Estudo do tempo gasto com exercícios ativos realizados por hemiparéticos crônicos submetidos a Fisioterapia em Grupo no formato de Circuito de Treinamento / Study of time spent in active exercises realized by chronic hemiparetic patients submitted to Physiotherapy in Group in the format of Training Circuit

Introdução: Hemiparéticos passam pouco tempo em atividades físicas funcionais em sessões de fisioterapia convencionais. Há evidências que a Fisioterapia de Grupo em Circuito de Treinamento (FGCT) é capaz de melhorar a capacidade funcional e aumentar a quantidade de tempo gasto durante a terapia. Objetivo: O objetivo deste trabalho foi avaliar o tempo gasto com exercícios ativos realizados por hemiparéticos crônicos submetidos a FGCT e correlacionar o tempo ativo com testes funcionais. Métodologia: Para verificar a normalidade dos dados, utilizou-se o teste Shapiro-Wilk; o teste t-student foi usado para amostras pareadas, para comparar o tempo ativo e inativo, considerando significante o valor de p < 0,05. O teste de Pearson foi para avaliar as correlações do Timed-Up-and-Go (TUG) e Escala de Equilíbrio de Berg (EEB) com o tempo ativo. Resultados: O valor médio obtido no TUG foi 19,43 ± 8,65 segundos e na EEB foi 43,83 ± 11,07 pontos. O Teste de Pearson mostrou correlação entre o EEB com as Atividades de Prática Ativas (APA) (r = 0,631, p ≤ 0,01) e entre TUG e APA (r = - 0,495, p ≤ 0,01). Conclusão: Os resultados demonstraram que o tempo gasto com exercícios ativos durante uma sessão de FGCT foi maior que o tempo inativo, e houve correlação moderada entre os valores de APA com os testes EEB e TUG.

Introduction: Hemiparetic patients spent little time in functional physical activities of conventional physiotherapy. There are evidences that the Physiotherapy of Group in Training Circuit (PGTC) is able to better the functional capacity and increase the quantity of time spent during the therapy. Objective: The objective of this work was to evaluate the time spent with active exercises realized by chronic hemiparetic patients submitted to PGTC, to correlating active time with functional tests. Methodology: It was verified the normality of the data with the Shapiro-Wilk test; the t-student test to paired samples, comparing active and inactive time, being significant the value of p < 0,05. The Pearson test was to evaluate the correlations of Timed-Up-and-Go (TUG) and Berg Balance Scale (BBS) with the active time. Results: The average value obtained in the TUG was 19,43 ± 8,65 seconds and in the BBS was 43,83 ± 11,07 points. Pearson test shows correlations between the BBS with the Active Practical Activities (APA) (r = 0,631, p ≤ 0,01) and between the TUG and the APA (r = -0,495, p ≤ 0,01). Conclusion: Results demonstrated that the time spent with active exercises during one session of PGTC was larger than the inactive time, and there was moderated correlation between the values of APA with the BBS and TUG tests.

Transcriptional network profile on synovial fluid T cells in psoriatic arthritis.

