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Biomedical subjects

S Finkelstein

Publications and source records attributed to S Finkelstein.

At least 55 records · Page 3Linked to original sources
PubMed1988

Distribution of anionic sites on the capillary endothelium in an experimental brain tumor model.

The distribution of anionic domains on the capillary endothelium of experimental brain tumors was determined using cationic ferritin (CF) in order to ascertain whether the pattern of these domains is different from that on normal cerebral capillaries. Tumors were induced by stereotaxic injection of cultured neoplastic glial cells, A15A5, into the caudate nucleus of Sprague-Dawley rats. Following a 14-21 day growth period tumors appeared as vascularized, sharply circumscribed masses which caused compression of the surrounding brain tissue. Anionic domains were distributed in a patchy and irregular pattern on the luminal plasma membrane of the endothelia of blood vessels in the tumors. Some variability in this pattern was observed infrequently in limited regions of the tumor where there was either a continuous layer of CF or an absence of CF binding. Plasmalemmal vesicles, coated vesicles, coated pits, multivesicular bodies, and some junctional complexes showed varying degrees of labeling with the probe. Capillaries in the tumor periphery and normal cerebral vessels showed a uniform distribution of anionic groups. These results indicate that there is an altered surface charge on the endothelial luminal plasma membrane of blood vessels in brain tumors. A correlation may exist between the altered surface charge and the degree to which the blood-brain barrier is impaired in these vessels.

Animals↗
PubMed1984

Liver ischemia increases the molecular order of microsomal membranes by increasing the cholesterol-to-phospholipid ratio.

An accelerated degradation of phospholipid is the likely basis of irreversible cell injury in ischemia, and the membranes of the endoplasmic reticulum of the liver are a convenient system with which to study the effect of such a disturbance on the structure and function of cellular membranes. In the present report, electron spin resonance spectroscopy has been used to evaluate changes in the molecular ordering of microsomal membrane phospholipids in the attempt to relate the loss of lipid to alterations in membrane structure. The order parameter, S, was calculated from spectra reflecting the anisotropic motion of 12-doxyl stearic acid incorporated into normal and 3-h ischemic microsomal membranes. Over the temperature range 4-40 degrees C, the molecular order (S) of ischemic membranes was increased by 8-10%. This increase was reproduced in the ordering of the phospholipids in liposomes prepared from total lipid extracts of the same membranes. In contrast, after removal of the neutral lipids, liposomes prepared from phospholipids of ischemic and control membranes had the same molecular order. There were no differences in the phospholipid species of control and ischemic membranes or in the fatty acid composition of the phospholipids. In the neutral lipid fraction of ischemic membranes, however, triglycerides and cholesterol were increased compared to control preparations. There were no free fatty acids. The total cholesterol content of the liver was unchanged after 3 h of ischemia. The cholesterol-to-phospholipid ratio of ischemic membranes, however, was increased by 22% from 0.258 to 0.315 as a consequence of the loss of phospholipid. Addition of cholesterol to the control total lipid extracts to give a cholesterol-to-phospholipid ratio the same as in ischemic membranes resulted in liposomes with order parameters similar to those of liposomes prepared from ischemic total lipids. It is concluded that the degradation of the phospholipids of the microsomal membrane results in a relative increase in the cholesterol-to-phospholipid ratio. This is accompanied, in turn, by an increased molecular order of the residual membrane phospholipids.

Animals↗
PubMed1984

Tricuspid valve obstruction due to intravenous leiomyomatosis.

A case is discussed of a 65-year-old woman who presented with tricuspid stenosis. She was evaluated with multiple imaging techniques including gated radionuclide angiography, cardiac sector scanning, and abdominal CT imaging. A review of the literature of the entity known as intravenous leiomyomatosis is presented.

Abdominal Neoplasms↗
PubMed1983

Altered heterogeneity of monocytes in acute myelomonocytic leukemia.

