Mon étude a porté sur le rôle du récepteur purinergique P2X7 (P2X7R) dans les processus physiopathologiques impliqués dans le développement des maladies auto-immunes de type lupique. Les souris MRL/lpr, déficientes en récepteurs d’apoptose Fas (mutation lpr), développent spontanément ces pathologies suite à l’accumulation lymphocytes T pathogéniques CD4−CD8− (DN) B220+ dans les organes lymphoïdes secondaires. Nous avons observé que ces lymphocytes ont également un déficit d’expression en P2X7R à leur surface. Cela nous a amené à postuler que P2X7R pourrait jouer un rôle clé dans l’homéostasie des lymphocytes T et le développement du lupus. Afin de vérifier notre hypothèse, nous avons produit des souris C57BL/6J (B6) déficientes simultanément pour Fas (lpr) et P2X7R (P2X7KO). Ces souris présentent une accumulation massive de lymphocytes T DN B220+ et des titres très élevés en auto-anticorps et en cytokines proinflammatoires ce qui n’est pas le cas pour les souris B6 simples mutantes lpr ou P2X7KO confirmant pour la première fois l’implication de P2X7R dans l’homéostasie des lymphocytes T, en synergie avec le récepteur Fas. Les lymphocytes T DN pathogéniques responsables de la lymphoaccumulation sont issues majoritairement de la sous populations des lymphocytes T CD8+. L’inflammation chronique présente chez les souris B6/lpr P2X7KO induit l’activation de l’ensemble des populations lymphocytaires T CD4+ et CD8+ naïves conduisant à l’accumulation de lymphocytes T Effecteurs/Mémoires : EM et CM et atteignent parfois le stade exhausted PD1+TIM3+. Ces cellules accumulées CD4+, CD8+ et DN B220+ ont une capacité de réactivation réduite. Ce biais fonctionnel et phénotypique a été confirmé en comparant la réponse immunitaire adaptative anti-adénovirus entre des souris déficientes en Fas et/ou P2X7R. Les réponses cellulaires et humorales sont moins importantes dans les souris B6/lpr P2X7KO que B6, B6-P2X7KO. Ces réponses antivirales sont intermédiaires dans les souris B6/lpr. L’ensemble de ces résultats renforcent notre hypothèse sur le rôle synergique des récepteurs Fas et P2X7R dans l’homéostasie des lymphocytes T. Le taux d’apoptose induit par l’activation des récepteurs Fas ou P2X7R séparément est moins important dans les lymphocytes T CD8+ par rapport au lymphocytes T CD4+. La synergie Fas-P2X7R serait donc nécessaire pour l’homéostasie des lymphocytes T CD8+. Afin de préciser les mécanismes à l’origine de la maladie et d’identifier l’influence de chaque récepteur sur l’expression des loci de susceptibilité, nous avons séquencé les ARNm exprimés dans la rate et les ganglions lymphatiques des souris MRL/lpr avant et après le développement de l’auto-immunité ainsi que chez les souris B6, B6/lpr, B6 P2X7KO et B6/lpr P2X7KO. / My project aims to determine the role of the purinergic receptor P2X7 (P2X7R) in the pathophysiological processes involved in the development of autoimmune lupus-like syndrome. MRL/lpr mice, deficient for the cell death receptor Fas (lpr mutation), spontaneously develop this pathology following the accumulation of pathogenic B220+CD4−CD8− (DN) T lymphocytes in secondary lymphoid organs. We have observed that these lymphocytes are also deficient in P2X7R cell surface expression. This led us to hypothesize that P2X7R could play a key role in T cell homeostasis and lupus development. To test our hypothesis, we produced B6 mice deficient for both Fas (lpr) and P2X7R (P2X7KO). These mice, but not single mutant B6 mice (lpr or P2X7KO), develop a massive accumulation of DN B220+ T lymphocytes and high levels of autoantibodies and proinflammatory cytokines, confirming for the first time the involvement of P2X7R in T-cell homeostasis. I have found that the pathogenic DN T lymphocytes are predominantly derived from the CD8+ T lymphocyte subpopulation. Chronic inflammation in B6/lpr P2X7KO mice induces the activation of the whole CD4+ and CD8+ naïve T lymphocyte subpopulations leading to the accumulation of Effector/Memory and exhausted T lymphocytes. Accumulated T-cells lose the ability to be reactivated. To confirm these results, I compared the adaptive immune response against adenovirus between mice deficient for Fas (lpr mutation), P2X7R-deficient mice or both receptors. The cellular and the humoral responses were lower in the B6/lpr-P2X7KO mouse strain compared to B6, B6-P2X7KO and B6/lpr mouse strains. The antiviral immune response in the B6/lpr mice was lower than in B6 and B6-P2X7KO mice. These results reinforce our hypothesis about the synergistic role of both receptors in the maintaining of T cell homeostasis. Ours results suggest that Fas and P2X7R play their synergistic role in T-cell homeostasis. In collaboration with a team from the University of Taiwan, we sequenced the mRNAs expressed in the spleen and lymph nodes of MRL/lpr mice before and after the onset of the diseases as well as in the B6, B6/lpr, B6 P2X7KO and B6/lpr P2X7KO mouse strains in order to better understand the mechanism triggering the disease and to identify the role of each receptor on the expression of the susceptibility loci.