The objective of the study was to quantify the transcriptional profile, as the main T cell lineage-transcription factors on synovial fluid (SF) T cells, in relation to SF cytokines and T cell frequencies (%) of psoriatic arthritis (PsA) patients. Reverse phase protein array was employed to identify interleukin (IL)-23Rp19-, FOXP3- and related orphan receptor gamma T (RORγt)- protein and Janus associated tyrosine kinases 1 (JAK1), signal transducer and activator and transcription 1 (STAT1), STAT3 and STAT5 phosphoproteins in total T cell lysates from SF of PsA patients. IL-1ß, IL-2, IL-6, IL-21 and interferon (INF)-γ were measured using a multiplex bead immunoassay in SF from PsA patients and peripheral blood (PB) from healthy controls (HC). Frequencies of CD4(+)CD25(-), CD4(+)CD25(high) FOXP3(+) and CD4(+)CD25(high) CD127(low) Treg, and either mean fluorescence intensity (MFI) of FOXP3(+) on CD4(+) Treg or MFI of classic IL-6 receptor (IL-6R) α expression on CD4(+)CD25(-) helper/effector T cells (Th/eff) and Treg cells, were quantified in SF of PsA patients and in PB from HC by flow cytometry (FC). In PsA SF samples, IL-2, IL-21 and IFN-γ were not detectable, whereas IL-6 and IL-1ß levels were higher than in SF of non-inflammatory osteoarthritis patients. Higher levels of IL-23R-, FOXP3- and RORγt proteins and JAK1, STAT1, STAT3 and STAT5 were found in total T cells from SF of PsA patients compared with PB from HC. Direct correlations between JAK1 Y1022/Y1023 and STAT5 Y694, and STAT3 Y705 and IL6, were found in SF of PsA patients. Increased proportion of CD4(+)CD25(high) FOXP3(+) and CD4(+)CD25(high) CD127(low) Treg cells and brighter MFI of IL-6Rα were observed both on CD4(+)CD25(high)- and CD4(+)CD25(-) T cells in PsA SF. The study showed a distinctive JAK1/STAT3/STAT5 transcriptional network on T cells in the joint microenvironment, outlining the interplay of IL-6, IL-23, IL-1ß and γC cytokines in the polarization and plasticity of Th17 and Treg cells, which might participate in the perpetuation of joint inflammation in PsA patients.

JAK/STAT/PKCδ molecular pathways in synovial fluid T lymphocytes reflect the in vivo T helper-17 expansion in psoriatic arthritis.

Looking to the sustained psoriatic arthritis (PsA) joint as a model of local human inflammation, this study was designed to assess the T lymphocyte signal transduction pathways potentially involved in this chronic immune-mediated inflammatory process, as characterized by direct ex vivo analysis of T helper (Th)-17 T effector (Teff) cell phenotypes in synovial fluid (SF) and peripheral blood (PB) of clinically active PsA patients. The reverse-phase protein arrays (RPPA) technique was employed to identify STAT3, STAT1, JAK1, JAK2, PKCδ and ERK1/2 phosphoprotein levels on total T cell lysates in SF samples of PsA patients. Frequencies of T CD4(+)IL-17A-F(+) and T CD4(+)IL-23R(+) Th17 cells were quantified in SF and matched PB of PsA patients by flow cytometry and compared with PB of healthy controls (HC). Increased levels of JAK1, STAT3, STAT1 and PKCδ phosphoproteins were found in SF T cells of PsA patients, compared with PB of HC. The expansion of T CD4(+)IL-17A-F(+) cells, as well as of T CD4(+) cells expressing IL-23Rp19 (T CD4(+) IL-23R(+)), considered as the pathogenic phenotype of effector Th17 cells, was found to be confined to the joints of PsA patients, as the frequencies of both populations were significantly higher in SF than in matched PB, or in PB of HC. In conclusion, T lymphocyte signal transduction pathway mapping revealed an enhanced activation of JAK1/STAT3/STAT1 and PKCδ phosphoproteins that may drive the local inflammatory process, characterized by the in vivo expansion of T CD4(+)IL-17A-F(+) and T CD4(+)IL-23R(+) Th17 Teff cells in SF of clinically active joints of PsA patients.

Cutting edge: Clec9A+ dendritic cells mediate the development of experimental cerebral malaria.

Plasmodium infections trigger strong innate and acquired immune responses, which can lead to severe complications, including the most feared and often fatal cerebral malaria (CM). To begin to dissect the roles of different dendritic cell (DC) subsets in Plasmodium-induced pathology, we have generated a transgenic strain, Clec9A-diphtheria toxin receptor that allows us to ablate in vivo Clec9A(+) DCs. Specifically, we have analyzed the in vivo contribution of this DC subset in an experimental CM model using Plasmodium berghei, and we provide strong evidence that the absence of this DC subset resulted in complete resistance to experimental CM. This was accompanied with dramatic reduction of brain CD8(+) T cells, and those few cerebral CD8(+) T cells present had a less activated phenotype, unlike their wildtype counterparts that expressed IFN-γ and especially granzyme B. This almost complete absence of local cellular responses was also associated with reduced parasite load in the brain.