Return-to-Work Coordinators' Perceptions of Their Roles Relative to Workers: A Discourse Analysis.

PURPOSE: This paper describes how Canadian Return to Work coordinators (RTWC) framed their job roles relative to workers in ways that went beyond the usual professional norms of helping worker recovery. METHODS: In-depth interviews were conducted with 47 RTWCs across Canada in 2018-2019. We used critical discourse analysis to analyze the way coordinators viewed workers in the complex, multi-stakeholder system of RTW. RESULTS: We identified four ways that RTWCs positioned themselves relative to workers: as trust builders, experts, detectives and motivators. These roles reflected RTWCs position within the system; however, their discourse also contributed to the construction of a moral hierarchy that valued worker motivation and framed some workers as attempting to exploit the RTW system. CONCLUSIONS: RTWCs' positions of power in the coordination process warrant further investigation of how they exercise judgement and discretion, particularly when the process depends on their ability to weigh evidence and manage cases in what might be seen as an objective and fair manner.

Systematic Review of the Impact on Return to Work of Return-to-Work Coordinators.

Purpose We conducted a systematic review to understand the impact that return-to-work coordinators (RTWCs) have on return to work (RTW) outcomes for sick/injured workers. Methods MEDLINE, EMBASE, CINAHL, PsycINFO, Web of Science, and ABI Inform were searched from January 1, 2000 to September 16, 2020. Of 2,927 retrieved and screened citations, 14 quantitative articles fulfilled the eligibility and quality criteria. Quality assessment, data extraction, and evidence synthesis followed article screening. Results We focused on the impact of RTWCs for outcomes of work absence, RTW rates, quality of life, and cost-benefit. Our final synthesis included 14 articles. We found strong evidence that work absence duration was reduced when workers had face-to-face contact with a RTWC. As well, there was strong evidence linking face-to-face RTWC interventions with higher RTW rates and moderate evidence that this reduced intervention costs. RTWC interventions involving the identification of barriers and facilitators to RTW also showed promising results. However, only limited evidence was found that RTWCs improved quality of life for workers. Conclusions Our synthesis identifies key features of RTW interventions that improve RTW outcomes. Future high-quality research should measure long-term outcomes of RTWC interventions to evaluate sustainability and consider the nature of work. They should also focus on RTWC impact on worker quality of life assessments and for older workers and workers with chronic health conditions.

Return to Work for Mental Ill-Health: A Scoping Review Exploring the Impact and Role of Return-to-Work Coordinators.

Purpose This scoping review was completed to explore the role and impact of having a return-to-work (RTW) coordinator when dealing with individuals with common mental ill-health conditions. Methods Peer reviewed articles published in English between 2000 and 2018 were considered. Our research team reviewed all articles to determine if an analytic focus on RTW coordinator and mental ill-health was present; consensus on inclusion was reached for all articles. Data were extracted for all relevant articles and synthesized for outcomes of interest. Results Our search of six databases yielded 1798 unique articles; 5 articles were found to be relevant. The searched yielded only quantitative studies. Of those, we found that studies grouped mental ill-health conditions together, did not consider quality of life, and used different titles to describe RTW coordinators. Included articles described roles of RTW coordinators but did not include information on their strategies and actions. Included articles suggest that RTW interventions for mental ill-health that utilize a RTW coordinator may result in delayed time to RTW. Conclusions Our limited findings suggest that interventions for mental ill-health that employ RTW coordinators may be more time consuming than conventional approaches and may not increase RTW rate or worker's self-efficacy for RTW. Research on this topic with long-term outcomes and varied research designs (including qualitative) is needed, as well as studies that clearly define RTW coordinator roles and strategies, delineate results by mental health condition, and address the impact of RTW coordinators on workers' quality of life.

The Populus holobiont: dissecting the effects of plant niches and genotype on the microbiome.

