Bakgrund: Intuberade patienter inom intensivvården har en hög risk för att erhålla en ventilator-associerad pneumoni (VAP). Det finns evidensbaserade riktlinjer för vuxna somförebygger VAP. För barn behövs det däremot mer forskning för att klargöra vilka omvårdnadsåtgärder som kan standardiseras. Syfte: Syftet är att beskriva vilka omvårdnadsåtgärder som förebygger VAP hos barn inom intensivvården, en litteraturöversikt. Metod: En deskriptiv litteraturstudie med kvantitativ induktiv ansats valdes. 16 kvantitativa studier analyserades med en innehållsanalys. Det samlade materialet kvalitetsgranskades med hjälp av GRADE. Resultat: Fem huvudteman identifierades utifrån studiernas resultat. Huvudteman var VAP-omvårdnadspaket, munvård med klorhexidin, skötsel av endotrakealtub, olika nutritionssonder, omvårdnadsutbildning. VAP-omvårdnadspaket och omvårdnadsutbildning visade sig statistiskt signifikant sänka VAP-prevalensen hos barn. Munvård med klorhexidin kunde inte sänka VAP-prevalensen. Slutsats: Med rätt evidensbaserad vård kan VAP-prevalensen sänkas. Forskning kring VAP-prevention till barn saknar evidens i nuläget och kan ej anses vara evidensbaserad vård. För att göra vården evidensbaserad, rekommenderas att globala riktlinjer för VAP-prevention till barn tas fram. / Background: Intubated patients admitted to an intensive care unit have a higher risk ofacquiring ventilator-associated pneumonia (VAP). There are evidence-based guidelines for adults that prevent VAP. For children there is a need for more research in this area to clarifywhich nursing methods can be standardized. Aim: The aim was to describe which nursing care measures prevent VAP in children admitted to the intensive care unit, a literature review. Method: A descriptive literature study with a quantitative inductive approach was used. A total of 16 quantitative studies was analysed with a content analysis. A GRADE system was used to assess the quality of the included studies. Results: Five main themes were identified from the study’s results. The main themes where VAP-care bundles, oral care with chlorhexidine, care of endotracheal tube, different nutritional catheters, and nursing care education. VAP-care bundles and nursing care education showed to have statistically and significantly lowered the prevalence of VAP in children. Oral care with Chlorhexidine did not lower the prevalence significantly of VAP. Conclusion: The prevalence of VAP can be lowered with the right evidence-based practice. At the current situation research on preventing VAP in children lack evidence and can’t be considered as evidence-based practice. To make the nursing care evidence based, it´s recommended to create global guidelines of VAP-prevention for children.

Bakgrund: Munhälsan hos intuberade patienter försämras successivt under vårdtiden. Risken att drabbas av VAP ökar dagligen och VAP anses vara en av de vanligaste komplikationerna till respiratorvård och patienter som drabbas kräver längre vårdtid. Munvård är en del av VAP-preventionen men det framgår inte vilka specifika munvårdsåtgärder som har effekt.    Syfte: Syftet med denna uppsats är att beskriva vilka munvårdsåtgärder som är mest effektiva avseende preventionen av VAP och därmed bör användas i intensivvårdssjuksköterskans dagliga arbete.   Metod: En systematisk litteraturöversikt med kvantitativ induktiv ansats. Sammanlagt 17 studier inkluderades i denna uppsats.    Resultat: Två huvudkategorier identifierades samt två subkategorier. Införandet av munvårdsprotokoll gav en statistiskt signifikant minskning av VAP-prevalens, klorhexidin kan vara effektivt mot VAP men det finns även andra antibakteriella lösningar som effektivt förebygger VAP.    Slutsats: För att bidra till ökad patientsäkerhet borde specialistsjuksköterskor inom intensivvård använda ett munvårdsprotokoll för att arbeta preventivt mot VAP. Utöver detta ska tandborstar regelbundet bytas ut, verksamheten borde även se över möjligheten att inkludera tandläkare. Dock är det aktuellt med ytterligare forskning om munvård för att i framtiden använda endast de munvårdsåtgärder som bevisats vara effektiva. / Background: The oral hygiene in intubated patients successively deteriorates during the period of care. The risk of contracting a VAP increases daily and VAP is considered to be one of the most common complications related to mechanical ventilation. The patients who are afflicted require a prolonged hospital stay. Oral hygiene is a part of VAP-prevention but it remains unclear as to which specific oral care measures are effective.    