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A Stark

Publications and source records attributed to A Stark.

136 records · Page 8Linked to original sources

Transplacental effects of a 15% olive-oil diet on chemically-induced tumorigenesis in offspring.

We evaluated whether feeding pregnant female rats a diet high in olive-oil, that showed a tumor-preventive effect in adults, has a similar preventive effect on chemically-induced cancer in offspring (i.e. mammary glands and colon cancer in rats). The control group was fed the same 7% corn-oil diet as their mothers. Experimental group I was fed a 7% corn-oil diet while their mothers received a 15% olive-oil diet. Experimental group II was fed the same 15% olive-oil diet as their mothers. Female offspring were twice administered 7,12-dimethylbenz(a)antracene (DMBA) in doses of 10 mg/rat. Male offspring were injected 6 times with 1, 2-dimethylhydrazine (DMH) in doses of 20 mg/kg body weight. Effect of DMBA was manifested in a high rate of tumorigenesis: the number of tumor-bearing rats in control offspring reached 52.0%. This effect increased to 60.6% among offspring of experimental group II and to 67.7% in offspring of experimental group I. The mean tumor size increased significantly in control offspring. Following administration of DMH number of tumor-bearing rats was similar in all groups of offspring: 36.7%, 40.7% and 42.8%. Tumor types differed: the majority of tumors in the control group were benign polyps and adenomas (72.1%) and the number of adenocarcinomas was low (27.9%). The number of malignant tumors increased to 37.5% in offspring of experimental group II and to 45.5% in offspring of experimental group I. In control group offspring, a distinct tendency to increased body weight and a significant increase in spleen weight were seen. The findings indicate that feeding mothers a diet high in fat concentrations, even those with known tumor preventive significance in adults, lose this cancer-inhibiting role in offspring.

1,2-Dimethylhydrazine↗

Comparative effects of dimethylbenz(a)anthacene and a 15% olive-oil diet on cellular components and expression of apoptosis-related proteins in the spleen and mammary gland tumors of rats.

We compared effects of a high fat diet and a carcinogen on cellular elements of the spleen and mammary gland tumors in rats. Animals were fed a 15% olive-oil diet and a group of them were exposed to a carcinogen, dimethylbenz(a)anthacene (DMBA), in two doses of 10 mg/rat. Results of the experiments were evaluated after 4 months. We studied changes in the areas of different zones of the spleen related to production of B and T lymphocytes and also the number of cells in the spleen and tumors with positive reaction to receptors related to manifestation of apoptosis (FasL and p53) and receptors related to inhibition of apoptosis (bcl-2). In the spleen, dietary fats as well as DMBA alone decreased the zones related to production of B lymphocytes and increased the number of T lymphocytes. The combined effect of a carcinogen and a high fat diet manifested in an increase in the number of lymphoid cells and macrophages. In tumors from rats fed a low-fat diet, an extremely high number of lymphoid cells was seen in the border of tumors with T cell killers as a main component of these infiltrates. In tumors from rats fed a 15% olive-oil diet, the main component of the infiltrates were macrophages. High levels of p53+ and bcl-2+ cells were found in the spleen of rats exposed to a carcinogen. The combined effect of a carcinogen and the 15% olive-oil diet inhibited production of FasL and p53 receptors and stimulated synthesis of bcl-2 protein. In tumors, a carcinogen alone stimulated the high expression of FasL and p53 proteins, but in combination with the 15% olive-oil diet synthesis of these receptors decreased while production of bcl-2 protein increased sharply. This observation may serve as an additional proof of tumor-promoter effects of a high fat diet.

9,10-Dimethyl-1,2-benzanthracene↗

Transplacental effect of a 15% olive-oil diet on functional activity of immune components in the spleen and colon tumors of rat offspring.

