AAV mediated carboxyl terminus of Hsp70 interacting protein overexpression mitigates the cognitive and pathological phenotypes of APP/PS1 mice

The E3 ubiquitin ligase,carboxyl terminus of heat shock protein 70(Hsp70)interacting protein(CHIP),also functions as a co-chaperone and plays a crucial role in the protein quality control system.In this study,we aimed to investigate the neuroprotective effect of overexpressed CHIP on Alzheimer’s disease.We used an adeno-associated virus vector that can cross the blood-brain barrier to mediate CHIP overexpression in APP/PS1 mouse brain.CHIP overexpression significantly ameliorated the performance of APP/PS1 mice in the Morris water maze and nest building tests,reduced amyloid-βplaques,and decreased the expression of both amyloid-βand phosphorylated tau.CHIP also alleviated the concentration of microglia and astrocytes around plaques.In APP/PS1 mice of a younger age,CHIP overexpression promoted an increase in ADAM10 expression and inhibitedβ-site APP cleaving enzyme 1,insulin degrading enzyme,and neprilysin expression.Levels of HSP70 and HSP40,which have functional relevance to CHIP,were also increased.Single nuclei transcriptome sequencing in the hippocampus of CHIP overexpressed mice showed that the lysosomal pathway and oligodendrocyte-related biological processes were up-regulated,which may also reflect a potential mechanism for the neuroprotective effect of CHIP.Our research shows that CHIP effectively reduces the behavior and pathological manifestations of APP/PS1 mice.Indeed,overexpression of CHIP could be a beneficial approach for the treatment of Alzheimer’s disease.

Dynamics of Non-Markovianity, Quantum Correlations and Information Scrambling of Three Qubits Systems Interacting via Rashba Interaction

The behavior of the quantum correlations, information scrambling and the non-Markovianity of three entangling qubits systems via Rashba is discussed. The results showed that, the three physical quantities oscillate between their upper and lower bounds, where the number of oscillations increases as the Rashba interaction strength increases. The exchanging rate of these three quantities depends on the Rashba strength, and whether the entangled state is generated via direct/indirect interaction. Moreover, the coherence parameter can be used as a control parameter to maximize or minimize the three physical quantities.

Interacting topological magnons in a checkerboard ferromagnet

This work is devoted to studying the magnon-magnon interaction effect in a two-dimensional checkerboard ferromagnet with the Dzyaloshinskii-Moriya interaction.Using a first-order Green function method,we analyze the influence of magnon-magnon interaction on the magnon band topology.We find that Chern numbers of two renormalized magnon bands are different above and below the critical temperature,which means that the magnon band gap-closing phenomenon is an indicator for one topological phase transition of the checkerboard ferromagnet.Our results show that the checkerboard ferromagnet possesses two topological phases,and its topological phase can be controlled either via the temperature or the applied magnetic field due to magnon-magnon interactions.Interestingly,it is found that the topological phase transition can occur twice with the increase in the temperature,which is different from the results of the honeycomb ferromagnet.

A new interacting capillary bundle model on the multiphase flow in micropores of tight rocks

Surfactants are widely used in the fracturing fluid to enhance the imbibition and thus the oil recovery rate. However, current numerical models cannot capture the physics behind capillary imbibition during the wettability alteration by surfactants. Although the interacting capillary bundle(ICB) model shows potential in characterizing imbibition rates in different pores during wettability alteration, the existing ICB models neglect the influence of wettability and viscosity ratio on the imbibition behavior, making it difficult to accurately describe the oil-water imbibition behavior within the porous media. In this work,a new ICB mathematical model is established by introducing pressure balance without assuming the position of the leading front to comprehensively describe the imbibition behavior in a porous medium under different conditions, including gas-liquid spontaneous imbibition and oil-water imbibition.When the pore size distribution of a tight rock is known, this new model can predict the changes of water saturation during the displacement process in the tight rock, and also determine the imbibition rate in pores of different sizes. The water saturation profiles obtained from the new model are validated against the waterflooding simulation results from the CMG, while the imbibition rates calculated by the model are validated against the experimental observations of gas-liquid spontaneous imbibition. The good match above indicates the newly proposed model can show the water saturation profile at a macroscopic scale while capture the underlying physics of the multiphase flow in a porous medium at a microscopic scale. Simulation results obtained from this model indicate that both wettability and viscosity ratio can affect the sequence of fluid imbibition into pores of different sizes during the multiphase flow, where less-viscous wetting fluid is preferentially imbibed into larger pores while more-viscous wetting fluid tends to be imbibed into smaller pores. Furthermore, this model provides an avenue to calculate the imbibition rate in pores of different sizes during wettability alteration and capture the non-Darcy effect in micro-and nano-scale pores.

