Delamination failure in a unidirectional curved composite laminate

Delamination failure in a unidirectional curved composite laminate was investigated. The curved laminate failed unstably by delaminations developing around the curved region of the laminate at different depths through the thickness until virtually all bending stiffness was lost. Delamination was assumed to initiate at the location of the highest radial stress in the curved region. A closed form curved beam elasticity solution and a 2-D finite element analysis (FEA) were conducted to determine this location. The variation in the strain energy release rate, G, with delamination growth was then determined using the FEA. A strength-based failure criteria adequately predicted the interlaminar tension failure which caused initial delamination onset. Using the G analysis the delamination was predicted to extend into the arm and leg of the laminate, predominantly in mode I. As the initial delamination grew arould the curved region, the maximum radial stress in the newly formed inner sublaminate increased to a level sufficient to cause a new delamination to initiate in the sublaminate with no increase in applied load. This failure progression was observed experimentally

Effect of initial delamination on Mode 1 and Mode 2 interlaminar fracture toughness and fatigue fracture threshold

Static and fatigue double-cantilever beam (DCB) and end-notch flexure (ENF) tests were conducted to determine the effect of the simulated initial delamination in interlaminar fracture toughness, G(sub c), and fatigue fracture threshold, G(sub th). Unidirectional, 24-ply specimens of S2/SP250 glass/epoxy were tested using Kapton inserts of four different thickness - 13, 25, 75, and 130 microns, at the midplane at one end, or with tension or shear precracks, to simulate an initial delamination. To determine G(sub c), the fatigue fracture threshold below which no delamination growth would occur in less than 1 x 10(exp 6) cycles, fatigue tests were conducted by cyclically loading specimens until delamination growth was detected. Consistent values of model 1 fracture toughness, G(sub Ic), were measured from DCB specimens with inserts of thickness 75 microns or thinner, or with shear precracks. The fatigue DCB tests gave similar values of G(sub Ith) for the 13, 25, and 75 microns specimens. Results for the shear precracked specimens were significantly lower that for specimens without precracks. Results for both the static and fatigue ENF tests showed that measured G(IIc) and G(IIth) values decreased with decreasing insert thickness, so that no limiting thickness could be determined. Results for specimens with inserts of 75 microns or thicker were significantly higher than the results for precracked specimens or specimens with 13 or 25 microns inserts

Results of ASTM round robin testing for mode 1 interlaminar fracture toughness of composite materials

The results are summarized of several interlaboratory 'round robin' test programs for measuring the mode 1 interlaminar fracture toughness of advanced fiber reinforced composite materials. Double Cantilever Beam (DCB) tests were conducted by participants in ASTM committee D30 on High Modulus Fibers and their Composites and by representatives of the European Group on Fracture (EGF) and the Japanese Industrial Standards Group (JIS). DCB tests were performed on three AS4 carbon fiber reinforced composite materials: AS4/3501-6 with a brittle epoxy matrix; AS4/BP907 with a tough epoxy matrix; and AS4/PEEK with a tough thermoplastic matrix. Difficulties encountered in manufacturing panels, as well as conducting the tests are discussed. Critical issues that developed during the course of the testing are highlighted. Results of the round robin testing used to determine the precision of the ASTM DCB test standard are summarized

Damage prediction in cross-plied curved composite laminates

Analytical and experimental work is detailed which is required to predict delamination onset and growth in a curved cross plied composite laminate subjected to static and fatigue loads. The composite used was AS4/3501/6, graphite/epoxy. Analytically, a closed form stress analysis and 2-D and 3-D finite element analyses were conducted to determine the stress distribution in an undamaged curved laminate. The finite element analysis was also used to determine values of strain energy release rate at a delamination emanating from a matrix crack in a 90 deg ply. Experimentally, transverse tensile strength and fatigue life were determined from flat 90 deg coupons. The interlaminar tensile strength and fatigue life were determined from double cantilevered beam specimens. Cross plied curved laminates were tested statically and in fatigue to give a comparison to the analytical predictions. A comparison of the fracture mechanics life prediction technique and the strength based prediction technique is given

Characterization of Mode 1 and Mode 2 delamination growth and thresholds in graphite/peek composites

Composite materials often fail by delamination. The onset and growth of delamination in AS4/PEEK, a tough thermoplastic matrix composite, was characterized for mode 1 and mode 2 loadings, using the Double Cantilever Beam (DCB) and the End Notched Flexure (ENF) test specimens. Delamination growth per fatigue cycle, da/dN, was related to strain energy release rate, G, by means of a power law. However, the exponents of these power laws were too large for them to be adequately used as a life prediction tool. A small error in the estimated applied loads could lead to large errors in the delamination growth rates. Hence strain energy release rate thresholds, G sub th, below which no delamination would occur were also measured. Mode 1 and 2 threshold G values for no delamination growth were found by monitoring the number of cycles to delamination onset in the DCB and ENF specimens. The maximum applied G for which no delamination growth had occurred until at least 1,000,000 cycles was considered the threshold strain energy release rate. Comments are given on how testing effects, facial interference or delamination front damage, may invalidate the experimental determination of the constants in the expression

Delamination onset in polymeric composite laminates under thermal and mechanical loads

