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  • Animals  (3)
  • body force method.  (2)
  • 2000-2004  (2)
  • 1995-1999  (3)
  • 1980-1984
  • 1
    Electronic Resource
    Electronic Resource
    Effect of crack shape, inclination angle, and friction coefficient in crack surface contact problems (2000)
    Springer
    International journal of fracture 105 (2000), S. 367-389 
    Details
    ISSN: 1573-2673
    Keywords: Stress intensity factor ; tribology ; contact problem ; friction coefficient ; fracture mechanics ; rolling contact fatigue ; surface crack ; body force method.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract In rolling/sliding contact fatigue, it is known that the crack propagates at a characteristic angle θ=15–30 deg to the surface. To analyze the mechanism, however, the body force method has been widely used assuming 3D crack models for θ=45–90. In this study, therefore, the unknown body force densities are newly approximated by using fundamental density functions and polynomials. Then, a semi-elliptical crack model is analyzed for θ=15–90 under compressive residual stresses and Hertzian contact loads. The stress intensity factors K II, K III are calculated with varying the crack shape b/a, inclination crack angle θ, and crack face friction coefficient μ. The calculations show that the present method is useful for the analysis for θ=15–30 deg with high accuracy. It is seen that the K II-values when b/a→0 are larger than the ones when b/a=1 by 0–24% for both under compressive residual stress and Hertzian contact load. Regarding the maximum K II values under Hertzian contact load, the results of θ=15 deg are smaller than the ones of θ=45 deg by 23–34%. Regarding the amplitude of (K II max−K II min), the results of θ=15 deg are smaller than the ones of θ=45 deg by 4–24%. With increasing the value of friction coefficient μ for crack faces the value of K II decreases significantly. When the crack is short and the inclination angle θ is small, the value of friction coefficient f for Hertzian contact load largely affect the K II value.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007688027669
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Variation of mixed modes stress intensity factors of an inclined semi-elliptical surface crack (1999)
    Springer
    International journal of fracture 100 (1999), S. 207-225 
    Details
    ISSN: 1573-2673
    Keywords: Semi-elliptical crack ; inclined crack ; stress intensity factor ; crack opening displacement ; singular integral equation ; body force method.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract In this paper, a singular integral equation method is applied to calculate the stress intensity factor along crack front of a 3D inclined semi-elliptical surface crack in a semi-infinite body under tension. The stress field induced by displacement discontinuities in a semi-infinite body is used as the fundamental solution. Then, the problem is formulated as a system of integral equations with singularities of the form r −3. In the numerical calculation, the unknown body force doublets are approximated by the product of fundamental density functions and polynomials. The results show that the present method yields smooth variations of mixed modes stress intensity factors along the crack front accurately for various geometrical conditions. The effects of inclination angle, elliptical shape, and Poisson's ratio are considered in the analysis. Crack mouth opening displacements are shown in figures to predict the crack depth and inclination angle. When the inclination angle is 60 degree, the mode I stress intensity factor F I has negative value in the limited region near free surface. Therefore, the actual crack surface seems to contact each other near the surface.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018666110597
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  • 3
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    Unknown
    Ventroptin: a BMP-4 antagonist expressed in a double-gradient pattern in the retina (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-07
    Description: In the visual system, the establishment of the anteroposterior and dorsoventral axes in the retina and tectum during development is important for topographic retinotectal projection. We identified chick Ventroptin, an antagonist of bone morphogenetic protein 4 (BMP-4), which is mainly expressed in the ventral retina, not only with a ventral high-dorsal low gradient but also with a nasal high-temporal low gradient at later stages. Misexpression of Ventroptin altered expression patterns of several topographic genes in the retina and projection of the retinal axons to the tectum along both axes. Thus, the topographic retinotectal projection appears to be specified by the double-gradient molecule Ventroptin along the two axes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sakuta, H -- Suzuki, R -- Takahashi, H -- Kato, A -- Shintani, T -- Iemura Si -- Yamamoto, T S -- Ueno, N -- Noda, M -- New York, N.Y. -- Science. 