Biomedical subjects

M Pollard

Publications and source records attributed to M Pollard.

At least 37 records · Page 2Linked to original sources

PubMed1987

Characterization of xenogeneic mouse-to-rat bone marrow chimeras. I. Examination of hematologic and immunologic function.

Eighteen xenogeneic chimeric rats (survival: greater than 100 days) were established by transplanting bone marrow cells from femurs of 10 gnotobiotic CFW mice into each germfree Sprague-Dawley or Wistar rat. The erythrocytes circulating in the rats were of mouse origin as determined by hemagglutination. Hemoglobin electrophoresis, radial immunodiffusion for IgG, and assay of granulocytic neutrophils for leukocyte alkaline phosphatase verified that true chimerism was achieved. The extent of hematological and immunological reconstitution varied. In general, hematocrit levels were low to normal, white blood cell counts and differentials were within normal limits, and serum protein levels were normal. Levels of circulating IgG of each species were comparable to those of germfree rat and mouse controls. Natural killer (NK) activity was depressed, a phenomenon that may be attributable to the radiation treatment of recipients, or to failure to transfer NK cells or precursors. Mitogenic stimulation reactions were varied, but most chimeric rats demonstrated moderately depressed responses. Reactions as a whole suggested that gnotobiotic rats with xenogeneic bone marrow are incompletely reconstituted, both hematologically and immunologically. No acute graft-versus-host reaction was seen.

Animals↗

PubMed1986

The beneficial effects of diphosphonate and piroxicam on the osteolytic and metastatic spread of rat prostate carcinoma cells.

Transplantable rat prostate adenocarcinoma III cells produce local tumors and osteolytic and osteoplastic lesions and they metastasize through defined lymphatic channels to the lungs in which they produce expanding focal tumors. The bone lesions were prevented by treatments with dichloromethane diphosphonate (Cl2MDP). Treatment of rats with piroxicam, a nonsteroidal antiinflammatory drug, suppressed to some extent tumor growth, bone destruction, and metastasis. However, simultaneous treatments of rats with both drugs (Cl2MDP and piroxicam) prevented bone damage and suppressed tumor growth and metastatic spread very significantly without evidence of toxicity.

Adenocarcinoma↗

PubMed1986

Promotional effects of testosterone and high fat diet on the development of autochthonous prostate cancer in rats.

Depots of testosterone implanted in Lobund-Wistar (L-W) rats, resulted in increased incidence of prostate adenocarcinomas (PAs) in the dorsal lateral lobe area. In testosterone-treated rats which had been fed the same diet plus 15% corn oil, the prostate tumors were more numerous and they appeared earlier. Rats consuming the same feed containing 15% corn oil (no testosterone) did not produce prostate tumors. Positive correlations were demonstrated between the development of PAs in L-W rats that were treated with testosterone and high fat diet.

Animals↗

PubMed1986

Production of autochthonous prostate cancer in Lobund-Wistar rats by treatments with N-nitroso-N-methylurea and testosterone.

More than 50% of Lobund-Wistar (L-W) strain rats developed large, palpable prostate adenocarcinomas (PAs) following treatments with N-nitroso-N-methylurea (CAS: 684-93-5) and testosterone propionate [(TP) CAS: 57-85-2], and most of the tumor-bearing rats manifested metastatic lesions. The incubation periods averaged 10.6 months. Within the same timeframe, no L-W rat developed a similar palpable PA when treated only with TP. In L-W rats, TP acted as a tumor enhancement agent, with primary emphasis on the development of prostate cancer.

Adenocarcinoma↗

PubMed1985

Promotional effects of testosterone and dietary fat on prostate carcinogenesis in genetically susceptible rats.

Germfree (GF) Lobund strain Wistar (LW) rats, fed vegetable diet L-485, have developed prostate adenocarcinomas spontaneously (10% incidence) at average age 34 months. Conventional LW rats, implanted with testosterone at age 4 months, developed a higher incidence of prostate cancer after an average interval of 14 months: 24% had developed gross tumors, and 40% when it included microscopic tumors. Preliminary results indicate that testosterone-treated LW rats that were fed the same diet, which was supplemented with corn oil up to 20% fat, developed prostate cancer after intervals of 6-12 months. Aged GF Sprague-Dawley (SD) rats have not developed prostate cancer spontaneously. Conventional SD rats fed diet L-485 and treated with testosterone developed only prostatitis. Experimental designs should consider genetic susceptibility as a basic prerequisite for studies on experimental prostate cancer.

Adenocarcinoma↗

PubMed1985

Prostate cancer in a Sprague-Dawley rat.

An adenocarcinoma of the prostate gland developed in one rat of the Lobund Sprague-Dawley (S-D) strain, following treatments with testosterone propionate in silastic membranes. The transplanted cells (PA-SD1) developed local tumors, metastasized through lymphatic channels to the lungs, and induced osteolytic lesions when deposited adjacent to the calvarium. In vitro-propagated PA-SD1 cells produced the same tumor type in Lobund strain S-D rats as that from which it was derived.

Adenocarcinoma↗

PubMed1985

The relationship of natural killer cells to metastasis of a transplantable prostate adenocarcinoma.

Natural killer (NK) cells have been proposed to play a significant role in the inhibition of metastasis. The prostate adenocarcinoma (PA-11) in the Lobund-Wistar (L-W) rat provides a unique model of spontaneous metastasis in which to study NK response. Cultured PA-11 tumor cells were shown to be resistant to NK lysis in vitro, and enhancement or inhibition of NK reactivity in vivo using drugs or antiserum did not change the rate or extent of metastasis evident at autopsy. Exposure to PA-11 tumor cells, supernatants from cultured tumor cells, or sera from rats with advanced PA-11 in vitro did not result in inhibition of NK activity. Exposure to PA-11 tumor cells in vivo also did not cause suppression of NK activity. These data indicate that, in the PA-11/L-W system, metastasis is independent of NK activity.

