A Doença de Wilson (DW) é uma moléstia hereditária, caracterizada pela deficiência de excreção do cobre pelo fígado devido à mutação do gene A TP7B. O distúrbio do olfato ocorre com frequência em doenças neurodegenerativas como na doença de Parkinson (DP) e na doença de Alzheimer (DA). A análise do olfato tem sido utilizada como um instrumento útil no diagnóstico diferencial das diversas formas de parkinsonismo degenerativo, e, especialmente, na diferenciação entre DP e tremor essencial. O diagnóstico precoce na DW é a chave para o sucesso do tratamento. Na hipótese de haver comprometimento do olfato em fases iniciais da doença, esse poderia ser um dado a mais para auxiliar no diagnóstico. Até o presente, há apenas um estudo relacionando a DW com a disfunção do olfato. O objetivo deste estudo foi avaliar o olfato em um grupo de pacientes com DW e confrontar com grupo- controle. No presente estudo, foram analisados 37 portadores de DW com manifestação neurológica, 24 portadores de DW sem manifestação neurológica e 59 controles. Todos os indivíduos foram analisados com relação à idade, ao gênero, ao grau de escolaridade, ao uso de tabaco e ao miniexame do estado mental (MEEM), e os portadores de DW foram avaliados quanto ao tempo de doença, tratamento medicamentoso e escore neurológico. O olfato foi avaliado por meio do teste de identificação de odor 8niffin\' 8ticks (88-16 canetas numeradas e quatro opções de resposta para cada uma). Vinte e quatro indivíduos eram pacientes da DW sem manifestação neurológica (45,83% do gênero feminino) e 37 pacientes apresentavam manifestações neurológicas (56,76% do gênero masculino). O qrupo-controle foi composto por 59 indivíduos, 35 (59,33%) do gênero masculino. As médias de- idade foram de 33,38 ± 9,79 anos no grupo de portadores de DW com manifestação neurológica; 29 ± 9,61 anos no grupo de portadores de DW sem manifestação neurológica e 33,81 ± 10,67 anos no grupo-controle. Todos os pacientes com DW estavam em tratamento: 47(77%) com penicilamina, 7 (11,5%) com trientine e 7 (11,5%) com sais de zinco. As médias de respostas corretas no teste de identificação do odor 88-16 foram: 12,03 ± 2, 21 no grupo de portadores de DW com manifestação neurológica, 12, 15 ± 2,07 no grupo de portadores de DW com manifestação hepática e 12,70 ± 2,03 para o grupo- controle. Na avaliação objetiva do olfato com o teste de identificação do odor SS-16, não foi evidenciada diferença significativa entre os três grupos analisados, mas observou-se que o MEEM e o grau de escolaridade influenciaram significativamente no escore do 88-16 na comparação do grupo de pacientes com DW com manifestação neurológica com os outros dois grupos (grupo-controle e o grupo de portadores de DW com manifestação hepática). No presente estudo, não foi evidenciada disfunção olfatória nos pacientes com DW, mas foi observada diminuição da percepção do olfato em alguns pacientes com DW (com e sem manifestação neurológica). Em relação à disfunção olfatória evidenciada em alguns pacientes com DW na presente análise, algumas considerações são pertinentes e poderiam ter influenciado na identificação do olfato neste grupo de pacientes com DW. O acúmulo de cobre e a produção de radicais livres no sistema nervoso central (SNC) podem desencadear processos de neurodegeneração em estruturas envolvidas no olfato, alterações metabólicas, acúmulo de substâncias neurotóxicas (amônia e manganês) e alterações de neurotransmissores, e contribuir para o surgimento da disfunção olfatória / Wilson\'s disease (WO) is a hereditary disease due to a mutation in ATP7B gene, characterized by deficiency of copper excretion by the liver. Smell disorders are frequently encountered in neurodegenerative diseases, such as Parkinson\'s disease (PO) and Alzheimer\'s disease (AO). Smell analysis has been a useful tool for the differential diagnosis of several forms of degenerative parkinsonism, and especially for the differentiation between PO and essential tremor. Early diagnosis in WO is the key for a successful treatment. If there were smell impairment in the early stages of the illness, it could be used as another clue to help on its diagnosis. To the present date, there is only one study connecting WO with smell problems, the aim of this study was to evaluate smell function in a group of WO patients and compare them with a control group. We analyzed 37 WO patients with and 24 WO patients without neurologic symptoms, and 59 controls. Ali subjects were evaluated regarding age, gender, schooling, tobacco use, Mini Mental State Examination (MMSE), and the WO