Spin-flip reflection at the normal metal-spin superconductor interface

We study spin transport through a normal metal-spin superconductor junction. A spin-flip reflection is demonstrated at the interface, where a spin-up electron incident from the normal metal can be reflected as a spin-down electron and the spin $2\times \hbar/2$ will be injected into the spin superconductor. When the (spin) voltage is smaller than the gap of the spin superconductor, the spin-flip reflection determines the transport properties of the junction. We consider both graphene-based (linear-dispersion-relation) and quadratic-dispersion-relation normal metal-spin superconductor junctions in detail. For the two-dimensional graphene-based junction, the spin-flip reflected electron can be along the specular direction (retro-direction) when the incident and reflected electron locates in the same band (different bands). A perfect spin-flip reflection can occur when the incident electron is normal to the interface, and the reflection coefficient is slightly suppressed for the oblique incident case. As a comparison, for the one-dimensional quadratic-dispersion-relation junction, the spin-flip reflection coefficient can reach 1 at certain incident energies. In addition, both the charge current and the spin current under a charge (spin) voltage are studied. The spin conductance is proportional to the spin-flip reflection coefficient when the spin voltage is less than the gap of the spin superconductor. These results will help us get a better understanding of spin transport through the normal metal-spin superconductor junction.Comment: 11 pages, 9 figure

Rosmarinic Acid Prevents Cisplatin-Induced Liver and Kidney Injury by Inhibiting Inflammatory Responses and Enhancing Total Antioxidant Capacity, Thereby Activating the Nrf2 Signaling Pathway

Drug-induced liver and kidney damage is an emergent clinical issue that should be addressed. Rosmarinic acid (RA) has obvious anti-inflammatory and antioxidant effects, so we evaluated the anti-inflammatory and antioxidant effects of RA pretreatment on serum and liver and kidney tissues of cisplatin (CP)-treated mice and explored the possible mechanisms. The results showed that RA pretreatment effectively downregulated the serum, liver, and kidney levels of ALT, AST, BUN, and CRE and the inflammatory factors IL-1β, IL-6, and TNF-α, and simultaneously enhanced the total antioxidant capacity of the liver and kidney. RA pretreatment significantly reduced the levels of MPO, MDA, and NO in liver and kidney tissue, inhibited the mRNA expression of IL-1β, IL-6, and TNF-α in liver and kidney tissue, activated the Nrf2 signaling pathway, and upregulated the mRNA expression of downstream target genes. Our findings show that RA could effectively prevent and alleviate acute liver and kidney injury caused by CP

Gamellia sinensis O.Ktze extract shows anti-colorectal cancer activity via MAPK/ERK signaling pathway

Purpose: To investigate the therapeutic effects of Gamellia sinensis O.Ktze extract (GSOE) on colorectal cancers, as well as the underlying mechanisms.Methods: The effect of GSOE on colorectal cancer cells HCT-116 or Caco-2 growth was tested, and then the apoptosis and invasion was analyzed by MTT, flow cytometry and Transwell assay in vitro. Next, the mice received three doses (200, 400 or 800 mg/kg/day, gastric perfusion) of GSOE to evaluate its effects on tumor growth. Lung metastasis in mouse xenograft models which were inoculated with HCT-116 or Caco-2 cells were also investigated. The expression of p-ERK and  p-MEK were evaluated by western blot analysis in HCT-116 and Caco-2 cells with or without GSOE treatment in vitro.Result: GSOE significantly inhibited colorectal cancer cell growth and induced  apoptosis or cell cycle arrest at G1- and S-phases in HCT-116 cells and Caco-2 cells in a dose-dependent manner. Moreover, GSOE effectively retarded tumor cell migration and invasion through ERK/MAPK signaling pathway suppression.Conclusion: These findings demonstrate that GSOE has an anti-tumor effect in colorectal cancer by inactivating ERK/MAPK signaling pathway.Keywords: Gamellia sinensis O.Ktze, Colorectal cancer, Invasion, Apoptosis, Cell cycle arrest ERK, MAPK

An Effective Way of J Wave Separation Based on Multilayer NMF

J wave is getting more and more important in the clinical diagnosis as a new index of the electrocardiogram (ECG) of ventricular bipolar, but its signal often mixed in normal ST segment, using the traditional electrocardiograph, and diagnosed by experience cannot meet the practical requirements. Therefore, a new method of multilayer nonnegative matrix factorization (NMF) in this paper is put forward, taking the hump shape J wave, for example, which can extract the original J wave signal from the ST segment and analyze the accuracy of extraction, showing the characteristics of hump shape J wave from the aspects of frequency domain, power spectrum, and spectral type, providing the basis for clinical diagnosis and increasing the reliability of the diagnosis of J wave

Real-time visualization of clustering and intracellular transport of gold nanoparticles by correlative imaging.

