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Nanoparticles for the treatment of spinal cord injury

Neural Regeneration Research 2025年第6期20卷 1665-1680页

作者： Qiwei Yang Di Lu Jiuping Wu Fuming Liang Huayi Wang Junjie Yang Ganggang Zhang Chen Wang Yanlian Yang Ling Zhu Xinzhi Sun Department of Orthopedic Surgery The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina CAS Key Laboratory of Standardization and Measurement for Nanotechnology CAS Key Laboratory for Biomedical Effects of Nanomaterials and NanosafetyCAS Center for Excellence in NanoscienceNational Center for Nanoscience and TechnologyBeijingChina University of Chinese Academy of Sciences BeijingChina Department of Neurosurgery The First Affiliated Hospital of Chongqing Medical UniversityChongqingChina

Spinal cord injuries lead to significant loss of motor, sensory, and autonomic functions, presenting major challenges in neural regeneration. Achieving effective therapeutic concentrations at injury sites has been a slow process, partly due to the difficulty of delivering drugs effectively. Nanoparticles, with their targeted delivery capabilities, biocompatibility, and enhanced bioavailability over conventional drugs, are garnering attention for spinal cord injury treatment. This review explores the current mechanisms and shortcomings of existing treatments, highlighting the benefits and progress of nanoparticle-based approaches. We detail nanoparticle delivery methods for spinal cord injury, including local and intravenous injections, oral delivery, and biomaterial-assisted implantation, alongside strategies such as drug loading and surface modification. The discussion extends to how nanoparticles aid in reducing oxidative stress, dampening inflammation, fostering neural regeneration, and promoting angiogenesis. We summarize the use of various types of nanoparticles for treating spinal cord injuries, including metallic, polymeric, protein-based, inorganic non-metallic, and lipid nanoparticles. We also discuss the challenges faced, such as biosafety, effectiveness in humans, precise dosage control, standardization of production and characterization, immune responses, and targeted delivery in vivo. Additionally, we explore future directions, such as improving biosafety, standardizing manufacturing and characterization processes, and advancing human trials. Nanoparticles have shown considerable progress in targeted delivery and enhancing treatment efficacy for spinal cord injuries, presenting significant potential for clinical use and drug development.

关键词： antioxidants axon regeneration biocompatible materials drug carriers nanoparticles nerve regeneration neuroinflammatory diseases neuroprotection spinal cord injury stem cells

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Factors Affecting the Genetic Diagnostic Rate in Congenital Heart Disease

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Congenital Heart Disease 2022年第6期17卷 653-673页

作者： Jun Sung Park Go Hun Seo Yunha Choi Soojin Hwang Minji Kang Hyo-Sang Do Young-Hwue Kim Jeong Jin Yu Ellen Ai-Rhan Kim Euiseok Jung Byong Sop Lee Jae Suk Baek Beom Hee Lee Department of Pediatrics Asan Medical CenterUniversity of Ulsan College of MedicineSeoulKorea 3 Billion Inc.SeoulKorea Genome Research center for Birth Defects and Genetic Diseases Asan Institute for Life SciencesAsan Medical CenterSeoulKorea Division of Cardiology Department of PediatricsAsan Medical CenterUniversity of Ulsan College of MedicineSeoulKorea Division of Neonatology Department of PediatricsAsan Medical CenterUniversity of Ulsan College of MedicineSeoulKorea medical Genetics center Asan Medical Center Children’s HospitalUniversity of Ulsan College of MedicineSeoulKorea