patients were also evaluated regarding duration of the illness, medication and neurologic scoring. Smell was analyzed by means of Sniffin\' Sticks smell identification test (SS-16 numbered pens and four options of answer for each pen). Twenty-four subjects with WO had no neurologic symptoms (45.83% female), and 37 patients had neurologic impairment (56,76% male). The control group was composed by 59 individuais, 35 (59,33%) male. Their age average were 33,38 ± 9,79 years for WO neurologic symptoms; 29 ± 9,61 years for WO without neurologic symptoms; and 33,81 ± 10,67 years for the control group. Ali WO patients were on treatment: 47(77%) with penicillamine, 7(11,5%) with trientine, and 7(11,5%) with zinc salt formulations. The average of correct answers in the SS-16 were: 12,03 ± 2,21 for the WO with neurologic symptoms group; 12,15 ± 2,07 for the WO without neurologic symptoms; and 12,70 ± 2,03 for the control group. In the smell testing with SS-16, there was no significant difference among the three groups, but the MMSE scoring and schooling had a significant influence over SS-16 score when comparing WO with neurologic symptoms patients with the other groups (WO patients without neurologic symptoms and control group). There was no smell dysfunction in WO patients in this study, but diminished smell perception was observed in some WO patients (either with or without neurologic impairment). Regarding smell impairment observed in some WO patients in the current analysis, some considerations must be made that could have influenced smell identification in these individuais. Copper accumulation and free radicais production in the central neNOUS system can trigger neurodegeneration processes in structures involved in srnell perception, metabolic impairment, building up of neurotoxic substances (such as ammonia and manganese), and neurotransmitter disorders, contributing to the emergence of srnell dysfunction

A doença de Wilson, moléstia hereditária, caracteriza-se pela deficiência de excreção de cobre pelo fígado, originária da mutação do gene ATP7B. As manifestações neurológicas na doença de Wilson são pleomórficas, observando-se distúrbios do movimento com início insidioso e em idade variável - geralmente na segunda ou terceira décadas de vida. Este estudo, dividido em duas partes, descreve as manifestações neurológicas iniciais em 119 pacientes com doença de Wilson (93 casos-índice e 26 familiares acometidos), avaliados entre 1963 e 2004 dos quais 109 foram através de análise retrospectiva dos prontuários médicos, enquanto aos 10 pacientes restantes se dispensou avaliação clínica prospectiva, a partir de 2002. O início dos sintomas ocorreu na média etária dos 19,4 anos (7-37), e o tempo médio do surgimento dos sintomas ao diagnóstico de 1,1 +/- 1,2 anos (0-5 anos). Entre as manifestações neurológicas mais freqüentes, observaram-se: disartria (91%), distúrbios da marcha (75%), risus sardonicus (72%), distonia (69%), rigidez (66%), tremor (60%) e disfagia (50%). A incidência das manifestações coréia e atetose, 16% e 14%, respectivamente, foi baixa. Manifestações atípicas incluíram convulsões (4,2%) e sinais piramidais (3%). A segunda parte do estudo trata da investigação do genótipo ATP7B em 41 pacientes e suas possíveis correlações com o fenótipo neurológico. Encontraram-se 23 mutações distintas, a mais comum das quais (p.A1135fs) com freqüência alélica de 31,7%. Expressiva associação (p<0,05) se deu entre essa mutação e a manifestação disfagia, ainda que limitada por amostra restrita de pacientes. Também sugestiva foi a associação entre a mutação p.A1135fs e quadros neurológicos precoces e graves. Este é o primeiro estudo a comparar o genótipo ATP7B com as manifestações neurológicas na doença de Wilson / Wilson disease, a rare inborn metabolic error, is characterized by deficient hepatic copper excretion, due to mutations in ATP7B gene. Neurological manifestations may vary, although there is commonly a movement disorder starting in the second or third decade of life. This study is divided in two parts, and it describes the neurological manifestations in 119 patients with Wilson disease (93 index cases and 26 affected family members), which were seen between 1963 and 2004 a retrospective analysis in 109 medical records and prospective clinical evaluation in 10 patients since 2002. The average age of symptoms onset was 19.4 years (ranging from 7 - 37 years), and the mean time between the first symptom and diagnosis was 1, 1 +/- 1, 2 years. The most frequent neurological manifestations observed were: dysarthria (91%), gait disturbance (75%), risus sardonicus (72%), dystonia (69%), rigidity (66%), tremor (60%), and dysphagia (50%). Less frequent manifestations were chorea (16%), and athetosis (14%). Rare neurological presentations were seizures (4,2%), and pyramidal signs (3%). In the second part of this study, we ascertain ATP7B genotype correlations with distinct neurological phenotypes in 41 Wilson disease patients. A total of 23 distinct mutations were detected, and the p.A1135fs frameshift had the highest allelic frequency (31.7%). An association between a p.A1135fs mutation and dysphagia was detected (p<0, 05), but the limited number of patients restricts valuable conclusions. This analysis also suggests an association between this mutation and early and severe neurological presentation. This present study is the first one to evaluate an ATP7B genotype correlation with specific neurological profile in Wilson disease

Submitted by Fabíola Silva (fabiola.silva@famerp.br) on 2017-03-01T19:46:36Z No. of bitstreams: 1 rogeriodelarco_dissert.pdf: 1300532 bytes, checksum: 8f79b58857fc2ea4ac77633ad6fd6445 (MD5) / Made available in DSpace on 2017-03-01T19:46:36Z (GMT). No. of bitstreams: 1 rogeriodelarco_dissert.pdf: 1300532 bytes, checksum: 8f79b58857fc2ea4ac77633ad6fd6445 (MD5) Previous issue date: 2014-08-21 / Introduction. Chronic pain in leprosy plays an important role for being responsible for the physical and psychological suffering that produces. Objectives: To identify the difficulties in diagnosing and treating neuropathic pain caused by Leprosy, as well as to investigate the main determinants of neuropathic pain. Methods: Eighty-five patients who completed treatment for leprosy with MDT/WHO were evaluated for neuropathic pain using the Douleur Neuropathic 4 test (DN4). A detailed questionnaire and neurological examination were employed to complement the results. Results: Forty-eight patients were excluded because they did not have pain at the time of this study. Of the 37 patients with pain, 22 (59.5%) reported neuropathic or mixed pain and 70.8% characterized their pain as moderate or severe; 81.8% had suffered with pain for more than 6 months. Only 12 (54.5%) patients had been diagnosed with the symptom and so the problem had not been identified in almost half of the cases (10; 45.5%). Of the 12 patients on medications for neuropathic pain, only 5 (41.6%) stated that it had improved with the pain of the other 7 patients (58.4%) remaining the same or getting worse. The difference in the improvement of pain between treated (n = 12) and untreated patients (n = 10) was significant (p-value = 0.020). Conclusion: Neuropathic pain is an important cause of suffering for patients with leprosy and is still neglected by the medical team because of difficulties to diagnose it. The appropriate recognition and treatment of this condition may relieve symptoms and improve the quality of life of patients. / Introdução: A dor crônica em hanseníase tem um papel importante por ser responsável pelo sofrimento físico e psicológico que produz. Objetivos: Avaliar a presença e as características de dor neuropática nas pessoas que tiveram hanseníase. Casuística e métodos: Oitenta e cinco (n=85) pacientes que completaram tratamento para hanseníase com PQT/OMS foram avaliados para dor neuropática por meio do teste Douleur Neuropathic 4 (DN4). Criterioso questionário e exame neurológico foram aplicados para complementar os dados. Resultados: Quarenta e oito pacientes foram excluídos por não apresentarem dor ou por se referirem a ela apenas no passado. Dos 37 pacientes com dor confirmou-se que 22 (59,5%) tinham dor neuropática ou mista e destes, 70,8% caracterizavam esta dor como de intensidade moderada ou grave, sendo que 81,8% sofriam por um período maior que 6 meses. Apenas 12 (54,5%) pacientes haviam sido diagnosticados com o problema e quase metade dos casos – 10 (45,5%) ainda estavam sem reconhecimento. Quanto ao tratamento medicamentoso (n=12) para a dor neuropática, apenas 5 (41,6%) responderam que tiveram melhora, os outros 7 (58,4%) ficaram igual ou pioraram comparado ao quadro inicial. A análise estatística comparando a melhora da dor entre os tratados – 12 pacientes, e os não tratados – 10 pacientes é significante (valor de p = 0,020). Conclusão: A dor neuropática é causa importante de sofrimento no paciente com hanseníase e mesmo assim é negligenciada pela equipe médica que tem dificuldade em diagnosticá-la. O adequado reconhecimento e tratamento desta condição podem aliviar sintomas e melhorar a qualidade de vida destes pacientes.

