An oasis of wellbeing : designing a backyard in Bergen city centre, with tools from Feng shui, colour theory and sensory design

Bergen is a city of rich history and culture. It consist of sacred/ listed buildings and places, and is surrounded by nature from the seven mountains. But despite its richness, the inner city lacks vegetated areas for relaxation. The area Vågsbunnen, in Bergen has gone through a severe transformation throughout the years of being a city. From being underneath water to one of the most popular meeting spots in the city with trading, craftsmen and being a seaport. From being all burned down to rebuilt, the city has left a great history. Today the city takes great pride of the history, its old buildings and its wellkept streets is a proof of Bergen`s history and culture. Therefore, many areas is listed and untouched like the backyard in Vågsbunnen. The city is quite well built and there are not many areas that has a need of change, but still the city lacks something different to be complete. Among the lacks, the city needs more sheltered vegetated areas for relaxation. In Vågsbunnen there is one of the biggest backyards in Bergen. Today it works as a parking lot. the adjacent streets may come across as dark, grey and narrow. Therefore one of the main strategies would be to open the backyard up for both people and more vegetation. To make this area in to a new meeting place. Some of the sub strategies would be to change the place through pleasant colours, shapes and vegetation. The thesis therefore focus on three topics; sensory gardens, colour theory and Feng shui in the aim to fulfil an oasis of wellbeing in the city. “An oasis of wellbeing” has been used as an example of how all kinds of cities can transform available places like backyards into vegetated areas filled with colours and shapes. All through using alternative but also basic design approaches.Bergen er en kulturhistorisk by som rommer både bevaringsverdige bygg og vernede plasser. Byen er omringet av natur fra «de syv fjell», men på tross av all dens prakt, mangler byen vegetasjonsrike områder for avslappning. Området vågsbunnen har gjennom historien som by, gått gjennom en stor transformasjon. Fra å være under vann til å bli ett av de mest folksomme gatene i Bergen med handel håndverkere og en travel havn. Men også fra å bli brent helt ned til bygd opp igjen, har dette medført en stor arv og historie til byen. I dag er Bergens innbyggere svært stolte av historien og den rike kulturen. Byggene og de velbevarte gatene og plassene er ett symbol på Bergen`s historie og kulturarv. Dette er grunnen til at de fleste steder og gamle bygg er uberørt og gjerne merket som fredet eller bevaringsverdig som for eksempel bakgården i Vågsbunnen. Byen er svært godt gjennomført og det er få områder som trenger store forandringer, men det er fortsatt behov for flere avskjermete parker eller steder som fungerer som «pusterom» i byen. Vågsbunnen er allerede ett avskjermet sted med smale gater, men kan virke grå og mørk. Og kan derfor trenge mer vegetasjon som for eksempel ved hjelp av en oase. I Vågsbunnen eksisterer en av Bergen`s største bakgårder. I dag står den ubrukt med unntak av litt parkering. Derfor blir en av hovedstrategiene å omgjøre bakgården til ett sted for mer vegetasjon og folk. Noen av del strategiene blir å endre stedet ved hjelp av behagelige farger, former og vegetasjon. Masteren`s problemstilling fokuserer derfor på sansehager, fargeteori/psykologi og Feng shui. Alt i håp om å skape en oase av velvære i byen. «En oase av velvære», har som mål om å være ett eksempel på hvordan de fleste byer kan forandre ubrukte plasser som bakgårder om til vegetasjonsrike områder, med farger som kontrast til byens «harde kanter». Dette med hjelp av alternative men også grunnleggende design prinsipper.submittedVersionM-L

Sodium channel b2 subunit promotes filopodia-like processes and expansion of the dendritic tree in developing rat hippocampal neurons

The b2 auxiliary subunit of voltage gated sodium channels (VGSCs) appears at early stages of brain development. It is abundantly expressed in the mammalian central nervous system where it forms complexes with different channel isoforms, including Nav1.2. From the structural point of view, b2 is a transmembrane protein: at its extracellular N-terminus an Ig-like type C2 domain mediates the binding to the pore forming alpha subunit with disulfide bonds and the interactions with the extracellular matrix. Given this structural versatility, b2 has been suggested to play multiple functions ranging from channel targeting to the plasma membrane and gating modulation to control of cell adhesion. We report that, when expressed in Chinese Hamster Ovary cells CHO-K1, the subunit accumulates at the perimetral region of adhesion and particularly in large lamellipodia-like membrane processes where it induces formation of filopodia-like structures. When overexpressed in developing embryonic rat hippocampal neurons in vitro, b2 specifically promotes formation of filopodia-like processes in dendrites leading to expansion of the arborisation tree, while axonal branching remains unaltered. In contrast to this striking and highly specific effect on dendritic morphology, the targeting of functional sodium channels to the plasma membrane, including the preferential localization of Nav1.2 at the axon, and their gating properties are only minimally affected. From these and previously reported observations it is suggested that b2, among its multiple functions, may contribute to promote dendritic outgrowth and to regulate neuronal wiring at specific stages of neuronal development

