Journal of toxicology. Clinical toxicology最新文献

{"title":"Diagnostic accuracy of urinary amanitin in suspected mushroom poisoning: a pilot study.","authors":"Raffaella Butera,&nbsp;Carlo Locatelli,&nbsp;Teresa Coccini,&nbsp;Luigi Manzo","doi":"10.1081/clt-200035472","DOIUrl":"https://doi.org/10.1081/clt-200035472","url":null,"abstract":"<p><strong>Background: </strong>Amatoxin-containing species are responsible for the most severe cases of mushroom poisoning, with high mortality rate. Therefore, this poisoning should be ruled out in all patients presenting gastrointestinal symptoms after wild mushroom ingestion.</p><p><strong>Objective: </strong>To determine sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic efficacy (DE) of urinary amanitin analysis in cases of suspected mushroom poisoning.</p><p><strong>Methods: </strong>All cases of mushroom ingestion referred to a Poison Center during a one-month period were analyzed. Amanitin measurements were performed by ELISA method (functional least detectable dose 1.5 ng/ml; cut-off value not clearly established). Gastrointestinal symptoms latency and initial clinical assessment were considered alternative diagnostic tools. Definitive diagnosis was used as the reference standard.</p><p><strong>Results: </strong>Among 61 patients included in the study, amatoxin poisoning was diagnosed in 10 cases. Urine samples were collected 5.5 to 92 hours after mushroom ingestion. Urinary amanitin DE was 91.8%, 93.4%, and 80.3%, based on the cut-off value considered (1.5, 5.0, and 10.0 ng/ml, respectively). Symptoms latency longer than 6 hours and initial clinical assessment DE were 70.5% and 67.2%, respectively. To identify amatoxin poisoning, initial clinical assessment resulted more sensitive and urinary amanitin analysis more specific.</p><p><strong>Conclusions: </strong>Urinary amanitin analysis is a valuable diagnostic tool and may significantly contribute to the management of suspected mushroom poisoning. At present, the best diagnostic accuracy can be obtained taking advantage of both the high sensitivity and negative predictive value of the clinical assessment performed by an experienced toxicologist, and the high specificity and positive predictive value that characterize urinary amanitin analysis.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"901-12"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035472","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802898","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}

{"title":"Carbon monoxide and cyanide poisoning in fire related deaths in Victoria, Australia.","authors":"Michael J Yeoh,&nbsp;George Braitberg","doi":"10.1081/clt-200035211","DOIUrl":"https://doi.org/10.1081/clt-200035211","url":null,"abstract":"<p><strong>Objective: </strong>This study was undertaken to examine the association of hydrogen cyanide and carboxyhaemoglobin in victims of fire related deaths in Australia. The secondary aim was to document demographic data about Australian fire related deaths.</p><p><strong>Methods: </strong>An observational retrospective study was undertaken of autopsy reports from the Victorian Institute of Forensic Medicine. Reports of fire related deaths were electronically searched using the terms burns, \"smoke\" or \"fire\" as a cause of death in the calender years 1992 to 1998. Data on the circumstances of the fire and results of toxicological screening were obtained on 178 persons. Additional whole blood cyanide levels were determined if blood samples were available in storage. Demographics of the victims were analysed, as well as the relationship between carboxyhaemoglobin and whole blood cyanide levels.</p><p><strong>Results: </strong>Most (82%) of the victims died at the scene, whilst 32 victims died after a period of hospitalisation (hours to weeks). Suicide as a result of self-immolation was the reported cause of death in 32 cases. Most of the fires were in houses (114) and cars (29). The blood ethanol level was zero in 112 cases; the remaining cases (53) had a mean level of 0.17%. Other central nervous system (CNS) depressants were recorded in 49 of the 134 cases that received a complete toxicological screen. Carboxyhaemoglobin levels were measured in only 154 of 178 cases. The carboxyhaemoglobin level was zero in 43 cases. The remaining cases (111) had a mean level of 40%; with 44 cases having a level greater than 50%, a level considered to be potentially lethal. Whole blood hydrogen cyanide levels were measured in only 138 of 178 cases. The hydrogen cyanide level was zero in 52 cases. The remaining cases (86) had a mean level of 1.65 mg/L; with 11 cases having a level greater than 3.0 mg/L (potentially fatal). Blood ethanol levels were significantly correlated with both carboxyhaemoglobin (R = 0.22, P < 0.01) and cyanide (R = 0.36, P < 0.001). In addition, a significant correlation (r = 0.34) between carboxyhaemoglobin and hydrogen cyanide levels was noted.</p><p><strong>Conclusions: </strong>This study showed a correlation between elevated blood ethanol and whole blood cyanide levels (r = 0.36, p < 0.001) and between elevated carboxyhaemoglobin and hydrogen cyanide levels (r = 0.34). Although the mean cyanide level was 1.3 mg/L (above the level some consider potentially toxic) in those cases with a carboxyhaemoglobin level of greater than 10%, there is insufficient data to permit recommendations for clinical care. Further studies are required on those victims that reach hospital alive.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"855-63"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035211","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802978","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}

