Untwisting of a Strained Cholesteric Elastomer by Disclination Loop Nucleation

The application of a sufficiently strong strain perpendicular to the pitch axis of a monodomain cholesteric elastomer unwinds the cholesteric helix. Previous theoretical analyses of this transition ignored the effects of Frank elasticity which we include here. We find that the strain needed to unwind the helix is reduced because of the Frank penalty and the cholesteric state becomes metastable above the transition. We consider in detail a previously proposed mechanism by which the topologically stable helical texture is removed in the metastable state, namely by the nucleation of twist disclination loops in the plane perpendicular to the pitch axis. We present an approximate calculation of the barrier energy for this nucleation process which neglects possible spatial variation of the strain fields in the elastomer, as well as a more accurate calculation based on a finite element modeling of the elastomer.Comment: 12 pages, 9 figure

Loss of the BMP Antagonist, SMOC-1, Causes Ophthalmo-Acromelic (Waardenburg Anophthalmia) Syndrome in Humans and Mice

Ophthalmo-acromelic syndrome (OAS), also known as Waardenburg Anophthalmia syndrome, is defined by the combination of eye malformations, most commonly bilateral anophthalmia, with post-axial oligosyndactyly. Homozygosity mapping and subsequent targeted mutation analysis of a locus on 14q24.2 identified homozygous mutations in SMOC1 (SPARC-related modular calcium binding 1) in eight unrelated families. Four of these mutations are nonsense, two frame-shift, and two missense. The missense mutations are both in the second Thyroglobulin Type-1 (Tg1) domain of the protein. The orthologous gene in the mouse, Smoc1, shows site- and stage-specific expression during eye, limb, craniofacial, and somite development. We also report a targeted pre-conditional gene-trap mutation of Smoc1 (Smoc1tm1a) that reduces mRNA to ∼10% of wild-type levels. This gene-trap results in highly penetrant hindlimb post-axial oligosyndactyly in homozygous mutant animals (Smoc1tm1a/tm1a). Eye malformations, most commonly coloboma, and cleft palate occur in a significant proportion of Smoc1tm1a/tm1a embryos and pups. Thus partial loss of Smoc-1 results in a convincing phenocopy of the human disease. SMOC-1 is one of the two mammalian paralogs of Drosophila Pentagone, an inhibitor of decapentaplegic. The orthologous gene in Xenopus laevis, Smoc-1, also functions as a Bone Morphogenic Protein (BMP) antagonist in early embryogenesis. Loss of BMP antagonism during mammalian development provides a plausible explanation for both the limb and eye phenotype in humans and mice

Spark-source mass spectra of several aromatic hydrocarbons using a spinning electrode /

"May 1967"--Cover.Bibliography: p. 11.Mode of access: Internet

Chemical reactions produced by exposing coal derivatives to ultrasonic energy /

"October 1967"--Cover.Bibliography: p. 11.Mode of access: Internet

Mass spectrometric analyses of coal-tar distillates and residues /

"August 1967"--Cover.Bibliography: p. 13-14.Mode of access: Internet

United States Bureau of Mines Bulletin 640

Report from the U.S. Bureau of mines discussing the use of infared and ultraviolet-visible spectrometry to study the structure of coal and coal extracts