Generation and regulation of electromagnetic pulses generated by femtosecond lasers interacting with multitargets

Ultrashort and powerful laser interactions with a target generate intense wideband electromagnetic pulses(EMPs).In this study,we report EMPs generated by the interactions between petawatt(30 fs,1.4×10^(20) W/cm^(2))femtosecond(fs)lasers with metal flat,plastic flat,and plastic nanowire-array(NWA)targets.Detailed analyses are conducted on the EMPs in terms of their spatial distribution,time and frequency domains,radiation energy,and protection.The results indicate that EMPs from metal targets exhibit larger amplitudes at varying angles than those generated by other types of targets and are enhanced significantly for NWA targets.Using a plastic target holder and increasing the laser focal spot can significantly decrease the radiation energy of the EMPs.Moreover,the composite shielding materials indicate an effective shielding effect against EMPs.The simulation results show that the NWA targets exert a collimating effect on thermal electrons,which directly affects the distribution of EMPs.This study provides guidance for regulating EMPs by controlling the laser focal spot,target parameters,and target rod material and is beneficial for electromagnetic-shielding design.

The DUF579 proteins GhIRX15s regulate cotton fiber development by interacting with proteins involved in xylan synthesis

Cotton provides the most abundant natural fiber for the textile industry.The mature cotton fiber largely consists of secondary cell walls with the highest proportion of cellulose and a small amount of hemicellulose and lignin.To dissect the roles of hemicellulosic polysaccharides during fiber development,four IRREGULAR XYLEM 15(IRX15)genes,GhIRX15-1/-2/-3/-4,were functionally characterized in cotton.These genes encode DUF579 domain-containing proteins,which are homologs of AtIRX15 involved in xylan biosynthesis.The four GhIRX15 genes were predominantly expressed during fiber secondary wall thickening,and the encoded proteins were localized to the Golgi apparatus.Each GhIRX15 gene could restore the xylan deficient phenotype in the Arabidopsis irx15irx15l double mutant.Silencing of GhIRX15s in cotton resulted in shorter mature fibers with a thinner cell wall and reduced cellulose content as compared to the wild type.Intriguingly,GhIRX15-2 and GhIRX15-4 formed homodimers and heterodimers.In addition,the GhIRX15s showed physical interaction with glycosyltransferases GhGT43C,GhGT47A and GhGT47B,which are responsible for synthesis of the xylan backbone and reducing end sequence.Moreover,the GhIRX15s can form heterocomplexes with enzymes involved in xylan modification and side chain synthesis,such as GhGUX1/2,GhGXM1/2 and GhTBL1.These findings suggest that GhIRX15s participate in fiber xylan biosynthesis and modulate fiber development via forming large multiprotein complexes.

