Competent Matrix Research Articles

Formation of mullions in two and three dimensions: Results from analogue modelling

Scale-model experiments, involving pure shear shortening of a single incompetent layer embedded in a competent matrix, were carried out to study the influence of the bulk strain geometry and an inclined layer on the growth rate and shape of mullions. The viscosity ratio between non-linear viscous layer and matrix varied from 1/4–1/35. If layer parallel shortening (eZ) is the same, the growth rate of mullions is highest under bulk constriction, moderate under bulk plane strain, and lowest under bulk flattening. Because of their low growth rate in a flattening strain field, formation of mullions is hardly possible. Initial layer inclination under bulk constriction led to antisymmetric mullions. Increasing the viscosity ratio between layer and matrix results in (1) faster rotation of the layer towards the main stretching axis, X, (2) earlier attainment of a stable mullion wavelength, and (3) earlier formation of flames. The style of deformation (coeval folding and boudinage vs. shearing) of a thin competent sheet, inserted into the incompetent layer, is controlled not only by the viscosity ratio, but also by the bonding between competent and incompetent material. The new results shed light on the deformation behavior of Sederholm-type dikes and sills at deep crustal levels.

In vitro maturation and in vivo stability of bioprinted human nasal cartilage

The removal of skin cancer lesions on the nose often results in the loss of nasal cartilage. The cartilage loss is either surgically replaced with autologous cartilage or synthetic grafts. However, these replacement options come with donor-site morbidity and resorption issues. 3-dimensional (3D) bioprinting technology offers the opportunity to engineer anatomical-shaped autologous nasal cartilage grafts. The 3D bioprinted cartilage grafts need to embody a mechanically competent extracellular matrix (ECM) to allow for surgical suturing and resistance to contraction during scar tissue formation. We investigated the effect of culture period on ECM formation and mechanical properties of 3D bioprinted constructs of human nasal chondrocytes (hNC)-laden type I collagen hydrogel in vitro and in vivo. Tissue-engineered nasal cartilage constructs developed from hNC culture in clinically approved collagen type I and type III semi-permeable membrane scaffold served as control. The resulting 3D bioprinted engineered nasal cartilage constructs were comparable or better than the controls both in vitro and in vivo. This study demonstrates that 3D bioprinted constructs of engineered nasal cartilage are feasible options in nasal cartilage reconstructive surgeries.

Adipose-derived stromal cell secreted factors induce the elastogenesis cascade within 3D aortic smooth muscle cell constructs

ObjectiveElastogenesis within the medial layer of the aortic wall involves a cascade of events orchestrated primarily by smooth muscle cells, including transcription of elastin and a cadre of elastin chaperone matricellular proteins, deposition and cross-linking of tropoelastin coacervates, and maturation of extracellular matrix fiber structures to form mechanically competent vascular tissue. Elastic fiber disruption is associated with aortic aneurysm; in aneurysmal disease a thin and weakened wall leads to a high risk of rupture if left untreated, and non-surgical treatments for small aortic aneurysms are currently limited. This study analyzed the effect of adipose-derived stromal cell secreted factors on each step of the smooth muscle cell elastogenesis cascade within a three-dimensional fibrin gel culture platform. Approach and resultsWe demonstrate that adipose-derived stromal cell secreted factors induce an increase in smooth muscle cell transcription of tropoelastin, fibrillin-1, and chaperone proteins fibulin-5, lysyl oxidase, and lysyl oxidase-like 1, formation of extracellular elastic fibers, insoluble elastin and collagen protein fractions in dynamically-active 30-day constructs, and a mechanically competent matrix after 30 days in culture. ConclusionOur results reveal a potential avenue for an elastin-targeted small aortic aneurysm therapeutic, acting as a supplement to the currently employed passive monitoring strategy. Additionally, the elastogenesis analysis workflow explored here could guide future mechanistic studies of elastin formation, which in turn could lead to new non-surgical treatment strategies.