Submitted by Erika Demachki (erikademachki@gmail.com) on 2017-01-04T19:50:51Z No. of bitstreams: 2 Dissertação - Thaís Bandeira Riesco - 2016.pdf: 4442276 bytes, checksum: fac73acc016bbd502cb80be355adc09d (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) / Approved for entry into archive by Luciana Ferreira (lucgeral@gmail.com) on 2017-01-05T10:04:44Z (GMT) No. of bitstreams: 2 Dissertação - Thaís Bandeira Riesco - 2016.pdf: 4442276 bytes, checksum: fac73acc016bbd502cb80be355adc09d (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) / Made available in DSpace on 2017-01-05T10:04:44Z (GMT). No. of bitstreams: 2 Dissertação - Thaís Bandeira Riesco - 2016.pdf: 4442276 bytes, checksum: fac73acc016bbd502cb80be355adc09d (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Previous issue date: 2016-12-09 / Introduction: Toxoplasma gondii is the etiological agent of a parasitic parasitic disease of universal distribution, with infected individuals in all countries. The main forms of contagion are through the ingestion of different parasite evolutionary forms present in raw meats or undercooked, unfiltered water, unpasteurized milk, contaminated soil handling and contact with infected cats. Clinical disease is less frequent and the most severe forms can be found when congenital transmission occurs and in immunocompromised patients. When the fetus touches this infectious agent and survive, it can present several problems such as: restriction in the intrauterine growth, premature birth, microcephaly, hydrocephalus, brain calcifications, pneumonitis, hepatosplenomegaly, skin rash, intellectual disability, among others. The consequences to the fetus are higher in the first trimester of pregnancy and the transmissibility in the third trimester is the highest. The degree of commitment of the newborn will depend on the gestational period in the moment of the first transmission of the illness and the pregnant woman. Objective: The objectives of this study were to evaluate perceptible alterations in the neuropsychomotor examination and in anthropometric measures of newborns (RNs) of chronically infected mothers by Toxoplasma gondii. Methods: The study was performed in a population of 79 children of puerperal mothers, 41 of them were children of mother with infection of toxoplasmosis and 38 were children of not infected mother by the protozoan. It was made out a sociodemographic interview with these mothers through a questionnaire and an examination of primitive reflexes in their respective children. The study was conducted in one maternity of standard for risk pregnancy, in the city of Goiânia, Goiás, in the period from June 2015 to June 2016. The analysis were performed with the aid of the statistical package SPSS®, version 23. The serologic testing for confirmation of toxoplasmosis infection and absence of anti-T gondii in the mothers serum was made by Immunoassay of Microparticles by Chemiluminescense (CMIA). Results: Neuropsychomotor examination the absence of reflection escape the suffocation was found in two children of chronically infected mothers. In the comparison of the thoracic perimeter and the cephalic perimeter 31/79 children were classified as inadequate and two children of mothers chronically infected were too small for their gestational age. Conclusion: In relation to the neuropsychomotor examination and anthropometric measurements, in the group of newborn of puerperal mothers chronically infected by Toxoplasma gondii could not detect any perceptible alterations when in comparison to the control group of susceptible mothers. / Introdução: Toxoplasma gondii é o agente etiológico de uma parasitose de distribuição universal, com indivíduos infectados em todos os países. As principais formas de contágio são através da ingestão de diferentes formas evolutivas do parasito presentes em carnes cruas ou mal cozidas, água não filtrada, leite não pasteurizado, manipulação de terra contaminada e convívio com gatos infectados. A doença clínica é pouco freqüente e as formas mais graves podem ser encontradas quando ocorre a transmissão congênita e em pacientes imunocomprometidos. Quando o feto entra em contato com esse agente infeccioso e sobrevive pode apresentar inúmeros problemas como: restrição de crescimento intrauterino, nascimento