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Machine learning applications in stroke medicine:advancements,challenges,and future prospectives

Neural Regeneration Research 2024年第4期19卷 769-773页

作者： Mario Daidone Sergio Ferrantelli Antonino Tuttolomondo Internal Medicine and Stroke Care Ward Department of Health PromotionMother and Child CareInternal Medicine and Medical SpecialtiesUniversity of Palermo Molecular and Clinical Medicine PhD Program University of Palermo

Stroke is a leading cause of disability and mortality worldwide,necessitating the development of advanced technologies to improve its diagnosis,treatment,and patient *** recent years,machine learning techniques have emerged as promising tools in stroke medicine,enabling efficient analysis of large-scale datasets and facilitating personalized and precision medicine *** abstract provides a comprehensive overview of machine learning’s applications,challenges,and future directions in stroke *** introduced machine learning algorithms have been extensively employed in all the fields of stroke *** learning models have demonstrated remarkable accuracy in imaging analysis,diagnosing stroke subtypes,risk stratifications,guiding medical treatment,and predicting patient *** the tremendous potential of machine learning in stroke medicine,several challenges must be *** include the need for standardized and interoperable data collection,robust model validation and generalization,and the ethical considerations surrounding privacy and *** addition,integrating machine learning models into clinical workflows and establishing regulatory frameworks are critical for ensuring their widespread adoption and impact in routine stroke *** learning promises to revolutionize stroke medicine by enabling precise diagnosis,tailored treatment selection,and improved *** research and collaboration among clinicians,researchers,and technologists are essential for overcoming challenges and realizing the full potential of machine learning in stroke care,ultimately leading to enhanced patient outcomes and quality of *** review aims to summarize all the current implications of machine learning in stroke diagnosis,treatment,and prognostic *** the same time,another purpose of this paper is to explore all the future perspectives these techniques can provide in combating this disabling dis

关键词： cerebrovascular disease deep learning machine learning reinforcement learning stroke stroke therapy supervised learning unsupervised learning

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Loss of homeostatic functions in microglia from a murine model of Friedreich's ataxia

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Genes & Diseases 2024年第6期11卷 60-64页

作者： Ilaria Della Valle Martina Milani Simona Rossi Riccardo Turchi Flavia Tortolici Valentina Nesci Alberto Ferri Cristiana Valle Daniele Lettieri-Bar-bato Katia Aquilano Mauro Cozzolino Savina Apolloni Nadia D'Ambrosi Department of Biology University of Rome Tor VergataRome 00133Italy PhD Program in Cellular and Molecular Biology University of Rome Tor VergataRome 00133Italy Institute of Translational Pharmacology National Research Council(CNR)Rome 00133Italy Santa Lucia Foundation IRCCS Rome 00179Italy Department of Systems Medicine "Tor Vergata"University of RomeRome 00133Italy

Friedreich's ataxia(FRDA)is a rare genetic disorder characterized by motor discoordination and cerebellar involvement due to mutations in the frataxin(FXN)gene,which encodes a mitochondrial protein involved in ironsulfur cluster biogenesis and iron handling."While progress has been made in understanding FRDA's pathophysiology and cerebellar degeneration caused by frataxin deficiency,the role of central nervous system(CNS)-resident nonneuronal cells,as microglia,necessitates further investigation.

关键词： involvement degeneration Friedreich

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RNA polymerase II at histone genes predicts outcome in human cancer

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Science (New York, N.Y.) 2025年第6735期387卷 737-743页

作者： Henikoff, Steven Zheng, Ye Paranal, Ronald M. Xu, Yiling Greene, Jacob E. Henikoff, Jorja G. Russell, Zachary R. Szulzewsky, Frank Thirimanne, H Nayanga Kugel, Sita Holland, Eric C. Ahmad, Kami Basic Sciences Division Fred Hutchinson Cancer Center Seattle WA United States Howard Hughes Medical Institute Chevy Chase MD United States Human Biology Division Fred Hutchinson Cancer Center Seattle WA United States Molecular Medicine and Mechanisms of Disease PhD Program University of Washington Seattle WA United States

