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FAST discovery of an extremely radio-faint millisecond pulsar from the Fermi-LAT unassociated source 3FGL J0318.1+0252

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Science China(Physics,mechanics & Astronomy) 2021年第12期64卷 10-17页

作者： Pei Wang Di Li Colin J.Clark pablo m.saz parkinson Xian Hou Weiwei Zhu Lei Qian Youling Yue Zhichen Pan Zhijie Liu Xuhong Yu Shanping You Xiaoyao Xie Qijun Zhi Hui Zhang Jumei Yao Jun Yan Chengmin Zhang Kwok Lung Fan Paul S.Ray matthew Kerr David A.Smith Peter F.michelson Elizabeth C.Ferrara David J.Thompson Zhiqiang Shen Na Wang FAST&Fermi-LAT Collaboration CAS Key Laboratory of FAST National Astronomical ObservatoriesChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Jodrell Bank Centre for Astrophysics Department of Physics and AstronomyUniversity of ManchesterManchester M139PLUK Department of Physics and Laboratory for Space Research University of Hong KongHong Kong 999077China Santa Cruz Institute for Particle Physics University of CaliforniaSanta Cruz CA 95064USA Yunnan Observatories Chinese Academy of SciencesKunming 650216China Key Laboratory for the Structure and Evolution of Celestial Objects Chinese Academy of SciencesKunming 650216China School of Computer Science and Technology Key Laboratory of Information and Computing Guizhou ProvinceGuizhou Normal UniversityGuiyang 550001China School of Physics and Electronic Science Guizhou Normal UniversityGuiyang 550001China Physics Department Stanford UniversityStanford CA 94305USA UmCP/CRESST/GSFC NASAGreenbeltMaryland MD 20771USA GSFC NASAGreenbeltMaryland MD 20771USA Centre d’´Etudes Nucl´eaires de Bordeaux Gradignan IN2P3/CNRSUniversit´e BordeauxGradignan 33175France Space Science Division U.S.Naval Research LaboratoryWashington DC 20375-5352USA Shanghai Astronomical Observatory Chinese Academy of SciencesShanghai 200030China Xinjiang Astronomical Observatory Urumqi 830011China Department of Physics University of MarylandCollege Park MD 20742USA NAOC-UKZN Computational Astrophysics Centre University of KwaZulu-NatalDurban 4000South Africa 不详

High sensitivity radio searches of unassociated γ-ray sources have proven to be an effective way of finding new pulsars. Using the Five-hundred-meter Aperture Spherical radio Telescope(FAST) during its commissioning phase, we have carried out a number of targeted deep searches of Fermi Large Area Telescope(LAT) γ-ray sources. On February 27, 2018 we discovered an isolated millisecond pulsar(mSP), PSR J0318+0253, coincident with the unassociated γ-ray source 3 FGL J0318.1+0252. PSR J0318+0253 has a spin period of 5.19 ms, a dispersion measure(Dm) of 26 pc cm-3 corresponding to a Dm distance of about 1.3 kpc, and a period-averaged flux density of(~11±2) μJy at L-band(1.05-1.45 GHz). Among all high energy mSPs, PSR J0318+0253 is the faintest ever detected in radio bands, by a factor of at least ~4 in terms of L-band fluxes. With the aid of the radio ephemeris, an analysis of 9.6 years of Fermi-LAT data revealed that PSR J0318+0253 also displays strong γ-ray pulsations. Follow-up observations carried out by both Arecibo and FAST suggest a likely spectral turn-over around 350 mHz. This is the first result from the collaboration between FAST and the Fermi-LAT teams as well as the first confirmed new mSP discovery by FAST, raising hopes for the detection of many more mSPs. Such discoveries will make a significant contribution to our understanding of the neutron star zoo while potentially contributing to the future detection of gravitational waves, via pulsar timing array(PTA) experiments.

