PubMed Health⌕ Search

Biomedical subjects

C C Fox

Publications and source records attributed to C C Fox.

28 records · Page 2Linked to original sources
PubMed1987

Dietary zinc deficiency increases the methylbenzylnitrosamine-induced formation of O6-methylguanine in the esophageal DNA of the rat.

Dietary zinc deficiency in combination with environmental exposure to methylbenzylnitrosamine (MBN) is associated with an increased incidence of esophageal carcinoma in man. The proposed mechanism of MBN-induced esophageal carcinoma is through metabolic activation of MBN to form benzaldehyde, and a carbonium ion which methylates DNA. MBN is known to methylate DNA forming O6-methylguanine (O6-MeG) adducts. These adducts can induce guanine to adenine point mutations and such mutations are responsible for certain carcinogen-induced tumors. Rats maintained on a zinc-deficient diet exhibit an increased incidence of MBN-induced esophageal carcinoma when compared with ad libitum and pair-fed controls. The caloric restriction of the pair-fed controls was associated with a lower incidence of MBN-induced esophageal carcinoma than was observed in the ad libitum controls. These differences in tumor incidence were associated with alterations in the formation and clearance of MBN-induced esophageal O6-MeG. Weanling male Sprague-Dawley rats were raised on egg protein diets containing 2.3 p.p.m. zinc (low zinc) or 50 p.p.m. zinc (control). One group of control animals was fed the control diet ad libitum and a second group pair-fed the control diet to match the intake of the zinc-deficient group. After 3 weeks on the diets the animals were injected with a single dose of MBN (2.0 mg/kg b.w.) and levels of esophageal O6-MeG were determined after 1, 3, 6 and 24 h. O6-MeG was significantly higher in the zinc-deficient animals than in controls, with the pair-fed controls demonstrating O6-MeG levels lower than the ad libitum controls. Thus, dietary zinc deficiency results in significantly increased levels of MBN-induced esophageal O6-MeG, and caloric restriction results in decreased levels of MBN-induced esophageal O6-MeG. These changes in esophageal O6-MeG may in part explain the increased incidence of MBN-induced esophageal carcinoma observed with dietary zinc deficiency.

Animals↗
PubMed1987

Evaluation of anaerobic culture and effect of culture medium supplementation with factor V on colonial morphology and efficacy of isolation of Streptococcus pneumoniae from sputum.

The use of anaerobic incubation for the culture of Streptococcus pneumoniae from sputum was compared with incubation in carbon dioxide in air. A coagglutination test for pneumococcal antigen was used as an index of the number of specimens containing pneumococci. A total of 334 specimens were examined. There was evidence of pneumococcal colonisation by culture or coagglutination, or both, in 48 (14.37%), of which 41 (12.27%) yielded S pneumoniae on culture. Anaerobic incubation was better than incubation in carbon dioxide in air for the primary culture of S pneumoniae from sputum. Primary isolation of S pneumoniae was achieved in 11 of the 41 strains (26.82%) by anaerobic incubation alone, by incubation only in carbon dioxide in air in one strain (2.43%), and by both anaerobic incubation and incubation in carbon dioxide in air in 29 strains (70.73%). Anaerobic incubation gave large moist or mucoid colonies that were easy to recognise, but it suppressed the typical draughtsman colony of S pneumoniae. The factor V supplement routinely used in our medium also inhibited the formation of draughtsman colonies. It is suggested that draughtsman colonies occur because of a relative lack of the coenzyme nicotinamide adenine dinucleotide (factor V), which is required as a reducing agent in aspartate and glutamate metabolism. This nutritional deficiency may lead to bacterial cell wall defect and hence to the autolysis which gives the typical draughtsman colony.

Agglutination Tests↗
PubMed1985

Role of human basophils and mast cells in the pathogenesis of allergic diseases.

The role of human basophils and mast cells in the pathogenesis of allergic diseases has been analyzed. Purified human basophils and mast cells release several known mediators of allergic reactions, including histamine, sulfidopeptide leukotrienes, kinin-forming enzymes, and, in the case of the mast cell, PGD2. These same mediators are released in vivo after experimental challenge in the upper airways with either allergen or cold, dry air, a stimulus used to simulate exercise-induced bronchospasm. The appearance of mast cell mediators in vivo after such challenges further implicates mast cells in the pathogenesis of allergic diseases of the airways that occur as a result of exposure to allergen or physical stimuli. During the LPR after experimental challenge of the upper airways, the pattern of mediators released (i.e., histamine, leukotrienes, and others, but no PGD2) suggests that basophils may contribute to the LPR. Antiallergic drugs that prevent mediator release in vitro, such as antihistamines, also prevent the appearance of mediators in vivo, strengthening both the validity of the in vitro test as a model of the disease and the hypothesis that mediator release is an essential element of the disease process. A model discussing the pathogenetic mechanism is presented.

Adrenal Cortex Hormones↗
PubMed1985

Isolation and characterization of human intestinal mucosal mast cells.

Study of the role of mast cells in the human gastrointestinal tract has suffered from the inability to examine these cells in vitro. In addition, work in rodent systems suggests that there are substantial differences between intestinal mast cells and those from other tissues, making extrapolation of data from other sources difficult. We report a method for producing mast cell-containing single cell suspensions from human intestinal tissue by mechanical and enzymatic dispersion. This method yields 4.5 X 10(5) mast cells per gram of tissue in purity of 3.1 +/- 2.1%. These mast cells were functionally intact as assessed by survival in short-term culture, low spontaneous release, and appropriate IgE-mediated histamine release. They were morphologically intact on electron microscopy and conformed to published descriptions of human lung mast cells. The intestinal mucosal mast cells were also indistinguishable from human lung mast cells in histamine content, goat anti-human IgE dose-response curves, kinetics of histamine release, unresponsiveness to f-met peptide, and production of arachidonic acid metabolites, prostaglandin D2, and leukotriene C4. This procedure produces human intestinal mast cell suspensions in sufficient numbers to make pharmacologic characterization and further purification of this cell feasible.

Cell Separation↗