Since the advent of computers numerous approaches have been taken to create hardware systems that provide a high degree of reliability even in the presence of errors. This study seeks to address the problem from a biological perspective using the human immune system as a source of inspiration. The immune system uses many ingenious methods to provide reliable operation in the body and so may suggest how similar methods can be used in the design of reliable systems. This study provides a brief introduction into a relatively new discipline: artificial immune systems (AIS) and demonstrates a new application of AIS with an immunologically inspired approach to fault tolerance. It is shown a finite state machine can be provided with a hardware immune system to provide a novel form of fault detection giving the ability to detect faulty states during a normal operating cycle. It is called immunotronics.

No description available.

The domain of Intrusion Detection Systems (IDS) has witnessed growing interest in recent years due to the escalating threats posed by cyberattacks. As Internet of Things (IoT) becomes increasingly integrated into our every day lives, we widen our attack surface and expose more of our personal lives to risk. In the same way the Human Immune System (HIS) safeguards our physical self, a similar solution is needed to safeguard our digital self. This thesis presents the Artificial Immune inspired Intrusion Detection System (AIS-IDS), an IDS modeled after the HIS. This thesis proposes an architecture for AIS-IDS, instantiates an AIS-IDS model for evaluation, conducts a robust set of experiments to ascertain the efficacy of the AIS-IDS, and answers key research questions aimed at evaluating the validity of the AIS-IDS. Finally, two expansions to the AIS-IDS are proposed with the goal of further infusing the HIS into AIS-IDS design.

Fungi represent one of the most diverse and abundant eukaryotes on earth. The interplay between mold exposure and the host immune system is still not fully elucidated. Literature research focusing on up-to-date publications is providing a heterogenous picture of evidence and opinions regarding the role of mold and mycotoxins in the development of immune diseases. While the induction of allergic immune responses by molds is generally acknowledged, other direct health effects like the toxic mold syndrome are controversially discussed. However, recent observations indicate a particular importance of mold/mycotoxin exposure in individuals with pre-existing dysregulation of the immune system, due to exacerbation of underlying pathophysiology including allergic and non-allergic chronic inflammatory diseases, autoimmune disorders, and even human immunodeficiency virus (HIV) disease progression. In this review, we focus on the impact of mycotoxins regarding their impact on disease progression in pre-existing immune dysregulation. This is complemented by experimental in vivo and in vitro findings to present cellular and molecular modes of action. Furthermore, we discuss hypothetical mechanisms of action, where evidence is missing since much remains to be discovered.

No description available.

