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: Sedimentary rocks follow certain rules. 1. Sedimentary rocks are formed with the oldest layers on the bottom and the youngest on top. 2. Sediments are deposited horizontally, so sedimentary rock layers are originally horizontal, as are some vol- canic rocks, such as ash falls. 3. Sedimentary rock layers that are not horizontal are deformed. Since sedimentary rocks follow these rules, they are useful for seeing the effects of stress on rocks. Sedimentary rocks that are not horizontal must have been deformed. You can trace the deformation a rock has experienced by seeing how it differs from its original horizontal, oldest- on-bottom position. This deformation produces geologic structures such as folds, joints, and faults that are caused by stresses. Youre standing in the Grand Canyon and you see rocks like those in the Figure 1.1. Using the rules listed above, try to figure out the geologic history of the geologic column. The Grand Canyon is full mostly of sedimentary rocks, which are important for deciphering the geologic history of a region. In the Grand Canyon, the rock layers are exposed like a layer cake. Each layer is made of sediments that were deposited in a particular environment - perhaps a lake bed, shallow offshore region, or a sand dune. (a) The rocks of the Grand Canyon are like a layer cake. (b) A geologic column showing the rocks of the Grand Canyon. In this geologic column of the Grand Canyon, the sedimentary rocks of groups 3 through 6 are still horizontal. Group 2 rocks have been tilted. Group 1 rocks are not sedimentary. The oldest layers are on the bottom and youngest are on the top. The ways geologists figure out the geological history of an area will be explored more in the chapter Earth History. Click image to the left or use the URL below. URL:
Question: the classic location to see layer cake geology is

Output: the grand canyon

Input: Consider Input: Context: It is unanimously accepted that there is an unmet need for pain medications that are both effective and safe. Unfortunately, no really novel analgesics have been approved over the past three decades. In view of both experimental and clinical evidence of a major role for nerve growth factor (NGF) in the generation and maintenance of a wide range of pain states, drug discovery efforts focusing on the development of anti-NGF agents have aroused particular interest. Several humanized anti-NGF monoclonal antibodies (mAbs) have entered clinical trials as potential analgesics. In this respect, tanezumab is at an advanced stage of clinical development while fulranumab, fasinumab and ABT-110, previously known as PG110, are in early phases of clinical development. This Current Opinion article aims at describing the rationale for targeting NGF for pain, reviewing the analgesic efficacy and safety of anti-NGF agents based on data from fully published studies, conference abstracts, and the US Food and Drug Administration (FDA) website, and discussing the possible future of these agents in managing chronic pain. Anti-NGF mAbs produced significant pain relief and functional improvement in patients with osteoarthritis of the knee and/or hip. Conversely, studies in non-specific lower back pain generated mixed results; overall, this condition appeared to be less responsive to anti-NGF agents than osteoarthritis. Finally, there was no conclusive evidence of the effectiveness of anti-NGF mAbs in some types of chronic visceral or neuropathic pain. Furthermore, these studies raised safety concerns about anti-NGF mAbs. As a class, these drugs may cause or worsen peripheral neuropathies. But the most problematic issue-which prompted the FDA to place studies of these compounds on clinical hold in 2010-was rapid joint destruction leading to joint replacement surgery. The aetiologies of these side effects have been much debated and their pathophysiology is poorly understood. After an Arthritis Advisory Committee meeting held in March 2012, pharmaceutical companies negotiated with the FDA on the conditions for restarting clinical studies. Although the FDA lifted its clinical hold, there remain many unresolved issues about the long-term efficacy and safety of anti-NGF mAbs. While acknowledging that the future of these drugs is unforeseeable, it appears that they may not be the safe and effective painkillers that have been awaited for decades.
Question: What is the target of tanezumab?

Output: ngf

Input: Consider Input: Context: Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Contrary to that of its phagocyte counterpart NOX2, the molecular basis of NOX1 regulation is not clear. Because NOXO1 lacks the phosphorylated region found in its homolog p47(PHOX), the current view is that NOX1 activation occurs without NOXO1 phosphorylation. Here, however, we demonstrate that phorbol myristate acetate (PMA) stimulates NOXO1 phosphorylation in a transfected human embryonic kidney (HEK) 293 epithelial cell model via protein kinase C and identify Ser-154 as the major phosphorylated site. Endogenous NOXO1 from T84 colon epithelial cells was also phosphorylated, suggesting that NOXO1 phosphorylation is physiologically relevant. In transfected HEK-293 cells, PMA-induced phosphorylation on Ser-154 enhanced NOXO1 binding to NOXA1 (+97%) and to the p22(PHOX) C-terminal region (+384%), increased NOXO1 colocalization with p22(PHOX), and allowed optimal ROS production by NOX1 as demonstrated by the use of S154A and S154D mutants compared with that by wild-type NOXO1 (P<0.05). Pulldown experiments revealed that phos-phorylation on Ser-154 was sufficient to markedly enhance NOXO1 binding to NOXA1, which in turn acts as a molecular switch, allowing optimal interaction of NOXO1 with p22(PHOX). This study unexpectedly revealed that full assembly and activation of NOX1 is a tightly regulated process in which NOXO1 phosphorylation on Ser-154 is the initial trigger.
Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nadph oxidase 1