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.

Ex Input:
Context: Patients affected by chronic lymphocytic leukemia (CLL) have an increased risk of developing a second cancer. There is not a definitive explanation for this phenomenon, although some hypotheses have been postulated. The aim of the present work was to assess the presence of second cancer in untreated patients with CLL who were cytogenetically characterized, and secondly to investigate if there is a correlation between the genetics of CLL and the emergence of second cancer.', 'We performed conventional cytogenetics and Fluorescent in situ hybridization analyses in a series of 106 patients.', 'We observed that nearly 8% of cases developed second cancer, mostly epithelial tumors. The majority of them presented two common features, del(13)(q14.3) and the presence of at least two genetic alterations.
Answer: We suggest that the genetic background of CLL, particularly the presence of several genetic alterations, influences the emergence of second cancer in patients affected by CLL.

Ex Output:
Does genetics of lymphocytes influence the emergence of second cancer in chronic lymphocytic leukemia?


Ex Input:
Context: Hypertrophic cardiomyopathy (HCM) patients are at risk of ventricular arrhythmias (VAs). We aimed to explore whether systolic function by strain echocardiography is related to VAs and to the extent of fibrosis by cardiac magnetic resonance imaging (CMR).', 'We included 150 HCM patients and 50 healthy individuals. VAs were defined as non-sustained and sustained ventricular tachycardia and aborted cardiac arrest. Left ventricular function was assessed by ejection fraction (EF) and by global longitudinal strain (GLS) assessed by speckle tracking echocardiography. Mechanical dispersion was calculated as standard deviation (SD) of time from Q/R on ECG to peak longitudinal strain in 16 left ventricular segments. Late gadolinium enhancement (LGE) was assessed by CMR. HCM patients had similar EF (61 ± 5% vs. 61 ± 8%, P = 0.77), but worse GLS (-15.7 ± 3.6% vs. -21.1 ± 1.9%, P < 0.001) and more pronounced mechanical dispersion (64 ± 22 vs. 36 ± 13 ms, P < 0.001) compared with healthy individuals. VAs were documented in 37 (25%) HCM patients. Patients with VAs had worse GLS (-14.1 ± 3.6% vs. -16.3 ± 3.4%, P < 0.01), more pronounced mechanical dispersion (79 ± 27 vs. 59 ± 16 ms, P < 0.001), and higher %LGE (6.1 ± 7.8% vs. 0.5 ± 1.4%, P < 0.001) than patients without VAs. Mechanical dispersion correlated with %LGE (R = 0.52, P < 0.001) and was independently associated with VAs (OR 1.6, 95% CI 1.1-2.3, P = 0.02) and improved risk stratification for VAs.
Answer: GLS, mechanical dispersion, and LGE were markers of VAs in HCM patients. Mechanical dispersion was a strong independent predictor of VAs and related to the extent of fibrosis. Strain echocardiography may improve risk stratification of VAs in HCM.

Ex Output:
Is strain echocardiography related to fibrosis and ventricular arrhythmias in hypertrophic cardiomyopathy?


Ex Input:
Context: Recently we reported that fluid shear stress promotes endothelial cell differentiation from a mouse embryo mesenchymal progenitor cell line C3H10T1/2. However, it is not clear whether the transforming growth factor-beta 1 (TGF-beta1) system is associated with shear-induced endothelial differentiation. The purpose of this study was to determine the effect of shear stress on the expression of TGF-beta1 and its signaling molecules in C3H10T1/2 cells.', 'Murine C3H10T1/2 cells were incubated on collagen Type 1-coated dishes, and subjected to a steady fluid shear stress of 15 dyn/cm(2) for 6, 12, and 24 h. The mRNA levels for TGF-beta1, TGF-beta receptors (TGF-beta R), and Smad molecules were determined with real-time PCR analysis and normalized to glyceraldehyde-3-phosphate dehydrogenase mRNA levels.', 'TGF-beta1 mRNA expression was down-regulated by 60% and 66% in shear stress-treated cells at 12 and 24 h, respectively, compared with static control group (P < 0.01). In addition, shear stress significantly decreased TGF-beta R1 mRNA levels by 30% and 50% in shear stress-treated cells at 12 and 24 h, respectively (P < 0.01). For TGF-beta R2, shear stress at 6, 12, and 24 h significantly reduced its expression by 93%, 95% and 97%, respectively, compared with static controls (P < 0.01). Furthermore, shear stress significant decreased mRNA levels of positive signaling molecules Smad2, Smad3, and Smad4 in a time-dependent manner (P < 0.01). However, shear stress significantly increased negative signaling molecule Smad7 mRNA levels by 100% at 24 h treatment compared with static control group (P < 0.01).
Answer: Fluid shear stress significantly suppresses TGF-beta1 functions through down-regulation of TGF-beta1, TGF-beta R, positive signaling molecules Smad2, Smad3, Smad4, and up-regulation of negative signaling molecule Smad7 in a mouse embryo mesenchymal progenitor cell line C3H10T1/2. This study suggests that the negative regulation of the TGF-beta1 system may be involved in shear-induced endothelial cell differentiation in C3H10T1/2.

Ex Output:

Does fluid shear stress regulate the expression of TGF-beta1 and its signaling molecules in mouse embryo mesenchymal progenitor cells?