Formation of dome-in-dome structures: Results from experimental studies and comparison with natural examples

Dome-in-dome structures are frequent in salt provinces and in high-grade rocks of orogens. Their origin is only poorly understood. In the present study we have modelled dome-in-dome structures, which result from constrictional (radial) in-plane shortening of a competent layer embedded in a rising less competent matrix. Both the layer and the matrix consist of non-linear viscous plasticine, which display a viscosity contrast of 5. The deforming competent layer is characterized by (1) a striking downward drag along the margins, (2) a sample-scale first-order dome, and (3) numerous second-order domes and basins straddling the first-order dome. With increasing layer thickness and strain, the amplitude, A, arc-length, L, and wavelength, λ, of the second-order domes and basins increase. However, their growth rate is significantly smaller than that of non-rising domes and basins, which result from a bidirectional flow. This restricted growth of rising domes and basins is attributed to the simultaneous growth of the first-order dome, and explains, why hair-pin type folds – typical for non-rising domes and basins - are lacking, even at higher finite strain.Similar dome-in-dome structures like those produced in the present study have been described from deeper levels of salt and gneiss domes or from foliation triple points of interfering diapirs.

Cartilaginous constructs using primary chondrocytes from continuous expansion culture seeded in dense collagen gels

Cell-based therapies such as autologous chondrocyte implantation require in vitro cell expansion. However, standard culture techniques require cell passaging, leading to dedifferentiation into a fibroblast-like cell type. Primary chondrocytes grown on continuously expanding culture dishes (CE culture) limits passaging and protects against dedifferentiation. The authors tested whether CE culture chondrocytes were advantageous for producing mechanically competent cartilage matrix when three-dimensionally seeded in dense collagen gels. Primary chondrocytes, grown either in CE culture or passaged twice on static silicone dishes (SS culture; comparable to standard methods), were seeded in dense collagen gels and cultured for 3weeks in the absence of exogenous chondrogenic growth factors. Compared with gels seeded with SS culture chondrocytes, CE chondrocyte-seeded gels had significantly higher chondrogenic gene expression after 2 and 3weeks in culture, correlating with significantly higher aggrecan and type II collagen protein accumulation. There was no obvious difference in glycosaminoglycan content from either culture condition, yet CE chondrocyte-seeded gels were significantly thicker and had a significantly higher dynamic compressive modulus than SS chondrocyte-seeded gels after 3weeks. Chondrocytes grown in CE culture and seeded in dense collagen gels produce more cartilaginous matrix with superior mechanical properties, making them more suitable than SS cultured cells for tissue engineering applications.

Phospholipases of Mineralization Competent Cells and Matrix Vesicles: Roles in Physiological and Pathological Mineralizations

The present review aims to systematically and critically analyze the current knowledge on phospholipases and their role in physiological and pathological mineralization undertaken by mineralization competent cells. Cellular lipid metabolism plays an important role in biological mineralization. The physiological mechanisms of mineralization are likely to take place in tissues other than in bones and teeth under specific pathological conditions. For instance, vascular calcification in arteries of patients with renal failure, diabetes mellitus or atherosclerosis recapitulates the mechanisms of bone formation. Osteoporosis—a bone resorbing disease—and rheumatoid arthritis originating from the inflammation in the synovium are also affected by cellular lipid metabolism. The focus is on the lipid metabolism due to the effects of dietary lipids on bone health. These and other phenomena indicate that phospholipases may participate in bone remodelling as evidenced by their expression in smooth muscle cells, in bone forming osteoblasts, chondrocytes and in bone resorbing osteoclasts. Among various enzymes involved, phospholipases A1 or A2, phospholipase C, phospholipase D, autotaxin and sphingomyelinase are engaged in membrane lipid remodelling during early stages of mineralization and cell maturation in mineralization-competent cells. Numerous experimental evidences suggested that phospholipases exert their action at various stages of mineralization by affecting intracellular signaling and cell differentiation. The lipid metabolites—such as arachidonic acid, lysophospholipids, and sphingosine-1-phosphate are involved in cell signaling and inflammation reactions. Phospholipases are also important members of the cellular machinery engaged in matrix vesicle (MV) biogenesis and exocytosis. They may favour mineral formation inside MVs, may catalyse MV membrane breakdown necessary for the release of mineral deposits into extracellular matrix (ECM), or participate in hydrolysis of ECM. The biological functions of phospholipases are discussed from the perspective of animal and cellular knockout models, as well as disease implications, development of potent inhibitors and therapeutic interventions.

What makes the permanent articular cartilage permanent?

