An acoustic emission technique is used to quantify and position microfracture events ahead of a growing opening mode crack in paper materials containing different amounts of added starch. A mechanical model based on gradient-enhanced elasticity, containing an intrinsic length parameter reflecting the fibre-based materials microstructure, is applied to analyse the results. It is found in experiments that the addition of starch increases the tensile strength of paper significantly while the level of onset of microfracture nucleation at the crack-tip is only slightly increased. It is also found that the height of the process zone (zone in which microfractures ahead of the crack predominantly take place), measured from the crack plane, decreases with increasing amount of starch. The experimental and analytical results suggest that adding cationic starch to paper reduces the material's sensitivity to gradients in the stress and strain fields and making the fibre network material more continuum-like'. The experimental observations are shown to be qualitatively in agreement with the numerical results and lend confidence to the applied model.

The twist stiffness of single and double-wall corrugated board is analyzed using first order shear deformation (FOSD) theory. Results are compared to finite element analysis (FEA) and dynamic test data for a large range of torsion loaded rectangular board specimens. The FOSD approach and FEA employ a homogenized core. In addition, a structural finite element model was developed where the web core is represented by shell elements. According to FOSD analysis, the twist stiffness is linearly dependent on the transverse shear moduli of the web core along both principal directions of the core. Good agreement between the torsional stiffness predictions by analytical and numerical approaches and test results is found for the range of single and double-wall boards examined. The FOSD solution is significantly less computationally demanding than FEA, and appears viable for prediction of the twist stiffness of corrugated board.

Nonlocal and gradient theories are capable of describing deformation of heterogeneous elastic materials better than classical elasticity theory. Crack-tip stress and strain fields in a gradient enhanced elastic material are derived on closed form. Physical requirements of finite stresses and strains at infinity and at the tip are applied to remove singularities. A fracture criterion is derived that links applied remote macroscopic stress via microscopic cohesive stress in the vicinity of the crack-tip to the Griffith's energy. A comparison to a classical nonlocal theory by Eringen is made. It is believed that the solutions will help engineers to deal with fracture analyses in elastic brittle heterogeneous materials. (C) 2012 Elsevier Ltd. All rights reserved.

A closed form relation for the strain energy density in the vicinity of a macroscopic mode I crack in a random fiber network is derived using an implicit gradient nonlocal continuum field theory. An expression for the characteristic length, used in the nonlocal formulations, in terms of microstructural properties is derived and it is found that the characteristic length is proportional to the average fiber segment length to the power of two. It is illustrated that the crack-tip singularity vanishes for a characteristic length greater than zero. An open fiber structure exhibits a distributed strain energy field in the crack tip vicinity. As the network becomes relatively denser, the characteristic length decreases and the networks mechanical behavior approaches the behavior of a classic elastic continuum. Only for an infinitely dense network is the r −1-singularity in strain energy field achieved. The theory explains why open network structures have difficulties in localizing failure to macroscopic cracks. It is found that there is a one-to-one relation between characteristic length and size of the smallest crack that can initiate macroscopic failure.

The problem of failure in the facings of a corrugated board is investigated by means of a mechanical model utilizing the principles of continuum damage mechanics. To evaluate the predictive capability of the model, experiments have been conducted on in-plane isotropic single- and two-ply paper sheets manufactured in the laboratory. It is found that there is a qualitative agreement between model and experiments. The model can predict if delamination will occur before the top-ply loses its in-plane load carrying capacity due to material degradation. To circumvent delamination problems, a material with low stiffness should be used in the top-ply (as compared to the bottom-ply) and a very thin top-ply should be avoided. It is exemplified that it is possible to steer the failure mode by optimizing the degree of beating or the ply thickness. It is demonstrated that plasticity may be omitted in the analysis if one is only interested in characterizing the expected type of failure mode. An important key result is that, if the circumstances are that severe damage growth takes place in the crack-tip region, then delamination most likely occur which may be in contradiction to what is anticipated from classical theories of fracture mechanics.

It is experimentally observed that the fracture process developed in an embossed paper sample having a periodic matrix organized pattern is distributed over several indentation rows in the region near a macroscopic crack. This observation suggests that the stresses at the tip of the crack is shielded by damage in neighboring rows of indentation: energy dissipation may occur not only at the tip of the main crack, but in several indentation rows parallel to the main crack.In this investigation, a model describing the in-plane fracture behavior of embossed low-basis-weight paper is developed. It is found that the model is capable of capturing the development of damage in rows parallel to the main crack and compares well with experimental results. (C) 2006 Elsevier Ltd. All rights reserved.