Studies on the temporal,structural,and interacting features of the clubroot resistance gene Rcr1 using CRISPR/Cas9-based systems

Clubroot disease is a severe threat to Brassica crops globally,particularly in western Canada.Genetic resistance,achieved through pyramiding clubroot resistance(CR)genes with different modes of action,is the most important strategy for managing the disease.However,studies on the CR gene functions are quite limited.In this study,we have conducted investigations into the temporal,structural,and interacting features of a newly cloned CR gene,Rcr1,using CRISPR/Cas9 technology.For temporal functionality,we developed a novel CRISPR/Cas9-based binary vector,pHHIGR-Hsp18.2,to deliver Rcr1 into a susceptible canola line(DH12075)and observed that early expression of Rcr1 is critical for conferring resistance.For structural functionality,several independent mutations in specific domains of Rcr1 resulted in loss-offunction,highlighting their importance for CR phenotype.In the study of the interacting features of Rcr1,a cysteine protease gene and its homologous allele in canola were successfully disrupted via CRISPR/Cas9 as an interacting component with Rcr1 protein,resulting in the conversion from clubroot resistant to susceptible in plants carrying intact Rcr1.These results indicated an indispensable role of these two cysteine proteases in Rcr1-mediated resistance response.This study,the first of its kind,provides valuable insights into the functionality of Rcr1.Further,the new vector p HHIGR-Hsp18.2 demonstrated an inducible feature on the removal of add-on traits,which should be useful for functional genomics and other similar research in brassica crops.

Potential regulatory mechanism and clinical significance of synaptotagmin binding cytoplasmic RNA interacting protein in colorectal cancer

BACKGROUND Colorectal cancer(CRC)causes many deaths worldwide.Synaptotagmin binding cytoplasmic RNA interacting protein(SYNCRIP)is an RNA-binding protein that plays an important role in multiple cancers by epigenetically targeting some genes.Our study will examine the expression,potential effect,biological function and clinical value of SYNCRIP in CRC.AIM To examine the expression,potential effect,biological function and clinical value METHODS The expression of SYNCRIP was examined by immunohistochemistry arrays and high-throughput data.The effect of SYNCRIP gene in CRC cell growth was evaluated by CRISPR-Cas9 technology.The target genes of SYNCRIP were calculated using various algorithms,and the molecular mechanism of SYNCRIP in CRC was explored by mutation analysis and pathway analysis.The clinical value of SYNCRIP in prognosis and radiotherapy was revealed via evidence-based medicine methods.RESULTS The protein and mRNA levels of SYNCRIP were both highly expressed in CRC samples compared to nontumorous tissue based on 330 immunohistochemistry arrays and 3640 CRC samples.Cells grew more slowly in eleven CRC cell lines after knocking out the SYNCRIP gene.SYNCRIP could epigenetically target genes to promote the occurrence and development of CRC by boosting the cell cycle and affecting the tumor microenvironment.In addition,CRC patients with high SYNCRIP expression are more sensitive to radiotherapy.CONCLUSION SYNCRIP is upregulated in CRC,and highly expressed SYNCRIP can accelerate CRC cell division by exerting its epigenetic regulatory effects.In addition,SYNCRIP is expected to become a potential biomarker to predict the effect of radiotherapy.

RETRACTED: Nuclear Structure Study of Odd-Odd Yttrium Nuclei within Interacting-Boson Fermi-Fermion Model (IBFFM)

Short Retraction NoticeThe paper does not meet the standards of "Journal of Applied Mathematics and Physics". This article has been retracted to straighten the academic record. In making this decision the Editorial Board follows COPE's Retraction Guidelines. The aim is to promote the circulation of scientific research by offering an ideal research publication platform with due consideration of internationally accepted standards on publication ethics. The Editorial Board would like to extend its sincere apologies for any inconvenience this retraction may have caused.Editor guiding this retraction: Prof. Wen-Xiu Ma (EiC of JAMP)The full retraction notice in PDF is preceding the original paper, which is marked "RETRACTED".

