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.

Input: Consider Input: 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).

Output: Does thermal microdebridement affect the time zero biomechanical properties of human patellar tendons?

Input: Consider Input: Alzheimer's disease (AD) is characterized by cerebral deposition of -amyloid peptide (A). A is produced by sequential cleavage of the Amyloid Precursor Protein (APP) by - and -secretases. Many studies have demonstrated that the internalization of APP from the cell surface can regulate A production, although the exact organelle in which A is produced remains contentious. A number of recent studies suggest that intracellular trafficking also plays a role in regulating A production, but these pathways are relatively under-studied. The goal of this study was to elucidate the intracellular trafficking of APP, and to examine the site of intracellular APP processing.", 'We have tagged APP on its C-terminal cytoplasmic tail with photoactivatable Green Fluorescent Protein (paGFP). By photoactivating APP-paGFP in the Golgi, using the Golgi marker Galactosyltranferase fused to Cyan Fluorescent Protein (GalT-CFP) as a target, we are able to follow a population of nascent APP molecules from the Golgi to downstream compartments identified with compartment markers tagged with red fluorescent protein (mRFP or mCherry); including rab5 (early endosomes) rab9 (late endosomes) and LAMP1 (lysosomes). Because -cleavage of APP releases the cytoplasmic tail of APP including the photoactivated GFP, resulting in loss of fluorescence, we are able to visualize the cleavage of APP in these compartments. Using APP-paGFP, we show that APP is rapidly trafficked from the Golgi apparatus to the lysosome; where it is rapidly cleared. Chloroquine and the highly selective -secretase inhibitor, L685, 458, cause the accumulation of APP in lysosomes implying that APP is being cleaved by secretases in the lysosome. The Swedish mutation dramatically increases the rate of lysosomal APP processing, which is also inhibited by chloroquine and L685, 458. By knocking down adaptor protein 3 (AP-3; a heterotetrameric protein complex required for trafficking many proteins to the lysosome) using siRNA, we are able to reduce this lysosomal transport. Blocking lysosomal transport of APP reduces A production by more than a third.

Output: Is the Amyloid Precursor Protein rapidly transported from the Golgi apparatus to the lysosome and where it is processed into beta-amyloid?

Input: Consider Input: This study characterizes ovariectomized (OVX)-induced osteoporotic fracture healing with focus on estrogen receptors (ERs). Callus formation plays a critical role in fracture healing, and ERs are well-known mechanosensors in osteogenic pathways. It was hypothesized that callus formation was related to and partially determined by the difference in expression patterns of ERs in both normal and OVX-induced osteoporotic fractures.', 'Closed femoral fracture in SHAM and ovariectomized rats were used in this study. Weekly callus width (CW) and area (CA), endpoint mechanical properties, gene expressions of Col-1, BMP-2, ER-, ER- and ER-:ER- ratios (ER-ratios), and correlations were assessed at 2, 4 and 8 weeks post-fracture.', 'CW and CA results confirmed that OVX-induced osteoporotic fracture was delayed at 2-4 weeks with impaired endpoint mechanical properties. Gene expressions of ER- and ER- were higher in the SHAM group at week 2 (p < 0.05) and later lowered at week 8; whereas the OVX group showed an opposing trend. Moderate correlation existed between ER- and BMP-2 (0.545, p = 0.003), and ER-ratio and BMP-2 (0.601, p = 0.001), and BMP-2 to CW and CA (r = 0.709, p = 0.000 and r = 0.588, p = 0.001, respectively). ER- and ER- proteins expressions were confirmed by immunohistochemistry at the fracture callus in reparative progenitor cells, osteoblasts- and osteoclasts-like cells.
Output: Is callus formation related to the expression ratios of estrogen receptors-alpha and -beta in ovariectomy-induced osteoporotic fracture healing?