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Aim: The current research aimed to study the association between exposure to low-dose radiation fallout after the Chernobyl accident in 1986 and the incidence of cancer in Sweden. Methods: A nationwide study population, selecting information from nine counties out of 21 in Sweden for the period from 1980 – 2010. In the first study, an ecological design was defined for two closed cohorts from 1980 and 1986. A possible exposure response pattern between the exposure to 137Cs on the ground and the cancer incidence after the Chernobyl nuclear power plant accident was investigated in the nine northernmost counties of Sweden (n=2.2 million). The activity of 137Cs at the county, municipality and parish level in 1986 was retrieved from the Swedish Radiation Safety Authority (SSI) and used as a proxy for received dose of ionizing radiation. Information about diagnoses of cancer (ICD-7 code 140-209) from 1958 – 2009 were received from the Swedish Cancer Registry, National Board of Health and Welfare (368,244 cases were reported for the period 1958 to 2009). The incidence rate ratios were calculated by using Poisson Regression for pre-Chernobyl (1980 – 1986) and post-Chernobyl (1986 – 2009) using average deposition of 137Cs at three geographical levels: county (n=9), municipality (n=95), and parish level (n=612). Also, a time trend analysis with age standardized cancer incidence in the study population and in the general Swedish population was drawn from 1980 – 2009. In the second study, a closed cohort was defined as all individuals living in the three most contaminated counties in mid-Sweden in 1986. Fallout of 137Cs was retrieved as a digital map from the Geological Survey of Sweden, demographic data from Statistics Sweden, and cancer diagnosis from the Swedish Cancer Registry, National Board of Health and Welfare. Individuals were assigned an annual 137Cs exposure based on their place of residence (1986 through 1990), from which 5-year cumulative 137Cs exposures were calculated, accounting for the physical decay of 137Cs and changing residencies. Hazard ratios for having cancer during the follow-up period, adjusted for age, sex, rural/non-rural residence, and pre-Chernobyl total cancer incidence, were calculated. Results: No obvious exposure-response pattern in the age-standardized total cancer incidence rate ratios could be seen in the first study. However, a spurious association between the fallout and cancer incidence was present, where areas with the lowest incidence of cancer before the accident coincidentally had the lowest fallout of cesium-137. Increasing the geographical resolution of exposure from the average values of nine counties to the average values of 612 parishes resulted in two to three times higher degree of variance explanation by regression model. There was a secular trend, with an increase in age standardized incidence of cancer from 1980 – 2009. This trend was stronger in the general Swedish population compared to the nine counties of the present study. In the second study, 734,537 people identified were divided into three exposure categories: the first quartile was low exposure (0.0 to 45.4 kBq/m2), the second and third quartiles were intermediate exposure (45.41 to 118.8 kBq/m2), and the fourth quartile was highest exposure (118.81 to 564.71 kBq/m2). Between 1991 and 2010, 82,495 cancer cases were registered in the three counties. Adjusted HRs (95% CI) were 1.03 (1.01 to 1.05) for intermediate exposure, and 1.05 (1.03 to 1.07) for the highest exposure, when comparing to the reference exposure. Conclusion: Using the ecological data, there was no exposure response trend; however, after refining the data to the individual level of exposure, there was an overall exposure response pattern. Nonetheless, due to the time dependency, these results were restricted to the age group of 25 – 49 among males. Using register-based data only, for determining the association between low-dose exposure to radiation and the risk of developing cancer, is difficult since we cannot control for other significant factors that are associated with cancer.

Bakgrund: Hjärt-kärlsjukdomar är den vanligaste orsaken till död och ateroskleros är den dominerande formen av hjärtkärlsjukdomar. Risken att drabbas av ateroskleros ökar hos kvinnor efter menopaus och därför undersöks det om östrogen kan skydda mot ateroskleros. Syfte: Syftet med studien var att undersöka om ateroskleros kan behandlas med östrogen hos postmenopausala kvinnor. Metod: Metoden som användes i litteraturarbetet var litteratursökningar i databasen Pubmed. Begränsningar till sökningar gjordes genom att endast kliniska studier från år 2012 eller efter användes. Sökord ” estrogen atherosclerosis” och ”estrogen LDL” användes. För att välja artiklar lästes deras abstract igenom för att sedan se om några artiklar besvarade litteraturstudiens frågeställning. Det var 5 artiklar som valdes ut och analyserades. Resultat: Östrogenbehandling till postmenopausala kvinnor ledde till att LDL minskade och HDL ökade. För att mäta aterosklerosutveckling användes förändringshastigheten i förtjockningen av halspulsådern vilket är ett mått på CIMT. För att mäta CIMT användes ultraljud. En förändring i CIMT sågs enbart i 1 av 4 studier. För att mäta inflammation användes C-reaktivt protein (CRP). CRP-nivåerna ökade i 2 av 3 studier. Diskussion: De olika studierna visar att effekten av östrogenbehandling är