Dynamics of the peel front and the nature of acoustic emission during peeling of an adhesive tape

We investigate the peel front dynamics and acoustic emission of an adhesive tape within the context of a recent model by including an additional dissipative energy that mimics bursts of acoustic signals. We find that the nature of the peeling front can vary from smooth to stuck-peeled configuration depending on the values of dissipation coefficient, inertia of the roller, mass of the tape. Interestingly, we find that the distribution of AE bursts shows a power law statistics with two scaling regimes with increasing pull velocity as observed in experiments. In this regimes, the stuck-peeled configuration is similar to the `edge of peeling' reminiscent of a system driven to a critical state.Comment: Accepted for publication in Phys. Rev. Let

Missing physics in stick-slip dynamics of a model for peeling of an adhesive tape

It is now known that the equations of motion for the contact point during peeling of an adhesive tape mounted on a roll introduced earlier are singular and do not support dynamical jumps across the two stable branches of the peel force function. By including the kinetic energy of the tape in the Lagrangian, we derive equations of motion that support stick-slip jumps as a natural consequence of the inherent dynamics. In the low mass limit, these equations reproduce solutions obtained using a differential-algebraic algorithm introduced for the earlier equations. Our analysis also shows that mass of the ribbon has a strong influence on the nature of the dynamics.Comment: Accepted for publication in Phys. Rev. E (Rapid Communication

Dynamics of stick-slip in peeling of an adhesive tape

We investigate the dynamics of peeling of an adhesive tape subjected to a constant pull speed. We derive the equations of motion for the angular speed of the roller tape, the peel angle and the pull force used in earlier investigations using a Lagrangian. Due to the constraint between the pull force, peel angle and the peel force, it falls into the category of differential-algebraic equations requiring an appropriate algorithm for its numerical solution. Using such a scheme, we show that stick-slip jumps emerge in a purely dynamical manner. Our detailed numerical study shows that these set of equations exhibit rich dynamics hitherto not reported. In particular, our analysis shows that inertia has considerable influence on the nature of the dynamics. Following studies in the Portevin-Le Chatelier effect, we suggest a phenomenological peel force function which includes the influence of the pull speed. This reproduces the decreasing nature of the rupture force with the pull speed observed in experiments. This rich dynamics is made transparent by using a set of approximations valid in different regimes of the parameter space. The approximate solutions capture major features of the exact numerical solutions and also produce reasonably accurate values for the various quantities of interest.Comment: 12 pages, 9 figures. Minor modifications as suggested by refere

Rat placentation: An experimental model for investigating the hemochorial maternal-fetal interface

The rat possesses hemochorial placentation with deep intrauterine trophoblast cell invasion and trophoblast-directed uterine spiral artery remodeling; features shared with human placentation. Recognition of these similarities spurred the establishment of in vitro and in vivo research methods using the rat as an animal model to address mechanistic questions regarding development of the hemochorial placenta. The purpose of this review is to provide the requisite background to help move the rat to the forefront in placentation research. © 2012 Elsevier Ltd. All rights reserved

Novel Therapeutic Strategies for Malignant Salivary Gland Tumors: Lessons Learned from Breast Cancer

Malignant salivary gland tumors (MSGTs) account for 2–6% of all head and neck cancers. Despite the rarity, MSGTs have been of great interest due to a wide variety of pathological features and high metastasis rates resulting in poor prognosis. Surgical resection followed by radiation therapy represents the main treatment of this malignancy. Adjuvant therapy is reserved for the management of local recurrence, no longer amenable to additional local therapy, and for metastasis. Based on the studies from other types of tumors, particularly breast cancer, the expression and function of sex steroid hormone receptors in cancer have been extensively studied and applied to diagnosis and treatment. Although a number of studies in MSGTs have been published, the rationale for hormone therapy is still controversial due to the disparate results and insufficient number of cases. However, some recent reports have demonstrated that certain salivary gland neoplasms are similar to breast cancer, not only in terms of the pathological features, but also at the molecular level. Here, we shed light on the biological similarity between MSGTs and certain types of breast cancer, and describe the potential use of hormone and additional therapies for MSGTs

