Experimental Dermatology最新文献

{"title":"Maternal and Infant Skin Microbiome Synchrony and Divergence: A Longitudinal Study of Skin Microbial Ecology and Early-Life Assembly","authors":"Doris Wilborn,&nbsp;Andria Constantinou,&nbsp;Agathe Franz,&nbsp;Rolf Schwarzer,&nbsp;Peter Menzel,&nbsp;Gabriela Engelhardt,&nbsp;Tsenka Tomova-Simitchieva,&nbsp;Ruhul Amin,&nbsp;Gavin Zhou,&nbsp;Kathrin Hillmann,&nbsp;Jan Kottner,&nbsp;Jann Ralle,&nbsp;Frank Konietschke,&nbsp;Ulrike Blume-Peytavi","doi":"10.1111/exd.70349","DOIUrl":"https://doi.org/10.1111/exd.70349","url":null,"abstract":"<p>During pregnancy and after childbirth, women's skin undergoes significant changes which may affect the skin's functional and structural characteristics and microbial diversity. Like their mothers, the newborns also experience various skin challenges in the months following birth. Temporal changes in skin microbiome in special groups such as pregnant women and newborns, as well as the interrelation between their skin's microbial diversity, have not been investigated. We followed women from pregnancy through 6 months after delivery, and their infants from 4 weeks to 6 months of age to investigate their skin characteristics and the microbiome, and potential associations. We enrolled 109 pregnant females residing in Berlin, Germany, with 93 mothers-infant pairs completing the study. Microbiome investigations included DNA isolation as single-site sampling using volar forearm skin swabs. Bioinformatic analysis involved OTU clustering at 97% sequence identity, taxonomic assignment using NCBI reference databases, and calculation of biodiversity metrics, including relative abundance of the dominant bacterial phylotypes, bacterial diversity and Shannon diversity index. The maternal skin microbiome showed mild to moderate changes throughout pregnancy and the 6 months postpartum period. In infants, alpha diversity significantly increased (mean species richness from 82.6 at 4 weeks to 116.1 at 6 months), although it did not reach maternal diversity levels (145.4 at 6 months postpartum). Regarding the microbiome consistency of the included women and infants, the within-pair similarity was always significantly higher than between-pair similarity for both time points. Therefore, we conclude that there is likely a relationship between the microbiome of the mother and that of her child.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70349","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148785193","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":"Beyond Histamine: Mast Cell-Neuron Communication in Chronic Pruritic and Pain Disorders","authors":"Tomer Kagan,&nbsp;Gil Yosipovitch","doi":"10.1111/exd.70320","DOIUrl":"https://doi.org/10.1111/exd.70320","url":null,"abstract":"<p>Chronic pruritic and cutaneous pain disorders are increasingly recognized as neuroimmune conditions driven by dynamic interactions between immune and sensory systems. While histamine has historically dominated models of mast cell-mediated itch, accumulating evidence indicates that non-histaminergic pathways are central to chronic disease. In this review, we synthesize current understanding of mast cell-neuron communication and propose a unifying framework in which these cells form functional neuroimmune units that sustain itch and pain through bidirectional signalling and feed-forward amplification. Mast cells release proteases, cytokines, lipid mediators, and neurotrophins that activate and sensitize sensory neurons via receptors including PAR-2, IL-31RA, TrkA, and transient receptor potential channels. In parallel, neuron-derived neuropeptides such as substance P and calcitonin gene-related peptide drive mast cell activation, notably through MRGPRX2-dependent mechanisms, reinforcing neurogenic inflammation. These interactions promote peripheral sensitization and structural remodelling of cutaneous innervation, providing a mechanistic basis for persistent symptoms across disorders such as atopic dermatitis, prurigo nodularis, urticaria, neuropathic itch, and chronic pruritus of unknown origin. Importantly, emerging therapies targeting key nodes of this axis - including IL-4Rα, IL-31RA, KIT, and Bruton's tyrosine kinase—offer clinical validation of this neuroimmune paradigm. We highlight critical gaps in translating these insights to human disease, including the need for spatially resolved biomarkers and real-time functional mapping of neuroimmune interactions. Advancing this framework may enable precision-targeted therapies for chronic itch and skin pain conditions that remain refractory to conventional treatment.