Drosophila suzukii

Den globala uppvärmningen och den ökade handeln mellan länder är den största anledningen till att främmande arter introduceras nya ekosystem. Den invasiva arten, Drosophila suzukii, orsakar i nuläget stora ekonomiska förluster för bär- och fruktodlare världen över. Tvåvingearten har sitt ursprung i Asien och har blivit en betydelsefull skadegörare på grund av flugans hastiga spridningsförmåga samt evolutionära tillgång,- förmåga att angripa omogen frukt. Till skillnad från ett flertal arter inom Drosophilidae, som vanligtvis konsumerar övermogen frukt, angriper D. suzukii bär och frukt under mognadsfas. D. suzukiis omfattande spridning på kort tid har resulterat i ökat behov av alternativa bekämpningsmetoder. Syftet med studien är att ta reda på vilka bekämpningsmetoder som finns tillgängliga för D. suzukii och vad det forskas omgällande bekämpningsstrategier. Arbetet ska även uppskatta Sveriges framtida påverkan av D. suzukii. Studiens resultat har tagits fram genom litteraturstudier, semistrukturerade kvalitativa intervjuer samt med hjälp av en enkätundersökning. Enkätundersökningen visade att det för närvarande finns ett otillräckligt utbud av biologisk bekämpning på marknaden, att flugan utgör stor ekonomisk skada och att det finns ett alarmerande behov av vidare utveckling av bekämpningsmetoder. Idag används övervakningsfällor för prognos av Drosophila suzukii- populationer. Forskare har upptäckt att olika jästarter attraherar D. suzukii och kunskapen kring området kan medföra att framgångsrika bekämpningsmetoder utvecklas. Predatorer och entomopatogena svampar kan i framtiden fungera som biologisk bekämpning, men vidare forskning kommer att behövas för att det ska vara praktiskt genomförbart. Det finns brist på mer skonsamma bekämpningsmetoder då D. suzukii idag bekämpas i stor utsträckning med insekticider. Slutligen kommer nyckeln till en lyckad bekämpning av D. suzukii bygga på en samordnad bekämpning bestående av flera åtgärder.Global warming and increased trade between countries are the main reasons why exotic species are introduced to new ecosystems. The invasive species, Drosophila suzukii, is now causing significant economic hardship for berry- and fruit growers worldwide. This fly originated in Asia and has become a major pest because of the fly's ability to rapidly spread and evolutionary asset for infesting unripe fruit; unlike a number of species within the Drosophilidae family, who normally consume over ripe fruit, D. suzukii attacks berries and fruit during maturation. D. suzukiis extensive spread in a short time has resulted in increased need for alternative pest control management. The purpose of this study is to find present control strategies against D. suzukii and summarize what is still being researched. The work also gives attention to the impact of D. suzukii in Sweden. Study results were obtained through literature study, semi-structured qualitative interviews and use of a questionnaire. The survey showed that there is currently an inadequate supply of biological control on the market, the fly represents great economic damage and that there is an urgent need for further development of control methods. Today, monitoring traps are used to forecast Drosophila suzukii- outbreak potential. Scientists have discovered that different yeast species attract D. suzukii and knowledge within this area can lead to the development of successful control methods. Predators and entomopathogenic fungi may, in the future, serve as biological control, but further research will be needed for it to be practical. There is a shortage of more environmentally sustainable control methods, as D. suzukii is fought largely with insecticides. Finally, the ultimate key to successful control of D. suzukii is based on implementation of various control measures, a coordinated fight

Detailed diesel exhaust characteristics including particle surface area and lung deposited dose for better understanding of health effects in human chamber exposure studies.

