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Perreault, Kyle. "The educational implications of childhood onset schizophrenia." Online version, 2008. http://www.uwstout.edu/lib/thesis/2008/2008perreaultk.pdf.
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Ruth, Natasha M. "Childhood-Onset Systemic Lupus Erythematosus: Neurocognitive Function." Cincinnati, Ohio : University of Cincinnati, 2006. http://www.ohiolink.edu/etd/view.cgi?acc_num=ucin1148060762.
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Thesis (M.S.)--University of Cincinnati, 2006.Advisor: Dr. Kim N. Dietrich. Title from electronic thesis title page (viewed June 3, 2009). Includes abstract. Keywords: Systemic Lupus Erythematosus; Neurocognitive Function; ANAM. Includes bibliographical references.
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McGurn, Brian. "Childhood mental ability and late-onset dementia." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/30480.
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Studying late-life cognitive change requires a measure of cognitive ability in early life. The Scottish Mental Survey of 1932 gives a valid measure of childhood mental ability age 11 years, the Moray House Test (MHT). Cases with vascular dementia had a lower MHT score than controls (mean MHT in cases = 34.0, mean MHT in controls 41.5, p=0.02). This translates to an odds ratio of 0.68 (95% CI 0.50 – 0.94; p=0.021) for every 10 point increase in MHT. There was no relationship demonstrated between childhood mental ability and late-onset AD. This association between childhood mental ability and vascular dementia has not been described previously. The estimation of pre-morbid mental ability is often required to demonstrate the cognitive decline required to diagnose dementia. The neuropsychological test most frequently used is the National Adult Reading Test (NART). NART scores were compared in cases with dementia (n=45) to healthy volunteers (n=550). Cases with dementia scored lower on the NART in old age, but also scored lower on MHT age 11. After adjusting the NART score for MHT age 11, the dementia and non-dementia groups no longer differed on NART scores. Pearson correlations between NART and MHT (measured more than 60 years apart) were similar in the dementia group (r =.60) and the non-dementia group (r =.63). These results confirm that the NART is a valid test of pre-morbid mental ability even in the presence of mild-moderate dementia. Changes on the resting electrocardiograph (ECG) can be considered a marker of vascular disease. Cognitive test scores were compared in a group of people with and without ECG changes. There was no difference in MHT between the two groups. Men with left ventricular hypertrophy had lower MMSE. Both left ventricular hypertrophy and conduction defects are associated with reduced scores on verbal fluency in women. Overall, this thesis establishes that lower childhood mental ability is associated with higher risk of dementia. This occurs for vascular but not Alzheimer’s dementia.
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Grafft, Amanda Jo. "Academic achievement following childhood onset brain injury." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3304.
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The degree of academic achievement following early onset brain injury is poorly understood. Furthermore, it is unclear if academic success can be predicted by age of onset or other lesion variables (e.g., size, laterality). The purpose of the current study was to describe patterns of academic achievement in individuals with childhood-onset focal brain lesions and to determine the role of variables in the plasticity or vulnerability of the developing brain with regard to achievement. Academic achievement data were collected from 58 individuals with childhood-onset focal brain lesions. The participants' reading, spelling, and arithmetic scores, as measured by the Wide Range Achievement Test, were analyzed in relation to several neuroanatomical variables, including lesion laterality, lesion site, and lesion size. The relationship between achievement and gender, age of onset, etiology, age at testing, and time since lesion onset was also identified.
As a group, achievement scores did not differ from normative data, and the majority of the sample demonstrated adequate skills in each domain. However, the frequency of deficits was larger than expected when compared to base rates, suggesting vulnerability to early insult. Achievement scores were correlated with intelligence scores, but did not differ based on lesion laterality, lesion site, age of onset, or etiology. Size of lesion was significantly correlated with reading and spelling but not with arithmetic outcomes. Gender differences were identified, with males performing significantly better on the arithmetic measure than females. The age of onset, age at testing, and time since lesion onset were not correlated with achievement scores in any domain. No interactions were found between lesion laterality and gender or lesion site and lesion laterality. An interaction between gender and lesion site was found, but the significance of the finding is unclear. The current findings provide mixed evidence for the plasticity-vulnerability debate, as many individuals were able to achieve adequate academic skills whereas others demonstrated significant impairments. Further research is needed to elucidate factors that may predict achievement outcomes in individuals with childhood-onset focal brain injury.
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Benn, Kelly Marie. "Parental coping following onset of childhood brain injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ52972.pdf.
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Dev, Borman Arundhati. "A genotype-phenotype study of childhood onset retinal dystrophies." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1476347/.
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Introduction The childhood onset retinal dystrophies comprise a clinically and molecularly heterogeneous group of disorders. To date, sixteen genes have been implicated in the pathogenesis of the spectrum of disorders comprising Leber Congenital Amaurosis (LCA) and Early Onset Retinal Dystrophy (EORD), accounting for approximately 70% of cases. Although a wide range of phenotypes have been observed within this spectrum, some genotype – phenotype associations are reported. Further detailed genotype – phenotype studies will be important for expanding our understanding of the effects of mutations in these genes on patients and their families. Our knowledge of the phenotypic effects of mutations in other genes implicated in childhood onset retinal dystrophies, such as the bestrophinopathies, continues to expand. Purpose To undertake detailed phenotypic studies into subjects with molecularly identified childhood onset retinal dystrophies, and to describe novel phenotypes. Methods Affected subjects and their families were recruited from Moorfields Eye Hospital to an ongoing Study into childhood onset retinal dystrophies. Subjects were examined clinically and those that were historically recruited to the Study were invited back for further phenotypic analyses, if their molecular cause was identified. Genetic analysis was performed using a variety of methods including DNA microarray analysis, autozygosity mapping, direct sequencing and whole exome sequencing. Results Between August 2008 and August 2011, 201 subjects from 186 families were recruited into the Childhood Onset Retinal Dystrophy Study, and categorised into 2 cohorts: cohort 1 - the generalised retinal dystrophies, comprising 177 subjects (166 families); and cohort 2 – subjects with a macular phenotype, comprising 24 subjects (20 families). The molecular cause was identified in 34.5% of subjects in cohort 1 and 25% of subjects in cohort 2. RDH12 accounted for 28% of mutations in cohort 1, 18% had mutations in CEP290, and 13% had mutations in RPE65. The subjects in cohort 2 with autosomal recessive bestrophinopathy all had bi-allelic mutations in BEST1. The phenotype associated with the different genes identified was expanded, and focused on those genes with limited reports of the phenotype, such as SPATA7, LRAT, RGR and BEST1. The phenotype associated with a gene not previously identified in human EORD, TUB, was studied, and the features associated with a novel macular phenotype named Benign Yellow Dot Dystrophy were characterised. Conclusions This study has expanded and refined our understanding of the phenotypes associated with mutations in genes that cause childhood onset retinal dystrophies, and has identified a novel phenotype. This work will allow accurate prognostic and genetic counselling to affected families, and provides phenotypic information that will be important in ascertaining disorders that may be suitable for clinical trials of novel therapies.
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Banerjee, Dipti, Bizu Gelaye, Qiu-Yue Zhong, Sixto E. Sanchez, and Michelle A. Williams. "Childhood abuse and adult-onset asthma among Peruvian women." Taylor and Francis Ltd, 2018. http://hdl.handle.net/10757/624658.