Adhésion et migration transendothéliale des cellules tumorales

Cancer metastasis is associated with 90% cancer-associated deaths, when cancer cells escape from the primary tumor and form metastatic colonies in secondary sites. Extravasation is an important step in cancer metastasis, where cancer cells carried in blood, adhere and transmigrate through the endothelium. Therefore identifying the key molecules involved during the adhesion process could enable to develop new anticancer cancer drugs able to inhibit the adhesion of cancer cells to the endothelium. We have previously shown that InterCellular Adhesion Molecule-1 (ICAM-1) expressed by endothelial cells is involved in the interactions of bladder cancer cells (BCs) with the endothelium. However the ICAM-1 ligands have never been investigated. In this study, we combined adhesion assays and Atomic Force Microscopy (AFM) to identify the ligands involved and to quantify the forces relevant in such interactions. We report the expression of MUC1 and CD43 on BCs and demonstrate that these ligands interact with ICAM-1 to mediate cancer cell-endothelial cell adhesion in the case of the more invasive BCs. AFM experiments were performed to quantify the force ranges involved by MUC1 and CD43 during their interaction with ICAM-1. AFM measurements combined with a Gaussian Mixture Model showed distinct force ranges for the interaction of ICAM-1 with MUC1 and ICAM-1 with CD43. Furthermore, a detailed analysis of the rupture events suggests that CD43 is strongly connected to the cytoskeleton and that its interaction with ICAM-1 mainly corresponds to force ramps followed by sudden jumps. On the contrary, MUC1 seems to be weakly connected to the cytoskeleton as its interactions with ICAM-1 are mainly associated with the formation of tethers. The forces involved during the transmigration of cancer cells through the endothelium was investigated using Traction Force Microscopy (TFM). Preliminary results showed that tractions exerted by cancer cells during transmigration can be studied and quantified using TFM.Les métastases sont responsables de 90 % des décès causés par le cancer. Les métastases sont des foyers cancéreux secondaires qui se forment à distance de la tumeur d’origine. Des cellules cancéreuses quittent la tumeur primaire, rejoignent la circulation sanguine puis colonisent des organes voisins par migration à travers l’endothélium vasculaire. Ce phénomène d’adhésion à l’endothélium et de migration à travers l’endothélium appelé l’extravasation est une étape clé du processus métastatique. L’identification des molécules impliquées constitue une priorité dans le but d’élaborer de nouvelles drogues anticancéreuses. Nous avons précédemment montré que la molécule d’adhésion cellulaire InterCellular Adhesion Molecule-1 (ICAM-1) exprimée par les cellules endothéliales, est impliquée dans l’interaction des cellules de cancer de la vessie (BCs) avec l’endothélium. Cependant les ligands d’ICAM-1 n’ont pas été étudiés. Dans cette étude, nous utilisons des tests d'adhésion cellulaire et la microscopie à force atomique (AFM) afin d’identifier les ligands d’ICAM-1 et de mesurer les forces impliquées dans l’interaction ligand-ICAM-1. Nous avons identifié que les protéines MUC1 et CD43 exprimées par les BCs les plus invasives se lient à ICAM-1 en développant des forces d’intensité différente selon le couple considéré. Une analyse détaillée des événements de rupture suggère que CD43 est fortement lié au cytosquelette et que son interaction avec ICAM-1 correspond principalement à des sauts brusques. Au contraire, MUC1 semble être lié faiblement au cytosquelette et ses interactions avec ICAM-1 sont principalement associées à la formation de filaments membranaires ou « tethers ». Les forces mises en jeu lors de la migration des cellules cancéreuses à travers l'endothélium ont été étudiées par microscopie de forces de traction (TFM). Les résultats préliminaires montrent que les tractions exercées par les cellules cancéreuses lors de l’extravasation sont mesurables par TFM

