Entanglement in Three-Atom Tavis-Cummings Model Induced by a Thermal Field

The explicit form of the evolution operator for the three-atom Tavis-Cummings model is given. The atoms can be entangled through their interaction with a thermal field. The degree of entanglement depends on the mean photon number of the thermal field and the initial state of the atoms.

Single-atom entropy squeezing and quantum entanglement in Tavis-Cummings model with atomic motion

We examine the single-atom entropy squeezing and the atom-field entanglement in a system of two moving twolevel atoms interacting with a single-mode coherent field in a lossless resonant cavity. Our numerical calculations indicate that the squeezing period, the squeezing time and the maximM squeezing can be controlled by appropriately choosing the atomic motion and the field-mode structure. The atomic motion leads to a periodical time evolution of entanglement between the two-atom and the field. Moreover, there exists corresponding relation between the time evolution properties of the atomic entropy squeezing and that of the entanglement between the two atoms and the field.

Measurement-induced disturbance between two atoms in Tavis-Cummings model with dipole dipole interaction

Quantum correlation, measured by measurement-induced disturbance （MID）, between two two-level atoms is investi- gated in detail in Tavis-Cummings model with dipole--dipole interaction （DDI）. We find that MID can be determined only by the dipole-dipole interaction between the two atoms when the cavity and atoms are at resonance. Moreover, DDI will have different effects on MID for two different kinds of initial states.

Entanglement of atoms in Tavis-Cummings model

Entanglement is used to measure correlation between separated subsystems, von Neumann entropy is used to study evolutions of entanglement of atoms in processes of interaction between atoms with the field prepared in coherent state. The effects of field intertsity and detuning on entanglement are investigated. It is shown that the entanglement exhibited oscillations in its evolutions, their amplitudes and mean values decrease with increasing field intensity. Oscillation frequencies increase with detuning, but the maximum values are almost independent of detuning.

Dissipative quantum phase transition in a biased Tavis-Cummings model

We study the dissipative quantum phase transition(QPT)in a biased Tavis–Cummings model consisting of an ensemble of two-level systems(TLSs)interacting with a cavity mode,where the TLSs are pumped by a drive field.In our proposal,we use a dissipative TLS ensemble and an active cavity with effective gain.In the weak drive-field limit,the QPT can occur under the combined actions of the loss and gain of the system.Owing to the active cavity,the QPT behavior can be much differentiated even for a finite strength of the drive field on the TLS ensemble.Also,we propose to implement our scheme based on the dissipative nitrogen-vacancy(NV)centers coupled to an active optical cavity made from the gainmedium-doped silica.Furthermore,we show that the QPT can be measured by probing the transmission spectrum of the cavity embedding the ensemble of the NV centers.

Aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders:progress of experimental models based on disease pathogenesis

Neuromyelitis optica spectrum disorders are neuroinflammatory demyelinating disorders that lead to permanent visual loss and motor dysfunction.To date,no effective treatment exists as the exact causative mechanism remains unknown.Therefore,experimental models of neuromyelitis optica spectrum disorders are essential for exploring its pathogenesis and in screening for therapeutic targets.Since most patients with neuromyelitis optica spectrum disorders are seropositive for IgG autoantibodies against aquaporin-4,which is highly expressed on the membrane of astrocyte endfeet,most current experimental models are based on aquaporin-4-IgG that initially targets astrocytes.These experimental models have successfully simulated many pathological features of neuromyelitis optica spectrum disorders,such as aquaporin-4 loss,astrocytopathy,granulocyte and macrophage infiltration,complement activation,demyelination,and neuronal loss;however,they do not fully capture the pathological process of human neuromyelitis optica spectrum disorders.In this review,we summarize the currently known pathogenic mechanisms and the development of associated experimental models in vitro,ex vivo,and in vivo for neuromyelitis optica spectrum disorders,suggest potential pathogenic mechanisms for further investigation,and provide guidance on experimental model choices.In addition,this review summarizes the latest information on pathologies and therapies for neuromyelitis optica spectrum disorders based on experimental models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders,offering further therapeutic targets and a theoretical basis for clinical trials.

