Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2004.TB00013.X
M. Youdim, M. Weinstock
{"title":"A Novel Neuroprotective Cholinesterase and Brain-Selective MAO Inhibitor with APP Processing Activity for the Treatment of Dementia Co-morbid with Depression and Parkinson's Disease","authors":"M. Youdim, M. Weinstock","doi":"10.1111/J.1527-3458.2004.TB00013.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2004.TB00013.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"34 1","pages":"191-191"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77537615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2001.TB00195.X
Jiang Ye, R. Ponnudurai, Rebecca Schaefer
Ondansetron is a selective 5-hydroxytryptamine(3) (5-HT(3)) receptor antagonist that has been introduced to clinical practice as an antiemetic for cancer treatment-induced and anesthesia-related nausea and vomiting. Its use under these circumstances is both prophylactic and therapeutic. It has a superior efficacy, safety and pharmacoeconomic profile compared with other groups of antiemetics, namely antidopaminergics, antihistamines and anticholinergics. However, its place in the management of anticipatory and delayed vomiting in cancer treatment and as a rescue antiemetic in surgical patients needs to be further explored. Furthermore, recent animal and human research also reflects its possible novel application in the treatment of other disease states, such as alcoholism, cocaine addiction, opioid withdrawal syndrome, anxiety disorders, gastrointestinal motility disorders, Tourette's syndrome and pruritus. This review revisits the widespread physiological and pathological effects of 5-HT and discusses both the basic science literature and the clinical developments responsible for the conventional and novel uses of ondansetron. In addition, new discoveries relating to the effects of ondansetron on other receptors/channels and their possible therapeutic applications are presented.
{"title":"Ondansetron: a selective 5-HT(3) receptor antagonist and its applications in CNS-related disorders.","authors":"Jiang Ye, R. Ponnudurai, Rebecca Schaefer","doi":"10.1111/J.1527-3458.2001.TB00195.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2001.TB00195.X","url":null,"abstract":"Ondansetron is a selective 5-hydroxytryptamine(3) (5-HT(3)) receptor antagonist that has been introduced to clinical practice as an antiemetic for cancer treatment-induced and anesthesia-related nausea and vomiting. Its use under these circumstances is both prophylactic and therapeutic. It has a superior efficacy, safety and pharmacoeconomic profile compared with other groups of antiemetics, namely antidopaminergics, antihistamines and anticholinergics. However, its place in the management of anticipatory and delayed vomiting in cancer treatment and as a rescue antiemetic in surgical patients needs to be further explored. Furthermore, recent animal and human research also reflects its possible novel application in the treatment of other disease states, such as alcoholism, cocaine addiction, opioid withdrawal syndrome, anxiety disorders, gastrointestinal motility disorders, Tourette's syndrome and pruritus. This review revisits the widespread physiological and pathological effects of 5-HT and discusses both the basic science literature and the clinical developments responsible for the conventional and novel uses of ondansetron. In addition, new discoveries relating to the effects of ondansetron on other receptors/channels and their possible therapeutic applications are presented.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"18 1","pages":"199-213"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90709643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2000.TB00173.X
M. Picciotto
{"title":"Role of Nicotinic Acetylcholine Receptors in Neurodegeneration or Neuroprotection During Aging","authors":"M. Picciotto","doi":"10.1111/J.1527-3458.2000.TB00173.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2000.TB00173.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"1 1","pages":"28-28"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83052335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2000.TB00142.X
F. Bordi, M. Mugnaini, A. Terron, R. Barnaby, A. Reggiani
Thromboembolic stroke is a severe, disabling disease characterized by an abrupt reduction of cerebral blood flow, which leads to deprivation of oxygen and nutrients to neuronal tissue, followed by permanent brain damage. Evidence has been accumulated to implicate excitotoxicity in the pathogenesis of ischemic brain injury. Overstimulation of excitatory amino acid receptors becomes deleterious for neuronal cell survival. Glutamate antagonists can ameliorate the ischemic injury by any of several mechanisms. Because blockade of the glycine site of the N-methyl-D-aspartate (NMDA) receptor seems to offer a better side-effect profile, glycine antagonists are attractive targets for blocking excitotoxicity following stroke. GV150526 is a selective and potent glycine antagonist at the NMDA receptor complex. It binds to the glycine site with both high affinity and high selectivity in in vitro binding studies. In vivo studies have shown that GV150526 significantly reduces infarct volume in the middle cerebral artery occlusion model of stroke. This effect remained statistically significant, even if treatment was delayed for as long as 6 h post-occlusion. GV150526 showed no evidence of adverse effects usually associated with NMDA receptor blockers, such as neuronal vacuolization in standard assays or cognitive impairment in behavioral tests. GV150526 had no significant treatment-related respiratory or cardiovascular effects or effects on behavior, body temperature, or blood pressure in mice or rats. Pharmacokinetic studies indicated that GV150526 has low clearance and volume of distribution in both the rat and the dog. Preclinical toxicology studies have shown that the compound is well tolerated in both species. Phase I/II studies were undertaken to assess the safety, tolerability, and pharmacokinetics of GV150526 in healthy volunteers and acute stroke patients, and from these a dose was selected to be studied in Phase III clinical trials. These efficacy studies have now completed recruitment and data reconciliation is ongoing. GV150526 has the potential to be an effective therapy for acute ischemic stroke.
