Given a passage, 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.

Example Input: To study the expression of small ubiquitin-like modifier 1 (SUMO-1) in aseptic loosening of prosthesis implants and to investigate its role in regulating the susceptibility of prosthesis-loosening fibroblast-like synoviocytes (FLS) to Fas-induced apoptosis.', 'Specimens of aseptically loosened tissue were obtained at revision surgery, and the expression of SUMO-1 was analyzed by in situ hybridization. SUMO-1 levels in FLS were determined by quantitative polymerase chain reaction and Western blot analysis. Immunohistochemistry and confocal microscopy were used to study the subcellular localization of SUMO-1. The functional role of SUMO-1 in Fas-induced apoptosis of prosthesis-loosening FLS was investigated by small interfering RNA-mediated knockdown of SUMO-1 and by gene transfer of the nuclear SUMO-specific protease SENP1.', 'SUMO-1 was expressed strongly in aseptically loosened tissue and was found prominently at sites adjacent to bone. Prosthesis-loosening FLS expressed levels of SUMO-1 similar to the levels expressed by rheumatoid arthritis (RA) FLS, with SUMO-1 being found mainly in promyelocytic leukemia protein nuclear bodies. Knockdown of SUMO-1 had no effect on spontaneous apoptosis but significantly increased the susceptibility of prosthesis-loosening FLS to Fas-induced apoptosis. Gene transfer of the nuclear SUMO-specific protease SENP1 reverted the apoptosis-inhibiting effects of SUMO-1.
Example Output: Does small ubiquitin-like modifier 1 [ corrected ] mediate the resistance of prosthesis-loosening fibroblast-like synoviocytes against Fas-induced apoptosis?

Example Input: To determine whether recent reimbursement cuts have resulted in a shift of outpatient MRI from private offices to hospital outpatient departments (HOPDs); and to study office MRI utilization trends among radiologists and other specialists.', 'The Medicare Part B Physician/Supplier Procedure Summary Master Files were used. MRI codes were aggregated, and total MRI volumes from 2002 to 2012 were studied. Medicare place-of-service codes were used to identify studies performed in private offices and HOPDs and create trend lines. Specialty codes were used to categorize private office MRI users as radiologists, orthopedic surgeons, other physicians, and independent diagnostic testing facilities.', 'Medicare office and HOPD utilization of MRI (all specialties) rose rapidly from 2002 to 2006, reaching 2,727,807 in offices and 2,355,641 in HOPDs. Thereafter, office volume steadily declined, whereas HOPD volume steadily increased. By 2012, more studies were done in HOPDs than in offices. Over the entire period from 2002 and 2012, office MRI volume among radiologists increased 27%, compared with 216% among orthopedic surgeons and 124% among other physicians.
Example Output: Do trends in outpatient MRI seem to reflect recent reimbursement cuts?

Example Input: The checkpoint kinase 1 (Chk1) functions not only in genotoxic stresses but also in normal cell cycle progression, particularly in the initiation, progression and fidelity of unperturbed mitosis. In this study, we investigated the role of Chk1 in regulating the metaphase-anaphase transition in mammalian cells.', 'The mitotic progression was monitored by flow cytometry analysis. The levels of cyclin B1, Cdc20 and Mad2 were measured by Western blotting. Metaphase chromosome alignment and the subcellular localization of Cdc20 and Mad2 were analyzed by immunofluorescence and confocal microscopy.', 'Cyclin B1 degradation and the metaphase-anaphase transition were severely blocked by Chk1 siRNA. Depletion of Chk1 induced chromosome alignment defect in metaphase cells. The kinetochore localization of Cdc20, Mad2 was disrupted in Chk1 depleted cells. Chk1 abrogation also dramatically reduced the protein expression levels of Cdc20 and Mad2.
Example Output:
Is chk1 required for the metaphase-anaphase transition via regulating the expression and localization of Cdc20 and Mad2?