Spin-current-mediated rapid magnon localisation and coalescence after ultrafast optical pumping of ferrimagnetic alloys.

Sub-picosecond magnetisation manipulation via femtosecond optical pumping has attracted wide attention ever since its original discovery in 1996. However, the spatial evolution of the magnetisation is not yet well understood, in part due to the difficulty in experimentally probing such rapid dynamics. Here, we find evidence of a universal rapid magnetic order recovery in ferrimagnets with perpendicular magnetic anisotropy via nonlinear magnon processes. We identify magnon localisation and coalescence processes, whereby localised magnetic textures nucleate and subsequently interact and grow in accordance with a power law formalism. A hydrodynamic representation of the numerical simulations indicates that the appearance of noncollinear magnetisation via optical pumping establishes exchange-mediated spin currents with an equivalent 100% spin polarised charge current density of 107 A cm-2. Such large spin currents precipitate rapid recovery of magnetic order after optical pumping. The magnon processes discussed here provide new insights for the stabilization of desired meta-stable states.

Ultrafast Self-Induced X-Ray Transparency and Loss of Magnetic Diffraction.

Using ultrafast ≃2.5 fs and ≃25 fs self-amplified spontaneous emission pulses of increasing intensity and a novel experimental scheme, we report the concurrent increase of stimulated emission in the forward direction and loss of out-of-beam diffraction contrast for a Co/Pd multilayer sample. The experimental results are quantitatively accounted for by a statistical description of the pulses in conjunction with the optical Bloch equations. The dependence of the stimulated sample response on the incident intensity, coherence time, and energy jitter of the employed pulses reveals the importance of increased control of x-ray free electron laser radiation.

Physiological role of Kvß2 (AKR6) in murine skeletal muscle growth and regulation.

AIM: Potassium channel accessory subunits (Kvß) play a key role in cardiac electrical activity through ion channel modulation. In this study, we hypothesize that Kvß2 regulates skeletal muscle growth and fibre phenotype via protein-protein interactions. METHODS: Kvß2 knockout mouse model was used for morphometric, immunohistochemical and biochemical analysis to evaluate the role of Kvß2 in skeletal muscle physiology. RESULTS: Deletion of Kvß2 gene in mice (Kvß2 knockout, KO) leads to significant decrease in body weight along with skeletal muscle size. Key hindlimb muscles such as biceps, soleus and gastrocnemius were significantly smaller in size in KO mice compared to that of wild type. Morphometric measurements and histological analysis clearly point that the fibre size is decreased in each of the muscle type in KO compared with wild-type mice. In addition, Kvß2 deletion contributes to fibre-type switching from fast to slow fibre as indicated by more abundant MHCI-expressing fibres in gastrocnemius and soleus muscles, which may underscore the smaller muscle size alongside increase in U3 ubiquitin ligase; NEDD4 expression. Using targeted siRNA knockdown approach, we identified that Kvß2 knockdown does not affect the myoblasts proliferation. However, Pax7 expression was significantly decreased in 4-week-old gastrocnemius muscle, suggesting that cellular reserve for growth may be deficient in KO mice. This is further supported by decreased migratory capacity of C2C12 cells upon siRNA-targeted Kvß2 knockdown. CONCLUSION: Overall, this is the first report identifying that genetic deletion of Kvß2 leads to decreased skeletal muscle size along with isotype switching.

Changes of microRNA-1, -15b and -21 levels in irradiated rat hearts after treatment with potentially radioprotective drugs.

