Research through a camera lens : a rhizomatic search for Lode’s Code

Every family culture is ruled by unspoken codes. Throughout the short film Lode's Code, Marieke Vandecasteele (the first author) searches for these codes within her own family in a visual-ethnographic way. In traditional research, families with a family member with a disability are often pinned down to individual categories linked with linear explanations. Vandecasteele's search for the code of her brother Lode and for her own position in the parental nest-with leaving home as a red thread-resulted in a hybrid animated documentary where subjective experiences prevail over the search for explanations. It shows how layered codes intra-act in the family machine and can (be) move(d). This paper focuses on the rhizomatic process of making the film. How were the keys to Vandecasteele's family code shaped and what was the role of animation film as a medium? An in-depth discussion shows how poetic research of this kind offers opportunities within the interdisciplinary research domain of Disability Studies to let the complexity inherent to a family with a member with a disability emerge in all its richness and multilayeredness

Rethinking agency as an assemblage from change management to collaborative work

The movement towards inclusion comes together with a neoliberal audit mentality whereby individuals are held responsible for the transformations. The Special Educational Needs Coordinators (SENCOs) are seen as change agents' whose task it is, to support teachers in adapting their approach to optimise the chances for children with special needs in regular schools. In this paper, we want to problematise the responsibility-blame discourse' and look differently at agency. By using a diffractive methodology based on collaborative work, in which we have used material images of the workplace of the SENCO, and read-the-data-while-thinking-with-theory, we deconstruct the individualisation of agency. The SENCOs are no longer seen as separate individual humanist subjects where agency is solely lodged in the body of an individual agent [Barad, K.2007. Meeting the Universe Halfway: Quantum Physics and the Entanglement of Matter and Meaning. Durham: Duke University Press] but the SENCOs are part of the intra-active entanglement of multiple agencies, of an assemblage. This re-conceptualisation of agency leads to a different approach to inclusion, in which the participants in any encounter can work as part of the assemblage to develop communities capable of re-thinking practice and transforming it into a place where children with special needs become legitimate members of the school

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Hilbrand De Vuyst Hout werkt. [Wood Works.]Slechts luttele personen stellen zich vermoedelijk een dergelijke vraag bij een molenbezoek. Zo vervreemd zijn we nu van het traditionele molenmakersambacht. Toch bepaalt nog steeds deze of gene afwerkingstechniek de belevingswaarde van het houten monument, zo verzekert ons Hilbrand De Vuyst, gespecialiseerd erfgoed-consulent. Voor omgang met hout is een grote vakkennis vereist. Molens vormen een ware encyclopedie van de houten bouw- en werktuigkunde. Ze zijn het product van intensief agrarisch en ambachtelijk genie. Met de molenrestauraties van de laatste jaren wordt opnieuw een aanzienlijke ambachtelijke kennis vergaard. Onze kennis neemt weer toe: vast en zeker, hout werkt.Dieter Nuytten Middeleeuwse dakkappen in het voormalige Hertogdom Brabant. [Mediaeval roof trusses in the former dukedom of Brabant.]Bij de middeleeuwse dakkappen van het voormalige hertogdom Brabant herkent men ruwweg twee -technologische groepen: sporenkappen en kappen met gebinten. Dieter Nuytten verkent een aantal Vlaams-Brabantse dakstructuren en stuit hierbij op dateringsmoeilijkheden. Een dendrochronologische datering kan in principe uitsluitsel geven over de precieze ouderdom van de houten structuren, maar er blijven nog tal van probleemgevallen. Vooral de Vlaamse eiken van vroeger geven hun leef-tijd niet prijs. Lokaal hout uit open bossen heeft immers een afwijkend groeipatroon.Inge Debacker Het behoud van houten buitenschrijnwerk: ramen. [The conservation of exterior woodwork: casements.]Houten ramen zijn kwetsbaar, ramen ouder dan de 18de eeuw zijn bijgevolg zelfs in historische gebouwen uiterst zeldzaam. Door de huidige isolatie-eisen, voortspruitend uit het begrip duurzaam bouwen, krijgt historisch raamwerk het bovendien steeds harder te verduren.Na een korte schets van de stilistische evolutie van 18de en 19de-eeuwse houten ramen, worden door Inge Debacker oplossingen tot behoud van historisch schrijnwerk aangereikt. Ze laat zich hierbij onder meer leiden door praktijkvoorbeelden uit Vlaams-Brabant. Ze illustreert treffend dat het begrip duurzaamheid verschillende ladingen dekt.Rudiger Van Hove De doelse Kogge(n). Maritiem erfgoed van Europees formaat. [The Doel cog, maritime heritage of european value.]In een geul in Doelpolder, de Deurganck of het Groot Gat, vindt men in september 2000 bij graafwerken een archeologische verrassing van formaat, een eikenhouten kogge van ruim 20 meter lang die uitzonderlijk goed is bewaard gebleven.De eertijds in dit gat geslagen en nu vakkundig opgegraven, geregistreerde en geborgen Doelse kogge is het centrale onderwerp van de bijdrage van Rudiger Van Hove, hoofd van de Archeologische Dienst Waasland. Samen met de beschrijving van het opgegraven maritiem erfgoed worden ook het onderzoekskader, de eigendom, het beheer en de diverse verantwoordelijkheden deskundig toegelicht.De auteur besluit met: wordt vervolgdSummar

