Photometric and Spectroscopic Observations of SN 1990E in NGC 1035: Observational Constraints for Models of Type II Supernovae

We present 126 photometric and 30 spectral observation of SN 1990E spanning from 12 days before B maximum to 600 days past discovery. These observations show that SN 1990E was of type II-P, displaying hydrogen in its spectrum, and the characteristic plateau in its light curve. SN 1990E is one of the few SNe II which has been well observed before maximum light, and we present evidence that this SN was discovered very soon after its explosion. In the earliest spectra we identify, for the first time, several N II lines. We present a new technique for measuring extinction to SNe II based on the evolution of absorption lines, and use this method to estimate the extinction to SN 1990E, Av=1.5+/-0.3 mag. From our photometric data we have constructed a bolometric light curve for SN 1990E and show that, even at the earliest times, the bolometric luminosity was falling rapidly. We use the late-time bolometric light curve to show that SN 1990E trapped a majority of the gamma rays produced by the radioactive decay of 56Co, and estimate that SN 1990E ejected 0.073 Mo of 56Ni, an amount virtually identical to that of SN 1987A. [excerpt

Steps toward determination of the size and structure of the broad-line region in active nuclei. 7: Variability of the optical spectrum of NGC 5548 over years

We report on the results of a continuation of a large monitoring program of optical spectroscopy of the Seyfert 1 galaxy NGC 5548. The new observations presented here were obtained between 1990 December and 1992 October, and extend the existing database to nearly 1400 days, dating back to 1988 December. The continuum variations are generally smooth and well-resolved, except during the third year of this 4 year project, when the variations were apparently more rapid and of lower amplitude than observed at other times. The broad H(beta) emission line is found to vary in response to the continuum variations with a lag of about 18 days, but with some changes from year to year. The H(beta) transfer functions for each of the 4 yr and for the entire 4 yr database are derived by using a maximum entropy method.Astronom

Análise da remodelação vascular na isquemia pulmonar experimental, nas fases aguda e crônica Analysis of acute and chronic vascular remodeling in an experimental model of pulmonary ischemia

INTRODUÇÃO: Alterações estruturais da circulação pulmonar traduzem processo de remodelação vascular e têm relação provável com variações locais de fluxo e isquemia. OBJETIVO: Definir as alterações histológicas na circulação pulmonar após obstrução experimental da artéria pulmonar. Correlacioná-las com os padrões de redistribuição sangüínea e remodelação vascular. MÉTODO: Foram submetidos à toracotomia esquerda 48 ratos Wistar, alocados aleatoriamente em dois grupos, com ligadura da artéria pulmonar e controle, e sacrificados com 1, 7, 30 e 60 dias. Nos pulmões retirados avaliou-se presença de sinais de injúria no parênquima e mensurou-se diâmetro externo e espessura da parede das arteríolas de bronquíolos terminais, respiratórios e alveolares. Diâmetro interno e porcentagem de espessura da parede foram calculados. RESULTADOS: Só ocorreu infarto, necrose e hemorragia no pulmão isquêmico. No não isquêmico houve aumento mantido dos diâmetros externo e interno das arteríolas, com redução inicial da espessura no 1º dia e valores semelhantes aos do grupo controle no 60º dia. No pulmão isquêmico houve redução transitória nos diâmetros externo e interno das arteríolas de bronquíolos terminais e respiratórios, com aumento, inicial e transitório, na sua espessura. As arteríolas alveolares apresentaram aumento do diâmetro externo e espessura da parede, com redução do diâmetro interno, mantida e progressiva. CONCLUSÃO: Este modelo reproduz arteriopatia distal em pacientes com tromboembolismo pulmonar crônico. A resposta vascular no pulmão não isquêmico é compatível com padrão de remodelação de hiperfluxo; a no pulmão isquêmico com hipofluxo e isquemia. Nas arteríolas de bronquíolos terminais e respiratórios a resposta foi transitória. Nas alveolares foi progressiva e mantida, pela provável ocorrência tardia de hiperfluxo local.<br>BACKGROUND: Structural alterations to the pulmonary circulation characterize the vascular remodeling process and are likely correlated with local variations in flow and ischemia. OBJECTIVE: To define the histological alterations to the pulmonary circulation seen after experimentally-induced ischemia of the pulmonary artery and to correlate those alterations with known patterns of blood redistribution and vascular remodeling. METHOD: Wistar rats (n = 48) were randomized into two groups with ligation of the pulmonary artery and without (controls) and were sacrificed on post-ischemia days 1, 7, 30 and 60. Lungs were removed and inspected for signs of parenchymal injury. External diameters, as well as wall thicknesses in the pulmonary, alveolar and bronchial end arterioles, were measured. Internal diameter and wall thickness percentage were calculated. RESULTS: Infarction, necrosis and hemorrhage occurred only in ischemic lungs. In nonischemic lungs, there was a sustained increase in the internal and external arteriolar diameters, with an initial reduction in wall thickness on day 1, and day-60 values were similar to those seen in controls. In ischemic lungs, there was a transitory reduction in the internal and external diameters of the pulmonary and bronchial end arterioles, together with an initial, equally transitory, increase in their wall thickness. The alveolar arterioles presented sustained and progressive increases in external diameter and wall thickness, with concomitant reductions in internal diameter. CONCLUSION: This model mimics distal arterial disease in patients with chronic pulmonary thromboembolism. The vascular response in nonischemic lungs was consistent with a pattern of flow remodeling, whereas that seen in ischemic lungs was more consistent with flow and ischemia. In the pulmonary and bronchial end arterioles, the response was transitory, in contrast to the sustained and progressive response seen in the alveolar arterioles, which was probably caused by delayed local flow