PMC:5623723 / 2202-3393 JSONTXT

{"project":"2_test","denotations":[{"id":"29021742-11459428-32379562","span":{"begin":90,"end":94},"obj":"11459428"},{"id":"29021742-6149259-32379563","span":{"begin":375,"end":379},"obj":"6149259"},{"id":"29021742-7905600-32379564","span":{"begin":403,"end":407},"obj":"7905600"},{"id":"29021742-1678302-32379565","span":{"begin":552,"end":556},"obj":"1678302"},{"id":"29021742-10541229-32379566","span":{"begin":573,"end":577},"obj":"10541229"},{"id":"29021742-11730442-32379567","span":{"begin":594,"end":598},"obj":"11730442"},{"id":"29021742-12849400-32379568","span":{"begin":623,"end":627},"obj":"12849400"},{"id":"29021742-8408318-32379569","span":{"begin":720,"end":724},"obj":"8408318"},{"id":"29021742-9519265-32379570","span":{"begin":740,"end":744},"obj":"9519265"},{"id":"29021742-16719807-32379571","span":{"begin":751,"end":755},"obj":"16719807"},{"id":"29021742-2883706-32379572","span":{"begin":937,"end":941},"obj":"2883706"},{"id":"29021742-22034391-32379573","span":{"begin":960,"end":964},"obj":"22034391"},{"id":"29021742-21152450-32379574","span":{"begin":1185,"end":1189},"obj":"21152450"}],"text":"Glutamate excitotoxicity is a major factor in ischemia-induced neuronal death (Nishizawa, 2001). Excess release of glutamate from presynaptic membranes induced by ischemia overactivates glutamate receptors leading to a series of events including intracellular calcium overload, excessive ROS production and mitochondrial stress and finally neuronal death (Benveniste et al., 1984; Lipton and Rosenberg, 1994). However, based on accumulating evidence in the literature, all clinical trials using glutamate receptor inhibitors have failed (Koh and Choi, 1991; Morris et al., 1999; Albers et al., 2001; Ikonomidou and Turski, 2002) although some of the inhibitors reduced ischemic damage in animal experiments (Lin et al., 1993; Reyes et al., 1998; Cai, 2006). It is known that glutamate receptors play important roles in maintaining physiological functions such as excitatory signal transduction, learning and memory (Mayer and Westbrook, 1987; Newcomer et al., 2000). Therefore, a more promising strategy for treating ischemic stroke may be through selectively blocking excitotoxicity while preserving important physiological aspects of glutamate receptor subunit function (Cho et al., 2010)."}

{"project":"MyTest","denotations":[{"id":"29021742-11459428-32379562","span":{"begin":90,"end":94},"obj":"11459428"},{"id":"29021742-6149259-32379563","span":{"begin":375,"end":379},"obj":"6149259"},{"id":"29021742-7905600-32379564","span":{"begin":403,"end":407},"obj":"7905600"},{"id":"29021742-1678302-32379565","span":{"begin":552,"end":556},"obj":"1678302"},{"id":"29021742-10541229-32379566","span":{"begin":573,"end":577},"obj":"10541229"},{"id":"29021742-11730442-32379567","span":{"begin":594,"end":598},"obj":"11730442"},{"id":"29021742-12849400-32379568","span":{"begin":623,"end":627},"obj":"12849400"},{"id":"29021742-8408318-32379569","span":{"begin":720,"end":724},"obj":"8408318"},{"id":"29021742-9519265-32379570","span":{"begin":740,"end":744},"obj":"9519265"},{"id":"29021742-16719807-32379571","span":{"begin":751,"end":755},"obj":"16719807"},{"id":"29021742-2883706-32379572","span":{"begin":937,"end":941},"obj":"2883706"},{"id":"29021742-22034391-32379573","span":{"begin":960,"end":964},"obj":"22034391"},{"id":"29021742-21152450-32379574","span":{"begin":1185,"end":1189},"obj":"21152450"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"Glutamate excitotoxicity is a major factor in ischemia-induced neuronal death (Nishizawa, 2001). Excess release of glutamate from presynaptic membranes induced by ischemia overactivates glutamate receptors leading to a series of events including intracellular calcium overload, excessive ROS production and mitochondrial stress and finally neuronal death (Benveniste et al., 1984; Lipton and Rosenberg, 1994). However, based on accumulating evidence in the literature, all clinical trials using glutamate receptor inhibitors have failed (Koh and Choi, 1991; Morris et al., 1999; Albers et al., 2001; Ikonomidou and Turski, 2002) although some of the inhibitors reduced ischemic damage in animal experiments (Lin et al., 1993; Reyes et al., 1998; Cai, 2006). It is known that glutamate receptors play important roles in maintaining physiological functions such as excitatory signal transduction, learning and memory (Mayer and Westbrook, 1987; Newcomer et al., 2000). Therefore, a more promising strategy for treating ischemic stroke may be through selectively blocking excitotoxicity while preserving important physiological aspects of glutamate receptor subunit function (Cho et al., 2010)."}