Tailoring Light–Matter Interactions in Overcoupled Resonator for Biomolecule Recognition and Detection

Plasmonic nanoantennas provide unique opportunities for precise control of light–matter coupling in surface-enhanced infrared absorption(SEIRA)spectroscopy,but most of the resonant systems realized so far suffer from the obstacles of low sensitivity,narrow bandwidth,and asymmetric Fano resonance perturbations.Here,we demonstrated an overcoupled resonator with a high plasmon-molecule coupling coefficient(μ)(OC-Hμresonator)by precisely controlling the radiation loss channel,the resonator-oscillator coupling channel,and the frequency detuning channel.We observed a strong dependence of the sensing performance on the coupling state,and demonstrated that OC-Hμresonator has excellent sensing properties of ultra-sensitive(7.25%nm^(−1)),ultra-broadband(3–10μm),and immune asymmetric Fano lineshapes.These characteristics represent a breakthrough in SEIRA technology and lay the foundation for specific recognition of biomolecules,trace detection,and protein secondary structure analysis using a single array(array size is 100×100μm^(2)).In addition,with the assistance of machine learning,mixture classification,concentration prediction and spectral reconstruction were achieved with the highest accuracy of 100%.Finally,we demonstrated the potential of OC-Hμresonator for SARS-CoV-2 detection.These findings will promote the wider application of SEIRA technology,while providing new ideas for other enhanced spectroscopy technologies,quantum photonics and studying light–matter interactions.

Catalyst–Support Interaction in Polyaniline‑Supported Ni_(3)Fe Oxide to Boost Oxygen Evolution Activities for Rechargeable Zn‑Air Batteries

Catalyst–support interaction plays a crucial role in improving the catalytic activity of oxygen evolution reaction(OER).Here we modulate the catalyst–support interaction in polyaniline-supported Ni_(3)Fe oxide(Ni_(3)Fe oxide/PANI)with a robust hetero-interface,which significantly improves oxygen evolution activities with an overpotential of 270 mV at 10 mA cm^(-2)and specific activity of 2.08 mA cm_(ECSA)^(-2)at overpotential of 300 mV,3.84-fold that of Ni_(3)Fe oxide.It is revealed that the catalyst–support interaction between Ni_(3)Fe oxide and PANI support enhances the Ni–O covalency via the interfacial Ni–N bond,thus promoting the charge and mass transfer on Ni_(3)Fe oxide.Considering the excellent activity and stability,rechargeable Zn-air batteries with optimum Ni_(3)Fe oxide/PANI are assembled,delivering a low charge voltage of 1.95 V to cycle for 400 h at 10 mA cm^(-2).The regulation of the effect of catalyst–support interaction on catalytic activity provides new possibilities for the future design of highly efficient OER catalysts.

T cell interactions with microglia in immune-inflammatory processes of ischemic stroke

The primary mechanism of secondary injury after cerebral ischemia may be the brain inflammation that emerges after an ischemic stroke,which promotes neuronal death and inhibits nerve tissue regeneration.As the first immune cells to be activated after an ischemic stroke,microglia play an important immunomodulatory role in the progression of the condition.After an ischemic stroke,peripheral blood immune cells(mainly T cells)are recruited to the central nervous system by chemokines secreted by immune cells in the brain,where they interact with central nervous system cells(mainly microglia)to trigger a secondary neuroimmune response.This review summarizes the interactions between T cells and microglia in the immune-inflammatory processes of ischemic stroke.We found that,during ischemic stroke,T cells and microglia demonstrate a more pronounced synergistic effect.Th1,Th17,and M1 microglia can co-secrete proinflammatory factors,such as interferon-γ,tumor necrosis factor-α,and interleukin-1β,to promote neuroinflammation and exacerbate brain injury.Th2,Treg,and M2 microglia jointly secrete anti-inflammatory factors,such as interleukin-4,interleukin-10,and transforming growth factor-β,to inhibit the progression of neuroinflammation,as well as growth factors such as brain-derived neurotrophic factor to promote nerve regeneration and repair brain injury.Immune interactions between microglia and T cells influence the direction of the subsequent neuroinflammation,which in turn determines the prognosis of ischemic stroke patients.Clinical trials have been conducted on the ways to modulate the interactions between T cells and microglia toward anti-inflammatory communication using the immunosuppressant fingolimod or overdosing with Treg cells to promote neural tissue repair and reduce the damage caused by ischemic stroke.However,such studies have been relatively infrequent,and clinical experience is still insufficient.In summary,in ischemic stroke,T cell subsets and activated microglia act synergistically to regulate inflammatory progression,mainly by secreting inflammatory factors.In the future,a key research direction for ischemic stroke treatment could be rooted in the enhancement of anti-inflammatory factor secretion by promoting the generation of Th2 and Treg cells,along with the activation of M2-type microglia.These approaches may alleviate neuroinflammation and facilitate the repair of neural tissues.

