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Synthesis and luminescence characteristics of terbium(Ⅲ) activated NaSrBO_3

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Journal of Rare Earths 2012年第9期30卷 856-859页

作者： p.a. Nagpure S.K. Omanwar Department of physics SGB Amravati University Amravati-444602 (M.S.) India

The thermoluminescence （TL） and photohmainescence （pL） properties of the phosphor NaSrBO3：Tb3＋ were reported and discussed. The combustion technique was used for the synthesis of polycrystalline samples of NaSrBO3：Th3＋. The TL glow curve of the compound had a simple structure with a single p.a. at 434 K. TL sensitivity of the phosphor was found to be more than that of （LiF：Mg,Cu,p）. The TL glow curve was studied as a function of concentration of dopant and dose of gamma ray irradiation. The kinetic parameters of the thermolumines- cence of NaSrBO3： Tb3＋were calculated employing the p.a. shape method. The photoluminescence （pL） properties of Tb3＋ doped in NaS- rBO3 were studied over the 200-400 nm excitation range. The excitation spectra of NaSrBO3：Tb3＋ consisted of single narrow band p.a.ing at about 236 nm. The emission spectra monitored at 236 nm excitation consisted of a series of sharp lines p.a.ing at 489, 544, 586 and 622 nm corresponding to the 5D4→7Fj （j=3,4,5,6） transitions within the 4f8 configurations of Tb3＋.

关键词： thermoluminescence photoluminescence terbium NaSrBO3 combustion synthesis rare earths

Unlocking hypoglycemia–associated brain microvascular dysfunction:critical insights from proteomic analysis

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Neural Regeneration Research 2025年第6期20卷 1707-1708页

作者： Siva S.V.p.Sakamuri Anil Sakamuri Department of Chemistry Auburn University at MontgomeryMontgomeryALUSA Vascular Biology Center and Department of Medicine Medical College of Georgia at Augusta UniversityAugustaGAUSA

Hypoglycemia-a critical complication linked to worsened brain function in diabetic subjects:Hypoglycemia is characterized by a decline in circulatory glucose levels below sta nda rd physiological *** hypoglycemia,classified as level 1 hypoglycemia,is defined by blood glucose levels below 70 mg/dL and can be effectively addressed through carbohydrate *** hypoglycemia,denoted by blood glucose levels less than 54 mg/dL,poses a life-threatening risk if left *** with type 1 and type 2 diabetes undergoing insulin treatment are particularly susceptible to hypoglycemia due to impaired counterregulatory mechanisms.

关键词： impaired intake critical

Small molecule inhibitor DDQ-treated hippocampal neuronal cells show improved neurite outgrowth and synaptic branching

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Neural Regeneration Research 2025年第9期20卷 2624-2632页

作者： Jangampalli Adi p.a.eepkiran priyanka Rawat Arubala p.Reddy Erika Orlov pHemachandra Reddy Department of Internal Medicine Texas Tech University Health Sciences CenterLubbockTXUSA Department of Nutritional Sciences College of Human SciencesTexas Tech UniversityLubbockTXUSA Department of p.a.macology&Neuroscience Texas Tech University Health Sciences CenterLubbockTXUSA Department of Neurology Texas Tech University Health Sciences CenterLubbockTXUSA Department of Speech Language and Hearing SciencesTexas Tech University Health Sciences CenterLubbockTXUSA Department of public Health Texas Tech University Health Sciences CenterLubbockTXUSA