We studied whether feeding pregnant female rats a 15% olive-oil diet affects the activity of lymph cells in the spleen and tumors in offspring with chemically-induced colon tumors. Rat mothers were fed either a 7% corn-oil or a 15% olive-oil diet. Five-week-old male offspring were divided into 3 groups. A control group was fed the 7% corn-oil diet similar to their mothers. The experimental group I was fed the 7% corn-oil diet whereas their mothers were fed the 15% olive-oil diet. The experimental group II was fed the same 15% olive-oil diet as their mothers. Experimental rats were injected weekly for 8 weeks with the carcinogen, 1,2-dimethylhydrazine (DMH), 20 mg/kg b.w. Results of experiments were studied 6 months later. The area of zones in the spleen responsible for producing B and T lymphocytes were measured and the number of cells counted. The activity of lymphoid elements of the spleen and of tumors were studied using immunohistochemical methods for evaluating the synthesis of CD8(+) lymphocytes and proliferative activity of lymphocytes in spleens and tumors. Feeding pregnant or lactating mothers with the 15% olive-oil diet had no marked tumor-protective effect on chemically-induced colon cancer in offspring. Diet-dependent changes were found at the cellular level. In the spleen of control offspring, the presence of a tumor was accompanied by an increase in the number of Ki-67(+) cells and CD8(+) lymphocytes in the red pulp. In experimental group I, DMH significantly increased the total cell number and the number of CD8(+) lymphocytes in the red pulp of the spleen in both tumor-bearing and tumor-free rats. In experimental group II, the total number of lymph cells and the number of CD8(+) lymphocytes increased compared to offspring fed a control diet. Tumor formation activated the proliferative activity of lymph elements. The total number of cells in infiltrates of the colon mucosa decreased in tumor-bearing rats compared to tumor-free counterparts, and this was seen in all three dietary groups of rats. In tumors from offspring of experimental group II, only the number of CD8(+) lymphocytes increased compared to those in offspring of experimental group I. The findings indicate that feeding mothers the 15% olive-oil diet had a cancer-inhibiting role in offspring, predominantly changes at the cellular level.

1,2-Dimethylhydrazine↗

Effects of a 15% orange-pulp diet on tumorigenesis and immune response in rats with colon tumors.

This study evaluated whether the feeding of rats with a 15% orange-pulp diet affects the lymphatic system and the tumorigenic response in rats exposed to a high dose of carcinogen. Five-week-old Sprague Dawley rats were divided into 2 groups fed a control chow diet or the same diet with 15% orange pulp. All rats were injected with 1,2-dimethylhydrazine (DMH) (20 mg/kg) weekly for 6 weeks. At 8 months, tumors, spleens and descending colon were taken from each group for analyses. Feeding rats the 15% orange-pulp diet did not reduce the tumor number but modified the number of adenocarcinomas found in the orange-pulp group compared to controls: 66.7% vs. 93.7%. The number of endophytic tumors was also significantly lower in the experimental group: 6.3% vs. 32.3% in controls. DMH affected the size of the splenic structures. The size of follicles and germinal centers decreased significantly in tumor-bearing rats compared to tumor-free rats. This effect was changed in rats fed the orange-pulp diet. In tumor-bearing rats from this group, only the area of the marginal zone decreased and the red pulp increased compared to tumor-free rats. The size of germinal centers significantly increased compared to tumor-bearing rats in controls. The total number of lymphoid cells decreased in germinal centers of spleens obtained from control tumor-bearing rats compared to tumor-free rats. DMH alone significantly increased the total number of cells in the colon mucosa of the rats fed the control diet. In tumor-bearing rats exposed to the carcinogen and fed the 15% orange-pulp diet, the total number of cells and the number of Ki-67+ cells increased in the depth of tumors whereas the number of CD8+ T cells increased in the colon mucosa, at the border of tumors and its depth. The caspase-3 protein a cysteine protease was elevated in tumors from rats fed the orange-pulp diet. Although the 15% orange-pulp diet did not change the number of tumors in the tumor-bearing rats, feeding rats orange pulp significantly decreased the number of endophytic tumors and increased the number of exophytic tumors. Increased activity of T cell killers in tumors and higher level of proteins involved with apoptosis following consumption of the orange pulp indicate a clear tumor suppressor effect of these dietary fibers.

Adenocarcinoma↗

What's the matter with business ethics?

