JID innovations : skin science from molecules to population health最新文献

{"title":"Patient journey and disparities in the diagnosis and treatment of patients with hidradenitis suppurativa","authors":"Raj Chovatiya ,&nbsp;Julie Gayle ,&nbsp;Robert Low ,&nbsp;Tae Oh ,&nbsp;Isabel Gomez ,&nbsp;Ning Rosenthal","doi":"10.1016/j.xjidi.2026.100462","DOIUrl":"10.1016/j.xjidi.2026.100462","url":null,"abstract":"<div><div>We compared the patient journey of adult and pediatric patients with hidradenitis suppurativa (HS) and suspected HS and of patients with HS stratified by race, ethnicity, and social determinants of health. Data were from the United States Premier Healthcare Database (including hospital discharge and billing data from inpatient and outpatient encounters) and its linked medical and pharmacy claims database. After diagnosis, adult patients (n = 3065) with HS initiated biologics more quickly and were less likely to have all-cause hospitalizations or all-cause emergency department visits than adult patients with suspected HS (n = 27,280). Adult patients with HS also reported more disease-related outpatient visits (mean ± SD: 3.7 ± 4.9 vs 2.9 ± 4.7) and lower overall costs ($22,128 ± $61,671 vs $36,359 ± $82,762) after diagnosis. Significant differences were found in the patient journey across ethnic groups (adult patients) and social vulnerability index categories (adult and pediatric patients). Differences in the patient journey were evident, particularly between adult patients with HS and adult patients with suspected HS. Although a confirmed diagnosis of HS is beneficial, disparities were prevalent. Increased awareness of these differences may minimize diagnostic delays, facilitate disease management, and reduce costs.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 3","pages":"Article 100462"},"PeriodicalIF":0.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147797659","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":"High-salt diet aggravates skin inflammation of psoriasis-like mouse model with CCL20‒CCR6 axis further activation","authors":"Mengyan Hu ,&nbsp;Han Cao ,&nbsp;Li Zhang ,&nbsp;Yuhan Xia ,&nbsp;Jiayi Zhang ,&nbsp;Feng Xue ,&nbsp;Xia Li ,&nbsp;Jie Zheng","doi":"10.1016/j.xjidi.2026.100451","DOIUrl":"10.1016/j.xjidi.2026.100451","url":null,"abstract":"<div><div>Epidermal keratinocytes are important for maintaining the skin barrier by interacting with immune cells and environmental stimuli. In this study, we reveal that a high-salt diet aggravated imiquimod-induced skin inflammation in a psoriasis-like mouse model, characterized by activation of the CCL20–CCR6 axis and increased infiltration of CCR6⁺ γδT cells in skin lesions. In the presence of additional sodium, the mRNA expression of <em>Ccl20</em> was upregulated in keratinocytes, mediated by JNK/p38–SGK1 pathway. Consistent with our experimental findings, a positive correlation between <em>SGK1</em> and <em>CCL20</em> gene expression was also observed in the skin of patients with psoriasis. Taken together, these data demonstrated that a high-salt diet aggravated skin inflammation in a psoriasis-like mouse model through further activation of the CCL20‒CCR6 axis.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100451"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146187844","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":"Dermoscopy-guided high-frequency ultrasound: Principles and applications in dermatology","authors":"Mehdi Boostani ,&nbsp;Ximena Wortsman ,&nbsp;Giovanni Pellacani ,&nbsp;Krisztián Füzesi ,&nbsp;Mariano Suppa ,&nbsp;Veronique Del Marmol ,&nbsp;Florencia Vera Morandini ,&nbsp;Javiera Perez-Anker ,&nbsp;Priscila Giavedoni ,&nbsp;Carmen Cantisani ,&nbsp;Lucas Boussingault ,&nbsp;Miklós Gyöngy ,&nbsp;Gyorgy Paragh ,&nbsp;Kamran Avanaki ,&nbsp;Norbert Kiss","doi":"10.1016/j.xjidi.2025.100446","DOIUrl":"10.1016/j.xjidi.2025.100446","url":null,"abstract":"<div><div>Conventional skin imaging modalities are often bulky, expensive, and impractical for routine dermatology practice. There is a need for a portable, multimodal imaging tool that integrates high-resolution surface and subsurface visualization at the point of care. The aim of this study was to describe the design, technical capabilities, and clinical application of dermoscopy-guided high-frequency ultrasound and to evaluate its performance across a range of dermatologic conditions. Dermoscopy-guided high-frequency ultrasound was applied to a total of 130 lesions from 122 patients at the Department of Dermatology, Semmelweis University (Budapest, Hungary); Université Libre de Bruxelles (Brussels, Belgium); and Hospital Clínic, Universidad de Barcelona (Barcelona, Spain). The examined cases included malignant skin cancers and inflammatory disorders. Dermoscopy-guided high-frequency ultrasound enabled simultaneous visualization and correlation of surface dermoscopic patterns with underlying structural alterations in real time. The device identified disease-specific imaging features for both malignant and inflammatory lesions. Artificial intelligence-based segmentation improved image interpretability. Dermoscopy-guided high-frequency ultrasound bridges a critical gap between surface and subsurface dermatologic imaging, offering a practical, portable, and cost-effective solution that could enhance noninvasive diagnosis and management in dermatologic care.