Disease Models & Mechanisms最新文献_第2页

Urinary sodium wasting and disrupted collecting duct function in mice with dRTA-causing SLC4A1 mutations. drta引起的SLC4A1突变小鼠的尿钠浪费和集尿管功能紊乱。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-28 DOI: 10.1242/dmm.052138

Priyanka Mungara, Kristina MacNaughton, A K M Shahid Ullah, Grace Essuman, Forough Chelangarimiyandoab, Rizwan Mumtaz, J Christopher Hennings, Christian A Hübner, Dominique Eladari, R Todd Alexander, Emmanuelle Cordat

{"title":"Urinary sodium wasting and disrupted collecting duct function in mice with dRTA-causing SLC4A1 mutations.","authors":"Priyanka Mungara, Kristina MacNaughton, A K M Shahid Ullah, Grace Essuman, Forough Chelangarimiyandoab, Rizwan Mumtaz, J Christopher Hennings, Christian A Hübner, Dominique Eladari, R Todd Alexander, Emmanuelle Cordat","doi":"10.1242/dmm.052138","DOIUrl":"https://doi.org/10.1242/dmm.052138","url":null,"abstract":"Distal renal tubular acidosis (dRTA) results in metabolic acidosis due to impaired urinary acidification and can result in an unexplained urinary sodium-wasting phenotype. We report the generation and characterization of a novel dRTA mutant mouse line, Ae1 L919X knockin (KI). Homozygous L919X KI mice exhibit typical dRTA features including a reduced ability to acidify urine in response to an acid load. This renal acidification defect was associated with a reduced number of Ae1-positive type A intercalated cells. To assess whether these mice exhibit urinary sodium-wasting, homozygous KI L919X and the previously described R607H KI mice were fed a salt-depleted acid diet. In line with human patients, both mouse strains exhibited urinary sodium loss. Additionally, we identified increased expression of tight junction proteins claudin-4 and -10b, suggesting a compensatory paracellular pathway. Consistent with data from human patients, L919X KI mice displayed a milder phenotype than R607H KI mice. Our findings reveal that both mouse strains are appropriate models for dRTA with a urinary salt-wasting phenotype and a compensatory up-regulation of the paracellular pathway.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A BALB/c mouse model of Mycobacterium abscessus lung infection based on once-weekly cyclophosphamide administration. 基于每周一次环磷酰胺给药的脓肿分枝杆菌肺部感染BALB/c小鼠模型。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-28 DOI: 10.1242/dmm.052310

Binayak Rimal, Chandra M Panthi, Ruth A Howe, Gyanu Lamichhane

{"title":"A BALB/c mouse model of Mycobacterium abscessus lung infection based on once-weekly cyclophosphamide administration.","authors":"Binayak Rimal, Chandra M Panthi, Ruth A Howe, Gyanu Lamichhane","doi":"10.1242/dmm.052310","DOIUrl":"https://doi.org/10.1242/dmm.052310","url":null,"abstract":"Mycobacterium abscessus is a fast-growing non-tuberculous mycobacterium that can cause chronic lung disease leading to rapid decline in lung function. There are no FDA-approved therapies for this disease. To support the development of new treatments, an animal model of M. abscessus lung infection that is simple to implement and requires minimal resources is crucial to encourage broad adoption. We present a mouse model using the immunocompetent BALB/c strain, which is both widely available and cost-effective. Since BALB/c mice naturally clear M. abscessus infections, immunosuppression is necessary to sustain bacterial growth in the lungs. Once-weekly intraperitoneal injections of 250 mg/kg cyclophosphamide successfully induced M. abscessus proliferation during the acute phase, followed by stabilization characteristic of chronic infection. This model demonstrated the efficacy of imipenem-an antibiotic commonly used in clinical settings-by significantly reducing bacterial burdens, mirroring their effects in human cases. However, clofazimine, which is also used to treat this disease, was bacteriostatic. This cost-effective and accessible mouse model is suitable for diverse laboratory environments and provides a valuable tool for preclinical evaluation of treatments for M. abscessus lung disease.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A precision image-guided murine model of stereotactic ablative radiotherapy for hepatocellular carcinoma. 一种精确图像引导的肝癌立体定向消融放疗小鼠模型。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-17 DOI: 10.1242/dmm.052301

Stephanie May, Katrina Stevenson, Bashaer Alqarafi, Kyi Lai Yin Swe, Algernon Bloom, Agata Mackintosh, Miryam Müller, Anastasia Georgakopoulou, Thomas M Drake, Christos Kiourtis, Saadia A Karim, Colin Nixon, Barbara Cadden, Aileen Duffton, Derek Grose, David Y Lewis, Karen Blyth, Anthony J Chalmers, Thomas G Bird

