Inter-physician agreement on the readiness of sick-listed employees to return to work

Purpose: To determine the agreement between occupational physician (OP) ratings of an employee's readiness to return to work (RRTW). Method: Anonymized written vignettes of 132 employees, sick-listed for at least 3 weeks, were reviewed by 5 OPs. The OPs intuitively rated RRTW as the ability (knowledge and skills) and willingness (motivation and confidence) of sick-listed employees to resume work. Inter-OP percentages of agreement were calculated and Cohen's kappas (kappa) were determined to correct for agreement by chance. Results: The percentage of agreement between OPs was 57% (range 39-89%) on the ability and 63% (range 48-87%) on the willingness of sick-listed employees to resume work. The mean. was 0.14 (range from -0.21 to 0.79) for ability and 0.25 (range from -0.11 to 0.74) for willingness. The OP-rating of RRTW of employees sick-listed with mental disorders did not differ from the OP-rating of RRTW of employees with musculoskeletal disorders. Conclusion: The inter-OP agreement on intuitively rated RRTW showed a wide variability, which accentuates the need for instruments to establish an employee's RRTW and for training in giving well founded return to work recommendations

Sickness absence frequency among women working in hospital care

Background Frequent short sickness absences result in understaffing and interfere with work processes. We need more knowledge about factors associated with this type of absence. Aims To investigate associations between the frequency of previous sickness absence and self-reported perceptions of health and work. Methods Cross-sectional study of female hospital care workers in which health, work characteristics and coping styles were assessed by questionnaire and linked to the number of sickness absence episodes recorded in the preceding 5 years using negative binomial regression analysis for counts distinguishing between short (1-7 days) and long (>7 days) episodes of absence after adjusting for age and duration of employment in December 2007 and hours worked between 2003 and 2007. Results Of 350 women employed for at least 5 years, 237 (68%) answered the questionnaire. The hours worked over the 5 year period [rate ratio (RR) = 1.2] and problem solving coping style score (RR = 1.1) were positively associated with the number of short sickness absence episodes. Age (RR = 0.8) and good general health (RR = 0.7) were inversely related to the number of both short and long episodes. Self-reported mental health and work characteristics were not shown to be related to the frequency of sickness absence. Conclusions Hours worked, problem-solving coping style, age and general health showed associations with the frequency of previous sickness absence among women who had worked at least 5 years in health care. Future prospective studies on the frequency of sickness absence should consider the impact of these factors further

Coping styles relate to health and work environment of Norwegian and Dutch hospital nurses:A comparative study

Nurses exposed to high nursing stress report no health complaints as long as they have high coping abilities. The purpose of this study was to investigate coping styles in relation to the health status and work environment of Norwegian and Dutch hospital nurses. This comparative study included a random sample of 5400 Norwegian nurses and a convenience sample of 588 Dutch nurses. Coping, health, and work environment were assessed by questionnaire in both samples and associations were investigated bivariately and multi-variately. We found that active problem-solving coping was associated with the health and work environment of Norwegian nurses but not with the health and work environment of Dutch. Passive coping (avoiding problems or waiting to see what happens) was found to relate to poor general health, poor mental health, low job control, and low job support in both Norwegian and Dutch nurses. Improvements in the nursing work environment may not only result in better mental health, but may also reduce passive coping

Modifications of the endosomal compartment in peripheral blood mononuclear cells and fibroblasts from Alzheimer’s disease patients

International audienceIdentification of blood-based biomarkers of Alzheimer’s disease (AD) remains a challenge. Neuropathological studies have identified enlarged endosomes in post-mortem brains as the earliest cellular change associated to AD. Here the presence of enlarged endosomes was investigated in peripheral blood mononuclear cells from 48 biologically defined AD patients (25 with mild cognitive impairment and 23 with dementia (AD-D)), and 23 age-matched healthy controls using immunocytochemistry and confocal microscopy. The volume and number of endosomes were not significantly different between AD and controls. However, the percentage of cells containing enlarged endosomes was significantly higher in the AD-D group as compared with controls. Furthermore, endosomal volumes significantly correlated to [C11]PiB cortical index measured by positron emission tomography in the AD group, independently of the APOE genotype, but not to the levels of amyloid-beta, tau and phosphorylated tau measured in the cerebrospinal fluid. Importantly, we confirmed the presence of enlarged endosomes in fibroblasts from six unrelated AD-D patients as compared with five cognitively normal controls. This study is the first, to our knowledge, to report morphological alterations of the endosomal compartment in peripheral cells from AD patients correlated to amyloid load that will now be evaluated as a possible biomarker