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70320","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784687","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":"Correction to ‘Attenuation of Subclinical TNF-α Signalling in Xerotic Skin by AIMP-1 Derived Peptide Containing Moisturiser Leads to Skin Barrier Recovery’","authors":"","doi":"10.1111/exd.70346","DOIUrl":"10.1111/exd.70346","url":null,"abstract":"<p>\u0000 <span>Y.H. Kim</span>, <span>S. J. Lee</span>, <span>H. S. Kim</span>, et al., “ <span>Attenuation of Subclinical TNF-α Signalling in Xerotic Skin by AIMP-1 Derived Peptide Containing Moisturiser Leads to Skin Barrier Recovery</span>,” <i>Experimental Dermatology</i> <span>34</span>, no. <span>12</span> (<span>2025</span>): e70183, https://doi.org/10.1111/exd.70183\u0000 </p><p>In the published article, the name of the fourth author was incorrect and has been updated from ‘Son Sun Woo’ to ‘Sun Woo Son’, with ‘Sun Woo’ as the first name and ‘Son’ as the last name.</p><p>The online version of this article has been corrected accordingly.</p><p>We apologise for this error.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70346","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758536","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":"Topical Application of Indole-3-Acetic Acid, Present in S. epidermidis Supernatant, Alleviates Atopic Dermatitis in Mice at Least via the Aryl Hydrocarbon Receptor Signalling Pathway","authors":"Piao Wang,&nbsp;Caixi Wang,&nbsp;Yanting Zhang,&nbsp;Lingbo Bi,&nbsp;Hanqing Zhao,&nbsp;Zining Xu,&nbsp;Ziyi Wang,&nbsp;Yujun Sheng,&nbsp;Yong Cui","doi":"10.1111/exd.70329","DOIUrl":"https://doi.org/10.1111/exd.70329","url":null,"abstract":"<div>\u0000 \u0000 <p>Dysbiosis of the skin microbiome, characterised by <i>Staphylococcus aureus</i> overgrowth and imbalance of commensals such as <i>Staphylococcus epidermidis</i> (<i>S. epidermidis</i>), is closely associated with atopic dermatitis (AD). However, the therapeutic relevance of defined <i>S. epidermidis</i>-associated indole metabolite, especially indole-3-acetic acid (IAA), in AD-like inflammation remains incompletely characterised. Here, we investigated the role of IAA, a tryptophan-derived metabolite enriched in the culture supernatant of the tested <i>S. epidermidis</i> strain, in AD-like inflammation. Public transcriptomic analyses suggested impaired AHR-associated and tryptophan-metabolism signatures in AD skin, particularly in lesional skin, while human metagenomic data indicated AD-associated staphylococcal alterations. Targeted metabolomics identified IAA as an enriched indole metabolite in <i>S. epidermidis</i> culture supernatant. In an MC903-induced AD-like mouse model, cutaneous IAA levels and <i>S. epidermidis</i> abundance were reduced. Topical IAA attenuated AD-like phenotypes, improved barrier-related proteins and reduced inflammatory indices. These protective effects were diminished by the AHR antagonist CH223191. Molecular docking predicted a possible interaction between IAA and AHR, and in vitro assays showed that IAA modulated keratinocyte AHR-associated inflammatory and barrier-related responses. Together, our findings support IAA as a microbiome-associated postbiotic candidate for AD management, at least partly through AHR-associated signalling.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148783596","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":"Differential Quantification of Cutibacterium acnes Phylotypes IA and IB/II on Healthy and Acne-Prone Human Skin","authors":"Cecilie Feidenhansl,&nbsp;Erinda Rruci,&nbsp;Nastassia Knödlseder,&nbsp;Hans B. Lomholt,&nbsp;Holger Brüggemann","doi":"10.1111/exd.70347","DOIUrl":"https://doi.org/10.1111/exd.70347","url":null,"abstract":"<p><i>Cutibacterium acnes</i> is a common skin bacterium that inhabits sebaceous follicles and comprises multiple phylotypes. Healthy skin is colonized by a <i>C. acnes</i> population dominated by phylotypes IA, IB, and II. In acne, this diversity is reduced, with a predominance of phylotype IA. Quantifying <i>C. acnes</i> phylotypes has been challenging due to the lack of specific methods. Here, we developed a droplet digital PCR (ddPCR) assay that separately quantifies phylotype IA and phylotypes IB/II, based on a difference in the hyaluronidase gene. The method was applied to skin swabs from 14 healthy individuals and 14 acne patients. Healthy skin contained nearly equal amounts of IA and IB/II, whereas acne samples showed a 111-fold predominance of IA over IB/II, due to a marked depletion of IB/II, instead of an increase of IA. After 4–6 months of isotretinoin treatment, <i>C. acnes</i> levels decreased drastically, with phylotype IA reduced by 50-fold. Twelve to 15 months after treatment, both phylotypes rebounded, although IB/II recovered only partially. Taken together, this ddPCR method can quantitatively distinguish the acne-dominant phylotype IA from healthy skin-associated phylotypes IB/II, and is thus a useful tool for skin microbiome studies and specifically for assessing <i>C. acnes</i> dysbiosis in acne.