Background: Fetal alcohol syndrome (FAS) is a devastating disorder whose mechanisms may be best investigated using animal models. Here we present a novel zebrafish FAS model to investigate the effects of low to moderate alcohol exposure during early development on learning. Methods: At 24-hours postfertilization zebrafish embryos were exposed to low doses of ethanol (external concentrations = 0.00, 0.25, 0.50, 0.75 and 1.00% vol/vol) for a very short duration (2 hours). Upon adulthood associative learning in the zebrafish was tested in a plus maze. Results: This exposure led to no gross anatomical abnormalities or increased morbidity or mortality. Overall activity was not significantly affected by embryonic ethanol exposure. A trend towards a dose-dependent decrease in learning and memory performance was observed. Conclusions: We suggest that zebrafish will be an appropriate model with which one can analyze the behavioural effects of embryonic alcohol exposure and the mechanisms of the ensuing abnormalities.

Background: Fetal alcohol syndrome (FAS) is a devastating disorder whose mechanisms may be best investigated using animal models. Here we present a novel zebrafish FAS model to investigate the effects of low to moderate alcohol exposure during early development on learning. Methods: At 24-hours postfertilization zebrafish embryos were exposed to low doses of ethanol (external concentrations = 0.00, 0.25, 0.50, 0.75 and 1.00% vol/vol) for a very short duration (2 hours). Upon adulthood associative learning in the zebrafish was tested in a plus maze. Results: This exposure led to no gross anatomical abnormalities or increased morbidity or mortality. Overall activity was not significantly affected by embryonic ethanol exposure. A trend towards a dose-dependent decrease in learning and memory performance was observed. Conclusions: We suggest that zebrafish will be an appropriate model with which one can analyze the behavioural effects of embryonic alcohol exposure and the mechanisms of the ensuing abnormalities.

Hepatitis C virus (HCV) infects millions of people worldwide and is one of the leading causes of liver damage. Infection with HCV is strongly correlated with an increased risk of steatosis, or fatty liver disease, which is caused by a build-up of fat deposits in hepatocytes. All genotypes of HCV appear to cause some degree of steatosis in approximately 50% of infected individuals, especially in the presence of contributing host factors such as diabetes, obesity and alcoholism. However, approximately 70% of genotype 3a infections exhibit steatosis. Furthermore, successful clearance of the genotype 3a virus results in eradication of the steatosis, suggesting the genotype 3a virus may be able to directly cause steatosis.<p> Research suggests a role for the core protein of HCV, which forms the capsid of the virus, in the alteration of lipid metabolism pathways during infection. As such, I hypothesized that: 1) HCV alters lipid metabolism pathways and causes the build up of lipid in hepatocytes and the development of steatosis; 2) HCV-3a core protein has a differential or increased effect on these pathways in comparison to 1b core protein; and 3) other HCV proteins could also play a role in the altering of lipid metabolism. My research characterized the subcellular localization on lipid droplets of the HCV-3a core protein in comparison to HCV-1b core protein. It was found that HCV-3a core causes increased transcriptional activity from the Fatty Acid Synthase (FAS) promoter, an important enzyme involved in the synthesis of triglycerides in hepatocytes. In addition, one specific amino acid of HCV-3a core was determined to be partially responsible for this effect. Further research determined that the effect of HCV-3a core on FAS was dependent on the transcription factor Sterol Response Element Binding Protein-1 (SREBP-1) and the presence of HCV-3a core increased the processing and activity of SREBP-1. HCV core was also able to increase activity of Akt 1 and Akt2; inhibition of Akt activity resulted in decreased SREBP-1 activity thereby indicating that HCV core partially mediates SREBP-1 via Akt. Further experiments examined the role of another HCV protein, NS2, in these same lipid metabolism pathways. NS2 was also able to increase transcription from the FAS promoter via SREBP-1, suggesting that this HCV protein may also be important in the development of steatosis during HCV infection.<p> The evidence provided in these studies shows a very important role for HCV in altering lipid metabolism during infection that may lead to the development of steatosis. Current research suggests that the SREBP-1 pathway may be critical in the life cycle of the virus and these studies have provided important information on how lipid metabolism pathways are being changed by the virus. Hopefully this work can help identify potential treatment options for HCV that can slow down disease progression by preventing the development of steatosis or by decreasing viral replication.

