Dose-Response最新文献

{"title":"Efficacy and Safety of Fibroblast Activation Protein Targeted Radioligand Therapy for Advanced Solid Tumour: A Systematic Review and Meta-Analysis.","authors":"Xiaoli Zhang, Jianpeng Cao, Xue Jiang, Yuxiao Xia, Ying Huang, Qian Liu, Lina Liu, Dongkun Xu, Hongjie Wu, Wenling Tu, Yuhong Shi","doi":"10.1177/15593258261437465","DOIUrl":"10.1177/15593258261437465","url":null,"abstract":"<p><strong>Objective: </strong>Fibroblast activation protein (FAP) is a promising cancer theranostic target. While FAP-based diagnostics have proven highly accurate, the efficacy and safety of FAP-targeted radioligand therapy (FAP-RLT) for advanced, treatment-refractory solid tumours are poorly characterized.</p><p><strong>Methods: </strong>We performed a systematic review and meta-analysis of clinical trials reporting therapeutic outcomes and adverse events of FAP-RLT up to 25 January 2025 (PubMed, ClinicalTrials.gov, Cochrane Library, Web of Science/MEDLINE). Primary endpoints were objective response rate (ORR), disease control rate (DCR), and incidence of grade ≥ 3 adverse events.</p><p><strong>Results: </strong>The objective response rate of FAP-RLT treatment was 11.7% (95%CI: 3.2%-23.2%; <i>p</i> < 0.001), and the disease control rate reached 44.4% (95%CI: 25.2%-64.5%; <i>p</i> = 0.004). Specifically, peptide ligands demonstrated superior therapeutic efficacy compared to small molecule ligands. Among radionuclides, ¹⁷⁷Lu exhibited better outcomes than ⁹⁰Y. In specific tumour types, patients with iodine-refractory thyroid cancer derived the greatest benefit from FAP-RLT, followed by those with lung cancer, sarcomas, and breast cancer. Conversely, patients with colorectal cancer and pancreatic cancer exhibited limited therapeutic responses. The pooled median overall survival was 7.26 months, while the median progression-free survival was 4.77 months. Grade ≥ 3 adverse reactions were observed in 2.2% (95%CI: 0.1%-6.0%; <i>p</i> = 0.018) of the cases, 11 out of 222 patients, mostly caused by hematotoxicity.</p><p><strong>Conclusion: </strong>FAP-RLT has demonstrated significant disease control in multiple advanced solid tumours while maintaining a favourable safety profile. These findings can contribute to clinical treatment expectations and support informed policy decision-making in oncology.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261437465"},"PeriodicalIF":2.8,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13195222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148013581","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":"Mechanisms, Clinical Phenotype and Potential Risk Prediction for Cardiovascular Toxicity Induced by Tyrosine Kinase Inhibitors In Chronic Myeloid Leukemia.","authors":"Hui Zheng, Chentong Huang, Zhanna Zhang, Manqi Su, Panruo Jiang, Gongqiang Wu","doi":"10.1177/15593258261454350","DOIUrl":"10.1177/15593258261454350","url":null,"abstract":"<p><p>Tyrosine kinase inhibitors (TKIs) form the cornerstone of targeted therapy for chronic myeloid leukemia (CML), significantly improving patient prognosis. However, long-term use of TKIs, particularly second-generation (e.g., nilotinib) and third-generation (e.g., ponatinib) drugs, has led to adverse cardiovascular events (CV-AEs). CV-AEs pose a critical challenge to patients' long-term quality of life and treatment adherence. This narrative review systematically elucidates the complex mechanisms underlying TKI-induced cardiovascular toxicity and proposes the \"Metabolism-Endothelium-Thrombosis Axis\" as a unifying conceptual framework, integrating endothelial dysfunction, metabolic impairment, oxidative stress, inflammatory responses, and abnormal platelet activation into a coherent pathophysiological cascade. These mechanisms collectively contribute to a spectrum of clinical phenotypes. At the clinical management level, identifying individuals at high risk is crucial. Multiple risk prediction models demonstrate predictive value for CV-AEs, particularly arterial occlusive events (AOEs). Future research should focus on elucidating TKI-specific toxicity pathways, validating and optimizing risk prediction models, and exploring effective cardioprotective strategies. Ultimately, this work will maximize cardiovascular risk reduction while preserving antileukemic efficacy.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261454350"},"PeriodicalIF":2.8,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13195214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148013603","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":"Daphnetin Ameliorates Pathological Damage in NK-92 Cells Induced by High-Glucose and High-free Fatty Acids.","authors":"Xiaodong Zhong, Yijun Nie, Ningrui Wang, Yuhuan Jiang, Wenjing Zhou, Yanan Chen, Hong Wu","doi":"10.1177/15593258261450781","DOIUrl":"10.1177/15593258261450781","url":null,"abstract":"<p><strong>Objectives: </strong>The present study aimed to characterize the protective role of daphnetin in attenuating HGHF-induced pathological injury in human NK-92 cells.