Background: Over 400 genes contribute to the development of congenital heart disease (CHD). Additionally,multisystemic manifestations accompanying syndromic CHD pose a higher risk of genetic diseases. This studyinvestigated the diagnostic yield of whole-exome sequencing (WES) in patients with sporadic syndromic CHDand the phenotypic factors affecting the genetic diagnostic rate. Methods: Sixty-four patients with sporadic syndromicCHD aged center,and the association between genetic testing data and extracardiac phenotypes was analyzed. Results: Extracardiacphenotypes were measured as 3.66 ± 3.05 (standard deviation, interquartile range: 2–5) items per patient. WESdetected diagnostic variants in 19 (29.7%) patients: seven (36.8%), seven (36.8%), and five (26.3%) with pathogenicvariants, likely pathogenic variants, and variants of unknown significance, respectively. Post-diagnosis surveillanceidentified the extracardiac phenotype in 54.5% (6/11) of patients. De novo variants accounted for 76.2%(15/19) of variants and autosomal dominant inheritance for 94.7% (18/19). Most diseases were ultra-rare. No significantdifferences were noted in cardiac and extracardiac phenotypes, single or combined (all P > 0.05), betweenthe groups with and without a diagnostic variant. However, patients with ≥3 extracardiac phenotypes had a significantlyhigher likelihood of having a diagnostic variant than those with ≤2 (38.3% vs. 5.9%, odds ratio = 9.93,95% confidence interval = 1.21–81.44, P = 0.013). Conclusions: The number of extracardiac phenotypes is importantin predicting the possibility of genetic diagnosis. Physicians will be able to select patients with a high probabilityof genetic diagnosis and provide appropriate genetic counseling based on the results of this study.

关键词： Heart defects congenital whole-exome sequencing genetic testing phenotype

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Inhibition of the cGAS–STING pathway:contributing to the treatment of cerebral ischemia-reperfusion injury

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Neural Regeneration Research 2025年第7期20卷 1900-1918页

作者： Hang Yang Yulei Xia Yue Ma Mingtong Gao Shuai Hou Shanshan Xu Yanqiang Wang School of Clinical Medicine Shandong Second Medical UniversityWeifangShandong ProvinceChina Department of Emergency The Affiliated Hospital of Weifang Medical UniversityWeifangShandong ProvinceChina Department of Neurology Ⅱ The Affiliated Hospital of Weifang Medical UniversityWeifangShandong ProvinceChina

The cGAS–STING pathway plays an important role in ischemia-reperfusion injury in the heart,liver,brain,and kidney,but its role and mechanisms in cerebral ischemia-reperfusion injury have not been systematically ***,we outline the components of the cGAS–STING pathway and then analyze its role in autophagy,ferroptosis,cellular pyroptosis,disequilibrium of calcium homeostasis,inflammatory responses,disruption of the blood–brain barrier,microglia transformation,and complement system activation following cerebral ischemia-reperfusion *** further analyze the value of cGAS–STING pathway inhibitors in the treatment of cerebral ischemia-reperfusion injury and conclude that the pathway can regulate cerebral ischemia-reperfusion injury through multiple *** of the cGAS–STING pathway may be helpful in the treatment of cerebral ischemia-reperfusion injury.

关键词： calcium homeostasis cellular autophagy cerebral ischemia-reperfusion injury cGAS–STING pathway ferroptosis gut–brain–microbiota axis inflammatory light chain 3 microglial cells Syntaxin-17 protein

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High Prevalence of Genetic Alterations in Infantile-Onset Cardiomyopathy

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Congenital Heart Disease 2021年第4期16卷 397-410页

作者： Junsung Park Go Hun Seo Yena Lee Yunha Choi Minji Kang Hyo-Sang Do Young-Hwue Kim Jeong Jin Yu Ellen Ai-Rhan Kim Euiseok Jung Byong Sop Lee Jae Suk Baek Beom Hee Lee Department of Pediatrics Asan Medical CenterUniversity of Ulsan College of MedicineSeoulKorea billion Inc.SeoulKorea Genome Research center for Birth Defects and Genetic Diseases Asan Institute for Life SciencesAsan Medical CenterSeoulKorea Division of Cardiology Department of PediatricsAsan Medical CenterUniversity of Ulsan College of MedicineSeoulKorea Division of Neonatology Department of PediatricsAsan Medical CenterUniversity of Ulsan College of MedicineSeoulKorea medical Genetics center Asan Medical Center Children’s HospitalUniversity of Ulsan College of MedicineSeoulKorea