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El texto completo de este trabajo no está disponible en el Repositorio Académico UPC por restricciones de la casa editorial donde ha sido publicado.Objective: Childhood abuse has been found to be associated with adult-onset asthma; however, this association has not been studied in low- and middle-income countries with a high burden of gender-based violence, including childhood abuse. We examined the odds of asthma diagnosed at age 18 or older in relation to history of physical and sexual abuse among Peruvian pregnant women. Methods: This cross-sectional study collected demographic characteristics, history of abuse and asthma diagnoses from 3081 pregnant women. Logistic regression procedures estimated adjusted odds ratios and 95% confidence intervals (aOR, [95% CI]) for asthma diagnoses in relation to abuse. Results: Overall, 71% of the women reported a history of abuse (<18 years), and asthma was diagnosed among 2.6% of the cohort participants. The prevalence of physical only, sexual only and both physical and sexual childhood abuse was 38, 8 and 25%, respectively. The history of physical only (1.16, [0.63–2.17]), sexual only (2.11, [0.92–4.84]) or both physical and sexual childhood abuse (1.75, [0.94–3.29]) was positively associated with increased odds of asthma, although the associations were not statistically significant in the multivariate analysis. However, the odds of asthma increased with increasing numbers of abuse events (ptrend = 0.01). Women who reported ≥3 abuse events had an increased odds of asthma (1.88, [1.06–3.34]). Conclusion: Our results do not provide convincing evidence that childhood abuse is associated with asthma among pregnant Peruvian women; however, we were able to demonstrate that an increased number of abuse events are associated with asthma. Further research is required to better understand the effects of abuse on asthma.
This research was supported by an award from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01-HD-059835). The NIH had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication. The authors wish to thank the dedicated staf f members of Asociacion Civil Proyectos en Salud (PROESA), Peru, and Instituto Especializado Materno Perinatal, Peru, for their expert technical assistance with this research.
Revisión por pares
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Foster, Kim Alison. "The clinical presentation of childhood-onset schizophrenia : a literature review." Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/50123.
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Assignment (MA) -- University of Stellenbosch, 2004.ENGLISH ABSTRACT: This literature review explores the research on the clinical presentation of childhood onset schizophrenia (COS) that has been conducted over the past ten years. A literature search was done using internet search engines and psychological databases to collect English language journals from 1994 onwards. Research indicates that COS is a stable diagnosis. Generally, there is a clear history of premorbid abnormalities, an insidious onset and a deteriorating course. For the majority of cases there seems to be a poor outcome. In conclusion, despite the limitations in the research conducted thus far, findings provide important insights regarding COS and several possibilities for future research.
AFRIKAANSE OPSOMMING: Hierdie literere oorsig fokus op navorsing wat die afgelope tien jaar gedoen is oor die kliniese aanbieding van skisofrenie wat in die kinderjare begin (COS). Daar is gebruik gemaak van Internet "soek enjins" en sielkundige databasisse ten einde Engelstalige joernale op te spoor wat vanaf 1994 tot nou oor die onderwerp verskyn het. Navorsing dui daarop dat COS 'n stabiele diagnose is. Oor die algemeen toon dit 'n duidelike geskiedenis van premorbiede abnormaliteite, 'n ongemerkte aanvang en verloop en agteruitgang oor tyd. In die meeste gevalle blyk daar 'n swak uitkoms te wees. Laastens bied die bevindinge belangrike insigte ten opsigte van COS en heelwat moontlikhede vir toekomstige navorsing, ten spyte van die beperkinge in die navorsing wat tot dusver gedoen is.
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Kurz, Susanne, Dyck Zoé van, Daniela Dremmel, Simone Munsch, and Anja Hilbert. "Variants of early-onset restrictive eating disturbances in middle childhood." Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-205393.
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Objective: This study sought to determine the factor structure of the newly developed self-report screening questionnaire Eating Disturbances in Youth-Questionnaire (EDY-Q) as well as to report the distribution of variants of early-onset restrictive eating disturbances characteristic of avoidant/restrictive food intake disorder (ARFID) in a middle childhood population sample. Method: Using the EDY-Q, a total of 1444 children aged 8-13 years were screened in elementary schools in Switzerland via self-report. The factor analysis of the 12 items covering ARFID related symptoms was performed using a principal component analysis (PCA). Results: The PCA showed a four factor solution, with clear allocation to the scales covering three variants of early-onset restrictive eating disturbances and weight problems. Inadequate overall food intake was reported by 19.3% of the children, a limited accepted amount of food by 26.1%, and food avoidance based on a specific underlying fear by 5.0%. Discussion: The postulated factor structure of the EDY-Q was confirmed, further supporting the existence of distinct variants of early-onset restrictive eating disturbances. Avoidant/restrictive eating behavior seems to be a common experience in middle childhood, but results have to be confirmed using validated interviews.
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Kurz, Susanne, Dyck Zoé van, Daniela Dremmel, Simone Munsch, and Anja Hilbert. "Variants of early-onset restrictive eating disturbances in middle childhood." International journal of eating disorders (2015) 49, 1, S. 102-106, 2015. https://ul.qucosa.de/id/qucosa%3A14781.
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Objective: This study sought to determine the factor structure of the newly developed self-report screening questionnaire Eating Disturbances in Youth-Questionnaire (EDY-Q) as well as to report the distribution of variants of early-onset restrictive eating disturbances characteristic of avoidant/restrictive food intake disorder (ARFID) in a middle childhood population sample. Method: Using the EDY-Q, a total of 1444 children aged 8-13 years were screened in elementary schools in Switzerland via self-report. The factor analysis of the 12 items covering ARFID related symptoms was performed using a principal component analysis (PCA). Results: The PCA showed a four factor solution, with clear allocation to the scales covering three variants of early-onset restrictive eating disturbances and weight problems. Inadequate overall food intake was reported by 19.3% of the children, a limited accepted amount of food by 26.1%, and food avoidance based on a specific underlying fear by 5.0%. Discussion: The postulated factor structure of the EDY-Q was confirmed, further supporting the existence of distinct variants of early-onset restrictive eating disturbances. Avoidant/restrictive eating behavior seems to be a common experience in middle childhood, but results have to be confirmed using validated interviews.
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Zaal, Ahmad. "Benchmarking the Quality of Medical Care of Childhood-Onset SLE." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427962136.
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Renoux, Christel. "Epidemiological study of childhood onset multiple sclerosis : course, prognosis and biases." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98777.
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The course and prognosis of childhood onset multiple sclerosis (MS) is not well defined unlike that with adult onset.A cohort of 380 patients with childhood onset (before the age of 16) MS and 3367 with adult onset were identified through the European Database for Multiple Sclerosis. The median time to reaching scores of four and six on the disability status scale was longer for childhood onset MS patients (20 and 29 years) compared with adult onset patients (12.8 and 23.7 years; p<0.0001). Two years after onset, the main prognostic factors of disability in childhood onset MS patients were age at onset, gender and the number of relapses during the first two years of MS. We showed that immortal time bias explains the previously reported protective effect of the time between the first two relapses on disability.
Childhood onset MS has a slower evolution to disability than adult onset MS.
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Tucciarone, Joseph T. Jr. "Adverse Childhood Experiences, Homeless Chronicity, and Age at Onset of Homelessness." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etd/3534.