Articular cartilage functions by providing a specialized mechanically competent extracellular matrix to withstand load bearing, thus protecting the underlying bones and allowing their near friction-free articulation in the joints. The resident chondrocytes maintain this function throughout life and do so by retaining a stable phenotype that resists hypertrophy and vascular invasion from the bone. This articular phenotype is distinct from the chondrocytes that drive endochondral ossification, which undergo hypertrophy and apoptosis followed by vascularization and bone formation (1). Unfortunately, stem cells used for cartilage repair seem to have a similar fate, making the repair tissue inadequate for normal joint function (2). How the articular chondrocyte avoids this and maintains its specialized phenotype is one of the fundamentally important issues in skeletal biology, yet the mechanisms remain unclear. Recent studies, however, have begun to provide some much needed insights. Although different growth factors (including transforming growth factor family members, bone morphogenetic proteins, and fibroblast growth factor family members) are important in skeletal development, there is relatively little evidence that these molecules are endogenously produced in physiologically significant amounts by adult articular cartilage. However, Klinger and colleagues, whose article appears elsewhere in this issue of Arthritis & Rheumatism (3), have identified a critical role for secreted matrix protein chondromodulin 1 in stabilizing the chondrocyte phenotype and inhibiting vascular invasion and endochondral ossification in stem cell–mediated articular cartilage repair (3). In their study, using a miniature pig model of cartilage repair, chondromodulin 1 was overexpressed in osteochondral progenitor cells (cells infected with adeno-associated virus vectors carrying chondromodulin 1 complementary DNA [AAV-Chm-1]), or AAV-Chm-1 vectors were directly administered to cartilage defects undergoing microfracture to induce repair. In both cases of chondromodulin 1 treatment, elaboration of a type II collagen–rich matrix was seen at 6 weeks, and most importantly, the tissue resisted calcification and vascular invasion over an extended experimental period (6 months). When progenitor cells were administered to cartilage defects with intact subchondral bone, although little calcification was observed, the repair tissue was fibrocartilaginous, with strong staining for type I collagen and less staining for type II collagen compared to the equivalent chondromodulin 1 treatment. Chondromodulin 1 has been shown to have antiangiogenic properties (4), but its mechanism of action is far from fully elucidated. Since Klinger and colleagues found no effect of chondromodulin 1 overexpression on VEGF mRNA levels, it appears not to inhibit this key angiogenic factor, at least in vitro. However, the situation in vivo is liable to be far more complex, and it will be of great interest to assess the levels of VEGF in chondromodulin 1–treated cartilage repair tissue. Klinger and colleagues also suggest that chondromodulin 1 prevents chondrocyte hypertrophy through suppression of type X collagen in cultured osteochondral progenitor cells. This in vitro finding must now be investigated in vivo, and it will also be of great interest to investigate if runt-related transcription factor 2 (RUNX-2) is down-regulated by chondromodulin 1, since this transcription factor plays an important role in endochondral ossification through regulation of type X collagen and induction of VEGFA (5,6). The role of SOX9 in this process should also be investigated further. SOX9 has been shown to be essential for early events in cartilage differentiation (7) and for expression of the cartilage-specific matrix genes in human articular chondrocytes (8). Moreover, mutations in SOX9 cause the severe skeletal abnormality of campomelic dysplasia (9). Interestingly, however, SOX9 is greatly down-regulated as chondrocytes undergo hyperChris L. Murphy, PhD: The Kennedy Institute and Imperial College London, London, UK. Address correspondence to Chris L. Murphy, PhD, The Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College London, 1 Aspenlea Road, London W6 8LH, UK. E-mail: c.murphy@imperial.ac.uk. Submitted for publication February 4, 2011; accepted in revised form March 1, 2011.

The origin of tablet boudinage: Results from experiments using power–law rock analogs

We used power–law viscous plasticine ( n = ca. 7) as a rock analog to simulate boudinage of rocks undergoing dislocation creep and brittle fracture. A competent plasticine layer, oriented perpendicular to the main shortening direction, Z, underwent bulk pure flattening inside a less competent plasticine matrix. Computer tomographic analyses of the deformed samples revealed that boudinage results from an initial phase of viscous necking followed by tensile failure along the previously formed necks. The resulting boudins display a polygonal shape in plan-view and are referred to as ‘tablet boudins’ (in contrast to the square to rectangular shaped chocolate-tablet boudins). The ratio between the plan-view long and short axis, R, ranges from 1.2 to 2.6. The polygonal, non-isometric shape of the tablet boudins can be explained by the strong interaction of concentric and radial tensile fractures. With increasing layer thickness, H i , the mean diameter of the boudin tablets, W a , increases, while the number of boudins, N, decreases. Progressive finite strain results in a higher number of the boudins and a smaller mean diameter. The thickness of the boudins, H f , is almost the same as the initial layer thickness, H i , while the aspect ratio ( W d = W a / H f ) decreases with layer thickness and finite strain. The mean W d values obtained from all experiments span from ca. 4 to ca. 11. Tablet boudins, described in the present paper, have yet not been described from natural outcrops. The reasons might be that pure flattening strain is not common in nature, and the characterization and evaluation of tablet boudins requires geometrical analysis in three dimensions, which is a difficult task when such structures occur in nature.

