Diabetes research (Edinburgh, Scotland)最新文献

{"title":"The effects of chronic diabetes and physiological insulin concentration on ketone bodies metabolism in the heart.","authors":"A M Sultan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In this study the effects of filter-type (Millipore and Whatman No. 54), albumin and insulin at physiological and non-physiological concentrations (12000, 1200, 600, 480, and 300 pM) on D-3-hydroxybutyrate (D-3-HB) utilization and oxidation and acetoacetate production by the isolated nonworking perfused heart from normal and diabetic (4-week) rats was investigated. The use of Whatman No. 54 paper filter to filter the perfusate, in contrast to Millipore filter (0.4 mm) porisity, resulted in the elevation of the rates of utilization and oxidation of D-3-HB and had no effect on acetoacetate production in hearts from normal or diabetic (4-week) rats. Albumin inhibited the utilization and oxidation of D-3-HB, suppressed the percentage of D-3-HB oxidation, increased the percentage of acetoacetate production and had no effect on acetoacetate production in hearts from normal or diabetic rats. Regardless of the filter type and the presence or absence of albumin, the utilization and oxidation of D-3-HB are inhibited and no effect on acetoacetate production was observed in hearts from diabetic rats. Insulin at physiological and non-physiological concentrations in the presence of albumin affects the metabolism of D-3-HB; the stimulations of D-3-HB utilization averaged 32% and 46% in hearts from normal and diabetic rats respectively. The stimulation of D-3-HB oxidation averaged 40% and 60% in hearts from normal and diabetic rats respectively. The D-3-HB utilization and oxidation rates were higher in the hearts isolated from normal rats. No effect of insulin on the rate of acetoacetate production in hearts from normal or diabetic rats was observed, with the exception of an insulin concentration of 1200 pM; there was a 54% reduction in hearts from normal rats. Insulin at 12000 pM had no effect on D-3-HB utilization and oxidation and acetoacetate production in hearts from normal or diabetic rats when perfused using Whatman paper filters in the absence of albumin, but it enhanced the utilization and oxidation of D-3-HB when Millipore paper filters were used.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"27 2","pages":"47-60"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18676286","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":"Occurrence of islet cell reactive autoantibodies in diabetes-prone BB/OK rats is not associated with the onset of diabetes: a cross-sectional study of BB rats and their diabetes-resistant congenic strains.","authors":"M Schlosser,&nbsp;B Ziegler,&nbsp;P Augstein,&nbsp;I Klöting,&nbsp;M Ziegler","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Diabetes-prone BB rats are one of the extensively studied animal models of human type 1 (insulin-dependent) diabetes. We have detected islet cell reactive autoantibodies (ICRA) in sera of age-matched (120 days of age) diabetic and non-diabetic diabetes-prone BB/OK rats compared to sex- and age-matched diabetes-resistant LEW.1A control rats by cellular enzyme-linked immunosorbent assay (CELISA) using either desiccated or viable rat insulinoma (RIN) cells as target. The antibody levels measured using desiccated RIN cells (mean O.D. +/- SD; prevalence) of the diabetic group (1.41 +/- 0.59; 94.1%) and the non-diabetic group (1.23 +/- 0.48; 100%) were significantly (p < 0.01) increased compared to those of the diabetes-resistant LEW.1A control rats (0.24 +/- 0.1; 3.2%). Additionally, in a 209-day-old group of non-diabetic diabetes-prone BB/OK rats the autoantibody levels were further significantly (p < 0.01) increased (2.65 +/- 0.48; 100%). Comparing both congenic rat strains BB.1A/OK and LEW.1BB/OK, only the BB.1A/OK rats which bears the genetic background of diabetes-prone BB/OK rats were found to be antibody positive (0.68 +/- 0.43; 63.1%). The results were confirmed by the CELISA using viable RIN cells. We conclude that the prevalence of islet cell autoantibodies in diabetes-prone BB/OK rats and congenic BB.1A/OK rats is closely associated with the genetic susceptibility to diabetes and may be independent of Beta-cell destruction, but they are not a predictive marker for the onset of the disease in this animal model.