Genome-wide hypertranscription is common in human cancer and predicts poor prognosis. To understand how hypertranscription might drive cancer, we applied our formalin-fixed paraffin-embedded (FFPE)-cleavage under targeted accessible chromatin method for mapping RNA polymerase II (RNAPII) genome-wide in FFPE sections. We demonstrate global RNAPII elevations in mouse gliomas and assorted human tumors in small clinical samples and discover regional elevations corresponding to de novo HER2 amplifications punctuated by likely selective sweeps. RNAPII occupancy at S-phase-dependent histone genes correlated with WHO grade in meningiomas, accurately predicted rapid recurrence, and corresponded to whole-arm chromosome losses. Elevated RNAPII at histone genes in meningiomas and diverse breast cancers is consistent with histone production being rate-limiting for S-phase progression and histone gene hypertranscription driving overproliferation and aneuploidy in cancer, with general implications for precision oncology.

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Targeting multiple signaling pathways:the new approach to acute myeloid leukemia therapy

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Signal Transduction and Targeted Therapy 2021年第1期6卷 41-69页

作者： Jenna LCarter Katie Hege Jay Yang Hasini AKalpage Yongwei Su Holly Edwards Maik Hüttemann Jeffrey WTaub Yubin Ge Cancer Biology Graduate Program Wayne State University School of MedicineDetroitMIUSA MD/PhD Program Wayne State University School of MedicineDetroitMIUSA Department of Oncology Wayne State University School of MedicineDetroitMIUSA Molecular Therapeutics Program Barbara Ann Karmanos Cancer InstituteWayne State University School of MedicineDetroitMIUSA Center for Molecular Medicine and Genetics Wayne State University School of MedicineDetroitMIUSA National Engineering Laboratory for AIDS Vaccine Key Laboratory for Molecular Enzymology and EngineeringThe Ministry of EducationSchool of Life SciencesJilin UniversityChangchunChina Division of Pediatric Hematology/Oncology Children’s Hospital of MichiganDetroitMIUSA Department of Pediatrics Wayne State University School of MedicineDetroitMIUSA

Acute myeloid leukemia(AML)is the most common form of acute leukemia in adults and the second most common form of acute leukemia in *** this,very little improvement in survival rates has been achieved over the past few *** is partially due to the heterogeneity of AML and the need for more targeted therapeutics than the traditional cytotoxic chemotherapies that have been a mainstay in therapy for the past 50 *** the past 20 years,research has been diversifying the approach to treating AML by investigating molecular pathways uniquely relevant to AML cell proliferation and *** we review the development of novel therapeutics in targeting apoptosis,receptor tyrosine kinase(RTK)signaling,hedgehog(HH)pathway,mitochondrial function,DNA repair,and c-Myc *** has been an impressive effort into better understanding the diversity of AML cell characteristics and here we highlight important preclinical studies that have supported therapeutic development and continue to promote new ways to target AML *** addition,we describe clinical investigations that have led to FDA approval of new targeted AML therapies and ongoing clinical trials of novel therapies targeting AML survival *** also describe the complexity of targeting leukemia stem cells(LSCs)as an approach to addressing relapse and remission in AML and targetable pathways that are unique to LSC *** comprehensive review details what we currently understand about the signaling pathways that support AML cell survival and the exceptional ways in which we disrupt them.

关键词： myeloid approach approval

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G-quadruplex-stalled eukaryotic replisome structure reveals helical inchworm DNA translocation

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Science (New York, N.Y.) 2025年第6738期387卷 eadt1978页

作者： Batra, Sahil Allwein, Benjamin Kumar, Charanya Devbhandari, Sujan Brüning, Jan-Gert Bahng, Soon Lee, Chong M. Marians, Kenneth J. Hite, Richard K. Remus, Dirk Molecular Biology Program Memorial Sloan Kettering Cancer Center New York NY USA Structural Biology Program Memorial Sloan Kettering Cancer Center New York NY USA BCMB Allied PhD Program Weill Cornell Medical Graduate School Weill Cornell Medicine New York NY USA

DNA G-quadruplexes (G4s) are non-B-form DNA secondary structures that threaten genome stability by impeding DNA replication. To elucidate how G4s induce replication fork arrest, we characterized fork collisions with preformed G4s in the parental DNA using reconstituted yeast and human replisomes. We demonstrate that a single G4 in the leading strand template is sufficient to stall replisomes by arresting the CMG helicase. Cryo-electron microscopy structures of stalled yeast and human CMG complexes reveal that the folded G4 is lodged inside the central CMG channel, arresting translocation. The G4 stabilizes the CMG at distinct translocation intermediates, suggesting an unprecedented helical inchworm mechanism for DNA translocation. These findings illuminate the eukaryotic replication fork mechanism under normal and perturbed conditions.

