Recomendações do enunciado CONSORT para o relato de estudos clínicos controlados e randomizados

Clinical strategies and decision making in health care should be supported by the best available scientific evidence not only on intuition neither on previous clinical experience. Randomized controlled trials (RCT) are considered the gold standard for the assessment of interventions efficacy but inadequate report difficulties their interpretation and identification of eventual bias. A group of scientists and editors developed the CONSORT Statement to improve the quality of reporting of RCTs. The CONSORT statement comprises a checklist of essential items that should be included in reports of RCTs and a diagram for documenting the flow of participants through a trial. Nowadays, the CONSORT are translated to several languages and it has been modified to attend different study designs. The present document intended to improve the comprehension of CONSORT recommendations and to spread its use on Portuguese language through a brief discussion of main aspects from the revised version of CONSORT statement.O raciocínio clínico e a tomada de decisão pelo profissional de saúde devem ter como base as evidências científicas relevantes e não apenas a intuição ou experiências clínicas prévias não-sistematizadas. Estas evidências são adequadamente obtidas a partir de estudos clínicos controlados randomizados (ECRs), cujas informações são frequentemente relatadas de forma incompleta, prejudicando a identificação de possíveis erros metodológicos. Com intuito de aprimorar o relato de ECR, um grupo de cientistas e editores de periódicos médicos elaborou o enunciado CONSORT, constituído de uma lista de checagem com 22 itens e um fluxograma dos participantes. Atualmente, o CONSORT se encontra traduzido em diversas línguas e em versões adaptadas para atender aos diferentes modelos de estudos. O presente trabalho pretendeu, portanto, facilitar a compreensão de tais instruções, assim como sua divulgação na língua portuguesa, ao abordar brevemente os principais aspectos contidos na versão revisada do enunciado CONSOR

Spontaneous B-cell lymphoma in hamster

Durante estudo anatomopatológico, incluindo imunoistoquímica, sobre pancreatite chagásica, experimentalmente induzida em hamsters machos, não-isogênicos, com quatro meses de idade, pesando 107,8 ± 10,9g, infiltração por linfoma foi observada em um animalcontrole normal, com 15 meses de idade. A neoplasia foi notada na ocasião da necropsia, 330 dias após o início do experimento. Lirifoma similar não foi achado nos demais controles normais (n=73), nem nos hamsters do grupo infectado, pareados para peso e idade (n=94). As alterações histopatológicas e imunoistoquímicas foram consistentes com linfoma difuso, não-Hodgkin, de grandes céiulas-B; porém, a hipótese de eventual origem leucêmica não foi inteiramente excluída. Linfomas experimentalmente induzidos têm sido relatados em animais de laboratório; entretanto, relatos de caso de linfoma, ocorrendo espontaneamente em hamsters, não têm sido freqüentes. No presente caso, o desenvolvimento da doença poderia ter alguma relação com o processo de envelhecimento.During anatomopathologic study, including immunohistochemistry, about chagasic pancreatitis experimentally induced in four month aged male non-isogenic hamsters, weighing 107.8 ± 10.9g, lymphoma infiltration was observed in a 15 month-aged normal control animal. The neoplasia was disclosed on the occasion of necropsy studies, 330 days after the beginning of experiment. Similar lymphoma was not found in the remainder normal controls (n=73), nor in the group of infected hamsters age and weight matched (n=94). The neoplasia histopathologic and immunohistochemical changes were consistent with non-Hodgkin diffuse large B-ceIl lymphoma; nevertheless, the hypothesis of eventual leukemic origin was not entirely excluded. Experimentally induced lymphomas have been related in laboratory animais; however, cases of spontaneously occurring lymphoma have been infrequently described in hamsters. In the present case, the development of the disease could have some relation with the animal aging process

Labeling mesenchymal cells with DMSA-coated gold and iron oxide nanoparticles : assessment of biocompatibility and potential applications

Nanoparticles’ unique features have been highly explored in cellular therapies. However, nanoparticles can be cytotoxic. The cytotoxicity can be overcome by coating the nanoparticles with an appropriated surface modification. Nanoparticle coating influences biocompatibility between nanoparticles and cells and may affect some cell properties. Here, we evaluated the biocompatibility of gold and maghemite nanoparticles functionalized with 2,3-dimercaptosuccinic acid (DMSA), Au-DMSA and γ-Fe2O3-DMSA respectively, with human mesenchymal stem cells. Also, we tested these nanoparticles as tracers for mesenchymal stem cells in vivo tracking by computed tomography and as agents for mesenchymal stem cells magnetic targeting

