PubMed Health⌕ Search

Biomedical subjects

D A Dempsey

Publications and source records attributed to D A Dempsey.

13 recordsLinked to original sources
PubMed2001

Risks and benefits of nicotine to aid smoking cessation in pregnancy.

Cigarette smoking during pregnancy is the single largest modifiable risk for pregnancy-related morbidity and mortality in the US. Addiction to nicotine prevents many pregnant women who wish to quit smoking from doing so. The safety and efficacy of nicotine replacement therapy (NRT) for smoking cessation during pregnancy have not been well studied. Nicotine is classified by the US Food and Drug Administration as a Pregnancy Category D drug. Animal studies indicate that nicotine adversely affects the developing fetal CNS, and nicotine effects on the brain may be involved in the pathophysiology of sudden infant death syndrome (SIDS). It has been assumed that the cardiovascular effects of nicotine resulting in reduced blood flow to the placenta (uteroplacental insufficiency) is the predominant mechanism of the reproductive toxicity of cigarette smoking during pregnancy. Short term high doses of nicotine in pregnant animals do adversely affect the maternal and fetal cardiovascular systems. However, studies of the acute effects of NRT in pregnant humans indicate that nicotine alone has minimal effects upon the maternal and fetal cardiovascular systems. Cigarette smoking delivers thousands of chemicals, some of which are well documented reproductive toxins (e.g. carbon monoxide and lead). A myriad of cellular and molecular biological abnormalities have been documented in placentas, fetuses, and newborns of pregnant women who smoke. The cumulative abnormalities produced by the various toxins in cigarette smoke are probably responsible for the numerous adverse reproductive outcomes associated with smoking. It is doubtful that the reproductive toxicity of cigarette smoking is primarily related to nicotine. We recommend the following. Efficacy trials of NRT as adjunctive therapy for smoking cessation during pregnancy should be conducted. The initial dose of nicotine in NRT should be similar to the dose of nicotine that the pregnant woman received from smoking. Intermittent-use formulations of NRT (gum, spray, inhaler) are preferred because the total dose of nicotine delivered to the fetus will be less than with continuous-use formulations (transdermal patch). A national registry for NRT use during pregnancy should be created to prospectively collect obstetrical outcome data from NRT efficacy trials and from individual use. The goal of this registry would be to determine the safety of NRT use during pregnancy, especially with respect to uncommon outcomes such as placental abruption. Finally, our review of the data indicate that minimal amounts of nicotine are excreted into breast milk and that NRT can be safely used by breast-feeding mothers.

Animals↗
PubMed2000

Tone abnormalities are associated with maternal cigarette smoking during pregnancy in in utero cocaine-exposed infants.

OBJECTIVE: Maternal cigarette smoking, alcohol use, and other factors confound studies of in utero cocaine exposure. Our goal was to determine whether in utero cocaine exposure is associated with an abnormal neurologic examination in infants, while controlling for concomitant cigarette smoke exposure and other confounding variables. DESIGN: Healthy newborns with birth weights > or =2000 g were prospectively enrolled into a race-matched study of cocaine-exposed and cocaine-unexposed infants. Urine and meconium samples were analyzed for illicit drugs, the cocaine metabolite, benzoylecgonine, and the nicotine metabolite, cotinine. A detailed neurological examination was performed at approximately 6 weeks of age by an examiner blinded to history. RESULTS: At 6 weeks of age, 40 cocaine-exposed infants and 56 cocaine-unexposed infants were examined. Tone abnormalities were the only neurologic abnormalities discovered, predominantly generalized hypertonia. Logistic models found that maternal urine cotinine levels were predictive of an abnormal neurologic examination, whereas cocaine exposure or benzoylecgonine levels were not. No interaction was found between maternal cigarette smoking and cocaine exposure. Race, ethanol exposure, prenatal care, homelessness, and head circumference were not predictive of an abnormal tone examination. The odds ratio for an abnormal examination was 2.9 (95% confidence interval: 1.04-8.25), if the maternal urine cotinine level was >200 ng/mL. CONCLUSION: Our findings suggest that maternal cigarette smoking may be the major predictor of tone abnormalities reported in cocaine-exposed infants.

Cocaine↗
PubMed1999

Impact of addictive and harmful substances on fetal brain development.

Animal models of alcohol, nicotine, and cocaine exposure have provided convincing evidence for prenatal effects on brain development caused by alterations in cell migration, signal transduction, and neurotransmitter function. The extrapolation to effects on the human nervous system is confounded by the multiplicity of factors affecting central nervous system development.

Animals↗
PubMed1998

Engineering disease and pest resistance in plants.

Improvements in transformation techniques and the isolation of many genes whose transcripts or protein products either have antimicrobial or insecticidal activity or are involved in the synthesis of products with such activities have provided valuable tools for engineering resistance in plants. Future exploitation of this technology should provide an environmentally friendly alternative to traditional disease and pest control measures.