</p><p><strong>Methods: </strong>The non-toxic concentration of daphnetin was determined using a the Cell Counting Kit-8 (CCK-8) assay. The levels of inflammatory cytokines(TNF-α, IFN-γ, IL-6 and IL-10), in cell supernatants were subsequently detected using the cytometric bead array method. Flow cytometric analysis was then performed to analyze the expression levels of perforin and granzyme B, as well as the cell apoptosis rate.</p><p><strong>Results: </strong>Daphnetin at a concentration of 10 μg/ml had no significant cytotoxicity on NK-92 cells, and therefore this concentration was selected for subsequent experiments. Compared with the control group, the HGHF group exhibited significantly reduced levels of TNF-α, IFN-γ, IL-6, IL-10, perforin and granzyme B (all P<0.05), along with a significantly increased cell apoptosis rate (P<0.05). Daphnetin treatment led to a marked upregulation of the levels of these inflammatory cytokines and intracellular molecules in both the control and the HGHF groups (all P<0.05); furthermore, the apoptosis rate was appreciably decreased in the HGHF-induced NK-92 cells (P<0.05).</p><p><strong>Conclusion: </strong>Daphnetin has been shown to alleviate HGHF-induced pathological damage in NK-92 cells both through upregulating the expression of inflammatory cytokines and intracellular molecules (namely, perforin and granzyme B), and via inhibiting cell apoptosis.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261450781"},"PeriodicalIF":2.8,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13195202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148013632","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":"Optimal Dose of Lorundrostat in Uncontrolled Hypertension: A Dose Response Meta-Analysis.","authors":"Omar Abdullah Gill, Miguel Leonardo Salcedo Monterrubio, Ayeman Rashid, Erum Habib, Asma Yasin, Ahmad Alam, Azhar Khan, Ramesha Tahir, Savika Bansal, Olivia Benny, Shivani Sabarish, Lakshmi Sheethal Arvapalli, Devanshi Bhanderi, Salau Ibrahim Layi, Hafiz Muhammad Haris, Dori Woldu","doi":"10.1177/15593258261449239","DOIUrl":"10.1177/15593258261449239","url":null,"abstract":"<p><strong>Background: </strong>Lorundrostat, an aldosterone synthase inhibitor, shows promise for hypertension management, though optimal dosing strategies remain poorly defined.</p><p><strong>Aims: </strong>To evaluate the efficacy, safety, and dose-response effects of Lorundrostat to identify the optimal therapeutic dose.</p><p><strong>Methods: </strong>We searched PubMed, Embase, Scopus, and ClinicalTrials.gov systematically for relevant RCTs. Using a random-effects model, data were pooled to calculate mean differences (MD) and risk ratios (RR) with 95% confidence intervals (CIs). Dose-response modeling was performed using \"dosresmeta\" and \"rcs\" packages in R (v4.4.3).</p><p><strong>Results: </strong>Three RCTs (n=1568) were included. Lorundrostat significantly reduced systolic BP at 4-8 weeks (MD: -7.66 mmHg, 95% CI: -10.42 to -4.89) and 12 weeks (MD: -10.19 mmHg, 95% CI: -13.57 to -6.82). Diastolic BP also decreased significantly (MD: -3.81). Sub-group analysis based on background medication count showed no significant differences (P=0.80). Aldosterone levels were significantly reduced (MD: -4.39). Dose-response modeling identified 60 mg as the optimal dose, with diminishing returns thereafter. While hyperkalemia risk increased (RR: 3.19), no significant differences were found in serious adverse events.</p><p><strong>Conclusion: </strong>Lorundrostat effectively lowers BP with a manageable safety profile. The modeling-based insights suggest 60 mg as the optimal dose, delineating a clearer therapeutic window.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261449239"},"PeriodicalIF":2.8,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13161659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147927567","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":"Heterogeneous Biological Responses to Low-Level Sodium Saccharin Exposure: An Integrated Computational Toxicology and Mendelian Randomization Study.","authors":"Zhao Xin, Wang Yanchun, Chen Xinwang, Wang Xuemei","doi":"10.1177/15593258261446844","DOIUrl":"10.1177/15593258261446844","url":null,"abstract":"<p><strong>Background: </strong>The long-term biological effects of low-level exposure to artificial sweeteners remain debated. We integrated computational toxicology and Mendelian randomization (MR) to explore potential biological responses associated with sodium saccharin across multiple cancer outcomes.</p><p><strong>Methods: </strong>Public databases were screened to identify saccharin-related targets, followed by protein-protein interaction network construction and enrichment analyses. Molecular docking assessed binding potential. Two-sample MR analyses were conducted using European genome-wide association study (GWAS) summary statistics to evaluate potential causal associations.