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100446"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078089","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":"Assessing T-Cell Profile Shifts through IL-23 Inhibition by Guselkumab on Psoriasis","authors":"Yoshifumi Kanayama ,&nbsp;Oki Watanabe ,&nbsp;Mai Sakurai ,&nbsp;Yuki Enomoto ,&nbsp;Aya Yamamoto ,&nbsp;Shunya Mashiko ,&nbsp;Yukako Sugiura ,&nbsp;Masahiko Miyashiro ,&nbsp;Junya Masuda ,&nbsp;Akimichi Morita","doi":"10.1016/j.xjidi.2025.100433","DOIUrl":"10.1016/j.xjidi.2025.100433","url":null,"abstract":"<div><div>Anti–IL-23 antibody therapies improve the underlying immunopathology of psoriasis. Immune profile dynamics after anti–IL-23 treatment and their association with the treatment response are unclear. Focusing on guselkumab, an anti–IL-23p19 antibody, we comprehensively analyzed immune cells, serum inflammatory molecules, and CD4⁺ T-cell transcriptomics to identify drug effects in psoriasis. Peripheral and lesional skin blood samples were collected from 24 biologic-naïve patients at baseline and after treatment with guselkumab. We conducted FACS analysis of regulatory T cells, resident memory T cells, and dendritic cells; measured serum cytokine and chemokine levels; and analyzed RNA-sequencing data for gene expression changes in peripheral CD4⁺ T cells. Guselkumab administration increased regulatory T cells and decreased resident memory T cells. Gene expression differences at baseline defined 2 groups on the basis of the treatment response: transcriptomic profile–based high responders and transcriptomic profile–based moderate responders. Expression of certain chemokines, such as CXCL1 and CXCL5, was higher in the moderate responders, suggesting their association with a lower treatment response. RNA-sequencing analysis revealed gene expression changes related to T helper 17 cells and regulatory T cell activity. We observed alterations in regulatory T cells and resident memory T cells in response to guselkumab treatment that may contribute to the long-term suppression of the IL-23–driven inflammatory pathology in psoriasis. Furthermore, baseline peripheral blood transcriptomic immune findings may predict therapeutic outcomes. The G-Grope trial was registered as jRCTs041200070 with the Japan Registry of Clinical Trials on December 8, 2020.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100433"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145697920","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":"Atopic Dermatitis–like mouse model using early inoculation of patient-derived S. aureus together with MC903","authors":"Aaroh Joshi ,&nbsp;Altan Cornu ,&nbsp;Josefa Luxner ,&nbsp;Gernot Zarfel ,&nbsp;Camille Braun ,&nbsp;Jean-Francois Nicolas ,&nbsp;Richard L. Gallo ,&nbsp;Marc Vocanson ,&nbsp;Peter Wolf ,&nbsp;Vijaykumar Patra","doi":"10.1016/j.xjidi.2025.100436","DOIUrl":"10.1016/j.xjidi.2025.100436","url":null,"abstract":"<div><div><em>Staphylococcus aureus</em> (<em>S. aureus</em>) worsens atopic dermatitis (AD), but how individual strains differ in pathogenicity remains unclear. Mouse models that mimic AD and allow direct manipulation of <em>S. aureus</em> in early stages of disease are limited. Moreover, these models rarely incorporate clinical <em>S. aureus</em> strains isolated from patients with AD. In this study, we investigated the inflammatory potential of clinical <em>S. aureus</em> and <em>S. epidermidis</em> isolates from patients with AD in a mouse model. Clinical <em>S. aureus</em> strains showed significant variability in their ability to elicit inflammation. The inflammation was associated with differences in virulence factor expression and, to a lesser extent, with genomic variation. In contrast, <em>S. epidermidis</em> strains (taken from the same lesional skin sites of patients) induced only mild but consistent inflammation, with less variability at the strain level. Next, we examined the impact of a pathogenic clinical <em>S. aureus</em> strains in the presence of an MC903-induced type 2 immune environment. Under these conditions, <em>S. aureus</em> enhanced colonization; increased inflammation; and promoted type 1, type 2, and type 17/22 immune responses. These responses were less evident with either treatment alone. Our findings suggest that clinical <em>S. aureus</em> strains from patients with AD differ in their capacity to modulate skin inflammation, particularly within a type 2–skewed environment. These results highlight the potential value of incorporating clinically relevant <em>S. aureus</em> isolates into early-stage in vivo models to better understand AD immunopathology and to inform microbiome-targeted therapeutic strategies.