dosberoende. Förhållandet mellan det dåliga och goda kolesterolet förbättrades. Också inflammationsbenägenheten ökade samtidigt som CIMT inte förändrades så mycket. Aterosklerosbehandling bör minska CIMT vilket östrogenbehandlingen misslyckas att göra. Östrogenbehandlingen höjde CRP och denna ökning speglar istället en ökad, inte minskad, inflammation och den ökningen innebär att östrogen i så fall kan vara en trolig riskfaktor för aterosklerosutveckling. Slutsats: Slutsatsen som dras i detta arbete är att ateroskleros inte kan behandlas med östrogen. De sammanfattade resultaten visar till del att östrogenbehandling gör att CRP ökar och östrogen kan inte heller, på ett övertygande sätt, minska CIMT. De gynnsamma förändringar av östrogen som ses i halterna HDL- och LDL-kolesterol verkar, enligt resultatet, inte ha den nyckelroll i aterosklerosutvecklingen som tidigare studier visat utan det är troligen istället inflammationen som spelar den rollen. Dagens behandling baseras på att förändra kolesterolvärdet samt LDL och HDL och de statiner som idag används har som sidoeffekt att minska inflammationen. Resultatet i detta arbete är hämtade från endast fem artiklar och det behövs fler studier för att helt kunna utvärdera effekten av östrogenbehandling i samband med aterosklerosutveckling. / Background: The most common reason in the Western world for death is cardiovascular disease and atherosclerosis is the predominant form of cardiovascular disease. The risk of atherosclerosis for women when they reach menopaus and therefore estrogen therapy is evaluated as treatment for atherosclerosis. Aim: The aim of this study was to examine the effects of estrogens on the progress of atherosclerosis and if atherosclerosis can be treated with estrogen in postmenopausal women. Method: The method used in this study was literature searches in the database Pubmed. Limitations to the searches were made by only using clinical trials published after year 2012. Key words “estrogen atherosclerosis” and “estrogen LDL” were used. To choose articles the abstract was read through to see if any of the articles answered the purpose of this study and five articles was chosen thereby for further evalution. Results: The results from the studies were that LDL-cholesterol decreased and HDL-cholesterol increased with estrogen therapy. The rate of change in the carotid intima-media thickness, CIMT, were used as a mesure of the atherosclerosis. A change in the rate of CIMT was found only in one out of four studies. The inflammation was measured by using C-reactive protein (CRP). CRP levels increased in two out of three studies.  Discussion: The different study show that the effects of estrogen therapy are dose-dependent. The ratio between LDL and HDL was improved which indicates better cholesterol levels. The inflammation was increased and very small effects on CIMT were seen. Treatment for atherosclerosis should decrease the rate of change of CIMT which estrogen therapy failed to do. Estrogen treatment increased CRP and this increase reflects an increased, not decreased, inflammation and the increase means that estrogen could likely be a factor of risk for developing atherosclerosis. Conclusion: The conclusion from this study is that atherosclerosis cannot be treated with estrogen. The results showed that estrogen treatment increased CRP and did not lead to a clinically significant decrease in CIMT. LDL and HDL levels as measured in this study could not be correlated to the development of atherosclerosis. It is instead likely that the inflammation has an important role in the development of atherosclerosis. Atherosclerosis is most often treated by statins nowadays, which on top of improving cholesterol blood levels also have anti-inflammatory effects. This literature study is based only on five studies, and more study needs to be done to be able to clarify the different effects of estrogen therapy on atherosclerosis.

Livsformerna på jorden delas systematiskt in i de tre domänerna bakterier, arkéer och eukaryoter. Arkéer är de mikroorganismer som lever i extrema miljöer såsom hetvattenkällor, sjöar med hög salthalt och i miljöer med extrema pH-värden. De kan existera i miljöer där inga andra organismer överlever men förekommer även rikligt överallt runtomkring oss, exempelvis i människans mage och som normalflora i munnen. Vissa bakterier och arkéer har genen för enzymet ammoniak monooxygenas (AMO). Detta enzym spelar en viktig roll vid rening av avloppsvatten genom att oxidera ammonium till nitrit. Syftet med detta examensarbete har varit att detektera arkéer i prover av aktivt slam vilket gjordes genom att optimera en Polymerase Chain Reaction (PCR) baserad metod. Först pelleterades slamproverna via centrifugering för att kunna preparera DNA. Detta DNA användes som templat för optimering av PCR med specifika primers för AMO genen hos arkéer. De PCR produkter som erhölls från det optimerade programmet klonades och transformerades in i Escherichia coli. Därefter sekvenserades PCR produkterna för att identifiera vilka ammonium oxiderande arkéer som fanns i proverna. De amplifierade gensekvenserna visade god överensstämmelse med den förväntade nukleotidsekvensen för arkéer. Samtliga gensekvenser passade bäst in på icke odlingsbara arkéer enligt databasen BLAST. Genom att välja bort icke odlingsbara arkéer i sökningen kunde arkéen Nitrosopumilus maritimus identifieras, vilket är en av få odlade arkéer med AMO-genen sekvens bestämd.