Aim: The aim of this study is to describe which oral care measures are the most effective in the prevention of VAP and therefore should be used by the intensive care nurse in the daily working routine.    Method: A systematic literature study with a qualitative inductive approach was used. A total of 17 studies were included in this essay.   Results: Two main categories were identified as well as two subcategories. The adoption of oral care protocols showed a statistically significant decrease of VAP, and chlorhexidine can be effective against VAP however there are also other antibacterial solutions which effectively prevent VAP.   Conclusion: In order to contribute to increased patient safety intensive care nurses should use an oral care protocol to prevent VAP. In addition to the protocol toothbrushes should be replaced regularly, and the ward should oversee the possibility of including dentists to optimize the oral care. Oral care requires additional research so that in the future it is possible to use only the oral care procedures that have been proven to be effective.

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Dans ce mémoire, je présenterai les outils que nous avons développés dans le cadre de ma maîtrise. Tout d'abord, je présenterai un outil d'analyse de données génomiques nommé Versatile Aggregrate Profiler (VAP). Ensuite, je présenterai un outil d'identification de profils agrégés similaires nommé vap_sim ainsi que la méthodologie utilisée afin d'obtenir un paramétrage adéquat de l'outil pouvant s'adapter assez facilement aux différents profils agrégés. Au troisième chapitre, je présenterai un outil de validation de formats génomiques nommé Genomic Format Validator (GFV) permettant d'identifier simplement et rapidement les erreurs de structure et de logique dans un fichier de données génomiques. Finalement, au dernier chapitre, je présenterai trois outils complémentaires à VAP.

La « semicarbazide-sensitive amine oxidase » (SSAO) catalyse la déamination oxydative des amines primaires en aldéhyde, peroxyde d’hydrogène et ammoniac. Elle participe à la différenciation cellulaires, l’inflammation et la transmigration leucocytaire à travers l’endothélium lymphatique. Nos objectifs ont été d’étudier le rôle de la SSAO (i) dans la différenciation chondrocytaire hypertrophique, en relation avec le développement de l’arthrose en utilisant des chondrocytes de rat en culture primaire et des genoux arthrosiques de patients (ii) dans le développement de l’athérosclérose en invalidant des souris ApoE-/- qui développent naturellement l’athérosclérose pour le gène de la SSAO. Au niveau articulaire, la SSAO a été détectée dans le cartilage de rat et humain. In vitro, la SSAO (activité et expression) augmentent au cours de la différenciation terminale de chondrocytes de rat. Son inhibition par le LJP1586 entraîne un retard de différenciation chondrocytaire. La SSAO augmente également dans les zones arthrosiques du cartilage humain parallèlement à l’augmentation de l’hypertrophie. La SSAO jouerait donc un rôle dans la différenciation terminale des chondrocytes (hypertrophie) possiblement via le transport de glucose et dans le développement de la maladie. Au niveau vasculaire, les souris femelles ApoE-/-SSAO-/- de 25 semaines présentent une augmentation de la surface des plaques d’athérome par rapport aux ApoE-/-. Ceci est associée à une diminution de l’expression d’α-actine dans le média sous les plaques et de smMHC dans l’aorte abdominale (AA) sans modification ni de l’infiltration des lymphocytes T; ni des monocytes/ macrophages dans la paroi artérielle, ni du profil cytokinique pro-/anti-inflammatoire dans la rate. A 15 semaines, les souris femelles ApoE-/-SSAO-/-, sm-MHC a diminué dans les AA de ces souris par rapport aux ApoE-/- ainsi qu’une réorientation du trafic des cellules immunitaires vers la paroi aortique sans modification significative de la surface des plaques a été détecté. La SSAO jouerait donc un rôle précoce dans le développement