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Neurofilament light chain is increased in the parahippocampal cortex and associates with pathological hallmarks in Parkinson’s disease dementia

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Translational Neurodegeneration 2023年第1期12卷 872-888页

作者： Irene Frigerio max A.Laansma Chen-Pei Lin Emma J.m.Hermans maud m.A.Bouwman John g.J.m.Bol Yvon galis-de graaf Dagmar H.Hepp Annemieke J.m.Rozemuller Frederik Barkhof Wilma D.J.van de Berg Laura E.Jonkman Section Clinical Neuroanatomy and Biobanking Department of Anatomy and NeurosciencesAmsterdam UMC Location Vrije Universiteit AmsterdamDe Boelelaan 1118AmsterdamThe Netherlands Amsterdam Neuroscience NeurodegenerationAmsterdamThe Netherlands Amsterdam Neurosci-ence Brain ImagingAmsterdamThe Netherlands Department of Neurology Amsterdam UMC Location Vrije Universiteit AmsterdamDe Boelelaan 1117AmsterdamThe Netherlands Department of Pathology Amsterdam UMC Location Vrije Universiteit AmsterdamDe Boelelaan 1117AmsterdamThe Netherlands Department of Radiology and Nuclear medicine Amsterdam UMC Location Vrije Universiteit AmsterdamDe Boelelaan 1117AmsterdamThe Netherlands Institutes of Neurology and Healthcare Engineering University College LondonLondonUK.

Background Increased neurofilament levels in biofluids are commonly used as a proxy for neurodegeneration in several neurodegenerative *** this study,we aimed to investigate the distribution of neurofilaments in the cerebral cortex of Parkinson’s disease(PD),PD with dementia(PDD)and dementia with Lewy bodies(DLB)donors,and its association with pathology load and mRI measures of atrophy and *** Using a within-subject post-mortem mRI-pathology approach,we included 9 PD,12 PDD/DLB and 18 age-matched control *** thickness and mean diffusivity(mD)metrics were extracted respectively from 3DT1 and DTI at 3T in-situ *** autopsy,pathological hallmarks(pSer129-αSyn,p-tau and amyloid-βload)together with neurofilament light-chain(NfL)and phosphorylated-neurofilament medium-and heavy-chain(p-Nfm/H)immunoreactivity were quantified in seven cortical regions,and studied in detail with confocal-laser scanning *** correlations between mRI and pathological measures were studied using linear mixed *** Compared to controls,p-Nfm/H immunoreactivity was increased in all cortical regions in PD and PDD/DLB,whereas NfL immunoreactivity was increased in the parahippocampal and entorhinal cortex in PDD/***-positive neurons showed degenerative morphological features and axonal *** increased p-Nfm/H correlated with p-tau load,and NfL correlated with pSer129-αSyn but more strongly with p-tau load in PDD/***,neuro-filament immunoreactivity correlated with cortical thinning in PD and with increased cortical mD in PDD/*** Taken together,increased neurofilament immunoreactivity suggests underlying axonal injury and neurofilament accumulation in morphologically altered neurons with increased pathological ***,we demonstrate that such neurofilament markers at least partly explain mRI measures that are associated with the neurodegenerative process.

关键词： Neurofilament NfL Axonal degeneration Parkinson’s disease Parkinson’s disease dementia Dementia with Lewy bodies Cortical thickness Cortical atrophy mean diffusivity

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IRAK4 inhibition: a promising strategy for treating RA joint inflammation and bone erosion

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Cellular & molecular Immunology 2021年第9期18卷 2199-2210页