{"title":"A precision image-guided murine model of stereotactic ablative radiotherapy for hepatocellular carcinoma.","authors":"Stephanie May, Katrina Stevenson, Bashaer Alqarafi, Kyi Lai Yin Swe, Algernon Bloom, Agata Mackintosh, Miryam Müller, Anastasia Georgakopoulou, Thomas M Drake, Christos Kiourtis, Saadia A Karim, Colin Nixon, Barbara Cadden, Aileen Duffton, Derek Grose, David Y Lewis, Karen Blyth, Anthony J Chalmers, Thomas G Bird","doi":"10.1242/dmm.052301","DOIUrl":"https://doi.org/10.1242/dmm.052301","url":null,"abstract":"Liver tumours, both primary and metastatic, are diseases of unmet clinical need. Hepatocellular carcinoma (HCC) the most common primary liver tumour, like many other cancers, may be treated by stereotactic ablative radiotherapy (SABR), reducing off-target effects of radiation on local anatomical structures. However, integrating all the necessary components for stereotactic irradiation of hepatocellular carcinoma in murine models has not yet been reported. Here we provide the development and detailed characterisation of a murine SABR model combining both MRI and CT image-guided delineation of the tumour, together with CT-guided liver tumour radiotherapy. The model enables accurate delivery of clinically relevant doses of radiotherapy with good tolerability and on-target tumour responses in models with otherwise universally progressive disease. The development of this preclinical modelling platform paves the way for its integration into multimodal therapeutic and mechanistic testing in preclinical murine models of both metastatic and primary liver tumours, including hepatocellular carcinoma.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Altered Huntingtin-Chromatin Interactions Predict Transcriptional and Epigenetic Changes in Huntington's Disease Mouse Models. 改变的亨廷顿蛋白-染色质相互作用预测亨廷顿病小鼠模型的转录和表观遗传变化。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-10 DOI: 10.1242/dmm.052282

Jocelynn R Pearl, Amol C Shetty, Jeffrey P Cantle, Dani E Bergey, Robert M Bragg, Sydney R Coffey, Holly B Kordasiewicz, Leroy E Hood, Nathan D Price, Seth A Ament, Jeffrey B Carroll

{"title":"Altered Huntingtin-Chromatin Interactions Predict Transcriptional and Epigenetic Changes in Huntington's Disease Mouse Models.","authors":"Jocelynn R Pearl, Amol C Shetty, Jeffrey P Cantle, Dani E Bergey, Robert M Bragg, Sydney R Coffey, Holly B Kordasiewicz, Leroy E Hood, Nathan D Price, Seth A Ament, Jeffrey B Carroll","doi":"10.1242/dmm.052282","DOIUrl":"https://doi.org/10.1242/dmm.052282","url":null,"abstract":"While progressive striatal gene expression changes and epigenetic alterations are a prominent feature of Huntington's disease (HD), the mechanistic basis remains poorly understood. Using chromatin immunoprecipitation and sequencing (ChIP-seq), we show that the huntingtin protein (HTT) reproducibly occupies specific locations in the mouse genome. Striatal HTT ChIP-seq peaks were enriched in coding regions of spiny projection neuron identity genes, which are found to have reduced expression in HD patients and mouse models, and had reduced occupancy in expanded polyglutamine HTT knock-in mice (HttQ111/Q111). Conversely, HTT occupancy was depleted near genes that are up-regulated in HD. ChIP-seq of striatal histone modifications revealed genotype-specific colocalization of HTT with active chromatin marks and enhancer of zeste homolog 2 (EZH2), a key enzymatic component of the PRC2 complex. Near genes that are differentially regulated in HD, greater HTT occupancy in HttQ111/Q111 vs. wildtype mice was associated with increased EZH2 binding, increased H3K4me3, and decreased H3K27me3. Our study suggests that huntingtin-chromatin interactions may play a role in organizing chromatin and promoting cell type-specific gene expression, with HTT occupancy predicting transcriptional dysregulation in HD.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oncogenic signaling in the Drosophila prostate-like accessory gland activates a pro-tumorigenic program in the absence of proliferation. 果蝇前列腺样副腺中的致癌信号在没有增殖的情况下激活了促肿瘤程序。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-01 Epub Date: 2025-04-30 DOI: 10.1242/dmm.052001

S Jaimian Church, Ajai J Pulianmackal, Joseph A Dixon, Luke V Loftus, Sarah R Amend, Kenneth Pienta, Frank C Cackowski, Laura A Buttitta

