Molecular genetics and metabolism最新文献

{"title":"Expanded characterization of glycosylation abnormalities and galactose therapy in a patient with CCDC115-CDG using semi-quantitative N-glycan analysis of total and fractionated plasma glycoproteins, in response to Geerts et al. [1]","authors":"Yupeng Liu , Christina Lam , Sheri Poskanzer , Jenny Thies , Holly Stevens , Wenyue Zhang , Eva Morava , Miao He","doi":"10.1016/j.ymgme.2025.109708","DOIUrl":"10.1016/j.ymgme.2025.109708","url":null,"abstract":"","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 3","pages":"Article 109708"},"PeriodicalIF":3.5,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurological and psychiatric issues in 187 adults with early-treated PKU: The ECOPHEN study","authors":"Chloé Giret ,&nbsp;Sybil Charrière ,&nbsp;François Feillet ,&nbsp;Alain Fouilhoux ,&nbsp;Leonardo Astudillo ,&nbsp;Christian Lavigne ,&nbsp;Jean-Baptiste Arnoux ,&nbsp;Sylvie Odent ,&nbsp;Claire Gay ,&nbsp;Manuel Schiff ,&nbsp;Karin Mazodier ,&nbsp;Alice Kuster ,&nbsp;Vincent Rigalleau ,&nbsp;Christel Thauvin ,&nbsp;Vanessa Leguy-Seguin ,&nbsp;Hervé Lêvesque ,&nbsp;Elise Sacaze ,&nbsp;Gérard Besson ,&nbsp;Benjamin Thoreau ,&nbsp;Amélie Le Gouge ,&nbsp;François Maillot","doi":"10.1016/j.ymgme.2025.109706","DOIUrl":"10.1016/j.ymgme.2025.109706","url":null,"abstract":"<div><h3>Introduction</h3><div>Phenylketonuria (PKU) is an autosomal recessive disorder caused by mutations in the PAH gene leading to phenylalanine hydroxylase deficiency. This results in the accumulation of phenylalanine (Phe) in blood and brain, causing neurological and psychiatric impairments if untreated. Newborn screening (NBS) introduced in the 1960s enables early PKU diagnosis, allowing prompt dietary or sapropterin treatment. The long-term outcomes in adults with early-treated PKU, however, may include subtle neurocognitive deficits alongside somatic neurological and psychiatric complications, which remain incompletely characterized.</div></div><div><h3>Patients and methods</h3><div>The ECOPHEN study was a French 5-year multicenter prospective cohort assessing neuropsychiatric disorders in adults with early-treated PKU.</div></div><div><h3>Results</h3><div>Here are presented the data at inclusion. The study recruited 187 patients who were classified by PKU severity—classic, mild, or mild persistent hyperphenylalaninemia—and diet adherence status.</div><div>Neurological history revealed symptoms in 11.2 % of patients, exclusively in classic PKU, including tremor, migraines, and balance disorders, without significant differences between diet groups. Neurological examination abnormalities predominantly included abnormal deep tendon reflexes in classic PKU patients. Psychiatric issues affected 25.7 % of patients across severity groups, mainly depressive episodes and anxiety, with no clear influence of diet adherence.</div></div><div><h3>Discussion/conclusion</h3><div>The present study highlights neurological complications persisting despite early treatment, particularly in classic PKU. Diet adherence and current plasma Phe levels did not correlate significantly with neurological or psychiatric outcomes, possibly due to suboptimal metabolic control. Limitations included the cross-sectional design, absence of control group, and retrospective data collection. Overall, adults with early-treated PKU show a generally favorable outcome but remain at risk for neuropsychiatric manifestations, supporting the need for lifelong follow-up including neurologic and psychiatric evaluation.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 1","pages":"Article 109706"},"PeriodicalIF":3.5,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and biochemical footprints of primary mitochondrial disorders: proposed nosology.","authors":"Martina Messina, Rebecca Ganetzky, Carlos R Ferreira, Nenad Blau, Shamima Rahman","doi":"10.1016/j.ymgme.2025.109704","DOIUrl":"https://doi.org/10.1016/j.ymgme.2025.109704","url":null,"abstract":"<p><p>Primary mitochondrial diseases (PMD) are a growing number of disorders caused by mitochondrial dysfunction. There is not yet a consensus on the precise definition of PMD. Therefore, this study presents an approach to developing a nosology for standardized, systematic classification of PMD, harmonized with ICIMD and IEMbase. A total of 452 PMD causative genes were included. The classification includes 18 categories: 1) Disorders of amino acid metabolism; 2) Disorders of peptide and amine metabolism; 3) Disorders of carbohydrate metabolism; 4) Disorders of fatty acid and ketone body metabolism; 5) Disorders of energy substrate metabolism; 6) Mitochondrial DNA-related disorders; 7) Nuclear-encoded disorders of oxidative phosphorylation; 8) Disorders of mitochondrial cofactor biosynthesis; 9) Disorders of