Diabetology International最新文献

{"title":"Anti-GAD antibody-negative, anti-IA2 antibody-positive slowly progressive insulin-dependent diabetes mellitus and Graves' disease preceded by childhood-onset minimal change nephrotic syndrome: a case report.","authors":"Yoshimi Kodama, Taijiro Okabe, Shuji Sasaki, Hisashi Yokomizo, Ryuichi Sakamoto, Kazuhiko Niimi, Yoshihiro Ogawa","doi":"10.1007/s13340-024-00787-6","DOIUrl":"10.1007/s13340-024-00787-6","url":null,"abstract":"<p><p>It is rare for a patient to have minimal change nephrotic syndrome, slowly progressive insulin-dependent diabetes mellitus, and Graves' disease in combination. In this case, a patient developed idiopathic nephrotic syndrome at the age of 11 years. She was diagnosed with frequently relapsing nephrotic syndrome and steroid-dependent nephrotic syndrome after repeated increases in urinary protein levels with prednisolone reduction. At the age of 14 years, steroid-induced diabetes was suspected because she was negative for anti-glutamic acid decarboxylase (GAD) antibody, and her glycemic control improved after medication. At the age of 16 years, her nephrotic syndrome was in remission, but even after discontinuation of cyclosporine, her glycemic control did not improve. Decreased insulin secretion and positive anti-insulinoma-associated protein-2 (IA2) antibody were found, and therefore she was diagnosed as having slowly progressive insulin-dependent diabetes mellitus (SPIDDM). Although her glycemic control was stable with insulin therapy, she was diagnosed with asymptomatic Graves' disease at the age of 28 years and started treatment. Human leukocyte antigen testing (HLA) was performed to evaluate the etiology of the disease, which revealed A*02:01, B*35:01, DQA1*03:01, DQB1*03:02, DQB1*04:01, DRB1*04:05, DRB1*08:02, and DPB1*05:01, suggesting genetic involvement of HLA for each disease susceptibility.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 2","pages":"421-426"},"PeriodicalIF":1.3,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term efficacy and safety of early sitagliptin initiation in individuals with type 2 diabetes: an extension of the SPIKE study.","authors":"Tomoya Mita, Naoto Katakami, Hidenori Yoshii, Tomio Onuma, Hideaki Kaneto, Takeshi Osonoi, Toshihiko Shiraiwa, Tetsuyuki Yasuda, Yutaka Umayahara, Tsunehiko Yamamoto, Hiroki Yokoyama, Nobuichi Kuribayashi, Kazunari Matsumoto, Masahiko Gosho, Iichiro Shimomura, Hirotaka Watada","doi":"10.1007/s13340-024-00786-7","DOIUrl":"10.1007/s13340-024-00786-7","url":null,"abstract":"<p><strong>Aims/instruction: </strong>We previously demonstrated that sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, slowed down the progression of carotid atherosclerosis in type 2 diabetes participants who were treated with insulin and had no history of cardiovascular disease in the Sitagliptin Preventive study of Intima-Media Thickness Evaluation (SPIKE) trial. This was an extension of the SPIKE trial that examined if early sitagliptin initiation improved long-term cardiovascular outcomes.</p><p><strong>Materials and methods: </strong>In the SPIKE trial, 282 participants were randomized to either sitagliptin or conventional treatment to examine the effects of sitagliptin on carotid atherosclerosis. All participants who completed the SPIKE trial were recruited to this prospective, observational, cohort study and followed for up to 520 weeks. The primary endpoint was the first occurrence of a major cardiovascular event, which included acute myocardial infarction, stroke, or total mortality.</p><p><strong>Results: </strong>Events of composite primary outcome occurred in only a few participants in each group (15 [12.6%] in the sitagliptin group and eight in the conventional treatment group [6.7%]). The incidence rate of the primary outcome did not differ significantly between two groups. In post hoc Poisson regression analysis, there were no significant between-group differences in the incidence rates of composite recurrence events for the same outcomes as the primary endpoint.</p><p><strong>Conclusions: </strong>Early initiation of sitagliptin as add-on therapy to insulin was not linked to reduced risk of composite cardiovascular disease. This may be due to low event numbers in both groups and/or relatively lower continuation rates of DPP-4 inhibitors in the sitagliptin group during the follow-up period.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s13340-024-00786-7.