Pigment Cell & Melanoma Research最新文献

{"title":"Disruption of mc1r Disturbs Skin Pigmentation in Xenopus tropicalis","authors":"Lanxin Li,&nbsp;Jixuan Huang,&nbsp;Yonglong Chen,&nbsp;Rensen Ran","doi":"10.1111/pcmr.70033","DOIUrl":"https://doi.org/10.1111/pcmr.70033","url":null,"abstract":"<p>The melanocortin 1 receptor (MC1R) is well-established as a pivotal regulator of pigmentation in various species. Despite a wealth of research focused on mammals and fish, the role of Mc1r in amphibians has remained largely unexplored. This study was designed to elucidate the contribution of Mc1r in <i>Xenopus tropicalis</i>. Our results reveal that targeted ablation of <i>mc1r</i> in <i>Xenopus tropicalis</i> led to a significant reduction in dorsal skin pigmentation, while simultaneously accelerating the onset of melanophore pigmentation in the ventral region. This dual effect resulted in a perturbation of the canonical countershading pattern. Additionally, knockout of <i>mc1r</i> disrupted the expression of multiple genes primarily associated with pigmentation. Collectively, these findings underscore the critical role of MC1R in the regulation of pigmentation and the development of countershading in amphibians, contributing to the growing body of literature on the evolution and function of MC1R across vertebrate species.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144299576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SASH1 Mutations and Hereditary Disorders of Pigmentation: Review of Literature","authors":"Anuradha Bishnoi,&nbsp;Aarushi Arunima,&nbsp;Keshavamurthy Vinay,&nbsp;Muthu Sendhil Kumaran,&nbsp;Davinder Parsad","doi":"10.1111/pcmr.70032","DOIUrl":"https://doi.org/10.1111/pcmr.70032","url":null,"abstract":"<p>Dyschromatosis universalis hereditaria (DUH) is a rare genodermatosis characterized by asymptomatic hyper- and hypopigmented macules appearing in infancy and persisting for life. Although mutations in ABCB6 account for many DUH cases, recently, the SAM and SH3 domain-containing 1 (SASH1) gene has emerged as a key player in DUH. Additionally, SASH1 mutations have been associated with the pure-lentiginous phenotype of familial pigmentation. In this review of literature, we found 22 different SASH1 mutations, most inherited in an autosomal dominant manner. These variants cause distinct phenotypes, including DUH, lentiginosis, and rarely, an autosomal recessive syndromic form with alopecia, palmoplantar keratoderma, and increased risk of malignancies. Functional studies have revealed that SASH1 acts as both a tumor suppressor and a pro-melanogenic factor. It modulates key pathways such as p53–POMC–α-MSH–MC1R–MITF and Gαs-SASH1–IQGAP1–E-cadherin pathways, affecting melanosome production, transport, and melanocyte migration. This unique dual role of SASH1 highlights its importance in melanocyte homeostasis and UV-induced pigmentation. Understanding the role of SASH1 in regulating pigmentation can help foster novel therapeutic approaches for these genodermatoses and related pigmentary anomalies, ultimately improving patient care and outcomes.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Neuro-Endocrinal Regulation in Vitiligo","authors":"Wei Liu,&nbsp;Wanlu Ma,&nbsp;Xiao Xue,&nbsp;Shanshan Li","doi":"10.1111/pcmr.70029","DOIUrl":"https://doi.org/10.1111/pcmr.70029","url":null,"abstract":"<p>Vitiligo is an acquired depigmentation disorder characterized by the loss of melanocytes. The specific etiology of vitiligo is not fully understood, but it is thought to result from a complex interplay of factors, including autoimmune responses, intrinsic melanocyte dysfunction, genetic susceptibility, oxidative stress, and neurogenic imbalances. The disfiguring nature of vitiligo significantly impacts the mental and physical health of patients, and psychological stress can further induce and exacerbate vitiligo. Recent research has underscored the potential mediating roles of the hypothalamic–pituitary–adrenal axis, hormones, and neuropeptides in the pathogenesis of vitiligo. Furthermore, individuals with vitiligo have been shown to have a notably higher prevalence of diabetes mellitus and metabolic syndrome compared to the general population. This evidence suggests that vitiligo is not merely a cosmetic issue confined to the skin but also a systemic disease with broader health implications. This review aims to explore the potential roles and mechanisms of neuroendocrine factors in the pathogenesis of vitiligo, shedding light on the multifaceted nature of this condition and its systemic associations.