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Childhood adversity is associated with numerous negative outcomes across multiple domains, including mental and physical health, interrelationships, and social functioning. Notably, research suggests that childhood adversity has a dose-response relationship with these outcomes; that is, greater numbers of adverse experiences in childhood are associated with worse outcomes. These outcomes overlap with many risk factors of homelessness. This study sought to address two questions: 1) Does a dose-response relationship exist between childhood adversity and chronic homelessness? 2) Does childhood adversity negatively predict the age at which homelessness first occurs? Adults experiencing homeless who are accessing homeless services in the Tri-Cities area of Northeast Tennessee responded to a brief instrument that includes measures of homeless chronicity, Adverse Childhood Experiences (ACEs), and age of onset of homelessness. Although relationships between ACEs and homeless chronicity was not observed, a relationship did emerge between number of ACEs and number of episodes and number of ACEs and age at initial onset of homelessness.
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Perreault, Kyle. "A comprehensive study and analysis of the implications of childhood onset schizophrenia." Menomonie, WI : University of Wisconsin--Stout, 2005. http://www.uwstout.edu/lib/thesis/2005/2005perreaultk.pdf.
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Zhao, Hongxin. "Epidemiological studies of childhood onset type 1 diabetes in Devon and Cornwall." Thesis, University of Plymouth, 2000. http://hdl.handle.net/10026.1/2398.
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A high quality register of children with type 1 diabetes, The Cornwall and Plymouth Children's Diabetes Register (CPCDR), has been successfully established in the far South West of England for this thesis. Children aged 0-15 years of age who were diagnosed with type I diabetes in the study area have been systematically registered on the database since 01 /01/1975 until the present day. Children are now registered prospectively, to provide a database of the disease in this region and to allow epidemiological studies. Basic descriptive studies on the occurrence of the disease based on the CPCDR between 1975-1996 have been carried out for this thesis. In addition, space-time clustering analysis of the disease has been conducted, as well as an exploration of the association of some chemical contents in domestic drinking water, serum minerals and birth weight to the risk of developing the disease. The incidence study demonstrated that the overall incidence rate of childhood onset type 1 diabetes was 14.9 cases/100 000/year in this area during the 22-year study period (1975-1996). The case ascertainment was 94.4% for the whole register. A significant increase (2.49% per year) of overall incidence has been observed, mainly due to a significant increase in the 0-4-year age group (6.32% per year). The incidence significantly differed among the 22 years with peak incidences seen in the years 1977, 1983, 1988, 1990 and 1993-94. Incidence increased with age, with a peak age of 12 years for girls and 14 years for boys. Girls had a significantly higher incidence than boys. The significant seasonal variations at diagnosis were detected with the peak incidence appearing in autumn and winter. Significant space-time clustering was found by the Knox test in the study region in the following combinations of critical cutoff values, 25, 35 and 50 km and 270 or 360 days (P values < 0.05), and 50 km and 90 days (P < 0.05) with the highest level of significance found at 35 km and 360 days (P < 0.01). Stronger clustering was found in the younger children (0-4 years). Therefore, there is evidence of space-time clustering in the onset of childhood diabetes in the far South West of England. These results lend some support to the hypothesis that viral infections in early life or other unknown environmental factor(s) may have a role to play in the development of childhood diabetes. The relationship between childhood diabetes and drinking water quality has been explored in the study area. The initial analysis with the Spearman's rank test and χ² test for trend on the tertiles of the dataset suggest that copper, magnesium and nitrate have some protective effect on children for developing type 1 diabetes. However, Poisson regression analyses revealed that zinc and magnesium were the main possible protective chemicals. The concentration ranges of zinc (22.27-27.00 µg/L) and magnesium (>= 2.61 mg/L) in domestic drinking water would significantly decrease the risk of childhood diabetes. The results indicated that zinc and magnesium in drinking water are protective factors against the development of childhood diabetes. No significant associations were detected between birth weight or serum minerals and the risk of developing the disease.
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Brodsky, Kimberly L. m. d. "Cognitive and genetic commonalities and differences in ADHD and childhood onset schizophrenia." Connect to online resource, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3315759.
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Spittal, Graeme William. "Characteristics of childhood-onset Systemic Lupus Erythematosus in Cape Town, South Africa." Master's thesis, University of Cape Town, 2014. http://hdl.handle.net/11427/6016.
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Holland, Michael J. "Measuring Disease Damage and its Severity in Childhood-Onset Systemic Lupus Erythematosus." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1527606864223975.
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Adib, Navid. "Disease impact and baseline correlates in recent onset childhood idiopathic inflammatory arthritis." Thesis, University of Manchester, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518865.
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Hsu, Lorena. "The comparison of obstetric complication histories of individuals with childhood-onset schizophrenia vs. adult-onset schizophrenia, a multi-site feasibility study." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0006/MQ45907.pdf.
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Cline, Jessie Irit. "Autonomic Nervous System Functioning and Callous-Unemotional Traits in Childhood-Onset Conduct Disorder." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/216568.
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PsychologyPh.D.
Although the current literature demonstrates relations between autonomic nervous system (ANS) functioning and conduct disorder (CD), there are inconsistencies across studies in the magnitude and direction of these associations, some of which may stem from heterogeneity within the CD diagnostic category. Considering callous-unemotional (CU) traits in research examining ANS functioning and CD relations could help to clarify these inconsistencies, given that CU traits identify a subgroup of youth with CD who exhibit a more severe and persistent course, as well as more negative correlates and sequelae than youth with CD without CU traits. However, there is a dearth of literature considering ANS processes among youth with CD with and without CU traits. Examining these relations, particularly during middle childhood when these processes may be amenable to intervention, has important implications for etiological, prevention, and intervention models. The present study examined relations among CD, CU, and ANS functioning among a sample of ethnic minority, urban children (N= 99, M= 9.87± 1.19 years old; 48.5% male; 94.9% African-American, 3% Latino/a). Specifically, I examined whether CU traits moderated the relations between CD and (a) parasympathetic nervous system (PNS) functioning and (b) sympathetic nervous system (SNS) functioning. In addition, I examined whether parenting behaviors (i.e., harsh parental discipline and parental warmth/involvement) influenced the relations between (a) CD and ANS functioning, and (b) CU and ANS functioning. Findings demonstrated that PNS functioning differed among children with high and low levels of CD symptoms depending on levels of CU traits. Within the current sample, among children with higher levels of CD symptoms, those with (a) higher CU symptom severity exhibited lower baseline respiratory sinus arrhythmia (RSA) and lower RSA reactivity (PNS withdrawal), compared to those with (b) lower CU symptom severity who demonstrated higher baseline RSA and higher RSA reactivity (PNS activation). Among children with lower CD symptom severity, those with (a) higher CU symptom severity exhibited higher baseline RSA and higher RSA reactivity, compared to those with (b) lower CU symptom severity who evidenced lower baseline RSA and lower RSA reactivity. Neither harsh parental discipline nor parental warmth/involvement moderated the relations between (a) CD and ANS functioning and (b) CU and ANS functioning. However, there were marginally significant associations between baseline RSA and (a) harsh parental discipline and (b) parental warmth/involvement, as well as between RSA reactivity and parental warmth/involvement in analyses examining CD, parenting, and ANS functioning. Furthermore, parental warmth/involvement tended to be associated with RSA reactivity in the analyses examining CU, parenting, and ANS functioning. Results have implications for facilitating the identification of children at risk for developing more pernicious subtypes of behavior problems, and contribute important information for the development of more individualized and potentially effective interventions for youth behavior problems, particularly among high-risk youth.