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100436"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145747576","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":"Corrigendum to ‘Superior Antiproliferative and Enhanced Synergistic Effects of a Rock Inhibitor in Multiple Models for Keloid Disease’ JID Innovations, Volume 5, Issue 6, November 2025, 100402","authors":"Zeinab Ghasemishahrestani ,&nbsp;Traci A. Wilgus ,&nbsp;Nonhlanhla P. Khumalo ,&nbsp;Ardeshir Bayat","doi":"10.1016/j.xjidi.2026.100452","DOIUrl":"10.1016/j.xjidi.2026.100452","url":null,"abstract":"","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100452"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146187843","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":"Abundances but not concentrations of circulating unsaturated fatty acids are associated with incident psoriatic diseases: Evidence from cohort and Mendelian randomization studies","authors":"Minxue Shen ,&nbsp;Zhiwei Wang ,&nbsp;Danrong Jing ,&nbsp;Songchun Yang ,&nbsp;Yi Xiao ,&nbsp;Xiang Chen","doi":"10.1016/j.xjidi.2025.100437","DOIUrl":"10.1016/j.xjidi.2025.100437","url":null,"abstract":"<div><div>Whether the levels of circulating fatty acids (FAs) are associated with psoriasis and psoriatic arthritis remains unknown. To examine the measured and predicted levels of circulating FAs in association with incident psoriatic disease, 2-sample Mendelian randomization analysis was performed to examine the causal relationship between monounsaturated FAs (MUFAs) and polyunsaturated FAs (PUFAs) and psoriasis, and a cohort study of the UK Biobank participants was conducted to validate the findings, in terms of the measured and dietarily predicted levels of FAs. Mendelian randomization analysis identified a positive association of genetically predicted MUFAs% but inverse associations of PUFAs% and PUFAs/MUFAs with psoriasis and psoriatic arthritis. In the cohort, higher MUFAs% was associated with increased risks of psoriasis (relative risk = 1.109, <em>P</em> = .004) and psoriatic arthritis (relative risk = 1.188, <em>P</em> = .016), whereas higher PUFAs% and PUFAs/MUFAs were associated with lower risks of psoriasis (relative risk = 0.891, <em>P</em> = .001) and psoriatic arthritis (relative risk = 0.874, <em>P</em> = .051). Dietary scores that predict PUFAs% and MUFAs% showed consistent results with larger effect sizes. The effects of PUFAs% and MUFAs% were not significant in under- or normal-weighted participants. In conclusion, circulating PUFAs% and MUFAs% are causal factors for incident psoriatic diseases, and the effects might be modified by obesity.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100437"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145841217","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":"Population- and haplotype-dependent variation around TYR rs1126809: An in silico study for melanoma risk research","authors":"Árpád Ármin Balogh ,&nbsp;Márta Széll ,&nbsp;Nikoletta Nagy","doi":"10.1016/j.xjidi.2025.100445","DOIUrl":"10.1016/j.xjidi.2025.100445","url":null,"abstract":"<div><div>The common missense variant rs1126809 in the <em>TYR</em> gene, encoding a key enzyme in melanin synthesis, is linked to both albinism and melanoma susceptibility. Although its role in hypopigmentation as part of a risk haplotype is established, its function in melanoma is less understood. To investigate population- and haplotype-dependent associations surrounding <em>TYR</em> rs1126809 that may suggest directions for future studies on melanoma risk and melanocyte biology, we analyzed melanoma GWAS summary statistics using FUMA to identify lead SNPs in linkage disequilibrium with rs1126809 and assessed their regulatory potential using chromatin state data from melanocytes, keratinocytes, and fibroblasts. Haplotype structures were examined in European, American, and South Asian populations using LDlink. rs1126809 emerged as lead SNP in the <em>TYR</em> locus. Thirty SNPs were in high linkage disequilibrium, 6 of which reside in melanocyte-specific regulatory regions. These variants form population-specific haplotypes that may modulate TYR expression. In Europeans and Americans, 2 distinct haplotypes carrying the risk allele showed different linked SNP profiles, suggesting haplotype-dependent effects. The findings suggest that variations surrounding <em>TYR</em> rs1126809 may exhibit population- and haplotype-dependent patterns relevant to melanoma risk, pointing to previously unreported directions for future research and refinement of polygenic risk modeling.