检索结果-南通市图书馆

Science China(Life Sciences) 2016年第10期59卷 1051-1054页

作者： Chao-Jun Wen Sai-Juan Chen Collaborative Innovation center of Systems Biomedicine National Research Center for Translational Medicine.Shanghai State Key Laboratory of Medical Genomics Shanghai Institute of Hematology Rui-Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine

In July 2013,the National Development and Reform Commission formally approved the'National Research center for translational medicine·Shanghai'(hereinafter'the center'),a piece of the national key scientific infrastruc-

关键词：基础设施医学转化上海科学国家发展基础结构共同管理

N^(6)-methyladenosine(m^(6)A)RNA modification in tumor immunity

在线全文

学校读者我要写书评

暂无评论

Cancer Biology & medicine 2022年第4期19卷 385-397页

作者： Siyi Zheng Hui Han Shuibin Lin center for translational medicine Precision Medicine InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Department of Otolaryngology Center for Translational MedicinePrecision Medicine InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China

Growing evidence supports that cancer progression is closely associated with the tumor microenvironment and immune evasion.Importantly,recent studies have revealed the crucial roles of epigenetic regulators in shaping the tumor microenvironment and restoring immune recognition.N^(6)-methyladenosine(m^(6)A)modification,the most prevalent epigenetic modification of mammalian mRNAs,has essential functions in regulating the processing and metabolism of its targeted RNAs,and therefore affects various biological processes including tumorigenesis and progression.Recent studies have demonstrated the critical functions and molecular mechanisms underlying abnormal m^(6)A modification in the regulation of tumor immunity.In this review,we summarize recent research progress in the potential roles of m^(6)A modification in tumor immunoregulation,with a special focus on the anti-tumor processes of immune cells and involvement in immune-associated molecules and pathways.Furthermore,we review current knowledge regarding the close correlation between m6A-related risk signatures and the tumor immune microenvironment landscape,and we discuss the prognostic value and therapeutic efficacy of m^(6)A regulators in a variety of cancer types.

关键词： N^(6)-methyladenosine(m^(6)A)modification immune evasion tumor microenvironment(TME) tumor immunology immune cells

Third Special Issue on Mechanisms of Pain and Itch

在线全文

学校读者我要写书评

暂无评论

Neuroscience Bulletin 2022年第4期38卷 339-341页

作者： Ru-Rong Ji Department of Anesthesiology and Neurobiology Center for Translational Pain MedicineDuke University Medical CenterDurhamNC 27710USA

We have published two special issues on pain and itch in Neuroscience Bulletin that cover their peripheral,central,and glial mechanisms[1,2],The first special was published in 2012[1],highlighting several topics such as Toll-like receptors,capsaicin receptor TRPVI,interactionof u-and 8-opioid receptors,and population coding of somatic sensations.In 2018,we published the second special issue[2],which covered a wide breath of research,including molecular and functional characterization of primary sensory neurons,neurocircuits of pain and itch,Na+channel expression in human sensory neurons,modulation ofpainand itch byspinal glia,infection,sex dimorphisms inpain。

关键词： sensation pain opioid

NLRP3 Inflammasome-Mediated Neuroinflammation and Related Mitochondrial Impairment in Parkinson's

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Neuroscience Bulletin 2023年第5期39卷 832-844页

作者： Qiu-Qin Han Weidong Le Shanghai University of medicine and Health Sciences Affiliated Zhoupu Hospital Shanghai 201318China center for Clinical and translational medicine Shanghai University of Medicine and Health SciencesShanghai 201318China

Parkinson's disease(PD)is a common neuro-degenerative disorder caused by the loss of dopamine neu-rons in the substantia nigra and the formation of Lewy bod-ies,which are mainly composed of alpha-synuclein fibrils.Alpha-synuclein plays a vital role in the neuroinflamma-tion mediated by the nucleotide-binding oligomerization domain-,leucine-rich repeat-,and pyrin domain-containing protein 3(NLRP3)inflammasome in PD.A better under-standing of the NLRP3 inflammasome-mediated neuroin-flammation and the related mitochondrial impairment during PD progression may facilitate the development of promis-ing therapies for PD.This review focuses on the molecular mechanisms underlying NLRP3 inflammasome activation,comprising priming and protein complex assembly,as well as the role of mitochondrial impairment and its subsequent inflammatory effects on the progression of neurodegenera-tion in PD.In addition,the therapeutic strategies targeting the NLRP3 inflammasome for PD treatment are discussed,including the inhibitors of NLRP3 inflammatory pathways,mitochondria-focused treatments,microRNAs,and other therapeutic compounds.

