New Phase Induced by Pressure in the Iron-Arsenide Superconductor K-Ba122

The electrical resistivity rho of the iron-arsenide superconductor Ba1-xKxFe2As2 was measured in applied pressures up to 2.6 GPa for four underdoped samples, with x = 0.16, 0.18, 0.19 and 0.21. The antiferromagnetic ordering temperature T_N, detected as a sharp anomaly in rho(T), decreases linearly with pressure. At pressures above around 1.0 GPa, a second sharp anomaly is detected at a lower temperature T_0, which rises with pressure. We attribute this second anomaly to the onset of a phase that causes a reconstruction of the Fermi surface. This new phase expands with increasing x and it competes with superconductivity. We discuss the possibility that a second spin-density wave orders at T_0, with a Q vector distinct from that of the spin-density wave that sets in at T_N.Comment: Two higher K concentrations were added, revealing a steady expansion of the new phase in the T-P phase diagra

The neonatal sepsis is diminished by cervical vagus nerve stimulation and tracked non-invasively by ECG: a preliminary report in the piglet model

In adults, vagus nerve stimulation (VNS) reduces inflammation. In neonates, the effects of VNS are not known. An electrocardiogram (ECG)-derived heart rate variability (HRV) index reliably tracks the inflammatory response induced by low-dose lipopolysaccharide (LPS) in near-term sheep fetuses. We evaluated the VNS effect on the systemic inflammatory response induced by a high dose of LPS in neonatal piglets to mimic late-onset neonatal sepsis. Next, we tested if our HRV inflammatory index tracks inflammation in piglets. Following anesthesia, electrodes were attached to the left vagal nerve; ECG and blood pressure (BP) were recorded throughout the experiment. Following baseline, the piglets were administered LPS as 2mg/kg IV bolus. In the VNS treated piglet, the vagus nerve was stimulated for 10 minutes prior to and 10 min after the injection of LPS. In both groups, every 15 min post LPS, the arterial blood sample was drawn for blood gas, metabolites, and inflammatory cytokines. At the end of the experiment, the piglets were euthanized. BP and HRV measures were calculated. The piglets developed a potent inflammatory response to the LPS injection with TNF-alpha, IL-1beta, IL-6 and IL-8 peaking between 45 and 90 min post-injection. VNS diminished the LPS-induced systemic inflammatory response varying across the measured cytokines from two to ten-fold. The HRV index tracked accurately the cytokines' temporal profile. This novel model allows manipulating and tracking neonatal sepsis: The HRV inflammatory index 1) applies across species pre- and postnatally and 2) performs well at different degrees of sepsis (i.e., nanogram and milligram doses of LPS); 3) the present VNS paradigm effectively suppresses LPS-induced inflammation, even at high doses of LPS. The potential of early postnatal VNS to counteract sepsis and of HRV monitoring to early detect and track it deserve further study

Decision, Sensation, and Habituation: A Multi-Layer Dynamic Field Model for Inhibition of Return

Inhibition of Return (IOR) is one of the most consistent and widely studied effects in experimental psychology. The effect refers to a delayed response to visual stimuli in a cued location after initial priming at that location. This article presents a dynamic field model for IOR. The model describes the evolution of three coupled activation fields. The decision field, inspired by the intermediate layer of the superior colliculus, receives endogenous input and input from a sensory field. The sensory field, inspired by earlier sensory processing, receives exogenous input. Habituation of the sensory field is implemented by a reciprocal coupling with a third field, the habituation field. The model generates IOR because, due to the habituation of the sensory field, the decision field receives a reduced target-induced input in cue-target-compatible situations. The model is consistent with single-unit recordings of neurons of monkeys that perform IOR tasks. Such recordings have revealed that IOR phenomena parallel the activity of neurons in the intermediate layer of the superior colliculus and that neurons in this layer receive reduced input in cue-target-compatible situations. The model is also consistent with behavioral data concerning temporal expectancy effects. In a discussion, the multi-layer dynamic field account of IOR is used to illustrate the broader view that behavior consists of a tuning of the organism to the environment that continuously and concurrently takes place at different spatiotemporal scales

Insulin Resistance and Metabolic Hepatocarcinogenesis with Parent-of-Origin Effects in A×B Mice

Insulin resistance is a defining feature of metabolic syndrome and type 2 diabetes mellitus but also may occur independently of these conditions. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of these disorders, increases the risk of hepatocellular carcinoma (HCC). However, mechanisms linking hyperinsulinemia to NAFLD and HCC require clarification. We describe a novel model of primary insulin resistance and HCC with strong parent-of-origin effects. Male AB6F1 (A/JCr dam × C57BL/6 sire) but not B6AF1 (B6 dam × A/J sire) mice developed spontaneous insulin resistance, NAFLD, and HCC without obesity or diabetes. A survey of mitochondrial, imprinted, and sex-linked traits revealed modest associations with X-linked genes. However, a diet-induced obesity study, including B6.A chromosome substitution–strain (consomic) mice, showed no segregation by sex chromosome. Thus, parent-of-origin effects were specified within the autosomal genome. Next, we interrogated mechanisms of insulin-associated hepatocarcinogenesis. Steatotic hepatocytes exhibited adipogenic transition characterized by vacuolar metaplasia and up-regulation of vimentin, adipsin, fatty acid translocase (CD36), peroxisome proliferator–activated receptor-γ, and related products. This profile was largely recapitulated in insulin-supplemented primary mouse hepatocyte cultures. Importantly, pyruvate kinase M2, a fetal anabolic enzyme implicated in the Warburg effect, was activated by insulin in vivo and in vitro. Thus, our study reveals parent-of-origin effects in heritable insulin resistance, implicating adipogenic transition with acquired anabolic metabolism in the progression from NAFLD to HCC.National Institutes of Health (U.S.) (NIH grant AA016563)National Institutes of Health (U.S.) (NIH grant CA067529)National Institutes of Health (U.S.) (NIH grant P01CA0267)National Institutes of Health (U.S.) (NIH grant P30ES02109)National Institutes of Health (U.S.) (NIH grant RR007036)National Institutes of Health (U.S.) (NIH grant CA158661)National Institutes of Health (U.S.) (NIH grant CA016086