Vacuum-UV negative photoion spectroscopy of CH4

Using synchrotron radiation in the range 12-35 eV, negative ions are detected by mass spectrometry following vacuum-UV photoexcitation of methane. Ion yields for H$^-$, CH$^-$ and CH$_2^-$ are recorded, the spectra of CH$^-$ and CH$_2^-$ for the first time. All ions display a linear dependence of signal with pressure, showing that they arise from unimolecular ion-pair dissociation. Cross sections for ion-pair formation are put onto an absolute scale by calibrating the signal strengths with those of F$^-$ from SF$_6$ and CF$_4$. Following normalisation to total vacuum-UV absorption cross sections, quantum yields for anion production are reported. There is a major discrepancy in the H$^-$ cross section with an earlier measurement, which remains unresolved. The anions arise from both direct and indirect ion-pair mechanisms. For a generic polyatomic molecule AB, the former is defined as AB $\rightarrow$ A$^-$ + B$^+$ (+ neutrals), the latter as the predissociative crossing of an initially-excited Rydberg state of AB by an ion-pair state. In a separate experiment, the threshold photoelectron spectrum of the second valence band of CH$_4$, ionisation to CH$_4^+$ A $^2$A$_1$ at 22.4 eV, is recorded with an instrumental resolution of 0.004 eV; many of the Rydberg states observed in indirect ion-pair formation converge to this state. The widths of the peaks are lifetime limited, increasing with increasing $v$ in the $v_1$ (a$_1$) vibrational ladder. They are the first direct measurement of an upper value to the dissociation rate of these levels into fragment ions

Altered functional brain network connectivity and glutamate system function in transgenic mice expressing truncated Disrupted-in-Schizophrenia 1

Considerable evidence implicates DISC1 as a susceptibility gene for multiple psychiatric diseases. DISC1 has been intensively studied at the molecular, cellular and behavioral level, but its role in regulating brain connectivity and brain network function remains unknown. Here, we utilize a set of complementary approaches to assess the functional brain network abnormalities present in mice expressing a truncated Disc1 gene (Disc1tr Hemi mice). Disc1tr Hemi mice exhibited hypometabolism in the prefrontal cortex (PFC) and reticular thalamus along with a reorganization of functional brain network connectivity that included compromised hippocampal–PFC connectivity. Altered hippocampal–PFC connectivity in Disc1tr Hemi mice was confirmed by electrophysiological analysis, with Disc1tr Hemi mice showing a reduced probability of presynaptic neurotransmitter release in the monosynaptic glutamatergic hippocampal CA1–PFC projection. Glutamate system dysfunction in Disc1tr Hemi mice was further supported by the attenuated cerebral metabolic response to the NMDA receptor (NMDAR) antagonist ketamine and decreased hippocampal expression of NMDAR subunits 2A and 2B in these animals. These data show that the Disc1 truncation in Disc1tr Hemi mice induces a range of translationally relevant endophenotypes underpinned by glutamate system dysfunction and altered brain connectivity

Purification and properties of white muscle lactate dehydrogenase from the anoxia-tolerant turtle, the red-eared slider, trachemys scripta elegans

Lactate dehydrogenase (LDH; E.C. 1.1.1.27) is a crucial enzyme involved in energy metabolism in muscle, facilitating the production of ATP via glycolysis during oxygen deprivation by recycling NAD+. The present study investigated purified LDH from the muscle of 20 h anoxic and normoxic T. s. elegans, and LDH from anoxic muscle showed a significantly lower (47%) K m for L-lactate and a higher V max value than the normoxic form. Several lines of evidence indicated that LDH was converted to a low phosphate form under anoxia: (a) stimulation of endogenously present protein phosphatases decreased the K m of L-lactate of control LDH to anoxic levels, whereas (b) stimulation of kinases increased the K m of L-lactate of anoxic LDH to normoxic levels, and (c) dot blot analysis shows significantly less serine (78%) and threonine (58%) phosphorylation in anoxic muscle LDH as compared to normoxic LDH. The physiological consequence of anoxia-induced LDH dephosphorylation appears to be an increase in LDH activity to promote the reduction of pyruvate in muscle tissue, converting the glycolytic end product to lactate to maintain a prolonged glycolytic flux under energy-stressed anoxic conditions