{"title":"Oncogenic signaling in the Drosophila prostate-like accessory gland activates a pro-tumorigenic program in the absence of proliferation.","authors":"S Jaimian Church, Ajai J Pulianmackal, Joseph A Dixon, Luke V Loftus, Sarah R Amend, Kenneth Pienta, Frank C Cackowski, Laura A Buttitta","doi":"10.1242/dmm.052001","DOIUrl":"https://doi.org/10.1242/dmm.052001","url":null,"abstract":"Drosophila models for tumorigenesis have revealed conserved mechanisms of signaling involved in mammalian cancer. Many of these models use highly mitotically active Drosophila tissues. Few Drosophila tumorigenesis models use adult tissues, when most cells are terminally differentiated and postmitotic. The Drosophila accessory glands are prostate-like tissues, and a model for prostate tumorigenesis using this tissue has been explored. In this prior model, oncogenic signaling was induced during the proliferative stages of accessory gland development, raising the question of how oncogenic activity impacts the terminally differentiated, postmitotic adult tissue. Here, we show that oncogenic signaling in the adult Drosophila accessory gland leads to activation of a conserved pro-tumorigenic program, similar to that of mitotic tissues, but in the absence of proliferation. In our experiments, oncogenic signaling in the adult gland led to tissue hypertrophy with nuclear anaplasia, in part through endoreduplication. Oncogene-induced gene expression changes in the adult Drosophila prostate-like model overlapped with those in polyploid prostate cancer cells after chemotherapy, which potentially mediate tumor recurrence. Thus, the adult accessory glands provide a useful model for aspects of prostate cancer progression that lack cellular proliferation.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":"18 4","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Glucose uptake in pigment glia suppresses Tau-induced inflammation and photoreceptor degeneration. 果蝇色素胶质细胞的葡萄糖摄取抑制tau诱导的炎症和光感受器变性。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-01 Epub Date: 2025-04-29 DOI: 10.1242/dmm.052057

Mikiko Oka, Sho Nakajima, Emiko Suzuki, Shinya Yamamoto, Kanae Ando

{"title":"Glucose uptake in pigment glia suppresses Tau-induced inflammation and photoreceptor degeneration.","authors":"Mikiko Oka, Sho Nakajima, Emiko Suzuki, Shinya Yamamoto, Kanae Ando","doi":"10.1242/dmm.052057","DOIUrl":"10.1242/dmm.052057","url":null,"abstract":"Brain inflammation contributes to the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD). Glucose hypometabolism and glial activation are pathological features seen in AD brains; however, the connection between the two is not fully understood. Using a Drosophila model of AD, we identified that glucose metabolism in glia plays a critical role in neuroinflammation under disease conditions. Expression of human MATP (hereafter referred to as Tau) in the retinal cells, including photoreceptor neurons and pigment glia, causes photoreceptor degeneration accompanied by the formation of dark-stained round inclusion-like structures and swelling of the lamina cortex. We found that inclusion-like structures are formed by glial phagocytosis, and swelling of the laminal cortex correlates with the expression of antimicrobial peptides. Coexpression of human glucose transporter 3 (SLC2A3, hereafter referred to as GLUT3) with Tau in the retina does not affect Tau levels but suppresses these inflammatory responses and photoreceptor degeneration. We also found that expression of GLUT3, specifically in the pigment glia, is sufficient to suppress inflammatory phenotypes and mitigate photoreceptor degeneration in the Tau-expressing retina. Our results suggest that glial glucose metabolism contributes to inflammatory responses and neurodegeneration in tauopathy.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143728836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anatomical and functional studies of vestibular neuroepithelia from patients with Ménière's disease. 分离的前庭神经上皮细胞的解剖和功能研究。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-01 Epub Date: 2025-04-15 DOI: 10.1242/dmm.052224

Hannah R Drury, Melissa A Tadros, Robert J Callister, Alan M Brichta, Robert Eisenberg, Rebecca Lim