The process of neurite outgrowth and branching is a crucial aspect of neuronal development and *** and dendrites,sometimes referred to as neurites,are extensions of a neuron's cellular body that are used to start *** we explored the effects of diethyl(3,4-dihydroxyphenethylamino)(quinolin-4-yl)methylphosphonate(DDQ)on neurite developmental features in HT22 neuronal *** this work,we examined the protective effects of DDQ on neuronal processes and synaptic outgrowth in differentiated HT22cells expressing mutant Tau(mTau)*** investigate DDQ chara cteristics,cell viability,biochemical,molecular,western blotting,and immunocytochemistry were *** outgrowth is evaluated through the segmentation and measurement of neural *** neural processes can be seen and measured with a fluorescence microscope by manually tracing and measuring the length of the neurite *** neuronal processes can be observed and quantified with a fluorescent microscope by manually tracing and measuring the length of the neuronal ***-treated mTau-HT22 cells(HT22 cells transfected with cDNA mutant Tau)were seen to disp.a. increased levels of synaptophysin,MAp-2,andβ-***,we confirmed and noted reduced levels of both total and p-Tau,as well as elevated levels of microtubule-associated protein 2,β-tubulin,synaptophysin,vesicular acetylcholine transporter,and the mitochondrial biogenesis protein-pe roxisome prolife rator-activated receptor-gamma coactivator-1α.In mTa u-expressed HT22 neurons,we observed DDQ enhanced the neurite characteristics and improved neurite development through increased synaptic *** findings conclude that mTa u-HT22(Alzheimer's disease)cells treated with DDQ have functional neurite developmental chara *** key finding is that,in mTa u-HT22 cells,DDQ preserves neuronal structure and may even enhance nerve development function with mTa u inhibition.

关键词： diethyl(3 4-dihydroxyphenethylamino)(quinolin-4-yl)methylphosphonate(DDQ) hippocampal neuronal cells HT22 neurite outgrowth neuronal development small molecule

NUMERICAL SOLUTION OF THE SCATTERING pROBLEM FOR ACOUSTIC WAVES BY A TWO-SIDED CRACK IN 2-DIMENSIONAL SpACE

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Journal of Computational Mathematics 2011年第2期29卷 141-166页

作者： Jijun Liu p.a. Krutitskii M. Sini Department of Mathematics Southeast University Nanjing 210096 China Keldysh Institute of Applied Mathematics Moscow 125047 Russia Johann Radon Institute for Computational and Applied Mathematics Austrian Academy of Sciences Linz A~40-40 Austria

The wave scattering problem by a crack F in R2 with impedance type boundary is considered. This problem models the diffraction of waves by thin two-sided cylindrical screens. A numerical method for solving the problem is developed. The solution of the problem is represented in the form of the combined angular potential and single-layer potential. The linear integral equations satisfied by the density functions are derived for general parameterized arcs. The weakly singular integrals and the Cauchy singular integral arising in these equations are computed using a highly accurate scheme with a truncation error analysis. The advantage of the scheme proposed in this paper is, in one hand, the fact that we do not need the analyticity property of the crack and we allow different complex valued surface impedances in both sides of the crack. In the other hand, we avoid the hyper-singular integrals. Numerical implementations showing the validity of the scheme are presented.

关键词： Wave scattering Impedance boundary Integral equations Singularity analysis,Numerics.

Adding new dimension to non-directed C（sp3）–H functionalizations

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Science China Chemistry 2025年

作者： Konstantin p.Bryliakov Laboratory of Selective Oxidation Catalysis N.D.Zelinsky Institute of Organic Chemistry RAS

Alip.a.ic C–H groups are among the most abundant yet least reactive functional groups in organic molecules. Nature has evolved metalloenzymes such as those of the cytochrome p450 superfamily that efficiently activate individual tertiary（3） and secondary （2） C（sp3）–H bonds in complex molecules with the highest level of regio-and stereoselectivity [1], thus encouraging studies aimed at engineering artificial metalloenzymes for synthetic applications [2].

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From single to combinatorial therapies in spinal cord injuries for structural and functional restoration

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Neural Regeneration Research 2025年第3期20卷 660-670页

作者： Ernesto Doncel-pérez Gabriel Guízar-Sahagún Israel Grijalva-Otero Hospital Nacional de parapléjicos de Toledo Servicio de Salud de Castilla La Mancha(SESCAM)ToledoSpain Medical Research Unit for Neurological Diseases UMAE Hospital de EspecialidadesCentro Médico Nacional Siglo XXIIMSSCiudad de MéxicoMéxico