Biomimetic Structures: Biological Implications of Dipeptide‐Substituted Polyphosphazene–Polyester Blend Nanofiber Matrices for Load‐Bearing Bone Regeneration

AbstractSuccessful bone regeneration benefits from three‐dimensional (3D) bioresorbable scaffolds that mimic the hierarchical architecture and mechanical characteristics of native tissue extracellular matrix (ECM). A scaffold platform that integrates unique material chemistry with nanotopography while mimicking the 3D hierarchical bone architecture and bone mechanics is reported. A biocompatible dipeptide polyphosphazene‐polyester blend is electrospun to produce fibers in the diameter range of 50–500 nm to emulate dimensions of collagen fibrils present in the natural bone ECM. Various electrospinning and process parameters are optimized to produce blend nanofibers with good uniformity, appropriate mechanical strength, and suitable porosity. Biomimetic 3D scaffolds are created by orienting blend nanofiber matrices in a concentric manner with an open central cavity to replicate bone marrow cavity, as well as the lamellar structure of bone. This biomimicry results in scaffold stress–strain curve similar to that of native bone with a compressive modulus in the mid‐range of values for human trabecular bone. Blend nanofiber matrices support adhesion and proliferation of osteoblasts and show an elevated phenotype expression compared to polyester nanofibers. Furthermore, the 3D structure encourages osteoblast infiltration and ECM secretion, bridging the gaps of scaffold concentric walls during in vitro culture. The results also highlight the importance of in situ ECM secretion by cells in maintaining scaffold mechanical properties following scaffold degradation with time. This study for the first time demonstrates the feasibility of developing a mechanically competent nanofiber matrix via a biomimetic strategy and the advantages of polyphosphazene blends in promoting osteoblast phenotype progression for bone regeneration.

Integrated biomimetic carbon nanotube composites for in vivo systems

As interest in using carbon nanotubes for developing biologically compatible systems continues to grow, biological inspiration is stimulating new directions for in vivo approaches. The ability to integrate nanotechnology-based systems in the body will provide greater successes if the implanted material is made to mimic elements of the biological milieu especially through tuning physical and chemical characteristics. Here, we demonstrate the highly successful capacity for in vivo implantation of a new carbon nanotube-based composite that is, itself, integrated with a hydroxyapatite-polymethyl methacrylate to create a nanocomposite. The success of this approach is grounded in finely tailoring the physical and chemical properties of this composite for the critical demands of biological integration. This is accomplished through controlling the surface modification scheme, which affects the interactions between carbon nanotubes and the hydroxyapatite-polymethyl methacrylate. Furthermore, we carefully examine cellular response with respect to adhesion and proliferation to examine in vitro compatibility capacity. Our results indicate that this new composite accelerates cell maturation through providing a mechanically competent bone matrix; this likely facilitates osteointegration in vivo. We believe that these results will have applications in a diversity of areas including carbon nanotube, regeneration, chemistry, and engineering research.

Fibrin and wound healing.

Although hemostasis is the major role of fibrin in wound repair, once the clot is present the wound cells must deal with it. The invasion and clearing of fibrin by these cells involves multiple complex processes that may go array XXX and delay wound repair. A good example, of the latter is leg ulcers. These chronic wounds contain a plethora of proteases that digest fibronectin and growth factors in the fibrin clot resulting in a corrupt provisional matrix that no longer supports reepithelialization or granulation tissue formation. Every good wound care provider knows that these wounds will not heal unless the corrupt matrix is removed by vigorous debridement that stimulates the accumulation of a competent provisional matrix.

