Contact stress analysis and optimization of single crystal turbine blade tenon/disk mortise structure considering thermal-solid coupling

Contact stress analysis and optimization design of single crystal turbine blade tenon/disk mortise structure considering thermal-solid coupling is proposed in this paper. Contact thermal conductivity analysis of turbine blade/disk mortise structure is carried out to obtain temperature distribution. Contact stress of mortise structure considering temperature influence is analyzed by FEM method. On basis of contact stress analysis, the optimization design method considering thermal-solid coupling is proposed. Broaching angle, wedge angle and gap distance are chosen as optimization design variables. The minimum Mises stress, average tensile stress and average compressive stress are chosen as optimization objectives. A three fir tree tenon/mortise structure is optimized to decrease the maximum Mises stress 14% by proposed method

Bone Protection by Inhibition of MicroRNA-182

Targeting microRNAs recently shows significant therapeutic promise; however, such progress is underdeveloped in treatment of skeletal diseases with osteolysis, such as osteoporosis and rheumatoid arthritis (RA). Here, we identified miR-182 as a key osteoclastogenic regulator in bone homeostasis and diseases. Myeloid-specific deletion of miR-182 protects mice against excessive osteoclastogenesis and bone resorption in disease models of ovariectomy-induced osteoporosis and inflammatory arthritis. Pharmacological treatment of these diseases with miR-182 inhibitors completely suppresses pathologic bone erosion. Mechanistically, we identify protein kinase double-stranded RNA-dependent (PKR) as a new and essential miR-182 target that is a novel inhibitor of osteoclastogenesis via regulation of the endogenous interferon (IFN)-β-mediated autocrine feedback loop. The expression levels of miR-182, PKR, and IFN-β are altered in RA and are significantly correlated with the osteoclastogenic capacity of RA monocytes. Our findings reveal a previously unrecognized regulatory network mediated by miR-182-PKR-IFN-β axis in osteoclastogenesis, and highlight the therapeutic implications of miR-182 inhibition in osteoprotection

Fermion-boson many-body interplay in a frustrated kagome paramagnet

Kagome-net, appearing in areas of fundamental physics, materials, photonic and cold-atom systems, hosts frustrated fermionic and bosonic excitations. However, it is extremely rare to find a system to study both fermionic and bosonic modes to gain insights into their many-body interplay. Here we use state-of-the-art scanning tunneling microscopy and spectroscopy to discover unusual electronic coupling to flat-band phonons in a layered kagome paramagnet. Our results reveal the kagome structure with unprecedented atomic resolution and observe the striking bosonic mode interacting with dispersive kagome electrons near the Fermi surface. At this mode energy, the fermionic quasi-particle dispersion exhibits a pronounced renormalization, signaling a giant coupling to bosons. Through a combination of self-energy analysis, first-principles calculation, and a lattice vibration model, we present evidence that this mode arises from the geometrically frustrated phonon flat-band, which is the lattice analog of kagome electron flat-band. Our findings provide the first example of kagome bosonic mode (flat-band phonon) in electronic excitations and its strong interaction with fermionic degrees of freedom in kagome-net materials.Comment: To appear in Nature Communications (2020

Genetic Deficiency of Glycogen Synthase Kinase-3β Corrects Diabetes in Mouse Models of Insulin Resistance