The aim of this study was to measure expression levels of microRNAs (miRNAs) (miRNA-1, -15b and -21) in the rat myocardium after a single dose of ionizing radiation (6-7 Gy/min, total 25 Gy). The rats were treated with selected drugs (Atorvastatin, acetylsalicylic acid (ASA), Tadalafil, Enbrel) for six weeks after irradiation. MiRNAs levels were measured by RT-qPCR. Irradiation down-regulated miRNA-1 in irradiated hearts. In Tadalafil- and Atorvastatin-treated groups, miRNA-1 expression levels were further decreased compared with irradiated controls. However, Enbrel increased miRNA-1 level in irradiated hearts similarly to that in non-irradiated untreated group. Increase of miRNA-15b is pro-apoptotic in relationship with ischemia. Irradiation caused down-regulation of miRNA-15b. Administration of ASA in the irradiated group resulted in the increase of miRNA-15b expression compared to non-treated controls without irradiation. After Enbrel administration, miRNA-15b levels were overexpressed compared to non-treated normal group. MiRNA-21 belongs to the most markedly up-regulated miRNAs in response to cardiogenic stress. MiRNA-21 was increased nearly 2-fold compared to non-treated hearts whereas Tadalafil reduced miRNA-21 levels (about 40 %). Our study suggests that Enbrel and Tadalafil changed miRNAs expression values of the irradiated rats to the values of non-irradiated controls, thus they might be helpful in mitigation of radiation-induced toxicity.

Photoinduced Enhancement of the Charge Density Wave Amplitude.

Symmetry breaking and the emergence of order is one of the most fascinating phenomena in condensed matter physics. It leads to a plethora of intriguing ground states found in antiferromagnets, Mott insulators, superconductors, and density-wave systems. Exploiting states of matter far from equilibrium can provide even more striking routes to symmetry-lowered, ordered states. Here, we demonstrate for the case of elemental chromium that moderate ultrafast photoexcitation can transiently enhance the charge-density-wave (CDW) amplitude by up to 30% above its equilibrium value, while strong excitations lead to an oscillating, large-amplitude CDW state that persists above the equilibrium transition temperature. Both effects result from dynamic electron-phonon interactions, providing an efficient mechanism to selectively transform a broad excitation of the electronic order into a well-defined, long-lived coherent lattice vibration. This mechanism may be exploited to transiently enhance order parameters in other systems with coupled degrees of freedom.

Correlation-Driven Insulator-Metal Transition in Near-Ideal Vanadium Dioxide Films.

We use polarization- and temperature-dependent x-ray absorption spectroscopy, in combination with photoelectron microscopy, x-ray diffraction, and electronic transport measurements, to study the driving force behind the insulator-metal transition in VO_{2}. We show that both the collapse of the insulating gap and the concomitant change in crystal symmetry in homogeneously strained single-crystalline VO_{2} films are preceded by the purely electronic softening of Coulomb correlations within V-V singlet dimers. This process starts 7 K (±0.3 K) below the transition temperature, as conventionally defined by electronic transport and x-ray diffraction measurements, and sets the energy scale for driving the near-room-temperature insulator-metal transition in this technologically promising material.

Direct observation and imaging of a spin-wave soliton with p-like symmetry.

Spin waves, the collective excitations of spins, can emerge as nonlinear solitons at the nanoscale when excited by an electrical current from a nanocontact. These solitons are expected to have essentially cylindrical symmetry (that is, s-like), but no direct experimental observation exists to confirm this picture. Using a high-sensitivity time-resolved magnetic X-ray microscopy with 50 ps temporal resolution and 35 nm spatial resolution, we are able to create a real-space spin-wave movie and observe the emergence of a localized soliton with a nodal line, that is, with p-like symmetry. Micromagnetic simulations explain the measurements and reveal that the symmetry of the soliton can be controlled by magnetic fields. Our results broaden the understanding of spin-wave dynamics at the nanoscale, with implications for the design of magnetic nanodevices.

Direct Observation of a Localized Magnetic Soliton in a Spin-Transfer Nanocontact.

We report the direct observation of a localized magnetic soliton in a spin-transfer nanocontact using scanning transmission x-ray microscopy. Experiments are conducted on a lithographically defined 150 nm diameter nanocontact to an ultrathin ferromagnetic multilayer with perpendicular magnetic anisotropy. Element-resolved x-ray magnetic circular dichroism images show an abrupt onset of a magnetic soliton excitation localized beneath the nanocontact at a threshold current. However, the amplitude of the excitation ≃25° at the contact center is far less than that predicted (⪅180°), showing that the spin dynamics is not described by existing models.

X-ray Detection of Transient Magnetic Moments Induced by a Spin Current in Cu.