BACKGROUND: Microorganisms serve important functions within numerous eukaryotic host organisms. An understanding of the variation in the plant niche-level microbiome, from rhizosphere soils to plant canopies, is imperative to gain a better understanding of how both the structural and functional processes of microbiomes impact the health of the overall plant holobiome. Using Populus trees as a model ecosystem, we characterized the archaeal/bacterial and fungal microbiome across 30 different tissue-level niches within replicated Populus deltoides and hybrid Populus trichocarpa × deltoides individuals using 16S and ITS2 rRNA gene analyses. RESULTS: Our analyses indicate that archaeal/bacterial and fungal microbiomes varied primarily across broader plant habitat classes (leaves, stems, roots, soils) regardless of plant genotype, except for fungal communities within leaf niches, which were greatly impacted by the host genotype. Differences between tree genotypes are evident in the elevated presence of two potential fungal pathogens, Marssonina brunnea and Septoria sp., on hybrid P. trichocarpa × deltoides trees which may in turn be contributing to divergence in overall microbiome composition. Archaeal/bacterial diversity increased from leaves, to stem, to root, and to soil habitats, whereas fungal diversity was the greatest in stems and soils. CONCLUSIONS: This study provides a holistic understanding of microbiome structure within a bioenergy relevant plant host, one of the most complete niche-level analyses of any plant. As such, it constitutes a detailed atlas or map for further hypothesis testing on the significance of individual microbial taxa within specific niches and habitats of Populus and a baseline for comparisons to other plant species.

Enhancing patient-based learning: introducing STRAC and the reflective history template.

The University of New South Wales School of Rural Health, Australia, like many other rural clinical schools, relies heavily on patient-based learning which is largely serendipitous. The learning is not driven by courses of lectures but by the patients who become available in a variety of settings. Students, who, in their first 3 years have been exposed to a very structured didactic learning experience, start their rural experience in Year IV with a curriculum mainly concerned with general medicine and surgery. They have to learn to adapt to a largely self-directed model. While their rural clinical experience is very much broader than that of their city-based peers, an excellent feature, it engenders feelings of insecurity and a perceived need for students and faculty to have a method of tracking patient encounters so they can ensure the syllabus is covered. Early attempts with a paper-based system and later a Reflective Learning Diary proved unsuccessful. This article presents Syllabus Tracking (STRAC) together with a Reflective Case History Template which encourages reflective learning from patients encountered. STRAC is a web-based solution that includes a reporting function, and is easily modified to suit the needs of the curriculum. It is believed it may also prove useful for future applications. Most rural clinical schools in Australia are young, as are these tools. They are not formally evaluated but are offered to other schools as a suggestion.

Sarcoidosis of the thoracic and lumbar spine: imaging findings with an emphasis on magnetic resonance imaging.

Vertebral sarcoidosis is exceedingly rare with only a few cases reported in the published literature. The case of a 40-year-old man with vertebral sarcoidosis is presented, emphasizing the role of MRI and biopsy in confirming the diagnosis. A brief review of the published literature is also presented.

Insulin potentiates EGFR activation and signaling in fibroblasts.

Insulin is an essential hormone for cell growth and potentiates the mitogenic actions of multiple growth factors, including EGF. While potentiation has been shown to be mediated by the upregulation of the cyclin/CDK system, the upstream mechanisms of such synergy have not been elucidated. Our study has examined whether insulin could mediate synergy by enhancing early signaling events of the EGF receptor (EGFR). Tyrosine phosphorylation at the cell periphery of confluent Swiss 3T3 fibroblasts induced by EGF was potentiated by insulin within 2 min of stimulation. Insulin potentiation of EGF-mediated phosphorylation of the EGFR occurred 2 min after stimulation. EGFR transactivation by insulin was not observed. In addition, downstream mitogenic signaling events including ERK1/2 activation and Elk-1 phosphorylation were enhanced in response to insulin and EGF coadministration. This study shows mitogenic synergy between insulin and EGF can occur at the earliest signaling event, receptor phosphorylation, and independent of transactivation.

A randomized, controlled trial of tea tree topical preparations versus a standard topical regimen for the clearance of MRSA colonization.

