Aspectos imunológicos do diabetes melito tipo 1

Universidade Federal de São Paulo (UNIFESP) Escola Paulista de MedicinaUNIFESP, EPMSciEL

O Aluno com Paralisia Cerebral em Contexto Educativo: Diferenciação de metodologias e estratégias

O modelo de Educação Inclusiva, atualmente implementado e defendido pelas organizações internacionais, pressupõe um único sistema educacional para TODOS os alunos, partindo da aceitação das diferenças individuais e da valorização da diversidade humana, como potenciadores de capacidades num mesmo processo educacional. A Educação Inclusiva não abrange somente crianças/jovens com deficiências, mas alarga a sua intervenção a todos os que, temporária ou permanentemente, apresentem necessidades especiais. Os alunos com Necessidades Educativas Especiais de carácter motor, especialmente Paralisia Cerebral, inseridos no ensino regular, pela especificidade das manifestações apresentadas e das significativas limitações ao nível da atividade e da participação, beneficiarão com a implementação de medidas educativas que diminuam a sua situação de desvantagem e promovam o desenvolvimento das suas potencialidades, recorrendo a metodologias e estratégias facilitadoras do seu desenvolvimento global, que abordaremos numa breve revisão da literatura

Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages

It has been well-documented that leukotrienes (LTs) are released in allergic lung inflammation and that they participate in the physiopathology of asthma. A role for LTs in innate immunity has recently emerged: Cys-LTs were shown to enhance Fc gamma R-mediated phagocytosis by alveolar macrophages (AMs). Thus, using a rat model of asthma, we evaluated Fc gamma R-mediated phagocytosis and killing of Klebsiella pneumoniae by AMs. the effect of treatment with a cys-LT antagonist (montelukast) on macrophage function was also investigated. Male Wistar rats were immunized twice with OVA/alumen intraperitoneally and challenged with OVA aerosol. After 24 h, the animals were killed, and the AMs were obtained by bronchoalveolar lavage. Macrophages were cultured with IgG-opsonized red blood cells (50: 1) or IgG-opsonized K. pneumoniae (30: 1), and phagocytosis or killing was evaluated. Leukotriene C(4) and nitric oxide were quantified by the EIA and Griess methods, respectively. the results showed that AMs from sensitized and challenged rats presented a markedly increased phagocytic capacity via Fc gamma R (10X compared to controls) and enhanced killing of K. pneumoniae (4X higher than controls). the increased phagocytosis was inhibited 15X and killing 3X by treatment of the rats with montelukast, as compared to the non-treated group. cys-LT addition increased phagocytosis in control AMs but had no effect on macrophages from allergic lungs. Montelukast reduced nitric oxide (39%) and LTC(4) (73%). These results suggest that LTs produced during allergic lung inflammation potentiate the capacity of AMs to phagocytose and kill K. pneumonia via Fc gamma R. Copyright (C) 2010 S. Karger AG, BaselConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Complex Fluids INCTFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo, Disciplina Nefrol, Dept Nefrol, Lab Imunol Clin & Expt, BR-04023900 São Paulo, BrazilUniv São Paulo, Dept Imunol, Lab Imunol Transplantes, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencias Biol, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Disciplina Nefrol, Dept Nefrol, Lab Imunol Clin & Expt, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencias Biol, BR-04023900 São Paulo, BrazilFAPESP: 07/07139-3FAPESP: 09/52119-6FAPESP: 10/01404-0Web of Scienc

Synergistic effect of mycophenolate mofetil and angiotensin-converting enzyme inhibitor in patients with chronic allograft nephropathy

Experimental data and few clinical non-randomized studies have shown that inhibition of the renin-angiotensin system by angiotensin-converting enzyme (ACE) associated or not with the use of mycophenolate mofetil (MMF) could delay or even halt the progression of chronic allograft nephropathy (CAN). In this retrospective historical study, we investigated whether ACE inhibition (ACEI) associated or not with the use of MMF has the same effect in humans as in experimental studies and what factors are associated with a clinical response. A total of 160 transplant patients with biopsy-proven CAN were enrolled. Eighty-one of them were on ACE therapy (G1) and 80 on ACEI_free therapy (G2). Patients were further stratified for the use of MMF. G1 patients showed a marked decrease in proteinuria and stabilized serum creatinine with time. Five-year graft survival after CAN diagnosis was more frequent in G1 (86.9 vs 67.7%; P < 0.05). In patients on ACEI-free therapy, the use of MMF was associated with better graft survival. The use of ACEI therapy protected 79% of the patients against graft loss (OR = 0.079, 95%CI = 0.015-0.426; P = 0.003). ACEI and MMF or the use of MMF alone after CAN diagnosis conferred protection against graft loss. This finding is well correlated with experimental studies in which ACEI and MMF interrupt the progression of chronic allograft dysfunction and injury. The use of ACEI alone or in combination with MMF significantly reduced proteinuria and stabilized serum creatinine, consequently improving renal allograft survival.Universidade Federal de São Paulo (UNIFESP) Hospital do Rim e Hipertensão Disciplina de NefrologiaUniversidade Federal de São Paulo (UNIFESP) Departamento de PatologiaUniversidade de São Paulo Instituto de Ciências Biomédicas IV Departamento de ImunologiaUNIFESP, Hospital do Rim e Hipertensão Disciplina de NefrologiaUNIFESP, Depto. de PatologiaSciEL

