A systematic review of parental involvement in cognitive behavioural therapy for adolescent anxiety disorders

Anxiety disorders are common among adolescents and lead to poor long-term outcomes. Cognitive Behavioural Therapy (CBT) is an evidenced-based intervention for adolescent anxiety disorders, but little is known about whether and how parents should be involved. This systematic review evaluated how parents have been involved and associated treatment outcomes in studies of CBT for adolescent anxiety disorders. Electronic systematic searches were conducted in PsycINFO, Embase, CINAHL, Medline, AMED databases, to identify studies investigating CBT for adolescent anxiety disorder(s) that included parents in treatment. Twenty-three studies were identified. Parents were involved in treatment in a number of different ways: by attending separate parent sessions, joint parent-adolescent sessions, or both, or through provision of a workbook while attending some adolescent sessions. Content varied but was most typically aimed at the parent developing an understanding of core CBT components and skills to help them manage their adolescent’s anxiety and avoidance. Treatment outcomes indicate that CBT with parental involvement is an effective intervention for adolescent anxiety disorders, however it is not possible to draw conclusions regarding whether parental involvement (generally or in any particular form) enhances treatment outcomes. Poor reporting and methodological issues also limit the conclusions. Further research is required to identify whether there are particular types of parental involvement in CBT that bring clinical benefits to adolescents with anxiety disorders generally, as well as in particular circumstances

A modelling framework for coupled hydrogen diffusion and mechanical behaviour of engineering components

In this paper, we propose a finite element formulation for solving coupled mechanical/diffusion problems. In particular, we study hydrogen diffusion in metals and its impact on their mechanical behaviour (i.e. hydrogen embrittlement). The formulation can be used to model hydrogen diffusion through a material and its accumulation within different microstructural features of the material (dislocations, precipitates, interfaces, etc.). Further, the effect of hydrogen on the plastic response and cohesive strength of different interfaces can be incorporated. The formulation adopts a standard Galerkin method in the discretisation of both the diffusion and mechanical equilibrium equations. Thus, a displacement-based finite element formulation with chemical potential as an additional degree of freedom, rather than the concentration, is employed. Consequently, the diffusion equation can be expressed fundamentally in terms of the gradient in chemical potential, which reduces the continuity requirements on the shape functions to zero degree, C0, i.e. linear functions, compared to the C1 continuity condition required when concentration is adopted. Additionally, a consistent interface element formulation can be achieved due to the continuity of the chemical potential across the interface—concentration can be discontinuous at an interface which can lead to numerical problems. As a result, the coding of the FE equations is more straightforward. The details of the physical problem, the finite element formulation and constitutive models are initially discussed. Numerical results for various example problems are then presented, in which the efficiency and accuracy of the proposed formulation are explored and a comparison with the concentration-based formulations is presented

Multi-scale modelling of creep cavity nucleation and growth in polycrystalline Type 316 stainless steel

 A common creep damage mode in Type 316 stainless steel under high-temperature power plant conditions is intergranular cavitation. A review of the literature has confirmed that cavitation in Type 316 is controlled by nucleation, which is not fully understood. In order to provide further insights into the physics of this process, existing strain-based empirical and stress-based (classical nucleation theory) nucleation models are modified in this study by considering experimentally-observed features of cavity nucleation in Type 316. The models are employed locally within a newly-developed crystal plasticity finite element (CPFE)-interface element framework. Modelling results suggest that the strain-based model as a function of local inelastic strain rate does not explain the physical nature of the nucleation process as observed experimentally. By contrast, the modified classical nucleation theory is able to capture features of the observed macroscopic failure response and the distribution of cavities in the microstructure. A number of missing features are identified in the mechanistic model, which need to be incorporated in future unified cavity nucleation theories. These findings highlight key aspects of the nucleation process, which need to be examined experimentally. </p

An improved method to model dislocation self-climb

Dislocations can provide short circuit diffusion paths for atoms resulting in a dislocation climb motion referred to as self-climb. A variational principle is presented for the analysis of problems in which fast dislocation core diffusion is the dominant mechanism for material redistribution. The linear element based self-climb model, developed in our previous work [1] Liu, Cocks and Tarleton (2020 J. Mech. Phys. Solids 135 103783), is significantly accelerated here, by employing a new finite element discretisation method. The speed-up in computation enables us to use the self-climb model as an effective numerical technique to simulate emergent dislocation behaviour involving both self-climb and glide. The formation of prismatic loops from the break-up of different types of edge dislocation dipoles are investigated based on this new method. We demonstrate that edge dipoles sequentially pinch-off prismatic loops, rather than spontaneously breaking-up into a string of loops, to rapidly decrease the total dislocation energy.</div

A Single Amino Acid Substitution Prevents Recognition of a Dominant Human Aquaporin-4 Determinant in the Context of HLA-DRB1*03:01 by a Murine TCR

BACKGROUND:Aquaporin 4 (AQP4) is considered a putative autoantigen in patients with Neuromyelitis optica (NMO), an autoinflammatory disorder of the central nervous system (CNS). HLA haplotype analyses of patients with NMO suggest a positive association with HLA-DRB1* 03:01. We previously showed that the human (h) AQP4 peptide 281-300 is the dominant immunogenic determinant of hAQP4 in the context of HLA-DRB1*03:01. This immunogenic peptide stimulates a strong Th1 and Th17 immune response. AQP4281-300-specific encephalitogenic CD4+ T cells should initiate CNS inflammation that results in a clinical phenotype in HLA-DRB1*03:01 transgenic mice. METHODS:Controlled study with humanized experimental animals. HLA-DRB1*03:01 transgenic mice were immunized with hAQP4281-300, or whole-length hAQP4 protein emulsified in complete Freund's adjuvant. Humoral immune responses to both antigens were assessed longitudinally. In vivo T cell frequencies were assessed by tetramer staining. Mice were followed clinically, and the anterior visual pathway was tested by pupillometry. CNS tissue was examined histologically post-mortem. Flow cytometry was utilized for MHC binding assays and to immunophenotype T cells, and T cell frequencies were determined by ELISpot assay. RESULTS:Immunization with hAQP4281-300 resulted in an in vivo expansion of antigen-specific CD4+ T cells, and an immunoglobulin isotype switch. HLA-DRB1*03:01 TG mice actively immunized with hAQP4281-300, or with whole-length hAQP4 protein were resistant to developing a neurological disease that resembles NMO. Experimental mice show no histological evidence of CNS inflammation, nor change in pupillary responses. Subsequent analysis reveals that a single amino acid substitution from aspartic acid in hAQP4 to glutamic acid in murine (m)AQP4 at position 290 prevents the recognition of hAQP4281-300 by the murine T cell receptor (TCR). CONCLUSION:Induction of a CNS inflammatory autoimmune disorder by active immunization of HLA-DRB1*03:01 TG mice with human hAQP4281-300 will be complex due to a single amino acid substitution. The pathogenic role of T cells in this disorder remains critical despite these observations