Linear Momentum Density in Quasistatic Electromagnetic Systems

We discuss a couple of simple quasistatic electromagnetic systems in which the density of electromagnetic linear momentum can be easily computed. The examples are also used to illustrate how the total electromagnetic linear momentum, which may also be calculated by using the vector potential, can be understood as a consequence of the violation of the action-reaction principle, because a non-null external force is required to maintain constant the mechanical linear momentum. We show how one can avoid the divergence in the interaction linear electromagnetic momentum of a system composed by an idealization often used in textbooks (an infinite straight current) and a point charge.Comment: 22 pages, 5 figures, to appear in Eur. J. Phy

The watchdogs of 'Washminster' – parliamentary scrutiny of executive patronage in the UK

The role of legislatures in scrutinising executive patronage has received scant attention in the context of parliamentary democracy. This article addresses this lacuna by focusing on the parliamentary scrutiny of public appointments in the UK. Presenting the results of an extensive programme of research, it reveals how select committees have accrued increasing powers to challenge ministerial appointments, and how this has resulted in a series of unintended consequences that raise critical concerns regarding the overall added-value of pre-appointment scrutiny. The article is therefore of comparative significance for theories of legislative scrutiny in particular and executive–legislature dynamics more broadly

Selecting and monitoring pheromone traps in insect pest management

Published December 1984. Facts and recommendations in this publication may no longer be valid. Please look for up-to-date information in the OSU Extension Catalog: http://extension.oregonstate.edu/catalo

IDOL regulates systemic energy balance through control of neuronal VLDLR expression.

Liver X receptors limit cellular lipid uptake by stimulating the transcription of Inducible Degrader of the LDL Receptor (IDOL), an E3 ubiquitin ligase that targets lipoprotein receptors for degradation. The function of IDOL in systemic metabolism is incompletely understood. Here we show that loss of IDOL in mice protects against the development of diet-induced obesity and metabolic dysfunction by altering food intake and thermogenesis. Unexpectedly, analysis of tissue-specific knockout mice revealed that IDOL affects energy balance, not through its actions in peripheral metabolic tissues (liver, adipose, endothelium, intestine, skeletal muscle), but by controlling lipoprotein receptor abundance in neurons. Single-cell RNA sequencing of the hypothalamus demonstrated that IDOL deletion altered gene expression linked to control of metabolism. Finally, we identify VLDLR rather than LDLR as the primary mediator of IDOL effects on energy balance. These studies identify a role for the neuronal IDOL-VLDLR pathway in metabolic homeostasis and diet-induced obesity

Hyperglycemia Induces a Dynamic Cooperativity of Histone Methylase and Demethylase Enzymes Associated With Gene-Activating Epigenetic Marks That Coexist on the Lysine Tail

OBJECTIVE: Results from the Diabetes Control Complications Trial (DCCT) and the subsequent Epidemiology of Diabetes Interventions and Complications (EDIC) Study and more recently from the U.K. Prospective Diabetes Study (UKPDS) have revealed that the deleterious end-organ effects that occurred in both conventional and more aggressively treated subjects continued to operate >5 years after the patients had returned to usual glycemic control and is interpreted as a legacy of past glycemia known as "hyperglycemic memory." We have hypothesized that transient hyperglycemia mediates persistent gene-activating events attributed to changes in epigenetic information. RESEARCH DESIGN AND METHODS: Models of transient hyperglycemia were used to link NFkappaB-p65 gene expression with H3K4 and H3K9 modifications mediated by the histone methyltransferases (Set7 and SuV39h1) and the lysine-specific demethylase (LSD1) by the immunopurification of soluble NFkappaB-p65 chromatin. RESULTS: The sustained upregulation of the NFkappaB-p65 gene as a result of ambient or prior hyperglycemia was associated with increased H3K4m1 but not H3K4m2 or H3K4m3. Furthermore, glucose was shown to have other epigenetic effects, including the suppression of H3K9m2 and H3K9m3 methylation on the p65 promoter. Finally, there was increased recruitment of the recently identified histone demethylase LSD1 to the p65 promoter as a result of prior hyperglycemia. CONCLUSIONS: These studies indicate that the active transcriptional state of the NFkappaB-p65 gene is linked with persisting epigenetic marks such as enhanced H3K4 and reduced H3K9 methylation, which appear to occur as a result of effects of the methyl-writing and methyl-erasing histone enzymes

Transverse-spin dependence of the p-p total cross section ΔσT from 0.8 to 2.5 GeV/c

The difference ΔσT=σ(↓↑)-σ(↑↑) between the proton-proton total cross sections for protons in pure transverse-spin states, was measured at incident momenta 0.8 to 2.5 GeV/c in experiments performed at the Los Alamos Clinton P. Anderson Meson Physics Facility and the Argonne Zero Gradient Synchrotron. In agreement with other data, peaks were observed at center-of-mass energies of 2.14 and 2.43 GeV/c2, where 1D2 and 1G4 dibaryon resonances have been proposed

Integrative analysis of the plasma proteome and polygenic risk of cardiometabolic diseases.