<p>To maintain homeostasis, T lymphocytes die through caspase&ndash;dependent apoptosis. However, blockage of caspase activity in T lymphocytes does not increase cell survival. The loss of caspase 8 activity leads to programmed necrosis (necroptosis) upon T cell receptor (TCR) stimulation in T lymphocytes. Necroptosis is correlated with excessive macroautophagy, an intracellular catabolic process characterized by the sequestration of cytoplasmic compartments through double&ndash;membrane vacuoles. Meanwhile, the proper induction of macroautophagy is required for T lymphocyte survival and function. Cellular caspase 8 (FLICE)&ndash;like inhibitory protein (c&ndash;FLIP) promotes survival in T lymphocytes. c&ndash;FLIP suppresses death receptor&ndash;induced apoptosis by modulating caspase 8 activation. Whether this modulation plays a role in the regulation of necroptosis has yet to be studied. Additionally, overexpression of c&ndash;FLIP reduces autophagy induction and promotes cell survival in cell lines. It remains unclear whether c&ndash;FLIP protects primary T lymphocytes by regulating the threshold at which autophagy occurs. In this study, c&ndash;FLIP isoform&ndash;specific conditional deletion models were used to study the role of c&ndash;FLIP in necroptosis and autophagy in primary T lymphocytes.</p><p>Our results showed that the long isoform of c&ndash;FLIP (c&ndash; FLIP_L) regulates necroptosis by inhibiting receptor interacting protein 1 (RIP&ndash;1). Upon TCR stimulation, c&ndash;FLIP_L&ndash;deficient T cells underwent RIP&ndash;1&ndash;dependent necroptosis. Interestingly, though previous studies have generally described necroptosis in the absence of caspase 8 activity and apoptosis, pro&ndash;apoptotic caspase 8 activity and the rate of apoptosis were also increased in c&ndash;FLIPL&ndash;deficient T lymphocytes. Moreover, c&ndash; FLIP_L&ndash;deficient T cells exhibited enhanced autophagy, which served a cytoprotective function. </p><p>Apoptosis can be induced by either death receptors on the plasma membrane (extrinsic pathway), or the damage of the genome and/or cellular organelles (intrinsic pathway). Previous studies in c&ndash;FLIP&ndash;deficient T lymphocytes suggested that c&ndash;FLIP promotes cell survival in the absence of death receptor signals. Independent of death receptor signaling, mitochondria sense apoptotic stimuli and mediate the activation of caspases. Whether c&ndash;FLIP regulates mitochondrion&ndash;dependent apoptotic signaling remains unknown. Here, by deleting the <italic>c&ndash;Flip <italic> gene in mature T lymphocytes, we showed a role for c&ndash;FLIP in the intrinsic apoptosis pathway. In naïve T cells stimulated with the apoptosis inducer, c&ndash;FLIP suppressed cytochrome c release from mitochondria. Bim&ndash;deletion rescued the enhanced apoptosis in c&ndash;FLIP&ndash;deficient T cells, while inhibition of caspase 8 did not. Different from activated T cells, there were no signs of necroptosis in c&ndash;FLIP&ndash;deficient naïve T cells. Together, our findings indicate that c&ndash;FLIP is a key regulator of apoptosis, necroptosis and autophagy in T lymphocytes.</p> / Dissertation

