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Biomedical subjects

L Goldschmidt

Publications and source records attributed to L Goldschmidt.

At least 19 recordsLinked to original sources

Prenatal tobacco exposure: is it a risk factor for early tobacco experimentation?

Few studies have considered the etiological role of the fetal environment on the offspring's substance use. This prospective study examines the relations between the mother's prenatal and current smoking and the offspring's smoking experimentation. A low SES birth cohort of 589 10-year-olds, who have been followed since their gestation, completed a self-report questionnaire about their substance use. Half were female, and 52% were African-American. Detailed data on exposure to tobacco and other substances in the prenatal and postnatal periods were collected from the mothers. During pregnancy, 52.6% of the mothers were smokers; 59.7% were smokers when their children were 10. Six per cent of the children (37/589) reported ever smoking cigarettes, 3% had had one full alcoholic drink, and none had started to use other drugs. Maternal smoking during pregnancy was significantly associated with an increased risk of the child's tobacco experimentation. Offspring exposed to more than 1/2 pack per day during gestation had a 5.5-fold increased risk for early experimentation. Structural equation modeling showed that prenatal tobacco exposure had a direct and significant effect on the child's smoking and that maternal current smoking was not significant. Prenatal tobacco exposure also predicted child anxiety/depression and externalizing behaviors, and these outcomes affected child smoking through the mediating effect of peer tobacco use.

Adolescent↗

Effects of prenatal tobacco exposure on preschoolers' behavior.

This is a longitudinal study of the relationship between prenatal tobacco exposure and the development of behavior problems in 672 children at the age of 3 years. Women from a prenatal clinic were interviewed about substance use at the end of each trimester of their pregnancy and at 3 years postpartum. Children were assessed at the age of 3 years with maternal ratings of behavior problems, activity, and attention. The prevalence of tobacco use was high in this cohort; 54.3% and 52.3% of the women smoked tobacco in the first and third trimesters of pregnancy, respectively. At 3 years postpartum, 61.6% of the women were smokers. There were significant effects of prenatal tobacco exposure on the children's behavior at age 3 years. Increases in scores on the Oppositional Behavior, Immaturity, Emotional Instability, Physical Aggression, and Activity scales and in the total score on the Toddler Behavior Checklist (TBC) were significantly associated with prenatal tobacco exposure. Smoking one pack of tobacco cigarettes per day during the third trimester of pregnancy was associated with an increase of 6 points in the total problem behavior score. Among the subscales of the TBC, tobacco exposure had the largest effect on oppositional behavior. Impulsivity and peer problems were associated with both prenatal and current tobacco exposure. Only current tobacco exposure predicted attention problems. Prenatal tobacco exposure had a significant negative effect on the development of behavior problems among preschoolers.

Adolescent↗

Growth of infants prenatally exposed to cocaine/crack: comparison of a prenatal care and a no prenatal care sample.

OBJECTIVE: It has not been possible to draw firm conclusions about the effects of prenatal cocaine exposure because of methodologic problems involved in the conduct of this research. This study, designed to overcome some of these methodologic problems, is a prospective, longitudinal investigation of the effects of prenatal cocaine/crack exposure on neonatal growth in two samples, one with and one without prenatal care (PC). METHODS: Women in the PC sample (n = 295) were interviewed at the end of each trimester about their use of cocaine, crack, alcohol, tobacco, marijuana, and other drugs. Women in the no prenatal care (NPC) sample (n = 98) were interviewed at delivery about their drug use during each trimester of pregnancy. In both samples, information was also obtained about sociodemographic, lifestyle, psychologic, and social support characteristics. Both samples consisted of women who were predominantly low income, single, and high school educated. Of the women, 48% in the PC sample were black; 81% in the NPC sample were black. Infants were examined during the postpartum hospital stay by project nurses who were blind to maternal substance use status. RESULTS: Women in both samples who used cocaine/crack during pregnancy were older, had lower family incomes, and used more alcohol than did women who did not use cocaine/crack during pregnancy. In addition, women in the NPC sample were more likely to be black, less educated, gained less weight during pregnancy, and used more alcohol than did women in the PC sample, regardless of cocaine use. In both samples, cocaine/crack use during early pregnancy predicted reduced gestational age, birth weight, length, and head circumference, after controlling for the significant covariates of cocaine use. In a comparison of the samples, the offspring of the NPC/cocaine group were significantly smaller than were the offspring of the PC/no cocaine group, whereas the offspring of the PC/cocaine and NPC/cocaine groups did not differ. CONCLUSIONS: These results indicate that exposure to cocaine/crack during early pregnancy decreases the intrauterine growth of exposed offspring in women with and without PC. Each of the growth parameters was affected indicating symmetric growth retardation. The adequacy of PC was not a significant factor in determining the difference between cocaine-exposed and nonexposed infants. These samples are being followed throughout childhood to determine whether there are long-term effects of prenatal cocaine/crack exposure on growth.

