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

Optical determination of the superconducting energy gap in electron-doped Pr_{1.85}Ce_{0.15}CuO_4

The optical properties of single crystal Pr_{1.85}Ce_{0.15}CuO_4 have been measured over a wide frequency range above and below the critical temperature (T_c \simeq 20 K). In the normal state the coherent part of the conductivity is described by the Drude model, from which the scattering rate just above T_c is determined to be 1/\tau \simeq 80 cm^{-1}. The condition that \hbar/\tau \approx 2k_B T near T_c appears to be a general result in many of the cuprate superconductors. Below T_c the formation of a superconducting energy gap is clearly visible in the reflectance, from which the gap maximum is estimated to be \Delta_0 \simeq 35 cm^{-1} (4.3 meV). The ability to observe the superconducting energy gap in the optical properties favors the nonmonotonic over the monotonic description of the d-wave gap. The penetration depth for T\ll T_c is \lambda \simeq 2000 \AA, which when taken with the estimated value for the dc conductivity just above T_c of \sigma_{dc} \simeq 35 \times 10^3 \Omega^{-1}cm^{-1} places this material on the general scaling line for the cuprates defined by 1/\lambda^2 \propto \sigma_{dc}(T\simeq T_c) \times T_c. This result is consistent with the observation that 1/\tau \approx 2\Delta_0, which implies that the material is not in the clean limit.Comment: Discussion has been expanded and reorganized; 9 pages, 6 figure

On the optical conductivity of Electron-Doped Cuprates I: Mott Physics

The doping and temperature dependent conductivity of electron-doped cuprates is analysed. The variation of kinetic energy with doping is shown to imply that the materials are approximately as strongly correlated as the hole-doped materials. The optical spectrum is fit to a quasiparticle scattering model; while the model fits the optical data well, gross inconsistencies with photoemission data are found, implying the presence of a large, strongly doping dependent Landau parameter

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

Pancreas Cancer-Associated Weight Loss.

Unintentional weight loss in patients with pancreatic cancer is highly prevalent and contributes to low therapeutic tolerance, reduced quality of life, and overall mortality. Weight loss in pancreatic cancer can be due to anorexia, malabsorption, and/or cachexia. Proper supportive care can stabilize or reverse weight loss in patients and improve outcomes. We review the literature on supportive care relevant to pancreatic cancer patients, and offer evidence-based recommendations that include expert nutritional assessment, counseling, supportive measures to ensure adequate caloric intake, pancreatic enzyme supplementation, nutritional supplement replacement, orexigenic agents, and exercise. Pancreatic Cancer Action Network-supported initiatives will spearhead the dissemination and adoption of these best supportive care practices. IMPLICATIONS FOR PRACTICE: Weight loss in pancreatic cancer patients is endemic, as 85% of pancreatic cancer patients meet the classic definition of cancer cachexia. Despite its significant prevalence and associated morbidity, there is no established approach to this disease entity. It is believed that this is due to an important knowledge gap in understanding the underlying biology and lack of optimal treatment approaches. This article reviews the literature regarding pancreas cancer-associated weight loss and establishes a new framework from which to view this complex clinical problem. An improved approach and understanding will help educate clinicians, improve clinical care, and provide more clarity for future clinical investigation

Cancer and Chemotherapy Contribute to Muscle Loss by Activating Common Signaling Pathways

Cachexia represents one of the primary complications of colorectal cancer due to its effects on depletion of muscle and fat. Evidence suggests that chemotherapeutic regimens, such as Folfiri, contribute to cachexia-related symptoms. The purpose of the present study was to investigate the cachexia signature in different conditions associated with severe muscle wasting, namely Colon-26 (C26) and Folfiri-associated cachexia. Using a quantitative LC-MS/MS approach, we identified significant changes in 386 proteins in the quadriceps muscle of Folfiri-treated mice, and 269 proteins differentially expressed in the C26 hosts (p < 0.05; -1.5 ≥ fold change ≥ +1.5). Comparative analysis isolated 240 proteins that were modulated in common, with a large majority (218) that were down-regulated in both experimental settings. Interestingly, metabolic (47.08%) and structural (21.25%) proteins were the most represented. Pathway analysis revealed mitochondrial dysfunctions in both experimental conditions, also consistent with reduced expression of mediators of mitochondrial fusion (OPA-1, mitofusin-2), fission (DRP-1) and biogenesis (Cytochrome C, PGC-1α). Alterations of oxidative phosphorylation within the TCA cycle, fatty acid metabolism, and Ca(2+) signaling were also detected. Overall, the proteomic signature in the presence of both chemotherapy and cancer suggests the activation of mechanisms associated with movement disorders, necrosis, muscle cell death, muscle weakness and muscle damage. Conversely, this is consistent with the inhibition of pathways that regulate nucleotide and fatty acid metabolism, synthesis of ATP, muscle and heart function, as well as ROS scavenging. Interestingly, strong up-regulation of pro-inflammatory acute-phase proteins and a more coordinated modulation of mitochondrial and lipidic metabolisms were observed in the muscle of the C26 hosts that were different from the Folfiri-treated animals. In conclusion, our results suggest that both cancer and chemotherapy contribute to muscle loss by activating common signaling pathways. These data support the undertaking of combination strategies that aim to both counteract tumor growth and reduce chemotherapy side effects

Bone Pain and Muscle Weakness in Cancer Patients

PURPOSE OF REVIEW: In this article, we will discuss the current understanding of bone pain and muscle weakness in cancer patients. We will describe the underlying physiology and mechanisms of cancer-induced bone pain (CIBP) and cancer-induced muscle wasting (CIMW), as well as current methods of diagnosis and treatment. We will discuss future therapies and research directions to help patients with these problems. RECENT FINDINGS: There are several pharmacologic therapies that are currently in preclinical and clinical testing that appear to be promising adjuncts to current CIBP and CIMW therapies. Such therapies include resiniferitoxin, which is a targeted inhibitor of noceciptive nerve fibers, and selective androgen receptor modulators, which show promise in increasing lean mass. CIBP and CIMW are significant causes of morbidity in affected patients. Current management is mostly palliative; however, targeted therapies are poised to revolutionize how these problems are treated