Influence of stress concentrators onto stress-strain state of elasto-plastic plates

На основі числового розв’язування крайових задач теорії малих пружно-пластичних деформацій для лінійно зміцнюваного матеріалу з урахуванням розвантаження з’ясовано вплив концентраторів напружень (отвору, розрізу, абсолютно жорсткого включення) в пластині на її напружено-деформований стан за одновісного розтягу.Effective numerical methods for solving 2D problems related to the theories of elasticity and plasticity have been worked out. The variation-difference method of building finite difference schemes is extended to domains with curvilinear boundaries and disconnected domains. The application of the variation-difference method for solving problems of the theory of small elasto-plastic deformations relatively the plates with a hole and a cut, taking into account the linear strengthening of the material and unloading, has been developed. For solving the resultant systems of nonlinear and linear equation, the Newton-Kantorovich method and combined iterative method (gradient and cyclic Chebyshev’s one) were proposed to be used. The choice of iteration parameters of the methods for solving the obtained systems of linear and nonlinear algebraic equations was made. The elaborated software ensures solving the problems with different boundary conditions, medium and domain parameters. A variety of problems concerning one-axis stretching of the plates with a disk hole (or rigid body instead of a hole) and a cut (or a thin rigid body instead of a cut) is numerically solved. The zones of evolution of plastic deformations for step enlarging of the loading are constructed, the residual strains and the limit loads are obtained. The influence of a disk hole, cut and rigid body instead of a hole or cut in the plates onto the stress magnitude was found. The presence of rigid bodies instead of a hole or a cut strengthen the plate in general, in particular, plastic strains in the plate with rigid bodies instead of a hole and a cut appear under tension stress in 2,75 times more, than in the plate with a disk hole and a cut, and yield limit arrives at tension stress in 1,79 times more. A long thin rigid body strengthens a plate more than a disk one. The residual strains around a rigid body in the plates with a disk rigid body and a cut, and in the plates with a disk hole and a thin rigid body do not arise, in general

Stress-strain state of elasto-plastic linearly strengthenable plates with two perpendicular cuts under all-round stretching

За допомогою числового розв’язування крайових задач теорії малих пружно-пластичних деформацій для лінійно зміцнюваного матеріалу з’ясовано напружено-деформований стан пружно-пластичних пластин з двома перпендикулярними розрізами за всебічного розтягу.Effective numerical methods for solving 2D problems related to the theories of elasticity and plasticity have been worked out. The variation-difference method of building finite difference schemes is extended to disconnected domains. The application of the variation-difference method for solving problems of the theory of small elasto-plastic deformations relatively the plates with cuts, taking into account the linear strengthening of the material and unloading, has been developed. For solving the resultant systems of nonlinear and linear equation, the Newton-Kantorovich method and combined iterative method (gradient and cyclic Chebyshev’s one) were proposed to be used. The choice of iteration parameters of the methods for solving the obtained systems of linear and nonlinear algebraic equations was made. The elaborated software ensures solving the problems with different boundary conditions, medium and domain parameters. A variety of problems concerning all-round stretching of the elasto-plastic plates with two perpendicular cuts is numerically solved. The zones of evolution of plastic deformations for step enlarging of the loading are constructed. There are found the stresses under which the yield limit and the strength limit are achieve in the plates. On the base of numerical analysis the following main regularities are found: under the close mutual location of cuts in the plate, the plastic deformations first appear under the stress which is 33% less than in the plate with the same cuts under the far mutual location; however, the strength limit in the plates in the both considered cases is achieve practically under the same stress

B7-H1-Deficiency Enhances the Potential of Tolerogenic Dendritic Cells by Activating CD1d-Restricted Type II NKT Cells

Background: Dendritic cells (DC) can act tolerogenic at a semi-mature stage by induction of protective CD4+ T cell and NKT cell responses. Methodology/Principal Findings: Here we studied the role of the co-inhibitory molecule B7-H1 (PD-L1, CD274) on semimature DC that were generated from bone marrow (BM) cells of B7-H12/2 mice and applied to the model of Experimental Autoimmune Encephalomyelitis (EAE). Injections of B7-H1-deficient DC showed increased EAE protection as compared to wild type (WT)-DC. Injections of B7-H12/2 TNF-DC induced higher release of peptide-specific IL-10 and IL-13 after restimulation in vitro together with elevated serum cytokines IL-4 and IL-13 produced by NKT cells, and reduced IL-17 and IFN-c production in the CNS. Experiments in CD1d2/2 and Ja2812/2 mice as well as with type I and II NKT cell lines indicated that only type II NKT cells but not type I NKT cells (invariant NKT cells) could be stimulated by an endogenous CD1d-ligand on DC and were responsible for the increased serum cytokine production in the absence of B7-H1. Conclusions/Significance: Together, our data indicate that BM-DC express an endogenous CD1d ligand and B7-H1 to ihibit type II but not type I NKT cells. In the absence of B7-H1 on these DC their tolerogenic potential to stimulate tolerogenic CD4+ and NKT cell responses is enhanced

