AgO investigated by photoelectron spectroscopy : Evidence for mixed valence

We present photoelectron spectroscopy investigations of in-situ prepared AgO. The sample was prepared by room temperature oxidation of Ag in an electron cyclotron resonance O2 plasma. In contrast to other measurements based on ex situ prepared AgO powder samples, our investigations show a distinct double peak structure of the O 1s signal with a remarkable chemical shift of 2.9 eV between the two O 1s components. These two components can not be motivated from a crystallographic point of view as the oxygen sites are all equivalent in the unit cell. We interpret this double peak structure as a characteristic feature of AgO and discuss it in terms of mixed valences

0128 : Sca-1 positive cells, but not c-kit positive cells, differentiate into mature cardiomyocytes after brain natriuretic peptide treatment

The Brain Natriuretic Peptide (BNP) is a cardiac hormone, which promotes the recovery of cardiac function and the preservation of cardiac tissue in animal models of heart diseases. Its cardiac protective role in animals was attributed to fibrosis inhibition, as well as to reduction of cardiomyocyte apoptosis and hypertrophy. Recently, we demonstrated that BNP induces heart regeneration via the stimulation of cardiac precursor cell (CPC) proliferation and differentiation into mature cardiomyocytes.The aim of our study was to identify which CPC’s subset is able to respond to BNP stimulation.Cardiac precursor cells identified as being Sca-1+ Nkx2.5+ or c-kit+ Nkx2.5+ cells, expressed in neonatal and adult hearts BNP’s receptors (NPR-A and NPR-B), showing their ability to be activated by BNP treatment. Cell sorting experiments based on the expression of Sca-1 or c-kit were performed on nonmyocyte cells isolated from neonatal wild-type hearts. Sca-1+ and c-kit+ cells were cultured up to 3 weeks with or without BNP in differentiating medium. Sca-1 positive cells, which contained few c-kit+ cells, responded clearly to BNP stimulation by upregulating mRNA levels of genes coding for Nkx2.5, Mlc-2v, c-kit, Sca-1, beta and alpha MHC. Furthermore, higher number of Troponin I+ cells was detected in BNP treated cells compared to untreated cells, suggesting that Sca-1+ cells differentiated after BNP stimulation into mature cardiomyocytes. BNP treatment of c-kit+ cells didn’t induce the upregulation of mRNA coding for cardiomyocyte specific genes. However, we determined that c-kit positive cells spontaneously differentiated into mature cardiomyocytes during the 3 weeks of cell culture without BNP stimulation.To determine which receptor is involved, Sca-1+ cells, isolated from neonatal hearts of NPR-A or NPR-B deficient mice, were treated with BNP. The effects of BNP on wild type and NPR-A KO cells did not differ substantially. However, Sca-1+ cells isolated from NPR-B deficient hearts couldn’t respond anymore to BNP stimulation.Thus, BNP specifically stimulates via NPR-B Sca-1+ cell differentiation into cardiomyocytes. c-kit+ cells display clearly a cardiogenic potential which is BNP independent

0232: A new role of the brain natriuretic peptide in the heart: Modulation of cardiac precursor cell proliferation and differentiation

The actual role of the brain natriuretic peptide (BNP) in the heart remains elusive despite its reported protective effect in ischemic animal hearts. Because recently BNP was shown to control the proliferation and differentiation of murine embryonic stem cells, we asked in this study whether BNP could influence the proliferation and differentiation of cardiac progenitor cells (CPC) in vitro and in vivo. We first identified a c-kit+ Sca-1+ cell population present in neonatal and adult hearts which expressed the NPR-A and NPR-B receptors. In vitro, these cells proliferated and in presence of BNP differentiated into CPCs (c-kit+ Sca-1+ Nkx2.5+) and into mature cardiomyocytes. In parallel, BNP was injected to newborn and adult healthy mice (n=6 mice per group). In the hearts of both neonatal and adult mice, BNP injection increased the number of newly formed cardiomyocytes (neonatal: + 23%, p= 0.009 and adult: +68%, p= 0.005) and the number of CPCs (neonatal: + 142%, p= 0.002 and adult: +134%, p= 0.04). BrdU injection to neonatal BNP treated mice demonstrated that BNP stimulated CPC proliferation. In anticipation that BNP might be used as a therapeutic agent, we injected BNP into mice undergoing myocardial infarction (n=6-7 mice per group). Higher numbers of Nkx2.5+ cells were detected in both the infarcted (+38%, p=0.03) and non infarcted areas (+69%, p=0.02) of BNP treated hearts one week after surgery. Finally, by isolating neonatal cardiac cells from the hearts of NPR-A or NPR-B deficient mice, we demonstrated that BNP modulates the fate of CPCs via NPRB binding and that long term BNP treatment is correlated in vitro and in vivo with decreased Protein Kinase G activity. Our results highlight a new key role for BNP in the control of CPC proliferation and/or differentiation. This new function of BNP should be evaluated in therapies aimed to induce cardiac cell regeneration and should reopen the debate about the therapeutic use of BNP for patients suffering from heart diseases

Natriuretic Peptide Receptor B modulates the proliferation of the cardiac cells expressing the Stem Cell Antigen-1.

