International Journal of Rheumatic Diseases最新文献

{"title":"Editorial: The Path in Psoriatic Disease—From Conceptual Clarity to Clinical Translation","authors":"An-Ping Huo, Tang-Kai Cheng, James Cheng-Chung Wei","doi":"10.1111/1756-185x.70858","DOIUrl":"10.1111/1756-185x.70858","url":null,"abstract":"<p>The management of psoriatic disease is at a transformative crossroads, shifting from reactive symptom control to proactive “disease interception” [<span>1</span>]. Psoriatic arthritis (PsA) develops in up to one-third of people with psoriasis, often following a prolonged subclinical phase that offers a unique window of opportunity for intervention. Despite this, diagnostic delays exceeding 2 years remain common, leading to irreversible joint damage and long-term disability. As we move toward a secondary prevention paradigm, we must address the fundamental challenges of defining the target, stratifying risk, and establishing robust trial endpoints.</p><p>A major challenge in interception is the lack of consensus on how to define the transition from psoriasis to PsA. For clinical practice and trial design, clear operational definitions are vital. “Subclinical PsA” typically denotes the presence of immunological or imaging-confirmed inflammation in individuals without clinical musculoskeletal symptoms. In contrast, aligning with the recent conceptual framework proposed by Ciccia and colleagues [<span>2</span>], “very early PsA” should be defined by the crucial threshold where subtle clinical musculoskeletal symptoms (such as mild arthralgia or early tenderness) co-occur with inflammation confirmed on imaging, prior to meeting the full Classification Criteria for Psoriatic Arthritis (CASPAR) [<span>2, 3</span>]. Current frameworks, such as those proposed by the European Alliance of Associations for Rheumatology (EULAR) and the Psoriasis and Psoriatic Arthritis Clinics Multicenter Advancement Network (PPACMAN), have historically differed in how they classify these stages [<span>3</span>]. Recent epidemiological insights suggest that harmonizing these definitions by focusing on this intrinsic biological transition is essential to ensure that interception trials are biologically grounded and ethically robust [<span>4</span>].</p><p>Effective interception requires identifying people at the highest risk of imminent transition. Clinical risk models utilize factors like psoriasis severity, nail involvement, and obesity to estimate risk. However, even at maximum risk, the 1-year absolute predicted probability remains modest. To improve precision, we must integrate these clinical markers with dynamic biological signals. Retrospective cohort studies utilizing the TriNetX network—employing rigorous propensity score matching to adjust for baseline demographics and medication use—have highlighted that comorbidities such as Type 2 diabetes and fatty liver significantly elevate transition risk, reinforcing the need for a multimodal approach [<span>5</span>]. Furthermore, the role of HLA-B27 as a marker for specific endotypes suggests that genetic susceptibility provides a fixed background risk that interacts with time-varying exposures [<span>5</span>].</p><p>The choice of trial endpoints remains a significant challenge. While PsA incidence (CASPAR-defined) is t","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185x.70858","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methodological Considerations on Relative Handgrip Strength and Cancer Risk in Older Adults","authors":"Chung-Chu Tung, Hui-Yuan Chen, Renin Chang, Sun-Lin Huang","doi":"10.1111/1756-185x.70812","DOIUrl":"10.1111/1756-185x.70812","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and Safety of Ultra-Low Starting Dose Febuxostat Titration in Male Patients With Primary Gout","authors":"Sun Huizhen,&nbsp;Li Yadi,&nbsp;Guo Lin,&nbsp;Sun Rui,&nbsp;Guo Xuemei,&nbsp;Li Ping","doi":"10.1111/1756-185x.70800","DOIUrl":"10.1111/1756-185x.70800","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Since gout is a common metabolic arthritis caused by urate crystal deposition, urate-lowering therapy (ULT) is clearly indicated, but the initiation of ULT frequently causes paradoxical acute flares that in turn impair patient adherence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study sought to assess the effectiveness and safety of an ultra-low-dose initiation strategy for febuxostat (10 mg/day) compared to the standard starting dose (20 mg/day) in reducing initiation-related flares while maintaining long-term urate control.