Journal of cardiovascular risk最新文献

{"title":"Risk factors for myocardial infarction among Swedish railway engine drivers during 10 years follow-up.","authors":"S Piros,&nbsp;S Karlehagen,&nbsp;G Lappas,&nbsp;L Wilhelmsen","doi":"10.1177/204748730000700513","DOIUrl":"https://doi.org/10.1177/204748730000700513","url":null,"abstract":"<p><strong>Background: </strong>Railway engine drivers have had an increased risk of myocardial infarction which could be due to reported low decision latitude and low social support but not to elevated somatic risk factors.</p><p><strong>Objective: </strong>To study somatic and psychosocial risk factors for myocardial infarction among railway engine drivers prospectively.</p><p><strong>Design: </strong>A prospective study of 2318 drivers followed for 10 years.</p><p><strong>Methods: </strong>Risk factors were surveyed in conjunction with periodic health checks at 15 different centres but with common methodology and commonly used questionnaires. Questionnaire and register information on myocardial infarction during follow-up was recorded.</p><p><strong>Results: </strong>Within this group of engine drivers, age, family history of myocardial infarction, systolic blood pressure and low body height were independent predictors of myocardial infarction, but diabetes, elevated serum cholesterol and smoking were not. Neither were a longer time in the occupation or work-related psychosocial factors. The drivers were all at the lower end of the decision authority and latitude scale and had low social support. With this limited span, it may be difficult to detect these variables as risk factors within this group.</p><p><strong>Conclusions: </strong>Several well-known, somatic risk factors for myocardial infarction were documented in this study, whereas psychosocial working conditions, which were common to all the drivers, were not significantly related to outcome.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 5","pages":"395-400"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21966010","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":"The impact of postprandial lipemia in accelerating atherothrombosis.","authors":"H M Roche,&nbsp;M J Gibney","doi":"10.1177/204748730000700504","DOIUrl":"https://doi.org/10.1177/204748730000700504","url":null,"abstract":"<p><p>Several clinical studies have shown that the magnitude and duration of postprandial lipemia is positively related to the pathogenesis and progression of coronary heart disease. Postprandial lipid metabolism refers to the series of metabolic events that occur following the ingestion of a meal containing fat. Dietary fat is principally composed of triacylglycerol, postprandial lipaemia therefore being characterized by an increase in plasma triacylglycerol concentration. This review will describe the nature of the postprandial response and show the direct and indirect pro-atherogenic effects of triacylglycerol-rich lipoprotein metabolism. An elevated postprandial lipemic response precipitates a number of adverse metabolic events, including the production of atherogenic chylomicron remnants, the formation of the highly atherogenic small, dense low-density lipoprotein particles, and a reduction in the concentration of the cardioprotective high-density lipoprotein fraction. Postprandial lipemia also interacts with the process of thrombosis, in that an elevated postprandial triacylglycerol-rich lipoprotein concentration has the ability to activate the coagulation factor VII and plasminogen activator inhibitor. In the light of the potential impact of an elevated postprandial lipemia on atherothrombosis, the genetic determinants of the magnitude of the postprandial response will be identified. Finally, the nutritional factors that modulate the postprandial response will also be discussed.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 5","pages":"317-24"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700504","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21966063","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":"Is there an optimal diet for the hypertriglyceridemic patient?","authors":"P M Kris-Etherton,&nbsp;D S Taylor,&nbsp;G Zhao","doi":"10.1177/204748730000700506","DOIUrl":"https://doi.org/10.1177/204748730000700506","url":null,"abstract":"<p><p>Many dietary factors affect plasma triglycerides. Those which decrease the triglyceride level include n-3 fatty acids from fish oil, weight loss, alcohol restriction, and a higher fat (unsaturated fat) diet, whereas a high-carbohydrate, low-fat diet increases triglycerides. The individual responses and the associated magnitude of change in triglycerides as a result of these different dietary factors will vary. For patients with hypertriglyceridemia, fish oil supplements will usually elicit the most potent effects. However, some patients can normalize their triglyceride level with weight loss plus exercise, by avoiding or limiting their alcohol intake, and by increasing the total fat content of their diet. In addition, fish oil supplements can help further to reduce plasma triglycerides. Thus, the combined effects of multiple dietary interventions provide the most potent means of maximally lowering the plasma triglyceride level.