Letteratura scientifica selezionata sul tema "Non auto immune"
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Articoli di riviste sul tema "Non auto immune":
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Leslie, R. D. G., e M. Hawa. "Twin Studies in Auto-immune Disease". Acta geneticae medicae et gemellologiae: twin research 43, n. 1-2 (aprile 1994): 71–81. http://dx.doi.org/10.1017/s000156600000297x.
Abstract (sommario):
AbstractImmune-mediated diseases affect up to 5% of the population and are a major cause of morbidity and mortality. These diseases can be organ specific, such as insulin-dependent diabetes (IDDM) and non-organ specific, such as Rheumatoid Arthritis (RA). Identical and non-identical twins have been used to establish whether these diseases are determined by genetic or environmental factors. The results of these studies have been collated in a new section of the Mendel Institute in Rome.Diseases included in these studies included IDDM, RA, Systemic Lupus Erythematosus (SLE), Multiple Sclerosis (MS) and Myasthenia. Striking differences in concordance rates between identical and non-identical twins in all these studies suggest that genetic factors are important in causing these diseases. All the diseases are known to be associated with HLA genes on chromosome 6 which may account for some or all of the genetic susceptibility. However, in the majority of pairs the affected twin has an unaffected co-twin. These observations suggest that non-genetically determined factors, probably environmental factors and not somatic mutations, are critical. The study of unaffected co-twins, who are at high disease-risk, has allowed the identification of changes which precede and predict the clinical disease. The immune-mediated destruction in many of these diseases is probably caused by T-lymphocytes. Twin studies have shown the importance of genetic factors in determining T-cell responses. Identical twins should, therefore, provide the perfect test bed to assess the role of T-cells in immune-mediated diseases.
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GARCIA, C., L. BORDIER, F. BANAL, F. DUTASTA, J. V. MALFUSON e O. BERETS. "Stratégie diagnostique devant une suspicion de polyendocrinopathie auto-immune." Médecine et Armées Vol. 40 No. 2, Volume 40, Numéro 2 (1 aprile 2012): 129–34. http://dx.doi.org/10.17184/eac.6600.
Abstract (sommario):
Les polyendocrinopathies auto-immunes de type 2 correspondent à une association d’au moins deux affections endocriniennes liées à une perturbation de la tolérance du système immunitaire. Nous rapportons l’observation d’une patiente, âgée de 38 ans, chez qui est découverte une maladie d’Addison, deux mois après l’introduction de lévothyroxine dans le traitement d’une thyroïdite à anticorps anti-thyroperoxydase, cette association étant auparavant connue sous l’appellation de syndrome de Schmidt. Ce cas clinique illustre les difficultés diagnostiques des polyendocrinopathies auto-immunes et permet de rappeler les principales associations rencontrées dans les polyendocrinopathie auto-immune de type 2. Enfin les modalités pratiques du dépistage systématique des endocrinopathies associées, non consensuelles, sont discutées.
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Trier, Nicole Hartwig, e Gunnar Houen. "Antibody Cross-Reactivity in Auto-Immune Diseases". International Journal of Molecular Sciences 24, n. 17 (2 settembre 2023): 13609. http://dx.doi.org/10.3390/ijms241713609.
Abstract (sommario):
Autoimmunity is defined by the presence of antibodies and/or T cells directed against self-components. Although of unknown etiology, autoimmunity commonly is associated with environmental factors such as infections, which have been reported to increase the risk of developing autoimmune diseases. Occasionally, similarities between infectious non-self and self-tissue antigens may contribute to immunological cross-reactivity in autoimmune diseases. These reactions may be interpreted as molecular mimicry, which describes cross-reactivity between foreign pathogens and self-antigens that have been reported to cause tissue damage and to contribute to the development of autoimmunity. By focusing on the nature of antibodies, cross-reactivity in general, and antibody–antigen interactions, this review aims to characterize the nature of potential cross-reactive immune reactions between infectious non-self and self-tissue antigens which may be associated with autoimmunity but may not actually be the cause of disease onset.
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Bouayad, Abdellatif, e Laila Benzekri. "Thyroïdite auto-immune et vitiligo non segmentaire : association avec DQB1 * 05". Transfusion Clinique et Biologique 24, n. 3 (settembre 2017): 350. http://dx.doi.org/10.1016/j.tracli.2017.06.217.
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Takeshita, Fumihiko, Kouji Kobiyama, Atsushi Miyawaki, Nao Jounai e Kenji Okuda. "The non-canonical role of Atg family members as suppressors of innate antiviral immune signaling". Autophagy 4, n. 1 (gennaio 2008): 67–69. http://dx.doi.org/10.4161/auto.5055.
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Nikolajczyk, Barbara S. "B cells as under-appreciated mediators of non-auto-immune inflammatory disease". Cytokine 50, n. 3 (giugno 2010): 234–42. http://dx.doi.org/10.1016/j.cyto.2010.02.022.
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Bhargava, Amit, e Nirupma Banerjee. "Rituximab in Lymphoma Associated Auto-Immune Haemolytic Anemia". Blood 116, n. 21 (19 novembre 2010): 4923. http://dx.doi.org/10.1182/blood.v116.21.4923.4923.
Abstract (sommario):
Abstract Abstract 4923 The association of Autoimmune hemolytic and Non Hodgkin's lymphoma is a known phenomenon. Cold hem agglutinin disease (CHD), is an uncommon Autoimmune hemolytic anemia, mediated by cold reactive auto antibodies that bind to erythrocyte carbohydrate antigen causing hem agglutination and complement mediated hemolysis. Cold agglutinin–mediated hemolysis occurs at low temperature which may be severe and difficult to treat. CHD may be primary when it is idiopathic or secondary as in lympho-proliferative disorder of bone marrow associated with clonal proliferation of CD20 B cells that produce monoclonal 1g M cold agglutinin (kappa /lamda). Rituximab has been used as an as a novel treatment option in Autoimmune hemolytic anemia. Rituximab is a genetically engineered chimeric monoclonal antibody that targets the CD20 antigen on B cells. Rituximab in autoimmune conditions possibly acts by destruction of CD20_clonotypic precursor B cells and/or CD20 plasma cells, thus is effective in controlling immunoglobulin-mediated diseases of B lymphocytes. We analysed four patients of lymphoma with severe CHD who were successfully treated with the chimeric anti-CD20 monoclonal Rituximab (375mg/ m2) intravenously every three weeks for four to six cycles, till the Agglutinins disappeared from the serum. Patient and method In this study patients diagnosed with lymphoma associated CHD were treated with Rituximab with a dose of 375mg/ meter square given every three weeks for four to six cycles, till the primary aim was achieved. The primary aim was correction of anemia, disappearance of cold hem-agglutinins from serum, assessed by complete blood counts and measuring cold agglutinins in serum. Four such patients were studied, all of them had NHL-DLBCL (IHC proven), with severe hemolysis and jaundice with Hemoglobin <5 gm/ dl. All had presence of cold agglutinins in the serum and were positive for direct and indirect coomb's test. Response All the patients showed significant improvement in the symptoms due to anemia and there was a rise in hemoglobin detected within the first week of Rituximab treatment. They achieved normal levels of hemoglobin with four to six weeks of treatment and in three patients cold agglutinins disappeared after completion of five cycles and the fourth patients had it after the sixth cycle. None of the patients was given any transfusion because of incompatibility issues. Conclusion Our experience with Rituximab was excellent in this indication and patients had a good overall outcome. Further trials need to be done for more evidence in this regard. Disclosures: No relevant conflicts of interest to declare.
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Rajavel, Sowndharya, Cade E. Ito, Keith Abe, Valerie Guerrero, Gene I. Uenishi, Andrew M. Scharenberg e Gregory J. Cost. "Chemically Controlled, Immunosuppression-Resistant, Anti-Bcma CAR-T Cells for Treatment of Antibody-Mediated Autoimmunity". Blood 132, Supplement 1 (29 novembre 2018): 2203. http://dx.doi.org/10.1182/blood-2018-99-117630.