Adhésion et migration transendothéliale des cellules tumorales

Cancer metastasis is associated with 90% cancer-associated deaths, when cancer cells escape from the primary tumor and form metastatic colonies in secondary sites. Extravasation is an important step in cancer metastasis, where cancer cells carried in blood, adhere and transmigrate through the endothelium. Therefore identifying the key molecules involved during the adhesion process could enable to develop new anticancer cancer drugs able to inhibit the adhesion of cancer cells to the endothelium. We have previously shown that InterCellular Adhesion Molecule-1 (ICAM-1) expressed by endothelial cells is involved in the interactions of bladder cancer cells (BCs) with the endothelium. However the ICAM-1 ligands have never been investigated. In this study, we combined adhesion assays and Atomic Force Microscopy (AFM) to identify the ligands involved and to quantify the forces relevant in such interactions. We report the expression of MUC1 and CD43 on BCs and demonstrate that these ligands interact with ICAM-1 to mediate cancer cell-endothelial cell adhesion in the case of the more invasive BCs. AFM experiments were performed to quantify the force ranges involved by MUC1 and CD43 during their interaction with ICAM-1. AFM measurements combined with a Gaussian Mixture Model showed distinct force ranges for the interaction of ICAM-1 with MUC1 and ICAM-1 with CD43. Furthermore, a detailed analysis of the rupture events suggests that CD43 is strongly connected to the cytoskeleton and that its interaction with ICAM-1 mainly corresponds to force ramps followed by sudden jumps. On the contrary, MUC1 seems to be weakly connected to the cytoskeleton as its interactions with ICAM-1 are mainly associated with the formation of tethers. The forces involved during the transmigration of cancer cells through the endothelium was investigated using Traction Force Microscopy (TFM). Preliminary results showed that tractions exerted by cancer cells during transmigration can be studied and quantified using TFM.Les métastases sont responsables de 90 % des décès causés par le cancer. Les métastases sont des foyers cancéreux secondaires qui se forment à distance de la tumeur d’origine. Des cellules cancéreuses quittent la tumeur primaire, rejoignent la circulation sanguine puis colonisent des organes voisins par migration à travers l’endothélium vasculaire. Ce phénomène d’adhésion à l’endothélium et de migration à travers l’endothélium appelé l’extravasation est une étape clé du processus métastatique. L’identification des molécules impliquées constitue une priorité dans le but d’élaborer de nouvelles drogues anticancéreuses. Nous avons précédemment montré que la molécule d’adhésion cellulaire InterCellular Adhesion Molecule-1 (ICAM-1) exprimée par les cellules endothéliales, est impliquée dans l’interaction des cellules de cancer de la vessie (BCs) avec l’endothélium. Cependant les ligands d’ICAM-1 n’ont pas été étudiés. Dans cette étude, nous utilisons des tests d'adhésion cellulaire et la microscopie à force atomique (AFM) afin d’identifier les ligands d’ICAM-1 et de mesurer les forces impliquées dans l’interaction ligand-ICAM-1. Nous avons identifié que les protéines MUC1 et CD43 exprimées par les BCs les plus invasives se lient à ICAM-1 en développant des forces d’intensité différente selon le couple considéré. Une analyse détaillée des événements de rupture suggère que CD43 est fortement lié au cytosquelette et que son interaction avec ICAM-1 correspond principalement à des sauts brusques. Au contraire, MUC1 semble être lié faiblement au cytosquelette et ses interactions avec ICAM-1 sont principalement associées à la formation de filaments membranaires ou « tethers ». Les forces mises en jeu lors de la migration des cellules cancéreuses à travers l'endothélium ont été étudiées par microscopie de forces de traction (TFM). Les résultats préliminaires montrent que les tractions exercées par les cellules cancéreuses lors de l’extravasation sont mesurables par TFM

