Dendritic Size Research Articles

The Effect of Cooling Rate on Solidification Characteristics and Grain Structure of Al-9Si Cast Alloy

A thermal analysis study is essential before the semisolid metal processing of a particular alloy. The surrounding environment, especially the cooling rate is also an important factor. This study investigated the influence of different cooling rates on the solidification characteristics and microstructure evolution of the Al-9Si cast alloy. Four cooling mediums were designed, and their cooling rates are 0.16 ℃/s, 1.0 ℃/s, 1.3 ℃/s, and 1.9 ℃/s, respectively. The results show that the primary dendrite size of the Al-9Si alloy was reduced from 162.61 μm to 86.86 μm as the cooling rate increased from 0.16 ℃/s to 1.9 ℃/s. Significant grain refinement was observed, however, the external cooling has a negligible impact on solid fraction. The optimal temperature range of the Al-9Si cast alloy for the semisolid metal processing at a solid fraction of 0.5 to 0.7 is between 554 ℃ and 563 ℃. With these thermal profiles provided, the relationship between the solid fraction and the solidification time could be expressed using the polynomial equation, which is also useful for point prediction in the subsequent semisolid metal processing.

Dendritic Spine Quantification Using an Automatic Three-Dimensional Neuron Reconstruction Software.

Synaptic connections allow for the exchange and processing of information between neurons. The post-synaptic site of excitatory synapses is often formed on dendritic spines. Dendritic spines are structures of great interest in research centered around synaptic plasticity, neurodevelopment, and neurological and psychiatric disorders. Dendritic spines undergo structural modifications during their lifespan, with properties such as total spine number, dendritic spine size, and morphologically defined subtype altering in response to different processes. Delineating the molecular mechanisms regulating these structural alterations of dendritic spines relies on morphological measurement. This mandates accurate and reproducible dendritic spine analysis to provide experimental evidence. The present study outlines a detailed protocol for dendritic spine quantification and classification using Neurolucida 360 (automatic three-dimensional neuron reconstruction software). This protocol allows for the determination of key dendritic spine properties such as total spine density, spine head volume, and classification into spine subtypes thus enabling effective analysis of dendritic spine structural phenotypes.

On tailored microstructure in AA 2024 alloy during in-situ microwave casting

In the present study, application of microwave energy was explored for tailoring the microstructure in AA 2024 alloy through directional solidification route. Microwave transparent (alumina) and absorbing (graphite) mould materials were utilized to investigate the effect of microwave interaction (electric and magnetic field components) with AA 2024 alloy on microstructure evolution in terms of dendrite size distribution and formation of eutectic phase. Results showed more pronounced eutectic phase gradient was developed using alumina mould. On the other hand, a more uniform distribution of the eutectic phase and grain size was observed with graphite mould. The development of the eutectic phase gradient is attributed to the effective microwave interaction with the AA 2024 alloy melt during solidification. This is primarily associated with the formation of an additional flux at the solid-liquid (S/L) interface of the alloy under the effect of magnetic field and an enhancement in diffusion flux due to mass transport caused by electric field component of microwave. Formation of AlCu, Al2Cu, and Al2CuMg intermetallic phases in both alumina and graphite mould casts was confirmed. Significantly higher hardness was observed at the higher eutectic phase sites within the alumina mould cast, whereas graphite mould casts exhibited better tensile properties.

BIN1 deficiency enhances ULK3-dependent autophagic flux and reduces dendritic size in mouse hippocampal neurons