Temple University--Theses
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Komulainen-Ebrahim, J. (Jonna). "Genetic aetiologies and phenotypic variations of childhood-onset epileptic encephalopathies and movement disorders." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526222356.
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Abstract Novel genetic aetiologies for epileptic encephalopathies and movement disorders have been discovered by using next-generation sequencing methods. The phenotypic and genotypic variability in these conditions is very wide. The aim of this study was to discover novel genetic causes and phenotypes of childhood-onset drug-resistant epilepsy and epileptic or developmental encephalopathies that occur separately or together with movement disorders, and familial movement disorders. Furthermore, the use of whole-exome sequencing (WES) as a diagnostic tool in clinical practice was evaluated. Altogether, 12 children with undefined aetiology, who fulfilled the inclusion criteria, were included in the study. GABRG2 gene was identified as a genetic cause of epileptic encephalopathies. Novel GABRG2-associated phenotypes included progressive neurodegeneration, epilepsy in infancy with migrating focal seizures, and autism spectrum disorder. New pathogenic variants, GABRG2 p.P282T and p.S306F, were discovered. The pathogenic NACC1 variant caused focal epilepsy, developmental disability, bilateral cataracts, and dysautonomia. The novel phenotype associated with the NACC1 p.R298W variant included hyperkinetic movement disorder. SAMD9L was found to be the genetic cause for the familial movement disorder. The phenotype associated with the novel SAMD9L p.I891T variant was very variable. Neuroradiological findings included cerebellar atrophy and periventricular white matter changes. After publication of these results, SAMD9L was reported to be one of the most common genetic aetiologies of childhood bone marrow failure and myelodysplastic syndrome. The pathogenic homozygous MTR variant was found to cause early-onset epileptic encephalopathy that occurred together with movement disorder and haematological disturbances. Drug resistant seizures responded to cofactor and vitamin treatments. Whole-exome sequencing for 10 patients with drug-resistant epilepsy or epileptic or developmental encephalopathy provided a genetic diagnosis for two patients (20%). This study confirmed that, for epileptic encephalopathies and movement disorders in which the genetic causes and phenotypes are heterogeneous and sometimes treatable, WES is a useful tool for diagnostics and in the search for novel aetiologies, which might turn out to be more common than expectedTiivistelmä Uusien sekvensointimenetelmien käyttöönotto on mahdollistanut epileptisten enkefalopatioiden ja liikehäiriöiden uusien geneettisten syiden löytymisen. Näissä sairausryhmissä geenien ja ilmiasujen vaihtelevuus on suurta. Tutkimuksen tarkoituksena oli löytää uusia geneettisiä syitä ja ilmiasuja lapsuusiällä alkavissa vaikeahoitoisissa epilepsioissa ja epileptisissä tai kehityksellisissä joko itsenäisesti tai yhdessä liikehäiriön kanssa esiintyvissä enkefalopatioissa sekä perheittäin esiintyvissä liikehäiriöissä. Lisäksi selvitettiin eksomisekvensoinnin käyttökelpoisuutta kliinisessä diagnostiikassa näiden potilasryhmien kohdalla. Tutkimukseen osallistui yhteensä 12 sisäänottokriteerit täyttävää lasta, joiden sairauden syy oli jäänyt tuntemattomaksi. GABRG2-geenin mutaatiot aiheuttivat epileptisiä enkefalopatioita, joiden uutena ilmiasuna oli etenevä taudinkuva, johon liittyivät aivojen rappeutuminen, migroiva imeväisiän paikallisalkuinen epilepsia sekä autismikirjon häiriö. Tutkimuksessa löydettiin uusia GABRG2-mutaatioita: p.P282T ja p.S306F. NACC1-geenin mutaatio aiheutti epilepsian, kehitysvammaisuuden, molemminpuolisen kaihin ja autonomisen hermoston toiminnan häiriön. Hyperkineettinen liikehäiriö oli uusi NACC1 p.R298W -mutaatioon liittyvä ilmiasu. SAMD9L-geenin mutaatio aiheutti perheessä esiintyvän liikehäiriön. Neurologinen ja hematologinen ilmiasu olivat hyvin vaihtelevia. Aivojen kuvantamislöydöksiin sisältyi pikkuaivojen rappeutumista ja valkoisen aivoaineen muutoksia aivokammioiden ympärillä. Näiden tutkimustulosten julkaisemisen jälkeen SAMD9L-geenin mutaatioiden on todettu olevan yksi yleisimmistä perinnöllisistä luuytimen vajaatoiminnan ja myelodysplasian syistä. Homotsygoottinen MTR-geenin mutaatio aiheutti varhain alkaneen epileptisen enkefalopatian, liikehäiriön ja hematologisen häiriön. Kofaktori- ja vitamiini hoidot vähensivät epileptisiä kohtauksia, joihin tavanomainen lääkitys ei tehonnut. Geneettiset syyt ja ilmiasut ovat epileptisissä enkefalopatioissa ja liikehäiriöissä hyvin vaihtelevia, ja osaan on olemassa spesifi hoito. Eksomisekvensointi on käyttökelpoinen diagnostiikan ja uusien geneettisten syiden etsimisen apuna. Tässä tutkimuksessa eksomisekvensoinnin avulla kymmenestä potilaasta kahdelle (20%) saatiin varmistettua geneettinen diagnoosi
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Giunta, Michele. "Exosomal protein deficiencies : how abnormal RNA metabolism results in childhood-onset neurological diseases." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3669.
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RNA metabolism is of critical importance for normal cellular functions and needs to be finely tuned in order to maintain stable conditions within the cell. The exosome complex is the most important RNA processing machinery, responsible for the correct processing of many different types of RNAs and interacting with different co-factors which bind and carry specific subtypes of RNA for degradation to the complex. Mutations in exosome complex subunits (EXOSC3, EXOSC8) were reported to cause severe childhood onset complex neurological disorders presenting with pontocerebellar hypoplasia type 1 (PCH1), spinal muscular atrophy (SMA) and central nervous system hypomyelination. We have recently identified a homozygous pathogenic mutation in RNA Binding Motif Protein 7 RBM7, a subunit of the nuclear exosome targeting (NEXT) complex in a single patient with SMA-like phenotype and proved that RBM7 is a novel human disease gene related to the exosome complex. In order to understand the disease mechanism in RBM7 deficiency and to explore the role of exosome complex in neurodevelopment, we performed gene expression studies (RT-PCR, RNA sequencing) in human cells of patients carrying mutations in EXOSC8 and RBM7. Furthermore we performed functional studies in zebrafish (D. rerio) by morpholino oligonucleotide mediated knock-down of rbm7, exosc8 and exosc3 and also by introducing pathogenic mutations in exosomal protein genes in zebrafish embryos by the CRISPR/Cas9 system. We showed that mutations in RBM7 and EXOSC8 mutant fibroblasts cause differential expression of several different transcripts, 62 of them being shared between the two cell lines. Altered gene expression of some AU-rich element containing genes may potentially contribute to the clinical presentation. Knock-down of rbm7, exosc8 and exosc3 caused impaired neurodevelopment in zebrafish, illustrated by abnormal growth of motor neuron axons and failure to differentiate cerebellar Purkinje cells. RT-PCR analysis in zebrafish showed a dramatic increase in expression of atxn1b (an AU-rich element containing homolog of the human ATXN1 gene) in rbm7, exosc8 and exosc3 downregulated fish, which may be responsible for the cerebellar defects. We have successfully introduced several germline mutations with CRISPR/Cas9 technology in rbm7. Phenotype of the F1 mutants is milder than what observed with the morpholino oligonucleotide injected fish. Mutants at a closer look do not show any morphological defect but further experiment may indicate similar characteristics to the morphants, although more iv subtle. Further studies on the CRISPR/Cas9 generated zebrafish models will extend our knowledge on the disease mechanisms caused by defective RNA metabolism.