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144197519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microfluidic Characterization and Analysis of Circulating Tumor Cells From Patients With Metastatic Melanoma","authors":"Matthew C. Mannino,&nbsp;Shuang G. Zhao,&nbsp;Benjamin K. Gibbs,&nbsp;Jennifer L. Schehr,&nbsp;Isabella G. Fernandez,&nbsp;Diego A. Eyzaguirre,&nbsp;Alyssa M. Hintz,&nbsp;Stephanie J. Davis,&nbsp;Manushi N. Vatani,&nbsp;Jacob C. Caceres,&nbsp;Alexander Birbrair,&nbsp;Joshua M. Lang,&nbsp;Vincent T. Ma","doi":"10.1111/pcmr.70030","DOIUrl":"https://doi.org/10.1111/pcmr.70030","url":null,"abstract":"<p>Circulating tumor cells (CTCs) can provide non-invasive insight into how a cancer patient responds to therapy. Their role in disease monitoring of advanced melanoma patients treated with immune checkpoint inhibitors (ICI) is unknown. CTC protein expression of human leukocyte antigen class-I (HLA I) and programmed death ligand-1 (PD-L1) may give insight into how a patient's disease evolves over the course of treatment. In our study, we utilize microfluidic Exclusion-based Sample Preparation (ESP) technology to isolate and characterize CTCs from patients with advanced-stage melanoma. CTC samples from melanoma patients are collected, captured, and stained. A range of 2 to 35 CTCs is observed in a cohort of 16 samples from 10 advanced-stage melanoma patients treated with ICI therapy. Single-cell protein expression data is generated from image cytometry analysis and used to calculate mean HLA I and PD-L1 expression. Using our ESP capture approach, we successfully detect phenotypic and numerical heterogeneity in CTCs from melanoma patients. Our assay shows sufficient capture sensitivity and promising prognostic and predictive information, as we illustrate in our case example. A greater clinical sample size will be necessary to confirm the diagnostic sensitivity and specificity of the assay in predicting clinical outcomes for patients with advanced-stage melanoma.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144197518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Drug–Drug Interactions on Clinical Outcomes in Metastatic Melanoma Patients Treated With Combined BRAF/MEK Inhibitors: A Real-World Study","authors":"Silvia Mezi,&nbsp;Andrea Botticelli,&nbsp;Giulia Pomati,&nbsp;Simone Scagnoli,&nbsp;Giulia Fiscon,&nbsp;Federica de Galitiis,&nbsp;Francesca Romana di Pietro,&nbsp;Sofia Verkhovskaia,&nbsp;Sasan Amirhassankhani,&nbsp;Giovanna Gentile,&nbsp;Maurizio Simmaco,&nbsp;Bjoern Gohlke,&nbsp;Robert Preissner,&nbsp;Daniele Santini,&nbsp;Paolo Marchetti","doi":"10.1111/pcmr.70026","DOIUrl":"https://doi.org/10.1111/pcmr.70026","url":null,"abstract":"<p>The unique pharmacokinetics of BRAF and MEK inhibitors make patients vulnerable to drug–drug interactions (DDIs), which may compromise treatment efficacy in metastatic melanoma. This study evaluates the impact of DDIs on clinical outcomes in patients with metastatic melanoma treated with BRAF/MEK inhibitors. This multicenter, observational, retrospective study assessed DDIs using the Drug-PIN software. Associations between the Drug-PIN continuous score, Drug-PIN light, and treatment outscomes were analyzed along with the specific drugs involved in the DDIs. A total of 177 patients with BRAF-mutant metastatic melanoma undergoing BRAF/MEK inhibitor therapy were included. Of these, 94 patients (55.9%) were exposed to complex drug regimens related to comorbidities, supportive care, and symptom management. A significant change in Drug-PIN scores was observed before and after therapy initiation. Patients with low-grade DDIs demonstrated significantly longer median overall survival (OS) and progression-free survival (PFS) compared to those with high-grade DDIs (log-rank <i>p</i> = 0.0045 and <i>p</i> = 0.012, respectively); this observation was further validated by multiple regression analysis. By combining clinical and DDI data, we identified four patient subgroups with distinct prognoses, showing statistically significant differences in OS and PFS (log-rank <i>p</i> &lt; 0.0001). The subgroup with the highest clinical risk and high DDI had markedly poorer outcomes (HR 2.87, 95% CI [1.7–4.8], <i>p</i> &lt; 0.001). The drugs involved in high-level pharmacological interactions were analyzed. DDIs significantly contribute to poorer OS and PFS outcomes, independent of other clinical risk factors. Optimizing pharmacological regimens to minimize DDIs should be prioritized to enhance treatment efficacy in oncology. Prospective clinical trials are warranted to further validate the advantages of individualized, preemptive therapy optimization.