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Low-dose imiquimod induces melanogenesis in melanoma cells through an ROS-mediated pathway

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Journal of Dermatological Science 2024年第1期113卷 18-25页

作者： Li, Zheng-Yi Chang, Shu-Hao Liu, Kuang-Ting Wu, Alaina Edelie Hsu, Chien-Sheng Huang, Shi-Wei Chung, Mu-Chi Wang, Shih-Chung Kao, Jun-Kai Chen, Yi-Ju Shieh, Jeng-Jer Institute of Biomedical Sciences National Chung Hsing University Taichung Taiwan Department of Pathology & Laboratory Medicine Taoyuan Armed Forces General Hospital Taoyuan Taiwan Frontier Molecular Medical Research Center in Children Changhua Christian Children Hospital Changhua County Taiwan Center for Cell Therapy and Translation Research China Medical University Hospital Taichung Taiwan Division of Nephrology Department of Medicine Taichung Veterans General Hospital Taichung Taiwan PhD Program in Translational Medicine National Chung Hsing University Taichung Taiwan Department of Biotechnology Asia University Taichung Taiwan Rong Hsing Research Center for Translational Medicine National Chung Hsing University Taichung Taiwan Division of Pediatric Hematology/Oncology Changhua Christian Children Hospital Changhua County Taiwan Department of Post-Baccalaureate Medicine College of Medicine National Chung Hsing University Taichung Taiwan Department of Dermatology Taichung Veterans General Hospital Taichung Taiwan Department of Education and Research Taichung Veterans General Hospital Taichung Taiwan

Background: Melanogenesis is the process of melanin maturation which not only protects skin from UV radiation but also plays an important role in antigenicity of melanomas. Imiquimod (IMQ) is a toll-like receptor 7 (TLR7) agonist that exhibits antiviral and anticancer activity. Objective: To explore whether IMQ could induce melanogenesis in melanoma cells. Methods: The mouse melanoma cell line B16F10, the mouse immortalized melanocyte Melan-A, and human melanoma cell lines MNT-1, C32 and A375 were utilized in this study. The pigmented level was observed by the centrifuged cell pellet. The intracellular and extracellular melanin levels were examined in the absorbance in NaOH-extracted cell lysate and cell-cultured medium, respectively. The expression of melanogenesis related proteins was examined by immunoblotting. The intracellular cyclic AMP amount was evaluated by the cAMP Glo assay kit. The activity of phosphodiesterase 4B (PDE4B) was investigated by CREB reporter assay with overexpressed PDE4B or not. Results: We demonstrated that a low dose of IMQ could trigger melanogenesis in B16F10 cells. IMQ induced microphthalmia-associated transcription factor (MITF) nuclear translocation, upregulated the expression of melanogenesis-related proteins, increased tyrosinase (TYR) activity, and led to pigmentation in B16F10 cells. Next, we found that IMQ-induced melanogenesis was activated by excessive intracellular cAMP accumulation, which was regulated through IMQ-mediated PDE4B inhibition. Finally, IMQ-induced ROS production was found to be involved in melanogenesis by its control of PDE4B activity. Conclusions: Low dose of IMQ could activate melanogenesis through the ROS/PDE4B/PKA pathway in melanoma cells. © 2023 Japanese Society for Investigative Dermatology

关键词： Imiquimod Melanogenesis Reactive oxygen species

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Chlorine-containing polyacetoxybriarane diterpenoids from the octocoral Junceella fragilis

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RSC Advances 2024年第24期14卷 17195-17201页