A desnutrição é capaz de induzir diversas alterações metabólicas afetando marcadamente a composição corporal e o sistema imunológico. O exercício físico, por sua vez, produz alterações no organismo para uma melhor capacidade de adaptação a situações de estresse. O desvio da situação de homeostase produzida pelo exercício físico induz uma reorganização de seus mecanismos funcionais, principalmente dos mecanismos endócrinos e imunológicos. Ainda é pouco conhecida a influência do exercício sobre a desnutrição e também as conseqüências sobre o sistema imunológico quando as duas variáveis são combinadas. Assim, esse trabalho teve como objetivo avaliar os efeitos do exercício físico de endurance sobre ratos submetidos a um protocolo de desnutrição crônica. Avaliamos ratos Wistar machos, desnutridos por 16 semanas, divididos em 4 grupos: eutrófico sedentário (ES), eutrófico treinado (ET), desnutrido sedentário (DS), desnutrido treinado (DT). O treinamento físico foi realizado em esteira, por 10 semanas, 5 vezes por semana, com intensidade aproximada de 60- 65% do consumo máximo de oxigênio. Avaliou-se a composição corporal, através da aferição do peso corporal, peso dos tecidos muscular esquelético e adiposo, do fígado, do conteúdo de gordura e proteína na carcaça, e a concentração de leptina, ACTH, glicose, insulina, e glutamina no plasma. Avaliamos também, através de citometria de fluxo, os marcadores de superfície celular CD3 e CD4, bem como a celularidade no timo. O consumo máximo de oxigênio e o desempenho através de um teste até a exaustão também foram analisados. A análise estatística utilizada foi o teste de variância ANOVA two-way com pós teste de Bonferroni e, nível de significância adotado de p<0,05. Os resultados encontrados demonstraram que o treinamento de endurance em ratos submetidos à desnutrição crônica promoveu uma acentuada redução do peso e da adiposidade corporal; um aumento da massa muscular relativa ao peso corporal; um restabelecimento da glicemia aos valores normais; uma melhor relação da concentração insulina/glicose, sugerindo uma sensibilidade à insulina aumentada; um aumento dos estoques de glicogênio muscular; um maior consumo máximo de oxigênio; e uma recuperação na morfologia e fisiologia tímica, uma maior resposta proliferativa do baço e linfonodos estimulados com IL2. Concluímos desta forma que o exercício foi capaz de recuperar a morfologia, como também a maturação timócitos CD3 e CD4 e sua celuraridade em ratos desnutridos. A resposta proliferativa à estimulação da IL2 também foi recuperada. / Malnutrition is capable of inducing diverse metabolic alterations, markedly affecting body composition and the immune system. Physical exercise, on the other hand, induces a renders the organism more capable of adaptation to stress. Still, little is known about the influence of exercise training upon malnutrition-related alterations and its consequences on the immune system. Our aim was to evaluate the effect of moderate intensity exercise training in rats submitted to a protocol (16wk) of chronic malnutrition. Male Wistar rats were divided in to 4 groups: sedentary, fed ad libitum (SF); trained fed ad libitum (TF); sedentary energy restricted (RES); and trained energy restricted (TER). Training was carried out on a treadmill for 10 weeks, 5 time wk, under an intensity of 60-65% of the maximal oxygen consumption. We evaluated the Corporal composition, the variation of body weight, and the weight of the skeletal muscle, adipose tissues, and liver; as well as fat and protein content in the carcass; and also plasma leptin, ACTH, glucose, insulin and glutamine concentration. We also examined through flow cytometry CD3 and CD4, as well as the celularity in the thymus. The maximum consumption of oxygen and the performance were also assessed. The results demonstrate that endurance training in rats submitted to the chronic malnutrition protocol promoted reduction of body weight and of corporal adiposity; an increase in the relative contribution of muscle to body weight; the reestablishment of glicemia; improval of insulin/glucose reason, suggesting increased sensitivy to insulin; an increase of muscle glycogen content; enhanced oxygen consumption; are recovery of the morphology and physiology of the thymus, together with a proliferative response of the spleen and lymph nodes stimulated with IL2. We conclude in such a way that moderate intensity training restored thymus morphology and the capacity of maturation of CD3 and CD4 and also timocyte number and the of proliferative response to IL2 stimulation.

