Fully relativistic first-principles calculations based on density functional theory are performed to study the spin-orbit-induced spin splitting in monolayer systems of the transition-metal dichalcogenides MoS 2 , MoSe 2 , WS 2 , and WSe 2 . All these systems are identified as direct-band-gap semiconductors. Giant spin splittings of 148-456 meV result from missing inversion symmetry. Full out-of-plane spin polarization is due to the two-dimensional nature of the electron motion and the potential gradient asymmetry. By suppression of the Dyakonov-Perel spin relaxation, spin lifetimes are expected to be very long. Because of the giant spin splittings, the studied materials have great potential in spintronics applications.

First-principles calculations are performed to investigate the effect of vacancies on the electronic structure and magnetic properties of the two prototypical half-Heusler semiconductors NiTiSn and CoTiSb. The spin degeneracy of the host materials is broken for all types of isolated vacancies under consideration, except for Ni-deficient NiTiSn. A half-metallic character is identified in Sn-deficient NiTiSn and Co/Ti/Sb-deficient CoTiSb. We can explain our findings by introducing an extending Slater-Pauling rule for systems with defects. A ferromagnetic ordering of the local moments due to double exchange appears to be likely.

Using first-principles calculations, we propose a two-dimensional diluted magnetic semiconductor: monolayer MoS 2 doped by transition metals. Doping of transition metal atoms from the IIIB to VIB groups results in nonmagnetic states, since the number of valence electrons is smaller or equal to that of Mo. Doping of atoms from the VIIB to IIB groups becomes energetically less and less favorable. Magnetism is observed for Mn, Fe, Co, Zn, Cd, and Hg doping, while for the other dopants from these groups it is suppressed by Jahn-Teller distortions. Analysis of the binding energies and magnetic properties indicates that (Mo,X)S 2 (X = Mn, Fe, Co, and Zn) are promising systems to explore two-dimensional diluted magnetic semiconductors.

The Rashba effect in quasi two-dimensional materials, such as noble metal surfaces and semiconductor heterostructures, has been investigated extensively, while interest in real twodimensional systems has just emerged with the discovery of graphene. We present ab initio electronic structure, phonon, and molecular-dynamics calculations to study the structural stability and spin-orbit-induced spin splitting in the transition metal dichalcogenide monolayers MXY (M = Mo, W and X, Y = S, Se, Te). In contrast to the non-polar systems with X = Y, in the polar systems with X = Y the Rashba splitting at the Γ-point for the uppermost valence band is caused by the broken mirror symmetry. An enhancement of the splitting can be achieved by increasing the spin-orbit coupling and/or the potential gradient.

Recently, a type-II Weyl fermion was theoretically predicted to appear at the contact of electron and hole Fermi surface pockets. A distinguishing feature of the surfaces of type-II Weyl semimetals is the existence of topological surface states, so-called Fermi arcs. Although WTe2 was the first material suggested as a type-II Weyl semimetal, the direct observation of its tilting Weyl cone and Fermi arc has not yet been successful. Here, we show strong evidence that WTe2 is a type-II Weyl semimetal by observing two unique transport properties simultaneously in one WTe2 nanoribbon. The negative magnetoresistance induced by a chiral anomaly is quite anisotropic in WTe2 nanoribbons, which is present in b-axis ribbon, but is absent in a-axis ribbon. An extra-quantum oscillation, arising from a Weyl orbit formed by the Fermi arc and bulk Landau levels, displays a two dimensional feature and decays as the thickness increases in WTe2 nanoribbon.

Exercise remains the most effective way to promote physical and metabolic wellbeing, but molecular mechanisms underlying exercise tolerance and its plasticity are only partially understood. In this study we identify musclin-a peptide with high homology to natriuretic peptides (NP)-as an exercise-responsive myokine that acts to enhance exercise capacity in mice. We use human primary myoblast culture and in vivo murine models to establish that the activity-related production of musclin is driven by Ca 2+ -dependent activation of Akt1 and the release of musclin-encoding gene (Ostn) transcription from forkhead box O1 transcription factor inhibition. Disruption of Ostn and elimination of musclin secretion in mice results in reduced exercise tolerance that can be rescued by treatment with recombinant musclin. Reduced exercise capacity in mice with disrupted musclin signaling is associated with a trend toward lower levels of plasma atrial NP (ANP) and significantly smaller levels of cyclic guanosine monophosphate (cGMP) and peroxisome proliferator-activated receptor gamma coactivator 1-α in skeletal muscles after exposure to exercise. Furthermore, in agreement with the established musclin ability to interact with NP clearance receptors, but not with NP guanyl cyclase-coupled signaling receptors, we demonstrate that musclin enhances cGMP production in cultured myoblasts only when applied together with ANP. Elimination of the activity-related musclin-dependent boost of ANP/ cGMP signaling results in significantly lower maximum aerobic capacity, mitochondrial protein content, respiratory complex protein expression, and succinate dehydrogenase activity in skeletal muscles. Together, these data indicate that musclin enhances physical endurance by promoting mitochondrial biogenesis.osteocrin | mitochondria | skeletal muscle | exercise | natriuretic peptide

