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.

Example Input: Prolonged re-exposure to a fear-eliciting cue in the absence of an aversive event extinguishes the fear response to the cue, and has been clinically used as an exposure therapy. Arc (also known as Arg3.1) is implicated in synaptic and experience-dependent plasticity. Arc is regulated by the transcription factor cAMP response element binding protein, which is upregulated with and necessary for fear extinction. Because Arc expression is also activated with fear extinction, we hypothesized that Arc expression is required for fear extinction.', 'Extinction training increased the proportion of Arc-labeled cells in the basolateral amygdala (BLA). Arc was transcribed during latter part of extinction training, which is possibly associated with fear extinction, as well as former part of extinction training. Intra-BLA infusions of Arc antisense oligodeoxynucleotide (ODN) before extinction training impaired long-term but not short-term extinction memory. Intra-BLA infusions of Arc antisense ODN 3h after extinction training had no effect on fear extinction.
Example Output: Does fear extinction require Arc/Arg3.1 expression in the basolateral amygdala?

Example Input: We recently proposed the existence of neurotoxic interactions between the cannabinoid type 1 (CB(1)) receptor and transient receptor potential vanilloid 1 (TRPV1) channels in rat mesencephalic cultures. This study seeks evidence for the mediator(s) and mechanisms underlying the neurotoxic interactions between CB(1) receptors and TRPV1 in vitro and in vivo.', 'The mediator(s) and mechanism(s) for the interactions between CB(1) receptors and TRPV1 were evaluated by cell viability assays, immunocytochemistry, Fura-2 calcium imaging, mitochondrial morphology assay, ELISA and Western blot assay in vitro in neuron-enriched mesencephalic cultures. Injections into the substantia nigra and subsequent cell counts were also used to confirm these interactions in vivo.', 'The neurotoxic interactions were mediated by 12(S)-hydroperoxyeicosatetraenoic acid (12(S)-HPETE), an endogenous TRPV1 agonist. CB(1) receptor agonists (HU210 and WIN55,212-2) increased the level of 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), a downstream metabolite of 12(S)-HPETE, which stimulates TRPV1-mediated death of mesencephalic neurons, both in vitro and in vivo. The neurotoxicity was mediated by increased intracellular Ca(2+) concentration ([Ca(2+)](i)) through TRPV1, consequently leading to mitochondrial damage and was attenuated by baicalein, a 12-lipoxygenase inhibitor.
Example Output: Are interactions between CB ( 1 ) receptors and TRPV1 channels mediated by 12-HPETE cytotoxic to mesencephalic dopaminergic neurons?

Example Input: A patient's baseline health status may affect the ability to survive an acute illness. Emergency medicine research requires tools to adjust for confounders such as comorbid illnesses. The Charlson Comorbidity Index has been validated in many settings but not extensively in the emergency department (ED). The purpose of this study was to examine the utility of the Charlson Index as a predictor of one-year mortality in a population of ED patients with suspected infection.", 'The comorbid illness components of the Charlson Index were prospectively abstracted from the medical records of adult (age older than 18 years) ED patients at risk for infection (indicated by the clinical decision to obtain a blood culture) and weighted. Charlson scores were grouped into four previously established indices: 0 points (none), 1-2 points (low), 3-4 points (moderate), and > or =5 points (high). The primary outcome was one-year mortality assessed using the National Death Index and medical records. Cox proportional-hazards ratios were calculated, adjusting for age, gender, and markers of 28-day in-hospital mortality.', 'Between February 1, 2000, and February 1, 2001, 3,102 unique patients (96% of eligible patients) were enrolled at an urban teaching hospital. Overall one-year mortality was 22% (667/3,102). Mortality rates increased with increasing Charlson scores: none, 7% (95% confidence interval [CI] = 5.4% to 8.5%); low, 22% (95% CI = 19% to 24%); moderate, 31% (95% CI = 27% to 35%); and high, 40% (95% CI = 36% to 44%). Controlling for age, gender, and factors associated with 28-day mortality, and using the "none" group as a reference group, the Charlson Index predicted mortality as follows: low, odds ratio of 2.0; moderate, odds ratio of 2.5; and high, odds ratio of 4.7.
Example Output:
Is charlson Index associated with one-year mortality in emergency department patients with suspected infection?