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Biomedical subjects

W K Silvers

Publications and source records attributed to W K Silvers.

At least 19 recordsLinked to original sources
PubMed1979

The behavior of H-Y-incompatible neonatal skin grafts in rats.

It has been well documented that virgin female rats previously systemically sensitized against H-Y antigen almost invariably reject male skin isografts of adult origin. However, when the donor is a neonatal animal, these H-Y-incompatible grafts are often permanently accepted. Furthermore, such neonatal male skin grafts are frequently able to induce a state of unresponsiveness to subsequent grafts of adult male skin. This ability to induce tolerance is evidently dependent upon the persistence of the neonatal skin graft as it does not occur if the neonatal graft is rejected. Thus, the behavior of H-Y-incompatible neonatal skin grafts in rats parallels their behavior in mice.

Animals↗
PubMed1979

Successful islet transplantation in spontaneous diabetes.

Optimism for islet transplantation is based on reversal of diabetes artificially induced in animals by pancreatectomy or beta cell toxins. In naturally occurring diabetes, implanted islets might be destroyed by the etiologic agent of the original disease; e.g., virus infection, genetic factors, or autoimmunity. Genetically determined diabetes in obese mice, in fact, is resistant to islet transplantation. Since these mice are hyperinsulinemic and not similar to human juvenile onset diabetes (JOD), more appropriate models were sought, "BB" rats spontaneously develop a syndrome remarkably similar to human JOD. We have studied 279 BB rats. In 31 rats the sudden onset of severe hyperglycemia was observed. Sinc BB rats proved to be AgB2 on serological typing, WF (AgB2) donors were selected. Six hundred Wistar-Furth isolated islets were transplanted intraportally in 10 BB diabetic rats immunosuppressed with antilymphocyte serum. All 10 recipients became normoglycemic, remaining so for 1 to 6 monts. An additional animal model studied was virus-induced diabetes in mice, since viral etiology of human diabetes seems likely. DBA mice receiving encephalomyocarditis virus became severely and persistently diabetic. Eight received syngeneic fetal pancreas to the renal subcapsule and became normoglycemic. Removal of the graft 30 days later demonstrated viable islets histologically and resulted in recurrent diabetes. That virally induced murine diabetes and one spontaneous syndrome in rats which is similar to human JOD responded to beta cell implantation argues that this treatment will be effective in man.

Animals↗
PubMed1977

H-Y antigen: behavior and function.

The factors are reviewed which affect the expression of H-Y antigen, a cell surface component that has been extensively analyzed in mice but which may be ubiquitous in all vertebrates. The phylogenetic stability of this antigen and its association with the Y chromosome indicate an important role in primary sex determination.

Androgens↗
PubMed1977

Islet transplantation in genetically determined diabetes.

Hyperglycemia induced in animals by beta cell toxins or by pancreatectomy can be reversed by pancreatic islet transplantation. Abnormal carbohydrate metabolism in juvenile onset human diabetics has also been corrected, albeit temporarily because of graft rejection, by pancreatic transplantation. It does not necessarily follow that naturally occurring diabetes in animals or adult onset diabetes in man would respond to similar treatment. Islet transplantation was studied in mice with chemically induced or genetically determined diabetes. Streptozotocin-induced diabetic mice were permanently cured by syngeneic islets and, when immunosuppressed, were rendered normoglycemic for six weeks after receiving xenogeneic rat islets. In contrast, histocompatible islets from normoglycemic coisogenic donors were ineffective in hyperglycemic db/db recipients as were xenogeneic rat islets in immunosuppressed db/db hosts. However, when islets were isolated from db/db donors and transplated to genetically normal coisogenic mice, which had been rendered hyperglycemic with streptozotocin, they became normoglycemic. Apparently the metabolic defect in the db/db mice, which is similar in some ways to human maturity onset diabetes, does not reside in their islets as these cells can function normally if transplanted to genetically nondiabetic hosts. In two other types of genetic diabetes (ob/ob and NZO) islet transplantation was more effective. Pancreatic transplantation is unlikely to be the proper treatment for all types of diabetes even if technical and immunological problems are overcome.

Animals↗
PubMed1976

The behavior of skin grafts incompatible with respect to skin alloantigens on mice rendered tolerant at birth with lymphoid cells.

It has been reported that lethally irradiated adult B6 mice restored with (A X B6) hemopoietic cells subsequently reject adult A-strain skin grafts because they are not tolerant of A-strain skin-specific (Sk) antigens. This thesis has been confirmed by a series of experiments conducted on neonatally treated animals. Thus sublethally irradiated neonatal B6 mice, inoculated with (A X B6) lymphoid cells, permanently accept these cells while subsequently rejecting adult strain A skin grafts. Further evidence that the destruction of these grafts results from the reaction of the host to Sk antigens, is provided by the fact that similarly treated recipients often permanently accept neonatal A-strain skin. Such grafts usually induce tolerance of adult A-strain skin grafts.

Age Factors↗
PubMed1976

The development of regional pigmentation patterns in black and tan (at) mice.

Mice which express the black and tan (at)allele at the agouti locus have black dorsal and yellow ventral hairs. To determine the site of action of this allele, the kind of hair pigment produced by various dermal-epidermal recombinations of dorsal and ventral black and tan (at/at), ventral nonagouti (a/a) and ventral yellow (Ay/a) embryonic skin has been investigated. The results indicate that it is the dermis which is responsible for the development of regional pigmentation patterns in black and tan mice.

Alleles↗