de l’athérosclérose via une modification du trafic des cellules immunitaires et du phénotype des CML dans la paroi / The semicarbazide-sensitive amine oxidase (SSAO) catalyzes the oxidative deamination of primary amines into aldehydes, hydrogen peroxide and ammonia. The SSAO was implicated in cellular differentiation, inflammation and transmigration of leukocyte through the lymphatic. The objectives of this work were to study the role of SSAO (i) in chondrocyte differentiation and in the development of osteoarthritis using rat chondrocyte primary cell culture and osteroarthritic samples from patients. (ii) in the development of atherosclerosis using ApoE-/- mice, which develop naturally atherosclerosis, invalidated for the SSAO gene. Concerning the articulation, the SSAO (expression and activity) was detected in the rat and human cartilage. In vitro, SSAO increases during chondrocyte terminal differentiation (hypertrophy) and the inhibition of its activity by LJP1586, decreases the level of differentiation. In human arthritic cartilage, SSAO was higher that in healthy cartilage, in association with an increase in hypertrophic markers. The SSAO plays a role in the terminal differentiation of chondrocytes and might be involved in the development of osteoarthritis. At the vascular level, 25 week-old female ApoE-/-SSAO-/- mice presented a 50% increase in plaque surface associated with an 80% decrease in α-actin expression in the media of aortic sinus and a decrease in sm-MCH in abdominal aortas (AA) compared to ApoE-/- mice. These results were not due neither to a modification of monocytes/ macrophages, Tcell infiltration in the plaque nor in a pro- or anti-inflammatory cytokine change in spleen. In 15 week-old ApoE-/-SSAO-/- mice, even if no modification of plaque surface was found, a decrease in sm-MHC was noticed in the AA from ApoE-/-SSAO-/- compare to ApoE-/- mice. More over, the immune cell trafficking was increased in the aortic wall of ApoE-/-SSAO-/- compared to ApoE-/- mice. Thus, SSAO is involved in the early development of atherosclerosis in changing the immune cell trafficking and the VSMC phenotype

Bakgrund: Ventilatorassocierad pneumoni, VAP, är en vårdrelaterad infektion inom intensivvården som ökar mortaliteten och vårdkostnaden. För att förebygga VAP finns olika åtgärder som beskrivs i kliniska riktlinjer. Dessa finns som stöd för hälso- och sjukvårdspersonal för att öka patientsäkerheten. I dagsläget finns inga nationella eller internationella VAP-förebyggande riktlinjer. Syfte: Syftet är att kvalitetsgranska och jämföra svenska intensivvårdsavdelningars lokala kliniska riktlinjer gällande VAP-förebyggande åtgärder för vuxna. Metod: Kvantitativ deskriptiv studie. De lokala kliniska riktlinjerna kvalitetsgranskades med hjälp av kvalitétbedömningsinstrumentet AGREE II.  Resultat: Totalt kvalitetsgranskades och jämfördes 34% (n=27) av Sveriges intensivvårdsavdelningars lokala kliniska riktlinjer gällande VAP-förebyggande åtgärder. Alla granskade lokala kliniska riktlinjerna var av låg kvalité. Den låga kvalitén var bland annat orsakad av låg noggrannhet vid framställningen av riktlinjen [md=5] och lågt redaktionellt oberoendet [md=0]. I jämförelsen av VAP-förebyggande åtgärderna beskrev 93–100% (n=25–27) av riktlinjerna möjlighet till subglottisaspiration, kufftryck mellan 25–30 cmH2O, höjd huvudända eller tippning till 30–45 grader och skriftliga rutiner.  Slutsats: Sveriges intensivvårdsavdelningars granskade lokala kliniska riktlinjer gällande förebyggande av ventilatorassocierad pneumoni, VAP, var av låg kvalité. De innehåller en stor variation av VAP-förebyggande åtgärder, som i vissa fall var motsägande.  Det finns behov av en uppdaterad och evidensbaserade nationell eller internationell klinisk riktlinje gällande förebyggande av VAP. Detta för att säkra patientsäkerheten på Sveriges intensivvårdsavdelningar. / Background: Ventilator associated-pneumonia, VAP is a hospital acquired-infection that increases the mortality and the healthcare cost in the intensive care. There are different methods to prevent VAP. These methods are described in clinical guidelines. These guidelines are there to support healthcare professionals and to increase patient safety. There exist no national or international clinical guidelines for VAP-preventions. Aim: The aim is to quality appraise and compare Swedish intensive care units´ local clinical guidelines of VAP-prevention for adults.  