A percepção de risco teratogênico equivocada pode levar à privação de uso de medicamentos seguros e à relutância ou não adesão ao tratamento farmacológico durante a gestação. Estudos prévios realizados em países desenvolvidos sugerem que a percepção de risco teratogênico ao uso de medicamentos é superestimada por gestantes, não gestantes e profissionais de saúde. Grande parte destes estudos foi realizada em centros de aconselhamento teratogênico e utilizou apenas uma técnica de aferição da percepção de risco (Escalas Visuais Analógicas). Com o objetivo de caracterizar a percepção de risco teratogênico por gestantes e mulheres em idade fértil, conduzimos um estudo que combinou métodos qualitativos e quantitativos de investigação. Participaram da pesquisa usuárias de serviços de saúde da rede básica municipal de Porto Alegre. Em termos qualitativos, foram realizados dois grupos focais com gestantes. Os dados quantitativos resultaram da realização de entrevistas estruturadas com 287 mulheres em idade fértil divididas em dois grupos: gestantes e não gestantes. A percepção de risco de malformações congênitas na população geral e as percepções de risco teratogênico das exposições a paracetamol, metoclopramida, misoprostol e radioterapia na gestação foram aferidas por duas técnicas: Escalas Visuais Analógicas (EVA) e perguntas numéricas. A concordância entre as duas técnicas de aferição foi avaliada pela análise gráfica de Bland-Altman. Não encontramos concordância entre as medidas obtidas por EVA e por pergunta para nenhuma das percepções de risco em estudo. As medianas das percepções de risco teratogênico medidas por EVA foram superiores às obtidas através da pergunta numérica, para todas as variáveis. Para ambas as técnicas de aferição, as medianas das percepções de risco teratogênico ao paracetamol e à metoclopramida foram mais baixas que para o risco de malformações congênitas na população geral. Já as medianas das percepções de risco ao misoprostol e à radioterapia apresentaram os maiores valores. Não foram encontradas diferenças significativas nas percepções de risco entre gestantes e não gestantes. A lógica acionada pelas mulheres na estimação do risco teratogênico é a da classificação dos medicamentos em fortes e fracos. Dentro desta lógica, os medicamentos e as exposições percebidos por elas como fracos não apresentam riscos, enquanto que aqueles percebidos como fortes são vistos como perigosos e devem ser evitados na gestação. Concluímos que o uso de EVA leva à superestimação das percepções de risco teratogênico. Além disso, frente à dificuldade em operar a lógica probabilística na estimação de risco, as mulheres operam uma lógica própria, classificando os medicamentos em fortes ou fracos. / An erroneous perception of teratogenic risk can lead to the non-use of safe medications and reluctance to or abstaining from pharmacological treatment during pregnancy. Previous studies conducted in developed countries suggest that the perception of teratogenic risk in the use of medications is overestimated by pregnant women, non-pregnant women and health professionals. Most of these studies were performed in teratogen counseling centers and only used one technique for measuring risk perception (Visual Analogue Scales). In order to characterize the perception of teratogenic risk by pregnant women and women of childbearing age, we conducted a study that combined qualitative and quantitative research methods. Public health care users from the city of Porto Alegre participated in the research. In qualitative terms, two focus groups were carried out with pregnant women. The quantitative data was derived from structured interviews with 287 women of childbearing age divided into two groups: pregnant and non-pregnant women. The perception of risk of congenital malformations in the general population and the perception of teratogenic risk through exposure to acetaminophen, metoclopramide, misoprostol and radiation therapy during pregnancy were measured via two techniques: Visual Analogue Scales (VAS) and numerical questions. The agreement between the two measurement techniques was evaluated using Bland-Altman graphic analysis. We did not find an agreement between the measurements obtained through VAS and those obtained through questions for any of the risk perceptions in the study. The medians of the perceptions of teratogenic risk measured by VAS were higher than those obtained by numerical questions, for all variables. For both measurement techniques, the medians of the perceptions of teratogenic risk with acetaminophen and metoclopramide were lower than those for the risk of congenital malformations in the general population. However, the medians of the perceptions of risk with misoprostol and radiation therapy presented the highest values. There were no significant differences in risk perceptions among pregnant and non-pregnant women. The logic employed by women in estimating teratogenic risk is the classification of drugs according to strong and weak. According to this logic, the drugs and exposure to them, perceived by these women as weak, do not present risks, while those perceived as strong are seen as hazardous and should be avoided during pregnancy. Our conclusion is that the use of VAS leads to the overestimation of teratogenic risk perceptions. Moreover, given the difficulty to engage in probabilistic logic for estimating risk, women engage in their own logic, classifying medications as strong or weak.