Abstract (sommario):
Abstract Auto-reactive antibody production by plasma cells is the direct cause of many auto-immune diseases. In such cases elimination of plasma cells would ameliorate the disease. Chimeric antigen receptor T (CAR-T) cells with cytotoxicity toward cells expressing B-cell maturation antigen (BCMA) have shown remarkable promise for the treatment of multiple myeloma, a plasma cell neoplasm. Elimination of non-malignant plasma cells is a side-effect of anti-BCMA CAR-T treatment of multiple myeloma, suggesting the use of these anti-BCMA CAR T cells for auto-immune indications. Unfortunately, CAR-T administration requires use of lymphodepletion to achieve efficient cell engraftment, and is often accompanied by cytokine release syndrome (CRS), a potentially life-threatening side-effect. As lymphodepletion and CRS pose morbidity/mortality risks that are unacceptable for therapy of many auto-immune diseases, we have utilized CRISPR-Cas9 gene editing to develop a controllable CAR-T cell platform that provides for (1) engraftment with non-cytotoxic transient immunosuppression; and (2) small-molecule dependent CAR T-cell expansion. We have implemented this platform using a unique dual targeting approach in which a BCMA CAR transgene is integrated into the TRAC locus, and additional payloads are integrated into a second locus, thus also enabling an allogeneic manufacturing process. Transgene integration occurred in >50% of cells individually with several percent of cells targeted at two loci. TRAC-targeted, anti-BCMA CAR T cells demonstrated CAR-dependent, target-cell-BCMA-dependent cytotoxicity towards both high-BCMA- and low-BCMA-expressing cell lines and in multiple myeloma cells xenografted into NSG mice. Drug-regulation properties and immunosuppression resistance are the subject of ongoing experiments. Anti-BCMA CAR T cells that are chemically controlled, incapable of graft-versus-host disease, and insensitive to immunosuppression may be an attractive treatment option a variety of antibody-mediated auto-immune conditions. Disclosures Rajavel: Casebia Therapeutics: Employment. Ito:Casebia Therapeutics: Employment. Abe:Casebia Therapeutics: Employment. Guerrero:Casebia Therapeutics: Employment. Uenishi:Casebia Therapeutics: Employment. Scharenberg:Casebia Therapeutics: Employment; Generation Bio: Equity Ownership; Alpine Immune Sciences: Equity Ownership. Cost:Casebia Therapeutics: Employment.
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Khungar, Jitendra Mohan, Hara Prasad Prasad Pati e Manoranjan Mahapatra. "Diagnosis of Auto Immune Hemolytic Anemia by Detection of RBC-Bound IgG Antibodies, Using Flow-Cytometry". Blood 120, n. 21 (16 novembre 2012): 5159. http://dx.doi.org/10.1182/blood.v120.21.5159.5159.
Abstract (sommario):
Abstract Abstract 5159 Introduction: Auto Immune Hemolytic Anemia (AIHA) is one of the most common types of acquired hemolytic anaemias. Its main cause is auto antibody mediated rapid destruction of RBCs. Detection of these autoantibodies to erythrocytes is of fundamental importance for diagnosis. A number of methodologies have been tried for detection & evaluation of these autoantibodies. Demonstration of a positive Direct Antiglobulin Test (DAT) against these autoantibodies is an important serological assay in the diagnosis of auto immune hemolytic anemia (AIHA). This test is also considered as pathognomonic of immune-mediated hemolysis. This routinely used direct antiglobulin test (DAT) has the disadvantage of low sensitivity and does not detect low levels of red cell auto antibodies leading sometimes to false negative results. Flow cytometry can effectively diagnose such patients of auto immune hemolytic anemia with low levels of autoantibodies. Role of flow cytometry in the diagnosis of several non-malignant haematological disorders is being explored & present study has been conducted with the same objective. Aims & Objectives: This study was conducted with the following aims and objectives: •To assess the utility of flow-cytometry (FCM) in the diagnosis of suspected AIHA patients. •Compare the sensitivity of flow-cytometry (FCM) with Direct Antiglobulin Test (DAT) by Gel-card Test (GT). •To assess the positivity in DAT negative cases by flow-cytometry in suspected AIHA cases. Material & Methods: This was a prospective study, carried out in Haematology Deptt of All India Institute of Medical Sciences, where patients with suspected auto immune hemolytic anemia (AIHA) were studied during two years period. Blood samples of suspected patients of AIHA were tested by Gel Card Test as well as by Flow cytometry for detection of RBC bound IgG. Results: A total of 50 patients with suspected diagnosis of auto immune hemolytic anemia (AIHA) were studied by flow-cytometry as well as by Gel card test (GT) for detection of RBC bound IgG. Out of these 50 cases, 41 cases have turned out to be positive and 9 were negative by flow-cytometry. The quantification of positivity by flow-cytometry was obtained by calculating percentage fluorescence. The same 50 cases were also tested by Gel card test (GT). By Gel card test, out of 50 cases, 34 were positive & 16 were negative. Therefore, there were 7 cases which were negative for RBC bound IgG by Gel card test and these were positive by flow-cytometry. The flow cytometry figures of these cases will be shown & discussed in the presentation. Conclusions: Flow-cytometry is a reliable and sensitive method of detecting RBC-bound IgG antibodies for the diagnosis of auto immune hemolytic anemia. This can be used as a new routine diagnostic technique for auto immune hemolytic anemia. Disclosures: No relevant conflicts of interest to declare.
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Pastva, Ondřej, e Kerstin Klein. "Long Non-Coding RNAs in Sjögren’s Disease". International Journal of Molecular Sciences 25, n. 10 (9 maggio 2024): 5162. http://dx.doi.org/10.3390/ijms25105162.
Abstract (sommario):
Sjögren’s disease (SjD) is a heterogeneous autoimmune disease characterized by severe dryness of mucosal surfaces, particularly the mouth and eyes; fatigue; and chronic pain. Chronic inflammation of the salivary and lacrimal glands, auto-antibody formation, and extra-glandular manifestations occur in subsets of patients with SjD. An aberrant expression of long, non-coding RNAs (lncRNAs) has been described in many autoimmune diseases, including SjD. Here, we review the current literature on lncRNAs in SjD and their role in regulating X chromosome inactivation, immune modulatory functions, and their potential as biomarkers.
Tesi sul tema "Non auto immune":
1
Denet, Sylvie. "Hyperthyroidie diffuse non auto-immune : nouveau concept physiopathologique ?" Nancy 1, 1992. http://www.theses.fr/1992NAN11217.
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Lipski, Deborah. "Study of the mechanisms of local auto-antigen presentation and inner blood-retinal barrier breakdown during non-infectious uveitis". Doctoral thesis, Universite Libre de Bruxelles, 2018. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/262873.