2001 Jul 6;293(5527):111-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, National Institute for Basic Biology, The Graduate University for Advanced Studies, 38 Nishigonaka, Myodaiji-cho, Okazaki 444-8585, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11441185" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Proteins/*antagonists & inhibitors/genetics/metabolism ; Chick Embryo ; Cloning, Molecular ; Electroporation ; Embryo, Nonmammalian/cytology/metabolism ; Eye Proteins/chemistry/genetics/*metabolism ; *Gene Expression Regulation, Developmental ; Gene Library ; Humans ; In Situ Hybridization ; Mice ; Microinjections ; Molecular Sequence Data ; *Morphogenesis ; Nerve Tissue Proteins ; Precipitin Tests ; Protein Binding ; Protein Isoforms/chemistry/genetics/metabolism ; RNA, Messenger/analysis/genetics ; Retina/*embryology/*metabolism ; Sequence Alignment ; Surface Plasmon Resonance ; Xenopus Proteins ; Xenopus laevis/embryology/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Altered cochlear fibrocytes in a mouse model of DFN3 nonsyndromic deafness (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: DFN3, an X chromosome-linked nonsyndromic mixed deafness, is caused by mutations in the BRN-4 gene, which encodes a POU transcription factor. Brn-4-deficient mice were created and found to exhibit profound deafness. No gross morphological changes were observed in the conductive ossicles or cochlea, although there was a dramatic reduction in endocochlear potential. Electron microscopy revealed severe ultrastructural alterations in cochlear spiral ligament fibrocytes. The findings suggest that these fibrocytes, which are mesenchymal in origin and for which a role in potassium ion homeostasis has been postulated, may play a critical role in auditory function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minowa, O -- Ikeda, K -- Sugitani, Y -- Oshima, T -- Nakai, S -- Katori, Y -- Suzuki, M -- Furukawa, M -- Kawase, T -- Zheng, Y -- Ogura, M -- Asada, Y -- Watanabe, K -- Yamanaka, H -- Gotoh, S -- Nishi-Takeshima, M -- Sugimoto, T -- Kikuchi, T -- Takasaka, T -- Noda, T -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Cancer Institute, Japanese Foundation for Cancer Research, 1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cochlear Duct/*metabolism/pathology ; *DNA-Binding Proteins ; Deafness/genetics/*metabolism/pathology ; Ear, Inner/metabolism/pathology ; Ear, Middle/pathology ; Endolymph/metabolism ; Evoked Potentials, Auditory, Brain Stem ; Female ; Gene Expression ; Gene Targeting ; Genetic Linkage ; In Situ Hybridization ; Ion Transport ; Male ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; *Nerve Tissue Proteins ; POU Domain Factors ; Potassium/*metabolism ; Transcription Factors/genetics/*metabolism ; X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Rapid colorectal adenoma formation initiated by conditional targeting of the Apc gene (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Familial adenomatous polyposis coli (FAP) is a disease characterized by the development of multiple colorectal adenomas, and affected individuals carry germline mutations in the APC gene. With the use of a conditional gene targeting system, a mouse model of FAP was created that circumvents the embryonic lethality of Apc deficiency and directs Apc inactivation specifically to the colorectal epithelium. loxP sites were inserted into the introns around Apc exon 14, and the resultant mutant allele (Apc580S) was introduced into the mouse germline. Mice homozygous for Apc580S were normal; however, upon infection of the colorectal region with an adenovirus encoding the Cre recombinase, the mice developed adenomas within 4 weeks. The adenomas showed deletion of Apc exon 14, indicating that the loss of Apc function was caused by Cre-loxP-mediated recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibata, H -- Toyama, K -- Shioya, H -- Ito, M -- Hirota, M -- Hasegawa, S -- Matsumoto, H -- Takano, H -- Akiyama, T -- Toyoshima, K -- Kanamaru, R -- Kanegae, Y -- Saito, I -- Nakamura, Y -- Shiba, K -- Noda, T -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Cancer Institute, Toshima-ku, Tokyo 170, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311916" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Adenomatous Polyposis Coli Protein ; Adenoviridae/genetics ; Animals ; Colon/metabolism ; Cytoskeletal Proteins/biosynthesis ; Disease Models, Animal ; Exons ; Female ; Frameshift Mutation ; Gene Deletion ; *Gene Targeting ; *Genes, APC ; Genetic Vectors ; Germ-Line Mutation ; Homozygote ; Integrases/genetics/metabolism ; Introns ; Male ; Mice ; Mice, Inbred C57BL ; Recombination, Genetic ; *Viral Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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