Background and Method:The genetic cause of infantile-onset cardiomyopathy is rarely ***,we conducted whole exome sequencing(WES)and mitochondrial DNA(mtDNA)sequencing in eight patients with infantile-onset cardiomyopathy to identify genetic ***:Among these patients,two(25%)had dilated cardiomyopathy(DCMP),two(25%)had left ventricular non-compaction(LVNC),and four(50%)had hypertrophic cardiomyopathy(HCMP).Except four patients identified prenatally,the remaining patients presented at a median age of 85.5 *** identified genetic variants in a total of seven(87.5%)patients and mtDNA sequencing in the other ***1 and MYH7 variants were identified in the two patients with DCMP;MYH11 and MYLK2 variants in the two patients with LVNC;HRAS,BRAF,and MYH7 variants in three patients with HCMP;and MT-ND1 variant in one patient with HCMP having high blood lactic acid *** the eight variants,four were classified as pathogenic or likely-pathogenic according to the American College of medical Genetics(ACMG)guidelines,and the remaining were identified as variants of unknown significance(VUSs).Three pathogenic mutations were de novo,whereas four(likely-pathogenic or VUSs)were inherited from a respective parent,excluding one variant where parental testing was unavailable,questioning whether these inherited variants are *** patients died before 3 months of ***:Genomic studies,such as WES with additional mtDNA sequencing,can identify a genetic variant in high proportions of patients with infantile-onset *** clinical implication of the parentally inherited variant needs to be assessed in a larger patient and family cohort with a longitudinal follow-up.

关键词： Cardiomyopathy whole exome sequencing infantile-onset

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Cerebral fat embolism following autologous fat injection in facial reconstruction:A case report

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World Journal of Clinical Cases 2025年第2期13卷 50-58页

作者： Xiu-Ying Chen Fa Shen Chang Cheng Yu-Han Wang Wen-Chao Cheng De-Zhi Yuan Wen Huang Department of Neurology Chongqing Emergency Medical CenterChongqing University Central HospitalChongqing 400000China Department of Neurology Xinqiao HospitalThe Army Medical University(Third Military Medical University)Chongqing 400000China

BACKGROUND Autologous fat injection in facial reconstruction is a common cosmetic *** cerebral fat embolism(CFE)as a complication is rare,it carries serious health *** SUMMARY We present a case of a 29-year-old female patient who developed acute CFE following facial fat filling *** the surgery,the patient experienced symptoms including headache,nausea,vomiting,and difficulty breathing,which was followed by neurological symptoms such as slurred speech and left-sided *** physical examination and auxiliary investigations,including blood tests,head and neck computed tomography angiography,and cranial magnetic resonance diffusion-weighted imaging,were performed upon *** clinical diagnosis was acute cerebral embolism following facial fat filling *** included measures to improve cerebral circulation,dehydration for intracranial pressure reduction,nutritional support,and rehabilitation therapy for left limb *** patient showed a significant improvement in symptoms after 2 weeks of *** recovered left limb muscle strength to grade 5,had clear speech,and experienced complete relief of *** Our case highlights the potential occurrence of severe complications in patients undergoing fat injection in facial *** prevent these complications,plastic surgeons should enhance their professional knowledge and skills.

关键词： Cerebral fat embolism Mechanical thrombectomy Thrombolysis Steroid therapy Symptomatic treatment Case report

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Therapeutic DC vaccination with IL-2 as a consolidation therapy for ovarian cancer patients： a phase Ⅰ/Ⅱ trial

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Cellular & Molecular Immunology 2015年第1期12卷 87-95页

作者： Soyoung Baek Yong-Man Kim Sung-Bae Kim Choung-Soo Kim Seog-Woon Kwon YongMan Kim HyunSoo Kim Hyunah Lee Office of Biomedical Professors Samsung Medical Center Sungkyunkwan University School of Medicine Seoul Korea Department of Gynecology Asan Medical Center University of Ulsan College of Medicine Seoul Korea Department of Oncology Asan Medical Center University of Ulsan College of Medicine Seoul Korean Department of Urology Asan Medical Center University of Ulsan College of Medicine Seoul Korean Department of Laboratory Medicine Asan Medical Center University of Ulsan College of Medicine Seoul Korea FCB-Pharmicell Co Ltd Seoul Korea

