Eva Lopez - Academia.edu (original) (raw)
Papers by Eva Lopez
Cardiovascular and Interventional Radiology, 1998
Purpose: To highlight the importance of detecting bronchial arteries of anomalous origin in patie... more Purpose: To highlight the importance of detecting bronchial arteries of anomalous origin in patients with massive or recurrent hemoptysis. Methods: In a series of 300 patients submitted to bronchial embolization in our hospital since 1986, we found 25 (8.3%) with 27 anomalous bronchial arteries. Eighteen patients presented with recurrent hemoptysis (10 massive) and seven with their first episode of massive hemoptysis. Results: Of the 27 anomalous bronchial arteries demonstrated, 24 originated from the aortic arch, one from the left thyrocervical trunk, one from the right subclavian artery, and one from the lower descending thoracic aorta; two of the arteries demonstrated showed no pathological findings. Hemoptysis resolved following the first embolization in 14 patients (56%). In nine patients (36%) more than one procedure was necessary to arrest hemorrhage. In two patients surgical intervention was required. One patient died from bleeding. Conclusions: In cases of hemorrhage when the cause is not easily identified, or in cases of recurrence in spite of accurate embolization of pathological arteries, the presence of bronchial arteries of anomalous origin should be considered. Embolization is more difficult in these cases and there is an increased risk of complications.
Neurobiology of Disease, 2000
Experimental evidence suggests that the massive release of glutamate during experimental brain is... more Experimental evidence suggests that the massive release of glutamate during experimental brain ischemia both directly and indirectly regulates downstream mechanisms of cell suicide. Cerebral ischemia was produced by distal, permanent occlusion of the middle cerebral artery (MCAO) in the rat. Sets of three animals and one sham-operated for each time-point were kept alive for 0 -30 min, 1, 4, 12, 24, and 48 h, and 4 days. Additional animals were treated by local administration of a 10 M (in 10 l) cocktail of caspase inhibitors (YVAD-cmk, DEVD-fmk, IETD). Immunohistochemistry was performed on free-floating tissue sections with goat polyclonal antibodies to procaspase-1, -2, -3, -6, and -8. Some sections were processed for double-labeling procaspase immunohistochemistry and in situ end-labeling of nuclear DNA fragmentation (TUNEL method). Both immunohistochemistry and doublelabeling procaspase immunohistochemistry and TUNEL method were carried out on formalin-fixed sections. For gel electrophoresis and Western blotting, we used antibodies to poly (ADP-ribose) polymerase (PARP), lamin B, and PKC-␦, as specific cleavage substrates of caspases. There was increased immunoreactivity ipsilaterally in the areas corresponding to the infarct and surrounding penumbra with the peak of immunoreactivity between 12 and 24 h for most of the procaspases. Procaspases were present early in the infarcted tissue neurones and their dendrites and axons. Additional procaspase expression occurred in astrocytes and microglial cells at different times following ischemia. Cells with positive in situ end-labeling of nuclear DNA fragmentation appeared in high number predominantly in the infarcted areas and at the edge of the infarction and colocalized with enhanced procaspase expression. These findings suggest increased procaspase expression in dying cells at the edge of the infarction. A major product of PARP degradation of about 89 kDa was found in the samples taken from the infarcted and penumbra areas. There was no difference in the intensity of the bands corresponding to lamin B or PKC-␦. Injection of procaspase inhibitors reduced the levels of major PARP products of 89 kDa and decreased the number of TUNEL-positive cells at 12 h post-MCAO. In conclusion, these results give support to further research on the use of caspase inhibitors as add-on therapeutic agents for the treatment of ischemia.
Cardiovascular and Interventional Radiology, 1998
Purpose: To highlight the importance of detecting bronchial arteries of anomalous origin in patie... more Purpose: To highlight the importance of detecting bronchial arteries of anomalous origin in patients with massive or recurrent hemoptysis. Methods: In a series of 300 patients submitted to bronchial embolization in our hospital since 1986, we found 25 (8.3%) with 27 anomalous bronchial arteries. Eighteen patients presented with recurrent hemoptysis (10 massive) and seven with their first episode of massive hemoptysis. Results: Of the 27 anomalous bronchial arteries demonstrated, 24 originated from the aortic arch, one from the left thyrocervical trunk, one from the right subclavian artery, and one from the lower descending thoracic aorta; two of the arteries demonstrated showed no pathological findings. Hemoptysis resolved following the first embolization in 14 patients (56%). In nine patients (36%) more than one procedure was necessary to arrest hemorrhage. In two patients surgical intervention was required. One patient died from bleeding. Conclusions: In cases of hemorrhage when the cause is not easily identified, or in cases of recurrence in spite of accurate embolization of pathological arteries, the presence of bronchial arteries of anomalous origin should be considered. Embolization is more difficult in these cases and there is an increased risk of complications.
Neurobiology of Disease, 2000
Experimental evidence suggests that the massive release of glutamate during experimental brain is... more Experimental evidence suggests that the massive release of glutamate during experimental brain ischemia both directly and indirectly regulates downstream mechanisms of cell suicide. Cerebral ischemia was produced by distal, permanent occlusion of the middle cerebral artery (MCAO) in the rat. Sets of three animals and one sham-operated for each time-point were kept alive for 0 -30 min, 1, 4, 12, 24, and 48 h, and 4 days. Additional animals were treated by local administration of a 10 M (in 10 l) cocktail of caspase inhibitors (YVAD-cmk, DEVD-fmk, IETD). Immunohistochemistry was performed on free-floating tissue sections with goat polyclonal antibodies to procaspase-1, -2, -3, -6, and -8. Some sections were processed for double-labeling procaspase immunohistochemistry and in situ end-labeling of nuclear DNA fragmentation (TUNEL method). Both immunohistochemistry and doublelabeling procaspase immunohistochemistry and TUNEL method were carried out on formalin-fixed sections. For gel electrophoresis and Western blotting, we used antibodies to poly (ADP-ribose) polymerase (PARP), lamin B, and PKC-␦, as specific cleavage substrates of caspases. There was increased immunoreactivity ipsilaterally in the areas corresponding to the infarct and surrounding penumbra with the peak of immunoreactivity between 12 and 24 h for most of the procaspases. Procaspases were present early in the infarcted tissue neurones and their dendrites and axons. Additional procaspase expression occurred in astrocytes and microglial cells at different times following ischemia. Cells with positive in situ end-labeling of nuclear DNA fragmentation appeared in high number predominantly in the infarcted areas and at the edge of the infarction and colocalized with enhanced procaspase expression. These findings suggest increased procaspase expression in dying cells at the edge of the infarction. A major product of PARP degradation of about 89 kDa was found in the samples taken from the infarcted and penumbra areas. There was no difference in the intensity of the bands corresponding to lamin B or PKC-␦. Injection of procaspase inhibitors reduced the levels of major PARP products of 89 kDa and decreased the number of TUNEL-positive cells at 12 h post-MCAO. In conclusion, these results give support to further research on the use of caspase inhibitors as add-on therapeutic agents for the treatment of ischemia.