作者： Sadiq Umar Karol Palasiewicz Katrien Van Raemdonck m.chael V.Volin Bianca Romay mAsif Amin Ryan K.Zomorrodi Shiva Arami mark gonzalez Vikram Rao Brian Zanotti David A.fox Nadera Sweiss Shiva Shahrara Jesse Brown VA medical Center ChicagoIL60612USA Department of medicine Division of RheumatologyUniversity of Illinois at ChicagoChicagoIL60612USA Department of microbiology and Immunology Midwestern UniversityDowners GroveIL60515USA Division of Rheumatology and Clinical Autoimmunity Center of Excellence University of MichiganAnn ArborMI481096USA Department of Orthopedic Surgery University of Illinois at ChicagoChicagoIL60612USA Pfizer Research CambridgeMA02139USA

Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis(RA)patients could reflect activation of innate immune ***,we show that a TLR7 gU-rich endogenous ligand,miR-Let7b,potentiates synovitis by amplifying RA monocyte and fibroblast(FLS)***-Let7b ligation to TLR7 in macrophages(mΦs)and FLSs expanded the synovial inflammatory ***,secretion of m1 monokines triggered by miR-Let7b enhanced Th1/Th17 cell *** showed that IRAK4 inhibitor(i)therapy attenuated RA disease activity by blocking TLR7-induced m1 mΦor FLS activation,as well as monokine-modulated Th1/Th17 cell ***4i therapy also disrupted RA osteoclastogenesis,which was amplified by miR-Let7b ligation to joint myeloid ***,the effectiveness of IRAK4i was compared with that of a TNF inhibitor(i)or anti-IL-6R treatment in collagen-induced arthritis(CIA)and miR-Let7b-mediated *** found that TNF or IL-6R blocking therapies mitigated CIA by reducing the infiltration of joint F480+iNOS+mΦs,the expression of certain monokines,and Th1 cell ***,these biologic therapies were unable to alleviate miR-Let7b-induced *** superior efficacy of IRAK4i over anti-TNF or anti-IL-6R therapy in miR-Let7b-induced arthritis or CIA was due to the ability of IRAK4i therapy to restrain the migration of joint F480+iNOS+mΦs,vimentin+fibroblasts,and CD3+T cells,in addition to negating the expression of a wide range of monokines,including IL-12,mIP2,and IRF5 and Th1/Th17 *** conclusion,IRAK4i therapy may provide a promising strategy for RA therapy by disconnecting critical links between inflammatory joint cells.

关键词： TLR7 mΦs RA FLSs osteoclasts T cells IRAK4

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造血生长因子与癌治疗

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国外医学情报 1993年第20期14卷 12-13页

作者： William P Sheridand Richard m fox 敏江

造血生长因子(HgF)或称集落刺激因子(CSF)属于糖蛋白激素族,其作用是调节骨髓祖细胞及其子代细胞的增殖、分化、移行和细胞功能。它们也控制各种白细胞的产生。调节红细胞生成的促红细胞生成素(erythropoitin)早已熟知。但单纯调节血小... 详细信息

造血生长因子(HgF)或称集落刺激因子(CSF)属于糖蛋白激素族,其作用是调节骨髓祖细胞及其子代细胞的增殖、分化、移行和细胞功能。它们也控制各种白细胞的产生。调节红细胞生成的促红细胞生成素(erythropoitin)早已熟知。但单纯调节血小板产生的调节因子尚未确定。 HgF现包括控制中性粒细胞、单核细胞和嗜酸细胞产生的激素。粒细胞集落刺激因子(g-CSF,filgrastim)和粒细胞-巨噬细胞集落刺激因子(gm-CSF,sargramostim)已在人类进行了广泛的研究。

关键词：造血生长因子巨噬细胞集落刺激因子粒细胞集落刺激因子促红细胞生成素中性细胞骨髓移植中性粒细胞糖蛋白激素血小板骨髓祖细胞

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血红素氧化酶基因启动子gT序列变化与冠状动脉支架术后再狭窄

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中国循环杂志 2006年第2期21卷 113-116页

作者：李萍 mohamedA.Elrayess AbuzeidH.gomma JuttaPalmen EmmaHawe Kimm.fox SteveE.Humphries 南昌大学第二附属医院心内科江西省南昌市330006 CentreforCardiovasculargeneticsBHFlaboratories UniversityCollegeLondon HeartandLungInstituteandRoyalBromptonHospital