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 2","pages":"272-284"},"PeriodicalIF":1.3,"publicationDate":"2025-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the pathophysiology of type 2 diabetes with a new selectively bred animal model, the Oikawa-Nagao mouse.","authors":"Mototsugu Nagao","doi":"10.1007/s13340-024-00784-9","DOIUrl":"10.1007/s13340-024-00784-9","url":null,"abstract":"<p><p>Type 2 diabetes (T2D) is a polygenic disease, and the development of animal models by selective breeding is crucial for understanding its etiology, pathophysiology, complications, and treatments. We recently developed a new T2D model, the Oikawa-Nagao (ON) mouse, by selectively breeding mice with inferior glucose tolerance [diabetes-prone (ON mouse DP®; ON-DP) strain] and superior glucose tolerance [diabetes-resistant (ON mouse DR®; ON-DR) strain] on a high-fat diet. ON-DP mice are predisposed to develop diabetes and obesity after being fed a high-fat diet, compared to ON-DR mice. These phenotypes provide valuable insights into the genetic and environmental interactions for the etiology of T2D. Our studies revealed that the emergence of these phenotypes is associated with novel pathophysiological mechanisms, such as low insulin secretion capacity associated with high CD36 expression in pancreatic β-cells and hypoleptinemia preceding obesity due to low leptin secretion capacity in adipocytes. In addition, ON-DP mice fed an atherogenic diet exhibit accelerated atherosclerosis, likely related to blood glucose fluctuations. These findings provide new perspectives on the pathogenesis of T2D and suggest potential prevention and treatment strategies. This review will present the development strategy of the ON mouse strain, representative metabolic phenotypes, and discuss the mechanisms driving these traits, and explore their relevance to human T2D and obesity.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 1","pages":"13-22"},"PeriodicalIF":1.3,"publicationDate":"2025-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes mellitus and peripheral artery disease.","authors":"Mitsuyoshi Takahara","doi":"10.1007/s13340-024-00785-8","DOIUrl":"10.1007/s13340-024-00785-8","url":null,"abstract":"<p><p>Atherosclerotic peripheral artery disease (PAD), that is, arteriosclerosis obliterans, is pathologically rooted in atherosclerosis, similar to other cardiovascular diseases. In addition to smoking, hypertension, and dyslipidemia, diabetes mellitus is a major risk factor. People with diabetes mellitus have an elevated risk of developing PAD. PAD in turn increases the risk of diabetic foot ulcers and gangrene in the population. Rest pain, nonhealing ulcers, and gangrene associated with chronic ischemia are known as chronic limb-threatening ischemia (CLTI). This article gives an overview of the link between atherosclerotic PAD, particularly CLTI, and diabetes mellitus. First, the clinical impact of CLTI among patients with diabetes mellitus is presented. Second, its clinical features, including prognosis, comorbidity, occurrence, and seasonality, are mentioned. The clinical management of CLTI is also discussed. Diabetes mellitus has notable clinical impact on CLTI and vice versa. CLTI has different clinical features from those of other atherosclerotic cardiovascular diseases. Its clinical profile also differs between individuals with both diabetes mellitus and CLTI and general people with diabetes mellitus. There is considerable room for improvement in CLTI treatment and management. Clinical measures taken before revascularization, including CLTI risk assessment, prompt diagnosis, and expedited referral to vascular specialists, may enhance CLTI outcomes. Further research is warranted to obtain more evidence.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 1","pages":"7-12"},"PeriodicalIF":1.3,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acknowledgment to the Reviewers.","authors":"","doi":"10.1007/s13340-024-00782-x","DOIUrl":"https://doi.org/10.1007/s13340-024-00782-x","url":null,"abstract":"","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 1","pages":"199-200"},"PeriodicalIF":1.3,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiological hallmarks in type 2 diabetes heterogeneity (review).","authors":"Dipamoy Datta, Raja Kundu, Rajdeep Basu, Partha Chakrabarti","doi":"10.1007/s13340-024-00783-w","DOIUrl":"10.1007/s13340-024-00783-w","url":null,"abstract":"<p><p>The mechanistic complexity in type 2 diabetes (T2DM) is primarily responsible for the degrees of heterogeneity and development of complications. A complex mode of interactions between different pathophysiological events and diabetogenic environmental factors support for the genesis of diabetes heterogeneity both in phenotypic and clinical contexts. The currently used diabetes classification strategies suffer from several inconsistencies that cannot fully capture the inherent heterogeneity among the diabetes patients. To effectively address this pathobiological and heterogeneity-related issue in diabetes research, the current review proposes nine pathophysiological hallmarks of T2DM that aims to mechanistically explain complexities of diabetes associated pathophysiological events and their underlying features. These pathophysiological hallmarks are pancreatic beta cell dysfunction, insulin sensitivity, insulin resistance, obesity, aging, subclinical inflammation, metabolic dysregulation, prothrombotic state induction and hypertension. Detail knowledge of these pathophysiological hallmarks with their key molecular mediators, influencing factors, clinical biomarkers and clinical assessment methodologies will greatly support precision medicine approaches in diabetes including patient stratification, subtype diagnosis and treatment.