mitochondrial DNA maintenance and replication; 10) Disorders of mitochondrial gene expression; 11) Other disorders of mitochondrial function; 12) Disorders of metabolite repair/proofreading; 13) Disorders of lipid metabolism; 14) Disorders of nucleobase, nucleotide and nucleic acid metabolism; 15) Disorders of tetrapyrrole metabolism; 16) Disorders of organelle biogenesis, dynamics and interaction; 17) Disorders of vitamin and cofactor metabolism and 18) Neurotransmitter disorders. We also describe the clinical involvement of 22 organs and systems and laboratory features. The most prevalent symptoms (per gene) were neurological (21.1%), ocular (10.3%), muscular (9.0%), gastrointestinal (8.3%), and cardiovascular (7.9%).</p>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 3","pages":"109704"},"PeriodicalIF":3.5,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complementary and alternative medicines and cannabis use among individuals with erythropoietic protoporphyria","authors":"Emma Draisin ,&nbsp;Chloe Paige Rome ,&nbsp;Karli Hedstrom ,&nbsp;Jessica Overbey ,&nbsp;Manisha Balwani ,&nbsp;Hetanshi Naik","doi":"10.1016/j.ymgme.2025.109703","DOIUrl":"10.1016/j.ymgme.2025.109703","url":null,"abstract":"<div><h3>Introduction</h3><div>Erythropoietic Protoporphyria (EPP) and X-Linked Protoporphyria (XLP) are rare, inherited disorders that present with severe cutaneous phototoxicity. Pain from phototoxic reactions does not respond to analgesics, and there is a need to identify therapies to address EPP-pain. Anecdotal reports from individuals with EPP indicate that cannabis may alleviate symptoms during phototoxic reactions. These reports warrant further systematic investigation. Therefore, this study aimed to explore how patients with EPP utilize cannabis and complementary and alternative medicines (CAM).</div></div><div><h3>Materials &amp; methods</h3><div>A cross-sectional survey assessing the use of CAMs and cannabis in individuals with EPP and XLP was conducted. The survey included demographics, EPP/XLP symptoms, CAM use (the International CAM Questionnaire and Daily Session (I-CAM-Q)), and cannabis use (the Frequency, Age of Onset and Quantity of Cannabis Use Inventory (DFAQ-CU)).</div></div><div><h3>Results</h3><div>A total of 149 participants completed the survey. More than half of participants (62.9 %, 78/124) reported having used cannabis, either currently or in the past. Among the cannabis users, 12.9 % (9/70) reported using it only for EPP symptoms, 34.2 % (24/70) only recreationally, and 47.4 % (37/70) for both reasons. Individuals reported that cannabis mitigated anxieties around symptoms, though it was not perceived to directly reduce EPP-pain. Participants with more severe symptoms reported higher cannabis use. Few participants reported seeing a CAM provider for symptoms related to EPP, with most seeing providers to improve general well-being or for other reasons not related to EPP. Additionally, 76.0 % (89/117) of participants used self-help practices, though generally not for their EPP symptoms.</div></div><div><h3>Discussion</h3><div>Overall, findings from this study suggest that cannabis may be impactful on secondary effects of EPP symptoms. Also, that individuals with EPP primarily used other CAMs to improve general well-being rather than as treatment for EPP-related symptoms or pain. Given the limited treatment options for EPP-pain and the findings here, additional research is needed to determine the effectiveness of cannabis on EPP symptoms.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 1","pages":"Article 109703"},"PeriodicalIF":3.5,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An update on clinical practice for Duarte galactosemia","authors":"Judith L. Fridovich-Keil ,&nbsp;Rani H. Singh","doi":"10.1016/j.ymgme.2025.109699","DOIUrl":"10.1016/j.ymgme.2025.109699","url":null,"abstract":"","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 1","pages":"Article 109699"},"PeriodicalIF":3.5,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145735011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Underrecognized need for early detection of inborn errors of metabolism in China: A population-based study of 14.31 million residents (2012−2023)","authors":"Ming-Jia Li ,&nbsp;Miao-Miao Zhao ,&nbsp;Qi Li ,&nbsp;Hanna Kim ,&nbsp;Ruo-Qi Feng ,&nbsp;Mo-Ning Guo ,&nbsp;Jian-Peng Zheng ,&nbsp;Chang Liu ,&nbsp;Jin-Kui Yang","doi":"10.1016/j.ymgme.2025.109702","DOIUrl":"10.1016/j.ymgme.2025.109702","url":null,"abstract":"<div><div>Inborn errors of metabolism (IEMs) are a major subgroup of rare diseases, comprising over 1000 genetic disorders that disrupt essential biochemical pathways. Globally, they cause an estimated 23,500 childhood deaths annually. Despite diagnostic advances indicating a cumulative incidence of ∼1 in 800 births, population-based data from China remain scarce.