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J Bax

Publications and source records attributed to J Bax.

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Modulation of putative preneoplastic foci in exocrine pancreas of rats and hamsters. I. Interaction of dietary fat and ethanol.

The effect of dietary fat and ethanol and their interactions on the development of putative, preneoplastic foci in exocrine pancreas was investigated in rats and hamsters. Rats were given a single i.p. injection of 30 mg azaserine per kg body wt at 19 days of age. Hamsters were injected s.c., with 20 mg N-nitrosobis(2-oxopropyl)amine (BOP)/kg body wt at 6 and 7 weeks of age. The animals were fed a low fat (LF) control diet (5% corn oil) or a high fat (HF) diet (25% corn oil). Ethanol was provided in drinking water at a 15% (w/v) concentration. The animals were given the respective diets and ethanol after the treatment with carcinogen. At 4 months post-initiation, the pancreata were quantitatively examined for the number and size of preneoplastic foci. In rats, acidophilic as well as basophilic foci were subject to modulation by HF and ethanol. The results point to a specific promoting effect of unsaturated fat on the growth potential of azaserine-induced acidophilic acinar cell foci in rat pancreas. There was no evidence of an interaction between HF and ethanol as far as acidophilic foci are concerned. Evaluation of the number and size of the basophilic foci demonstrated an enhancing effect of ethanol on the modulation of pancreatic carcinogenesis by fat, pointing to a possible interaction between these two lifestyle factors. This suggestion was supported by the finding that six out of 20 rats in the HF with ethanol group exhibited a carcinoma in situ, whereas in the HF and in the ethanol group such an advanced lesion was found in one animal only. Unlike in rats, ethanol had no modulating effect on number and growth of putative, preneoplastic lesions in hamsters, either in combination with LF or in combination with HF. A HF diet, however, caused a significant increase in number as well as an increase in percentage of pancreatic tissue occupied by early lesions induced in hamster pancreas by BOP.

Adenosine Triphosphatases↗

Suppression of antibody-mediated accumulation of eosinophils in chronic inflammatory lesions by concomitant delayed hypersensitivity reactions.

Studies were carried out in order to explain the often small contribution of eosinophils to immunologically mediated chronic inflammatory reactions. A chronic inflammation model was used in which large numbers of eosinophils accumulated in the peritoneal injections with PPD or ovalbumin (OA). Eosinophil accumulation could be strongly suppressed by pre-immunization with a mycobacteria-containing adjuvant, which induces delayed hypersensitivity to the stimulating antigen. Suppression of OA-induced eosinophil accumulation could be obtained in a non-specific way by concomitant delayed hypersensitivity reactions to PPD. The absence o eosinophil accumulation was not related to a lack of relevant antibodies. Histological studies suggested that similar numbers of basophils were locally available in both non-pre-immunized and pre-immunized groups to allow for the attraction of eosinophils by the expression of basophil anaphylactic reactivity. Skin tests and macrophage migration inhibition measurements provided further support for the hypothesis that local lymphokine release may suppress the accumulation of eosinophils in chronic inflammatory lesions.

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Alteration of colony-stimulating factor output, endotoxemia, and granulopoiesis in cyclic neutropenia.

Cellular and humoral factors involved in the regulation of granulopoiesis were evaluated in two patients with cyclic neutropenia by utilizing the agar-gel marrow culture technique to serially study marrow granulocytic colony-forming capacity (CFC) and the urinary output of colony-stimulating factor (CSF). CSF output varied inversely with peripheral neutrophil counts and directly with monocyte counts and evidence for infection (endotoxemia and/or staphylococcal abscesses). Following autologous infusion of one patient's plasma obtained during a period of neutropenia, increased urinary excretion of CSF occurred concomitant with increments in both marrow CFC and the proportion of granulocytic progenitor cells in DNA synthesis. Neutrophil periodicity was not altered by the administration of the neutropenic plasma. These findings are consistent with the hypothesis that cyclic neutropenia is caused by a quantitatively decreased entry of stem cells or granulocytic progenitor cells into granulopoiesis.

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