793 research outputs found
Quantitative Determination of the Critical Points of Mott Metal-Insulator Transition in Strongly Correlated Systems
The Mottness is at the heart of the essential physics in a strongly
correlated system as many novel quantum phenomena occur at the metallic phase
near the Mott metal-insulator transition. We investigate the Mott
metal-insulator transition in a strongly-correlated electron system based on
the Hubbard model. The on-site moment evaluated by the dynamical mean-field
theory is employed to depict the Mott metal-insulator transition. Conveniently,
the on-site moment is a more proper order parameter to quantitatively determine
the Mott critical point, in comparison with the corresponding quasiparticle
coherent weight. Moreover, this order parameter also gives a consistent
description of two distinct forms of the critical points of the Mott
metal-insulator transition.Comment: 6 pages, 4 figure
Defect-engineered graphene for bulk supercapacitors with high energy and power densities
The development of high-energy and high-power density supercapacitors (SCs)
is critical for enabling next-generation energy storage applications.
Nanocarbons are excellent SC electrode materials due to their economic
viability, high-surface area, and high stability. Although nanocarbons have
high theoretical surface area and hence high double layer capacitance, the net
amount of energy stored in nanocarbon-SCs is much below theoretical limits due
to two inherent bottlenecks: i) their low quantum capacitance and ii) limited
ion-accessible surface area. Here, we demonstrate that defects in graphene
could be effectively used to mitigate these bottlenecks by drastically
increasing the quantum capacitance and opening new channels to facilitate ion
diffusion in otherwise closed interlayer spaces. Our results support the
emergence of a new energy paradigm in SCs with 250% enhancement in double layer
capacitance beyond the theoretical limit. Furthermore, we demonstrate prototype
defect engineered bulk SC devices with energy densities 500% higher than
state-of-the-art commercial SCs without compromising the power density.Comment: 15 pages, 5 figures, and 8 supplemental figure
Review of Evidence Suggesting That the Fascia Network Could Be the Anatomical Basis for Acupoints and Meridians in the Human Body
The anatomical basis for the concept of meridians in traditional Chinese medicine (TCM) has not been resolved. This paper reviews the evidence supporting a relationship between acupuncture points/meridians and fascia. The reviewed evidence supports the view that the human body's fascia network may be the physical substrate represented by the meridians of TCM. Specifically, this hypothesis is supported by anatomical observations of body scan data demonstrating that the fascia network resembles the theoretical meridian system in salient ways, as well as physiological, histological, and clinical observations. This view represents a theoretical basis and means for applying modern biomedical research to examining TCM principles and therapies, and it favors a holistic approach to diagnosis and treatment
The Resistance Phenotype and Molecular Epidemiology of Klebsiella pneumoniae in Bloodstream Infections in Shanghai, China, 2012–2015
Neuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer’s disease
Abstract: Subjective cognitive decline (SCD) is regarded as the first clinical manifestation in the Alzheimer’s disease (AD) continuum. Investigating populations with SCD is important for understanding the early pathological mechanisms of AD and identifying SCD-related biomarkers, which are critical for the early detection of AD. With the advent of advanced neuroimaging techniques, such as positron emission tomography (PET) and magnetic resonance imaging (MRI), accumulating evidence has revealed structural and functional brain alterations related to the symptoms of SCD. In this review, we summarize the main imaging features and key findings regarding SCD related to AD, from local and regional data to connectivity-based imaging measures, with the aim of delineating a multimodal imaging signature of SCD due to AD. Additionally, the interaction of SCD with other risk factors for dementia due to AD, such as age and the Apolipoprotein E (ApoE) ɛ4 status, has also been described. Finally, the possible explanations for the inconsistent and heterogeneous neuroimaging findings observed in individuals with SCD are discussed, along with future directions. Overall, the literature reveals a preferential vulnerability of AD signature regions in SCD in the context of AD, supporting the notion that individuals with SCD share a similar pattern of brain alterations with patients with mild cognitive impairment (MCI) and dementia due to AD. We conclude that these neuroimaging techniques, particularly multimodal neuroimaging techniques, have great potential for identifying the underlying pathological alterations associated with SCD. More longitudinal studies with larger sample sizes combined with more advanced imaging modeling approaches such as artificial intelligence are still warranted to establish their clinical utility
LPS-induced down-regulation of signal regulatory protein α contributes to innate immune activation in macrophages
Activation of the mitogen-activated protein kinases (MAPKs) and nuclear factor κB (NF-κB) cascades after Toll-like receptor (TLR) stimulation contributes to innate immune responses. Signal regulatory protein (SIRP) α, a member of the SIRP family that is abundantly expressed in macrophages, has been implicated in regulating MAPK and NF-κB signaling pathways. In addition, SIRPα can negatively regulate the phagocytosis of host cells by macrophages, indicating an inhibitory role of SIRPα in innate immunity. We provide evidences that SIRPα is an essential endogenous regulator of the innate immune activation upon lipopolysaccharide (LPS) exposure. SIRPα expression was promptly reduced in macrophages after LPS stimulation. The decrease in SIRPα expression levels was required for initiation of LPS-induced innate immune responses because overexpression of SIRPα reduced macrophage responses to LPS. Knockdown of SIRPα caused prolonged activation of MAPKs and NF-κB pathways and augmented production of proinflammatory cytokines and type I interferon (IFN). Mice transferred with SIRPα-depleted macrophages were highly susceptible to endotoxic shock, developing multiple organ failure and exhibiting a remarkable increase in mortality. SIRPα may accomplish this mainly through its association and sequestration of the LPS signal transducer SHP-2. Thus, SIRPα functions as a biologically important modulator of TLR signaling and innate immunity
Altered landscape of total RNA, tRNA and sncRNA modifications in the liver and spleen of mice infected by Toxoplasma gondii
BackgroundPathogens can impact host RNA modification machinery to establish a favorable cellular environment for their replication. In the present study, we investigated the effect of Toxoplasma gondii infection on host RNA modification profiles and explored how these modifications may influence the host-parasite interaction.Methodology/principal findingsWe analyzed the modification levels of ∼ 80 nt tRNA and 17–50 nt sncRNAs in mouse liver, spleen, and serum using liquid chromatography and tandem mass spectrometry analysis. The results revealed alterations in RNA modification profiles, particularly during acute infection. The liver exhibited more differentially abundant RNA modifications than the spleen. RNA modification levels in serum were mostly downregulated during acute infection compared to control mice. Correlations were detected between different RNA modifications in the liver and spleen during infection and between several RNA modifications and many cytokines. Alterations in RNA modifications affected tRNA stability and protein translation.Conclusions/significanceThese findings provide new insight into the role of RNA modifications in mediating the murine host response to T. gondii infection
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