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Mikkonen, K. (Kirsi). "Endocrine function and growth in young patients with childhood- or adolescence-onset epilepsy." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514274229.
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Abstract
Endocrine disorders are common in adults with epilepsy on
antiepileptic drugs (AEDs). This study aimed to evaluate endocrine
function, lipid metabolism and growth in patients with childhood- or
adolescence-onset epilepsy.
Altogether 148 patients with epilepsy on carbamazepine (CBZ),
oxcarbazepine (OXC), valproate (VPA) or lamotrigine monotherapy during
pubertal maturation and 124 healthy controls participated in this
population-based cohort study. Boys and young men (n = 140)
underwent cross-sectional evaluation once, and girls and young women
(n = 132) twice at an approximate interval of 6 years.
Gonadal structure and serum reproductive and thyroid hormone and lipid
concentrations were evaluated and growth data were gathered.
Elevated serum testosterone and androstenedione levels and
polycystic ovary syndrome (PCOS) were common in female subjects whose
medication, especially VPA, continued into young adulthood. Serum
reproductive hormone concentrations and ovarian structure were similar
in patients off medication and controls in young adulthood. CBZ was
associated with elevated serum sex hormone binding globulin and
decreased dehydroepiandrosterone sulfate levels and VPA with elevated
serum androstenedione concentrations in male patients. Testicular
structure was similar in patients and controls. CBZ, OXC and VPA were
associated with changes in serum thyroid hormone, thyrotropin and lipid
levels during pubertal maturation in female patients, but these levels
returned to normal after withdrawal of medication. Linear growth and
final height were normal in female patients, but overweight was common
if they had been obese and on VPA medication during pubertal maturation.
Elevated serum androgen levels, PCOS and overweight are common if
epilepsy and AED use, especially VPA, continue into young adulthood.
These untoward changes or alterations in serum thyroid hormone or lipid
concentrations are not present in young women with medication withdrawn.
CBZ and VPA are associated with changes in serum sex hormone levels in
boys and young men with epilepsy. Epilepsy and AED use during pubertal
maturation does not seem to affect growth.
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Owen, Nicholas. "Molecular genetics of spinal muscular atrophy." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342635.
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Proal, Fernández Erika. "Brain anatomy of attention deficit/hyperactivity disorder in children and adults with childhood onset." Doctoral thesis, Universitat Autònoma de Barcelona, 2011. http://hdl.handle.net/10803/51438.
Full textAbstract:
El trastorno por déficit de atención e hiperactividad (TDAH) es uno de los trastornos del neurodesarrollo más comunes en niños. Los principales síntomas son la inatención, impulsividad e hiperactividad. El TDAH se presenta en un 8 a 12% de la población escolar mundial; la mayoría (60-85%) continua presentando los criterios diagnósticos durante la adolescencia.
Estudios de neuroimagen volumétricos en niños con TDAH han encontrado de manera consistente reducciones globales del volumen total cerebral con una mayor tendencia a la reducción de regiones fronto-estriatales, cerebelo y parietales-temporales comparándolos con niños controles (desarrollo típico). El diagnostico de TDAH en adultos requiere de haberse presentado en la niñez, en la actualidad ya se ha confirmado que la persistencia de los síntomas puede continuar hasta la edad adulta.
El uso de diferentes técnicas de neuroimagen realizados por diferentes grupos de investigación han ayudado a la mejora del entendimiento de los sustratos neurológicos que están por detrás de la patofisiología de TDAH. Hoy en día, los investigadores han hecho énfasis en las contribuciones potenciales de la disfunción de circuitos cerebrales, en vez de enfocarse solamente en anormalidades de regiones por separado. En consecuencia, el objetivo principal de la presente tesis es examinar los sustratos neurales del TDAH aplicando tres diferentes técnicas de neuroimagen. El objetivo secundario es analizar si estas diferencias están relacionadas con el diagnostico de TDAH en la niñez o si están relacionadas con la persistencia de los síntomas en la edad adulta.
Los resultados del presente estudio están divididos en dos principalmente. Primero, en una muestra grande de niños y adolescentes con TDAH, se encontró una reducción volumétrica significativa en el estriado ventral, una región considerada como clave en los procesos de recompensa y relacionada con los circuitos cortico-striato-thalamo-coticales (circuito de recompenza). En segundo lugar, los adultos que fueron diagnosticados con TDAH en la niñez, mostraron una reducción tanto en el grosor cortical como el volumen de la sustancia gris en regiones parietales y motoras (Circuito dorsal atencional). La mayoría de estas diferencias se observaron independientemente del diagnóstico actual de los sujetos. En otras palabras, estas diferencias fueron, estas diferencias fueron encontradas en aquellos sujetos que persistieron con los síntomas en la edad adulta y también en los que remitieron el diagnostico. En contraste, las regiones implicadas en el circuito de recompensa fueron disminuidas en los que persistieron pero no en los que remitieron. Por lo tanto, las diferencias en estas ultimas regiones (estriado ventral en niños, corteza orbitofrontal, parahipocampo, tálamo, polo frontal en adultos con TDAH) están relacionadas con el diagnostico actual del trastorno; mientras que las diferencias en el circuito dorsal atencional parecen estar más implicado con haber tenido TDAH en edad temprana.
Nuestros datos nos permiten sugerir una hipótesis integrativa de disfunción en el circuito de la recompesa, que esta particularmente afectado en niños y adolescentes con TDAH y en adultos con persistencia de TDAH; a su vez el circuito atencional dorsal está más relacionado con funciones ejecutivas y atencionales y esto se ve reflejado en los sujetos que han tenido TDAH en la niñez sin importar que en la actualidad (edad adulta) presenten o no síntomas de TDAH.