</p><p><strong>Results: </strong>Among 191 identified targets, 160 overlapped with genes implicated across 36 cancer types. Hub genes included <i>TP53, IL6, and MAPK3</i>, with docking indicating moderate binding affinity. Enrichment analyses highlighted inflammatory pathways including interleukin-17 signaling. MR analyses suggested inverse associations with non-melanoma skin cancer (odds ratio [OR] = 0.38, <i>P</i> = 0.006) and colon cancer (OR = 0.56, <i>P</i> < 0.001), while a preliminary positive signal was observed for Kaposi sarcoma (OR = 3.73, <i>P</i> = 0.044). No significant associations were detected for most other cancers.</p><p><strong>Conclusion: </strong>Sodium saccharin may interact with cancer-related molecular networks; however, population-level evidence indicates heterogeneous and context-dependent associations rather than a generalized carcinogenic effect under low-level exposure conditions.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261446844"},"PeriodicalIF":2.8,"publicationDate":"2026-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147867214","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":"Naringenin-Loaded Zinc Nitrate and Manganese Nitrate Nanoparticles Induce Caspase-Dependent Apoptosis in Kidney Cancer A-498 Cells.","authors":"Xi Guo, Jiyu Yang, Shuxian Zhu, Abdurahman Hajinur Hirad, Palanisamy Arulselvan, Zhengxian Hu","doi":"10.1177/15593258261446840","DOIUrl":"10.1177/15593258261446840","url":null,"abstract":"<p><strong>Objective: </strong>Kidney cancer remains a major clinical concern due to its complex biology and resistance to conventional therapies. This study aimed to synthesize and characterize naringenin-loaded zinc nitrate and manganese nitrate nanoparticles (Naringenin-Zn/Mn NPs) and to evaluate their anticancer efficacy against A-498 kidney cancer cells.</p><p><strong>Methods: </strong>The formulated nanoparticles were characterized using X-ray diffraction (XRD), UV-visible spectroscopy, energy-dispersive X-ray (EDX) analysis, scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, photoluminescence (PL), and dynamic light scattering (DLS). Cytotoxicity was determined by MTT assay. Apoptosis was assessed using dual staining, while oxidative stress parameters and caspase enzyme activities were measured using standard biochemical assay kits.</p><p><strong>Results: </strong>Characterization analyses confirmed the successful formation of crystalline, spherical Naringenin-Zn/Mn NPs with an average size of 135.90 nm and appropriate elemental composition. The nanoparticles significantly reduced A-498 cell viability in a dose-dependent manner (1-40 µg/ml). Treated cells showed elevated caspase activity, decreased antioxidant levels, and increased oxidative stress. Dual staining further demonstrated prominent apoptotic changes in nanoparticle-treated cells.</p><p><strong>Conclusion: </strong>Naringenin-Zn/Mn NPs effectively inhibited proliferation and induced caspase-dependent apoptosis in A-498 kidney cancer cells. These findings suggest that the formulated nanoparticles may represent a promising nanotherapeutic strategy for kidney cancer management.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261446840"},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147867148","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":"Dexmedetomidine Improves BBB and Neuronal Damage in Subarachnoid Hemorrhage by Repressing S100A4-Mediated Astrocytic Reactivity.","authors":"Jiaxiang Yin, Qiaomin Xu, Kuan Lu, Jinchao Wu, Weiwei Cai","doi":"10.1177/15593258261445031","DOIUrl":"10.1177/15593258261445031","url":null,"abstract":"<p><strong>Objectives: </strong>Following subarachnoid hemorrhage (SAH), long-lasting inflammation triggered by activated glial cells has adverse effects on neurological recovery. As an α2 adrenoceptor agonist commonly utilized for sedative purposes, dexmedetomidine (DEX) has demonstrated the ability to confer neuroprotective effects across diverse physiological or pathological conditions. This study was designed to determine whether DEX protects against SAH by altering astrocytic reactivity.</p><p><strong>Methods: </strong>Eight-week-old male C57BL/6 mice were subjected to experimental SAH. They were treated with DEX in the presence or absence of the α2 adrenoceptor antagonist atipamezole (ATI) via intraperitoneal injection. Neurological function was evaluated on the basis of a modified Garcia score and beam balance test. TUNEL staining was conducted to assess neuronal apoptosis. Western blotting was carried out to determine the expression of Bcl-2, Bax, and cleaved caspase-3 in the hippocampus and ZO-1 and occludin in the cortex, and ELISA was conducted to measure TNF-α, IL-6, IL-1β, and HMGB1 expression. The wet‒dry method was employed to measure the water content in the brain tissue. The permeability of the blood‒brain barrier (BBB) was assessed via Evans blue staining. Primary astrocytes were treated with S100A4 and/or DEX. The expression levels of GFAP, C3, GBP2, Serping 1, PTX3, S100A10, S100A4, and the NF-κB pathway were also determined.