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.

Example Input: Context: Mutations of the caspase-activating recruitment domain 15 (CARD15) gene on chromosome 16 are associated with chronic inflammatory granulomatous bowel disease (Crohn's disease). Sarcoidosis is a systemic granulomatous disease with unknown etiology, which shares histological features with Crohn's disease.", 'To evaluate whether ethnic Danes with sarcoidosis have an increased frequency of CARD15 mutations compared to healthy control subjects.', 'Genotyping for CARD15 mutations R702W, G908R, and L1007fsinsC, also designated single nucleotide polymorphism (SNP) SNP8, SNP12 and SNP13, respectively, were performed by capillary electrophoresis single-strand confirmation polymorphism in 53 patients with histologically verified sarcoidosis and in 103 healthy controls.', 'The frequencies of CARD15 mutations in sarcoidosis patients were: SNP8, 4/106 chromosomes (3.8%); SNP12, 2/106 chromosomes (1.9%); SNP13, 2/106 chromosomes (1.9%); SNP8+SNP12+SNP13, 8/106 chromosomes (7.6%). All 8 patients were heterozygous. The frequencies in controls were: SNP8, 9/206 chromosomes (4.4%); SNP12, 2/206 chromosomes (1.0%); SNP13, 4/206 chromosomes (1.9%); SNP8+SNP12+SNP13, 15/206 chromosomes (7.3%). All controls were heterozygous. The differences were not statistically significant (p>0.05). Furthermore, the course of disease was not significantly different in the 8 patients with CARD15 mutations and the 45 patients without mutations.
Answer: The frequency of CARD15 mutations is not increased in ethnic Danish patients with sarcoidosis, and heterozygosity for such mutations apparently has no influence on the course of disease.
Example Output: Are cARD15 single nucleotide polymorphisms 8 , 12 and 13 increased in ethnic Danes with sarcoidosis?

Example Input: Context: To conduct clinical and genetic studies in a European family with autosomal dominant Stargardt-like macular dystrophy (adSTGD-like MD) and to investigate the functional consequences of a novel ELOVL4 mutation.', 'Ophthalmic examination and mutation screening by direct sequencing of the ELOVL4 gene was performed in two affected individuals. Wild-type and mutant ELOVL4 genes were expressed as enhanced green fluorescent protein (EGFP) fusion proteins in transient transfection in NIH-3T3 and HEK293 cells. To determine the subcellular localization of ELOVL4, an endoplasmic-reticulum (ER)-specific marker for pDsRed2-ER was cotransfected with ELOVL4 constructs. Transfected cells were viewed by confocal microscopy. Western blot analysis was performed to assess protein expression using an anti-GFP antibody.', 'Affected patients exhibited macular atrophy with surrounding flecks characteristic of adSTGD-like MD. A novel ELOVL4 p.Tyr270X mutation was detected in affected individuals. In cell-transfection studies, wild-type ELOVL4 localized preferentially to the ER. In contrast, the mutant protein appeared to be mislocalized within transfected cells.
Answer: In a European family with adSTGD-like MD, a novel ELOVL4 mutation was found to underlie the disorder. Transfection studies indicated that, unlike wild-type ELOVL4, the mutant protein does not localize to the ER but rather appears to be sequestered elsewhere in an aggregated pattern in the cytoplasm. Further analysis of the function of normal and mutant ELOVL4 will provide insight into the mechanism of macular degeneration.
Example Output: Does a novel mutation in the ELOVL4 gene cause autosomal dominant Stargardt-like macular dystrophy?

Example Input: Context: Postictal inhibition (PI) is a decrease in excitability that follows an epileptic seizure and decreases probability of new seizure occurrence. PI may involve both increased inhibition and persisting elevated excitation. Our experiments tested whether shorter trains of weak stimuli are able to unmask this residual increase of excitability during the PI.', 'Four epileptic afterdischarges (ADs) were evoked by intense electrical stimulation (20 s, 8 Hz, current intensity at 5x threshold) of the neocortex in two groups (A, B) of Wistar rats. Before the first AD and during the 10-min interictal period, 8-Hz trains of four weak pulses (half of the intensity used for the AD triggering; 4P) were applied every 20 s in group B and a single pulse with similar parameters in group A.', 'The number of interictal epileptiform events evoked by 4P in the group B was significantly higher than that in the group A (evoked by single pulses) except after the second AD. Epileptic events were triggered by 4P also immediately after the AD termination.
Answer: It is apparent that weak stimulation can trigger epileptic phenomena during PI. Our results indicate that it is no longer possible to perceive PI only as persisting extreme and active inhibition. An appropriate stimulation can reveal more subtle (but important) excitatory events contributing to the functional status during the postictal period.
Example Output:
Do short bursts of weak pulses break postictal inhibition in the neocortex of Wistar rats?