prematuro, microcefalia, hidrocefalia, calcificações cerebrais, pneumonite, hepatoesplenomegalia, erupção cutânea, retardo mental, entre outros. As conseqüências para o feto são mais graves no primeiro trimestre de gestação, e a transmissibilidade no terceiro trimestre é mais elevada. O grau de comprometimento do recémnascido irá depender da fase em que a gestação se encontrava no momento do primeiro contágio da gestante com o parasito. Objetivos: Os objetivos deste estudo foram avaliar alterações perceptíveis no exame neuropsicomotor e nas medidas antropométricas de recém-nascidos (RNs) de mães cronicamente infectadas pelo Toxoplasma gondii. Métodos: A população do estudo foi composta por 79 filhos de puérperas, os quais 41 eram filhos de mães com toxoplasmose crônica e 38 filhos de mães não infectadas pelo protozoário. Foi realizada uma entrevista sociodemográfica com essas mães através de um questionário e um exame de reflexos primitivos em seus respectivos filhos. O estudo foi realizado em uma maternidade de referência para gestações de risco, na cidade de Goiânia, Goiás, no período de junho de 2015 a junho de 2016. As análises foram realizadas com o auxílio do pacote estatístico SPSS ®, versão 23. O teste sorológico para confirmação da toxoplasmose infecção e ausência de anticorpos anti-T gondii no soro das mães foi feito por Imunoensaio de Micropartículas por Quimioluminescência (CMIA). Resultados: No exame neuropsicomotor a ausência do reflexo de fuga ao sufocamento foi encontrada em duas crianças filhas de mães cronicamente infectadas. Na comparação entre perímetro torácico e perímetro cefálico 31/79 crianças foram classificadas como inadequadas e duas crianças de mães cronicamente infectadas estavam pequenas para a idade gestacional. Conclusão: Em relação ao exame neuropsicomotor e as medidas antropométricas no grupo de recém-nascidos filhos de puérperas cronicamente infectadas pelo Toxoplasma gondii não foi possível detectar alterações perceptíveis quando em comparação ao grupo controle de mães suscetíveis.

Long-chain polyunsaturated fatty acids (LCPUFA) are essential for proper neural and retinal development in many mammalian species. One objective of this research was to investigate the effects of dietary &#945;-linolenic acid (ALA) and LCPUFA on the fatty acid composition of canine plasma phospholipids (PL) and milk during the gestation and lactation periods. The fatty acid composition of plasma PL and the retinal development of puppies reared on the same experimental diets as their mothers were also investigated. Enriching the canine gestation/lactation diet with ALA (6.8% DM) does not result in enrichment of docosahexaenoic acid (DHA) in the milk. From this data it can be inferred that peroxisomal elongation and desaturation of LCPUFA does not occur in canine mammary tissue. Dose responses of linoleic acid (LA), ALA and DHA were observed in the plasma of adult dogs during gestation and lactation and in puppies during both the suckling and post-weaning periods. Plasma PL fatty acid data from puppies indicate that canine neonates are capable of synthesizing LCPUFA from ALA, but that plasma enrichment of the newly-synthesized DHA does not compare with that obtained from preformed DHA in the diet. Visual function was assessed via electroretinography (ERG) in 12-wk old canines. One-way ANOVA revealed significantly better visual performance in dogs fed the highest amounts of n-3 LCPUFA. Puppies in this group demonstrated the greatest rod response as measured by the amplitude and implicit time of the a-wave. Neonates reared on the lowest dietary levels of both ALA and n-3 LCPUFA exhibited the poorest visual function. A novel parameter devised in this study was the threshold intensity, which was the initial intensity at which the a-wave was detectable. Again, puppies consuming the greatest concentrations of n-3 LCPUFA responded significantly sooner, i.e. exhibited greater rod sensitivity, than other diet groups. The findings of this research underscore the importance of preformed n-3 LCPUFA in the diet, rather than ALA, as a means of enriching neural tissues in DHA during the developmental period. Moreover, dietary DHA appears to be related to improved visual performance in developing canines.

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 120-128).