Human peripheral blood monocytes isolated from normal donors and patients with acute myelomonocytic leukemia (AMML) were separated on a discontinuous density gradient of bovine serum albumin (BSA) into five fractions. Cells from each fraction were assayed for cell surface markers, prostaglandin E2 (PGE2) production, ability to affect proliferation in response to antigen by autologous peripheral blood lymphocytes previously depleted of monocytes, and ability to regulate immunoglobulin (Ig) synthesis by allogeneic B-lymphocytes. Fractions 1-5 from normal donors contained 11, 10, 23, 34, and 22%, respectively, of the total number of monocytes. In contrast, in 6 patients with AMML fraction 3 was considerably larger (52%) than any other fraction, in 1 patient comprising 87% of her monocytes. Cells from each fraction differed markedly in accessory function. In general, cells from fraction 3 were poorer as helper cells than cells from other fractions. They also produced after stimulation larger amounts of PGE2 than did cells from other fractions of the gradient. These data show that PBL contain a subpopulation of monocytes, which either helps poorly or suppresses in vitro immunologic function of T-cells (proliferation) and B-cells (lg synthesis), and that this subpopulation is increased in the blood of patients with AMML.

B-Lymphocytes↗
PubMed1982

Angiolymphoid hyperplasia with eosinophilia: a bone lesion pathologically resembling Kimura's disease of skin. A report of two cases.

Primary osseous lesions morphologically identical to the soft tissue entity known as angiolymphoid hyperplasia with eosinophilia were diagnosed by means of light and electron microscopy in two men, ages 20 and 27 years, respectively. The characteristics of the lesions were reactive rather than neoplastic. The soft tissue counterpart of this lesion has shown no indication of aggressive behavior nor of a potential to metastasize. Further investigations are necessary to determine whether a similar benign behavior can be established for angiolymphoid hyperplasia with eosinophilia arising primarily in bone.

Adult↗
PubMed1980

A comparison between Frank and SVEC III lead systems in normal subjects.

The Frank and the SVEC III lead systems were used to record the vectorcardiograms (VCGs) of 10 normal subjects. The VCGs obtained using the two leads were compared. The QRS and the T magnitudes of the Frank lead were 25-30% and 13%, respectively, larger than those of the SVEC III. The maximum QRS vectors of the Frank lead were less inferiorly and less posteriorly oriented. Maximal T vectors of the Frank lead were less inferiorly and less anteriorly oriented. When the VCGs of 318 adult male Minnesotans (Minnesota group) recorded by the SVEC III lead system were compared with the VCGs of 510 adults from Washington, D.C. (Draper group) recorded by the Frank system, the magnitudes of QRS and T of the Draper group were larger. The percent increase of voltage was comparable to that seen when the two leads were compared in the same population. There were angular differences between the Draper and the Minnesota groups which could not be explained by lead differences. The differences were attributed to the differences in populations. It was also noted that there are significant differences in the normal values published by various authors and that the normal values obtained from one population should be applied with caution to other populations.

Adult↗
PubMed1978

Broca aphasia: pathologic and clinical.

The speech disturbance resulting from infarction limited to the Broca area has been delineated; it differs from the speech disorder called Broca aphasia, which results from damage extending far outside the Broca area. Nor does Broca area infarction cause Broca aphasia. The lesions in 20 cases observed since 1972 were documented by autopsy, computerized tomography, or arteriogram; the autopsy records from the Massachusetts General hospital for the past 20 years and the published cases since 1820 were also reviewed. The findings suggest that infarction affecting the Broca area and its immediate environs, even deep into the brain, causes a mutism that is replaced by rapidly improving dyspraxic and effortful articulation, but that no significant distrubance in language function persists. The more complex syndrome traditionally referred to as Broca aphasia, including Broca's original case, is characterized by protracted mutism, verbal stereotypes, and agrammatism. It is associated with a considerably larger infarct which encompasses the operculum, including the Broca area, insula, and adjacent cerebrum, in the territory supplied by the upper division of the left middle cerebral artery.

Adult↗