Modelling Fatigue Crack Growth in High-Density Polyethylene and Acrylonitrile Butadiene Styrene Polymers.

Prior studies into fatigue crack growth (FCG) in fibre-reinforced polymer composites have shown that the two methodologies of Simple-Scaling and the Hartman-Schijve crack growth equation, which is based on relating the FCG rate to the Schwalbe crack driving force, Δ, were able to account for differences observed in the measured delamination growth curves. The present paper reveals that these two approaches are also able to account for differences seen in plots of the rate of crack growth, , versus the range of the imposed stress intensity factor, Δ, associated with fatigue tests on different grades of high-density polyethylene (HDPE) polymers, before and after electron-beam irradiation, and for tests conducted at different ratios. Also, these studies are successfully extended to consider FCG in an acrylonitrile butadiene styrene (ABS) polymer that is processed using both conventional injection moulding and additive-manufactured (AM) 3D printing.

On Cyclic-Fatigue Crack Growth in Carbon-Fibre-Reinforced Epoxy-Polymer Composites.

The growth of cracks between plies, i.e., delamination, in continuous fibre polymer matrix composites under cyclic-fatigue loading in operational aircraft structures has always been a very important factor, which has the potential to significantly decrease the service life of such structures.

Experimental and numerical investigations on the impact behaviour of pristine and patch-repaired composite laminates.

The present paper investigates the impact behaviour of both pristine carbon-fibre-reinforced-plastic (CFRP) composite laminates and repaired CFRP laminates. For the patch-repaired CFRP specimen, the pristine CFRP panel specimen has been damaged by cutting out a central disc of the CFRP material and then repaired using an adhesively bonded patch of CFRP to cover the hole. Drop-weight, impact tests are performed on these two types of specimens and a numerical elastic-plastic, three-dimensional damage model is developed and employed to simulate the impact behaviour of both types of specimen.

Innate-like self-reactive B cells infiltrate human renal allografts during transplant rejection.

Intrarenal B cells in human renal allografts indicate transplant recipients with a poor prognosis, but how these cells contribute to rejection is unclear. Here we show using single-cell RNA sequencing that intrarenal class-switched B cells have an innate cell transcriptional state resembling mouse peritoneal B1 or B-innate (Bin) cells. Antibodies generated by Bin cells do not bind donor-specific antigens nor are they enriched for reactivity to ubiquitously expressed self-antigens.

Fatigue crack growth in epoxy polymer nanocomposites.

The present paper describes detailed analyses of experimental data for the cyclic-fatigue behaviour of epoxy nanocomposite polymers. It has been shown that the data may be interpreted using the Hartman-Schijve relationship to yield a unique, 'master', linear relationship for each epoxy nanocomposite polymer. By fitting the experimental data to the Hartman-Schijve relationship, two key materials parameters may be deduced: (i) the term , which may be thought of as the fatigue equivalent to the quasi-static value of the fracture energy, , and (ii) the fatigue threshold value, [Formula: see text], below which no significant fatigue crack growth (FCG) occurs.

Machine Learning to Quantify Humoral Selection in Human Lupus Tubulointerstitial Inflammation.

In human lupus nephritis, tubulointerstitial inflammation (TII) is associated with expansion of B cells expressing anti-vimentin antibodies (AVAs). The mechanism by which AVAs are selected is unclear. Herein, we demonstrate that AVA somatic hypermutation (SHM) and selection increase affinity for vimentin.

Antibodies in cerebral cavernous malformations react with cytoskeleton autoantigens in the lesional milieu.

Previous studies have reported robust inflammatory cell infiltration, synthesis of IgG, B-cell clonal expansion, deposition of immune complexes and complement within cerebral cavernous malformation (CCM) lesions. B-cell depletion has also been shown to reduce the maturation of CCM in murine models. We hypothesize that antigen(s) within the lesional milieu perpetuate the pathogenetic immune responses in CCMs.

Anti-vimentin antibodies: a unique antibody class associated with therapy-resistant lupus nephritis.

Background:: Tubulointerstitial inflammation (TII) in lupus nephritis (LN) is associated with a worse prognosis. Vimentin, a filamental antigen, is commonly targeted by activated B-cells in TII. The prognostic importance of high serum anti-vimentin antibodies (AVAs) in LN and their relationship with common lupus autoantibody specificities is unknown.