Strains, computed by the finite element method, are evaluated and compared to an experimentally determined strain field. The analyzed low-density paper has been designed to ensure bond–breakage as the dominating damage mechanism and the paper material is approximately in-plane isotropic. An optical non-contact displacement measuring system has been used in fracture tests to determine the strain field in the crack-tip region of a pre-fabricated crack. Additionally, acoustic emission monitored tensile tests have been conducted to determine onset and evolution of damage processes and thereby enabling calibration of required constitutive parameters. The results suggest that the investigated paper material can tolerate significantly higher strains than what is predicted by a classic elastic–plastic J2-flow theory. Immediately before onset of the final fracture (i.e., localization), the experimental measured normal strain in the near-tip region is around 60% higher than the computed strain when using exclusively an elastic–plastic theory for the corresponding load while the strain computed utilizing a non-local damage theory is of the same order of magnitude as the experimentally measured strain. Hence, it seems essential to include a non-local continuum theory to describe strains in the near-tip region quantitatively correct for paper materials. It is demonstrated that path independence of the well-known J-integral does not prevail for this class of material models. Only for the special situation of a homogenous damage field in the crack-tip region may the stress and strain fields be described by the well-known HRR-solutions.

The mechanical behavior of a layered paper structure subjected to a combined load of bending and tension is studied. A finite element analysis is performed to include a gradient enhanced continuum damage theory since a non-local theory has to be used when stress gradients are present. Despite the anisotropic nature of paper materials, each layer is modeled as isotropic and homogenous where material parameters are estimated from the in-plane properties of the paper sheet. The two failure modes, material failure and delamination between top and base layer is analyzed within the frameworks of fracture and continuum damage mechanics. Delamination is assumed to be in shearing mode since the crack surfaces are predominantly sliding and crack opening is vanishing. An analytic solution for the fracture energy release rate is derived utilizing engineering beam theory assuming small deformations. Different combinations of stiffness and thickness ratios between the top and base layer are examined in order to judge the risk for having material failure or delamination failure of the multi-ply linerboard. Having a thick and weak top layer, compared to the base layer, increases the probability to obtain through-thickness damage failure in favor of delamination. On the other hand, having a stiff and thin top layer, compared to the base layer, increases the probability to obtain delamination prior to rupture of the top layer. Experiments performed on two-ply linerboards consisting of one ply of mainly virgin fibers and one ply of recycled fibers confirm the predictions made by the model.

Continuum damage mechanics (CDM) is used to describe the post-elastic behavior of low-basis-weight paper. The relevance of undertaking studies of the mechanical behavior of low-basis-weight paper is that it enables characterization, optimization and quality control. In accordance with a CDM theory, an internal variable is introduced that represent the degree to which the material has degraded in a continuum sense and details inherent in a damage evolution law contain information about the rupture mechanism. To account for long ranging micro-structural effects, because of the fiber structure in the paper material, a non-local formulation of the constitutive law is considered. Of particular interest is the fracture toughness of the material, i.e. the ability to resist further crack propagation, as it is often a good measure of flaw tolerance and durability in the context of paper. The constitutive model discussed is verified against tensile tests on rectangular paper specimens containing pre-fabricated cracks. Acoustic emission was used to study the damage evolution in paper specimens during tensile loading. An orthotropic material description has been utilized. The model is contrasted with a purely isotropic formulation. It seems that for the type of problem analyzed in this work, an orthotropic material description does not significantly improve the predictive capability as compared to an isotropic formulation. It is concluded that the model can be used to evaluate the influence of arbitrary defect geometries, defect size and loading conditions and can easily be incorporated into a finite element code.

The mechanical behavior of two packaging paper materials subjected to tensile loading up to complete breakage has been investigated. A model for isotropic strain hardening elastic anisotropic plasticity, coupled to anisotropic damage, is discussed. The constitutive relations, including a gradient enhanced damage model, are developed within a thermodynamical framework. The Helmholtz free energy in the continuum is assumed to depend not only on the strain and stress components but also on the damage in the material.The model has been analyzed in a non-linear finite element procedure. The capability of the model to properly capture and simulate the failure of a paper material subjected to tensile loading is demonstrated by means of several numerical examples that are compared to, and verified with, experiments on packaging paper specimens of varying geometry. (C) 2004 Elsevier Ltd. All rights reserved.