Birth Weight↗

Prenatal alcohol use and offspring size at 10 years of age.

The Maternal Health Practices and Child Development Project is a longitudinal study of the effects of prenatal exposure to alcohol and other substances. Women were selected from a prenatal clinic and interviewed at the 4th and 7th months of pregnancy. Their offspring were examined at delivery, at 8 and 18 months, and at 3, 6, and 10 years. This report examined 610 offspring, at age 10, who were exposed prenatally to alcohol. Most alcohol use in this low-income cohort was light to moderate, although the entire spectrum of alcohol use is represented. The weight, length, head circumference, and skinfold thickness of the offspring were measured. At each assessment phase, we found a significant association between size and prenatal exposure to alcohol. At age 10, the children who were prenatally exposed to alcohol continued to be significantly smaller in weight, height, head circumference, and skinfold thickness. These results indicate that prenatal alcohol exposure has a long-term impact on offspring growth.

Alcohol Drinking↗

Effects of prenatal substance exposure: altered maturation of visual evoked potentials.

We investigated the effects of prenatal substance use on visual evoked potentials (VEPs). Seventy-four children were tested at birth and 1 month of age with binocular flash VEPs and at 4, 8, and 18 months of age with binocular pattern VEPs. Regressions were run by trimester to assess the independent effects of substance exposure. Variables included in the regression model were alcohol, marijuana, tobacco, other drug use for each trimester, maternal age, education, income, race, marital status, infant sex, birthweight, and Dubowitz score. Changes in specific components of the binocular VEP were both substance- and trimester-specific. First trimester alcohol use was associated with prolonged P1 wave latencies at 1 month of age. Prolonged P1 wave latencies at birth and 18 months were associated with tobacco use during each of the three trimesters, at 1 and 18 months with third trimester marijuana use, and at 1 and 18 months with first trimester other illicit drug use. Although these women were moderate substance users during pregnancy, their offspring exhibited maturational changes in components of the VEP in the absence of neonatal behavioral disturbances.

Aging↗

Prenatal alcohol exposure and academic achievement at age six: a nonlinear fit.

This is a report on the effects of prenatal alcohol exposure on the academic achievement of children at 6 years of age. In this longitudinal study, women were interviewed at the end of each trimester of pregnancy, at delivery, and at 8, 18, 36, and 72 months postpartum. The women were of lower socioeconomic status, high school-educated, and moderate users of alcohol. The offspring received age-appropriate physical and developmental assessments at each follow-up. Linear regression and nonlinear curve fitting were used to investigate the nature and shape of the relationship between prenatal alcohol exposure and achievement. In addition, the role of child IQ in this relationship was explored. Alcohol exposure during the second trimester predicted deficits in each of the three subtests of the Wide Range Achievement Test-Revised (WRAT-R): reading, spelling, and arithmetic. The relationship was partially reduced by the addition of IQ to the model, but prenatal alcohol exposure still predicted significant deficits in achievement, even after controlling for IQ. Tests for the shape of the relationship demonstrated that the effect of prenatal exposure on the arithmetic subtest of the WRAT-R was a linear or dose-response relationship. By contrast, the relationships between prenatal alcohol exposure and performance on the spelling and reading subtests of the WRAT-R were better modeled as threshold effects. The thresholds for both were approximately 1 drink/day in the second trimester.

Achievement↗

A longitudinal analysis of the effect of prenatal alcohol exposure on growth.

Cross-sectional analyses have demonstrated that prenatal exposure to alcohol can result in growth deficits at birth and in early childhood. However, there have been few longitudinal analyses of this relationship. This study presents an analysis of the longitudinal effect of prenatal alcohol exposure on growth. The model used for analysis was a general unbalanced repeated-measures model with a fully parameterized covariance matrix. Application of the model demonstrated that for length and head circumference, the effect of prenatal alcohol exposure was constant over time. The relationship between prenatal alcohol exposure and growth in weight was more complex. Prenatal alcohol exposure affected the rate of growth between birth and the eight month. Subsequently, the relationship between weight and prenatal alcohol exposure was constant. Therefore, for length and head circumference, prenatal alcohol exposure suppresses the rate of growth in the fetus but not at subsequent time points. For weight, exposure affects the rate of growth through the eighth month but not at subsequent time points. For each of the growth parameters, there is no catch-up growth, and the smaller size observed in the offspring is maintained.