Nutrient and light limitation of algal biomass in selected streams in Ireland

This study was undertaken to improve knowledge on the role of both phosphorus and nitrogen in eutrophication of riverine systems. The potential for nutrient limitation of algal biomass was examined during the early growth season in 4 good water quality Irish streams. Four treatments using nutrient diffusing substrata were employed in each river to test algal growth responses to addition of nitrogen (N), phosphorus (P), and a combination of N and P at 3 concentrations (0.05, 0.1, and 0.5 mol/L) as well as a control (agar only) in open and closed canopy over a 21 d period. The ambient streamwater nutrient concentrations from all streams remained at low levels with high N:P ratios. Results indicated that algal biomass as chlorophyll a (Chl-a) was significantly greater at all sites located in open canopy than at the closed canopy sites, implicating light as the first limiting factor in the studied streams. Periphyton response to the nutrient treatments was varied: one stream responded significantly to N addition, indicating N limitation; 2 streams were co-limited by both N and P; and a fourth stream did not show significant responses to any treatment. Phosphorus did not seem to be the sole limiting nutrient for algal biofilm in 4 examined Irish streams at this time of year (May–Jun). There was no significant difference in Chl-a concentrations in response to the applied nutrient concentrations for most sites in the open canopy; there was some response in the closed-canopy sites

Cervical MR Myelography: 3D TSE optimized acquisition technique

info:eu-repo/semantics/nonPublishe

Strain localization and shear band propagation in ductile materials

A model of a shear band as a zero-thickness nonlinear interface is proposed and tested using finite element simulations. An imperfection approach is used in this model where a shear band, that is assumed to lie in a ductile matrix material (obeying von Mises plasticity with linear hardening), is present from the beginning of loading and is considered to be a zone in which yielding occurs before the rest of the matrix. This approach is contrasted with a perturbative approach, developed for a J2-deformation theory material, in which the shear band is modelled to emerge at a certain stage of a uniform deformation. Both approaches concur in showing thatthe shear bands (differently from cracks) propagate rectilinearly under shear loading and that a strong stress concentration should be expected to be present at the tip of the shear band, two key features in the understanding of failure mechanisms of ductile materials

CALCIUM-SENSING RECEPTORS OF HUMAN NEURAL CELLS PLAY CRUCIAL ROLES IN ALZHEIMER’S DISEASE

In aged subjects, late-onset Alzheimer’s disease (LOAD) starts in the lateral entorhinal allocortex where a failure of clearance mechanisms triggers an accumulation neurotoxic of amyloid-β42 oligomers (Aβ42-os). In neurons and astrocytes, Aβ42-os enhance the transcription of Aβ precursor protein (APP) and β-secretase/BACE1 genes. Thus, by acting together with γ-secretase, the surpluses of APP and BACE1 amplify the endogenous production of Aβ42-os which pile up, damage mitochondria, and are oversecreted. At the plasmalemma, exogenous Aβ42-os bind neurons' and astrocytes' calcium-sensing receptors (CaSRs) activating a set of intracellular signalling pathways which upkeep Aβ42-os intracellular accumulation and oversecretion by hindering Aβ42-os proteolysis. In addition, Aβ42-os accumulating in the extracellular milieu spread and reach mounting numbers of adjacent and remoter teams of neurons and astrocytes which in turn are recruited, again via Aβ42-osCaSR-governed mechanisms, to produce and release additional Aβ42-os amounts. This relentless self-sustaining mechanism drives AD progression towards upper cortical areas. Later on accumulating Aβ42-os elicit the advent of hyperphosphorylated (p)-Tau oligomers which acting together with Aβ42-os and other glial neurotoxins cooperatively destroy wider and wider cognition-related cortical areas. In parallel, Aβ42-osCaSR signals also elicit an excess production and secretion of nitric oxide and vascular endothelial growth factor-A from astrocytes, of Aβ42-os and myelin basic protein from oligodendrocytes, and of proinflammatory cytokines, nitric oxide and (likely) Aβ42-os from microglia. Activated astrocytes and microglia survive the toxic onslaught, whereas neurons and oligodendrocytes increasingly die. However, we have shown that highly selective allosteric CaSR antagonists (calcilytics), like NPS 2143 and NPS 89626, efficiently suppress all the neurotoxic effects Aβ42-osCaSR signalling drives in cultured cortical untransformed human neurons and astrocytes. In fact, calcilytics increase Aβ42 proteolysis and discontinue the oversecretion of Aβ42-os, nitric oxide, and vascular endothelial growth factor-A from both astrocytes and neurons. Seemingly, calcilytics would also benefit the other types of glial cells and cerebrovascular cells otherwise damaged by the effects of Aβ42-osCaSR signalling. Thus, given at amnestic minor cognitive impairment (aMCI) or initial symptomatic stages, calcilytics could prevent or terminate the propagation of LOAD neuropathology and preserve human neurons' viability and hence patients’ cognitive abilities