Amyloid β oligomers disrupt blood-CSF barrier integrity by activating matrix metalloproteinases

The blood-CSF barrier (BCSFB) consists of a monolayer of choroid plexus epithelial (CPE) cells that maintain CNS homeostasis by producing CSF and restricting the passage of undesirable molecules and pathogens into the brain. Alzheimer's disease is the most common progressive neurodegenerative disorder and is characterized by the presence of amyloid beta (A beta) plaques and neurofibrillary tangles in the brain. Recent research shows that Alzheimer's disease is associated with morphological changes in CPE cells and compromised production of CSF. Here, we studied the direct effects of A beta on the functionality of the BCSFB. Intracerebroventricular injection of A beta 1-42 oligomers into the cerebral ventricles of mice, a validated Alzheimer's disease model, caused induction of a cascade of detrimental events, including increased inflammatory gene expression in CPE cells and increased levels of proinflammatory cytokines and chemokines in the CSF. It also rapidly affected CPE cell morphology and tight junction protein levels. These changes were associated with loss of BCSFB integrity, as shown by an increase in BCSFB leakage. A beta 1-42 oligomers also increased matrix metalloproteinase (MMP) gene expression in the CPE and its activity in CSF. Interestingly, BCSFB disruption induced by A beta 1-42 oligomers did not occur in the presence of a broad-spectrum MMP inhibitor or in MMP3-deficient mice. These data provide evidence that MMPs are essential for the BCSFB leakage induced by A beta 1-42 oligomers. Our results reveal that Alzheimer's disease-associated soluble A beta 1-42 oligomers induce BCSFB dysfunction and suggest MMPs as a possible therapeutic target

MMP-3 deficiency alleviates endotoxin-induced acute inflammation in the posterior eye segment

Matrix metalloproteinase-3 (MMP-3) is known to mediate neuroinflammatory processes by activating microglia, disrupting blood-central nervous system barriers and supporting neutrophil influx into the brain. In addition, the posterior part of the eye, more specifically the retina, the retinal pigment epithelium (RPE) and the blood-retinal barrier, is affected upon neuroinflammation, but a role for MMP-3 during ocular inflammation remains elusive. We investigated whether MMP-3 contributes to acute inflammation in the eye using the endotoxin-induced uveitis (EIU) model. Systemic administration of lipopolysaccharide induced an increase in MMP-3 mRNA and protein expression level in the posterior part of the eye. MMP-3 deficiency or knockdown suppressed retinal leukocyte adhesion and leukocyte infiltration into the vitreous cavity in mice subjected to EIU. Moreover, retinal and RPE mRNA levels of intercellular adhesion molecule 1 (Icam1), interleukin 6 (Il6), cytokine-inducible nitrogen oxide synthase (Nos2) and tumor necrosis factor alpha (Tnf alpha), which are key molecules involved in EIU, were clearly reduced in MMP-3 deficient mice. In addition, loss of MMP-3 repressed the upregulation of the chemokines monocyte chemoattractant protein (MCP)-1 and (C-X-C motif) ligand 1 (CXCL1). These findings suggest a contribution of MMP-3 during EIU, and its potential use as a therapeutic drug target in reducing ocular inflammation

A defective cerebellar morphogenesis in mice deficient for matrix metalloproteinase-3.

