Pharmacology Research & Perspectives最新文献

{"title":"Deciphering the Functional Mechanisms of eIF3f in Tumors and Exploring Targeted Therapies.","authors":"Yujinpeng Hao, Jun Shao, Naqi Lian, Mianli Bian","doi":"10.1002/prp2.70292","DOIUrl":"10.1002/prp2.70292","url":null,"abstract":"<p><p>Eukaryotic translation initiation factor 3 subunit F (eIF3f) is a critical component of the eIF3 complex and plays a pivotal role in diverse biological processes, including cell proliferation, apoptosis, adhesion, and transcriptional regulation. Recent studies have revealed that eIF3f is aberrantly expressed in multiple malignancies and exhibits a striking context-dependent functional profile. In solid tumors such as hepatocellular carcinoma (HCC), colorectal cancer (CRC), and prostate cancer (PCa), elevated eIF3f expression correlates with poor patient prognosis, indicating an oncogenic role. Conversely, in pancreatic cancer (PC) and melanoma (MM), reduced or absent eIF3f expression promotes tumor progression, suggesting a tumor-suppressive function. This functional plasticity indicates that eIF3f is not a simple oncogenic driver but rather a molecular hub that integrates diverse cellular signals. This review systematically delineates the structural characteristics and biological functions of eIF3f, summarizing its expression patterns and underlying molecular mechanisms across various malignancies. Building on this, we propose an integrated mechanistic framework that attributes the functional plasticity of eIF3f to differential upstream signaling networks, heterogeneity in post-translational modification profiles, and the remodeling status of the tumor microenvironment (TME). Furthermore, we critically evaluate the strength of evidence supporting eIF3f as a diagnostic and prognostic biomarker, identify methodological bottlenecks and translational challenges in current targeting strategies, and outline priority research directions, including elucidating the structural biological basis of its functional plasticity and developing context-specific intervention strategies. By integrating mechanistic insights with clinical relevance, this review aims to establish a conceptually coherent and mechanistically testable theoretical framework for eIF3f research, guiding the design of precision stratified therapeutic approaches and facilitating its substantive translation from basic research to clinical application.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70292"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148369484","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":"Potent and Sustained Lowering of Serum Uric Acid by YJH-012-D, a GalNAc-Conjugated siRNA Targeting Xanthine Dehydrogenase.","authors":"Tingke Tang, Qiuying Li, Chenguang Zhang, Yongxing Wang, Lu Yang, Haibin Huang, Yujun He, Zhi Zheng, Dong Liang, Meng Wang, Yingyu Wu, Chengjiang Zhao, Wenhao Cui","doi":"10.1002/prp2.70308","DOIUrl":"10.1002/prp2.70308","url":null,"abstract":"<p><p>Hyperuricemia (HUA) is primarily driven by hepatic overproduction of urate, mediated by xanthine dehydrogenase (XDH). This preclinical study evaluates YJH-012-D, a N-acetylgalactosamine (GalNAc)-conjugated small interfering RNA (siRNA) targeting hepatic XDH. Functional assays demonstrated that YJH-012-D potently suppressed both XDH mRNA and protein expression in primary hepatocytes. In mice, a single subcutaneous dose of 8 mg/kg significantly reduced serum uric acid levels and suppressed hepatic XDH expression for more than 42 days. In cynomolgus monkeys, administration of YJH-012-D at 10 mg/kg lowered serum uric acid for up to 180 days, with sustained XDH inhibition observed for 120 days. Pharmacokinetic analysis revealed a high liver-to-plasma area under the curve (AUC) ratio (2000-6100) and a hepatic half-life exceeding 10 days, consistent with prolonged pharmacological activity. Comprehensive toxicity assessments-including clinical biochemistry, histopathology, and RNA sequencing (RNA-seq)-based off-target profiling-identified no significant adverse effects. Collectively, YJH-012-D exhibits potent, durable urate-lowering efficacy and a favorable safety profile, underscoring its potential as a novel therapeutic candidate for HUA.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70308"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13428038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148648994","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":"Leveraging Administrative Health Data to Capture Rare Adverse Drug Reactions: Identifying Pediatric Patients With Trimethoprim-Sulfamethoxazole Acute Respiratory Distress Syndrome.","authors":"Keith Feldman, Jenna O Miller, Katherine Doane, Laura Loftis, James W Antoon, Kevin J Downes, Jennifer L Goldman","doi":"10.1002/prp2.70289","DOIUrl":"10.1002/prp2.70289","url":null,"abstract":"<p><p>Rare adverse drug reactions (ADRs) are underrecognized and underreported in the electronic medical record (EMR). These events often require clinical review, making systematic identification challenging. The study aim was to develop an approach to prioritize identification and