Brain Natriuretic Peptide (BNP) injections in adult "healthy" or infarcted mice led to increased number of non-myocyte cells (NMCs) expressing the nuclear transcription factor Nkx2.5. The aim of this study was to identify the nature of the cells able to respond to BNP as well as the signaling pathway involved. BNP treatment of neonatal mouse NMCs stimulated Sca-1 <sup>+</sup> cell proliferation. The Sca-1 <sup>+</sup> cells were characterized as being a mixed cell population involving fibroblasts and multipotent precursor cells. Thus, BNP treatment led also to increased number of Sca-1 <sup>+</sup> cells expressing Nkx2.5, in Sca-1 <sup>+</sup> cell cultures in vitro and in vivo, in the hearts of neonatal and adult infarcted mice. Whereas BNP induced Sca-1 <sup>+</sup> cell proliferation via NPR-B receptor and protein kinase G activation, CNP stimulated Sca-1 <sup>+</sup> cell proliferation via NPR-B and a PKG-independent mechanism. We highlighted here a new role for the natriuretic peptide receptor B which was identified as a target able to modulate the proliferation of the Sca-1 <sup>+</sup> cells. The involvement of NPR-B signaling in heart regeneration has, however, to be further investigated

A multichannel wireless sEMG sensor endowing a 0.13 μm CMOS mixed-signal SoC

This paper presents a wireless multichannel surface electromyography (sEMG) sensor which features a custom 0.13μm CMOS mixed-signal system-on-chip (SoC) analog frontend circuit. The proposed sensor includes 10 sEMG recording channels with tunable bandwidth (BW) and analog-to-digital converter (ADC) resolution. The SoC includes 10x bioamplifiers, 10x 3 rd order ΔΣ MASH 1-1-1 ADC, and 10x on-chip decimation filters (DF). This SoC provides the sEMG samples data through a serial peripheral interface (SPI) bus to a microcontroller unit (MCU) that then transfers the data to a wireless transceiver. We report sEMG waveforms acquired using a custom multichannel electrode module, and a comparison with a commercial grade system. Results show that the proposed integrated wireless SoC-based system compares well with the commercial grade sEMG recording system. The sensor has an input-referred noise of 2.5 μVrms (BW of 10-500 Hz), an input-dynamic range of 6 mVpp, a programmable sampling rate of 2 ksps, for sEMG, while consuming only 7.1 μW/Ch for the SoC (w/ ADC & DF) and 21.8 mW of power for the sensor (Transceiver, MCU, etc.). The system lies on a 1.5 × 2.0 cm 2 printed circuit board and weights <; 1 g

Receptor binding proteins of Listeria monocytogenes bacteriophages A118 and P35 recognize serovar-specific teichoic acids

Adsorption of a bacteriophage to the host requires recognition of a cell wall-associated receptor by a receptor binding protein (RBP). This recognition is specific, and high affinity binding is essential for efficient virus attachment. The molecular details of phage adsorption to the Gram-positive cell are poorly understood. We present the first description of receptor binding proteins and a tail tip structure for the siphovirus group infecting Listeria monocytogenes. The host-range determining factors in two phages, A118 and P35 specific for L. monocytogenes serovar 1/2 have been determined. Two proteins were identified as RBPs in phage A118. Rhamnose residues in wall teichoic acids represent the binding ligands for both proteins. In phage P35, protein gp16 could be identified as RBP and the role of both rhamnose and N-acetylglucosamine in phage adsorption was confirmed. Immunogold-labeling and transmission electron microscopy allowed the creation of a topological model of the A118 phage tail

Fatigue, Induced via Repetitive Upper-Limb Motor Tasks, Influences Trunk and Shoulder Kinematics During an Upper Limb Reaching Task in a Virtual Reality Environment

Background Efficient shoulder movement depends on the ability of central nervous system to integrate sensory information and to create an appropriate motor command. Various daily encountered factors can potentially compromise the execution of the command, such as fatigue. This study explored how fatigue influences shoulder movements during upper limb reaching. Methods Forty healthy participants were randomly assigned to one of two groups: Control or Fatigue Group. All participants completed an upper limb reaching task at baseline and post-experimental, during which they reached four targets located at 90° of shoulder abduction, 90° external rotation at 90° abduction, 120° scaption, and 120° flexion in a virtual reality environment. Following the baseline phase, the Fatigue Group completed a shoulder fatigue protocol, while Controls took a 10-minute break. Thereafter, the reaching task was repeated. Upper limb kinematic (joint angles and excursions) and spatiotemporal (speed and accuracy) data were collected during the reaching task. Electromyographic activity of the anterior and middle deltoids were also collected to characterize fatigue. Two-way repeated-measures ANOVA were performed to determine the effects of Time, Group and of the interaction between these factors. Results The Fatigue group showed decreased mean median power frequency and increased electromyographic amplitudes of the anterior deltoid (p \u3c 0.05) following the fatigue protocol. Less glenohumeral elevation, increased trunk flexion and rotation and sternoclavicular elevation were also observed in the Fatigue group (Group x Time interaction, p \u3c 0.05). The Control group improved their movement speed and accuracy in post-experimental phase, while the Fatigue group showed a decrease of movement speed and no accuracy improvement (Group x Time interaction, p \u3c 0.05). Conclusion In a fatigued state, changes in movement strategy were observed during the reaching task, including increased trunk and sternoclavicular movements and less glenohumeral movement. Performance was altered as shown by the lack of accuracy improvement over time and a decrease in movement speed in the Fatigue group