Anti-Infective Agents↗
PubMed1998

A single amino acid change in turnip crinkle virus movement protein p8 affects RNA binding and virulence on Arabidopsis thaliana.

Comparison of the symptoms caused by turnip crinkle virus strain M (TCV-M) and TCV-B infection of a resistant Arabidopsis thaliana line termed Di-17 demonstrates that TCV-B has a greater ability to spread in planta. This ability is due to a single amino acid change in the viral movement protein p8 and inversely correlates with p8 RNA binding affinity.

Arabidopsis↗
PubMed1997

Identification of an Arabidopsis locus required for resistance to turnip crinkle virus.

Inoculation of turnip crinkle virus (TCV) into a (TCV)-resistant line of Arabidopsis thaliana, Di-17, results in the development of a hypersensitive response (HR) on the inoculated leaves. In contrast, an HR does not occur when leaves of the TCV-susceptible Di-3 line or the susceptible ecotypes Columbia (Col-0), or Landsberg erecta (Ler) are inoculated. Genetic analysis of progeny from crosses between Di-17 and either Di-3, Col-0 or Ler demonstrates that the development of an HR is regulated by a single dominant nuclear locus, herein designated HRT. Using progeny from a Di-17 x Col-0 cross, HRT was mapped to chromosome 5, where it is tightly linked to the DFR locus. We also demonstrate that a variety of resistance-associated phenomena, including the TCV-induced accumulation of salicylic acid, camalexin and autofluorescent cell-wall material, correlate with the HR, suggesting the possibility that HRT is required for their activation.

Arabidopsis↗
PubMed1994

Salicylic acid, active oxygen species and systemic acquired resistance in plants.

Infection of plants, particularly by a necrotizing pathogen, usually induces a long-lasting, broad-based, systemic resistance to secondary pathogen attack. Many studies implicate salicylic acid as an essential signal in the development of such systemic acquired resistance in several plant species. Salicylic acid appears to mediate plant defence by binding to and inhibiting catalase, thus increasing the concentration of H(2)O(2) and other active oxygen species. Active oxygen species may then act as second messengers that induce plant defence gene expression, analogous to their activation of gene expression in mammalian cells.

Journal Article↗
PubMed1994

Cocaine metabolites in the neonate: potential for toxicity.

Recent reports indicate that cocaine metabolites have biologic activity and could be toxic. To explore this possibility, two studies were initiated. The first study aimed to define the distribution of cocaine species by quantifying levels of cocaine and its metabolites norcocaine, benzoylecgonine, and benzoylnorecgonine in newborn cord blood and meconium. The second study sought to determine whether they produced a clinical effect. Compared to cord blood, meconium had a greater number of metabolites and a higher concentration of cocaine metabolites, including the previously undetectable norcocaine and benzoylnorecgonine derivatives. Benzoylecgonine was the most common species found in both sources and was usually lower in concentration in blood. An inverse relation existed between meconium benzoylecgonine levels and the serum catabolic enzyme pseudocholinesterase, implying genetic variability in cocaine metabolism. To determine whether cocaine and/or its metabolites could be linked to a distinct clinical state, a second study focusing on newborn behavior was performed with an independent large cohort of cocaine-exposed infants. Neonates with increased signs of "neuroexcitation" had benzoylecgonine and no cocaine in urine, whereas lethargic neonates had detectable urinary cocaine. These findings support the hypothesis that cocaine metabolites, especially benzoylecgonine, may play a role in altering newborn behavior and produce a clinical syndrome distinct from that related to the parent compound.

Butyrylcholinesterase↗
PubMedDate not supplied

Cocaine, nicotine, caffeine, and metabolite plasma concentrations in neonates.

The objective of this study was to measure the umbilical cord plasma levels of cocaine, nicotine, caffeine, and their metabolites. Thirty-six neonates at risk for prenatal cocaine exposure were prospectively enrolled. Umbilical cord plasma was analyzed by gas chromatography-mass spectroscopy for cocaine, cocaethylene, benzoylecgonine (BZE), nicotine, cotinine, and caffeine. Eighteen neonates were plasma positive for BZE, and 50% of these were also positive for cocaine. Cocaethylene was not found. The maximum plasma cocaine concentration was 88 ng/mL (mean, 39 ng/mL). The maximum plasma BZE concentration was 3880 ng/mL (mean, 844 ng/mL). Among BZE-positive babies, the mean plasma drug levels were as follows: nicotine, 1.8 ng/mL; cotinine, 94 ng/mL; and caffeine, 1205 ng/mL. Among the BZE-negative babies, the mean plasma drug levels were as follows: nicotine, 5.2 ng/mL; cotinine, 97 ng/mL; and caffeine, 1440 ng/mL. These cocaine levels raise the possibility of pharmacological effects of cocaine in the early neonatal period.

Caffeine↗