Indflydelse i arbejdslivet – status, muligheder, alternativer?

I de formende konflikter på arbejdsmarkedet i slutningen af det 19. århundrede var indfl ydelse i arbejdet et centralt konfliktpunkt, i Danmark og i den industrialiserede verden i øvrigt. Arbejdsgivere og fagforeninger var i konflikt om, hvem der havde retten til at lede og fordele arbejdet. Med Septemberforliget i 1899 blev Danmark det første land i verden, hvor der blev indgået et nationalt kompromis om indfl ydelse. Arbejdsgiverne vandt ledelsesretten, og fagforeningerne vandt retten til at forhandle løn og arbejdsvilkår og indgå overenskomster om disse spørgsmål (Galeson, 1955, Christensen et al., 2015). Dermed var spørgsmålet om indflydelse dog langt fra afklaret. I årtierne efter Septemberforliget tilkæmpede fagforeningerne sig gradvist mere indflydelse. Indflydelsen på løn og arbejdsforhold blev udbygget. Overenskomstsystemet blev mere omfattende. Medarbejderne fik ret til at vælge tillidsrepræsentanter, som arbejdsgiverne havde pligt til at inddrage i beslutningsprocesserne. Samarbejdsudvalg og senere arbejdsmiljøudvalg blev etableret. Endelig fik medarbejdere i aktieselskaber ret til at vælge repræsentanter til selskabernes bestyrelser. I tiden efter 2. verdenskrig voksede en anden mere konsensusorienteret strømning til udvikling af indflydelse i arbejdet frem. Denne strømning har siden forgrenet sig i variationer og antaget mange forskellige navne, bl.a. Human Relations og Human Resources, Socioteknik, High Performance Work Systems samt Workplace Innovation. En af grundlæggerne var Kurt Lewin, som allerede i 1940erne blev kendt for sin formulering af principper for en involverende arbejdsorganisation og demokratisk ledelse (Lewin et al., 1939). Socioteknikken, som blev udviklet i 1950erne, havde som målsætning at udvikle en arbejdsorganisation, hvor hensynet til det sociale system og det teknisk/økonomiske system var ligeværdigt (Trist & Bamforth, 1951). En sådan ligeværdighed kunne etableres i en arbejdsorganisation, hvor medarbejderne havde en stor grad af autonomi i et gruppeorganiseret arbejde, samtidig med at medarbejderne havde ansvar overfor virksomheden

Decreased plasma levels of soluble CD18 link leukocyte infiltration with disease activity in spondyloarthritis

INTRODUCTION: Spondyloarthritis (SpA) comprises a group of diseases often associated with HLA-B27 and characterized by inflammation of the entheses and joints of the axial skeleton. The inflammatory process in SpA is presumably driven by innate immune cells but is still poorly understood. Thus, new tools for monitoring and treating inflammation are needed. The family of CD18 integrins is pivotal in guiding leukocytes to sites of inflammation, and CD18 hypomorphic mice develop a disease resembling SpA. Previously, we demonstrated that altered soluble CD18 (sCD18) complexes in the blood and synovial fluid of patients with arthritis have anti-inflammatory functions. Here, we study the mechanisms for these alterations and their association with SpA disease activity. METHODS: Plasma levels of sCD18 in a study population with 84 patients with SpA and matched healthy controls were analyzed with a time-resolved immunoflourometric assay (TRIFMA). Binding of sCD18 to endothelial cells and fibroblast-like synoviocytes (FLSs) was studied with confocal microscopy. Shedding of CD18 from peripheral blood mononuclear cells (PBMCs) was studied with flow cytometry and TRIFMA. RESULTS: Plasma levels of sCD18 were decreased in patients with SpA compared with healthy volunteers (P <0.001), and the lowest levels were in the HLA-B27-positive subgroup (P <0.05). In a multiple regression model, the sCD18 levels exhibited an inverse correlation with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) (P <0.05), the level of morning stiffness (P <0.05), the Bath Ankylosing Spondilitis Metrology Index (P <0.05), the physician global assessment score (P <0.01), and the sacroiliac magnetic resonance imaging activity score (P <0.05). The mechanisms for these changes could be simulated in vitro. First, sCD18 in plasma adhered to inflammation-induced intercellular adhesion molecule 1 (ICAM-1) on endothelial cells and FLS, indicating increased consumption. Second, CD18 shedding from SpA PBMCs correlated inversely with the BASDAI (P <0.05), suggesting insufficient generation. CD18 was shed primarily from intermediate CD14(++) CD16(+) monocytes, supporting the view that alterations in innate immunity can regulate the inflammatory processes in SpA. CONCLUSIONS: Taken together, the failure of patients with SpA to maintain adequate sCD18 levels may reflect insufficient CD18 shedding from monocytes to counterbalance the capture of sCD18 complexes to inflammation-induced ICAM-1. This could increase the availability of ICAM-1 molecules on the endothelium and in the synovium, facilitating leukocyte migration to the entheses and joints and aggregating disease activity