Submitted by Renata Lopes (renatasil82@gmail.com) on 2016-10-26T12:56:35Z No. of bitstreams: 1 rosanadepaivaoliveira.pdf: 518922 bytes, checksum: ada6fbbe3e06a4a6b09ddb9b371b9336 (MD5) / Approved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2016-12-15T12:41:46Z (GMT) No. of bitstreams: 1 rosanadepaivaoliveira.pdf: 518922 bytes, checksum: ada6fbbe3e06a4a6b09ddb9b371b9336 (MD5) / Made available in DSpace on 2016-12-15T12:41:46Z (GMT). No. of bitstreams: 1 rosanadepaivaoliveira.pdf: 518922 bytes, checksum: ada6fbbe3e06a4a6b09ddb9b371b9336 (MD5) Previous issue date: 2007-09-19 / FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais / O ultra-som terapêutico tem amplo uso em diversas disfunções estéticas, cujo tratamento é procurado por mulheres jovens que podem se expor à irradiação em período precoce de gestação. Estudos sobre o efeito do ultra-som terapêutico na gestação são antigos, apresentam resultados controversos, foram realizados com metodologia nem sempre compatível com a clínica, com métodos e técnicas diversas, nenhuma reproduzida em dois trabalhos semelhantes e poucos envolveram as fases precoces de gestação. Os efeitos do ultra-som devem-se ao aumento da permeabilidade por vasodilatação, alteração de difusão de íons, modificação da posição de partículas intra e extracelular e alterações da configuração normal da célula, as quais podem acarretar alteração na sua atividade. Durante a fase precoce do desenvolvimento embrionário as células dependem de síntese protéica e de diversas sinalizações processadas através de canais de sódio e potássio. Além disso, microtúbulos e microfilamentos são extremamente importantes na morfogênese. Portanto, a exposição ao ultra-som poderia acarretar lesões no concepto. No presente estudo, avalia-se o efeito da exposição de ratas, no início da prenhez, ao ultra-som terapêutico por ondas pulsadas e ondas contínuas. A metodologia consistiu em utilizar ratas em dois períodos: pré-implantação (grupos A1, A2 e A3) e implantação (grupos B1, B2 e B3). Os animais foram sedados e expostos ao ultra-som terapêutico de freqüência 3 MHz e intensidade de 0,6 W/cm2 (SATA), por 5min. Os grupos A1 e B1 receberam ondas pulsadas; os grupos A2 e B2, ondas contínuas e os grupos A3 e B3 ultra-som simulado. As ratas foram eutanasiadas no 20o dia pós-inseminação. No sangue coletado procedeu-se à análise do hematócrito, da hemoglobina, dos leucócitos totais, do aspartato aminotransferase (AST/TGO), da alanina aminotransferase (ALT/TGP), do colesterol, dos triglicérides e da creatinina. Posteriormente, os animais foram submetidos à autópsia para identificação de lesões de órgãos internos, remoção e pesagem de fígado, rins e ovários. Foram contados os fetos vivos, malformados, mortos e reabsorvidos; seus cérebros, pulmões, fígados, rins e placentas foram pesados. Os dados obtidos foram analisados por ANOVA - uma via - seguida de teste de Dunnett. Dados não paramétricos foram submetidos aos testes do Qui quadrado ou Kruskall Walis. A hipótese nula foi rejeitada quando p< 0,05. Nas mães não foram observadas alterações de peso corporal e de órgãos, nem da capacidade reprodutiva. Nos fetos o peso relativo do coração, fígado, pulmão e dos rins aumentou no grupo A2; no grupo B2 o coração e o cérebro tiveram seu peso aumentado, e o peso da placenta diminuiu no grupo B1. Em conclusão, no modelo experimental usado, não foram observados efeitos tóxicos do ultra-som sobre o organismo materno, exceto pelo aumento dos triglicerídeos. O ultra-som pulsado no período de pré-implantação não alterou os fetos, mas as ondas contínuas induziram aumento do peso relativo do coração, fígado, dos pulmões e rins. No período de implantação, o ultra-som pulsado causou diminuição do peso da placenta, e as ondas contínuas acarretaram aumento do peso absoluto do cérebro e do coração fetais. / Therapeutic ultrasound is widely used in different aesthetic treatment by young women, who can be irradiated during early gestation. Researches regarding the effects of therapeutic ultrasound on gestation present controversial results. Methodologies incompatible with clinical aspects are used and different methods and technics were employed. However none of them were reproduced in two similar works and only a few observed the early gestation, period when pregnancy is commonly unnoticed. The ultrasound causes increased cell membrane permeability, alterations