A 1.8 million year history of Amazon vegetation

During the Pleistocene, long-term trends in global climate were controlled by orbital cycles leading to high amplitude glacial-interglacial variability. The history of Amazonian vegetation during this period is largely unknown since no continuous record from the lowland basin extends significantly beyond the last glacial stage. Here we present a paleoenvironmental record spanning the last 1800 kyr based on palynological data, biome reconstructions, and biodiversity metrics from a marine sediment core that preserves a continuous archive of sediments from the Amazon River. Tropical rainforests dominated the Amazonian lowlands during the last 1800 ka interchanging with surrounding warm-temperate rainforests and tropical seasonal forests. Between 1800 and 1000 ka, rainforest biomes were present in the Amazon drainage basin, along with extensive riparian wetland vegetation. Tropical rainforest expansion occurred during the relatively warm Marine Isotope Stages 33 and 31 (ca. 1110 to 1060 ka), followed by a contraction of both forests and wetlands until ca. 800 ka. Between 800 and 400 ka, low pollen concentration and low diversity of palynological assemblages renders difficult the interpretation of Amazonian vegetation. A strong synchronicity between vegetation changes and glacial-interglacial global climate cycles was established around 400 ka. After 400 ka, interglacial vegetation was dominated by lowland tropical rainforest in association with warmer temperatures and higher CO2. During cooler temperatures and lower CO2 of glacial stages, tropical seasonal forests expanded, presumably towards eastern Amazonia. While this study provides no evidence supporting a significant expansion of savanna or steppe vegetation within the Amazonian lowlands during glacial periods, there were changes in the rainforest composition in some parts of the basin towards a higher proportion of deciduous elements, pointing to less humid conditions and/or greater seasonality of precipitation. Nevertheless, rainforest persisted during both glacial and interglacial periods. These findings confirm the sensitivity of tropical lowland vegetation to changes in CO2, temperature, and moisture availability and the most suitable conditions for tropical rainforests occurred during the warmest stages of the Mid Pleistocene Transition and during the interglacial stages of the past 400 kyr

Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells.

Background: Epidemiologic studies have highlighted the association of environmental factors with the development and progression of autoimmune and chronic inflammatory diseases. Among the environmental factors, smoking has been associated with increased susceptibility and poor prognosis in rheumatoid arthritis (RA). However, the immune and molecular mechanism of smoking-induced arthritis aggravation remains unclear. The transcription factor aryl hydrocarbon receptor (AHR) regulates the generation of Th17 cells, CD4 T cells linked the development of autoimmune diseases. AHR is activated by organic compounds including polycyclic aromatic hydrocarbons (PAHs), which are environmental pollutants that are also present in cigarette smoke. In this study, we investigated the role of AHR activation in the aggravation of experiment arthritis induced by exposure to cigarette smoke. Methods: Mice were exposed to cigarette smoke during the developmental phase of antigen-induced arthritis and collagen-induced arthritis to evaluate the effects of smoking on disease development. Aggravation of articular inflammation was assessed by measuring neutrophil migration to the joints, increase in articular hyperalgesia and changes in the frequencies of Th17 cells. In vitro studies were performed to evaluate the direct effects of cigarette smoke and PAH on Th17 differentiation. We also used mice genetically deficient for AHR (Ahr KO) and IL-17Ra (Il17ra KO) to determine the in vivo mechanism of smoking-induced arthritis aggravation. Results: We found that smoking induces arthritis aggravation and increase in the frequencies of Th17 cells. The absence of IL-17 signaling (Il17ra KO) conferred protection to smoking-induced arthritis aggravation. Moreover, in vitro experiments showed that cigarette smoke can directly increase Th17 differentiation of T cells by inducing AHR activation. Indeed, Ahr KO mice were protected from cigarette smoke-induced arthritis aggravation and did not display increase in TH17 frequencies, suggesting that AHR activation is an important mechanism for cigarette smoke effects on arthritis. Finally, we demonstrate that PAHs are also able to induce arthritis aggravation. Conclusions: Our data demonstrate that the disease-exacerbating effects of cigarette smoking are AHR dependent and environmental pollutants with AHR agonist activity can induce arthritis aggravation by directly enhancing Th17 cell development

Influence of migration on prevalence of serological hepatitis B markers in a rural community: 2 - Comparative analysis of some characteristics of the population studied

The association between prevalence of hepatitis B serological markers and birthplace, in a study carried out in a small rural county of S. Paulo State, Brazil, suggests different risk factors for hepatitis B between migrants and nonmigrant populations. These two groups were compared with regard to the following variables: level of education, professional occupation, number of previous hospitalizations, past history of blood transfusions and type of dental treatment. Migrants, mainly those from other states of Brazil, showed a low-level of education, a high proportion of people employed in agricultural activities, a higher number of past hospitalizations and higher exposure to blood transfusion and to more aggressive dental procedures. Associations were observed between the prevalence of serological markers and the following variables: level of education, professional occupation, number of previous hospitalizations and type of dental procedures, even though the last two associations did not justify the higher prevalences observed among migrants. The different distribution of hepatitis B markers seems to be dependent on the migrants' worse socio-economic condition, demonstrated by their lower level of education and by the predominance of secondary occupations.A associação entre prevalência de marcadores sorológicos de hepatite B e local de nascimento, verificado em estudo realizado num município de características rurais do Estado de São Paulo, Cássia dos Coqueiros, sugere existirem diferenças entre migrantes e não-migrantes no que diz respeito a fatores de risco para hepatite B. Esses dois grupos foram analisados segundo as variáveis escolaridade, ocupação profissional, número de hospitalizações, antecedente de transfusões sangüíneas e tipo de tratamento dentário prévio. A comparação entre os grupos mostra que migrantes, particularmente de outros Estados do País, apresentam baixos níveis de escolaridade, elevadas proporções de lavradores empregados, maior número de internações prévias e maiores exposições a transfusões sangüíneas e a procedimentos odontológicos mais agressivos. Observaram-se ainda associações entre a prevalência de marcadores de hepatite B e as variáveis escolaridade, ocupação profissional, número de hospitalizações e tipo de tratamento odontológico, muito embora as duas últimas não justifiquem as maiores prevalências entre os migrantes. A distribuição diferenciada de marcadores de hepatite B parece ser resultado da pior condição socioeconômica dos migrantes, refletida pelo seu nível inferior de escolaridade e pela predominância de ocupações secundárias