Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

M.A. / Patterns of substance abuse within the family is a widespread phenomenon that occurs through generations. Although various factors can be a symptom of a dysfunctional family, the dynamics that maintain the transgenerational patterns of substance abuse are of great interest. The family in which the abuse of alcohol is repetitive through generations, is seen as a dysfunctional family system. It appears that a circular pattern exists in the family that maintains the alcohol abuse. Although the family as a whole has an influence on individual members, these individual members enter their families with their own preconceived mind maps of past experiences that also have a great influence on the family dynamics. Family dynamics are seen as those factors that impact either positively or negatively on the family and its individual members. The alcoholic parent and adult child of the alcoholic parent are the subjects of concern in this study because it is assumed that parental inputs have been the most influential in the respondent’s lives. A qualitative method of research was implemented to describe this explorative study and was decided on because it describes the phenomenon of transgenerational patterns of alcohol abuse from the viewpoint of the respondent. The aim of this research study was to determine the dynamics that contribute to transgenerational patterns of alcohol abuse, with specific reference to the respondent’s family history of alcohol abuse, their co-dependency (alcohol abuse) and the maintenance of these dynamics throughout generations. These dynamics will be explained in terms of the Living Systems Theory and the Object Relations Theory. These theories form the theoretical foundation from which these dynamics were explained. From these theories a strategy of data-gathering was developed with specific focus on the genogram, family tree and general questions. A focused sampling method was implemented in this research study, and the research units consisted of five respondents with families that have a history of alcohol abuse. Data-gathering was done through phenomenological and semi-structured interviews. The interviews were audiotaped and fieldnotes were made, although limited and only to confirm some of the findings of the research study. The data was analysed according to a specific strategy. Preliminary coding was done by using the audiotapes (transcriptions) and fieldnotes. After the preliminary coding was completed, these categories were used to derive central themes from the findings and all the categories were then divided under one or several of these themes. These central themes were compared with existing literature in order to confirm the findings of this research study and to enhance the trustworthiness. From the study, certain recommendations with regard to methodology and content were made. / Dr. E. Oliphant

Graduation date: 1994

No description available.

E realizado o estudo epidemiológico das meningites de etiologia indeterminada no Municlpio de São Paulo, no período de 1960 a 1977. O trabalho é apresentado em quatro partes. Na primeira parte são apresentados e discutidos os diferentes modos de diagnóstico etiológico das meningites (presuntivos e de certeza) e é enfatizada a necessidade do estudo das meningites indeterminadas. Na segunda parte é apresentado o comportamento epidemiológico da doença meningocócica no Município de São Paulo, no período 1960 a 1977. Esta apresentação é feita visando comparar e procurando verificar a influência da doença meningocócica no comportamento epidemiológico das meningites de etiologia indeterminada. Na terceira e quarta partes são apresentados os caracteres epidemiológicos das meningites de etiologia indeterminada. Inicialmente os casos são classificados em meningites indeterminadas de provavel etiologia bacteriana ou viral, utilizando-se como parâmetro para a classificação o percentual de neutrófilos no liquor. Em seguida são apresentados e analisados os comportamentos segundo variaveis da pessoa (idade e sexo), do local de residência (segundo distritos e areas homogêneas do município), do tempo (variação anual e mensal), modo diagnóstico, evolução clinica, tempo de hospitalização. O estudo mostra que entre 1972 e 1977 ocorreu no Município de São Paulo um aumento significativo de casos de meningite de etiologia indeterminada; grande parte dos casos, provavelmente, era constituída por casos de meningite meningocócica, dos quais não foi possivel a determinação etiológica. Ocorreu também, concomitantemente, um aumento significativo de meningites de provável etiologia viral. O percentual de neutrófilos no liquor (primeiro exame) em épocas epidêmicas, pode ser utilizado como parâmetro para classificacão epidemiológica meningites segundo etiologia provavelmente bacteriana ou viral. / The epidemiological behaviour of the meningitis of undetermined etiology within the Municipality of São Paulo, during the period from 1860 to 1977, is studied. The work consists of four parts. In the first part, the different forms of etiological diagnosis of meningitis (either presumptives ar certain) are submitted and discussed, as well as the need study of the undetermined meningitis. In the second part the epidemiological behaviour of the meningococcal diseases within the Municipality of São Paulo, during the period from 1960 to 1977, is submitted. Such a presentation is made with the purpose of comparison, and trying to verify the influence of the meningococcal disease on the epidemiological behaviour of the meningitis of undetermined etiology. In the third and fourth parts, the epidemiologic characters of the meningitis of undetermined etiology are submitted. At first, the cases are classified as undetermined meningitis of probable bacterial or viral etiology, using as parameter for the classification the percentile number of neutrophiles in the liquor (first examination). Then, there are submitted and analysed the behaviour as per the variables of the person (age and sex), place of residence (according to districts and homogeneous areas within the Municipality), time (annual and monthly variation), form of diagnosis, clinic evolution, and hospitalization period. It is concluded that between 1972 and 1977 there was in the Municipality of São Paulo, an epidemics of meningitis of undetermined etiology; most of the cases were, probably, constituted by cases of meningococcic meningitis, of which it was not possible to make the etiologic determination. There was, also, al the same time, an important increase of diagnosis of meningitis of probable viral etiology. The percentile number of neutrophiles in the Liquor (first examination), in epidemic times, may be used as an epidemiological parameter for the classification of the meningitis, as per the etiology, probably bacterial or viral.

