Effects of electron-phonon interactions on the electron tunneling spectrum of PbS quantum dots

We present a tunnel spectroscopy study of single PbS Quantum Dots (QDs) as function of temperature and gate voltage. Three distinct signatures of strong electron-phonon coupling are observed in the Electron Tunneling Spectrum (ETS) of these QDs. In the shell-filling regime, the $8\times$ degeneracy of the electronic levels is lifted by the Coulomb interactions and allows the observation of phonon sub-bands that result from the emission of optical phonons. At low bias, a gap is observed in the ETS that cannot be closed with the gate voltage, which is a distinguishing feature of the Franck-Condon (FC) blockade. From the data, a Huang-Rhys factor in the range $S\sim 1.7 - 2.5$ is obtained. Finally, in the shell tunneling regime, the optical phonons appear in the inelastic ETS $d^2I/dV^2$.Comment: 5 pages, 5 figure

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

STAT3 in the systemic inflammation of cancer cachexia

Weight loss is diagnostic of cachexia, a debilitating syndrome contributing mightily to morbidity and mortality in cancer. Most research has probed mechanisms leading to muscle atrophy and adipose wasting in cachexia; however cachexia is a truly systemic phenomenon. Presence of the tumor elicits an inflammatory response and profound metabolic derangements involving not only muscle and fat, but also the hypothalamus, liver, heart, blood, spleen and likely other organs. This global response is orchestrated in part through circulating cytokines that rise in conditions of cachexia. Exogenous Interleukin-6 (IL6) and related cytokines can induce most cachexia symptomatology, including muscle and fat wasting, the acute phase response and anemia, while IL-6 inhibition reduces muscle loss in cancer. Although mechanistic studies are ongoing, certain of these cachexia phenotypes have been causally linked to the cytokine-activated transcription factor, STAT3, including skeletal muscle wasting, cardiac dysfunction and hypothalamic inflammation. Correlative studies implicate STAT3 in fat wasting and the acute phase response in cancer cachexia. Parallel data in non-cancer models and disease states suggest both pathological and protective functions for STAT3 in other organs during cachexia. STAT3 also contributes to cancer cachexia through enhancing tumorigenesis, metastasis and immune suppression, particularly in tumors associated with high prevalence of cachexia. This review examines the evidence linking STAT3 to multi-organ manifestations of cachexia and the potential and perils for targeting STAT3 to reduce cachexia and prolong survival in cancer patients

Interleukin-6/ GP80-dependent pathways role in physiologic cachexia during liver regeneration after partial hepatectomy

poster abstractLiver has a unique capacity to regenerate its mass after tissue loss. Many of the cytokines and growth factors were shown to be critical in liver regeneration. Studies with interleukin-6 (IL-6) – deficient mice demonstrated that IL-6 plays central role in hepatocyte proliferation via activating signal transducer and activator of transcription 3 (STAT3). The biological activities of IL-6 are potentiated when it binds to an 80 kDa IL-6 (IL-6Ra) receptor located on target cells. IL-6 and Il-6Ra complex then associates with another glycoprotein, gp130, to initiate intracellular signaling. Another of many IL-6 functions is metabolic control of the body. Increased activation of IL6 and STAT3 due to acute body injury, such as partial hepatectomy, causes metabolic dysregulation associated with sustained muscle and adipose tissue loss, a condition called physiologic Cachexia. Two lines of trangenic mice with conditional knockout of gp 80 in the liver and conditional knockout of gp 80 in the muscle were generated to investigate the role of Il6 in liver regeneration and concomitant muscle wasting after partial hepatectomy. Here, we report that specific interruption of IL-6 pathway in the liver was presented with normal liver regeneration but associated with increased animal mortality after partial hepatectomy. Conversely, specific abrogation of IL-6 pathway in muscle lead to increased liver regeneration that did not increase muscle or adipose tissue wasting. These findings suggest that IL-6 pathway may play a central role in the liver regeneration and muscle wasting axis

In Vitro, In Vivo, and In Silico Methods for Assessment of Muscle Size and Muscle Growth Regulation

Trauma, burn injury, sepsis, and ischemia lead to acute and chronic loss of skeletal muscle mass and function. Healthy muscle is essential for eating, posture, respiration, reproduction, and mobility, as well as for appropriate function of the senses including taste, vision, and hearing. Beyond providing support and contraction, skeletal muscle also exerts essential roles in temperature regulation, metabolism, and overall health. As the primary reservoir for amino acids, skeletal muscle regulates whole-body protein and glucose metabolism by providing substrate for protein synthesis and supporting hepatic gluconeogenesis during illness and starvation. Overall, greater muscle mass is linked to greater insulin sensitivity and glucose disposal, strength, power, and longevity. In contrast, low muscle mass correlates with dysmetabolism, dysmobility, and poor survival. Muscle mass is highly plastic, appropriate to its role as reservoir, and subject to striking genetic control. Defining mechanisms of muscle growth regulation holds significant promise to find interventions that promote health and diminish morbidity and mortality after trauma, sepsis, inflammation, and other systemic insults. In this invited review, we summarize techniques and methods to assess and manipulate muscle size and muscle mass in experimental systems, including cell culture and rodent models. These approaches have utility for studies of myopenia, sarcopenia, cachexia, and acute muscle growth or atrophy in the setting of health or injury

Infrared Signature of the Superconducting State in Pr(2-x)Ce(x)CuO(4)

We measured the far infrared reflectivity of two superconducting Pr(2-x)Ce(x)CuO(4) films above and below Tc. The reflectivity in the superconducting state increases and the optical conductivity drops at low energies, in agreement with the opening of a (possibly) anisotropic superconducting gap. The maximum energy of the gap scales roughly with Tc as 2 Delta_{max} / kB Tc ~ 4.7. We determined absolute values of the penetration depth at 5 K as lambda_{ab} = (3300 +/- 700) A for x = 0.15 and lambda_{ab} = (2000 +/- 300) A for x = 0.17. A spectral weight analysis shows that the Ferrell-Glover-Tinkham sum rule is satisfied at conventional low energy scales \~ 4 Delta_{max}.Comment: 4 pages, 4 figure

Multimodal Action of Mas Activation for Systemic Cancer Cachexia Therapy

Cancer cachexia remains a largely intractable, deadly condition for patients with no approved, effective therapies. However, research progress over the past few decades demonstrates that cachexia is a disease with specific, targetable mechanisms. New work by Murphy and colleagues in this issue of Cancer Research suggests that activation of the alternative renin–angiotensin system with the nonpeptide Mas receptor agonist AVE 0991 holds promise for reducing muscle wasting in cancer. Their cell studies demonstrate on-target activity in skeletal muscle cells, whereas their mouse results suggest potentially more important systemic effects