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"26 2","pages":"67-77"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18561400","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":"Methodological issues in the application of the minimal model: effects of glucose dose, basal glucose concentration, test duration and modelling constraint.","authors":"I F Godsland,&nbsp;S Luzio,&nbsp;V Wynn,&nbsp;D R Owens","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>An intravenous glucose tolerance test (IVGTT) glucose dose of 0.3 g/kg has been adopted for measurement of insulin sensitivity using the minimal model. Traditionally, however, a dose of 0.5 g/kg has been used, which might be expected to improve the IVGTT insulin response and hence the effectiveness of minimal model analysis. In a preliminary study of 5 subjects given 0.3 and 0.5 g/kg IVGTTs, each lasting 120 minutes, we found a 53% increase in IVGTT insulin response at the higher dose, but there was a marked discrepancy in the difference between fasting and final glucose concentrations (-0.17 mmol.l-1 at 0.3 g/kg and -1.01 mmol.l-1 at 0.5 g/kg). Good agreement obtained between estimates of Si derived from 0.3 and 0.5 g/kg IVGTTs (mean Si: 0.3 g/kg test = 6.0 min-1.microU-1.ml, 0.5 g/kg test = 5.8 min-1.microU-1.ml: r = 0.97, p < 0.001) providing the final IVGTT glucose concentration rather than the fasting concentration was taken as the basal level for modelling analysis. These findings were confirmed and extended in two further studies; firstly in an analysis of the effects of choice of basal glucose concentration and the application of various modelling constraints in a cross-section of 66 subjects with a wide range of insulin sensitivities; then in a further study in which seven subjects were each given two 0.3 g/kg IVGTTs and one 0.5 g/kg IVGTT, with each test being prolonged to 300 minutes. Agreement between estimates of Si at the two different doses was again only achieved by taking the final IVGTT glucose concentration as basal (mean Si: 0.3 g/kg test = 4.7 min-1.microU-1.ml, 0.5 g/kg test = 3.8 min-1.microU-1.ml: r = 0.75, p < 0.05), although one anomalous test required that a constraint be applied to the modelling process for this agreement to obtain. Closest agreement between the 300 minute 0.3 and 0.5 g/kg IVGTTs was found when tests were modelled up to 180 minutes. An IVGTT duration of 180 minutes appears to be optimum for re-establishing the basal concentration necessary for effective modelling analysis. Application of constraints can markedly affect certain analyses and may introduce some bias; their use should be carefully monitored, although their effect on large datasets is likely to be small.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"26 4","pages":"139-53"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18651661","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":"C-peptide response to glucagon in type 2 diabetes mellitus: a comparison with oral glucose tolerance test.","authors":"Y Iwasaki,&nbsp;K Kondo,&nbsp;H Hasegawa,&nbsp;Y Oiso","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>C-peptide immunoreactivity (CPR) response during glucagon test (intravenous injection of 1 mg glucagon) was compared with CPR response during 75 g oral glucose tolerance test (oGTT) in 58 patients with newly-diagnosed, untreated type 2 (non-insulin-dependent) diabetes mellitus. Both tests were also repeated after blood glucose was well controlled with sulfonylurea or insulin in 17 patients. CPR secretory response was estimated by delta CPR, i.e. the difference between maximal and basal levels of CPR during each test. In the 58 untreated patients, the mean fasting plasma glucose (FPG) level was 12.8 +/- 0.6 mmol/L (M +/- SE), and there was no significant correlation between delta CPR during glucagon test and delta CPR during oGTT. The therapy for diabetes mellitus in 17 patients resulted in a fall in FPG (from 15.1 +/- 0.5 to 6.7 +/- 0.3 mmol/L) and a marked increase in delta CPR during oGTT (from 0.28 +/- 0.06 to 1.18 +/- 0.17 nmol/L, P < 0.01), but did not influence delta CPR during glucagon test (from 0.39 +/- 0.06 to 0.42 +/- 0.06 nmol/L, N.S.). In these patients, delta CPR during glucagon test before therapy correlated significantly with delta CPR during oGTT after therapy. Of the 13 patients who showed impaired CPR response during oGTT (delta CPR < 0.5 nmol/L) but substantial response during glucagon test (delta CPR > or = 0.5 nmol/L), 12 were successfully controlled without insulin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"25 3","pages":"129-37"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18676284","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":"Blood coagulation and fibrinolysis in obese NIDDM patients.","authors":"G Avellone,&nbsp;V Di Garbo,&nbsp;R Cordova,&nbsp;G Rotolo,&nbsp;G Abruzzese,&nbsp;G Raneli,&nbsp;R De Simone,&nbsp;G D Bompiani","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Four group of age- and sex-matched patients were studied: 1. nondiabetic subjects (n = 20) with a body mass index (BMI) < 25 Kg/m2 (lean control subjects); 2. obese non diabetic subjects (n = 22) with a BMI > 30 Kg/m2 (obese control subjects); 3. lean NIDDM subjects (n = 22); and 4. obese NIDDM subjects (n = 24). We determined: total cholesterol, triglycerides, HDL-cholesterol, blood glucose, Apolipoproteins A1 and B, insulin, Lp(a), Factor VII, fibrinogen, plasminogen, t-PA(Ag) pre and post venous occlusion (VO) and PAI activity pre and post VO. In addition to metabolic abnormalities obese non diabetic subjects and lean and obese NIDDM patients displayed significantly higher levels of fibrinogen, Factor VII, plasminogen, PAI pre and post VO and tPA(Ag) pre VO and significantly lower levels of t-PA(Ag) post VO. Our findings demonstrate an impairment of the haemostatic and fibrinolytic mechanisms which may be a key role in the pathogenesis of atherosclerotic vascular complications in obesity and in NIDDM.