The more business ethics secures its status in campuses across the country, the more bewildering it appears to actual managers. It's not that managers dislike the idea of doing the right thing. As University of Toronto Assistant Professor Andrew Stark argues, far too many business ethicists just haven't offered them the practical advice they need. Before business ethics became a formal discipline, advocates of corporate social responsibility claimed that the market would ultimately reward ethical behavior. But ethics and interests did not always intersect so fruitfully in the real world. And when they did not, managers were left in the dark to grope for the right ethical course. In the 1970s, the brand-new field of business ethics came onto the scene to address this issue. Critical of the "ethics pays" approach, academics held that ethics and interests can and do conflict. Still, scholars took an equally unrealistic line. To them, a manager's motivation could be either altruistic or self-interested, but never both. In short, ethicists still weren't addressing the difficult moral dilemmas that managers face on a day-to-day basis, and only recently have they begun to do so. After some initial stumbles, ethicists are getting their hands dirty and seriously considering the costs of doing the right thing. Finally, a new business ethics is emerging that acknowledges and accepts the messy world of mixed motives. As a result, novel concepts are springing up: moderation, pragmatism, minimalism, among others.(ABSTRACT TRUNCATED AT 250 WORDS)

Administrative Personnel↗

[The relationship between the chemical structure and anti-arrhythmia action of a number of omega-aminoacyl-3-carbalcoxyaminodibenzazepines].

The antiarrhythmic activity of 20 derivatives of dibenzazepine (the effects on the maximal effective rabbit heart auricle contraction rate, aconitine-induced arrhythmia in rats under or without anesthesia) was studied. It was shown that the most active compounds are those with carbethoxyamine group in position 3 in combination with dimethylamino- or diethylamino-acetyl groups in position 5 of dibenzazepine ring. 5-dimethyl-aminoacetyl-10,11-dihydro-5H-dibenz b, f azepine (GS-015, bonnecor) was selected for the further detailed investigation.

Aconitine↗

Malrotation following Ender nailing.

External malrotation is a frequent complication following Ender nailing. Biomechanical studies demonstrate that the standard Ender nail tends to produce external malrotation when the fracture is unstable. This type of malrotation does not develop to the same degree if the nails are bent into a 25 degree angle of anteversion. The anteversion nail follows the natural anteversion curve of the upper femur and does not build up a torsional stress that might be released in an unstable fracture situation. It is recommended that anteversion nails be used in condylocephalic nailing.

Biomechanical Phenomena↗

Effects of dietary fiber on the rat intestinal mucosa exposed to low doses of a carcinogen.

BACKGROUND: Changes in morphological and immunohistochemical parameters were studied in the rat intestinal mucosa exposed to low doses of a carcinogen and administered with dietary fibers. METHODS: Tumors were induced by five subcutaneous injections of 1,2-dimethylhydrazine, 10 mg/kg rat, once a week. Rats were fed a semi-synthetic fiber-free diet (control) or a high-fiber diets (15%) derived from cellulose, tomato peels or white grape. The rats were sacrificed 24 weeks after the first carcinogen's injection. The ileum, colon and tumors were removed for the study. Areas of the mucosal stroma and of lymph infiltrations, and mitotic index were studied along with morphological parameters. Immunohistochemical parameters included determination of Ki-67 proliferating protein and apoptotic index. RESULTS: Areas of the stroma in colon tumors increased in rats fed tomato peels. Changes in areas of lymphoid infiltrates were related to the type of diet and tumor presence. Lymphoid infiltrations were found to be highly developed in the colon area close to tumors, especially in rats fed the white-grape diet. Mitotic index and Ki-67 protein increased significantly in the colon area close to a tumor and in tumors themselves without any relation to the fiber varieties consumed. Changes in the rate of apoptosis were not related to the preventive effect of diets: apoptotic index was high in tumors obtained from rats fed the high-cellulose diet with high tumor-preventive effects and also from rats fed the high-tomato-peel diet with low tumor-preventive effects. CONCLUSIONS: No morphological changes were found in the ileum of rats exposed to a carcinogen and fed different dietary fibers. In the colon, a carcinogen even in low concentrations inhibited the lymphoid system in the mucosa located far from the tumor or close to the tumor. An increase in the proliferation rate in the colon close to the tumor may reflect the development of precanceromatous processes or may be related to the effect of growth factors expressed by tumor cells. Finding adenoma-like dysplasia near tumors may be possible in early stages of the development of new tumors. In addition, activation of the lymphoid system of the colon following consumption to specific dietary fiber may be a mechanism by which fiber protect against cancer.

1,2-Dimethylhydrazine↗