Abstract (sommario):
Le développement de l’uvéite auto-immune expérimentale (UAE) se fait en plusieurs étapes, commençant par l’activation en périphérie de lymphocytes T auxiliaires auto-réactifs spécifiques d’antigènes rétiniens, leur migration vers l’œil, où ils sont réactivés de façon antigène-spécifique et CMH II (complexe majeur d’histocompatibilité de classe II)-dépendante pour enfin induire la rupture de la barrière hémato-rétinienne (BHR), permettant le recrutement aspécifique de cellules inflammatoires responsables des dommages tissulaires. Tous ces processus représentent des cibles potentielles pour des thérapies biologiques ciblées. Dans cette perspective, notre travail a pour but d’approfondir la compréhension des mécanismes impliqués dans le recrutement de cellules inflammatoires, la présentation locale d’antigènes rétiniens et la rupture de la BHR interne lors de l’induction de l’UAE par transfert adoptif.L’expression de molécules d’adhésion par les cellules de la BHR joue un rôle central dans l’infiltration de cellules inflammatoires dans l’œil. Dans ce contexte, nous avons d’abord montré qu’à l’instar de ce que nous avions démontré pour VCAM-1, l’expression d’ICAM-1 est fortement induite dans la rétine durant l’UAE, avec une intensité et une extension corrélées à la sévérité de la maladie. Cependant, alors que VCAM-1 est uniquement inductible, une expression basale d’ICAM-1 est détectée dans la rétine naïve. Le ligand d’ICAM-1, LFA-1, est exprimé de façon ubiquitaire par les cellules immunes circulantes, contrairement au ligand de VCAM-1, VLA-4, qui n’est exprimé que par une minorité de cellules. Par ailleurs, nous avons observé une répartition tissulaire différente de ces deux molécules d’adhésion dans la rétine. En effet, si ICAM-1 prédomine dans l’épithélium pigmentaire rétinien, VCAM-1 est fortement exprimé au niveau des lésions de vasculite, à la fois sur les cellules endothéliales et gliales péri- vasculaires. Ces 2 sites correspondent respectivement à la BHR externe et interne. Ces différences majeures en termes de distribution rétinienne des molécules d’adhésion pourraient refléter des voies d’entrée distinctes pour les cellules inflammatoires lors de leur pénétration dans l’œil.Comme les lymphocytes T auto-réactifs n’induisent la maladie qu’après avoir localement reconnu leur antigène, nous nous sommes ensuite intéressés à identifier les cellules présentatrices d’antigène (CPA) potentielles exprimant du CMH II dans la rétine lors de l’UAE. Nous avons tout d’abord observé une forte induction de l’expression de molécules du CMH II dans la rétine lors de l’inflammation intraoculaire, corrélée avec la sévérité de la maladie. Celle-ci est associée avec l’induction de l’expression de molécules de co-stimulation, particulièrement sur les cellules exprimant fortement le CMH II. L’expression la plus forte de CMH II se retrouve dans la rétine interne, au niveau des vaisseaux enflammés et s’étend vers les couches externes de la rétine et l’espace sous-rétinien dans les uvéites sévères. Nous avons identifié 3 populations de CPA potentielles exprimant le CMH II dans la rétine :des cellules CD45-CD11b- non-hématopoïétiques exprimant faiblement le CMH II et des cellules CD45+CD11b+ hématopoïétiques exprimant plus fortement le CMH II, pouvant être subdivisées en cellules Ly6C+ et Ly6C-. L’analyse bio-informatique à l’aveugle du transcriptome de ces 3 populations mène à une ségrégation claire des échantillons, avec un enrichissement en marqueurs de macrophages et de microglie dans les cellules Ly6C+ et Ly6C-, respectivement. Cependant, l’expression de Ly6C ne permet pas une ségrégation absolue entre macrophages infiltrants et microglie résidente. L’analyse fonctionnelle à l’aide de DAVID (Database for Annotation, Visualization and Integrated Discovery) révèle que les 2 populations de cellules hématopoïétiques sont plus compétentes dans la présentation d’antigène associée au CMH II et l’activation des lymphocytes T que les cellules non-hématopoïétiques.Paradoxalement, nos données n’ont pas mis en évidence d’expression de CMH II par les principales cellules de la BHR que sont les cellules endothéliales et les cellules de l’épithélium pigmentaire rétinien. Cependant, il est bien établi que les cellules endothéliales rétiniennes subissent un changement majeur de phénotype lors du développement d’une UAE. Afin d’investiguer de façon globale les mécanismes sous-jacents à la rupture de la BHR interne, nous avons étudié la régulation de l’expression génique des cellules endothéliales rétiniennes lors de l’uvéite non-infectieuse. En accord avec les données de nos travaux précédents, l’analyse du transcriptome des cellules endothéliales rétiniennes n’a pas mis en évidence d’expression de CMH II lors de l’UAE. En revanche, cette approche nous a permis d’identifier 65 gènes modulés dans les cellules endothéliales rétiniennes lors du développement d’une UAE, confirmant non seulement l’implication de certaines molécules dont le rôle pathogénique est déjà connu, mais procurant également une liste de nouveaux gènes candidats et de voies fonctionnelles potentiellement associées à la rupture de la BHR lors d’une uvéite non- infectieuse.Doctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished
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EL, KHALID ABDELLATIF. "Aspergillose pulmonaire chez le non immunodeprime : a propos d'un cas survenu au cours d'une infection a cytomegalovirus compliquee de thrombopenie auto-immune". Dijon, 1994. http://www.theses.fr/1994DIJOM110.
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Le, Collen Lauriane. "Médecine de précision du diabète de type 2 et des obésités génétiques". Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS042.
Abstract (sommario):
Cette thèse de sciences s'est consacrée à une exploration approfondie de la composante génétique de cas de diabète, d'obésité et de lipodystrophies familiales (FPLD). Ces maladies métaboliques d'origine multifactorielle sont des enjeux de santé cruciaux en raison de leurs impact majeur sur l'espérance et la qualité de vie des malades, mais aussi sur les systèmes collectifs de santé. L'objectif central était d'exploiter les capacités du séquençage de nouvelle génération (NGS), par exome, pour détecter des variants au sein de gènes déjà associés à ces affections chez des patients en errance diagnostic. Il est maintenant démontré qu'au moins 2% des cas de diabète de type 2 peuvent être attribués à des variants pathogènes dans des gènes liés au diabète Maturity-Onset Diabetes of the Young (MODY). Cette étude avait pour objectif d'améliorer le processus de diagnostic et d'optimiser la prise en charge thérapeutique de ces patients, tout en démontrant l'efficacité de l'approche de séquençage dans la gestion globale de ces affections complexes. Dans un premier cas, nous avons démontré l'importance de cette démarche en examinant un patient présentant un diabète atypique de forme syndromique. Nous avons identifié un variant hétérozygote pathogène dans WFS1, transmis par le père atteint de diabète. Cette découverte a eu un impact majeur sur le traitement de ce patient, mettant en évidence l'efficacité d'un traitement par analogue du GLP1 pour optimiser la gestion de son diabète. Notre étude a aussi examiné l'impact d'une délétion en 16q24.2 de novo, ayant le potentiel d'affecter la régulation d'un gène voisin, FOXC2, impliqué dans le syndrome lymphœdème-distichiasis. Ce cas soulevait aussi des questions sur les troubles neurodéveloppementaux, liés potentiellement à la délétion et à un variant hérité de sa mère dans USP9X. Ces résultats mettent en lumière l'importance cruciale du diagnostic précis dans le choix des traitements appropriés. Notre recherche a aussi porté sur PDX1 (MODY4), en analysant les porteurs hétérozygotes de variants pathogènes. Nos investigations ont révélé une pénétrance complète du diabète, une augmentation de l'indice de masse corporelle et un risque accru d'insuffisance pancréatique chez ces individus. Une fois de plus, l'utilisation d'analogues du GLP1 s'est révélée bénéfique pour optimiser la gestion de la glycémie.Ensuite, nous avons exploré le cas d'une patiente souffrant d'obésité morbide, présentant un déficit hypophysaire combiné et une hétérozygotie composite en POMC. Cette observation a remis en question la notion selon laquelle l'hétérozygotie en POMC pouvait être la cause d'une obésité monogénique. Cela soulève la question de l'efficacité du traitement par agonistes de MC4R chez ces