血栓栓塞性中风是一种严重的致残疾病，其特征是脑血流量突然减少，导致神经元组织缺氧和营养缺乏，随后是永久性脑损伤。越来越多的证据表明，兴奋性毒性参与缺血性脑损伤的发病机制。兴奋性氨基酸受体的过度刺激对神经元细胞的存活是有害的。谷氨酸拮抗剂可以通过多种机制改善缺血性损伤。由于阻断n -甲基- d -天冬氨酸(NMDA)受体的甘氨酸位点似乎提供了更好的副作用，甘氨酸拮抗剂是阻断卒中后兴奋性毒性的有吸引力的靶点。GV150526是一种选择性和有效的甘氨酸拮抗剂，作用于NMDA受体复合物。在体外结合研究中，它以高亲和力和高选择性与甘氨酸位点结合。体内研究表明，GV150526可显著降低脑卒中大脑中动脉闭塞模型的梗死体积。即使治疗延迟至闭塞后6小时，这种效果仍然具有统计学意义。GV150526没有显示出通常与NMDA受体阻滞剂相关的不良反应的证据，例如标准测定中的神经元空泡化或行为测试中的认知障碍。GV150526对小鼠或大鼠的呼吸或心血管没有明显的治疗相关作用，也没有对行为、体温或血压的影响。药代动力学研究表明，GV150526在大鼠和狗体内具有低清除率和分布量。临床前毒理学研究表明，该化合物在这两个物种中都具有良好的耐受性。开展I/II期研究，评估GV150526在健康志愿者和急性中风患者中的安全性、耐受性和药代动力学，并从中选择一种剂量进行III期临床试验。这些疗效研究现已完成招募，数据核对正在进行中。GV150526有潜力成为治疗急性缺血性脑卒中的有效药物。
{"title":"GV150526: A Neuroprotective Agent","authors":"F. Bordi, M. Mugnaini, A. Terron, R. Barnaby, A. Reggiani","doi":"10.1111/J.1527-3458.2000.TB00142.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2000.TB00142.X","url":null,"abstract":"Thromboembolic stroke is a severe, disabling disease characterized by an abrupt reduction of cerebral blood flow, which leads to deprivation of oxygen and nutrients to neuronal tissue, followed by permanent brain damage. Evidence has been accumulated to implicate excitotoxicity in the pathogenesis of ischemic brain injury. Overstimulation of excitatory amino acid receptors becomes deleterious for neuronal cell survival. Glutamate antagonists can ameliorate the ischemic injury by any of several mechanisms. Because blockade of the glycine site of the N-methyl-D-aspartate (NMDA) receptor seems to offer a better side-effect profile, glycine antagonists are attractive targets for blocking excitotoxicity following stroke. \u0000 \u0000 \u0000 \u0000GV150526 is a selective and potent glycine antagonist at the NMDA receptor complex. It binds to the glycine site with both high affinity and high selectivity in in vitro binding studies. In vivo studies have shown that GV150526 significantly reduces infarct volume in the middle cerebral artery occlusion model of stroke. This effect remained statistically significant, even if treatment was delayed for as long as 6 h post-occlusion. GV150526 showed no evidence of adverse effects usually associated with NMDA receptor blockers, such as neuronal vacuolization in standard assays or cognitive impairment in behavioral tests. GV150526 had no significant treatment-related respiratory or cardiovascular effects or effects on behavior, body temperature, or blood pressure in mice or rats. Pharmacokinetic studies indicated that GV150526 has low clearance and volume of distribution in both the rat and the dog. Preclinical toxicology studies have shown that the compound is well tolerated in both species. Phase I/II studies were undertaken to assess the safety, tolerability, and pharmacokinetics of GV150526 in healthy volunteers and acute stroke patients, and from these a dose was selected to be studied in Phase III clinical trials. These efficacy studies have now completed recruitment and data reconciliation is ongoing. GV150526 has the potential to be an effective therapy for acute ischemic stroke.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"1 1","pages":"135-152"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81177821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2000.TB00183.X
Z. Sarnyai, E. Sibille, C. Pavlides, Robert J. Fenster, B. McEwen, M. Toth
KO animals showedimpairments in hippocampal-dependent learning and memory tests, such as the hiddenplatform (spatial) version of the Morris water maze (MWM) and the delayed version ofY-maze. Performance of KO mice was not impaired in non-hippocampal memory taskssuch as the visible platform (non-spatial) version of the MWM, the immediate version ofthe Y-maze, and the spontaneous alternation test of working memory. These resultsdemonstrate that 5HT
{"title":"Functional Abnormalities in the Hippocampus and Impaired Hippocampal‐dependent Learning in Mice Lacking the 5HT1A Receptors","authors":"Z. Sarnyai, E. Sibille, C. Pavlides, Robert J. Fenster, B. McEwen, M. Toth","doi":"10.1111/J.1527-3458.2000.TB00183.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2000.TB00183.X","url":null,"abstract":"KO animals showedimpairments in hippocampal-dependent learning and memory tests, such as the hiddenplatform (spatial) version of the Morris water maze (MWM) and the delayed version ofY-maze. Performance of KO mice was not impaired in non-hippocampal memory taskssuch as the visible platform (non-spatial) version of the MWM, the immediate version ofthe Y-maze, and the spontaneous alternation test of working memory. These resultsdemonstrate that 5HT","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"69 1","pages":"40-40"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90632234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2000.TB00175.X
