Thesis (M.S.)--University of Wisconsin--Madison, 1981. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves [152]-157).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1983. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 165-169).

This study was designed to increase our understanding of remitted major depressive disorder among parents and how it relates to child externalizing problems. Specifically, various facets that may differentiate one remitted clinical depressive presentation from another were investigated: past depression severity, past depression chronicity, and residual or current levels of depressive symptoms. Relations of these characteristics of parent depression with youth externalizing symptomatology, as well as the mediating role of negative parenting, were studied among 118 parent-child dyads across two sites. Specifically, three hypotheses were tested: (1) all three indicators of parental depression would have a significant relationship with adolescent externalizing problems when examined individually; (2) when examined simultaneously, past depression chronicity and current depressive symptoms, but not past depression severity, would each have a unique association with young adolescent externalizing outcomes; and (3) negative parenting would partially mediate the relationship of each of the three indicators (i.e., current parental symptoms, past depression chronicity, past depression severity) with child externalizing behavior. Results revealed that residual parent depressive symptoms were most salient in their association with youth externalizing behavior. Further, negative parenting mediated this relationship for parent, but not child, report of child problem behavior. Findings highlight the importance of further research to investigate remitted clinical depression in parent populations, and the impact on child behavioral adjustment. As well, implications for preventive and other intervention efforts are considered.

No description available.

Abstract The purpose of this research was to assess the role of antibodies to glutamic acid decarboxylase (GAD) in children with newly diagnosed type 1 diabetes in relation to other disease-associated autoantibodies and HLA-defined genetic disease susceptibility, to evaluate the role of GAD antibodies (GADA) in relation to clinical characteristics at the diagnosis of type 1 diabetes and to compare the frequency and levels of GADA between adult and childhood onset type 1 diabetes.The study population comprised altogether 999 children and adolescents with type 1 diabetes, 100 affected adult subjects and more than 370 non-diabetic controls. GADA were measured with a liquid radioligand assay, and a similar assay was used for the analysis of antibodies to the islet antigen 2 (IA-2) molecule. Islet cell antibodies (ICA) were determined with conventional immunofluorescence and insulin autoantibodies (IAA) with a liquid phase radioimmunoassay either in a tube or a plate format (microassay). GADA were detected at diagnosis in 68 to 73% of the children and adolescents with type 1 diabetes. GADA were more frequent in girls and in those older than 10 years of age at clinical disease manifestation. Subjects testing positive for GADA had higher levels of ICA and IAA than those negative for GADA. Multiple antibodies ( 2) were observed more often in girls and in children under the age of 5 years. Children with the HLA DR3/non-DR4 phenotype had the highest GADA levels, significantly higher than those seen in children with the DR4/non-DR3 combination. The highest prevalence of multiple autoantibodies was seen in subjects heterozygous for DR3/4. When studying HLA DQB1 genotypes those with the DQB1*02/y (y = other than *0302) genotype had the highest GADA levels as expected since DQB1*02 and DR3 are in strong linkage disease equilibrium. The same group had the lowest frequency of multiple antibodies among the children younger than 10 years of age.Patients diagnosed with type 1 diabetes before the age of 20 had a higher frequency of all four autoantibodies analysed than those presenting with clinical disease after the age of 20. The proportion of subjects testing negative for all four antibodies was substantially higher among adults than in those under the age of 20. The smallest age-related difference in antibody frequencies was observed for GADA, and the GADA-positive adult patients had on an average about three times higher antibody levels than the GADA-positive children. No association was observed between positivity for GADA and the degree of metabolic decompensation at the clinical presentation of type 1 diabetes. No significant differences were either seen between the subjects who tested positive for GADA at diagnosis and those who were negative in serum C-peptide concentrations, metabolic control or exogenous insulin requirement over the first 2 years of observation. The proportion of children in clinical remission was, however, lower among GADA-positive subjects than in GADA-negative patients at 18 months after the clinical manifestation. Positivity for multiple antibodies was associated with accelerated beta-cell destruction and increased exogenous insulin requirements over the 2-year observation period. The observations that GADA are related to female gender, older age and the HLA-DR3/ DQB1*02 haplotype suggest that a strong humoral immune response to GAD may reflect a propensity to general autoimmunity rather than specific beta-cell destruction.

