Historical Perspective: The Historical Development of the Society for Occupational Health Psychology

The Society for Occupational Health Psychology (SOHP) is the first professional group of its kind in the United States. The development of the Society can be traced to the development of the field of occupational health psychology (OHP). OHP is an interdisciplinary partnership of the psychological and occupational health sciences. The goals of this partnership include the improvement of the quality of people’s working lives and the enhancement of the safety, health, and well-being of workers. To our knowledge the first time the term occupational health psychology became visible in the research literature is in 1986 in a book chapter by George Everly, Jr.; the concept of integrating occupational health and psychology, however, has been around much longer (see Julian Barling and Amanda Griffiths’s fine history in a chapter in James Campbell Quick and Lois Tetrick’s Handbook of Occupational Health Psychology, APA Books)

UK survey of academics 2015

Research is changing. New technology brings increased computational power and virtual representation of physical objects, allowing us to pose and answer previously unimaginable research questions. Big data can be mixed, linked and mined to reveal new unsuspected connections. Enhanced connectivity allows us to collaborate beyond traditional geographic and disciplinary boundaries. Funders demand greater demonstration of impact and engagement with non-academic communities and audiences. As research changes, so do researchers. Their behaviour and expectations shift, evolving to take advantage of new opportunities or responding to changing requirements from their funders or institutions. The researcher of today works in a very different environment to that of even just 20 years ago. Those, either on or above campus, whose role it is to support researchers need to understand these changes, adapt the services they offer to new requirements and anticipate future changes. In an ideal world they would even develop these services before the researchers realised they needed them! This report is the second Ithaka S+R/ Jisc / RLUK survey of UK academics. It asks of the UK research community their views on resource discovery, their use of these resources (online and digital), attitudes to research data management, and much more. It provides a powerful insight into how researchers view their own behaviour and the research environment within the UK today

Fatty liver in familial hypobetalipoproteinemia: Triglyceride assembly into VLDL particles is affected by the extent of hepatic steatosis

Familial hypobetalipoproteinemia (FHBL) subjects may develop fatty liver. Liver fat was assessed in 21 FHBL with six different apolipoprotein B (apoB) truncations (apoB-4 to apoB-89) and 14 controls by magnetic resonance spectroscopy (MRS). Liver fat percentages were 16.7 ± 11.5 and 3.3 ± 2.9 (mean ± SD) (P = 0.001). Liver fat percentage was positively correlated with body mass index, waist circumference, and areas under the insulin curves of 2 h glucose tolerance tests, suggesting that obesity may affect the severity of liver fat accumulation in both groups. Despite 5-fold differences in liver fat percentage, mean values for obesity and insulin indexes were similar. Thus, for similar degrees of obesity, FHBL subjects have more hepatic fat. VLDL-triglyceride (TG)-fatty acids arise from plasma and nonplasma sources (liver and splanchnic tissues). To assess the relative contributions of each, [2H2] palmitate was infused over 12 h in 13 FHBL subjects and 11 controls. Isotopic enrichment of plasma free palmitate and VLDL-TG-palmitate was determined by mass spectrometry. Nonplasma sources contributed 51 ± 15% in FHBL and 37 ± 13% in controls (P = 0.02). Correlations of liver fat percentage and percent VLDL-TG-palmitate from liver were r = 0.89 (P = 0.0001) for FHBL subjects and r = 0.69 (P = 0.01) for controls. Thus, apoB truncation-producing mutations result in fatty liver and in altered assembly of VLDL-TG

Three-dimensional N=4 supersymmetry in harmonic N=3 superspace

We consider the map of three-dimensional N=4 superfields to N=3 harmonic superspace. The left and right representations of the N=4 superconformal group are constructed on N=3 analytic superfields. These representations are convenient for the description of N=4 superconformal couplings of the Abelian gauge superfields with hypermultiplets. We analyze the N=4 invariance in the non-Abelian N=3 Yang-Mills theory.Comment: Latex file, 22 pages; v2 two references adde

Replication of linkage of familial hypobetalipoproteinemia to chromosome 3p in six kindreds

Familial hypobetalipoproteinemia (FHBL) is a genetically heterogeneous condition characterized by very low apolipoprotein B (apoB) concentrations in plasma and/or low levels of LDL-cholesterol (LDL-C) with a propensity to developing fatty liver. In a minority of cases, truncation-specifying mutations of the apoB gene (APOB) are etiologic, but the genetic basis of most cases is unknown. We previously reported linkage of FHBL to a 10 cM region on 3p21.1-22 in one kindred. The objectives of the current study were to identify other FHBL families with linkage to 3p and to narrow the FHBL susceptibility region on 3p. Six additional FHBL kindreds unlinked to the APOB region on chromosome 2 were genotyped with polymorphic markers spanning a region of approximately 13 cM on chromosome 3. Quantitative linkage analyses indicated that the FHBL in these families was linked to 3p21.1-22. Haplotype analysis identified several meiotic crossover events, allowing us to narrow the critical region from 10 cM to 2.0 cM, between markers D3S2407 and D3S1767