El present treball es basa en l'estudi del efecte de dues proteïnes identificades com antagonistes de la mort induïda pel receptor Fas, FAIM i FLIP, en el sistema nerviós. Malgrat que totes dues molècules promouen el creixement neurític, existeixen diferències mecanístiques que es detallaran de forma separada. Inicialment, hem procedit a la caracterització de la proteïna FAIM (Fas Apoptosis Inhibitory Molecule), de la qual n'existeixen dues úniques referències, en la bibliografia. Hem demostrat que l'expressió forçada de FAIM no protegeix les neurones de la retirada de factors tròfics, però exerceix una clara acció promotora del creixement neurític en els diversos sistemes neuronals estudiats. D'una banda, l'expressió forçada de FAIM incrementa la longitud i el grau d'arborització de les neurites induïts pel factor de creixement nerviós (NGF), tant en la línia cel·lular PC12 com en cultius primaris de neurones del gangli cervical superior (SCG). Per altra banda, si es redueixen els nivells endògens de FAIM mitjançant la tècnica del ARN d'interferència, el creixement neurític induït pel NGF es veu dràsticament afectat de forma negativa en els dos models cel·lulars utilitzats. L'expressió exògena de FAIM promou l'activació de la via NF-&#954;B, mentre que el bloqueig d'aquesta via, mitjançant la transfecció d'una forma mutada d'I&#954;B&#945; no degradable o bé usant neurones corticals de ratolins nuls que manquen de la subunitat p65 de NF-&#954;B, evita el creixement neurític promogut per NGF. L'efecte estimulador del creixement neurític també pot ser bloquejat per la inhibició de la via de Ras/ERK. Finalment, hem demostrat que FAIM interacciona amb els dos receptors de la neurotrofina NGF, p75NTR i TrkA, d'una forma depenent de lligand. Aquests resultats revelen una nova funció de FAIM com promotor de creixement neurític mitjançant un mecanisme depenent de NF-&#954;B. En el cas de FLIP, s'ha descrit la seva funció com inhibidor endogen de la apoptosi induïda per Fas, però, també s'ha vist implicat en promoció de proliferació. El treball descriu per primera vegada una funció, fins ara desconeguda, de FLIP en el sistema nerviós. FLIP s'expressa en motoneurones, en neurones SCGs i cèl·lules PC12. Malgrat això, la seva expressió forçada, només pot protegir el cultiu de motoneurones de ratolí de la mort cel·lular induïda per la retirada de factors tròfics. De totes maneres, aquesta expressió augmenta de forma considerable el creixement neurític en els tres models després de l'estímul neurotròfic apropiat per a cadascun d'ells. De forma interessant, i sense excepció, la reducció dels nivells endògens de FLIP inhibeix la neuritogènesis en aquests models. Les vies intracel·lulars regulades per FLIP impliquen tant ERK com NF-&#954;B. L'expressió forçada de FLIP promou un increment en la seva activitat, mentre que la reducció de la seva expressió provoca una disminució d'aquesta, després de l'estímul de NGF en cèl·lules PC12. Finalment, es demostra que FLIP interacciona amb el receptor del NGF, TrkA d'una manera depenent d'estímul. Aquests resultats revelen una nova funció neuritogènica de FLIP a través d'un mecanisme que implica l'activació de les vies MAPK/ERK i NF-&#954;B, i que no està relacionada amb la seva clàssica funció antiapoptòtica. / El presente trabajo se basa en el estudio del efecto de dos proteínas identificadas como antagonistas de la muerte inducida por el receptor de muerte Fas, FAIM y FLIP, en el sistema nervioso. Para ello, y pese a que comparten el fenotipo de promoción del crecimiento neurítico, existen diferencias mecanísticas que detallaremos de forma separada. Inicialmente, caracterizamos la proteína FAIM (Fas Apoptosis Inhibitory Molecule), de la cual existen dos únicas referencias en la bibliografía. Hemos demostrado que la expresión forzada de FAIM no protege las neuronas de la retirada de suporte trófico, pero ejerce una clara acción promotora del crecimiento neurítico en los diversos sistemas neuronales estudiados. Por una parte, la expresión forzada de FAIM incrementa la longitud y el grado de arborización de las neuritas inducidos por el factor de crecimiento nervioso (NGF), tanto en línea celular PC12 como en cultivos primarios de neuronas del ganglio cervical superior (SCG). Por otra parte, si se reducen los niveles endógenos de FAIM mediante la técnica del ARN de interferencia, se disminuye el crecimiento neurítico en dichas células. La expresión forzada de FAIM promueve la activación de la vía NF-&#954;B, mientras que el bloqueo de esta vía, mediante