Self-Reported Tobacco Use and Correlation with Umbilical Cord Blood Cotinine levels at Delivery among Appalachian Gravidas

The detrimental effects of cigarette use during pregnancy are well documented. Studies have shown that cigarette smoking while pregnant is associated with multiple adverse outcomes including: pre-term birth, placental abruption, placenta previa, fetal growth restriction, stillbirth, increased rate of birth defects, and increased risk of sudden infant death syndrome. Cotinine is the primary metabolite of nicotine and allows for measurement of active as well as passive exposure. Cotinine freely cross the placental barrier and maternal concentrations are closely correlated with newborn plasma levels. The aim of this study was to compare maternally reported rates of tobacco use to fetal umbilical cord blood cotinine levels at the time of delivery. A cross-sectional study was conducted on 172 patients. Patients were asked a single yes or no question in regards to their cigarette use during pregnancy. Cord blood was collected at the time of delivery and analyzed for serum concentrations of cotinine. Cotinine levels greater than 3.0 ng/mL were considered consistent with the use of tobacco or tobacco cessation products. Maternal self-reporting of tobacco use indicates a reported tobacco use rate of 27.3% and an actual use rate of 30.2%. The reported tobacco non-use rate was 72.7% and the actual non-use rate was 66.3%. The prevalence of tobacco use during pregnancy in our study was 30.2%, while the overall rate in the United States is reported to be 12.3%. Our findings indicate that self-reported smoking prevalence and verified umbilical cord blood cotinine levels at the time of delivery have excellent correlation (kappa=0.76). Compared to the national average our study group also had nearly double the rate of tobacco use. Due to the deleterious effects of cigarette use during pregnancy continued efforts to educate patients regarding cigarette cessation is of utmost importance as cessation of tobacco products will improve and promote maternal and fetal well-being

Istraživanje mehanizma toksičnosti anilina u eritrocitima

Strategies for the use of bio-indicators in the prediction of environmental damage should include mechanistic research. This study involves the relationship between the chemical structure and hemotoxic markers of aniline and its halogenated analogs. Aniline-induced methemoglobinemia, loss of circulating blood cells, blood stability, glutathione depletion and membrane cytoskeletal changes were assessed following exposure to phenylhydroxylamine (PHA), para-fluoro-, para-bromo-, and para-iodo in male Sprague-Dawley rats. Methemoglobin was determined spectrophotometrically at 635 nm. Erythrocyte depletion was investigated by loss of radioactivity in chromium-labeled red blood cells in vivo. Membrane proteins were analyzed by SDS-PAGE using red blood ghost cells treated with various aniline analogs. Results showed dose- and time-dependent changes in the induction of methemoglobin of up to 78 % with para-bromo PHA and 75 % with para-iodo PHA compared to 3 % to 5 % in control. Treated animals lost up to three times more blood from circulation compared to control within 14 days after treatment. Erythrocytes were more stable in buffer solution than in para-iodo-treated cells. Depletion of reduced glutathione in PHA and para-iodo-PHA treated red cells was also observed. Analysis of red cell skeletal membrane treated with para-iodo-PHA showed that protein band 2.1 became broader and band 2.2 diminished completely in some treatments. Dose- and time-dependent changes suggested the use of hemotoxic endpoints as potential biomarkers for assessing chemical and drug safetyStrategije primjene biopokazatelja za predviđanje štete u okolišu trebaju u obzir uzeti istraživanja mehanizama djelovanja. Ovo istraživanje propituje odnos između kemijske strukture i hemotoksičnih pokazatelja djelovanja anilina i njegovh halogeniranih analoga. Nakon izlaganja mužjaka štakora soja Sprague-Dawley para-fluoro-, para-bromo- i para-jodofenilhidroksilaminu, utvrđena je methemoglobinemija uzrokovana anilinom te pad broja krvnih stanica u krvotoku i stabilnosti krvi, gubitak glutationa i promjene na membrani stanice. Methemoglobin je određivan spektrofotometrijski na 635 nm. Pad broja eritrocita mjeren je in vivo s pomoću eritrocita obilježenih radioaktivnim kromom. Membranske su bjelančevine analizirane s pomoću SDS-PAGE, rabeći eritrocite bez hemoglobina (engl. ghost cells) kojima su dodani različiti analozi anilina. Nalazi upućuju na promjene indukcije methemoglobina ovisno o dozi i vremenu djelovanja do 78 % s para-bromo-fenilhidroksilaminom te do 75 % s para-jodofenilhidroksilaminom u usporedbi s 3 % do 5 % u kontrolnih uzoraka. U razdoblju od 14 dana nakon tretiranja izložene životinje izgubile su tri puta više krvi iz krvotoka od kontrolnih. Eritrociti su bili stabilniji u puferskoj otopini negoli u stanicama kojima je dodan para-jodofenilhidroksilamin. Zamijećen je i pad glutationa u eritrocitima kojima je dodan fenilhidroksilamin odnosno para-jodofenilhidroksilamin. Analizom membrane eritrocita kojima je dodan para-jodofenilhidroksilamin zamijećeno je da se u pojedinih obrada raširila proteinska vrpca 2.1, a potpuno smanjila proteinska vrpca 2.2. Zamijećene promjene uvjetovane dozom i vremenom upućuju na primjenu hemotoksičnih parametara kao mogućih biopokazatelja u procjeni sigurnosti lijeka odnosno kemikalije

Impairment of endothelium-dependent but not of endothelium-independent dilatation in guinea-pig aorta rings incubated in the presence of elevated glucose

1. Purine compounds such as ATP and adenosine, respectively endothelium-dependent and-independent vasodilators, are largely involved in the control of vascular tone and vascular reactivity to contracting stimuli. We investigated the relaxing activity of ATP and adenosine in guinea-pig aorta rings exposed for 6 h to elevated glucose concentration (50 mM), in order to mimic hyperglycaemic conditions. Guinea-pigs were reserpine-treated (2 mg kg(−1), i.p., 48 and 24 h before death). 2. Rings of aortae incubated in 50 mM glucose, contracted submaximally by 1 μM noradrenaline, lost endothelium-dependent relaxation in response to acetylcholine (10 nM to 10 μM). Aortae incubated with 50 mM mannose, as a hyperosmotic control, relaxed to acetylcholine normally. Rings of aortae incubated in 50 mM glucose, contracted submaximally by 3 mM 4-aminopyridine, lost endothelium-dependent relaxation in response to ATP (30 μM) whereas endothelium-independent relaxation in response to adenosine (0.3 mM) was well preserved. 3. The relaxation induced by A23187 or sodium nitroprusside (10 nM to 0.1 μM) did not differ between rings exposed to control (5.5 mM) or elevated glucose (50 mM) and contracted submaximally by 3 mM 4-aminopyridine. 4. When incubated with aortic tissue in the presence of elevated glucose, the cyclo-oxygenase inhibitors, indomethacin (10 μM) and mefenamic acid (30 μM), or the scavenger of superoxide anions, superoxide dismutase (150 u ml(−1)), prevented the impairment of ATP-mediated relaxation. 5. The present results indicate that endothelium-dependent, receptor-induced relaxation in response to acetylcholine and ATP is impaired in guinea-pig aorta rings exposed to elevated glucose. The endothelial dysfunction caused by glucose might be located at a step between receptor activation and intracellular calcium increase, and might be related to an increased metabolism of arachidonic acid coupled to an increased production, or to a reduced inactivation of superoxide anions