<p>Detta är en korrelationsstudie med avsikt att undersöka förhållandet mellan personlighetsegenskaper och kognitiva förmågor samt detta förhållandes inverkan på prestation. Studien är baserad på övningstestningar (n = 176) med WAIS-III, FAS, det lexikala beslutstestet SLDT samt personlighetsformuläret SSP, genomförda under informella former. Signifikanta negativa korrelationer förelåg mellan resultat på kognitiva test och personlighetsvariablerna Bitterhet, Somatisk Ångestbenägenhet, Psykisk Ångestbenägenhet, Stresskänslighet och Misstroende. Ett starkt positivt samband framkom mellan Somatisk ångestbenägenhet och antalet som riktiga ord skattade pseudoord i SLDT. Ett starkt negativt samband framkom mellan Bitterhet och samtliga skalindex i WAIS-III. Signifikanta negativa korrelationer förelåg vidare mellan en genom komponentanalys erhållen Neuroticism-faktor och resultat på WAIS-III. Jämförda med tidigare forskningsresultat är flera här redovisade korrelationer anmärkningsvärt starka. Som en bland flera tänkbara förklaringar till detta diskuteras möjligheten av stärkt ekologisk validitet vid testning under informella omständigheter. Vidare diskuteras bl a möjliga kopplingar mellan Somatisk ångestbenägenhet och alexitymi respektive verbal rigiditet samt mellan Bitterhet och flytande intelligens respektive exekutiva funktioner.</p>

Spinal cord injury (SCI) is a debilitating condition accompanied by motor and sensory deficits and a reduced quality of life. Current treatment options are limited and are associated with variable efficacy and a risk of adverse effects. The pathophysiology of SCI is initiated by a primary mechanical insult to the spinal cord, followed by a complex series of deleterious events known as secondary injury. Secondary injury processes include free radical formation, glutamate excitotoxicity, inflammation and cell death. Apoptotic cell death in particular plays a key role in the secondary injury processes and exacerbates tissue degradation and loss of function. The role of Fas-mediated apoptosis in SCI pathophysiology is poorly defined in the literature to date. Correlative evidence suggests that this form of cell death is delayed and occurs in white matter adjacent to sites of primary damage. The cellular and temporal mechanisms of Fas-mediated apoptosis following experimental SCI were evaluated using a clinically relevant clip compression SCI model in the rat. Furthermore, therapeutic manipulation of Fas activation using a soluble form of the Fas receptor (sFasR) was carried out to establish the efficacy and clinical relevance of targeting this aspect of secondary injury. This work shows that Fas-mediated apoptosis is an important contributor to secondary SCI pathology. Oligodendrocytes are targeted by this form of cell death in a delayed fashion post-injury, providing an opportunity for therapeutic intervention. Intrathecal administration of sFasR following SCI reduced post-traumatic apoptosis, improved cell survival, enhanced tissue preservation and resulted in an improved motor recovery. Administration of sFasR was effectively delayed by up to 24 hours post-injury, however a shorter delay of 8 hours post-injury was most efficacious. A surprising result emerged from this work. Delayed intrathecal administration of IgG following SCI showed significant efficacy in both cellular and tissue level outcomes, as well as at the functional level. Fas-mediated apoptosis is an important aspect of secondary SCI pathophysiology and is an attractive therapeutic target. The beneficial outcomes of manipulating Fas activation using sFasR provide further evidence for this. Future work will refine this treatment strategy, bringing it into the SCI patient population.

