Kidney360最新文献

{"title":"Alterations in Coagulation and Endothelial Function in Nephrotic Syndrome: A Multi-Center, Cross-Sectional Analysis.","authors":"Sarah Kelddal, Erik L Grove, Camilla L Duus, Louis B Nygaard, Tilde Kristensen, Frank H Mose, Jon W Gregersen, Anne-Mette Hvas, Henrik Birn","doi":"10.34067/KID.0000000865","DOIUrl":"https://doi.org/10.34067/KID.0000000865","url":null,"abstract":"<p><strong>Background: </strong>Nephrotic syndrome is associated with an increased risk of venous thromboembolism, but the underlying mechanism remains incompletely understood. The efficacy of prophylactic anticoagulant strategies is also poorly documented. To optimize preventive therapy, this study aimed to characterize the coagulation abnormalities in patients with nephrotic syndrome.</p><p><strong>Methods: </strong>This Danish multicenter, cross-sectional study included 47 adult patients with nephrotic syndrome, defined by plasma-albumin < 30g/L and urine albumin-creatinine ratio >2200mg/g. Exclusion criteria included estimated glomerular filtration rate < 30 mL/min/1.73m2, ongoing anticoagulant treatment, thrombophilia, prior thrombosis, malignancy, or pregnancy. Markers of endothelial cell function, platelet function, thrombin generation and fibrinolysis were compared to those of healthy individuals (n ranging from 10 to 174 depending on assay).</p><p><strong>Results: </strong>Patients with nephrotic syndrome (n = 47) had significantly increased thrombin generation markers compared to healthy individuals, as indicated by elevated prothrombin fragment 1+2 (509 pmol/L, 95% CI 426-592 vs. 183 pmol/L, 95% CI 171-196; p <0.001) and thrombin-antithrombin complex (3.5 µg/L, 95% CI 3.2-3.8 vs. 2.5 µg/L, 95% CI 2.3-2.7; p <0.001). Fibrinolysis was impaired, as demonstrated by prolonged 50% clot lysis time (1281 s, 95% CI 1101-1462 vs.: 964 s, 95% CI 843-1085; p = 0.004). Endothelial cell markers, including thrombomodulin, syndecan-1, and von Willebrand factor, were significantly elevated. In contrast, platelet function, natural anticoagulants, and other coagulation markers did not differ.</p><p><strong>Conclusions: </strong>Our results indicate that the prothrombotic state in nephrotic syndrome is driven by excessive thrombin generation and impaired fibrinolysis rather than increased platelet aggregation. In line with current guideline recommendations, this supports the rationale for antithrombotic strategies targeting secondary hemostasis rather than platelet function in patients with nephrotic syndrome.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248573","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":"Prevalence of Kidney Stones in US Hispanic/Latino Adults: Findings from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL).","authors":"Marcelino E Rivera, Ana C Ricardo, Jinsong Chen, Jennifer L Ennis, Joseph J Crivelli, Robert Burk, Jianwen Cai, Martha L Daviglus, James P Lash","doi":"10.34067/KID.0000000882","DOIUrl":"https://doi.org/10.34067/KID.0000000882","url":null,"abstract":"","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248574","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":"Financial Toxicity in ESKD.","authors":"Lindsey M Maclay, Kyle Woodward, Natalie Strohmayer, Miko E Yu, Sumit Mohan, Anne M Huml, Syed Ali Husain","doi":"10.34067/KID.0000000857","DOIUrl":"https://doi.org/10.34067/KID.0000000857","url":null,"abstract":"<p><strong>Background: </strong>Patients with kidney failure require treatments that are demanding and time-intensive, potentially interfering with employability and leading to indirect costs. We sought to characterize the prevalence of, and risk factors for financial toxicity among patients with kidney failure.</p><p><strong>Methods: </strong>We conducted a cross-sectional survey study of 112 participants with kidney failure at a large, urban, academic medical center. Financial toxicity was assessed via a survey which included the validated CoST tool as well as additional items to evaluate self-reported changes to material conditions and financial coping behaviors. Participants were grouped according to kidney replacement therapy modality (dialysis, transplant after dialysis, or preemptive transplant) Descriptive statistics were used to summarize demographic and clinical characteristics of the study population and to compare those with above-median vs below-medial CoST scores, and by modality of kidney replacement therapy.</p><p><strong>Results: </strong>Median CoST score was 17 with 71% of participants experiencing at least mild financial toxicity. Participants experiencing financial toxicity were less likely to have White race, and more likely to be receiving dialysis. Over half of participants reported reduction in employment (61%) or income (57%) following kidney failure onset with the greatest likelihood of these among participants with any dialysis.</p><p><strong>Conclusions: </strong>Adults with kidney failure experience significant financial toxicity as measured by the CoST score and report significant negative changes in employment and income. Although this toxicity persists through many stages of treatment, treatment modality may impact financial burdens experienced by patients with kidney failure.