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Biomedical subjects

D D Porter

Publications and source records attributed to D D Porter.

At least 73 records · Page 4Linked to original sources
PubMed1975

Accumulation of mononuclear cells in tumors with growth slowing and elevation in host splenic histidine decarboxylase activity following repeated tumor injections with bradykinin.

Repeated intratumor injections of SV-40 virus-induced and transplaned syngenic fibrosarcomsa in hamsters with bradykinin (BK) has produced markded slowing of tumor growth in comparison with control saline injections. Growth slowing was greatest when the injections were daily, with a decrease in growth slowing as injections became less frequent. The growth slowing also was dose dependent (greater with 250 mug BK injections than with 50 mug BK injections). BK-injected tumors, on histological study, were found to have marked infiltration with mononuclear cells. This was not encountered in noninjected or saline-injected tumors. Significant mononuclear cell infiltration of noninjected tumors was found in two tumor animals which had had one tumor injectecd with BK. Splenic histidine decarboxylase (HDC) activity was higher in BK tumor-injected animals than in saline tumor-injected animals. Splenic HDC activity was higher when studed nearer the period of daily intratumor injections. The findings of this study suggest a potential role of inportance for inter-related vasoactive substances which act as mediators of inflammation in the study and therapy of neoplasia.

Animals↗
PubMed1975

Spontaneous lesions and parasites of the Mongolian gerbil, Meriones unguiculatus.

Four-hundred-eighty Mongolian gerbils, Meriones unguiculatus [Uclp:(MON)], most of which were experimentally infected with filarial worms, were examined for spontaneous lesions. Previously unrecognized lesions included cutaneous squamous cell carcinoma, duodenal adenocarcinoma, malignant blue nevus, hepatic choleangiocarcinoma, malignant hemangiopericytoma of the uterus, ovarian teratoma, chronic interstitial nephritis, renal cortical retention cysts, splenic hemangiomas, and various histologic abnormalities of the lung. Previously reported lesions also seen in the present study were a malignant melanoma, adrenal cortical adenoma or carcinoma, uterine leiomyoma, sebaceous gland adenoma, hepatic lymphangioma, and renal hemangioma. Hymenolepis diminuta (Cestoda) and Tyrophagus castellani (Acarina) were accidentally recovered from experimental animals. Tritichomonas caviae and a species of Entamoeba were the most common intestinal protozoa. Tyzzer's disease, however, was clearly the most significant infectious disease of gerbils in the UCLA School of Public Health colony.

Adenoma↗
PubMed1974

Nature of the scrapie agent: evidence against a viroid.

The postulated viroid nature of scrapie agent was tested. Since the agent could not be recovered after a carefully controlled phenol extraction of infected mouse brains, it is suggested that this agent is not a viroid.

Animals↗
PubMed1974

Studies on a murine form of spontaneous lower motor neuron degeneration--the wobbler (wa) mouse.

The wobbler (wr) mouse has been considered an animal model of spontaneous lower motor neuron degeneration which is inherited as an autosomal recessive trait. Previously available data are, however, also compatible with genetic factors playing a necessary though not exclusive role in the expression of the wobbler trait. The present report describes the results of chromosome analyses, electromyography and selected histochemical studies on wobbler mice, as well as studies exploring the possible participation of infectious agents, transneuronal effects, retrograde effects, aging, circulating toxins and immunologic factors in the pathogenesis of the wobbler disorder. The data obtained do not implicate any of these mechanisms in the pathogenesis of the wobbler trait and also indicate that the wobbler mouse is not a clinical variant of the recently described type C oncornavirus-induced murine paralytic disease.

Aging↗
PubMed1973

The pathogenesis of Aleutian disease of mink. 3. Immune complex arteritis.

Mink chronically infected with Aleutian disease virus develop a severe necrotizing arteritis affecting muscular arteries. Acute, subacute and healing lesions may be found. Extracellular deposits of host immunoglobulin and complement and, after acid elution, viral antigen can be shown by immunofluorescence technics in areas of fibrinoid necrosis and between proliferating endothelial cells. No intracellular viral antigen was found, indicating that the virus probably does not replicate in vascular structures. The arteritis of Aleutian disease appears to be the result of immune complex deposits in vessel walls.

Aleutian Mink Disease↗
PubMed1969

The pathogenesis of Aleutian disease of mink. I. In vivo viral replication and the host antibody response to viral antigen.

Mink inoculated with 1 x 10(5)ID(50) of Aleutian disease virus revealed very high virus titers in the tissues 8-18 days later. The highest virus titers observed were 5 x 10(8)ID(50) per g of spleen and 1 x 10(9)ID(50) per g of liver 10 days after inoculation. Concomitant with the increase in infectious virus titers, viral antigen(s) was found in the cytoplasm of macrophages in the spleen and lymph nodes and in Kupffer cells in the liver. Antiviral antibody was assayed by indirect immunofluorescence, using sections of infected liver as the source of antigen. A few mink infected for 9 days and all those infected 10 days or more developed antibody to Aleutian disease virus antigen(s). By 60 days after infection, when hypergammaglobulinemia was marked, the mink had an exceptionally high mean antibody titer of 100,000. The pathogenesis of the glomerulonephritis of Aleutian disease is apparently related to formation of viral antigen-antibody-complement complexes which lodge in glomerular capillaries. No evidence was found that viral infection of the kidney took place, and no autoimmune responses were found. In this "slow-virus" disease the virus replicates rapidly and the morphologic and biochemical manifestations of disease are apparently due to the continuing interplay between a replicating antigen and the host immune response.

Animals↗