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"25 2","pages":"85-92"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18651655","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 endothelin levels in NIDDM patients with macroangiopathy.","authors":"M Donatelli,&nbsp;I Colletti,&nbsp;M L Bucalo,&nbsp;V Russo,&nbsp;S Verga","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To determine whether plasma endothelin, a potent vasoconstrictive peptide, is elevated in NIDDM patients, we compared a group of 15 NIDDM patients with macroangiopathy of mean age 60.60 +/- 2.33 years with 15 NIDDM randomly selected matched patients without macroangiopathy. Plasma endothelin levels were significantly increased in NIDDM patients with macroangiopathy (4.22 +/- 0.57 pmol/L) and in NIDDM patients without macroangiopathy (3.81 +/- 0.51 pmol/L). Although endothelin values did not differ between NIDDM groups, both represented significant difference from control values (2.46 +/- 0.24 pmol/L). No significant correlations were found between plasma endothelin and age (rs = 0.11), duration of diabetes mellitus (rs = 0.06), BMI (rs = 0.19), plasma glucose (rs = 0.15), plasma fructosamine (rs = 0.02). These findings confirm that in diabetes mellitus a primary disturbance in endothelin production from vascular endothelium exists as an early phenomenon rather than a result of advanced stage of the disease.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"25 4","pages":"159-64"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18651658","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 effects of in vitro and in vivo exposure to insulin upon prostaglandin E1 stimulation of platelet adenylate cyclase activity in healthy subjects.","authors":"T S Jap,&nbsp;C F Kwok,&nbsp;M C Wong,&nbsp;H Chiang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Insulin treatment of platelets is associated with increased prostaglandin E1-stimulated adenylyl cyclase activity and decreased platelet aggregation. Because non-insulin dependent (Type II) diabetes mellitus is associated with hyperinsulinemia, we sought to determine the effect of insulin treatment in vivo and in vitro upon stimulation of platelet adenylyl cyclase by prostaglandin E1. Incubation of platelet-rich plasma obtained from normal subjects with 2 microM prostaglandin E1 resulted in a 16-fold increase in cAMP accumulation. Pre-incubation of platelet-rich plasma with 0.7 nM insulin resulted in a 62% increase in prostaglandin E1 (2 microM)-stimulated cAMP accumulation (p < 0.005). Pretreatment of platelets with cholera toxin prior to incubation with insulin had no effect on subsequent prostaglandin E1-stimulated cAMP accumulation. By contrast, pretreatment of platelets with pertussis toxin prior to incubation with insulin resulted in a nearly 2-fold increase in prostaglandin E1-stimulated cAMP accumulation (p < 0.005). To determine whether platelets exposed in vivo to elevated concentrations of insulin would show similar responses, we isolated platelet-rich plasma from subjects before and after a 120 minute euglycemic clamp study in which insulin was infused (40 mU m-2min-1) intravenously. Patients who underwent the euglycemic clamp study achieved steady state serum levels on insulin of 0.70 +/- 0.19 pmol/ml. Platelets obtained after insulin infusion had a 65% increase in prostaglandin E1-stimulated cAMP. Our results indicate that serum levels of insulin that are common in patients with type II diabetes mellitus can increase the sensitivity of platelet adenylyl cyclase to stimulation by prostaglandin E1.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"27 1","pages":"39-46"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18652292","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 comparison of the metabolic profiles of fetal and maternal plasma and placenta in normal and diabetic rats by 1H magnetic resonance spectroscopy.","authors":"K J Brooks,&nbsp;C Lowy,&nbsp;C R Thomas","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Spectral analysis of spin-echo 1H magnetic resonance spectroscopy (MRS) data has revealed differences in the metabolic profiles of maternal and fetal plasma and placental extracts. Resonances from low-molecular weight components of the normal maternal and fetal plasma were attributed to glucose, lactate, creatine, citrate, amino acids and ketone bodies. There were