Learning disabilities and performance on the Pennsylvania System of School Assessment.

The No Child Left Behind Act mandates all students in schools receiving Title I funds show proficiency in reading by 2014. This stricture applies to students with diagnosed learning disabilities as well as to students without learning disabilities. Multiple regression analyses on data for seniors attending a Grade 9-12 predominately white, comprehensive vocational-technical school indicated that, when absenteeism, socioeconomic status, and sex were held constant, the 26 students with diagnosed learning disabilities scored 246.

Supraphysiological acetaldehyde levels suppress growth in chicken embryos.

Although exposure to ethanol is known to cause growth inhibition in a developing embryo, the contributing effect of acetaldehyde on growth is not as well documented. In this study, we measured acetaldehyde-induced growth suppression in three different chicken strains: Peterson x Hubbard, HY x Hubbard, and W36 Ginther White Leghorn. The chicken embryo provides a useful model for studying fetal alcohol syndrome (FAS) and has been used extensively in our laboratory.

Differential expression of glucose transporters during chick embryogenesis.

The patterns of Glut1 and Glut3 glucose transporter protein and mRNA expression were assessed during embryogenesis of chicken brain and skeletal muscle, Glut4 protein levels were also evaluated in skeletal muscle and heart, and Glut1 was examined in the developing heart and liver. Glut1 protein expression was detectable throughout brain ontogeny but was highest during early development. Glut1 mRNA levels in the brain remained very high throughout development.

Ethanol-induced decrease of developmental PKC isoform expression in the embryonic chick brain.

Prenatal ethanol exposure can cause a number of physiological deficits known as fetal alcohol syndrome (FAS). Because protein kinase C (PKC) regulates the cell cycle and has been linked to growth, we examined the effect of ethanol on PKC isoform expression in a developing chick brain. Ethanol exposure causes decreased head weight in chickens at day 5 in a dose-dependent manner and a decreased brain weight at days 7 and 10 at an ethanol concentration of 1.

Increased intracellular localization of brain GLUT-1 transporter in response to ethanol during chick embryogenesis.

Fetal exposure to ethanol is associated with growth retardation of the developing central nervous system. We have previously described a chick model to study the molecular mechanism of ethanol effects on glucose metabolism in ovo. Total membrane fractions were prepared from day 4, day 5, and day 7 chick embryos exposed in ovo to ethanol or to vehicle.

Experimental models used to measure direct and indirect ethanol teratogenicity.

The teratogenic effects of ethanol have been widely studied in a variety of experimental models. In humans, ethanol teratogenicity results from both direct and indirect effects. This paper reviews the differences between direct and indirect effects of ethanol on the developing fetus.

Teratogenicity of ethanol in different chicken strains.

This study investigated the teratogenicity of ethanol in several different strains of chickens. The chick embryo provides a useful model for studying the fetal alcohol syndrome. Two broad classifications of chicks, each containing many strains, are commercially available for use: broilers and layers.

Sodium ion-dependent (N-methylamino)-alpha-isobutyric [correction of isobutryic] acid uptake by embryonic chick cells exposed to ethanol in ovo:response to the stimulation/downregulation of protein kinases.

Amino acid uptake, critical for embryonic development, was studied in cultured chick cells isolated from 5-day-old chick embryos that had received treatment in ovo with either vehicle (sterile chick Ringer's solution) or vehicle plus ethanol (1.5 g/kg). Upon being placed in culture, the cells were grown in the absence of ethanol per se.

Changes in brain glucose levels and glucose transporter protein isoforms in alcohol- or nicotine-treated chick embryos.

Suppression of fetal brain growth during pregnancy as the result of maternal smoking or alcohol consumption leads to significant problems for the offspring as well as for the society who must care for these individuals. Chronic maternal intake of cigarette smoke is frequently observed in humans and studies using animal models suggest that in utero nicotine exposure is an important component of the growth suppression that results. Similarly, maternal consumption of alcohol (ethanol) has a profound, negative effect on fetal growth.

Metabolic and mitotic changes associated with the fetal alcohol syndrome.

In the USA, fetal alcohol syndrome (FAS) is the leading known cause of mental retardation. FAS is estimated to affect 4000 infants yearly in the USA with an additional 7000 children suffering various forms of fetal alcohol effects in the absence of the full syndrome. A comparable incidence would be expected in other industrialized countries, but essentially no data are available from either developing or third world countries.

Ethanol differentially affects metabolic and mitotic processes in chick embryonic cells.

Our laboratory has been investigating the mechanisms by which ethanol-induced growth inhibition occurs in a developing embryo, and our studies have focused on disruption of cellular signaling pathways. Previous work on ethanol-induced changes in signaling systems that regulate ornithine decarboxylase activity indicated that the pathways containing protein kinase A, protein kinase C (PKC), and insulin-dependent tyrosine kinase were important for the control of ornithine decarboxylase in chick embryonic cells. Herein, we report ethanol's effect on the regulation of glucose uptake and thymidine uptake by these same kinase pathways.

Insulin signaling in chick embryos exposed to alcohol.

Although insulin is known to be an important generator of regulatory signals during fetal growth and development, neither the immediate nor long-term effects of alcohol (ethanol) on insulin action are well understood. In the rat, fetal exposure to alcohol has been shown to be correlated with a subsequent abnormal response to a glucose load in the neonate and adult. Further, fetal hypoplasia secondary to maternal alcohol consumption is correlated with decreased placental glucose transport and with a lowering of the glucose levels in fetal tissues.

Ethanol's effect on tissue polyamines and ornithine decarboxylase activity: a concise review.

An extraordinarily diverse literature describes the cellular/tissue systems in which the molecular effects of both acute and chronic alcohol exposure seem to be mediated by changes in polyamine levels and/or ornithine decarboxylase (ODC) activity. The single unifying factor that links most of these studies is that they all, in some way, involve tissues that are undergoing relatively rapid cell division. Non-dividing cells expressing the NMDA receptor are a notable exception in that ethanol and the polyamines seem to act via discrete regions of that receptor.

Signaling pathways regulating ornithine decarboxylase activity in the embryonic chicken.

The pathways regulating ornithine decarboxylase (ODC) activity in the chick embryo were studied to determine which kinase-signaling pathways regulate ODC activity levels during development. Insulin-dependent tyrosine kinase, protein kinase C and cAMP-dependent protein kinase were activated by the addition of insulin, tetradecanoylphorbol-12,13-acetate, and forskolin, respectively. All three drugs increased ODC activity and forskolin combined with insulin increased ODC activity above the increase caused by either drug alone.

Biochemical changes, early brain growth suppression and impaired detour learning in nicotine-treated chicks.

Fetal growth suppression associated with chronic maternal intake of cigarette smoke is frequently observed in humans and studies using animal models suggest that in utero nicotine exposure is an important component of this growth suppression. The developing fetal central nervous system (CNS) is sensitive to the growth inhibitory effect of nicotine and morphological as well as functional CNS deficits may result from fetal nicotine exposure. The studies presented here show that nicotine exposure during early embryonic development ultimately inhibits the ability of 7-11 day old chicks to learn a detour task.

Deoxyguanosine-resistant leukemia L1210 cells. Loss of specific deoxyribonucleoside kinase activity.

A mouse leukemia L1210 cell line was selected for resistance to deoxyguanosine. The deoxyguanosine-resistant cells (dGuo-R) were 126-fold less sensitive to deoxyguanosine than the wild-type cells. The IC50 values for araC and araG were increased, but only 10-12-fold in the dGuo-R cells when compared with the wild-type cells.