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234477","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":"Association of Cannabis Use With Access to Kidney Transplantation and Post-Transplant Outcomes.","authors":"Danielle S Kroll, Kyle J Woodward, Syed Ali Husain","doi":"10.34067/KID.0000000858","DOIUrl":"https://doi.org/10.34067/KID.0000000858","url":null,"abstract":"","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225843","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":"Nfkb1 Removal from Proximal Tubule Cells Improves Renal Tubular Outcomes Following Ischemia Reperfusion Injury.","authors":"Shun-Yang Cheng, Kari Koppitch, Jinjin Guo, Nathan Moy, Taylor L Simonian, Parker C Wilson, Andrew P McMahon","doi":"10.34067/KID.0000000868","DOIUrl":"https://doi.org/10.34067/KID.0000000868","url":null,"abstract":"<p><strong>Background: </strong>CKD is a significant global health burden. AKI is a risk factor for progression to CKD. Recent studies have linked a failure in proximal tubule repair as a potential contributing factor to CKD in mouse and human studies. Failed repair proximal tubule cells (FR-PTCs), initially present at the site of maximal sensitivity to ischemia reperfusion injury and spreading to more cortical regions over time, adopt a senescence-associated secretory phenotype (SASP) linked to activation of the NF-kB pathway. Several transcriptional regulatory factors mediate NF-kB pathway action. Of these, Nfkb1 is prominent within FR-PTCs and chromatin studies predict Nfkb1 interactions with pathology-associated gene targets.</p><p><strong>Methods: </strong>To examine the role of NF-kB in nephron injury outcomes, we removed Nfkb1 activity within the nephron lineage of the mouse kidney and examined the kidney's response to bilateral ischemia reperfusion injury (Bi-IRI).</p><p><strong>Results: </strong>Single cell transcriptional analysis showed a significant reduction of inflammation-associated gene expression, including Ccl2, Birc3, Spp1, Cd47, and Traf1, in Nfkb1 deficient FR-PTCs. A reduced pathological signature correlated with normalized expression of genes associated with healthy proximal tubule function including Cubn, Kap, and a number of solute carriers. Single-nucleus ATAC-seq analysis linked transcriptomic changes to enhancer regulation, in particular, marked opening of chromatin for targets of HNF-family members associated with normal regulation of gene expression in PTCs.</p><p><strong>Conclusions: </strong>Examining ATAC-seq motif predictions and performing direct immunolabelling studies suggested Relb, another transcriptional mediator of NF-κB transcriptional responses with overlapping targeting specificity to Nfkb1, may partially compensate for the loss of Nfkb1. These studies support future efforts to remove ongoing NF-κB signaling within nephrons as a potential therapeutic strategy to target the AKI-to-CKD transition.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225845","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":"CKD-Induced Oxidative Twitch Muscle Atrophy is Mediated by Transforming Growth Factor-β.","authors":"Kyoka Homma, Yuki Enoki, Kazuaki Taguchi, Kazuaki Matsumoto","doi":"10.34067/KID.0000000852","DOIUrl":"https://doi.org/10.34067/KID.0000000852","url":null,"abstract":"<p><strong>Background: </strong>Understanding the vicious cycle driving renal impairment progression and skeletal muscle atrophy in chronic kidney disease (CKD) is crucial. Therefore, this study aimed to examine the role of transforming growth factor-beta (TGF-β) in promoting skeletal muscle atrophy in CKD.</p><p><strong>Methods: </strong>A combined model of 2/3 nephrectomy and unilateral ureteral ligation, as we previously reported, was used for CKD mice. Skeletal muscle weight and changes in skeletal muscle fiber twitch type were evaluated. Using C2C12 cells, a skeletal muscle myoblast cell line, molecules that induce a reduction in type IIa muscle fibers in CKD were identified. The identified molecule, TGF-β, was administered to mice to investigate its effects on muscle fiber-type changes. Furthermore, the effects of administering a TGF-β inhibitor to CKD mice were evaluated.</p><p><strong>Results: </strong>In CKD mice, myosin heavy chain (MyHC)-specific antibody immunostaining showed an increase in atrophied MyHC IIa (oxidative twitch) muscle fibers. CKD mouse serum preferentially induces MyHC IIa fiber atrophy in C2C12 cells. TGF-β-treated mice had reduced levels of oxidative metabolic skeletal muscle and oxidative type IIa fiber, similar to CKD mice. Furthermore, TGF-β inhibitor treatment prevented the CKD-associated decrease in oxidative type IIa muscle fiber size and reduced exercise capacity.</p><p><strong>Conclusions: </strong>These findings indicate that TGF-β causes skeletal muscle deterioration in CKD by reducing oxidative metabolism and inducing type IIa fiber atrophy. In addition, our results emphasize that reversing the disrupted MyHC phenotype in CKD is a potential therapeutic target for CKD-induced muscle atrophy.