778 research outputs found
Integral equation method for the electromagnetic wave propagation in stratified anisotropic dielectric-magnetic materials
We investigate the propagation of electromagnetic waves in stratified
anisotropic dielectric-magnetic materials using the integral equation method
(IEM). Based on the superposition principle, we use Hertz vector formulations
of radiated fields to study the interaction of wave with matter. We derive in a
new way the dispersion relation, Snell's law and reflection/transmission
coefficients by self-consistent analyses. Moreover, we find two new forms of
the generalized extinction theorem. Applying the IEM, we investigate the wave
propagation through a slab and disclose the underlying physics which are
further verified by numerical simulations. The results lead to a unified
framework of the IEM for the propagation of wave incident either from a medium
or vacuum in stratified dielectric-magnetic materials.Comment: 14pages, 3figure
Coherent phonon Rabi oscillations with a high frequency carbon nanotube phonon cavity
Phonon-cavity electromechanics allows the manipulation of mechanical
oscillations similar to photon-cavity systems. Many advances on this subject
have been achieved in various materials. In addition, the coherent phonon
transfer (phonon Rabi oscillations) between the phonon cavity mode and another
oscillation mode has attracted many interest in nano-science. Here we
demonstrate coherent phonon transfer in a carbon nanotube phonon-cavity system
with two mechanical modes exhibiting strong dynamical coupling. The
gate-tunable phonon oscillation modes are manipulated and detected by extending
the red-detuned pump idea of photonic cavity electromechanics. The first- and
second-order coherent phonon transfers are observed with Rabi frequencies 591
kHz and 125 kHz, respectively. The frequency quality factor product
fQ_m~2=10^12 Hz achieved here is larger thank k_B T_base/h, which may enable
the future realization of Rabi oscillations in the quantum regime
Clinical evaluation of cetuximab combined with an S-1 and oxaliplatin regimen for Chinese patients with advanced gastric cancer
The significance of Notch ligand expression in the peripheral blood of children with hand, foot and mouth disease (HFMD)
BACKGROUND: Hand, foot and mouth disease (HFMD), a virus-induced infectious disease that usually affects infants and children, has an increased incidence in China in recent years. This study attempted to investigate the role of the Notch signaling pathway in the pathogenesis of HFMD. METHODS: Eighty-two children diagnosed with HFMD were enrolled into this study. The HFMD group was further divided into the uncomplicated HFMD and HFMD with encephalitis groups. The control group included 40 children who underwent elective surgery for treatment of inguinal hernias. RESULTS: Children with HFMD displayed significantly reduced CD3+, CD3+CD4+ and CD3+CD8+ cell subsets, but substantially enhanced CD3−CD19+ cell subset (p < 0.05 versus control subjects). The expression levels of Notch ligands Dll1 and Dll4 in the peripheral blood of the HFMD group were significantly higher than those in the control group (p < 0.05). There were statistically significant differences in CD3+, CD3+CD4+ and CD3−CD19+ cell subsets, but not in Notch ligand expression, between the uncomplicated HFMD and HFMD with encephalitis groups. Dll4 expression in HFMD subjects correlated negatively with the CD3+ and CD3+CD8+ cell subsets (p < 0.05), but positively with the CD3−CD19+ cell subset (p < 0.05). Furthermore, Dll4 expression in HFMD with encephalitis subjects correlated positively with total white blood cell (WBC) counts and total protein contents in cerebrospinal fluid (CSF) (p < 0.05). CONCLUSIONS: The Notch ligand Dll4 exhibits a strong correlation with the CD3+, CD3+CD8+ and CD3−CD19+ cell subsets in children with HFMD, indicating that the Notch signaling may be involved in the development of HFMD by affecting the number and status of peripheral lymphocytes
Highly branched cobalt phosphide nanostructures for hydrogen-evolution electrocatalysis
Plant toxin β-ODAP activates integrin β1 and focal adhesion : a critical pathway to cause neurolathyrism
Neurolathyrism is a unique neurodegeneration disease caused by beta-N-oxalyl-L-alpha, beta-diaminopropionic (beta-ODAP) present in grass pea seed (Lathyrus stativus L.) and its pathogenetic mechanism is unclear. This issue has become a critical restriction to take full advantage of drought-tolerant grass pea as an elite germplasm resource under climate change. We found that, in a human glioma cell line, beta-ODAP treatment decreased mitochondrial membrane potential, leading to outside release and overfall of Ca2+ from mitochondria to cellular matrix. Increased Ca2+ in cellular matrix activated the pathway of ECM, and brought about the overexpression of beta 1 integrin on cytomembrane surface and the phosphorylation of focal adhesion kinase (FAK). The formation of high concentration of FA units on the cell microfilaments further induced overexpression of paxillin, and then inhibited cytoskeleton polymerization. This phenomenon turned to cause serious cell microfilaments distortion and ultimately cytoskeleton collapse. We also conducted qRT-PCR verification on RNA-sequence data using 8 randomly chosen genes of pathway enrichment, and confirmed that the data was statistically reliable. For the first time, we proposed a relatively complete signal pathway to neurolathyrism. This work would help open a new window to cure neurolathyrism, and fully utilize grass pea germplasm resource under climate change
Novel norcantharidin-loaded liver targeting chitosan nanoparticles to enhance intestinal absorption
In this paper, two novel liver-targeting nanoparticles, norcantharidin-loaded chitosan nanoparticles (NCTD-CS-NPs) and norcantharidin-associated galactosylated chitosan nanoparticles (NCTD-GC-NPs), were prepared using ionic cross-linkage. The physical properties, particle size, encapsulation efficiency, and drug release characteristics of the nanoparticles were investigated in vitro. To investigate the intestinal absorption mechanisms of the two preparations, a series of experiments was carried out, including in situ circulation method, in vitro everted gut sacs, and Ussing chamber perfusion technique. The absorption rate constants (Ka) of NCTD at different segments were found to be duodenum > jejunum > ileum > colon. The concentration had no distinctive effect on absorption kinetics, suggesting that drug absorption is not dose-dependent. The transport of NCTD was found to be inhibited by P-glycoprotein (P-gp) inhibitor, indicating that NCTD might be the substrate of P-gp. The order of the absorption enhancer effects were as follows: low molecular weight chitosan (CS-8kDa) > high molecular weight chitosan (CS-30kDa) > Poloxamer > sodium dodecyl sulfate (SDS) > sodium deoxycholate (SDCh). The results indicate that the chitosan nanoparticles can improve intestinal absorption of NCTD
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
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