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Biomedical subjects

E Ben-David

Publications and source records attributed to E Ben-David.

36 records · Page 2Linked to original sources
PubMed1986

Neuromuscular involvement in glycogen storage disease type III.

Sixteen patients with glycogen storage disease type III (GSD III) aged 3 to 22 years underwent a detailed neuromuscular evaluation. A minimal impairment of skeletal muscle function was presented in eight patients, slight impairment in four and severe impairment in one patient. Serum creatinine phosphokinase (CPK) was elevated in all patients studied. In the nine patients, in whom electromyography (EMG) was performed; six exhibited a myopathic pattern while a "mixed" (neurogenic-myopathic) pattern was present in three. Muscle biopsies performed in 12 patients, revealed in all cases amylo-1,6,-glucosidase deficiency and biochemical as well as morphological evidence of glycogen accumulation. Two brothers suffered from late onset myopathy, which in the older sibling was associated with clinical, EMG and EM findings of a peripheral neuropathy. Fifteen patients had either electrocardiographic and or echographic evidence of cardiomyopathy. Observations based on this patient material suggest a widespread myopathy in GSD III patients with heterogeneous expression, while peripheral nerve involvement is rarely encountered.

Adolescent↗
PubMed1983

Murine interleukin-2 generates glycogen-rich and mucus-secreting NK cells.

Colonies of cells termed 'giant granular leucocytes' (GGL) displaying natural killer (NK) activity were generated in cell culture. The prominent feature of these cells was the formation of large cytoplasmic pool--the 'theca'--filled up with glycogen. This was demonstrated by the strong positive red staining of the theca with periodic acid Schiff reagent (PAS) which was abolished by prior treatment with amylase. Two different procedures were employed for obtaining colonies of NK-GGL. In the first, mice were injected either with killed Corynebacterium parvum or with killed Bordetella pertusis preparations and their mesenteric lymph-node cells were grown on syngeneic X-irradiated embryonic skin fibroblast monolayers. At the foci of GGL formation the fibroblasts were killed and the cleared areas thus formed were populated by adherent GGL. In the second procedure, supernates from rat or mouse spleen cultures stimulated with concanavalin A (Con A)--Interleukin-2 (IL-2)--were added to cultures of spleen and lymph-node cells prepared from either ordinary or from athymic nude mice. Richest GGL populations developed when rat IL-2 was added to cells of nude mice. Mouse IL-2 was less consistent. With nude mouse cells it stimulated, either mast cells or GGL, or both; rat IL-2 did not stimulate mast-cell differentiation in nude mouse cultures. In contrast, supernates from lymph-node cell cultures prepared from mice infected with Schistosoma mansoni. Mucosal mast cell-stimulating factor (MMSF) stimulated the formation of colonies of mast cells but not GGL. When MMSF was added as late as 23 days, colonies of young mast cells appeared and mast cells progressively increased in number. When rat IL-2 was added to such mature mast-cell cultures on the 30th day, colonies of cytolytic-GGL appeared. These observations indicate that precursors of mast cells and GGL persist in the cultures and preserve their potential to be stimulated by T-cell factors. GGL-NK cells developed on monolayers prepared from whole embryos released substance that displayed morphology and staining characteristic of mucus. Evidence gathered from in-vitro and in-vivo studies links the in-vitro GGL-NK cells to motile cells that inhabit the mucosal epithelium. Based on the observations, a hypothesis on the function of NK cytotoxicity is brought forward. It proposes the replacement of ordinary epithelial cells, which are killed during a proliferative and differentiative response of other cells at the onset of an infection course.

Amylases↗
PubMed1982

Feedback inhibition of thymic secretory activity in mice treated by the thymic extract TP-1 (thymostimulin).

The ultrastructural changes occurring in the medullary epithelium of the thymus of young mice, as a result of repeated injections of thymic extract, TP-1 (thymostimulin) was investigated. After daily injection of TP-1 for 3 weeks, no changes in thymus architecture could be observed by light microscopy. However, by electron microscopy, specific changes were noticed in the epithelial cells. The secretory granules became dilated and engorged; diameter of granules in normal control thymus was approximately 200-250 nm, but reached 1000 nm in treated mice. Degenerative changes appeared in some of these granules, including myelin bodies, distorted configuration and fat droplets. Signs of involution of whole cells and presence of cellular debri within macrophages were observed. Acid phosphatase staining disclosed many lysosomes containing ingested granules. No such findings were observed in control untreated mice, or in mice treated by a heart extract similarly prepared to TP-1. All these findings can be taken as ultrastructural evidence for feedback inhibition of thymic secretory activity, in analogy to the changes occurring other feedback inhibited, peptide hormone secreting glands. The data indicate that (i) the thymus respond to feedback inhibitory stimuli, as other endocrine glands do; (ii)TP-1, the thymic extract under study, contains a physiologically significant thymic hormone, which, when introduced in high doses can exert specific feedback inhibition. This can be taken as an additional, new criterion for the definition of thymic hormones.

Animals↗
PubMed1982

Mast cell growth on fibroblast monolayers: two-cell entities.