Spinal cord injury results in paralysis, sensory disturbances, sphincter dysfunction, and multiple systemic secondary conditions, most arising from autonomic dysregulation. All this produces profound negative psychosocial implications for affected people, their families, and their communities;the financial costs can be challenging for their families and health institutions. Treatments aimed at restoring the spinal cord after spinal cord injury, which have been tested in animal models or clinical trials, generally seek to counteract one or more of the secondary mechanisms of injury to limit the extent of the initial damage. Most published works on structural/functional restoration in acute and chronic spinal cord injury stages use a single type of treatment: a drug or trophic factor, transp.a.t of a cell type, and imp.a.tation of a biomaterial. Despite the significant benefits reported in animal models, when translating these successful therapeutic strategies to humans, the result in clinical trials has been considered of little relevance because the improvement, when present, is usually insufficient. Until now, most studies designed to promote neuroprotection or regeneration at different stages after spinal cord injury have used single treatments. Considering the occurrence of various secondary mechanisms of injury in the acute and sub-acute p.a.es of spinal cord injury, it is reasonable to speculate that more than one therapeutic agent could be required to promote structural and functional restoration of the damaged spinal cord. Treatments that combine several therapeutic agents, targeting different mechanisms of injury, which, when used as a single therapy, have shown some benefits, allow us to assume that they will have synergistic beneficial effects. Thus, this narrative review article aims to summarize current trends in the use of strategies that combine therapeutic agents administered simultaneously or sequentially, seeking structural and functional restoratio

关键词： neural regeneration neuroprotection spinal cord injury repair spinal cord injury treatments structural restoration of spinal cord injury

Spastin and alsin protein interactome analyses begin to reveal key canonical pathways and suggest novel druggable targets

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Neural Regeneration Research 2025年第3期20卷 725-739页

作者： Benjamin R.Helmold Angela Ahrens Zachary Fitzgerald p.Hande Ozdinler Department of Neurology Feinberg School of MedicineNorthwestern UniversityChicagoILUSA Center for Molecular Innovation and Drug Discovery Center for Developmental TherapeuticsChemistry of Life Processes InstituteNorthwestern UniversityEvanstonILUSA Mesulam Center for Cognitive Neurology and Alzheimer’s Disease Feinberg School of MedicineNorthwestern UniversityChicagoILUSA Feinberg School of Medicine Les Turner ALS Center at Northwestern UniversityChicagoILUSA

Developing effective and long-term treatment strategies for rare and complex neurodegenerative diseases is challenging. One of the major roadblocks is the extensive heterogeneity among patients. This hinders understanding the underlying disease-causing mechanisms and building solutions that have implications for a broad spectrum of patients. One potential solution is to develop personalized medicine approaches based on strategies that target the most prevalent cellular events that are perturbed in patients. Especially in patients with a known genetic mutation, it may be possible to understand how these mutations contribute to problems that lead to neurodegeneration. protein–protein interaction analyses offer great advantages for revealing how proteins interact, which cellular events are primarily involved in these interactions, and how they become affected when key genes are mutated in patients. This line of investigation also suggests novel druggable targets for patients with different mutations. Here, we focus on alsin and spastin, two proteins that are identified as “causative” for amyotrophic lateral sclerosis and hereditary spastic paraplegia, respectively, when mutated. Our review analyzes the protein interactome for alsin and spastin, the canonical pathways that are primarily important for each protein domain, as well as compounds that are either Food and Drug Administration–approved or are in active clinical trials concerning the affected cellular pathways. This line of research begins to pave the way for personalized medicine approaches that are desperately needed for rare neurodegenerative diseases that are complex and heterogeneous.