A fracture mechanics damage methodology to predict edge delamination is described. The methodology accounts for residual thermal stresses, cyclic thermal stresses, and cyclic mechanical stresses. The modeling is based on the classical lamination theory and a sublaminate theory. The prediction methodology determines the strain energy release rate, G, at the edge of a laminate and compares it with the fatigue and fracture toughness of the composite. To verify the methodology, isothermal static tests at 23, 125, and 175 C and tension-tension fatigue tests at 23 and 175 C were conducted on laminates. The material system used was a carbon/bismaleimide, IM7/5260. Two quasi-isotropic layups were used. Also, 24 ply unidirectional double cantilever beam specimens were tested to determine the fatigue and fracture toughness of the composite at different temperatures. Raising the temperature had the effect of increasing the value of G at the edge for these layups and also to lower the fatigue and fracture toughness of the composite. The static stress to edge delamination was not affected by temperature but the number of cycles to edge delamination decreased

Evaluation of the split cantilever beam for Mode 3 delamination testing

A test rig for testing a thick split cantilever beam for scissoring delamination (mode 3) fracture toughness was developed. A 3-D finite element analysis was conducted on the test specimen to determine the strain energy release rate, G, distribution along the delamination front. The virtual crack closure technique was used to calculate the G components resulting from interlaminar tension, GI, interlaminar sliding shear, GII, and interlaminar tearing shear, GIII. The finite element analysis showed that at the delamination front no GI component existed, but a GII component was present in addition to a GIII component. Furthermore, near the free edges, the GII component was significantly higher than the GIII component. The GII/GIII ratio was found to increase with delamination length but was insensitive to the beam depth. The presence of GII at the delamination front was verified experimentally by examination of the failure surfaces. At the center of the beam, where the failure was in mode 3, there was significant fiber bridging. However, at the edges of the beam where the failure was in mode 3, there was no fiber bridging and mode 2 shear hackles were observed. Therefore, it was concluded that the split cantilever beam configuration does not represent a pure mode 3 test. The experimental work showed that the mode 2 fracture toughness, GIIc, must be less than the mode 3 fracture toughness, GIIIc. Therefore, a conservative approach to characterizing mode 3 delamination is to equate GIIIc to GIIc

An update on nuclear calcium signalling

Over the past 15 years or so, numerous studies have sought to characterise how nuclear calcium (Ca2+) signals are generated and reversed, and to understand how events that occur in the nucleoplasm influence cellular Ca2+ activity, and vice versa. In this Commentary, we describe mechanisms of nuclear Ca2+ signalling and discuss what is known about the origin and physiological significance of nuclear Ca2+ transients. In particular, we focus on the idea that the nucleus has an autonomous Ca2+ signalling system that can generate its own Ca2+ transients that modulate processes such as gene transcription. We also discuss the role of nuclear pores and the nuclear envelope in controlling ion flux into the nucleoplasm

Oncogenic K-Ras suppresses IP₃-dependent Ca²⁺ release through remodeling of IP₃Rs isoform composition and ER luminal Ca²⁺ levels in colorectal cancer cell lines

The GTPase Ras is a molecular switch engaged downstream of G-protein coupled receptors and receptor tyrosine inases that controls multiple cell fate-determining signalling athways. Ras signalling is frequently deregulated in cancer underlying associated changes in cell phenotype. Although Ca2+ signalling pathways control some overlapping functions with Ras, and altered Ca2+ signalling pathways are emerging as important players in oncogenic transformation, how Ca2+ signalling is remodelled during transformation and whether it has a causal role remains unclear. We have investigated Ca2+ signalling in two human colorectal cancer cell lines and their isogenic derivatives in which the mutated K-Ras allele (G13D) has been deleted by homologous recombination. We show that agonist-induced Ca2+ release from intracellular stores is enhanced by loss of K-RasG13D through an increase in the ER store content and a modification of IP3R subtype abundance. Consistently, uptake of Ca2+ into mitochondria and sensitivity to apoptosis was enhanced as a result of KRasG13D loss. These results suggest that suppression of Ca2+ signalling is a common response to naturally occurring levels of K-RasG13D that contributes to a survival advantage during oncogenic transformation

Alzheimer’s disease-associated peptide Aβ₄₂ mobilizes ER Ca²⁺ via InsP₃R-dependent and -independent mechanisms

Dysregulation of Ca2+ homeostasis is considered to contribute to the toxic action of the Alzheimer’s Disease (AD) associated Amyloid β-peptide (Aβ). Ca2+ fluxes across the plasma membrane and release from intracellular stores have both been reported to underlie the Ca2+ fluxes induced by Aβ42. Here, we investigated the contribution of Ca2+ release from the endoplasmic reticulum (ER) to the effects of Aβ42 upon Ca2+ homeostasis and the mechanism by which Aβ42 elicited these effects. Consistent with previous reports, application of soluble oligomeric forms of Aβ42 exhibited Ca2+ mobilizing properties. The Aβ42-stimulated Ca2+ signals persisted in the absence of extracellular Ca2+ indicating a significant contribution of Ca2+ release from the ER Ca2+ store to the generation of these signals. Moreover, inositol 1,4,5-trisphosphate (InsP3) signaling contributed to Aβ42-stimulated Ca2+ release. The Ca2+ mobilizing effect of Aβ42 was also observed when applied to permeabilized cells deficient in InsP3 receptors revealing an additional direct effect of internalized Aβ42 upon the ER, and a mechanism for induction of toxicity by intracellular Aβ42