la transfección de una forma mutada de I&#954;B&#945; no degradable o bien usando neuronas corticales de ratones nulos que carecen de la subunidad p65 de NF-&#954;B, previene el crecimiento neurítico promovido por NGF. El efecto estimulador del crecimiento neurítico también puede ser bloqueado por la inhibición de la vía de Ras/ERK. Finalmente, demostramos que FAIM interacciona con los dos receptores de la neurotrofina NGF, p75NTR y TrkA, de una forma dependiente de ligando. Estos resultados revelan una nueva función de FAIM como promotor de crecimiento neurítico mediante un mecanismo dependiente de NF-&#954;B. En el caso de FLIP, se ha descrito su función como inhibidor endógeno de la apoptosis mediada por Fas, pero, también se ha visto implicado en promoción de proliferación. El trabajo describe por primera vez una función, hasta ahora desconocida, de FLIP en el sistema nervioso. FLIP se expresa en motoneuronas, en neuronas SCGs y células PC12, aunque su expresión forzada, únicamente protege de la muerte celular inducida por la retirada de factores tróficos en motoneuronas. De todos modos, dicha expresión aumenta de forma considerable el crecimiento neurítico en los tres modelos, después del estímulo neurotrófico apropiado. De forma interesante, y sin excepción, la reducción de los niveles endógenos de FLIP inhibe la neuritogénesis en estos modelos. Las vías intracelulares reguladas por FLIP implican tanto ERK como NF-&#954;B. La expresión forzada de FLIP promueve un incremento en su actividad, mientras que la reducción de su expresión provoca una disminución de ésta, después de un estímulo de NGF en células PC12. Finalmente, demostramos que FLIP interacciona con el receptor del NGF, TrkA de una manera dependiente de estímulo. Estos resultados revelan una nueva función para FLIP, la neuritogénesis, a través de un mecanismo que implica la activación de las vías Ras/ERK y NF-&#954;B, y que no está relacionada con su clásica función antiapoptótica. / The present work studies the effect of two proteins identified as Fas-induced cell death antagonists, FAIM and FLIP, in the nervous system. Although they share the neuritogenesis promoting effect, there are mechanistical differences that will be detailed separately. Fas apoptosis inhibitory molecule (FAIM) is a protein identified as an antagonist of Fas-induced cell death. We show here that FAIM over expression fails to rescue neurons from trophic factor deprivation, but exerts a marked neurite growth -promoting action in different neuronal systems. Whereas FAIM over expression greatly enhanced neurite outgrowth from PC12 cells and sympathetic neurons grown with nerve growth factor (NGF), reduction of endogenous FAIM levels by RNAi decreased neurite outgrowth in these cells. FAIM over expression promoted NF-&#954;B activation, and blocking this activation by using a super repressor I&#954;B&#945; or by carrying out experiments using cortical neurons from mice that lack the p65 NF-&#954;B subunit prevented FAIM-induced neurite outgrowth. The effect of FAIM on neurite outgrowth was also blocked by inhibition of the Ras-ERK pathway. Finally, we show that FAIM interacts with both TrkA and p75NTR NGF receptors in a ligand-dependent manner. These results reveal a new function of FAIM in promoting neurite outgrowth by a mechanism involving activation of the Ras-ERK pathway and NF-&#954;B. Cellular FLIP (c-FLIP) is an endogenous inhibitor of the signaling pathway triggered by Fas activation implicated in apoptosis as well as in proliferation processes. Here, we demonstrate for the first time an unexpected role of FLIP in the nervous system. FLIP is expressed in motoneurons, SCGs and PC12 cells. However, its over expression is only able to protect mouse isolated motoneurons from growth factor deprivation-induced cell death. Whereas FLIP over expression greatly enhanced neurite outgrowth in the three neuronal models after appropriate neurotrophin stimuli, reduction of endogenous FLIP levels by RNAi decreased neuritogenesis in these cells. The intracellular signals regulated by FLIP implicate both ERK and NF-&#954;B pathways. Over expression of FLIP promotes an increased activity, whereas its downregulation provokes a reduction after NGF stimulus in PC12 cells. Finally, we demonstrate that FLIP interacts with TrkA receptor in a NGF dependent manner. These results reveal a new function of FLIP in neuritogenesis by a mechanism involving activation of Ras/ERK pathway and NF-&#954;B that can be separated from its classical antiapoptotic function.