CNKSR2 interactome analysis indicates its association with the centrosome/microtubule system

The protein connector enhancer of kinase suppressor of Ras 2(CNKSR2),present in both the postsynaptic density and cytoplasm of neurons,is a scaffolding protein with several protein-binding domains.Variants of the CNKSR2 gene have been implicated in neurodevelopmental disorders,particularly intellectual disability,although the precise mechanism involved has not yet been fully understood.Research has demonstrated that CNKSR2 plays a role in facilitating the localization of postsynaptic density protein complexes to the membrane,thereby influencing synaptic signaling and the morphogenesis of dendritic spines.However,the function of CNKSR2 in the cytoplasm remains to be elucidated.In this study,we used immunoprecipitation and high-resolution liquid chromatography-mass spectrometry to identify the interactors of CNKSR2.Through a combination of bioinformatic analysis and cytological experiments,we found that the CNKSR2 interactors were significantly enriched in the proteome of the centrosome.We also showed that CNKSR2 interacted with the microtubule protein DYNC1H1 and with the centrosome marker CEP290.Subsequent colocalization analysis confirmed the centrosomal localization of CNKSR2.When we downregulated CNKSR2 expression in mouse neuroblastoma cells(Neuro 2A),we observed significant changes in the expression of numerous centrosomal genes.This manipulation also affected centrosome-related functions,including cell size and shape,cell proliferation,and motility.Furthermore,we found that CNKSR2 interactors were highly enriched in de novo variants associated with intellectual disability and autism spectrum disorder.Our findings establish a connection between CNKSR2 and the centrosome,and offer new insights into the underlying mechanisms of neurodevelopmental disorders.

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

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.

An interacting multiple model-based two-stage Kalman filter for vehicle positioning

To address the problem that a general augmented state Kalman filter or a two-stage Kalman filter cannot achieve satisfactory positioning performance when facing uncertain noise of the micro-electro-mechanical system（MEMS） inertial sensors, a novel interacting multiple model-based two-stage Kalman filter（IMM-TSKF） is proposed to adapt to the uncertain inertial sensor noise. Three bias filters are developed based on different noise characteristics to cover a wide range of noise levels. Then, an accurate estimation of biases is calculated by the interacting multiple model algorithm to correct the bias-free filter. Thus, the vehicle positioning system can achieve good performance when suffering from uncertain inertial sensor noise. The experimental results indicate that the average position error of the proposed IMMTSKF is 25% lower than that of the general TSKF.

Maneuvering target tracking using threshold interacting multiple model algorithm

To avoid missing track caused by the target maneuvers in automatic target tracking system, a new maneuvering target tracking technique called threshold interacting multiple model （TIMM） is proposed. This algorithm is based on the interacting multiple model （IMM） method and applies a threshold controller to improve tracking accuracy. It is also applicable to other advanced algorithms of IMM. In this research, we also compare the position and velocity root mean square （RMS） errors of TIMM and IMM algorithms with two different examples. Simulation results show that the TIMM algorithm is superior to the traditional IMM alzorithm in estimation accuracy.