Two topical MRSA eradication regimes were compared in hospital patients: a standard treatment included mupirocin 2% nasal ointment, chlorhexidine gluconate 4% soap, silver sulfadiazine 1% cream versus a tea tree oil regimen, which included tea tree 10% cream, tea tree 5% body wash, both given for five days. One hundred and fourteen patients received standard treatment and 56 (49%) were cleared of MRSA carriage. One hundred and ten received tea tree oil regimen and 46 (41%) were cleared. There was no significant difference between treatment regimens (Fisher's exact test; P = 0.0286). Mupirocin was significantly more effective at clearing nasal carriage (78%) than tea tree cream (47%; P = 0.0001) but tea tree treatment was more effective than chlorhexidine or silver sulfadiazine at clearing superficial skin sites and skin lesions. The tea tree preparations were effective, safe and well tolerated and could be considered in regimens for eradication of MRSA carriage.

The complex fibronectin--Trichomonas vaginalis interactions and Trichomonosis.

Trichomonosis is the vaginitis caused by Trichomonas vaginalis. This sexually transmitted agent achieves successful host parasitism through various means including: (1). acquisition of nutrients through specific receptors; (2). recognition and binding to mucin followed by cytoadherence mediated by adhesins that resemble metabolic enzymes; (3). evasion of immune responses through (i). masking of organisms by host proteins, (ii). shedding of trichomonad proteins into the secretions and (iii). secretions of cysteine proteinases that degrade all immunoglobulin subclasses and complement; (4). alternating surface expression of at least two antigen repertoires; and (5) alternate and coordinate expression of virulence genes in response to host environmental factors. The fact that the parasite survives long term in the varying and adverse environment of the vagina attests to the highly evolved nature of this protist. An understanding of the non-self-limiting nature of this infection may come from recent findings illustrating the complexity of Trichomonas vaginalis-fibronectin (FN) interactions. The parasite readily attaches to surfaces with immobilized FN and binds to FN in a highly specific receptor-mediated fashion. The amount and affinity of bound FN by live organisms is influenced by concentrations in medium of both iron and calcium. De novo protein synthesis is required for optimal FN acquisition in the presence of calcium. Furthermore, the parasites bind with differing affinities to the N-terminal domain (NTD), the cell-binding domain (CBD) and the gelatin-binding domain (GBD) of FN. Iron modulates binding of NTD similar to that of FN. This minireview summarizes recent findings on the T. vaginalis-FN associations.

The phosphoinositide 3-kinase and p70 S6 kinase regulate long-term potentiation in hippocampal neurons.

The mechanisms by which long-term changes in synaptic efficacy (e.g., long-term potentiation) are maintained are not well understood. There is evidence that reorganization of the neuronal actin cytoskeleton is important for consolidation of long-term potentiation. In non-neuronal cells, phosphoinositide 3-kinase and p70 S6 kinase have been shown to regulate actin polymerization. We have investigated the subcellular localization of these enzymes in cultured hippocampal pyramidal neurons and their possible role in hippocampal long-term potentiation. Immunohistochemical analysis revealed enrichment of both enzymes in the growth cones and filopodia of extending neurites, whereas p70 S6 kinase was also present at the soma. Antibodies to the phosphorylated form of p70 S6 kinase confirmed its activity in these locations. Interestingly, both enzymes displayed strong colocalization with F-actin in discrete regions of developing neurites. In hippocampal slices, the maintenance of long-term potentiation was attenuated by either rapamycin or 2-(4-morpholinyl)-8-phenyl-1(4H)-1-benzopyran-4-one, inhibitors of p70 S6 kinase and phosphoinositide 3-kinase, respectively. Our findings provide evidence for a novel biochemical pathway involving phosphoinositide 3-kinase and p70 S6 kinase that is important for the maintenance of hippocampal long-term potentiation, possibly via regulation of actin dynamics.

Differentiation of bipolar CG-4 line oligodendrocytes is associated with regulation of CREB, MAP kinase and PKC signalling pathways.