by Lit Choi Wan. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 119-127). / ACKNOWLEDGEMENTS / SUMMARY / LIST OF TABLES / LIST OF FIGURES / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Terminology & Overview --- p.2 / Chapter 1.2 --- Gell & Coombs Classification of Hypersensitivity --- p.3 / Chapter 1.2.1 --- Type I - Immediate Hypersensitivity --- p.4 / Chapter 1.2.2 --- Type II - Antibody Dependent Cytotoxic Hypersensitivity --- p.4 / Chapter 1.2.3 --- Type III - Immune-Complex Mediated Hypersensitivity --- p.6 / Chapter 1.2.4 --- Type IV - Cell-Mediated (Delayed-Type) Hypersensitivity --- p.6 / Chapter 1.3 --- Historical Review of IgE-Mediated Hypersensitivity --- p.7 / Chapter 1.4 --- The Clinical Biochemistry of IgE --- p.8 / Chapter 1.4.1 --- Structure and Properties --- p.9 / Chapter 1.4.2 --- The Fcε Receptors --- p.11 / Chapter 1.4.3 --- Production and Tissue Localisation --- p.11 / Chapter 1.4.4 --- Turnover in Blood and on Mast Cells --- p.13 / Chapter 1.4.5 --- Control of Synthesis --- p.13 / Chapter 1.4.6 --- The Role of IgE in Health and Disease --- p.14 / Chapter 1.5 --- Pathophysiology of IgE-Mediated Hypersensitivity --- p.20 / Chapter 1.5.1 --- Cell Activation and IgE Synthesis --- p.20 / Chapter 1.5.2 --- Activation of Mast Cells and Basophils --- p.22 / Chapter 1.6 --- Allergens --- p.25 / Chapter 1.7 --- Factors Predisposing to Allergy --- p.30 / Chapter 1.7.1 --- Genetic Predisposition --- p.30 / Chapter 1.7.2 --- Environmental Exposure --- p.32 / Chapter 1.7.3 --- Underlying Infection and Immune Status --- p.32 / Chapter 1.8 --- Epidemiology --- p.33 / Chapter 1.8.1 --- Allergic Diseases Worldwide --- p.33 / Chapter 1.8.2 --- Allergic Diseases in Hong Kong --- p.34 / Chapter 1.9 --- Diagnosis of IgE-Mediated Allergy --- p.36 / Chapter 1.9.1 --- Medical History and Physical Examination --- p.36 / Chapter 1.9.2 --- Introduction to Diagnostic Tests --- p.36 / Chapter 1.9.3 --- Skin Tests --- p.37 / Chapter 1.9.4 --- In Vitro Tests --- p.38 / Chapter 1.9.5 --- Serum Total IgE Assay --- p.41 / Chapter (1) --- Test Principle --- p.41 / Chapter (2) --- Normal Values of Serum Total IgE Concentration --- p.42 / Chapter 1.9.6 --- Allergen Specific IgE Concentration --- p.44 / Chapter (1) --- Principle of RAST --- p.44 / Chapter (2) --- Clinical Usefulness of RAST --- p.44 / Chapter 1.9.7 --- The CAP System --- p.46 / Chapter 1.9.8 --- Mixed Aeroallergen Specific IgE Assay (Phadiatop´ёØ) --- p.46 / Chapter 1.10 --- Further Notes on Allergic Rhinitis --- p.48 / Chapter 1.10.1 --- A Prevalent and Costly Health Problem --- p.48 / Chapter 1.10.2 --- Epidemiology --- p.48 / Chapter 1.10.3 --- Symptoms of Allergic Rhinitis --- p.49 / Chapter 1.10.4 --- ENT Examination --- p.49 / Chapter 1.11 --- Aims of This Study --- p.51 / Chapter CHAPTER 2 --- MATERIALS AND METHOD I Evaluation of The Pharmacia CAP System --- p.52 / Chapter 2.1 --- Materials --- p.53 / Chapter 2.1.1 --- Pharmacia Reagents --- p.53 / Chapter 2.1.2 --- Abbott Reagents --- p.54 / Chapter 2.1.3 --- In-House Reagents --- p.54 / Chapter 2.2 --- Apparatus and Equipment --- p.55 / Chapter 2.2.1 --- Components and Accessories of the CAP System --- p.55 / Chapter 2.2.2 --- Abbott IMx Analyser --- p.55 / Chapter 2.3 --- Methods for