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: Mice with functional ablation of the neurokinin-1 receptor gene (NK1R(-/-)) display behavioural abnormalities which resemble the hyperactivity, inattention and impulsivity seen in Attention Deficit Hyperactivity Disorder (ADHD). Here, we investigated whether the established ADHD treatment, atomoxetine, alleviates these abnormalities when tested in the light/dark exploration box (LDEB) and 5-Choice Serial Reaction-Time Task (5-CSRTT).', 'Separate cohorts of mice were tested in the 5-CSRTT and LDEB after treatment with no injection, vehicle or atomoxetine (5-CSRTT: 0.3, 3 or 10mg/kg; LDEB: 1, 3 or 10mg/kg).', 'Atomoxetine reduced the hyperactivity displayed by NK1R(-/-) mice in the LDEB at a dose (3mg/kg) which did not affect the locomotor activity of wildtypes. Atomoxetine (10mg/kg) also reduced impulsivity in NK1R(-/-) mice, but not wildtypes, in the 5-CSRTT. No dose of drug affected attention in either genotype.
Answer: This evidence that atomoxetine reduces hyperactive/impulsive behaviours in NK1R(-/-) mice consolidates the validity of using NK1R(-/-) mice in research of the aetiology and treatment of ADHD.

Ex Output:
Does atomoxetine reduce hyperactive/impulsive behaviours in neurokinin-1 receptor 'knockout ' mice?


Ex Input:
Context: Vessel formation is a crucial event in tissue repair after injury. Thus, one assumption of innovative therapeutic approaches is the understanding of its molecular mechanisms. Notwithstanding our knowledge of the role of Protein Kinase C epsilon (PKCε) in cardio-protection and vascular restenosis, its role in vessel progenitor differentiation remains elusive.', 'Given the availability of PKCε pharmacological modulators already tested in clinical trials, the specific aim of this study is to unravel the role of PKCε in vessel progenitor differentiation, with implications in vascular pathology and vasculogenesis.', 'Mouse Peri-Vascular Adipose Tissue (PVAT) was used as source of mesenchymal vessel progenitors. VEGF-induced differentiation of PVAT cells down-regulates both PKCε and p-PAK1 protein expression levels. PKCε overexpression and activation: i) reduced the expression levels of SMA and PECAM in endothelial differentiation of PVAT cells; ii) completely abrogated tubules formation in collagen gel assays; iii) increased the expression of p-PAK1.
Answer: PKCε negatively interferes with vessel progenitor differentiation via interaction with PAK-1.

Ex Output:
Is pKCε a negative regulator of PVAT-derived vessel formation?


Ex Input:
Context: Low serum levels of vitamin D have been associated with depression in non-stroke subjects. Our aim was to examine the possible association between serum vitamin D levels and the development of post-stroke depression (PSD).', 'In total, 189 patients with acute ischaemic stroke were consecutively recruited. Serum levels of 25-hydroxyvitamin D [25(OH)D] were measured by competitive protein-binding assay within 24 h after admission. The 17-item Hamilton Depression Scale was used for screening for the existence of depressive symptoms at 1 month after stroke. Patients with a Hamilton Depression Scale score of ≥7 were given the Structured Clinical Interview of the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, for diagnosis of PSD. Meanwhile, 100 healthy control subjects were also recruited and underwent measurement of 25(OH)D.', 'Fifty-five patients (29.1%) were diagnosed as having PSD at 1 month. Serum vitamin D levels within 24 h after admission were significantly lower in both non-PSD patients and PSD patients than in normal controls. PSD patients had significantly lower vitamin D than non-PSD patients. Serum vitamin D levels (≤37.1 and ≥64.1 nmol/l) were independently associated with the development of PSD (odds ratio 8.824, 95% confidence interval 2.011-38.720, P = 0.004, and odds ratio 0.127, 95% confidence interval 0.022-0.718, P = 0.020, respectively).
Answer: Serum vitamin D levels within 24 h after admission are found to be associated with PSD and may predict its development at 1 month post-stroke.

Ex Output:

Are low serum levels of vitamin D associated with post-stroke depression?