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.

[EX 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).
[EX A]: Does thermal microdebridement affect the time zero biomechanical properties of human patellar tendons?

[EX Q]: Increased placental growth secondary to reduced apoptosis may contribute to the development of macrosomia in GDM pregnancies. We hypothesize that reduced apoptosis in GDM placentas is caused by dysregulation of apoptosis related genes from death receptors or mitochondrial pathway or both to enhance placental growth in GDM pregnancies.', 'Newborn and placental weights from women with no pregnancy complications (controls; N=5), or with GDM (N=5) were recorded. Placental villi from both groups were either fixed for TUNEL assay, or snap frozen for gene expression analysis by apoptosis PCR microarrays and qPCR.', 'Maternal, placental and newborn weights were significantly higher in the GDM group vs. Controls. Apoptotic index of placentas from the GDM group was markedly lower than the Controls. At a significant threshold of 1.5, seven genes (BCL10, BIRC6, BIRC7, CASP5, CASP8P2, CFLAR, and FAS) were down regulated, and 13 genes (BCL2, BCL2L1, BCL2L11, CASP4, DAPK1, IBE, MCL1, NFBIZ, NOD1, PEA15, TNF, TNFRSF25, and XIAP) were unregulated in the GDM placentas. qPCR confirmed the consistency of the PCR microarray. Using Western blotting we found significantly decreased placental pro-apoptotic FAS receptor and FAS ligand (FASL), and increased mitochondrial anti-apoptotic BCL2 post GDM insult. Notably, caspase-3, which plays a central role in the execution-phase of apoptosis, and its substrate poly (ADP-ribose) polymerase (PARP) were significantly down regulated in GDM placentas, as compared to non-diabetic Control placentas.
[EX A]: Does gestational diabetes mellitus alter apoptotic and inflammatory gene expression of trophobasts from human term placenta?

[EX Q]: Flow-mediated dilation (FMD) is a complex mechanism involving several mediators, and different hemodynamic forces. Temporally distinct FMD patterns can be elicited by ischemic stimulus. Some subjects dilate early after cuff release, while others dilate later or do not dilate at all. Aim of the present research was to verify if hemorheological and hemodynamic factors might influence different FMD pattern.', '148 free-living subjects were studied. FMD was measured at 50 s, 2 min and 3 min. Blood viscosity was measured and shear stress calculated. Shear stress stimulus was quantified as the area under the curve after ischemia (SSAUC) over the first 40-s post-occlusion.', 'Based on the timing or absence of arterial dilation, 82 subjects were classified as Early dilators, 37 as Late dilators and 29 as No dilators. Peak FMD was 7.9 4.3 % in Early dilators, and 9.1 5.7 in Late dilators (p = NS). SSAUC was not significantly different among three groups, while blood viscosity was significantly higher in Late FMD subjects. Regression analyses showed the independent predictive role of age and blood viscosity on FMD patterns, and the lack of any association between FMD pattern and the magnitude of SS.
[EX A]:
Does blood viscosity but not shear stress associate with delayed flow-mediated dilation?