Myocardial mitochondrial Ca 2+ entry enables physiological stress responses but in excess promotes injury and death. However, tissue-specific in vivo systems for testing the role of mitochondrial Ca 2+ are lacking. We developed a mouse model with myocardial delimited transgenic expression of a dominant negative (DN) form of the mitochondrial Ca 2+ uniporter (MCU). DN-MCU mice lack MCU-mediated mitochondrial Ca 2+ entry in myocardium, but, surprisingly, isolated perfused hearts exhibited higher O 2 consumption rates (OCR) and impaired pacing induced mechanical performance compared with wild-type (WT) littermate controls. In contrast, OCR in DN-MCU-permeabilized myocardial fibers or isolated mitochondria in low Ca 2+ were not increased compared with WT, suggesting that DN-MCU expression increased OCR by enhanced energetic demands related to extramitochondrial Ca 2+ homeostasis. Consistent with this, we found that DN-MCU ventricular cardiomyocytes exhibited elevated cytoplasmic [Ca 2+ ] that was partially reversed by ATP dialysis, suggesting that metabolic defects arising from loss of MCU function impaired physiological intracellular Ca 2+ homeostasis. Mitochondrial Ca 2+ overload is thought to dissipate the inner mitochondrial membrane potential (ΔΨm) and enhance formation of reactive oxygen species (ROS) as a consequence of ischemia-reperfusion injury. Our data show that DN-MCU hearts had preserved ΔΨm and reduced ROS during ischemia reperfusion but were not protected from myocardial death compared with WT. Taken together, our findings show that chronic myocardial MCU inhibition leads to previously unanticipated compensatory changes that affect cytoplasmic Ca 2+ homeostasis, reprogram transcription, increase OCR, reduce performance, and prevent anticipated therapeutic responses to ischemia-reperfusion injury.myocardium | mitochondrial calcium uniporter | ischemia-reperfusion injury E ntry of Ca 2+ into the mitochondrial matrix is a central event for Ca 2+ homeostasis in cardiomyocytes (1) as well as for coordinating fundamental and diverse responses to physiological (2) and pathological stress (3). The paradigm for Ca 2+ as a physiological second messenger that enhances oxidative phosphorylation to enable fight-or-flight responses but in excess contributes to disease and dysfunction is well established in myocardium (4). The molecular identity of the mitochondrial Ca 2+ uniporter (MCU) was recently discovered, enabling development of new genetic models to understand the role of MCU in vivo. MCU is an ion channel protein that acts as the primary pathway for Ca 2+ entry into the mitochondrial matrix (5, 6). Recent findings in global Mcu −/− mice (7) suggest that the MCU pathway is dispensable for regulating cellular energy production, except under extreme physiological stress, and for activation of pathways leading to cell death; however, the effect of selective myocardial MCU inhibition is unknown. We developed a new transgenic mouse model with myocardial delimited dominant negative (DN)-MCU protein overexpressio...

Summary Metabolic processes that regulate muscle energy use are major determinants of bodily energy balance. Here we find that sarcolemmal ATP-sensitive K+ (KATP) channels, which couple membrane excitability with cellular metabolic pathways, set muscle energy expenditure under physiological stimuli. Disruption of KATP channel function provoked, in conditions of unaltered locomotor activity and blood substrate availability, an extra energy cost of cardiac and skeletal muscle performance. Inefficient fuel metabolism in KATP channel-deficient striated muscles reduced glycogen and fat body depots promoting a lean phenotype. The propensity to lesser body weight imposed by KATP channel deficit persisted under a high-fat diet, yet obesity restriction was achieved at the cost of compromised physical endurance. Thus, sarcolemmal KATP channels govern muscle energy economy, and their down-regulation in a tissue-specific manner could present an anti-obesity strategy by rendering muscle increasingly thermogenic at rest and less fuel efficient during exercise.