JNK3 is abundant in insulin-secreting cells and protects against cytokine-induced apoptosis

Aims/hypothesis: In insulin-secreting cells, activation of the c-Jun NH2-terminal kinase (JNK) pathway triggers apoptosis. Whereas JNK1 and JNK2 are ubiquitously produced, JNK3 has been described exclusively in neurons. This report aims to characterise the expression and role in apoptosis of the three JNK isoforms in insulin-secreting cells exposed to cytokines. Methods: Sections of human and mouse pancreases were used for immunohistochemistry studies with isoform-specific anti-JNK antibodies. Human, pig, mouse and rat pancreatic islets were isolated by enzymatic digestion and RNA or protein extracts were prepared. RNA and protein levels were determined by quantitative RT-PCR and western blotting respectively, using JNK-isoform-specific primers and isoform-specific antibodies; activities of the three JNK isoforms were determined by kinase assays following quantitative immunoprecipitation/depletion of JNK3. JNK silencing was performed with small interfering RNAs and apoptotic rates were determined in INS-1E cells by scoring cells displaying pycnotic nuclei. Results: JNK3 and JNK2 mRNAs are the predominant isoforms expressed in human pancreatic islets. JNK3 is nuclear while JNK2 is also cytoplasmic. In INS-1E cells, JNK3 knockdown increases c-Jun levels and caspase-3 cleavage and sensitises cells to cytokine-induced apoptosis; in contrast, JNK1 or JNK2 knockdown is protective. Conclusions/interpretation: In insulin-secreting cells, JNK3 plays an active role in preserving pancreatic beta cell mass from cytokine attacks. The specific localisation of JNK3 in the nucleus, its recruitment by cytokines, and its effects on key transcription factors such as c-Jun, indicate that JNK3 is certainly an important player in the transcriptional control of genes expressed in insulin-secreting cell

Impact of aerobic exercise type on blood flow, muscle energy metabolism, and mitochondrial biogenesis in experimental lower extremity artery disease.

Exercise training (ET) is recommended for lower extremity artery disease (LEAD) management. However, there is still little information on the hemodynamic and metabolic adaptations by skeletal muscle with ET. We examined whether hindlimb perfusion/vascularization and muscle energy metabolism are altered differently by three types of aerobic ET. ApoE &lt;sup&gt;-/-&lt;/sup&gt; mice with LEAD were assigned to one of four groups for 4 weeks: sedentary (SED), forced treadmill running (FTR), voluntary wheel running (VWR), or forced swimming (FS). Voluntary exercise capacity was improved and equally as efficient with FTR and VWR, but remained unchanged with FS. Neither ischemic hindlimb perfusion and oxygenation, nor arteriolar density and mRNA expression of arteriogenic-related genes differed between groups. &lt;sup&gt;18&lt;/sup&gt; FDG PET imaging revealed no difference in the steady-state levels of phosphorylated &lt;sup&gt;18&lt;/sup&gt; FDG in ischemic and non-ischemic hindlimb muscle between groups, nor was glycogen content or mRNA and protein expression of glucose metabolism-related genes in ischemic muscle modified. mRNA (but not protein) expression of lipid metabolism-related genes was upregulated across all exercise groups, particularly by non-ischemic muscle. Markers of mitochondrial content (mitochondrial DNA content and citrate synthase activity) as well as mRNA expression of mitochondrial biogenesis-related genes in muscle were not increased with ET. Contrary to FTR and VWR, swimming was ineffective in improving voluntary exercise capacity. The underlying hindlimb hemodynamics or muscle energy metabolism are unable to explain the benefits of running exercise

Chemical contrast in STM imaging of transition metal aluminides

The present manuscript reviews recent scanning tunnelling microscopy (STM) studies of transition metal (TM) aluminide surfaces. It provides a general perspective on the contrast between Al atoms and TM atoms in STM imaging. A general trend is the much stronger bias dependence of TM atoms, or TM-rich regions of the surface. This dependence can be attenuated by the local chemical arrangements and environments. Al atoms can show a stronger bias dependence when their chemical environment, such as their immediate subsurface, is populated with TM. All this is well explained in light of combined results of STM and both theoretical and experimental electronic and crystallographic structure determinations. Since STM probes the Fermi surface, the electronic structure in the vicinity of the Fermi level (EF) is essential forunderstanding contrast and bias dependence. Hence, partial density of states provides information about the TM d band position and width, s–p–d hybridization or interactions, or charge transfer between constituent elements. In addition, recent developments in STM image simulations are very interesting for elucidating chemical contrast at Al–TM alloy surfaces, and allow direct atomic identification, when the surface does not show too much disorder. Overall, we show that chemically-specific imaging is often possible at these surfaces