Análise das redes interpessoais: aplicação na realidade de uma equipe de enfermagem atuando em unidade de hematologia

A equipe de Enfermagem do Serviço de Hematologia depara-se constantemente com situações de sofrimento intenso, podendo afetar sua homeostase. Considerando o postulado acerca da tendência à atualização do ser humano, as redes interpessoais podem ser benéficas, disponibilizando suportes para atualização da pessoa, que passa a transformar sua energia em comportamento útil, favorecendo o desempenho de funções e promovendo saúde. Este estudo foi realizado sobre a metodologia de análise das redes sociais, com o objetivo de analisar a rede interpessoal dos componentes de uma equipe de Enfermagem, que atua em unidade de hematologia de um hospital-escola na cidade de Fortaleza-CE. Foi realizado no ano de 2009, com 10 informantes-chaves. Os dados foram coletados no questionário gerador de nomes e qualificador da relação, processados nos programas: UCINET 6.123 e NETDRAW 2.38. O emprego da metodologia de análise de redes sociais permitiu reunir elementos elucidativos acerca da estrutura do grupo, sendo possível, a partir daí, tecer considerações acerca da posição ocupada pelos indivíduos, bem como do núcleo de relações constituído ao redor de cada um.The nursing team of the Hematology Service are constantly facing situations of intense suffering and this can affect their homeostasis. Considering the premise according to which human beings tend to upgrade themselves, interpersonal networks may be beneficial, providing support so that the person can upgrade herself, and starts to transform her energy into useful behavior, favoring the performance of duties and promoting health. This study employed the methodology of Social Network Analysis, and it aimed to analyze the interpersonal network of the members of a nursing team that work in the hematology unit of a hospital-school in the city of Fortaleza, Northeastern Brazil. The study was conducted in 2006, with ten key informants. Data were collected through a questionnaire that generates names and evaluates the relationship, and were processed by the programs: UCINET 6.123 and NETDRAW 2.38. The use of Social Network Analysis enabled us to learn about the structure of the group. Based on this, it was possible to make considerations about the position occupied by the individuals and about the nucleus of relationships constituted around each one of them

The Genome of Anopheles darlingi, the main neotropical malaria vector

Anopheles darlingi is the principal neotropical malaria vector, responsible for more than a million cases of malaria per year on the American continent. Anopheles darlingi diverged from the African and Asian malaria vectors ∼100 million years ago (mya) and successfully adapted to the New World environment. Here we present an annotated reference A. darlingi genome, sequenced from a wild population of males and females collected in the Brazilian Amazon. A total of 10 481 predicted protein-coding genes were annotated, 72% of which have their closest counterpart in Anopheles gambiae and 21% have highest similarity with other mosquito species. In spite of a long period of divergent evolution, conserved gene synteny was observed between A. darlingi and A. gambiae. More than 10 million single nucleotide polymorphisms and short indels with potential use as genetic markers were identified. Transposable elements correspond to 2.3% of the A. darlingi genome. Genes associated with hematophagy, immunity and insecticide resistance, directly involved in vectorhuman and vectorparasite interactions, were identified and discussed. This study represents the first effort to sequence the genome of a neotropical malaria vector, and opens a new window through which we can contemplate the evolutionary history of anopheline mosquitoes. It also provides valuable information that may lead to novel strategies to reduce malaria transmission on the South American continent. The A. darlingi genome is accessible at www.labinfo.lncc.br/index.php/anopheles- darlingi. © 2013 The Author(s)

Reduction of bacterial adhesion to biocompatible polymer surfaces via plasma processing

Plasma processing of the surfaces of biomaterials is interesting because it enables modification of the characteristics of a surface without affecting bulk properties. In addition, the results are strongly influenced by the conditions of the treatment. Therefore, by adjusting the plasma parameters it is possible to tailor the surface properties to best fulfill the requirements of a given application. In this work, polyurethane substrates have been subjected to sulfur hexafluoride glow discharge plasmas. The influences of different SF 6 plasma exposure times and pressures on the adhesion of Staphylococcus aureus and Pseudomonas aeruginosa to the polymer have been investigated. The wettability and surface free energy have been evaluated via contact angle measurements. At low pressure (6.7 Pa) the contact angle decreases with increasing exposure time in the 180 s to 540 s interval, but at higher pressure (13.3 Pa) it increases as a function of the same variable. Bacterial adhesion has been quantified from in vitro experiments by determining the growth of colonies on Petri dishes treated with agar nutrient. It has been observed that the surface properties play an important role in microbe adhesion. For instance, the density of adhered P. aeruginosa decreased as the surface contact angle increased. S. aureus preferred to adhere to hydrophobic surfaces. © 2011 by Begell House, Inc