En base a nuestros datos, se propone un modelo de fisiopatología del TDAH que envuelve dos circuitos principalmente. El circuito dorsal atencional, que parece estar más reflejado con factores genéticos. Por el contrario, diferencias anatómicas en el circuito de recompensa está relacionado con los síntomas actuales de TDAH. Sin embargo no podemos diferenciar con nuestros datos, si las diferencias encontradas son la base de la remisión de los síntomas o si son cambios en los circuitos cerebrales que están reflejando una remodelación secundaria de los efectos del comportamiento, como aprendizaje o refuerzo selectivo. Esta pregunta deberá intentar abordarse en futuras investigaciones longitudinales y con técnicas de neuroimagen que incorporen también factores genéticos y métodos de seguimiento del tratamiento.Attention-Deficit/Hyperactivity Disorder (ADHD) is one of the most common neurodevelopmental disorders occurring in childhood. The main symptoms are developmentally excessive levels of inattention, impulsivity and hyperactivity. ADHD occurs in 8 to 12% of school age children worldwide; the majority (60%-85%) continues to meet criteria for the disorder during their teenage years. Volumetric studies in children with Attention-Deficit/Hyperactivity Disorder (ADHD) have consistently found global reductions of total brain volume with frontal-striatal regions, cerebellum and parieto-temporal regions particularly affected relative to typically developing subjects. The adult diagnosis of ADHD requires onset in childhood, but persistence of ADHD into adulthood is now well documented. This longitudinal course together with smaller brain volumes in children with ADHD has raised questions about brain development into adulthood. The use of different neuroimaging techniques by independent groups is leading to an improved understanding of the neural substrates underlying the pathophysiology of ADHD. Nowadays, researchers have begun to place more emphasis on the potential contributions of dysfunctional brain circuits, rather than isolated regional abnormalities. Therefore, the aim of this thesis is to examine the neural substrates of ADHD by applying three different anatomic neuroimaging approaches. A secondary aim is to analyze whether these brain differences are related with the diagnosis of ADHD in childhood or whether it is associated with the persistence of the diagnosis in adulthood. The results of the present dissertation are two-fold. First, in a large sample of children and adolescents with ADHD, we found a striking volumetric reduction in the ventral striatum, a region critically involved in reward processes that is a key relay in cortical-striatal-thalamo-cortical circuits (reward circuit). Second, in adults diagnosed with ADHD in childhood, we found reduced cortical thickness and voxel-based morphometry (VBM) gray matter volume in parietal and motor regions (Dorsal attentional network). Most of these differences were independent of current adult diagnoses status. In other words, these differences were largely found in both individuals with persistent ADHD and in those who were in remission. By contrast, reward-related regions were diminished in probands with persistent ADHD compared to controls but not in those who were in remission. Thus differences in reward-related circuitry (ventral striatum in children, orbitofrontal cortex, parahippocampus, thalamus, and frontal pole in adults) were associated with the current diagnosis of ADHD, whereas frontal-parietal motor cortex differences in adults with ADHD seem to reflect the trait of having had ADHD in childhood. Our data allow us to suggest an overall integrative hypothesis that dysfunction in the reward circuit, which was particularly prominent in children and adolescents with ADHD and in the adults with persistent ADHD, reflects ongoing symptoms of ADHD. By contrast, abnormalities in the top-down control dorsal attentional network seem to be related to the trait of having had ADHD in childhood, as the abnormalities were comparable in adults who had remitted or who had persistent ADHD. On the basis of our data, we propose a model of ADHD physiopathology in which two main circuits interact. These are the dorsal attentional network, which seems to be anatomically abnormal in individuals with a history of ADHD, whether or not they are currently affected. As such, we hypothesize that dorsal attentional network deficiencies may be related to the genetic factors associated with ADHD. By contrast, anatomic abnormalities in the reward circuit appear to be related to current ADHD symptoms. Based on our data, we cannot differentiate whether anatomic changes in the reward circuits are the basis for symptomatic remission, or whether such changes in brain circuits reflect brain remodeling secondary to behavioral effects, such as learning and selective reinforcement. This question will have to be addressed in the future through longitudinal brain imaging studies that can incorporate genetic factors and treatment tracking methods.
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Alexander-Bloch, Aaron Felix. "Brain networks in magnetic resonance imaging studies of typical development and childhood-onset schizophrenia." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608247.
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Batty, Allison. "Integrating the Unconscious Into Conscious Reality| A Jungian Approach to Treating Early Onset Psychosis." Thesis, Pacifica Graduate Institute, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10254363.
Full textAbstract:
Limited research exists on effective treatment modalities for early onset trauma-based psychosis during the latency period of childhood. This thesis reviews research on the benefits of using Jungian play therapy to treat trauma-based psychosis. Depth psychologists have theorized that the conscious reality of individuals experiencing psychosis is flooded by unconscious complexes, resulting in symptoms of psychosis and intolerance to emotions experienced. Using hermeneutic and heuristic methodologies, this thesis focuses on how, using Jungian play therapy, therapists can form therapeutic alliances with children experiencing psychosis, assist the child with integrating their unconscious experiences, affect, and thoughts into conscious reality thereby managing distressing emotions, contributing to healthy ego development, and reducing psychotic symptoms. Psychological literature and a friend of the author’s experience of psychosis are examined to demonstrate how the integration of unconscious material leads to the potential to heal the fragmentation of the psyche caused by trauma and psychosis.
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Harper, Jessica C. "Early Onset of Obesity and Treatment Outcome in a Behavioral Weight Loss Program." Bowling Green State University / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1122041149.
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Abdalrahaman, Naiemh. "The assessment of bone health in young women with childhood-onset type one diabetes mellitus." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8413/.
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The risk of hip fracture in people with type one diabetes mellitus (T1DM) is reported to be 7 to 12 times greater than in those without T1DM, and this increased risk is evident in both children and young adults. This fracture risk is higher than expected bone mineral density (BMD) measurements, which indicates the likelihood that other skeletal factors, not captured by DXA, may contribute toward increased fracture risk. There is increasing evidence that alteration in trabecular bone microarchitecture and increased bone marrow adiposity (BMA) are causes for excess skeletal fragility, yet these data are lacking in people with T1DM. Recent technological advances in magnetic resonance imaging (MRI) have allowed the quantification of trabecular bone architecture. In addition, MRI can quantify the amount of intra-abdominal fat, and magnetic resonance spectroscopy (MRS) can also be used to assess BMA. These advances may enhance our understanding of the underlying causes of diabetic osteopathy which may lead to improved fracture risk predictors and preventive measures in patients with T1DM beyond that provided by dual energy x-ray absorptiometry (DXA). The overall objective of this thesis was to improve the understanding of the bone pathology of young adult women with childhood-onset T1DM by using high resolution MRI. A cross-sectional study was first carried out to assess trabecular bone microarchitecture of the tibia, vertebral BMA and abdominal adiposity in patients with childhood onset T1DM (n=30) compared with healthy controls (n=28). Additionally, the biochemical markers of bone turnover, adiposity and GH/IGF-1 axis (IGF-1, IGFBP3, and ALS) were examined to evaluate the underlying mechanism that might result in bone deficit in this group of people. We found that young women with childhood onset T1DM had reduced apparent trabecular bone volume (appBV/TV) and apparent trabecular number (appTbN) and greater apparent trabecular separation (appTbSp) than women without T1DM. Interestingly, these differences remained significant after adjustment for multiple confounders. Furthermore, these abnormalities were markedly obvious in those with microvascular complication compared with those without microvascular complication. Although women with T1DM had greater abdominal adiposity compared with healthy controls, there was no significant difference in BMA between the groups. However, BMA showed positive significant association with current glycaemic control (r= 0.45, p=0.02). Women with T1DM had lower bone turnover and decreased GH/IGF axis compared with healthy controls. Osteocalcin and ALS were negatively correlated with trabecular separation in women with T1DM. III Next, a one-year prospective study was conducted in a subset (n=28) of the participants involved in the cross-sectional study. The aim of this study was to compare one year changes in trabecular bone microarchitecture and BMA in women with and without T1DM. Additionally, the study aimed to evaluate the effect of glycaemic control on these changes over this period. After adjustment for relevant confounders, the cases (n=17) had a lower median appTbN and a higher median appTbSp at baseline and 12 months compared with healthy controls (n=11). Although the sample size was small at follow-up, the trabecular bone deficits were clearly noticeable in those with retinopathy compared with those without retinopathy. Similarly, there was no difference in median BMA which was 26.2% (12.1, 62.1) and 22.4% (9.6, 41.9) in cases and controls, respectively (p=0.57). Additionally, over the 12 month period, there was no significant change in MRI-measured parameters in cases or in controls, and no differences in the change of these variables between the two groups. Mixed model effect analysis showed that age was a negative predictor of percent changes of appBV/TV, appTbN and appTbSp in both cases and controls (p=0.02, p=0.02, p=0.002, respectively). Interestingly, there was a strong correlation between change in HbA1c and change in BMA (r=0.8; p=0.002). In the third study, we aimed to assess adiposity-based determinants of bone mineral density and bone microarchitecture in healthy young women and women with T1DM. Additionally, we aimed to compare the feasibility of using DXA and MRI-measured bone parameters to differentiate women with and without T1DM. In addition to high resolution MRI we used DXA scans to measure BMD and body composition from the same participants (n=26) involved in the longitudinal study. Vertebral BMA was positively correlated with VAT. Additionally, we demonstrated evidence of an inverse association of vertebral BMA and DXA-measured bone parameters of femoral neck, lumbar spine and total body independent of demographics and body composition in healthy young women and women with T1DM. These finding support the hypothesis that BMA is linked with low bone density, and may contribute to excess bone fragility. Moreover, this study suggested that MRI-measured trabecular bone measurements were able to differentiate between T1DM with and without microvascular complication compared with DXA-measured BMD. In summary, differences in MRI-measured trabecular microarchitecture parameters identified in this body of work provide preliminary explanations for elevated fracture risk in young women with childhood onset T1DM. Additionally, these findings provide potential insight into a number of possible underlying mechanisms of diabetic osteopathy.