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 5","pages":"333-7"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700506","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21966065","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":"Triglycerides and coronary heart disease: a global perspective.","authors":"I Ahmad,&nbsp;M Miller","doi":"10.1177/204748730000700502","DOIUrl":"https://doi.org/10.1177/204748730000700502","url":null,"abstract":"1350-6277 © 2000 Lippincott Williams & Wilkins Introduction Epidemiologic studies have convincingly demonstrated a strong positive and independent correlation between serum cholesterol level and coronary heart disease (CHD) [1]. In recent years, this association has been solidified because clinical endpoint data have consistently demonstrated that lowering an elevated cholesterol level reduces the CHD event and mortality rates [2]. Whether and to what extent triglycerides independently contribute to CHD has been widely debated in the literature. Some have argued that elevated triglycerides do not cause CHD per se, but rather serve as a marker for metabolic abnormalities (e.g. glucose intolerance) associated with a reduced catabolism of triglyceride-rich lipoproteins [3]. Others have pointed out that although triglycerides are associated with CHD in univariate analysis, the strength of this association is reduced after adjustment for other co-variates such as high-density lipoprotein (HDL) cholesterol [4].","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 5","pages":"303-7"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700502","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21966061","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":"Variation of candidate genes in triglyceride metabolism.","authors":"C P Busch,&nbsp;R A Hegele","doi":"10.1177/204748730000700503","DOIUrl":"https://doi.org/10.1177/204748730000700503","url":null,"abstract":"<p><p>After more than a decade of study, investigators are grappling for a consensus regarding the relationship between variation in candidate genes and plasma triglyceride concentration. Certain variants of LPL--both rare variants, in the case of loss-of-function mutations in kindreds with chylomicronemia, and common variants, in the case of the D9N and N291S variants--appear to be fairly consistently associated with an elevated plasma triglyceride level. In addition, the variation of the recognition site for Sstl within the 3'-untranslated region of APOC3 has consistently shown an association with a variation in plasma triglycerides. The LPL and APOC3 variants thus have at least a chance in future clinical applications, but this will require more study. Common variants of some other promising candidate genes, such as HL, have not shown as consistent an association with the variation in plasma triglyceride level. Finally, studies of variants of newer candidates, such as the mitochondrial genome, LMNA, and IL-6, indicate that many different genes might be important determinants of plasma triglyceride concentration in the general population. As always, the associations of genes with a complex intermediate trait such as plasma triglyceride level depend upon interactions with modulatory factors such as genetic background and/or secondary genetic effects, in addition to the effects of gender, age, hormone replacement, and postprandial status. A key attribute for increasing confidence in the biologic or potential clinical validity of the associations of candidate gene variation with plasma triglyceride will be the development of assays that will provide a more direct mechanistic link between the genetic variant and the elevated plasma triglyceride.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 5","pages":"309-15"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700503","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21966062","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":"Respiratory decline in smokers and ex-smokers--an independent risk factor for cardiovascular disease and death.","authors":"G Engström,&nbsp;B Hedblad,&nbsp;L Janzon,&nbsp;S Valind","doi":"10.1177/204748730000700404","DOIUrl":"https://doi.org/10.1177/204748730000700404","url":null,"abstract":"<p><strong>Background and objective: </strong>Although smoking is associated with an increased incidence of cardiovascular disease and death, many smokers remain healthy after many years of smoking. Our objective was to assess whether this variation is related to rate of decline of respiratory function.</p><p><strong>Design: </strong>This was a population-based cohort study, its subjects being men born in 1914 from Malmö, Sweden.</p><p><strong>Methods: </strong>All 291 smokers who since the baseline examination in 1969 had remained in Malmö were invited to a follow-up examination in 1982. Of the 242 participants, 199 men without history of myocardial infarction or stroke were included in the study. Eighty-four of them had quit smoking. The incidence of cardiovascular disease and death during 14 years was studied in relation to the decline in lung function [forced expiratory volume during 1 second (FEV1.0) and vital capacity] between 55 and 68 years of age.</p><p><strong>Results: </strong>Fifty-nine (51%) smokers and 43 (51%) ex-smokers died. Forty-four (38%) smokers and 29 (35%) ex-smokers suffered a cardiovascular event. The mortality rate among smokers in the high, middle and low thirds with regard to the decline in FEV1.0 was 66.5, 44.0, and 37.6, respectively, per 1000 person-years (P for trend = 0.04). The corresponding figures in ex-smokers were 88.7, 42.0, and 35.1 (P for trend = 0.002). The cardiovascular event rate among smokers in these three groups was 56.0, 41.0, and 22.7 events, respectively, per 1000 person-years (P for trend = 0.01). The association remained significant after adjustments for potential confounders. A change in vital capacity was associated with a similar pattern of disease and death.