ABSTRACT
With careful selection of patients, complete resection of pulmonary metastases from breast carcinoma may be a useful therapeutic option. Such a treatment appears to offer a significant survival benefit when compared with medical treatment alone, or with incomplete resection.
Subject(s)
Breast Neoplasms/pathology , Carcinoma/secondary , Lung Neoplasms/secondary , Antineoplastic Agents/therapeutic use , Antineoplastic Agents, Hormonal/therapeutic use , Carcinoma/diagnosis , Carcinoma/drug therapy , Carcinoma/surgery , Combined Modality Therapy , Female , Humans , Lung Neoplasms/diagnosis , Lung Neoplasms/drug therapy , Lung Neoplasms/surgery , Neoplasm, Residual/pathology , Patient Selection , Pneumonectomy , Survival RateABSTRACT
We investigated the effect of an anti-CD11b monoclonal antibody (1B6c) on ischemic cell damage after transient middle cerebral artery occlusion. We divided animals into three groups: MAb 1 group (n = 5)--rats were subjected to 2 hours of transient occlusion and 1B6c (1 mg/kg) was administered intravenously at 0 and 22 hours of reperfusion; MAb 2 group (n = 5)--same experimental protocol as MAb 1 group, except that the initial dose of 1B6c was increased to 2 mg/kg; and control group (n = 5)--same experimental protocol as MAb 2 group, except that an isotype-matched control antibody was administered. Animals were weighed and tested for neurological function before and after occlusion of the middle cerebral artery. Forty-six hours after reperfusion, brain sections were stained with hematoxylin and eosin for histology evaluation. We observed a significant reduction of weight loss and improvement in neurological function after ischemia in the MAb 2 animals compared to MAb 1 and vehicle-treated animals (p < 0.05). The lesion volume was significantly smaller in the MAb 2 group (19.5 +/- 1.9%) compared to MAb 1 (29.9 +/- 2.6%) and vehicle-treated (34.2 +/- 5.4%) groups (p < 0.01). Tissue polymorphonuclear cell numbers were reduced in both 1B6c-administered groups. Our data demonstrate that administration of anti-CD11b antibody results in a dose-dependent, significant functional improvement and reduction of ischemic cell damage after transient focal cerebral ischemia in the rat.
Subject(s)
Antibodies, Monoclonal/therapeutic use , Ischemic Attack, Transient/therapy , Macrophage-1 Antigen/immunology , Animals , Blood Gas Analysis , Blood Pressure/physiology , Brain/pathology , Ischemic Attack, Transient/pathology , Ischemic Attack, Transient/physiopathology , Male , Rats , Rats, WistarABSTRACT
The temporal evolution and spatial distribution of ischemic cell injury was investigated after transient middle cerebral artery (MCA) occlusion. Male Wistar rats (n = 61) were subjected to 2 h of MCA occlusion induced by advancing a nylon monofilament into the right internal carotid artery. Animals were killed after different durations of reperfusion, ranging from 4 to 166 h (n = 6-11 for each group). Neuronal injury and astrocytic reaction were evaluated using hematoxylin and eosin (H & E) and glial fibrillary acidic protein (GFAP) immunohistochemistry, respectively. Eosinophilic neurons were detected at 4 h of reperfusion in the basal ganglia, and at 10 h of reperfusion in the cortex. Focal brain infarct developed by 46 h of reperfusion, both in the cortex and the basal ganglia, and the volume remained constant between 46 and 166 h of reperfusion. Significant differences in astrocytic reaction were detected between the lesion and the periphery of the lesion at reperfusion times from 46 to 166 h; GFAP staining decreased in the core of the lesion and increased in the peripheral areas. Our data suggest that, after 2 h of MCA occlusion, brain tissue progresses from isolated neuronal injury to infarct with a time course dependent on anatomical site; and astrocytic reactivity, expressed by GFAP staining, reflects the outcome of the ischemic injury.
Subject(s)
Astrocytes/physiology , Cerebral Arteries/physiology , Ischemic Attack, Transient/pathology , Neurons/physiology , Animals , Basal Ganglia/metabolism , Basal Ganglia/pathology , Blood Gas Analysis , Cerebral Cortex/metabolism , Cerebral Cortex/pathology , Glial Fibrillary Acidic Protein/immunology , Glial Fibrillary Acidic Protein/metabolism , Immunohistochemistry , Ischemic Attack, Transient/etiology , Male , Paraffin Embedding , Rats , Rats, WistarABSTRACT
The role of cerebral depolarizations in focal cerebral ischemia is unknown. We therefore measured the direct current (DC) electrical activity in the cortex of Wistar rats subjected to transient occlusion of the middle cerebral artery (MCA). Focal ischemia was induced for 90 min by insertion of an intraluminal filament to occlude the MCA. To modulate cell damage, we subjected the rats to hypothermic (30 degrees C, n = 4), normothermic (37 degrees C, n = 4), and hyperthermic (40 degrees C, n = 6) ischemia. Controlled temperatures were also maintained during 1 h of reperfusion. Continuous cortical DC potential changes were measured using two active Ag-AgCl electrodes placed in the cortical lesion. Animals were killed 1 week after ischemia. The brains were sectioned and stained with hematoxylin and eosin, for evaluation of neuronal damage, and calculation of infarct volume. All animals exhibited an initial depolarization within 30 min of ischemia, followed by a single depolarization event in hypothermic animals, and multiple periodic depolarization events in both normothermic and hyperthermic animals. Hyperthermic animals exhibited significantly more (p < 0.05) DC potential deflections (n = 6.17 +/- 0.67) than normothermic animals (n = 2.75 +/- 0.96). The ischemic infarct volume (% of hemisphere) was significantly different for the various groups; hypothermic animals exhibited no measurable infarct volume, while the ischemic infarct volume was 10.2 +/- 12.3% in normothermic animals and 36.5 +/- 3.4% in hyperthermic animals (p < 0.05). A significant correlation was detected between the volume of infarct and number of depolarization events (r = 0.90, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
