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In the pharmaceutical industry, it is always important to have reproducible processes and raw materials of high quality to ensure good quality products. AstraZeneca, that is a leading manufacturer of different pharmaceuticals, works according to GMP to make sure that their processes deliver products of the same quality every time. A problem that has occurred at AstraZeneca is when a raw material is not properly understood and variations in the raw material affects the final product. Variations in drug release in one of AstraZeneca´s products, Product X, has been linked to the cushioning excipient Microcrystalline cellulose (MCC). Variations in drug release has been noticed during change from one batch of MCC to another. The aim of this study was to investigate which material attributes of MCC that contributes to variations in the final product. Particle size and moisture content were identified as critical material attributes (CMA´s) and were therefore chosen to be investigated more thoroughly. By variating particle size and moisture content during manufacturing of Product X, the influence of these attributes could be investigated using Design of Experiment (DoE). An additional experiment that compared two MCC batches from different suppliers was also performed during this study. The results from these experiments showed that the particle size and moisture content of MCC does affect the drug release. Large particles and high moisture content gave rise to a faster drug release compared to small particles and low moisture content that gave rise to a slower drug release. It is however hard to draw conclusions regarding how small differences in particle size and moisture content could affect the drug release.

Bakgrund En stor del av de patienter som frekvent söker vård lider av psykosomatiska sjukdomar (MUPS) och somatiseringssyndrom (MUS). Båda dessa tillstånd grundar sig i psykiska påfrestningar men yttrar sig i form av fysiska symptom. Stress är en psykisk påfrestning som är mycket utbredd i vårt samhälle idag. När människan utsätts för stress startar en rad olika fysiska processer i kroppen, som en del av vår överlevnadsinstinkt. Trots det är det många som stressar sig sjuka. Då kroppen inte får chans till återhämtning ökar risken för ohälsa med risk för psykosomatiska sjukdomar och somatiseringssyndrom som följd. Syfte Studiens syfte var att belysa upplevelser hos patienter med psykosomatiska sjukdomar och somatiseringssyndrom i den somatiska vården. Metod En litteraturöversikt valdes som metod, där 16 artiklar inkluderades. Artiklarna var av kvantitativ eller kvalitativ metod och analyserades enligt metoden integrerad analys. Resultat Patienter med MUPS/MUS lider av ohälsa och remitteras runt till olika vårdenheter utan att få den hjälp de behöver. Detta innebär ytterligare påfrestning på hälsan hos dessa patienter. Starka känslor såsom utanförskap, oro, skam och rädsla för sin egna ohälsan genomsyrar dessa patienters upplevelser. Kunskapen för dessa sjukdomstillstånd är bristfällig och det saknas tydliga riktlinjer och behandlingsmetoder inom vården. Slutsats Stigmatisering kring psykisk ohälsa skapar skam och utanförskap, vilket patienter med MUPS/MUS i stor utsträckning upplever. Bristande kunskap har visat på ineffektiv behandling vilket dessutom medför enorma kostnad för samhället. Sambandet mellan kropp och själ får inte förbises. Sjukvårdspersonal bör därför utbildas i att se den psykologiska faktorn bakom de fysiologiska symptomen. / Background A large proportion of patients who frequently seek health care suffer from psychophysiologic disorders (MUPS) and somatoform disorders (MUS). Both of these conditions derive from mental illness yet they manifest as physical symptoms. Stress is a psychological phenomenon which is widely spread in our society today. When a person is exposed to stress, a variety of physical reactions commence within our body, due to our survival instinct. In spite of this, a lot of people become physically and mentally ill from stress. When our body is deprived of recovery, there is a higher probability for lack of health and therefore the risk of developing psychophysiologic disorder and somatoform syndromes increases. Aim The purpose of the study was to illuminate patients with psychophysiologic disorders and somatoform disorders and their experiences within the somatic healthcare. Method A literature review has been conducted with an including total of 16 articles. The chosen articles consisted of quantitative or qualitative methods, analyzed according to the integrated analysis method. Results Patients with MUPS/MUS suffer from lack of health and are often referred to various care units without getting the help they need. This leads to further distress with a decreased health experience. Strong emotions such as exclusion, anxiety, shame and fear of lacking health permeate these patients' experiences. The knowledge regarding these conditions are insufficient and no distinct guidelines nor clear treatments exist within the healthcare system. Conclusions The stigmatization regarding mental illness leads to feelings of shame and exclusion for these patients. The lack of knowledge leads to ineffective treatment, which also entails an increased economic burden for the society. The relationship between the body and the soul must not be overlooked. Healthcare professionals need to be educated in the ability to recognize the underlying psychological factors behind the physiological symptoms.