Requirements and Variability Affecting the Durability of Bonded Joints.

This paper firstly reveals that when assessing if a bonded joint meets the certification requirements inherent in MIL-STD-1530D and the US Joint Services Standard JSSG2006 it is necessary to ensure that: (a) There is no yielding at all in the adhesive layer at 115% of design limit load (DLL), and (b) that the joint must be able to withstand design ultimate load (DUL). Secondly, it is revealed that fatigue crack growth in both nano-reinforced epoxies, and structural adhesives can be captured using the Hartman-Schijve crack growth equation, and that the scatter in crack growth in adhesives can be modelled by allowing for variability in the fatigue threshold. Thirdly, a methodology was established for estimating a valid upper-bound curve, for cohesive failure in the adhesive, which encompasses all the experimental data and provides a conservative fatigue crack growth curve.

Humoral Immunity to Vimentin in HLA-DRB1*03 Patients With Pulmonary Sarcoidosis.

Vimentin has been implicated in pulmonary sarcoidosis as a T-cell autoantigen, particularly in the context of , the Vα2.3/Vβ22 T-cell receptor (TCR), and Löfgren's syndrome. As vimentin is a known antigenic target in B-cell-mediated autoimmunity, we investigated humoral anti-vimentin responses in pulmonary sarcoidosis and their relationship with .

A systematic approach to the formulation of anti-onychomycotic nail patches.

Nail patches have a potential role as drug carriers for the topical treatment of nail diseases such as onychomycosis, a common condition. Our aim was therefore to develop a systematic and novel approach to the formulation of a simple drug-in-adhesive ungual patch. Twelve pressure-sensitive adhesives (PSAs), four backing membranes, two release liners and three drugs were screened for pharmaceutical and mechanical properties.

Novel Electrically Conductive Porous PDMS/Carbon Nanofiber Composites for Deformable Strain Sensors and Conductors.

Highly flexible and deformable electrically conductive materials are vital for the emerging field of wearable electronics. To address the challenge of flexible materials with a relatively high electrical conductivity and a high elastic limit, we report a new and facile method to prepare porous polydimethylsiloxane/carbon nanofiber composites (denoted by p-PDMS/CNF). This method involves using sugar particles coated with carbon nanofibers (CNFs) as the templates.

A facile way to produce epoxy nanocomposites having excellent thermal conductivity with low contents of reduced graphene oxide.

A well-dispersed phase of exfoliated graphene oxide (GO) nanosheets was initially prepared in water. This was concentrated by centrifugation and was mixed with a liquid epoxy resin. The remaining water was removed by evaporation, leaving a GO dispersion in epoxy resin.

Strain Sensors with Adjustable Sensitivity by Tailoring the Microstructure of Graphene Aerogel/PDMS Nanocomposites.

Strain sensors with high elastic limit and high sensitivity are required to meet the rising demand for wearable electronics. Here, we present the fabrication of highly sensitive strain sensors based on nanocomposites consisting of graphene aerogel (GA) and polydimethylsiloxane (PDMS), with the primary focus being to tune the sensitivity of the sensors by tailoring the cellular microstructure through controlling the manufacturing processes. The resultant nanocomposite sensors exhibit a high sensitivity with a gauge factor of up to approximately 61.

From matrix nano- and micro-phase tougheners to composite macro-properties.

In this paper, firstly, the morphology and toughness of a range of bulk epoxy polymers, which incorporate a second phase of well-dispersed silica nanoparticles and/or rubber microparticles, have been determined. Secondly, the macro-properties of natural-fibre reinforced-plastic (NFRP) composites based upon these epoxy polymers have been ascertained, using (i) unidirectional flax fibres or (ii) regenerated-cellulose fibres in the architecture of a plain-woven fabric. Thirdly, the toughening mechanisms which are induced in these materials by the presence of the silica nanoparticles, the rubber microparticles and the natural fibres have been identified.

In situ thermally reduced graphene oxide/epoxy composites: thermal and mechanical properties.

Graphene has excellent mechanical, thermal, optical and electrical properties and this has made it a prime target for use as a filler material in the development of multifunctional polymeric composites. However, several challenges need to be overcome to take full advantage of the aforementioned properties of graphene. These include achieving good dispersion and interfacial properties between the graphene filler and the polymeric matrix.