Enamel Biomineralization Defects Result from Alterations to Amelogenin Self-Assembly

Enamel formation is a powerful model for the study of biomineralization. A key feature common to all biomineralizing systems is their dependency upon the biosynthesis of an extracellular organic matrix that is competent to direct the formation of the subsequent mineral phase. The major organic component of forming mouse enamel is the 180-amino-acid amelogenin protein (M180), whose ability to undergo self-assembly is believed to contribute to biomineralization of vertebrate enamel. Two recently defined domains (A and B) within amelogenin appear essential for this self-assembly. The significance of these two domains has been demonstrated previously by the yeast two-hybrid system, atomic force microscopy, and dynamic light scattering. Transgenic animals were used to test the hypothesis that the self-assembly domains identified with in vitro model systems also operate in vivo. Transgenic animals bearing either a domain-A-deleted or domain-B-deleted amelogenin transgene expressed the altered amelogenin exclusively in ameloblasts. This altered amelogenin participates in the formation an organic enamel extracellular matrix and, in turn, this matrix is defective in its ability to direct enamel mineralization. At the nanoscale level, the forming matrix adjacent to the secretory face of the ameloblast shows alteration in the size of the amelogenin nanospheres for either transgenic animal line. At the mesoscale level of enamel structural hierarchy, 6-week-old enamel exhibits defects in enamel rod organization due to perturbed organization of the precursor organic matrix. These studies reflect the critical dependency of amelogenin self-assembly in forming a competent enamel organic matrix and that alterations to the matrix are reflected as defects in the structural organization of enamel.

Progressive deformation of single layers under constantly oriented boundary stresses

Competent single layers embedded in incompetent rock display a variety of structures if deformed by shortening or stretching: folds, boudins, or pinch-and-swells. Similarly, incompetent single layers hosted by more competent matrix rock may develop mullions, inverse folds, or both. The change in length of material planes with time is controlled by the type of bulk deformation and the initial layer orientation. The length and rotation history of material planes in a unit volume of rock is studied systematically by using, for the first time, deviatoric stresses of arbitrary-but constant-orientation making use of a fundamental deformation tensor. The traces of the eight planes in the unit volume of rock used in the analysis are in the plane of deformation and are treated as passive marker lines. The change in the length of these material lines is computed for arbitrary orientations of the principal deviatoric stresses. The history of the length change and rotation of the passive marker planes, carefully scaled against time, is subsequently used to predict the structures which would evolve in similarly oriented single layers of either competent or incompetent rock. The theoretical range of structural patterns evolving in the model is controlled by the orientations of the principal deviatoric stress. Conversely, the geometry of deformation patterns in nature can be used to constrain the possible orientations of the palaeostress axes.

Crystallographic preferred orientation development in a buckled single layer: a computer simulation

The development of crystallographic preferred orientation in a single-layer buckling assembly has been numerically simulated using an explicit, finite difference computer code, FLAC. The model treats the materials in the single competent layer and the embedding less competent matrix as a polycrystalline aggregate with one slip system, which exhibits elastic-perfectly-plastic behaviour, and assumes dislocation glide as the dominant strain accommodation mechanism. The results show that the preferred orientation of slip planes is much better developed in the less competent matrix than in the buckled competent layer. This correlates with the low strains developed in the layer and the high strains in the matrix. The competency contrast in the model also influences the fabric development, since changing the contrast effectively alters the final buckle size and strain distributions. The patterns of the preferred orientations vary throughout the assembly, showing different orientation relationships to the fold axial plane. The slip planes are generally preferably oriented approximately parallel to the local principal extension direction.

Effect of caffeine on parameters of osteoblast growth and differentiation of a mineralized extracellular matrix in vitro

The effects of caffeine exposure on bone formation were examined using a chick osteoblast culture system. Secondary cultures of normal diploid osteoblasts were exposed to chronic doses of 0, 0.1, 0.2, or 0.4 mM caffeine beginning on day 0 through day 28. Neither the rate of cell proliferation nor cell number, as measured by total DNA, was decreased for any of the doses examined. In contrast, osteocalcin levels, alkaline phosphatase activity, and total calcium levels showed a dose-related decrease in cultures treated with caffeine. These parameters were significantly decreased at the highest dose of 0.4 mM. The reduction in total protein levels ranged from 29 to 66% of control values and was independent of dose. In contrast, total collagen levels were more affected by the dose of caffeine used. Inhibition of collagen levels was most apparent on days 17 and 21, time points during the period of active formation of the matrix immediately preceding the deposition of mineral. By day 28 collagen levels in cultures exposed to the lower doses of caffeine had returned to control levels, and only the cultures exposed to the highest dose (0.4 mM) remained significantly inhibited with respect to both collagen and mineral. Histochemically, alkaline phosphatase and mineral staining of day 28 cultures mirrored the biochemical events with the 0.4 mM caffeine exposure. The results indicate that one of the effects of caffeine on bone development is to inhibit the formation of a competent extracellular matrix during the osteoblast differentiation sequence, which results in the inhibition of mineralization analogous to the delayed ossification observed in fetal animals after prenatal caffeine exposure.