L. Kaczmarek, E. Jonas
{"title":"Regulation of Synaptic Stability by Bcl-2 Family Proteins","authors":"L. Kaczmarek, E. Jonas","doi":"10.1111/J.1527-3458.2000.TB00175.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2000.TB00175.X","url":null,"abstract":"","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"8 1","pages":"30-31"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77841610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2001.TB00206.X
Jie Zhu, E. Mix, B. Winblad
Rolipram is a selective inhibitor of phosphodiesterases (PDE) IV, especially of the subtype PDE IVB. These phosphodiesterases are responsible for hydrolysis of the cyclic nucleotides cAMP and cGMP, particularly in nerve and immune cells. Consequences of rolipram-induced elevation of intracellular cAMP are increased synthesis and release of norepinephrine, which enhance central noradrenergic transmission, and suppress expression of proinflammatory cytokines and other mediators of inflammation. In humans and animals rolipram produces thereby a variety of biological effects. These effects include attenuation of endogenous depression and inflammation in the central nervous system (CNS), both effects are of potential clinical relevance. There are some discrepancies between in vitro and in vivo effects of rolipram, as well as between results obtained in animal models and clinical studies. The clinical use of rolipram is limited because of its behavioral and other side effects. Newly developed selective PDE IV inhibitors with presumably higher potency and lower toxicity are currently under investigation.
{"title":"The antidepressant and antiinflammatory effects of rolipram in the central nervous system.","authors":"Jie Zhu, E. Mix, B. Winblad","doi":"10.1111/J.1527-3458.2001.TB00206.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2001.TB00206.X","url":null,"abstract":"Rolipram is a selective inhibitor of phosphodiesterases (PDE) IV, especially of the subtype PDE IVB. These phosphodiesterases are responsible for hydrolysis of the cyclic nucleotides cAMP and cGMP, particularly in nerve and immune cells. Consequences of rolipram-induced elevation of intracellular cAMP are increased synthesis and release of norepinephrine, which enhance central noradrenergic transmission, and suppress expression of proinflammatory cytokines and other mediators of inflammation. In humans and animals rolipram produces thereby a variety of biological effects. These effects include attenuation of endogenous depression and inflammation in the central nervous system (CNS), both effects are of potential clinical relevance. There are some discrepancies between in vitro and in vivo effects of rolipram, as well as between results obtained in animal models and clinical studies. The clinical use of rolipram is limited because of its behavioral and other side effects. Newly developed selective PDE IV inhibitors with presumably higher potency and lower toxicity are currently under investigation.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"64 1","pages":"387-98"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79119599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2000.TB00147.X
V. Matteo, G. Giovanni, E. Esposito
SB 242084 is the most potent and selective 5-HT2C receptor antagonist thus far available. Thus, SB 242084 has high affinity for the cloned human 5-HT2C receptor with a pKi of 9.0, a much lower affinity for the human cloned 5-HT2B (pKi 7.0) and 5-HT2A (pKi 6.8) receptors, and low affinity for other 5-HT, dopamine, and adrenergic receptors. In the 5-HT-stimulated PI hydrolysis model of 5-HT2C receptor function, SB 242084 was found to be a competitive antagonist with a pKB of 9.3. A series of in vivo studies have shown that SB 242084 is a very effective antagonist of behavioral responses mediated by 5-HT2C receptors such as penile erections, and the hypophagic and hypolocomotor effect of mCPP in rats. In addition, this compound has anxiolytic-like properties. Moreover, SB 242084 increases the basal activity of dopaminergic neurons in the VTA and the in vivo DA release in the nucleus accumbens, and it is capable of blocking the inhibitory effects of mCPP and RO 60-0175 on mesolimbic dopaminergic activity. These data are consistent with the evidence that 5-HT2C receptors exert an inhibitory control upon the mesolimbic dopaminergic system. Taken togheter, the available data on SB 242084 might have implication for the possible use of this compound in the treatment of anxiety, depression, and the negative symptoms of schizophrenia.