We have used a MHz lock-in x-ray spectromicroscopy technique to directly detect changes in magnetic moment of Cu due to spin injection from an adjacent Co layer. The elemental and chemical specificity of x rays allows us to distinguish two spin current induced effects. We detect the creation of transient magnetic moments of 3×10^{-5}µ_{B} on Cu atoms within the bulk of the 28 nm thick Cu film due to spin accumulation. The moment value is compared to predictions by Mott's two current model. We also observe that the hybridization induced existing magnetic moments at the Cu interface atoms are transiently increased by about 10% or 4×10^{-3}µ_{B} per atom. This reveals the dominance of spin-torque alignment over Joule heat induced disorder of the interfacial Cu moments during current flow.

Speed limit of the insulator-metal transition in magnetite.

As the oldest known magnetic material, magnetite (Fe3O4) has fascinated mankind for millennia. As the first oxide in which a relationship between electrical conductivity and fluctuating/localized electronic order was shown, magnetite represents a model system for understanding correlated oxides in general. Nevertheless, the exact mechanism of the insulator-metal, or Verwey, transition has long remained inaccessible. Recently, three-Fe-site lattice distortions called trimerons were identified as the characteristic building blocks of the low-temperature insulating electronically ordered phase. Here we investigate the Verwey transition with pump-probe X-ray diffraction and optical reflectivity techniques, and show how trimerons become mobile across the insulator-metal transition. We find this to be a two-step process. After an initial 300 fs destruction of individual trimerons, phase separation occurs on a 1.5±0.2 ps timescale to yield residual insulating and metallic regions. This work establishes the speed limit for switching in future oxide electronics.

Cardiovascular protection with sildenafil following chronic inhibition of nitric oxide synthase.

During the past 18 years, sildenafil has evolved from a potential anti-angina drug to an on-demand treatment for erectile dysfunction and more recently to a new orally active treatment for pulmonary hypertension. Recent studies suggest that the drug has powerful cardioprotective effect against ischemia/reperfusion injury, doxorubicin-induced cardiomyopathy and anti-hypertensive effect induced by chronic inhibition of nitric oxide synthase in animals. Based on several recent basic and clinical studies, it is clear that sildenafil and other clinically approved type-5 phosphodiesterase-5 inhibitors including vardenafil and tadalafil will eventually be developed for several cardiovascular indications including essential hypertension, endothelial dysfunction, ischemia/reperfusion injury, myocardial infarction, ventricular remodeling and heart failure.

Secondary post-tonsillectomy haemorrhage and informed consent.

This is a prospective incidence study of 250 secondary post-tonsillectomy haemorrhages from a population of 2706 tonsillectomies performed over a seven-year period, which aims to ascertain the incidence and character of post-tonsillectomy secondary haemorrhage. Out of 250 post-tonsillectomy secondary bleeds (9.2 per cent of total; 95 per cent CI = 8.2 per cent - 10.4 per cent), 39 patients had a severe bleed (1.4 per cent; 95 per cent CI = 1.2 per cent - 2.1 per cent). The incidence of secondary tonsillectomy haemorrhage increased with age, peaking at 30-34 years in both men and women (p < 0.001), with no statistically significant difference between the two sexes (p = 0.23). The incidence of serious haemorrhage increases in the older age categories (p = 0.005) but is not influenced by gender (p = 0.50). The majority of secondary tonsillectomy haemorrhages presented between the fourth and seventh day post-operation (69.8 per cent). These results now provide the basis for informed consent for a tonsillectomy in our department.

Ultrastructural examination of rabbit aortic wall following high-fat diet feeding and selenium supplementation: a transmission electron microscopy study.

Experiments were carried out to examine the changes occurring in the wall of rabbit aortae following high-fat diet (HFD) feeding as well as HFD + selenium supplementation. Male New Zealand White rabbits were divided into three groups-control, HFD-fed and HFD + Se supplementation-and were treated for three months. The study depicted that levels of serum total cholesterol and triglycerides were markedly increased in the HFD-fed group as compared with control animals. However, in the HFD + Se-fed group, these levels were markedly suppressed vis-à-vis animals fed on HFD only. Development of atherogenic and atheromatic plaques has been shown at the light microscopy level in HFD-fed rabbits, whereas these developments were not visible in the HFD + Se-fed rabbits. Transmission electron microscopy findings indicated altered ultrastructure in the endothelial cells of the intimal layer as well as smooth-muscle cells of the medial layer in HFD-fed animals. However, these findings indicated normal ultrastructure in most of the cells, with little ultrastructural alterations from animals supplemented with Se along with HFD feeding. The study on the whole depicted the ability of Se to inhibit the onset of progression of aortic disease and hence has relevance to its therapeutic potential.

