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Biomedical subjects

Y Ben-Shaul

Publications and source records attributed to Y Ben-Shaul.

At least 37 records · Page 2Linked to original sources
PubMed1985

Formation of lentoids from retina gliocytes: ultrastructural study.

In primary monolayer cultures of dispersed neural retina cells from 13-day chick embryo, gliocytes (Müller glia cells) multiply and rapidly change into a lentoidal (lens-like) phenotype. They express lens proteins, including MP26 (a lens plasma-membrane antigen) and ultra-structurally appear to resemble lens cells. A significant aspect of this modification is that the glia-derived lentoidal cells no longer display contact-affinity for neurons but become preferentially adhesive to each other; in aggregates, they assemble into compact lentoids. A likely explanation for this change in cell affinities is that the modified gliocytes express little or no R-cognin, a retinal cell-surface antigen implicated in mutual recognition and adhesion of retina cells. Although lentoidal cells express MP26, a gap-junction component in the lens, no gap junctions could be found in the lentoids.

Animals↗
PubMed1984

Separation of induction and expression of tight junction formation mediated by proteinases.

The formation of tight junctions can be induced in the human adenocarcinoma cell line HT 29 by treatment with trypsin at 37 degrees C. In contrast, after treatment of the cells with trypsin at low temperature (3 degrees C), no tight junctions were observed. However, abundant formation of tight junctions occurred when cells were treated with trypsin at 3 degrees C, washed with soybean trypsin inhibitor, and subsequently incubated at 37 degrees C. Thus, this protocol allows for the first time the temporal separation of the induction and assembly of tight junctions.

Adenocarcinoma↗
PubMed1984

Cell disorganization and malformation in neural retina caused by antibodies to R-cognin: ultrastructural study.

Retina tissue from 6-day chick embryos was organ-cultured for 3 days in the presence of antibodies to R-cognin, a surface antigen of retina cells. The antibodies which are known to bind to this antigen caused a striking malformation: interruption of the outer limiting membrane and extensive cell disorganization resulting in exteriorization of many cells and forming of chaotic masses on the surface of the tissue. Controls did not show these effects. These results further confirm that R-cognin is involved in the mechanism of histotypic contacts and recognition of retina cells, and that it plays an essential role in cell organization and histogenesis in the retina.

Animals↗
PubMed1983

Localization of retina cognin in embryonic neural retina tissue by immuno-scanning electron microscopy.

The retina cognin (a retina-specific cell-surface glycosylated protein that mediates self-recognition and morphogenetic contact associations of embryonic retina cells) was visualized by immunolabeling and scanning electron microscopy on the surface of cells within retina tissue of 9- and 16-day chick embryos. The photoreceptor processes which are free of contact with cells in the neural retina, were found to be devoid of surface cognin from early on in their development. These results extend previous studies on cognin localization and regeneration on separated retina cells in vitro and conclusively correlate its presence and surface topology with its postulated role.

Animals↗
PubMed1983

Immunoscanning electron microscopy of antigenic determinants of T/t-complex (tw18) mouse embryos.

tw18 antigen(s) have been localized by immunoscanning electron microscopy in 7.5-day mutant embryos using a primary antiserum to tw18 made and defined on male germ cells and a secondary rabbit anti-mouse Ig antibody coupled to hemocyanin. Homozygotes (tw18/tw18) diagnosed on morphological grounds are more densely labeled primarily on those cell types affected by genetically caused dysfunction. Eight-celled tw18 embryos are not labeled. This finding of embryonic cell type specificity, together with the available evidence for stage specificity, implicate a function for t-antigens in embryonic development.

Animals↗
PubMed1981

Cell surface labeling of embryonic neural retina cells exposed to low temperature, energy inhibitors, cytochalasin B and colchicin.

Large blebs devoid of receptors for hemocyanin-labeled concanavalin A appear on neural retina cells from 8-day chick embryos exposed to low temperature or to potassium cyanide or 2,4(alpha)-dinitrophenol at room temperature. Labeling with mixed antibodies against a crude retina membrane preparation and with goat anti-rabbit-hemocyanin conjugate showed the same results. Determination of cell ATP content indicated a drop in ATP concentration after exposure to low temperature or to respiration inhibitors. Disruption of microtubules by colchicin inhibited the formation of 'naked' large blebs, whereas cytochalasin B had no such inhibitory effect.

2,4-Dinitrophenol↗
PubMed1980

Corneal endothelial changes under induced intraocular pressure elevation: a scanning and transmission electron microscopic study in rabbits.

Intraocular pressure was artificially raised to 60--70 mmHg in 7 albino rabbits for periods of 15 minutes to 4 hours. The corneal endothelium of these eyes was studied by transmission and scanning electron microscopy. A correlation between exposure time to elevated IOP, clinical signs observed by slit-lamp examination, and extent of morphological damage is clearly shown. In eyes exposed to high pressure for 15 and 30 minutes corneas remained transparent and only minimal changes could be detected by SEM, which consisted of small areas of cell with unevenness of their surface, occasional cellular ruptures, and diminution of cilia and microvilli. After 1--2 hours of exposure small, solitary corneal opacifications appeared. In these eyes more severe morphological changes affecting larger areas were observed, with additional cellular blebbing, excariocytosis, cellular rupture, disintegration, and disappearance seen in SEM. Thin sections revealed swelling of mitochondria, disorganisation of endoplasmic reticulum, and the existence of myelin bodies. In eyes exposed for 3 and 4 hours to high IOP corneal haziness, implying stromal oedema, appeared. In these eyes the areas affected were larger, the extent of damage being more severe. Many areas were bare of endothelium, surrounded by scattered cellular debris, and showed cells with ballooning surfaces and multiple ruptures. Even in severe cellular damage cellular junctions appeared intact. It is assumed that endothelial cells are more sensitive to IOP elevation than the cellular junctions and that injury to the active pump system due to morphological damage is responsible for the resultant corneal oedema.