in ionic diffusion, vasodilation; modifies the intra and extracellular particles position and alter the normal configuration of cells, leading to functional alterations. During early embryo development, cells depend upon protein synthesis and on sinalizations triggered by sodium and potassium channels. Furthermore the participation of microtubules and microfilaments on morphogenesis are extremely important. All this indicates the exposition to ultrasound could cause lesions on the conceptus. In the present work the effects of therapeutic ultrasound with pulsed and continous waves during early pregnancy of the rat were assesed. The methodology consisted in rats exposition to ultrasound in two periods: preimplantion (groups A1, A2 and A3) and implantation (groups B1, B2 and B3). The animals were sedated and exposed to therapeutic ultrasound, frequence of 3 MHz, intensity of 0.6 W/cm2 (SATA), during five minutes. Groups A1 and B1 received pulsed waves, groups A2 and B2 received continuous waves whereas the groups A3 and B3 were sham-exposed. The rats were euthanatized by an overdose of anesthesic 20 days after insemination. The hematocrit, hemoglobin, total leukocytes, and the level of aspartate aminotransferases, alanine transaminase, cholesterol, triglycerides and creatinine were analysed. The dams underwent authopsy for the identification of lesions in the internal organs and removal and weghing of the liver, kidneys and ovaries. The number of resorptions, live, dead and malformed fetuses were counted. The fetal brain, lungs, liver, kidneys and placentae were weighed. The data were processed using the one-way analysis of variance (ANOVA) followed by Dunnett's test. Non parametric data were analyse using the Chi-Square or Kruskal-Wallis tests. The null hyphotesis was reject when p< 0.05. No alterarions were detected on body and maternal organs’ weights, and reproductive performance. The relative weights of heart, liver, kidneys and lungs were higher in group A2. Heart and brain were heavier in group B2, and the weight of placentae decreased in group B1. In conclusion, in the experimental model used, the ultrasound showed no toxic effects on the maternal organism, except for the increased triglyceride levels. The pulsed -wave ultrasound presented no fetal toxic effects on the preimplantation period, but the continuous waves induced an increase on the relative weights of heart, liver, kidneys and lungs. During the implantation period, the pulsedwave ultrasound caused a decrease in placentae weights, and the continuous waves induced an increased on the aboslute weights of fetal brain and heart.

Charles University, Faculty of Pharmacy, Hradec Králové Department: Department of Pharmacognosy Head of thesis: doc. PharmDr. Lenka T mová, Csc. Student: Bc. Rut Łu ská Title of the thesis: Teratogenic drugs The aim of this diploma thesis is to give an overview of teratogenic drugs. The work approaches the problems of teratogenesis, factors affecting teratogenicity, distribution of teratogens, classification of medication in pregnancy and methods of teratogenicity study. An overview of teratogenic plants broken down by family with manifestation of teratogenicity and substances responsible for teratogenicity is given here. Most teratogenic plants were found in the Fabacae, Compositae and Lamiacae families. Alkaloids and terpenes are most often responsible for teratogenic effects. In addition, the work focuses on the negative effects of cannabis, tobacco smoking and caffeine on the course of pregnancy. Keywords: teratogen, medicinal plant, drug, pregnancy

In two separate experiments, weight adjusted doses of nocodazole and acrylamide were injected intraperitoneally at various time intervals into twelve week old female mice. Within the nocodazole experiment, the doses were injected at varying time intervals before and after mating. On day seventeen of gestation, the female mice were sacrificed and their uterine contents examined. Nocodazole induced a significant increase in reproductive pathology per total implants when administered one hour after mating to the (SECxC57BL)F, stock: 5.00% total deads, 70.23% moles, and 3.41% abnormal fetuses. Acrylamide treatment produced a significant reduction in live births when administered six hours after mating: 50.86% moles and 46.46% living fetuses per total implants.

No description available.