Evaluation of the Pharmacia CAP System --- p.56 / Chapter 2.3.1 --- Principle of the Pharmacia CAP System RAST FEIA Fluorescence Enzyme Immunoassay --- p.56 / Chapter 2.3.2 --- Assay Preparation and Procedure --- p.58 / Chapter 2.3.3 --- Evaluation Experiments --- p.59 / Chapter (1) --- Elution Efficiency of Assay Washer96 --- p.59 / Chapter - --- Gross Assessment of Assay Washer96 --- p.59 / Chapter - --- Precision of Elution Volume in Each Well --- p.60 / Chapter - --- Overall Precision and Accuracy of Elution through ImmunoCAP --- p.60 / Chapter (2) --- Precision of RAST FEIA --- p.60 / Chapter (3) --- Accuracy --- p.61 / Chapter (4) --- Linearity and Detection Limits --- p.61 / Chapter (5) --- Recovery Study --- p.61 / Chapter CHAPTER 3 MATERIALS --- AND METHOD II Aetiology of Allergic Rhinitis in Hong Kong --- p.62 / Chapter 3.1 --- Patients and Controls --- p.63 / Chapter 3.2 --- Blood Samples --- p.63 / Chapter 3.3 --- Serum Total IgE Assay --- p.65 / Chapter 3.4 --- Mixed Aeroallergen Specific IgE (Phadiatop) --- p.67 / Chapter 3.5 --- Statistical Analysis --- p.67 / Chapter CHAPTER 4 --- RESULTS I Evaluation of The Pharmacia CAP System --- p.70 / Chapter 4.1 --- Elution Efficiency of Assay Washer96 --- p.71 / Chapter 4.1.1 --- Gross Assessment of Elution Volume --- p.71 / Chapter 4.1.2 --- Precision of Elution Volume in Each Well --- p.72 / Chapter 4.1.3 --- Overall Precision and Accuracy of Elution through ImmunoCAP --- p.75 / Chapter 4.2 --- Precision of RAST FEIA --- p.75 / Chapter 4.3 --- Accuracy --- p.75 / Chapter 4.4 --- Linearity and Detection Limit --- p.79 / Chapter 4.5 --- Recovery --- p.79 / Chapter CHAPTER 5 --- RESULTS II Aetiology of Allergic Rhinitis in Hong Kong --- p.83 / Chapter 5.1 --- Patients and Controls --- p.84 / Chapter 5.2 --- "Serum Total IgE, Mixed Aeroallergen IgE (Phadiatop) and Specific IgE Concentrations in Patients and Controls" --- p.84 / Chapter 5.2.1 --- Total IgE Concentration --- p.84 / Chapter 5.2.2 --- Phadiatop´ёØ --- p.84 / Chapter 5.2.3 --- Specific IgE Concentration --- p.93 / Chapter 5.2.4 --- Degree and Severity of Sensitization --- p.93 / Chapter 5.2.5 --- Single and Multiple Allergy --- p.94 / Chapter 5.2.6 --- Usefulness of Phadiatop´ёØ --- p.94 / Chapter CHAPTER 6 --- DISCUSSION I Evaluation of the Pharmacia CAP System --- p.95 / Chapter 6.1 --- Elution Efficiency of Assay Washer96 --- p.96 / Chapter 6.2 --- "Within-Batch and Between-Batch Precision, Accuracy, Linearity and Detection Limit, and Recovery of FEIA" --- p.97 / Chapter 6.3 --- Overall Evaluation --- p.98 / Chapter CHAPTER 7 --- DISCUSSION II Aetiology of Allergic Rhinitis in Hong Kong --- p.100 / Chapter 7.1 --- Patients and Controls --- p.101 / Chapter 7.2 --- Serum Total IgE Concentration --- p.102 / Chapter 7.3 --- Efficiency of Phadiatop´ёØ Screening Test --- p.103 / Chapter 7.4 --- Serum Specific IgE Assay and Aetiology of Allergic Rhinitis in Hong Kong --- p.107 / Chapter 7.4.1 --- Major Allergens in Allergic Rhinitis --- p.107 / Chapter 7.4.2 --- House Dust Mite --- p.108 / Chapter 7.4.3 --- Cockroach --- p.111 / Chapter 7.4.4 --- Cat and Dog --- p.111 / Chapter 7.4.5 --- Pollens --- p.112 / Chapter 7.4.6 --- Moulds --- p.113 / Chapter 7.4.7 --- Summary --- p.115 / REFERENCES --- p.118