No description available.

Cancer survivors typically adapt well to life following remission; however, some patients still experience lingering negative moods that may develop into depression. There are multiple factors that can contribute to depressive symptoms from somatic symptoms, to emotion and social concerns. When analyzing these contributing factors, an underlying theory of a connection between the symptoms of depression and inflammation was revealed. Although this was not shown to be a causal association, it set forward some theories on the pathogenesis of depression in cancer survivors who may have persistent inflammation following treatment. As cancer patients are a growing group due to improvements in treatment and an aging general population, early identification of high-risk survivors and research into new treatment methods is essential. Depression in survivors can lead to an inability to follow through on medical care, decreased quality of life and poorer patient health outcomes. Currently, depressive symptoms are treated primarily on an individual basis, determining if there is a common underlying biological mechanism that could help scientists develop new guidelines for the treatment of survivors. Research studies demonstrated interdependence between conditions such as chronic pain, fatigue, sleep disturbance, cognitive impairment and depression. Current published literature on each of these conditions was explored and while each of these conditions have demonstrated connections to inflammatory pathways and specific cytokines, there does not appear to be one common underlying mechanism. Preliminary research has presented some options for future treatments that can mitigate the severity of the inflammation caused during traditional cancer therapies. These preventative measures address certain cytokine pathways that have been associated with negative side effects. As emotional and social concerns can add to a survivor’s stress causing stimulation of inflammatory pathways, evidence-based methods for reducing stress have been discussed and include exercise, psychosocial and occupational therapy interventions as well as legislative advocacy for better insurance coverage. There are some limitations in the current literature on the topic as much of the survivor research centers on patients who were diagnosed with breast cancer. There are several diverse subgroups of cancer survivors including childhood, adolescent and young adult, and adult cancer survivors, and comprehensive research should be conducted across these cohorts to ascertain which groups are at a higher risk for certain symptoms and stresses. Furthermore, research into novel treatment options has focused mainly on pharmacological solutions to the negative impacts of chemotherapy. While several studies have theorized about possible, persistent biological mechanisms underlying radiotherapy, few drugs have been suggested or developed to combat the late effects of inflammation including fibrosis. Many of the suggested treatments can be given as a co-treatment alongside of chemotherapy, radiotherapy or surgery; in the future, research should be conducted on the effects of reducing inflammatory levels in patients already in remission.

Objective. To examine the natural course of social anxiety disorder (SAD) in the community and to explore predictors for adverse long-term outcomes. Method. A community sample of N=3,021 subjects aged 14-24 was followed-up over 10 years using the DSM-IV/M-CIDI. Persistence of SAD is based on a composite score reflecting the proportion of years affected since onset. Diagnostic stability is the proportion of SAD subjects still affected at follow-up. Results. SAD reveals considerable persistence with more than half of the years observed since onset spent with symptoms. 56.7% of SAD cases revealed stability with at least symptomatic expressions at follow-up; 15.5% met SAD threshold criteria again. 15.1% were completely remitted (no SAD symptoms and no other mental disorders during follow-up). Several clinical features (early onset, generalized subtype, more anxiety cognitions, severe avoidance and impairment, co-occurring panic) and vulnerability characteristics (parental SAD and depression, behavioural inhibition, harm avoidance) predicted higher SAD persistence and -less impressively- diagnostic stability. Conclusion. A persistent course with a considerable degree of fluctuations in symptom severity is characteristic for SAD. Both, consistently meeting full threshold diagnostic criteria and complete remissions are rare. Vulnerability and clinical severity indicators predict poor prognosis and might be helpful markers for intervention needs.

No description available.

Thesis (M.C.P.)--Massachusetts Institute of Technology, Dept. of Urban Studies and Planning, 1982. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ROTCH / Bibliography: leaves 61-62. / by Arne Steven Abramson. / M.C.P.