Professionele ruimte en gespreid leiderschap

Professionele ruimte voor leraren staat hoog op de politieke agenda. Op dit moment is er een wetsvoorstel over dit thema in behandeling bij de Tweede Kamer. Professionele ruimte zou moeten leiden tot een grotere inhoudelijke ontwikkelingstaak van leraren, en tot meer reflectie en ideeënuitwisseling. Professionele ruimte is daarmee direct gekoppeld aan vraagstukken rond de professionele ontwikkeling van leraren. Hoe professionele ruimte vorm moet krijgen, is echter de vraag. Uit diverse onderzoeken blijkt dat de rol van de leidinggevende cruciaal is, maar hoe die rol er precies uitziet is onduidelijk. Er is behoefte aan een nieuw type onderzoek naar de wijze waarop leraren professionele ruimte krijgen en nemen.\ud Deze reviewstudie heeft als doel om het perspectief van gespreid leiderschap nader te duiden en in verband te brengen met de professionele ruimte die leraren ervaren in scholen. De literatuur rondom gespreid leiderschap en professionele ruimte wordt verkend en er wordt een conceptueel model voorgesteld om deze begrippen met elkaar in verband te brengen. Op basis hiervan wordt toegewerkt naar een ontwerp van een praktijknabij onderzoeksinstrument om dit verband inzichtelijk te maken

Continuous registration of thrombin generation in plasma:Its use for the determination of the thrombin potential

A method is described by which the time-course of thrombin generation in plasma can be obtained from a continuous optical density recording of p-nitroaniline (pNA) production in a 2:3 diluted plasma. A chromogenic substrate, methylmalonyl-methylanalyl-arginyl-pNA (SQ 68), is used that is specifically split by thrombin but at a low rate. The thrombin that appears and disappears in the plasma does not split more than 5% of the substrate added, so the rate of substrate conversion is in good approximation proportional to the amidolytic activity in the plasma over the entire period of thrombin generation. The course of the enzyme concentration can be calculated from the amidolytic activity curve. It is shown that the thrombin generation curves obtained in this way are essentially identical to those obtained via the classical subsampling method.The presence of SO 68 influences the amount of free thrombin that appears in plasma because it competitively inhibits the inactivation of thrombin by AT III and alpha2 macroglobulin. The inhibition of the thrombin peak by heparin, relative to an uninhibited control, remains unaltered by the presence of the substrate.From the course of thrombin activity and the prevailing decay constants, the course of prothrombin conversion velocity can be calculated. Prothrombin conversion was seen to be inhibited at high (>500 muM) substrate concentrations only, and experimental conditions are found under which the inhibition of the clotting process by the substrate is negligible.The amidolytic activity is the sum of the activities of free thrombin and of the alpha2 macroglobulin-thrombin complex formed. Via a mathematical procedure the amount of SQ 68 that has been split by thrombin alone and not by the alpha2 macroglobulin-thrombin complex, can be derived from the course of the optical density.The total amount of SQ 68 eventually split by thrombin alone is proportional to the surface under the thrombin generation curve, i. e. to the time-integral of free thrombin. This value, that we call the thrombin potential (TP), directly indicates how much of any physiological substrate can potentially be split by the thrombin being generated in the plasma

GluR1 links structural and functional plasticity at excitatory synapses

Long-term potentiation (LTP), a cellular model of learning and memory, produces both an enhancement of synaptic function and an increase in the size of the associated dendritic spine. Synaptic insertion of AMPA receptors is known to play an important role in mediating the increase in synaptic strength during LTP, whereas the role of AMPA receptor trafficking in structural changes remains unexplored. Here, we examine how the cell maintains the correlation between spine size and synapse strength during LTP. We found that cells exploit an elegant solution by linking both processes to a single molecule: the AMPA-type glutamate receptor subunit 1 (GluR1). Synaptic insertion of GluR1 is required to permit a stable increase in spine size, both in hippocampal slice cultures and in vivo. Synaptic insertion of GluR1 is not sufficient to drive structural plasticity. Although crucial to the expression of LTP, the ion channel function of GluR1 is not required for the LTP-driven spine size enhancement. Remarkably, a recombinant cytosolic C-terminal fragment (C-tail) of GluR1 is driven to the postsynaptic density after an LTP stimulus, and the synaptic incorporation of this isolated GluR1 C-tail is sufficient to permit spine enlargement even when postsynaptic exocytosis of endogenous GluR1 is blocked. We conclude that during plasticity, synaptic insertion of GluR1 has two functions: the established role of increasing synaptic strength via its ligand-gated ion channel, and a novel role through the structurally stabilizing effect of its C terminus that permits an increase in spine size

Measurement of thrombin generation in whole blood:The effect of heparin and aspirin

A technique has been developed to monitor the development of thrombin in freshly collected whole blood in the absence of anticoagulants. It is based on the centrifugal separation of the cellular components from subsamples of blood drawn from non-anticoagulated clotting whole blood which are diluted in buffer containing a chromogenic substrate.It is shown that the burst of thrombin generation after triggering coagulation with trace amounts of tissue thromboplastin occurs sooner in non-anticoagulated whole blood than in citrated whole blood. Heparin is shown to prolong the lag-time of thrombin generation more in native blood than in recalcified citrated blood.It is also demonstrated that intake of 500 mg of aspirin significantly delays and inhibits thrombin generation in non-anticoagulated, thromboplastin triggered whole blood, whereas it has no effect on the coagulation in citrated plasma. The effect of aspirin intake on thrombin generation in blood is roughly equal to that of 0.03 U/ml of unfractionated heparin. This demonstrates that platelet reactions and the coagulation system are closely linked processes. It further lends support to the hypothesis that inhibition of thrombin generation is a common denominator of antithrombotic therapy