Die Todesrezeptoren Fas, TRAILR1 und TRAILR2 werden seit einigen Jahren aufgrund ihrer Fähigkeit, Apoptose zu induzieren, als therapeutisch interessantes Ziel bei der Therapie maligner Tumoren angesehen. Gleichzeitig werden immer mehr Entitäten von Tumoren beschrieben, die eine Resistenz gegen die Todesrezeptor-induzierte Apoptose aufweisen. In dieser Konstellation können neben den blockierten proapoptotischen Signalen insbesondere auch Todesrezeptor-assoziierte, protumoral wirksame Signalwege sichtbar werden, die unter anderen Umständen durch die Apoptose maskiert werden. In dieser Arbeit wurde die von FasL- und TRAIL-induzierte Signaltransduktion in einer apoptoseresistenten Variante der kolorektalen Karzinomzelllinie HCT116 untersucht. Eine aktivierende Mutation des PIK3CA-Gens protektiert diese Zellen aufgrund der konstitutiven Aktivierung des onkogenen PI3K/Akt-Signalweges gegenüber Todesrezeptor-vermittelter Apoptose. Durch Vergleich isogener Zelllinien, welche für den PIK3CA-Locus funktionell haploid waren und entweder ein Wildtyp oder ein mutiertes Allel trugen, konnte die Signaltransduktion von Fas und der TRAIL-Todesrezeptoren in apoptoseresistenten Tumorzellen, sowie deren Zusammenspiel mit dem PI3K/Akt-Signalweg im Detail untersucht werden. So wurde in dieser Arbeit gezeigt, dass nach Stimulation der HCT116 PIK3CA-mut protektierten Zellen mit FasL oder TRAIL die initialen Schritte der Apoptoseinduktion durch Todesrezeptoren bis hin zur Bildung des DISC und der Aktivierung von Caspase-8 ungestört vonstatten gehen. Der durch die PIK3CA-Mutation induzierte Schutzmechanismus muss deshalb unterhalb dieser frühen apoptoseinduzierenden Ereignisse wirksam werden. Darüber hinaus zeigte sich, dass Todesliganden in HCT116 PIK3CA-mut Zellen den proinflammatorischen NF&#954;B-Signalweg aktivieren, wohingegen dieser Signalweg in HCT116 PIK3CA-wt Zellen durch die ablaufende Apoptose inhibiert wurde. Während HCT116 PIK3CA-wt Zellen nach Stimulation von Fas oder den TRAIL-Todesrezeptoren morphologisch die klassischen Anzeichen des apoptotischen Zelltods zeigten, veränderten die HCT116 PIK3CA-mut protektierten Zellen ihre Morphologie von einer mesenchymal-länglichen hin zu einer amöboid-abgerundeten Form, die Zellen blieben jedoch vital. Die Änderung der Zellmorphologie konnte mit dem Vorhandensein enzymatisch aktiver Casapse-8 verknüpft werden, generiert durch den Todesrezeptor-assoziierten DISC. Caspase-8 vermittelte die Reorganisation des Aktinzytoskeletts durch Spaltung und der damit einhergehenden Aktivierung von ROCK-1. Blockade der Caspase-8 Aktivierung in HCT116 PIK3CA-mut Zellen durch pharmakologische Inhibitoren oder ektope Überexpression von cFLIPS verhinderte entsprechend den FasL- oder TRAIL-induzierten Übergang zur amöboid-abgerundeten Zellform. Funktionell zeigten die amöboid-abgerundeten HCT116 PIK3CA-mut Zellen im Vergleich zu unstimulierten HCT116 PIK3CA-mut Zellen eine erhöhte Invasivität, was anhand erhöhter Spiegel an Urokinase im Überstand nachgewiesen werden konnte. Diese Arbeit beschreibt mit der Induktion einer amöboid-abgerundeten Zellmorphologie erstmals eine nicht-apoptotische Funktion von Caspase-8 im Kontext der Todesrezeptor-Signaltransduktion, die von der enzymatischen Aktivität abhängig ist. Weiterhin konnte ROCK-1 als Caspase-8 Substrat identifiziert werden. Ob durch die Aktivierung von ROCK-1 und die Reorganisation des Aktinzytoskeletts neben der Ausbildung einer amöboiden Zellmorphologie auch der amöboide Typ der Zellmigration in Gang gesetzt wird, müssen zukünftige Studien zeigen. / During the last years, the death receptors Fas, TRAILR1 and TRAILR2 emerged as promising therapeutic targets in cancer therapy. On the contrary, the number of tumor entities showing resistance against death receptor-induced apoptosis is still rising, thereby limiting the effectiveness of a therapeutic approach. Furthermore, under conditions where death receptor-induced apoptosis is blocked, cell death induction is not the only signal emanating from Fas and TRAIL death receptors. Non-apoptotic and even tumor-promoting signaling pathways may become apparent which are otherwise masked by ongoing apoptosis. This study provides insight in FasL- and TRAIL-induced signaling in an apoptosis resistant variant of HCT116 colorectal cancer cells. An activating mutation in the PIK3CA gene protected these cells against death receptor-induced apoptosis by constitutive activation of the oncogenic PI3K/Akt pathway. Comparing isogenic cell lines either harboring a PIK3CA wild-type allele or an activating mutated allele allowed investigation of signal transduction events associated with Fas and TRAIL death receptors in apoptosis resistant cells as well as their interplay with the PI3K/Akt signaling pathway. Upon stimulation with FasL or TRAIL, PIK3CA-mut protected HCT116 cells were still capable of initiating the first