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1.
Chest ; 132(3): 930-5, 2007 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-17646225

RESUMEN

BACKGROUND: Stereotactic radiosurgery (Cyberknife; Accuray Incorporated; Sunnyvale, CA) is a treatment option for patients who are medically unfit to undergo lung tumor resection. For precise tumor ablation, the Cyberknife requires fiducial marker placement in or near the target tumor. Fiducial placement under transthoracic CT guidance is associated with a high risk of iatrogenic pneumothorax. Electromagnetic navigation bronchoscopy (ENB) may offer a less morbid alternative to accurately deploy fiducials to bronchoscopically invisible peripheral lung lesions. OBJECTIVE: Open-label, feasibility study to assess fiducial placement in peripheral lung tumors by ENB. METHOD: Consecutive patients with peripheral lung tumors and who were evaluated to be nonsurgical candidates underwent fiducial placement under ENB. This procedure was considered successful if fiducials were placed in or near the tumors and remained in place without migration for radiosurgery to proceed. The need for alternative or additional intrathoracic fiducial placement was documented as procedure failure. RESULTS: A total of 39 fiducials markers were successfully deployed in eight of nine patients (89%). Of these eight successful cases, seven had fiducials placed directly within the tumor (88%). At Cyberknife planning, 7 to 10 days after fiducial placement, 35 of 39 fiducial markers (90%) were still in place and were adequate to allow radiosurgery to proceed. No immediate bronchoscopic complications were observed. One patient had a COPD exacerbation. Another patient returned within 1 day with transient, self-limiting fever. CONCLUSIONS: ENB can be used to deploy fiducial markers for Cyberknife radiosurgery of lung tumors safely and accurately without the complications associated with transthoracic placement.


Asunto(s)
Broncoscopía/métodos , Carcinoma/cirugía , Fenómenos Electromagnéticos , Neoplasias Pulmonares/cirugía , Radiocirugia/instrumentación , Cirugía Asistida por Computador/métodos , Anciano , Anciano de 80 o más Años , Carcinoma/patología , Estudios de Factibilidad , Femenino , Humanos , Neoplasias Pulmonares/patología , Masculino , Persona de Mediana Edad , Robótica
2.
Arch Med Res ; 38(1): 39-44, 2007 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-17174721

RESUMEN

BACKGROUND: Alkaline phosphatase (ALPase) is found in blood plasma or serum and leukocytes and regulates intercellular processes, maintaining phosphoryl metabolites in a steady state, as well as synthesizing and hydrolyzing phosphate esters on membranes. ALPase supervises the active transport of inorganic phosphates, fats, proteins, carbohydrates and the sodium/potassium pump mechanisms. The formed elements of blood such as polymorphonuclear (PMNs) leucocytes, macrophages (MP) and some lymphocytes are high in ALPase concentrations. METHODS: In this study we have tested whether the interleukin-1 receptor antagonist (IL-lra) could influence ALPase generation in IL-1beta or lipopolysaccharide (LPS)-stimulated neutrophils and MP. Human neutrophils were isolated from heparin-anticoagulated blood drawn from healthy individuals by centrifugation in a two-step gradient, Ficoll-Hypaque. ALPase activity was assessed spectrophotometrically in test tubes containing isolated neutrophils and adherence PBMCs treated with LPS, IL-1beta and IL-1ra, alone or in combination. RESULTS: IL-lbeta or LPS enhanced ALPase in both PMNs and MP, whereas IL-1ra could not inhibit ALPase activity. We performed time course experiments at 0 min, 5 min, 1 h, 24 h, and 43 h (LPS 20 microg/mL, IL-1beta 10 ng/mL). No significant increase in ALPase activity was seen until 1 h; however, there was a rapid rise over the next few hours. In another set of experiments using IL-1ra (500 ng/mL), there was no difference between treated cells and control cells. The combination of IL-1beta plus IL-1ra did not reduce the ability of IL-1beta to induce ALPase activity. CONCLUSIONS: These data suggest that IL-1beta stimulates ALPase through other mechanisms than the release of arachidonic acid products, which are inhibited by IL-lra.


Asunto(s)
Fosfatasa Alcalina/metabolismo , Interleucina-1beta/farmacología , Monocitos/efectos de los fármacos , Fagocitos/efectos de los fármacos , Fosfatasa Alcalina/antagonistas & inhibidores , Humanos , Proteína Antagonista del Receptor de Interleucina 1/farmacología , Lipopolisacáridos/farmacología , Monocitos/enzimología , Neutrófilos/efectos de los fármacos , Neutrófilos/enzimología , Fagocitos/enzimología , Regulación hacia Arriba
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