Nephron最新文献

{"title":"Further Clinical and Biochemical Phenotype of GLA p.A143T: a Fabry Disease Newborn Screening Experience.","authors":"Allison M Paltzer, Allegra M Quadri, Carly Rasmussen, Raphael Schiffmann, Joel Charrow, Carlos E Prada","doi":"10.1159/000543920","DOIUrl":"https://doi.org/10.1159/000543920","url":null,"abstract":"<p><strong>Background: </strong>In 2015, Illinois added Fabry disease to the newborn screening (NBS) panel, and numerous individuals who have the controversial p.A143T GLA variant were identified. Ann &amp; Robert H. Lurie Children's Hospital of Chicago identified 80 individuals with this variant.</p><p><strong>Summary: </strong>Of the 80 individuals, 34/80 were identified by NBS, 2/80 were identified by gene panel testing, and 44/80 were identified by cascade testing. These individuals were from 36 families and ranged in age from 7 months to 71 years. Most individuals identified by NBS were male (90.9%) and 35.96% had the p.A143T variant. All newborns with known pathogenic or likely pathogenic variants in GLA had enzyme leukocyte activities below 20% of the percentage of mean of normal. This threshold could serve as a guideline for determining risk of symptom development for p.A143T and other variants of unknown significance. No person with p.A143T had significant lyso-GL3 elevation in this cohort.</p><p><strong>Key messages: </strong>These data suggest the variant impacts enzyme levels, but its effect on health outcomes remains unclear. We further characterize clinical and biochemical data on individuals with the p.A143T GLA variant to help provide guidance on its clinical significance.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-14"},"PeriodicalIF":2.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation between plasma aldosterone concentrations and simple renal cyst in hypertensive patients.","authors":"Huimin Ma, Xintian Cai, Shuaiwei Song, Qing Zhu, Junli Hu, Di Shen, Wenbo Yang, Yingying Zhang, Rui Ma, Pan Zhou, Delian Zhang, Qin Luo, Jing Hong, Nanfang Li","doi":"10.1159/000545105","DOIUrl":"https://doi.org/10.1159/000545105","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have linked primary aldosteronism to simple renal cysts (SRC), but the relationship between plasma aldosterone concentration (PAC) and SRC remains unclear. This study aimed to investigate the association between PAC and SRC in hypertensive patients.</p><p><strong>Methods: </strong>A total of 30,135 hypertensive patients who visited our hospital from January 2014 to December 2023 were included. Logistic regression analyses were conducted to explore the relationship between PAC and SRC, while restricted cubic splines (RCS) assessed the dose-response relationship. SRC were further categorized by size (≥ 2 cm) and number (≥ 2). Subgroup analyses were performed to evaluate PAC effects across different conditions.</p><p><strong>Results: </strong>Multivariate logistic regression showed a positive association between PACPAC levels (per 5-ng/dL increase) and SRC (OR: 1.20, 95% CI: 1.17 ~ 1.23) after adjusting for confounders. Compared to the lowest PAC quartile (Q1), the Q2, Q3, and Q4 groups had progressively higher risks of SRC, with ORs of 1.03 (95% CI: 0.95 ~ 1.12), 1.25 (95% CI: 1.15 ~ 1.35), and 1.65 (95% CI: 1.52 ~ 1.78), respectively. Combining Q3 and Q4 (PAC ≥ 14.92) yielded an OR of 1.41 compared to Q1 and Q2 (< 14.92). Similar trends were observed for SRC size ≥ 2 cm and number ≥ 2. RCS analysis confirmed a linear dose-response relationship between PAC and SRC risk. Subgroup and sensitivity analyses consistently supported these findings.</p><p><strong>Conclusions: </strong>Elevated PAC levels have been linked to an increased risk of SRC in hypertensive patients. Regulating PAC levels may help mitigate SRC formation; however, further prospective studies are required to confirm this causal relationship.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-20"},"PeriodicalIF":2.3,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Second Opinion SGLT2 Inhibitors and Uric acid.","authors":"Laura G Sanchez-Lozada, Miguel A Lanaspa, Bernardo Rodriguez-Iturbe, Jared M Brown, Magdalena Madero, Richard J Johnson","doi":"10.1159/000545131","DOIUrl":"https://doi.org/10.1159/000545131","url":null,"abstract":"<p><p>The use of SGLT2 inhibitors have had remarkable success in the management of chronic kidney disease, by both slowing progression and reducing cardiovascular mortality. Among their many actions, SGLT2 inhibitors have also been found to lower serum uric acid, likely by both enhancing urinary excretion and blocking urate production. A recent study by Mayne et al reported that SGLT2 inhibitors lowered uric acid levels in the EMPA-Kidney trial, but did not provide any significant protection from gout nor have effect on kidney outcomes. However, there is increasing evidence that lowering of uric acid by SGLT2 inhibitors in subjects with diabetes or heart failure can reduce acute episodes of gout as well as urate kidney stones. Given the frequency of hyperuricemia and gout in the subject with CKD, we believe that more studies are needed, and that likely there is some benefit in hyperuricemic subjects with CKD.