Undifferentiated bipolar CG-4 cell line oligodendrocytes provide a model system for the O-2A progenitor cell from which oligodendrocytes are derived both in vivo and in vitro. The exchange of neuroblastoma conditioned basal media for basal media causes differentiation of undifferentiated bipolar CG-4 cells into multipolar oligodendrocyte-like cells whilst replacement with basal media containing 20% foetal bovine serum favours the formation of type-2 astrocyte-like cells. Here, we demonstrate that activation of these differentiation pathways correlates with distinct changes both in cell metabolism and in signal transduction. Exchange of neuroblastoma conditioned media for basal media correlates with stimulation of basal metabolic activity, reduced phosphorylation of p44/42 MAP kinase and reduced phosphorylation of the transcription factor CREB. In contrast, differentiation with basal medium containing 20% foetal bovine serum (FBS), into type 2 astrocyte-like cells, correlates with reduction in basal metabolic activity, increased phosphorylation of p44/42 MAP kinase and increased phosphorylation of the transcription factor CREB. Inhibition of protein kinase C blocked both the metabolic and morphological changes associated with differentiation towards mature multipolar oligodendrocyte-like cells. Inhibition of PKA and MEK did not effect metabolic activity. The rapid return of neuroblastoma conditioned basal media to cells treated with basal media, increased phosphorylation of CREB and MAP kinase. These results demonstrate that protein kinase C and p44/42 MAP kinase signalling pathways are modulated during bipolar CG-4 cell differentiation and demonstrate that the transcription factor CREB may play a pivotal role in differentiation along oligodendrocyte-or astrocyte-lineages.

Lysophosphatidic acid activates the 70-kDa S6 kinase via the lipoxygenase pathway.

Many hormones are known to activate the 70-kDa S6 kinase (p70(S6K)). The signalling pathways mediating p70(S6K) activation are only partially characterized. We investigate, in this report, the mechanisms by which lysophosphatidic acid (LPA) activates p70(S6K). We observed that p70(S6K) activation was conventional, in that it was sensitive to both rapamycin and PI3 kinase inhibition. p70(S6K) activation appeared to be caused by the activation of several phospholipase pathways. LPA was an effective stimulus of phospholipase C induced intracellular calcium mobilization, which appeared to participate in p70(S6K) activation. Similarly, the effect of LPA on p70(S6K) activity was antagonized by butan-1-ol but not butan-2-ol suggesting the involvement of agonist stimulated phospholipase D activity. Further, antagonism of the phospholipase A(2) and lipoxygenase pathways attenuated p70(S6K) activation indicating a novel mechanism of p70(S6K) regulation. We conclude that in Swiss 3T3 cells LPA coordinates activation of several phospholipases to regulate p70(S6K).

MEK, ERK, and p90RSK are present on mitotic tubulin in Swiss 3T3 cells: a role for the MAP kinase pathway in regulating mitotic exit.

The mitogen-activated protein (MAP) kinase pathway has been implicated in cell cycle control for some time. Several reports have suggested a role for this pathway in growth factor stimulation of DNA synthesis, while other reports have proposed a role in the transition of cells through mitosis. Here, we have examined the potential involvement of the extracellular signal-related kinase (ERK)1/2 MAP kinases, their upstream regulators, and downstream effectors in the regulation of mitosis. Inhibition of MAP kinase/ERK kinase (MEK) activity reduced the serum-stimulated DNA synthesis and proliferation of Swiss 3T3 cells. To study the potential mechanisms of this effect, we examined the subcellular localization of members of the MAP kinase pathway including regulators (MEK1/2), substrates (90-kDa ribosomal S6 kinases (RSKs): RSK1, RSK2 and RSK3), and ERK itself. We show that there is enrichment of ERK, MEK, and the RSK enzymes on both the spindle and midbody tubulin of dividing cells. Inhibition of MEK1/2 activity in cells released from mitotic arrest results in an inability of cells to complete mitosis. This failure to exit mitosis correlated with altered cyclin-dependent kinase (cdk) activities. Thus, the MAP kinase pathway may act to coordinate passage through mitosis in Swiss 3T3 fibroblasts by regulation of cdk activity.

