Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Context: A cross-sectional study.', 'This study aims to investigate the correlation of the cervical canal and spinal cord size, and evaluate whether the size of the spinal cord relative to the spinal canal is a risk factor for development of cervical spinal cord compression (SCC).', 'There is little knowledge regarding the relationship between cervical bony canal and spinal cord diameters. Although developmental canal stenosis has been recognized as a risk factor for SCC, the size of the spinal cord relative to the spinal canal has not been similarly discussed.', 'Cervical canal anteroposterior (AP) diameters on X-rays and AP diameters and cross-sectional areas of dural sacs and spinal cords on magnetic resonance imaging (MRI) were measured in 1211 healthy volunteers. Correlation between cervical canal diameter on X-rays and AP diameter and cross-sectional area of dural sacs and spinal cords on MRI were assessed. The ratio of the AP diameter of the spinal cord/dural sac was compared between subjects with and without SCC.', 'Spinal canal diameters were not highly correlated with spinal cord AP diameters and cross-sectional areas, although spinal canal diameters were significantly correlated with dural sac AP diameters. The individual difference in the ratio of the AP diameter of the spinal cord/dural sac was large (35%-93%), and the ratio was significantly larger in the subjects with SCC. An AP diameter ratio more than 62% at the C2 to C3 disc level is a risk factor for developing SCC.
Answer: The spinal cord diameter was independent of the spinal canal diameter and the relative size of a spinal cord and spinal canal differed on an individual basis. In addition, the ratio of spinal cord/dural sac in subjects with SCC was significantly larger. Therefore, a relatively large spinal cord could be a risk factor for SCC.
Is relatively Large Cervical Spinal Cord for Spinal Canal a Risk factor for Development of Cervical Spinal Cord Compression : A Cross-Sectional Study of 1211 Subjects?

Context: Postoperative neurologic deficits after thoracic aortic reconstruction vary widely. Our previous study showed that delayed ischemic preconditioning could prevent spinal cord injury caused by occlusion of the descending thoracic aorta in pigs. We investigated early ischemic preconditioning in the same model.', 'Twenty-eight pigs were divided into 4 groups: group 1 (n = 6) underwent a sham operation, group 2 (n = 6) underwent aortic occlusion for 20 minutes, group 3 (n = 8) underwent aortic occlusion for 35 minutes, and group 4 (n = 8) underwent aortic occlusion for 20 minutes and underwent aortic occlusion 80 minutes later without hypotension for 35 minutes. Aortic occlusion was accomplished by using 2 balloon occlusion catheters placed fluoroscopically at T6 to T8 above the diaphragm and at the aortic bifurcation. Neurologic evaluation was performed by an independent observer according to the Tarlov scale (0-4). The lower thoracic and lumbar spinal cords were harvested at 120 hours and examined histologically with hematoxylin-and-eosin stain. Histologic results (number of neurons and grade of inflammation) were scored (0-4) and were similarly analyzed. Statistical analysis was by means of the Kruskal-Wallis test.', 'Group 4 had a better neurologic outcome at 24, 48, and 120 hours in comparison with group 3 (P <.001). The histologic changes were proportional to the neurologic test scores, with the more severe and extensive gray matter damage in animals of group 3 (number of neurons, P <.001; grade of inflammation, P <.001).
Answer: Early ischemic preconditioning without hypotension protects against spinal cord injury after aortic occlusion, as confirmed by using the Tarlov score and histopathology.
Does early ischemic preconditioning without hypotension prevent spinal cord injury caused by descending thoracic aortic occlusion?

Context: The antileukemic drug asparaginase, a key component in the treatment of acute lymphoblastic leukemia, acts by depleting asparagine from the blood. However, little is known about its pharmacokinetics and mechanisms of therapy resistance are poorly understood. Here, we explored the in vivo biodistribution of radiolabeled asparaginase, using a combination of in vivo imaging and biochemical techniques, and provide evidence for tissue specific clearance mechanisms, which could reduce effectiveness of the drug at these specific sites.', 'In vivo localization of Indium-111-labeled E.coli asparaginase was carried out in C57Bl/6 mice by both microSPECT/CT and by ex vivo biodistribution studies. Mice were treated with liposomal clodronate to investigate the effect of macrophage depletion on tracer localization and drug clearance in vivo. Moreover, macrophage cell line models RAW264.7 and THP-1, as well as cathepsin B deficient mice, were used to identify the cellular and molecular components controlling asparaginase pharmacokinetics.', 'In vivo imaging and biodistribution studies showed a rapid accumulation of asparaginase in macrophage-rich tissues such as liver, spleen and in particular bone marrow. Clodronate-mediated depletion of phagocytic cells markedly prolonged the serum half-life of asparaginase in vivo and decreased drug uptake in target organs. Immunohistochemistry and in vitro binding assays confirmed the involvement of macrophage-like cells in the uptake of asparaginase. We identified the activity of the lysosomal protease cathepsin B in macrophages as a rate-limiting factor in degrading asparaginase both in vitro and in vivo.
Answer: We show that asparaginase is rapidly cleared from the serum by liver, spleen and bone marrow-resident phagocytic cells. As a consequence of this efficient uptake and protease mediated degradation, particularly bone marrow resident macrophages may provide a protective niche to leukemic cells.
Does in vivo imaging of antileukemic drug asparaginase reveal a rapid macrophage mediated clearance from the bone marrow?