Determining the Distribution of Hydraulic Conductivity in a Fractured Limestone Aquifer by Simultaneous Injection and Geophysical Logging

ABSTRACTA field technique for assessing the vertical distribution of hydraulic conductivity in an aquifer was applied to a fractured carbonate formation in southeastern Nevada. The technique combines the simultaneous use of fluid injection and geophysical logging to measure in situ vertical distributions of fluid velocity and hydraulic head down the borehole; these data subsequently are analyzed to arrive at quantitative estimates of hydraulic conductivity across discrete intervals in the aquifer. The diagnostic capabilities of the analysis were found to be constrained by the accuracy and resolution of the logging tools as well as by the hydraulic characteristics of the formation. Despite these limitations, this injection/logging technique appears to be practical and effective under the conditions encountered in this application. The results of this analysis identified the contact margin between the Anchor and Dawn Members of the Monte Cristo Limestone as being the dominant transmissive unit. This section is extensively fractured, and quantitative estimates of its hydraulic conductivity are at least two orders of magnitude larger than that of the surrounding competent rock matrix. This transmissive zone also correlates strongly with an interval where the drilling rate was reported to be quite rapid. Aquifer transmissivity was computed from the profile of hydraulic conductivity and found to be 7.6 × 105 ft2/day, a value that is in close agreement with that determined from a conventional constant‐discharge test. Discrepancies between the two estimates may be scale‐dependent, a function of the different formation volumes investigated by each method. The friction factor, a parameter derived from the differential pressure and velocity logs, appears to be a good indicator of borehole rugosity across intervals where fluid velocity remains virtually unchanged, and vertical flow is turbulent.

Endothelial cell response to pulsed electromagnetic fields: Stimulation of growth rate and angiogenesis in vitro

The effects of pulsed electromagnetic fields on the repopulation rate of denuded regions of endothelial cell monolayers and on endothelial cell reorganization into complex vessellike structures was monitored in vitro by using human umbilical vein and bovine aortic endothelial cells. A small (20-40%) but statistically significant enhancement in growth rate of partially denuded endothelial cell monolayers as determined by tritiated thymidine incorporation was observed in the presence of pulsed electromagnetic fields. Morphologically, endothelial cells entering the denuded regions were observed to be elongated, often connecting end to end to form a mycelial or "sprouting" pattern when exposed to pulsed electromagnetic fields. This was in contrast to cells outside of the field which had a more cuboidal morphology. Complete disruption of the endothelial cell monolayer by passaging the cells with EDTA-trypsin resulted in reorganization of some of the cells into three-dimensional vessellike structures after as little as 5-8 hours in the presence of the pulsed electromagnetic field. This reorganization occurred in the presence of heparin, endothelial cell growth factor, and a competent fibronectin matrix. Vascularization for comparable cultures outside of the field did not occur during the time-course of the experiments. Discrete stages of neovascularization were observed in the presence of the field that were qualitatively similar to stages of angiogenesis observed in vivo.

Extracting Information from Folds in Rocks

Folds in rocks form by three processes: buckling, in which an instability arises when rocks are compressed parallel to the layering; bending, in which differential transverse forces are applied to the layering; and passive folding, in which the layers have no mechanical significance. Geometrical properties and strain distribution help us identify which processes produced natural folds, and also provide information about the mechanical properties and relative competence of the rocks, and the sense of shear in shear zones. For single competent layers and matrix of given compositions, the characteristic features of buckle folds are: (1) a preferred arclength/thickness (L/h) ratio; (2) a tendency for the competent layer to maintain constant thickness; (3) rapid decay of folds away from the competent layer; and (4) cuspate interfaces between layers, with cusps pointing toward the competent layer. The average value of L/h provides a measure of viscosity contrast and, if the strain in the competent layer is know...