{"title":"Anatomical and functional studies of vestibular neuroepithelia from patients with Ménière's disease.","authors":"Hannah R Drury, Melissa A Tadros, Robert J Callister, Alan M Brichta, Robert Eisenberg, Rebecca Lim","doi":"10.1242/dmm.052224","DOIUrl":"10.1242/dmm.052224","url":null,"abstract":"Surgical removal of vestibular end organs is a final treatment option for people with intractable Ménière's disease (MD). Here, we used surgically excised vestibular neuroepithelium from patients with MD for (1) anatomical investigation of hair cell and nerve fibre markers using immunohistochemistry, and (2) functional studies using electrophysiological recordings of voltage-activated currents. Our data show considerable reduction in and disorganisation of vestibular hair cells in the cristae ampullares. Nerve fibres maintain contact with remaining sensory receptors but appear thin in regions in which hair cells are absent. Electrophysiological recordings of voltage-activated potassium currents from surviving hair cells demonstrated normal activity in both type I and type II vestibular hair cells. Current-voltage plots from type I vestibular hair cells are consistent with the presence of a surrounding calyx afferent terminal. These data indicate that the surviving hair cells that were sampled in patients with MD remain functional and capable of transmitting sensory information to the central nervous system. Determining functionality of vestibular receptors and nerves is critical for vestibular implant research to restore balance in people with MD.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12032548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An appetite for research: an interview with Sadaf Farooqi. 对研究的兴趣：对Sadaf Farooqi的采访。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-01 Epub Date: 2025-04-28 DOI: 10.1242/dmm.052379

Sadaf Farooqi

{"title":"An appetite for research: an interview with Sadaf Farooqi.","authors":"Sadaf Farooqi","doi":"10.1242/dmm.052379","DOIUrl":"https://doi.org/10.1242/dmm.052379","url":null,"abstract":"Professor Sadaf Farooqi is a clinician and researcher investigating the genetics underpinning obesity. Her research uncovered the first known genes that cause severe obesity, highlighting the significant role of appetite in regulating weight gain. Sadaf's work has been instrumental in proving that many observations in mice are also true in humans, paving the way for novel treatments and shifts in policy. After studying medicine at the University of Birmingham, Birmingham, UK, Sadaf completed her PhD on the genetics of severe childhood obesity at the University of Cambridge, Cambridge, UK, marking the beginning of her impressive research career in this field. She is currently Professor of Metabolism and Medicine at the University of Cambridge and Honorary Consultant in Diabetes and Endocrinology at Addenbrooke's Hospital, Cambridge, UK. Sadaf previously served on the Board of Directors for Disease Models & Mechanisms' publisher, The Company of Biologists. Here, we discuss the fascinating insights from her work on obesity and appetite, her approach to exploring new research questions, and how these discoveries can ultimately impact patients and society.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":"18 4","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: A novel mouse model of Duchenne muscular dystrophy carrying a multi-exonic Dmd deletion exhibits progressive muscular dystrophy and early-onset cardiomyopathy. 更正：一种携带多外显子Dmd缺失的杜氏肌营养不良小鼠模型表现出进行性肌营养不良和早发性心肌病。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-01 Epub Date: 2025-04-04 DOI: 10.1242/dmm.052372

Tatianna Wai, Ying Wong, Abdalla Ahmed, Grace Yang, Eleonora Maino, Sydney Steiman, Elzbieta Hyatt, Parry Chan, Kyle Lindsay, Nicole Wong, Diane Golebiowski, Joel Schneider, Paul Delgado-Olguı N, Evgueni A Ivakine, Ronald D Cohn

引用次数: 0

Expanding the neuroimmune research toolkit with in vivo brain organoid technologies. 用体内脑类器官技术扩展神经免疫研究工具箱。

IF 4 3区医学

Disease Models & Mechanisms Pub Date : 2025-04-01 Epub Date: 2025-04-15 DOI: 10.1242/dmm.052200

Ai Tian, Afrin Bhattacharya, Julien Muffat, Yun Li

{"title":"Expanding the neuroimmune research toolkit with in vivo brain organoid technologies.","authors":"Ai Tian, Afrin Bhattacharya, Julien Muffat, Yun Li","doi":"10.1242/dmm.052200","DOIUrl":"https://doi.org/10.1242/dmm.052200","url":null,"abstract":"Human pluripotent stem cell-derived microglia-like cells (MLCs) and brain organoid systems have revolutionized the study of neuroimmune interactions, providing new opportunities to model human-specific brain development and disease. Over the past decade, advances in protocol design have improved the fidelity, reproducibility and scalability of MLC and brain organoid generation. Co-culturing of MLCs and brain organoids have enabled direct investigations of human microglial interactions in vitro, although opportunities remain to improve microglial maturation and long-term survival. To address these limitations, innovative xenotransplantation approaches have introduced MLCs, organoids or neuroimmune organoids into the rodent brain, providing a vascularized environment that supports prolonged development and potential behavioral readouts. These expanding in vitro and in vivo toolkits offer complementary strategies to study neuroimmune interactions in health and disease. In this Perspective, we discuss the strengths, limitations and synergies of these models, highlighting important considerations for their future applications.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":"18 4","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12032547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0