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

{"title":"Evaluation of Actinic Keratosis as a Risk Factor for Subsequent Nonskin Cancer Risk","authors":"Alexander R. Gomez-Lara ,&nbsp;Christopher D. George ,&nbsp;Chen Jiang ,&nbsp;Jie Yin ,&nbsp;Yuhree Kim ,&nbsp;Charles P. Quesenberry ,&nbsp;Eric Jorgenson ,&nbsp;Shabnam Madani ,&nbsp;Maryam M. Asgari ,&nbsp;Hélène Choquet","doi":"10.1016/j.xjidi.2025.100374","DOIUrl":"10.1016/j.xjidi.2025.100374","url":null,"abstract":"<div><div>Actinic keratosis (AK) is a precancerous lesion that develops on chronically sun-exposed skin. Immunosuppression is known to increase the risk of both AK and other cancers, highlighting the need to evaluate potential associations between AK and subsequent nonskin cancers. To determine whether a diagnosis of AK is associated with an increased subsequent incident of nonskin cancers, we conducted a retrospective case-control study within a large integrated healthcare delivery system. The study included 53,778 patients with AK and 152,896 controls without prior cancer diagnoses at enrollment. AK was more prevalent in males (30.7 vs 23.5% in females). AK was not associated with increased risk of overall nonskin cancers after adjusting for demographic (age, sex), clinical (body mass index, immunosuppression history), behavioral (smoking, alcohol use), and healthcare utilization factors (adjusted hazard ratio = 0.99, 95% confidence interval = 0.95–1.02). However, significant associations were observed between AK and breast (adjusted hazard ratio = 1.11, 95% confidence interval = 1.03–1.19) and prostate (adjusted hazard ratio =1.14, 95% confidence interval = 1.03–1.26) cancers. This large study reveals that AK may be a predictor of risk for subsequent cancers, notably breast and prostate cancers. These findings emphasize the need for increased surveillance for these cancer types in individuals with AK.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 4","pages":"Article 100374"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923032","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":"The Role of Skin Dysbiosis and Quorum Sensing in Atopic Dermatitis","authors":"Hiroki Okamoto ,&nbsp;Shuo Li ,&nbsp;Yuumi Nakamura","doi":"10.1016/j.xjidi.2025.100377","DOIUrl":"10.1016/j.xjidi.2025.100377","url":null,"abstract":"<div><div>The skin microbiome plays a crucial role in the pathogenesis of atopic dermatitis (AD), a chronic inflammatory skin disorder strongly associated with microbial dysbiosis, particularly <em>Staphylococcus aureus</em> colonization. However, the mechanisms linking <em>S aureus</em> to AD remain insufficiently understood. This review explores the impact of the quorum-sensing (QS) system, particularly the accessory gene regulator Agr, in AD development and progression. By examining key microbial–host interactions, we provide insights into how QS influences skin inflammation and dysbiosis. Furthermore, we discuss the potential of microbiome-targeted therapeutic strategies to mitigate or prevent AD, highlighting their implications for future research and clinical applications.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 4","pages":"Article 100377"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155003","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":"Wnt Signaling in Male Genital Lichen Sclerosus, Differentiated Penile Intraepithelial Neoplasia, and Penile Squamous Cell Carcinoma","authors":"Georgios Kravvas ,&nbsp;Boyu Xie ,&nbsp;Michael Millar ,&nbsp;Alex Freeman ,&nbsp;Aiman Haider ,&nbsp;Hussain M. Alnajjar ,&nbsp;Asif Muneer ,&nbsp;Aamir Ahmed ,&nbsp;Christopher Barry Bunker","doi":"10.1016/j.xjidi.2025.100372","DOIUrl":"10.1016/j.xjidi.2025.100372","url":null,"abstract":"<div><h3>Introduction</h3><div>Male genital lichen sclerosus (MGLSc) is a chronic inflammatory disease causing scarring and significant morbidity, and predisposing individuals to differentiated penile intraepithelial neoplasia (dPeIN) and penile squamous cell carcinoma (PeSCC). Penile carcinogenesis follows two pathways: HPV-related and non-HPV-related. While HPV drives undifferentiated PeIN and warty/basaloid PeSCC, MGLSc is implicated in non-HPV-related dPeIN and \"usual\" PeSCC. Wnt signalling, pivotal in carcinogenesis, remains underexplored in MGLSc and PeIN.</div></div><div><h3>Methods</h3><div>Tissue arrays from 114 archival samples of MGLSc, dPeIN, and PeSCC were analyzed using multi-label fluorescence staining and confocal microscopy for Wnt4, cyclin D1, c-MYC, and MMP7 expression.</div></div><div><h3>Results</h3><div>Wnt signalling proteins were upregulated in PeSCC: cyclin D1 (2.3-fold), Wnt4 (2-fold), c-MYC (2.5-fold), and MMP7 (1.8-fold). Wnt4 expression increased in MGLSc (p=0.02), while dPeIN showed minimal changes. Altered co-localization of Wnt4/MMP7 (p=0.04) was observed in MGLSc and significant co-localization alterations of several protein pairs were also identified in PeSCC.