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3D Printed Intelligently Graded Functional Stiffness Foam for Sturdier Multi Stiffness Materials
Foams are ubiquitous, being used in applications such as padding, insulation, and noise isolation.
Bonding different density foams together produces undesired stress concentrations and boundary
effects. Creating controlled gradients in foam properties has been a challenge for traditional and
AM processes. Here we show how to use a form of material extrusion called Viscous Thread
APrinting (VTP) to produce foams with multiple stiffnesses and continuous gradients between
different stiffnesses. We do so by varying the path speed during extrusion to control the
production of microstructures. We compare the process of producing discrete components and
those with gradients, showing that those with gradients have higher strength in plane during
tension, have no discontinuities in out of plane stiffness, and are less prone to forming cracks at
the boundaries. We demonstrate the process in thermoplastic polyurethane (TPU).Mechanical Engineerin
Experimental Signature of Medium Modifications for rho and omega Mesons in the 12 GeV p + A Reactions
The invariant mass spectra of e+e- pairs produced in 12-GeV proton-induced
nuclear reactions are measured at the KEK Proton-Synchrotron. On the low-mass
side of the omega meson peak, a significant enhancement over the known hadronic
sources has been observed. The mass spectra, including the excess, are well
reproduced by a model that takes into account the density dependence of the
vector meson mass modification, as theoretically predicted.Comment: 4 pages, 3 figures, Version accepted for Physical Review Lette
Nuclear mass number dependence of inclusive production of omega and phi mesons in 12 GeV p + A collisions
The inclusive production of omega and phi mesons is studied in the backward
region of the interaction of 12 GeV protons with polyethylene, carbon, and
copper targets. The mesons are measured in e^+ e^- decay channels. The
production cross sections of the mesons are presented as functions of rapidity
y and transverse momentum p_T. The nuclear mass number dependences (A
dependences) are found to be A^{0.710 +/- 0.021(stat) +/- 0.037(syst)} for
omega mesons and A^{0.937 +/- 0.049(stat) +/- 0.018(syst)} for phi mesons in
the region of 0.9 < y < 1.7 and p_T < 0.75 GeV/c.Comment: 12 pages, 8 figures; typos adde
Nuclear-matter modification of decay widths in the and channels
The invariant mass spectra of are measured in 12 GeV
reactions in order to search for the in-medium modification of
mesons. The observed spectra are well reproduced by the
relativistic Breit-Wigner function with a combinatorial background shape in
three regions between 1.0 and 3.5. The nuclear mass-number
dependence of the yields of the decay channel is compared to the
simultaneously measured decay channel for carbon and copper
targets. We parameterize the production yields as and obtain to be
0.14 0.12. Limits are obtained for the partial decay widths of
mesons in nuclear matter.Comment: 5 pages, 4 figure
Regulation of vascular smooth muscle cell calcification by syndecan-4/FGF-2/PKCα signaling and cross-talk with TGFβ
Aims: Vascular calcification is a major cause of morbidity and mortality. Fibroblast growth factor-2 (FGF-2) plays an instructive role in osteogenesis and bone development, but its role in vascular calcification was unknown. Therefore, we investigated the involvement of FGF-2 in vascular calcification and determined the mechanism by which it regulates this process. Methods and Results: We demonstrate that FGF-2 expression is increased in vascular smooth muscle cells (VSMCs) induced to deposit a mineralized matrix by incubation with β-glycerophosphate. FGF-2 is also localized to sites of calcification within human atherosclerotic plaques. The expression of syndecan-4, a heparan sulfate proteoglycan which regulates FGF-2 signaling, is also increased in mineralizing VSMCs and co-localizes with FGF-2 in human calcified atherosclerotic plaques. Exogenous FGF-2 inhibits VSMC mineralization, and this inhibition is reduced when syndecan-4 expression is knocked-down using siRNA. Biochemical inhibition of FGFR signaling using a pan FGFR inhibitor (BGJ398) or knocking-down syndecan-4 expression in VSMCs using siRNA increases VSMC mineralization. These increases are prevented by inhibiting transforming growth factor-β (TGFβ) signaling with SB431542, suggesting cross-talk between FGF-2 and TGFβ signaling is crucial for the regulation of VSMC mineralization. Syndecan-4 can also regulate FGF-2 signaling directly via protein kinase Cα (PKCα) activation. Biochemical inhibition of PKCα activity using Gö6976, or siRNA-mediated suppression of PKCα expression increases VSMC mineralization; this increase is also prevented with SB431542. Finally, the ability of FGF-2 to inhibit VSMC mineralization is reduced when PKCα expression is knocked-down. Conclusion: This is the first demonstration that syndecan-4 promotes FGF-2 signaling, and in turn, suppresses VSMC mineralization by down-regulating TGFβ signaling. Our discoveries that FGF-2 and syndecan-4 expression is increased in mineralizing VSMCs and that PKCα regulates FGF-2 and TGFβ signaling in VSMCs suggests that the syndecan-4/FGF-2/TGFβ signaling axis could represent a new therapeutic target for vascular calcification