Clonal mast cell differentiation occurs when mesenteric lymph node cells from mice immunized with an antigen are grown in its presence on fibroblast monolayers prepared from mouse embryonic skin. Two types of mast cell clones are identified: the first, originates from a precursor present in the lymphoid cell suspension and the second, from a precursor in the fibroblast monolayer. Clones of the first type fail to appear when T cells are eliminated from the suspension; but they grow luxuriantly in the presence of fluid, harvested from cultures containing the antigen-sensitive T cells exposed to the antigen. The two mast cells differ in the clonal size and rate of growth, life span, cell size, shape and size of the granules and numbers of IgE receptors. It is concluded that the rapidly multiplying lymphoid mast cells associate with the mucosae of the respiratory and gastrointestinal tracts and appear in large number in response to immunological stimuli; the long lived mast cells derived from the embryonic skin monolayer are found in the general connective tissue.

Animals↗
PubMed1980

beta 1-Adrenergic receptors in kidney tubular cell membrane in the rat.

We used a beta-adrenergic antagonist, (-) 3H-dihydroalprenolol, to demonstrate binding sites in purified rat kidney preparations that consistsed of plasma membranes of cells from tubules. The tubular origin of these plasma membranes was shown by electron microscopy and Na-K-ATPase enrichment. The binding was rapid (t1/2, 78 sec) and rapidly reversible (t1/2, 48 sec). The binding sites were saturable and bound 69.8 +/- (SD) 29.1 fmoles/mg of membrane protein. The binding was stereospecific with the isomers of beta-adrenergic agonists and beta-adrenergic antagonist propranolol, the (-) isomers being about 40 times more potent than the (+) isomers incompeting for these sites. (-) 3H-dihydroalprenolol had a high affinity for the binding sites, expressed by the mean equilibrium dissociation constant (KD) (KD, 7.1 nM). The beta-adrenergic antagonist (-) propranolol also showed high affinity (KD, 62.8 nM). The order of potency for inhibition of binding by beta-adrenergic agonists was: (-) isoproterenol (KD, 0.66 microM) greater than (-) epinephrine (KD, 4.3 microM) greater than or equal to (-) norepinephrine (KD, 13.5 microM). Conclusion. The (-) 3H-dihydroalprenolol binding sites in the rat kidney tubular cell membrane are beta-adrenergic receptor of the beta1 subgroup.

Alprenolol↗
PubMed1979

Mitogenic activity of Mycoplasma pulmonis. I. Stimulation of rat B and T lymphocytes.

The mitogenic activity of Mycoplasma pulmonis towards both rat B and T lymphocytes has been demonstrated. The data summarized in this report show that spleen cells obtained from T X BM rats were extensively activated by M. pulmonis. Furthermore, M. pulmonis has been demonstrated to induce the development of antibody producing cells, as attested by the appearance of direct plaque forming cells against SRBC and TNP-SRBC in spleen cultures exposed to this mitogen. It was also demonstrated that rat thymus cells and a part of the lymph node T-cell population responding to either Con A or PWM, were stimulated by M. pulmonis, the response being weaker than that of rat B-cell populations. It was thus concluded that M. pulmonis activates both rat B and T lymphocytes. This mitogenic stimulation, however, is not equally exerted on both these populations, being strongly effective upon B cells and less so on T cells.

Animals↗
PubMed1979

Histamine levels in ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome was produced in rabbits by administration of human menopausal gonadotropin (hMG) and human chorionic gonadotropin (hCG). Histamine levels in the animals' plasma were determined by an enzymatic-isotopic assay. The results of this study show that there is no statistically significant difference between histamine levels in ovarian hyperstimulated animals as compared with control animals. Furthermore, no differences in the number of mast cells in the ovaries could be demonstrated between the 2 groups. It is concluded that histamine probably does not play a role in the pathogenesis of this syndrome. The relevance of this suggestion to other proposed mechanisms on the etiology of ovarian hyperstimulation syndrome is discussed.

Animals↗
PubMedDate not supplied

The role of lysosomes in the healing process of cutaneous leishmaniasis.

Biopsy material in early and late stages of cutaneous leishmaniasis was obtained. The ultrastructural study using acid phosphatase reaction as a marker for lysosomes showed that in early stages parasites proliferate undisturbed within macrophage cytoplasm. At later stages numerous degenerating parasites were seen and macrophage lysosomes were observed adhering to and pouring their contents into the parasite. It is assumed that activated macrophages control intracellular parasitism by lysosomal activity.

Adult↗
PubMedDate not supplied

Arterial hypertension injures brain capillaries. Definition of the lesions. Possible pathogenesis.

Systemic hypertension (secondary to aortic coarctation) produces in monkeys, multifocal brain lesions where capillaries show increased diameter, endothelial degeneration and deposition of collagen and other substances in the basement membrane. In one animal, capillary changes were detected as early as 8 weeks after induction of hypertension. Similar capillary alterations were demonstrated in brain samples of hypertensive humans obtained at autopsy. We suggest that the above abnormalities may be the result of successive episodes of regional ischemia and/or hyperperfusion. Validation of these observations requires careful evaluation of additional human and animal brains.

Animals↗