patients, qu'il convient de réserver aux cas dont l'étiologie génétique est avérée.Enfin, nous avons étudié une famille présentant un syndrome métabolique associé à une possible FPLD. L'analyse génétique a révélé un variant dans ZMPSTE24, déjà identifié dans la même région géographique, ce qui a soulevé la question d'un variant fondateur. Cependant, la contribution de ce variant hétérozygote à la FPLD reste à confirmer, nécessitant des études complémentaires pour établir définitivement son rôle.En conclusion, cette thèse a mis en évidence l'efficacité du NGS pour élucider des cas complexes de diabète et d'obésité atypiques, mettant en avant des formes monogéniques de ces affections. Cette recherche a élargi la portée de ses investigations en examinant ces données à l'échelle de la population générale, grâce à une revue de la littérature et à l'analyse de différentes bases de données, telles que Human Gene Mutation Database, RaDIO et UK Biobank. Nous espérons que ces résultats convaincants contribueront à encourager une adoption plus répandue du séquençage génétique, ouvrant ainsi la voie à une personnalisation accrue des traitements en fonction du génotype des patients dans un avenir procheThis scientific thesis delves deeply into critical health issues, specifically diabetes, obesity, and rare familial lipodystrophies. These health concerns hold immense importance due to their substantial medical and financial implications, impacting individuals, healthcare systems, and national economies. The central aim of this research was to harness the capabilities of next-generation sequencing (NGS), such as exome sequencing, to detect genetic mutations within genes already associated with these conditions in diagnostically challenging patients. It is now established that up to 2% of cases of type 2 diabetes can be attributed to pathogenic variants in genes related to Maturity-Onset Diabetes of the Young (MODY). This study sought to enhance the diagnostic process and optimize therapeutic management for these complex conditions while demonstrating the effectiveness of the sequencing approach in comprehensive disease management.In a first case, we showcased the significance of this approach by examining a patient with an atypical syndromic form of diabetes. Through in-depth genetic analysis using NGS, we identified a pathogenic heterozygous variant in the WFS1 gene inherited from the diabetic father. This discovery had a profound impact on the patient's treatment, highlighting the effectiveness of GLP1 analog therapy in optimizing diabetes management. Furthermore, our study investigated the impact of a de novo deletion in 16q24.2, which had the potential to affect the regulation of a neighboring gene, FOXC2, implicated in lymphedema-distichiasis syndrome. This case also raised questions about neurodevelopmental disorders, potentially linked to this deletion and a variant located in USP9X inherited from the patient's mother. These results underscore the critical importance of precise diagnosis in selecting appropriate treatments.In a second article, our research focused on the PDX1 gene, responsible for MODY 4, by analyzing heterozygous carriers of pathogenic variants. Our investigations revealed complete penetrance of diabetes, an increase in body mass index, and an elevated risk of pancreatic insufficiency in these individuals. Once again, the judicious use of GLP1 analogs proved beneficial in optimizing glycemic control.Next, we explored the case of a patient suffering from morbid obesity, presenting with combined pituitary deficiency and composite heterozygosity in POMC. This observation challenged the previous notion that heterozygosity in POMC could cause monogenic obesity. This reconsideration raises crucial questions about the effectiveness of targeted treatment with MC4R agonists in POMC heterozygotes, posing significant financial challenges for its use in this indication.Finally, we studied a large family with a severe metabolic syndrome associated with partial lipodystrophy. Genetic analysis revealed a variant in the ZMPSTE24 gene, previously identified in the same geographic region, raising the question of a founder variant. However, the contribution of this heterozygous variant to partial lipodystrophy remains to be confirmed, necessitating further studies to definitively establish its role.In conclusion, this thesis has highlighted the remarkable efficacy of next-generation sequencing in elucidating complex cases of atypical diabetes and obesity, shedding light on monogenic forms of these conditions. Moreover, this research expanded its investigations to the broader population through comprehensive literature reviews and analysis of various databases, including the Human Gene Mutation Database, RaDIO, and UK Biobank. We hope that these compelling results will encourage wider adoption of genetic sequencing, paving the way for increased customization of treatments based on patients' genotypes in the near future
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Deruytter, Nathalie. "De nouveaux gènes de prédisposition au diabète auto-immun liés au complexe majeur d'histocompatibilité chez la souris Non Obese Diabetic (NOD)". Paris 6, 2004. http://www.theses.fr/2004PA066088.
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Laloux, Véronique. "Rôle immuno-régulateur des lymphocytes TNK". Paris 6, 2002. http://www.theses.fr/2002PA066206.
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Hussain, Munther Jaffar. "Role of cytokines in the pathogenesis of type 1 diabetes". Thesis, Brunel University, 1996. http://bura.brunel.ac.uk/handle/2438/3655.
Abstract (sommario):
T lymphocytes and macrophages appear to play an important role in mediating ß-cell damage and causing Type 1 diabetes. Both activated T cells and macrophages operate and interact through the release of soluble factors called cytokines, which influence the type and magnitude of immune responses. It has been suggested that cytokines such as TNF-α and IL-1α can damage the N-cell directly. In Type 1 diabetes, cytokines are likely to have a critical role in individuals whose immune system is unbalanced allowing the emergence of self-destructive processes. To investigate this possibility, sensitive assays to detect a range of cytokines of potential relevance to the immune pathogenesis of diabetes were establised. Using these, serum levels of IL-1α, IL-1N, TNF-α and IL-6 (macrophage-derived cytokines), IFN-γ and IL-2 (T helper 1 cytokine profile) and IL-4 and IL-10 (T helper 2 profile) have been measured in patients with Type 1 diabetes of different disease duration. Increased levels of TNF-α, IL-1α, IL-2 and IFN-γ were found in recently diagnosed patients with Type 1 diabetes when compared with both disease and metabolic control subjects and with normal controls. The presence of this profile of cytokines implies activation of the TH1 subset of helper cells near to diagnosis of Type 1 diabetes
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Zhu, Ren. "Dissection des fonctions régulatrices des lymphocytes iNKT en situation auto-immune dans le modèle de la souris NOD". Phd thesis, Université René Descartes - Paris V, 2006. http://tel.archives-ouvertes.fr/tel-00084227.
Abstract (sommario):
Les cellules iNKT ont des propriétés régulatrices qui suscitent un intérêt particulier en immunopathologie. Mon travail de thèse a eu pour objectif de mesurer l'impact du défaut des cellules iNKT de la souris NOD dans deux situations auto-immunes : 1) le diabète de type 1, une maladie développée spontanément par la souris NOD dans laquelle nous avons montré que les cellules iNKT, tout en constituant des cibles thérapeutiques sous l'impulsion de leur ligand a-GalCer n'ont pas d'activité protectrice spontanée; 2) l'hépatite induite par la ConA, dont la moindre susceptibilité chez la souris NOD a révélé le caractère dominant du rôle délétère de la production d'IL-4 assurée surtout par les cellules iNKT spléniques et non hépatiques et qui est directement potentialisée par l'IL-12, une cytokine qui exacerbe la maladie. En conclusion, notre travail ouvre une nouvelle voie thérapeutique tout en illustrant le caractère ambivalent « mi ange, mi démon » des cellules iNKT en situation auto-immune.
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Bourdenet, Gwladys. "Étude physiopathologique de la myopathie auto-immune des souris NOD invalidées pour la voie de costimulation ICOS/ICOSL". Thesis, Normandie, 2017. http://www.theses.fr/2017NORMR062/document.