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-8"},"PeriodicalIF":2.3,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dapagliflozin Treatment Attenuates the Interaction Between the Renal Sodium Chloride co-transporter and Ezrin in Hypertensive Diabetic db/db Mice.","authors":"Mohammed F Gholam, Abdel A Alli","doi":"10.1159/000543336","DOIUrl":"https://doi.org/10.1159/000543336","url":null,"abstract":"<p><strong>Introduction: </strong>Ezrin is a protein that links the actin cytoskeleton to membrane proteins. The sodium chloride cotransporter (NCC) plays a key role in regulating total body electrolyte homeostasis and systemic blood pressure. Dapagliflozin, an SGLT2 inhibitor, is used to manage type 2 diabetes mellitus. We hypothesize dapagliflozin reduces sodium reabsorption and blood pressure by inhibiting the interaction between NCC and ezrin in the distal convoluted tubules of salt-loaded hypertensive mice.</p><p><strong>Methods: </strong>Male diabetic db/db mice were salt loaded to induce hypertension and then given dapagliflozin or vehicle by oral gavage. The mice were subject to metabolic cage experiments and blood pressure was assessed using the tail-cuff method to study the impact of dapagliflozin compared to the vehicle. Protein expression of NCC and ezrin were evaluated using immunohistochemistry and Western blotting.</p><p><strong>Results: </strong>Treatment with dapagliflozin lowered systolic blood pressure, raised urine sodium excretion, and lowered urinary potassium excretion. A decrease in phospho-NCC and ezrin proteins was observed in db/db mice treated with dapagliflozin. There was less co-localization of ezrin and phosphorylated NCC in dapagliflozin treated mice.</p><p><strong>Conclusions: </strong>Collectively, we demonstrate that dapagliflozin reduces sodium retention and blood pressure via decreasing the density of renal NCC at the luminal membrane and the interaction between NCC and the actin cytoskeleton.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-30"},"PeriodicalIF":2.3,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lysosomal storage-independent Fabry disease variants with α-galactosidase A misprocessing-induced ER stress and the unfolded protein response.","authors":"Martina Živná, Malte Lenders, Stanislav Kmoch","doi":"10.1159/000545388","DOIUrl":"https://doi.org/10.1159/000545388","url":null,"abstract":"<p><strong>Background: </strong>Clinical findings in Fabry disease have classically been attributed to loss-of- function variants in the GLA gene that result in α-galactosidase A deficiency, intracellular accumulation of globotriaosylceramides and clinical manifestations. However, over time, increasing number of patients have been identified with GLA variants causing either non-classic Fabry disease or having unclear clinical effects.</p><p><strong>Summary: </strong>Searching for additional etiologic and lysosomal storage-independent factors, investigators have recently identified that certain missense GLA variants not only affect enzymatic activity, but also encode for misfolded α-galactosidase A that itself induces chronic endoplasmic reticulum stress and the unfolded protein response. Thus, Fabry disease pathogenesis may be caused by decreased enzymatic activity as well as cellular toxicity from accumulation of the misfolded α-galactosidase A protein, with the contribution of each factor determined by the type of the genetic variant and host factors.</p><p><strong>Key messages: </strong>Defective proteostasis and misfolding of certain missense α-galactosidase A variants induce chronic endoplasmic reticulum stress and the unfolded protein response that may contribute to intra-familial and inter-familial variation in disease penetrance and clinical expressivity. Pharmacologic modulation of defective proteostasis may have therapeutic implications in Fabry disease.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-17"},"PeriodicalIF":2.3,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the Molecular Nexus Between Ankylosing Spondylitis and IgA Nephropathy: Insights from Mendelian Randomization and Bioinformatics Analysis.","authors":"Ningjun Shao, Kuibi Tan, Ping Chen, Qun Luo","doi":"10.1159/000544970","DOIUrl":"https://doi.org/10.1159/000544970","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Renal complications are frequently observed in patients with ankylosing spondylitis (AS), with IgA nephropathy (IgAN) being a particularly significant concern. Although anecdotal evidence suggests a potential association between AS and IgAN, robust epidemiological data remain limited. Previous studies have reported varying prevalence rates of IgAN among AS patients, but these studies are often constrained by small sample sizes and inconsistent methodologies. Establishing a causal relationship between AS and IgAN through conventional observational studies has proven challenging due to confounding factors and reverse causality. Mendelian randomization (MR) offers a promising alternative, utilizing genetic variants to explore causal relationships. This study employs MR combined with bioinformatics analysis to investigate the molecular link between AS and IgAN, aiming to identify potential therapeutic targets.