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>120 male patients with primary gout presenting with acute arthritis were randomly assigned to initiate febuxostat at 10 mg/day (Group A) or 20 mg/day (Group B), with protocol-mandated biweekly titration. The primary outcomes were gout flare frequency over 24 weeks (assessed using Poisson regression), serum uric acid (SUA) target attainment, and the incidence of adverse events.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Although both groups achieved comparable target SUA levels by week 24, Group A demonstrated a significantly lower overall flare incidence (36.7% vs. 70.0%; <i>p</i> &lt; 0.001), along with a greater percentage of flare-free patients (70.0% vs. 46.7%; <i>p</i> = 0.016). Multivariable Poisson regression revealed that Group B had an approximately twofold higher risk of flares compared to Group A (Incidence Rate Ratio = 1.95; <i>p</i> = 0.012), with obese patients deriving the most pronounced benefit from the ultra-low-dose approach. To avert one additional flare, the calculated number needed to treat was 4.3. Additionally, the occurrence of clinically significant liver injury (ALT/AST &gt; 3× ULN) was low in both groups, with 3.3% in Group A and 1.7% in Group B. Multivariable regression analysis confirmed that LDL-C is an independent predictor of ALT (β = 12.90, <i>p</i> = 0.009), while febuxostat dosage was not linked to hepatotoxicity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Initiating febuxostat at a dose of 10 mg/day with gradual titration demonstrates a superior safety profile by effectively reducing early acute flares without compromising long-term urate control, which is particularly advantageous for high-risk cohorts, including obese patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13548448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Inflammation: Breaking the Vicious Cycle of Matrix Stiffness and Mechanotransduction in Systemic Sclerosis","authors":"Tang-Kai Cheng,&nbsp;Durga Prasanna Misra,&nbsp;James Cheng-Chung Wei","doi":"10.1111/1756-185x.70835","DOIUrl":"10.1111/1756-185x.70835","url":null,"abstract":"&lt;p&gt;Systemic sclerosis (SSc) remains a formidable challenge in clinical rheumatology, characterized by progressive tissue fibrosis that often resists conventional immunosuppressive therapies [&lt;span&gt;1&lt;/span&gt;]. Managing this disease frequently presents a frustrating clinical bottleneck: while initial inflammatory phases may be mitigated with current therapeutic arsenals, the relentless progression of fibrosis often continues unchecked. The systemic burden of SSc—ranging from profound cutaneous induration to life-threatening interstitial lung disease and major adverse cardiovascular events—highlights an urgent need to rethink our approach to fibrogenesis [&lt;span&gt;2&lt;/span&gt;]. Traditionally, the rheumatology community has viewed the pathogenesis of SSc predominantly through an immunological lens, focusing on how autoantibodies and inflammatory cytokines continuously activate fibroblasts [&lt;span&gt;3&lt;/span&gt;]. However, recent breakthroughs suggest that extracellular matrix (ECM) stiffness is not merely an endpoint of the disease but a plausible feed-forward amplifier. This editorial explores the clinical implications of identifying mechanosensitive fibroblast progenitor populations and targeting mechanical stiffness to better understand the self-sustaining cycle of fibrosis in SSc.&lt;/p&gt;&lt;p&gt;Recent original research published in the Annals of the Rheumatic Diseases by Ueberall et al. provides a compelling perspective: the physical rigidity of the ECM itself acts as a signal that may further amplify disease progression [&lt;span&gt;4&lt;/span&gt;]. This builds upon an existing, broader mechanobiology paradigm involving integrin-mediated mechanotransduction, YAP/TAZ signaling, TGF-beta activation, LOX-dependent matrix crosslinking, and FAK signaling. The recent work challenges the classical “chicken-or-egg” dilemma in fibrosis by demonstrating in experimental contexts that once the tissue stiffens, this mechanical signal becomes a plausible feed-forward amplifier for further deterioration.