The c-Jun N-terminal kinases (JNKs) are MAPK family members and are activated by stress, growth factors and cytokines. They are encoded by three separate genes (jnk 1, 2, and 3), spliced alternately creating 10 isoforms. JNK signaling promotes both cell death and cell survival in a stimuli and tissue specic manner and is also implicated in tumorigenesis. Using the Polyoma Virus Middle T Antigen (PyVMT) transgenic mouse model where jnk2 was either expressed or deleted, we found that the PyVMTjnk2-/- tumors expressed higher Epidermal Growth Factor Receptor Substrate 8 (EPS8) mRNA and protein. EPS8 regulates EGFR signaling from Ras to Rac and EGFR tracking via Rab5 and RN-Tre. EPS8 is a prime candidate for connecting the EGFR signaling to actin cytoskeleton remodeling, thus mediating cell migration, a critical step in metastasis. In migration assays, PyVMTjnk2+/+ cells migrated ve fold more than the PyVMTjnk2-/- cells. Re-expression of JNK2[alpha] in the PyVMTjnk2-/- cells rescued this phenotype. Expression of shRNA EPS8 in the PyVMTjnk2-/- cell increased migration in vitro. EPS8 localization at dorsal rues and internalization of EGF-EGFR complexes coincided with JNK2 expression. Expression of shEPS8 in the PyVMTjnk2-/- cells increased EGF internalization suggesting that in absence of JNK2, EPS8 participates in Rab5-RN-Tre complex that inhibits EGFR internalization. Finally, we report that in absence of JNK2, EPS8 protein stability is greatly increased, suggesting that JNK2 is essential for endosomal sorting and degradation of EGFR associated cargo, of which EPS8 is a critical part. In contrast, silencing JNK1 (p46) in 4T1.2 mammary tumor cells, consistently enhanced cell invasion and tumor growth. Tumors derived from orthotopic injection of the 4T1.2shJNK1 expressing cells into the mammary fat pad reached target volume signicantly earlier than non-silencing vector expressing tumors. When injected intravenously, signicantly higher lung metastasis was observed in the 4T1.2shJNK1 group. The more aggressive behavior of 4T1.2shJNK1 tumors was associated with an increase in CCR5 and pAkt as detected by microarray analysis. Taken together, our data suggest that JNK1 suppresses the expression of proteins associated with tumor growth and invasive phenotype, contributing to tumor progression. / text

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