</p><p><strong>Results: </strong>DEX improved early neurological deficits in SAH mice, mitigated the permeability of the BBB, and reduced the brain water content. DEX attenuated neuronal apoptosis and proinflammatory cytokine (TNF-α, IL-6, IL-1β and HMGB1) expression in the cortex. However, DEX-mediated protective effects were attenuated by ATI administration. Additionally, DEX attenuated GFAP, C3, Serping1, S100A4, and NF-κB pathway activation in the brain and in S100A4-treated primary astrocytes, whereas ATI reversed the effects of DEX.</p><p><strong>Conclusion: </strong>DEX has neuroprotective and anti-inflammatory effects in SAH through the inhibition of S100A4-mediated astrocytic \"A1\" polarization via the activation of the α2A adrenoceptor.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261445031"},"PeriodicalIF":2.8,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13125827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812371","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":"Understanding the Radiation Adaptive Response: General Methodology and Theoretical Approaches to the Study of the Radioadaptation Phenomenon.","authors":"Julianna Krasowska, Jan Kłos, Jan Ostrowski, Krzysztof W Fornalski","doi":"10.1177/15593258261442577","DOIUrl":"10.1177/15593258261442577","url":null,"abstract":"<p><strong>Objectives: </strong>The radiation-induced adaptive response (RAR), also referred to as radioadaptation, describes modifications of biological radiation sensitivity following prior exposure to low doses or low dose-rates of ionizing radiation. Despite extensive experimental evidence, RAR remains difficult to reproduce consistently and lacks a unified quantitative and methodological framework. The objective of this study was to develop a systematic biophysical approach enabling coherent analysis and comparison of RAR experiments performed under different irradiation protocols.</p><p><strong>Methods: </strong>We formulated a dose- and time-dependent adaptive response function characterized by transient, memory-like dynamics. On this basis, we derived analytical expressions describing RAR under multiple irradiation schemes, including priming-challenge protocols, radiation training, constant low dose-rate exposure, and variable dose-rate scenarios. A unified relative endpoint parameter was introduced to quantify the magnitude of the adaptive response across experimental designs.</p><p><strong>Results: </strong>The proposed framework yields explicit expressions for the adaptive response parameter under diverse exposure conditions and demonstrates how RAR magnitude depends on dose, dose-rate, and time interval between exposures. The methodology enables consistent normalization of experimental endpoints, facilitates parameter estimation from empirical data, and clarifies conditions under which adaptive effects are expected to emerge or vanish.</p><p><strong>Conclusion: </strong>This work provides a coherent and transferable methodological foundation for quantitative RAR research. The framework improves comparability between experimental studies and supports mechanistic interpretation of low dose adaptive effects, while remaining primarily applicable to controlled experimental systems rather than population-level radiation risk assessment.</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261442577"},"PeriodicalIF":2.8,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765580","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":"Retraction: Vitamin C and Turmeric Attenuate Bax and Bcl-2 Proteins' Expressions and DNA Damage in Lead Acetate-Induced Liver Injury.","authors":"","doi":"10.1177/15593258261433295","DOIUrl":"10.1177/15593258261433295","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1177/1559325819885782.].</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261433295"},"PeriodicalIF":2.8,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765611","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":"Retraction: Quercetin and Idebenone Ameliorate Oxidative Stress, Inflammation, DNA Damage, and Apoptosis Induced by Titanium Dioxide Nanoparticles in Rat Liver.","authors":"","doi":"10.1177/15593258261433232","DOIUrl":"10.1177/15593258261433232","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1177/1559325818812188.].</p>","PeriodicalId":11285,"journal":{"name":"Dose-Response","volume":"24 2","pages":"15593258261433232"},"PeriodicalIF":2.8,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765544","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}