目的:观察I型血红素氧化酶(HO-1)基因启动子gT重复长短对冠状动脉支架置入术后再狭窄的影响。方法:187例行冠状动脉支架置入术者,6个月时随访再狭窄情况。PCR和DNA测序仪确定HO-1启动子gT重复次数。高敏法测术前及术后24h、48h血浆白介... 详细信息

目的:观察I型血红素氧化酶(HO-1)基因启动子gT重复长短对冠状动脉支架置入术后再狭窄的影响。方法:187例行冠状动脉支架置入术者,6个月时随访再狭窄情况。PCR和DNA测序仪确定HO-1启动子gT重复次数。高敏法测术前及术后24h、48h血浆白介素-6(IL-6)和C反应蛋白(CRP)值。结果:各基因型间术后IL-6和CRP水平及再狭窄发生率无差异,携较短gT者术前血浆IL-6水平比非短gT序列携带者低约33．3％(P=0．0008)。结论:HO-1基因多态性不影响支架置入术后炎症介质水平及再狭窄,但可能影响动脉粥样硬化形成的炎症过程。

关键词：血红素氧化酶 gT重复序列再狭窄

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南京国金中心

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建筑实践 2024年第Z1期 196-203页

作者： Kohn Pedersen fox Associates KPF建筑设计事务所

南京国金中心地处河西中央商业区，位于双地铁交汇的元通站上方。其设计灵感来源于自然几何图形，3座水晶塔楼通过商业裙楼相连，象征着城市新中央商务区的发展。南京国金中心的裙楼内设有一系列商店和餐厅，在其上方则是设有362间客房...

南京国金中心地处河西中央商业区，位于双地铁交汇的元通站上方。其设计灵感来源于自然几何图形，3座水晶塔楼通过商业裙楼相连，象征着城市新中央商务区的发展。南京国金中心的裙楼内设有一系列商店和餐厅，在其上方则是设有362间客房的安达仕酒店和两座办公塔楼：国金中心一号和二号塔楼。该项目的主入口位于一号和二号塔楼之间的4层通高中庭，同时也作为一个聚会空间，其30m高的玻璃立面赋予建筑整体以雕塑感。此外，商业空间另设专门的雨篷入口。

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应用mRI测量口腔-盲肠通过时间

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国际医学放射学杂志 2015年第4期 399-400页

作者： E.Savarino V.Savarino m.fox g.D.Leo m.Furnari E.marabotto 刘春明 Division of gastroenterology Department of SurgicalOncological and Gastroenterological Sciences

摘要目的前瞻性地评估乳果糖氢呼气试验(LHBT)和mRI测量健康个体口腔-盲肠通过时间(OCTT)的一致性。方法所有志愿者均行空腹及摄入乳果糖(10 g/125 m L)后的

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伦敦帕丁顿中心Two Kingdom Street项目

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城市建筑 2010年第8期7卷 84-87页

作者： Kohn Pedersen fox Associates KPF建筑师事务所

KPF设计师事务所已完成了Two Kingdom Street项目设计。该项目投资8800万英镑,由Development Securities公司开发,为Aviva Investors公司和Quinlan Private公司所有。该项目提供了2.2万m2的最佳办公空间,是帕丁顿中心项目第二阶段的最... 详细信息

KPF设计师事务所已完成了Two Kingdom Street项目设计。该项目投资8800万英镑,由Development Securities公司开发,为Aviva Investors公司和Quinlan Private公司所有。该项目提供了2.2万m2的最佳办公空间,是帕丁顿中心项目第二阶段的最新增加项目,位于帕丁顿火车站附近的大型综合开发区内。

关键词： Private 伦敦项目设计项目投资办公空间开发区事务所设计师

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美国放射学院适宜性标准:肩关节置换术后影像学检查(续)

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中华肩肘外科电子杂志 2017年第4期5卷 299-304页