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s13340-024-00783-w.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 2","pages":"201-222"},"PeriodicalIF":1.3,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term effects of esaxerenone in patients with type 2 diabetes, diabetic kidney disease, and hypertension (JDDM77).","authors":"Daigaku Uchida, Yasunori Sato, Azuma Kanatsuka, Nobuichi Kuribayashi, Susumu Nakamura, Shigetake Ko, Hiroshi Maegawa","doi":"10.1007/s13340-024-00779-6","DOIUrl":"10.1007/s13340-024-00779-6","url":null,"abstract":"<p><strong>Objectives: </strong>This clinical study assessed the three-year, long-term effects of esaxerenone, a non-steroidal aldosterone receptor blocker, on Japanese patients with type 2 diabetes, diabetic kidney disease, and hypertension who were receiving renin-angiotensin system inhibitors.</p><p><strong>Materials and methods: </strong>Data from a computerized diabetic care database were used to retrospectively compare esaxerenone users (Group A) with non-esaxerenone users (Group B). Propensity score weighting was applied to Group B. The study primarily focused on percent changes in the Urine Albumin-Creatinine Ratio (UACR) from baseline and also examined the estimated Glomerular Filtration Rate (eGFR), blood pressure, serum potassium levels, and HbA1c.</p><p><strong>Results: </strong>There were 199 patients in Group A and 199 in Group B, matched 1:1 using propensity scores. UACR and blood pressure were significantly lower in Group A than in Group B. Geometric mean percent changes in UACR from baseline between the two groups were as follows: - 62.7% at 1 year (95% Confidence Interval (CI): - 91.0 to - 34.1%), - 48.9% at 2 years (95% CI: - 79.4 to - 19.3%), and - 63.8% at 3 years (95% CI: - 107.4 to - 20.2%). Additionally, the present study examined the impact of combining esaxerenone with SGLT2 inhibitors and GLP-1 receptor agonists and showed consistent effects on UACR irrespective of these medications. Esaxerenone slightly lowered eGFR with a low risk of hyperkalemia but did not adversely impact glucose metabolism.</p><p><strong>Conclusions: </strong>Esaxerenone exerted antihypertensive and antialbuminuric effects in patients with type 2 diabetes, diabetic kidney disease, and hypertension.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 1","pages":"153-161"},"PeriodicalIF":1.3,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined associations of education and health literacy with preventive dental visits in patients with diabetes: a nationwide cross-sectional study.","authors":"Kyoko Saito, Yuki Kawai, Hirono Ishikawa, Takahiro Tabuchi, Keisuke Kuwahara","doi":"10.1007/s13340-024-00780-z","DOIUrl":"10.1007/s13340-024-00780-z","url":null,"abstract":"<p><strong>Aim: </strong>Oral health is important in patients with diabetes. While health literacy may promote preventive dental visits, the evidence is sparse among them. Additionally, because education is indicated as a determinant of health literacy, none clarified whether health literacy can mitigate educational inequalities in healthcare-seeking behaviors. We examined combined associations of education and health literacy with preventive dental visits in patients with diabetes.</p><p><strong>Methods: </strong>We used cross-sectional data from the Japan COVID-19 and Society Internet Survey (JACSIS) in 2020. We included 1441 patients reporting to have diabetes currently. Educational level was self-reported. Health literacy was measured using the validated scale. Preventive dental visits in the past 12 months were self-reported. We estimated multivariable-adjusted prevalence ratio (PR) for preventive dental visits.</p><p><strong>Results: </strong>54% of the participants had preventive dental visits; 35% had high health literacy. Overall, high health literacy was significantly associated with preventive dental visits. Being more educated and/or having high health literacy were associated with an increased prevalence of preventive dental visits (<i>P</i> for trend < 0.001). Compared with less education and low health literacy group, adjusted PRs (95% confidence intervals) of preventive dental visits were 1.10 (0.93, 1.31) for less education and high health literacy group, 1.14 (1.00, 1.30) for more education and low health literacy group, and 1.29 (1.13, 1.48) for more education and high health literacy group.