In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
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Question: Context: To demonstrate the effect in vivo of the myocilin gene mutation Thr377Met on outflow facility of aqueous humor, as measured by tonography.', 'Forty-two members of a pedigree known to carry the Thr377Met mutation were examined for glaucoma, evaluated with tonography, and screened for myocilin mutations. Tonography was used to calculate the coefficient of aqueous outflow facility (C), as well as the ratio of the resting intraocular pressure to C (P(0)/C). Subjects were reexamined for glaucoma 5 years after tonography.', "Seven subjects were excluded because of previous treatment known to alter facility of aqueous outflow. The mean outflow facility of the eyes of the 12 subjects carrying the Thr377Met mutation was significantly reduced compared with the 23 non-carriers' eyes using both C (P<0.001) and P(0)/C (P<0.001). Reduced outflow facility was also demonstrated in those mutation carriers who were not yet expressing clinical signs of glaucoma or ocular hypertension when measured using C (P = 0.015) and P(0)/C (P = 0.001). After 5 years, progression towards glaucoma had occurred in 5 of the myocilin mutation-carriers, 2 of whom showed bilateral progression; 3 carriers remained completely normal. Four subjects had bilateral glaucoma at the outset and remained unchanged. The carriers' eyes that progressed towards glaucoma had reduced outflow facility compared with those that remained normal, although the difference was not statistically significant.\Question: Does tonography demonstrate reduced facility of outflow of aqueous humor in myocilin mutation carriers?

Answer: Carriers of the myocilin Thr377Met mutation have reduced outflow facility, which may be detected prior to developing glaucoma. Tonography was not seen to be clinically useful in predicting progression towards glaucoma.

Question: Context: The aim of this study was to examine the efficacy and surgical success rates of amniotic membrane (AM) transplantation performed for corneal perforation closure using a novel technique.', 'This study included 6 eyes from 6 patients with corneal perforation who had received AM transplantation between May 2011 and April 2012. The AM was collected from human placenta shortly after cesarean section. In surgery, the AM was folded into pleats and used to plug the wound using 10-0 nylon suture. The wound was then covered with an AM seal. After reepithelialization and AM scarring, sutures were removed.', 'All 6 patients had successful wound closure with 1 surgery. One patient underwent optical keratoplasty later, and 1 patient required combined preserved sclera transplantation. The absolute value of astigmatism decreased to <3.50 diopters (D) 3 months after surgery and to <3.00 D 6 months after surgery in patients with peripheral AM transplants. The visual acuity gradually improved over the first 3 months after surgery, and visual acuity gains were maintained at the 6-month postoperative mark.\Question: Do '' Pleats fold '' technique of amniotic membrane transplantation for management of corneal perforations?

Answer: The AM transplantation procedure may be an effective option for treating corneal perforations when the wound is circular or irregular, except for incised wounds. Our "Pleats Fold" AM transplantation technique can achieve definite closure and effectively repair wounds of various sizes. Postoperative astigmatic values were acceptable. Therefore, we recommend this procedure for repairing lesions <3 mm in diameter that do not involve the central cornea and that are infection free.

Question: Context: Acute lung injury (ALI) induced by excessive hyperoxia has been employed as a model of oxidative stress imitating acute respiratory distress syndrome. Under hyperoxic conditions, overloading quantities of reactive oxygen species (ROS) are generated in both lung epithelial and endothelial cells, leading to ALI. Some NADPH oxidase (NOX) family enzymes are responsible for hyperoxia-induced ROS generation in lung epithelial and endothelial cells. However, the molecular mechanisms of ROS production in type II alveolar epithelial cells (AECs) and ALI induced by hyperoxia are poorly understood.', 'In this study, we show that dual oxidase 2 (DUOX2) is a key NOX enzyme that affects hyperoxia-induced ROS production, particularly in type II AECs, leading to lung injury. In DUOX2 mutant mice (DUOX2(thyd/thyd)) or mice in which DUOX2 expression is knocked down in the lungs, hyperoxia-induced ALI was significantly lower than in wild-type (WT) mice. DUOX2 was mainly expressed in type II AECs, but not endothelial cells, and hyperoxia-induced ROS production was markedly reduced in primary type II AECs isolated from DUOX2(thyd/thyd) mice. Furthermore, DUOX2-generated ROS are responsible for caspase-mediated cell death, inducing ERK and JNK phophorylation in type II AECs.', 'To date, no role for DUOX2 has been defined in hyperoxia-mediated ALI despite it being a NOX homologue and major ROS source in lung epithelium.\Question: Is dual oxidase 2 in lung epithelia essential for hyperoxia-induced acute lung injury in mice?

Answer:
Here, we present the novel finding that DUOX2-generated ROS induce AEC death, leading to hyperoxia-induced lung injury.