Interaction between thermal convection and mean flow in a rotating system with a tilted axis

Thermal convection in a sine-type horizontal shear flow in a rotating system with the rotation axis tilted from the vertical direction is investigated, sweeping three parameters: Taylor number, tilt angle of the rotation axis (i.e. latitude) and Rayleigh number. Nonlinear time evolutions show that there is not only a regime in which roll convections of a herringbone pattern accelerate a mean flow but also a regime in which a large-scale east–west roll convection accelerates the mean flow strongly. The parameter region in which this type of stable steady two-dimensional (2D) roll solution exists is determined by linear stability analyses. Even when the 2D steady solution is not linearly stable, unsteady quasi-periodic solutions oscillating around the steady solution can be found in the nonlinear time evolutions. Finally, a simple mechanism for the acceleration of the mean flow by the large-scale east–west roll convection is described in detail, in which both the tilt of the rotation axis and the sine-type horizontal shear of the flow are important

Magnetization and AC-Susceptibility of Fe-Zr Amorphous Alloys

Measurements of magnetization and ac-susceptibility of Fe-Zr amorphous alloys over the wide composition range have been carried out. The spin glass like behavior appears in two different regions of composition. The spin glass behavior in Fe-rich Fe amorphous alloys (around 90 at.% Zr) is due to the frustration of antiferromagnetic coupling between spins. The other behavior around 50 at.% is due to the dilution of atoms with magnetic moment. They are explained by the local environment effect

Spin Glass Behaviour of Fe-7.6 at% Zr Amorphous Alloy Studied by AC-Susceptibility and Magnetic Viscosity

The spin glass behaviour of the Fe-7.6 at% Zr amorphous alloy was studied by ac-susceptibility and dc-magnetization measurements. A cusp of linear susceptibility and a sharp negative peak of non-linear susceptibility characterize the spin glass transition. This transition is also accompanied by the remarkable relaxation of the dc-magnetization

A novel Rac1-GSPT1 signaling pathway controls astrogliosis following central nervous system injury

Astrogliosis (i.e. glial scar), which is comprised primarily of proliferated astrocytes at the lesion site and migrated astrocytes from neighboring regions, is one of the key reactions in determining outcomes after CNS injury. In an effort to identify potential molecules/pathways that regulate astrogliosis, we sought to determine whether Rac/Rac-mediated signaling in astrocytes represents a novel candidate for therapeutic intervention following CNS injury. For these studies, we generated mice with Rac1 deletion under the control of the GFAP (glial fibrillary acidic protein) promoter (GFAP-Cre;Rac1(flox/flox)). GFAP-Cre;Rac1(flox/flox) (Rac1-KO) mice exhibited better recovery after spinal cord injury and exhibited reduced astrogliosis at the lesion site relative to control. Reduced astrogliosis was also observed in Rac1-KO mice following microbeam irradiation-induced injury. Moreover, knockdown (KD) or KO of Rac1 in astrocytes (LN229 cells, primary astrocytes, or primary astrocytes from Rac1-KO mice) led to delayed cell cycle progression and reduced cell migration. Rac1-KD or Rac1-KO astrocytes additionally had decreased levels of GSPT1 (G(1) to S phase transition 1) expression and reduced responses of IL-1β and GSPT1 to LPS treatment, indicating that IL-1β and GSPT1 are downstream molecules of Rac1 associated with inflammatory condition. Furthermore, GSPT1-KD astrocytes had cell cycle delay, with no effect on cell migration. The cell cycle delay induced by Rac1-KD was rescued by overexpression of GSPT1. Based on these results, we propose that Rac1-GSPT1 represents a novel signaling axis in astrocytes that accelerates proliferation in response to inflammation, which is one important factor in the development of astrogliosis/glial scar following CNS injury

A role for PKC-ɛ in FcγR-mediated phagocytosis by RAW 264.7 cells

Protein kinase C (PKC) plays a prominent role in immune signaling, and the paradigms for isoform selective signaling are beginning to be elucidated. Real-time microscopy was combined with molecular and biochemical approaches to demonstrate a role for PKC-ɛ in Fcγ receptor (FcγR)–dependent phagocytosis. RAW 264.7 macrophages were transfected with GFP-conjugated PKC isoforms, and GFP movement was followed during phagocytosis of fluorescent IgG–opsonized beads. PKC-ɛ, but not PKC-δ, concentrated around the beads. PKC-ɛ accumulation was transient; apparent as a “flash” on target ingestion. Similarly, endogenous PKC-ɛ was specifically recruited to the nascent phagosomes in a time-dependent manner. Overexpression of PKC-ɛ, but not PKC-α, PKC-δ, or PKC-γ enhanced bead uptake 1.8-fold. Additionally, the rate of phagocytosis in GFP PKC-ɛ expressors was twice that of cells expressing GFP PKC-δ. Expression of the regulatory domain (ɛRD) and the first variable region (ɛV1) of PKC-ɛ inhibited uptake, whereas the corresponding PKC-δ region had no effect. Actin polymerization was enhanced on expression of GFP PKC-ɛ and ɛRD, but decreased in cells expressing ɛV1, suggesting that the ɛRD and ɛV1 inhibition of phagocytosis is not due to effects on actin polymerization. These results demonstrate a role for PKC-ɛ in FcγR-mediated phagocytosis that is independent of its effects on actin assembly

Pathophysiology and Treatment of Diabetic Cardiomyopathy and Heart Failure in Patients with Diabetes Mellitus

There is a close relationship between diabetes mellitus and heart failure, and diabetes is an independent risk factor for heart failure. Diabetes and heart failure are linked by not only the complication of ischemic heart disease, but also by metabolic disorders such as glucose toxicity and lipotoxicity based on insulin resistance. Cardiac dysfunction in the absence of coronary artery disease, hypertension, and valvular disease is called diabetic cardiomyopathy. Diabetes-induced hyperglycemia and hyperinsulinemia lead to capillary damage, myocardial fibrosis, and myocardial hypertrophy with mitochondrial dysfunction. Lipotoxicity with extensive fat deposits or lipid droplets is observed on cardiomyocytes. Furthermore, increased oxidative stress and inflammation cause cardiac fibrosis and hypertrophy. Treatment with a sodium glucose cotransporter 2 (SGLT2) inhibitor is currently one of the most effective treatments for heart failure associated with diabetes. However, an effective treatment for lipotoxicity of the myocardium has not yet been established, and the establishment of an effective treatment is needed in the future. This review provides an overview of heart failure in diabetic patients for the clinical practice of clinicians