Tse Man. / Accompanying booklet titled: Dietary assessment food portion booklet. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 101-122). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / Abstract (Chinese version) --- p.iv / Table of contents --- p.vi / List of figures --- p.x / List of tables --- p.xi / List of abbreviations --- p.xiv / Chapter Chapter one: --- Introduction --- p.1 / Breast cancer trends in Hong Kong --- p.1 / Risk factors for breast cancer occurrence --- p.4 / "Body weight, obesity, hormones and breast cancer" --- p.4 / Evidence for postmenopausal women --- p.4 / Evidence for premenopausal women --- p.6 / Hormones and breast cancer --- p.7 / Dietary factors: Foods and nutrients --- p.11 / Animal foods and fats --- p.11 / Dietary fats --- p.13 / Other animal foods --- p.14 / Fruit and vegetable intakes --- p.14 / Positive family history --- p.15 / Alcohol consumption and cigarette smoking --- p.15 / Physical Activity --- p.17 / "Cancer, obesity and immunity" --- p.17 / Aims and scope of the study --- p.19 / Chapter Chapter two: --- Methodology --- p.22 / Questionnaires and their derivation --- p.22 / Literature derivation of the questionnaires --- p.22 / Pretest of the questionnaires --- p.25 / Research ethics --- p.26 / Subject recruitment --- p.26 / Anthropometric measurements --- p.27 / Interviews --- p.28 / First interview --- p.28 / Second and third telephone interviews --- p.29 / Immunoassays --- p.30 / Materials for immunoassays --- p.30 / Immunophenotyping of cells --- p.30 / MultiTEST´ёØ four-color direct immunofluorescence reagent kit --- p.32 / Human tumor neurosis factor-alpha (TNF-α) Quantikine® high sensitivity enzyme-linked immunosorbent assay (ELISA) kit --- p.33 / Methods for immunoassays --- p.33 / Flow cytometric analysis --- p.34 / TNF-α Quantikine® high sensitivity ELISA assay --- p.35 / Data management --- p.35 / Statistical methods --- p.35 / Data analysis --- p.36 / Dietary analysis --- p.36 / Definition of weight status --- p.37 / Measurements of immune cell levels --- p.37 / Chapter Chapter three: --- Results --- p.39 / Participation rate --- p.39 / Characteristics of the patients --- p.40 / Demographics --- p.40 / Pregnancy and breast-feeding experiences --- p.42 / Medical history --- p.43 / Body weight and obesity status --- p.45 / Dietary patterns --- p.46 / Fat and oil removal habit when eating meat and poultry --- p.46 / Perceived fat consumption --- p.46 / Eating out habits --- p.47 / Vegetarian diet adoption and food allergy or intolerance --- p.48 / Cooking methods --- p.48 / Alcohol consumption and supplementation habits --- p.50 / Preferences and perceived amounts of consumption on food groups --- p.51 / Cooking oils used at home --- p.52 / Nutrient intake patterns from dietary recalls --- p.53 / Soy intakes --- p.55 / Meal locations --- p.55 / Energy intakes by weight status --- p.56 / Food group intakes by FFQ --- p.57 / Food items not covered by FFQ --- p.62 / Top ten fat and fiber contributors by FFQ --- p.63 / Daily fruit and vegetable intakes by FFQ and 3 days' dietary recalls --- p.64 / Correlation of FFQ and 3 days' dietary recalls by food group intakes --- p.64 / Correlation of FFQ and 3 days' dietary recalls by fat and fiber intakes --- p.65 / Fat and fiber intakes by weight status --- p.66 / Other lifestyle patterns --- p.68 / Exercise participation and smoking habits --- p.68 / Daily activities' participation by weight status --- p.69 / Immune status / Overview of general immune cell levels --- p.71 / Immune status and BMI weight grouping --- p.72 / Immune status and overweight --- p.74 / Immune status and percent body fat --- p.76 / Immune status and waist-hip ratio --- p.77 / "Weight status, adiposity and immune status: summary" --- p.78 / Immune status and protein intakes --- p.82 / Immune status and fat intakes --- p.83 / Immune status and fiber intake --- p.84 / Immune status and vitamin C intake --- p.85 / Immune status and menopausal status --- p.86 / Chapter Chapter four: --- Discussion / Implications of findings --- p.88 / Interpreting the Immune status of the subjects --- p.88 / Lymphocyte and NK cell levels --- p.89 / Regulatory T cell (Treg) levels --- p.89 / TNF-α levels --- p.90 / Immune status and nutrient intakes --- p.90 / Typical dietary patterns of the subjects --- p.91 / Physical activity patterns --- p.94 / Weight status --- p.95 / "Subjects' fat, fiber intakes and anthropometric measurements compared to previous research" --- p.96 / Limitations of the study --- p.96 / Future directions of research --- p.98 / Chapter Chapter five: --- Conclusion --- p.99 / References --- p.101 / Appendices --- p.123 / Chapter A1 --- Questionnaire (Chinese version) --- p.123 / Chapter A2 --- Questionnaire (English version) --- p.138 / Chapter B1 --- Food frequency questionnaire (Chinese version) --- p.153 / Chapter B2 --- Food frequency questionnaire (English version) --- p.156 / Chapter C --- Dietary assessment food portion booklet --- p.160 / Chapter D1 --- 3 days dietary recall questionnaire (Chinese version) --- p.161 / Chapter D2 --- 3 days dietary recall questionnaire (English version) --- p.174 / Chapter El --- Consent form (Chinese version) --- p.187 / Chapter E2 --- Consent form (English version) --- p.189 / Chapter F --- Results of patient invitation to participate during recruitment period --- p.191