Abstract (sommario):
Les myopathies inflammatoires (MI) représentent un groupe hétérogène de maladies caractérisépar une faiblesse musculaire chronique et symétrique associée à une augmentation du taux sérique decréatine phosphokinase (CPK). Les MI sont actuellement subdivisées en 5 entitées : les dermatomyosites,les myopathies nécrosantes auto-immunes, la myosite à inclusion, la polymyosite et les myosites dechevauchement. A ce jour, le diagnostic des MI repose sur l’association de signes cliniques, decaractéristiques anatomopathologiques sur la biopsie musculaire et la présence d’auto-anticorps (aAc). Eneffet, la découverte d’aAc spécifiques et/ou associés aux myosites (MSA/MAA) a considérablementamélioré le diagnostic et le pronostic de la maladie. Cependant, un nombre non négligeable de patientsatteints de MI sont séronégatifs pour les MSA/MAA connus. Par ailleurs, la biopsie musculaire nécessaireau diagnostic est parfois guidée par imagerie par résonance magnétique (IRM), bien qu’il n’ait pas étéprouvé que les données d’imagerie soient corrélées aux signes histologiques. Enfin, le traitement des MIrepose sur l’utilisation d’immunosuppresseurs systémiques, une approche non spécifique de laphysiopathologie de la maladie. Les modèles animaux de MI les plus utilisés sont induits et nonspontanés : ils reposent principalement sur l’immunisation d’animaux contre des protéines telles que lamyosine, la protéine C ou l’histidyl-tRNA synthétase.Les souris NOD (non obese diabetic) sont le modèle classique d’étude du diabète de type 1.Lorsque ces souris sont invalidées pour la voie de costimulation lymphocytaire ICOS/ICOSL, les souris nedéveloppent plus de diabète mais présentent alors une atteinte musculaire. Dans ce travail, nous avonsétudié le phénotype et caractérisé l’atteinte musculaire des souris NOD Icos-/- et NOD Icosl-/-. Nous avonsainsi établi le 1er modèle murin spontané de MI, dont la physiopathologie est médiée par leslymphocytes T CD4+ et la sécrétion d’IFN-γ. Par ailleurs, ces souris présentent un déficit en lymphocytes Trégulateurs. Nous avons également identifié 4 auto-antigènes (aAg) candidats cibles d’aAc chez ces souris.La recherche des aAc correspondants aux aAg orthologues dans le sérum des patients atteints de MI apermis d’identifier, pour l’un d’entre eux, une minorité d’individus séropositifs grâce au développementd’un nouveau test ALBIA (addressable laser bead immunoassay). Il pourrait donc s’agir d’un nouveaubiomarqueur. Dans la perspective de nouvelles évaluations thérapeutiques, nous avons établi desdonnées préliminaires montrant que l’interleukine 2 à faibles doses permet de retarder l’apparition de lamaladie. Enfin, nous avons mis à profit ce modèle et démontré la corrélation entre les données généréespar IRM et par analyse histologique de l’inflammation, confortant le rôle de cette technique d’imagerie àla fois pour le diagnostic et le suivi des MIInflammatory Myopathies (IM) are a heterogeneous group of diseases characterized bychronic and symmetrical muscle weakness associated to increased creatine phosphokinase (CPK)levels, according to entity concerned. Currently, IM are divided into 5 main entities:dematomyositis, immune-mediated necrotizing myopathies, inclusion body myositis, polymyositisand overlap myositis. Nowadays, IM diagnosis is based on clinical signs associated to pathologicfeatures on muscle biopsy and presence of auto-antibodies (aAb). Indeed, the discovery of myositisspecific and/or associated auto-antibodies (MSA/MAA) had considerably improve disease diagnosisand prognosis. However, substantial proportion of IM patients do not display any knownMSA/MAA. Furthermore, diagnosis requires muscle biopsy. This biopsy is sometimes guided bymagnetic resonance imaging (MRI), even though correlation between MRI findings and pathologicalfeatures is not established. Lastly, therapeutics used in IM treatment are systemicimmunosuppressive agents, i.e. not specific to IM pathophysiology. Animal models of IM are mainlybased on active immunization against different proteins as myosin, C protein orhistidyl-tRNA synthetase, while spontaneous models are required to identify pathophysiologicalmechanisms that new therapeutics should target.NOD (non obese diabetic) mice are the main model of type 1 diabetes. When invalidatedfor ICOS/ICOSL costimulation pathway, these mice do not develop diabetes but present musculardisorders. In this work, we study Icos-/- and Icosl-/- NOD mice phenotype and characterize theremuscle lesion. Thus, we have established this model as the first paradigm of IM. Pathophysiologicalstudy in these mice demonstrated that disease is CD4+ T cell dependent and associated to IFN-γproduction. Furthermore, we shown a quantitative defect in regulatory T cells. We have alsoidentified 4 candidate autoantigens (aAg) in Icos-/- and Icosl-/- NOD mice. Searching forcorresponding aAb against ortholog proteins in patients with IM, we identified for one of them, alow percentage of seropositive individuals using a new ALBIA (addressable laser beadimmunoassay). It could be identified as a new biomarker. In order to evaluate new therapies, weestablished preliminary data showing that low dose interleukin 2 therapy allow to delay diseaseonset. Lastly, we took advantage of this new model to demonstrate the correlation betweenMRI findings and histological inflammation features, confirming the valuable role of MRI for thediagnosis and monitoring of IM
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Fakir, Mohammed. "Prévention du diabète auto-immun par greffe macro-encapsulée de tissus sécréteurs d'insuline chez la souris NOD". Dijon, 1998. http://www.theses.fr/1998DIJOMU15.
Libri sul tema "Non auto immune":
1
Foster, Charles. On Being Not Depressed. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198801900.003.0003.
Abstract (sommario):
This chapter is written from the perspective of someone who claims never to have suffered from depression. When asked if he has ever been depressed, the author of this chapter reports that he responds vaguely. He states he can be evasive and pompous, insisting that he does not think he satisfies all the clinical criteria. The reason why he is reluctant to accept the notion that he is depressed is not because he feels ashamed about being depressive. On the contrary, he feels that he does not belong to the community of the depressed—an elite club with a black, glorious fellowship of agony in which he cannot share. Another reason is that depression and its symptoms are impossible to describe, even if the will to describe them is intense. No metaphors or similes are sufficient to describe what happens. The author says he is better off with the unnamed and unnamable. He concludes by suggesting that the least unsatisfactory picture is of auto-immune disease: self-consumption.
2
Paintal, Harman S., e Rajinder K. Chitkara. Zoonotic infections with filarial nematodes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0067.
Abstract (sommario):
Filarial nematodes have been known to cause human disease for many centuries. Lymphatic filariasis is a common disease in the developing part of the world and much has been written about diagnosis and treatment of this scourge. Wuchereria , Brugia and Onchocerca (especially O. volvulus) have a wide pattern of distribution with severe morbidity. Given the years of scientific work in this field, many drugs that work against these parasites are available today and are attempting to control these infections. In this chapter, the focus is on those filarial nematodes that do not have humans as their primary host. Instead, the filarial organisms that usually parasitize other animals and cause human infection due to a variety of factors are discussed. These factors include: 1. Proximity of humans to the primary host, 2. Proximity of humans to the vector, 3. Changing ecology with introduction of different animals (both host and vector) into new environments, 4. Increasing human mobility, 5. Special scenarios concerning humans, including altered immune function (immunosuppressed due to drugs, auto-immune illness, immunosuppressive diseases), There has been a recent interest in this field because newer diagnostic techniques, including polymerase chain reaction (PCR) assays, DNA primers and electron microscopy have become widespread in use. This will eventually enhance our understanding of the pathophysiology of infections with these seemingly rare filarial organisms.Much of the early work in this field was done in a few specialized centers. As information about these parasites (through the worldwide web) and diagnostic techniques are now widely available, it is our hope that more work regarding these nematodes will be carried out in the developing countries where these infections are common. In this chapter, we focus on Dirofi laria, Meningonema, Loaina, Dipetalonema and certain species of Onchocerca and Brugia.
3
Sternbach, Marion. Apheresis in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0268.