Fluid absorption during percutaneous nephrolithotomy: does it matter?

BACKGROUND AND PURPOSE: Large amounts of irrigating fluid are used during percutaneous nephrolithotomy (PCNL). This use may be associated with migrating calculus debris, infection, and fluid absorption. This study evaluated the presence of fluid absorption during PCNL, its clinical and biochemical significance, and maneuvers to reduce it. PATIENTS AND METHODS: Fluid absorption during PCNL was evaluated in 148 patients by estimating the expired breath ethanol concentration. Factors thought to affect the amount of fluid absorbed were studied, including the amount of irrigating fluid used, the number of nephrostomy tracts, the presence of a low-pressure system, the presence of existing tracts, and complications such as bleeding or perforation of the pelvicaliceal wall. RESULTS: Fluid absorption was evident in all patients, although no patient had any clinical or biochemical evidence of intraoperative or postoperative electrolyte imbalance. Creating a low-pressure system by using an Amplatz sheath, reducing the amount of irrigating fluid used, and staging the procedure significantly reduced the amount of fluid absorbed. CONCLUSIONS: Fluid absorption does take place during PCNL. This may be clinically significant in patients with compromised cardiorespiratory or renal status and in pediatric patients, leading to fluid overload. Using a low-pressure system, reducing the nephroscopy time and the amount of irrigating fluid used, and staging the procedure for large renal stone burdens, especially in the presence of complications such as perforation of the pelvicaliceal system, reduces fluid absorption and avoids volume overload. Fluid absorption may also be associated with both infective and noninfective pyrexia, necessitating adequate preoperative control of urinary infection.

p38 Triggers late preconditioning elicited by anisomycin in heart: involvement of NF-kappaB and iNOS.

We investigated the role of stress-activated p38 MAP kinase (p38/SAPK-2) signaling in delayed preconditioning of the heart. Adult male out-bred ICR mice were treated with p38 activator, anisomycin (0.1 mg/kg IP), or vehicle (5% DMSO). Twenty-four hours later, hearts were perfused in Langendorff mode and subjected to 30 minutes of ischemia and 30 minutes of reperfusion. Improvement in postischemic recovery of end-diastolic pressure and reduction in infarct size was observed, which was abolished by SB203580, a specific p38 inhibitor, and pyrrolidinediethyldithiocarbamate (PDTC), the NF-kappaB inhibitor, but not by PD 98059, a specific inhibitor for MEK1 or 2. Transient increase in p38 phosphorylation was observed 15 minutes after anisomycin treatment which subsided by 30 minutes. Electrophoretic mobility shift assay demonstrated rapid activation of NF-kappaB DNA binding with anisomycin, peaking at 30 minutes. Western blot confirmed the accumulation of p50 and p65 in nuclear extracts after anisomycin treatment. Anisomycin-induced NF-kappaB DNA binding activity was inhibited by SB203580 and PDTC. Expression of inducible nitric oxide synthase (iNOS) mRNA, protein, and nitric oxide (NO) synthesis were enhanced in anisomycin-treated mice. SB203580 and PDTC blocked the increased expression of iNOS and increase in synthesis of NO. Selective iNOS inhibitor S-methylisothiourea abolished the protective effect of anisomycin. Furthermore, postischemic cardioprotective effect of anisomycin was absent in mice with targeted ablation of iNOS gene but not in the wild-type B6.129 mice. For the first time, these results suggest that direct pharmacological activation of p38 triggers delayed preconditioning by signaling mechanism involving NF-kappaB activation and synthesis of NO from iNOS.

Whole body hyperthermia and preconditioning of the heart: basic concepts, complexity, and potential mechanisms.

