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

Input: Consider Input: Nowadays they are giving homework even during the holidays and I hate that very much. But I think there is a reason for it. Homework is given so that we can remember whatever we have learnt. Regular drilling and repetition make perfect. But teachers have started to give too much homework. Anything in excess is bad. Jane What's the use of just homework without allowing children to get an insight into the subject? It just makes them bookworms but nothing else. Homework such as writing some things 5 times at home will just make them memorize things but not put them into use. I regret to say that teachers find it easy to bundle the children with homework rather than making them get interested to understand what they learn. The same trend continues even in college. I find that most of the so-called high scorers are unable to answer simple things in an interview. Sally It is OK to give homework. But it should be given less. We are spending most of our time in school and at least we must be free in our home. If you give homework, we will be very tired and we wouldn't be able to pay attention to extra-curricular activities, which in turn may affect our physical and mental health. So please give less homework to us. Johnson It is part of our work to give students homework. There will be some punishments if we won't do our work. So I have to do that though I know such a teacher is not liked by students.

Output: Who thinks homework should help students learn something practical?


Input: Consider Input: 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.

Output: What is the target of tanezumab?


Input: Consider Input: The plasma membrane Na(+)/Ca(2+) exchanger (NCX) is a bidirectional ion transporter that couples the translocation of Na(+) in one direction with that of Ca(2+) in the opposite direction. This system contributes to the regulation of intracellular Ca(2+) concentration via the forward mode (Ca(2+) efflux) or the reverse mode (Ca(2+) influx). We have previously demonstrated that the Ca(2+) paradox, an in vitro reperfusion model, causes the sustained activation of the reverse mode of the NCX, the disruption of Ca(2+) homeostasis, and subsequent delayed apoptotic-like death in astrocytes. In addition, we found that the nitric oxide (NO)-cyclic GMP signaling pathway inhibits Ca(2+) paradox-mediated astrocyte apoptosis, while a high concentration of NO induces cytotoxicity. In this way, Ca(2+) and NO may work together in the pathogenesis of several cells in the central nervous system. Concerning the role of NCX in NO cytotoxicity, we have found, using the specific inhibitor of NCX 2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline (SEA0400), that NCX is involved in NO-induced cytotoxicity in cultured microglia, astrocytes, and neuronal cells. This review summarizes the pathological roles of the NCX as a new target for NO-mediated cellular toxicity, based on our studies on NO-NCX-mediated glial toxicity.


Output: The small molecule SEA0400 is an inhibitor of which ion antiporter/exchanger?