Method: A quantitative descriptive study. The local clinical guidelines were appraised with the qualitative appraisal instrument AGREE-II.  Main result: In total 34% (n=27) of the Swedish intensive care units clinical guidelines for VAP-preventions were quality appraised and compared. All reviewed local clinical guidelines were of low quality. The low quality was caused by low accuracy in the preparation of the guideline [md=5] and low editorial independence [md=0]. In the comparison of VAP-preventions 93–100% (n=25–27) of the clinical guidelines described the possibility of subglottic aspiration, cuff-pressure between 25–35 cmH20, elevated head of the bed to 30–45 degrees and written guidelines.  Conclusion: The local Swedish intensive care units reviewed clinical guidelines for prevention of ventilator associated pneumonia, VAP had low quality.  They included a large variation of different VAP-preventions, and some of the preventions were contradictory. There is a need for an updated and evidence based national or international clinical guideline to prevent VAP. There is a need to ensure the patient safety in Sweden's intensive care units.

<p>Plasma activity of the enzyme semicarbazide-sensitive amine oxidase (SSAO; EC.1.4.3.6) has been reported to be high in disorders such as diabetes mellitus, chronic congestive heart failure and liver cirrhosis. Little is known of how the activity is regulated and, consequently, the cause for these findings is not well understood. Due to the early occurrence of increased enzyme activity in diabetes, in conjunction with the production of highly cytotoxic substances in SSAO-catalysed reactions, it has been speculated that there could be a causal relationship between high SSAO activity and vascular damage. Aminoacetone and methylamine are the best currently known endogenous substrates for human SSAO and the resulting aldehyde-products are methylglyoxal and formaldehyde, respectively. Both of these aldehydes have been shown to be implicated in the formation of advanced glycation end products (AGEs).</p><p>This thesis is based on studies exploring the regulation of SSAO activity and its possible involvement in the development of vascular damage. The results further strengthen the connection between high SSAO activity and the occurrence of vascular damage, since type 2 diabetic patients with retinopathy were found to have higher plasma activities of SSAO and lower urinary concentrations of methylamine than patients with uncomplicated diabetes. From studies on mice, it was also found that an SSAO inhibitor potently reduces the incorporation of methylamine-metabolite in the tissues. By quantifying SSAO-gene expression in alloxan-induced diabetes, increased transcription could be ruled out as a cause for the increased enzyme activity, thereby opening up for the possibility that the activity is regulated post-translationally. In fact, increased enzyme activity in adipose tissue was accompanied by decreased mRNA-levels, suggesting that the gene expression could be negatively controlled by the enzyme activity.</p>

<p>Semicarbazide-sensitive amine oxidase (SSAO, EC 1.4.3.6) belongs to a family of copper-containing amine oxidases. SSAO exists as a membrane bound protein in endothelial-, smooth muscle-, and adipose cells as well as soluble in plasma. SSAO catalyses oxidative deamination of primary monoamines, which results in the production of corresponding aldehydes, hydrogen peroxide and ammonia. These compounds are very reactive and potentially cytotoxic, and are able to induce vascular damage if produced in high levels. Patients with diabetes mellitus, and with diabetic complications in particular, have a higher SSAO activity in plasma compared to healthy controls. It has therefore been speculated that high SSAO activity is involved in the development of vascular complications associated with diabetes. The aim of this thesis is to investigate the importance of SSAO in the development of disorders of a vascular origin. We have studied the transcriptional regulation of the SSAO gene, by inducing diabetes in NMRI and in transgenic