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

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.

In general, AD is diagnosed based on Hanifin and Rajka's diagnostic criteria or the UK working diagnostic criteria. The atopic status of study participants was evaluated clinically by (1) the presence of atopic symptoms including allergie rhinitis, asthma or hyperactive airway disease in patients, parents, and/or siblings, (2) measuring the concentrations of total and allergen-specific IgE in their peripheral blood, and/or (3) positive skin prick tests to common aeroallergens or food allergens. The severity of AD was assessed either clinically by validated disease scores, objective serum parameters such as serum chemokine levels, or physiological parameters such as nocturnal wrist movements. Quality of life (QoL) is assessed with the Cantonese version of the Children's Dermatology Life Quality Index (CDLQI). Although not a gold standard, ail assessment tools were compared against SCORAD. / Research Hypotheses or aims: (1) To investigate if AD severity as determined by a 12-month-severity score correlates with a validated acute severity score. The research aims to establish a chronic severity scores for local use in AD research. (2) To explore if correlations exist between objective and subjective symptoms. (3) To evaluate if quality of life (QoL) correlates with disease severity. (4) To assess if age and gender may affect quality of life. (5) To explore if serum markers (CTACK, IL-18, BDNF, and substance P.) correlate with disease severity or quality of life score. (6) To evaluate if urine LTE4 as a non-serum marker correlates with disease severity. (7) To evaluate if nocturnal wrist movements correlate with various clinical and laboratory markers. (8) To evaluate if skin hydration (SH) and transepidermal water loss (TEWL) correlate with severity and QoL. (9) In a final chapter, we give a number of clinical studies to illustrate the application of these methods in clinical research. / The objectives of the MD thesis are to explore various clinical scores, quality of life evaluation, laboratory tests, and mechano-physiological parameters as assessment tools for the evaluation of AD. The research hypotheses are that many aspects of the disease can be objectively measured by these new scores and markers. The application of some of these assessment tools in clinical trials will be described. In all of the studies reported, I am the principal investigator and the first author of the publications in indexed medical journals. / Kam Lun Ellis Hon. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3419. / Thesis (M.D.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 192-213). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / School code: 1307.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 5 uppsatser.

Includes bibliographical references and index.

INTRODUÇÃO: A dermatite atópica (DA) é uma doença cutânea inflamatória, acompanhada por prurido intenso e xerose cutânea. A etiopatogenia da DA é multifatorial, envolvendo fatores genéticos, ambientais e imunológicos, dentre outros. OBJETIVOS: Avaliar a influência das enterotoxinas A e B do Staphylococcus aureus (SEA e SEB) na resposta mediada por células Th17 e Th22 nos indivíduos adultos com DA. MÉTODOS: Foram selecionados 38 pacientes adultos com DA e um grupo controle com 40 indivíduos adultos, pareados por idade e gênero Os métodos utilizados foram: 1) ELISA: dosagem dos níveis séricos de IL-6, IL-17, IL-22 e IL-12p40/IL-23 e em sobrenadantes de culturas de células mononucleares do sangue periférico (PBMC) estimuladas com SEA e SEB; 2) Imuno-histoquímica: análise da expressão de IL-17 em fragmentos de pele; 3) Citometria de fluxo: a) análise das citocinas circulantes em amostras de soro: IL-2, IL-4, IL-5, IL-6, IL-10, TNF, IL-17A e IFN-y b)avaliação das células T CD4+ mono e polifuncionais secretoras de IL-17, IL-22, TNF, IFN-y, MIP-1beta, e expressão do marcador de ativação celular CD38; c) células Th22 e Tc22 estimuladas com SEA e SEB. RESULTADOS: 1) Através do ELISA, a secreção de IL-22 sérica e em PBMC induzidas por SEA e SEB foi significativamente mais elevada, quando comparada ao grupo controle; 2) houve aumento na expressão de IL-17 em amostras de pele de doentes de DA através da imuno-histoquímica; 3) Através da citometria de fluxo, foram detectados: a) níveis séricos de IL-2, 5, 6, 10, 17A e IFN-y elevados no grupo com DA em relação aos controles; houve diferença significativa nos níveis circulantes de IL-17A nos pacientes com DA moderada e grave; b) na avaliação monofuncional das células T CD4+ sob estímulo de SEA/SEB, houve redução da expressão das citocinas IFN-y, IL-17A, IL-22 ou TNF na DA, quando comparadas ao grupo controle; na análise polifuncional das células T CD4+/CD8+, ocorreu redução da resposta na DA em relação aos controles; nos pacientes atópicos encontramos aumento da resposta em situação basal na dependência de CD38, e redução na resposta frente a SEA/SEB na ausência de CD38; c) encontramos resposta reduzida das células Th22, e elevada de células Tc22 frente aos estímulos SEA e SEB, nos pacientes com DA. CONCLUSÕES: O estudo corrobora o papel patogênico das enterotoxinas estafilocócicas na DA. A ativação crônica com superantígenos estafilocócicos pode contribuir com a alta frequência de células T CD4+ CD38+ polifuncionais, e com a resposta polifuncional anérgica, mediadas por células T CD38- / BACKGROUND: Atopic dermatitis (AD) is an inflammatory skin disease with intense itching and xerosis. AD pathogenesis is multifactorial, involving genetic, environmental, and immunological factors, among others. OBJECTIVES: To evaluate the influence of enterotoxins A and B from Staphylococcus aureus (SEA and SEB) in Th17 and Th22 cell response in adults with AD. METHODS: We evaluated 38 adult patients with AD, and a control group of 40 adults, age and gender matched. Assays: 1) ELISA: evaluation of IL-6, IL-17, IL-12p40/IL-23 and IL-22 serum levels and in supernatants of mononuclear cell cultures from peripheral blood (PBMC), stimulated with SEA/SEB; 2) Immunohistochemistry: analysis of IL-17 expression in skin specimens; 3) Flow cytometry: a) analysis of circulating cytokines in serum samples: IL-2, IL-4, IL-5, IL-6, IL-10, TNF, IL-17A and IFN-y b) evaluation of mono and polyfunctional TCD4+ cells that secrete IL-17, IL-22, TNF, IFN-y, MIP-1beta, and expression of the activation marker CD38; c) analysis of Tc22 and Th22 cells stimulated with SEA and SEB. RESULTS: 1) Secretion of IL-22 in the serum and from supernatants of cell cultures from PBMC, stimulated with SEA and SEB were higher in AD patients, when compared to the control group by ELISA; 2) there was an increase of IL-17 expression in skin samples by immunohistochemistry; 3) Flow cytometry showed: a) elevated serum levels of IL-2, 5, 6, 10, 17A and IFN-y in AD, when compared to controls; there was a significant difference in circulating levels of IL-17A in patients with moderate and severe disease; b) monofunctional evaluation of T CD4+ cells under SEA/SEB stimuli showed reduced expression of IFN-y, IL-17A, IL-22 or TNF cytokines in AD, compared to controls; the same was observed for polyfunctional CD4+/CD8+ T cells analysis, exhibiting a diminished response in AD. In atopic patients under basal conditions, there was an augmented CD38- dependent response and reduced pattern to SEA/SEB in the absence of CD38; c) finally, we observed a reduced response of Th22 cells and enhanced Tc22 cells under SEA/SEB stimuli in patients with AD. CONCLUSIONS: This study corroborates the pathogenic role of staphylococcal enterotoxins in AD. Chronic activation with staphylococcal superantigens may contribute to the high frequency of polyfunctional CD4 +CD38+ T cells and with the anergic polyfunctional response mediated by T CD38- T cells

