Retrato da epidemiologia da meningite no Estado do Pará entre 2015 e 2018/Portrait of the epidemiology of meningitis in the State of Pará between 2015 and 2018

A meningite é um processo inflamatório das membranas cerebrais e do líquido cefalorraquidiano que envolvem o sistema nervoso, podendo ser causado por fatores de natureza infecciosa ou não infecciosa. Assim, o objetivo deste estudo é traçar o perfil epidemiológico da meningite no Estado do Pará no período de 2015 a 2018. Trata-se de um estudo descritivo, retrospectivo e foi utilizado como fontes de informação o Sistema de Informação de Agravos de Notificação, cujos dados são disponibilizados pelo Departamento de Informática do SUS. Os dados obtidos foram organizados em planilhas do programa Microsoft® Excel 2016, onde foram analisados por meio da confecção de gráficos e tabelas. De Janeiro de 2015 à Dezembro de 2018 foram notificados 1974 casos de Meningite no Estado do Pará. No ano de 2017 houve um maior número de casos notificados (n 509) em relação aos demais anos avaliados. A faixa etária mais acometida pela doença foi entre 20-39 anos, representando aproximadamente 34% (n 678) dos casos confirmados e a etiologia dos casos de meningite pode variar entre as faixas etárias. Portanto, se faz necessário que divulgue na população os meios de prevenção da doença, e seus manejos corretos em casos suspeitos, a fim de evitar o máximo de sequelas, além de reforçar a importância da notificação junto à Vigilância Epidemiológica para que viabilize a implementação de estratégias adequadas de combate à doença

Oral treatment with the extract of Euterpe oleracea Mart. improves motor dysfunction and reduces brain injury in rats subjected to ischemic stroke

PROPESP-UFPA.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. Centre for the Valorization of Amazonian Bioactive Compounds. Belém, PA, Brazil.Federal University of Pará. Centre for the Valorization of Amazonian Bioactive Compounds. Belém, PA, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde e Ambiente. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Federal University of Pará. Institute Biological Science. Laboratory of Pharmacology and Toxicology of Natural Products. Belém, PA, Brazil.Federal University of Pará. Institute Biological Science. Laboratory of Pharmacology and Toxicology of Natural Products. Belém, PA, Brazil.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. João de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Ischemic stroke is one of the principal causes of morbidity and mortality around the world. The pathophysiological mechanisms that lead to the formation of the stroke lesions range from the bioenergetic failure of the cells and the intense production of reactive oxygen species to neuroinflammation. The fruit of the açaí palm, Euterpe oleracea Mart. (EO), is consumed by traditional populations in the Brazilian Amazon region, and it is known to have antioxidant and anti-inflammatory properties. We evaluated whether the clarified extract of EO was capable of reducing the area of lesion and promoting neuronal survival following ischemic stroke in rats. Animals submitted to ischemic stroke and treated with EO extract presented a significant improvement in their neurological deficit from the ninth day onward. We also observed a reduction in the extent of the cerebral injury and the preservation of the neurons of the cortical layers. Taken together, our findings indicate that treatment with EO extract in the acute phase following a stroke can trigger signaling pathways that culminate in neuronal survival and promote the partial recovery of neurological scores. However, further detailed studies of the intracellular signaling pathways are needed to better understand the mechanisms involved

The anthelmintic drug mebendazole inhibits growth, migration and invasion in gastric cancer cell model

AbstractThe present study aimed to investigate the effects of MBZ on a human malignant ascites cell line derived from a primary gastric cancer tumor. Our data reveal that MBZ showed high cytotoxicity in vitro, displaying an IC50 of 0.39μM and 1.25μM in ACP-02 and ACP-03, respectively. The association between MBZ and 5-FU increased slightly the cytotoxicity when compared to MBZ and 5-FU alone. Furthermore, MBZ disrupted the microtubule structure of AGP-01 cells and inhibited significantly the invasion and migration of these cells. Activity of active MMP-2 significantly decreased at all tested concentration of MBZ compared to negative control. These results support the indication of MBZ in combination with chemotherapeutic agents as a possible adjuvant therapy for the management/treatment of patients with advanced gastric cancer since MBZ is a drug of low cost with acceptable safety profile and reduced toxicity to normal cells. However, clinical trials must be performed in o to evaluate its efficacy in gastric cancer patients

Mebendazole induces apoptosis via C-MYC inactivation in malignant ascites cell line (AGP01)