Architecture and dynamics of the jasmonic acid gene regulatory network

Jasmonic acid (JA) is a critical hormonal regulator of plant growth and defense. To advance our understanding of the architecture and dynamic regulation of the JA gene regulatory network, we performed a high-resolution RNA-seq time series of methyl JA-treated Arabidopsis thaliana at 15 time points over a 16-h period. Computational analysis showed that methyl JA (MeJA) induces a burst of transcriptional activity, generating diverse expression patterns over time that partition into distinct sectors of the JA response targeting specific biological processes. The presence of transcription factor (TF) DNA binding motifs correlated with specific TF activity during temporal MeJA-induced transcriptional reprogramming. Insight into the underlying dynamic transcriptional regulation mechanisms was captured in a chronological model of the JA gene regulatory network. Several TFs, including MYB59 and bHLH27, were uncovered as early network components with a role in pathogen and insect resistance. Analysis of subnetworks surrounding the TFs ORA47, RAP2.6L, MYB59, and ANAC055, using transcriptome profiling of overexpressors and mutants, provided insights into their regulatory role in defined modules of the JA network. Collectively, our work illuminates the complexity of the JA gene regulatory network, pinpoints and validates previously unknown regulators, and provides a valuable resource for functional studies on JA signaling components in plant defense and development

Effects of intranasal TNFα on granulocyte recruitment and activity in healthy subjects and patients with allergic rhinitis

<p>Abstract</p> <p>Background</p> <p>TNFα may contribute to the pathophysiology of airway inflammation. For example, we have recently shown that nasal administration of TNFα produces late phase co-appearance of granulocyte and plasma exudation markers on the mucosal surface. The objective of the present study was to examine indices of granulocyte presence and activity in response to intranasal TNFα challenge.</p> <p>Methods</p> <p>Healthy subjects and patients with allergic rhinitis (examined out of season) were subjected to nasal challenge with TNFα (10 μg) in a sham-controlled and crossover design. Nasal lavages were carried out prior to and 24 hours post challenge. Nasal biopsies were obtained post challenge. Nasal lavage fluid levels of myeloperoxidase (MPO) and eosinophil cationic protein (ECP) were analyzed as indices of neutrophil and eosinophil activity. Moreover, IL-8 and α₂-macroglobulin were analyzed as markers of pro-inflammatory cytokine production and plasma exudation. Nasal biopsy numbers of neutrophils and eosinophils were monitored.</p> <p>Results</p> <p>Nasal lavage fluid levels of MPO recorded 24 hours post TNFα challenge were increased in healthy subjects (p = 0.0081) and in patients with allergic rhinitis (p = 0.0081) (<it>c.f</it>. sham challenge). Similarly, α₂-macroglobulin was increased in healthy subjects (p = 0.014) and in patients with allergic rhinitis (p = 0.0034). Lavage fluid levels of ECP and IL-8 were not affected by TNFα challenge. TNFα increased the numbers of subepithelial neutrophils (p = 0.0021), but not the numbers of eosinophils.</p> <p>Conclusion</p> <p>TNFα produces a nasal inflammatory response in humans that is characterised by late phase (i.e., 24 hours post challenge) neutrophil activity and plasma exudation.</p

ParadisEO-MOEO: A Software Framework for Evolutionary Multi-Objective Optimization