validation of a rare ADR to trimethoprim-sulfamethoxazole causing acute respiratory distress syndrome (TMP-SMX ARDS) across medical institutions. We developed a clinical phenotype based on 2 local TMP-SMX ARDS cases mapped to standardized elements of a national comparative healthcare database (PHIS). We validated identification of TMP-SMX ARDS at scale across medical institutions. A set of scoring criteria was created to prioritize cases and generate a center-specific top 10 list of candidate encounters. External validation at 3 PHIS contributing hospitals with a known TMP-SMX ARDS case was performed by reviewing the top 10 candidate list for the known case. The review period was January 1, 2012-January 1, 2025. EMR data extracted from 2 TMP-SMX ARDS cases included patients that both required extracorporeal membrane oxygenation for > 100 days, experienced air leak early in hospital presentation, required tracheostomy placement, and were hospitalized for > 440 days. Based on the TMP-SMX ARDS phenotype, the local cases ranked 1st and 3rd on the PHIS generated top 10 candidate list for internal validation. For external validation, known cases were identified on their respective hospital top 10 lists, ranking 3rd, 3rd, and 5th. Applying a TMP-SMX ARDS phenotype to a national health care database paired with clinical review of candidate cases may be an effective approach to identify underrecognized ADRs.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70289"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13275549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148272548","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":"The JAK1/2 Inhibitor Baricitinib Ameliorates Neuroinflammation and Symptoms in an Animal Model of Essential Tremor.","authors":"Mehran Ilaghi, Fatemeh Shahsavari, Monavareh Soti, Sina Elyasifar, Leila Bagherzadeh, Zeynab Pirmoradi, Mohammad Shabani","doi":"10.1002/prp2.70299","DOIUrl":"10.1002/prp2.70299","url":null,"abstract":"<p><p>Essential tremor (ET) is one of the most prevalent adult-onset movement disorders, which significantly impairs quality of life. So far, there are few therapeutic options with limited efficacy. This study investigated the therapeutic potential of baricitinib, a selective JAK1/2 inhibitor, in the harmaline-induced model of ET. Male Swiss mice were randomly assigned to five groups (n = 8): control, harmaline, and harmaline plus baricitinib at 10, 20, or 50 mg/kg doses. ET was induced using harmaline (10 mg/kg, i.p.). Baricitinib was administered orally daily for 14 days. Assessments included behavioral tests and cerebellar gene expression analysis of inflammatory markers (TNF-α, IL-6, NF-κB), neurotrophic factors (BDNF), ET-related targets (Lingo-1, NMDA receptor), and histopathological evaluation. Baricitinib reduced harmaline-induced tremor severity. The drug also significantly ameliorated anxiety-like behaviors in elevated plus maze and open field tests, while reducing depressive-like behavior in the tail suspension test. Passive avoidance outcomes changed in a direction suggestive of improved retention; however, the high-dose findings should be interpreted cautiously because 50 mg/kg was associated with motor coordination impairment. Molecular analyses revealed baricitinib completely normalized cerebellar pro-inflammatory cytokines TNF-α and IL-6 and suppressed NF-κB expression. The drug restored BDNF levels and reduced Lingo-1 expression. Histopathological examination also suggested reduced Purkinje cell degeneration, with 20 and 50 mg/kg doses reducing Purkinje cell degeneration to control levels. Baricitinib reduced tremor and affective behaviors in a harmaline-induced ET model, though gait abnormalities persisted. Cognitive benefits at lower doses were observed, with cautious interpretation required for the high dose due to motor effects. Molecular and histological analyses supported anti-inflammatory and neuroprotective effects, indicating selective benefits via neuroinflammatory modulation.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70299"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148423114","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":"Alterations in Abdominal Blood Flows After Drinking Coffee.","authors":"Soshi Owada, Shohei Shibasaki, Yoriko Sei, Keiichiro Harashima, Hiroaki Ohnishi, Takashi Watanabe, Konomi Sakata, Tomonori Kishino","doi":"10.1002/prp2.70296","DOIUrl":"10.1002/prp2.70296","url":null,"abstract":"<p><p>Coffee exerts beneficial effects on health, such as suppressing type 2 diabetes, cardiovascular disease, and fatty liver. Coffee also relieves headaches by the caffeine component decreasing blood flow in the cerebral arteries. Caffeine is also used to treat apnea in premature infants, but blood flow in the superior mesenteric artery (SMA) decreases as a side effect. However, whether drinking coffee decreases abdominal blood flows in adults remains uncertain. If drinking coffee decreases SMA blood flow in adults, subsequent blood flows via the portal vein (PV) to the liver might also decrease, which could be a contributor to the beneficial suppression of fatty liver. The present study aimed to clarify hemodynamics in the SMA and PV under fasting conditions after drinking coffee or water in 32 healthy young men (mean age, 21 ± 1 years). Flow volume decreased on sonography 30 min after drinking coffee in the SMA (median -13.4%, interquartile range [IQR] -18.6% to -9.6%; p < 0.001) together with an increase in pulsatility index (median 9.0%, IQR -1.1% to 14.5%; p < 0.001), and a decrease in PV (median -11.3%, IQR -14.5% to -5.3%; p < 0.001). These phenomena were observed 90 min after drinking coffee and were particularly prominent in habitual low caffeine consumers, but were largely absent after drinking water. Drinking coffee decreases SMA and PV blood flows in adults.