A resposta proliferativa das células mononucleares do sangue periférico dos adultos com dermatite atópica mostrou-se diminuída após estímulos com mitógenos (enterotoxinas estafilocócicas A e B, "pokeweed" e fitohemaglutinina) e antígenos (toxóide tetânico e Candida albicans). A correlação positiva dos níveis séricos de interleucina-18, IgE e escore de gravidade da doença sugerem que esta citocina seria um marcador de atividade da dermatite atópica do adulto / A reduced proliferative response of peripheral blood mononuclear cells in adults with atopic dermatitis was detected when stimuli with mitogens (staphylococcal enterotoxins A and B, phytohemaglutinin, pokeweed), and with antigens (tetanus toxoid and Candida albicans) were performed. A positive correlation of interleukin-18, IgE levels and severity scores of the disease suggest that this cytokine could be a marker of disease activity in adult atopic dermatitis

A resposta proliferativa das células mononucleares do sangue periférico dos adultos com dermatite atópica mostrou-se diminuída após estímulos com mitógenos (enterotoxinas estafilocócicas A e B, "pokeweed" e fitohemaglutinina) e antígenos (toxóide tetânico e Candida albicans). A correlação positiva dos níveis séricos de interleucina-18, IgE e escore de gravidade da doença sugerem que esta citocina seria um marcador de atividade da dermatite atópica do adulto / A reduced proliferative response of peripheral blood mononuclear cells in adults with atopic dermatitis was detected when stimuli with mitogens (staphylococcal enterotoxins A and B, phytohemaglutinin, pokeweed), and with antigens (tetanus toxoid and Candida albicans) were performed. A positive correlation of interleukin-18, IgE levels and severity scores of the disease suggest that this cytokine could be a marker of disease activity in adult atopic dermatitis

INTRODUÇÃO: A dermatite atópica (DA) é uma doença cutânea inflamatória, acompanhada por prurido intenso e xerose cutânea. A etiopatogenia da DA é multifatorial, envolvendo fatores genéticos, ambientais e imunológicos, dentre outros. OBJETIVOS: Avaliar a influência das enterotoxinas A e B do Staphylococcus aureus (SEA e SEB) na resposta mediada por células Th17 e Th22 nos indivíduos adultos com DA. MÉTODOS: Foram selecionados 38 pacientes adultos com DA e um grupo controle com 40 indivíduos adultos, pareados por idade e gênero Os métodos utilizados foram: 1) ELISA: dosagem dos níveis séricos de IL-6, IL-17, IL-22 e IL-12p40/IL-23 e em sobrenadantes de culturas de células mononucleares do sangue periférico (PBMC) estimuladas com SEA e SEB; 2) Imuno-histoquímica: análise da expressão de IL-17 em fragmentos de pele; 3) Citometria de fluxo: a) análise das citocinas circulantes em amostras de soro: IL-2, IL-4, IL-5, IL-6, IL-10, TNF, IL-17A e IFN-y b)avaliação das células T CD4+ mono e polifuncionais secretoras de IL-17, IL-22, TNF, IFN-y, MIP-1beta, e expressão do marcador de ativação celular CD38; c) células Th22 e Tc22 estimuladas com SEA e SEB. RESULTADOS: 1) Através do ELISA, a secreção de IL-22 sérica e em PBMC induzidas por SEA e SEB foi significativamente mais elevada, quando comparada ao grupo controle; 2) houve aumento na expressão de IL-17 em amostras de pele de doentes de DA através da imuno-histoquímica; 3) Através da citometria de fluxo, foram detectados: a) níveis séricos de IL-2, 5, 6, 10, 17A e IFN-y elevados no grupo com DA em relação aos controles; houve diferença significativa nos níveis circulantes de IL-17A nos pacientes com DA moderada e grave; b) na avaliação monofuncional das células T CD4+ sob estímulo de SEA/SEB, houve redução da expressão das citocinas IFN-y, IL-17A, IL-22 ou TNF na DA, quando comparadas ao grupo controle; na análise polifuncional das células T CD4+/CD8+, ocorreu redução da