Altered extracellular vesicle microrna expression in ischemic stroke and small vessel disease

Active transport of microRNAs (miRNA) in extracellular vesicles (EV) occurs in disease. Circulating EV-packaged miRNAs in the serum of stroke patients were compared to stroke mimics with matched cardio- and cerebrovascular risk factors, with corroboration of results in a pre-clinical model. An unbiased miRNA microarray was performed in stroke vs stroke mimic patients (n=39). Results were validated (n=173 patients) by real-time quantitative polymerase chain reaction. miRNA expression was quantified in total serum/EV (n=5-7) of naïve adult spontaneously hypertensive stroke-prone rats (SHRSP), their normotensive reference strain (Wistar Kyoto, WKY) and in circulating EV (n=3), peri-infarct brain (n=6) or EV derived from this region (n=3) in SHRSP following transient middle cerebral artery occlusion (tMCAO). Circulating EV concentration did not differ between stroke and stroke mimic patients. The microarray identified many altered EV-packaged miRNAs: levels of miRNA-17-5p, -20b-5p and -93-5p (miRNA-17 family members) and miRNA-27b-3p were significantly (p≤0.05) increased in stroke vs stroke mimic patients. Patients with small vessel disease (SVD) consistently had the highest miRNA levels. Circulating EV concentration was unaltered between naïve SHRSP and WKY but levels of miRNA-17-5p and -93-5p were significantly increased in SHRSP. tMCAO in SHRSP did not further alter circulating EV miRNA-17 family member expression and nor did it change total miRNA-17 family levels in peri-infarct brain tissue or in EV isolated from this region at 24hrs post-tMCAO. Changes in EV packaged miRNA expression was validated in patients with stroke, particularly those with SVD, and corroborated pre-clinically. Together, altered circulating EV levels of miRNA-17 family members may reflect the chronic sequelae underlying cerebrovascular SVD rather than the acute ischemic stroke itself

Magnetic field generation through angular momentum exchange between circularly polarized radiation and charged particles

The interaction between circularly polarized (CP) radiation and charged particles can lead to generation of magnetic field through an inverse Faraday effect. The spin of the circularly polarized electromagnetic wave can be converted into the angular momentum of the charged particles so long as there is dissipation. We demonstrate this by considering two mechanisms of angular momentum absorption relevant for laser-plasma interactions: electron-ion collisions and ionization. The precise dissipative mechanism, however, plays a role in determining the efficiency of the magnetic field generation

Asymptotic properties of Born-improved amplitudes with gauge bosons in the final state

For processes with gauge bosons in the final state we show how to continuously connect with a single Born-improved amplitude the resonant region, where resummation effects are important, with the asymptotic region far away from the resonance, where the amplitude must reduce to its tree-level form. While doing so all known field-theoretical constraints are respected, most notably gauge-invariance, unitarity and the equivalence theorem. The calculations presented are based on the process $f\bar{f}\to ZZ$, mediated by a possibly resonant Higgs boson; this process captures all the essential features, and can serve as a prototype for a variety of similar calculations. By virtue of massive cancellations the resulting closed expressions for the differential and total cross-sections are particularly compact.Comment: 23 pages, Latex, 4 Figures, uses axodra

Socially impaired robots: Human social disorders and robots’ socio-emotional intelligence

© Springer International Publishing Switzerland 2014. Social robots need intelligence in order to safely coexist and interact with humans. Robots without functional abilities in understanding others and unable to empathise might be a societal risk and they may lead to a society of socially impaired robots. In this work we provide a survey of three relevant human social disorders, namely autism, psychopathy and schizophrenia, as a means to gain a better understanding of social robots’ future capability requirements.We provide evidence supporting the idea that social robots will require a combination of emotional intelligence and social intelligence, namely socio-emotional intelligence. We argue that a robot with a simple socio-emotional process requires a simulation-driven model of intelligence. Finally, we provide some critical guidelines for designing future socio-emotional robots