steps of apoptosis induction as was evident from DISC-formation and activating caspase-8. This indicated that the PIK3CA-mut-granted blocking of the apoptotic program must act downstream of these early events. Furthermore, the proinflammatory NF&#954;B pathway was turned on, as demonstrated by the phosphorylation of crucial signaling components and the enhanced expression of NF&#954;B controlled target genes. Activation of the NF&#954;B pathway, however, was masked in HCT116 PIK3CA-wt cells by ongoing apoptosis. After stimulation of Fas or TRAIL death receptors, HCT116 PIK3CA-wt cells exhibited classical morphological apoptotic features. Interestingly, stimulation of HCT116 PIK3CA-mut cells induced transition to an amoeboid-like morphology without affecting the viability. The changes in cellular morphology were crucially dependent on enzymatically active caspase-8 generated at the DISC. Caspase-8 cleaved and thereby activated ROCK-1, a key player in reorganisation of the actin cytoskeleton. Interfering with caspase-8 activation by ectopic expression of cFLIPS or pharmacological inhibitors abrogated the changes in cellular morphology. Additionally, HCT116 PIK3CA-mut cells showed upon FasL- or TRAIL-treatment increased invasiveness, demonstrated by elevated levels of urokinase in the supernatant of the cells. To date, the FasL- or TRAIL-induced transition of HCT116 PIK3CA-mut cells to an amoeboid-like cellular morphology is the first clearly demonstrated non-apoptotic function of caspase-8 in context of death receptor signaling, that is dependent on the enzymatic activity of the molecule. Furthermore, this study identifies ROCK-1 as a novel substrate of caspase-8. Further investigations will have to clarify the role of caspase-8 mediated activation of ROCK-1 and accompanied reorganization of the actin cytoskeleton with respect to the induction of the amoeboid-type of cell migration.

Alcohol use during pregnancy is common and its consequences often result in a broad range of negative, lifelong developmental outcomes. This study describes the effects of prenatal alcohol exposure and interacting socio-demographic factors on early childhood development. One hundred and twenty one children from the Northern Cape, South Africa, were clinically examined using standard diagnostic procedures and assessed using the Griffiths Mental Development Scales (GMDS/ER) at 7-12 months (Time 1) and 5 years of age (Time 2). Participants were assigned to either: a Fetal Alcohol Syndrome (FAS/Partial Fetal Alcohol Syndrome (PFAS); a Prenatal Alcohol Exposed (PAE); or a Control group based on the diagnosis at 5 years. Mothers/caregivers were interviewed to ascertain socio-demographic information, including prenatal alcohol exposure. During infancy, the FAS/PFAS group showed significantly lower gross motor and language abilities, with delays in higher-order executive functioning becoming more apparent with age. No significant differences were noted during infancy between the PAE and Control groups over any developmental subscales. However, with age, higher-order executive function delays were reported in the PAE group. Performance on the infant and child versions of the GMDS was not significantly correlated, suggesting that the tests may be measuring different developmental constructs. Lower maternal education, unemployment and later recognition of pregnancy were associated with reduced social adaptive functioning, and language and eye hand coordination abilities, irrespective of amount of prenatal alcohol exposure over both time points. Larger anthropometric birth measurements and longer duration of breastfeeding were significantly related to increased performance on the GMDS at 5 years within the groups exposed to prenatal alcohol. Socio–demographic variables are likely to complicate developmental profiles for all three groups, with prenatal and postnatal nutrition emerging as possible protective factors for positive developmental outcomes at 5 years of age.

"This paper describes our work in exploring trading strategies for the leveraged exchange-traded funds, Direxion Daily Financial Bull 3X (FAS) and Direxion Daily Financial Bear 3X (FAZ) over the first three quarters of 2009. Using minute-by-minute stock data we are able to verify the accuracy of these ETFs in regards to their target of the Russell 1000 Financial Index (RIFIN). We are then able to quantify the returns and risks involved with trading strategies that seek to exploit the ETFs objectives, specifically momentum trades, tracking-error discrepancy trades, and a combination of the two strategies we term “discount-and-up.” Bootstrap simulation techniques are employed to measure values at risk and conditional tail expectations over 30 day time horizons for each strategy. Lastly, we demonstrate the dangers of traditional buy-and-hold investing with regards to leveraged ETFs."

