Kondo Spin Screening Cloud in Two-dimensional Electron Gas with Spin-orbit Couplings

A spin-1/2 Anderson impurity in a semiconductor quantum well with Rashba and Dresselhaus spin-orbit couplings is studied by using a variational wave function method. The local magnetic moment is found to be quenched at low temperatures. The spin-spin correlations of the impurity and the conduction electron density show anisotropy in both spatial and spin spaces, which interpolates the Kondo spin screenings of a conventional metal and of a surface of three-dimensional topological insulators.Comment: accepted by the Journal of Physics: Condensed Matte

Anderson Impurity in Helical Metal

We use a trial wave function to study the spin-1/2 Kondo effect of a helical metal on the surface of a three-dimensional topological insulator. While the impurity spin is quenched by conduction electrons, the spin-spin correlation of the conduction electron and impurity is strongly anisotropic in both spin and spatial spaces. As a result of strong spin-orbit coupling, the out-of-plane component of the impurity spin is found to be fully screened by the orbital angular momentum of the conduction electrons.Comment: The published versio

Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions.

Rationale: Cigarette smoking is a well-established risk factor for myocardial infarction and sudden cardiac death. The deleterious effects are mainly due to nicotine, but the mechanisms involved and theranostics remain unclear. Thus, we tested the hypothesis that nicotine exposure increases the heart sensitivity to ischemia/reperfusion injury and dysfunction, which can be rescued by autophagy inhibitor. Methods: Nicotine or saline was administered to adult rats via subcutaneous osmotic minipumps in the absence or presence of an autophagy inhibitor, 3-methyladenine (3-MA). After 30 days of nicotine treatment, the rats underwent the cardiac ischemia/reperfusion (I/R) procedure and echocardiography analysis, and the heart tissues were isolated for molecular biological studies. Results: Nicotine exposure increased I/R-induced cardiac injury and cardiac dysfunction as compared to the control. The levels of autophagy-related proteins including LC3 II, P62, Beclin1, and Atg5 were upregulated in the reperfused hearts isolated from nicotine-treated group. In addition, nicotine enhanced cardiac and plasma ROS production, and increased the phosphorylation of GSK3β (ser9) in the left ventricle tissues. Treatment with 3-MA abolished nicotine-mediated increase in the levels of autophagy-related proteins and phosphorylation of GSK3β, but had no effect on ROS production. Of importance, 3-MA ameliorated the augmented I/R-induced cardiac injury and dysfunction in the nicotine-treated group as compared to the control. Conclusion: Our results demonstrate that nicotine exposure enhances autophagy signaling pathway, resulting in development of ischemic-sensitive phenotype of heart. It suggests a potentially novel therapeutic strategy of autophagy inhibition for the treatment of ischemic heart disease

NH 3 sensing property and mechanisms of quartz surface acoustic wave sensors deposited with SiO 2 , TiO 2 , and SiO 2 -TiO 2 composite films

Pristine SiO2, TiO2 and composite SiO2-TiO2 films of 200 nm thick were coated on surface of quartz acoustic wave (SAW) sensors with sol-gel and spin coating technique. Their performance and mechanisms for sensing NH3 were systematically investigated. Sensors made with the TiO2 and SiO2-TiO2 films showed positive frequency shifts, whereas SiO2 film exhibits a negative frequency shift to NH3 gas. it is believed that the negative frequency shift was mainly caused by the increase of NH3 mass loading on the sensitive film while the positive frequency shift was associated to the condensation of the hydroxyl groups (-OH) on the film making the film stiffer and lighter, when exposed to NH3 gas. It demonstrated that humidity played a significant factor on the sensing performance. Comparative studies exhibited that the sensor based on the composite SiO2-TiO2 film had a much better sensitivity to NH3 at a low concentration level (1 ppm) with a response of 2 KHz, and also showed fast response and recovery, excellent selectivity, stability and reproducibility