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144190818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alteration of Hair Melanin in Patients With Mowat–Wilson Syndrome: The Role of the ZEB2 Gene in Regulating Melanogenesis Through SLC45A2","authors":"Mayuko Yamamoto,&nbsp;Hiroyuki Morisaka,&nbsp;Yuka Shibata,&nbsp;Mika Teraishi,&nbsp;Kentaro Ohko,&nbsp;Mikiro Takaishi,&nbsp;Kimiko Nakajima,&nbsp;Kazumasa Wakamatsu,&nbsp;Shosuke Ito,&nbsp;Shigetoshi Sano","doi":"10.1111/pcmr.70028","DOIUrl":"https://doi.org/10.1111/pcmr.70028","url":null,"abstract":"<div>\u0000 \u0000 <p>Mowat–Wilson syndrome (MOWS) is a congenital disease characterized by intellectual disability, delayed motor development, characteristic facial features, epilepsy, and a wide spectrum of neurocristopathies. MOWS is caused by de novo heterozygous loss-of-function mutations or deletions in the zinc finger E-box-binding homeobox2 (<i>ZEB2</i>) gene, which is a multifunctional regulator of neuronal development and cancer progression/metastasis through epithelial-to-mesenchymal transition. We recognized that patients with MOWS have brown to red hair. In the present study, we report that hair from patients with MOWS has reduced eumelanin and elevated pheomelanin contents, resulting in an increased pheomelanin-to-eumelanin ratio. Furthermore, <i>ZEB2</i>-mutated human epidermal melanocytes show a predominance of pheomelanin biosynthesis over eumelanin and decreased expression of <i>SLC45A2</i>, the gene responsible for oculocutaneous albinism 4. Our results suggest that ZEB2 plays a role in mixed melanogenesis by regulating the melanosomal ion transporter gene, <i>SLC45A2</i>.</p>\u0000 </div>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Profiling of Acral Lentiginous Melanoma Reveals Downregulated Immune Activation Compared to Cutaneous Melanoma","authors":"Stephanie J. Wang,&nbsp;Joanne Xiu,&nbsp;Katherine M. Butcher,&nbsp;Brittney K. DeClerck,&nbsp;Gene H. Kim,&nbsp;Justin Moser,&nbsp;Geoffrey T. Gibney,&nbsp;Leonel F. Hernandez-Aya,&nbsp;Jose Lutzky,&nbsp;Farah Abdulla,&nbsp;Kim A. Margolin,&nbsp;Patrícia Abrão Possik,&nbsp;Carla Daniela Robles-Espinoza,&nbsp;Fumito Ito,&nbsp;Gino K. In","doi":"10.1111/pcmr.70027","DOIUrl":"https://doi.org/10.1111/pcmr.70027","url":null,"abstract":"<p>Acral lentiginous melanoma (ALM) is a rare and insufficiently understood subtype of melanoma lacking in effective treatment options. Recent work has demonstrated that the response of ALM to immune checkpoint blockade is inferior to that of cutaneous melanoma (CM). Here we performed bulk genomic and transcriptomic sequencing of tumor tissue from 28 ALM and 5692 CM cases. Similar to prior studies, ALM was associated with a significantly lower incidence of point mutations, including in the <i>TERT</i> promoter and <i>BRAF</i>, but increased numbers of gene amplifications, notably of <i>CCND1</i>, <i>HMGA2</i>, and <i>MDM2</i>. Reactome pathway analysis revealed enhancement of keratinization and PI3K/AKT signaling pathways. Overall immunogenicity was decreased in ALM, which possessed lower IFNγ (<i>p</i> &lt; 0.001) and T-cell inflammatory (<i>p</i> = 0.03) pathway scores than CM. Despite higher computationally inferred levels of myeloid dendritic cells (<i>p</i> = 0.006), neoantigen load independent of predicted HLA binding affinity was lower (<i>p</i> &lt; 0.01) in ALM versus CM. Assessment of classical and nonclassical HLA mRNA levels revealed upregulation of HLA-G, suggesting alternative ALM immune evasion pathways in the setting of lower PD-L1 expression (<i>p</i> = 0.005). Additional research is needed to better understand and therapeutically target signaling networks in the ALM tumor microenvironment.