Demokrati gennem sociokrati?

Der farer demokratiske vinde igennem arbejdslivet. Det er nyt. I mange år er udviklingen gået mod centraliseret styring og mere kontrol, og det gør den i vid udstrækning stadig. Men der tages nu også initiativer til forandring, der fører arbejdet i en mere demokratisk retning (Hvid, Møller & Ajslev, 2020; internationalt se fx #Democratizingwork eller Responsive.org). Der er veletablerede metoder, tilgange og traditioner for den centraliserede og hierarkiske ledelse, og det er svært at forestille sig en professionel organisation uden. Men i disse år sker der noget nyt. Der udvikles nu koncepter for etablering og udvikling af selvledende organisationer, hvor alle indgår i ledelse, og hvor ingen er dedikeret til ledelse (Lee & Edmondson, 2017). Vi vil her præsentere tre forbundne koncepter, der tilbyder udvikling af den selvledende organisation: sociokrati, holakrati og TEAL. De tre koncepter er tæt relaterede, og vi tillader os at præsentere dem under et. Sociokrati er det oprindelige begreb, som kan føres tilbage til ”sociologiens fader” Auguste Comte i 1850’erne. Vi tillader os derfor at ophøje sociokrati som den fælles betegnelse og holakrati og TEAL som varianter af sociokrati. Sociokratiet sætter i disse år sine spor, både i den private og den offentlige sektor. F.eks. afprøver flertallet af landets kommuner netop nu forsøg med at gøre hjemmeplejen (mere) selvledende. Inspirationen kommer fra den succesfulde hollandske virksomhed Buurtzog, der udbyder hjemmepleje på sociokratiske principper. Også inden for andre dele af den offentlige sektor afprøves sociokratiske idéer under paraplyen ”frisættelse af den offentlige sektor”. Hensigten er at tiltrække og fastholde medarbejdere, involvere borgerne og skabe mere individuelt tilpassede ydelser, som vi kommer ind på senere. Selv om sociokrati er et fænomen, der breder sig i disse år, har den akademiske interesse for fænomenet været begrænset indtil nu. I denne kronik vil vi præsentere, hvad sociokrati er – hvilket har vist sig ikke at være nogen let opgave. Vi er fuldt bevidste om, at én ting er idéen, noget andet er praksis, men vi tror, at afstanden mellem idé og praksis bliver større, hvis praksis slet ikke kender ideén. Derfor har vi sat os for at præsentere sociokratiet som idé og kun ganske kort nævne steder, hvor den sociokratiske idé afprøves

Treatment of wastewater solutions from anodizing industry by membrane distillation and membrane crystallization

The treatment of wastewater containing various metal ions is a challenging issue in the anodizing industry. The current study investigates the application of membrane distillation/crystallization (MD/MCr) for the simultaneous recovery of freshwater and sodium sulfate from wastewater originating from a Danish anodizing industry. MD/MCr experiments were performed on supernatant from wastewater obtained after centrifugation. The effect of various feed temperatures and cross-flow velocities on flux and crystal characteristics was investigated. The crystal growth in the feed tank was monitored through the use of an online PaticleView microscope. The crystals’ morphology and form were determined by using scanning electron microscope (SEM) and X-ray powder diffraction (XRD), respectively, while inductively coupled plasma (ICP) was applied to determine the purity of the obtained crystals. The weight and dimensions of the MD/MCr unit that were required to treat the specific amount of wastewater were evaluated as a function of the feed inlet temperature. It was demonstrated that the application of MCr allows extracting high-purity sodium sulfate crystals and more than 80% freshwater from the wastewater

Structural changes during water-mediated amorphization of semiconducting two-dimensional thiostannates

Owing to their combined open-framework structures and semiconducting properties, two-dimensional thio­stannates show great potential for catalytic and sensing applications. One such class of crystalline materials consists of porous polymeric [Sn$_3$S$_7$$^{2−}$]n sheets with molecular cations embedded in-between. The compounds are denoted R-SnS-1, where R is the cation. Dependent on the cation, some R-SnS-1 thio­stannates transition into amorphous phases upon dispersion in water. Knowledge about the fundamental chemical properties of the thio­stannates, including their water stability and the nature of the amorphous products, has not yet been established. This paper presents a time-resolved study of the transition from the crystalline to the amorphous phase of two violet-light absorbing thio­stannates, i.e. AEPz-SnS-1 [AEPz = 1-(2-amino­ethyl)­piperazine] and trenH-SnS-1 [tren = tris­(2-amino­ethyl)­amine]. X-ray total scattering data and pair distribution function analysis reveal no change in the local intralayer coordination during the amorphization. However, a rapid decrease in the crystalline domain sizes upon suspension in water is demonstrated. Although scanning electron microscopy shows no significant decrease of the micrometre-sized particles, transmission electron microscopy reveals the formation of small particles (∼200–400 nm) in addition to the larger particles. The amorphization is associated with disorder of the thio­stannate nanosheet stacking. For example, an average decrease in the interlayer distance (from 19.0 to 15.6 Å) is connected to the substantial loss of the organic components as shown by elemental analysis and X-ray photoelectron spectroscopy. Despite the structural changes, the light absorption properties of the amorphisized R-SnS-1 compounds remain intact, which is encouraging for future water-based applications of such materials

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

Semaglutide treatment attenuates vessel remodelling in ApoE-/- mice following vascular injury and blood flow perturbation.

BACKGROUND AND AIMS Randomized clinical studies have shown a reduction in cardiovascular outcomes with glucagon-like peptide 1 receptor agonist (GLP-1RA) treatment with the hypothesized mechanisms being an underlying effect on atherosclerosis. Here, we aimed to assess the pharmacological effects of semaglutide in an atheroprone murine model that recapitulates central mechanisms related to vascular smooth muscle cell (VSMC) phenotypic switching and endothelial dysfunction known to operate within the atherosclerotic plaque. METHODS In study A, we employed an electrical current to the carotid artery in ApoE-/- mice to induce severe VSMC injury and death, after which the arteries were allowed to heal for 4 weeks. In study B, a constrictive cuff was added for 6 h at the site of the healed segment to induce a disturbance in blood flow. RESULTS Compared to vehicle, semaglutide treatment reduced the intimal and medial area by ∼66% (p = 0.007) and ∼11% (p = 0.0002), respectively. Following cuff placement, expression of the pro-inflammatory marker osteopontin and macrophage marker Mac-2 was reduced (p < 0.05) in the semaglutide-treated group compared to vehicle. GLP-1R were not expressed in murine carotid artery and human coronary vessels with and without atherosclerotic plaques, and semaglutide treatment did not affect proliferation of cultured primary human VSMCs. CONCLUSIONS Semaglutide treatment reduced vessel remodelling following electrical injury and blood flow perturbation in an atheroprone mouse model. This effect appears to be driven by anti-inflammatory and -proliferative mechanisms independent of GLP-1 receptor-mediated signalling in the resident vascular cells. This mechanism of action may be important for cardiovascular protection.This study was supported by a grant from the LifePharm Centre of In Vivo Pharmacology.S

Progression of esophageal dysplasia to cancer

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108637/1/nyas12523.pd