Open Access Publishing in Business Research: The Authors’ Perspective

Open access (OA) publishing is now accepted as an integral part of the emerging trends within scholarly communication. Business librarians, like their subject specialist colleagues in other disciplines, are increasingly called upon to interpret scholarly communication trends to their faculty. This study surveys 1,293 business faculty from American schools of business accredited by the Association to Advance Collegiate Schools of Business. Issues explored include business faculty publishing practices within the discipline and how these affect academic advancement, obtaining articles for their own research, electronic publishing, self-archiving, and their perceptions about OA publishing generally.With support from the Emerald Publishing Research Award 2009

Failure of Gauge Invariance in the Nonperturbative Formulation of Massless Lorentz-Violating QED

We consider a Lorentz-violating modification to the fermionic Lagrangian of QED that is known to produce a finite Chern-Simons term at leading order. We compute the second order correction to the one-loop photon self-energy in the massless case using an exact propagator and a nonperturbative formulation of the theory. This nonperturbative theory assigns a definite value to the coefficient of the induced Chern-Simons term; however, we find that the theory fails to preserve gauge invariance at higher orders. We conclude that the specific nonperturbative value of the Chern-Simons coefficient has no special significance.Comment: 8 pages, very minor change

Estrogen Up-regulates Apolipoprotein E (ApoE) Gene Expression by Increasing ApoE mRNA in the Translating Pool via the Estrogen Receptor α-Mediated Pathway

The antiatherogenic property of estrogens is mediated via at least two mechanisms: first by affecting plasma lipoprotein profiles, and second by affecting the components of the vessel wall. Raising plasma apolipoprotein E (apoE) in mice protects them against diet-induced atherosclerosis (Shimano, H., Yamada, N., Katsuki, M., Gotoda, T., Harada, K., Murase, T., Fukuzawa, C., Takaku, F., and Yazaka, Y. (1992) Proc. Natl. Acad. Sci. U. S. A. 89, 1750-1754). It is possible that estrogen may be antiatherogenic at least in part by increasing plasma apoE levels. Therefore, we studied the regulation of apoE by estrogen. A survey of 15 inbred strains of mice showed that some mouse strains responded to injections or subcutaneously implanted pellets of estradiol by raising their apoB and apoE levels and some did not. We performed detailed studies in two "responder" strains, C57L and C57BL, and two "non-responder" strains, C3H and BALBc. Responders increased their plasma apoE levels 2.5-fold. Non-responders' levels were altered +/-10%. In the responders the distribution of apoE among the plasma lipoproteins shifted from high density lipoprotein toward the apoB-containing lipoprotein fractions. In nonresponders the shift was toward high density lipoprotein. Hepatic apoE mRNA levels and relative rates of apoE mRNA transcription were unchanged in all strains, suggesting that apoE regulation occurred at posttranscriptional loci. Therefore, we measured apoE synthesis in fresh liver slices and on isolated hepatic polysomes. Two-fold increases were noted but only in responders accompanied by selective 1.5-fold increases in polysomal apoE mRNA levels. Similar increases in apoE synthesis were also observed in castrated C57BL mice given either physiological or pharmacological replacement doses of estradiol, but not testosterone, suggesting that the effect of estradiol was specific on the distribution of apoE mRNA in the translationally active polysomal pool. Next, we examined whether the effects of estrogen on apoE translation were mediated by estrogen receptors (ER). ER-alpha knock-out mice and their wild-type littermates were administered estradiol. As expected, apoE levels and hepatic apoE synthesis increased more than 2-fold in the wild-type littermates, but only 20% increases in the plasma apoE and hepatic synthesis were observed in the ER knock-out mice. Hepatic apoE mRNA levels did not change in either the wild-type or the ER knock-out mice. Thus, estradiol up-regulates apoE gene expression by increasing levels of apoE mRNA in the polysomal translating pool. Furthermore, the increased polysomal recruitment of apoE mRNA is largely mediated by estrogen receptors

Exact calculation of the radiatively-induced Lorentz and CPT violation in QED

Radiative corrections arising from the axial coupling of charged fermions to a constant vector b_\mu can induce a Lorentz- and CPT-violating Chern-Simons term in the QED action. We calculate the exact one-loop correction to this term keeping the full b_\mu dependence, and show that in the physically interesting cases it coincides with the lowest-order result. The effect of regularization and renormalization and the implications of the result are briefly discussed.Comment: LaTex, 8 pages; minor correction

Central charge and renormalization in supersymmetric theories with vortices

Some quantum features of vortices in supersymmetric theories in 1+2 dimensions are studied in a manifestly supersymmetric setting of the superfield formalism. A close examination of the supercurrent that accommodates the central charge and super-Poincare charges in a supermultiplet reveals that there is no genuine quantum anomaly in the supertrace identity and in the supercharge algebra, with the central-charge operator given by the bare Fayet-Iliopoulos term alone. The central charge and the vortex spectrum undergo renormalization on taking the expectation value of the central-charge operator. It is shown that the vortex spectrum is exactly determined at one loop while the spectrum of the elementary excitations receives higher-order corrections.Comment: 9 pages, revte