ABSTRACT Genome-wide association studies identified variants around the BIN1 (bridging integrator 1) gene locus as prominent risk factors for late-onset Alzheimer disease. In the present study, we decreased the expression of BIN1 in mouse hippocampal neurons to investigate its neuronal function. Bin1 knockdown via RNAi reduced the dendritic arbor size in primary cultured hippocampal neurons as well as in mature Cornu Ammonis 1 excitatory neurons. The AAV-mediated Bin1 RNAi knockdown also generated a significant regional volume loss around the injection sites at the organ level, as revealed by 7-Tesla structural magnetic resonance imaging, and an impaired spatial reference memory performance in the Barnes maze test. Unexpectedly, Bin1 knockdown led to concurrent activation of both macroautophagy/autophagy and MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1). Autophagy inhibition with the lysosome inhibitor chloroquine effectively mitigated the Bin1 knockdown-induced dendritic regression. The subsequent molecular studydemonstrated that increased expression of ULK3 (unc-51 like kinase 3), which is MTOR-insensitive, supported autophagosome formation in BIN1 deficiency. Reducing ULK3 activity with SU6668, a receptor tyrosine kinase inhibitor, or decreasing neuronal ULK3 expression through AAV-mediated RNAi, significantly attenuated Bin1 knockdown-induced hippocampal volume loss and spatial memory decline. In Alzheimer disease patients, the major neuronal isoform of BIN1 is specifically reduced. Our work suggests this reduction is probably an important molecular event that increases the autophagy level, which might subsequently promote brain atrophy and cognitive impairment through reducing dendritic structures, and ULK3 is a potential interventional target for relieving these detrimental effects.Abbreviations: AV: adeno-associated virus; Aβ: amyloid-β; ACTB: actin, beta; AD: Alzheimer disease; Aduk: Another Drosophila Unc-51-like kinase; AKT1: thymoma viral proto-oncogene 1; AMPK: AMP-activated protein kinase; AP: autophagosome; BafA1: bafilomycin A1; BDNF: brain derived neurotrophic factor; BIN1: bridging integrator 1; BIN1-iso1: BIN1, isoform 1; CA1: cornu Ammonis 1; CA3: cornu Ammonis 3; CLAP: clathrin and adapter binding; CQ: chloroquine; DMEM: Dulbecco’s modified Eagle medium; EGFP: enhanced green fluorescent protein; GWAS: genome-wide association study; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MRI: magnetic resonance imaging; MTOR; mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; PET: positron emission tomography; qRT-PCR: real-time quantitative reverse transcription PCR; ROS: reactive oxygen species; RPS6KB1: ribosomal protein S6 kinase B1; TFEB: transcription factor EB; ULK1: unc-51 like kinase 1; ULK3: unc-51 like kinase 3.

Targeting LIMK1 in Alzheimer's Disease: A Multifaceted Computational Investigation Involving ADMET, Virtual Screening, Molecular Docking, and Molecular Dynamics

LIM domain kinases (LIMKs), which include LIMK1 and LIMK2, are key proteins in actin dynamics. On this basis, the inhibition of LIMK1 enhances dendritic spine density and size in dementia, reducing Alzheimer's disease (AD) effects. Therefore, several small molecules were discovered as potential therapeutic targets for AD. Herein, a pharmacophore-based virtual screening was employed to identify novel potential LIMK1 inhibitors. The pharmacophore model derived from the co-crystallized receptor structure of PubChem-329823760: LIMK1 (PDB ID: 5NXC) was then used for virtual screening. After applying Lipinski's rules and pharmacophore filters, 29 potential hits were identified. Molecular docking simulations were performed to determine the binding affinities of these candidates against LIMK1, with results ranging from -5.20 to -10.60 kcal/mol. Notably, PubChem-136621040 showed the highest binding affinity against the target protein, with a docking score of -10.60 kcal/mol, slightly surpassing the native ligand, PubChem-329823760, possessing a lower docking score of -9.80 kcal/mol. The drug-likeness and toxicity properties of target compounds were assessed through ADMET evaluations. A series of 75 nanosecond molecular dynamics (MD) simulations were conducted on the complexes generated by the best-docked molecule and the native ligand. RMSD, RMSF, SASA, and Rg calculations of their trajectories were also calculated. PubChem-136621040 possessed an average RMSD value of 0.23 nm, lower than the native ligand's 0.31 nm, indicating a greater binding stability. The RMSF results also revealed that the best-docked compound had a lower value (0.10 nm), while the native ligand possessed a value of 0.12 nm. The SASA values for both the native ligand and the best-docked compound were nearly identical, at 150.20 nm2 and 150.80 nm2, respectively. The Rg results demonstrated that both complexes maintained their rigidity throughout the simulation, with similar average values of 2.04 nm for the native ligand and 2.06 nm for the best-docked compound.

