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.

[Q]: Thermal microdebridement for the treatment of chronic tendinopathy has recently been introduced. The effect of thermal microdebridement on the biomechanical properties of human tendons, however, remains unknown.', 'Thermal microdebridement does not affect the biomechanical properties of human patellar tendons in a cadaveric model at the time of initial treatment.', 'Controlled laboratory study.', 'The central 15 mm of 12 matched, human (mean age, 71 years; 8 male, 4 female), fresh-frozen patellar tendons was divided into 3 equal 5-mm specimens. The treatment group (n = 12) underwent thermal microdebridement with a radiofrequency probe. A sham treatment group (n = 12) underwent insertion of a deactivated probe. The control group (n = 12) underwent no treatment. After treatment, each specimen was tested to failure in a servo-hydraulic materials testing machine at an elongation rate of 3 mm/s. One-way repeated measures analysis of variance was used to determine differences between groups.', 'No significant difference in ultimate stress at failure, elastic modulus, strain energy density, or strain at maximum load was found between the groups. The ultimate stress at failure for the treatment, sham, and control groups was 61.0, 66.7, and 63.0 MPa, respectively (P = .653), and the strain at maximum load was 0.12, 0.11, and 0.09, respectively (P = .279).
[A]: Does thermal microdebridement affect the time zero biomechanical properties of human patellar tendons?


[Q]: A distinct velocity pattern represented by a "notch" is observed during the time interval between the end of the systolic and the onset of the early diastolic velocity wave on longitudinal myocardial velocity curve. The origin of the post-systolic velocity notch (PSN) has not been resolved.', 'The high frame rate color tissue Doppler imaging of the apical longitudinal axis was performed in 32 healthy subjects.', 'The time delays of the PSN onset at the posterior aortic wall (AW), the mid anteroseptal wall (MAS) and the posterior mitral annulus (MA) relatively to the anterior aortic annulus (AA) were found to be significantly longer than zero (5.1 ± 2.2, 6.0 ± 2.3, 6.8 ± 2.8 ms; p < 0.001). The amplitude was the highest at the AA when compared to the AW, the MAS and the MA (4.77 ± 1.28 vs. 2.88 ± 1.11, 2.15 ± 0.73, 2.44 ± 1.17 cm/s; p < 0.001). A second PSN spike was identifiable in 10/32 (31%) of the studied subjects at the AA. Of these, 9 (28%) exhibited a second PSN spike at the AW, 3 (9%) at the MAS and no one at the MA.
[A]: Does the tissue Doppler imaging derived post-systolic velocity notch originate at the aortic annulus?


[Q]: Heat shock protein-27 (HSP-27) belongs to the group of small heat shock proteins that become induced in response to various pathologic conditions. HSP-27 has been shown to protect cells and subcellular structures, particularly mitochondria, and serves as a carrier for estradiol. It is a reliable marker for tissues affected by oxidative stress. Oxidative stress and related cellular defence mechanisms are currently thought to play a major role during experimentally induced epileptic neuropathology. We addressed the question whether HSP-27 becomes induced in the neocortex resected from patients with pharmacoresistant epilepsy.', "Human epileptic temporal neocortex was obtained during neurosurgery, and control tissue was obtained at autopsy from subjects without known neurologic diseases. The tissues were either frozen for Western blot analysis or fixed in Zamboni's fixative for the topographic detection of HSP-27 at the cellular level by means of immunohistochemistry.", 'HSP-27 was highly expressed in all epilepsy specimens and in the cortex of a patient who died in the final stage of multiple sclerosis (positive control), whereas only low amounts of HSP-27 were detectable in control brains. In epilepsy patients, HSP-27 was present in astrocytes and in the walls of blood vessels. The intracortical distribution patterns varied strongly among the epilepsy specimens.
[A]:
Is heat shock protein-27 upregulated in the temporal cortex of patients with epilepsy?