Biomedical subjects

A Sandra

Publications and source records attributed to A Sandra.

75 records · Page 5Linked to original sources

PubMed1977

Suppression of myoblast fusion by concanavalin A: possible involvement of membrane fluidity.

Experimental evidence is presented which is consistent with the involvement of membrane fluidity during myoblast fusion. Treatment of pretrypsinized myoblasts with tetrameric Con A, but not with the dimeric succinyl derivate, inhibits fusion. Inhibition is reversed by treatment with alpha-methyl-D-mannoside or subsequent trypsinization. No inhibition is observed when the lectin is incubated with cells at 4 degrees C unless the incubation is followed by treatment with glycogen, a multivalent Con A cross-linking agent. This effect of glycogen is reversed by subsequent treatment with alpha-amylase. Direct observation of Con A-binding site topography by transmission electron microscopy of membrane replicas of cells labelled with Con A and haemocyanin reveals that inhibition of fusion correlates with a clustered distribution of Con A-binding sites, whereas normal fusion correlates with a dispersed distribution.

Animals↗

PubMed1977

Modulation of lipids in the chick liver by "hypophysectomy" and replacement.

The effect of "hypophysectomy" by means of surgical decapitation upon total lipids in developing chick embryo liver has been studied from 10.5 to 18.5 days of incubation. "Hypophysectomy" results in subnormal levels of hepatic lipid per whole liver throughout this period. Data expressed as mg lipid per 100 mg liver corrected wet weight also results in decreased liver lipid concentrations after day 14.5. In "hypophysectomized" embryos bearing pituitary transplants, liver total lipid amounts and concentrations are significantly increased toward normal values. The possible role(s) of the pituitary in the control of embryonic liver lipid metabolism is discussed.

Animals↗

PubMedDate not supplied

Expression of c-KIT and its ligand, stem cell factor, in normal and subfertile human testicular tissue.

The c-KIT proto-oncogene encodes for a transmembrane receptor and is associated with maturation of several cell types, including germ cells. The ligand of the receptor has been identified as stem cell factor (SCF). Loss or alteration of the expression of either of these factors leads to anemia, albinism, and/or sterility in mice. We examined the expression of c-KIT and SCF by immunohistochemistry in specimens from normal and infertile human testis. All specimens were obtained in the evaluation of male subfertility. We were able to demonstrate staining for c-KIT in Leydig cells in all specimens. Normal testis stained for c-KIT in the cytoplasm of early spermatogenic cells, as well as the acrosomal granules of the round spermatids and the acrosome of testicular spermatozoa. However, staining in testis demonstrating maturation arrest failed to demonstrate acrosomal staining, and Sertoli-only specimens demonstrated staining for c-KIT in Leydig cells only. The results for SCF demonstrated an overall uniform staining of Leydig cells in all specimens. The intensity of staining of Sertoli cells increased from normal to maturation arrest to Sertoli-only specimens. Germ cell staining was consistently negative. We hypothesize that these staining patterns for SCF are due to either lack of staining of the receptor-ligand complex or overexpression of the kit ligand in tissue that does not express the kit receptor. It appears that the c-kit receptor is expressed in the acrosome of developing germ cells, as well as in Leydig cells and early spermatogenic cells, suggesting a role in the acrosome reaction, as well as germ cell maturation and differentiation.

Adult↗