Sofosbuvir protects Zika virus-infected mice from mortality, preventing short- and long-term sequelae

Submitted by Sandra Infurna ([email protected]) on 2017-10-17T12:58:25Z No. of bitstreams: 1 andre_ferreira_etal_IOC_2017.pdf: 1574700 bytes, checksum: 1cbe13c85078c5cb11c6954145f48296 (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2017-10-17T13:16:07Z (GMT) No. of bitstreams: 1 andre_ferreira_etal_IOC_2017.pdf: 1574700 bytes, checksum: 1cbe13c85078c5cb11c6954145f48296 (MD5)Made available in DSpace on 2017-10-17T13:16:07Z (GMT). No. of bitstreams: 1 andre_ferreira_etal_IOC_2017.pdf: 1574700 bytes, checksum: 1cbe13c85078c5cb11c6954145f48296 (MD5) Previous issue date: 2017Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Universidade Federal do Rio de Janeiro. Instituto de Ciências Biomédicas. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biologia. Rio de Janeiro, RJ, BrasilBMK Consortium: Blanver Farmoquímica Ltda; Microbiológica Química e Farmacêutica Ltda, Karin Bruning & Cia. Ltda. Taboão da Serra, SP, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil. / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde. Instituto Nacional de Ciência e Tecnologia de Inovação em Doenças Negligenciadas. Rio de Janeiro, RJ, Brasil.Zika virus (ZIKV) causes significant public health concerns because of its association with congenital malformations, neurological disorders in adults, and, more recently, death. Considering the necessity to mitigate ZIKV-associated diseases, antiviral interventions are an urgent necessity. Sofosbuvir, a drug in clinical use against hepatitis C virus (HCV), is among the FDA-approved substances endowed with anti-ZIKV activity. In this work, we further investigated the in vivo activity of sofosbuvir against ZIKV. Neonatal Swiss mice were infected with ZIKV (2 × 10(7) PFU) and treated with sofosbuvir at 20 mg/kg/day, a concentration compatible with pre-clinical development of this drug. We found that sofosbuvir reduced acute levels of ZIKV from 60 to 90% in different anatomical compartments, such as the blood plasma, spleen, kidney, and brain. Early treatment with sofosbuvir doubled the percentage and time of survival of ZIKV-infected animals. Sofosbuvir also prevented the acute neuromotor impairment triggered by ZIKV. In the long-term behavioural analysis of ZIKV-associated sequelae, sofosbuvir prevented loss of hippocampal- and amygdala-dependent memory. Our results indicate that sofosbuvir inhibits ZIKV replication in vivo, which is consistent with the prospective necessity of antiviral drugs to treat ZIKV-infected individuals

Analgesic and anti-inflammatory activity of the aqueous extract of Rheedia longifolia Planch & Triana

Rheedia longifolia Planch et Triana belongs to the Clusiaceae family. This plant is widely distributed in Brazil, but its chemical and pharmacological properties have not yet been studied. We report here that leaves aqueous extract of R. longifolia (LAE) shows analgesic and anti-inflammatory effects. Oral or intraperitoneal administration of this extract dose-dependently inhibited the abdominal constrictions induced by acetic acid in mice. The analgesic effect and the duration of action were similar to those observed with sodium diclofenac, a classical non-steroidal analgesic. In addition to the effect seen in the abdominal constriction model, LAE was also able to inhibit the hyperalgesia induced by lipopolysaccharide from gram-negative bacteria (LPS) in rats. We also found that R. longifolia LAE inhibited an inflammatory reaction induced by LPS in the pleural cavity of mice. Acute toxicity was evaluated in mice treated with the extract for seven days with 50 mg/kg/day. Neither death, nor alterations in weight, blood leukocyte counts or hematocrit were noted. Our results suggest that aqueous extract from R. longifolia leaves has analgesic and anti-inflammatory activity with minimal toxicity and are therefore endowed with a potential for pharmacological control of pain and inflammation

