Phonon-driven spin-Floquet magneto-valleytronics in MoS2

Two-dimensional materials equipped with strong spin-orbit coupling can display novel electronic, spintronic, and topological properties originating from the breaking of time or inversion symmetry. A lot of interest has focused on the valley degrees of freedom that can be used to encode binary information. By performing ab initio time-dependent density functional simulation on MoS2, here we show that the spin is not only locked to the valley momenta but strongly coupled to the optical E '' phonon that lifts the lattice mirror symmetry. Once the phonon is pumped so as to break time-reversal symmetry, the resulting Floquet spectra of the phonon-dressed spins carry a net out-of-plane magnetization (approximate to 0.024 mu(B) for single-phonon quantum) even though the original system is non-magnetic. This dichroic magnetic response of the valley states is general for all 2H semiconducting transition-metal dichalcogenides and can be probed and controlled by infrared coherent laser excitation

Rasa3 Controls Megakaryocyte Rap1 Activation, Integrin Signaling and Differentiation into Proplatelet

Rasa3 is a GTPase activating protein of the GAP1 family which targets Ras and Rap1. Ubiquitous Rasa3 catalytic inactivation in mouse results in early embryonic lethality. Here, we show that Rasa3 catalytic inactivation in mouse hematopoietic cells results in a lethal syndrome characterized by severe defects during megakaryopoiesis, thrombocytopenia and a predisposition to develop preleukemia. The main objective of this study was to define the cellular and the molecular mechanisms of terminal megakaryopoiesis alterations. We found that Rasa3 catalytic inactivation altered megakaryocyte development, adherence, migration, actin cytoskeleton organization and differentiation into proplatelet forming megakaryocytes. These megakaryocyte alterations were associated with an increased active Rap1 level and a constitutive integrin activation. Thus, these mice presented a severe thrombocytopenia, bleeding and anemia associated with an increased percentage of megakaryocytes in the bone marrow, bone marrow fibrosis, extramedular hematopoiesis, splenomegaly and premature death. Altogether, our results indicate that Rasa3 catalytic activity controls Rap1 activation and integrin signaling during megakaryocyte differentiation in mouse

Do diabetes, metabolic syndrome or their association equally affect biventricular function? A tissue Doppler study

Metabolic syndrome (MetS) and type 2 diabetes (T2DM) have been associated with an impairment of left (LV) and right ventricular (RV) function as well as an increased risk of heart failure (HF). However, it remains unclear whether these clinical entities or their associations promote a similar derangement of biventricular function. Overall, 345 patients without overt cardiovascular disease consecutively underwent routine blood chemistry including high-sensitivity C reactive protein (hs-CRP) and echocardiographical examination with conventional and tissue Doppler imaging (TDI) of both ventricles. According to the ATP III criteria and fasting glucose levels, the study population was stratified into four groups: (1) healthy controls (n = 120); (2) MetS without T2DM (n = 84); (3) T2DM without MetS (n = 49); and (4) MetS + T2DM (n = 92). The Myocardial performance index (MPI) of the RV and LV was obtained with a multi-segmental approach using TDI. Patients with MetS and T2DM exhibited a similar impairment of biventricular function compared with healthy controls, whereas a further decline was observed in patients having both MetS and T2DM. In addition to MetS markers, hs-CRP exhibited the strongest association with the MPI of both ventricles. Regression analyses indicated that individual MetS markers were inferior to MetS in identifying subtle cardiac dysfunction. Independent associations of MetS and T2DM with biventricular dysfunction were comparable, and the coexistence of MetS and T2DM exhibited the highest risk for biventricular dysfunction. Our findings emphasize the importance of MetS as an equivalent of T2DM and support a synergic effect of these clinical conditions on cardiac organ damage requiring more aggressive therapeutic strategies to prevent HF. Hypertension Research (2013) 36, 36-42; doi:10.1038/hr.2012.137; published online 6 September 201