</div><div>We conducted a population-based study of 14.31 million permanent residents in the Great Beijing Area (2012–2023) using the municipal disease registry. Rare diseases were identified using ICD-10 codes mapped to the 2018 and 2023 National Rare Disease Catalog, from which 13 classified as IEMs were included in this study. Age-standardized incidence rates (ASIRs) were calculated, and disease patterns were compared with international newborn screening (NBS) data.</div><div>Of 12,371 rare disease diagnoses, 314 (2.5 %) were IEMs. The ASIR was 0.180 per 100,000 person-years (95 % CI: 0.031–0.565) in 2012 and remained stable at 0.159 (95 % CI: 0.023–0.532) in 2023. Early-onset cases (&lt;1 year) comprised 41.7 %. The mean diagnostic age was 11.0 years, with a median of 1.0 year. Methylmalonic acidemia without homocystinuria (40.8 %), phenylketonuria (29.9 %), and Fabry disease (6.7 %) were most common; males accounted for 60.5 % of cases. Although the prevalence of certain IEMs was broadly consistent with global data, the markedly low ASIR suggests substantial underdiagnosis of IEMs in China.</div><div>This first large-scale, population-based study of IEMs in China reveals underestimation of true disease burden. Expanding and standardizing NBS coverage, broadening genetic testing, implementing mandatory screening, and integrating long-term care into health systems are urgent policy priorities.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 1","pages":"Article 109702"},"PeriodicalIF":3.5,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145724811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Navigating molecular therapies: The emerging role of mRNA in treating inherited metabolic diseases","authors":"J.A. Castro-Alpízar ,&nbsp;M.J. Lenderink ,&nbsp;E.E.S. Nieuwenhuis ,&nbsp;S.A.A. Kooijmans ,&nbsp;S.A. Fuchs","doi":"10.1016/j.ymgme.2025.109698","DOIUrl":"10.1016/j.ymgme.2025.109698","url":null,"abstract":"<div><div>Inherited metabolic diseases (IMDs) are a diverse group of rare genetic disorders caused by enzymatic deficiencies that disrupt essential biochemical pathways. Current treatments remain largely supportive and fail to address the molecular root cause. Messenger RNA (mRNA)-based therapeutics, delivered by lipid nanoparticles (LNPs), have recently emerged as a powerful treatment strategy: mRNA enables transient and programmable protein expression, while LNPs provide an effective, non-viral vehicle with natural liver tropism. Initial phase I/II clinical trials and <em>n</em> = 1 cases in liver-dominant IMDs have shown encouraging results. Yet, given the rarity of each IMD and the small patient numbers in individual trials, definitive insights into efficacy and safety require integrating evidence across multiple disorders. In this review, we synthesize the emerging clinical trial evidence of mRNA-LNP therapies across IMDs, highlighting both enzyme replacement and genome editing strategies. We discuss the clinical promise and modularity of these approaches, alongside remaining challenges related to durability, immunogenicity, and extrahepatic delivery. The recent and anticipated evolving developments position mRNA-LNP therapeutics at the forefront of precision medicine, offering a flexible therapeutic platform with applications ranging from bridge therapy to long-term stabilization or potential one-time disease-modifying interventions, transforming the prospect of IMD management.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 1","pages":"Article 109698"},"PeriodicalIF":3.5,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145756227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predicting subtypes of glycogen storage disease type IV: Challenges of hepatic subtypes and genotype-phenotype correlation","authors":"Anne Taylor ,&nbsp;Desale Yacob ,&nbsp;Bonita Fung ,&nbsp;Shamlal Mangray ,&nbsp;Daniel R. Boué ,&nbsp;Kevin M. Flanigan ,&nbsp;Rebecca L. Koch ,&nbsp;Priya S. Kishnani ,&nbsp;Deeksha Bali ,&nbsp;Alexander Weymann ,&nbsp;Mari Mori","doi":"10.1016/j.ymgme.2025.109293","DOIUrl":"10.1016/j.ymgme.2025.109293","url":null,"abstract":"<div><div>Glycogen storage disease type IV (GSD IV) is a rare autosomal recessive disease caused by the deficiency of the glycogen branching enzyme encoded by <em>GBE1</em>. GSD IV can present with variable age of onset and severity of disease processes involving liver, central and peripheral nerves, muscles, and heart. Adult Polyglucosan Body Disease (APBD) is now increasingly recognized as a continuum of the GSDIV spectrum. If the clinical disease presentation includes progressive liver failure, treatment may require liver transplant to prevent morbidity and mortality. The variable presentation of GSD IV, including the hepatic phenotypes, creates diagnostic and treatment challenges. Here we describe a girl presenting with hypotonia and hepatomegaly at age 4 years; genetic analysis revealed compound heterozygosity in <em>GBE1</em>: c.1621A&gt;G p.