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Jones, Jordan T. "Pain, Fatigue and Psychological Impact on Health-related Quality of Life in Childhood-onset Lupus." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427797527.
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Smitherman, Emily A. "Improving Quality of Care for Childhood-onset Systemic Lupus Erythematosus: Cardiovascular and Bone Health Screenings." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535381218464551.
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Brunner, Hermine Isabella. "Investigation of the relationship between disease activity and disease damage in childhood-onset systemic lupus erythematosus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ58818.pdf.
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Turner, Claudia. "Infant and early childhood pneumonia and early onset neonatal sepsis in Maela camp for displaced persons." Thesis, Open University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.594753.
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Background An estimated nine million children under five years of age die each year. The largest numbers of deaths are from pneumonia. Another common cause of death is early onset neonatal sepsis (EONS), with an estimated half a million neonates dying annually. Methods This thesis comprises three studies that were conducted over a five-year period in Maela camp for displaced persons on the Thailand-Myanmar border. The first study: a cohort study focussed on pneumorua that followed 955 children from birth until two years of age. Pneumonia episodes were diagnosed using WHO criteria and investigations taken included chest x-ray, complete blood count, C-reactive protein, serum sodium, blood culture and a nasopharyngeal aspirate. Potential risk factors for pneumonia were examined. The second study: a three year observational study capturing all episodes of clinically diagnosed EONS occurring in infants born in Maela camp. The final study: a cross sectional study of Group B Streptococcus (GBS) carriage. Vaginal-rectal swabs, collected during labour from 675 women were processed to determine the GBS carriage rate and serotype prevalence, Results The incidence of clinical pneumonia was 0.73 (95% CI 0.7O-D.75) episodes per child year, with one third of cases being associated with RSV infection. From April 2009 until April 2012 the incidence of EONS was 42.1 per 1000 live births. None were associated with proven GBS infection. The maternal GBS carriage rate in the study population was 12.0% (95% CI 9.4- II 15.0). Conclusion We found a high incidence of WHO defined clinical pneumonia in children less than two years of age living in a crowded but rural community in Thailand, with RSV being commonly detected during a pneumonia episode. Despite EONS being a common cause of neonatal death globally, there were no deaths from EONS in the study described in this thesis.
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Vega-Fernandez, Patricia. "Cognitive Performance Scores for the Pediatric Automated Neuropsychological Assessment Metrics in Childhood-Onset Systemic Lupus Erythematosus." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406901194.
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Harry, Onengiya M. D. "Feasibility, Acceptability, and Preliminary Efficacy of an Innovative Adherence Intervention for Young Adults with Childhood-Onset Systemic Lupus Erythematosus." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1562674805687393.
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Hamilton-Shield, J. P. "Sub-clinical manifestations of microvascular disease in childhood onset insulin dependent diabetes mellitus (IDDM) : a follow up study on the 'Avon Childhood Diabetes Cohort'." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387992.
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Schmidt, Ulrike Hermine. "The role of traumatic childhood experiences and life stresses before onset in the origins of eating disorders." Thesis, King's College London (University of London), 1997. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-traumatic-childhood-experiences-and-life-stresses-before-onset-in-the-origins-of-eating-disorders(d98b57d8-0910-4843-90ea-31ac398d10d5).html.
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Alexander, Melannie. "Analysis of the Association of Pesticide Exposure and Onset of Wheeze and Asthma in Early Childhood among Puerto Rican Children in New York City, 2002-2004." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/iph_theses/76.
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INTRODUCTION: Asthma is one of the most common chronic diseases in the United States, affecting the quality of life of at least 20 million Americans. Almost half of the affected (approximately 9.5 million) are children under the age of 18. While Hispanics overall (5.4%) had lower asthma prevalence compared to non-Hispanics (7.4%), those of Puerto Rican descent (14.5%) have a higher burden of asthma than those of Mexican descent (3.9%). AIM: The purpose of this study was to use data collected from a cohort of Puerto Rican infants born in New York City to examine associations between indoor pesticides use and wheeze and asthma in the first two years of life. The data were collected in a prospective birth cohort of Puerto Rican children born to mothers with a history of allergy or asthma. METHODS: Data analysis was conducted using SAS. Descriptive statistics were calculated and reported as percentages. Bivariate statistics were carried out to test independent associations. Logistic regression models for asthma and wheeze at each time point and generalized estimating equation (GEE) models (for wheeze at the end of the study period) were then created with adjustment of potential confounders. RESULTS: After controlling for confounders, no forms of pesticides were associated with wheeze using logistic regression and GEE. However, use of rodenticides at baseline yielded a hazardous relationship with asthma at two years of age (OR = 3.64, 95% CI = 1.26 - 10.52). DISCUSSION: The strong association with exposure to rodenticides at baseline reveals the importance of early life exposures, specifically those that occur prenatally or perinatally. Because rodenticide exposures have not been specifically identified as a possible risk factor in previous scientific literature, it is difficult to ascertain the mechanism behind exposure and asthma onset. Findings from this study and previous studies indicate that more research is needed to further elucidate the role of pesticides and physiological processes, specifically lung and immune system development, in children, especially those in highly allergenic environments.
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Judge, Abigail M. Penn David L. "Prospective identification of clinically relevant risk factors influencing illness course in childhood- and adolescent-onset psychotic disorders." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2528.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.Title from electronic title page (viewed Oct. 5, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Psychology Clinical." Discipline: Psychology; Department/School: Psychology.
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Murphy, Christel A. "The Development of an Educational and Vocational Needs Survey for Adults with Childhood-Onset Chronic Health Conditions." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1540565225128269.
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McDonald, Joseph. "Major Salivary Gland Ultrasound: Pilot Study of Findings and Feasibility in Childhood-Onset Systemic Lupus Erythematosus (cSLE)." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1583999153546294.
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O'Donnell, Cedar W. "Development of conduct problems in girls: Testing theoretical models and examining the role of puberty." ScholarWorks@UNO, 2007. http://scholarworks.uno.edu/td/574.
