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.

Q: Context: Week 10 featured the top-ranked defenses (by yardage against) in each conference, as the Lions hosted the Dolphins. Detroit got off to a quick start. Matt Prater kicked a 26-yard field goal on the opening drive of the game. Later in the first quarter, Calvin Johnson, playing in his first game since Week 5, caught a 49-yard TD pass from Matthew Stafford for a 10-0 lead. Miami managed a 23-yard Caleb Sturgis field goal before halftime, making the score 10-3. The Dolphins took the lead in the third, starting with a 50-yard Stugis field goal. Next, Earl Mitchell blocked Prater's 42-yard field goal attempt, and Dion Jordan returned the ball to the Lions 3-yard line. On the next play, Ryan Tannehill connected with Mike Wallace for the touchdown, putting Miami ahead, 13-10. Prater made good on a 50-yard field goal early in the fourth quarter to knot the score at 13-13, but Sturgis' 20-yarder put Miami back on top by 3. As in the previous two games, the Lions had to rally on their final drive to win the game. Starting at their own 26 with 3:13 left in the game, the drive culminated with Stafford's 11-yard touchdown pass to Theo Riddick, putting the Lions ahead for good, 20-16. This was the third straight game in which the Lions trailed at the two-minute warning, then went ahead on their final drive. It was the second time in a month that Miami had lost a game in the final seconds, following a Week 7 loss to Green Bay in which the final touchdown was scored with 3 seconds remaining. According to STATS Inc., this is the first time Detroit has started a season 7-2 since 1993. 
 Question: Which player threw the last touchdown pass of the game?

A: matthew stafford
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Q: Context: In the present study, we tested the hypothesis that having migraine in middle age is related to late-life parkinsonism and a related disorder, restless legs syndrome (RLS), also known as Willis-Ekbom disease (WED). The AGES-Reykjavik cohort (born 1907-1935) has been followed since 1967. Headaches were classified based on symptoms assessed in middle age. From 2002 to 2006, 5,764 participants were reexamined to assess symptoms of parkinsonism, diagnosis of Parkinson disease (PD), family history of PD, and RLS/WED. Subjects with midlife migraine, particularly migraine with aura (MA), were in later life more likely than others to report parkinsonian symptoms (odds ratio [OR]MA = 3.6 [95% CI 2.7-4.8]) and diagnosed PD (ORMA = 2.5 [95% CI 1.2-5.2]). Women with MA were more likely than others to have a parent (ORMA = 2.26 [95% CI 1.3-4.0]) or sibling (ORMA = 1.78 [95% CI 1.1-2.9]) with PD. Late-life RLS/WED was increased for headache generally. Associations were independent of cardiovascular disease and MRI-evident presumed ischemic lesions. These findings suggest there may be a common vulnerability to, or consequences of, migraine and multiple indicators of parkinsonism. Additional genetic and longitudinal observational studies are needed to identify candidate pathways that may account for the comorbid constellation of symptoms. 
 Question: Willis-Ekbom disease is also known as?

A: restless legs syndrome
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Q: Context: SEA0400 is a selective inhibitor of the Na(+)/Ca(2+) exchanger having equal potencies to suppress both the forward and reverse mode operation of the Na(+)/Ca(2+) exchanger. Present experiments were designed to study the effect of partial blockade of Na(+)/Ca(2+) exchanger on Ca(2+) handling in isolated rat ventricular myocytes. Intracellular Ca(2+) transient and cell shortening were measured in ventricular myocytes loaded with Fura-2-AM fluorescent dye. Partial blockade of Na(+)/Ca(2+) exchanger was induced by superfusion of the cells with SEA0400 at a concentration of 0.3 microM. Amplitude of the intracellular Ca(2+) transient and cell shortening was significantly increased by SEA0400 in both field stimulated and voltage clamped myocytes, without significant elevation of diastolic Ca(2+) level and the decay time constant of the Ca(2+) transient. In patch clamped myocytes the SEA0400 induced increase in the Ca(2+) transient and cell shortening was accompanied by significant reduction of peak L-type Ca(2+) current. These effects can be explained by the autoregulative nature of cardiac Ca(2+) handling, as the reduced Ca(2+) efflux from the cell results in an increased Ca(2+) load to the sarcoplasmic reticulum leading to increased Ca(2+) release, which in turn may decrease the L-type Ca(2+) current by accelaration of Ca(2+) dependent inactivation of L-type Ca(2+) current. Our results suggest that complex changes in the Ca(2+) cycling can occur after selective pharmacological inhibition of the Na(+)/Ca(2+) exchanger. 
 Question: The small molecule SEA0400 is an inhibitor of which ion antiporter/exchanger?

A:
na(+)/ca(2+) exchanger
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