{"title":"SB 242084: A Selective 5‐HT2C Receptor Antagonist","authors":"V. Matteo, G. Giovanni, E. Esposito","doi":"10.1111/J.1527-3458.2000.TB00147.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2000.TB00147.X","url":null,"abstract":"SB 242084 is the most potent and selective 5-HT2C receptor antagonist thus far available. Thus, SB 242084 has high affinity for the cloned human 5-HT2C receptor with a pKi of 9.0, a much lower affinity for the human cloned 5-HT2B (pKi 7.0) and 5-HT2A (pKi 6.8) receptors, and low affinity for other 5-HT, dopamine, and adrenergic receptors. In the 5-HT-stimulated PI hydrolysis model of 5-HT2C receptor function, SB 242084 was found to be a competitive antagonist with a pKB of 9.3. A series of in vivo studies have shown that SB 242084 is a very effective antagonist of behavioral responses mediated by 5-HT2C receptors such as penile erections, and the hypophagic and hypolocomotor effect of mCPP in rats. In addition, this compound has anxiolytic-like properties. Moreover, SB 242084 increases the basal activity of dopaminergic neurons in the VTA and the in vivo DA release in the nucleus accumbens, and it is capable of blocking the inhibitory effects of mCPP and RO 60-0175 on mesolimbic dopaminergic activity. These data are consistent with the evidence that 5-HT2C receptors exert an inhibitory control upon the mesolimbic dopaminergic system. \u0000 \u0000 \u0000 \u0000Taken togheter, the available data on SB 242084 might have implication for the possible use of this compound in the treatment of anxiety, depression, and the negative symptoms of schizophrenia.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"37 1","pages":"195-205"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82924058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-06-07DOI: 10.1111/J.1527-3458.2001.TB00196.X
Ming Li, H. Lester
In the last decade, advances in molecular genetics and cellular electrophysiology have increased our understanding of ion channel function. A number of diseases termed "channelopathies" have been discovered that are caused by ion channel dysfunction. Channelopathies can be caused by autoimmune, iatrogenic, toxic or genetic mechanisms. Mutations in genes encoding ion channel proteins that disrupt channel function are now the most commonly identified cause of channelopathies, perhaps because gene disruption is readily detected by the methods of molecular genetics. Ion channels are abundant in the central nervous system (CNS), but CNS channelopathies are rare; however, they overlap with some important neurological disorders, such as epilepsy, ataxia, migraine, schizophrenia, Alzheimer's disease and other neurodegenerative diseases. It is possible that more CNS channelopathies will be discovered when additional ion channels are characterized and the complex mechanisms of brain function are better understood. At present, increased knowledge of the identity, structure and function of ion channels is facilitating diagnosis and treatment of many channelopathies.
{"title":"Ion channel diseases of the central nervous system.","authors":"Ming Li, H. Lester","doi":"10.1111/J.1527-3458.2001.TB00196.X","DOIUrl":"https://doi.org/10.1111/J.1527-3458.2001.TB00196.X","url":null,"abstract":"In the last decade, advances in molecular genetics and cellular electrophysiology have increased our understanding of ion channel function. A number of diseases termed \"channelopathies\" have been discovered that are caused by ion channel dysfunction. Channelopathies can be caused by autoimmune, iatrogenic, toxic or genetic mechanisms. Mutations in genes encoding ion channel proteins that disrupt channel function are now the most commonly identified cause of channelopathies, perhaps because gene disruption is readily detected by the methods of molecular genetics. Ion channels are abundant in the central nervous system (CNS), but CNS channelopathies are rare; however, they overlap with some important neurological disorders, such as epilepsy, ataxia, migraine, schizophrenia, Alzheimer's disease and other neurodegenerative diseases. It is possible that more CNS channelopathies will be discovered when additional ion channels are characterized and the complex mechanisms of brain function are better understood. At present, increased knowledge of the identity, structure and function of ion channels is facilitating diagnosis and treatment of many channelopathies.","PeriodicalId":10499,"journal":{"name":"CNS drug reviews","volume":"11 1","pages":"214-40"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82443464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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