Exploiting fly models to investigate rare human neurological disorders

Rare neurological diseases,while individually are rare,collectively impact millions globally,leading to diverse and often severe neurological symptoms.Often attributed to genetic mutations that disrupt protein function or structure,understanding their genetic basis is crucial for accurate diagnosis and targeted therapies.To investigate the underlying pathogenesis of these conditions,researchers often use non-mammalian model organisms,such as Drosophila(fruit flies),which is valued for their genetic manipulability,cost-efficiency,and preservation of genes and biological functions across evolutionary time.Genetic tools available in Drosophila,including CRISPR-Cas9,offer a means to manipulate gene expression,allowing for a deep exploration of the genetic underpinnings of rare neurological diseases.Drosophila boasts a versatile genetic toolkit,rapid generation turnover,and ease of large-scale experimentation,making it an invaluable resource for identifying potential drug candidates.Researchers can expose flies carrying disease-associated mutations to various compounds,rapidly pinpointing promising therapeutic agents for further investigation in mammalian models and,ultimately,clinical trials.In this comprehensive review,we explore rare neurological diseases where fly research has significantly contributed to our understanding of their genetic basis,pathophysiology,and potential therapeutic implications.We discuss rare diseases associated with both neuron-expressed and glial-expressed genes.Specific cases include mutations in CDK19 resulting in epilepsy and developmental delay,mutations in TIAM1 leading to a neurodevelopmental disorder with seizures and language delay,and mutations in IRF2BPL causing seizures,a neurodevelopmental disorder with regression,loss of speech,and abnormal movements.And we explore mutations in EMC1 related to cerebellar atrophy,visual impairment,psychomotor retardation,and gain-of-function mutations in ACOX1 causing Mitchell syndrome.Loss-of-function mutations in ACOX1 result in ACOX1 deficiency,characterized by very-long-chain fatty acid accumulation and glial degeneration.Notably,this review highlights how modeling these diseases in Drosophila has provided valuable insights into their pathophysiology,offering a platform for the rapid identification of potential therapeutic interventions.Rare neurological diseases involve a wide range of expression systems,and sometimes common phenotypes can be found among different genes that cause abnormalities in neurons or glia.Furthermore,mutations within the same gene may result in varying functional outcomes,such as complete loss of function,partial loss of function,or gain-of-function mutations.The phenotypes observed in patients can differ significantly,underscoring the complexity of these conditions.In conclusion,Drosophila represents an indispensable and cost-effective tool for investigating rare neurological diseases.By facilitating the modeling of these conditions,Drosophila contributes to a deeper understanding of their genetic basis,pathophysiology,and potential therapies.This approach accelerates the discovery of promising drug candidates,ultimately benefiting patients affected by these complex and understudied diseases.

A promising approach for quantifying focal stroke modeling and assessing stroke progression:optical resolution photoacoustic microscopy photothrombosis

To investigate the mechanisms underlying the onset and progression of ischemic stroke,some methods have been proposed that can simultaneously monitor and create embolisms in the animal cerebral cortex.However,these methods often require complex systems and the effect of age on cerebral embolism has not been adequately studied,although ischemic stroke is strongly age-related.In this study,we propose an optical-resolution photoacoustic microscopy-based visualized photothrombosis methodology to create and monitor ischemic stroke in mice simultaneously using a 532 nm pulsed laser.We observed the molding process in mice of different ages and presented age-dependent vascular embolism differentiation.Moreover,we integrated optical coherence tomography angiography to investigate age-associated trends in cerebrovascular variability following a stroke.Our imaging data and quantitative analyses underscore the differential cerebrovascular responses to stroke in mice of different ages,thereby highlighting the technique's potential for evaluating cerebrovascular health and unraveling age-related mechanisms involved in ischemic strokes.

Reduced mesencephalic astrocyte-derived neurotrophic factor expression by mutant androgen receptor contributes to neurodegeneration in a model of spinal and bulbar muscular atrophy pathology

Spinal and bulbar muscular atrophy is a neurodegenerative disease caused by extended CAG trinucleotide repeats in the androgen receptor gene,which encodes a ligand-dependent transcription facto r.The mutant androgen receptor protein,characterized by polyglutamine expansion,is prone to misfolding and forms aggregates in both the nucleus and cytoplasm in the brain in spinal and bulbar muscular atrophy patients.These aggregates alter protein-protein interactions and compromise transcriptional activity.In this study,we reported that in both cultured N2a cells and mouse brain,mutant androgen receptor with polyglutamine expansion causes reduced expression of mesencephalic astrocyte-de rived neurotrophic factor.Overexpressio n of mesencephalic astrocyte-derived neurotrophic factor amelio rated the neurotoxicity of mutant androgen receptor through the inhibition of mutant androgen receptor aggregation.Conversely.knocking down endogenous mesencephalic astrocyte-derived neurotrophic factor in the mouse brain exacerbated neuronal damage and mutant androgen receptor aggregation.Our findings suggest that inhibition of mesencephalic astrocyte-derived neurotrophic factor expression by mutant androgen receptor is a potential mechanism underlying neurodegeneration in spinal and bulbar muscular atrophy.

