Student Mobility and Research Capacity: A Global Health Experience

Global South countries struggle to train and retain researchers and practitioners to address local, regional, and global health challenges. Therefore, it is necessary to train a new generation of Global South scientists adequately, aiming to develop these low- and middle-income countries’ research capacity. In this regard, international student mobility fosters collaboration among institutions and promotes global health education while building capacity. The International Federation of Medical Students’ Associations (IFMSA) operates the largest student-run medical exchange program worldwide, providing research exchange programs since 1991. This article aims to report the experience of a Brazilian medical student, a Global South country, in Germany, a Global North country in an IFMSA research exchange. The 4-week research exchange occurred in February of 2020 at the Medical Faculty of Ruhr Universität Bochum in Bochum, Germany. The student assisted on various research projects at the institution's neurophysiology department. Educational activities also included journal clubs, lectures, workshops, and a conference. All activities were in English and under supervision. In terms of assessment, the student work was detailed in a logbook, which was shared with supervisors. During the exchange experience, the student learned through being exposed to different environments, people, and scientific methodologies. This resulted in the acquisition and improvement of research-related skills including research design and implementation, ethics, and professionalism, besides fostering intercultural learning. Additionally, this report demonstrates how student mobility fosters more collaborative environments and enhances scientific and networking possibilities

Involvement of Astrocytes in the Process of Metabolic Syndrome

Astrocytes constitute a very heterogeneous population of cells, which regulate pH, extracellular levels of ions and neurotransmitters, and energy metabolism in addition to actively participating in neurotransmission. In situations of damage to the CNS, the typical response is the degree of reactive gliosis, which can form glial scars. On the other hand, chronic diseases such as obesity, type 2 diabetes, hypertension, and atherosclerosis have been causally related to low-grade chronic inflammation in various metabolic tissues. It has been pointed out that the identification of hypothalamic inflammatory alterations are triggered by overnutrition, orchestrated by the hypothalamic immune system, and sustained by the pathophysiology associated with the metabolic syndrome. We discuss here the effects of astrocytes and the main astrocyte mechanisms involved in the metabolic syndrome and its comorbidities

Diethylcarbamazine Reduces Chronic Inflammation and Fibrosis in Carbon Tetrachloride- (CCl 4

This study investigated the anti-inflammatory effects of DEC on the CCl4-induced hepatotoxicity in C57BL/6 mice. Chronic inflammation was induced by i.p. administration of CCl4 0.5 μL/g of body weight through two injections a week for 6 weeks. DEC (50 mg/kg) was administered by gavage for 12 days before finishing the CCl4 induction. Histological analyses of the DEC-treated group exhibited reduced inflammatory process and prevented liver necrosis and fibrosis. Immunohistochemical and immunofluorescence analyses of the DEC-treated group showed reduced COX-2, IL1β, MDA, TGF-β, and αSMA immunopositivity, besides exhibiting decreased IL1β, COX-2, NFκB, IFNγ, and TGFβ expressions in the western blot analysis. The DEC group enhanced significantly the IL-10 expression. The reduction of hepatic injury in the DEC-treated group was confirmed by the COX-2 and iNOS mRNA expression levels. Based on the results of the present study, DEC can be used as a potential anti-inflammatory drug for chronic hepatic inflammation

Citogenotoxicidade e mutagenicidade do sulfato de cobre em diferentes variedades de allium cepa linn / Cytogenotoxicity and mutagenicity of copper sulphate in different varieties of allium cea linn