also signals from lipoprotein molecules associated with lipid-transporting moeties contained in the plasma. The placental extract showed a similar composition to the plasma samples however the spectra were dominated by a large signal attributed to betaine, there was also an absence of signals from citrate, acetoacetate, acetone and lipoproteins. Diabetes caused profound changes in all tissue types indicating high levels of glucose and ketogenic activity. In both the maternal and fetal plasma there were increases in glucose, ketone bodies and valine in the diabetic rats, increases in lactate and alanine were confined to the fetal plasma and placenta. This study indicates that diabetes causes major changes in the composition of fetal plasma which in turn could interfere with the development of the fetus.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"26 3","pages":"117-25"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18627035","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":"Analysis of serum apolipoprotein A-I in elderly non-insulin-dependent diabetic patients.","authors":"M Folin,&nbsp;E Contiero,&nbsp;R Ferrari,&nbsp;G M Vaselli","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Quantitative and qualitative modifications of plasma apolipoproteins could provide additional information in predicting coronary heart disease (CHD) in non-insulin-dependent diabetes mellitus (NIDDM). We examined 17 men and 15 women aged over 65 years affected by NIDDM. Alcohol intake, smoking habits, antidiabetic therapy, body weight, stature, and body mass index were considered. Furthermore, serum lipids and apolipoprotein A-I and B levels were determined. Apo A-I was characterized by isoelectric focusing (IEF) and immunoblotting. The men were heavier and taller than the women. The women had significantly higher serum levels of total cholesterol, HDL-cholesterol, and apo A-I than the men. The levels of HDL-cholesterol, apo A-I and B were significantly influenced by an interaction between sex and the duration of diabetes. An invariant pattern was observed for apo A-I isoforms in samples from diabetic subjects of both sexes. The percentage distribution of serum apo A-I isoforms determined by densitometry is quite different from that previously reported in the literature for the general population. Quantitative modification in apo A-I isoforms could be due to the specific pathology and these variations could partly explain reduced levels of HDL-cholesterol in diabetic patients.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"26 4","pages":"155-71"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18652287","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":"Disparate effects of castration on renal structure and function in the streptozotocin diabetic rat.","authors":"L A Bach,&nbsp;M E Cooper,&nbsp;D Vranes,&nbsp;T J Allen,&nbsp;J Rumble,&nbsp;G Jerums","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Diabetic children are protected from the complications of diabetes until puberty, suggesting the involvement of a hormonal mechanism. In order to investigate the contribution of sex steroids to the development of diabetic nephropathy, castrated Wistar-Kyoto rats were made diabetic with streptozotocin and compared with intact diabetic rats. In intact rats, 32 weeks of diabetes resulted in hyperfiltration (p = 0.0001) and a marked increase in albuminuria (control, 1.3 x/divided by 1.3 vs diabetes intact, 11.8 x/divided by 1.3 mg/day, p < 0.001). Concomitant structural changes included glomerular basement membrane thickening (diabetes, 199.2 +/- 7.9 vs control, 175.9 +/- 3.9 nm, p = 0.02) and increased mesangial volume (diabetes, 194 +/- 14 vs control, 129 +/- 20 microns 3, p = 0.02). Although castration resulted in blood pressure lowering of 12 mmHg (p = 0.0003), albuminuria increased to the same extent in intact and castrated diabetic rats (castrated diabetic 10.5 x/divided by 1.3 mg/day). Glomerular filtration rate was lower in castrated rats than in intact rats prior to induction of diabetes, but increased similarly with induction of diabetes. Castrated diabetic rats had increased mesangial volume (castrated diabetic, 213 +/- 20 microns 3), but glomerular basement membrane thickness was lower than in intact diabetic rats (castrated diabetic, 179.5 +/- 4.5 nm). Thus, there is a dissociation between basement membrane thickening and albuminuria in this model of diabetic kidney disease. The mechanism of action of castration on glomerular function and structure remains to be elucidated but may relate to indirect effects such as reduction of blood pressure or renal polyol accumulation or a direct effect of sex steroids.</p>","PeriodicalId":77108,"journal":{"name":"Diabetes research (Edinburgh, Scotland)","volume":"27 1","pages":"27-38"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18652291","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}