L-type Ca2+ channel activation of STIM1–Orai1 signaling remodels the dendritic spine ER to maintain long-term structural plasticity

Learning and memory require coordinated structural and functional plasticity at neuronal glutamatergic synapses located on dendritic spines. Here, we investigated how the endoplasmic reticulum (ER) controls postsynaptic Ca2+ signaling and long-term potentiation of dendritic spine size, i.e., sLTP that accompanies functional strengthening of glutamatergic synaptic transmission. In most ER-containing (ER+) spines, high-frequency optical glutamate uncaging (HFGU) induced long-lasting sLTP that was accompanied by a persistent increase in spine ER content downstream of a signaling cascade engaged by N-methyl-D-aspartate receptors (NMDARs), L-type Ca2+ channels (LTCCs), and Orai1 channels, the latter being activated by stromal interaction molecule 1 (STIM1) in response to ER Ca2+ release. In contrast, HFGU stimulation of ER-lacking (ER-) spines expressed only transient sLTP and exhibited weaker Ca2+ signals noticeably lacking Orai1 and ER contributions. Consistent with spine ER regulating structural metaplasticity, delivery of a second stimulus to ER- spines induced ER recruitment along with persistent sLTP, whereas ER+ spines showed no additional increases in size or ER content in response to sequential stimulation. Surprisingly, the physical interaction between STIM1 and Orai1 induced by ER Ca2+ release, but not the resulting Ca2+ entry through Orai1 channels, proved necessary for the persistent increases in both spine size and ER content required for expression of long-lasting late sLTP.

Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling.

Neuronal excitatory synapses are primarily located on small dendritic protrusions called spines. During synaptic plasticity underlying learning and memory, Ca2+ influx through postsynaptic NMDA-type glutamate receptors (NMDARs) initiates signaling pathways that coordinate changes in dendritic spine structure and synaptic function. During long-term potentiation (LTP), high levels of NMDAR Ca2+ influx promote increases in both synaptic strength and dendritic spine size through activation of Ca2+-dependent protein kinases. In contrast, during long-term depression (LTD), low levels of NMDAR Ca2+ influx promote decreased synaptic strength and spine shrinkage and elimination through activation of the Ca2+-dependent protein phosphatase calcineurin (CaN), which is anchored at synapses via the scaffold protein A-kinase anchoring protein (AKAP)150. In Alzheimer's disease (AD), the pathological agent amyloid-β (Aβ) may impair learning and memory through biasing NMDAR Ca2+ signaling pathways toward LTD and spine elimination. By employing AKAP150 knock-in mice of both sexes with a mutation that disrupts CaN anchoring to AKAP150, we revealed that local, postsynaptic AKAP-CaN-LTD signaling was required for Aβ-mediated impairment of NMDAR synaptic Ca2+ influx, inhibition of LTP, and dendritic spine loss. Additionally, we found that Aβ acutely engages AKAP-CaN signaling through activation of G-protein-coupled metabotropic glutamate receptor 1 (mGluR1) leading to dephosphorylation of NMDAR GluN2B subunits, which decreases Ca2+ influx to favor LTD over LTP, and cofilin, which promotes F-actin severing to destabilize dendritic spines. These findings reveal a novel interplay between NMDAR and mGluR1 signaling that converges on AKAP-anchored CaN to coordinate dephosphorylation of postsynaptic substrates linked to multiple aspects of Aβ-mediated synaptic dysfunction.

A Comparative Study on the Performance and Microstructure of 304NG Stainless Steel in Underwater and Air Laser Welding.

