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.

Example Input: Context: To study the effect of removal of YY1 binding sites within the LCR region of HPV 16 on viral transforming activity.', 'Previously we had generated new plasmids carrying HPV 16 whole genome, which contained naturally occurred mutated LCR sequences. The viral transforming abilities on mouse fibroblasts were evaluated in anchorage-independent assays, while the expression and activity of YY1 protein in fibroblasts were tested with EMSA and luciferase assays.', 'YY1 protein was expressed in mouse fibroblasts C127, with ability for DNA binding and repression on P97 activity. Both HPV 16 wild-type DNA and mutated DNAs were transfected into C127 cells and spread to the soft-agarose mediums after selecting with G 418. The growth numbers of the cells transfected with mutated HPV 16 DNAs were 2-10 fold more than that with wild-type HPV 16 DNA.
Answer: Like in epithelial cells or cell lines, transcription regulator YY1 is widely expressed in rodent fibroblasts. Removal of YY1 binding motifs can elevate in the context of the whole genome, the anchorage independent growth ability and the transforming capacity of HPV 16 on the mouse fibroblasts.
Example Output: Does [ Removal of YY1 binding sites in HPV 16 LCR increase viral transforming activities on mouse fibroblasts ]?

Example Input: Context: Osteoarthritis (OA) is associated with a gradual reduction in the interstitial osmotic pressure within articular cartilage. The aim of this study was to compare the effects of sudden and gradual hypo-osmotic challenge on chondrocyte morphology and biomechanics.', 'Bovine articular chondrocytes were exposed to a reduction in extracellular osmolality from 327 to 153 mOsmol/kg applied either suddenly (<5 s) or gradually (over 180 min). Temporal changes in cell diameter and the existence of regulatory volume decrease (RVD) were quantified along with changes in cortical actin and chromatin condensation. The cellular viscoelastic mechanical properties were determined by micropipette aspiration.', 'In response to a sudden hypo-osmotic stress, 66% of chondrocytes exhibited an increase in diameter followed by RVD, whilst 25% showed no RVD. By contrast, cells exposed to gradual hypo-osmotic stress exhibited reduced cell swelling without subsequent RVD. There was an increase in the equilibrium modulus for cells exposed to sudden hypo-osmotic stress. However, gradual hypo-osmotic challenge had no effect on cell mechanical properties. This cell stiffening response to sudden hypo-osmotic challenge was abolished when actin organization was disrupted with cytochalasin D or RVD inhibited with REV5901. Both sudden and gradual hypo-osmotic challenge reduced cortical F-actin distribution and caused chromatin decondensation.
Answer: Sudden hypo-osmotic challenge increases chondrocyte mechanics by activation of RVD and interaction with the actin cytoskeleton. Moreover, the rate of hypo-osmotic challenge is shown to have a profound effect on chondrocyte morphology and biomechanics. This important phenomenon needs to be considered when studying the response of chondrocytes to pathological hypo-osmotic stress.
Example Output: Does the rate of hypo-osmotic challenge influence regulatory volume decrease ( RVD ) and mechanical properties of articular chondrocytes?

Example Input: Context: Peripheral arterial disease (PAD) is common in patients with acute cerebral ischemia. Indexes of resistance derived from the systolic and diastolic velocities are routinely used in diagnostic transcranial Doppler (TCD) to detect intracranial arterial disease. We sought to explore whether these indexes can predict the presence of PAD in acute cerebral ischemia.', 'We prospectively evaluated consecutive patients with acute cerebral ischemia. On TCD, peak-systolic and end-diastolic velocities in both middle cerebral and basilar arteries were manually measured to calculate pulsatility index (PI) and resistance index (RI). Increased resistance was defined as PI equal to 1.2 or more and RI equal to .75 or more. Ankle-brachial index (ABI) measurements were performed and an ABI equal to .9 or more was considered predictive of definite PAD.', 'We included 95 patients (45 male, 50 female) aged 66 9 years with a median National Institutes Health Stroke Scale score of 3 (interquartile range, 8) points. The ABI was abnormal and consistent with definite PAD in 24 of 95 (25.3%; 95% confidence interval [CI], 16.4-34.2) patients. Increased PI did not differ among patients with and without PAD (20.8% vs. 28.2%, P = .60). Only 1 patient with PAD had increased RI as opposed to 4 patients without PAD (4.2% vs. 5.6%, P = 1.0). Increased PI was not found to be an independent predictor of PAD (odds ratio [OR], .68; 95% CI, .22-2.12; P = .51). Increases in both PI and RI independently predicted arterial hypertension (OR, 1.62; 95% CI, 1.19-2.21; P = .002 and OR, 3.20; 95% CI, 1.51-6.77; P = .002, respectively).
Answer: Our findings indicate that PAD cannot be inferred from intracranial flow parameters predictive of arterial disease and risk factors such as hypertension among patients with acute cerebral ischemia.
Example Output:
Does increased pulsatility of the intracranial blood flow spectral waveform on transcranial Doppler point to peripheral arterial disease in stroke patients?