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100445"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078088","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":"Deep intronic MSH2 variant confirms Muir-Torre subtype of Lynch syndrome","authors":"Fiona Chan-Pak-Choon ,&nbsp;Andrew Y. Shuen ,&nbsp;Evan Weber ,&nbsp;Lili Fu ,&nbsp;Barbara Rivera ,&nbsp;William D. Foulkes","doi":"10.1016/j.xjidi.2025.100438","DOIUrl":"10.1016/j.xjidi.2025.100438","url":null,"abstract":"<div><div>Whole-genome sequencing can uncover clinically significant noncoding variants missed by standard germline testing, as demonstrated in this report in a patient with Muir–Torre syndrome, a subtype of Lynch syndrome. In this case, despite a convincing clinical phenotype and immunohistochemical loss of MSH2/MSH6 in 1 of the patient’s tumors, conventional gene panel testing failed to detect a germline pathogenic variant. Whole-genome sequencing identified a deep intronic <em>MSH2</em> variant, and tumor sequencing revealed somatic <em>MSH2</em> mutations (second hits) across multiple tumors, confirming mismatch repair deficiency and establishing a Muir-Torre syndrome diagnosis. This report underscores the limitations of routine genetic testing and highlights the clinical utility of whole-genome sequencing in identifying pathogenic variants in noncoding regions. It also emphasizes the role of dermatologists in recognizing cutaneous markers of hereditary cancer syndromes and the importance of interdisciplinary evaluation in guiding both patient care and familial risk assessment.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100438"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939040","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 standardized approach to test missense PNPLA1 rare genetic variants of uncertain significance in epidermal differentiation disorders","authors":"Nuria Pell ,&nbsp;Pauline Bernard ,&nbsp;Séverine Courrech ,&nbsp;Lukas Opalka ,&nbsp;Aina Millán-Sánchez ,&nbsp;Elise Levy ,&nbsp;Séverine Garnier ,&nbsp;Cyrielle Clément ,&nbsp;Pauline Le Faouder ,&nbsp;Katerina Vávrová ,&nbsp;Olga López ,&nbsp;Justine Bertrand-Michel ,&nbsp;Corinne Leprince ,&nbsp;Isabelle Fourquaux ,&nbsp;José-Enrique Mejia ,&nbsp;Jean-Christophe Pagès ,&nbsp;Juliette Mazereeuw-Hautier ,&nbsp;Nathalie Jonca","doi":"10.1016/j.xjidi.2025.100442","DOIUrl":"10.1016/j.xjidi.2025.100442","url":null,"abstract":"<div><div>Congenital ichthyoses, now renamed epidermal differentiation disorders (EDDs) (syndromic EDD or nonsyndromic EDD), are rare, disabling conditions caused by sequence variations in epidermal barrier genes. However, 5–10% of variants, called “variants of uncertain significance” (VUS), remain uncharacterized, and their pathogenicity is not demonstrated. We developed an approach for classifying VUS in nonsyndromic EDD associated with variant in <em>PNPLA1</em>. We generated <em>PNPLA1</em>-knockout human keratinocytes. PNPLA1, encoded by a missense VUS or by the reference coding sequence, was expressed after lentiviral transduction in the <em>PNPLA1</em>-knockout cells. Transduced cells were used to produce human epidermal equivalents, and the functionality of the normal or VUS-encoded proteins was evaluated. Compared with <em>PNPLA1</em>-knockout human epidermal equivalents re-expressing normal PNPLA1, <em>PNPLA1</em>-knockout human epidermal equivalents showed disrupted synthesis of ω-O-acylceramide, the normal product of PNPLA1, as well as abnormal vesicle-like structures and immature cornified envelopes, characteristic of the epidermis of patients with <em>PNPLA1</em> variants. Human epidermal equivalents expressing the <em>PNPLA1</em> VUS showed similar abnormalities, consistent with an impaired PNPLA1 function. This work demonstrated a feasible strategy to help reclassifying missense VUS, which can be extended to other EDD-related genes. Although further efforts are needed to translate this approach into clinical practice and help overcome current diagnostic limitations, such models are valuable tools for pathophysiological and preclinical research on EDDs.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"6 2","pages":"Article 100442"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037969","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}