In order to facilitate the application of underwater laser welding technology in in situ repairs of nuclear power plants, this study conducted comparative experiments between local dry underwater laser welding and laser welding in air on 304NG nitrogen-controlled stainless steel. The aim was to explore its microstructural evolution and mechanical properties in underwater environments. It was found that, near the fusion line of laser welding in air, columnar dendrites gradually evolved into cellular dendrites toward the weld center, eventually disappearing, resulting in a skeletal ferrite and serrated austenite structure. The underwater laser welding joints exhibited similar characteristics yet with more pronounced alternation between columnar and cellular dendrites. Additionally, the size of cellular dendrites decreased significantly, and needle-like ferrite was observed at the weld center. The hardness of underwater laser welded joints was slightly higher than that of in-air laser welded joints. Compared to laser welding in air, the strength of underwater laser welding joints increased from 443 MPa to 471 MPa, and the displacement increased from 2.95 mm to 3.45 mm, both types of welded joints exhibited a mixed mode fracture characterized by plasticity and brittleness.

Dendritic Morphology of Developing Hippocampal Neurons in Cyp11a1 Null Mice.

Neurosteroids have a variety of neurological functions, such as neurite growth, neuroprotection, myelination, and neurogenesis. P450scc, encoded by CYP11A1 gene, is the cholesterol side chain cleavage enzyme that catalyzes the first and rate-limiting step in steroidogenesis. In this study, we examine the dendritic morphology in developing hippocampal neurons of Cyp11a1 null mice at P15, a critical period for synapse formation and maturation. Knockout mice were maintained until P15 with hormone administration. The Golgi-Cox method stained CA1 and CA3 pyramidal neurons in the hippocampus to reveal dendritic morphology. We demonstrated that Cyp11a1 null mice usually die within 7 days after birth and thus collected brain samples at postnatal day 5 (P5) for examination. There was significant shrinkage of dendrite size and diminishment of dendritic branching in CA1 and CA3 pyramidal neurons in the hippocampus of Cyp11a1 null mice, suggesting a developmental delay. We wonder if this delay may catch up later in life. Since the age of P15 is a critical period for synapse formation and maturation, the Cyp11a1 null mice were rescued by receiving hormone administration until P15 that the dendritic morphology in the developing hippocampal neurons could be examined. The results indicated that the total dendritic length, the number of dendritic branches, as well as dendritic arborization in the CA1 and CA3 pyramidal neurons are significantly decreased in P15 knockout mice when compared to the wild type. The spine densities were also significantly decreased. In addition, the Western blot analysis revealed decreased PSD-95 expression levels in the knockout mice compared to the wild type at P15. These results suggested that Cyp11a1 deficiency impairs the dendritic structures in the developing hippocampal pyramidal neurons.

Effect of remelting on cracking of Inconel 939 fabricated via laser powder bed fusion

Laser remelting of each layer during laser powder bed fusion (L-PBF) is an important strategy used for enhancing the quality of components. However, the impact of remelting on internal cracking has not been completely understood. This study investigates the feasibility of employing remelting to mitigate internal cracking using Inconel 939 (IN939) as an example, a high-temperature nickel-based alloy with high susceptibility to cracking during L-PBF. The effects of remelting parameters, strategies, and the number of remelting cycles on microstructure features and defects were studied. The residual stresses in remelted samples and initial melt samples were measured for different laser scanning strategies. Reduction in residual stresses is identified as a key factor in minimizing cracking, with the lowest residual stresses observed in remelted samples using the chess strategy. Additionally, crack density in remelted samples was decreased with reducing cellular dendrite size in the fabricated sample. In comparison to initial melt samples, remelted samples exhibited an 85% reduction in crack density and a 60% reduction in porosity. These findings present a potential approach for defect inhibition during L-PBF processing of IN939 and other high-temperature alloys.

