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Biomedical subjects

R L Carter

Publications and source records attributed to R L Carter.

At least 163 records · Page 9Linked to original sources
PubMed1977

Balkan (endemic) nephropathy and a toxin-producing strain of Penicillium verrucosum var cyclopium: An experimental model in rats.

Cultures of an isolate of Penicillium verrucosum var. cyclopium, obtained from stored maize in an area of Balkan (endemic) nephropathy--Vratza, Bulgaria--has consistently induced renal tubular lesions when force-fed to rats for 20 days. The lesions, confined to the lower reaches of the proximal convoluted tublues (pars recta and junctional zone), closely resemble the tubular changes in patients with Balkan nephropathy. Preliminary evidence suggests that this nephrotoxin-producing strain of P. verrucosum var. cyclopium may be implicated in the aetiology of Balkan nephropathy.

Animals↗
PubMed1977

Tracer and freeze fracture observations on developing tight junctions in fetal rat thyroid.

The development of tight junctions in fetal rat thyroid from the sixteenth to the twentieth days of gestation was examined with conventional ultrastructural methods and freeze-fracture preparations. These results were compared with those obtained using lanthanum hydroxide and horseradish peroxidase (HRP) tracers. Tight junctions appear to arise on the plasma membranes of fetal thyroid cells by the aggregation and fusion of linear particle chains which appear at several discrete sites on the plasma membrane of developing follicular cells. Tracer studies show that they are effective barriers to the passage of HRP from the outset, are freely penetrated by La3+ at the sixteenth and seventeenth days of gestation, but progressively lose permeability to La3+ from the seventeenth to twentieth days of gestation. However, freeze-fracture observations suggest that La3+ must penetrate into the follicular lumen through the tight junction elements, for the follicular lumen, when it appears, is always completely surrounded by a continuous though sometimes rudimentary meshwork of tight junction elements. The results suggest that the tight junction forms an effective barrier to the passage of large macromolecules, e.g. thyroglobulin, from very early stages in its development. The La3+ results suggest that decreased resistance of the intercellular pathway, possibly related to the development of transepithelial potentials, may occur during this period in development.

Animals↗
PubMed1977

The immunological response of CBA mice to P. yoelii. I. General characteristics, the effects of T-cell deprivation and reconstitution with thymus grafts.

Experimental infection of normal CBA mice with the parasite Plasmodium berghei yoelii (P. yoelii) resulted in a mild, non-fatal and self-limiting infection which lasted for 15-17 days. Animals which recovered from the primary infection were immune to reinfection though parasites could be detected in the kidneys of such mice 4 weeks after recovery from infection. (No plasmodia were demonstrated in the peripheral blood and other tissues examined.) In T cell-deprived mice, P. yoelii infections resulted in a progressive parasitaemia and proved fatal in 35-40 days. Studies of fluorescent antibody levels and morphological changes in the spleens of infected normal and T cell-deprived mice showed that while normal mice produced high levels of IgG1, IgG2 and IgM antiplasmodial antibodies and developed a strong and sustained germinal centre response, in T cell-deprived animals the production of IgG1 antibodies was almost completely abolished and the germinal centre response severely impaired. Reconstitution of T cell-deprived mice with syngeneic thymus grafts resulted in partial restoration of immunological responsiveness. P. yoelii infections in these reconstituted animals ran a self-limiting course akin to that seen in normal CBA mice; the level of protective immunity and the germinal centre response correlated with the degree of reconstitution achieved.

Animals↗
PubMed1976

Growth of a transplantable lymphoma and its modification in mice infected with the inducing virus.

The growth of a transplantable lymphoma was examined in normal mice and in mice previously infected with the lymphoma-inducing virus (ULV). Normal BALB/c mice respond to a footpad injection of X-irradiated lymphoma cells (ULMC) with popliteal lymph node (PLN) enlargement; mice previously infected with ULV do not. 106 viable ULMC injected into the footpads of ULV-infected mice grew progressively, and the animals died with disseminating malignant lymphoma. In contrast, this dose of cells injected into normal animals evoked strong host responses in the foot and draining lymph node, and no progressive growth of the lymphoma occurred. This increased susceptibility of the ULV-infected animals was also observed when ULMC were injected s.c. into the back or i.m. into the calf muscle, but not after s.c. injection of an unrelated 3-methylcholanthrene-induced sarcoma. Resistance to tumour growth after i.v. injection of ULMC is clearly ineffective, since 10 cells can grow and kill the animal, and in this case no increased susceptibility of ULV-infected animals was observed.

Animals↗
PubMed1975

Infectious mononucleosis: model for self-limiting lymphoproliferation.

Evidence for the extensive lymphoproliferation which characterises infectious mononucleosis (I.M.) is summarised, and some of the mechanisms which are though to control lymphoproliferative activity in this disease are discussed. The main host responses which appear to limit lymphoproliferation in I.M. include the development of humoral antibodies against the Epstein-Barr (E.B.) virus-associated membrane antigen (present on the E.B. viral envelope and on E.B.-virus-infected cells) and cellular immune responses directed against E.B.-virus-containing lymphocytes. Recent evidence is reviewed which indicates that E.B. virus preferentially infects B lymphocytes and that these E.B.-virus-containing cells, which are altered antigenically, evoke a massive response in the host T cells which do not carry E.B. virus; in the presence of E.B.-virus-infected B cells, T cells are transformed and become cytotoxic for B cells. Some of the general implications of the predominant T-cell response in I.M. are discussed with particular relation to autoantibody formation and antigenic competition. The possible role of the distinctive heterophil antigens and antibodies in determining the self-limiting course of I.M. is briefly considered. The general status of I.M. as a self-limiting, albeit intense, lymphoproliferative disease is appraised and the tenuous relationship between I.M. and irreversible lymphoproliferative states is discussed.

Antibodies, Heterophile↗