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225844","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 Novel Ultrafiltration Rate Feedback Controller for Use in Hemodialysis First Clinical Experience: First Clinical Experience: An Interventional Pilot Study.","authors":"Stephan Thijssen, Lemuel Rivera Fuentes, Leticia Mirell Tapia Silva, Xiaoling Ye, Sabrina Casper, Doris H Fuertinger, Stefan Fuertinger, Peter Kotanko","doi":"10.34067/KID.0000000839","DOIUrl":"https://doi.org/10.34067/KID.0000000839","url":null,"abstract":"<p><strong>Background: </strong>Relative blood volume (RBV) monitors are increasingly being used during hemodialysis. Manual ultrafiltration rate (UFR) adjustments to establish a favorable RBV trajectory are not feasible in routine practice. The goal of this study was to characterize the behavior of a new UFR feedback controller in vivo.</p><p><strong>Methods: </strong>In this pilot trial, chronic hemodialysis patients were prospectively studied during up to six successful study dialysis treatments each. During each study visit, the feedback controller generated UFR recommendations designed to guide the subject's RBV curve towards a pre-defined target trajectory. Each recommendation was evaluated by licensed healthcare staff and then either implemented or disregarded. Results were compared to standard-of-care treatments in the same subjects.</p><p><strong>Results: </strong>Fifteen subjects (age 59 ± 15 years, 8 males) were studied during a total of 63 treatments. The controller functioned as intended and issued a total of 1 037 recommendations. Compared to standard-of-care treatments, its use was associated with a higher probability of RBV target range attainment (69% vs. 47%) and lower nadir systolic (106 vs. 111 mmHg) and diastolic (55 vs. 59 mmHg) blood pressure.</p><p><strong>Conclusions: </strong>The UFR feedback controller operated as intended, and its use led to a substantial increase in the rate of RBV target range attainment. This technology holds promise for improving fluid management in chronic hemodialysis patients.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225842","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 Gut Microbiome in Autosomal Dominant Polycystic Kidney Disease: A Cross-Sectional Study.","authors":"Fabian Woestmann, Sebastian Strubl, Fedja Farowski, Sita Arjune, Anastasia Tsakmaklis, Polina Todorova, Martin R Späth, Susanne Brodesser, Till Baar, Franziska Grundmann, Maria J G T Vehreschild, Roman-Ulrich Müller","doi":"10.34067/KID.0000000836","DOIUrl":"https://doi.org/10.34067/KID.0000000836","url":null,"abstract":"<p><strong>Background: </strong>Changes in gut microbiota signatures have been associated with chronic kidney disease and nephrolithiasis and may thus be a factor explaining variability of outcome in ADPKD. We aimed to characterize the intestinal microbiome in a cross-sectional study of patients with ADPKD and to explore the potential impact of microbiome signatures on PKD disease progression.</p><p><strong>Methods: </strong>This observational cross-sectional pilot study recruited 25 patients from the AD(H)PKD patient cohort and 12 healthy, age- and sex matched control subjects. The gut microbiome was analyzed by 16S rRNA gene profiling of stool samples. Bacteria-derived serum uremic toxins were measured using liquid chromatography coupled to tandem mass spectrometry. Microbiome data was correlated with age, kidney function, and markers of PKD disease progression like Mayo classification and arterial hypertension <35 years of age.</p><p><strong>Results: </strong>Patients with ADPKD displayed a significantly decreased abundance of Actinobacteria including probiotic Bifidobacteriaceae and significantly increased abundance of Enterobacteriaceae. Those findings were independent of kidney function. Most notably, Streptococcaceae were significantly overrepresented in patients with Mayo Classes 1D and 1E compared to 1A-1C. Additionally, early onset of hypertension (< 35 years of age) was associated with an increased abundance of Proteobacteria and a decreased abundance of Tannerelleaceae. Furthermore, patients with ADPKD revealed an increased abundance of Peptococcaceae with increasing age and declining kidney function. Finally, serum uremic toxin levels were significantly increased in patients with ADPKD, highly correlating with eGFR.</p><p><strong>Conclusions: </strong>This pilot study suggests relevant changes in gut microbiota signatures of patients with ADPKD which might be associated with rapid disease progression. These findings indicate that composition of the gut microbiota could potentially contribute to disease progression of ADPKD and the individual disease variability. Further investigation is warranted to assess the gut microbiota as a potential therapeutic target in ADPKD.