Umbilical cord tissue performs as well as meconium in assessing fetal drug exposure to amphetamines, opiates, cocaine, and cannabinoids. Results of studies using the cord may have a more rapid return to the clinician, because waiting for meconium to be passed sometimes requires several days. Moreover, in some cases the meconium is passed in utero making collection impossible, whereas cord should always be available for drug testing.
Hepatic enzyme-inducing antiepileptic drugs (AEDs) lower oral contraceptive (OC) sex hormone levels approximately 40% and increase the risk of unplanned pregnancies in women with epilepsy. AEDs also increase the risk of birth defects in offspring of women with epilepsy. We performed a national survey to determine obstetricians' and neurologists' knowledge of OC and AED interactions and the risk of birth defects for women with epilepsy taking AEDs. We received responses to a mailed questionnaire from 160 of 1,000 neurologists (16%) and 147 of 1,000 obstetricians (15%) from 47 states. Practice demographics and ages of responders were typical for U.S. neurologists and obstetricians. Ninety-one percent of neurologists and 75% of obstetricians said they treat women with epilepsy of child-bearing age. Only 4% of the neurologists and none of the obstetricians, however, knew the effects of the six most common AEDs on OCs, even though 27% of neurologists and 21% of obstetricians reported OC failures in their patients taking AEDs. Although increasing OC doses can compensate for insufficient OC sex hormone levels due to AEDs, most physicians do not increase the doses. Even though the risk of birth defects for the offspring of women with epilepsy is 4 to 6%, up from the background level of 2%, 44% of neurologists thought the risk was lower (0 to 3%), and some of the respondents guessed that it was as high as 50%. Many neurologists and obstetricians do not have accurate information to counsel women with epilepsy properly about their contraceptive and pregnancy choices.
The effects of trypsin on Escherichia coli cells that have been treated with colicins have been examined. By the use of trypsin, it has been possible to demonstrate that the action of several colicins (El, E2, and K) proceeds through at least two stages. Stage I is a period after colicin adsorption when trypsin can restore colonyforming ability to a colicin-treated cell./ Stage I is followed by a period when trypsin is unable to restore colony-forming ability (stage II). The transition between stage I and stage II follows first-order kinetics, with a rate proportional to the number of killing units of colicin adsorbed.A quantitative comparison of the effects of colicin K on colony-forming ability and on several cellular processes indicates that colicin damage to these processes occurs in the stage II period of colicin action and is not subject to reversal by the trypsin treatment that restores viability to cells in stage I. The implications of these findings for an understanding of the mode of action of colicins are discussed.The idea that colicins act from the surface of bacterial cells has arisen from reports that agents that presumably do not penetrate the outer membrane, such as trypsin (1-4) or colicin-specific antiserum (5), can reverse the effects of certain colicins. In the case of colicin K, it has been shown that some of the colicin-produced damage on Escherichia coli B cells can be repaired by prolonged exposure of colicin-treated cells to trypsin (1). Other observations indicate that reversibility of the effects of colicin K by trypsin is limited. Wendt (6) has presented data indicating that trypsin completely reverses colicin K effects on colony-forming ability of E. coli K-12 Bacterial Strain, Media, and Grnwth Conditions. The bacterial strain used throughout this study was LA319 [F-lac-(i-z-y+) pro-strr] from our laboratory collection. LA319 was routinely grown at 370 in Ozeki medium base (10), supplemented with D,L-lactate (0.5%/), i-proline (100 gg/ml), and thiamine (3 MM), to a cell density of 100 Klett units (no. 54 filter). One Klett unit corresponds to about 5 X 106f cells/ml. Cultures (20 ml) were incubated in 300-ml flasks shaken in a New Brunswick Gyratory Shaker. The cultures were harvested at room temperature, washed once with Ozeki medium, and resuspended in this medium containing lactate and thiamine, at a density of about 2 X 109 cells/ml.
Aims This study aimed to evaluate the performance of ethyl glucuronide (EtG) in hair and fingernails as a long-term alcohol biomarker. Design Cross-sectional survey with probability sampling. Setting Midwestern United States. Participants Participants were 606 undergraduate college students between the ages of 18 and 25 at the time of selection for potential study participation. Measurements EtG concentrations in hair and fingernails were measured by Liquid Chromatography-Tandem Mass Spectrometry at three thresholds (30 picograms (pg) per milligram (mg); 20 pg/mg; and 8 pg/mg). Any weekly alcohol use, increasing-risk drinking, and high-risk drinking on average during the past 12 weeks was assessed by participant interview using the TimeLine Followback. Findings In both hair and fingernails at all three EtG thresholds, sensitivity was greatest for the high-risk drinking group (hair: 0.43, Confidence Interval (CI) = [0.17, 0.69] at 30 pg/mg, 0.71, CI = [0.47, 0.95] at 20 pg/mg; 0.93, CI = [0.79, 1.00] at 8 pg/mg; fingernails: 1.00, CI = [1.00–1.00] at 30, 20 and 8 pg/mg), and specificity was greatest for any alcohol use (hair: 1.00, CI = [1.00, 1.00] at 30 and 20 pg/mg; 0.97, CI = [0.92–0.99] at 8 pg/mg; fingernails: 1.00, CI = [1.00–1.00] at 30, 20, and 8 pg/mg). Areas under the receiver operating characteristic curves were significantly higher for EtG concentration in fingernails than hair for any weekly alcohol use (p = 0.02, DeLong test, two-tailed) and increasing-risk drinking (p = 0.02, DeLong test, two-tailed). Conclusions Ethyl glucuronide, especially in fingernails, may have potential as a quantitative indicator of alcohol use.
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