Beyond Members of the Flaviviridae Family, Sofosbuvir Also Inhibits Chikungunya Virus Replication

Submitted by Sandra Infurna ([email protected]) on 2019-02-28T15:34:15Z No. of bitstreams: 1 carolinaq_sacramento_etal_IOC_2019.pdf: 2000356 bytes, checksum: 1bca1940789c6699df11840402c4da0f (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2019-02-28T15:54:29Z (GMT) No. of bitstreams: 1 carolinaq_sacramento_etal_IOC_2019.pdf: 2000356 bytes, checksum: 1bca1940789c6699df11840402c4da0f (MD5)Made available in DSpace on 2019-02-28T15:54:29Z (GMT). No. of bitstreams: 1 carolinaq_sacramento_etal_IOC_2019.pdf: 2000356 bytes, checksum: 1bca1940789c6699df11840402c4da0f (MD5) Previous issue date: 2019Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz, Instituto Nacional de Ciência e Tecnologia sobre Inovação em Doenças de Populações Negligenciada. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz. Instituto Nacional de Ciência e Tecnologia sobre Inovação em Doenças de Populações Negligenciada. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz, Instituto Nacional de Ciência e Tecnologia sobre Inovação em Doenças de Populações Negligenciada. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Tecnologia de Fármacos. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto de Tecnologia de Fármacos. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz, Instituto Nacional de Ciência e Tecnologia sobre Inovação em Doenças de Populações Negligenciada. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz, Instituto Nacional de Ciência e Tecnologia sobre Inovação em Doenças de Populações Negligenciada. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Instituto D`OR de Pesquisa e Educação. Rio de Janeiro, RJ, Brasil.Instituto D`OR de Pesquisa e Educação. Rio de Janeiro, RJ, Brasil.Instituto D`OR de Pesquisa e Educação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz, Instituto Nacional de Ciência e Tecnologia sobre Inovação em Doenças de Populações Negligenciada. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto de Tecnologia em Fármacos. Rio de Janeiro, RJ, Brasil.Instituto D`OR de Pesquisa e Educação. Rio de Janeiro, RJ, Brasil / Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Rio de Janeiro, RJ, Brasil.BMK Consortium. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil .Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil / Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz, Instituto Nacional de Ciência e Tecnologia sobre Inovação em Doenças de Populações Negligenciada. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.Chikungunya virus (CHIKV) causes a febrile disease associated with chronic arthralgia, which may progress to neurological impairment. Chikungunya fever (CF) is an ongoing public health problem in tropical and subtropical regions of the world, where control of the CHIKV vector, Aedes mosquitos, has failed. As there is no vaccine or specific treatment for CHIKV, patients receive only palliative care to alleviate pain and arthralgia. Thus, drug repurposing is necessary to identify antivirals against CHIKV. CHIKV RNA polymerase is similar to the orthologue enzyme of other positive-sense RNA viruses, such as members of the Flaviviridae family. Among the Flaviviridae, not only is hepatitis C virus RNA polymerase susceptible to sofosbuvir, a clinically approved nucleotide analogue, but so is dengue, Zika, and yellow fever virus replication. Here, we found that sofosbuvir was three times more selective in inhibiting CHIKV production in human hepatoma cells than ribavirin, a pan-antiviral drug. Although CHIKV replication in human induced pluripotent stem cell-derived astrocytes was less susceptible to sofosbuvir than were hepatoma cells, sofosbuvir nevertheless impaired virus production and cell death in a multiplicity of infection-dependent manner. Sofosbuvir also exhibited antiviral activity in vivo by preventing CHIKV-induced paw edema in adult mice at a dose of 20 mg/kg of body weight/day and prevented mortality in a neonate mouse model at 40- and 80-mg/kg/day doses. Our data demonstrate that a prototypic alphavirus, CHIKV, is also susceptible to sofosbuvir. As sofosbuvir is a clinically approved drug, our findings could pave the way to it becoming a therapeutic option against CF