</div></div><div><h3>Conclusion</h3><div>Wnt signalling plays a role in progression from MGLSc to PeSCC through protein dysregulation. Overexpression and altered interactions in PeSCC highlight its potential as a diagnostic, prognostic, and therapeutic target.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 4","pages":"Article 100372"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143942202","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":"Genetic and Phenotypic Features of 2 Northern Italy Families with Dowling-Degos Disease Type 4","authors":"Dario Tomasini ,&nbsp;Carlo F. Tomasini ,&nbsp;Andrea Michelerio ,&nbsp;Eloisa Arbustini ,&nbsp;Fabio Sirchia ,&nbsp;Alrun Hotz ,&nbsp;Judith Fischer ,&nbsp;Svenja Rademacher","doi":"10.1016/j.xjidi.2025.100364","DOIUrl":"10.1016/j.xjidi.2025.100364","url":null,"abstract":"<div><div>Dowling-Degos disease (DDD) is an autosomal dominant genodermatosis involving the folds with lentiginous hyperpigmentation and reddish–brown papules. Four main types of DDD with variable clinical presentations likely related to the heterogeneity of the gene variant landscape have been implicated. Pathogenic keratin 5 gene <em>K5</em> gene variants favor a reticular distribution with predominant fold involvement, whereas pathogenic variants in <em>POGLUT1</em> lead to a widespread form with acantholytic features previously named Galli–Galli disease, now belonging to the disease spectrum of DDD and renamed DDD type 4. This study details the clinical and histopathological features associated with the sequence variant c.205C&gt;T, p.(Arg69∗) in <em>POGLUT1</em> of 2 families from northern Italy affected by DDD4. Despite sharing the same variant, clinical manifestations varied among the affected members of the 2 families. Environmental factors probably contributed to phenotypic variability and symptoms exacerbation. Histopathology was sustained by digitiform rete ridges, suprabasal acantholysis, and dyskeratosis. Moreover, we detected aberrant keratin 5 gene <em>K5</em> expression in 2 biopsies. A review of the literature on <em>POGLUT1</em>-related DDD subtypes contextualizes these findings. The fact that several patients have been reported to carry the variant c.205C&gt;T, p.(Arg69∗) might point to a potential mutational hotspot.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 4","pages":"Article 100364"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143916783","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 Direct Comparative Analysis of HPV DNA with Single-Molecule RNA and p16INK4a Protein Expression in Lichen Sclerosus: Implications for Diagnostics and Pathogenesis","authors":"Georgios Kravvas ,&nbsp;Boyu Xie ,&nbsp;Clarisse Ganier ,&nbsp;Henk van den Munckhof ,&nbsp;Ellen van den Munckhof ,&nbsp;Maurits de Koning ,&nbsp;Sandra Jerkovic Gulin ,&nbsp;Alex Freeman ,&nbsp;Aiman Haider ,&nbsp;Hussain Alnajjar ,&nbsp;Asif Muneer ,&nbsp;Magnus Lynch ,&nbsp;Michael Millar ,&nbsp;Aamir Ahmed ,&nbsp;Christopher Barry Bunker","doi":"10.1016/j.xjidi.2025.100367","DOIUrl":"10.1016/j.xjidi.2025.100367","url":null,"abstract":"<div><h3>Introduction</h3><div>Emerging evidence suggests a relationship between chronic, intermittent, occluded exposure of a susceptible epithelium to urine and male genital lichen sclerosus (MGLSc), although human papillomavirus (HPV) may also play a role.</div></div><div><h3>Aims and methods</h3><div>This study investigated the association between MGLSc and HPV across the prepuce. Preputial samples from uncircumcised patients with MGLSc undergoing circumcision were tested for MGLSc distribution, HPV genotyping, RNAscope, and p16^INK4a detection.</div></div><div><h3>Results</h3><div>Preputial samples from 9 patients with MGLSc were analyzed, with 9 distinct areas per prepuce, yielding 81 samples. These included MGLSc, non-MGLSc, and indeterminate regions. Various mucosal and beta HPV types were detected, most commonly HPV24, HPV23, HPV36, and HPV9. HPV DNA was found in all patients, and high-risk HPV types were found in 6. No significant differences were observed in total HPV (<em>P</em> = .1) or oncogenic HPV (<em>P</em> = .6) between MGLSc and non-MGLSc tissues. Transcriptionally active HPV was absent in all samples on the basis of independent RNAscope and p16^INK4a staining.</div></div><div><h3>Discussion</h3><div>HPV DNA was detected in a mosaic pattern across the prepuce, with no significant differences between MGLSc and non-MGLSc skin. The absence of transcriptional activity suggests that HPV in MGLSc is incidental and may not contribute toward pathogenesis.