 Neuropsychiatric systemic erythematosus (NPSLE) is a complicated complication of systemic erythematosus (SLE). Asian patients are associated with high prevalence of systemic disease and mortality It increases patients’ morbidity and mortality (Samanta et al., 1991). But the detailed pathology and pathogenesis are still remained unclear. Our study’s purpose is to use advanced functional imaging method, including diffusion tensor imaging (DTI) and magnetic resonance spectroscopy imaging (MRSI) to detect intracranial volumetry, functional and other metabolite changes in NPSLE patients. We recruited 3 age-matched female groups, one patient group with NPSLE (20 patients), one patient group with SLE (20 patients) and one control group (15 normal controls). Each patient was applied to structural 3D-T1 and axial T2, DTI and MRSI. Whole brain volumetry and hippocampus volumetry were analyzed by FSL and MARINA software from T1 images. White matter hyperintensity was calculated manually. Whole brain FA and other indices were collected. Regional FA was also collected and was collected with MRS over corpus callosum slice. The result showed no significant whole brain atrophy in NPSLE patients and SLE patients compared with controls. But with segmentation of grey matter, white matter and CSF, NPSLE patients showed significant decrease volume from SLE patients in white matter. Left hippocampus showed significant decreased volume in white matter and grey matter compared with control, while right hippocampus showed significant decreased volume in white matter. No other significant difference was found between NPSLE vs SLE and SLE vs controls. Whole brain FA was significantly decreased in NPSLE compared to SLE and controls, but not significantly different between SLE and controls. MD, λ∥ and λ⊥ were significantly increased in NPSLE and SLE compared with controls, but not significantly different between SLE and controls. White matter hyperintensity score was consistent with MD, λ∥ and λ⊥ results, showed significantly higher scores in two patients groups compared to controls. Regional FA, involving frontal lobes and corpus callosum, periventricular regions adjacent to centrum semiovale and posterior lateral temporal lobe, confirmed the regional FA decrease showed in whole brain FA statistical color map and NPSLE patients’ regional FA decrease correlated with MRS metabolic changes. N-acetyl aspartate (NAA)/ Creatine (Cr), the marker of neurons, decreased significantly in NPSLE patients compared with SLE and controls. Choline (Cho)/Cr showed significant increase of tendency of significant increase in NPSLE and SLE patients in some ROIs compared with controls. Our finding suggested that, although the whole brain atrophy is not obvious in NPSLE, the hippocampus and white matter suffered atrophy in NPSLE patients. These atrophy in white matter of whole brain and hippocampus combined with functional imaging results of DTI and MRS, indicated that NPSLE endured more severe axonal damage than SLE, which might be due to a variety of lesions, such as demyelination, microangiopathy, large vessel thrombosis, cytokine, etc. Varying ratio of NAA/Cr and Cho/Cr may be associated with the severity of axonal damage, probably due to demyelination in the background of inflammatory/ischemic/vasculitic changes. / published_or_final_version / Diagnostic Radiology / Master / Master of Philosophy

Theory of mind is the ability to have mental states about mental states. Among theories concerning the structure and role of theory of mind is the view that theory of mind is the cognitive component of empathy. It is proposed that there is partial dissociation within theory of mind between emotional state representation and non-emotional state representation. In trying to test this hypothesis, an instrument was developed and implemented in a pilot study. Current theory of mind tests are reviewed and design features discussed in relation to the new hypothesis. The instrument aims to measure emotional and non-emotional state representation on separate subscales, as well as coding representations from emotional stories and non-emotional stories separately. The instrument was administered to 33 third level or higher students from the University of KwaZulu-Natal. Groups were chosen from science major (n = 9) and humanities major (n = 24) students. The findings fail to show the group performance patterns reported in literature, for example that humanities students tend to score higher in ToM tests than science students. A number of factors might contribute to the finding, but principally, low sample size and unequal general cognitive ability between groups are proposed as vital. Problems with the pilot study are identified and improvements suggested for subsequent testing. / Thesis (M.A.)-University of KwaZulu-Natal, Durban, 2010.

Thesis (Ph.D). / Written for the Dept. of Human Genetics. Title from title page of PDF (viewed 2009/06/08). Includes bibliographical references.

Thesis (M.S. Ed.) - - Bank Street College of Education, New York, 2005. / Includes bibliographical references and abstract.