Forming high-strength and softening-resistant AlxHf0.5Mo0.5NbTa0.5TiVZr dual-phase refractory high-entropy alloys

Refractory high-entropy alloys AlxHf0.5Mo0.5NbTa0.5TiVZr with the addition of different amounts of low-density aluminum were developed to improve the strength and softening resistance at elevated temperatures. The microstructure and phase formation were investigated, and the mechanical properties and deformation behavior at various temperatures were studied. The primary dendrites consisted of body-centered cubic (Mo,Nb,Ta)-rich multicomponent phase, and the latter solidified interdendrites contained Al-(Hf,V,Zr)-rich second phase initiating from grain boundaries. With an increased aluminum content, the size of dendrites decreased, and the portion of the network-like second phase increased. The hard precipitates improved the yield strength and softening resistance but sacrificed the ductility of the alloys. At an appropriate aluminum content of x = 0.5, the Al0.5Hf0.5Mo0.5NbTa0.5TiVZr alloy showed promising softening resistance at 600 °C with a retained strength of 1240 MPa and a compressive strain of 13 %. A large number of dislocations formed a tangled dislocation forest than glided in a planar way, additionally enhancing the work hardening and improving the softening resistance. However, an excessive accumulation of dislocations at the phase boundaries caused the brittle fracture in the latter stage.

Effect of Ce and solidification cooling rate on the microstructure and mechanical properties of AA2017 aluminum alloy

Controlling dendritic growth and grain size in new Ce-containing Al-based alloys becomes crucial due to new envisioned applications and Ce rising demand in casting processes. In the present work Ce effect on the 2xxx Al series microstructures at various industrial-scale solidification cooling rates was investigated. The directional solidification technique is crucial in this endeavor since can generate several solidified samples related to several cooling rates. The AA2017 alloy and a modified version containing 3 wt % of Ce were both produced under directional solidification and various microstructure aspects were characterized. The mechanical behavior was analyzed by microhardness and compression tests. The Ce addition reduced primary and secondary dendritic spacing without impacting grain size. Cells were only observed to form on the Ce-containing alloy at cooling rates of approximately 19 °C/s; while dendritic configurations dominated all other conditions. While round pockets composed of Al+Al2Cu+Mg2Si ternary eutectic formed the interdendritic zones in the AA2017 alloy, the AA2017-Ce alloy microstructure was mainly constituted by elongated AlCeSi + Al8CeCu4 interdendritic phases. Finally, the addition of Ce favored an increase in the microhardness and compressive strength values of the AA2017 alloy, which is attributed to the refinement of the solidification structure, as well as the formation of a greater fraction of secondary reinforcement phases.

New insights on dislocation forming mechanism of nickel-based superalloy fabricated by laser powder bed fusion

In this work, the forming mechanism of dislocation in laser powder bed fusion (LPBF) built IN738LC alloy was elucidated by studying the intrinsic relationships between the density and distribution of dislocation and the orientation and size of dendrite. The substructures with different dislocation densities and cell spacings were customized by controlling solidification conditions, and analyzed by multi-scale characterizing methods. The results show that an increase in geometrically necessary dislocation (GND) density from 1.48 × 1014 to 1.82 × 1014m−2 is accompanied by a decrease in cell spacing from 1046 nm to 640 nm as the solidification rate increases. However, the relationship between GND density and cell spacing doesn't follow Ashby's model. This indicates that GNDs are not entirely generated by thermal strain itself. On the other hand, the characterization results of cell structures show that a number of misfit dislocations are formed by the thermal strain induced deflection growth of the dendrites. These prove that the dislocations are comprehensively generated by thermal strain itself and dendritic deflection growth.