作者：张晓萌陈建海 Soterios gyftopoulos Zehava S.Rosenberg Catherine C.Roberts Jenny T.Bencardino marc Appel Steven J.Baccei R.Carter Cassidy Eric Y.Chang m.chael g.fox Bennett S.greenspan mary g.Hochman Jon A.Jacobson Douglas N.mintz Joel S.Newman Nehal A.Shah Kirstin m.Small Barbara N.Weissman 北京大学人民医院创伤骨科 100044 纽约大学医疗中心纽约市纽约关节病医院纽约市梅奥诊所亚利桑那州凤凰城纽约大学医学院纽约市 James J.Peters VA医疗中心纽约市马萨诸塞大学医疗中心伍斯特英国医疗脊柱和全关节服务列克星敦 VA圣地亚哥医疗系统圣地亚哥弗吉尼亚卫生系统夏洛茨维尔奥古斯塔大学佐治亚州医学院奥古斯塔贝斯以色列女执事医疗中心波士顿密歇根大学医疗中心安娜堡纽约特种外科医院纽约市新英格兰浸信会医院波士顿布列根和妇女医院波士顿

过去的20年里,在美国实施的肩关节置换术的数量迅速增长,其中包括部分或全肱骨头表面置换术、半肩置换术、全肩关节置换术和反式全肩关节置换术。影像学检查在诊断这些肩关节置换术引起的并发症方面起到了重要作用。本综述分为两个部分... 详细信息

过去的20年里,在美国实施的肩关节置换术的数量迅速增长,其中包括部分或全肱骨头表面置换术、半肩置换术、全肩关节置换术和反式全肩关节置换术。影像学检查在诊断这些肩关节置换术引起的并发症方面起到了重要作用。本综述分为两个部分。第一部分阐述了对各种影像学检查模式的总体探讨,包括X线片、计算机断层扫描、核磁共振成像、超声、核医学以及它们提供有益的以治疗为导向的信息时所发挥的作用。第二部分重点研究最佳影像学方法的选择,用于肩关节置换术的并发症,包括无菌性松动、感染、骨折、肩袖肌腱撕裂和神经损伤。在本报告中所提供的美国放射学院适宜性标准循证指南,是通过广泛分析来自同行评审期刊的现有医学文献,并应用行之有效的方法学而完成的(兰德/加州大学洛杉矶分校的适宜性方法以及推荐评价、发展和评估分级),它们用于特殊临床情况下的影像学检查和治疗措施的适宜性评价。多学科专家小组对指南进行了进一步的分析和审查。由于用于推荐合适成像算法的数据会出现不足或模棱两可,在这种情况下,专家意见可能对现有证据进行补充。为此,将美国《放射学院适宜性标准:肩关节置换术后影像学检查》翻译成中文,供同道参考。

关键词：全肩关节置换术美国放射学院影像学检查适宜性标准核磁共振成像计算机断层扫描循证指南

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A focus on parietal cells as a renewing cell population

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World Journal of gastroenterology 2010年第5期16卷 538-546页

作者： Sherif m Karam Department of Anatomy Faculty of Medicine and Health Sciences United Arab Emirates University Al-Ain PO Box 17666 United Arab Emirates