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216293","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":"Clinicopathological Characteristics and Long-Term Kidney Outcomes in Biopsy-Proven Renal Sarcoidosis.","authors":"Jing Miao, Charat Thongprayoon, Wisit Cheungpasitporn, Alessia Buglioni, Ladan Zand, Fernando Fervenza","doi":"10.34067/KID.0000000842","DOIUrl":"https://doi.org/10.34067/KID.0000000842","url":null,"abstract":"<p><strong>Background: </strong>Renal sarcoidosis (RS) is a rare but potentially severe manifestation of sarcoidosis, primarily affecting the kidneys through granulomatous interstitial nephritis (GIN) and calcium metabolic disturbances. This study evaluates the clinicopathological features and renal outcomes of biopsy-proven RS, focusing on identifying predictors of renal recovery and disease progression.</p><p><strong>Methods: </strong>This retrospective study included 43 biopsy-proven RS at Mayo Clinic (2012-2024). Demographic, clinical, laboratory, and histopathological data were analyzed. Renal recovery within six months was classified as complete, partial, or no recovery based on serum creatinine (sCr) changes. Long-term adverse composite outcomes included the chronic kidney disease (CKD) onset, CKD progression, end-stage kidney disease, dialysis initiation, or death. Logistic regression and Cox proportional hazards regression were used to assess predictors of renal outcomes.</p><p><strong>Results: </strong>Among cohort, 84% exhibited interstitial nephritis, with GIN in 33%. Calcium phosphate deposits were found in 58% of cases. Hypercalciuria (90%) was more common than hypercalcemia (74%). Within six months, 86% achieved recovery (74% complete, 12% partial), while 40% experienced long-term adverse composite outcomes. Higher sCr at biopsy (≥ 2.4 mg/dL) and moderate-to-severe interstitial fibrosis and tubular atrophy (IFTA) were associated with reduced complete recovery and worse long-term outcomes; while pre-existing CKD significantly increased the risk of adverse long-term outcomes. Steroid therapy significantly increased the likelihood of complete recovery and reduced the risk of adverse long-term outcomes.</p><p><strong>Conclusions: </strong>Pre-existing CKD, elevated sCr at biopsy, IFTA, and steroid therapy are key predictors of renal outcomes in RS. Early diagnosis and intervention are crucial to preventing irreversible kidney damage.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208899","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":"Comparative Analysis of Human Kidney Organoid and Tubuloid Models.","authors":"Ana B Nunez-Nescolarde, Leilani L Santos, Lingyun Kong, Elif Ekinci, Paddy Moore, Evdokia Dimitriadis, David J Nikolic-Paterson, Alexander N Combes","doi":"10.34067/KID.0000000834","DOIUrl":"https://doi.org/10.34067/KID.0000000834","url":null,"abstract":"<p><strong>Background: </strong>Epithelial kidney organoids (tubuloids) made from kidney biopsies, urine, or iPSC-derived kidney organoids offer new opportunities in experimental and clinical nephrology. Yet, we have limited knowledge of how tubuloid models differ from each other, from iPSC-derived kidney organoids and from the human kidney. New insight is required to guide model selection for studies in kidney physiology and disease.</p><p><strong>Methods: </strong>Tubuloids were generated from adult nephrectomy samples (adult tubuloids n=3), iPSC-derived kidney organoids (iTubuloids n=3), and for the first time, from human fetal kidneys (fetal tubuloids n=3). Kidney organoid and tubuloid models were compared to each other and to adult human kidney using bulk RNA sequencing. As a proof of principle study, the potential to investigate the tubular response to repeated hypoxic insults was examined in iTubuloids.</p><p><strong>Results: </strong>Expression signatures of proximal and distal tubules were stronger in adult kidneys than any organoid or tubuloid model. iPSC-derived kidney organoids expressed proximal tubule markers at higher levels than any tubuloid culture, despite adult tubuloids being derived from mature kidneys. Collecting duct signatures were enriched in adult and fetal tubuloids. Adult tubuloids showed stronger signatures of ageing and inflammation, while fetal tubuloids had enhanced ureteric tip progenitor signatures. Over 80 genes linked to inherited disorders were expressed in all tubuloid cultures, while a further 54 were expressed at higher levels in either adult, fetal or iTubuloids. iTubuloids subject to a single hypoxic injury effectively recovered by the end of the passage, while cultures exposed to hypoxia over three passages expressed markers of maladaptive repair.</p><p><strong>Conclusions: </strong>This study provides new transcriptome-wide reference data to aid in the selection and optimization of disease modelling for the human kidney. It defines common and unique opportunities to model inherited disorders in adult, fetal and iTubuloid models and illustrates new potential to model repetitive injury in long-lived tubuloid cultures.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150968","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}