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70296"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148339629","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":"A Tale of Two Cell Lines: Characterization of Differential Efficacy of Small Molecule Drugs Cediranib and NU-7441 on Primary Versus Metastatic Colorectal Cancer.","authors":"Josephine D Tsang, Cai M Roberts","doi":"10.1002/prp2.70298","DOIUrl":"10.1002/prp2.70298","url":null,"abstract":"<p><p>Colorectal cancer is recognized as one of the leading causes of cancer death amongst both sexes in the U.S. Despite rigorous screening, those diagnosed with colon cancer often face poor prognosis, and approximately 70% of affected patients will develop metastatic relapse. The investigation of colon carcinoma cell lines' genetic variability and response to chemotherapy panels may aid in targeting therapies to improve outcomes. This study aims to find correlations between metastasis status, gene variability, and drug response. We used two cell lines that were isolated from the same 51-year-old male with colorectal adenocarcinoma: a primary tumor-derived line (SW480) and a secondary metastasis-derived line (SW620). Live cell imaging using time-lapse microscopy over 3 days exhibited differential cell death responses following treatment with multiple chemotherapeutic agents, particularly cediranib and Nu-7441, with SW620 demonstrating greater sensitivity. Western blots revealed changes in DNA repair machinery expression (particularly NHEJ proteins) between SW480 and SW620. RNA sequencing and Gene Ontology analysis corroborated our findings, demonstrating upregulated DNA repair and metabolic survival genes including TGM2 in SW620 and PROM1 in SW480. An SW620 line grown in non-attachment plates and then reattached (SW620F) exhibited high DNA-PKcs activation and drug sensitivity. Correlation between drug response and gene expression crucial to cell growth and successful metastasis may reveal new biomarkers to target potential treatments.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70298"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148423121","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":"Special Issue on the Promise of Psychedelic Pharmacology in Neuropsychiatric Drug Development.","authors":"Andreas Halman, Ross Corriden","doi":"10.1002/prp2.70309","DOIUrl":"10.1002/prp2.70309","url":null,"abstract":"","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70309"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13420331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148621057","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":"Hirudin Attenuates Uric Acid-Induced Renal Tubular Injury via TNFRSF6B-Mediated Suppression of NF-κB Signaling.","authors":"Yingxue Zhao, Yongjie Qin, Lanzhi He, Haikun Luo, Ying Mo, Weihai Zhou, Huamei He, Ganping Zhou, Xihua Liu","doi":"10.1002/prp2.70305","DOIUrl":"10.1002/prp2.70305","url":null,"abstract":"<p><p>Hyperuricemia, characterized by elevated serum uric acid (SUA) levels, is increasingly recognized as a pathological contributor to renal injury through oxidative stress, inflammation, and apoptosis. Hirudin, a thrombin inhibitor derived from leech saliva, has recently been noted for its anti-inflammatory properties, yet its role in hyperuricemia remains unclear. This study aimed to investigate the protective effects and underlying mechanisms of hirudin in a uric acid (UA)-induced renal tubular epithelial injury model. Using HK-2 cells, we found that hirudin enhanced cell viability and reduced apoptosis in UA-treated conditions. Mechanistically, these protective effects were mediated through downregulation of TNFRSF6B, a decoy receptor involved in inflammatory and apoptotic signaling. TNFRSF6B knockdown potentiated hirudin's cytoprotective effects, whereas its overexpression reversed them. Hirudin treatment attenuated UA-induced expression of urate transporters (URAT1, GLUT9, and OAT4) and pro-inflammatory cytokine IL-1β, both at the transcriptional and protein levels. Moreover, hirudin suppressed activation of the NF-κB signaling pathway, a critical mediator of inflammation and apoptosis in hyperuricemia, with transcriptomic and immunoblotting data confirming downregulation of NF-κB-associated targets. Co-treatment with JSH-23, an NF-κB inhibitor, further reinforced these findings and highlighted a TNFRSF6B/NF-κB axis as a key regulatory mechanism. Collectively, these findings reveal a novel protective role for hirudin in UA-induced renal injury, mediated via modulation of TNFRSF6B and suppression of NF-κB signaling. This study provides new insight into the potential therapeutic application of hirudin in hyperuricemia-associated kidney damage.