Dagens konkurrensutsatta arbetsmarknad bidrar till att nya krav ställs på individen. För att vara attraktiv på arbetsmarknaden krävs det att man besitter vissa faktorer för att bli anställd.Man talar om att en person är anställningsbar på arbetsmarknaden och om personen har en anställningsbarhet som lämpar sig för det utvalda området. Idag finns det arbetsmarknadspolitiska program för att få folk anställningsbara, som ligger som uppdrag hos Arbetsförmedlingen. Det som fick oss intresserade av ämnet var hur manarbetar kring personers anställningsbarhet och med dem som varit ifrån arbetsmarknadenunder en längre period. Syftet är att undersöka hur förmedlare på Arbetsförmedlingen ser på begreppet anställningsbarhet samt arbetet kring de arbetssökande i fas 1. De frågeställningarvi utgått ifrån för att svara på vårt syfte är vad begreppet anställningsbarhet innebär för arbetsförmedlaren, deras arbetssätt och förutsättningar för att få de arbetssökandeanställningsbara. Samt om det finns ett särskilt förhållningssätt till anställningsbarheten hos de arbetssökande i jobb- och utvecklingsgarantins fas 1. Vi har utfört undersökningen kvalitativt med individuellt genomförda semistrukturerade intervjuer. De intervjuade är sexarbetsförmedlare som arbetar runt om i Västra Götalands län. De viktigaste slutsatserna vi fått fram med studien är att arbetsförmedlarna använder sig framförallt av en förståelsebaserad syn på anställningsbarhet och i arbetet med de arbetssökande. Förutsättningarna som råder för arbetsförmedlarna i deras arbete upplevs styrt genom politiska och ekonomiska faktorer. Arbetet med den arbetssökandes anställningsbarhet i fas 1 skiljer sig inte nämnvärt gentemot arbetssökande i andra instanser. Istället erbjuds fler åtgärder för att få de arbetssökande i åtgärdersprogrammet mer anställningsbara. / Program: Organisations- och personalutvecklare i samhället

<p> </p><p>Syftet med denna studie var att beskriva arbetsterapeutiska insatser för patienter i den akuta fasen efter stroke. Metoden som användes var en systematisk litteraturstudie med deskriptiv ansats där 12 vetenskapliga studier stod till grund för resultatet. Resultatet visade att de arbetsterapeutiska insatserna för patienter i akut fas efter stroke består av bedömning, träning och mobilisering. Bedömning sker mestadels inom funktionsdomänen men ibland även inom aktivitetsdomänen. Det framkommer att interventionerna består av arm-/handfunktionsträning, aktivitetsträning samt att tidig mobilisering praktiseras. Det är inte alltid tydligt vilka interventions- eller bedömningsområden arbetsterapeuten ansvarar för. Ofta talar man om hela teamets insatser och terapeutiska insatser var för sig eller tillsammans med sjukgymnast. Tydligt är att det handlar om tidiga insatser så snart som möjligt efter sjukdomen oavsett profession. Indelning av olika faser vid stroke samt vad arbetsterapin består av är sällan tydligt beskrivet i studierna. Uttryck som arbetsterapi, standardiserad behandling samt traditionell arbetsterapi omnämns utan att tydligt och enkelt klargöra vad detta innebär.</p><p>Slutsatsen författarna drar av denna studie är att det i granskad vetenskaplig litteratur saknas enhetliga beskrivningar av arbetsterapeutiska insatser i den akuta fasen efter stroke.</p><p> </p>

<p>Funktionsinriktad musikterapi (FMT) kan användas till att utveckla personer med olika funktionsnedsättningar oavsett ålder. I detta examensarbete beskriver jag arbetet med ett barn och en vuxen som har funktionsnedsättningar på grund av hjärnskada. Den ena har en förvärvad och den andra en medfödd skada.</p><p>Det har funnits skillnader i arbetet med dessa båda personer men likheterna har övervägt. Även i resultatet finns en tydlig överensstämmelse mellan de båda. Min erfarenhet säger att FMT med sin tydliga struktur skänker ro att få tillgång till den egna förmågan. Tryggheten, lugnet och lagom stora utmaningar har visat sig vara helt rätt för dessa personer. Tack vare impulser till hjärnan har flera funktioner som saknats eller varit ofullständiga börjat fungera. Vi har funnit de nya vägar vi sökt.</p>