Local tunneling spectroscopy of the electron-doped cuprate Sm1.85Ce0.15CuO4

We present local tunneling spectroscopy in the optimally electron-doped cuprate Sm2-xCexCuO4 x=0.15. A clear signature of the superconducting gap is observed with an amplitude ranging from place to place and from sample to sample (Delta~3.5-6meV). Another spectroscopic feature is simultaneously observed at high energy above \pm 50meV. Its energy scale and temperature evolution is found to be compatible with previous photoemission and optical experiments. If interpreted as the signature of antiferromagnetic order in the samples, these results could suggest the coexistence on the local scale of antiferromagnetism and superconductivity on the electron-doped side of cuprate superconductors

Increase in muscle mitochondrial biogenesis does not prevent muscle loss but increased tumor size in a mouse model of acute cancer-induced cachexia.

Cancer-associated cachexia is a complex metabolic condition characterized by the progressive loss of body fat and deterioration of muscle mass. Although the cellular and molecular mechanisms of cachexia are incompletely understood, previous studies have suggested mitochondrial dysfunction in murine models of cancer cachexia. To better understand the metabolic shift in cancer-induced cachexia, we studied the effects of enhanced oxidative capacity on muscle wasting using transgenic mice over-expressing Peroxisome Proliferator-Activated Receptor gamma Co-activator-1α (PGC-1α) in skeletal muscle in a Lewis lung carcinoma-implanted model. Increased mitochondrial biogenesis was observed in the skeletal muscle of tumor-implanted mice. However, these increases did not prevent or reverse muscle wasting in mice harboring tumors. Moreover, tumor size was increased in muscle PGC-1α over-expressing mice. We found similar levels of circulating inflammatory cytokines in tumor-implanted animals, which was not affected by increased muscle expression of PGC-1α. Our data indicated that increased mitochondrial biogenesis in skeletal muscle is not sufficient to rescue tumor-associated, acute muscle loss, and could promote tumor growth, possibly through the release of myokines

Influence of ion implantation on the magnetic and transport properties of manganite films

We have used oxygen ions irradiation to generate controlled structural disorder in thin manganite films. Conductive atomic force microscopy CAFM), transport and magnetic measurements were performed to analyze the influence of the implantation process in the physical properties of the films. CAFM images show regions with different conductivity values, probably due to the random distribution of point defect or inhomogeneous changes of the local Mn3+/4+ ratio to reduce lattice strains of the irradiated areas. The transport and magnetic properties of these systems are interpreted in this context. Metal-insulator transition can be described in the frame of a percolative model. Disorder increases the distance between conducting regions, lowering the observed TMI. Point defect disorder increases localization of the carriers due to increased disorder and locally enhanced strain field. Remarkably, even with the inhomogeneous nature of the samples, no sign of low field magnetoresistance was found. Point defect disorder decreases the system magnetization but doesn t seem to change the magnetic transition temperature. As a consequence, an important decoupling between the magnetic and the metal-insulator transition is found for ion irradiated films as opposed to the classical double exchange model scenario.Comment: 27 pages, 11 Figure

Strength of Correlations in electron and hole doped cuprates

High temperature superconductivity was achieved by introducing holes in a parent compound consisting of copper oxide layers separated by spacer layers. It is possible to dope some of the parent compounds with electrons, and their physical properties are bearing some similarities but also significant differences from the hole doped counterparts. Here, we use a recently developed first principles method, to study the electron doped cuprates and elucidate the deep physical reasons why their behavior is so different than the hole doped materials. We find that electron doped compounds are Slater insulators, e.g. a material where the insulating behavior is the result of the presence of magnetic long range order. This is in sharp contrast with the hole doped materials, where the parent compound is a Mott charge transfer insulator, namely a material which is insulating due to the strong electronic correlations but not due to the magnetic order.Comment: submitted to Nature Physic

Serum Concentrations of Myostatin and Myostatin-Interacting Proteins do not differ between young and Scarcopenic elderly men

Peer reviewedPostprin

Spin correlations in the electron-doped high-transition-temperature superconductor Nd{2-x}Ce{x}CuO{4+/-delta}

High-transition-temperature (high-Tc) superconductivity develops near antiferromagnetic phases, and it is possible that magnetic excitations contribute to the superconducting pairing mechanism. To assess the role of antiferromagnetism, it is essential to understand the doping and temperature dependence of the two-dimensional antiferromagnetic spin correlations. The phase diagram is asymmetric with respect to electron and hole doping, and for the comparatively less-studied electron-doped materials, the antiferromagnetic phase extends much further with doping [1, 2] and appears to overlap with the superconducting phase. The archetypical electron-doped compound Nd{2-x}Ce{x}CuO{4\pm\delta} (NCCO) shows bulk superconductivity above x \approx 0.13 [3, 4], while evidence for antiferromagnetic order has been found up to x \approx 0.17 [2, 5, 6]. Here we report inelastic magnetic neutron-scattering measurements that point to the distinct possibility that genuine long-range antiferromagnetism and superconductivity do not coexist. The data reveal a magnetic quantum critical point where superconductivity first appears, consistent with an exotic quantum phase transition between the two phases [7]. We also demonstrate that the pseudogap phenomenon in the electron-doped materials, which is associated with pronounced charge anomalies [8-11], arises from a build-up of spin correlations, in agreement with recent theoretical proposals [12, 13].Comment: 5 pages, 4 figure