Whole body hyperthermia (WBH) is a distinctive pathophysiological condition with significant impact on tissue metabolism and organ functions. WBH has been investigated as a promising adjunct therapy to the conventional chemo- or radiotherapy for treating certain types of cancer. Numerous studies have shown that WBH is associated with induction of heat shock proteins (HSPs), which in turn modulate cellular survival or death. A brief period of WBH (40-42 degrees C; 15-20 min) can induce delayed protection against lethal endotoxemia as well as various forms of injury in brain, heart, liver, lungs, small intestine, and skeletal muscle. This review article focuses on discussing the WBH-induced myocardial protection against ischemia/reperfusion injury. Most recently, possible involvement of protein kinase C, mitogen-activated protein kinases, nitric oxide, ATP-sensitive potassium channels, and neural peptides in the signal transduction pathways has been demonstrated. On the other hand, whether HSPs or antioxidant enzymes are the primary end-effector of the cardioprotection continues to be a matter of ongoing debates. It has also been recognized that the complex nature of WBH may be the responsible factor for the discordant results among various studies, especially across different animal species or strains, in terms of the time course and potency of WBH-induced cardioprotection. Nevertheless, a better understanding of the WBH-elicited myocardial ischemic resistance may have a wide spectrum of clinical implications as well as insightful inputs into the hyperthermic biology.

Deoxycholic acid (DCA) causes ligand-independent activation of epidermal growth factor receptor (EGFR) and FAS receptor in primary hepatocytes: inhibition of EGFR/mitogen-activated protein kinase-signaling module enhances DCA-induced apoptosis.

Previous studies have argued that enhanced activity of the epidermal growth factor receptor (EGFR) and the mitogen-activated protein kinase (MAPK) pathway can promote tumor cell survival in response to cytotoxic insults. In this study, we examined the impact of MAPK signaling on the survival of primary hepatocytes exposed to low concentrations of deoxycholic acid (DCA, 50 microM). Treatment of hepatocytes with DCA caused MAPK activation, which was dependent upon ligand independent activation of EGFR, and downstream signaling through Ras and PI(3) kinase. Neither inhibition of MAPK signaling alone by MEK1/2 inhibitors, nor exposure to DCA alone, enhanced basal hepatocyte apoptosis, whereas inhibition of DCA-induced MAPK activation caused approximately 25% apoptosis within 6 h. Similar data were also obtained when either dominant negative EGFR-CD533 or dominant negative Ras N17 were used to block MAPK activation. DCA-induced apoptosis correlated with sequential cleavage of procaspase 8, BID, procaspase 9, and procaspase 3. Inhibition of MAPK potentiated bile acid-induced apoptosis in hepatocytes with mutant FAS-ligand, but did not enhance in hepatocytes that were null for FAS receptor expression. These data argues that DCA is causing ligand independent activation of the FAS receptor to stimulate an apoptotic response, which is counteracted by enhanced ligand-independent EGFR/MAPK signaling. In agreement with FAS-mediated cell killing, inhibition of caspase function with the use of dominant negative Fas-associated protein with death domain, a caspase 8 inhibitor (Ile-Glu-Thr-Asp-p-nitroanilide [IETD]) or dominant negative procaspase 8 blocked the potentiation of bile acid-induced apoptosis. Inhibition of bile acid-induced MAPK signaling enhanced the cleavage of BID and release of cytochrome c from mitochondria, which were all blocked by IETD. Despite activation of caspase 8, expression of dominant negative procaspase 9 blocked procaspase 3 cleavage and the potentiation of DCA-induced apoptosis. Treatment of hepatocytes with DCA transiently increased expression of the caspase 8 inhibitor proteins c-FLIP-(S) and c-FLIP-(L) that were reduced by inhibition of MAPK or PI(3) kinase. Constitutive overexpression of c-FLIP-(s) abolished the potentiation of bile acid-induced apoptosis. Collectively, our data argue that loss of DCA-induced EGFR/Ras/MAPK pathway function potentiates DCA-stimulated FAS-induced hepatocyte cell death via a reduction in the expression of c-FLIP isoforms.