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In an attempt to understand girls' involvement conduct problems, this dissertation first reviews two existing theoretical approaches that provide an explanation for the development of conduct problems. Specifically, the available literature on the development and correlates of conduct problems in boys suggests the subtypes of conduct disorder represent two developmental trajectories. The adolescent-onset pathway is associated with deviant peers and few characterological problems, where as the childhood-onset pathway is associated with emotion regulation deficits, negative parenting, callous and unemotional traits, and neurological deficits. Research also suggests a gender-specific model, the delayed-onset model, for the development of conduct problems in girls. Following this theoretical review, differential predictions made by the competing theoretical models are tested in a community sample of school-aged girls and boys. Participants were 202 children (87 males and 115 females) in grades 5-9. The students ranged in age from 10 to 17 years old (M = 13.16). Similar to the total student body, the ethnic breakdown of the sample was as follows: African-American (60%), Caucasian (24%), Hispanic (6%), and Other (5%). Data was also collected from the students' parents and teachers. Results indicated that girls conduct problems did not follow either model in a consistent manner. Specifically, adolescent-onset conduct problem girls, childhood-onset conduct problem boys, and adolescentonset conduct problem boys differed from non-conduct problem children but did not differ significantly amongst themselves on study variables (e.g., deviant peer association, hyperactivity/impulsivity, emotional dysregulation, callous/unemotional traits). However, results suggest that gender-specific risk factors should be taken into account when developing theoretical models for girls' conduct problems. For example, early pubertal maturation is a particularly salient risk factor for conduct problems in girls, and pubertal development interacts with emotion regulation problems to place girls at high risk for deviant behavior. Finally, implications for prevention and intervention as well as future research are discussed.
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Chalhoub, Nathalie E. "Establishing Clinical Variables towards the Development of Corticosteroid Treatment Algorithms in Pediatric Proliferative Lupus Nephritis." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1554214478116667.
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Amatya, Kaushalendra. "Witnessing Partner Violence in Childhood: Factors Influencing Emotion Regulation Difficulties in College Students." Diss., Virginia Tech, 2014. http://hdl.handle.net/10919/63887.
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Witnessing partner violence (WPV) in childhood and adolescence can have significant impact on psychological functioning throughout development. Studies have shown that parenting factors, perceived social support, coping strategies, age at exposure, and gender can influence the relationship between WPV and outcomes. Although WPV can have serious implications towards emotion regulation abilities, empirical research on the link between WPV and emotion regulation is inadequate. The current study examined the associations between the frequency and types of WPV in childhood and adolescence and emotion dysregulation in adulthood. The study further explored the roles of parental bonds, social support, coping strategies, age at exposure, and gender as moderators in the relationship between WPV and emotion dysregulation. Data were collected using an undergraduate sample at Virginia Tech (N = 1040). Results indicated that verbal violence exposure was a significant predictor of emotion dysregulation while physical violence and total WPV were not. Parental warmth moderated the relationship between all three types of WPV and emotion dysregulation, while parental control and age of onset were moderators for total and physical WPV. Social support moderated the relationship between verbal violence exposure and emotion dysregulation. Coping strategies and gender were not found to be significant moderators. Exploratory analyses were conducted to further explore these relationships. The findings and their implications are discussed.Ph. D.
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Rosser, Casey Lynnell. "Analyzing the Relationship Between Exclusive Breastfeeding and the Onset of Childhood Obesity at 9-12 Months of Age." Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/297750.
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Childhood obesity is a public health crisis prevalent in the United States, particularly among Hispanics in Southern Arizona. There is much speculation that breastfeeding may be linked to a decreased risk of childhood obesity/overweight, but the association is unknown. Our purpose is to investigate the potential benefit of breastfeeding as a way to combat the obesity epidemic in Southern Arizona. The Ready.Set.StartSmart!(RSSS) database from a childhood obesity prevention study underway at The University of Arizona was used to examine whether there is a difference in the weight status of children who are exclusively breastfed compared to those who are bottle fed. We found children who were exclusively breastfed to be five times less likely to be overweight/obese at one year of age than those who were bottle fed(p=0.062). Despite the lack of statistical significance, our results indicate that breastfeeding may be a way to minimize the incidence of childhood obesity and overweight, though a larger sample size is needed. Other variables analyzed were: insurance status, primary language, birth order, mother’s age and pre-pregnancy BMI, RSSS intervention, and length of pregnancy. Of these, only the RSSS intervention status seemed to affect the overweight/obesity prevalence at one year of age.
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Ting, Tracy V. "Text Messaging: a Possible New Intervention to Improve Visit Adherence Among Childhood-onset Systemic Lupus Erythematosus (cSLE) Patients." Cincinnati, Ohio : University of Cincinnati, 2009. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1250702988.
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Thesis (M.S.)--University of Cincinnati, 2009.Advisor: Paul Succop. Title from electronic thesis title page (viewed Jan. 13, 2010). Includes abstract. Keywords: childhood SLE; adherence; text messaging. Includes bibliographical references.
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Milward, Sophie Jane. "Learning to act as a team : developmental onset, underlying processes and pre-requisites of co-representation in early childhood." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5651/.
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Co-representation has been argued to be a mechanism in adult joint action that allows participants in a joint task to co-ordinate their actions with a partner. Substantial evidence for this mechanism has come from tasks such as the joint Simon task (Sebanz, Knoblich & Prinz, 2003), which show interference from a partner’s task on one’s own performance. The following studies aim to use this mechanism as a measure of children’s joint action abilities and a way of directly comparing adult and child behaviours. Chapter 1 presents three studies which suggest a developmental onset of co-representation effects at around 4 years old. Chapter 2 attempts to uncover what type of representations may be formed in joint tasks at this age. Chapter 3 presents an individual differences study, suggesting that both Inhibitory Control and explicit Theory of Mind, but not Working Memory, play an indirect role in avoiding interference from co-representation. These findings contribute to the Joint Action Development literature, by demonstrating at least one way in which adult and child joint action may not be comparable. They also shed light on the adult co-representation literature, by highlighting cognitive skills that may interact with co-representation in order to reduce potential interference.
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Kurz, Susanne, Dyck Zoé van, Daniela Dremmel, Simone Munsch, and Anja Hilbert. "Early-onset restrictive eating disturbances in primary school boys and girls." Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-205300.
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Background. This study sought to determine the distribution of early-onset restrictive eating disturbances characteristic of the new DSM-5 diagnosis, avoidant/restrictive food intake disorder (ARFID) in middle childhood, as well as to evaluate the screening instrument, Eating Disturbances in Youth-Questionnaire (EDY-Q).
Methods. A total of 1444 8- to 13-year-old children were screened in regular schools (3rd to 6th grade) in Switzerland using the self-report measure EDY-Q, consisting of 12 items based on the DSM-5 criteria for ARFID.
Results. Forty-six children (3.2%) reported features of ARFID in the self-rating. Group differences were found for body mass index, with underweight children reporting features of ARFID more often than normal- and overweight children. The EDY-Q revealed good psychometric properties, including adequate discriminant and convergent validity.
Conclusions. Early-onset restrictive eating disturbances are commonly reported in middle childhood. Because of possible negative short- and long-term impact, early detection is essential. Further studies with structured interviews and parent reports are needed to confirm this study’s findings.
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Green, Ryan Liam. "Investigating the role of FUS, TDP-43 and DYNC1H1 mutations in the etiology of adult and childhood-onset motor neuron disease." Thesis, University of Sussex, 2017. http://sro.sussex.ac.uk/id/eprint/67574/.
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