Microstructure, mechanical properties and sensitization of ultra-low nickel Cr–Mn austenitic stainless steels

The present study deals with the effect of shielded metal arc welding (SMAW) and gas metal arc welding (GMAW) processes with different welding speeds on microstructural and mechanical properties including intergranular corrosion susceptibility of ultra-low nickel chrome-manganese austenitic stainless steel (ASS). The microstructural analysis was performed by an optical microscope. The Fisher Ferritscope was used for determining ferrite content in the weldment. The microstructural analysis shows that the size of dendrites of δ ferrite and the width of heat affected zone (HAZ) decreases when welding speed increases. It was found more δ-ferrite in SMAW weld compared to GMAW weld. It was also found that when welding speed increases, tensile strength, impact strength and hardness values decrease for both welding processes. From the U-bending test, it was found that the welded joints are strong enough to withstand bend at 1800 without any cracks for both welding processes. It was also found that Cr-Mn ASS weld becomes susceptible to intergranular corrosion on welding. For both welding processes, the degree of sensitization value decreases with an increase in welding speed for both the welding processes as evaluated by the double loop electrochemical potentiodynamic reactivation (DLEPR) test. Also, the weld joint made using the GMAW process is more susceptible to intergranular corrosion than that made using the SMAW process.

The Effect of Heat Treatment on the Microstructure and Mechanical Properties of Plasma-Cladded CoCrFeNiMn Coatings on Compacted Graphite Iron

CoCrFeNiMn high-entropy alloy coatings were deposited on compacted graphite iron (CGI) by plasma transfer arc cladding to strengthen and improve the wear resistance (performance) of the surface. The effects of different heat treatment processes on the microstructure and mechanical properties of the CoCrFeNiMn coatings were investigated. Compared with the deposited coating, the single FCC phase in the heat-treated coatings was retained, the grain size of the columnar dendrites decreased, the spacing between the dendrites increased, and the Cr-rich precipitated phase in the grain boundary increased. The heat treatment process had a positive influence on the microhardness and wear resistance of the coatings. The microhardness of the coatings increased after heat treatment. After heat treatment at 660 °C for 90 min, the coating had the highest microhardness of 563 ± 6.9 HV0.2, and it had the best wear resistance.

The E3 ubiquitin ligase TRIM9 regulates synaptic function and actin dynamics in response to netrin-1.

During neuronal development, dynamic filopodia emerge from dendrites and mature into functional dendritic spines during synaptogenesis. Dendritic filopodia and spines respond to extracellular cues, influencing dendritic spine shape and size as well as synaptic function. Previously, the E3 ubiquitin ligase TRIM9 was shown to regulate filopodia in early stages of neuronal development, including netrin-1-dependent axon guidance and branching. Here, we demonstrate that TRIM9 also localizes to dendritic filopodia and spines of murine cortical and hippocampal neurons during synaptogenesis and is required for synaptic responses to netrin. In particular, TRIM9 is enriched in the postsynaptic density (PSD) within dendritic spines and loss of Trim9 alters the PSD proteome, including the actin cytoskeleton landscape. While netrin exposure induces accumulation of the Arp2/3 complex and filamentous actin in dendritic spine heads, this response is disrupted by genetic deletion of Trim9. In addition, we document changes in the synaptic receptors associated with loss of Trim9. These defects converge on a loss of netrin-dependent increases in neuronal firing rates, indicating TRIM9 is required downstream of synaptic netrin-1 signaling. We propose that TRIM9 regulates cytoskeletal dynamics in dendritic spines and is required for the proper response to synaptic stimuli.

Nickel-aluminide cladding on a steel substrate using dual wire arc additive manufacturing