mice, overexpressing the human form of SSAO in smooth muscle cells. We found that the increase in SSAO activity in diabetes is accompanied by reduced mRNA levels of the endogenous mouse gene, suggesting a negative feedback on the transcription of the SSAO gene. In addition, the transgenic mice exhibited an abnormal phenotype in the elastic tissue of aorta and renal artery. These mice have a lower mean artery pressure and an elevated pulse pressure. These results indicate that high SSAO activity in smooth muscle cells is associated with a change in the morphology of large arteries. This is likely contributing to the development of vascular complications in diabetes.</p>

Plasma activity of the enzyme semicarbazide-sensitive amine oxidase (SSAO; EC.1.4.3.6) has been reported to be high in disorders such as diabetes mellitus, chronic congestive heart failure and liver cirrhosis. Little is known of how the activity is regulated and, consequently, the cause for these findings is not well understood. Due to the early occurrence of increased enzyme activity in diabetes, in conjunction with the production of highly cytotoxic substances in SSAO-catalysed reactions, it has been speculated that there could be a causal relationship between high SSAO activity and vascular damage. Aminoacetone and methylamine are the best currently known endogenous substrates for human SSAO and the resulting aldehyde-products are methylglyoxal and formaldehyde, respectively. Both of these aldehydes have been shown to be implicated in the formation of advanced glycation end products (AGEs). This thesis is based on studies exploring the regulation of SSAO activity and its possible involvement in the development of vascular damage. The results further strengthen the connection between high SSAO activity and the occurrence of vascular damage, since type 2 diabetic patients with retinopathy were found to have higher plasma activities of SSAO and lower urinary concentrations of methylamine than patients with uncomplicated diabetes. From studies on mice, it was also found that an SSAO inhibitor potently reduces the incorporation of methylamine-metabolite in the tissues. By quantifying SSAO-gene expression in alloxan-induced diabetes, increased transcription could be ruled out as a cause for the increased enzyme activity, thereby opening up for the possibility that the activity is regulated post-translationally. In fact, increased enzyme activity in adipose tissue was accompanied by decreased mRNA-levels, suggesting that the gene expression could be negatively controlled by the enzyme activity.

Semicarbazide-sensitive amine oxidase (SSAO, EC 1.4.3.6) belongs to a family of copper-containing amine oxidases. SSAO exists as a membrane bound protein in endothelial-, smooth muscle-, and adipose cells as well as soluble in plasma. SSAO catalyses oxidative deamination of primary monoamines, which results in the production of corresponding aldehydes, hydrogen peroxide and ammonia. These compounds are very reactive and potentially cytotoxic, and are able to induce vascular damage if produced in high levels. Patients with diabetes mellitus, and with diabetic complications in particular, have a higher SSAO activity in plasma compared to healthy controls. It has therefore been speculated that high SSAO activity is involved in the development of vascular complications associated with diabetes. The aim of this thesis is to investigate the importance of SSAO in the development of disorders of a vascular origin. We have studied the transcriptional regulation of the SSAO gene, by inducing diabetes in NMRI and in transgenic mice, overexpressing the human form of SSAO in smooth muscle cells. We found that the increase in SSAO activity in diabetes is accompanied by reduced mRNA levels of the endogenous mouse gene, suggesting a negative feedback on the transcription of the SSAO gene. In addition, the transgenic mice exhibited an abnormal phenotype in the elastic tissue of aorta and renal artery. These mice have a lower mean artery pressure and an elevated pulse pressure. These results indicate that high SSAO activity in smooth muscle cells is associated with a change in the morphology of large arteries. This is likely contributing to the development of vascular complications in diabetes.