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EN
Observation of nature is often the inspiration for unconventional and innovative ideas, proposals, suggestions, overall concepts for carrying out modeling phenomena and technical processes, economic, processing and analysis of statistical data. Artificial neural networks, genetic algorithms and evolutionary algorithms were created as an imitation of biological solutions. In recent years, the rapid development of immunological algorithms which are based on the action of the human immune system, has occurred. These algorithms are used in mathematics, engineering, problem solving in decision making, management, economics, finance. At the beginning of this article we describe the action of the human immune system, which is the basis for the construction of immune algorithms. Then we present the most important mechanisms influencing the operation and construction of the algorithms based on biological mechanisms of the immune system, in particular the negative selection, immune network, clonal selection. Then we describe how the elements and mechanisms of artificial immune system algorithms are represented to enable modeling, processing and analysis of data. In the last part of the article to illustrate the wide range of possibilities of using immune algorithms to solve various sorts of problems from a completely different fields, we present examples of applications that involve the assessment of bank borrowers, the task of coloring a graph belonging to combinatorial optimization problems, a multi-dimensional classification, fault detection.
EN
ObjectivesAs a chronic, recurrent, immunologically mediated systemic disease and a common cause of dermatological problems, psoriasis is often a subject of scientific research. Skin changes located on the hands can cause difficulties and limitations in the performance of professional activities, especially manual ones. The main role in pathogenesis is played by immunological factors – improper functioning of the components of the immune system, among others, T lymphocytes and cytokines like interleukin-12 (IL-12), interleukin-22 (IL-22) and interferon gamma (IFN-γ).Material and MethodsThe obtained tissue and blood were destined for RNA isolation. The RNA was then subjected to a reverse transcription reaction. The relative gene expression level was evaluated by the real-time polymerase chain reaction for IL-12B, IL-22 and IFN-γ genes, and presented as the relative quantification (RQ) value, relative to the reference gene GAPDH. In addition, a correlation analysis of the expression level of selected genes with the clinical course of the disease, as assessed by the Psoriasis Area and Severity Index (PASI), the Body Surface Area (BSA) and the Dermatology Life Quality Index (DLQI) scores was performed.ResultsStatistical analysis confirmed a significant increase in RQ values for IL-12B, IL-22 and IFN-γ in the group of psoriatic patients vs. the control group. A positive correlation was also found between BSA and PASI and RQ for the IL-12B gene.ConclusionsIncreased expression levels of IL-12B, IL-22 and IFN-γ genes in psoriatic skin confirm that selected cytokines play an important role in the initiation and sustenance of psoriasis.
EN
Coeliac disease is a small intestine disorder caused by gluten intolerance. It has a long history and had developed when the humans started to cultivate grains. The first written records of coeliac disease come from the 1st and 2nd centuries AD, given by Aretaeus of Cappadocia. Samuel Gee gave the first clear description of this condition in 1888 and suggested dietary treatment with shellfish. In 1950 Wim Dicke prooved that the exclusion of wheat, rye and oats rom the diet led to improvement in coeliac patients. His collegues, Weijers and Van de Kamer stated that gluten is responsible for the disease, especially one of its fractions - gliadin. First description of histological abnormalities of the lining of the small intestine were presented by Paulley in 1954 and first description of per-oral biopsy technique was published in 1955 by Royer. In 1965 MacDonald established the hereditary nature of the disease. His followers in the 80’s and 90’s discovered the predisposing genes HLA-DQ2/DQ8. In 1983 Tadeusz Chorzelski described the immunological mechanism of coeliac disease and discovered the anti-endomysial antibodies, that serve as an immunological marker of the disease till present. Nowadays many research centres are performing studies aimed to facilitate the diagnosis and improve the dietary treatment.
PL
Celiakia, inaczej choroba trzewna, jest chorobą jelita cienkiego, spowodowaną nadwrażliwością na gluten. Jej historia sięga czasów, kiedy zaczęto uprawiać zboża. Pierwsze zapiski na temat celiakii sporządził Areteusz z Kapadocji na przełomie I i II w. W 1888 r. Samuel Gee dokonał pierwszego pełniejszego opisu choroby, zaproponował leczenie dietetyczne skorupiakami. W 1950 r. Wim Dicke odkrył, że eliminacja z diety pszenicy, żyta i owsa prowadzi do poprawy klinicznej w celiakii. Z kolei jego współpracownicy, Weijers i Van de Kamer zauważyli, że gluten i jego frakcja zawarta w pszenicy – gliadyna, odpowiadają za chorobę. Pierwszy opis zmian histologicznych w celiakii w jelicie cienkim sporządził Paulley w 1954r., natomiast endoskopową technikę biopsyjną opisał Royer w 1955r. MacDonald dowiódł tła genetycznego choroby w 1965r., a jego następcy w latach 80-tych. i 90-tych. odkryli układ genów HLA-DQ2/DQ8 predysponujący do celiakii. W 1983r. Tadeusz Chorzelski opisał autoimmunologiczny charakter choroby i odkrył przeciwciała endomozyjalne służące do dziś w diagnostyce. Obecnie wiele ośrodków naukowych na świecie prowadzi dalsze badania, celem coraz lepszej diagnostyki i opieki nad chorymi.
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