关键词： FAST pulsar radio gamma rays

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parkinson’s disease and diabetes mellitus: common mechanisms and treatment repurposing

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Neural Regeneration Research 2022年第8期17卷 1652-1658页

作者： Carmen m.Labandeira Arturo Fraga-Bau David Arias Ron Elena Alvarez-Rodriguez pablo Vicente-Alba Javier Lago-Garma Ana I.Rodriguez-Perez Department of Clinical Neurology Hospital Alvaro CunqueiroUniversity Hospital ComplexVigoSpain Laboratory of Cellular and molecular Neurobiology of parkinson’s Disease Research Center for Molecular Medicine and Chronic Diseases(CIMUS)IDISUniversity of Santiago de CompostelaSantiago de CompostelaSpain Department of Clinical Oncology University Hospital ComplexOurenseSpain Department of Endocrinology Hospital MeixoeiroUniversity Hospital ComplexVigoSpain Networking Research Center on Neurodegenerative Diseases(CiberNed) MadridSpain

In the last decade,attention has become greater to the relationship between neurodegeneration and abnormal insulin signaling in the central nervous system,as insulin in the brain is implicated in neuronal survival,plasticity,oxidative stress and neuroinflammation.Diabetes mellitus and parkinson’s disease are both aging-associated diseases that are turning into epidemics worldwide.Diabetes mellitus and insulin resistance not only increase the possibility of developing parkinson’s disease but can also determine the prognosis and progression of parkinsonian symptoms.Today,there are no available curative or disease modifying treatments for parkinson’s disease,but the role of insulin and antidiabetic medications in neurodegeneration opens a door to treatment repurposing to fight against parkinson’s disease,both in diabetic and nondiabetic parkinsonian patients.Furthermore,it is essential to comprehend how a frequent and treatable disease such as diabetes can influence the progression of neurodegeneration in a challenging disease such as parkinson’s disease.Here,we review the present evidence on the connection between parkinson’s disease and diabetes and the consequential implications of the existing antidiabetic molecules in the severity and development of parkinsonism,with a particular focus on glucagon-like peptide-1 receptor agonists.

关键词： antidiabetic diabetes mellitus dopamine exenatide glucagon-like peptide-1 insulin neurodegeneration neuroinflammation parkinson’s disease repurposing

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Vicious cycle of lipid peroxidation and iron accumulation in neurodegeneration

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Neural Regeneration Research 2023年第6期18卷 1196-1202页

作者： Instituto de Salud Carlos III Irene Villalón-García Suleva Povea-Cabello mónicaÁlvarez-Córdoba marta Talaverón-Rey Juan mSuárez-Rivero Alejandra Suárez-Carrillo manuel munuera-Cabeza Diana Reche-López Paula Cilleros-Holgado Rocío Piñero-Pérez JoséA.Sánchez-Alcázar Centro Andaluz de Biología del Desarrollo(CABD-CSIC-Universidad pablo de Olavide de Sevilla) and Centro de Investigación Biomédica en Red:Enfermedades RarasInstituto de Salud Carlos IIISevillaSpain

Lipid peroxidation and iron accumulation are closely associated with neurodegenerative diseases,such as Alzheimer’s,parkinson’s,and Huntington’s diseases,or neurodegeneration with brain iron accumulation disorders.mitochondrial dysfunction,lipofuscin accumulation,autophagy disruption,and ferroptosis have been implicated as the critical pathomechanisms of lipid peroxidation and iron accumulation in these disorders.Currently,the connection between lipid peroxidation and iron accumulation and the initial cause or consequence in neurodegeneration processes is unclear.In this review,we have compiled the known mechanisms by which lipid peroxidation triggers iron accumulation and lipofuscin formation,and the effect of iron overload on lipid peroxidation and cellular function.The vicious cycle established between both pathological alterations may lead to the development of neurodegeneration.Therefore,the investigation of these mechanisms is essential for exploring therapeutic strategies to restrict neurodegeneration.In addition,we discuss the interplay between lipid peroxidation and iron accumulation in neurodegeneration,particularly in PLA2G6-associated neurodegeneration,a rare neurodegenerative disease with autosomal recessive inheritance,which belongs to the group of neurodegeneration with brain iron accumulation disorders.