{"title":"A Near‐Fatal Overdose of Carisoprodol (SOMA): Case Report","authors":"M. Siddiqi, C. Jennings","doi":"10.1081/CLT-120030952","DOIUrl":"https://doi.org/10.1081/CLT-120030952","url":null,"abstract":"Carisoprodol is a centrally acting skeletal muscle relaxant, structurally and pharmacologically related to meprobamate (1). It was first introduced in the 1950s for the relief of back pain and muscle spasms. Carisoprodol is metabolized to meprobamate, a potent and addictive sedative. Carisoprodol also has weak anticholinergic, antipyretic, and analgesic properties (2,3). Poisoning with carisoprodol is reported infrequently. Following ingestion of a large dose, death is attributed to CNS depression with respiratory failure. Ingestion of 3.5 g of carisoprodol has resulted in the death of a 4-year-old (4). Seizures and coma persisting for 33h (5) followed ingestion of up to 14.7 g of carisoprodol in an adult, whereas ingestion of 9.45 g has resulted in milder CNS effects (2). We report a 40-year-old white male who ingested 21 g (60 tablets) of carisoprodol along with an unknown quantity of chlordiazepoxide and temazepam. This case is worth reporting because it illustrates one of the highest-reported blood levels of carisoprodol. The patient was found unresponsive by the paramedics at a video store, where he underwent emergent endotracheal intubation and received artificial ventilation. On arrival to the Emergency Department, he was unresponsive to painful stimuli. He had a HR of 130 bpm, BP 220/118 mm HG, a temperature of 100.5 F, and was manually ventilated. The patient also demonstrated anticholinergic signs. Pupils were symmetric, dilated, and sluggishly reactive to light. Breath sounds were coarse with rales on the right side. Abdominal exam revealed absent bowel sounds as often seen in an anticholinergic toxidrome. He was deeply comatose, with absent tendon and plantar reflexes. His skin was warm and dry. The patient had a past medical history significant for psychiatric illness, substance abuse, chronic back pain, and hypertension. Initial blood gas analysis revealed a mild respiratory acidosis with a ph of 7.31 and a pCO2 of 50.1 mmHg (partially compensated with artificial ventilation). Other baseline labs were normal. The toxicology urine immunoassay was positive for cocaine metabolites and benzodiazepines. Chest radiographs showed a right upper lobe infiltrate. EKG revealed sinus tachycardia with a prolonged QT interval (exact measurements no longer available) mimicking a possible tricyclic overdose. In view of the possibility of multiple-drug ingestion and since he presented to the ER within an hour after his ingestion, the treatment in the emergency department consisted of gastric lavage and activated charcoal with sorbitol. Naloxone was used as part of the coma cocktail, and sodium bicarbonate was used to reverse cardiac toxicity from a tricyclic antidepressant. The use of flumazenil to reverse the possible benzodiazepine component of his presentation was considered ill-advised as the patient was on chronic benzodiazepine therapy, thus increasing the risk of withdrawal seizures. Intravenous clindamycin was initiated for aspiration pneumo","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"101 1","pages":"239 - 240"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75858371","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}