Student Number : 9502128Y - MSc dissertation - School of Anatomical Sciences - Faculty of Science / Retinoic acid, the active metabolite of Vitamin A is known to play a major role in embryonic growth and differentiation during development. It has been shown that either excess or deficiency of retinoic acid during embryogenesis can be teratogenic. In order to study the teratogenic effects of retinoic acid, the aim of the present study was therefore to investigate the effect of all-trans retinoic acid on the migration and fate of neural crest cells in vitro and in vivo. In addition, the study investigated the effect of retinoic acid on the cytoskeletal elements of neural crest cells and on Rac and Rho, two members of the Rho family of GTPases. The neural tubes containing neural crest cells of quail embryos were removed at cranial levels and cultured on fibronectin as a substrate. The neural tubes were cultured in either Dulbecco’s minimal essential medium (DMEM) or in DMEM+Dimethylsulphoxide (DMSO) as controls. In order to test the effect of retinoic acid, the neural tubes were cultured in 10-5M all-trans retinoic acid (RA) which was reconstituted in DMSO. The distance of migration of the cultured quail neural crest cells was measured and compared between the controls and the experimentals. To study the effect of RA on the cell actin cytoskeleton in vitro, cultured neural crest cells were stained with rhodamine phalloidin. In addition, following 24 hours of culture, the quail neural crest cells were brought into suspension and micro-injected into 36 hour-old chick hosts. While the migration of neural crest cells was extensive in the control cultures in vitro, migration was inhibited in the retinoic acid-treated neural crest cells. In addition, retinoic-acid treated neural crest cells showed pigmentation and neuronal processes earlier than did the control neural crest cells. Retinoic acid-treated neural crest cells showed a disarray of the cytoskeletal elements as they were devoid of stress fibres and focal adhesions. In addition, retinoic acid appears to decrease the expression of Rac and Rho of cultured quail neural crest cells. Following micro-injection of cultured control and RA-treated quail neural crest into the cranial region of chick hosts, the control cells populated the beak area, whereas the retinoic acid-treated quail neural crest cells migrated to the retina of the eye, a region they normally do not populate. These results suggest that retinoic acid disturbs the migration of neural crest cells. It appears to do this by affecting the cytoskeletal elements of neural crest cells and the genes that are involved in forming these elements.

Methamphetamine (MA) is a well-known, easily accessible and powerful psychostimulant, and its abuse has become a global problem. MA abuse affects millions of people worldwide and places an enormous burden on public healthcare resources. Documented consequences of MA abuse include cardiotoxic, neurotoxic and teratogenic effects, as well as long-term consequences of chronic abuse including affective disorders such as schizophrenia and major depressive disorder (MDD). MDD is a highly prevalent mood disorder in both adults and children, documented to contribute to approximately 850 000 suicides annually. This disorder is projected to become the 2nd leading disease of global burden by 2020, preceded only by ischemic heart disease. Depressive-like behaviour is documented as a symptom of chronic MA abuse and particularly during extensive MA withdrawal. Also, MA abuse during pregnancy is documented to cause neurodevelopmental changes that persist into later life. However, current understanding thereof is limited and warrants further investigation of the effects of early-life exposure to MA on outcome in adulthood, particularly in terms of mood disorders. The aim of the current study was to determine the effect of chronic exposure to MA on the depressive-like behaviour later in life in stress-sensitive (Flinders Sensitive Line) and control (Flinders Resistant Line) rats. Rats were exposed during one of the following natal day (ND) age groups: prenatal (ND-13 to ND+02), postnatal (ND+03 to ND+18), prepuberty (ND+19 to ND+34) or puberty (ND+35 to ND+50). These age groups represent different stages in neurodevelopment, as also seen in humans. For prenatal exposure, pregnant dams received 5 mg/kg daily subcutaneously (s.c.), and pups from postnatal, prepuberty and puberty age groups received an escalating dose regimen to simulate “binge-dosing” commonly seen in humans abusing MA. After MA exposure, rats were housed normally until behavioural testing on postnatal day 60 (ND+60), which included the novel object recognition test (NOR), open field test (OFT) and forced swim test (FST), measuring cognitive function, locomotor activity and depressive-like behaviour respectively. The FST data showed increased immobility behaviour of saline-treated FSL rats relative to that of FRL rats, in line with previous data validating FSL rats as a genetic rodent model of depression. Practically significant MA-induced increases in immobility behaviour were observed in all FSL and FRL treatment groups in the FST, reaching statistical significance in prenatally treated FRL rats, and in postnatally, prepuberty and puberty treated FSL rats. The data suggest that early-life MA exposure may alter neurodevelopment to predispose the rats to display depressive-like behaviour in early adulthood, and suggests that this