Modern tests of Lorentz invariance

Motivated by ideas about quantum gravity, a tremendous amount of effort over the past decade has gone into testing Lorentz invariance in various regimes. This review summarizes both the theoretical frameworks for tests of Lorentz invariance and experimental advances that have made new high precision tests possible. The current constraints on Lorentz violating effects from both terrestrial experiments and astrophysical observations are presented.Comment: Modified and expanded discussions of various points. Numerous references added. Version matches that accepted by Living Reviews in Relativit

Plasma Cholesterol-Induced Lesion Networks Activated before Regression of Early, Mature, and Advanced Atherosclerosis

Plasma cholesterol lowering (PCL) slows and sometimes prevents progression of atherosclerosis and may even lead to regression. Little is known about how molecular processes in the atherosclerotic arterial wall respond to PCL and modify responses to atherosclerosis regression. We studied atherosclerosis regression and global gene expression responses to PCL (>= 80%) and to atherosclerosis regression itself in early, mature, and advanced lesions. In atherosclerotic aortic wall from Ldlr(-/-)Apob(100/100)Mttp(flox/flox)Mx1-Cre mice, atherosclerosis regressed after PCL regardless of lesion stage. However, near-complete regression was observed only in mice with early lesions; mice with mature and advanced lesions were left with regression-resistant, relatively unstable plaque remnants. Atherosclerosis genes responding to PCL before regression, unlike those responding to the regression itself, were enriched in inherited risk for coronary artery disease and myocardial infarction, indicating causality. Inference of transcription factor (TF) regulatory networks of these PCL-responsive gene sets revealed largely different networks in early, mature, and advanced lesions. In early lesions, PPARG was identified as a specific master regulator of the PCL-responsive atherosclerosis TF-regulatory network, whereas in mature and advanced lesions, the specific master regulators were MLL5 and SRSF10/XRN2, respectively. In a THP-1 foam cell model of atherosclerosis regression, siRNA targeting of these master regulators activated the time-point-specific TF-regulatory networks and altered the accumulation of cholesterol esters. We conclude that PCL leads to complete atherosclerosis regression only in mice with early lesions. Identified master regulators and related PCL-responsive TF-regulatory networks will be interesting targets to enhance PCL-mediated regression of mature and advanced atherosclerotic lesions. Author Summary The main underlying cause of heart attacks and strokes is atherosclerosis. One strategy to prevent these often deadly clinical events is therefore either to slow atherosclerosis progression or better, induce regression of atherosclerotic plaques making them more stable. Plasma cholesterol lowering (PCL) is the most efficient way to induce atherosclerosis regression but sometimes fails to do so. In our study, we used a mouse model with elevated LDL cholesterol levels, similar to humans who develop early atherosclerosis, and a genetic switch to lower plasma cholesterol at any time during atherosclerosis progression. In this model, we examined atherosclerosis gene expression and regression in response to PCL at three different stages of atherosclerosis progression. PCL led to complete regression in mice with early lesions but was incomplete in mice with mature and advanced lesions, indicating that early prevention with PCL in individuals with increased risk for heart attack or stroke would be particularly useful. In addition, by inferring PCL-responsive gene networks in early, mature and advanced atherosclerotic lesions, we identified key drivers specific for regression of early (PPARG), mature (MLL5) and advanced (SRSF10/XRN2) atherosclerosis. These key drivers should be interesting therapeutic targets to enhance PCL-mediated regression of atherosclerosis

Elektriskt ledande filter : funktionoch prestanda

Denna rapport ger en bild över luftfilteroch dess funktioner. Syftet med arbetet var att undersöka hur elektriskt ledande luftfilter tillsammans med en joniseringsenhet fungerar samt hur de står sig i förhållande till de mekaniska.Det låg även i syftet att titta på hur andra parametrar påverkar filtrering såsom tjocklek och innehåll av olika andel konduktivt material. Bakgrunden till arbetet var att VokesAir AB hade testat att tillverka elektriskt ledande filter med jonisering i filtret vilket hade fungerat i lite skala men inte i större. Det gjorde att man i detta arbete ville titta på om det kunde fungera om man satte joniseringen utanför filtret istället. Nio stycken luftfilter tillverkades i ennon-woven konstruktion med olika andel konduktivt material och i olika tjocklekar. Utförandetav testerna gjordes i entestriggliknande den i EN779:2012dock med vissa modifieringar. En av dem varatt ett joniseringsrörsomvar fäst före filtretsom tillverkar joner som i sin tur kan fastna på partiklar vilket ger partiklar en laddning. När partiklar tillsammans med joner sedan kommernära luftfiltret innehållande konduktivt material kan de fastnai filtret.Resultatet visade att deelektriska ledande filtrena hade en högre effektivitet när det gällde filtrering av partiklar än de mekaniska. Dock visade inte resultaten någon tydlig skillnad vad det gäller effektiviteten. När det gäller hur tjockleken och andelen konduktivt material påverkade filtreringsförmågan var det svårt att utläsa några tydliga trender. Andelen konduktivt material hade en viss riktning åt att mera andel konduktivtProgram: Textilingenjörsutbildninge