</p><p><strong>Conclusions: </strong>The present data suggest that health literacy may help promote preventive dental visits and do not deny the possibility that health literacy can mitigate educational inequalities in patients with diabetes.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s13340-024-00780-z.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 1","pages":"145-152"},"PeriodicalIF":1.3,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of CK2 against endoplasmic reticulum stress in pancreatic β cells.","authors":"Tomoko Takai, Shun-Ichiro Asahara, Hiroko Ikushiro, Kenta Kobayashi, Takato Yano, Yoshiaki Kido, Wataru Ogawa","doi":"10.1007/s13340-024-00775-w","DOIUrl":"10.1007/s13340-024-00775-w","url":null,"abstract":"<p><p>Endoplasmic reticulum (ER) stress due to obesity or systemic insulin resistance is an important pathogenic factor that could lead to pancreatic β-cell failure. We have previously reported that CCAAT/enhancer-binding protein β (C/EBPβ) is highly induced by ER stress in pancreatic β cells. Moreover, its accumulation hampers the response of these cells to ER stress by inhibiting the induction of the molecular chaperone 78 kDa glucose-regulated protein (GRP78). We also demonstrated that C/EBPβ is phosphorylated by CK2, which is reportedly associated with the ER stress signal. In the present study, we aimed to clarify the mechanisms underlying the effect of CK2 on pancreatic β cells using a CK2-specific inhibitor, CX4945, and shRNA-mediated knockdown and overexpression of CK2β, the regulatory subunit of CK2. The results indicate that CK2 was activated in MIN6 cells under ER stress and in pancreatic β cells of a diabetic mouse model. Under normal conditions, CK2 interacted with FL-ATF6α in MIN6 cells and regulated the expression of GRP78 and ERAD-associated proteins. Mechanistically, CK2 activation in MIN6 cells upon the overexpression of the CK2β subunit reduced ER stress signals and the accumulation of unfolded proteins via an increase in GRP78 and ERAD-associated protein levels. These results highlight the important role of CK2 in protecting against ER stress-induced apoptosis by regulating GRP78 and ERAD proteins. CK2 contributed to the clearance of unfolded or misfolded proteins in MIN6 cells under both normal and ER stress conditions. Therefore, CK2 activation could be a promising novel approach for preventing type 2 diabetes.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s13340-024-00775-w.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 1","pages":"131-144"},"PeriodicalIF":1.3,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differentiation, reduction, and proliferation of pancreatic β-cells and their regulatory factors.","authors":"Akari Inada","doi":"10.1007/s13340-024-00774-x","DOIUrl":"10.1007/s13340-024-00774-x","url":null,"abstract":"<p><p>The prevalence of diabetes has increased rapidly in recent years, and many types of therapeutic agents have been developed. However, the main purpose of these drugs is to lower blood glucose levels, and they are not fundamental solutions. In contrast, our research has been aimed at stimulating and inducing β-cell proliferation in vivo and replenishing β-cells. We demonstrated that pancreatic ductal cells are a source of β-cells both after birth and during regeneration after partial duct ligation: cell lineage tracing showed that 39% of growing islets and 50% of adult islets during tissue regeneration contained β-cells differentiated from duct cells. We also examined the factors contributing to β-cell depletion. Insulin and cyclin A genes are tightly regulated by transcriptional activators and repressors, and we found that imbalanced and excessive levels of repressors result in a drastic reduction of insulin and β-cell numbers, leading to severe diabetes. Thus, we searched for factors that induce β-cell proliferation in vivo. In our transgenic (Tg) mice, there was a sex difference in the progression of diabetes and sex steroid hormones were shown to contribute to this. Surprisingly, in diabetic male Tg mice, modulation of sex steroid hormones under certain conditions resulted in a marked increase of β-cells. We identified Greb1 as a factor inducing β-cell proliferation in response to a rapid elevation of E2 levels. This series of studies has demonstrated that islet cells exhibit plasticity and indicates that changes of islet cell mass and function are dynamic and recoverable.</p>","PeriodicalId":11340,"journal":{"name":"Diabetology International","volume":"16 1","pages":"23-29"},"PeriodicalIF":1.3,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}