Abstract (sommario):
This chapter describes therapeutic plasma exchange, as well as cytapheresis for hyperleukocytosis and essential thrombocythemia, as well as harvesting haematological stem cells (HSC) for transplantation. Instrumentation and techniques are mostly density centrifugation, much less column adsorption for antibodies or membrane filtration for noxious molecules. Pathophysiology of apheresis is dealt with in great detail with emphasis on prevention and treatment of side effects, much more critical in the intensive care unit (ICU) setting. Main manifestations are: hypocalcaemia due to chelation by anticoagulants, hypo- and less hypervolaemia, allergic reactions to sedimenting and volume replacement starches or plasma, depletion of coagulation factors, vitamin K, immunoglobulins, lymphocytes with long lifespan and platelets. Wash-out of drugs for comorbid or underlying conditions occurs inadvertently. Main indications for plasma exchange are thrombotic thrombocytopenic purpura (TTP)/haemolytic uraemic syndrome (HUS) with plasma or cryo-poor supernatant (based on RCT), hyperviscosity syndromes, post-transfusion purpura (PTP) and auto-immune haemolytic anaemia (AIHA), where all other treatments have failed. In cold agglutinin disease, cryoglobulinaemia, coagulation factor inhibitors and ABO incompatible HSC transplants, plasmapheresis has proven useful. Myeloma with renal failure does not seem to benefit significantly from plasma exchange (randomized controlled trials proven).
4
Morgan Wortham, Simon. Lupus (Adler and Freud). Edinburgh University Press, 2018. http://dx.doi.org/10.3366/edinburgh/9781474429603.003.0010.
Abstract (sommario):
This chapter examines phobia as a question of psychoanalysis itself, a means to assess its complex and problematic conditions of possibility. In 1929, Alfred Adler produced a case study of ‘Miss R.’ in which he analysed her lupus phobia. Lupus is an auto-immune disease that reached its heights during the nineteenth century. Found at the crossroads between the sprawl of the city and the birth of the clinic, lupus’s historic arc reflects the early history of psychoanalysis. Adler associates Miss R.’s phobias with a desire to avoid her own inferiorization within the family and a fear about life on the outside. The case study offers a clue to the relationship between analyst and analysand: Adler interprets the young girl’s behaviour in terms of an egotistic desire to hold centre-stage; yet the case history is constructed out of extemporized remarks made before a captive audience, presumably to show off Adler’s analytic brilliance (in contrast to Freud’s, whom he takes every opportunity to disparage). We wonder whether Adler might be talking about himself as much as Miss R., and the case study begins to offer some insights not only into the split with Freud in 1911 but indeed the resistances of psychoanalysis itself.
Capitoli di libri sul tema "Non auto immune":
1
Greco, Raffaella, e Dominique Farge. "CART Cells and Other Cell Therapies (ie MSC, Tregs) in Autoimmune Diseases". In The EBMT Handbook, 837–48. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_93.
Abstract (sommario):
AbstractAuto-immune diseases (AD) are heterogeneous conditions, characterized by polyclonal activation of the immune system with a defect of B or T lymphocyte selection and altered lymphocytic reactions to auto-antigens components (Burnet 1959a, b), although it is rare to identify a single antigenic epitope. The native immune system and its tissue environment play an important role to determine if exposure to a given antigen will induce an immune response or tolerance or anergy. The role of the genes coding for the major histocompatibility system molecules, but also of many other genes, is important in the regulation of the immune response, although this does not explain all the observed phenomena during loss of tolerance (Matzinger 1994; Rioux and Abbas 2005).
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Wolfe, Cary. "(Auto)Immunity In Esposito And Derrida". In Roberto Esposito, a cura di Tilottama Rajan e Antonio Calcagno, 153–73. Edinburgh University Press, 2021. http://dx.doi.org/10.3366/edinburgh/9781474480338.003.0008.
Abstract (sommario):
This essay compares the paradigm of (auto)immunity and its centrality to the reconceptualization of biopolitical thought in the work of Jacques Derrida and Roberto Esposito. While Esposito and Derrida share an ‘ecologised’ understanding of the immune system, the alterity of temporality that is operative in the organism/environment relationship (as emphasized in immune system discourse itself in biology) is formalized more rigorously in Derrida than in Esposito – and this has serious consequences for the concept of ‘community’ and more generally for the attempt to craft an ‘affirmative’ biopolitics, in which Esposito is quite invested. The missing link between Derrida’s more creative or productive sense of (auto)immunity and its underpinnings in theoretical biology is the radical alterity of temporality at work in the tech[1]nicity or machinalité of iterability (specifically, the iterability of the organism/ environment relationship and its non-linear character, as it unfolds in real time). This, in turn, is central to his own denaturalisation and deconstruc[1]tion of the difference between the organic (or biological) and the technical (or mechanical), and eventually to his own reconceptualisation of ‘Life’, all of which is key to a non-reductionist and non-vitalist concept of (auto)immunity for biopolitical thought.
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Shimpi, Pooja, Smita Pillewan e Vandana S. Nikam. "Diseases and Disorders Associated with Immune System". In Natural Immunomodulators: Promising Therapy for Disease Management, 41–74. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815123258123010005.
Abstract (sommario):
The human immune system is one of the complex systems of the body, which works against both external and internal invasion. It has two parts: the innate and the acquired immune systems. We have been born with the innate system which gives a quick response for the invading pathogen non-specifically. To deal with the typical environmental antigens, immune system adapts to changes. The acquired (or adaptive) component develops over time and produces antibodies that “remember” invaders to fight them if they return. Failure of it could be due to genetic defect (weak natural immunity), inability to adapt to the change, hyper-responsiveness, or inability to distinguish self from foreign, leading to various diseases and disorders. Various genetic defects of the immune system are at the core of Primary Immune disorders (PIDs), while overactivity is responsible for allergic diseases. Autoimmune diseases are mostly due to malfunction of the adaptive immune system, while in Systemic Auto-inflammatory Disorders (SAIDs), the innate immune system is affected. Advancements in technology and genetics have improved our understanding of the pathogenesis, diagnosis, and management of these diseases.
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Reséndiz-Mora, Albany, Alonso Tescucano, Giovanna Barrera-Aveleida, Anahi Sotelo-Rodríguez, Christian-Irene Nevárez-Lechuga, Iván Galarce-Sosa, Isabel Wong-Baeza, Isabel Baeza e Carlos Wong-Baeza. "Anti-Non-Bilayer Phospholipid Arrangement Antibodies Trigger an Autoimmune Disease Similar to Systemic Lupus Erythematosus in Mice". In Systemic Lupus Erythematosus - Pathogenesis and Management [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106373.
Abstract (sommario):
Anti-lipid antibodies are present in some infectious and autoimmune diseases, such as Systemic Lupus Erythematosus (SLE). Particularly, anti-non-bilayer phospholipid arrangement (NPA) antibodies have been detected in patients with SLE, and these antibodies trigger a disease similar to human lupus in mice. NPA are lipid associations different from the lipid bilayer of cellular membranes and, since they are transient, they are not immunogenic. However, if NPA are stabilized by drugs, they induce an immune response with the production of anti-NPA antibodies, which bind to NPA on cell membranes and generate cell lysis. As a result, intracellular antigens are exposed and trigger an immune response that generates more auto-antibodies. In this chapter, we describe the formation and stabilization of NPA, the induction of B cell responses to generate anti-NPA antibodies, and the characteristics that the disease caused by these antibodies in mice shares with human lupus.
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Jardetzky, T. "The Interaction of Antigens and Superantigens with the Human Class II Major Histocompatibility Complex Molecule HLA-DR1". In Biological NMR Spectroscopy. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780195094688.003.0022.