Power Laws, Precursors and Predictability During Failure

We investigate the dynamics of a modified Burridge-Knopoff model by introducing a dissipative term to mimic the bursts of acoustic emission (AE) from rock samples. The model explains many features of the statistics of AE signals observed in experiments such as the crossover in the exponent value from relatively small amplitude AE signals to larger regime, and their dependence on the pulling speed. Significantly, we find that the cumulative energy dissipated identified with acoustic emission can be used to predict a major slip event. We also find a data collapse of the acoustic activity for several major slip events describable by a universal stretched exponential with corrections in terms of time-to-failure.Comment: 7 pages, 6 figures, Final version with minor change

Structural Basis for Activation of Calcineurin by Calmodulin

The highly conserved phosphatase calcineurin (CaN) plays vital roles in numerous processes including T-cell activation, development and function of the central nervous system, and cardiac growth. It is activated by the calcium sensor calmodulin (CaM). CaM binds to a regulatory domain (RD) within CaN, causing a conformational change that displaces an autoinhibitory domain (AID) from the active site, resulting in activation of the phosphatase. This is the same general mechanism by which CaM activates CaM-dependent protein kinases. Previously published data have hinted that the RD of CaN is intrinsically disordered. In this work, we demonstrate that the RD is unstructured and that it folds upon binding CaM, ousting the AID from the catalytic site. The RD is 95 residues long, with the AID attached to its C-terminal end and the 24-residue CaM binding region toward the N-terminal end. This is unlike the CaM-dependent protein kinases that have CaM binding sites and AIDs immediately adjacent in sequence. Our data demonstrate that not only does the CaM binding region folds but also an ∼25- to 30-residue region between it and the AID folds, resulting in over half of the RD adopting α-helical structure. This appears to be the first observation of CaM inducing folding of this scale outside of its binding site on a target protein

Structural basis for activation of calcineurin by calmodulin

The highly conserved phosphatase calcineurin plays vital roles in numerous processes including T-cell activation, development and function of the central nervous system, and cardiac growth. It is activated by the calcium sensor calmodulin. Calmodulin binds to a regulatory domain within calcineurin, causing a conformational change that displaces an autoinhibitory domain from the active site, resulting in activation of the phosphatase. This is the same general mechanism by which calmodulin activates calmodulin-dependent protein kinases. Previously published data has hinted that the regulatory domain of calcineurin is intrinsically disordered. In this work we demonstrate that the regulatory domain is unstructured and that it folds upon binding calmodulin, ousting the autoinhibitory domain from the catalytic site. The regulatory domain is 95 residues long, with the autoinhibitory domain attached to its C-terminal end and the 24 residue calmodulin binding region towards the N-terminal end. This is unlike the calmodulin-dependent protein kinases which have calmodulin binding sites and autoinhibitory domains immediately adjacent in sequence. Our data demonstrate that not only does the calmodulin binding region fold, but that an ~25-30 residue region between it and the autoinhibitory domain also folds, resulting in over half of the regulatory domain adopting α-helical structure. This appears to be the first observation of calmodulin inducing folding of this scale outside of its binding site on a target protein

Germline and somatic JAK2 mutations and susceptibility to chronic myeloproliferative neoplasms

Myeloproliferative neoplasms (MPNs) are a group of closely related stem-cell-derived clonal proliferative diseases. Most cases are sporadic but first-degree relatives of MPN patients have a five- to seven-fold increased risk for developing an MPN. The tumors of most patients carry a mutation in the Janus kinase 2 gene (JAK2V617F). Recently, three groups have described a strong association of JAK2 germline polymorphisms with MPN in patients positive for JAK2V617F. The somatic mutation occurs primarily on one particular germline JAK2 haplotype, which may account for as much as 50% of the risk to first-degree relatives. This finding provides new directions for unraveling the pathogenesis of MPN