关键词： 4-hidroxynonenal ferroptosis iron lipid peroxidation lipofuscin neurodegeneration neurodegeneration with brain iron accumulation oxidative stress PLA2G6-associated neurodegeneration

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Precision medicine in pantothenate kinase-associated neurodegeneration

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Neural Regeneration Research 2019年第7期14卷 1177-1185页

作者： mónica álvarez-Córdoba marina Villanueva-Paz Irene Villalón-García Suleva Povea-Cabello Juan m.Suárez-Rivero marta Talaverón-Rey Javier Abril-Jaramillo Ana Belén Vintimilla-Tosi José A.Sánchez-Alcázar Centro Andaluz de Biología del Desarrollo(CABD-CSIC-Universidad pablo de Olavide) and Centro de Investigación Biomédica en Red:Enfermedades RarasInstituto de Salud Carlos Ⅲ Centro de Neurología Avanzada Centro Civet

Neurodegeneration with brain iron accumulation is a broad term that describes a heterogeneous group of progressive and invalidating neurologic disorders in which iron deposits in certain brain areas,mainly the basal ganglia.The predominant clinical symptoms include spasticity,progressive dystonia,parkinson's disease-like symptoms,neuropsychiatric alterations,and retinal degeneration.Among the neurodegeneration with brain iron accumulation disorders,the most frequent subtype is pantothenate kinase-associated neurodegeneration(PKAN) caused by defects in the gene encoding the enzyme pantothenate kinase 2(PANK2)which catalyzed the first reaction of the coenzyme A biosynthesis pathway.Currently there is no effective treatment to prevent the inexorable course of these disorders.The aim of this review is to open up a discussion on the utility of using cellular models derived from patients as a valuable tool for the development of precision medicine in PKAN.Recently,we have described that dermal fibroblasts obtained from PKAN patients can manifest the main pathological changes of the disease such as intracellular iron accumulation accompanied by large amounts of lipofuscin granules,mitochondrial dysfunction and a pronounced increase of markers of oxidative stress.In addition,PKAN fibroblasts showed a morphological senescence-like phenotype.Interestingly,pantothenate supplementation,the substrate of the PANK2 enzyme,corrected all pathophysiological alterations in responder PKAN fibroblasts with low/residual PANK2 enzyme expression.However,pantothenate treatment had no favourable effect on PKAN fibroblasts harbouring mutations associated with the expression of a truncated/incomplete protein.The correction of pathological alterations by pantothenate in individual mutations was also verified in induced neurons obtained by direct reprograming of PKAN fibroblasts.Our observations indicate that pantothenate supplementation can increase/stabilize the expression levels of PANK2 in specific mutations.Fibroblasts and induced neuron

关键词： neurodegeneration with brain iron accumulation pantothenate kinase-associated neurodegeneration pantothenate kinase 2 pantothenate induced neurons precision medicine induced neuron fibroblast

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帕金森病的LRRK2基因突变

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世界核心医学期刊文摘(神经病学分册) 2006年第1期 41-41页

作者： Farrer m. Stone J. mata I.F. 张殿增 Department of Neuroscience mayo Clinic College of medicine Birdsall Bldg. 4500 San pablo Road Jacksonville FL 32224 United States Dr.

To determine the frequency of LRRK2 mutations in idiopathic parkinson disease (PD), the authors studied 786 PD probands, 32 affected siblings, 1,044 unaffected siblings, and 278 unrelated controls. The authors designed allelic discrimination assays for nine LRRK2 mutations and identified these in six probands with PD, one affected sibling, one unaffected sibling, and one unrelated control. Thus LRRK2 mutations only rarely cause idiopathic PD.

关键词：基因突变 RK 点突变 LRRK2 先证者

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