Previous studies have shown that in the early phase of sepsis, the plasma concentration of arginine vasopressin (AVP) is increased, but in the late phase, its levels remain inadequately low, despite of persistent hypotension. One hypothesis suggested for this relative deficiency is apoptosis of vasopressinergic neurons. Here, we investigated apoptosis pathways in the hypothalamus during sepsis, as well as mechanisms underlying this process. Male Wistar rats were submitted to sepsis by cecal ligation and puncture (CLP) or nonmanipulated (naive) as control. After 6 and 24 h, the animals were decapitated and brain and blood were collected to assess hypothalamic apoptotic markers, IFN-γ plasma levels, and evidence for breakdown of the blood-brain barrier (BBB). Sepsis caused a decrease in mitochondrial antiapoptotic proteins (Bcl-2, Bcl-xL) in the hypothalamus, but had no effect on markers of cell death mediated by death receptors or immune cells. In the supraoptic nuclei of these animals, microglia morphology was consistent with activation, associated with an increase in plasma IFN-γ. A transitory breakdown of BBB in the hypothalamus was seen at 6 h following CLP. The results indicate that the intrinsic but not extrinsic apoptosis pathway is involved in the cell death observed in vasopressinergic neurons, and that this condition is temporally associated with microglial activation and BBB leaking.

The global emergence and re-emergence of arthropod-borne viruses (arboviruses) over the past four decades have become a public health crisis of international concern, especially in tropical and subtropical countries. A limited number of vaccines against arboviruses are available for use in humans; therefore, there is an urgent need to develop antiviral compounds. Snake venoms are rich sources of bioactive compounds with potential for antiviral prospection. The major component of Crotalus durissus terrificus venom is a heterodimeric complex called crotoxin, which is constituted by an inactive peptide (crotapotin) and a phospholipase A 2 (PLA 2-CB). We showed previously the antiviral effect of PLA 2-CB against dengue virus, yellow fever virus and other enveloped viruses. The aims of this study were to express two PLA 2-CB isoforms in a prokaryotic system and to evaluate their virucidal effects. The sequences encoding the PLA 2-CB isoforms were optimized and cloned into a plasmid vector (pG21a) for recombinant protein expression. The recombinant proteins were expressed in the E. coli BL21(DE3) strain as insoluble inclusion bodies; therefore, the purification was performed under denaturing conditions, using urea for protein solubilization. The solubilized proteins were applied to a nickel affinity chromatography matrix for binding. The immobilized recombinant proteins were subjected to an innovative protein refolding step, which consisted of the application of a decreasing linear gradient of urea and dithiothreitol (DTT) concentrations in combination with the detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate hydrate (CHAPS) as a protein stabilizer. The refolded recombinant proteins showed phospholipase activity and virucidal effects against chikungunya virus, dengue virus, yellow fever virus and Zika virus.

Data from the International Diabetes Federation (IDF) indicate that 8.8% of the world's population suffers from diabetes. Glycemic dosage is one of the most important laboratory parameters for the diagnosis and monitoring of the disease. That is why it is of paramount importance to guarantee doctors and the patient a reliable, safe and error-free report. It is known that the majority of the population uses medications randomly and without a prescription. Many drugs can interfere with the analytical methods of various laboratory tests. The objective of this study was to evaluate the in vitro interference of the drug paracetamol in glycemic dosage by the glucose oxidase method, which the literature reports is the most used method in glycemic dosages and which is susceptible to interference by paracetamol. Glycemic measurement of a control sample was performed with commercial serum of known value, at a concentration of 100 mg/dl, and commercial serum samples submitted to different concentrations of paracetamol, ranging from 10 μg/ml to 5 mg/ml. A significant decrease (p<0.0001) in blood glucose was observed in the samples with the presence of paracetamol at concentrations of 200 μg/ml and 5mg/ml. The present study demonstrated a negative correlation between increasing concentrations of acetaminophen and glycemic dosage.

SANTOS-JUNIOR, N. N. Neuroimmunoendocrine alterations in sepsis survivor animals 2018. 98f. Tese (Doutorado)

Introdução: a síndrome pós-COVID-19 trata-se do termo aplicado a diversos sintomas, alguns cognitivos, persistentes da COVID-19, mesmo após o final da fase aguda da infecção. Objetivo: apresentar os efeitos cognitivos da síndrome pós-COVID-19 por meio de dados coletados e analisar a relação entre a infecção do SARS-CoV-2 e o desenvolvimento dessas manifestações clínicas. Metodologia: foi realizada uma revisão sistemática de literatura, com base na busca de ensaios clínicos nos portais PubMED e Scielo. Seis estudos foram selecionados para a revisão. Resultados: no geral, os estudos acerca dos efeitos cognitivos da síndrome pós-COVID-19 foram pequenos e se basearam em testes e autoavaliações, mas mostram que confusão mental, perda de memória e dificuldade de concentração são as principais queixas relatadas pelos pacientes. Discussão:  evidências apontam que os efeitos cognitivos da síndrome pós-COVID-19 podem estar relacionados com a gravidade da infecção pelo COVID-19 e a doenças neurológicas prévias. A relação entre doenças virais e efeitos cognitivos já é bem estabelecida, o que torna possível pensar que o COVID-19 também é capaz de afetar o sistema nervoso. O sistema de saúde deve se preparar para enfrentar uma grande demanda relacionada a sequelas cognitivas, sendo necessário realizar reformas em sua estrutura. Conclusão: a continuação dos estudos acerca da síndrome pós-COVID-19 é essencial para a compreensão de uma condição que se mostra relacionada a tantos efeitos cognitivos.