Albinism↗
PubMed1980

Age-dependent differences in cognin regeneration on embryonic retina cells: immunolabeling and SEM studies.

The retina cognin (a glycoprotein isolated from the surface membrane of neural retina cells of chick embryos and postulated to mediate self-recognition and histogenetic association of retina cells) has been visualized by SEM on the surface of embryonic retina cells in vitro following immunolabeling of the cells with antibodies to the purified cognin and with polystyrene latex microbeads. Trypsin dissociation of retina tissue into separated cells resulted in cognin depletion from the cell surface; following incubation at 37 degrees C the cells regenerated the cognin. Regeneration was fastest and most abundant on cells from the youngest retinas examined; it declined markedly with the embryonic age of the cells, suggesting an age-dependent decrease in cell capacity for cognin formation. Evidence is discussed that the rate and amount of cognin regeneration on the cell surface are temporally-causally correlated with the capacity of the cells to reaggregate into retinotypic tissue. The results support the suggested role of the cognin in the mechanism of self-affinity and morphogenetic association of embryonic neural retinal cells.

Animals↗
PubMed1980

Tight junctions in epithelial cells of human fetal hindgut, normal colon, and colon adenocarcinoma.

The structural patterns of tight junctions in normal human colon mucosa, colon adenocarcinomas, and fetal colon were studied and compared by the freeze-fracturing technique. The zonula occludens of the normal colon cells at the upper, more differentiated part of the crypts of Lieberkühn appeared as continuous belts made of about eight parallel strands. At the less differentiated bases of the crypts, the zonula occludens was less regular and contained fewer, mostly beaded strands. In the colons of 10-week fetuses, early stages of tight junction assembly were observed. At the same time, vesicles bearing remnants of tight junction elements were observed within the cytoplasm. This finding suggested that during the early development and organization of the fetal gut, mechanisms of assembly and disassembly of tight junctions are operating concomitantly. In well-differentiated adenocarcinomas, the cells in the luminal region retained their polarity and had seven or eight parallel junctional elements. In infiltrating cells, however, tight junctions appeared as fascia occludens and resembled the junctional organization of 10-week fetuses.

Adenocarcinoma↗
PubMed1979

Tight junctions of dissociated and reaggregated embryonic lung cells.

Treatment of embryonic lung tissue with trypsin resulted in clustering of intramembrane particles (IMP) and gradual disassembly of tight junctions. In dissociated single cells kept in trypsin-free medium, IMP are randomly distributed but degradation of tight junctions continue. Vesicles containing tight junction elements were observed within the cytoplasm. It is therefore assumed that tight junctions may be degraded in two ways: breakdown of elements to IMP, and endocytosis. In cells reaggregated by rotation tight junctions reassembled only in hystotypic aggregates. Cycloheximide which interferes with histotypic reaggregation prevents the reassembly of tight junctions.

Animals↗
PubMed1979

Degradation of tight junctions in HT29, a human colon adenocarcinoma cell line.

The process of tight junction degradation was followed in a cell line of human colon adenocarcinoma. Tight junctions are degraded by 2 mechanisms: (1) breakdown of junctional elements to intramembrane particles; (2) bleb formation by which tight-junctional elements are internalized into the cytoplasm or excluded into the medium. It is suggested that the first mechanism allows preservation of membrane particles for re-use, whereas the second is a mechanism by which the cells eliminate unneeded junctional elements.

Adenocarcinoma↗
PubMed1977

The human coronary microcirculation: an electron microscopic study.

The ultrastructure of the terminal vascular bed of human coronary arteries was studied in the myocardial tissue obtained at surgery from different locations in the heart in five patients. The following vessels were identified: (1) Arterioles; slender and prolonged endothelial cells, flat nuclei and two to three layers of smooth muscle cells. (2) Precapillary sphincters: short endothelial cells, large nuclei bulging into the lumen, close myoendothelial junctions and a single layer of circular smooth muscle. (3) Capillaries: composed of one or more slender endothelial cells. (4) Venules: flat endothelial cells and nuclei, no muscular layer, rich collagen tissue. The function of these structures is believed to be as follows: the arterioles are the smallest blood-distributing arteries in the heart. The precapillary sphincters control blood flow to the capillaries; pressor substances present in the blood are picked up by endothelial cells, pass rapidly through the myoendothelial junctions and cause contractions of the smooth circular muscle layer; the bulging nuclei of endothelial cells then passively obstruct the lumen almost completely. The main exchange of gases and nourishing substances takes place in the capillaries. We postulate that in some pathologic conditions, abnormal constriction of the sphincters may cause diminished flow and be the basis for some well defined or unclear ischemic events.

Coronary Circulation↗
PubMed1976

Membrane-bound ATPase in chloroplasts of Euglena gracilis.

Membrane-bound ATPase activities in chloroplasts of Euglena were examined. Ca2+- and Mg2+-dependent activities were relatively high in membrane preparations and could not be further activated by a number of procedures. The enzyme was found to be highly specific for purine nucleotides and was inhibited by the usual inhibitors of photophosphorylation. Km values of Ca2+ and Mg2+ ATPase for ATP were 2.5 and 2.1 mM, respectively. Both activities were competitively inhibited by ADP and inorganic phosphate. A relationship was found between Ca2+- or Mg2+-dependent ATPase activities and chloroplast completeness. The possibilities that these activities result from one enzyme depending on Ca2+ or Mg2+ or from two different enzymes are discussed.

Adenosine Triphosphatases↗