Several diesel exhaust (DE) characteristics, comprising both particle and gas phase, recognized as important when linking with health effects, are not reported in human chamber exposure studies. In order to understand effects of DE on humans there is a need for better characterization of DE when performing exposure studies. The aim of this study was to determine and quantify detailed DE characteristics during human chamber exposure. Additionally to compare to reported DE properties in conducted human exposures. A wide battery of particle and gas phase measurement techniques have been used to provide detailed DE characteristics including the DE particles (DEP) surface area, fraction and dose deposited in the lungs, chemical composition of both particle and gas phase such as NO, NO2, CO, CO2, volatile organic compounds (including aldehydes, benzene, toluene) and polycyclic aromatic hydrocarbons (PAHs). Eyes, nose and throat irritation effects were determined. Exposure conditions with PM1 (<1 mm) mass concentration 280 mg m3, number concentration 4 105 cm3 and elemental to total carbon fraction of 82% were generated from a diesel vehicle at idling. When estimating the lung deposited dose it was found that using the size dependent effective density (in contrast to assuming unity density) reduced the estimated respiratory dose by 132% by mass. Accounting for agglomerated structure of DEP prevented underestimation of lung deposited dose by surface area by 37% in comparison to assuming spherical particles. Comparison of DE characteristics reported in conducted chamber exposures showed that DE properties vary to a great extent under the same DEP mass concentration and engine load. This highlights the need for detailed and standardized approach for measuring and reporting of DE properties. Eyes irritation effects, most probably caused by aldehydes in the gas phase, as well as nose irritation were observed at exposure levels below current occupational exposure limit values given for exhaust fumes. Reporting detailed DE characteristics that include DEP properties (such as mass and number concentration, size resolved information, surface area, chemical composition, lung deposited dose by number, mass and surface) and detailed gas phase including components known for their carcinogenic and irritation effect (e.g. aldehydes, benzene, PAHs) can help in determination of key parameters responsible for observed health effects and comparison of chamber exposure studies

Whole Blood Profiling of T-cell-Derived microRNA Allows the Development of Prognostic models in Inflammatory Bowel Disease

Background: MicroRNAs [miRNAs] are cell-specific small non-coding RNAs that can regulate gene expression and have been implicated in inflammatory bowel disease [IBD] pathogenesis. Here we define the cell-specific miRNA profiles and investigate its biomarker potential in IBD. Methods: In a two-stage prospective multi-centre case control study, next generation sequencing was performed on a discovery cohort of immunomagnetically separated leukocytes from 32 patients (nine Crohn''s disease [CD], 14 ulcerative colitis [UC], eight healthy controls) and differentially expressed signals were validated in whole blood in 294 patients [97 UC, 98 CD, 98 non-IBD, 1 IBDU] using quantitative PCR. Correlations were analysed with phenotype, including need for early treatment escalation as a marker of progressive disease using Cox proportional hazards. Results: In stage 1, each leukocyte subset [CD4+ and CD8+ T-cells and CD14+ monocytes] was analysed in IBD and controls. Three specific miRNAs differentiated IBD from controls in CD4+ T-cells, including miR-1307-3p [p = 0.01], miR-3615 [p = 0.02] and miR-4792 [p = 0.01]. In the extension cohort, in stage 2, miR-1307-3p was able to predict disease progression in IBD (hazard ratio [HR] 1.98, interquartile range [IQR]: 1.20-3.27; logrank p = 1.80 × 10-3), in particular CD [HR 2.81; IQR: 1.11-3.53, p = 6.50 × 10-4]. Using blood-based multimarker miRNA models, the estimated chance of escalation in CD was 83% if two or more criteria were met and 90% for UC if three or more criteria are met. Interpretation: We have identified and validated unique CD4+ T-cell miRNAs that are differentially regulated in IBD. These miRNAs may be able to predict treatment escalation and have the potential for clinical translation; further prospective evaluation is now indicated

Systemic Inflammation in Preclinical Ulcerative Colitis

Background & Aims: Preclinical ulcerative colitis is poorly defined. We aimed to characterize the preclinical systemic inflammation in ulcerative colitis, using a comprehensive set of proteins. Methods: We obtained plasma samples biobanked from individuals who developed ulcerative colitis later in life (n = 72) and matched healthy controls (n = 140) within a population-based screening cohort. We measured 92 proteins related to inflammation using a proximity extension assay. The biologic relevance of these findings was validated in an inception cohort of patients with ulcerative colitis (n = 101) and healthy controls (n = 50). To examine the influence of genetic and environmental factors on these markers, a cohort of healthy twin siblings of patients with ulcerative colitis (n = 41) and matched healthy controls (n = 37) were explored. Results: Six proteins (MMP10, CXCL9, CCL11, SLAMF1, CXCL11 and MCP-1) were up-regulated (P < .05) in preclinical ulcerative colitis compared with controls based on both univariate and multivariable models. Ingenuity Pathway Analyses identified several potential key regulators, including interleukin-1ß, tumor necrosis factor, interferon-gamma, oncostatin M, nuclear factor-¿B, interleukin-6, and interleukin-4. For validation, we built a multivariable model to predict disease in the inception cohort. The model discriminated treatment-naïve patients with ulcerative colitis from controls with leave-one-out cross-validation (area under the curve = 0.92). Consistently, MMP10, CXCL9, CXCL11, and MCP-1, but not CCL11 and SLAMF1, were significantly up-regulated among the healthy twin siblings, even though their relative abundances seemed higher in incident ulcerative colitis. Conclusions: A set of inflammatory proteins are up-regulated several years before a diagnosis of ulcerative colitis. These proteins were highly predictive of an ulcerative colitis diagnosis, and some seemed to be up-regulated already at exposure to genetic and environmental risk factors. © 2021 The Author

