Reflexões sobre a utilização do Teste de Progresso na avaliação programática do estudante

Resumo: Introdução: O Teste de Progresso (TP) constitui modalidade estabelecida e bem-sucedida de avaliação de conhecimentos do estudante das profissões da saúde, principalmente os de Medicina, com potencial de contribuir substancialmente para as finalidades formativa e informativa (controle de qualidade e indicação de melhoria nos processos de ensino e aprendizagem). Adicionalmente, o TP apresenta características adequadas à sua inclusão em sistemas institucionais de avaliação que privilegiem a finalidade formativa, como a avaliação programática (AP), mas que cumprem também a somativa. Nas escolas que vêm definindo ações visando à introdução da AP em seus cursos de graduação, é necessária a reflexão sobre as fortalezas e limitações da utilização do TP no sistema de avaliação. Desenvolvimento: A partir das considerações de um grupo de trabalho representativo de toda a instituição, incumbido de propor meios de introdução da AP em um novo currículo para o curso de Medicina, contando com assessoria internacional com experiência tanto no TP como na AP, elaborou-se reflexão sobre esse tema, baseada na experiência dos autores e em dados da literatura. Propõe-se que, dentro da perspectiva longitudinal da AP, o TP constitua um dos pilares na avaliação de conhecimentos. O TP pode servir de base para acompanhamento do estudante, no contexto da sua turma (coorte), e seus resultados devem ser discutidos com o mentor que o acompanha e lhe dá suporte. O TP deve ter também papel central na gestão, como fonte de informações para eventual revisão e qualificação do currículo e das suas atividades de ensino e aprendizagem. É previsível que a utilização do TP na AP traga diferentes desafios e barreiras, que serão mais facilmente superados se houver na instituição experiências já consolidadas de aplicação de exames institucionais e de desenvolvimento docente para a elaboração de questões objetivas de boa qualidade. Conclusão: A efetividade do TP dentro do sistema institucional de AP vai depender de medidas que visem aumentar a sua efetividade na avaliação e que estimulem a participação ativa do estudante, refletindo sobre seu desempenho no TP, com o apoio do seu mentor, de modo a se engajar em ações que fomentem a autorregulação da aprendizagem

Effect of Ang II vaccine on SHR.

<p>A) Experimental protocol is shown. Ang II-KLH (Ang II-KLH group, n = 5) or saline (saline group, n = 5) were injected on days 0, 14, and 21 in twenty-four-week old male SHR. The anti-Ang II antibody titer and systolic BP were measured on days 0, 14, and 28. The Ang II-KLH group rats were immunized with 5 µg Ang II-KLH with CFA on day 0 and with 5 µg Ang II-KLH with IFA on day 14 and 21. B) Anti-Ang II antibody titers in the sera of immunized rats on days 0, 14, 28, and that of saline injected rats on day 28 were examined. *<i>P</i><0.01 vs. day 0. C) Systolic BP on days 0, 14, and 28 were shown. The data are expressed as the mean systolic BP ± standard error (SE) of the mean. *<i>P</i><0.05. vs. Saline.</p

Histochemical analysis of kidney and heart after vaccination.

<p>(A and B) Kidney (upper panel) or heart with coronary artery (lower panel) was stained with H&E in control (saline) or immunized mice (1,000 ng Ang II-KLH with adjuvant) . The scale bar represents 100 µm in the upper panel or 20 µm in the lower panel. The results were examined (A) at day 42 after vaccination and (B) after Ang II infusion (day 56 after vaccination).</p

Conceptual schematic of the experiment.

<p>(A)Immunization step (Ang II-KLH: an antigen) (Step1) The antigen presenting cells (APCs) phagocytose the Ang II-KLH conjugate and present a T cell epitope of KLH to T cells through the major histocompatibility complex (MHC). T cells recognize it through T cell receptors and become activated. (Step2) B cells specific to Ang II (pentagons) differentiate to plasmacytes and proliferate with the help of activated T cells. Then, B cells produce anti-Ang II antibody. (B)Post-Immunization step (response to Ang II) (Step1) The APCs do not present the T cell epitope of Ang II to T cells. Therefore, T cells do not recognize it and are not activated by Ang II. (Step2) B cells specific to Ang II (pentagons) differentiate and proliferate in response to Ang II. Therefore, Ang II does not stimulate the production of anti-AngII antibody.</p

Neutralizing antibody production induced by Ang II vaccine.

<p>(A) The antibody titers in the sera of mice immunized with saline, Ang II, KLH or Ang II-KLH (dose: 25 ng/mouse) with or without Freund’s adjuvant (FA) are shown. †<i>P</i><0.001 vs. saline. ELISA was performed using the sera of mice on day 42. (B) The serum antibody titers elicited by various doses (10, 25, 100, 300, 1000 ng/mouse) of Ang II-KLH with Freund’s adjuvant (FA). *<i>P</i><0.05 vs. 10 ng. The titer is expressed as the dilution of serum giving half-maximal binding (optical density: OD 50%) ± SE of the mean. (C) Western blot using anti-phosphorylated ERK (P-ERK) and anti-ERK antibodies. The total protein was extracted from HASMCs treated with 10⁻⁷ M Ang II that was previously incubated with 1 % serum. (D) Promoter activity of <i>c-fos</i> was measured using luciferase activity. HASMCs were transfected with <i>c-fos</i> luciferase reporter gene and stimulated by pre-incubated Ang II (10⁻⁷ M) with 1 % serum of the control or immunized mice for 24 hours. The results from 3 samples are expressed as the mean of the ratio to no stimulation ± SE of the mean. ‘‘Control serum’’ indicates serum from mice immunized by KLH (1 mg, with adjuvant), and ‘‘Immunized serum’’ indicates serum from mice immunized by Ang II-KLH (1,000 ng, with adjuvant). All serum was obtained on day 42. †<i>P</i><0.01.</p

T cell activation by Ang II-KLH, KLH or Ang II.

<p>(A) T cell proliferation was determined by analyzing [³H]-thymidine incorporation. Splenocytes from mice on day 42 were stimulated for 36 hours with Ang II-KLH, KLH, Ang II or angiotensinogen (AGT) at a concentration of 10 µg/ml. The stimulation index is expressed as the ratio of stimulation to no stimulation. The data are expressed as the mean stimulation index ± the standard error of the mean per 10⁶ splenocytes. *<i>P</i><0.001 vs. no stimulation. (B) A representative photograph from the ELISPOT assay. The ELISPOT assay detected splenocytes that produced IL-4 and/or IFN-γ? Splenocytes from mice on day 42 were stimulated for 48 hours with 10 µg/ml Ang II-KLH, KLH, Ang II or angiotensinogen (AGT). (C) The quantification of spots in the ELISPOT assay. The data are expressed as the mean number of spots ± SEM per 10⁶ splenocytes. *<i>P</i><0.001 vs. saline. (a,c) The results are from 6 control mice (saline) and 6 experimental mice (1,000 ng Ang II-KLH with adjuvant).</p

Effect of Ang II vaccine on Ang II-induced hypertension.

<p>(A) Systolic BP at steady state and under Ang II infusion on day 49. The control mice were immunized with 1 mg KLH. The experimental mice were immunized with 100ng or 1,000 ng Ang II-KLH. All groups contained 6 to 8 mice. The data are expressed as the mean systolic BP ± standard error (SE) of the mean. †<i>P</i><0.01 *<i>P</i><0.05. (B) The correlation between systolic BP under Ang II infusion and the anti-Ang II antibody titers in the sera of immunized mice. The titer is expressed as the dilution of serum giving half-maximal binding (optical density: OD 50%).</p

Effect of Ang II vaccine on cardiac remodeling induced by Ang II.

<p>(A) The mouse heart weights are shown. The results are expressed as the mean heart weight per body weight ± the standard error of the mean. (B) The cardiac tissue was stained with Masson trichrome and analyzed for cardiac fibrosis. Representative photographs are shown. The scale bar represents 20 µm. The results are expressed as the mean of the fibrotic area ± SE of the mean. (C) The mRNA levels of collagen type I (collagen I), collagen type III (collagen III), atrial natriuretic factor (ANF) and β-myosin heavy chain (β-MHC) were evaluated using RT-PCR. The results are expressed as the ratio of gene expression in the experimental mice to gene expression in the control mice ± SE of the mean. Control mice were immunized with KLH (1 mg, with adjuvant) and experimental mice were immunized with Ang II-KLH (1,000 ng, with adjuvant). All groups contained 6 to 8 mice on day 56. *<i>P</i><0.05.</p