In this study the nickel-aluminide intermetallic cladded on AISI 1010 steed using dual wire arc process. The nickel-aluminide is fabricated in situ through an arc provided by a gas tungsten arc welding process and changing aluminum wire feeding rate. The research findings reveal that at a constant Ni wire feeding rate of 450 mm/min, by decreasing the Al wire feeding rate lower than 800 mm/min, the instability of the melt pool prevents the formation of a uniform deposit on the substrate. Although deposition has been done at an Al wire feeding rate higher than 1600 mm/min, transverse cracks have formed in the clad layer. Increasing the aluminum wire feeding rate from 1000 to 1400 mm/min decreases the dendritic arm size from 9.2 ± 0.1 to 4.1 ± 0.3 μm. Although unreacted nickel is visible in the microstructure at the Al wire feeding rate of 1000 mm/min, at a high feeding rate (1400 mm/min), most of the microstructure contains AlNi and Ni3Al intermetallic compounds. With the rise in Al wire feeding rate from 1000 to 1400 mm/min, both yield strength and ultimate tensile strength increase from 521.45 ± 14.16 to 620.89 ± 16.08 MPa and from 762.11 ± 19.89 to 855.65 ± 21.54 MPa, respectively. Intriguingly, the clad layer's tensile toughness decreases from 26.51 ± 2.43 to 18.32 ± 2.56 MJ m−3. By increasing the wire feeding rate from 1000 to 1400 mm/min, the wear rate at room temperature, 500 °C, and 800 °C increases by 61.2, 45.7, and 44.3%, respectively.

Magnitude of Type I Interferon Responses by Plasmacytoid Dendritic Cells After TLR7 Stimulation Is Associated With Human Immunodeficiency Virus Type 1 (HIV-1) Reservoir Sizes in Cisgender Women With HIV-1 on Antiretroviral Therapy.

Human immunodeficiency virus type 1 (HIV-1) disease manifestations differ between cisgender women and men, including better control of viral replication during primary infection and less frequent residual HIV-1 replication on antiretroviral therapy (ART) in cisgender women with HIV-1 (WWH). Investigating plasmacytoid dendritic cell (pDC) functions and HIV-1 reservoir sizes in 20 WWH on stable ART, we observed inverse correlations between interferon-α and tumor necrosis factor responses of pDCs to Toll-like receptor 7/8 stimulation and intact/total proviral HIV-1 DNA levels. Additionally, ISG15 mRNA levels in peripheral blood mononuclear cells correlated with cytokine responses of pDCs. These findings demonstrate an association between higher type I interferon responses and lower HIV-1 reservoir sizes in WWH on ART, warranting studies to identify the underlying mechanisms.

Microstructure and molten pool morphology of TiB2/ AlSi7Mg composites fabricated by infrared-blue hybrid laser powder bed fusion

A hybrid laser composed of infrared and blue laser is applied in fabricating TiB2/AlSi7Mg composites on AlSi7Mg substrate by LPBF. The effect on formability, molten pool morphology, molten pool size and microstructure under infrared, blue and hybrid laser were compared. It was confirmed that hybrid laser can make up for the unbalanced energy distribution of infrared laser and the low energy density of blue laser. The increased energy input improves the molten pool size and cellular dendrites size. Therefore, the hybrid laser can improve the formability and forming stability in the LPBF process of low absorption rate alloys.

Dendrites contribute to the gradient of intrinsic timescales encompassing cortical and subcortical brain networks.

Cytoarchitectonic studies have uncovered a correlation between higher levels of cortical hierarchy and reduced dendritic size. This hierarchical organization extends to the brain's timescales, revealing longer intrinsic timescales at higher hierarchical levels. However, estimating the contribution of single-neuron dendritic morphology to the hierarchy of timescales, which is typically characterized at a macroscopic level, remains challenging. Here we mapped the intrinsic timescales of six functional networks using functional magnetic resonance imaging (fMRI) data, and characterized the influence of neuronal dendritic size on intrinsic timescales of brain regions, utilizing a multicompartmental neuronal modeling approach based on digitally reconstructed neurons. The fMRI results revealed a hierarchy of intrinsic timescales encompassing both cortical and subcortical brain regions. The neuronal modeling indicated that neurons with larger dendritic structures exhibit shorter intrinsic timescales. Together these findings highlight the contribution of dendrites at the neuronal level to the hierarchy of intrinsic timescales at the whole-brain level. This study sheds light on the intricate relationship between neuronal structure, cytoarchitectonic maps, and the hierarchy of timescales in the brain.