Tavis-Cummings模型中两原子纠缠的时间演化

基于两个子系统的复合体系的纠缠度可以用复合体系密度矩阵的部分转置矩阵负本征值来定义的特性,利用数值模拟方法研究了与单模粒子数场进行相互作用的Tavis-Cummings模型中两原子的纠缠的时间演化．当考虑两原子初始处于混态时,结果表明,粒子数场的初始态、两原子的初始态以及两原子与粒子数光场的耦合常数的大小都对两个原子间纠缠度的时间演化特性有着显著的影响．

Tavis-Cummings模型中原子信息熵压缩的演化特性

本文研究了Tavis-Cummings模型中,在共振时的原子信息熵压缩随时间的演化特性。在初始为相干光场和两原子分别为各种相干叠加态时,精确求解了二原子信息熵的各压缩分量,数值计算表明:该体系中原子信息熵的压缩将随二原子所处的初始状态、光场的强度、原子间及原子与场间的耦合系数的变化而变化.

双光子Tavis-Cummings模型中的量子纠缠

我们对两个全同二能级原子通过双光子跃迁与单模辐射场发生相互作用的Tavis-Cummings(T-C)模型中的量子纠缠特性进行了研究.通过数值计算与分析,结果表明:双光子T-C模型的量子纠缠比单光子T-C模型的量子纠缠要保持得好一些;另外分析了双光子T-C模型中原子间偶极-偶极相互作用强度系数、原子与场的耦合系数、光子数对两原子间纠缠特性与场熵的影响.

多模简并多光子Tavis-Cummings模型中的量子纠缠特性(英文)

利用冯·纽曼约化熵理论研究了多模相干态光场与两等同二能级原子简并多光子相互作用系统量子纠缠演化特性,得到了多模光场量子纠缠的解析表达式,并给出了双模光场与两原子相互作用时量子纠缠的数值计算结果.结果表明:量子纠缠随着光子简并度的增大而增强;随着初始平均光子数的增加,量子纠缠演化的周期性变得越来越明显;当场与原子远离共振时,量子纠缠随着频率失谐量的增大而减弱;当失谐量足够大时,场与原子几乎总是处于纠缠状态.这些结论对于纠缠态或纯态的制备及获取光学系统中的量子信息研究中有一定参考价值.

Stark位移对两全同原子Tavis-Cummings模型中的原子纠缠的影响

通过研究两全同原子初始处于最大纠缠态,光场处于单模时的原子纠缠动力学及Tavis-Cummings模型(T-C模型),分析了在T-C模型全同原子系统的Hamilton量中加入Stark位移时对原子纠缠的退相干时间的影响.结果表明:不考虑Stark位移时两原子在系统演化过程中周期性地出现退纠缠现象;考虑Stark位移时,两全同原子长时间地纠缠.

Tavis-Cummings模型中的量子态平均保真度

运用全量子理论,研究了Tavis-Cummings模型中量子态平均保真度的演化特性,对原子和光场的初态以及两原子的关联程度对平均保真度的影响进行了研究.结果表明,原子、光场和系统的平均保真度依赖于初态时2个原子处在基态的几率以及光场处于真空态的几率;初态两原子在基态无关联,光场处于真空态,体系不失真.

Tavis-Cummings模型中Stark移位对三体纠缠量的影响(英文)

Tavis-Cummings模型中,我们通过考虑原子的碰撞引起的Stark移位来研究系统的纠缠量的变化,结果发现纠缠量受Stark移位影响很大。

非线性Tavis-Cummings模型压缩光场的Pancharatnam相位特性

研究了存在非线性Kerr介质时耦合双原子与单模压缩真空场相互作用系统的Pancharatnam相位特性、选取合适的初始条件并运用旋波近似,通过解薛定谔方程求出Pancharatnam相位的表示形式,并对此相位进行数值分析、结果表明:耦合双原子处于任意初态,随着原子与光场相互作用强度、两个二能级原子偶极-偶极耦合强度和非线性Kerr介质非线性的增大,Pancharatnam相位演化的频率都显著增长、耦合双原子初态同处激发态时,Pancharatnam相位演化有明显的振荡上升(或振荡下降)趋势、耦合双原子初态只有一个处于激发态时,随着Kerr介质非线性作用的增强,Pancharatnam相位演化变混乱、

非简并双光子Tavis-Cummings模型中的纠缠演化

研究了2对非相互作用、空间分离的原子在双模腔场作用下的三体和两体纠缠动力学行为。对非简并双光子Tavis-Cummings模型进行了研究,通过数值计算分析了纠缠初始状态、原子与腔场以及光纤模与腔场的耦合强度对纠缠的影响.结果表明:纠缠初始状态对原子间的纠缠有显著影响;较大的场和光纤模的耦合强度可以实现原子与原子间最大纠缠的转移;较大的原子与腔场耦合强度有助于两原子与腔场构成三体纠缠。

高斯型耦合Tavis-Cummings模型中原子的熵压缩

利用全量子理论研究了高斯型耦合Tavis-Cummings模型中一个原子的熵压缩,运用数值计算方法讨论了原子垂直于腔轴的运动速度、光场强度以及两原子的初态对单个原子熵压缩的影响.结果表明,原子的熵压缩时间由原子的运动速度决定,压缩程度由光场强度决定,压缩时间和压缩程度还决定于原子的初始状态.