resposta na DA em relação aos controles; nos pacientes atópicos encontramos aumento da resposta em situação basal na dependência de CD38, e redução na resposta frente a SEA/SEB na ausência de CD38; c) encontramos resposta reduzida das células Th22, e elevada de células Tc22 frente aos estímulos SEA e SEB, nos pacientes com DA. CONCLUSÕES: O estudo corrobora o papel patogênico das enterotoxinas estafilocócicas na DA. A ativação crônica com superantígenos estafilocócicos pode contribuir com a alta frequência de células T CD4+ CD38+ polifuncionais, e com a resposta polifuncional anérgica, mediadas por células T CD38- / BACKGROUND: Atopic dermatitis (AD) is an inflammatory skin disease with intense itching and xerosis. AD pathogenesis is multifactorial, involving genetic, environmental, and immunological factors, among others. OBJECTIVES: To evaluate the influence of enterotoxins A and B from Staphylococcus aureus (SEA and SEB) in Th17 and Th22 cell response in adults with AD. METHODS: We evaluated 38 adult patients with AD, and a control group of 40 adults, age and gender matched. Assays: 1) ELISA: evaluation of IL-6, IL-17, IL-12p40/IL-23 and IL-22 serum levels and in supernatants of mononuclear cell cultures from peripheral blood (PBMC), stimulated with SEA/SEB; 2) Immunohistochemistry: analysis of IL-17 expression in skin specimens; 3) Flow cytometry: a) analysis of circulating cytokines in serum samples: IL-2, IL-4, IL-5, IL-6, IL-10, TNF, IL-17A and IFN-y b) evaluation of mono and polyfunctional TCD4+ cells that secrete IL-17, IL-22, TNF, IFN-y, MIP-1beta, and expression of the activation marker CD38; c) analysis of Tc22 and Th22 cells stimulated with SEA and SEB. RESULTS: 1) Secretion of IL-22 in the serum and from supernatants of cell cultures from PBMC, stimulated with SEA and SEB were higher in AD patients, when compared to the control group by ELISA; 2) there was an increase of IL-17 expression in skin samples by immunohistochemistry; 3) Flow cytometry showed: a) elevated serum levels of IL-2, 5, 6, 10, 17A and IFN-y in AD, when compared to controls; there was a significant difference in circulating levels of IL-17A in patients with moderate and severe disease; b) monofunctional evaluation of T CD4+ cells under SEA/SEB stimuli showed reduced expression of IFN-y, IL-17A, IL-22 or TNF cytokines in AD, compared to controls; the same was observed for polyfunctional CD4+/CD8+ T cells analysis, exhibiting a diminished response in AD. In atopic patients under basal conditions, there was an augmented CD38- dependent response and reduced pattern to SEA/SEB in the absence of CD38; c) finally, we observed a reduced response of Th22 cells and enhanced Tc22 cells under SEA/SEB stimuli in patients with AD. CONCLUSIONS: This study corroborates the pathogenic role of staphylococcal enterotoxins in AD. Chronic activation with staphylococcal superantigens may contribute to the high frequency of polyfunctional CD4 +CD38+ T cells and with the anergic polyfunctional response mediated by T CD38- T cells

Wong Kin Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 151-166). / Abstracts in English and Chinese. / Chapter (I) --- ABSTRACT (IN ENGLISH) --- p.i / Chapter (II) --- Abstract (in Chinese) --- p.iv / Chapter (III) --- ACKNOWLEDGEMENTS --- p.vii / Chapter (IV) --- PERSONAL CONTRIBUTION TO THE WORK --- p.ix / Chapter (V) --- PUBLICATIONS --- p.x / Chapter (VI) --- TABLE OF CONTENTS --- p.xi / Chapter (VII) --- List of Abbreviations --- p.xvi / Chapter (VIII) --- LIST OF FIGURES --- p.xx / Chapter (IX) --- LIST OF TABLES --- p.xxii / Chapter Section 1: --- GENERAL INTRODUCTION / Chapter CHAPTER 1 --- General Introduction of Atopic Dermatitis --- p.1-8 / Chapter 1.1. --- Definition of Atopic Dermatitis --- p.1 / Chapter 1.2. --- Epidemiology and Classification --- p.3 / Chapter 1.3. --- Factors Provoking Flares of AD / Chapter 1.3.1. --- Genetics --- p.5 / Chapter 1.3.2. --- "Allergens-Food Allergens, Aeroallergens and Autoallergens" --- p.6 / Chapter 1.3.3. --- Microbial Colonization: Staphylococcus Aureus (S. aureus) --- p.7 / Chapter CHAPTER 2 --- Measurements of AD Severity and Quality of Life Impairment --- p.9-14 / Chapter 2.1. --- Scoring of Atopic Dermatitis severity and the SCORing Atopic Dermatitis (SCORAD) Index --- p.9 / Chapter 2.2. --- Quality of life Measurement --- p.10 / Chapter 2.3. --- The Children's Dermatology Life Quality Index --- p.11 / Chapter CHAPTER 3 --- Management of AD --- p.15-19 / Chapter 3.1. --- Current Management of AD and Their Drawbacks --- p.15 / Chapter 3.2. --- Traditional Chinese Herbal Medicne (TCHM) / Chapter 3.2.1. --- General Principle of TCHM --- p.17 / Chapter 3.2.2. --- Side Effects of Using TCHM --- p.18 / Chapter 3.2.3. --- Literature Reviews of TCHM Use in Treating AD --- p.18 / Chapter CHAPTER 4 --- The Pentaherbs Formula for AD Treatment --- p.20-26 / Chapter 4.1. --- Pilot study: Pentaherbs Capsule as Treatment Option of AD Children --- p.20 / Chapter 4.2. --- Literature Review: Nature of Five Herbs / Chapter 4.2.1. --- PHF as Treatment Option of AD under TCHM Concepts --- p.22 / Chapter 4.2.2. --- PHF as Treatment Option of AD from Modern Research Literature --- p.22 / Chapter CHAPTER 5 --- Pathobiology of Atopic Dermatitis --- p.27-40 / Chapter 5.1. --- Nature of Complexity of Pathogenesis --- p.27 / Chapter 5.2. --- Skin barrier-impairment of epidermal barrier --- p.28 / Chapter 5.3. --- Biphasic T cell response in skin of AD --- p.29 / Chapter 5.4. --- Nature of Immunoglobulin-E and its Role in Atopic Dermatitis --- p.32 / Chapter 5.5. --- Innate Immunity Defect in AD --- p.33 / Chapter 5.6. --- Role of Superantigen in Pathogenesis of AD --- p.35 / Chapter 5.7. --- "Cytokines, Chemokines and Inflammatory Mediators in Pathogenesis of Atopic Dermatitis" / Chapter 5.7.1. --- Proinflammatory Cytokines --- p.37 / Chapter 5.7.2. --- Th1/Th2 Cytokines --- p.37 / Chapter 5.7.3. --- Chemokines --- p.38 / Chapter 5.7.4. --- Pruritus Mediators --- p.39 / Chapter Section 2: --- CLINICAL TRIAL OF PENTAHERBS / Chapter CHAPTER 1 --- Objective --- p.41 / Chapter CHAPTER 2 --- Materials and Methods (RCT) --- p.42-51 / Chapter 2.1. --- Materials / Chapter 2.1.1. --- SCORAD worksheet --- p.42 / Chapter 2.1.2. --- CDLQI questionnaire --- p.42 / Chapter 2.1.3. --- Allergic Rhinitis Score (ARS) --- p.43 / Chapter 2.1.4. --- ELISA Assay Kits --- p.43 / Chapter 2.1.5. --- EDTA blood collestion tubes --- p.43 / Chapter 2.2. --- Methods / Chapter 2.2.1. --- Design --- p.45 / Chapter 2.2.2. --- Intervention --- p.45 / Chapter 2.2.3. --- Treatment / Chapter 2.2.3.1 --- The Pentaherbs Formula --- p.45 / Chapter 2.2.3.2 --- Randomization --- p.48 / Chapter 2.2.3.3 --- Concomitant Treatment in Study Period --- p.48 / Chapter 2.2.4. --- Participants --- p.49 / Chapter 2.2.5. --- Outcome Measures --- p.50 / Chapter 2.2.6. --- Statistical Analysis --- p.50 / Chapter CHAPTER 3 --- Results (RCT) --- p.52-67 / Chapter 3.1. --- Demographics --- p.52 / Chapter 3.2. --- Drug Compliance --- p.55 / Chapter 3.3. --- Efficacy / Chapter 3.3.1. --- SCORAD Score --- p.56 / Chapter 3.3.2. --- Quality of Life Score --- p.56 / Chapter 3.3.3. --- Duration and Amount of CS Usage --- p.59 / Chapter 3.3.4. --- Amount of Antihistamine Usage --- p.61 / Chapter 3.3.5. --- Allergic Rhinitis Score --- p.61 / Chapter 3.3.6. --- Blood chemistry and Haematology --- p.63 / Chapter 3.3.7. --- Plasma TARC and BDNF level --- p.63 / Chapter 3.4. --- Tolerability --- p.65 / Chapter Section 3: --- IN VITRO STUDY OF PENTAHERBS / Chapter CHAPTER 1 --- Objectives and Study Design --- p.68 / Chapter CHAPTER 2 --- Materials and Methods (In vitro Study) --- p.69-86 / Chapter 2.1. --- Materials for in vitro study / Chapter 2.1.1. --- Preparation of the Water Extracts of PHF Capsules --- p.69 / Chapter 2.1.2. --- Endotoxin Assay --- p.69 / Chapter 2.1.3. --- Cell isolation and culture ofPBMC / Chapter 2.1.3.1 . --- Cell Isolation from Human Peripheral Blood --- p.70 / Chapter 2.1.3.2. --- Culture of Peripheral Blood Mononuclear Cells --- p.70 / Chapter 2.1.4. --- Trypan Blue Exclusion Assay --- p.72 / Chapter 2.1.5. --- [3H]-Thymidine incorporation Assay --- p.72 / Chapter 2.1.6. --- Supernatant Collection and ELISA --- p.72 / Chapter 2.1.7. --- RNA Extraction and RT-PCR / Chapter 2.1.7.1. --- Reagents for RNA Extraction --- p.73 / Chapter 2.1.7.2. --- Reagents for Reverse Transcription --- p.73 / Chapter 2.1.7.3. --- Reagents for Polymerase Chain Reaction --- p.74 / Chapter 2.1.7.4. --- Reagents for Gel Electrophoresis --- p.74 / Chapter 2.2. --- Methods / Chapter 2.2.1. --- Isolation and Culture PBMC / Chapter 2.2.1.1. --- Isolation of PBMC --- p.76 / Chapter 2.2.1.2. --- Culture of Isolated PBMC --- p.76 / Chapter 2.2.1.3. --- PHA/SEB Treatment --- p.77 / Chapter 2.2.2. --- Preparation of PHF Water Extracts and Endotoxin Level / Chapter 2.2.2.1. --- Hot Water Extraction --- p.78 / Chapter 2.2.2.2. --- Limulus Amebocyte Lysate Assay --- p.78 / Chapter 2.2.3. --- Study on the Cytotoxic and Mitogenic Effects of PHF on PBMC / Chapter 2.2.3.1. --- Trypan Blue Exclusion Assay --- p.80 / Chapter 2.2.3.2. --- [3H]-Thymidine Incorporation Assay --- p.80 / Chapter 2.2.4. --- Study on the Effect of PHF on PBMC Inflammatory Mediator Production / Chapter 2.2.4.1. --- Determination of Inflammatory Mediator Expression Levels by ELISA --- p.82 / Chapter 2.2.4.2. --- Semi-quantification of Inflammatory Mediator mRNA Levels by RT-PCR --- p.83 / Chapter 2.2.5. --- Statistical Analysis --- p.86 / Chapter CHAPTER 3 --- Results(In vitro) --- p.87-114 / Chapter 3.1. --- preparation of PHF Water Extracts and Endotxin Level --- p.87 / Chapter 3.2. --- Cytotoxicity Effect of PHF on PBMC --- p.88 / Chapter 3.3. --- Mitogenicity Effect of PHF on PBMC --- p.93 / Chapter 3.4. --- Effects of PHF on Expression of Inflammatory Mediators from PBMC Following Mitogen (PHA) Stimulation / Chapter 3.4.1. --- Effects of PHF on mRNA Expression of Inflammatory Mediators from PHA-stimulated PBMC --- p.98 / Chapter 3.4.2. --- Effects of PHF on Secretion of Inflammatory Mediators from PHA-stimulated PBMC --- p.101 / Chapter 3.5 --- Effects of PHF on Expression of Inflammatory Mediators from SEB-stimulated PBMC / Chapter 3.5.1. --- Effects of PHF on mRNA Expression of Inflammatory --- p.106 / Chapter 3.5.2. --- Effescts of PHF on secretion of inflammatory Mediatorsfrom SEM-Stimulated PBMC --- p.109 / Chapter 3.6. --- Summarization of Effects of PHF on Expression of Inflammatory Mediators from PHA- and SEB-stimulated PBMC / Chapter 3.6.1. --- Mitogen (PHA) Stimulation --- p.114 / Chapter 3.6.2. --- Superantigen (SEB) Stimulation --- p.114 / Chapter Section 4: --- DISCUSSIONS / Chapter CHAPTER 1 --- Discussions on RCT of PHF --- p.115-122 / Chapter 1.1. --- Clinical Efficacy and Tolerability of PHF for Treatment of Children AD: a RCT study / Chapter 1.2. --- Efficacy of PHF for Treatment of Children with AD --- p.117 / Chapter 1.3. --- Safety and Tolerability of PHF Use for Treatment of Children with AD --- p.119 / Chapter 1.4. --- Rounding up --- p.121 / Chapter CHAPTER 2 --- Discussions on In vitro Immunomodulatory Activities of PHF --- p.123-130 / Chapter 2.1. --- General Effects of PHF on PBMC --- p.123 / Chapter 2.2. --- Effects of PHF on Inflammatory Mediators Expression in PBMC --- p.124 / Chapter CHAPTER 3 --- Limitations of the Present Study --- p.131-132 / Chapter Section 5: --- CONCLUSIONS AND FUTURE PROSPECTS / Chapter CHAPTER 1 --- Conclusions --- p.133 / Chapter CHAPTER 2 --- Future Prospects --- p.134-135 / Chapter Section 6: --- APPENDICES / Appendix1 --- p.137 / Appendix2 --- p.142 / Appendix3 --- p.149 / Chapter Section 7: --- BIBLIOGRAPHY --- p.151-166