Search PubMed⌕ Search

Biomedical subjects

J D FELDMAN

Publications and source records attributed to J D FELDMAN.

At least 37 records · Page 2Linked to original sources
PubMed1961

Passive transfer of tuberculin sensitivity by tritiated thymidine-labeled lymphoid cells.

Passive transfer of tritiated thymidine-labeled BCG sensitized lymphoid cells into homologous guinea pigs resulted in positive tuberculin skin reactions 24 hours after testing with PPD. Labeled cells were found specifically attracted to these sites. Labeled non-sensitized lymphoid cells did not appear at PPD injection sites, nor did labeled sensitized cells accumulate in non-specific inflammatory lesions. The specifically reacting tritiated cells were small, medium, and large lymphocytes and stem or immature cells of the lymphoid series. In the homologous system employed, positive skin tests were either minimal or absent 3 days after transfusion of activated cells. The injected labeled sensitized cells were rapidly cleared from the circulating blood and lodged in the lungs, spleen, and lymph nodes. Upon application of specific antigen they reappeared at the skin test site at 6 hours and then increased in number for the next 18 hours.

Animals↗
PubMed1961

Experimental glomerulonephritis. The pathogenesis of a laboratory model resembling the spectrum of human glomerulonephritis.

Daily injections of any one of several foreign serum proteins produced in rabbits functional and morphological alterations similar to those seen in acute, subacute, and chronic human glomerulonephritis. The critical factor determining whether a rabbit would develop renal disease and the type of disease developed was the amount of antibody the rabbit formed. Those responding with much antibody were likely to develop an acute, self-limited glomerulonephritis and to be subsequently immune to further renal damage. Those responding with antibody barely sufficient to neutralize the antigen injected developed subacute and chronic glomerulonephritis. In the circulation of the rabbits with chronic glomerulonephritis, there was a daily recurring antigen-antibody reaction in the region of near antigen excess to near antibody excess which presumably led to the disease. Antigen apparently in the form of antigen-antibody complexes was deposited along the renal capillary basement membranes coincident with the development of subacute and chronic glomerulonephritis. Once developed, the morphologic stigmata of chronic glomerulonephritis persisted even after injections of antigen were stopped. However, in milder instances the renal function recovered in part after stopping antigen. This experimental model has several implications: first, the renal injury is precipitated by antigens with no known affinity for, or immunologic relationship to, kidney; second, antigen antibody complexes localize in the kidney, apparently on the basis of non-immunologic factors, and may be an etiologic agent of renal injury; third, severe hypersensitivity disorders can be related specifically to relatively poor as well as to good antibody responses; and finally, the pathogenesis suggested here offers an alternative to that of nephrotoxic serum nephritis for the experimental approach to the study of human glomerulonephritis.

Animals↗
PubMed1961

Maturation of the rat fetal thyroid.

Maturation of the rat fetal thyroid was studied with the aid of I(131) and of fluorescence and electron microscopy. The I(131) concentration of the fetal gland increased exponentially from day 17 to day 20 of gestation and was related to the weight of the fetus (and presumably the weight of the thyroid) and also to the quantity of I(131) accumulated by the fetus. In the 17-day gland, thyroglobulin or immunologically similar material was sparsely present in the incipient lumens of some cell clusters. With maturation, this material increased and was also observed within follicular cells on days 18 to 19 of gestation. On day 20, the specifically reacting material was present in the follicular lumens and was absent from the cytoplasm of follicular epithelium. Ultrastructurally, the earliest thyroid cells examined were replete with all the organelles found in the more mature epithelium. No direct correlation could be made between the cytoplasmic structures and the presence of thyroglobulin, although the granular endoplasmic reticulum was most likely the organelle responsible for synthesis of thyroglobulin. Thyroglobulin or a precursor was found in fetal thyroid cells before measurable quantities of I(131) were concentrated and before cytoplasmic droplets appeared.

Animals↗
PubMed1958

Electron microscopy of serum sickness nephritis.

The renal lesions of serum sickness were studied with the electron microscope. The most prominent change was a marked swelling and proliferation of glomernlar endothelial cells causing obliteration of the capillary lumen. The basement membrane also showed focal thickenings and excrescences. Deposits of electron-dense material blended into the basement membrane. On the extracapillary side epithelial foot processes were reduced in number and replaced by broad sheets of cytoplasm which were closely applied to the basement membrane. From a comparison of electron and fluorescent microscopic studies of the glomerulus in serum sickness, it would seem that antigen-antibody complexes initiated injury in endothelial cells, although the possibility of the primary reaction occurring on basement membrane cannot be excluded.

Antigen-Antibody Complex↗