In early studies, herpes simplex virus 1 (HSV-1) proteins were identified on the basis of two criteria. The first consisted of characterization of proteins contained in virions purified from cells whose proteins were labeled prior to infection. These proteins designated by the prefix VP were numbered in the order of decreasing apparent molecular weight or, conversely, ascending electrophoretic mobility in denaturing gels (147). The second criterion identified putative viral proteins accumulating in infected cells but absent from uninfected cells. These proteins, designated infected-cell proteins (ICPs), were also numbered in order of decreasing apparent molecular weight (73). One protein, however, while clearly apparent only in infected cells, varied with respect to electrophoretic mobility depending on the composition of the denaturing gel (74). This anomalously migrating protein was designated ICP0 (74). In subsequent studies, viral proteins were designated either by their known primary function (e.g., DNA polymerase, etc.) or the position of the gene along the unique long (UL) or short (US) components of the viral genome (105, 107). The original ICP designation, however, was retained primarily for five proteins recognized in early studies as being the products of α or immediate-early genes expressed after infection in the absence of de novo viral protein synthesis (74, 75). The five proteins, ICP0, ICP4, ICP22, ICP27, and ICP47, have been extensively studied, and for the most part, there is at least a semblance of concordance between the phenotype of cells infected with the mutant lacking the gene, the behavior of the protein in transduced cells, and the molecular functions expressed by the protein (reviewed in reference 132). ICP4 is an essential positive and negative regulator of gene expression (reviewed in reference 132). The protein blocks gene expression by binding to high-affinity DNA consensus sites located at transcription initiation sites of at least two genes. The mechanism of gene activation is less understood, although ICP4’s affinity for transcription factors and binding to highly degenerate or nonconsensus sites are suggestive of how it might act. ICP27 is also a multifunctional protein whose phenotype can be largely explained by its ability to block RNA splicing but not transport of unspliced RNA early in infection and by its activity as a chaperone of newly made viral mRNA across the nuclear membranes at late times after infection (reviewed in reference 137). Available data indicate that the carboxyl-terminal half of ICP22 enables full expression of a subset of late (γ2) viral genes by causing cdc2 cyclin-dependent kinase activity to survive the degradation of its physiologic partners cyclins A and B, by an aberrant partnership with the UL42 DNA polymerase processivity factor (2, 5, 6, 19, 141). Optimal transcription of late genes requires binding and posttranslational modification of topoisomerase IIα by the two proteins (7). The sole known mission of ICP47 is to bind to and preclude TAP1/TAP2 from enabling the transport of antigenic peptides into the endoplasmic reticulum for eventual presentation on the cell surface (50, 71, 161). Despite 3 decades of research and enormous interest, it is not known how the functions encoded in ICP0 account for its phenotype in either infected or transduced cells. However, available evidence suggests that ICP0 is a multifunctional protein and that its role in viral infection reflects the sum of its multiple and diverse functions (132). Studies published nearly 20 years ago established that ICP0 activates genes introduced into cells by transfection or infection (29, 30, 54, 118, 129). Furthermore, ICP0 also activates a specific subset of cellular genes, including several p53-responsive genes that it activates independently of p53 (72). ICP0 is considered a promiscuous transactivator, inasmuch as it activates transcription from HSV (16, 22, 104) and heterologous (58, 114, 143) promoter elements independently of a single cis-acting element (40). ICP0 activates transcription of viral genes in synergy with or independent of ICP4 (29, 31, 55, 129). ICP0 has been shown to interact with ICP4, and this interaction is believed to mediate cooperative activation of gene expression, as it maps to a region of ICP0 (residues 617 to 775) that contains the domain involved in synergy with ICP4 (residues 680 to 767) (33, 159). In most cell lines infected at low multiplicity with mutants lacking the gene encoding ICP0 (Δα0), viral yields are 10- to 100-fold lower than those from cells infected with wild-type virus (34, 136, 148). At higher multiplicities of infection, viral yields and protein expression are similar to those of wild-type virus (34, 136, 148). Exceptions are a few cell lines, exemplified by the line U20S, in which Δα0 mutants replicate as well as wild-type viruses (160). Because of the lethargy of Δα0 mutants, ICP0 has been held responsible for the establishment of latency and a myriad of other functions. Nevertheless, none of these phenotypic properties of ICP0 correlate directly with the emerging patterns of interaction of ICP0 with cellular proteins—the subject of this review.