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70305"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13428022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148648978","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":"Could NAPQI Contribute to Paracetamol Analgesia? Redox Modulation of Kv7 Ion Channels.","authors":"Sara M-Alicante, Janire Urrutia, Arantza Muguruza-Montero, Miren Revuelta, Ane Arrizabalaga-Iriondo, Alvaro Villarroel, Eider Nuñez","doi":"10.1002/prp2.70283","DOIUrl":"10.1002/prp2.70283","url":null,"abstract":"<p><p>Paracetamol (acetaminophen, APAP) is one of the most widely used analgesic and antipyretic drugs worldwide, yet its mechanism of action remains incompletely understood. While several pathways have been proposed, including cyclooxygenase inhibition and endocannabinoid modulation via AM404, none fully account for its pharmacological profile. The reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI) is classically associated with hepatotoxicity, but electrophilic species can also modulate protein function through covalent modification of redox-sensitive residues. Recent evidence indicates that NAPQI can enhance neuronal Kv7 (KCNQ) channel activity, reducing neuronal excitability. Here, we examine the hypothesis that NAPQI formation during therapeutic APAP metabolism may contribute to analgesia via redox-dependent modulation of nociceptive ion channels. We integrate current knowledge on APAP metabolism, ion channel redox regulation, and neuronal excitability, and complement this with order-of-magnitude quantitative estimates and sensitivity analyzes. These analyzes indicate that the expected magnitude of NAPQI formation in neural tissue is likely to remain below current analytical detection limits while still being compatible with transient, spatially restricted concentrations in cellular microdomains that could modulate nearby targets. Although direct in vivo evidence remains lacking, this framework raises the possibility that localized and transient NAPQI signaling may contribute to APAP-induced modulation of neuronal excitability while remaining difficult to detect using conventional bulk analytical approaches. We outline key experimental strategies required to test this hypothesis and discuss its implications for understanding APAP pharmacology and the broader role of electrophilic metabolites in physiological signaling.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70283"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13337544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148397434","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":"Promoting Sustainable Prescribing-A Case Study Presenting Experiences From Two Swedish Drug and Therapeutics Committees.","authors":"Björn Ericsson, Ulf Lindahl, Johanna Villén, Marmar Nekoro, Helena Ramström, Björn Wettermark","doi":"10.1002/prp2.70279","DOIUrl":"10.1002/prp2.70279","url":null,"abstract":"<p><p>During the past two decades, it has become evident that pharmaceuticals is an emerging environmental problem. In this study, we present the experiences from two Swedish Drug & Therapeutics Committees (DTCs) on how they integrate environmental considerations into their formularies and continuous professional education activities. A cross sectional study was performed describing activities to promote sustainable prescribing conducted during two decades by the DTCs in the Swedish regions of Gävleborg and Västernorrland, along with trends in sales of diclofenac and fluoroquinolones between 2000 and 2024. The two DTCs integrate environmental considerations in their formularies and continuous professional education activities. Further acitivities include monitoring of prescribing, dialogue with water suppliers and pharmacies, as well as information and communication to the general public. The total utilization of diclofenac for systemic use peaked with 127 kg in Gävleborg and 137 kg in Västernorrland in 2011, after which the amounts declined. The topical formulations were mainly sold as over-the-counter and increased until 2016, when it started to decline. The amounts of ciprofloxacin and norfloxacin increased until 2012 when they started to decline. This case study from two Swedish regions illustrates how environmental considerations can be incorporated into the DTC's mission to promote rational and responsible medication use. We believe it may be valuable for different stakeholders to show potential ways in how to promote a more sustainable use of medicines.</p>","PeriodicalId":19948,"journal":{"name":"Pharmacology Research & Perspectives","volume":"14 4","pages":"e70279"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13283205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295763","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}