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Continuum-based analyses for laterally loaded piles with rectangular and circular cross sections are presented using solutions that can be obtained quickly without requiring any elaborate inputs for the geometry and numerical mesh. The analysis is developed by solving the differential equations governing the displacements of the pile-soil system derived using the variational principles of mechanics. Parametric studies are performed to investigate the influence of the pile cross-sectional shape, soil layering, pile slenderness ratio, and pile-soil modulus ratio on the response of laterally loaded piles in heterogeneous soil in which the soil shear modulus varies continuously or discretely with depth. The results show that piles with the same second moment of inertia have similar lateral-load response. The lateral responses of piles in two-layer systems were mainly affected by the thickness and stiffness of the top soil layer. Soil layering also influences the lateral response of piles in three-layer soil deposits consisting of two thin layers overlying the third layer. Algebraic equations for estimating the pile-head deflection and maximum bending moment are proposed that can be readily used in design. A user-friendly spreadsheet program is developed as a tool to perform calculations of pile response using the analysis. Numerical examples demonstrating the use of the analysis are provided. [ABSTRACT FROM AUTHOR]

SUMMARY The paper presents a constitutive model for simulating the high strain-rate behavior of sands. Based on the concepts of critical-state soil mechanics, the bounding surface plasticity theory and the overstress theory of viscoplasticity, the constitutive model simulates the high strain-rate behavior of sands under uniaxial, triaxial and multi-axial loading conditions. The model parameters are determined for Ottawa and Fontainebleau sands, and the performance of the model under extreme transient loading conditions is demonstrated through simulations of split Hopkinson pressure bar tests up to a strain rate of 2000/s. The constitutive model is implemented in a finite-element analysis software Abaqus to analyze underground tunnels in sandy soil subjected to internal blast loads. Parametric studies are conducted to examine the effect of relative density and type of sand and of the depth of tunnel on the variation of stresses and deformations in the soil adjacent to the tunnels. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

SUMMARY Analytical solutions for the steady-state response of an infinite beam resting on a visco-elastic foundation and subjected to a concentrated load moving with a constant velocity are developed in this paper. The beam responses investigated are deflection, bending moment, shear force and contact pressure. The mechanical resistance of the foundation is modeled using two parameters ks and ts - ks accounts for soil resistance due to compressive strains in the soil and ts accounts for the resistance due to shear strains. Since this model represents the ground behavior more accurately than the Winkler spring model, the developed solutions produce beam responses that are closer to reality than those obtained using the existing solutions for Winkler model. The dynamic beam responses depend on the damping present in the system and on the velocity of the moving load. Based on the study, dynamic amplification curves are developed for beam deflection. Such amplification curves for deflection, bending moment, shear force and contact pressure can be developed for any beam-foundation system and can be used in design. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Separase is an endopeptidase that separates sister chromatids by cleaving cohesin Rad21 during the metaphase-to-anaphase transition. Conditional expression of Separase in tetracycline-inducible diploid FSK3 mouse mammary epithelial cells with both p53 WT and mutant (Ser-233-234) alleles of unknown physiological significance develops aneuploidy within 5 days of Separase induction in vitro. Overexpression of Separase induces premature separation of chromatids. lagging chromosomes, and anaphase bridges. In an in vivo mouse mammary transplant model, induction of Separase expression in the transplanted FSK3 cells for 3-4 weeks results in the formation of aneuploid tumors in the mammary gland. Xenograft studies combined with histological and cytogenetic analysis reveal that Separase-induced tumors are clonal in their genomic complements and have a mesenchymal phenotype suggestive of an epithelial- mesenchymal transition. Induction of Separase resulted in trisomies for chromosomes 8. 15, and 17; monosomy for chromosome 10; and amplification of the distal region of chromosomes 8 and 11. Separase protein is found to be significantly overexpressed in human breast tumors compared with matched normal tissue. These results collectively suggest that Separase is an oncogene, whose overexpression alone in mammary epithelial cells is sufficient to induce aneuploidy and tumorigenesis in a p53 mutant background. [ABSTRACT FROM AUTHOR]

A correction to the article "Response of Laterally Loaded Rectangular and Circular Piles in Soils With Properties Varying With Depth" by Yoon Seok Choi and colleagues, that was published in the journal in 2013 is presented.

Background: Omipalisib has been found to affect the viability of cancer cells. However, its effect on clonogenicity - a feature of cancer stem cells, is not clear. Cells isolated from neurocutaneous melanocytosis (NCM) patients' lesions grow clonogenically. The aim of this study was to investigate the effect of omipalisib treatment on clonogenic growth of NCM cells in vitro., Materials and Methods: Clonogenic growth efficiency was evaluated by colony formation assays with or without specific growth factors. Activation of MEK and Akt was determined by immunoblots. Colony formation and cell viability were assessed upon pharmacological inhibition of MEK, Akt and mToR., Results: Clonogenicity appeared to depend on bFGF and IGF1signaling through ERK and Akt. Omipalisib treatment prevented colony formation and induced autophagic cell death., Conclusion: Signaling through Akt is important for survival of clonogenic cells in NCM, and omipalisib treatment as a monotherapy or in combination with MEK162 could be an effective therapeutic strategy to inhibit clonogenic growth., (Copyright© 2018, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Maturation of vertebrate oocytes is regulated by maturation inducing hormone (MIH), which is progesterone in all vertebrates except in fish, where it is 17alpha, 20beta dihydroxy progesterone. Once the full growth of the oocytes is achieved, they arrest at prophase of meiosis I. MIH releases oocytes from this arrest. MIH promotes the formation of a dimeric protein kinase complex known as maturation promoting factor (MPF), the regulatory component of which is cyclin B and the catalytic component is cell division cycle (Cdc2) kinase. This complex is activated by phosphorylation at Thrl61 but remains inactive due to the inhibitory phosphorylation at Thrl4 and Tyrl5. MIH stimulates Cdc25, a dual specific phosphatase, that dephosphorylates both Thrl4 and Tyrl5 and converts pre- or inactive MPF to active MPF. Germinal vesicle break down (GVBD) is the marker of oocyte maturation. In an Indian freshwater perch, Anabas testudineus, MIH induced GVBD between 18-20 h. MIH induced oocytes extract in SDS-PAGE showed over-expression of a 30 kDa protein, which is confirmed to be cyclin B by using both monoclonal and polyclonal anti-cyclin B antibodies from various sources. The size of cyclin B in other vertebrates including mammals lies between 46-55 kDa. We have cloned cyclin B gene from perch oocyte and found it to contain the domains required for its function and immunological recognition. We also cloned Cdkl gene, which is very similar to other vertebrates Cdkl. Perch oocyte Cdc25 is overexpressed prior to GVBD converting inactive MPF to active MPF that affect GVBD. The objective of this overview is to deal with the molecular regulation of MPF activation which causes final maturation of oocytes.