{"title":"Acute poisoning with emamectin benzoate.","authors":"Tzung-Hai Yen,&nbsp;Ja-Liang Lin","doi":"10.1081/clt-200026968","DOIUrl":"https://doi.org/10.1081/clt-200026968","url":null,"abstract":"<p><strong>Background: </strong>Emamectin benzoate is the 4'-deoxy-4'-epi-methyl-amino benzoate salt of avermectin B1 (abamectin), which is similar structurally to natural fermentation products of Streptomyces avermitilis. Emamectin benzoate is being developed as a newer broad-spectrum insecticide for vegetables and has a very low application rate. The mechanism of action involves stimulation of high-affinity GABA receptors and a consequent increase in membrane chloride ion permeability. Animal studies indicate a wide margin of safety because mammalian species are much less sensitive due to lower GABA receptor affinities and relative impermeability of the blood-brain barrier. Notably, the literature has not reported human exposure resulting in toxicity.</p><p><strong>Case report: </strong>This paper describes a case of acute poisoning with Proclaim insecticide (Syngenta, Taiwan), consisting of 2.15% w/w emamectin benzoate in 2, 6-bis (1, 1-dimethylethyl)-4-methyl-phenol and 1-hexanol. The clinical manifestation was transient gastrointestinal upset with endoscopy-proven gastric erosion and superficial gastritis, mild central nervous system depression, and aspiration pneumonia. No specific antidote exists for emamectin benzoate intoxication; this patient was treated successfully with gastric lavage, administration of activated charcoal, and empiric antibiotics. Drugs that enhance GABA activity such as barbiturates and benzodiazepines were avoided.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 5","pages":"657-61"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200026968","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40901026","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}

{"title":"Treatment of severe pediatric ethylene glycol intoxication without hemodialysis.","authors":"E Martin Caravati,&nbsp;Heather L Heileson,&nbsp;Michael Jones","doi":"10.1081/clt-120037424","DOIUrl":"https://doi.org/10.1081/clt-120037424","url":null,"abstract":"<p><strong>Background: </strong>There is limited experience treating severe ethylene glycol poisoning in children without hemodialysis. The objective of this study was to describe the clinical course and outcome of severe pediatric ethylene glycol poisoning treated without hemodialysis.</p><p><strong>Methods: </strong>Patient records were identified retrospectively by hospital discharge diagnosis (ICD-9 code) of ethylene glycol poisoning from 1999 through 2002 at a pediatric medial center. Patients with initial serum ethylene glycol concentrations less than 50 mg/dL or those who received hemodialysis were excluded.</p><p><strong>Results: </strong>Six patients with an age range of 22 months to 14 years were admitted for treatment of ethylene glycol poisoning over a four-year period. Initial serum ethylene glycol concentrations ranged from 62 to 304 mg/dL (mean 174.0 mg/dL). The lowest-measured individual serum bicarbonates ranged from 4 to 17 mEq/L. All patients were initially admitted to intensive care. One patient received ethanol only, two patients received fomepizole only, and three patients received a loading dose of ethanol and then were converted to fomepizole therapy. None of the patients received hemodialysis. Treatment was continued until the serum ethylene glycol was less than 10 mg/dL. Metabolic acidosis resolved with intravenous fluid and supplemental bicarbonate within 24h. All patients had a normal creatinine upon presentation and at discharge. The mean length of stay in intensive care was 21h and on the ward was 33.7h. One episode of hypoglycemia occurred in a 22-month-old. All patients recovered without evidence of renal insufficiency or other major complications at discharge.</p><p><strong>Conclusion: </strong>Six pediatric patients with severe ethylene glycol intoxication and normal renal function were successfully treated without hemodialysis.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"255-9"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037424","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24677034","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}

{"title":"Oral sumatriptan-induced myocardial infarction.","authors":"Jason B Hack","doi":"10.1081/clt-120037434","DOIUrl":"https://doi.org/10.1081/clt-120037434","url":null,"abstract":"<p><strong>Background: </strong>Sumatriptan has been used in the treatment of migraine and other vascular headaches since 1993 in the United States. Its side effects include chest pains in 3% to 8% of patients who have known cardiac risk factors. This is a case report of a 45-year-old woman with no history of cardiac risk factors who had a myocardial infarction after her monthly dose of oral sumatriptan.</p><p><strong>Methods: </strong>The patient was examined in the emergency room, evaluated by electrocardiography, and serial evaluations of cardiac enzymes over the next 24 h. She was admitted to the cardiology ward. A cardiac catherization and additional laboratory studies were performed the following day.</p><p><strong>Results: </strong>The catherization revealed normal heart function, but a 60% to 70% non-flowing stenosis within the first septal perforator. Laboratory indices for cardiac risk were within normal ranges.</p><p><strong>Conclusions: </strong>Patients without cardiac risk factors may experience myocardial infarction following an oral dose of sumatriptan.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"309-11"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037434","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678093","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}