Abstract (sommario):
The initiation and maintenance of an immune response to pathogens requires the interactions of cells and proteins that together are able to distinguish appropriate non-self targets from the myriadof self-proteins (Janeway and Bottomly, 1994). This discrimination between self and non-self is in part accomplished by three groups of proteins of the immune system that have direct and specific interactions with antigens: antibodies, T cell receptors (TcR) and major histocompatibility complex (MHC) proteins. Antibodies and TcR molecules are clonally expressed by the B and T cells of the immune system, respectively, defining each progenitor cell with a unique specificity for antigen. In these cell types both antibodies and TcR proteins undergo similar recombination events to generate a variable antigen combining site and thus produce a nearly unlimited number of proteins of different specificities. TcR molecules are further selected to recognize antigenic peptides bound to MHC proteins, during a process known as thymic selection, restricting the repertoire of T cells to the recognition of antigens presented by cells that express MHC proteins at their surface. Thymic selection of TcR and the subsequent restricted recognition of peptide-MHC complexes by peripheral T cells provides a fundamental molecular basis for the discrimination of self from non-sell and the regulation of the immune response (Allen, 1994; Nossal, 1994; von Boehmer, 1994). For example, different classes of T cells are used to recognize and kill infected cells (cytotoxic T cells) arid to provide lymphokiries that induce the niajority of soluble antibody responses of B cells (helper T cells). In contrast to the vast combinatorial and clonal diversity of antibodies and TcRs, a small set of MHC molecules is used to recognize a potentially unlimited universe of foreign peptide antigens for antigen presentation to T cells (Germain, 1994). This poses the problem of how each MHC molecule is capable of recognizing enough peptides to insure an immune response to pathogens. In addition, the specificity of the TcR interaction with MHC-peptide complexes is clearly crucial to the problem of self :non-self discrimination, with implications for both protective immunity and auto-immune disease.
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Pandya, Purvi M., Ekta N. Jayswal e Yash Shah. "Spread of Tuberculosis Among Smokers". In Mathematical Models of Infectious Diseases and Social Issues, 49–73. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-3741-1.ch003.
Abstract (sommario):
Smoking tobacco has some hazardous implications on an individual's physical, physiological, and psychological health; health of the passive smokers near him or her; and on the surrounding environment. From carcinomas to auto-immune disorders, smoking has a role to play. Therefore, there arises a need to frame a systemic pathway to decipher relationship between smoking and a perilous disease such as tuberculosis. This research work focuses on how drugs or medications can affect individuals who are susceptible to tuberculosis because of smoking habits and also on individuals who have already developed symptoms of tuberculosis due to their smoking addiction. The mathematical model is formulated using non-linear ordinary differential equations, and then threshold is calculated for different equilibrium points using next generation matrix method. Stability analysis along with numerical simulations are carried out to validate the data.
7
Aggarwal, Pallvi. "Biological Potential of Nanoparticles as Effective Pharmacological Agents". In Plant Mediated Synthesis of Metal Nanoparticles, 57–87. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815256352124010005.
Abstract (sommario):
Green nanoparticles are being used in the field of pharmaceutical industry to convert them into pharmacologically effective agents that are used to cure many dangerous diseases. Inventions have been done in this area to prepare non-toxic and pharmacologically beneficial drugs to save life of humans and to preserve the environment to its originality. This chapter gives information about the different types of nanoparticles that are used in the form of drugs such as Dendrimers, Micelles, Drug conjugates, Protein nanoparticles, Nano-gels, Nanotubes of carbon and Nano-diamonds etc. It has been found that incorporation of green nanoparticles into drug reduces the toxicity level of the drug and used to cure Cancer, Infectious disorders, Auto-immune disorders, Cardiovascular Diseases, Neurodegenerative diseases, Disorders of the eye and lungs etc. Along with this, the chapter describes the various route of administration of nanoparticles with appropriate mechanisms.
8
Ghate, Utkarsh, e Hema Kulkarni. "Polyphenols, Spices and Vegetarian Diet for Immunity and Anti-Inflammatory Drug Design". In Biosynthesis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97661.
Abstract (sommario):
Much lower COVID-19 incidence and mortality in India compared to the Europe and northern America may relate to higher immunity possibly due to the low consumption of fast/packed food, liquour, tobacco, meat, HFSS- high fat, salt, sugar, besides higher exposure and a key blood protein. Indian spice intake is also double the world average and healthy cooking oil use such as Mustard, and may also explain it. Inflammation is the foundation for many ailments and challenges the immunity and vital in non-communicable ailments are at the centre stage in an aeing world. Polypehnols are crucial anti-inflammatory chemicals from spices that can for wellbeing and reduce adverse drug rections. We show this using Arthritis- a chronic auto-immune disorder, with the hlep of pharmacokinetic studies. Molecular Docking study was performed on the key bioactive compounds of important spices regarding COX2 active site (PDB ID 5IKR). Piperine in Black Pepper had most stability (Black Pepper, −9.99 Kcal/mol) followed by ‘Apigenin’ (Coriander, −9.63), and ‘Curcumin’ (Turmeric, −8.66) like quercetin in literature, and higher than the methotrexate (−8.6), the standard drug. Hence, their synergistic combination in fat medium such as clarified butter can lead the future drug design.
9
Omkar, S. N., Dheevatsa Mudigere, J. Senthilnath e M. Vijaya Kumar. "Identification of Helicopter Dynamics based on Flight Data using Nature Inspired Techniques". In Deep Learning and Neural Networks, 257–73. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-0414-7.ch016.
Abstract (sommario):
The complexity of helicopter flight dynamics makes modeling and helicopter system identification a very difficult task. Most of the traditional techniques require a model structure to be defined a priori and in case of helicopter dynamics, this is difficult due to its complexity and the interplay between various subsystems. To overcome this difficulty, non-parametric approaches are commonly adopted for helicopter system identification. Artificial Neural Network are a widely used class of algorithms for non-parametric system identification, among them, the Nonlinear Auto Regressive eXogeneous input network (NARX) model is very popular, but it also necessitates some in-depth knowledge regarding the system being modelled. There have been many approaches proposed to circumvent this and yet still retain the advantageous characteristics. In this paper, the authors carry out an extensive study of one such newly proposed approach - using a modified NARX model with a II-tiered, externally driven recurrent neural network architecture. This is coupled with an outer optimization routine for evolving the order of the system. This generic architecture is comprehensively explored to ascertain its usability and critically asses its potential. Different implementations of this architecture, based on nature inspired techniques, namely, Artificial Bee Colony (ABC), Artificial Immune System (AIS) and Particle Swarm Optimization (PSO) are evaluated and critically compared in this paper. Simulations have been carried out for identifying the longitudinally uncoupled dynamics. Results of identification indicate a quite close correlation between the actual and the predicted response of the helicopter for all the models.
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Vital, David. "Auto—emancipation?" In A People Apart, 346–475. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780198219804.003.0006.
Abstract (sommario):
Abstract European Jewry was now divided. It was divided defacto and more than ever before in conscience. It was one thing to observe events in Russia from without and at the immense distance in space and mind separating the barbarities inflicted on the Pale of Jewish Settlement from the comparative order and civilization of central and western Europe. It was another to suffer, or even merely to observe, them at first hand from within the empire itself. Sympathy and benign concern for the easterners when contemplating their disasters were not un-common sentiments in Berlin, Vienna, Budapest, London, and Paris, as we have seen. For the Jews of Russia and Poland themselves matters were of course vastly more immediate, depressing, and, above all, urgent. For the great majority within the Pale, but also for the very small minority allowed to live outside it, for the rich, for the poor, for the high and for the low, for firmly orthodox believers no less than for those who had been touched (or more) by secularism and by indigenous Russian culture, for those who had escaped molestation almost as much as for those who had suffered it at the hands of the mob or those of the authorities-for all these, for all classes, some sort of reckoning had now to be made.
Atti di convegni sul tema "Non auto immune":
1
Gupta, Krati, Arnav Bhavsar e Anil K. Sao. "Mitotic v/s non-mitotic HEp-2 cells classification for CAD based auto-immune disorder detection". In CoDS-COMAD '18: The ACM India Joint International Conference on Data Science & Management of Data. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3152494.3167987.