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144117843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Function of Melanin-Based Colour Polymorphism in Cattle, Sheep and Goats","authors":"Venkatesh K.M.,&nbsp;Alexandre Roulin","doi":"10.1111/pcmr.70024","DOIUrl":"https://doi.org/10.1111/pcmr.70024","url":null,"abstract":"<p>Natural selection has rarely promoted the evolution of colour polymorphism in wild mammals. However, it is more common in domestic mammals due to artificial selection. For this reason, domestication could provide valuable insights into the mechanisms underlying the evolution of colour diversity. This raises the question of whether the associations between coat colour and other phenotypes in domestic animals are similar to those in free-living animals. Our literature review of cows, goats and sheep suggests that these associations can differ not only between species but also within and between breeds. This pattern holds for all the traits that we considered: morphology, behaviour, physiology, reproduction, milk production and parasitism. The only consistent association we found in the literature was the attraction of flies towards dark-coloured cows. The relationships between same colour morph, cortisol and thermoregulation varied across environments, suggesting a possible condition-dependent expression of multiple traits. We conclude that artificial selection may lead to a different integration of multiple phenotypes compared to animals living in the wild. Therefore, colour variation may not always serve the same functional roles in domestic animals as it does in wild ones.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144100415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Dominant Mutation in Gαs-Protein Increases Hair Pigmentation","authors":"Philip S. Goff,&nbsp;Peter Budd,&nbsp;Darren W. Logan,&nbsp;Margaret Keighren,&nbsp;Marta Cantero,&nbsp;Lisa McKie,&nbsp;Lluis Montoliu,&nbsp;Ian J. Jackson,&nbsp;Elena V. Sviderskaya","doi":"10.1111/pcmr.70025","DOIUrl":"https://doi.org/10.1111/pcmr.70025","url":null,"abstract":"<p>We have identified a chemically induced mouse mutation which increases the eumelanic hair pigmentation. We identify a coding mutation, A3533G, resulting in an amino acid substitution Y1133C, in the <i>Gnas</i> gene encoding the G_αs subunit of the tripartite G-protein, consistent with an activation of signalling via MC1R. In addition heterozygous mutant females are significantly lighter than wild type littermates. In cultured melanocytes, derived from mutant mice crossed to C57BL6 mice carrying <i>Cdkn2a</i>^{<i>tm1Rdp</i>}, basal pigmentation is higher than wild type melanocytes derived from litter mates. However, the addition of exogenous NDP-MSH does not increase pigmentation in mutant melanocytes in contrast to the pigmentation response of non-mutant melanocytes. The mutant and wild type cells respond in the same way to agouti signalling protein (ASP), consistent with ASP signalling mediated through a pathway other than G_αs-protein.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143938853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cutaneous Pigment Cell Distributions and Skin Structure of Xenopus","authors":"Weizheng Liang,&nbsp;Chenyang Hou,&nbsp;Zhenpeng Zhu,&nbsp;Peng Wang,&nbsp;Xiran Wang,&nbsp;Zhongwu Li,&nbsp;Jun Xue,&nbsp;Rensen Ran","doi":"10.1111/pcmr.70022","DOIUrl":"https://doi.org/10.1111/pcmr.70022","url":null,"abstract":"<p>Pigment cells not only are intrinsic factors to determine animal patterns, but also play vital roles in numerous behavioral and physiological processes as well as health, such as melanomas originating from melanocytes. Model organisms are commonly used to study pigment cell development and the mechanisms underlying related diseases, with zebrafish and mice, and <i>Xenopus</i> being well-established examples. <i>Xenopus tropicalis</i>, a diploid amphibian model, offers advantages such as high fecundity and easily observable pigment cell development. Recent advancements in gene-editing techniques have increased its prominence in research on pigment cell biology and melanoma pathogenesis. Here, we compare the skin pigment cell distribution as well as the skin structure in <i>X. tropicalis</i>, zebrafish, mice, and humans and point out the potential value of using <i>X. tropicalis</i> to model human skin diseases, such as melanoma.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/pcmr.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}