作者： Do, Hai Nhat Chen, Yu-Ta Chien, Su-Ying Chen, You-Ying Zhang, Mingzi M. Tsou, Lun Kelvin Chen, Jih-Jung Wen, Zhi-Hong Lo, Yi-Hao Zheng, Li-Guo Sung, Ping-Jyun Department of Marine Biotechnology and Resources National Sun Yat-sen University Kaohsiung804201 Taiwan National Museum of Marine Biology & Aquarium Pingtung944401 Taiwan Department of Family Medicine Zuoying Armed Forces General Hospital Kaohsiung813204 Taiwan Instrumentation Center National Taiwan University Taipei106319 Taiwan Institute of Molecular and Genomic Medicine National Health Research Institutes Miaoli350401 Taiwan Institute of Biotechnology and Pharmaceutical Research National Health Research Institutes Miaoli350401 Taiwan Department of Pharmacy School of Pharmaceutical Sciences National Yang Ming Chia Tung University Taipei112304 Taiwan Shu-Zen Junior College of Medicine and Management Kaohsiung821004 Taiwan Institute of Medical Science and Technology National Sun Yat-sen University Kaohsiung804201 Taiwan Doctoral Degree Program in Marine Biotechnology National Sun Yat-sen University Kaohsiung804201 Taiwan Chinese Medicine Research and Development Center China Medical University Hospital Taichung404394 Taiwan Graduate Institute of Natural Products Kaohsiung Medical University Kaohsiung807378 Taiwan PhD Program in Pharmaceutical Biotechnology Fu Jen Catholic University New Taipei City242062 Taiwan

The chemical screening of an octocoral identifed as Junceella fragilis has led to the isolation of five chlorinated briarane-type diterpenoids, including three known metabolites, gemmacolide X (1), frajunolide I (2), and fragilide F (3), along with two new analogs, 12α-acetoxyfragilide F (4) and 12α-acetoxyjunceellin (5). Single-crystal X-ray diffraction analysis was carried out to determine the absolute configurations of 1 and 2, while the structures of new compounds 4 and 5 were ascertained with 2D NMR experiments. Briaranes 1 and 3-5 were active in enhancing alkaline phosphatase (ALP) activity. © 2024 The Royal Society of Chemistry.

关键词： Metabolites

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The mystery of phospho-Drp1 with four adaptors in cell cycle: when mitochondrial fission couples to cell fate decisions

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Cell Cycle 2023年第21-22期22卷 2485-2503页

作者： Wu, Nian-Siou Ma, I-Chu Lin, Yi-Fan Ko, Huey-Jiun Loh, Joon-Khim Hong, Yi-Ren Department of Education Hsin-Chu Branch National Taiwan University Hospital Hsinchu Taiwan PhD Program in Molecular Medicine National Tsing Hua University Hsinchu Taiwan Division of Neurology China Medical University Hospital Taichung Taiwan Department of Education National Taiwan University Hospital Taipei Taiwan Department of Biochemistry College of Medicine Kaohsiung Medical University Kaohsiung Taiwan Department of Neurosurgery Kaohsiung Medical University Hospital Kaohsiung Taiwan Graduate Institutes of Medicine College of Medicine Kaohsiung Medical University Kaohsiung Taiwan Department of Biological Sciences National Sun Yat-Sen University Kaohsiung Taiwan Department of Medical Research Kaohsiung Medical University Hospital Kaohsiung Taiwan Center for Cancer Research Kaohsiung Medical University Kaohsiung Taiwan Neuroscience Research Center Kaohsiung Medical University Kaohsiung Taiwan

Recent study had deepened our knowledge of the mitochondrial dynamics to classify mitochondrial fission into two types. To further clarify the relationship between the two distinct fission machinery and the four major adaptors of Drp1, we propose a model of mechanism elucidating the multiple functions of phospho-Drp1 with its adaptors during cell cycle and providing in-depth insights into the molecular basis and evolutionary implications in depth. The model highlights not only the clustering characteristics of different phospho-Drp1 with respective subsets of mitochondrial pro-fission adaptors but also the correlation, crosstalk and shifting between different clustering of phosphorylated Drp1-adaptors during different key fission situations. Particularly, phospho-Drp1 (Ser616) couples with Mff/MiD51 to exert mitochondrial division and phospho-Drp1 (Ser637) couples with MiD49/Fis1 to execute mitophagy in M-phase. We then apply the model to address the relationship of mitochondrial dynamics to Parkinson’s disease (PD) and carcinogenesis. Our proposed model is indeed compatible with current research results and pathological observations, providing promising directions for future treatment design. © 2023 Informa UK Limited, trading as Taylor & Francis Group.

