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Biomedical subjects

C A Norman

Publications and source records attributed to C A Norman.

6 recordsLinked to original sources
PubMed1990

Is carbon monoxide a workplace teratogen? A review and evaluation of the literature.

Sixty case reports of carbon monoxide exposures involving pregnant women are reviewed. The circumstances under which carbon monoxide exposures adversely affected pregnancy and the types of effects seen are summarized. Severe acute exposures to carbon monoxide caused foetal death or toxic effects, including anatomical malformations and functional alterations. Foetal outcome was related to two major indices of carbon monoxide exposure: maternal blood carboxyhaemoglobin levels and maternal toxicity.

Abnormalities, Drug-Induced↗
PubMed1990

Formation and persistence of DNA adducts in rats following intraperitoneal administration of 1,8-dinitropyrene.

DNA adduct formation was examined in rat tissues following a single i.p. injection with 1,8-dinitropyrene (1,8-DNP). A single common adduct was observed in mammary, mesentery, bladder, lung, kidney and liver tissue using the 32P-postlabelling technique. Adduct levels were highest in mammary and mesentery tissue. The mammary gland and soft tissues of the peritoneal cavity are primary tumour sites in rats injected i.p. with 1,8-DNP. Adducts were not detected in the small intestine, heart or reproductive tissue. Pretreatment of rats with Aroclor 1254, an inducer of hepatic oxidative enzymes, did not alter qualitative or quantitative aspects of adduct formation. Over a 2 week period the relative adduct labelling values declined in all tissues. The loss of DNA adducts was biphasic, with an initial rapid decrease followed by a slower rate of adduct removal.

Animals↗
PubMed1989

DNA adduct formation in primary rabbit tracheal epithelial cells following treatment with 1,8-dinitropyrene and its partially reduced derivative, 1-nitro-8-nitrosopyrene.

Formation of DNA adducts, following treatment of primary rabbit tracheal epithelial cells (RTEC) with 1,8-dinitropyrene (1,8-DNP) and its partially reduced derivative, 1-nitro-8-nitrosopyrene (1,8-NONO2), was examined using the 32P-post-labelling technique. Treatment of aerobic cells with 1,8-DNP or 1,8-NONO2 produced qualitatively similar results. Cochromatography showed that the major adduct observed corresponded to the major adduct seen following treatment of poly(dG.dC) with N-hydroxyl-1-amino-8-nitropyrene, generated from 1,8-NONO2. A minor adduct migrated to the same area on the TLC plate as the major compound observed following a similar treatment with poly(dA.dT). Relative adduct labelling (RAL) values were consistently an order of magnitude higher with 1,8-NONO2 than with 1,8-DNP, suggesting that reduction of a nitro group of 1,8-DNP to a nitroso group may be a rate-limiting step in the cells. In studies on the formation and persistence of the 1,8-NONO2 adduct in RTEC maximum binding was observed at 1 h. Fifteen hours later the RAL value was less than 15% of this maximum level.

Animals↗
PubMedDate not supplied

Kindergarten screening predictive inaccuracy: first-grade teacher variability.

Screening kindergarten students to predict first-grade achievement is characterized by rather gross errors over identification and under identification. This lack of predictive validity may be the consequence of overly simplistic conceptualizations that fail to take into account differences in first-grade teachers. This study attempted to evaluate the extent to which first-teachers differ in their preferences, requirements, and expectancies of students. Twenty-one teachers ranked 86 student descriptors on a continuum ranging from "absolutely contributes to student success" to "absolutely contributes to student failure." Results suggest that teachers vary considerably in the way they rank student descriptors and that these variations may be a factor in the predictive inaccuracy of kindergarten screening.

Aptitude Tests↗
PubMedDate not supplied

Pretranslational suppression of cytochrome P-450h (IIC11) gene expression in rat liver after administration of interferon inducers.

Administration of the interferon inducer polyriboinosinic acid.polyribocytidylic acid (poly rl.poly rC) (10 mg/kg, ip) to male rats suppressed the constitutive hepatic expression of the male-specific cytochrome P-450 [AH, reduced-flavoprotein/oxygen oxidoreductase (RH hydroxylating), EC 1.14.14.1] isozyme P450IIC11 (P-450h) to 21% of control levels within 24 hr. The mRNA for P-450h was more rapidly suppressed by the drug, being significantly suppressed to 56% of control values within 6 hr of administration. P-450h mRNA levels were further lowered to 10% of control by 24 hr. The kinetics of suppression of P-450h apoprotein and mRNA by poly rl.poly rC indicate that the primary mechanism(s) is (are) at a pretranslational level. Tilorone analog R11-877DA (TA) (50 mg/kg, ip), also an interferon inducer, produced qualitatively similar effects to those of poly rl.poly rC, although the TA produced lesser (51% and 59%) decreases in P-450h protein and mRNA, respectively, 24 hr after injection. Again, the results indicate a pretranslational mechanism of P-450h suppression. Although both interferon inducers suppressed hepatic P-450h expression, the magnitudes of these effects were not notably greater than those on total hepatic P-450, indicating that suppression of rat liver P-450 isozymes by interferon inducers is not confined to P-450h.

Animals↗