Cardiometabolic diseases are frequently polygenic in architecture, comprising a large number of risk alleles with small effects spread across the genome1-3. Polygenic scores (PGS) aggregate these into a metric representing an individual's genetic predisposition to disease. PGS have shown promise for early risk prediction4-7 and there is an open question as to whether PGS can also be used to understand disease biology8. Here, we demonstrate that cardiometabolic disease PGS can be used to elucidate the proteins underlying disease pathogenesis. In 3,087 healthy individuals, we found that PGS for coronary artery disease, type 2 diabetes, chronic kidney disease and ischaemic stroke are associated with the levels of 49 plasma proteins. Associations were polygenic in architecture, largely independent of cis and trans protein quantitative trait loci and present for proteins without quantitative trait loci. Over a follow-up of 7.7 years, 28 of these proteins associated with future myocardial infarction or type 2 diabetes events, 16 of which were mediators between polygenic risk and incident disease. Twelve of these were druggable targets with therapeutic potential. Our results demonstrate the potential for PGS to uncover causal disease biology and targets with therapeutic potential, including those that may be missed by approaches utilizing information at a single locus

FXR activation protects against NAFLD via bile-acid-dependent reductions in lipid absorption

FXR agonists are used to treat non-alcoholic fatty liver disease (NAFLD), in part because they reduce hepatic lipids. Here, we show that FXR activation with the FXR agonist GSK2324 controls hepatic lipids via reduced absorption and selective decreases in fatty acid synthesis. Using comprehensive lipidomic analyses, we show that FXR activation in mice or humans specifically reduces hepatic levels of mono- and polyunsaturated fatty acids (MUFA and PUFA). Decreases in MUFA are due to FXR-dependent repression of Scd1, Dgat2, and Lpin1 expression, which is independent of SHP and SREBP1c. FXR-dependent decreases in PUFAs are mediated by decreases in lipid absorption. Replenishing bile acids in the diet prevented decreased lipid absorption in GSK2324-treated mice, suggesting that FXR reduces absorption via decreased bile acids. We used tissue-specific FXR KO mice to show that hepatic FXR controls lipogenic genes, whereas intestinal FXR controls lipid absorption. Together, our studies establish two distinct pathways by which FXR regulates hepatic lipids

Collaborating around digital tabletops: children’s physical strategies from the UK, India and Finland

We present a study of children collaborating around interactive tabletops in three different countries: the United Kingdom, India and Finland. Our data highlights the key distinctive physical strategies used by children when performing collaborative tasks during this study. Children in the UK tend to prefer static positioning with minimal physical contact and simultaneous object movement. Children in India employed dynamic positioning with frequent physical contact and simultaneous object movement. Children in Finland used a mixture of dynamic and static positioning with minimal physical contact and object movement. Our findings indicate the importance of understanding collaboration strategies and behaviours when designing and deploying interactive tabletops in heterogeneous educational environments. We conclude with a discussion on how designers of tabletops for schools can provide opportunities for children in different countries to define and shape their own collaboration strategies for small group learning that take into account their different classroom practices

Deletion of Trim28 in committed adipocytes promotes obesity but preserves glucose tolerance.

The effective storage of lipids in white adipose tissue (WAT) critically impacts whole body energy homeostasis. Many genes have been implicated in WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms in embryonic development. However, in the current study we demonstrate that mice with deletion of Trim28 specifically in committed adipocytes, also develop obesity similar to global Trim28 deletion models, highlighting a post-developmental role for Trim28. These effects were exacerbated in female mice, contributing to the growing notion that Trim28 is a sex-specific regulator of obesity. Mechanistically, this phenotype involves alterations in lipolysis and triglyceride metabolism, explained in part by loss of Klf14 expression, a gene previously demonstrated to modulate adipocyte size and body composition in a sex-specific manner. Thus, these findings provide evidence that Trim28 is a bona fide, sex specific regulator of post-developmental adiposity and WAT function