关键词： Parkinson's disease NLRP3 inflammasome Neuroinflammation Mitochondrial impairment Microglia

Synaptosome microRNAs:emerging synapse players in aging and Alzheimer’s disease

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Neural Regeneration Research 2023年第6期18卷 1275-1276页

作者： Subodh Kumar center of Emphasis in Neuroscience Department of Molecular and Translational Medicine Paul L.Foster School of medicine Texas Tech University Health Sciences CenterEl PasoTXUSA

Synaptosome:Synapses are the most critical portion of neuron connections,necessary for cellular organization of the brain.Synapse integrity is uttermost important for healthy brain functioning.Any perturbation in the synapse structure and/or function initiates neurological disorders.Synapses are the prime targets that are smashed in almost all neurodegenerative diseases.The vital components of synapse are essential for neurotransmission,synaptic plasticity and overall synapse function.Synapse dysfunctions are well studied in Alzheimer’s disease(AD)and other neurodegenerative diseases(Gowda et al.,2021).The best way to study the synapse dysfunctions in neurological diseases is the biochemical analysis of“synaptosome”.

关键词： Alzheimer diseases

A pancreatic player in dementia:pathological role for islet amyloid polypeptide accumulation in the brain

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2023年第10期18卷 2141-2146页

作者： Angelina S.Bortoletto Ronald J.Parchem center for Cell and Gene Therapy Stem Cell and Regenerative Medicine CenterDepartment of NeuroscienceDepartment of Molecular and Cellular BiologyTranslational Biology and Molecular Medicine ProgramMedical Scientist Training ProgramBaylor College of MedicineHoustonTXUSA

Type 2 diabetes mellitus patients have a markedly higher risk of developing dementia.While multiple factors contribute to this predisposition,one of these involves the increased secretion of amylin,or islet amyloid polypeptide,that accompanies the pathophysiology of type 2 diabetes mellitus.Islet amyloid polypeptide accumulation has undoubtedly been implicated in various forms of dementia,including Alzheimer’s disease and vascular dementia,but the exact mechanisms underlying islet amyloid polypeptide’s causative role in dementia are unclear.In this review,we have summarized the literature supporting the various mechanisms by which islet amyloid polypeptide accumulation may cause neuronal damage,ultimately leading to the clinical symptoms of dementia.We discuss the evidence for islet amyloid polypeptide deposition in the brain,islet amyloid polypeptide interaction with other amyloids implicated in neurodegeneration,neuroinflammation caused by islet amyloid polypeptide deposition,vascular damage induced by islet amyloid polypeptide accumulation,and islet amyloid polypeptide-induced cytotoxicity.There are very few therapies approved for the treatment of dementia,and of these,clinical responses have been controversial at best.Therefore,investigating new,targetable pathways is vital for identifying novel therapeutic strategies for treating dementia.As such,we conclude this review by discussing islet amyloid polypeptide accumulation as a potential therapeutic target not only in treating type 2 diabetes mellitus but as a future target in treating or even preventing dementia associated with type 2 diabetes mellitus.

关键词： Alzheimer’s disease amylin amyloid dementia diabetes human islet amyloid polypeptide islet amyloid polypeptide protofibrils type 2 diabetes mellitus vascular dementia

Zinc finger protein ZPR1:promising survival motor neuron protein-dependent modifier for the rescue of spinal muscular atrophy

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2022年第10期17卷 2225-2227页

作者： Juliana Cuartas Laxman Gangwani center of Emphasis in Neurosciences Department of Molecular and Translational MedicinePaul L.Foster School of MedicineTexas Tech University Health Sciences Center El PasoEl PasoTXUSA

neuromuscular disease caused by the homozygous mutation or deletion of the survival motor neuron 1(SMN1)gene.A second copy,SMN2,is similar to SMN1,but produces only~10%SMN protein because of a single-point mutation(C>T)in coding exon 7 causing a splicing defect which leads to the exclusion of exon 7,resulting in a majority(~90%)of transcripts lacking exon 7 that translate into mutant SMN(SMNΔ7)protein.SMA is caused by chronic low levels of SMN and is characterized by the degeneration of the spinal cord motor neurons leading to symmetrical skeletal muscle atrophy,respiratory failure,and death(Ahmad et al.,2012).Chronic low levels of SMN cause the accumulation of pathogenic R-loops and double-stranded breaks(DSBs)in DNA,leading to genomic instability and neurodegeneration in SMA(Kannan et al.,2018).The severity of SMA disease correlates inversely with SMN levels.