Ectopic Expression Reveals a Conserved PHYB Homolog in Soybean

Phytochromes sense red/far-red light and trigger a cascade of physiological responses in plant. Here, a phytochrome B homolog, GmPHYB1, was amplified from the soybean genome, and its expression profiles were obtained for various parts of the plant and at various developmental stages. The gene was ectopically expressed in Arabidopsis thaliana, driven by CaMV 35S promoter, to study the physiological functions of the gene product. The overexpressors of GmPHYB1 behaved similarly to those of AtPHYB, but with some subtle differences with respect to the acceleration of flowering under short day conditions and the growth of the hypocotyl under certain light fluence rate. The results suggested that this soybean PHYB homolog was well conserved both at the level of sequence and physiological function

Glucagon-like peptide-1 enhances cardiac L-type Ca2+ currents via activation of the cAMP-dependent protein kinase A pathway

<p>Abstract</p> <p>Background</p> <p>Glucagon-like peptide-1 (GLP-1) is a hormone predominately synthesized and secreted by intestinal L-cells. GLP-1 modulates multiple cellular functions and its receptor agonists are now used clinically for diabetic treatment. Interestingly, preclinical and clinical evidence suggests that GLP-1 agonists produce beneficial effects on dysfunctional hearts via acting on myocardial GLP-1 receptors. As the effects of GLP-1 on myocyte electrophysiology are largely unknown, this study was to assess if GLP-1 could affect the cardiac voltage-gated L-type Ca²⁺current (I_Ca).</p> <p>Methods</p> <p>The whole-cell patch clamp method was used to record I_Caand action potentials in enzymatically isolated cardiomyocytes from adult canine left ventricles.</p> <p>Results</p> <p>Extracellular perfusion of GLP-1 (7-36 amide) at 5 nM increased I_Caby 23 ± 8% (<it>p </it>< 0.05, n = 7). Simultaneous bath perfusion of 5 nM GLP-1 plus 100 nM Exendin (9-39), a GLP-1 receptor antagonist, was unable to block the GLP-1-induced increase in I_Ca; however, the increase in I_Cawas abolished if Exendin (9-39) was pre-applied 5 min prior to GLP-1 administration. Intracellular dialysis with a protein kinase A inhibitor also blocked the GLP-1-enhanced I_Ca. In addition, GLP-1 at 5 nM prolonged the durations of the action potentials by 128 ± 36 ms (<it>p </it>< 0.01) and 199 ± 76 ms (<it>p </it>< 0.05) at 50% and 90% repolarization (n = 6), respectively.</p> <p>Conclusions</p> <p>Our data demonstrate that GLP-1 enhances I_Cain canine cardiomyocytes. The enhancement of I_Cais likely via the cAMP-dependent protein kinase A mechanism and may contribute, at least partially, to the prolongation of the action potential duration.</p

Repression of the Glucocorticoid Receptor Aggravates Acute Ischemic Brain Injuries in Adult Mice.

Strokes are one of the leading causes of mortality and chronic morbidity in the world, yet with only limited successful interventions available at present. Our previous studies revealed the potential role of the glucocorticoid receptor (GR) in the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE). In the present study, we investigate the effect of GR knockdown on acute ischemic brain injuries in a model of focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) in adult male CD1 mice. GR siRNAs and the negative control were administered via intracerebroventricular (i.c.v.) injection 48 h prior to MCAO. The cerebral infarction volume and neurobehavioral deficits were determined 48 h after MCAO. RT-qPCR was employed to assess the inflammation-related gene expression profiles in the brain before and after MCAO. Western Blotting was used to evaluate the expression levels of GR, the mineralocorticoid receptor (MR) and the brain-derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) signaling. The siRNAs treatment decreased GR, but not MR, protein expression, and significantly enhanced expression levels of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) in the brain. Of interest, GR knockdown suppressed BDNF/TrkB signaling in adult mice brains. Importantly, GR siRNA pretreatment significantly increased the infarction size and exacerbated the neurobehavioral deficits induced by MCAO in comparison to the control group. Thus, the present study demonstrates the important role of GR in the regulation of the inflammatory responses and neurotrophic BDNF/TrkB signaling pathway in acute ischemic brain injuries in adult mice, revealing a new insight into the pathogenesis and therapeutic potential in acute ischemic strokes