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.

Input: Consider Input: Context: Duchenne muscular dystrophy (DMD) is a devastating muscle disease caused by a mutation in DMD encoding dystrophin. Oxidative stress accounts for dystrophic muscle pathologies in DMD. We examined the effects of molecular hydrogen in mdx mice, a model animal for DMD.', 'The pregnant mother started to take supersaturated hydrogen water (>5\u2005ppm) ad libitum from E15.5 up to weaning of the offspring. The mdx mice took supersaturated hydrogen water from weaning until age 10 or 24 weeks when they were sacrificed.', 'Hydrogen water prevented abnormal body mass gain that is commonly observed in mdx mice. Hydrogen improved the spontaneous running distance that was estimated by a counter-equipped running-wheel, and extended the duration on the rota-rod. Plasma creatine kinase activities were decreased by hydrogen at ages 10 and 24 weeks. Hydrogen also decreased the number of central nuclei of muscle fibers at ages 10 and 24 weeks, and immunostaining for nitrotyrosine in gastrocnemius muscle at age 24 weeks. Additionally, hydrogen tended to increase protein expressions of antioxidant glutathione peroxidase 1, as well as anti-apoptotic Bcl-2, in skeletal muscle at age 10 weeks.
Answer: Although molecular mechanisms of the diverse effects of hydrogen remain to be elucidated, hydrogen potentially improves muscular dystrophy in DMD patients.

Output: Does molecular hydrogen alleviate motor deficits and muscle degeneration in mdx mice?


Input: Consider Input: Context: A cross-sectional study.', 'This study aims to investigate the correlation of the cervical canal and spinal cord size, and evaluate whether the size of the spinal cord relative to the spinal canal is a risk factor for development of cervical spinal cord compression (SCC).', 'There is little knowledge regarding the relationship between cervical bony canal and spinal cord diameters. Although developmental canal stenosis has been recognized as a risk factor for SCC, the size of the spinal cord relative to the spinal canal has not been similarly discussed.', 'Cervical canal anteroposterior (AP) diameters on X-rays and AP diameters and cross-sectional areas of dural sacs and spinal cords on magnetic resonance imaging (MRI) were measured in 1211 healthy volunteers. Correlation between cervical canal diameter on X-rays and AP diameter and cross-sectional area of dural sacs and spinal cords on MRI were assessed. The ratio of the AP diameter of the spinal cord/dural sac was compared between subjects with and without SCC.', 'Spinal canal diameters were not highly correlated with spinal cord AP diameters and cross-sectional areas, although spinal canal diameters were significantly correlated with dural sac AP diameters. The individual difference in the ratio of the AP diameter of the spinal cord/dural sac was large (35%-93%), and the ratio was significantly larger in the subjects with SCC. An AP diameter ratio more than 62% at the C2 to C3 disc level is a risk factor for developing SCC.
Answer: The spinal cord diameter was independent of the spinal canal diameter and the relative size of a spinal cord and spinal canal differed on an individual basis. In addition, the ratio of spinal cord/dural sac in subjects with SCC was significantly larger. Therefore, a relatively large spinal cord could be a risk factor for SCC.

Output: Is relatively Large Cervical Spinal Cord for Spinal Canal a Risk factor for Development of Cervical Spinal Cord Compression : A Cross-Sectional Study of 1211 Subjects?


Input: Consider Input: Context: To investigate the effect of antisense non-coding RNA in the INK4 locus (ANRIL) on invasion and metastasis of thyroid cancer (TC).', 'ANRIL expression was significantly up-regulated in TC tissues and cells (P < 0.001), and ANRIL expression was significantly different regarding histological grade and LNM (both P < 0.01). The siRNA-mediated ANRIL silencing inhibits proliferation, invasion, and metastasis of TPC-1 and SW579 cells, and lung metastasis, which can be reversed by TGF-β1 siRNA. The mRNA levels of p15INK4b, p14ARF and p16INK4a in TPC-1 and SW579 cells increased significantly after silencing ANRIL (all P < 0.001), and TGF-β1 siRNA could reverse the ANRIL siRNA induced increase of p15INK4b; expressions of TGF-β1 and p-Smad2/3 were increased after silencing ANRIL (both P < 0.05).', 'TC and adjacent normal tissues were collected from 105 TC patients. LncRNA ANRIL expressions were detected by qRT-PCR. The siRNA ANRIL and siRNA TGF-β1 were constructed for TPC-1 and SW579 cell line transfection: si-ANRIL group, si-TGF-β1 group, si-ANRIL + si-TGF-β1 group, negative control group and blank group. Effects of ANRIL silencing on proliferation, invasion and metastasis of TC cells was detected by MTT assay, Transwell assay and tail vein injection of nude mice in vitro and in vivo. TGF-β1 and p-Smad2/3 expressions in TGF-β/Smad signaling pathway were detected by western blot.
Answer: ANRIL may reduce p15INK4B expression through inhibiting TGF-β/Smad signaling pathway, promoting invasion and metastasis of TC cells, and the silencing of ANRIL inhibits the invasion and metastasis of TPC-1 cells.


Output: Does long non-coding RNA ANRIL promote the invasion and metastasis of thyroid cancer cells through TGF-β/Smad signaling pathway?