While ovarian cancer （OvCa） responds well to surgery and conventional chemotherapy, a high recurrence rate of advanced OvCa is observed. In this phase Ⅰ/Ⅱ study, 10 OvCa patients with minimal residual disease were treated with autologous dendritic cells （DCs） and IL-2 to evaluate the safety and feasibility of this therapeutic strategy and to characterize the antigen-specific immune alterations induced through this treatment. Approximately 4 months after initial debulking and chemotherapy, patients received two subcutaneous doses of autologous monocyte-derived DCs pulsed with autologous tumor lysate and keyhole limpet hemocyanin （KLH） at 4-week intervals. After each DC inoculation, low-dose （200 mlU） IL-2 was introduced for 14 consecutive days as an immune adjuvant. The vaccination was well tolerated. In three out of 10 patients, the inclusion status after the initial therapy showed the maintenance of complete remission （CR） after DC vaccination for 83, 80.9 and 38.2 months without disease relapse. One patient with stable disease （SD） experienced the complete disappearance of tumor after DC vaccination, and this status was maintained for 50.8 months until tumor recurrence. In two patients with partial response （PR） was not responding to DC vaccination and their disease recurred. In the three patients with disease free long-term survival, significant immune alterations were observed, including increased natural killer （NK） activity, IFN-γ-secreting T cells, immune-stimulatory cytokine secretion and reduced immune-suppressive factor secretion after DC vaccination. Thus, in patients with NED status and increased overall survival, DC vaccination induced tumor-related immunity, potentially associated with long-term clinical responses against OvCa.

关键词： dendritic cell vaccine immune response ovarian cancer phase Ⅰ/Ⅱ trial

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Relief of YAP-mediated inhibition by IKKε promotes innate antiviral immunity

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Cellular & Molecular Immunology 2018年第6期15卷 642-644页

作者： Nayoung Kim Yun-Yong Park Chul Hyun Joo Hun Sik Kim Department of Convergence Medicine Asan Medical CenterUniversity of Ulsan College of MedicineSeoul 05505Korea asan Institute for Life Sciences Asan Medical CenterUniversity of Ulsan College of MedicineSeoul 05505Korea Department of Microbiology Asan Medical CenterUniversity of Ulsan College of MedicineSeoul 05505Korea Department of Biomedical Sciences Asan Medical CenterUniversity of Ulsan College of MedicineSeoul 05505Korea

The innate immune response to invading viruses is critical for the mounting of protective immunity,in which type I interferons(IFN),for example,IFN-αandβ,are potent effector molecules.1 Most cell types,particularly fibroblasts and epithelial cells,produce IFN-β,whereas hematopoietic cells,notably plasmacytoid dendritic cells,are the predominant sources of IFN-α.IFNs potently stimulate a variety of innate and adaptive immune cells,including macrophages,NK cells and T *** binding of type I IFN to its cognate receptor triggers the activation of the Janus kinase signal transducer and activator of transcription pathway,which results in the transcription of IFNstimulated genes that play key roles in host resistance to viral infections.

关键词： immunity protective mount

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Tilting homeostatic and dyshomeostatic microglial balance in health and disease:transforming growth factor-beta1 as a critical protagonist

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Neural Regeneration Research 2025年第10期20卷 2895-2897页

作者： Nicolas Hugues Yu Luo Department of Molecular and Cellular Biosciences University of CincinnatiCincinnatiOHUSA Neuroscience Graduate Program University of CincinnatiCincinnatiOHUSA Division of Immunobiology Cincinnati Children’s Hospital Medical CenterUniversity of Cincinnati College of MedicineCincinnatiOHUSA

Adult microglia,by continuously sensing changes in their environment and communicating with nearly all brain cell types,are considered to be the immune sentinels of the *** the healthy central nervous system(CNS),microglia display a unique molecular homeostatic signature(i.e.,Tmem119,P2ry12,Sall1,Siglech,Gpr34,and Hexb)(Figure 1A).

关键词： Figure signature critical

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FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

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Neural Regeneration Research 2025年第7期20卷 2068-2083页

作者： Jing Yao Yuan Li Xi Liu Wenping Liang Yu Li Liyong Wu Zhe Wang Weihong Song The National Clinical Research center for Geriatric Disease Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina Department of Neurosurgery Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Pediatrics The Second Affiliated Hospital and Yuying Children’s HospitalKey Laboratory of Alzheimer’s Disease of Zhejiang ProvinceInstitute of AgingWenzhou Medical UniversityWenzhouZhejiang ProvinceChina Oujiang Laboratory(Zhejiang Laboratory for Regenerative Medicine Visionand Brain Health)WenzhouZhejiang ProvinceChina

