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Additional file 1: Figure S1. Anti-IL-23p19 treatment decreases the activation of SCs and inflammation in EAMG muscle after 2 weeks of treatment. mRNA expression of Pax7 (A), MyoD (B), MyoG (C), Il-6 (D), Il-6r (E), Tgf-β (F) and Il-17a (G) in the Tibialis anterior muscle of CFA and EAMG mice treated with or without anti-IL-23p19 antibody. mRNA analyses were performed in duplicate after 2 weeks treatment. Data were obtained from 2 independent experiments. There were n > 4 mice per group. Each point represents an individual mouse. mRNA expression were determined in duplicate by quantitative RT-PCR. mRNA levels are expressed as arbitrary unit (AU) and normalized to Cypa. P values were obtained with a t-test. P value are δ = 0.06 to 0.05; * < 0.05;**0.005; *** 0.0007. Figure S2. Effect of anti-IL-23p19 treatment on human Th17/Treg cells and antibodies in the spleen and blood of engrafted NSG mice. Analysis by flow cytometry of human T cells in the spleens of NSG-MG mice (A). ELISA analysis of human anti-AChR antibodies in the blood of NSG-MG mice 28 days after thymic engraftment (B). Flow cytometry analyses were performed at day 42 after thymic engraftment in NSG-MG mice treated with saline solution (NaCl) or anti-IL-23p19 antibody. Each point represents the mean value per experiment for each thymic biopsy obtained from one donor. Each point is from at least 4 mice. All data are from at least 4 different experiments done with thymic biopsies obtained from different AChR+ MG patients. P values were obtained with Wilcoxon matched paired test. Figure S3. Anti-IL-23p19 treatment does not induce global physiological changes in the NSG-MG mouse model. mRNA expression levels of Keratin 14 (A) in AChR+ MG thymuses engrafted in NSG-MG mice. Representative images of vascularized human MG thymuses after engraftment in mice without (B) or with treatment (C). Flow cytometry analyses of human T cells in engrafted human MG thymuses (D), in the blood (E) and in spleens (F) of NSG mice. ELISA quantification of total human immunoglobulins in the serum of NSG-MG mice (G). Images were acquired with a Zeiss Axio Observer Z1 inverted microscope using 20× magnification. In the flow cytometry graphs, each point represents the mean of the percentage of cells for an experiment. All analyses were performed at day 42 after engraftment in NSG-MG mice treated with saline solution (NaCl) or anti-IL-23p19 antibody. The data are from at least 3 different experiments performed with at least 3 thymic biopsies obtained from different MG patients. For each thymic biopsy, there were n > 3 mice per treatment condition. P values were obtained using the Wilcoxon matched paired test (A–F) and an ANOVA test (G). Figure S4. Anti-IL-23p19 tends to reduce markers of eGCs in the spleens of EAMG mice. mRNA expression of Il-6 (A), Podoplanin (B) and Aid (C) in the spleens of CFA and EAMG mice treated with or without anti-IL-23p19 antibody. mRNA analyses were performed in duplicate after 2 weeks or 4 weeks of treatment by quantitative RT-PCR. For each treatment time, data were obtained from 2 independent experiments. n > 4 mice per group. Each point represents an individual mouse. The mRNA results are expressed as arbitrary unit (AU) and normalized to Gapdh. P values were obtained with an ANOVA test. P value are as follows * < 0.05;**0.004; ****0.0001. Figure S5. Anti-IL-23p19 modifies markers of pathogenic Th17 cells in the spleens of EAMG mice. mRNA expression of Tgf-β1 (A), Tgf-β3 (B), Il-17a (C), Il-22 (D), Il-10 (E) in the spleens of CFA and EAMG mice treated with or without anti-IL-23p19 antibody. mRNA analyses were performed in duplicate after 2 weeks or 4 weeks of treatment by quantitative RT-PCR. For each treatment time, data were obtained from 2 independent experiments. n > 4 mice per group. Each point represents an individual mouse. The mRNA results are expressed as arbitrary unit (AU) and normalized to Gapdh. P values were obtained with an ANOVA test (δ = 0.05; * < 0.05;**0.007; ***0.001; ****0.0001).

Additional file 8: Table S1. RT-qPCR primer sequences list.

Dissertação (mestrado)—Universidade de Brasília, Instituto de Psicologia, Departamento de Psicologia Clínica, Programa de Pós-Graduação em Psicologia Clínica e Cultura, 2011. Modelos teóricos de impacto sobre a evasão universitária associam o fenômeno à interação entre características de (1) estudantes, (2) contextos não-universitários e (3) contextos universitários. O objetivo dessa pesquisa consistiu em identificar os precursores psicológicos do trancamento de matrícula por motivo de saúde mental, uma modalidade temporária de evasão universitária. Foi utilizada metolodologia qualitativa de pesquisa, constituída de análise documental dos processos de trancamento e análise clínica e de conteúdo e de entrevistas psicológicas de dez estudantes de graduação. Como resultado, obteve-se que os fatores individuais dos estudantes, principalmente as características de pré-ingresso mostraram-se muito relevantes no desencadeamento desse trancamento. A constatação de que mais da metade dos universitários em trancamento já tinha transtorno mental antes da entrada na universidade chamou a atenção para a vulnerabilidade que muitos estudantes universitários levam para a universidade. Dentre os fatores individuais encontraram-se isolamento social, introversão, identidade frágil, transtorno mental, perfeccionismo, alterações cognitivas e ideação suicida. A categoria fatores do contexto não-universitário dividiu-se em dificuldades com relacionamentos íntimos e dependência emocional com a parentalidade. E os fatores do contexto universitário envolveram ausência/superficialidade de relacionamento com coordenadores de curso; dificuldades de relacionamento entre estudantes e professores; dificuldades de relacionamento entre estudantes e falta de suporte do contexto universitário. Novas pesquisas sobre fatores dos contextos não-universitários e universitários relacionados ao trancamento de matrícula por motivo de saúde mental fazem-se necessárias para subsidiar programas de prevenção à evasão e aos problemas de saúde mental. _________________________________________________________________________________ ABSTRACT Theoretical models of impact on college dropout associate it to the interaction among the following factors: (1) students, (2) non-university contexts and (3) university contexts. The objective of this research was to identify the psychological precursors of college stopout for mental health reasons, a type of dropout characterized by a temporary interruption of the college course, without necessarily the permanent interruption of the regular link with the university. Documental analysis of college stopout procedures and clinical and content analysis of psychological interviews of students were performed with ten undergraduate students. Results showed that students`individual factors, especially the characteristics before university were very relevant in the onset of college stopout. The finding that over half of university students stopout had a mental disorder before the university entrance drew attention to the vulnerability that many students bring to college. Among the individual factors were found social isolation, shyness, fragile identity, mental illness, perfectionism, cognitive disorders and suicide ideation. The non-university category was divided into difficulties with intimate relationships and emotional dependency with parenting. University context factors involved no/superficial relationship with course coordinators, relationship problems between students and teachers and students and lack of support by university. New researches about university and non university factors related to college stopout for mental health reasons are necessary to support college dropout and mental health problems prevention programs.