Current concepts in osteogenesis imperfecta:bone structure, biomechanics and medical management

The majority of patients with osteogenesis imperfecta (OI) have mutations in the COL1A1 or COL1A2 gene, which has consequences for the composition of the bone matrix and bone architecture. The mutations result in overmodified collagen molecules, thinner collagen fibres and hypermineralization of bone tissue at a bone matrix level. Trabecular bone in OI is characterized by a lower trabecular number and connectivity as well as a lower trabecular thickness and volumetric bone mass. Cortical bone shows a decreased cortical thickness with less mechanical anisotropy and an increased pore percentage as a result of increased osteocyte lacunae and vascular porosity. Most OI patients have mutations at different locations in the COL1 gene. Disease severity in OI is probably partly determined by the nature of the primary collagen defect and its location with respect to the C-terminus of the collagen protein. The overall bone biomechanics result in a relatively weak and brittle structure. Since this is a result of all of the above-mentioned factors as well as their interactions, there is - considerable variation between patients, and accurate prediction on bone strength in the individual patient with OI is difficult. Current treatment of OI focuses on adequate vitamin-D levels and interventions in the bone turnover cycle with bisphosphonates. Bisphosphonates increase bone mineral density, but the evidence on improvement of clinical status remains limited. Effects of newer drugs such as antibodies against RANKL and sclerostin are currently under investigation. This paper was written under the guidance of the Study Group Genetics and Metabolic Diseases of the European Paediatric Orthopaedic Society

Induction of Interferon-Stimulated Genes by Chlamydia pneumoniae in Fibroblasts Is Mediated by Intracellular Nucleotide-Sensing Receptors

BACKGROUND: Recognition of microorganisms by the innate immune system is mediated by pattern recognition receptors, including Toll-like receptors and cytoplasmic RIG-I-like receptors. Chlamydia, which include several human pathogenic species, are obligate intracellular gram-negative bacteria that replicate in cytoplasmic vacuoles. The infection triggers a host response contributing to both bacterial clearance and tissue damage. For instance, type I interferons (IFN)s have been demonstrated to exacerbate the course of Chlamydial lung infections in mice. METHODS/PRINCIPAL FINDINGS: Here we show that Chlamydia pneumoniae induces expression of IFN-stimulated genes (ISG)s dependent on recognition by nucleotide-sensing Toll-like receptors and RIG-I-like receptors, localized in endosomes and the cytoplasm, respectively. The ISG response was induced with a delayed kinetics, compared to virus infections, and was dependent on bacterial replication and the bacterial type III secretion system (T3SS). CONCLUSIONS/SIGNIFICANCE: Activation of the IFN response during C. pneumoniae infection is mediated by intracellular nucleotide-sensing PRRs, which operate through a mechanism dependent on the bacterial T3SS. Strategies to inhibit the chlamydial T3SS may be used to limit the detrimental effects of the type I IFN system in the host response to Chlamydia infection