O sistema Allium cepa Linn. é utilizado na avaliação dos efeitos deletérios aos cromossomos. O objetivo desse estudo foi analisar o efeito citogenotóxico e mutagênico do sulfato de cobre nas variedades de cebola, Red creole, White creole e Texas early. As sementes foram colocadas para germinar em placas de Petri em água destilada (controle) e sulfato de cobre 0,006 g/L (tratado). Após a germinação procedeu-se a coleta do meristema radicular com fixação em Carnoy. Foram contadas 5000 células por grupo. A citogenotoxicidade foi avaliada pelo cálculo do índice mitótico e a avaliação mutagênica pelas alterações cromossômicas (micronúcleos, brotos, perdas e quebras cromossômicas). Diferenças significativas foram registradas no grupo controle entre as variedades Red creole e Texas early e entre as variedades Texas early e White creole. As variedades analisadas sofreram de forma significativa a ação agressiva do sulfato de cobre, que agiu de forma diferenciada entre as variedades analisadas. Pode-se concluir que a variedade Red creole demonstrou ser a mais resistente enquanto a White creole e a Texas early as mais sensíveis. Os resultados devem ser avaliados com cautela uma vez que podem implicar, dependendo da variedade escolhida, em respostas tendenciosas para refutar ou confirmar uma ação de um suposto agente estudado.

Involvement of AMPK, IKβα-NFκB and eNOS in the sildenafil anti-inflammatory mechanism in a demyelination model

Sildenafil (Viagra®) has recently been found to have a neuroprotective effect, which occurs through the inhibition of inflammation and demyelination in the cerebellum. However, the mechanism of action of sildenafil remains unknown. AMPK, the regulatory protein of the lipid and glucose metabolism, plays a protective role by activating the eNOS enzyme. The production of a nanomolar concentration of NO by eNOS has an anti-inflammatory effect through the cGMP signaling pathway and plays an important role in the regulation of the nuclear transcription factor (NFkB), preventing the expression of inflammatory genes. The present study investigated whether AMPK-eNOS-NO-cGMP-IКβα-NFkB is involved in the mechanism of action of sildenafil in a cuprizone-demyelination model. Neuroinflammation and demyelination induced by cuprizone in rodents have been widely used as a model of MS. In the present study, five male C57BL/6 mice (7-10 weeks old) were used. Over a four week period, the groups received: cuprizone (CPZ) 0.2% mixed in feed; CPZ in the diet, combined with the administration of sildenafil (Viagra®, Pfizer, 25mg/kg) orally in drinking water, starting concurrently (sild-T0) or 15 days (sild-T15) after the start of CPZ. Control animals received pure food and water. The cerebella of the mice were dissected and processed for immunohistochemistry, immunofluorescence (frozen), western blotting and dosage of cytokines (Elisa). CPZ induced an increase in the expression of GFAP, IL-1β TNF-α, total NFkB and inactive AMPK, and prompt microglia activation. CPZ also induced a reduction of IKβα. The administration of sildenafil reduced the expression of the pro-inflammatory cytokines IL-1β and TNF-α and increased the expression of the anti-inflammatory cytokine IL-10. In addition, the administration of sildenafil reduced expression of GFAP, NFkB, inactive AMPK and iNOS, and increased IKβα. Interestingly, sildenafil also reduced levels of NGF. In general, the sild-T0 group was more effective than sild-T15 in improving clinical status and promoting the control of neuroinflammation. The present study offers evidence that sildenafil has anti-inflammatory and neuroprotective effects, which are probably achieved through modulation of AMPK-IKβα-NFκB signaling. In addition, eNOS may play a role in the sildenafil neuroprotective mechanism, contributing to the activation of AMPK. However, other pathways such as MAPK-NFkB and the downstream proteins AMPK (AMPK-SIRT1-NFκB) should also be further investigated. An understanding of these mechanisms of action is critical for the clinical use of sildenafil to control neuroinflammation in neurodegenerative diseases such as MS.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Diethylcarbamazine reduces chronic inflammation and fibrosis in carbon tetrachloride- (CCl₄-) induced liver injury in mice