{"title":"Neuroleptic malignant syndrome in a child treated with an atypical antipsychotic.","authors":"Ibrahim Abu-Kishk,&nbsp;Michal Toledano,&nbsp;Ahuva Reis,&nbsp;David Daniel,&nbsp;Matitiahu Berkovitch","doi":"10.1081/clt-200035214","DOIUrl":"https://doi.org/10.1081/clt-200035214","url":null,"abstract":"<p><p>Neuroleptic malignant syndrome (NMS) is an uncommon potentially fatal side effect of neuroleptic drugs, characterized by movement disorder, altered mental status and autonomic instability. A single dose of clotiapine was administered to an 11-year old male with acute psychosis. The previously healthy child had signs consistent with NMS including hyperthermia, hypertension, motor and mental changes. Repeat examination performed two weeks later, demonstrated that while his hyperthermia subsided, his mental status deteriorated. Olanzapine was administered, after which the child had hyperthermia, dystonia and more pronounced restlessness, once again consistent with NMS. He developed respiratory failure and was intubated and mechanically ventilated. Lorazepam, dantrolene and bromocriptine were administered as treatment of possible NMS. His mental condition, movement disorder and autonomic dysfunction improved significantly. Two weeks later, the patient was discharged in good general condition without the need for any ongoing medical treatment. There are only few case reports of NMS in children treated with olanzapine, an atypical antipsychotic. In children, caution must be exercised when prescribing antipsychotics, particularly atypical antipsychotics as these drugs may cause NMS. Because of the low incidence of NMS, a high index of suspicion is needed to identify cases so prompt treatment can be undertaken.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"921-5"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035214","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802901","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}

{"title":"Comment on \"Treatment of hyperkalemia in a patient with unrecognized digitalis toxicity\".","authors":"Philip D Walson","doi":"10.1081/clt-120028758","DOIUrl":"https://doi.org/10.1081/clt-120028758","url":null,"abstract":"","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"119"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028758","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467194","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}

{"title":"Comment on \"The abrupt cessation of therapeutically administered sodium oxybate (GHB) may cause withdrawal symptoms\".","authors":"Deborah L Zvosec,&nbsp;Stephen W Smith","doi":"10.1081/clt-120028759","DOIUrl":"https://doi.org/10.1081/clt-120028759","url":null,"abstract":"","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"121-3; author reply 125-7"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028759","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467195","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}

{"title":"Position Paper on urine alkalinization.","authors":"A T Proudfoot,&nbsp;E P Krenzelok,&nbsp;J A Vale","doi":"10.1081/clt-120028740","DOIUrl":"https://doi.org/10.1081/clt-120028740","url":null,"abstract":"<p><p>This Position Paper was prepared using the methodology agreed by the American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT). All relevant scientific literature was identified and reviewed critically by acknowledged experts using set criteria. Well-conducted clinical and experimental studies were given precedence over anecdotal case reports and abstracts were not considered. A draft Position Paper was then produced and presented at the North American Congress of Clinical Toxicology in October 2001 and at the EAPCCT Congress in May 2002 to allow participants to comment on the draft after which a revised draft was produced. The Position Paper was subjected to detailed peer review by an international group of clinical toxicologists chosen by the AACT and the EAPCCT, and a final draft was approved by the boards of the two societies. The Position Paper includes a summary statement (Position Statement) for ease of use, which will also be published separately, as well as the detailed scientific evidence on which the conclusions of the Position Paper are based. Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. The term urine alkalinization emphasizes that urine pH manipulation rather than a diuresis is the prime objective of treatment; the terms forced alkaline diuresis and alkaline diuresis should therefore be discontinued. Urine alkalinization increases the urine elimination of chlorpropamide, 2,4-dichlorophenoxyacetic acid, diflunisal, fluoride, mecoprop, methotrexate, phenobarbital, and salicylate. Based on volunteer and clinical studies, urine alkalinization should be considered as first line treatment for patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization cannot be recommended as first line treatment in cases of phenobarbital poisoning as multiple-dose activated charcoal is superior. Supportive care, including the infusion of dextrose, is invariably adequate in chlorpropamide poisoning. A substantial diuresis is required in addition to urine alkalinization in the chlorophenoxy herbicides, 2,4-dichlorophenoxyacetic acid, and mecoprop, if clinically important herbicide elimination is to be achieved. Volunteer studies strongly suggest that urine alkalinization increases fluoride elimination, but this is yet to be confirmed in clinical studies. Although urine alkalinization is employed clinically in methotrexate toxicity, currently there is only one study that supports its use. Urine alkalinization enhances diflunisal excretion, but this technique is unlikely to be of value in diflunisal poisoning. In conclusion, urine alkalinization should be considered first line treatment in patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine a","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"1-26"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028740","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467278","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}