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 4","pages":"Article 100367"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143863352","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":"The PAR2 Antagonist Larazotide Can Mitigate Acute Histamine-Stimulated Epithelial Barrier Disruption in Keratinocytes: A Potential Adjunct Treatment for Atopic Dermatitis","authors":"Danielle M. Glinka ,&nbsp;Gordon G. MacGregor","doi":"10.1016/j.xjidi.2025.100369","DOIUrl":"10.1016/j.xjidi.2025.100369","url":null,"abstract":"<div><div>Atopic dermatitis (AD) is a chronic inflammatory skin condition with evidence of defects in the barrier properties of the epidermis. Changes in the permeability properties of the tight junction have been reported in AD, and reversing this leaky tight junction may be a potential treatment for AD. This study aimed to determine the effect of larazotide, an antagonist of the protease-activated receptor 2, on the permeability and barrier properties of the tight junctions in keratinocyte monolayers. Normal human epithelial keratinocytes were grown in culture on permeable supports. The effects of larazotide on transepithelial resistance and permeability properties of keratinocyte monolayers were studied before and after histamine challenge. Larazotide mitigated the disruptive effect of histamine on epithelial permeability by increasing the electrical resistance and decreasing epithelial permeability. Larazotide may be beneficial as a topical therapeutic for AD; however, the permeability properties of the short-peptide larazotide through the uppers layers of the epidermis is currently unknown. In conclusion, the protease-activated receptor 2 antagonist larazotide has a protective effect on keratinocyte monolayers and may be useful as an adjunct therapeutic agent to enhance barrier function and promote epidermal healing in AD.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 4","pages":"Article 100369"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143869058","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":"Using Durometers to Quantify Stiffness as an Outcome Measure for Cutaneous Neurofibroma in Neurofibromatosis Type 1","authors":"Bahir Chamseddin ,&nbsp;Renee M. McKay ,&nbsp;Ruyun Jin ,&nbsp;Hong Zhu ,&nbsp;Lu Q. Le","doi":"10.1016/j.xjidi.2025.100380","DOIUrl":"10.1016/j.xjidi.2025.100380","url":null,"abstract":"<div><div>Patients with neurofibromatosis type 1 develop multiple cutaneous neurofibromas (cNFs) for which no effective drug therapy exists; mainstay treatment remains physical removal. However, clinical trials testing new drugs are ongoing, and quantitative techniques based on cNF biology are needed to measure changes in cNF after treatment. cNF tumor bulk is composed of extracellular matrix and inflammatory cells that dictate their stiffness. No studies have reported measuring the stiffness change in neurofibromas, which would indicate shrinking of the tumor bulk. The goal of this study was to evaluate 2 different instruments—the Rex Gauge durometer (denoted as REX) and the Delfin SkinFibroMeter (denoted as DELFIN)—in reproducibly measuring cNF stiffness. Ninety-seven neurofibromas from patients with neurofibromatosis type 1 on different skin areas were measured at each of 2 visits about 2 weeks apart. The DELFIN had moderate within-tumor agreement (intraclass correlation coefficient = 0.607, 95% confidence interval = 0.512–0.691) and moderate within-visit agreement (intraclass correlation coefficient = 0.732, 95% confidence interval = 0.665–0.786), and the REX had moderate within-tumor agreement (intraclass correlation coefficient = 0.740, 95% confidence interval = 0.631–0.816) and excellent within-visit agreement (intraclass correlation coefficient = 0.937, 95% confidence interval = 0.913–0.953), while accounting for repeated visits and tumor measurements clustered within each patient. We found that both the DELFIN and REX are easy to use and reliable, providing consistent quantification of cNF stiffness.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 4","pages":"Article 100380"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203569","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":"Integration of Longitudinal Clinical, Immunologic, and Environmental Data for Enhanced Disease Monitoring and Management in Pemphigus Vulgaris: A Case Study","authors":"Justin Baroukhian ,&nbsp;Kristina Seiffert-Sinha ,&nbsp;Animesh A. Sinha","doi":"10.1016/j.xjidi.2025.100358","DOIUrl":"10.1016/j.xjidi.2025.100358","url":null,"abstract":"<div><div>We present a case study of a patient with pemphigus vulgaris using an integrative, longitudinal approach to resolve the identities and potential contributions of a network of environmental exposures of possible clinical relevance in a genetically predisposed individual. Our comprehensive methodology tracked exposomal factors, disease evolution, and biological variables across the patient's lifespan. Our patient reported multiple predisease onset exposures historically associated with pemphigus vulgaris, including multiple psychosocial and physical/chemical stressors. After disease onset, despite standard pharmacologic treatment, disease activity fluctuated