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753766","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":"Bullous Pemphigoid: A Focused Review on Antigen Epitopes","authors":"Jishu Li,&nbsp;Xun Feng,&nbsp;Min Zou,&nbsp;Mintong Wei,&nbsp;Wei Li","doi":"10.1111/exd.70345","DOIUrl":"https://doi.org/10.1111/exd.70345","url":null,"abstract":"<p>Bullous pemphigoid (BP) is the most common subepidermal autoimmune blistering disease, characterized by autoantibodies against BP180 and BP230. Although the NC16A domain of BP180 is the immunodominant epitope, increasing evidence indicates that non-NC16A epitopes also contribute to the clinical heterogeneity of BP. This review summarizes the immunological characteristics and clinical significance of BP180 and BP230 epitopes, and discusses their associations with disease phenotypes, treatment responses, and prognosis. We also outline the pathogenesis and animal models of BP, and highlight the rarity of validated models for non-NC16A epitopes and their limited mechanistic scope. Emerging targeted therapies are critically reviewed in relation to current knowledge of epitope-specific immune responses. Although epitope profiling may eventually contribute to disease stratification and biomarker development, current evidence is insufficient to support routine epitope-guided therapeutic decision-making. Despite current progress, challenges remain in clarifying the pathogenicity of non-NC16A epitopes and establishing standardized detection. Future research should focus on epitope–phenotype correlations and large-cohort studies to promote the development of precision therapy for BP.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70345","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148754165","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":"Diet-Induced Obesity Promotes Alopecia Through Oxidative Stress and Androgen Signalling in Female Mice","authors":"Yi-An Tu,&nbsp;Chia-Hung Chou,&nbsp;Koping Chang,&nbsp;Chu-Chun Huang,&nbsp;Hong-Nerng Ho,&nbsp;Mei-Jou Chen","doi":"10.1111/exd.70343","DOIUrl":"10.1111/exd.70343","url":null,"abstract":"<div>\u0000 \u0000 <p>Female-pattern hair loss is common in obese women with polycystic ovary syndrome (PCOS), recently proposed as polyendocrine metabolic ovarian syndrome (PMOS) and is often associated with hypertriglyceridemia (TG), although the underlying mechanisms remain unclear. This study investigated how metabolic factors and androgens contribute to hair loss in female mice exposed to a high-fat diet (HFD). A controlled, parallel-group study using 8-week-old female C57BL/6 mice fed either an HFD (60% kcal fat) or a standard diet for 16 weeks. Mice were sacrificed at baseline and 4-week intervals for serial evaluation of metabolic, hormonal and skin changes (<i>n</i> = 6/group/time point). Hair loss was quantified from digital photographs using the ImageJ and further supported by histological examination. Circulating metabolic and hormonal profiles were measured. In dorsal skin, oxidative stress (malondialdehyde, MDA) and androgen-related markers—5-alpha-reductase type II (5αR2), dihydrotestosterone (DHT) and androgen receptor (AR)—were evaluated using immunohistochemistry, Western blot and enzyme-linked immunosorbent assay. From Week 12 onward, HFD-fed mice exhibited greater weight gain, pronounced dorsal hair thinning and elevated TG, insulin and free androgen index (FAI) levels. Skin MDA, 5αR2, DHT and AR levels also progressively increased. In the second experiment, 8-week-old female mice were assigned to four groups (<i>n</i> = 6/group): HFD with N-acetylcysteine (NAC), finasteride, spironolactone, or vehicle administered by oral gavage for 12 weeks. Compared with HFD-vehicle, antioxidant or anti-androgen co-treatment significantly lowered serum TG, tissue MDA and ameliorated hair thinning despite similar weight gain and 5αR2 levels. NAC reduced TG, FAI and decreased tissue MDA, DHT and AR. Finasteride lowered TG, MDA, DHT and AR, whereas spironolactone reduced TG and MDA. HFD-induced obesity exacerbates hair loss in female mice by enhancing oxidative stress and activating androgen signalling in the skin. Targeting these pathways, such as antioxidants and antiandrogens, may mitigate HFD-accelerated hair loss.