Interleukin-6, MCP-1, IP-10, and MIG are sequentially expressed in cerebrospinal fluid after subarachnoid hemorrhage
Cardiac involvement in Beagle-based canine X-linked muscular dystrophy in Japan (CXMD(J)): electrocardiographic, echocardiographic, and morphologic studies
BACKGROUND: Cardiac mortality in Duchenne muscular dystrophy (DMD) has recently become important, because risk of respiratory failure has been reduced due to widespread use of the respirator. The cardiac involvement is characterized by distinctive electrocardiographic abnormalities or dilated cardiomyopathy, but the pathogenesis has remained obscure. In research on DMD, Golden retriever-based muscular dystrophy (GRMD) has attracted much attention as an animal model because it resembles DMD, but GRMD is very difficult to maintain because of their severe phenotypes. We therefore established a line of dogs with Beagle-based canine X-linked muscular dystrophy in Japan (CXMD(J)) and examined the cardiac involvement. METHODS: The cardiac phenotypes of eight CXMD(J )and four normal male dogs 2 to 21 months of age were evaluated using electrocardiography, echocardiography, and histopathological examinations. RESULTS: Increases in the heart rate and decreases in PQ interval compared to a normal littermate were detected in two littermate CXMD(J )dogs at 15 months of age or older. Distinct deep Q-waves and increase in Q/R ratios in leads II, III, and aVF were detected by 6–7 months of age in all CXMD(J )dogs. In the echocardiogram, one of eight of CXMD(J )dogs showed a hyperechoic lesion in the left ventricular posterior wall at 5 months of age, but the rest had not by 6–7 months of age. The left ventricular function in the echocardiogram indicated no abnormality in all CXMD(J )dogs by 6–7 months of age. Histopathology revealed myocardial fibrosis, especially in the left ventricular posterobasal wall, in three of eight CXMD(J )dogs by 21 months of age. CONCLUSION: Cardiac involvement in CXMD(J )dogs is milder and has slower progression than that described in GRMD dogs. The distinct deep Q-waves have been ascribed to myocardial fibrosis in the posterobasal region of the left ventricle, but our data showed that they precede the lesion on echocardiogram and histopathology. These findings imply that studies of CXMD(J )may reveal not only another causative mechanism of the deep Q-waves but also more information on the pathogenesis in the dystrophin-deficient heart
Genome-wide association of multiple complex traits in outbred mice by ultra low-coverage sequencing
The authors wish to acknowledge excellent technical assistance from A. Kurioka, L. Swadling, C. de Lara, J. Ussher, R. Townsend, S. Lionikaite, A.S. Lionikiene, R. Wolswinkel and I. van der Made. We would like to thank T.M. Keane and A.G. Doran for their help in annotating variants and adding the FVB/NJ strain to the MGP. We thank the High-Throughput Genomics Group at the Wellcome Trust Centre for Human Genetics and the Wellcome Trust Sanger Institute for the generation of the sequencing data. This work was funded by Wellcome Trust grant 090532/Z/09/Z (J.F.). Primary phenotyping of the mice was supported by the Mary Lyon Centre and Mammalian Genetics Unit (Medical Research Council, UK Hub grant G0900747 91070 and Medical Research Council, UK grant MC U142684172). D.A.B. acknowledges support from NIH R01AR056280. The sleep work was supported by the state of Vaud (Switzerland) and the Swiss National Science Foundation (SNF 14694 and 136201 to P.F.). The ECG work was supported by the Netherlands CardioVascular Research Initiative (Dutch Heart Foundation, Dutch Federation of University Medical Centres, Netherlands Organization for Health Research and Development and the Royal Netherlands Academy of Sciences) PREDICT project, InterUniversity Cardiology Institute of the Netherlands (ICIN; 061.02; C.A.R. and C.R.B.). N.C. is supported by the Agency of Science, Technology and Research (A*STAR) Graduate Academy. R.W.D. is supported by a grant from the Wellcome Trust (097308/Z/11/Z).Peer reviewedPostprin
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