Adolescent↗

The effects of prenatal alcohol use on the growth of children at three years of age.

In this prospective study of substance use during pregnancy, women were interviewed in their 4th and 7th prenatal months, and women and children were assessed at 24 hr, 8, 18, and 36 months postpartum. Data are presented on the outcome of 519 children at age 3. At 3 years, children who were exposed prenatally to alcohol were smaller in weight, length, and head circumference. They also had an increased number of minor physical anomalies. These effects were found even after controlling for nutritional and environmental factors. The persistence of growth effects at age 3 suggests that children exposed to alcohol prenatally may have a diminished capacity for growth.

Body Height↗

Prenatal alcohol exposure and offspring growth at 18 months of age: the predictive validity of two measures of drinking.

This is an analysis of the effect of prenatal alcohol exposure on growth of the offspring at 18 months of age. In this prospective study, a cohort of women was interviewed at the end of each trimester of pregnancy, at delivery, and at 8 and 18 months. Offspring were examined at each follow-up point. Two drinking scales, average daily volume (ADV) and frequent heavy drinking (FHD), were used to explore the effect of different patterns of drinking. We found significant relationships between both prenatal FHD and ADV and offspring growth at 18 months. A significant and inverse relationship was found between ADV during the second and the third trimesters of pregnancy and weight, height, and head circumference at 18 months. Frequent heavy drinking during all three trimesters predicted a significant decrease in head circumference at 18 months. FHD during the second trimester was significantly related to weight and height at 18 months. Analyses demonstrated that ADV was a better predictor of growth deficits than FHD.

Adult↗

The immune response to homologous lens crystallin. I. Antibody production after lens injury.

Using a sensitive radioimmunoassay to homologous mouse alpha-crystallin, it was established that autoantibodies are produced to this self constituent in mice after rupture of the lens capsule by needling. Antibody to lens crystallin was detected within 4 days of lens rupture and persisted for 24 days, suggesting that these mice are not tolerant to alpha-crystallin at the B cell level. However, T cells from mice immunized with homologous crystallin cannot be stimulated to proliferate by either homologous or heterologous crystallin. On the other hand, lymphocytes from mice immunized with bovine alpha-crystallin can be stimulated to proliferate to bovine crystallin, but not to either unfractionated mouse crystallin (MC) or purified mouse alpha-crystallin. At the level of detection, therefore, T cells appear to be tolerant to homologous alpha-crystallin, but not to heterologous alpha-crystallin. LPS resulting from bacterial contamination after needling was ruled out as a necessity for antibody production because antibody to mouse alpha-crystallin was produced after sterile lens rupture with a laser. However, LPS and poly A:U did enhance the antibody response to alpha-crystallin. These data suggest that T cells, but not B cells, are tolerant to homologous crystallin and that antibody results from circumvention of specific helper T cell requirements for antibody synthesis. The implications of these findings for tolerance and autoimmune uveitis are discussed.

Animals↗

Remodeling on a shoestring improves pharmacy's efficiency.

A hospital's pharmacy renovated its existing outdated and highly restricted departmental space to help ensure more efficient operation until the master plan for hospitalwide improvements could be completed and implemented. This temporary renovation was accomplished at very low cost and yielded improvements ranging from better use of space and personnel to better communication between the nursing and the pharmacy departments.

Efficiency↗

Mechanisms of genetic resistance to Friend virus leukemia in mice. IV. Identification of a gene (Fv-3) regulating immunosuppression in vitro, and its distinction from Fv-2 and genes regulating marrow allograft reactivity.

Friend leukemia viru (FV) suppresses the proliferative response of normal lymphocytes to mitogens. The in vitro suppressive effect of FV on lymphocyte mitogenesis is mediated by T-suppressor cells and is under host genetic control. Lymphocytes from strains of mice of the C57BL background (e.g., C57BL/6) are resistant while cells from other strains (e.g., 129 and DBA/2) are susceptible. Genetic analyses utilizing resistant and susceptible parental strains, their F1, intercross and backcross progeny indicated that susceptibility to in vitro suppression is regulated by a single autosomal gene, dominant for susceptibility to suppression. This gene, which is not linked to the H-2 complex, segregated independently of the Fv-2 gene which controls resistance to spleen focus formation in vivo. The gene is also unlinked to the Ir-like genes which regulate the ability of H-2d mice to reject H-2b bone marrow grafts. The gene is therefore designated as Fv-3. Fv-3 may mediate its effect by regulating the numbers and/or functions of T-suppressor cells.

Animals↗