Direct observation of electronic inhomogeneities induced by point defect disorder in manganite films

We have investigated the influence of point defect disorder in the electronic properties of manganite films. Real-time mapping of ion irradiated samples conductivity was performed though conductive atomic force microscopy (CAFM). CAFM images show electronic inhomogeneities in the samples with different physical properties due to spatial fluctuations in the point defect distribution. As disorder increases, the distance between conducting regions increases and the metal-insulator transition shifts to lower temperatures. Transport properties in these systems can be interpreted in terms of a percolative model. The samples saturation magnetization decreases as the irradiation dose increases whereas the Curie temperature remains unchanged

GDF-15 is abundantly expressed in plexiform lesions in patients with pulmonary arterial hypertension and affects proliferation and apoptosis of pulmonary endothelial cells

<p>Abstract</p> <p>Background</p> <p>Growth-differentiation factor-15 (GDF-15) is a stress-responsive, transforming growth factor-β-related cytokine, which has recently been reported to be elevated in serum of patients with idiopathic pulmonary arterial hypertension (IPAH). The aim of the study was to examine the expression and biological roles of GDF-15 in the lung of patients with pulmonary arterial hypertension (PAH).</p> <p>Methods</p> <p>GDF-15 expression in normal lungs and lung specimens of PAH patients were studied by real-time RT-PCR and immunohistochemistry. Using laser-assisted micro-dissection, GDF-15 expression was further analyzed within vascular compartments of PAH lungs. To elucidate the role of GDF-15 on endothelial cells, human pulmonary microvascular endothelial cells (HPMEC) were exposed to hypoxia and laminar shear stress. The effects of GDF-15 on the proliferation and cell death of HPMEC were studied using recombinant GDF-15 protein.</p> <p>Results</p> <p>GDF-15 expression was found to be increased in lung specimens from PAH patients, com-pared to normal lungs. GDF-15 was abundantly expressed in pulmonary vascular endothelial cells with a strong signal in the core of plexiform lesions. HPMEC responded with marked upregulation of GDF-15 to hypoxia and laminar shear stress. Apoptotic cell death of HPMEC was diminished, whereas HPMEC proliferation was either increased or decreased depending of the concentration of recombinant GDF-15 protein.</p> <p>Conclusions</p> <p>GDF-15 expression is increased in PAH lungs and appears predominantly located in vascular endothelial cells. The expression pattern as well as the observed effects on proliferation and apoptosis of pulmonary endothelial cells suggest a role of GDF-15 in the homeostasis of endothelial cells in PAH patients.</p

STAT3 Activation in Skeletal Muscle Links Muscle Wasting and the Acute Phase Response in Cancer Cachexia

Cachexia, or weight loss despite adequate nutrition, significantly impairs quality of life and response to therapy in cancer patients. In cancer patients, skeletal muscle wasting, weight loss and mortality are all positively associated with increased serum cytokines, particularly Interleukin-6 (IL-6), and the presence of the acute phase response. Acute phase proteins, including fibrinogen and serum amyloid A (SAA) are synthesized by hepatocytes in response to IL-6 as part of the innate immune response. To gain insight into the relationships among these observations, we studied mice with moderate and severe Colon-26 (C26)-carcinoma cachexia.Moderate and severe C26 cachexia was associated with high serum IL-6 and IL-6 family cytokines and highly similar patterns of skeletal muscle gene expression. The top canonical pathways up-regulated in both were the complement/coagulation cascade, proteasome, MAPK signaling, and the IL-6 and STAT3 pathways. Cachexia was associated with increased muscle pY705-STAT3 and increased STAT3 localization in myonuclei. STAT3 target genes, including SOCS3 mRNA and acute phase response proteins, were highly induced in cachectic muscle. IL-6 treatment and STAT3 activation both also induced fibrinogen in cultured C2C12 myotubes. Quantitation of muscle versus liver fibrinogen and SAA protein levels indicates that muscle contributes a large fraction of serum acute phase proteins in cancer.These results suggest that the STAT3 transcriptome is a major mechanism for wasting in cancer. Through IL-6/STAT3 activation, skeletal muscle is induced to synthesize acute phase proteins, thus establishing a molecular link between the observations of high IL-6, increased acute phase response proteins and muscle wasting in cancer. These results suggest a mechanism by which STAT3 might causally influence muscle wasting by altering the profile of genes expressed and translated in muscle such that amino acids liberated by increased proteolysis in cachexia are synthesized into acute phase proteins and exported into the blood