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711918","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":"Antimicrobial Peptides of the Skin: Roles in Skin Cancer and Clinical Applications","authors":"Elizabeth Botto,&nbsp;Zoe M. Lipman,&nbsp;Laurie A. Temiz,&nbsp;Lilia Corea-Selm,&nbsp;James M. Grichnik","doi":"10.1111/exd.70341","DOIUrl":"10.1111/exd.70341","url":null,"abstract":"<p>Cutaneous antimicrobial peptides (AMPs) are increasingly recognized for their multifaceted roles in skin disease and cancer, and thus application for therapeutic potential. Beyond their contributions to innate defence and the skin's microbiome, AMPs have been implicated in inflammatory skin conditions and cutaneous malignancies. Comprehensive summaries of AMPs' roles in skin cancer and related current clinical developments remain scarce, despite abundant emerging evidence of pro- and anti-tumour properties in other fields. This review provides a comprehensive discussion of AMPs, including dermcidin, psoriasin (S100A7), human cathelicidin (LL-37), RNase-7 and the human β-defensins, in the context of skin cancer research and clinical developments. These AMPs influence skin tumorigenesis through microbiome regulation, innate immune pathways and chronic inflammation, and although the mechanistic details are subject to scrutiny, several AMP-derived therapies, including LL-37 and LTX-315, have been developed for their potential in cutaneous oncology.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70341","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705912","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":"Gene Therapy for Dystrophic Epidermolysis Bullosa","authors":"Cristina Has,&nbsp;Meropi Karakioulaki","doi":"10.1111/exd.70339","DOIUrl":"10.1111/exd.70339","url":null,"abstract":"<p>Dystrophic epidermolysis bullosa (DEB) is a rare, debilitating genodermatosis caused by loss-of-function variants in <i>COL7A1,</i> resulting in type VII collagen (C7) deficiency and defective anchoring fibrils, which are essential for dermal–epidermal adhesion. <i>COL7A1</i> is a large gene, and C7 is synthesized by both keratinocytes and fibroblasts, and extracellularly secreted, where it forms a supramolecular network that stabilizes the dermal–epidermal junction. Human genotype–phenotype correlations suggest that residual C7 expression (~10% of normal levels) may confer a milder disease phenotype, whereas complete absence results in generalized skin fragility with scarring and systemic complications. Thus, restoring C7 expression remains a central therapeutic objective. Since the discovery of <i>COL7A1</i>, thousands of pathogenic variants have been described, including amino acid substitutions in the triple-helical domain that allow partial C7 function, whereas null alleles are associated with severe phenotypes. Gene- and cell-based strategies have evolved to address the large <i>COL7A1</i> size and delivery challenges. Ex vivo gene/cell therapies (keratinocytes or fibroblasts engineered to express <i>COL7A1</i>) have demonstrated partial, wound-specific C7 restoration but with durability limitations, as grafted cells may be outcompeted or lose transgene expression over time; select patients show sustained anchoring fibril formation and improved wound healing; however, long-term outcomes remain variable. In vivo topical gene therapy has achieved clinically meaningful wound closure in DEB, illustrating a paradigm shift toward accessible and patient-friendly therapeutic approaches, albeit with real-world considerations on durability and wound recurrence. A multidisciplinary framework integrating EB expert centers, drug-delivery pharmacy services, wound management, and patient-support programs can further enhance treatment access and adherence. General factors such as nutritional status, infection and comorbidities also influence both wound healing and the response to gene therapy. Revertant mosaicism offers a natural gene-therapy substrate: cultured epidermal autografts derived from revertant patches have yielded substantial, yet heterogeneous, epithelization, with outcomes contingent on revertant cell proportion and culture fidelity. Collectively, these advances highlight the emerging potential of gene- and cell-based therapies to achieve durable disease modification in DEB.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13451533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148688814","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":"Low-Risk Basal Cell Carcinoma: Surgery First, but Not Surgery Only—Toward Protocolised Active Surveillance","authors":"Vincenzo De Giorgi,&nbsp;Gabriella Perillo,&nbsp;Giovanni Cecchi,&nbsp;Federica Fazzari,&nbsp;Biancamaria Zuccaro","doi":"10.1111/exd.70340","DOIUrl":"10.1111/exd.70340","url":null,"abstract":"","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673212","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}