Gastrointestinal microflora has been shown to have a bi-directional relationship with the host immune system. A variety of fermentable carbohydrate polymers largely pass through the small intestine, providing fermentable substrates for gut microflora. Dietary fibre supplementation may provide a strategy for manipulating the intestinal bacterial profile, changing the interaction with the mucosal immune system, thereby modulating the host immune system. We used a BBc rat animal model to evaluate the effects of oat bran and wheat bran dietary fibre on the immune system. Previous collaborative efforts have shown that these dietary fibres can change the intestinal microflora, with wheat bran fibre showing a greater ability to influence colonic microbial community diversity. We have shown that dietary wheat bran fibre led to reduced IL-4 levels in the liver and T lymphocyte numbers in the Mesenteric Lymph Node and may be involved in reduced IgA levels in the cecal contents. In addition, IgA in the cecal contents was decreased while MLN B cell numbers increased in response to dietary wheat bran fibre. It was observed that neither wheat bran or oat bran treatments exerted any pro-inflammatory effects, with oat bran actually improving antioxidant status. These results suggest that both oat and wheat bran fibre treatments induce changes in the intestinal microflora, and that the microflora changes due to wheat fibre are associated with immunomodulatory effects on the host. This type of dietary fibre supplementation could ultimately provide a potential strategy for promoting health through microflora-associated effects on the immune system.

Professional antigen presenting cells (APCs) represent an important link between the innate and adaptive immune system. Macrophages (MΦs) and dendritic cells (DCs) serve as sentinels in the periphery collecting samples from their environment and processing this information. These cells then present antigenic fragments to T cells in the context of self-MHC molecules. Although a clear role for both of these APCs in the stimulation of already activated or memory T cells has been established, the ability of MΦs to activate naive T cells is still unknown. In this thesis the ability of bone marrow-derived MΦs and DCs to prime naive CD8+ and CD4+ T cells was investigated. Using adoptively transferred transgenic CFSE-Iabeled P-14 T cells, specific for gp33 from lymphocytic choriomeningitis virus in the context of Db, we were able to demonstrate the ability of both MΦs and DCs to induce naive CD8+ T cells proliferation. Once primed by MΦs these T cells gained effector function as shown by interferon- γ (IFN-γ) production and in vivo cytolysis. In addition, immunization of wild type animals with gp33-pulsed MΦs, as well as DCs, led to greater than a 95% reduction in lymphocytic choriomeningitis virus titers. To rule out the role of cross-presentation in the observed priming, two models were used. In the first model, lethally irradiated F1 bxs chimeras reconstituted with either H-2s or H-2b bone marrow were used as host for the adoptive transfer experiments. Since the gp33 peptide binds to Db, the H-2s reconstituted animals should be unable to cross-present the peptide to the P-14 T cells. Using this model, we were able to clearly demonstrate the ability of MΦs to activate naive P-14 T cells to undergo division. Additional experiments, demonstrated that these MΦ primed T cells went on to develop into effector cells. Finally, the ability of the MΦ primed T cells to develop into functional memory cells was demonstrated. To confirm the chimera results, these experiments were repeated using β2 microglobulin deficient animals (whose cells don't express MHC I) as host in adoptive experiments. MΦs were able to stimulate the naive P-14 T cells to divide and gain effector function as demonstrated by the ability to produce IFN-γ. In contrast to the CD8 system, MΦ were poor stimulators of D011.10 CD4+ T cell proliferation. Additionally, D011.10 T cells stimulated by DCs were able to produce interleukin-2 (IL-2), IL-4, tumor necrosis factor and granulocyte-macrophage colony stimulating factor where as MΦ stimulated D011.10 T cells were only able to produce IL-2. In conclusion this body of work clearly demonstrates the in vivo ability of MΦ to stimulate CD8+ T cell proliferation, effector function, as well as the formation of functional CD8+ T cell memory. Whether or not the nature of the memory pools stimulated by the two APCs is exactly the same is still unknown and needs further investigation. The ability of APCs other than DCs to stimulate functional protective memory needs to be considered in the quest to design vaccines that offer broad-spectrum protection.

