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

Q: 1. In order to investigate the biological function of the human CLN3 gene that is defective in Batten disease, we created a yeast strain by PCR-targeted disruption of the yeast gene (YHC3), which is a homologue of the human CLN3 gene. 2. The phenotypic characterization revealed that the yhc3 delta mutants are more sensitive to combined heat and alkaline stress than the wild-type strains as determined by inhibition of cell proliferation. 3. This suggests that the yhc3 delta mutant is a good model to investigate the biological function of human CLN3 gene in mammalian cells and to understand the pathophysiology of juvenile Batten disease.

A: What is the effect of a defective CLN3 gene?
****
Q: The fourteenth week of the season featured a game between 5-7 teams as the Washington Redskins visited Soldier Field. In 48 games, the Redskins led the series 24-23-1 and had won the last five meetings. The Chicago offense took on a Washington defense that excelled against passers, being ranked tenth in the category; Dashon Goldson led all defensive backs in tackles with 95, while Bashaud Breeland led the team in passes defended with 13. The Redskins defensive rush, which had 20 sacks in 2015, was led by Ryan Kerrigan, who has 6.5. Despite such performances, the Redskins rush defense was ranked 29th in yards per carry with 4.64 and 25th in average rushing yards at 124.2. Jeff Joniak writes that the Bears could exploit this with the three-man rushing attack of Matt Forte, Jeremy Langford, and Ka'Deem Carey. On defense, the Bears faced a Kirk Cousins-led offense that focuses on quick passes; Cousins completed a league-high 68.6 percent of his passes, with 7.1 yards per pass. One of Cousins' main targets was tight end Jordan Reed, who scored six touchdowns and led the Redskins in yards after the catch. Rankings-wise, the pass attack was ranked 17th in the league in passing yards per game and 16th for yards per play. Joniak states that the Bears had to force turnovers, and an area was on third down, as five of Cousins' interceptions had been on third down. The Bears won the coin toss and elected to defer. Washington recorded a 15-play, 80-yard drive en route to scoring on Alfred Morris' one-yard touchdown run. After the Bears punted, the Redskins scored again with Cousins' fake read option leading to a three-yard touchdown run in the second quarter. Chicago's woes continued when the offense began the next drive on their own seven-yard line, and despite reaching the Washington 49, Jay Cutler was strip-sacked by Trent Murphy, who recovered the fumble. The Redskins failed to capitalize on the turnover and punted; the following two drives also ended with punts. With 52 seconds left in the first half, the Bears took over at their own 42, and managed to score with 18 seconds left when Cutler threw a 20-yard touchdown pass to Alshon Jeffery. Cousins kneeled once to end the half. After the Bears punted on the first drive of the second half, Cousins threw a five-yard touchdown pass to Reed. The Bears responded with Cutler's nine-yard touchdown pass to Zach Miller, who managed to escape DeAngelo Hall and made contact with Goldson as he reached the endzone. The score was the Bears' first third quarter touchdown of 2015. Afterwards, Cousins' pass for Pierre Garcon was intercepted by Kyle Fuller, and the Bears took advantage with Forte's seven-yard touchdown run to tie the score. Dustin Hopkins gave the Redskins the 24-21 lead on the first drive of the final quarter with a 47-yard field goal. Five drives later, the Bears attempted a 50-yard field goal with 1:40 left in the game. However, Robbie Gould's kick sailed wide left, and the Redskins ran the ball three times to end the game.

A: Who scored the first touchdown of the game?
****
Q: Disease patterns in RA vary between the sexes; the condition is more commonly seen in women, who exhibit a more aggressive disease and a poorer long-term outcome. Men, however, are more likely than women to die from extra-articular complications of rheumatoid disease. This chapter discusses the outcome and mortality studies that substantiate these conclusions and then examines the possible mechanisms that may account for them, including the HLA system, seropositivity, compliance, response to therapy and pain threshold. In particular, sex and sex hormones emerge as independent risk factors in rheumatoid disease. The epidemiological evidence points towards a peak age of onset of RA at the time of the menopause in women and towards later in life in men. Premenopausal women may fare better than postmenopausal women with RA. The possible protective effects of the oral contraceptive pill and the dramatic amelioration with pregnancy are well documented. In vivo and in vitro studies have demonstrated that sex hormones interfere with a number of the putative processes involved in the pathogenesis of RA, including immunoregulation, interaction with inflammatory mediators and the cytokine system, and direct effects on cartilage itself. All these observations point towards the importance of gonadal hormones. However, trials on the potential therapeutic use of sex hormones in RA are limited and, as yet, disappointing. Further work is necessary to determine whether the roles of sex hormones are as central protagonists or just supporting cast in the complex arena of rheumatoid disease.

A:
Is Rheumatoid Arthritis more common in men or women?
****