关键词： cell cycle Drp1 Mitochondrial Adaptors mitophagy phosphorylation

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Coexpression of CD163 and CD141 identifies human circulating IL-10-producing dendritic cells (DC-10)

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Cellular & molecular Immunology 2020年第1期17卷 95-107页

作者： Michela Comi Daniele Avancini Francesca Santoni de Sio Matteo Villa Molly Javier Uyeda Matteo Floris Daniela Tomasoni Alessandro Bulfone Maria Grazia Roncarolo Silvia Gregori San Raffaele Telethon Institute for Gene Therapy(SR-TIGET) San Raffaele Scientific Institute(IRCCS)MilanItaly PhD Program in Translational and Molecular Medicine(DIMET) University of Milan-BicoccaMilanItaly Division of Stem Cell Transplantation and Regenerative Medicine Department of PediatricsISCBRMStanford School of MedicineStanfordCAUSA CRS4 Technology Park PolarisPulaItaly

Tolerogenic dendritic cells(DCs)are key players in maintaining immunological homeostasis,dampening immune responses,and promoting ***-10,a tolerogenic population of human IL-10-producing DCs characterized by the expression of HLA-G and ILT4,play a pivotal role in promoting tolerance via T regulatory type 1(Tr1)*** far,the absence of markers that uniquely identify DC-10 has limited in vivo *** in vitro gene expression profiling of differentiated human DCs,we identified CD141 and CD163 as surface markers for *** coexpression of CD141 and CD163 in combination with CD14 and CD16 enables the ex vivo isolation of DC-10 from the peripheral ***14+CD16+CD141+CD163+cells isolated from the peripheral blood of healthy subjects(ex vivo DC-10)produced spontaneously and upon activation of IL-10 and limited levels of ***,in vitro stimulation of allogeneic naive CD4+T cells with ex vivo DC-10 induced the differentiation of alloantigen-specific CD49b+LAG-3+Tr1 ***,ex vivo DC-10 and in vitro generated DC-10 exhibited a similar transcriptional profile,which are characterized by an anti-inflammatory and pro-tolerogenic *** results provide new insights into the phenotype and molecular signature of DC-10 and highlight the tolerogenic properties of circulating *** findings open the opportunity to track DC-10 in vivo and to define their role in physiological and pathological settings.

关键词： Dendritic cells IL-10 T regulatory type 1(Tr1)cells Tolerance

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An atlas of single-cell eQTLs dissects autoimmune disease genes and identifies novel drug classes for treatment

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Cell Genomics 2025年第4期5卷 100820-100820页

作者： Wang, Lida Markus, Havell Chen, Dieyi Chen, Siyuan Zhang, Fan Gao, Shuang Khunsriraksakul, Chachrit Chen, Fang Olsen, Nancy Foulke, Galen Jiang, Bibo Carrel, Laura Liu, Dajiang J. Department of Public Health Sciences Pennsylvania State University College of Medicine Hershey 17033 PA United States Bioinformatics and Genomics PhD Program Pennsylvania State University College of Medicine Hershey 17033 PA United States Institute for Personalized Medicine Pennsylvania State University College of Medicine Hershey 17033 PA United States Department of Biochemistry and Molecular Biology Pennsylvania State University College of Medicine Hershey 17033 PA United States Department of Medicine Penn State University College of Medicine Hershey 17033 PA United States Department of Dermatology Penn State University College of Medicine Hershey 17033 PA United States

Most variants identified from genome-wide association studies (GWASs) are non-coding and regulate gene expression. However, many risk loci fail to colocalize with expression quantitative trait loci (eQTLs), potentially due to limited GWAS and eQTL analysis power or cellular heterogeneity. Population-scale single-cell RNA-sequencing (scRNA-seq) datasets are emerging, enabling mapping of eQTLs in different cell types (sc-eQTLs). Compared to eQTL data from bulk tissues (bk-eQTLs), sc-eQTL datasets are smaller. We propose a joint model of bk-eQTLs as a weighted sum of sc-eQTLs (JOBS) from constituent cell types to improve power. Applying JOBS to One1K1K and eQTLGen data, we identify 586% more eQTLs, matching the power of 4× the sample sizes of OneK1K. Integrating sc-eQTLs with GWAS data creates an atlas for 14 immune-mediated disorders, colocalizing 29.9% or 32.2% more loci than using sc-eQTL or bk-eQTL alone. Extending JOBS, we develop a drug-repurposing pipeline and identify novel drugs validated by real-world data. © 2025 The Author(s)

关键词： autoimmune disease bulk eQTL colocalization drug repurposing GWAS scRNAseq sequencing design single cell eQTL transcriptome

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