detrimental effect of MA may be more expressed in stress-sensitive rats. Furthermore, all FSL groups plus prenatally and puberty treated FRL rats revealed practically and statistically significant decreases in swimming behaviour in the FST, whereas decreases in swimming behaviour in prepuberty treated FRL rats were practically significant but did not reach statistical significance. These data suggest that MA-induced depressive-like behaviour in FSL rats may be related to impaired serotonergic neurotransmission, and that this appears to be more robust in FSL rats. Climbing behaviour in the FST was generally not altered by early-life MA exposure, with a notable exception being a practically and statistically significant increase in puberty treated FRL rats. These data suggest that in general early-life MA exposure does not affect noradrenergic neurotransmission in early adulthood, except when normal rats were treated at puberty. The reason for the latter observation is not clear. The data from the NOR test revealed no discernible trends of MA-induced effects on memory and cognition, except for a small albeit practically significant increase in exploration time in prepuberty treated FRL rats and a practically and statistically significant decrease in exploration time in puberty-treated FRL rats. Lastly, locomotor activity in the OFT was mostly unaffected by MA treatments, except for practically significant decreases in locomotor activity in postnatally-and prepuberty-treated FRL rats and practically and statistically significant decreases in locomotor activity of prepuberty treated FSL rats. Altered locomotor activity is therefore not expected to explain any of the immobility results of the FST. In final conclusion, the study confirms that early-life MA exposure results in a depressogenic effect later in life in stress-sensitive (FSL) and control (FRL) rats, but appears to be more robust in stress-sensitive animals. Furthermore the data suggest that long-lasting MA-induced depressogenic effects may relate to impaired serotonergic neurotransmission. / MSc (Pharmacology), North-West University, Potchefstroom Campus, 2014

Methamphetamine (MA) is a well-known, easily accessible and powerful psychostimulant, and its abuse has become a global problem. MA abuse affects millions of people worldwide and places an enormous burden on public healthcare resources. Documented consequences of MA abuse include cardiotoxic, neurotoxic and teratogenic effects, as well as long-term consequences of chronic abuse including affective disorders such as schizophrenia and major depressive disorder (MDD). MDD is a highly prevalent mood disorder in both adults and children, documented to contribute to approximately 850 000 suicides annually. This disorder is projected to become the 2nd leading disease of global burden by 2020, preceded only by ischemic heart disease. Depressive-like behaviour is documented as a symptom of chronic MA abuse and particularly during extensive MA withdrawal. Also, MA abuse during pregnancy is documented to cause neurodevelopmental changes that persist into later life. However, current understanding thereof is limited and warrants further investigation of the effects of early-life exposure to MA on outcome in adulthood, particularly in terms of mood disorders. The aim of the current study was to determine the effect of chronic exposure to MA on the depressive-like behaviour later in life in stress-sensitive (Flinders Sensitive Line) and control (Flinders Resistant Line) rats. Rats were exposed during one of the following natal day (ND) age groups: prenatal (ND-13 to ND+02), postnatal (ND+03 to ND+18), prepuberty (ND+19 to ND+34) or puberty (ND+35 to ND+50). These age groups represent different stages in neurodevelopment, as also seen in humans. For prenatal exposure, pregnant dams received 5 mg/kg daily subcutaneously (s.c.), and pups from postnatal, prepuberty and puberty age groups received an escalating dose regimen to simulate “binge-dosing” commonly seen in humans abusing MA. After MA exposure, rats were housed normally until behavioural testing on postnatal day 60 (ND+60), which included the novel object recognition test (NOR), open field test (OFT) and forced swim test (FST), measuring cognitive function, locomotor activity and depressive-like behaviour respectively. The FST data showed increased immobility behaviour of saline-treated FSL rats relative to that of FRL rats, in line with previous data validating FSL rats as a genetic rodent model of depression. Practically significant MA-induced increases in immobility behaviour were observed in all FSL and FRL treatment groups in the FST, reaching statistical significance in prenatally treated FRL rats, and in postnatally, prepuberty and puberty treated FSL rats. The data suggest that early-life MA exposure may alter neurodevelopment to predispose the rats to display depressive-like behaviour in early adulthood, and suggests that this detrimental effect of MA may be more expressed in stress-sensitive rats. Furthermore, all FSL groups plus prenatally and puberty treated FRL rats revealed practically and statistically significant decreases in swimming behaviour in the FST, whereas decreases in swimming behaviour in prepuberty treated FRL rats were practically significant but did not reach statistical significance. These data suggest that MA-induced depressive-like behaviour in FSL rats may be related to impaired serotonergic neurotransmission, and that this appears to be