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Two publicly available datasets were utilized: a genome-wide association study (GWAS) of AS (dataset ID: ebi-a-GCST005529) with 9,069 AS cases and 13,578 controls, and IgAN data from the FinnGen project, which included 653 cases and 411,528 controls. Instrumental variables were selected based on stringent criteria. MR analysis was conducted using the inverse variance weighted (IVW), weighted median (WM), and MR-Egger methods to assess the causal relationship between AS and IgAN. Reverse MR analysis and sensitivity analysis were conducted to validate the findings. Bioinformatics analysis involved acquiring gene expression data from the GEO database and identifying differentially expressed genes (DEGs) using the Limma package. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein-protein interaction (PPI) network construction, and hub gene identification were performed to elucidate the biological functions involved.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;24 independent single nucleotide polymorphisms (SNPs) associated with AS were identified through stringent SNP selection. MR analysis revealed a protective causal relationship between AS and IgAN [odds ratio (OR) =0.552, 95% confidence interval (CI), 0.339-0.900; P = 0.017]. Analysis of DEGs identified 332 DEGs for IgAN and 5,521 DEGs for AS, with 59 common DEGs shared between the two diseases. Functional enrichment analysis highlighted significant changes in biological processes, cellular components, molecular functions, and KEGG pathways. PPI network analysis identified eight hub genes, including CX3CR1, which links AS and IgAN. External validation confirmed CX3CR1 as a crucial gene associated with both diseases.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This study provides evidence of a protective causal relationship between AS and IgAN using MR analysis. Furthermore, bioinformatics analysis identifies CX3CR1 as a key gene, suggesting its role in mediating the protective link between AS and IgAN. T","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-22"},"PeriodicalIF":2.3,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comments regarding \"Adoption of CKD-EPI (2021) for GFR estimation - implications for UK practice\".","authors":"Paul T Williams","doi":"10.1159/000545104","DOIUrl":"https://doi.org/10.1159/000545104","url":null,"abstract":"","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-7"},"PeriodicalIF":2.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developing and Tailoring a Person-Centred Pathway for Mental Health Care for People Receiving Dialysis.","authors":"Kara Schick-Makaroff, Charlotte Berendonk, Marlo Salum, Peter Yoeun, Jenny Wichart, Marni Armstrong, Stephanie Thompson, Meghan Elliott, Loretta Lee, Terry Smith, Frances Reintjes, Denise Fillier, Scott Klarenbach, Richard Sawatzky","doi":"10.1159/000544058","DOIUrl":"10.1159/000544058","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Mental health symptoms are underdiagnosed and undertreated among people receiving dialysis treatment. Despite a high prevalence of depression (40%) and anxiety (42%) symptoms in this population, international guidance does not exist. To address this gap, a multi-phase project involved collaboration by diverse groups in Alberta, Canada to develop and tailor a pathway that supports person-centred mental health care for Albertans receiving dialysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This mixed methods patient-oriented research was conducted in two phases. Phase 1 included: (a) an online clinician survey (n = 199), (b) 11 focus groups and 2 interviews involving 10 people with lived experience and 44 clinicians and administrators, and (c) a scoping review of evidence-based pharmacological treatment. Descriptive analyses of the survey data and summative content analysis of qualitative data (written survey comments and data from focus groups and interviews) were conducted to understand current processes, health services, and interventions for mental health care in Alberta Kidney Care for people receiving dialysis, and to determine appropriateness and opportunities of existing mental health services and interventions. The results were used to develop preliminary statements to inform development of the pathway. Attributes of centeredness in health care - being unique, being heard, and shared responsibility - guided pathway development. Phase 2 involved building consensus on these statements via two rounds of modified Delphi surveys (n = 59 and 51 for rounds 1 and 2, respectively), followed by a consensus call on a virtual platform for discussion and voting involving 27 participants. Voters rated their agreement for each statement using a 3-point Likert scale. Consensus was defined a priori as ≥80% agreement by two groups of voters: people with lived experience and clinicians/others.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Phase 1 results informed the development of 68 statements in round 1 of Delphi voting; 42 were approved. Based on voter comments, 11 new statements were developed and 23 statements were revised. Round 2 of Delphi voting included 34 statements. A call was held with people with lived experience to understand why they voted differently than clinicians/others. We learned that some statement language was too technical, such as \"assessment\" or \"score.