The mechanical response and the evolution of director orientation are characterized in a smectic, main-chain liquid crystalline elastomer (LCE) as it undergoes the familiar polydomain−monodomain (P−M) transition. Under uniaxial tension, the LCE behaves like an ordinary rubber-like network at low strains, and local director rotations are shown to slightly favor the perpendicular (“anomalous”) orientation of chain axes with respect to the draw direction. As strain increases, a well-defined yield stress is observed due to the onset of a necking instability. Macroscopic elongation proceeds by growth of the necked monodomain region, which appears to consume the non-necked polydomain region(s) at its boundaries. Within the necked region, the parallel (“normal”) orientation of chain axes with respect to the draw direction is strongly favored. The P−M transition is attributed to a change in the conformation of the elastic polymer backbones from hairpinned coils to extended chains. Under the conditions of temperature and strain rate studied, buckling of the smectic layers is observed as the fully necked monodomain state is approached.
Smectic main-chain liquid crystalline elastomers (MCLCE) with polydomain morphology are rare examples of elastomers that can form a neck and undergo cold drawing under tension. However, not all previous studies of the mechanical behavior of smectic MCLCE reported neck formation. The mechanical response of a polydomain smectic MCLCE has therefore been characterized by elongation at varying strain rates and temperatures to identify factors favoring mechanical instability. Yielding and neck formation are increasingly favored as the strain rate increases at constant temperature, or as the temperature decreases toward T g . As cold drawing pro-ceeds, significant creep occurs continuously within the neck, in contrast to the behavior of certain linear polymers that exhibit a ''natural'' draw ratio. Thermal imaging during elongation indicates that viscous heating is not a prerequisite for neck formation. Rather, inherent softening of the material during yielding due to morphological changes leads to an enhanced rate of deformation and contraction at the neck. V C 2011 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 49: 591-598, 2011
The genomic DNA polymorphism of the beta chain of the T cell receptor was examined. The restriction fragment length polymorphism distribution was similar in systemic lupus erythematosus patients, their relatives, and normal controls. Our observations suggest that these genes are not coinberited with genes responsible for systemic lupus erythematosus.Systemic lupus erythematosus (SLE) is an autoimmune illness characterized by multiple abnormalities of lymphocyte activation and regulation. Many studies offer evidence of a genetic influence in SLE including: familial aggregation (I), concordance in identical twins (2), the presence of autoantibodies in unaffected relatives of SLE patients (3), an increased frequency of certain histocompatibility (4) and Gm markers (9, low levels of erythrocyte C3b receptors (6), and abnormal T cell suppressor function in healthy relatives of SLE patients (7). Abnormal recognition of antigen and/or major histocompatibility antigens by a -~ defective T cell receptor (8) could result in loss of tolerance to self-antigens, with ensuing autoantibody production and resulting tissue injury.The recent cloning of the beta chain of the T cell receptor (9) and the description of a characteristic restriction fragment length polymorphism (RFLP) in normal individuals (10) permit the examination of this genomic DNA polymorphism in SLE patients in order to assess this protein's role in the predisposition for lupus, Kotzin et a1 (1 1) have recently suggested that defects in the mouse T cell beta chain may be involved in murine lupus.We have demonstrated that this RFLP has a similar distribution in SLE patients, their unaffected relatives, and in normal individuals. These findings suggest that the genes encoding the beta chain of the T cell receptor are not coinherited with a gene whose product is responsible for the development of SLE.Patients and methods. DNA was extracted from washed, lysed, and pelleted cells from peripheral blood of 14 patients who met the American Rheumatism Association 1982 revised criteria for SLE (12), 13 healthy relatives of the SLE patients, and 6 healthy, unrelated normal individuals. The genomic DNA was digested with the restriction enzyme Bgl I1 (New England Nuclear, Boston, MA), size-fractionated by agarose gel electrophoresis, and transferred onto nitrocellulose membranes according to the Southern method (13). The fractionated DNA was hybridized as described previously (10). The probe consisted of the Eco RI-Bgl I1 fragment of the human T cell receptor beta chain locus at the 5' end of the second constant region. The hybridized blots were placed onto radio-
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.