Att utveckla IT-system som löser de problem det är ämnat att lösa är en förutsättning för systemutvecklingen. Trots att detta kan ses som en självklarhet samt att forskning sker inom området klarar inte verksamheterna, som utvecklingen ser ut idag, alltid av att lösa detta problem (Standish Group 1994; Standish Group 2003). Andra exempel på problem som kan finnas i ett systemutvecklingsprojekt är dålig kommunikation i projektgruppen, otydliga mål inom den, dålig grund att stå på och att en helhetsbild av verksamheten saknas (Goldkuhl &amp; Röstlinger 1988). Vi har tagit fram en alternativ lösning för att tillgodose dessa behov, vilket erbjuder ett alternativt arbetssätt med avsikt att minska risken för att dessa problem uppstår. Vi presenterar ett arbetssätt som utgår från metoden Dialogseminarium, en metod för kunskaps- och erfarenhetsutveckling, vilken har som huvudsyfte att: • Etablera ett gemensamt språk • Skapa en yrkespraxis • Utveckla ett reflektivt och analogiskt tänkande • Bygga kunskap • Utveckla erfarenhetsbaserade kunskaper I det presenterade arbetssättet används Dialogseminariet i början och slutet av systemutvecklingsprojekt samt som ett moment inför och mellan dess olika systemutvecklingsfaser där de bäst lämpar sig att användas. Genom att arbeta på detta sätt hoppas vi bland annat att arbetssättet ska kunna generera i en bättre kommunikation inom projektgruppen och att en gemensam förståelse för projektet skapas med Dialogseminariet. Under projektets gång ska kontinuerlig reflektion och bearbetning bland annat bidra till att problem förs upp till ytan och att till exempel grunden inför nästa systemutvecklingsfas läggs. Vi vill även att kunskap och erfarenhet om hur projektet genomförts ska skapas, vilka ska kunna komma att användas vid framtida systemutvecklingsprojekt. Då arbetssättet förutsätter att det finns ett längre investeringsperspektiv krävs ett engagemang från verksamheten. Om verksamheterna får den information som krävs för ett sådan införande tror vi att detta kan bli ett naturligt sätt att arbeta efter. / Developing IT-systems which solve the intended problem is a necessity for systems development. Although this can be seen as obvious and that research is performed within the subject, organisations are not able to handle these problems (Standish Group 1994; Standish Group 2003). Other problems that can occur in a systems development project is bad communication within the project group, ambiguous goals, weak foundation to stand on and that an overall picture of the project is missing (Goldkuhl &amp; Röstlinger 1988). We have developed a possible solution to manage these needs, which should be able to offer an alternative work procedure so that the possibilities of problems occurring will decrease. We will present a work procedure that is based on the Dialogue seminar method, a method for knowledge- and experience extraction, which has the main purposes to: • Establish a common language • Create a work practice • Develop reflective and analogical thinking • Build knowledge • Develop experience based knowledge In our presented work procedure the Dialogue seminar is used in the beginning and at the end of the systems development project and as an element before and in between different systems development phases where the use of it is best suited. By working this way we are hoping that the work procedure will generate better communication within the project group and that a common under-standing for the project will be created. During the project a continuous reflection and refining will contribute to avoid problems and for example build a foundation prior to future system developing phases. We also want to create knowledge and experience about how projects are carried out, which will be used in future system development projects. When the work procedure requires that there is a longer investment perspective, a commitment from the organisation is needed. If the organisation receives the information needed for establishing this work procedure, we believe that this can be a natural way of working.