Matrix metalloproteinases (MMPs) belong to a large family of endopeptidases able to cleave all matrix proteins and to (in)activate important signaling molecules. As such, MMPs contribute to a wide variety of biological processes, both under physiological and pathophysiological circumstances. Besides their frequently reported detrimental role in neurological diseases, it is becoming increasingly clear that these proteinases are also supporting development, functioning and repair in the central nervous system (CNS). As MMPs can be both friends and foes in the CNS, the challenges for a better understanding of the MMP biology in specific conditions are considerable, especially in order to wisely apply non-selective/selective MMP inhibitors as potential therapeutic drugs. MMP-3 has a very broad degradome, indicating its importance in mediating a wide range of processes. Importantly, MMP-3 has been shown to contribute to many pathologies such as cancer, asthma and rheumatoid arthritis and has also been associated with neurodegenerative diseases. As such, MMP-3 supports neuroinflammation and neuronal apoptosis and contributes to the pathogenesis of Parkinson s and Alzheimer s disease. However, MMP-3 also seems to be involved in neurite outgrowth, axonal guidance and plasticity in the CNS. To further unravel a role for MMP-3 in brain development and neuronal wiring, we choose the cerebellar cortex as model system, mainly because of its rather simple anatomy and well-known circuitry. MMP-2, -3, -9 and MT5-MMP are known to be expressed in the developing rat cerebellum, yet, only MMP-9 has been functionally investigated in more detail. Here, we aimed to analyse the spatiotemporal expression pattern of MMP-3 during postnatal mouse development and to characterize a possibly altered cerebellar phenotype and behavior in mice deficient for MMP-3. Moreover, we tried to define the molecular mechanisms via which MMP-3 regulates neural pattern formation and wiring in the mouse cerebellum.RT-PCR and immunohistochemistry revealed increased MMP-3 mRNA and protein levels from the second postnatal week on, with most prominent staining in Purkinje cells (PCs). Histomorphometric investigations showed, from postnatal day 8 (P8) on, a thicker external granular layer (EGL) and an increased number of granule cells (GCs) in the EGL of MMP-3-/- cerebella, as compared to wild-type (WT) cerebella. No abnormalities in GC proliferation or GC apoptosis in the EGL were found. BrdU pulse studies combined with TAG-1 and p27 immunostainings revealed a stalling of radially migrating GCs in the deeper EGL between P6 and P8. In addition, prolonged parallel fibers and an increased number of migrating GCs, processes which possibly underlie the delayed radial GC migration, were found in ex vivo cerebellar explant cultures, harvested from MMP-3-/- mice. These GC migration anomalies, which result in a thicker and persistent EGL in MMP-3-/- mice, as well as the consequent disturbed synaptogenesis of GCs on PCs, seemed to be caused by an abnormal PC dendritogenesis. Indeed, although no overt abnormalities were found in PC number, alignment and soma diameter, detailed analysis of PC morphology revealed a defective dendritogenesis. More specifically, the PC primary dendrite length and tree size were reduced during development, resulting in an aberrant PC morphology in adulthood. Of note, the delayed GC arrival in the internal granular layer (IGL) and the abnormal PC dendritic development resulted in a delayed interneuron migration, a retarded synaptogenesis on PCs and a sustained GC proliferation rate at later stages during cerebellar development in MMP-3-/- animals. Importantly, the observed anatomical developmental alterations were accompanied by mild deficits in balance and motor behavior in postnatal and adult MMP-3-/- mice. In order to define the mechanisms underlying the observed developmental defects in the MMP-3-/- cerebella, a proteomic study was initiated. Data obtained from a 2D-DIGE experiment on P8 cerebellar extracts revealed multiple differential spots, which are currently awaiting identification by mass spectrometry. In conclusion, the results obtained in this study have shed some new light on the involvement of MMP-3 in the development of the postnatal cerebellar cortex, thereby supporting the increasing evidence for a functional role of MMP-3 in neuronal development and wiring. Besides its more frequently reported role in neurodegeneration, these data may stimulate further research investigating the beneficial involvement of MMP-3 in the developing and injured CNS.nrpages: 110status: publishe