Federal University of Pará. Biological Science Institute. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Ceará. Drug Research and Development Center. Laboratory of Pharmacogenetics. Fortaleza, CE, Brazil.Federal University of Pará. Biological Science Institute. Laboratory of Human Cytogenetics. Belém, PA, Brazil.Federal University of Ceará. Drug Research and Development Center. Laboratory of Pharmacogenetics. Fortaleza, CE, Brazil.Federal University of Pará. Laboratory of Structural and Functional Biology Science. Belém, PA, Brazil / Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Cultura Celular e Citogenética. Ananindeua, PA, Brasil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Cultura Celular e Citogenética. Ananindeua, PA, Brasil.Federal University of Pará. Biological Science Institute. Laboratory of Human Cytogenetics. Belém, PA, Brazil.Federal University of Ceará. Drug Research and Development Center. Laboratory of Pharmacogenetics. Fortaleza, CE, Brazil.The objective of study was to examine the role of MBZ on malignant ascites cells and the involvement of C-MYC. Comet assay was used to assess the genotoxic effects of MBZ in AGP01 cells and human lymphocytes; differential staining by ethidium bromide and acridine orange, caspase 3/7 and flow cytometry assay was done to access the mechanisms of apoptosis and cell cycle analysis of MBZ in AGP01 cells. C-MYC amplification, C-MYC mRNA and C-MYC protein expression were evaluated by FISH, RT-qPCR and Western blotting, respectively. In addition, cytotoxicity of MBZ was evaluated in AGP01 and AGP01 shRNA MYC by MTT. MBZ significantly increased the damage index and no produced in human lymphocytes. MBZ caused remarkable cell cycle arrest in G0/G1 and G2/M phases at 0.5μM and 1.0 μM, respectively and induced significantly apoptosis in higher concentrations. Additionally, MBZ (0.5 μM and 1.0 μM) increased caspase 3 and 7 activities. MBZ decreased signals, C-MYC mRNA and C-MYC protein expression in AGP01 cells. MBZ induced lower cell viability in AGP01 cells compared AGP01 shRNA MYC in the same concentration. Therefore, our results show the evidence of C-MYC gene as one of the pathways by which MBZ induces cell death in gastric cancer cells

The GPER1 agonist G1 reduces brain injury and improves the qEEG and behavioral outcome of experimental ischemic stroke

PROPESP-UFPAFederal University of Pará. Joao de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. Joao de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. Joao de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. Joao de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. Joao de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde e Ambiente. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Federal University of Pará. Joao de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Federal University of Pará. Biological Sciences Institute. Laboratory of Pharmacology and Toxicology of Natural Products. Belém, PA, Brazil.Federal University of Pará. Joao de Barros Barreto University Hospital. Laboratory of Experimental Neuropathology. Belém, PA, Brazil.Stroke is one of the principal cerebrovascular diseases in human populations and contributes to a majority of the functional impairments in the elderly. Recent discoveries have led to the inclusion of electroencephalography (EEG) in the complementary prognostic evaluation of patients. The present study describes the EEG, behavioral, and histological changes that occur following cerebral ischemia associated with treatment by G1, a potent and selective G protein-coupled estrogen receptor 1 (GPER1) agonist in a rat model. Treatment with G1 attenuated the neurological deficits induced by ischemic stroke from the second day onward, and reduced areas of infarction. Treatment with G1 also improved the total brainwave power, as well as the theta and alpha wave activity, specifically, and restored the delta band power to levels similar to those observed in the controls. Treatment with G1 also attenuated the peaks of harmful activity observed in the EEG indices. These improvements in brainwave activity indicate that GPER1 plays a fundamental role in the mediation of cerebral injury and in the behavioral outcome of ischemic brain injuries, which points to treatment with G1 as a potential pharmacological strategy for the therapy of stroke

Synthesis and Biological Evaluation of Novel 6-Hydroxy-benzo[d][1,3]oxathiol-2-one Schiff Bases as Potential Anticancer Agents

With the aim of discovering new anticancer agents, we have designed and synthesized novel 6-hydroxy-benzo[d][1,3]oxathiol-2-one Schiff bases. The synthesis started with the selective nitration at 5-position of 6-hydroxybenzo[d][1,3]oxathiol-2-one (1) leading to the nitro derivative 2. The nitro group of 2 was reduced to give the amino intermediate 3. Schiff bases 4a–r were obtained from coupling reactions between 3 and various benzaldehydes and heteroaromatic aldehydes. All the new compounds were fully identified and characterized by NMR (1H and 13C) and specifically for 4q by X-ray crystallography. The in vitro cytotoxicity of the compounds was evaluated against cancer cell lines (ACP-03, SKMEL-19 and HCT-116) by using MTT assay. Schiff bases 4b and 4o exhibited promising cytotoxicity against ACP-03 and SKMEL-19, respectively, with IC50 values lower than 5 μM. This class of compounds can be considered as a good starting point for the development of new lead molecules in the fight against cancer

Layered double hydroxide–indomethacin hybrid: A promising biocompatible compound for the treatment of neuroinflammatory diseases

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