&lt;/p&gt;&lt;p&gt;The identification of specific cellular populations provides a mechanistic link for this phenomenon. A subset of fibroblast progenitor cells, defined as PI16+, possess specialized mechanoreceptors like PIEZO1/2 that allow them to continuously monitor matrix rigidity [&lt;span&gt;4&lt;/span&gt;]. In a rigid microenvironment, these precursor cells appear driven to differentiate into SFRP2+ COMP+ myofibroblasts, which act as a key profibrotic myofibroblast subset responsible for excessive collagen production. This creates a vicious, self-sustaining feedback loop: a stiffened ECM “educates” precursor cells to become fibrotic effectors, which in turn secrete more matrix, further increasing tissue stiffness within the localized environment [&lt;span&gt;4&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;For clinicians and researchers investigating the epidemiological and systemic impact of SSc—such as the significantly increased risks of cardiovascular comorbidities [&lt;span&gt;2&lt;/span&gt;] or premature ovarian insufficiency [&lt;span&gt;5&lt;/span&gt;] frequently ","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13548438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-Sectional and Longitudinal Association Between Biological Aging Acceleration and the Risk of Osteoarthritis: A Cohort Study From UK Biobank","authors":"Sisi Liu,&nbsp;Weishu Wang,&nbsp;Chengxu Li,&nbsp;Yuxin Lai,&nbsp;Zhounan Zhou,&nbsp;Menglin Han,&nbsp;Yujie Zhang,&nbsp;Yan Zhang,&nbsp;Ke Tang,&nbsp;Haitao Sun,&nbsp;Qian Yang,&nbsp;Muhui Zeng,&nbsp;Tianxiang Fan,&nbsp;Zhong Alan Li,&nbsp;GO Consortium,&nbsp;Changhai Ding,&nbsp;David J. Hunter,&nbsp;Zhaohua Zhu","doi":"10.1111/1756-185x.70853","DOIUrl":"10.1111/1756-185x.70853","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To evaluate the relationship between biological ages and the prevalence and incidence of osteoarthritis (OA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>332 261 participants from UK Biobank were analyzed. Biological aging was measured using phenotypic age (PhenoAge) and Klemera–Doubal (KDMAge). KDMAge was derived from nine clinical biomarkers to gauge system integrity decline, while PhenoAge was computed from chronological age and nine clinical biomarkers to gauge mortality risk. Biological aging accelerations were computed as residuals from regressing KDMAge and PhenoAge against chronological age. The associations between biological aging and prevalence and incidence of OA were analyzed using logistic and Cox regression models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>At baseline, 55.4% of included individuals had younger PhenoAge aging acceleration. In cross-sectional analyses, individuals with accelerated aging had higher odds of OA compared to those with non-accelerated aging (odds ratios [OR]: 1.12 [95% CI: 1.09–1.14] for PhenoAge acceleration and 1.05 [1.03–1.08] for KDMAge acceleration). In the longitudinal analyses, increased PhenoAge acceleration was associated with a higher risk of incident OA (hazard ratios [HR]: 1.12 [1.10–1.15]). However, the association between KDMAge acceleration and the incidence of OA was not statistically significant (HR: 0.99 [0.97–1.01]). Accelerated biological aging showed a more pronounced association with OA among individuals &gt; 60 years. No additive or multiplicative interactions were found between OA polygenic risk score (PRS) and biological aging.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Advanced biological aging may increase the risk of OA, independent of OA genetic risk, particularly in individuals aged over 60 years. The two biological aging indicators hold potential as novel composite clinical biomarkers, directing prevention and intervention strategies for high-risk populations for OA.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose–Response Meta-Analysis: A Quantitative Perspective on Rheumatic Diseases","authors":"Yu Lei,&nbsp;Ting Tang,&nbsp;Aihua Du,&nbsp;Liye Xu,&nbsp;William Tao-Hsin Tung","doi":"10.1111/1756-185x.70852","DOIUrl":"10.1111/1756-185x.70852","url":null,"abstract":"&lt;p&gt;Rheumatic and immune-mediated diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), gout, and ankylosing spondylitis (AS), arise from the interplay of multiple factors in their development, including genetic susceptibility, metabolic disorders, immune imbalances, and environmental exposures. These diseases exhibit significant heterogeneity in their phenotypes and disease progression [&lt;span&gt;1&lt;/span&gt;]. Our long-term research examines the relationship between various exposure factors—including metabolic indicators, nutritional