Strain distribution across an experimental single-layer fold

Experiments have been carried out to study the effects of progressive deformation on the shape of folds and the variation in two-dimensional strains on cross-sections of singlelayer folds in a less competent matrix, in a pure-shear plane-strain deformation box with no volume change. The layer shortening continues after buckling has set in, leading to thickening of the fold hinge and with progressive buckling the layer elongates. During the layer elongation stage of folding the hinges continue to thicken, whereas the limbs thin out. Concentric folds are a combination of Class 1a type in the outer arc which gradually change to Class Ib type and then to Class 3 folds of Ramsay (1967) in the inner arc. Tangential longitudinal strains and shearing strains predominate in the fold-hinge zone and in the fold limbs of the buckling layer, respectively. Initially, uniform layer-flattening strains perpendicular to the layering develop which become extensive strains in the outer fold arc and compressive strains in the inner fold arc with progressive buckling. In the outer fold arc the extensive strains are distributed laterally over a wider zone and are of a lower magnitude than the compressive strains which are restricted to a narrow zone in the inner fold arc. The neutral surface first appears when the initial layer-flattening strains are removed due to extensive strains on the outer arc and with progressive buckling migrates towards the inner fold arc and extends laterally on the outer fold arc.

Uyak Complex, Kodiak Islands, Alaska: A Cretaceous subduction complex

The Uyak Complex is a chaotic assemblage of gray chert and argillite, wacke, greenstone, radiolarian chert, and gabbroic and ultramafic rocks. The simplest interpretation of these rocks is that the gabbroic and ultramafic rocks and greenstone represent basal oceanic crust upon which the radiolarian chert, gray chert and argillite, and wacke were deposited, respectively, at a mid-ocean rise, on the abyssal ocean floor, and in an oceanic trench. Fossils are scarce in the complex and range in age from mid-Permian to mid–Early Cretaceous. The Uyak Complex was emplaced by underthrusting to the northwest beneath lower Mesozoic metamorphic, igneous, and sedimentary rocks. During underthrusting, brittle rock types were broken into phacoids of all sizes and suspended in the less competent matrix of gray chert and argillite with their longest dimensions aligned subparallel to cataclastic foliation. Prehnite and pumpellyite developed extensively in lithologies of suitable composition. The Uyak Complex correlates to the northeast with a similar assemblage of deep-sea rocks on the Barren Islands and with the McHugh Complex on the Kenai Peninsula and near Anchorage. The Uyak-McHugh belt defines a probable subduction complex trending northeast for at least 600 km along the margin of southwestern Alaska. The time of emplacement of this melange is uncertain, but fossils present indicate that it occurred after mid–Early Cretaceous time. To the southeast, the Uyak is underthrust by deformed turbidites of the Kodiak Formation, which are interpreted to have been deposited in an oceanic trench and accreted to the Alaskan margin in Late Cretaceous time. The relationship between the Uyak Complex and Kodiak Formation is uncertain, but they may represent two phases, or two facies, of Late Cretaceous accretion. Two large bodies of schist, referred to as the Kodiak Islands schist terrane, occur along the northwest border of the Uyak. The Kodiak Islands schist terrane is a blueschist-bearing metamorphic belt that has yielded mainly Early Jurassic K-Ar mineral ages. Similarities in K-Ar ages, metamorphism, and tectonic setting support a correlation between the Kodiak Islands schists and the Seldovia schist terrane on southern Kenai Peninsula. The Upper Triassic Shuyak Formation structurally overlies the Kodiak Islands schist terrane and Uyak Complex but is separated from them by a long, narrow pluton emplaced in Early Jurassic time. The Shuyak is a little-deformed formation of volcanic and volcaniclastic rocks. It correlates with similar rocks on the Alaska and Kenai Peninsulas, which together outline a lower Mesozoic forearc basin; K-Ar ages show that much of the Alaska-Aleutian Range batholith was intruded coeval with deposition in this forearc basin. A likely interpretation of these rocks is that the Kodiak-Seldovia schists are the only vestige of a subduction complex emplaced along the margin of southwestern Alaska during the prominent early Mesozoic volcanoplutonic activity recorded on the Alaska and Kenai Peninsulas and the Kodiak Islands.