关键词： atrophy degeneration Zinc

Withdrawal of anti-tumour necrosis factor α therapy in inflammatory bowel disease

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2015年第16期21卷 4773-4778页

作者： Konstantinos Papamichael Severine Vermeire Department of Clinical and Experimental medicine Translational Research Center for Gastrointestinal Disorders

Anti-tumour necrosis factor α(anti-TNFα) therapy is an established treatment in inflammatory bowel disease.However, this treatment is associated with high costs and the possibility of severe adverse events representing a true challenge for patients, clinicians and health care systems.Consequently, a crucial question is raised namely if therapy can be stopped once remission is achieved and if so, how and in whom.Additionally, in a real-life clinical setting, discontinuation may also be considered for other reasons such as the patient's preference, pregnancy, social reasons as moving to countries or continents with less access, or different local policy or reimbursement.In contrast to initiation of anti-TNFα therapy guidelines regarding stopping of this treatment are missing.As a result, the decision of discontinuation is still a challenging aspect in the use of anti-TNFα therapy.Currently this is typically based on an estimated, case-by-case, benefit-risk ratio.This editorial is intended to provide an overview of recent data on this topic and shed light on the proposed drug withdrawal strategies.

关键词： Inflammatory bowel disease Anti-tumournecrosis factor α therapy Withdrawal Remission Infliximab

Kidney disease models:tools to identify mechanisms and potential therapeutic targets

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Zoological Research 2018年第2期39卷 72-86页

作者： Yin-Wu Bao Yuan Yuan Jiang-Hua Chen Wei-Qiang Lin Kidney Disease center First Affiliated Hospital School of Medicine Zhejiang University Institute of translational medicine School of Medicine Zhejiang University

Acute kidney injury （AKI） and chronic kidney disease （CKD） are worldwide public health problems affecting millions of people and have rapidly increased in prevalence in recent years. Due to the multiple causes of renal failure, many animal models have been developed to advance our understanding of human nephropathy. Among these experimental models, rodents have been extensively used to enable mechanistic understanding of kidney disease induction and progression, as well as to identify potential targets for therapy. In this review, we discuss AKI models induced by surgical operation and drugs or toxins, as well as a variety of CKD models （mainly genetically modified mouse models）. Results from recent and ongoing clinical trials and conceptual advances derived from animal models are also explored.

关键词： Acute kidney injury Chronic kidneydisease Mouse models Transgenic mice

β-Estradiol 17-acetate enhances the in vitro vitality of endothelial cells isolated from the brain of patients subjected to neurosurgery

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2023年第2期18卷 389-395页

作者： Sonia Guzzo Pasquale De Bonis Barbara Pavan Luciano Fadiga Department of Neuroscience and Rehabilitation Section of PhysiologyUniversity of FerraraFerraraItaly center for translational Neurophysiology of Speech and Communication(CTNSC) Italian Institute of Technology(IIT)FerraraItaly Department of translational medicine and for Romagna University of FerraraFerraraItaly

In the current landscape of endothelial cell isolation for building in vitro models of the blood-brain barrier,our work moves towards reproducing the features of the neurovascular unit to achieve glial compliance through an innovative biomimetic coating technology for brain chronic implants.We hypothesized that the autologous origin of human brain mic rovascular endothelial cells(hBMECs)is the first requirement for the suitable coating to prevent the glial inflammato ry response trigge red by foreign neuroprosthetics.Therefo re,this study established a new procedure to preserve the in vitro viability of hBMECs isolated from gray and white matter specimens taken from neurosurge ry patients.Culturing adult hBMECs is generally considered a challenging task due to the difficult survival ex vivo and progressive reduction in proliferation of these cells.The addition of 10 nMβ-estradiol 17-acetate to the hBMEC culture medium was found to be an essential and discriminating factor promoting adhesion and proliferation both after isolation and thawing,suppo rting the well-known protective role played by estrogens on microvessels.In particular,β-estradiol 17-acetate was critical for both freshly isolated and thawed female-derived hBMECs,while it was not necessary for freshly isolated male-derived hBMECs;however,it did countera ct the decay in the viability of the latter after thawing.The tumo r-free hBMECs were thus cultured for up to 2 months and their growth efficiency was assessed befo re and after two periods of cryopreservation.Des pite the thermal stress,the hBMECs remained viable and suitable for re-freezing and storage for several months.This approach increasing in vitro viability of hBMECs opens new perspectives for the use of cryopreserved autologous hBMECs as biomimetic therapeutic tools,offering the potential to avoid additional surgical sampling for each patient.

关键词： β-estradiol 17-acetate 17β-estradiol cryopreservation gender-specific gray matter human brain microvascular endothelial cells surgical resections vascular protection white matter