The fact that the acidsecreting parietal cells undergo continuous renewal has been ignored by many gastroenterologists and cell biologists. In the past, it was thought that these cells were static. However, by using 3Hthymidine radioautography in combination with electron microscopy, it was possible to demonstrate that parietal cells belong to a continuously renewing epithelial cell lineage. In the gastric glands, stem cells anchored in the isthmus region are responsible for the production of parietal cells. The stem cells give rise to three main progenitors: prepit, preneck and preparietal cells. Parietal cells develop either directly from the noncycling preparietal cells or less commonly via differentiation of the cycling prepit and preneck cell progenitors. The formation of a parietal cell is a sequential process which involves diminishment of glycocalyx, production of cytoplasmic tubulovesicles, an increase in number and length of microvilli, an increase in number and size of mitochondria, and fi nally, expansion and invagination of the apical membrane with the formation of an intracellular canalicular system. Little is known about the genetic counterparts of these morphological events. However, the time dimension of parietal cell production and the consequences of its alteration on the biological features of the gastric gland are well documented. The production of a new parietal cell takes about 2 d. However, mature parietal cells have a long lifespan during which they migrate bidirectionally while their functional activity for acid secretion gradually diminishes. Following an average lifespan of about 54 d, in mice, old parietal cells undergo degeneration and elimination. Various approaches for genetic alteration of the development of parietal cells have provided evidence in support of their role as governors of the stem/progenitor cell proliferation and differentiation programs. Revealing the dynamic features and the various roles of parietal cells would help

关键词： Cell differentiation Cell dynamics Cell renewal Oxyntic gland Oxyntic mucosa Parietal cell Preparietal cell

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macrophages are the primary effector cells in IL-7-induced arthritis

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Cellular & molecular Immunology 2020年第7期17卷 728-740页

作者： Seung-jae Kim Huan J.Chang m.chael VVolin Sadiq Umar Katrien Van Raemdonck Aimee Chevalier Karol Palasiewicz John W.Christman Suncica Volkov Shiva Arami mehrdad maz Anjali mehta Ryan K.Zomorrodi David A.fox Nadera Sweiss Shiva Shahrara Division of Rheumatology Jesse Brown VAMedical CenterChicagoIL 60612USA Department of medicine Division of RheumatologyUniversity of Illinois at ChicagoChicagoIL 60612USA Department of microbiology and Immunology Chicago College of Osteopathic MedicineMidwestern UniversityDowners GroveIL 60515USA Pulmonary Critical Care and Sleep MedicineOhio State University Wexner Medical CenterDavis Heart and Lung Research InstituteColumbusOH 43210USA Division of Allergy Clinical Immunology and RheumatologyThe University of Kansas Medical CenterKansas CityKS 66160USA Division of Rheumatology and Clinical Autoimmunity Center of Excellence University of MichiganAnn ArborMI 481096USA

Synovial macrophages are crucial in the development of joint inflammation and bone damage;however, the pathways that controlmacrophage remodeling in inflammatory m1 cells or bone-eroding osteoclasts are not fully understood. We determined thatelevated IL-7R/CD127 expression is the hallmark of rheumatoid arthritis (RA) m1 macrophages and that these cells are highlyresponsive to interleukin-7 (IL-7)-driven osteoclastogenesis. We established that lipopolysaccharide (LPS), interferon-γ (IFNγ), andtumor necrosis factor-α (TNFα), the classic m1 macrophage mediators, enhance IL-7R expression in RA and murine *** local expression of IL-7 provokes arthritis, predominantly through escalating the number of F480^(+)iNOS^(+) cells rather than CD3^(+)T cells. Ectopic LPS injection stabilizes IL-7-induced arthritis by increasing myeloid IL-7R expression, in part via IFNγ ***, in RAg−/− mice, IL-7-mediated arthritis is suppressed because of the reduction in myeloid IL-7R expression due to the lackof IFNγ. moreover, the amelioration of IL-7-induced arthritis by anti-TNF therapy is due to a decrease in the number of cells in theunique F480^(+)iNOS^(+)IL-7R^(+)CCL5^(+) subset, with no impact on the F480^(+)Arginase^(+) cell or CD3^(+) T cell frequency. Consistent with thepreclinical findings, the findings of a phase 4 study performed with RA patients following 6 months of anti-TNF therapy revealedthat IL-7R expression was reduced without affecting the levels of IL-7. This study shifts the paradigm by discovering that IL-7-induced arthritis is dependent on F480^(+)iNOS^(+)IL-7R^(+)CCL5^(+) cell function, which activates TH-1 cells to amplify myeloid IL-7Rexpression and disease severity.

关键词： myeloid elevated inflammation

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