widely. Notably, within 14 months after substantial dietary changes and body mass index reduction, the patient achieved long-lasting complete clinical remission off therapy. Our results reinforce the significance of the gene–environment interplay in pemphigus vulgaris, emphasizing the role of diet in autoimmune regulation. This study serves as proof of concept regarding the power of detailed longitudinal mapping of disease expression and contemporaneous monitoring of the \"exposome\" and \"behaviorome\" to reveal previously unrecognized disease-modifying elements and suggest targeted and personalized lifestyle modifications to augment established treatments. Our study design and strategy offer a template for a hyperpersonalized approach to medicine through comprehensive lifespan data collection and integrative analyses to yield enhanced insights into disease development, with the goal of uncovering actionable interventions in future clinical care settings in the management of autoimmune disorders.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100358"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antimicrobial Peptide Signaling in Skin Diseases","authors":"Sharan Kumar Balaji ,&nbsp;Bhavani Balasundarasekar ,&nbsp;Waris Muhammad Khuwaja ,&nbsp;Keean Michael Dolan ,&nbsp;Xintong Dong","doi":"10.1016/j.xjidi.2025.100354","DOIUrl":"10.1016/j.xjidi.2025.100354","url":null,"abstract":"<div><div>Antimicrobial peptides (AMPs) are important innate immune molecules at microbe–host interfaces. The biophysical properties of AMPs that facilitate direct killing of microbes have been extensively reviewed. In this article, we focus on how AMPs perform immunomodulatory functions through interaction with host receptors on epithelial, immune, and neuronal cell types. We summarize the current knowledge of known AMPs in the skin, the receptors that respond to AMPs, and the downstream intracellular signaling pathways. In the end, we discuss the roles of AMP signaling systems in skin diseases.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100354"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143521194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary Sugar and Atopic Dermatitis in a Longitudinal Birth Cohort","authors":"Judy Shan ,&nbsp;Morgan Ye ,&nbsp;Sheng-Pei Wang ,&nbsp;Hannah Kang ,&nbsp;Ahnna Lee ,&nbsp;Sinéad M. Langan ,&nbsp;Erin L. Van Blarigan ,&nbsp;Katrina Abuabara","doi":"10.1016/j.xjidi.2025.100366","DOIUrl":"10.1016/j.xjidi.2025.100366","url":null,"abstract":"<div><h3>Importance</h3><div>The association of diet with atopic dermatitis (AD) in children is understudied and may present an opportunity to optimize AD management in a cost-effective and low-risk manner.</div></div><div><h3>Objective</h3><div>The aim of this study was to determine the extent to which dietary sugar is associated with AD period prevalence and severity in a longitudinal pediatric cohort.</div></div><div><h3>Design, setting, and participants</h3><div>This was a longitudinal cohort study of children from the Avon Longitudinal Study of Parents and Children with food frequency questionnaire data to estimate dietary carbohydrate and sugar at 1, 3, 5, 7, 10, and 13 years.</div></div><div><h3>Exposure</h3><div>The exposure was dietary sugar as a proportion of total caloric intake.</div></div><div><h3>Main outcome and measure</h3><div>The primary outcome was AD based on a maternal- or self-reported questionnaire that asked about disease activity and severity over the past 12 months. Logistic regression models adjusted for sex, race, maternal delivery age, highest parental education level, social class assessed through parental occupation, body mass index, total caloric intake, and maternal history of AD.</div></div><div><h3>Results</h3><div>The study population included 5372 unique participants, 50% of whom were female, and 20–30% of whom reported AD at any time point. No significant associations were found at ages 1, 3, 5, and 7 years. At age 13 years, logistic regression revealed that a 10% increase in dietary sugar as a proportion of total caloric intake was associated with a 22% (95% confidence interval = 7–40%) increase in odds of AD overall. There was a dose–response relationship with disease severity: there was a 19% (95% confidence interval = 0–42%) increase in the odds of mild AD and 32% (95% confidence interval = 5–86%) increase in the odds of moderate–severe AD. When examining subtypes of dietary sugar, the effect was limited to nonmilk extrinsic sugars.</div></div><div><h3>Conclusions and relevance</h3><div>Given the known health benefits, reduction of nonmilk sugars could be studied as a cost-effective and low-risk intervention for AD in late childhood and early adolescence.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100366"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143825584","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}