The domain matrix method: a new calculation scheme for diffraction profiles

A new calculation scheme for diffraction profiles is presented that combines the matrix method with domain approaches. Based on a generalized Markov chain, the method allows the exact solution of the diffraction problem from any one-dimensionally disordered domain structure. The main advantage of this model is that a domain statistic is used instead of a cell statistic and that the domain-length distribution can be chosen independently from the domain-type stacking. A recursive relation is derived for the correlations between the domains and a double recursive algorithm, not reducible to a simpler one, is obtained as solution. The algorithm developed here is referred to as the domain matrix method. Results and applications of the new approach are discussed

Dimer bond geometry in D/Ge(100)-(2×1): A low-energy electron-diffraction structure analysis

The asymmetry of the Ge dimer in the (2×1) reconstruction of Ge(100) is removed upon adsorption of deuterium D. The R-factor analysis indicates a slight remaining asymmetry which is attributed to the coexistence of bare and D-covered dimers. The Ge-Ge bond length of 2.4(2) Å in the dimer does not change within the error limits when compared to the clean surface. The D atoms bond on top of the Ge atoms, exhibiting a Ge-D bond length of 1.6(2) Å

Adsorption induced reconstruction of the Cu(110) surface

The formation of the O/Cu(110)-(2 × 1) and H/Cu(110)-(1 × 2) superstructures has been investigated by a LEED beam profile analysis. The oxygen induced reconstruction proceeds at later stages by creation of holes on flat terraces. This could not be observed at the hydrogen induced missing row reconstruction. The formation of the missing row structure proceeds most probably via nucleation at steps and subsequent growth of (1 × 2) islands. The influence of different distributions of steps and islands on beam profiles is discussed

IL-27 Imparts Immunoregulatory Function to Human NK Cell Subsets

Interleukin-27 (IL-27) is a cytokine with multiple roles in regulating the immune response, but its effect on human CD56bright and CD56dim NK cell subsets is unknown. NK cell subsets interact with other components of the immune system, leading to cytotoxicity or immunoregulation depending on stimulating factors. We found that IL-27 treatment results in increased IL-10 and IFN-γ expression, increased viability and decreased proliferation in both CD56bright and CD56dim NK cell subsets. More importantly, IL-27 treatment imparts regulatory activity to CD56bright NK cells, which mediates its suppressive function on T cells in a contact-dependent manner. There is growing evidence that CD56bright NK cell-mediated immunoregulation plays an important role in the control of autoimmunity. Thus, understanding the role of IL-27 in NK cell function has important implications for treatment of autoimmune disorders

Reducing drug related deaths : a pre-implementation assessment of knowledge,barriers and enablers for naloxone distribution through general practice

Peer reviewedPublisher PD

Site‐specific weed management—constraints and opportunities for the weed research community: Insights from a workshop

The adoption of site‐specific weed management (SSWM) technologies by farmers is not aligned with the scientific achievements in this field. While scientists have demonstrated significant success in real‐time weed identification, phenotyping and accurate weed mapping by using various sensors and platforms, the integration by farmers of SSWM and weed phenotyping tools into weed management protocols is limited. This gap was therefore a central topic of discussion at the most recent workshop of the SSWM Working Group arranged by the European Weed Research Society (EWRS). This insight paper aims to summarise the presentations and discussions of some of the workshop panels and to highlight different aspects of weed identification and spray application that were thought to hinder SSWM adoption. It also aims to share views and thoughts regarding steps that can be taken to facilitate future implementation of SSWM

The first report of RPSA polymorphisms, also called 37/67 kDa LRP/LR gene, in sporadic Creutzfeldt-Jakob disease (CJD)

<p>Abstract</p> <p>Background</p> <p>Although polymorphisms of <it>PRNP</it>, the gene encoding prion protein, are known as a determinant affecting prion disease susceptibility, other genes also influence prion incubation time. This finding offers the opportunity to identify other genetic or environmental factor (s) modulating susceptibility to prion disease. Ribosomal protein SA (<it>RPSA</it>), also called 37 kDa laminin receptor precursor (LRP)/67 kDa laminin receptor (LR), acts as a receptor for laminin, viruses and prion proteins. The binding/internalization of prion protein is dependent for LRP/LR.</p> <p>Methods</p> <p>To identify other susceptibility genes involved in prion disease, we performed genetic analysis of <it>RPSA</it>. For this case-control study, we included 180 sporadic Creutzfeldt-Jakob disease (CJD) patients and 189 healthy Koreans. We investigated genotype and allele frequencies of polymorphism on <it>RPSA </it>by direct sequencing or restriction fragment length polymorphism (RFLP) analysis.</p> <p>Results</p> <p>We observed four single nucleotide polymorphisms (SNPs), including -8T>C (rs1803893) in the 5'-untranslated region (UTR) of exon 2, 134-32C>T (rs3772138) in the intron, 519G>A (rs2269350) in the intron and 793+58C>T (rs2723) in the intron on the <it>RPSA</it>. The 519G>A (at codon 173) is located in the direct PrP binding site. The genotypes and allele frequencies of the <it>RPSA </it>polymorphisms showed no significant differences between the controls and sporadic CJD patients.</p> <p>Conclusion</p> <p>These results suggest that these <it>RPSA </it>polymorphisms have no direct influence on the susceptibility to sporadic CJD. This was the first genetic association study of the polymorphisms of <it>RPSA </it>gene with sporadic CJD.</p

IL-27 supports germinal center function by enhancing IL-21 production and the function of T follicular helper cells

IL-27 signaling directly into T cells is needed for follicular T helper cell survival, germinal center formation, and the production of T cell–dependent high-affinity antibodies in mice

Effects of Hepatitis B Surface Antigen on Virus-specific and Global T Cells in Patients With Chronic HBV infection

10.1053/j.gastro.2020.04.019Gastroenterolog

IL-27 Regulates IL-18 Binding Protein in Skin Resident Cells

IL-18 is an important mediator involved in chronic inflammatory conditions such as cutaneous lupus erythematosus, psoriasis and chronic eczema. An imbalance between IL-18 and its endogenous antagonist IL-18 binding protein (BP) may account for increased IL-18 activity. IL-27 is a cytokine with dual function displaying pro- and anti-inflammatory properties. Here we provide evidence for a yet not described anti-inflammatory mode of action on skin resident cells. Human keratinocytes and surprisingly also fibroblasts (which do not produce any IL-18) show a robust, dose-dependent and highly inducible mRNA expression and secretion of IL-18BP upon IL-27 stimulation. Other IL-12 family members failed to induce IL-18BP. The production of IL-18BP peaked between 48–72 h after stimulation and was sustained for up to 96 h. Investigation of the signalling pathway showed that IL-27 activates STAT1 in human keratinocytes and that a proximal GAS site at the IL-18BP promoter is of importance for the functional activity of IL-27. The data are in support of a significant anti-inflammatory effect of IL-27 on skin resident cells. An important novel property of IL-27 in skin pathobiology may be to counter-regulate IL-18 activities by acting on keratinocytes and importantly also on dermal fibroblasts