Magnetoresistance and electronic structure of asymmetric GaAs/AlGaAs double quantum wells in the in-plane/tilted magnetic field

Bilayer two-dimensional electron systems formed by a thin barrier in the GaAs buffer of a standard heterostructure were investigated by magnetotransport measurements. In magnetic fields oriented parallel to the electron layers, the magnetoresistance exhibits an oscillation associated with the depopulation of the higher occupied subband and the field-induced transition into a decoupled bilayer. Shubnikov-de Haas oscillations in slightly tilted magnetic fields allow to reconstruct the evolution of the electron concentration in the individual subbands as a function of the in-plane magnetic field. The characteristics of the system derived experimentally are in quantitative agreement with numerical self-consistent-field calculations of the electronic structure.Comment: 6 pages, 5 figure

Magneto-Gyrotropic Photogalvanic Effects in Semiconductor Quantum Wells

We show that free-carrier (Drude) absorption of both polarized and unpolarized terahertz radiation in quantum well (QW) structures causes an electric photocurrent in the presence of an in-plane magnetic field. Experimental and theoretical analysis evidences that the observed photocurrents are spin-dependent and related to the gyrotropy of the QWs. Microscopic models for the photogalvanic effects in QWs based on asymmetry of photoexcitation and relaxation processes are proposed. In most of the investigated structures the observed magneto-induced photocurrents are caused by spin-dependent relaxation of non-equilibrium carriers

Derangements of amino acids in cachectic skeletal muscle are caused by mitochondrial dysfunction.

Background Cachexia is the direct cause of at least 20% of cancer-associated deaths. Muscle wasting in skeletal muscle results in weakness, immobility, and death secondary to impaired respiratory muscle function. Muscle proteins are massively degraded in cachexia; nevertheless, the molecular mechanisms related to this process are poorly understood. Previous studies have reported conflicting results regarding the amino acid abundances in cachectic skeletal muscle tissues. There is a clear need to identify the molecular processes of muscle metabolism in the context of cachexia, especially how different types of molecules are involved in the muscle wasting process. Methods New in situ -omics techniques were used to produce a more comprehensive picture of amino acid metabolism in cachectic muscles by determining the quantities of amino acids, proteins, and cellular metabolites. Using matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging, we determined the in situ concentrations of amino acids and proteins, as well as energy and other cellular metabolites, in skeletal muscle tissues from genetic mouse cancer models (n = 21) and from patients with cancer (n = 6). Combined results from three individual MALDI mass spectrometry imaging methods were obtained and interpreted. Immunohistochemistry staining for mitochondrial proteins and myosin heavy chain expression, digital image analysis, and transmission electron microscopy complemented the MALDI mass spectrometry imaging results. Results Metabolic derangements in cachectic mouse muscle tissues were detected, with significantly increased quantities of lysine, arginine, proline, and tyrosine (P = 0.0037, P = 0.0048, P = 0.0430, and P = 0.0357, respectively) and significantly reduced quantities of glutamate and aspartate (P = 0.0008 and P = 0.0124). Human skeletal muscle tissues revealed similar tendencies. A majority of altered amino acids were released by the breakdown of proteins involved in oxidative phosphorylation. Decreased energy charge was observed in cachectic muscle tissues (P = 0.0101), which was related to the breakdown of specific proteins. Additionally, expression of the cationic amino acid transporter CAT1 was significantly decreased in the mitochondria of cachectic mouse muscles (P = 0.0133); this decrease may play an important role in the alterations of cationic amino acid metabolism and decreased quantity of glutamate observed in cachexia. Conclusions Our results suggest that mitochondrial dysfunction has a substantial influence on amino acid metabolism in cachectic skeletal muscles, which appears to be triggered by diminished CAT1 expression, as well as the degradation of mitochondrial proteins. These findings provide new insights into the pathobiochemistry of muscle wasting

Learning to Look in Different Environments: An Active-Vision Model which Learns and Readapts Visual Routines

One of the main claims of the active vision framework is that nding data on the basis of task requirements is more ecient than reconstructing the whole scene by performing a complete visual scan. To be successful, this approach requires that agents learn visual routines to direct overt attention to locations with the information needed to accomplish the task. In ecological conditions, learning such visual routines is dicult due to the partial observability of the world, the changes in the environment, and the fact that learning signals might be indirect. This paper uses a reinforcement-learning actor-critic model to study how visual routines can be formed, and then adapted when the environment changes, in a system endowed with a controllable gaze and reaching capabilities. The tests of the model show that: (a) the autonomouslydeveloped visual routines are strongly dependent on the task and the statistical properties of the environment; (b) when the statistics of the environment change, the performance of the system remains rather stable thanks to the re-use of previously discovered visual routines while the visual exploration policy remains for long time sub-optimal. We conclude that the model has a robust behaviour but the acquisition of an optimal visual exploration policy is particularly hard given its complex dependence on statistical properties of the environment, showing another of the diculties that adaptive active vision agents must face

Perception and recognition of faces in adolescence

Most studies on the development of face cognition abilities have focussed on childhood, with early maturation accounts contending that face cognition abilities are mature by 3–5 years. Late maturation accounts, in contrast, propose that some aspects of face cognition are not mature until at least 10 years. Here, we measured face memory and face perception, two core face cognition abilities, in 661 participants (397 females) in four age groups (younger adolescents (11.27–13.38 years); mid-adolescents (13.39–15.89 years); older adolescents (15.90–18.00 years); and adults (18.01–33.15 years)) while controlling for differences in general cognitive ability. We showed that both face cognition abilities mature relatively late, at around 16 years, with a female advantage in face memory, but not in face perception, both in adolescence and adulthood. Late maturation in the face perception task was driven mainly by protracted development in identity perception, while gaze perception abilities were already comparatively mature in early adolescence. These improvements in the ability to memorize, recognize and perceive faces during adolescence may be related to increasing exploratory behaviour and exposure to novel faces during this period of life