In this paper, we present some analytical and numerical results concerning the zero-span testing method, frequently used for quality control of cellulose fiber for papermaking. Of particular interest is the relationship between an apparent modulus obtained from the zero-span testing method and the elastic properties of the fibers. The apparent elasticity modulus is estimated using two energy theorems in elasto-statics in which the role of span length is explored. Analytical results, derived under the assumption that slippage between specimen and clamps does not occur, clearly show that the apparent modulus strongly depends on the span length. This is verified by the numerical results obtained using the finite element method. In addition to the above analysis, the effect of slippage is investigated, also by utilizing the finite element method, and it is found that for a specific case, the contribution from slippage to the total displacement depends strongly on the length of the span. Tensile tests at nominal zero span were conducted in an effort to further validate the analysis with relevant experimental data and it was concluded that there is qualitative agreement between the experimental results and the result of the analysis.

ABSTRACT Herpes simplex virus type 1 (HSV-1) infected cell protein 0 (ICP0) is a multifunctional protein that functions as a promiscuous transactivator and promotes the degradation of multiple cellular proteins. In vitro studies indicated that it encodes two physically separated functional E3 ubiquitin ligase domains. One, designated herpesvirus ubiquitin ligase 1 (HUL-1), maps to a region encoded by exon 3 and is contained between residues 543 and 680. Deletion of amino acids 621 to 625 abolishes this activity. The second, designated HUL-2, maps to the RING finger domain present in ICP0 encoded by exon 2. Earlier studies have shown that ICP0 stabilizes cyclins D1 and D3, and several lines of investigation led to the hypothesis that this function of ICP0 is the consequence of degradation of the E2 enzyme cdc34, known to be involved in the proteasome-dependent degradation of D-type cyclins. Consistent with this hypothesis, we have previously shown that cdc34 physically interacts with ICP0 at or near aspartate 199 and at amino acids 621 to 625 and that the former site is required for effective ubiquitylation and degradation of cdc34. Furthermore, the ICP0 HUL-1 domain promotes the polyubiquitination of cdc34 in vitro. If the mechanism by which D-type cyclins are salvaged in wild-type-infected cells is dependent on polyubiquitination and consequent destruction of cdc34, than the mutant virus R6701, which was constructed for these studies and lacks ICP0 residues 621 to 625, should destabilize the D cyclins and preclude the degradation of cdc34. We report that ICP0 residues 621 to 625 are essential for degradation of cdc34 in infected cells and for the ICP0-mediated stabilization of D-type cyclins, that a mutation that specifically disrupted the ring finger domain of the HUL-2 site had no effect on the degradation of cdc34 in infected cells, and that deletion of ICP0 residues 621 to 625 decreased the replicative capacity of the virus in growth-arrested but not in dividing cells and resulted in diminished pathogenicity on intracerebral inoculation of mice. We conclude that the ICP0 HUL-1 domain acts in infected cells to degrade cdc34 and that this function requires the interaction of cdc34 with sequences in exons 2 and 3 but does not involve the HUL-2 RING finger E3 domain.

The fracture toughness of a polymer-metal laminate composite is obtained by mechanical testing of a specimen containing a pre-crack. The laminate is a material used for packaging. It consists of a thin aluminium foil and a polymer coating. A centre cracked panel test geometry is used. Each of the layers forming the laminate is also tested separately. The result is compared with the measured fracture strength of the individual layers. It is observed that the load carrying capacity increases dramatically for the laminate. At the strain when peak load is reached for the laminate only aluminium is expected to carry any substantial load because of the low stiffness of the LDPE. However, the strength of the laminate is almost twice the strength of the aluminium foil. The reason seems to be that the aluminium forces the polymer to absorb large quantities of energy at small nominal strain. The toughness compares well with the accumulated toughness of all involved layers. Possible fracture of the interface between the layers is discussed.