Submitted by Kamylla Nascimento ([email protected]) on 2017-11-16T13:07:55Z No. of bitstreams: 1 art. Diethylcarbamazine Reduces - rocha.pdf: 5582953 bytes, checksum: 562326c09cbcfb6e9d9e7d22e6d0890a (MD5)Approved for entry into archive by Kamylla Nascimento ([email protected]) on 2017-11-16T13:20:48Z (GMT) No. of bitstreams: 1 art. Diethylcarbamazine Reduces - rocha.pdf: 5582953 bytes, checksum: 562326c09cbcfb6e9d9e7d22e6d0890a (MD5)Made available in DSpace on 2017-11-16T13:20:48Z (GMT). No. of bitstreams: 1 art. Diethylcarbamazine Reduces - rocha.pdf: 5582953 bytes, checksum: 562326c09cbcfb6e9d9e7d22e6d0890a (MD5) Previous issue date: 2014Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.This study investigated the anti-inflammatory effects of DEC on the CCl4-induced hepatotoxicity in C57BL/6 mice. Chronic inflammation was induced by i.p. administration of CCl4 0.5 μL/g of body weight through two injections a week for 6 weeks. DEC (50 mg/kg) was administered by gavage for 12 days before finishing the CCl4 induction. Histological analyses of the DEC-treated group exhibited reduced inflammatory process and prevented liver necrosis and fibrosis. Immunohistochemical and immunofluorescence analyses of the DEC-treated group showed reduced COX-2, IL1β, MDA, TGF-β, and αSMA immunopositivity, besides exhibiting decreased IL1β, COX-2, NFκB, IFNγ, and TGFβ expressions in the western blot analysis. The DEC group enhanced significantly the IL-10 expression. The reduction of hepatic injury in the DEC-treated group was confirmed by the COX-2 and iNOS mRNA expression levels. Based on the results of the present study, DEC can be used as a potential anti-inflammatory drug for chronic hepatic inflammation

Diethylcarbamazine attenuates the development of carrageenan-induced lung injury in mice

Submitted by Kamylla Nascimento ([email protected]) on 2017-11-29T11:36:50Z No. of bitstreams: 1 art. Diethylcarbamazine Attenuates - ribeiro.pdf: 6007802 bytes, checksum: ac1b6700ec4b292331a13203cb3744f4 (MD5)Approved for entry into archive by Kamylla Nascimento ([email protected]) on 2017-11-29T12:18:36Z (GMT) No. of bitstreams: 1 art. Diethylcarbamazine Attenuates - ribeiro.pdf: 6007802 bytes, checksum: ac1b6700ec4b292331a13203cb3744f4 (MD5)Made available in DSpace on 2017-11-29T12:18:36Z (GMT). No. of bitstreams: 1 art. Diethylcarbamazine Attenuates - ribeiro.pdf: 6007802 bytes, checksum: ac1b6700ec4b292331a13203cb3744f4 (MD5) Previous issue date: 2014Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil / Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brazil.Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil.Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil.Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil.Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil.Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil.Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil.Universidade Federal de Pernambuco. Pós-Graduação em Ciências Biológicas. Recife, PE, Brazil.Universidade Federal Rural de Pernambuco. Departamento de Morfologia e Fisiologia Animal. Recife, PE, Brazil.Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Laboratorio de Ultraestrutura. Recife, PE, Brazil.Diethylcarbamazine (DEC) is an antifilarial drug with potent anti-inflammatory properties as a result of its interference with the metabolism of arachidonic acid. The aim of the present study was to evaluate the anti-inflammatory activity of DEC in a mouse model of acute inflammation (carrageenan-induced pleurisy). The injection of carrageenan into the pleural cavity induced the accumulation of fluid containing a large number of polymorphonuclear cells (PMNs) as well as infiltration of PMNs in lung tissues and increased production of nitrite and tumor necrosis factor-α and increased expression of interleukin-1β, cyclooxygenase (COX-2), and inducible nitric oxide synthase. Carrageenan also induced the expression of nuclear factor-κB. The oral administration of DEC (50 mg/Kg) three days prior to the carrageenan challenge led to a significant reduction in all inflammation markers. The present findings demonstrate that DEC is a potential drug for the treatment of acute lung inflammation