</p><p><strong>Conclusion: </strong>Although smoking is associated with an accelerated respiratory decline, there are marked differences between smokers. The increased cardiovascular event and death rates among those whose lung function declined the most suggests that the change in respiratory function can be used as a measure of individual susceptibility.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 4","pages":"267-72"},"PeriodicalIF":0.0,"publicationDate":"2000-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700404","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21839444","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":"Leisure-time physical activity and coronary risk factors in women.","authors":"W D Ashton,&nbsp;K Nanchahal,&nbsp;D A Wood","doi":"10.1177/204748730000700403","DOIUrl":"https://doi.org/10.1177/204748730000700403","url":null,"abstract":"<p><strong>Background: </strong>Evidence that physical activity is cardioprotective in women is not as strong as that observed in men. Furthermore, the extent to which exercise protects against coronary heart disease via its influence on classical risk factors remains unclear. This study examines the relationship between reported physical activity, a range of coronary heart disease risk factors and a 10-year predicted coronary heart disease risk score.</p><p><strong>Methods: </strong>A cross-sectional study of 14,077 female employees aged 30-64 years who were screened between 1988 and 1991 was employed. Measurements included systolic and diastolic blood pressure, body mass index, serum total cholesterol, high-density lipoprotein cholesterol, total cholesterol:high-density lipoprotein cholesterol ratio, low-density lipoprotein cholesterol, triglycerides, apolipoprotein A1, apolipoprotein B, lipoprotein a and fasting blood glucose. Participants were divided into three groups according to reported average frequency of vigorous leisure-time physical activity, that is zero, one to two, or three or more episodes per week.</p><p><strong>Results: </strong>Increasing activity frequency was associated with lower systolic and diastolic blood pressure, total cholesterol, total cholesterol:high-density lipoprotein cholesterol ratio, triglycerides and body mass index (all P < 0.001), low-density lipoprotein cholesterol (P = 0.003), apolipoprotein B (P = 0.04) and blood glucose (P = 0.01) and higher high-density lipoprotein cholesterol (P < 0.001) and apolipoprotein A1 (P = 0.03). There was no association with lipoprotein a. After controlling for possible confounders, these relationships remained statistically significant except for apolipoprotein B and glucose. The odds ratios for being in the top quintile of predicted 10-year coronary heart disease risk for individuals in each category of activity were 1.0 (inactive), 0.70 (one to two episodes of activity per week) and 0.77 (three or more episodes of activity per week).</p><p><strong>Conclusion: </strong>Women engaging in vigorous, leisure-time physical activity have a less atherogenic coronary heart disease risk factor profile than those who do not, which translates into a potential reduction of approximately 30% in coronary heart disease risk.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 4","pages":"259-66"},"PeriodicalIF":0.0,"publicationDate":"2000-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700403","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21839443","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":"Socioeconomic status, ABO phenotypes and risk of ischaemic heart disease: an 8-year follow-up in the Copenhagen Male Study.","authors":"P Suadicani,&nbsp;H O Hein,&nbsp;F Gyntelberg","doi":"10.1177/204748730000700406","DOIUrl":"https://doi.org/10.1177/204748730000700406","url":null,"abstract":"<p><strong>Objectives: </strong>The association of socioeconomic status with the risk of ischaemic heart disease is only partly explained by the uneven distribution of conventional risk factors. We tested the hypothesis that an uneven socioeconomic distribution of ABO phenotypes could contribute to the explanation.</p><p><strong>Design: </strong>A prospective study controlling for age and other relevant potential confounders: smoking, physical activity, wine consumption, height, weight, serum lipids, blood pressure, hypertension, type II diabetes, serum selenium concentration and soldering fumes exposure.</p><p><strong>Setting: </strong>The Copenhagen Male Study, Denmark.</p><p><strong>Study participants: </strong>Two thousand, nine hundred and ninety-three men aged 53-74 years without overt ischaemic heart disease.</p><p><strong>Main outcome measure: </strong>Incidence of ischaemic heart disease in an 8-year follow-up.</p><p><strong>Results: </strong>Two hundred and forty-two men (8.1%) had a first ischaemic heart disease event. There was no association between socioeconomic status and the ABO blood group phenotypes and, in accordance with this, ABO phenotype was not a confounder for the association of socioeconomic status with the risk of ischaemic heart disease. However, ABO blood group was a strong risk or effect modifier. Only among men with the O phenotype was socioeconomic status (social classes IV and V versus social classes I, II and III) associated with a significant excess risk (relative risk 1.7, 95% confidence interval 1.1-2.7 and P = 0.02 after adjustment for confounders; the corresponding relative risks among the A and B/AB phenotypes comparing low social classes with the higher social classes were 1.08 (P = 0.77) and 1.08 (P = 0.89), respectively).