\" We talked through each statement and people with lived experience verbally approved the intention of all statements. Through this dialogue, and round 2 voting, 20 statements were approved. A consensus call was held, concluding with voting on 5 statements previously not approved by both groups; 3 were approved. In total, 66 statements were approved for use in development of a pathway addressing symptoms of depression and anxiety, as well as coping. Approved statements guided depiction of the pathway as an algorithm for initial conversations, assessment, follow-up (includin","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-19"},"PeriodicalIF":2.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When Proteins Go Berserk: The Unfolded Protein Response and ER stress.","authors":"Doria Meiseles, Narkis Arbeli, Moran Dvela-Levitt","doi":"10.1159/000544971","DOIUrl":"https://doi.org/10.1159/000544971","url":null,"abstract":"<p><p>Background The cellular proteostasis machinery is essential for maintaining protein homeostasis by employing quality control systems that identify, sequester, and eliminate damaged or misfolded proteins. However, the accumulation of misfolded proteins can overwhelm these protective mechanisms, disrupting proteostasis. This phenomenon is a hallmark of numerous pathologies, including a variety of genetic disorders. In the secretory pathway, the buildup of misfolded proteins triggers endoplasmic reticulum (ER) stress, which activates the unfolded protein response (UPR). The UPR serves as an adaptive mechanism, aiming to alleviate stress and restore cellular homeostasis. However, if ER stress is prolonged or severe, the UPR may fail to restore balance and apoptosis is induced. Summary This review introduces the intricate signaling pathways activated by the three UPR transmembrane sensors: protein-kinase R-like endoplasmic reticulum kinase (PERK), inositol requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6). We briefly present the roles of the distinct transcriptional programs activated by each sensor in modulating the cellular response to protein stress and in determining cell fate. We discuss how genetic variants and environmental factors contribute to the heterogeneity observed in protein misfolding diseases. Finally, we critically evaluate select therapeutic strategies, specifically protein stabilization, trafficking modulation, and UPR sensor targeting approaches. Key message This review introduces the potential consequences of protein misfolding, which may not only impair protein function, but can also lead to toxic protein accumulation and stress induction. Using Fabry disease as a compelling example, we suggest that future therapeutic intervention may require nuanced, combination approaches that address both loss and gain of protein function.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-14"},"PeriodicalIF":2.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Home-based dialysis and person-centered care: A scoping review.","authors":"Beate Nygaard-Andersen, Astrid Torbjørnsen, Peter Forde Hougaard, Ann-Chatrin Linqvist Leonardsen, Axel Wolf, Jeanette Finderup","doi":"10.1159/000544699","DOIUrl":"https://doi.org/10.1159/000544699","url":null,"abstract":"<p><p>Introduction Managing dialysis at home requires the involvement of the patient in decisions, treatment, and their illness and health. Evidence-based person-centered care interventions focus on listening to the patient's narrative, establishing a partnership between patients and healthcare professionals, and documenting care and treatment in a shared health plan. Therefore, a person-centered care intervention is expected to enhance the patient's ability to manage dialysis at home. This study aimed to identify and map evidence for person-centered interventions and home-based dialysis for individuals with kidney failure. Methods A scoping review was conducted based on the approach of Arksey and O'Malley. A systematic search was carried out in Medline, CINAHL, and Scopus for articles in all languages and without time restrictions. Person-centered care interventions concerning home dialysis were included. Two independent researchers assessed the literature. Data were extracted using NVIVO, and a relational analytical framework was employed to synthesise the data. Results The search identified 9,443 articles, of which 16 met the inclusion criteria. A total of 13 person-centered care interventions were identified. Eight interventions aimed to involve the patient in the decision regarding the type of dialysis modality, with six interventions identified to involve the patient in treatment, illness, and health. Only one intervention was identified to involve the patient in the decisions that follow once the patient has commenced dialysis treatment. Five interventions showed a correlation between a person-centered care intervention and the number of patients in home dialysis. Conclusion There is a need for interventions for patients in home dialysis to be adapted to a more person-centered care approach, particularly regarding the involvement of the patient in their treatment, illness and health, as well as the decisions that follow the initiation of dialysis treatment.</p>","PeriodicalId":18998,"journal":{"name":"Nephron","volume":" ","pages":"1-25"},"PeriodicalIF":2.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}