Adenocarcinoma↗

PubMed1985

The relationship between natural killer cells and drugs that modify metastasis of PA-III cells.

Rat prostate adenocarcinoma III (PA-III) cells produce in L-W rats local tumors at the implant site, osteolytic and osteoblastic lesions and metastatic tumors in the lungs. Treatment of rats with dichloromethylene diphosphonate (Cl2MDP) prevented the osteolytic lesions, but the drug showed little beneficial effect on the local and/or metastatic spread of tumor cells. While treatment of rats with piroxicam inhibited PA-III cell metastasis, it manifested only moderate protection against the development of osteolytic lesions. Treatments with both Cl2MDP and piroxicam resulted in smaller tumors, no osteolysis and significantly reduced metastasis. Comparisons of natural killer (NK) cell activities in normal and in tumor-bearing rats, with and without drug treatments, showed that NK cell activity was suppressed by Cl2MDP, and enhanced by piroxicam. When treatments included both drugs, NK cell activity was enhanced. Thus, the suppression of NK cell activity resulting from treatment with Cl2MDP was reversed by piroxicam with resultant benefits from both drugs.

Adenocarcinoma↗

PubMed1985

Relative value of glucose and amino acids in preserving exercise capacity in the postoperative period.

The value of crystalline amino acids compared with glucose in maintaining functional muscle mass (maximum exercise capacity) in the perioperative period was studied. Twelve surgical patients received 100 g of glucose (Group 1) for 7 to 10 days perioperatively, and 12 (Group 2) received 90 g of crystalline amino acids for a similar period. Maximum exercise capacity, nitrogen balance, and serum albumin were studied. The use of amino acids instead of glucose spared nitrogen. Net nitrogen loss was 64.7 +/- 6.7 g in Group 1 compared with 34.7 +/- 4 g in Group 2 (p less than or equal to 0.001). Exercise capacity decreased 13.8 +/- 4.5 percent in Group 1 and 13.3 +/- 2.9 percent in group 2. The serum albumin level decreased by 0.30 +/- 0.2 g/100 ml in Group 1 compared with 0.34 +/- 0.15 g/100 ml in Group 2. These differences were not significant. Changes in serum albumin were correlated with changes in exercise capacity (r = 0.7, p less than or equal to 0.002), but neither was significantly correlated with nitrogen loss. We concluded that the use of amino acids instead of glucose during moderate periods of semi-starvation associated with moderate trauma will not influence loss of exercise capacity significantly, although some nitrogen will be spared; patients undergoing moderately severe surgical procedures accompanied by moderate periods of semistarvation will lose approximately 14 percent of their exercise capacity; and loss of exercise capacity is not correlated with loss of nitrogen under these conditions but is loosely correlated with changes in serum albumin levels.

Adult↗

PubMed1985

Effects of dichloromethylene diphosphonate on the osteolytic and osteoplastic effects of rat prostate adenocarcinoma cells.

A model system of prostate adenocarcinoma (PA) in Lobund-Wistar rats is described in which the transplanted tumor cells (PA-III) were inoculated sc over the calvaria. A local tumor developed that, when attached to the bone, caused erosion and fragmentation of the bone, with adjacent osteoplastic changes and metastases to the lungs. The attachment of the tumor to the bone was enhanced if the periosteum was scratched during the inoculation of tumor cells. The destructive effect on bone structure was also induced by in vivo transplanted PA-I and PA-IV cells, but not by PA-II cells. In rats that were pretreated with dichloromethylene diphosphonate, the local PA-III tumors developed with metastases to the lungs, but the calvariae were intact.

Adenocarcinoma↗

PubMed1985

Protected environment and its utility in experimental allogeneic and xenogeneic bone marrow transplantation.

Allogeneic bone marrow (BM) chimerism can be established in germfree (GF) rats and mice without the manifestations of graft vs host (GvH) disease that develop in conventional counterpart animals. This procedure has been applied with prophylactic and therapeutic benefits in mice predestined to develop leukemia and reticulum cell sarcoma. Xenogeneic BM chimerism has been accomplished in rats with mouse bone marrow cells, without evidence of GvH disease; and over long periods they produce blood cells with characteristics of mouse species. A critical factor in allogeneic and xenogeneic BM chimerism is the microbial status of the animals.

Animals↗

PubMed1985

Tumorigenic effects of direct- and indirect-acting chemical carcinogens in rats on a restricted diet.

The influence of diet restriction on induction of intestinal tumors in Sprague-Dawley rats by two unique carcinogenic agents was investigated: methylazoxymethanol acetate [(MAM) CAS: 592-62-1], which requires metabolic activation, and N-methylnitrosourea [(MNU) CAS: 684-93-5], which is a direct-acting carcinogen. Most of the tumors induced by MAM developed in the small intestine and less frequently in the colon, but MNU produced tumors predominantly in the colon. Among rats fed the restricted diet (12 g/day), the production of tumors by MAM was significantly reduced compared to that of counterpart rats on the ad libitum diet. However, dietary restriction did not modify the production of tumors in rats by MNU. The same relationship of diet restriction to tumor induction was demonstrable when MAM and MNU were administered to the same test rats: Numbers of MAM-related tumors, especially in the small intestine, were reduced and numbers of MNU-related tumors in the colon were unchanged. Dietary restriction modified the tumorigenic response of rats to MAM but not to MNU.

Animals↗

PubMed1985