE) were analyzed. Seven children with meningitis later developed focal neurologic signs of SDE. The CT scans showed prominent subdural lesions with medial membrane enhancement; only one child had a parenchymal lesion, which represented a brain abscess. Two lesions were multiloculated, which was delineated by the CT finding of medial enhancing bands separating the compartments of the hypodense lesions. Of eight adolescents and adults with SDE, seven had sinusitis. These patients presented initially with fever and meningeal signs in addition to altered levels of consciousness. They latter developed focal neurologic signs or seizures. In seven cases, CT showed hemispheric mass effect with a thin subdural lesion and a medial enhancing membrane. One scan showed a prominent subdural lesion with minimal hemispheric mass effect.

Adolescent↗
PubMed1978

The Klüver-Bucy syndrome in man.

It is apparent that the importance of the limbic system is essentially for survival. The inability to discriminate enemy from friend as well as loss of the proper affective response to what is dangerous or safe to the organism may be thought of as more central to survival than what is described as "other higher intellectual functions." The case described is a dramatic expression of such a transient limbic dementia originally described by Klüver and Bucy in their syndrome. Since Klüver and Bucy originally described their syndrome, the structural and functional understanding of the limbic system has been greatly increased. Although a rare occurrence in man, the Klüver-Bucy syndrome serves as a demonstration of an unusual brain syndrome whose theoretical and experimental basis has been greatly enlarged since first described.

Adult↗
PubMed1977

Computed tomographic evaluation of increased intracranial pressure without localizing signs.

A total of 29 alert patients with papilledema and no localizing neurological signs were evaluated by computed tomography. Lesions were demonstrated in 8 who exhibited ventricular enlargement or abnormal tissue density; 19 had normal ventricles which suggested pseudotumor cerebri and only 6 of these patients underwent subsequent pneumoencephalography. In alert patients with papilledema alone, CT can demonstrate ventricular abnormalities and abnormal densities, and assist in the diagnosis of benign intracranial hypertension without pneumoencephalography or angiography.

Adolescent↗
PubMedDate not supplied

Tuberous sclerosis: CT findings and differential diagnosis.

The CT findings in a patient with tuberous sclerosis are described with special emphasis upon the differential diagnosis. The presence of multiple bilateral subependymal nodular nonenhancing hyperdense calcified lesions is relatively characteristic of tuberous sclerosis when combined with the appropriate clinical findings. In some cases, cerebral cortical heterotopias are visualized as hypodense nonenhancing subependymal lesions. The finding of a subependymal giant cell astrocytoma is sometimes seen in patients with tuberous sclerosis, and the finding of a subependymal hyperdense enhancing lesion is consistent with this diagnosis.

Calcinosis↗
PubMedDate not supplied

Computed tomographic findings in brain swelling.

Vasogenic edema is due to a breakdown of the blood-brain barrier. This is the most common type of brain edema encountered in clinical medicine. In vasogenic edema, CT shows hypodense frond-like regions located within the white matter. This edema surrounds the underlying pathological lesion. The edema may be quite extensive in relation to the size of the lesion. Cytotoxic edema is due to impaired brain metabolism with swelling of neurons, glial, and endothelial cells. In cytotoxic edema, CT shows diffuse hypodense subcortical regions. Ischemic edema is due to impaired tissue perfusion. The CT appearance is that of a hypodense region with a specific arterial vascular distribution. Interstitial edema is due to hydrocephalus, CT shows hypodense regions directly capping the ventricles or the mass lesion. Based upon the CT findings, it is frequently possible to determine the type of edema present and to predict with greater accuracy the nature of the underlying pathological process.

Brain Edema↗