Pentastomiasis is a rare zoonotic disease. Almost all recorded cases of human pentastomiasis had been incidental findings at autopsy. We report an unusual case of human pentastomiasis mimicking liver tumor successfully treated by liver resection. This clinical presentation is uncommon and it was probably caused by a pentastomid that exited its cyst and migrated to the liver causing an infarct that was mistaken as a primary liver tumor. Diagnosis could not be made before the surgery. This is the first reported case of human pentastomiasis in Brazil.
Temperate bacteriophage Mu-1 was used to generate a lysogenic derivative of the F'lac episome of Escherichia coli. Intact, covalently circular molecules of F'lac and lysogenic F'lac Mu+ deoxyribonucleic acid (DNA) were isolated and examined by electron microscopy. The mean contour lengths of F'lac and F'lac Mu+ molecules were 37.6 + 0.4 Am and 53.2 + 0.4 ,um, respectively. The mean difference, 15.6 Am, is similar to the mean contour length of 12.9 + 0.1 Am obtained for linear DNA molecules released by osmotic shock from mature phage Mu-1 virions. These results provide direct physical evidence that phage Mu-1 integrates by linear insertion of its genome into the DNA of lysogenic host bacteria. Chemical and physical analyses of phage Mu-1 DNA indicate that it is similar to E. coli DNA in respect of gross base composition, buoyant density, and molting temperature.
Night admission is an independent risk factor for mortality in Night admission is an independent risk factor for mortality in Night admission is an independent risk factor for mortality in Night admission is an independent risk factor for mortality in Night admission is an independent risk factor for mortality in trauma patients -a systemic error approach trauma patients -a systemic error approach trauma patients -a systemic error approach trauma patients -a systemic error approach trauma patients -a systemic error approach Admissão noturna é fator de risco independente para mortalidade em pacientes Admissão noturna é fator de risco independente para mortalidade em pacientes Admissão noturna é fator de risco independente para mortalidade em pacientes Admissão noturna é fator de risco independente para mortalidade em pacientes Admissão noturna é fator de risco independente para mortalidade em pacientes vítimas de trauma -uma abordagem ao erro sistêmico vítimas de trauma -uma abordagem ao erro sistêmico vítimas de trauma -uma abordagem ao erro sistêmico vítimas de trauma -uma abordagem ao erro sistêmico vítimas de trauma -uma abordagem ao erro sistêmico LEONARDO DE [1][2][3] . Fatigue and lack of supervision to attending physicians may contribute to increased complications and hospital mortality. Such situations, also added to the circadian rhythm and dynamics of abnormal operating changes can be crucial factors for the worst performance in these periods. The cumulative presence of a number of unfavorable conditions is remarkable and very common in these periods, situations that favor and increase vulnerability to error [1][2][3][4][5][6][7][8][9][10] . Specific studies in patients with acute myocardial infarction, ischemic stroke and the Intensive Care Units showed higher rate of clinical complications and hospital mortality in the "off-hours" periods (nighttime or weekends) [4][5][6][7][8][9][10][11][12] . The volume of evidence demonstrating higher incidence of unfavorable outcomes in these adverse conditions weakens the idea of occasional errors as the cause of these events [4][5][6][7][8][9][10] . This highlights the need to analyze these situations trough of a model to interpret the error with a systemic view.Due to the lack of Brazilian studies, this study aimed to verify the impact of the shift of admission of patients who have suffered trauma, underwent surgery, in hospital mortality. According to these results, interpretation models and error correction are discussed.
METHODS
METHODS METHODS METHODS METHODSThis is a cohort study with retrospective collection of data, which were selected through electronic medical records, patients admitted from November 2011 to March 2012 in the emergency of Hospital do Subúrbio (HS) -a public hospital attending urgency and emergency and public-private administrative nature, in Subúrbio Ferroviá-rio, district of the city of Salvador, Bahia. The study included trauma patients admitted to the emergency HS who underwent surgery and were classified according to Internatio...
RESUMO -Racional -A lesão de isquemia e reperfusão hepática é um evento comum e responsável por considerável morbidade e mortalidade.Objetivo -Avaliar efeitos de inibidor da glicoproteína IIb/IIIa, cloridrato de tirofiban, nas alterações hepáticas e pulmonares da lesão de isquemia e reperfusão de fígado de ratos. Método -Vinte e três ratos Wistar divididos em três grupos: laparotomia (n = 6), isquemia e reperfusão que receberam solução fisiológica (n = 8), e submetidos a isquemia e reperfusão e tratados com o cloridrato de tirofiban (n = 9). Foram realizadas dosagens das aminotransferases e análise histológica hepática. Avaliação pulmonar foi realizada pelo teste do azul de Evans e pela dosagem tecidual da mieloperoxidase no parênquima pulmonar. A oxidação e fosforilação mitocondrial das células hepáticas também foram avaliadas. Resultados -O grupo tratado com cloridrato de tirofiban apresentou menores níveis de aminotransferases, assim como alterações histológicas menos intensas. Avaliação pulmonar demonstrou diminuição no teste de azul de Evans no grupo tratado com cloridrato de tirofiban. Grupo tratado com cloridrato de tirofiban apresentou aumento significativo do estado 3 da respiração mitocondrial e das relações adenosina difosfato utilizado para fosforilação sobre o oxigênio consumido na reação e de coeficiente respiratório. Conclusões -O uso do cloridrato de tirofiban exerceu papel protetor da lesão hepática de isquemia e reperfusão e impediu o aumento da permeabilidade vascular secundária à lesão de reperfusão hepática. DESCRITORES -Traumatismo por reperfusão. Fígado. Hepatectomia. Glicoproteínas da membrana de plaquetas. Ratos.
INTRODUÇÃOA lesão de isquemia e reperfusão é a principal determinante da disfunção hepática após hepatectomias, e também, a causa mais importante da disfunção primária do enxerto hepático (2,3,23)
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