more robust in FSL rats. Climbing behaviour in the FST was generally not altered by early-life MA exposure, with a notable exception being a practically and statistically significant increase in puberty treated FRL rats. These data suggest that in general early-life MA exposure does not affect noradrenergic neurotransmission in early adulthood, except when normal rats were treated at puberty. The reason for the latter observation is not clear. The data from the NOR test revealed no discernible trends of MA-induced effects on memory and cognition, except for a small albeit practically significant increase in exploration time in prepuberty treated FRL rats and a practically and statistically significant decrease in exploration time in puberty-treated FRL rats. Lastly, locomotor activity in the OFT was mostly unaffected by MA treatments, except for practically significant decreases in locomotor activity in postnatally-and prepuberty-treated FRL rats and practically and statistically significant decreases in locomotor activity of prepuberty treated FSL rats. Altered locomotor activity is therefore not expected to explain any of the immobility results of the FST. In final conclusion, the study confirms that early-life MA exposure results in a depressogenic effect later in life in stress-sensitive (FSL) and control (FRL) rats, but appears to be more robust in stress-sensitive animals. Furthermore the data suggest that long-lasting MA-induced depressogenic effects may relate to impaired serotonergic neurotransmission. / MSc (Pharmacology), North-West University, Potchefstroom Campus, 2014

The amphibian decline phenomenon now involves in excess of a third of the roughly 6000 species of amphibians on the planet. The problems that drive the declines are diverse with no end in sight. The Amphibian Conservation Action Plan (ACAP) aims to stem amphibian decline through four recommended actions by researchers and conservation biologists: (1) Expand scientific understanding of amphibian declines and extinctions; (2) continue to document amphibian diversity and ecology and how they are changing; (3) develop and implement long-term conservation programs; (4) prepare emergency response actions for eminent crises. This Dissertation focused on two of those recommendations: expanding scientific understanding of amphibian declines and extinctions and continuing to document amphibian diversity and ecology and how they are changing. The first chapter is a review of the amphibian decline phenomenon. The second, third, and fourth chapters focus on expanding scientific understanding of amphibian diversity and ecology with the description of a formerly unknown species (chapter 2), and ecological papers on two poorly known species (chapters 3 and 4). Chapter five focuses on the first ACAP recommendation in improving scientific understanding of the causes behind amphibian decline. The chapter is an experimental examination of two related species and their developmental reactions to common heavy metal contaminants. The goal of this Dissertation is to contribute toward the general amphibian knowledge base relative to the recommendations of ACAP.

Previous research has shown a relationship between prenatal teratogenic exposure and impaired cognitive functioning. However, data regarding the long-term outcome of prenatal teratogenic exposure are minimal. The present study investigated the long-term neuropsychological functioning (specifically attention and memory) of adults prenatally exposed to alcohol or phenylalanine, and examined whether there was evidence to suggest that there are effects specific to individual teratogens. Using a battery of attention and memory measures the performance of 17 adults diagnosed with Fetal Alcohol Syndrome (FAS) and 13 adults with Maternal Phenylketonuria Syndrome (MPKUS) was assessed. In order to identify the pattern of deficits associated with prenatal teratogenic exposure, an age and CA and IQ matched control group was assessed. Attention was broadly assessed using Mirsky et al.'s (1991) neuropsychological model of attention. The memory and learning tests administered included a number of well standardized measures of verbal learning, verbal and visual recall, delayed recall, and recognition. Paired comparisons between the FAS group and age and CA and IQ matched controls indicated a unique pattern of attention and memory deficits consistent with previous research with children and adolescents. Specifically, adult individuals with FAS appear to have deficits in acquisition of new material, delayed recall of verbal material and in response inhibition. Paired comparisons between the MPKUS group and CA and IQ matched controls indicated that the pattern of attention and memory deficits seen in adults with MPKUS is difficult to distinguish when the effect of IQ is removed. A randomized block design using IQ as the blocking variable and group (FAS, MPKUS, or Controls) as the treatment variable was utilized to examine the question of whether the two prenatal teratogen groups differ from one another and from Controls in terms of attention and memory ability. Ten blocks of three participants (FAS, MPKUS and Control) matched on IQ were formed. The randomized block analyses revealed few differences between the groups and failed to reveal a number of the differences found in the paired comparisons between the prenatal teratogen groups and the CA and IQ matched Control group. Possible reasons for these differences are discussed.