Acute Kidney Injury Reduces Phagocytic and Microbicidal Capacities of Alveolar Macrophages

Background/Aims: Renal ischaemia-reperfusion injury (IRI) is a systemic inflammatory process in which Th1 responses predominate affecting other organs including the lungs. the present study explored the phagocytic and microbicidal capacity of macrophages in rats with lung inflammation that underwent IRI. Methods: the alveolar macrophages of rats sensitised to OVA were evaluated for phagocytosis and bacterial killing 24h after antigen challenge in animals with or without prior submission to 60 min of renal ischaemia. Results: Bronchoalveolar lavage had a high level of cellular infiltrate in immunised animals (420%) compared with control animals; IRI significantly reduced this infiltration (52%). Macrophages from animals immunised and challenged with OVA presented a 10x increase in phagocytic capacity compared to the control group, whereas immunised animals subjected to IRI showed a reduction in the phagocytic index of 68%. the killing of Klebsiella pneumoniae by macrophages from immunised animals was higher (56%) compared with the control group but reduced in animals submitted to IRI (45%). Immunised and challenged group showed an increase in gene expression levels of IL-10(450%), HO-1 (259%), INF-gamma (460%) and MCP-1 (370%) compared to the immunised group subjected to IRI. Conclusions: Renal ischaemia and reperfusion injury apparently alters the phagocytic and microbicidal capacity of macrophages, reducing lung inflammation to OVA. Copyright (C) 2013 S. Karger AG, BaselFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)INCT Complex FluidsFADA-UNIFESPUniversidade Federal de São Paulo, Disciplina Nefrol, Lab Imunol Clin & Expt, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Inst Ciencias Ambientais Quim & Farmaceut, Lab Inflamacao & Farmacol Vasc, BR-04023900 São Paulo, BrazilUniv São Paulo, Inst Ciencias Biomed, Dept Imunol, Lab Imunobiol Transplante, BR-05508 São Paulo, BrazilUniversidade Federal de São Paulo, Disciplina Nefrol, Lab Imunol Clin & Expt, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Inst Ciencias Ambientais Quim & Farmaceut, Lab Inflamacao & Farmacol Vasc, BR-04023900 São Paulo, BrazilFAPESP: 07/07139-3FAPESP: 10/52180-4FAPESP: 10/01404-0FAPESP: 12/02270-0FAPESP: 12/51104-8Web of Scienc

Glomerular damage as a predictor of renal allograft loss

Interstitial fibrosis and tubular atrophy (IF/TA) are the most common cause of renal graft failure. Chronic transplant glomerulopathy (CTG) is present in approximately 1.5-3.0% of all renal grafts. We retrospectively studied the contribution of CTG and recurrent post-transplant glomerulopathies (RGN) to graft loss. We analyzed 123 patients with chronic renal allograft dysfunction and divided them into three groups: CTG (N = 37), RGN (N = 21), and IF/TA (N = 65). Demographic data were analyzed and the variables related to graft function identified by statistical methods. CTG had a significantly lower allograft survival than IF/TA. In a multivariate analysis, protective factors for allograft outcomes were: use of angiotensin-converting enzyme inhibitor (ACEI; hazard ratio (HR) = 0.12, P = 0.001), mycophenolate mofetil (MMF; HR = 0.17, P = 0.026), hepatitis C virus (HR = 7.29, P = 0.003), delayed graft function (HR = 5.32, P = 0.016), serum creatinine ≥1.5 mg/dL at the 1st year post-transplant (HR = 0.20, P = 0.011), and proteinuria ≥0.5 g/24 h at the 1st year post-transplant (HR = 0.14, P = 0.004). The presence of glomerular damage is a risk factor for allograft loss (HR = 4.55, P = 0.015). The presence of some degree of chronic glomerular damage in addition to the diagnosis of IF/TA was the most important risk factor associated with allograft loss since it could indicate chronic active antibody-mediated rejection. ACEI and MMF were associated with better outcomes, indicating that they might improve graft survival.Universidade Federal de São Paulo (UNIFESP) Departamento de Medicina Disciplina de NefrologiaHospital Universitario Central de Asturias Servicio de NefrologíaFundación Renal Iñigo Alvarez de Toledo Y Fundación Carolina-BBVAUniversidade de São Paulo Instituto de Ciências Biomédicas IV Departamento de ImunologiaUniversidade Federal de São Paulo (UNIFESP) Departamento de PatologiaUNIFESP, Depto. de Medicina Disciplina de NefrologiaUNIFESP, Depto. de PatologiaSciEL