(Asn541Asp) and c.1655C&gt;T p.(Pro552Leu). Based on her presentation and genotypes, her phenotypic prognosis was not immediately clear. She was monitored closely for liver disease progression including, synthetic dysfunction, cholestasis, or cirrhosis, but her liver function proved stable over time.</div><div>Recent analysis suggested that liver disease progression is a spectrum and some develop a progressive/severe hepatic form and others stabilize with an attenuated hepatic form. Previous reviews of GSD IV genotype-phenotype correlations have not adequately addressed the prediction of hepatic phenotype based on <em>GBE1</em> genotypes. We performed an updated comprehensive literature search and genotype-phenotype analysis, while updating the <em>GBE1</em> genotypes according to the HGVS nomenclature.</div><div>Our detailed and comprehensive review of GSDIV adds to the previously published literature available on GSD IV genotypes (Li et al. 2010, Iijima 2018, Souza et al. 2021).</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 4","pages":"Article 109293"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145621093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cover 2 / Ed. Board","authors":"","doi":"10.1016/S1096-7192(25)00683-3","DOIUrl":"10.1016/S1096-7192(25)00683-3","url":null,"abstract":"","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 4","pages":"Article 109691"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145732903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genotype-phenotype correlations of GFAP variants in type I Alexander disease subtypes","authors":"Tiziana Bachetti ,&nbsp;Ylenia Vaia ,&nbsp;Alice Grossi ,&nbsp;Francesca Rosamilia ,&nbsp;Enrico Bertini ,&nbsp;Francesco Nicita ,&nbsp;Deianira Bellitto ,&nbsp;Florian Eichler ,&nbsp;Geneviève Bernard ,&nbsp;Amanda Nagy ,&nbsp;Ayelet Zerem ,&nbsp;Morteza Heidari ,&nbsp;Ali Reza Tavasoli ,&nbsp;Isabella Moroni ,&nbsp;Isabella Ceccherini ,&nbsp;Davide Tonduti ,&nbsp;AxD Type I Study Group","doi":"10.1016/j.ymgme.2025.109689","DOIUrl":"10.1016/j.ymgme.2025.109689","url":null,"abstract":"<div><h3>Introduction</h3><div>Alexander disease (AxD) is a rare and progressive leukodystrophy caused by variants in the Glial Fibrillary Acidic Protein (GFAP) gene. AxD presents as Type I and Type II, based on clinical and neuroradiological features. However, Type I patients variable disease progression has led to sub-classify them into subtypes Ia-Ib-Ic-Id. Our study investigated genotype-phenotype correlations in Type I AxD across these subtypes.</div></div><div><h3>Methods</h3><div>A cohort of 74 genetically confirmed Type I AxD patients was analysed, with variants classified according to the clinical subtypes Ia, Ib, Ic, and Id. Genotypic–phenotypic correlations were explored both across all subtype groups and in stratified analyses based on patients' ability to achieve independent ambulation versus those who never acquired this milestone. To investigate the functional consequences of a representative variant, in vitro assays were performed. Selected mutant GFAP protein was expressed and their ability to assemble into intermediate filament networks was assessed.</div></div><div><h3>Results</h3><div>The study revealed a progressive decrease in GFAP allelic heterogeneity across disease subtypes from Ia to Id. Additionally, <em>GFAP</em> pathogenic variants in exon 1 were more frequent in milder forms, whereas mutations in exon 4 were predominantly observed in severe phenotypes. In addition, changes at p.R239 and p.R79 residues showed an opposite trend, with variants affecting p.R239 never detected in Id subtype, while variants affecting p.R79 never detected in Ia. Specific aminoacidic changes at the p.R79 residue were able to stratify patients based on ability to acquire independent ambulation or not. Furthermore, the distribution of Combined Annotation Dependent Depletion (CADD) scores showed an inverse correlation with the acquisition of autonomous ambulation.</div></div><div><h3>Conclusions</h3><div>These results suggest that specific <em>GFAP</em> variants could be potential predictors for disease progression in Type I AxD, supporting patients' subclassification and underscoring the importance of considering both genetic and clinical factors in AxD management, particularly as therapeutic interventions are being developed.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"147 1","pages":"Article 109689"},"PeriodicalIF":3.5,"publicationDate":"2025-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}