Interacting Multiple Model Algorithm with the Unscented Particle Filter (UPF)

Combining interacting multiple model （IMM） and unscented particle filter （UPF）, a new multiple model filtering algorithm is presented. Multiple models can be adapted to targets＇ high maneu- vering. Particle filter can be used to deal with the nonlinear or non-Gaussian problems and the unscented Kalman filter （UKF） can improve the approximate accuracy. Compared with other interacting multiple model algorithms in the simulations, the results demonstrate the validity of the new filtering method.

VANISHING VISCOSITY FOR NON-ISENTROPIC GAS DYNAMICS WITH INTERACTING SHOCKS

In this paper, we study the vanishing viscosity limit for non-isentropic gas dy- namics with interacting shocks. Given any entropy solution of non-isentropic gas dynamics which consists of two different families of shocks interacting at some positive time, we show that such solution is the vanishing viscosity limit of a family of smooth global solutions for a viscous system of conservation law. We remark that, after the interacting time, not only shocks but also contact discontinuity are generated.

Effects of ethanol on the proteasome interacting proteins

Proteasome dysfunction has been repeatedly reported in alcoholic liver disease. Ethanol metabolism endproducts affect the structure of the proteasome, and, therefore, change the proteasome interaction with its regulatory complexes 19S and PA28, as well as its interacting proteins. Chronic ethanol feeding alters the ubiquitin-proteasome activity by altering the interaction between the 19S and the 20S proteasome interaction. The degradation of oxidized and damaged proteins is thus decreased and leads to accumulation of insoluble protein aggregates, such as Mallory-Denk bodies. Ethanol also affects the immunoproteasome formation. PA28a/b interactions with the 20S proteasome are decreased in the proteasome fraction isolated from the liver of rats fed ethanol chronically, thus affecting the cellular antigen presentation and defense against pathogenic agents. Recently, it has been shown that ethanol also affects the proteasome interacting proteins (PIPs). Interaction of the proteasome with Ecm29 and with deubiquitinating enzymes Rpn11, UCH37, and Usp14 has been found to decrease. However, the two UBL-ubiquitin-associated domain (UBA) PIPs p62 and valosin-containing protein are upregulated when the proteasome is inhibited. The increase of these UBL-UBA proteins, as well as the increase in Hsp70 and Hsp25 levels, compensated for the proteasome failure and helped in the unfolding/docking of misfolded proteins. Chronic alcohol feeding to rats causes a significant inhibition of the proteasome pathway and this inhibition results from a decreases of the interaction between the 20S proteasome and the regulatory complexes, PIPs, and the ubiquitin system components.

MicroRNA-760 acts as a tumor suppressor in gastric cancer development via inhibiting G-protein-coupled receptor kinase interacting protein-1 transcription

BACKGROUND Gastric cancer(GC)has become a serious threat to people's health.Accumulative evidence reveals that dysregulation of numerous microRNAs(miRNAs)has been found during malignant formation.So far,the role of microRNA-760(miR-760)in the development of GC is largely unknown.AIM To measure the expression level of miR-760 in GC and investigate its role in gastric tumorigenesis.METHODS Real-time quantitative polymerase chain reaction and Western blot analysis were used to measure the expression of miR-760 and G-protein-coupled receptor kinase interacting protein-1(GIT1).Cell growth was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT)and cell colony formation assays.Apoptosis was assessed by flow cytometric analysis.The relationship between miR-760 and GIT1 was verified by luciferase reporter assay.RESULTS The results showed that the expression of miR-760 was decreased in GC and associated with poor clinical outcomes in GC patients.Furthermore,miR-760 restrained cell proliferation and cell colony formation and induced apoptosis in GC cells.In addition,miR-760 directly targeted GIT1 and negatively regulated its expression in GC.GIT1 was upregulated in GC and predicted a worse prognosis in GC patients.We also found that upregulation of GIT1 weakened the inhibitory CONCLUSION In conclusion,miR-760 targets GIT1 to inhibit cell growth and promote apoptosis in GC cells.Our data demonstrate that miR-760 may be a potential target for the treatment of GC.