Alzheimer's disease is characterized by deposition of amyloid-β,which forms extracellular neuritic plaques,and accumulation of hyperphosphorylated tau,which aggregates to form intraneuronal neurofibrillary tangles,in the *** NLRP3 inflammasome may play a role in the transition from amyloid-βdeposition to tau phosphorylation and *** NLRP3 is primarily found in brain microglia,and tau is predominantly located in neurons,it has been suggested that NLRP3 expressed by microglia indirectly triggers tau phosphorylation by upregulating the expression of pro-inflammatory ***,we found that neurons also express NLRP3 in vitro and in vivo,and that neuronal NLRP3 regulates tau *** biochemical methods,we mapped the minimal NLRP3 promoter and identified FUBP3 as a transcription factor regulating NLRP3 expression in *** primary neurons and the neuroblastoma cell line Neuro2A,FUBP3 is required for endogenous NLRP3 expression and tau phosphorylation only when amyloid-βis *** the brains of aged wild-type mice and a mouse model of Alzheimer's disease,FUBP3 expression was markedly increased in cortical *** analysis suggested that FUBP3 plays a role in neuron-mediated immune *** also found that FUBP3 trimmed the 5′end of DNA fragments that it bound,implying that FUBP3 functions in stress-induced *** findings suggest that neuronal NLRP3 may be more directly involved in the amyloid-β-to–phospho-tau transition than microglial NLRP3,and that amyloid-βfundamentally alters the regulatory mechanism of NLRP3 expression in *** that FUBP3 was only expressed at low levels in young wild-type mice and was strongly upregulated in the brains of aged mice and Alzheimer's disease mice,FUBP3 could be a safe therapeutic target for preventing Alzheimer's disease progression.

关键词： 5′end trimming Alzheimer's disease amyloid-beta amyloid-β-dependent transcription FUBP3 inflammasome inflammation neuron NLRP3 tau transcription factor

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AAV2-PDE6B restores retinal structure and function in the retinal degeneration 10 mouse model of retinitis pigmentosa by promoting phototransduction and inhibiting apoptosis

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Neural Regeneration Research 2025年第8期20卷 2408-2419页

作者： Ruiqi Qiu Mingzhu Yang Xiuxiu Jin Jingyang Liu Weiping Wang Xiaoli Zhang Jinfeng Han Bo Lei Henan Eye Hospital Henan Provincial People’s HospitalPeople’s Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina Eye Institute Henan Academy of Innovations in Medical ScienceZhengzhouHenan ProvinceChina Branch of National Clinical Research center for Ocular Disease Henan Provincial People’s HospitalZhengzhouHenan ProvinceChina Academy of medical Science Zhengzhou UniversityZhengzhouHenan ProvinceChina

Retinitis pigmentosa is a group of inherited diseases that lead to retinal degeneration and photoreceptor cell ***,there is no effective treatment for retinitis pigmentosa caused by PDE6B ***-associated virus(AAV)-mediated gene therapy is a promising strategy for treating retinitis *** aim of this study was to explore the molecular mechanisms by which AAV2-PDE6B rescues retinal *** do this,we injected retinal degeneration 10(rd10)mice subretinally with AAV2-PDE6B and assessed the therapeutic effects on retinal function and structure using dark-and light-adapted electroretinogram,optical coherence tomography,and ***-independent acquisition-mass spectrometry-based proteomic analysis was conducted to investigate protein expression levels and pathway enrichment,and the results from this analysis were verified by real-time polymerase chain reaction and western ***2-PDE6B injection significantly upregulated PDE6βexpression,preserved electroretinogram responses,and preserved outer nuclear layer thickness in rd10 *** expressed proteins between wild-type and rd10 mice were closely related to visual perception,and treating rd10 mice with AAV2-PDE6B restored differentially expressed protein expression to levels similar to those seen in wild-type *** Encyclopedia of Genes and Genome analysis showed that the differentially expressed proteins whose expression was most significantly altered by AAV2-PDE6B injection were enriched in phototransduction ***,the phototransductionrelated proteins Pde6α,Rom1,Rho,Aldh1a1,and Rbp1 exhibited opposite expression patterns in rd10 mice with or without AAV2-PDE6B ***,Bax/Bcl-2,p-ERK/ERK,and p-c-Fos/c-Fos expression levels decreased in rd10 mice following AAV2-PDE6B *** data suggest that AAV2-PDE6B-mediated gene therapy promotes phototransduction and inhibits apoptosis by inhibiting the ERK signaling pathway and upr

关键词： apoptosis AAV2-PDE6B ERK1/2 gene therapy phototransduction proteomics rd10 retinitis pigmentosa

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