This chapter presents ParadisEO-MOEO, a white-box object-oriented software framework dedicated to the flexible design of metaheuristics for multi-objective optimization. This paradigm-free software proposes a unified view for major evolutionary multi-objective metaheuristics. It embeds some features and techniques for multi-objective resolution and aims to provide a set of classes allowing to ease and speed up the development of computationally efficient programs. It is based on a clear conceptual distinction between the solution methods and the problems they are intended to solve. This separation confers a maximum design and code reuse. This general-purpose framework provides a broad range of fitness assignment strategies, the most common diversity preservation mechanisms, some elitistrelated features as well as statistical tools. Furthermore, a number of state-of-the-art search methods, including NSGA-II, SPEA2 and IBEA, have been implemented in a user-friendly way, based on the fine-grained ParadisEO-MOEO components

Cell-type specific transcriptomics reveals roles for root hairs and endodermal barriers in interaction with beneficial rhizobacterium

Growth-promoting bacteria can boost crop productivity in a sustainable way. Pseudomonas simiae WCS417 is a well-studied bacterium that promotes growth of many plant species. Upon colonization, WCS417 affects root system architecture resulting in an expanded root system. Both immunity and root system architecture, are controlled by root-cell-type specific biological mechanisms, but it is unknown how WCS417 affects these mechanisms. Therefore, here, we transcriptionally profiled five Arabidopsis thaliana root cell types following WCS417 colonization. The cortex and endodermis displayed the most differentially expressed genes, even though they were not in direct contact with this epiphytic bacterium. Many of these genes are associated with reduced cell wall biogenesis, possibly facilitating the root architectural changes observed in WCS417-colonized roots. Comparison of the transcriptome profiles in the two epidermal cell types that were in direct contact with WCS417 -- trichoblasts that form root hairs and atrichoblasts that do not -- imply functional specialization. Whereas basal expression levels of nutrient uptake-related genes and defense-related genes are highest in trichoblasts and atrichoblasts, respectively, upon exposure to WCS417 these roles revert. This suggests that root hairs participate in the activation of root immunity, further supported by attenuation of immunity in a root hairless mutant. Furthermore, we observed elevated expression of suberin biosynthesis genes and increased deposition of suberin in the endodermis in WCS417-colonized roots. Using an endodermal barrier mutant we show the importance of endodermal barrier integrity for optimal plant-beneficial bacterium association. Altogether, we highlight the strength of cell-type-specific transcriptional profiling to uncover masked biological mechanisms underlying successful plant-microbe associations

Vascular Endothelial Growth Factor (VEGF) isoform expression and activity in human and murine lung injury

<p>Abstract</p> <p>Background</p> <p>The properties of vascular endothelial growth factor (VEGF) as a potent vascular permogen and mitogen have led to investigation of its potential role in lung injury. Alternate spliced VEGF transcript generates several isoforms with potentially differing functions. The purpose of this study was to determine VEGF isoform expression and source in normal and ARDS subjects and investigate the expression and regulation of VEGF isoforms by human alveolar type 2 (ATII) cells.</p> <p>Methods</p> <p>VEGF protein expression was assessed immunohistochemically in archival normal and ARDS human lung tissue. VEGF isoform mRNA expression was assessed in human and murine lung tissue. Purified ATII cells were cultured with proinflammatory cytokines prior to RNA extraction/cell supernatant sampling/proliferation assay.</p> <p>Measurements and Main Results</p> <p>VEGF was expressed on alveolar epithelium, vascular endothelium and alveolar macrophages in normal and ARDS human lung tissue. Increases in VEGF expression were detected in later ARDS in comparison to both normal subjects and early ARDS (p < 0.001). VEGF₁₂₁, VEGF₁₆₅and VEGF₁₈₉isoform mRNA expression increased in later ARDS (p < 0.05). The ratio of soluble to cell-associated isoforms was lower in early ARDS than normal subjects and later ARDS and also in murine lung injury. ATII cells constitutionally produced VEGF₁₆₅and VEGF₁₂₁protein which was increased by LPS (p < 0.05). VEGF₁₆₅upregulated ATII cell proliferation (p < 0.001) that was inhibited by soluble VEGF receptor 1 (<it>sflt</it>) (p < 0.05).</p> <p>Conclusion</p> <p>These data demonstrate that changes in VEGF isoform expression occur in ARDS which may be related to their production by and mitogenic effect on ATII cells; with potentially significant clinical consequences.</p

Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells

BACKGROUND: Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. METHODS: Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. RESULTS: RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. CONCLUSION: RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling