The Arabidopsis R2R3 MYB transcription factor MYB15 is a key regulator of lignin biosynthesis in effector-triggered immunity

Lignin, a major component of the secondary cell wall, is important for plant growth and development. Moreover, lignin plays a pivotal role in plant innate immunity. Lignin is readily deposited upon pathogen infection and functions as a physical barrier that limits the spread of pathogens. In this study, we show that an Arabidopsis MYB transcription factor MYB15 is required for the activation of lignin biosynthesis genes such as PAL, C4H, 4CL, HCT, C3′H, COMT, and CAD, and consequently lignin formation during effector-triggered immune responses. Upon challenge with the avirulent bacterial pathogen Pst DC3000 (AvrRpm1), lignin deposition and disease resistance were reduced in myb15 mutant plants. Furthermore, whereas invading pathogens, together with hypersensitive cell death, were restricted to the infection site in wild-type leaves, they spread beyond the infected area in myb15 mutants. The exogenous supply of the lignin monomer coniferyl alcohol restored lignin production and rescued immune defects in myb15 plants. These results demonstrate that regulation at the transcriptional level is key to pathogen-induced lignification and that MYB15 plays a central role in this process

Monte Carlo simulation method for Laughlin-like states in a disk geometry

We discuss an alternative accurate Monte Carlo method to calculate the ground-state energy and related quantities for Laughlin states of the fractional quantum Hall effect in a disk geometry. This alternative approach allows us to obtain accurate bulk regime (thermodynamic limit) values for various quantities from Monte Carlo simulations with a small number of particles (much smaller than that needed with standard Monte Carlo approaches).Comment: 13 pages, 6 figures, 2 table

Assessment of wear resistance of tin and tin alloy coatings

Tin alloy coatings have traditionally been used as corrosion resistant bamens due to their inert nature and comprehensive coverage, and have seldom been considered in physically demanding applications, such as wear resistant coatings owing to misconceptions associated with the soft nature of tin metal. The alloying of tin with copper has already been shown to significantly increase its mechanical properties, as demonstrated by the adoption of tin-copper alloys for use as bearing materials. Unfortunately, its cyanide plating technology makes tin-copper environmentally unsustainable, whilst the process requires constant regulation and monitoring, and there are disposal costs associated with the cyanide waste products. The tin-nickel alloy, however, can be produced with minimal supervision and its plating process uses less harmful precursors, making it an alternative consideration. The research documented in this thesis assesses this increase by quantifying the resistance of tin, tin-nickel and tin-copper coatings to removal from sliding wear. As tin is a soft material and behaves dissimilarly to conventional coatings in a sliding wear environment, traditional wear assessment techniques are not appropriate. A novel approach is therefore devised and implemented, and this involves the continually monitoring the effect of damage introduced to the surface of the tin and tin alloy coatings, from an abrading ceramic ball. Using an elemental detection tool, it is possible to analyse wear scars that exhibit progressively depleted coating material, by identifying the underlying substrate material as it becomes exposed. In this way, it is possible to quantify the improvements made to tin from alloying with nickel and copper. The large volume of data acquired from this research is presented in a matrix format to enable simultaneous depiction of multiple parameters, and to allow quick and easy interpretation. The tin-nickel coating is found to be comparable to tin-copper in terms of resistance to removal. Despite tin-copper being slightly superior over the range of test conditions used, tin-nickel as been shown to be an environmentally friendly and cost effective alternative coating alloy to tin-copper.EThOS - Electronic Theses Online ServiceITRI LtdGBUnited Kingdo

Parkinson's VPS35[D620N] mutation induces LRRK2-mediated lysosomal association of RILPL1 and TMEM55B

We demonstrate that the Parkinson's VPS35[D620N] mutation alters the expression of ~220 lysosomal proteins and stimulates recruitment and phosphorylation of Rab proteins at the lysosome. This recruits the phospho-Rab effector protein RILPL1 to the lysosome where it binds to the lysosomal integral membrane protein TMEM55B. We identify highly conserved regions of RILPL1 and TMEM55B that interact and design mutations that block binding. In mouse fibroblasts, brain, and lung, we demonstrate that the VPS35[D620N] mutation reduces RILPL1 levels, in a manner reversed by LRRK2 inhibition and proteasome inhibitors. Knockout of RILPL1 enhances phosphorylation of Rab substrates, and knockout of TMEM55B increases RILPL1 levels. The lysosomotropic agent LLOMe also induced LRRK2 kinase-mediated association of RILPL1 to the lysosome, but to a lower extent than the D620N mutation. Our study uncovers a pathway through which dysfunctional lysosomes resulting from the VPS35[D620N] mutation recruit and activate LRRK2 on the lysosomal surface, driving assembly of the RILPL1-TMEM55B complex.</p

Spine-GFlow: A hybrid learning framework for robust multi-tissue segmentation in lumbar MRI without manual annotation

Most learning-based magnetic resonance image (MRI) segmentation methods rely on the manual annotation to provide supervision, which is extremely tedious, especially when multiple anatomical structures are required. In this work, we aim to develop a hybrid framework named Spine-GFlow that combines the image features learned by a CNN model and anatomical priors for multi-tissue segmentation in a sagittal lumbar MRI. Our framework does not require any manual annotation and is robust against image feature variation caused by different image settings and/or underlying pathology. Our contributions include: 1) a rule-based method that automatically generates the weak annotation (initial seed area), 2) a novel proposal generation method that integrates the multi-scale image features and anatomical prior, 3) a comprehensive loss for CNN training that optimizes the pixel classification and feature distribution simultaneously. Our Spine-GFlow has been validated on 2 independent datasets: HKDDC (containing images obtained from 3 different machines) and IVDM3Seg. The segmentation results of vertebral bodies (VB), intervertebral discs (IVD), and spinal canal (SC) are evaluated quantitatively using intersection over union (IoU) and the Dice coefficient. Results show that our method, without requiring manual annotation, has achieved a segmentation performance comparable to a model trained with full supervision (mean Dice 0.914 vs 0.916)

Parkinson's VPS35[D620N] mutation induces LRRK2-mediated lysosomal association of RILPL1 and TMEM55B

We demonstrate that the Parkinson's VPS35[D620N] mutation alters the expression of ~220 lysosomal proteins and stimulates recruitment and phosphorylation of Rab proteins at the lysosome. This recruits the phospho-Rab effector protein RILPL1 to the lysosome where it binds to the lysosomal integral membrane protein TMEM55B. We identify highly conserved regions of RILPL1 and TMEM55B that interact and design mutations that block binding. In mouse fibroblasts, brain, and lung, we demonstrate that the VPS35[D620N] mutation reduces RILPL1 levels, in a manner reversed by LRRK2 inhibition and proteasome inhibitors. Knockout of RILPL1 enhances phosphorylation of Rab substrates, and knockout of TMEM55B increases RILPL1 levels. The lysosomotropic agent LLOMe also induced LRRK2 kinase-mediated association of RILPL1 to the lysosome, but to a lower extent than the D620N mutation. Our study uncovers a pathway through which dysfunctional lysosomes resulting from the VPS35[D620N] mutation recruit and activate LRRK2 on the lysosomal surface, driving assembly of the RILPL1-TMEM55B complex.</p

Speak-up culture in an intensive care unit in Hong Kong: a cross-sectional survey exploring the communication openness perceptions of Chinese doctors and nurses

Objectives Despite growing recognition of the importance of speaking up to protect patient safety in critical care, little research has been performed in this area in an intensive care unit (ICU) context. This study explored the communication openness perceptions of Chinese doctors and nurses and identified their perceptions of issues in ICU communication, their reasons for speaking up and the possible factors and strategies involved in promoting the practice of speaking up. Design A mixed-methods design with quantitative and sequential qualitative components was used. Setting and participants Eighty ICU staff members from a large public hospital in Hong Kong completed a questionnaire regarding their perceptions of communication openness. Ten clinicians whose survey responses indicated support for open communication were then interviewed about their speak-up practices. Results The participating ICU staff members had similar perceptions of their openness to communication. However, the doctors responded more positively than the nurses to many aspects of communication openness. The two groups also had different perceptions of speaking up. The interviewed ICU staff members who indicated a high level of communication openness reported that their primary reasons for speaking up were to seek and clarify information, which was achieved by asking questions. Other factors perceived to influence the motivation to speak up included seniority, relationships and familiarity with patient cases. Conclusions Creating an atmosphere of safety and equality in which team members feel confident in expressing their personal views without fear of reprisal or embarrassment is necessary to encourage ICU staff members, regardless of their position, to speak up. Because harmony and saving face is valued in Chinese culture, training nurses and doctors to speak up by focusing on human factors and values rather than simply addressing conflict management is desirable in this context.This work was supported by funding from the Hospital Authority’s Kowloon Central Cluster Research Grant (grant number: KCC/RC/G/1516-B03)

Manganese Superoxide Dismutase and Chemokine Genes Polymorphisms in Chinese Patients with Anterior Uveitis

PURPOSE. To investigate the association of single-nucleotide polymorphisms (SNPs) in the manganese superoxide dismutase (MnSOD) and two chemokine genes (CCL2 and CCL5) in patients with anterior uveitis (AU). METHODS. Seventy-nine Chinese patients with acute AU were recruited, and genotyping of four SNPs including MnSOD 47, CCL2 Ϫ2518, CCL2 Ϫ2076, and CCL5 Ϫ403 alleles was performed with SNP genotyping assays. The genotype and allele frequencies were compared between patients with AU and 206 healthy control subjects. Analyses were also stratified according to the HLA-B27 status of the patients. RESULTS. There were significant increases in the frequency of the AA homozygosity in the MnSOD 47 SNP (P ϭ 0.049) and in the CCL2 Ϫ2518G allele frequency and GG homozygosity in patients with AU compared with control subjects (P ϭ 0.017 and P ϭ 0.024, respectively). No significant association was found between AU with the CCL2 Ϫ2076 and CCL5 Ϫ403 SNPs. Subgroup analyses showed that the MnSOD 47A polymorphism was significantly associated with AU in HLA-B27-positive patients, but not in HLA-B27-negative patients, whereas the CCL2 Ϫ2518G polymorphism was significantly associated with AU in HLA-B27-negative patients, but not in HLA-B27-positive patients. CONCLUSIONS. The 47A polymorphism in the MnSOD gene and the Ϫ2518G polymorphism in the CCL2 gene are associated with the development of AU in HLA-B27-positive and -negative Chinese patients, respectively. Further studies to evaluate the interactions of the HLA-B27 status and these SNPs are warranted. (Invest Ophthalmol Vis Sci