In 1996, the Institute of Medicine made an initial step towards addressing the confusion and controversy regarding the diagnosis of fetal alcohol syndrome (FAS) by proposing a classification scheme and calling for research to evaluate its validity and clinical utility. Previous research evaluated memory, executive functions, and behaviour problems in FAS. Prior to the present study, however, there had not been an empirical evaluation of the existence of a spectrum of diagnostic subgroups or an evaluation of subgroup functioning on neuropsychological components of attention during the pre-teen and adolescent years. Part 1 of this study used categorical data regarding diagnostic domains to determine if an a priori spectrum of four subgroups could be identified. This spectrum included FAS and three fetal alcohol effect (FAE) subgroups, which were defined using teratogenic theory, previous research findings, and logic. The sample consisted of 112 children with a confirmed history of excessive prenatal alcohol exposure. Part 2 evaluated the continuity and comparability of the CNS dysfunction subgroups exhibited by assessing neuropsychological components of attention using models by Mirsky and Conners. The sample consisted of 30 children and subgroups were matched on age, sex, and living situation. Results identified 3 of the 4 potential subgroups. All subgroups exhibited a clinically significant attention deficit. After adjusting for IQ, the FAS and FAE subgroups had comparable levels of functioning on all components of attention with one exception. On the sustain component, the FAE subgroups had more difficulties than the FAS subgroup in maintaining a consistent response-speed in response to changes in the length of time between targets. This study provides empirical and theoretical support for the validity and clinical utility of a spectrum of fetal alcohol subgroups consistent with the IOM's classification. It furthers a theoretical understanding of the dose-response effects of alcohol as a teratogenic agent. It suggests that attention regulation functions are especially vulnerable to the damage caused by prenatal alcohol exposure. The findings emphasize the importance of obtaining a history of prenatal alcohol exposure in individuals presenting with neuropsychological difficulties, and developing treatment programs for pregnant women with an alcohol addiction.

Hepatitis C virus (HCV) infects millions of people worldwide and is one of the leading causes of liver damage. Infection with HCV is strongly correlated with an increased risk of steatosis, or fatty liver disease, which is caused by a build-up of fat deposits in hepatocytes. All genotypes of HCV appear to cause some degree of steatosis in approximately 50% of infected individuals, especially in the presence of contributing host factors such as diabetes, obesity and alcoholism. However, approximately 70% of genotype 3a infections exhibit steatosis. Furthermore, successful clearance of the genotype 3a virus results in eradication of the steatosis, suggesting the genotype 3a virus may be able to directly cause steatosis.<p> Research suggests a role for the core protein of HCV, which forms the capsid of the virus, in the alteration of lipid metabolism pathways during infection. As such, I hypothesized that: 1) HCV alters lipid metabolism pathways and causes the build up of lipid in hepatocytes and the development of steatosis; 2) HCV-3a core protein has a differential or increased effect on these pathways in comparison to 1b core protein; and 3) other HCV proteins could also play a role in the altering of lipid metabolism. My research characterized the subcellular localization on lipid droplets of the HCV-3a core protein in comparison to HCV-1b core protein. It was found that HCV-3a core causes increased transcriptional activity from the Fatty Acid Synthase (FAS) promoter, an important enzyme involved in the synthesis of triglycerides in hepatocytes. In addition, one specific amino acid of HCV-3a core was determined to be partially responsible for this effect. Further research determined that the effect of HCV-3a core on FAS was dependent on the transcription factor Sterol Response Element Binding Protein-1 (SREBP-1) and the presence of HCV-3a core increased the processing and activity of SREBP-1. HCV core was also able to increase activity of Akt 1 and Akt2; inhibition of Akt activity resulted in decreased SREBP-1 activity thereby indicating that HCV core partially mediates SREBP-1 via Akt. Further experiments examined the role of another HCV protein, NS2, in these same lipid metabolism pathways. NS2 was also able to increase transcription from the FAS promoter via SREBP-1, suggesting that this HCV protein may also be important in the development of steatosis during HCV infection.<p> The evidence provided in these studies shows a very important role for HCV in altering lipid metabolism during infection that may lead to the development of steatosis. Current research suggests that the SREBP-1 pathway may be critical in the life cycle of the virus and these studies have provided important information on how lipid metabolism pathways are being changed by the virus. Hopefully this work can help identify potential treatment options for HCV that can slow down disease progression by preventing the development of steatosis or by decreasing viral replication.