</p><p><strong>Conclusion: </strong>ABO phenotypes did not contribute directly to the explanation of socioeconomic inequalities in the risk of ischaemic heart disease. However, the finding of ABO phenotypes being effect modifiers for the association of socioeconomic status with the risk of ischaemic heart disease may open up new possibilities of clarifying the roles of socioeconomic status and ABO blood group as cardiovascular disease risk factors.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 4","pages":"277-83"},"PeriodicalIF":0.0,"publicationDate":"2000-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700406","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21839446","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":"Re-survey of the Whitehall study of London civil servants: changes in risk factors for cardiovascular disease during 29 years of follow-up.","authors":"R Clarke, E Breeze, L Youngman, P Sherliker, P Bell, S Shah, M Shipley, R Collins, D Leon, M Marmot, A Fletcher","doi":"10.1177/204748730000700402","DOIUrl":"10.1177/204748730000700402","url":null,"abstract":"<p><strong>Background: </strong>Substantial uncertainty persists about the relevance of blood pressure and cholesterol to the risk of cardiovascular disease in the elderly.</p><p><strong>Objective: </strong>To investigate the determinants of cardiovascular risk in old age, and the relevance of such risk factors when recorded in middle and old age.</p><p><strong>Methods: </strong>A re-survey in 1997 of 8537 survivors of a cohort of men who were originally examined in 1967-1970 when aged 40-69 years.</p><p><strong>Results: </strong>Completed questionnaires were received from 7050 (82%) of the survivors, and blood pressure and blood samples from 5427 (64%). The response rate declined with increasing age, was inversely related to markers of socioeconomic status in 1967-70 and in 1997, and was lower in those who had been current smokers or had a higher blood pressure level in 1967-70. After excluding those with reported cardiovascular disease (25% of respondents), the mean levels of total cholesterol and apolipoprotein B were lower in older age groups, whereas apolipoprotein A1 levels did not vary much with age. Among those with risk factors recorded both in 1967-70 and 1997, the prevalence of smoking had declined by two-thirds (32% in 1970 and 12% in 1997), the prevalence of diabetes had increased (0.3% versus 4.5%), and the mean systolic blood pressure had increased by 16 mmHg (130 versus 146 mmHg), but the diastolic blood pressure had not changed materially (80 versus 81 mmHg), and the measured levels of total cholesterol had increased by 0.5 mmol/l (although that change may be artefactual).</p><p><strong>Conclusion: </strong>Follow-up of vital status in this cohort should permit an assessment of the relevance of risk factors recorded in middle and old age to cardiovascular disease in old age.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 4","pages":"251-7"},"PeriodicalIF":0.0,"publicationDate":"2000-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21839442","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":"Plasma-induced endothelial activation associated with incident atherosclerosis: prospective results from the Bruneck Study.","authors":"P Schratzberger,&nbsp;S Kiechl,&nbsp;S Dunzendorfer,&nbsp;C M Kähler,&nbsp;J R Patsch,&nbsp;J Willeit,&nbsp;C J Wiedermann","doi":"10.1177/204748730000700407","DOIUrl":"https://doi.org/10.1177/204748730000700407","url":null,"abstract":"<p><strong>Background: </strong>Whether systemic inflammation is an epiphenomenon of atherosclerosis or whether it is part of the atherosclerosis causal pathway requires further study.</p><p><strong>Design: </strong>As part of a prospective population survey on the course and aetiology of atherosclerosis, we investigated the effects of plasma on the endothelial monolayers inducing activation for leukocyte transmigration.</p><p><strong>Methods: </strong>An age- and sex-stratified random sample of inhabitants of Bruneck (Italy) with and without atherosclerotic disease aged 50-69 years was selected. Carotid arteries were evaluated by duplex sonography at baseline (1990). Carotid arteries were re-evaluated for the development of new plaques 5 years later (1995). Frozen plasma samples from baseline were available for a random sample of 152 men. Monolayers of endothelial cells cultured in micropore filter insets were pre-treated with plasma, then normal human neutrophils were added to the endothelial cells and subsequent transmigration through the monolayers and micropore filters was measured.</p><p><strong>Results: </strong>The endothelial monolayers were activated for transmigration of leukocytes more potently by plasma from participants with carotid artery plaques than participants without it. Increased endothelial activation with plasma at baseline was associated with the development of new atherosclerotic lesions during a period of 5 years.</p><p><strong>Conclusions: </strong>Plasma from individuals with prevalent atherosclerosis of the carotid arteries activates the endothelium for leukocyte transmigration, suggesting the presence of systemic pro-inflammatory mediators. In an epidemiological survey, follow-up data on new lesion formation after 5 years indicated that plasma-mediated endothelium activation for interaction with leukocytes precedes the development of atherosclerotic lesions.</p>","PeriodicalId":79345,"journal":{"name":"Journal of cardiovascular risk","volume":"7 4","pages":"285-91"},"PeriodicalIF":0.0,"publicationDate":"2000-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/204748730000700407","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21839447","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}