RESUMO Objetivo: Comparar as características antropométricas, bioquímicas, hormonais e a presença de polimorfismos genéticos de leptina, adiponectina e fator de necrose tumoral alfa (TNF-α) entre crianças e adolescentes eutróficos e obesos. Métodos: Trata-se de um estudo caso-controle conduzido com 104 crianças e adolescentes. Todos os indivíduos foram avaliados quanto às características antropométricas e parâmetros clínicos, laboratoriais e de polimorfismo genético. A amostra foi selecionada no ambulatório de endocrinologia pediátrica especializado no tratamento da obesidade em crianças e adolescentes de acordo com a classificação do Centers for Disease Control and Prevention (CDC), e os controles foram selecionados no mesmo local, porém no ambulatório de pediatria geral. Resultados: Alguns parâmetros foram associados à obesidade em nosso estudo: cor preta, pais obesos, pais hipertensos e desmame precoce. Níveis aumentados de insulina, triglicerídeos, colesterol total, colesterol LDL, PCR-U, AST, ALT, GGT, T4 Livre, IGF-1, ácido úrico e níveis baixos de colesterol HDL estão associados a uma chance maior de obesidade. A presença de polimorfismos AG/AA na leptina está associada a uma chance 290% (OR 3,9) maior de obesidade, enquanto para os genes da adiponectina as chances são 740% (OR 8,4) maiores. Nessas crianças e adolescentes obesos com haplótipos AG/AA, os níveis séricos de leptina aumentaram e os níveis de adiponectina diminuíram em relação aos eutróficos, já os níveis séricos de TNF-α não se alteraram. Conclusões: Concluiu-se que os polimorfismos AG/AA nos genes da leptina e adiponectina alteram os níveis séricos dessas adipocinas e predispõem à obesidade precoce, e muitos marcadores antropométricos, bioquímicos e hormonais ficam alterados, trazendo consequências para a saúde dessas crianças e adolescentes.

ABSTRACT Objective: The aim of this study was to compare the anthropometric, biochemical, and hormonal characteristics and the presence of genetic polymorphisms of leptin, adiponectin, and tumor necrosis factor alpha (TNF-α) between eutrophic and obese children and adolescents. Methods: This is a case–control study involving 104 children and adolescents. All subjects were assessed for anthropometric characteristics and clinical, laboratory, and genetic polymorphism parameters. The sample was selected from the pediatric endocrinology outpatient clinic specialized in the treatment of obesity in children and adolescents according to the Centers for Disease Control and Prevention (CDC) classification, and controls were selected from the same location in the general pediatric outpatient clinic. Results: As a result, the parameters, such as black color, obese parents, hypertensive parents, and early weaning, were found to be associated with obesity. Increased levels of insulin, triglyceride, total cholesterol, LDL cholesterol, CRP-U, AST, ALT, GGT, free T4, IGF-1, and uric acid and low levels of HDL cholesterol are found to be associated with a higher chance of obesity. The presence of AG/AA polymorphisms in the leptin is associated with a 290% (OR 3.9) higher chance of obesity, and for adiponectin genes, the chances are 740% (OR 8.4) higher. In these obese children and adolescents with AG/AA haplotypes, serum leptin levels were increased and adiponectin levels were decreased in eutrophic individuals, whereas serum TNF-α levels did not change. Conclusions: The AG/AA polymorphisms in the leptin and adiponectin genes alter the serum levels of these adipokines and predispose them to obesity, and many anthropometric, biochemical, and hormonal markers are altered, demonstrating early consequences for the health of these obese children and adolescents.

Despite major improvements in its treatment and diagnosis, sepsis is still a leading cause of death and admittance to the intensive care unit (ICU). Failure to identify patients at high risk of developing septic shock contributes to an increase in the sepsis burden and rapid molecular tests are currently the most promising avenue to aid in patient risk determination and therapeutic anticipation. The primary goal of this study was to evaluate the genetic susceptibility that affects sepsis outcome in 72 sepsis patients admitted to the ICU. Seven polymorphisms were genotyped in key inflammatory response genes in sepsis, including tumour necrosis factor-α,interlelukin (IL)-1β, IL-10,IL-8, Toll-like receptor 4, CXCR1and CXCR2. The primary finding showed that patients who were homozygous for the major A allele in IL-10rs1800896 had almost five times higher chance to develop septic shock compared to heterozygotes. Similarly, selected clinical features and CXCR2rs1126579 single nucleotide polymorphisms modulated septic shock susceptibility without affecting survival. These data support the hypothesis that molecular testing has clinical usefulness to improve sepsis prognostic models. Therefore, enrichment of the ICU portfolio by including these biomarkers will aid in the early identification of sepsis patients who may develop septic shock.

Vaccinia virus is responsible for a zoonosis that usually affects cattle and human beings in Brazil. The initial clinical signs of the infection are focal red skin areas, fever, and general symptoms similar to those of a cold. Then, pustules and ulcerated lesions surrounded by edema and erythema follow, as well as local lymphadenopathy that can last for weeks. Cure and healing of the lesions occur over several weeks, leaving a typical scar in the skin of people and animals affected. The infection definitive diagnosis is made through morphological characterization of the virus by use of electron microscopy, followed by PCR for specific viral genes. Since 1963, circulating orthopoxviruses in infectious outbreaks in several regions of Brazil have been reported. Later, the etiological agent of those infections was characterized as samples of Vaccinia virus. In addition, the widespread use of those viruses in research laboratories and mass vaccination of militaries have contributed to increase the cases of those infections worldwide. Thus, several epidemiological and clinical studies are required, as well as studies of viral immunology, public health, and economic impact, because little is known about those Vaccinia virus outbreaks in Brazil.

Despite the wealth of information generated by trans-disciplinary research in Chagas disease, knowledge about its multifaceted pathogenesis is still fragmented. Here we review the body of experimental studies in animal models supporting the concept that persistent infection by Trypanosoma cruzi is crucial for the development of chronic myocarditis. Complementing this review, we will make an effort to reconcile seemingly contradictory results concerning the immune profiles of chronic patients from Argentina and Brazil. Finally, we will review the results of molecular studies suggesting that parasite-induced inflammation and tissue damage is, at least in part, mediated by the activities of trans-sialidase, mucin-linked lipid anchors (TLR2 ligand) and cruzipain (a kinin-releasing cysteine protease). One hundred years after the discovery of Chagas disease, it is reassuring that basic and clinical research tends to converge, raising new perspectives for the treatment of chronic Chagas disease.