Interfaces often play a significant role in many physical properties and phenomena of nanocrystalline materials (NcMs). In the present paper, the interface effects on the effective elastic property ...of NcMs are investigated. First, an atomic potential method is suggested for estimating the effective elastic modulus of an interface phase. Then, the Mori-Tanaka effective field method is employed to determine the overall effective elastic moduli of a nanocrystalline material, which is regarded as a binary composite consisting of a crystal or inclusion phase with regular lattice connected by an amorphous-like interface or matrix phase. Finally, the stiffening effects of strain gradients are examined on the effective elastic property by using the strain gradient theory to analyze a representative unit cell. Our analysis shows two physical mechanisms of interfaces that influence the effective stiffness and other mechanical properties of materials. One is the softening effect due to the distorted atomic structures and the increased atomic spacings in interface regions, and another is the baffling effect due to the existence of boundary layers between the interface phase and the crystalline phase.
The density distributions of large nuclei are typically modeled with a Woods-Saxon distribution characterized by a radius \(R_{0}\) and skin depth \(a\). Deformation parameters \(\beta\) are then ...introduced to describe non-spherical nuclei using an expansion in spherical harmonics \(R_{0}(1+\beta_2Y^0_2+\beta_4Y^0_4)\). But when a nucleus is non-spherical, the \(R_{0}\) and \(a\) inferred from electron scattering experiments that integrate over all nuclear orientations cannot be used directly as the parameters in the Woods-Saxon distribution. In addition, the \(\beta_2\) values typically derived from the reduced electric quadrupole transition probability B(E2)\(\uparrow\) are not directly related to the \(\beta_2\) values used in the spherical harmonic expansion. B(E2)\(\uparrow\) is more accurately related to the intrinsic quadrupole moment \(Q_{0}\) than to \(\beta_2\). One can however calculate \(Q_0\) for a given \(\beta_2\) and then derive B(E2)\(\uparrow\) from \(Q_0\). In this paper we calculate and tabulate the \(R_0\), \(a\), and \(\beta_2\) values that when used in a Woods-Saxon distribution, will give results consistent with electron scattering data. We then present calculations of the eccentricity \(\varepsilon_2\) and \(\varepsilon_3\) with the new and old parameters. We demonstrate that \(\varepsilon_3\) is particularly sensitive to \(a\) and argue that using the incorrect value of \(a\) has important implications for the extraction of \(\eta/s\) from the QGP created in Heavy Ion collisions.
Cancer-associated fibroblasts induce malignant behavior in genetically initiated but nontumorigenic human prostatic epithelium. The genetic basis for such transformation is still unknown. By using ...Affymetrix GeneChip technology, we profiled genomewide gene expression of transformed tumorigenic benign prostatic hyperplasia (BPH1)CAFTD and parental (nontumorigenic BPH1) cells. We identified differentially expressed genes, which are associated with tumorigenesis or tumor progression. One striking finding is that a significant portion of the down-regulated genes belongs to interferon (IFN)-inducible molecules. We show that IFN inhibited the tumorigenic BPH1CAFTDcell proliferation and colony formation in vitro and inhibited tumor growth in xenografts in vivo. Expression of the IFN-inducible molecules correlates with the growth-inhibiting effects of IFN. In addition, these genes are reported to be mapped mainly to two chromosomal regions, 10q23-26 and 17q21, which are frequently deleted in human prostate cancers. Furthermore, in silico data-mining with the GeneLogic database revealed that expression of the IFN-inducible genes was down-regulated in approximately 30% of the 49 clinically characterized samples of prostatic adenocarcinomas. Collectively, we show that there seems to be a direct link between IFN-inducible molecules and prostatic tumor progression. These findings suggest IFN-inducible molecules as potential therapeutic targets for the treatment of prostate cancer.
Sonic hedgehog (Shh), a vertebrate homologue of the Drosophila segment-polarity gene hedgehog, has been reported to play an important role during normal development of various tissues.
Abnormal ...activities of Shh signaling pathway have been implicated in tumorigenesis such as basal cell carcinomas and medulloblastomas.
Here we show that Shh signaling negatively regulates prostatic epithelial ductal morphogenesis. In organotypic cultures of
developing rat prostates, Shh inhibited cell proliferation and promoted differentiation of luminal epithelial cells. The expression
pattern of Shh and its receptors suggests a paracrine mechanism of action. The Shh receptors Ptc1 ( P
a tc hed
1 ) and Ptc2 were found to be expressed in prostatic stromal cells adjacent to the epithelium, where Shh itself was produced.
This paracrine model was confirmed by co-culturing the developing prostate in the presence of stromal cells transfected with
a vector expressing a constitutively active form of Smoothened , the real effector of the Shh signaling pathway. Furthermore, expression of activin A and TGF-β1 that were shown previously
to inhibit prostatic epithelial branching was up-regulated following Shh treatment in the organotypic cultures. Taken together,
these results suggest that Shh negatively regulates prostatic ductal branching indirectly by acting on the surrounding stromal
cells, at least partly via up-regulating expression of activin A and TGF-β1.
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