169 resultados para interleukin 1 gene
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To establish guidelines based on cientific evidences for the management of cryopyrin associated periodic syndromes. The Guideline was prepared from 4 clinical questions that were structured through Pico (Patient, Intervention or indicator, Comparison and Outcome), to search in key primary scientific information databases. After defining the potential studies to support the recommendations, these were graduated considering their strength of evidence and grade of recommendation. 1215 articles were retrieved and evaluated by title and abstract; from these, 42 articles were selected to support the recommendations. 1. The diagnosis of Caps is based on clinical history and clinical manifestations, and later confirmed by genetic study. Caps may manifest itself in three phenotypes: FCAS (mild form), MWS (intermediate form) and Cinca (severe form). Neurological, ophthalmic, otorhinolaryngological and radiological assessments may be highly valuable in distinguishing between syndromes; 2. The genetic diagnosis with NLRP3 gene analysis must be conducted in suspected cases of Caps, i.e., individuals presenting before 20 years of age, recurrent episodes of inflammation expressed by a mild fever and urticaria; 3. Laboratory abnormalities include leukocytosis and elevated serum levels of inflammatory proteins; 4. Targeted therapies directed against interleukin-1 lead to rapid remission of symptoms in most patients. However, there are important limitations on the long-term safety. None of the three anti-IL-1β inhibitors prevents progression of bone lesions.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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High protein content in the diet during childhood and adolescence has been associated to the onset insulin-dependent diabetes mellitus. We investigated the effect of interleukin-1 beta (IL-I beta) on insulin secretion, glucose metabolism, and nitrite formation by islets isolated from rats fed with normal protein (NP, 17%) or low protein (LP, 6%) after weaning. Pretreatment of islets with IL-1 beta for 1 h or 34 h inhibited the insulin secretion induced by glucose in both groups, but it was less marked in LP than in NP group. Islets from LP rats exhibited a decreased IL-1 beta -induced nitric oxide (NO) production, lower inhibition of D-[(UC)-C-14]-glucose oxidation to (CO2)-C-14, and less pronounced effect of IL-1 beta on alpha -ketoisocaproic acid-induced insulin secretion than NP islets. However, when the islets were stimulated by high concentrations of K+ the inhibitory effect of IL-1 beta on insulin secretion was not different between groups. In conclusion, protein restriction protects beta -cells of the deleterious effect of IL-1 beta, apparently, by decreasing NO production. The lower NO generation in islets from protein deprived rats may be due to increased free fatty acids oxidation and consequent alteration in Ca2+ homeostasis. (C) 2001 Elsevier B.V. All rights reserved.
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OBJETIVO: Investigar a influência do inibidor não-seletivo da ciclooxigenase, cetoprofeno (ceto) intravenoso, em alterações histológicas e dos níveis das citocinas renais - fator α de necrose tumoral (TNF- α) e interleucina 1 (IL-1) - após hemorragia de 30% da volemia (10%, três vezes, em intervalos de 10 min). MÉTODOS: Sob anestesia com sevoflurano (sevo), os grupos sevo e sevo+ceto (10 ratos cada) foram preparados cirurgicamente para leitura de pressão arterial média (PAM) e administração de solução de Ringer (5 mL/kg/h) e de cetoprofeno (1,5 mg/kg), no início da anestesia, no grupo sevo+ceto. Mediu-se temperatura retal continuamente. Os valores de temperatura e PAM foram observados antes da primeira hemorragia (T1), após a terceira hemorragia (T2) e 30 min após T2 (T3). Realizada nefrectomia bilateral nos dois grupos para análise histológica e imuno-histoquímica. RESULTADOS: Nos dois grupos, temperatura e PAM diminuíram com relação aos valores basais. Hipotermia foi mais acentuada no grupo sevo (p=0,0002). Necrose tubular foi mais frequente no grupo sevo (p=0,02). As citocinas estiveram igualmente presentes nos rins dos dois grupos. CONCLUSÃO: Cetoprofeno foi mais protetor no rim de rato durante anestesia com sevoflurano e hipovolemia, porém parece que TNF- α e IL-1 não estão envolvidas nessa proteção.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Small blue round cell tumors (SBRCTs) are a set of malignancies that have a particular proclivity for the pediatric age group. These tumors are notoriously difficult to distinguish by histologic evaluation alone, and in recent years a number of new immunohistochemical markers have emerged that can aid in the correct categorization of these lesions. Myogenin, a muscle-restricted nuclear transcription factor, has been demonstrated to be a highly sensitive and specific marker of rhabdomyosarcoma, and is superior to previous markers such as myoglobin, muscle actins, and desmin. The FlI-1 gene product is expressed as part of the EWS/FLI-1 novel chimeric protein that results from the t(11;22)(q24;q12) translocation that occurs in approximately two-thirds of cases of PNET/Ewings sarcoma. Immunohistochemical detection of the FLI-1 gene product can thus complement detection of CD99/MIC2 for the positive identification of PNET/Ewings sarcoma. Markers of neuroblastoma include neural markers, such as chromogranin A, neurofilaments, and synaptophysin. Desmoplastic small round cell tumor (DSRCT) is a tumor with an unusual immunophenotype, including co-expression of cytokeratin, vimentin, and desmin; recent studies have also documented the use of antibodies to the WT-1 gene product as a marker of the chimeric EWS/WT-1 protein formed as a result of the t(11;22)(p13;q12) translocation that characterizes this unique tumor. In summary, there now exists a panel of antibodies defining immunohistochemical markers of individual SBRCTs that can identify rhabdomyosarcoma, PNET/Ewings sarcoma, neuroblastoma, and DSRCT with high sensitivity and specificity.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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A caquexia relacionada à artrite reumatoide é conceituada como perda involuntária de massa magra, predominantemente de músculo esquelético, que também ocorre em vísceras e sistema imune, com massa gorda estável ou um pouco elevada e com pequena ou nenhuma perda de peso. A causa é multifatorial, incluindo a produção acentuada de citocinas, principalmente TNF± e IL-1², diminuição da ação periférica da insulina e pouca atividade física. A caquexia se faz presente em doentes com AR ativa ou mesmo inativa. Neste artigo discutem-se aspectos relacionados à patogenia, implicações clínicas e possíveis opções terapêuticas.
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The aim of this study was to investigate cellular migration induced by calcium hydroxide to air-pouch cavities in mice. The migration was more specific to neutrophil and was dose and time dependent (peaking 96 h after stimulation). This migration was inhibited by pretreatment with thalidomide, indomethacin, MK886, meloxicam, dexamethasone, MK886 associated with indomethacin, and MK886 associated with indomethacin and dexamethasone. The air-pouch exudate from animals stimulated with calcium hydroxide showed an increase of leukotriene-B4 (LTB4), interleukin-1 beta, tumor necrosis factor alpha (TNF-alpha), cytokine-induced neutrophil chemoattractant (KC), and macrophage inflammatory protein 2 (MIP-2) release. Pretreatment with 3% thioglycollate increased the macrophage population in the air pouch but did not change neutrophil migration. Depleting the resident mast cells through chronic pretreatment with compound 48/80 did not alter neutrophil migration in response to calcium hydroxide. It was possible to conclude that calcium hydroxide-induced neutrophil migration to the air-pouch cavity in mice is mediated by LTB4, TNF-alpha, KC, MIP-2, and prostaglandins, but it was not dependent on macrophages or mast cells.