Mechanistic understanding of the endocytosis and intracellular trafficking of nanoparticles is essential for designing smart theranostic carriers. Physico-chemical properties, including size, clustering and surface chemistry of nanoparticles regulate their cellular uptake and transport. Significantly, even single nanoparticles could cluster intracellularly, yet their clustering state and subsequent trafficking are not well understood. Here, we used DNA-decorated gold (fPlas-gold) nanoparticles as a dually emissive fluorescent and plasmonic probe to examine their clustering states and intracellular transport. Evidence from correlative fluorescence and plasmonic imaging shows that endocytosis of fPlas-gold follows multiple pathways. In the early stages of endocytosis, fPlas-gold nanoparticles appear mostly as single particles and they cluster during the vesicular transport and maturation. The speed of encapsulated fPlas-gold transport was critically dependent on the size of clusters but not on the types of organelle such as endosomes and lysosomes. Our results provide key strategies for engineering theranostic nanocarriers for efficient health management

Effect of hydroalcohol extract of lemon (Citrus limon) peel on a rat model of type 2 diabetes

Purpose: To determine the effect of the hydroalcohol extract of lemon peel (LP) on a rat model of type 2 diabetes (T2D).Method: The rat model of T2D by injection of streptozotocin was established. The effects of a hydroalcoholic extract of LP was characterised on a rat model of type 2 diabetes based on body weight, food intake, fasting blood glucose (FBG), glucose tolerance test, and insulin tolerance test. Antioxidant activity and oxidative stress were analysed by superoxide dismutase (SOD) and malonaldehyde (MDA) assays.Results: In acute toxicity studies, administration of LP extract at 2000 mg/kg orally did not cause any symptoms of poisoning or death after 14 days. The body weight of rats increased after treatment with LP extracts. Food intake in diabetic rats decreased with LP extract treatment. Continual treatment with LP extracts for 35 days significantly reduced blood glucose levels in diabetic rats. Glucose tolerance improved, and insulin resistance was reduced after treatment with LP extracts. SOD and MDA data indicate that treatment with LP extract alleviated the oxidative stress in diabetic rats as well as enhanced the antioxidant activity of liver in a dosage-dependent manner.Conclusion: LP extract decreased food intake and FBG, but increased body weight in rats. The effect of LP on T2D is likely related to improved antioxidant activity and reduced oxidative stress. Thus, LP extract has potentials for the treatment of T2D.Keywords: Lemon peel, Type 2 diabetes, Antioxidant activity, Glucose tolerance, Insulin toleranc

Angiotensin II mediates the high-glucose-induced endothelial-to-mesenchymal transition in human aortic endothelial cells

<p>Abstract</p> <p>Background</p> <p>Substantial evidence suggests that high glucose (HG) causes endothelial cell damage; however, the potential mechanism therein has yet to be clarified. The aim of this study was to investigate the influence of HG on the endothelial-to-mesenchymal transition (EndMT) and its relevance to the activation of the renin-angiotensin system.</p> <p>Methods</p> <p>Primary human aortic endothelial cells (HAECs) were divided into three groups: a normal glucose (NG) group, HG group, and irbesartan (1 μM)-treated (HG+irbesartan) group. The concentration of angiotensin II in the supernatant was detected by radioimmunoassay. Pathological changes were investigated using fluorescence microscopy and electron microscopy. Immunofluorescence staining was performed to detect the co-expression of CD31 and fibroblast markers, such as fibroblast-specific protein 1 (FSP1). The expressions of FSP1 and α-SMA were detected by RT-PCR and Western blot.</p> <p>Results</p> <p>The treatment of HAECs in the HG group resulted in significant increases in the expressions of FSP1 and angiotensin II in dose-and time-dependent manners. The incubation of HAECs exposure to HG resulted in a fibroblast-like phenotype, wherein increased microfilamentation and a roughened endoplasmic reticulum structure were observed in the cytoplasm. The expressions of FSP1 and α-SMA were significantly increased in the HG group, and these changes were inhibited by irbesartan treatment (<it>P </it>< 0.05). Double staining of the HAECs indicated a co-localization of CD31 and FSP1 and that some cells acquired spindle-shaped morphologies and a loss of CD31 staining; however, treatment with irbesartan attenuated the expression of EndMT (<it>P </it>< 0.05).</p> <p>Conclusions</p> <p>These findings suggest a novel mechanism in HG-induced endothelial damage via the mediation of the EndMT by angiotensin II, which was inhibited by Irbesartan.</p