Binding of fibronectin by Trichomonas vaginalis is influenced by iron and calcium.

We have reported that Trichomonas vaginalis, the causative agent of the most common, non-viral sexually transmitted disease, bound to cover slips coated with fibronectin (FN) (Crouch & Alderete, Microbiol 1999 145: 2835-43). In this study, we extend that observation by showing that FN binding is specific, and we present data on the requirements of FN binding by T. vaginalis. Immunofluorescence and immuno-gold labelling readily detected FN throughout the trichomonal surface. Parasites bound to(125)I-labelled FN in a time- and concentration-dependent fashion. In the absence of protease inhibitor, iodinated FN was released from the trichomonad surface. Unlabelled FN specifically competed for binding in a concentration-dependent fashion with the(125)I-labelled FN. Interestingly, the amount of FN bound by T. vaginalis organisms was dependent on iron. High-iron-grown trichomonads acquired lower numbers of molecules but with 10-fold higher affinity than low-iron-grown organisms. Further, we show that for iron-replete organisms, calcium (Ca(2+)) at physiological levels increased amounts of bound FN. The increase in binding was rapid, occurring within 5 min of Ca(2+)addition, and required de novo protein synthesis. Co-incubation of live parasites with Ca(2+)in the presence of FN was necessary to increase the amount of FN bound. Treatment of trichomonads with okadaic acid, but not other phosphatase inhibitors, resulted in a 50% decrease in binding of FN, regardless of the presence of Ca(2+), suggesting a role for phosphatase in FN association. These results indicate that depending on the iron status of T. vaginalis organisms in vivo, Ca(2+)may influence trichomonad recognition and binding to FN during host parasitism.

Trichomonas vaginalis has two fibronectin-like iron-regulated genes.

BACKGROUND: Trichomonas vaginalis, a protozoan parasite of the human urogenital tract, interacts with fibronectin (FN), a glycoprotein of the extracellular matrix. We, therefore, attempted to identify genes of this eukaryote encoding FN-binding proteins. METHODS: A cDNA clone, C1, representing an incomplete gene was obtained from an expression library based on its FN-binding ability and was characterized. The full-length 378-bp gene encoding a 14.8-kDa protein of 125 amino acids was obtained. RESULTS: The amino acid sequences revealed homology with the type III-14 repeat of the heparin-binding domain at the carboxyl terminal end of FN. This fibronectin-like protein gene, flp1, was single copy in all the T. vaginalis isolates examined. Levels of flp1 transcript were elevated in cells grown under low-iron conditions. Another low-iron-regulated gene, flp2, with 70 and 67.5% identity to flp1 at the nucleotide and amino acid levels, respectively, was recovered from the trichomonad genome. Both flp1 and flp2 had consensus Inr promoter-like elements immediately adjacent to the start codon. flp2 also contained an additional Inr element followed by an ATG 24-bp within the gene. CONCLUSIONS: Unlike flp2, the flp1 gene had AU-rich destabilizing elements in the 3'-untranslated region (UTR).

Activation of endogenous thrombin receptors causes clustering and sensitization of epidermal growth factor receptors of swiss 3T3 cells without transactivation.