Additional file 1: of C9orf72 is differentially expressed in the central nervous system and myeloid cells and consistently reduced in C9orf72, MAPT and GRN mutation carriers

Supplementary Data. Figure S1: Definition of TSSs at the C9orf72 locus; Figure S2: C9orf72 expression changes in challenged CD14+ monocytes. Figure S3: Distinct TSSs expression at C9orf72 locus in CNS, myeloid and lymphoid cells. Figure S4: Sense and antisense C9orf72 transcripts at the C9orf72 locus. Figure S5: Distinct C9orf72 TSSs expression in control brains. Figure S6: C9orf72 expression in adult and fetal cortex. Figure S7: C9orf72 expression level in CD14+ monocytes, brain tissue and microglia. Figure S8: C9orf72 expression in brains of patients with different neurodegenerative diseases. Figure S9: C9orf72 expression in CD14+ monocytes. Suppl. excel File 1: WGCNA results. Suppl. excel File 2: Correlations values between C9orf72 TSS(s) and all the other TSSs in the co-expressed modules. Table S1: Expression of C9orf72 TSSs as defined in CAGEseq dataset 1. Table S2: Expression of C9orf72 TSSs as defined in CAGEseq dataset 2. Table S3: List of primers used in this study. Table S4: Biological functions significant to the three modules related to C9orf72 TSSs as identified by WGCNA. Table S5: Biological functions significant for genes that correlate with C9orf72 TSSs in the WGCNA identified modules. Table S6: Summary of the Mann-Whitney test performed on NRQ values from qPCR experiments on medial frontal gyrus. (ZIP 20675ย�kb

Sensing Tissue Damage by Myeloid C-Type Lectin Receptors

After both sterile and infectious insults, damage is inflicted on tissues leading to accidental or programmed cell death. In addition, events of programmed cell death also take place under homeostatic conditions, such as in embryo development or in the turnover of hematopoietic cells. Mammalian tissues are seeded with myeloid immune cells, which harbor a plethora of receptors that allow the detection of cell death, modulating immune responses. The myeloid C-type lectin receptors (CLRs) are one of the most prominent families of receptors involved in tailoring immunity after sensing dead cells. In this chapter, we will cover a diversity of signals arising from different forms of cell death and how they are recognized by myeloid CLRs. We will also explore how myeloid cells develop their sentinel function, exploring how some of these CLRs identify cell death and the type of responses triggered thereof. In particular, we will focus on DNGR-1 (CLEC9A), Mincle (CLEC4E), CLL-1 (CLEC12A), LOX-1 (OLR1), CD301 (CLEC10A) and DEC-205 (LY75) as paradigmatic death-sensing CLRs expressed by myeloid cells. The molecular processes triggered after cell death recognition by myeloid CLRs contribute to the regulation of immune responses in pathologies associated with tissue damage, such as infection, autoimmunity and cancer. A better understanding of these processes may help to improve the current approaches for therapeutic intervention.Carlos Del Fresno is supported by AECC Foundation (INVES192DELF). Francisco Javier Cueto is the recipient of a Ph.D. “La Caixa” fellowship (LCF/BQ/ES14/10320011). Work in the DS laboratory is funded by the CNIC; by the European Research Council (ERC-2016-Consolidator Grant 725091); by the European Commission (635122-PROCROP H2020); by Ministerio de Ciencia, Innovación e Universidades (MICINN), Agencia Estatal de Investigación and Fondo Europeo de Desarrollo Regional (FEDER) (SAF2016-79040-R); by Comunidad de Madrid (B2017/BMD-3733 Immunothercan-CM); by FIS-Instituto de Salud Carlos III, MICINN and FEDER (RD16/0015/0018-REEM); by Acteria Foundation; by Atresmedia (Constantes y Vitales prize) and by Fundació La Marató de TV3 (201723). The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the MICINN and the Pro-CNIC Foundation and is a Severo Ochoa Center of Excellence (SEV-2015-0505).S

The Dendritic Cell Receptor Clec9A Binds Damaged Cells via Exposed Actin Filaments

10.1016/j.immuni.2012.03.009Immunity364646-657IUNI