关键词： ALS2 alsin amyotrophic lateral sclerosis hereditary spastic paraplegia neurodegenerative diseases personalized medicine precision medicine protein interactome protein-protein interactions SpAST spastin

peptides radiolabeled with Re-186/188 and Tc-99m as potential diagnostic and therapeutic agents

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Nuclear Science and Techniques 2007年第2期18卷 88-100页

作者： E. GARCíA-GARAYOA R. SCHIBLI p.a. SCHUBIGER Center for Radiop.a.maceutical Science of the ETH Zurich-paul Scherrer Institut-University Hospital Zurich CH-5232 Villigen PSI Switzerland Center for Radiop.a.maceutical Science of the ETH Zurich-paul Scherrer Institut-University Hospital Zurich CH-5232 Villigen PSI Switzerland Department of Chemistry and Applied Biosciences ETH Zurich 8093 Zurich Switzerland

Small peptide-based compounds have attracted an enormous interest as carrier molecules to selectively de- liver radionuclides to target tissues, sparing critical normal organs. When looking for "matched pairs" of radionuclides, suitable for radiolabeling of peptides for diagnosis and therapy, technetium and rhenium represent an almost ideal constellation. The important role of technetium-99m and Re-186/188 is based on the decay characteristics, suitable for tumor diagnosis and therapy. Tc-99m and Re-188 are readily available by either a 99Mo/99mTc or the 188W/188Re ra- dionuclide generator system. Furthermore, technetium and rhenium are chemically related and share structural as well as reactive similarities, which prompt an attractive "matched-pair" situation. This article shows an overview of 99mTc- and 186/188Re-radiolabeled peptides that have been tested for their potential use as imaging and therapeutic agents in oncological diseases.

关键词：放射性同位素标记肽类铼186/188 锝99m 诊断药物治疗药物

Impacts of pI3K/protein kinase B pathway activation in reactive astrocytes: from detrimental effects to protective functions

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Neural Regeneration Research 2025年第4期20卷 1031-1041页

作者： Ramón pérez-Núñez María Fernanda González Ana María Avalos Lisette Leyton Cellular Communication Laboratory Programa de Biología Celular y MolecularCenter for Studies on ExerciseMetabolism and Cancer(CEMC)Instituto de Ciencias Biomédicas(ICBM)Facultad de MedicinaUniversidad de ChileSantiagoChile Advanced Center for Chronic Diseases(ACCDiS) Faculty of Chemical and Pharmaceutical Sciences&Faculty of MedicineUniversidad de ChileSantiagoChile Instituto de Ciencias Biomédicas Facultad de Ciencias de la SaludUniversidad Autónoma de ChileSantiagoChile

Astrocytes are the most abundant type of glial cell in the central nervous *** injury and inflammation,astrocytes become reactive and undergo morphological and functional *** on their phenotypic classification as A1 or A2,reactive astrocytes contribute to both neurotoxic and neuroprotective responses,***,this binary classification does not fully capture the diversity of astrocyte responses observed across different diseases and *** analysis has revealed that reactive astrocytes have a complex landscape of gene expression profiles,which emp.a.izes the heterogeneous nature of their *** actively participate in regulating central nervous system inflammation by interacting with microglia and other cell types,releasing cytokines,and influencing the immune *** phosphoinositide 3-kinase(pI3K)/protein kinase B(AKT)signaling pathway is a central p.a.er in astrocyte reactivity and impacts various aspects of astrocyte behavior,as evidenced by in silico,in vitro,and in vivo *** astrocytes,inflammatory cues trigger a cascade of molecular events,where nuclear factor-κB serves as a central mediator of the pro-inflammatory ***,we review the heterogeneity of reactive astrocytes and the molecular mechanisms underlying their *** highlight the involvement of various signaling pathways that regulate astrocyte reactivity,including the pI3K/AKT/mammalian target of rapamycin(mTOR),αvβ3 integrin/pI3K/AKT/connexin 43,and Notch/pI3K/AKT *** targeting the inactivation of the pI3K/AKT cellular signaling pathway to control reactive astrocytes and prevent central nervous system damage,evidence suggests that activating this pathway could also yield beneficial *** dual function of the pI3K/AKT pathway underscores its complexity in astrocyte reactivity and brain function *** review emp.a.izes the importance of employing astrocyte-exclusive models to underst

关键词： inflammation integrins neuroprotective neurotoxic phosp.a.idylinositol 3-kinase reactive astrocytes signal transduction Thy-1(CD90)