A desnutrição é capaz de induzir diversas alterações metabólicas afetando marcadamente a composição corporal e o sistema imunológico. O exercício físico, por sua vez, produz alterações no organismo para uma melhor capacidade de adaptação a situações de estresse. O desvio da situação de homeostase produzida pelo exercício físico induz uma reorganização de seus mecanismos funcionais, principalmente dos mecanismos endócrinos e imunológicos. Ainda é pouco conhecida a influência do exercício sobre a desnutrição e também as conseqüências sobre o sistema imunológico quando as duas variáveis são combinadas. Assim, esse trabalho teve como objetivo avaliar os efeitos do exercício físico de endurance sobre ratos submetidos a um protocolo de desnutrição crônica. Avaliamos ratos Wistar machos, desnutridos por 16 semanas, divididos em 4 grupos: eutrófico sedentário (ES), eutrófico treinado (ET), desnutrido sedentário (DS), desnutrido treinado (DT). O treinamento físico foi realizado em esteira, por 10 semanas, 5 vezes por semana, com intensidade aproximada de 60- 65% do consumo máximo de oxigênio. Avaliou-se a composição corporal, através da aferição do peso corporal, peso dos tecidos muscular esquelético e adiposo, do fígado, do conteúdo de gordura e proteína na carcaça, e a concentração de leptina, ACTH, glicose, insulina, e glutamina no plasma. Avaliamos também, através de citometria de fluxo, os marcadores de superfície celular CD3 e CD4, bem como a celularidade no timo. O consumo máximo de oxigênio e o desempenho através de um teste até a exaustão também foram analisados. A análise estatística utilizada foi o teste de variância ANOVA two-way com pós teste de Bonferroni e, nível de significância adotado de p<0,05. Os resultados encontrados demonstraram que o treinamento de endurance em ratos submetidos à desnutrição crônica promoveu uma acentuada redução do peso e da adiposidade corporal; um aumento da massa muscular relativa ao peso corporal; um restabelecimento da glicemia aos valores normais; uma melhor relação da concentração insulina/glicose, sugerindo uma sensibilidade à insulina aumentada; um aumento dos estoques de glicogênio muscular; um maior consumo máximo de oxigênio; e uma recuperação na morfologia e fisiologia tímica, uma maior resposta proliferativa do baço e linfonodos estimulados com IL2. Concluímos desta forma que o exercício foi capaz de recuperar a morfologia, como também a maturação timócitos CD3 e CD4 e sua celuraridade em ratos desnutridos. A resposta proliferativa à estimulação da IL2 também foi recuperada. / Malnutrition is capable of inducing diverse metabolic alterations, markedly affecting body composition and the immune system. Physical exercise, on the other hand, induces a renders the organism more capable of adaptation to stress. Still, little is known about the influence of exercise training upon malnutrition-related alterations and its consequences on the immune system. Our aim was to evaluate the effect of moderate intensity exercise training in rats submitted to a protocol (16wk) of chronic malnutrition. Male Wistar rats were divided in to 4 groups: sedentary, fed ad libitum (SF); trained fed ad libitum (TF); sedentary energy restricted (RES); and trained energy restricted (TER). Training was carried out on a treadmill for 10 weeks, 5 time wk, under an intensity of 60-65% of the maximal oxygen consumption. We evaluated the Corporal composition, the variation of body weight, and the weight of the skeletal muscle, adipose tissues, and liver; as well as fat and protein content in the carcass; and also plasma leptin, ACTH, glucose, insulin and glutamine concentration. We also examined through flow cytometry CD3 and CD4, as well as the celularity in the thymus. The maximum consumption of oxygen and the performance were also assessed. The results demonstrate that endurance training in rats submitted to the chronic malnutrition protocol promoted reduction of body weight and of corporal adiposity; an increase in the relative contribution of muscle to body weight; the reestablishment of glicemia; improval of insulin/glucose reason, suggesting increased sensitivy to insulin; an increase of muscle glycogen content; enhanced oxygen consumption; are recovery of the morphology and physiology of the thymus, together with a proliferative response of the spleen and lymph nodes stimulated with IL2. We conclude in such a way that moderate intensity training restored thymus morphology and the capacity of maturation of CD3 and CD4 and also timocyte number and the of proliferative response to IL2 stimulation.