components, and drug dosages—and disease risk or therapeutic efficacy. Traditional meta-analyses typically compare “exposed” versus “unexposed” groups or high versus low exposure levels, often overlooking the gradient information of exposure intensity. This binary research approach limits our capacity to identify the actual trend in disease risk as exposure doses change [&lt;span&gt;2&lt;/span&gt;]. Dose–response meta-analysis (DRMA) is a specialized technique that builds on the traditional meta-analysis/meta-regression framework. It reconstructs and combines study-specific dose–response functions by integrating stratified exposure data across studies and accounting for intra-study correlations, such as through the Greenland-Longnecker method [&lt;span&gt;3, 4&lt;/span&gt;]. Models can explore quadratic or fractional polynomial regression, though they more commonly use restricted cubic splines (RCS) for flexible nonlinear fitting [&lt;span&gt;5, 6&lt;/span&gt;]. Given the complex, multifactorial etiology of these conditions, DRMA provides a quantitative framework to move beyond simple binary associations and uncover critical thresholds, thereby refining our understanding of how environmental, nutritional, and therapeutic factors shape disease trajectories across the rheumatology spectrum.&lt;/p&gt;&lt;p&gt;Numerous studies have used DRMA to investigate the dose–response relationship between nutritional intake and the risk of rheumatic and immune diseases. For example, the consumption of fruits, vegetables, and oily fish exhibits a nonlinear dose–response relationship with RA risk, where the risk decreases once intake exceeds a specific threshold [&lt;span&gt;7&lt;/span&gt;]. Notably, DRMA allows researchers to more precisely assess specific levels of alcohol consumption or tobacco exposure that significantly increase disease risk. In terms of alcohol consumption, Jin et al.'s 2014 study revealed a J-shaped nonlinear relationship. Compared to abstinence, daily intake of about 3 g of alcohol resulted in an RR = 0.93 (95% CI 0.88–0.98), and 9 g/day resulted in an RR = 0.86 (95% CI 0.76–0.97), suggesting that low-to-moderate drinking may be linked to a reduced RA risk. However, when alcohol intake reached approximately 30 g/day, the risk increased (RR = 1.28, 95% CI 0.94–1.73), indicating that beyond a certain threshold, the protective effect disappears and may even become harmful [&lt;span&gt;8&lt;/span&gt;]. Furthermore, studies show that compared to lifelong non-smoker","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148865014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Risk to Treatment: Clinical Updates in Osteoporosis Management.","authors":"Karam Alchi, Antoni Chan","doi":"10.1111/1756-185x.70862","DOIUrl":"10.1111/1756-185x.70862","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":"e70862"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report: Serum Protein Electrophoresis Incidentally Reveals Alpha-1 Antitrypsin Deficiency in p-ANCA-Positive Crescentic Glomerulonephritis.","authors":"Andac Komac, Nergis Serin, Duygu Temiz Karadag, Serap Argun Baris, Ayse Cefle","doi":"10.1111/1756-185x.70871","DOIUrl":"10.1111/1756-185x.70871","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":"e70871"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13574492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148968585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incremental Benefit of Combining Etanercept and Tofacitinib in Treatment-Refractory Axial Spondyloarthritis: A Series of Four Cases.","authors":"Maria Sunny, Justin George, Prakashini Mruthyunjaya, Sakir Ahmed, Padmanabha Shenoy Devakumar","doi":"10.1111/1756-185x.70881","DOIUrl":"https://doi.org/10.1111/1756-185x.70881","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":"e70881"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149008355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radiological Change in Interstitial Lung Abnormalities and Interstitial Lung Disease in Patients With Rheumatoid Arthritis at 1 Year.","authors":"Takeshi Mochizuki, Shinji Katayanagi, Motoaki Sato, Koichiro Yano, Ken Okazaki","doi":"10.1111/1756-185x.70864","DOIUrl":"10.1111/1756-185x.70864","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":"e70864"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13574495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148968555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}