Diacylglycerol acyltransferase (DGAT) is a key for the synthesis of triacylglycerol (TAG) from diacylglycerol in the unicellular green alga Chlamydomonas reinhardtii.Acetyl-CoA carboxylase (ACCase) and fatty acid synthase (FAS) are responsible for the synthesis of fatty acids. We found the TAG and fatty acid synthesis related genes in C. reinhardtii, including five DGAT (DGAT1 (JGI 184281), DGAT2 (JGI 400751), DGAT3 (JGI 285889), DGAT4 (JGI 141301), and DGAT5 (JGI 190539)), three £] ketoacyl-ACP reductase isoforms ( (JGI 153976), (JGI 153976), and (JGI 194728)) and two £] ketoacyl-ACP synthase isofroms ( (JGI 139619) and (JGI 205887)) for FAS, and ACC £\ (NCBI XP_001696945.1), ACC £] (NCBI XP_001703187.1) and ACC biotin carboxylase ( NCBI XP_001702319.1)) for ACCase in C. reinhardtii. This investigation designed the primers of the above genes to determine whether acetate influences their mRNA expression levels in cell-wall less strain CC400 in the nitrogen starvation condition. The results showed that the absence of nitrogen in the medium triggered the lipid accumulation for the strains of CC400 in the condition of 50 £gE light. DGAT3 mRNA levels were increased by nitrogen starvation. For the FAS genes, in the strain of CC400 showed no increased mRNA levels upon exposure to nitrogen starvation. The mRNA levels of ACC£\, ACC £] and ACC biotin carboxylase were more or less decreased by nitrogen starvation in CC400 strains. Thus, the responses of DGAT gene expression to acetate supplement were checked. The absence of acetate from the medium partly inhibited the nitrogen starvation induced increases in lipid and DGAT3 mRNA levels, and the mRNA levels of DGAT1 and DGAT2 in the nitrogen starvation condition. However, DGAT4 mRNA levels were significantly induced by the absence of acetate from the medium. In conclusion, the present study demonstrate that acetate is required for the nitrogen starvation induced DGAT3 gene expression (mRNA levels) and lipid accumulation in C. reinhardtii.

<p>Background: A harmonisation of accounting directions has been taken place, which for most countries has meant an adjustment to the directions of the United States. The Swedish directions of group accounting, RR 1:00, is one such adaptation. At the same time, a new direction of group goodwill, FAS 142, is introduced in the US. </p><p>Purpose: The purpose of this thesis is to map out the Swedish actors’, mainly the companies’, opinion about the direction of group goodwill accounting. </p><p>Procedure: Information from three actors in the market of accounting (accountants at the firms, users, in the form of analysts, and authorised accountants and one issuer of the directions) was collected via questionnaire and complementary telephone interviews. </p><p>Summary: From the investigation we found out that the Swedish actors are content with the Swedish directions of group goodwill accounting but they think that an adjustment to the American direction FAS 142 is inevitable. The analysts had a positive attitude towards FAS 142 while the other actors were a little more doubtful.</p>

<p>Vid min praktiktid på avdelningen för undersökning av förorenade områden vid SWECO VBB VIAK, Linköping utvecklades en förståelse för hur komplext problemet är med riskklassning av förorenade områden. Idag används uteslutande metodiken i MIFO-modellen, men ett önskemål yttrades om kunskaper om andra metodiker. Jag föreslogs att i mitt följande examensarbete ta fram någon annan metod än MIFO-modellen för vad man bör undersöka för att kunna riskklassa ett förorenat område. Då det finns många olika slags förorenade områden och därmed olika faktorer att ta hänsyn till för att kunna riskklassa ett förorenat område gjordes en avgränsning för att arbetet skulle rymmas inom en 10-poängs kandidatexamensuppsats. </p><p>Med kunskap om i vilken fas en deponi befinner sig i, samt vilka skyddssystem som deponien har, kan man få indikation om tillstånd och möjlighet att förutse emissioner från deponien. Detta är en av förutsättningarna då man vill riskklassa deponien. </p><p>Som förorenat område valdes undersökning av deponi. Som analysfaktorer valdes att undersöka vilka variabler som kan bestämma i vilken fas en deponi befinner sig i samt vilka variabler som behövs avseende en deponis barriärsystem för att kunna riskbedöma emissioner från deponien. Dessutom valdes att göra en fallstudie på ett mindre objekt. Som objekt valdes Nykvarns deponi i Linköping. Som sidoprojekt var det också intressant att undersöka om Nykvarns deponi efter de åtgärder som gjorts motsvarar dagens krav på avslutade deponier. </p><p>Syftet med den här studien har varit att införskaffa kunskap om hur man undersöker i vilken fas en deponi befinner sig i samt vilket barriärsystem den har. </p><p>Studiens utgångspunkt har varit att besvara följande frågeställningar: Med vilka variabler kan en deponis fas bedömas? Med vilka variabler kan en deponis barriärsystem bedömas? Vilka variabler finns att tillgå för Nykvarns deponi? Vilka ytterligare variabler behövs för att kunna fastställa Nykvarns deponis fas respektive för att fastställa om barriärsystemet motsvarar de krav som ställs i lagar och förordningar?</p>