The G protein-coupled thrombin receptor can induce cellular responses in some systems by transactivating the epidermal growth factor (EGF) receptor. This is in part due to the stimulation of ectoproteases that generate EGF receptor ligands. We show here that this cannot account for the stimulation of proliferation or migration by thrombin of Swiss 3T3 cells. Thrombin has no direct effect on the activation state of the EGF receptor or of its downstream effectors. However, thrombin induces the subcellular clustering of the EGF receptor at filamentous actin-containing structures at the leading edge and actin arcs of migrating cells in association with other signaling molecules, including Shc and phospholipase Cgamma1. In these thrombin-primed cells, the subsequent migratory response to EGF is potentiated. Thrombin did not potentiate the EGF-stimulated EGF receptor phosphorylation. Thus, in Swiss 3T3 cells the G protein-coupled thrombin receptor can potentiate the EGF tyrosine kinase receptor response when activated by EGF, and this appears to be due to the subcellular concentration of the receptor with downstream effectors and not to the overall ability of EGF to induce receptor transphosphorylation. Thus, the EGF receptor subcellular localization which is altered by thrombin appears to be an important determinant of the efficacy of downstream EGF receptor signaling in cell migration.

Effective use of statins to prevent coronary heart disease.

Primary and secondary prevention trials have shown that use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (also known as statins) to lower an elevated low-density lipoprotein cholesterol level can substantially reduce coronary events and death from coronary heart disease. In 1987 and 1993, the National Cholesterol Education Program promulgated guidelines for cholesterol screening and treatment. Thus far, however, primary care physicians have inadequately adopted these guidelines in clinical practice. A 1991 study found that cholesterol screening was performed in only 23 percent of patients. Consequently, many patients with elevated low-density lipoprotein levels and a high risk of primary or recurrent ischemic events remain unidentified and untreated. A study published in 1998 found that fewer than 15 percent of patients with known coronary heart disease have low-density lipoprotein levels at the recommended level of below 100 mg per dL (2.60 mmol per L). By identifying patients with elevated low-density lipoprotein levels and instituting appropriate lipid-lowering therapy, family physicians could help prevent cardiovascular events and death in many of their patients.

The flightless I protein colocalizes with actin- and microtubule-based structures in motile Swiss 3T3 fibroblasts: evidence for the involvement of PI 3-kinase and Ras-related small GTPases.

The flightless I protein contains an actin-binding domain with homology to the gelsolin family and is likely to be involved in actin cytoskeletal rearrangements. It has been suggested that this protein is involved in linking the cytoskeletal network with signal transduction pathways. We have developed antibodies directed toward the leucine rich repeat and gelsolin-like domains of the human and mouse homologues of flightless I that specifically recognize expressed and endogenous forms of the protein. We have also constructed a flightless I-enhanced green fluorescent fusion vector and used this to examine the localization of the expressed protein in Swiss 3T3 fibroblasts. The flightless I protein localizes predominantly to the nucleus and translocates to the cytoplasm following serum stimulation. In cells stimulated to migrate, the flightless I protein colocalizes with beta-tubulin- and actin-based structures. Members of the small GTPase family, also implicated in cytoskeletal control, were found to colocalize with flightless I in migrating Swiss 3T3 fibroblasts. LY294002, a specific inhibitor of PI 3-kinase, inhibits the translocation of flightless I to actin-based structures. Our results suggest that PI 3-kinase and the small GTPases, Ras, RhoA and Cdc42 may be part of a common functional pathway involved in Fliih-mediated cytoskeletal regulation. Functionally, we suggest that flightless I may act to prepare actin filaments or provide factors required for cytoskeletal rearrangements necessary for cell migration and/or adhesion.

NASA strategic planning for 2000 and beyond.

This short paper outlines the United States National Aeronautics and Space Administration's development of its 2000 Strategic Plan.

Nuclear and cytoskeletal translocation and localization of heterotrimeric G-proteins.

Heterotrimeric GTP-binding proteins (G-proteins) are involved in a diverse array of signalling pathways. They are generally thought to be membrane-bound proteins, which disassociate on receptor activation and binding of GTP. A model to explain this has been proposed, which is often described as 'the G-protein cycle'. The 'G-protein cycle' is discussed in the present paper in relation to evidence that now exists regarding the non- membranous localization of G-proteins. Specifically, the experimental evidence demonstrating association of G-proteins with the cytoskeleton and the nucleus, and the mechanisms by which G-proteins translocate to these sites are reviewed. Furthermore, the possible effector pathways and the physiological function of G-proteins at these sites are discussed.