Vimentin is a dominant target of in situ humoral immunity in human lupus tubulointerstitial nephritis.

Objective: In lupus nephritis (LN), severe tubulointerstitial inflammation (TII) predicts progression to renal failure. Severe TII is associated with tertiary lymphoid neogenesis and in situ antigen-driven clonal B cell selection. The autoantigen(s) driving in situ B cell selection in TII are not known.

Immune complex formation and in situ B-cell clonal expansion in human cerebral cavernous malformations.

Cerebral cavernous malformations (CCMs) represent clusters of dilated vascular channels, predisposing to hemorrhagic stroke and seizures. They are associated with defective blood brain barrier, hemorrhages of different ages and a robust inflammatory cell infiltrate. We report for the first time evidence of co-localized IgG and complement membrane attack complexes in CCM lesions.

Immunization with Porphyromonas gingivalis enolase induces autoimmunity to mammalian α-enolase and arthritis in DR4-IE-transgenic mice.

Objective: To examine the hypothesis that the subset of rheumatoid arthritis (RA) characterized by antibodies to citrullinated α-enolase is mediated by Porphyromonas gingivalis enolase in the context of DR4 alleles.

Methods: Recombinant human α-enolase and P gingivalis enolase, either citrullinated or uncitrullinated, were used to immunize DR4-IE-transgenic mice and control mice (class II major histocompatibility complex-deficient [class II MHC(-/-)] and C57BL/6 wild-type mice). Arthritis was quantified by measurement of ankle swelling in the hind paws and histologic examination.

Citrullination of autoantigens: upstream of TNFα in the pathogenesis of rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by synovial inflammation and destruction of joints. Over 20 years ago, tumour necrosis factor alpha (TNFα) was identified as a key player in a cytokine network, whose multifunctional effects could account for both the inflammation and destruction in RA. The remarkable efficacy of TNF inhibitors in the treatment of RA has resulted in extensive research addressing the regulation of TNFα production responsible for this excessive production.

Clinical applications of autoimmunity to citrullinated proteins in rheumatoid arthritis, from improving diagnostics to future therapies.

Rheumatoid arthritis (RA), although widely considered to be the most commonly occurring autoimmune disease, has only truly been substantiated as a distinct autoimmune disease very recently. The lack of understanding of the specific autoimmune system/s at work in rheumatoid patients resulted in an absence of robust diagnostic tools and had meant that the rational choice for use and design of therapy was based on broad-spectrum immunosuppression. The revelation that the autoimmune response specific for patients with RA is to particular protein antigens bearing the post-translational modification 'citrulline' has therefore revolutionized diagnostics and has helped explain why patients carrying particular MHC alleles are predisposed to the disease.

A critical role for LTA4H in limiting chronic pulmonary neutrophilic inflammation.

Leukotriene A(4) hydrolase (LTA(4)H) is a proinflammatory enzyme that generates the inflammatory mediator leukotriene B(4) (LTB(4)). LTA(4)H also possesses aminopeptidase activity with unknown substrate and physiological importance; we identified the neutrophil chemoattractant proline-glycine-proline (PGP) as this physiological substrate. PGP is a biomarker for chronic obstructive pulmonary disease (COPD) and is implicated in neutrophil persistence in the lung.

Peptidylarginine deiminase from Porphyromonas gingivalis citrullinates human fibrinogen and α-enolase: implications for autoimmunity in rheumatoid arthritis.

Objective: To investigate protein citrullination by the periodontal pathogen Porphyromonas gingivalis as a potential mechanism for breaking tolerance to citrullinated proteins in rheumatoid arthritis (RA).

Methods: The expression of endogenous citrullinated proteins was analyzed by immunoblotting of cell extracts from P gingivalis and 10 other oral bacteria. P gingivalis-knockout strains lacking the bacterial peptidylarginine deiminases (PADs) or gingipains were created to assess the role of these enzymes in citrullination.

Autoimmunity to specific citrullinated proteins gives the first clues to the etiology of rheumatoid arthritis.

Rheumatoid arthritis (RA) is now clearly a true autoimmune disease with accumulating evidence of pathogenic disease-specific autoimmunity to citrullinated proteins. Citrullination, also termed deimination, is a modification of arginine side chains catalyzed by peptidylarginine deiminase (PAD) enzymes. This post-translational modification has the potential to alter the structure, antigenicity, and function of proteins.