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Adil Mansoor, AL-Husnah. "Role of Interleukin-35 In The Pathogenesis of Hashimoto’s Thyroiditis Disease". In X INTERNATIONAL CONGRESS OF PURE AND APPLIED TECHNOLOGICAL SCIENCES. Rimar Academy, 2023. http://dx.doi.org/10.47832/minarcongress10-1.
Abstract (sommario):
The immune system has the ability to distinguish between self and non-self. Also, Regulatory T-cells are a portion of Tcells that are in charge of preserving regulation of the immune system and immune tolerance through active immunerepression. Immune tolerance is very important to prevent the immune system from interacting against itself and thus to avoid the development of autoimmune diseasesInterleukin-35 (IL-35), which is a member of the interleukin-12 (IL12) cytokine family, is an anti-inflammatory immune response that plays the important function in the obstruction of the development of autoimmune diseases in different tests autoimmunities. When loss of self-tolerance occurs becuses many genetic and environmental factors, this causes the absence of balanced anti-inflammatory immune responses, which reduces the in vivo suppressive capacity of Treg, which is taken to be a regular T-cell-linked autoimmune disease., especially Hashimoto’s thyroiditis (HT). Methods: The current study included 90 samples. 60 hypothyroid HT patients (Group 1) and 30 healthy controls (Group 2) were enrolled in the study. Blood samples were collected and separated into serum from the two groups to be used to measure the functions of the thyroid gland by measuring the levels of thyroid hormone and thyroid stimulating hormone, measuring the level of anti-thyroid auto-antibodies, and determining the standard of serum Interloukin-35 through ELISA. Results: The results of the current study Through statistical analysis using the program SPSS version 22, it was shown that serum IL-35 levels were inversely Correlation used Pearson test with TSH, TPO-Ab, and TG-Ab in patients HT (-.292 (P≥0.01), -.245 (P≥0.02), -.269 (P≥0.01). While serum IL-35 levels were directly correlated with TSH, TPO-Ab, and TGAb in healthy controls (.151 (P≥0.01),.192 (P≥0.01),.097 (P≥0.01). The results of the current study showed a highly significant difference in TSH and FT4, respectively (P≥0.01), between the control and hypothyroid groups. Hypothyroidism is more common in females than males, and the incidence of hypothyroidism steadily increases with advancing age. Thyroid hormone concentrations show a significant change in patients with hormonal hypothyroidism compared with the control group. Conclusion: Our findings indicate an effective role for interleukin 35 in the reverse association with auto-antibodies and the development of autoimmune diseases, especially Hashmoto's disease
3
Gandolfo, John, Mohit Kumar, Mingyang Gao, Benjamin Lawler e Brian Gainey. "Analysis <!--<QUERY id="Q01" name="John Gandolfo"><p text_align="left">Redo plots of compression stroke timing sweep.</p></QUERY>--> of a Split Injection Strategy to Enable High Load, High Compression Ratio Spark Ignition with Hydrous Ethanol". In Energy & Propulsion Conference & Exhibition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2023. http://dx.doi.org/10.4271/2023-01-1616.
Abstract (sommario):
<div class="section abstract"><div class="htmlview paragraph">High compression ratios are critical to increasing the efficiency of spark ignition engines, but the trend in downsized and down sped configurations has brought attention to the nominally low compression ratios used to avoid knock. Knock is an abnormal combustion event defined by the acoustic sound caused by end-gas auto-ignition ahead of the flame front. In order to avoid engine-damaging levels of knock, low compression ratios and retarded combustion phasing at high loads are used, both of which lower efficiency. Low carbon alternative fuels such as ethanol or water-based alcohol fuels combine strong chemical auto-ignition resistance with large charge cooling characteristics that can suppress knock and enable optimal combustion phasing, thus allowing an increase in the compression ratio.</div><div class="htmlview paragraph">Of course, these high cooling potential fuels are not immune to knock at high loads at high enough compression ratios and are subject to the same combustion phasing strategies (i.e., spark retard) that diminish efficiency. In this work, an injection strategy is characterized in which the cooling potential of water-based alcohol fuel such as hydrous ethanol (WE92 - 190 proof, 92% ethanol, 8% water by mass) is taken advantage of in order to suppress knock at high load conditions. This work explores the implications of extending the injection window into the compression stroke. The results demonstrated a maximum 1 percentage point increase in net fuel conversion efficiency and 2.0 degree CA50 advance at 17 bar IMEPn with 15% of the total fuel injected in the compression stroke.</div></div>
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Horellou, M. H., C. Capelle, T. Lecompte, C. Kaplan, C. Lecrubier, J. M. James, R. Le Menn, J. Y. Muller e M. Samama. "PSEUDO-THROMBOCYTOPENIA ASSOCIATED WITH AN ANTICOAGULANT INDEPENDENT IgM PLATELET AGGLUTININ IN A PATIENT WITH PROLONGED BLEEDING TIME". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643975.
Abstract (sommario):
An original observation of platelet agglutination was found in a 63 y.o. man during 5 years following, without spontaneous bleeding. Low platelet counts (10 × 109/liter) and large agglutinates were observed on blood specimens collected into EDTA (1 to 15 mg/ml whole blood WB), citrate (1/10 volume citrate 0.11 M), sodium heparin (100 units/ml WB), citrate plus acetyl salicylic acid (5 to 100 mg/ml WB), citrate plus prostacyclin (Upjohn 10−5 to 10−6 M)? and buffering anticoagulant (0.8 M citrate, pH 4.65). Low platelet count and large agglutinates were also observed in capillary blood obtained by finger puncture kept at 22° or 37°C. All techniques revealed significant clumping making assessment of overall platelet number impossible. Bleeding time Ivy horizontal incision is longer than 20 minutes.Patient's serum induced normal platelets agglutination up to a 1/512 dilution at 22°and 37°C temperature. Lack of agglutination after treatment of the serum by IgM and indirect immunofluorescence tests identified the IgM nature of the agglutinating factor. This antibody reacted with Glanzmann thrombasthenia platelets ruling out the IIb/IIIa complex as the target of this agglutinin.There was no evidence of platelet activation following agglutination of autologous or alldgenic platelets : electronic microscopy of native blood platelets clumps did not show any sign of activation, and plasma level of B-thromboglobulin was normal in this patient. Normal platelets agglutination by patient's serum was not accompanied with ATP secretion (luciferin-luciferase).This IgM agglutinin was associated with elevation of IgM (700 mg/dl) without clinical or biological signs of auto-immune disease.No similar case with irreversible platelet agglutination in both capillary or venous blood has been reported before. The significance of the observation remains obscure.
Rapporti di organizzazioni sul tema "Non auto immune":
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LI, jianhong, Zhuang LI, Yalin SHE e Guohua LIN. Assessment of acupuncture for treating herpes zoster:a protocol for an umbrella systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2022. http://dx.doi.org/10.37766/inplasy2022.4.0010.
Abstract (sommario):
Review question / Objective: Patients who suffer from HZ in line with the consensus of Chinese experts will be included, regardless of sex, race and time of onset . Those who diagnosed with PHN, auto-immune diseases, pregnant women will be excluded.Acupuncture, electroacupuncture, fire needle, skin acupuncture, plum blossom needle, auriculo-acupuncture all these such therapies in treating herpes zoster will be included.The control group’s treatment includes drug therapy (such as antiviral acyclovir nutritional nerve medicine or traditional Chinese medicine, etc.) ，sham acupuncture, placebo, no treatment, and so on except acupuncture therapy. efficacy rate (with reference to the guiding principles of Clinical Research of New drugs in China (trial)).pain evaluation (pain relief time, pain intensity, visual analogue score, VAS), incidence of residual neuralgia PHN.