Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Coming off their divisional road win over the Dolphins, the Jets flew to Ralph Wilson Stadium for a Week 4 AFC East duel with the throwback-clad Buffalo Bills. New York scored in the first quarter as running back LaDainian Tomlinson got a 1-yard touchdown run. The Jets added onto their lead in the second quarter with a 19-yard field goal from kicker Nick Folk, followed by quarterback Mark Sanchez completing a 41-yard touchdown pass to wide receiver Braylon Edwards. The Bills closed out the half with quarterback Ryan Fitzpatrick finding tight end David Martin on a 4-yard touchdown pass. New York pulled away in the third quarter as tight end Dustin Keller caught a 3-yard touchdown pass from wide receiver/quarterback Brad Smith, followed by his 2-yard touchdown reception thrown by Sanchez. Afterwards, Tomlinson's 26-yard touchdown run effectively secured the victory. Buffalo closed out the game in the fourth quarter as Fitzpatrick threw a touchdown pass to wide receiver Steve Johnson.
Which player scored multiple touchdowns?

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a small vessel disease of the brain caused by mutations in the NOTCH3 gene. CADASIL progresses, in some cases, to subcortical dementia with a particular cognitive impairment. Different diseases in the dementia spectrum share a central cholinergic and sensorimotor plasticity alteration. We aimed to study different intracortical circuits and sensorimotor plasticity in CADASIL patients using transcranial magnetic stimulation protocols, and to determine whether these characteristics correlated with the results of clinical neuropsychological evaluation. Ten CADASIL patients and 10 healthy subjects were included in the study. All subjects underwent a transcranial magnetic stimulation study examining different intracortical circuits. Sensorimotor plasticity was also assessed using a paired associative stimulation and extensive neuropsychological tests. CADASIL patients showed a lack of intracortical facilitation, short latency afferent inhibition and sensorimotor plasticity when compared with control subjects. CADASIL patients also showed an altered neuropsychological profile. Correlation between sensorimotor plasticity and neuropsychological alterations was observed in CADASIL patients. These results suggest that acetylcholine and glutamate could be involved in the dementia process in CADASIL and that abnormal sensorimotor plasticity correlates with the neuropsychological profile in CADASIL patients.
Which gene is involved in CADASIL?

Acute lung injury is a life-threatening condition characterized by surfactant dysfunction and raised secretory phospholipase A2 (sPLA2) activity. Varespladib is a sPLA2 inhibitor shown to be effective in animal models of acute lung injury. We aimed at investigating the effect of co-administration of surfactant and varespladib on sPLA2 activity. Alveolar macrophages were cultured and stimulated with lipopolysaccharide and then treated with either varespladib, surfactant, varespladib followed by surfactant or nothing. sPLA2 activity, free fatty acids, tumour necrosis factor- (TNF-) and protein concentrations were measured in culture supernatants. Treatment with varespladib (p=0.019) and varespladib + surfactant (p=0.013), reduced the enzyme activity by approximately 15% from the basal level measured in the untreated cultures. Surfactant, varespladib and varespladib + surfactant, respectively decreased free fatty acids by -45% (p=0.045), - 62% (p=0.009) and -48% (p=0.015), from the baseline concentration of the untreated cultures. Varespladib and poractant- co-administration reduces sPLA2 activity and free fatty acids release in cultured rat alveolar macrophages, although a clear drug synergy was not evident. Since co-administration may be useful to reduce inflammation and surfactant inactivation in acute lung injury, further in vivo studies are warranted to verify its clinical usefulness.

Which enzyme is inhibited by Varespladib?