Die Erkrankung Huntington s Chorea ist eine autosomal dominant vererbte Erkrankung, die gewöhnlich im mittleren Lebensabschnitt beginnt und unausweichlich zum Tode führt. In unserem Bestreben, Proteine zu identifizieren, welche an Prozessen "Upstream" oder "Downstream" des krankheitsverursachenden Proteins Huntingtin beteiligt sind, wurde das Proteom eines sehr gut etablierten Mausmodells mit Hilfe der Großgel 2D-Elektrophorese untersucht. Es konnte zum ersten Mal auf Proteinebene nachweisen werden, dass die Expression von zwei Serinproteasehemmern, alpha1-Antitrypsin und Contraspin und darüber hinaus eines Chaperons, alphaB-Kristallin, im Verlauf der Erkrankung abnimmt. Reduzierte Expression von alpha1-Antitrypsin und Contraspin konnte in Gehirn, Leber, Herz und Testes nahe dem Endstadium der Erkrankung nachgewiesen werden. Hier ist es wichtig festzustellen, dass die Expressionsabnahme von alpha1-Antitrypsin im Gehirn der Abnahme in der Leber im Herzen und in den Testes vorangeht. Eine verminderte Expression des Chaperons alphaB-Kristallin wurde nur im Gehirn gefunden. Für ein weiteres Protein, das Major Urinary Protein, wurde eine verminderte Expression in der Leber und im Urin von betroffenen Mäusen festgestellt. Damit konnte demonstriert werden, dass die Erkrankung auf Proteinebene auch ein Protein, das im Gehirn von transgenen Mäusen nicht vorkommt, beeinflusst. Bei Untersuchungen am Menschen wurde in drei Gehirnregionen von Postmortem-Gehirnen von Huntington s Chorea Patienten eine veränderte Expression von alpha1-Antitrypsin festgestellt. Wenn gewährleistet werden kann, dass die Konzentration von alpha1-Antitrypsin und alphaB-Kristallin während Huntington s Chorea im Gewebe nicht absinkt, könnte dies vielleicht neuronalen Zelltod verhindern und somit bei der Verzögerung des Krankheitsverlaufs nutzbringend eingesetzt werden. / Huntington disease is an autosomal dominantly inherited disease that usually starts in midlife and inevitably leads to death. In an effort to identify proteins involved in processes upstream or downstream of the disease causing huntingtin, the proteome of a well-established mouse model was studied by large-gel 2D electrophoresis. It could be demonstrated for the first time at the protein level that two serin protease inhibitors, alpha1-antitrypsin and contraspin and the chaperone alphaB-crystallin decrease in expression over the course of disease. Importantly, the alpha1-antitrypsin decrease in the brain precedes that in liver, heart and testes in mice. Reduced expression of alpha1-antitrypsin and contraspin could be detected in the brain, liver heart and testes close to terminal disease. Decreased expression of the chaperone alphaB-crystallin was found exclusively in the brain. Reduced expression of the liver specific major urinary proteins not found in the brain, was seen in affected mice, demonstrating that the disease exerts its influence on a protein not present in the brain of transgenic mice at the protein level. When investigating three human brain regions obtained post-mortem from Huntington s disease patients, alpha1-antitrypsin expression was also altered. Maintaining alpha1-antitrypsin and alphaB-crystallin availability during the course of Huntington s disease might prevent neuronal cell death and therefore could be useful in delaying the disease progression.