Given a question and a context passage, generate the answer having the word or phrase from the context passage. Here, the answer should be a shortest continous span from the passage.

Input: Consider Input: Context: Coming off their bye week, the Lions played a Week 5 Black and Blue Division duel at home with the Chicago Bears. In the first quarter, Detroit trailed early as Bears kicker Robbie Gould got a 37-yard field goal. In the second quarter, the Lions continued to trail as QB Kyle Orton completed a 9-yard TD pass to RB Matt Forte and a 12-yard TD pass to WR/KR Devin Hester. In the third quarter, Chicago continued its domination as Forte got a 1-yard TD run, and CB Charles Tillman returned an interception 26 yards for a touchdown. Afterwards, Detroit got its only score of the game as rookie RB Kevin Smith scored on a 12-yard TD run. In the fourth quarter, the Bears sealed the win when Gould nailed a 45-yard field goal.
Question: How was the ball received ending in the longest touchdown run?

Output: interception

Input: Consider Input: Context: Mutations in the solute carrier family 9, subfamily A member 6 (SLC9A6) gene, encoding the endosomal Na+/H+ exchanger 6 (NHE6) are associated with Christianson syndrome, a syndromic form of X-linked intellectual disability characterized by microcephaly, severe global developmental delay, autistic behavior, early onset seizures and ataxia. In a 7-year-old boy with characteristic clinical and neuroimaging features of Christianson syndrome and epileptic encephalopathy with continuous spikes and waves during sleep, we identified a novel splice site mutation (IVS10-1G>A) in SLC9A6. These findings expand the clinical spectrum of the syndrome and indicate NHE6 dysfunction as a new cause of electrical status epilepticus during slow-wave sleep (ESES).
Question: Mutation of which gene is implicated in the Christianson syndrome?

Output: slc9a6

Input: Consider Input: Context: One of the major histopathological hallmarks of Alzheimer's disease (AD) is cerebral deposits of extracellular -amyloid peptides. Preclinical studies have pointed to glucagon-like peptide 1 (GLP-1) receptors as a potential novel target in the treatment of AD. GLP-1 receptor agonists, including exendin-4 and liraglutide, have been shown to promote plaque-lowering and mnemonic effects of in a number of experimental models of AD. Transgenic mouse models carrying genetic mutations of amyloid protein precursor (APP) and presenilin-1 (PS1) are commonly used to assess the pharmacodynamics of potential amyloidosis-lowering and pro-cognitive compounds. In this study, effects of long-term liraglutide treatment were therefore determined in two double APP/PS1 transgenic mouse models of Alzheimer's disease carrying different clinical APP/PS1 mutations, i.e. the 'London' (hAPPLon/PS1A246E) and 'Swedish' mutation variant (hAPPSwe/PS1E9) of APP, with co-expression of distinct PS1 variants. Liraglutide was administered in 5 month-old hAPPLon/PS1A246E mice for 3 months (100 or 500 ng/kg/day, s.c.), or 7 month-old hAPPSwe/PS1E9 mice for 5 months (500 ng/kg/day, s.c.). In both models, regional plaque load was quantified throughout the brain using stereological methods. Vehicle-dosed hAPPSwe/PS1E9 mice exhibited considerably higher cerebral plaque load than hAPPLon/PS1A246E control mice. Compared to vehicle-dosed transgenic controls, liraglutide treatment had no effect on the plaque levels in hAPPLon/PS1A246E and hAPPSwe/PS1E9 mice. In conclusion, long-term liraglutide treatment exhibited no effect on cerebral plaque load in two transgenic mouse models of low- and high-grade amyloidosis, which suggests differential sensitivity to long-term liraglutide treatment in various transgenic mouse models mimicking distinct pathological hallmarks of AD.
Question: Which disease the London mutation involved in?
Output: alzheimer's disease