An ALS-Linked Mutant SOD1 Produces a Locomotor Defect Associated with Aggregation and Synaptic Dysfunction When Expressed in Neurons of Caenorhabditis elegans

The nature of toxic effects exerted on neurons by misfolded proteins, occurring in a number of neurodegenerative diseases, is poorly understood. One approach to this problem is to measure effects when such proteins are expressed in heterologous neurons. We report on effects of an ALS-associated, misfolding-prone mutant human SOD1, G85R, when expressed in the neurons of Caenorhabditis elegans. Stable mutant transgenic animals, but not wild-type human SOD1 transgenics, exhibited a strong locomotor defect associated with the presence, specifically in mutant animals, of both soluble oligomers and insoluble aggregates of G85R protein. A whole-genome RNAi screen identified chaperones and other components whose deficiency increased aggregation and further diminished locomotion. The nature of the locomotor defect was investigated. Mutant animals were resistant to paralysis by the cholinesterase inhibitor aldicarb, while exhibiting normal sensitivity to the cholinergic agonist levamisole and normal muscle morphology. When fluorescently labeled presynaptic components were examined in the dorsal nerve cord, decreased numbers of puncta corresponding to neuromuscular junctions were observed in mutant animals and brightness was also diminished. At the EM level, mutant animals exhibited a reduced number of synaptic vesicles. Neurotoxicity in this system thus appears to be mediated by misfolded SOD1 and is exerted on synaptic vesicle biogenesis and/or trafficking

The prevalence and transcriptional activity of the mucosal microbiota of ulcerative colitis patients

Active microbes likely have larger impact on gut health status compared to inactive or dormant microbes. We investigate the composition of active and total mucosal microbiota of treatment-naïve ulcerative colitis (UC) patients to determine the microbial picture at the start-up phase of disease, using both a 16S rRNA transcript and gene amplicon sequencing. DNA and RNA were isolated from the same mucosal colonic biopsies. Our aim was to identify active microbial members of the microbiota in early stages of disease and reveal which members are present, but do not act as major players. We demonstrated differences in active and total microbiota of UC patients when comparing inflamed to non-inflamed tissue. Several taxa, among them the Proteobacteria phyla and families therein, revealed lower transcriptional activity despite a high presence. The Bifidobacteriaceae family of the Actinobacteria phylum showed lower abundance in the active microbiota, although no difference in presence was detected. The most abundant microbiota members of the inflamed tissue in UC patients were not the most active. Knowledge of active members of microbiota in UC patients could enhance our understanding of disease etiology. The active microbial community composition did not deviate from the total when comparing UC patients to non-IBD controls

Integrative epigenome-wide analysis demonstrates that DNA methylation may mediate genetic risk in inflammatory bowel disease

Epigenetic alterations may provide important insights into gene-environment interaction in inflammatory bowel disease (IBD). Here we observe epigenome-wide DNA methylation differences in 240 newly-diagnosed IBD cases and 190 controls. These include 439 differentially methylated positions (DMPs) and 5 differentially methylated regions (DMRs), which we study in detail using whole genome bisulphite sequencing. We replicate the top DMP (RPS6KA2) and DMRs (VMP1, ITGB2 and TXK) in an independent cohort. Using paired genetic and epigenetic data, we delineate methylation quantitative trait loci; VMP1/microRNA-21 methylation associates with two polymorphisms in linkage disequilibrium with a known IBD susceptibility variant. Separated cell data shows that IBD-associated hypermethylation within the TXK promoter region negatively correlates with gene expression in whole-blood and CD8+ T cells, but not other cell types. Thus, site-specific DNA methylation changes in IBD relate to underlying genotype and associate with cell-specific alteration in gene expression