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.
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Question: Brain-derived neurotrophic factor (BDNF) acts rapidly to modulate synaptic neurotransmission in the brain. Although present in neurons, glial cells, and mucosal cells of the colon, and in higher concentrations than in brain, the action of BDNF in gut have not been characterized. The aim of this study was to identify the role of BDNF in mediating the peristaltic reflex.', 'BDNF and a specific antiserum were examined for their effects on the peristaltic reflex and release of the sensory mediators serotonin and calcitonin gene-related peptide in rat colon. The peristaltic reflex and release of serotonin and calcitonin gene-related peptide were also examined in genetically modified mice (BDNF(+/-)) with reduced levels of BDNF.', 'Endogenous brain-derived neurotrophic factor was released into the sensory compartment in a stimulus-dependent manner during the peristaltic reflex induced by mucosal stimulation but not muscle stretch. BDNF stimulated and immunoneutralization of endogenous BDNF reduced ascending contraction and descending relaxation of circular muscle and release of serotonin and calcitonin gene-related peptide during the peristaltic reflex induced by mucosal stimulation but not muscle stretch. The peristaltic reflex and release of serotonin and calcitonin gene-related peptide during the peristaltic reflex induced by mucosal stimulation but not muscle stretch were significantly reduced in BDNF(+/-) mice.

Answer: Does brain-derived neurotrophic factor augment peristalsis by augmenting 5-HT and calcitonin gene-related peptide release?


Question: Precise long-term assessment of movement and physical function following Achilles tendon rupture is required for the development and evaluation of treatment, including different regimens of physical therapy.', 'To assess intermediate-term (<10 years by conventional thinking) objective measures of physical function following Achilles tendon rupture treated nonsurgically and to compare these with self-reported measures of physical function.', 'Cross-sectional study; Level of evidence, 3.', 'Two to 5 years after Achilles tendon rupture, 9 women and 43 men (mean age, 49.2 years; range, 26-68 years) were assessed by physical examination, performance of 1-legged jumps, and 3-dimensional gait analysis (including calculation of muscle work). Self-reported scores for foot function (Achilles tendon rupture score) and level of physical activity were collected. Twenty age- and sex-matched controls were assessed in the same manner.', 'Physical examination of patients with the knee extended revealed 11.1° of dorsiflexion on the injured side and 9.2° on the uninjured side (P = .020), indicating gastrocnemius muscle lengthening. The 1-legged jump distance was shorter on the injured side (89.5 vs 96.2 cm; P < .001). Gait analysis showed higher peak dorsiflexion (14.3° vs 13.3°; P = .016) and lower concentric (positive) plantar flexor work (16.6 vs 19.9 J/kg; P = .001) in the ankle on the uninjured side. At the same time, eccentric (negative) dorsiflexor work was higher on the injured side (13.2 vs 11.9 J/kg; P = .010). Self-perceived foot function and physical activity were lower in patients than in healthy controls (mean Achilles tendon rupture score, 78.6 and 99.8, respectively).

Answer: Does three-Dimensional Gait Analysis Following Achilles Tendon Rupture With Nonsurgical Treatment reveal Long-Term Deficiencies in Muscle Strength and Function?


Question: Lamin A and C are nuclear filament proteins encoded by the LMNA gene. Mutations in the LMNA gene cause many congenital diseases known as laminopathies, including Emery-Dreifuss muscular dystrophy, Hutchinson-Gilford progeria syndrome, and familial dilated cardiomyopathy (DCM) with conduction disease. A missense mutation (N195K) in the A-type lamins results in familial DCM and sudden arrhythmic death.', 'The purpose of this study was to investigate the ion current mechanism of arrhythmia and DCM caused by the LaminA-N195K variant.', 'A homozygous mouse line expressing the Lmna-N195K mutation (Lmna', 'Both peak and late I

Answer:
Does inhibition of late sodium current attenuate ionic arrhythmia mechanism in ventricular myocytes expressing LaminA-N195K mutation?