Despite treatment with agents that enhance β-cell function and insulin action, reduction in β-cell mass is relentless in patients with insulin resistance and type 2 diabetes mellitus. Insulin resistance is characterized by impaired signaling through the insulin/insulin receptor/insulin receptor substrate/PI-3K/Akt pathway, leading to elevation of negatively regulated substrates such as glycogen synthase kinase-3β (Gsk-3β). When elevated, this enzyme has antiproliferative and proapoptotic properties. In these studies, we designed experiments to determine the contribution of Gsk-3β to regulation of β-cell mass in two mouse models of insulin resistance. Mice lacking one allele of the insulin receptor (Ir+/−) exhibit insulin resistance and a doubling of β-cell mass. Crossing these mice with those having haploinsufficiency for Gsk-3β (Gsk-3β+/−) reduced insulin resistance by augmenting whole-body glucose disposal, and significantly reduced β-cell mass. In the second model, mice missing two alleles of the insulin receptor substrate 2 (Irs2−/−), like the Ir+/− mice, are insulin resistant, but develop profound β-cell loss, resulting in early diabetes. We found that islets from these mice had a 4-fold elevation of Gsk-3β activity associated with a marked reduction of β-cell proliferation and increased apoptosis. Irs2−/− mice crossed with Gsk-3β+/− mice preserved β-cell mass by reversing the negative effects on proliferation and apoptosis, preventing onset of diabetes. Previous studies had shown that islets of Irs2−/− mice had increased cyclin-dependent kinase inhibitor p27kip1 that was limiting for β-cell replication, and reduced Pdx1 levels associated with increased cell death. Preservation of β-cell mass in Gsk-3β+/−Irs2−/− mice was accompanied by suppressed p27kip1 levels and increased Pdx1 levels. To separate peripheral versus β-cell–specific effects of reduction of Gsk3β activity on preservation of β-cell mass, mice homozygous for a floxed Gsk-3β allele (Gsk-3F/F) were then crossed with rat insulin promoter-Cre (RIP-Cre) mice to produce β-cell–specific knockout of Gsk-3β (βGsk-3β−/−). Like Gsk-3β+/− mice, βGsk-3β−/− mice also prevented the diabetes of the Irs2−/− mice. The results of these studies now define a new, negatively regulated substrate of the insulin signaling pathway specifically within β-cells that when elevated, can impair replication and increase apoptosis, resulting in loss of β-cells and diabetes. These results thus form the rationale for developing agents to inhibit this enzyme in obese insulin-resistant individuals to preserve β-cells and prevent diabetes onset

Contact stress analysis and optimization of single crystal turbine blade tenon/disk mortise structure considering thermal-solid coupling

Contact stress analysis and optimization design of single crystal turbine blade tenon/disk mortise structure considering thermal-solid coupling is proposed in this paper. Contact thermal conductivity analysis of turbine blade/disk mortise structure is carried out to obtain temperature distribution. Contact stress of mortise structure considering temperature influence is analyzed by FEM method. On basis of contact stress analysis, the optimization design method considering thermal-solid coupling is proposed. Broaching angle, wedge angle and gap distance are chosen as optimization design variables. The minimum Mises stress, average tensile stress and average compressive stress are chosen as optimization objectives. A three fir tree tenon/mortise structure is optimized to decrease the maximum Mises stress 14% by proposed method

Contact stress analysis and optimization of single crystal turbine blade tenon/disk mortise structure considering thermal-solid coupling

Contact stress analysis and optimization design of single crystal turbine blade tenon/disk mortise structure considering thermal-solid coupling is proposed in this paper. Contact thermal conductivity analysis of turbine blade/disk mortise structure is carried out to obtain temperature distribution. Contact stress of mortise structure considering temperature influence is analyzed by FEM method. On basis of contact stress analysis, the optimization design method considering thermal-solid coupling is proposed. Broaching angle, wedge angle and gap distance are chosen as optimization design variables. The minimum Mises stress, average tensile stress and average compressive stress are chosen as optimization objectives. A three fir tree tenon/mortise structure is optimized to decrease the maximum Mises stress 14% by proposed method

Cleanliness improvement and microstructure refinement of H13 die steel by laboratory magnetic-controlled electroslag remelting

The current work investigated the impact of transverse static magnetic field (TSMF) with varied magnetic flux density (MFD) on cleanliness and microstructure of laboratory scale electroslag remelted H13 die steel. The inclusion morphology and microstructure evolution of electroslag remelted ingots were examined utilizing scanning electron and optical microscopes, respectively. The number and size of inclusions in ingots were detected using the FEI Aspex Explorer. The results demonstrated that the number/size of inclusions in H13 electroslag remelted ingots were decreased as the MFD of applied TSMF increased. This resulted from the application of the TSMF, which produced the thinner liquid melting film (LMF), smaller droplets, and shallower metal molten pool, strengthening the kinetic conditions for inclusion migration to the slag-metal interface and the removal process. When the MFD of the applied TSMF was higher (95 mT and 140 mT), the LMF became thinner, the droplets became smaller, and the metal pool became shallower were more visible. Moreover, the metal pool became shallower and the local solidification time became shorter after applying TSMF with larger MFD, resulting in finer dendritic structure and carbides