Pumpejet - den lydløse propell

I denne oppgaven har problemstillingen: "Vil pumpejet være en god propulsjonsløsning for nye undervannsfarkoster i marinen?" blitt besvart. Ved hjelp av en litteraturstudie har forfatterne funnet teori og nødvendige data for å gjennomføre propell -og pumpejetberegninger. Det er blitt definert et fiktivt fartøy basert på tall fra et slepeforsøk gjennomført av Monesoon, javadi, Charmdooz og Mikhailovich (2013). På bakgrunn av disse data har forfatterne gjennomført propelldimensjonering tilpasset dette fartøyet. Det har videre blitt gjort utregninger for virkningsgrad, rekkevidde og propellbelastning. Med propellberegningene som utgangspunkt er det til slutt blitt gjort utregninger for en akselererende pumpejet. Resultatene fra beregningene er blitt diskutert opp mot hverandre og sett i lys av teori funnet i litteraturstudien. Forskjell i kavitasjon, akustikk og økonomi er ikke med i beregningene og er av den grunn kun drøftet på bakgrunn av innhentet teori fra litteraturstudiet. Oppgavens konklusjon er todelt da kravene og operasjonsmønstrene til ulike fartøyet vil variere. Forfatterne konkluderer med at pumpejeten vil være en god propulsjonsløsning for en ny undervannsfarkost som er tiltenkt å operere med høye hastigheter eller høye akselrasjonskrav. Dette fordi resultatene og diskusjonen viser til at pumpejeten har en suveren evne til å motstå kavitasjon sammenlignet med propellen. Videre vil det for et fartøy som opererer slik at det ikke vil være fare for kavitasjon, være anbefalt å nytte en konvensjonell propell. Dette for å utnytte propellens gode virkningsgrad og billige vedlikeholdsrutiner

Разработка избирательного усилителя для приема сигналов поисковой системы

STUDY DESIGN: National registry cohort studyObjective. To investigate the effect of surgical stabilisation on survival of spinal fractures related to ankylosing spondylitis (AS). SUMMARY OF BACKGROUND DATA: Spinal fractures related to AS are associated with considerable morbidity and mortality. Multiple studies suggest a beneficial effect of surgical stabilisation in these patients. METHODS: In the Swedish patient registry all patients treated in an inpatient facility are registered with diagnosis and treatment codes. The Swedish mortality registry collects date and cause of death for all fatalities. Registry extracts of all patients with AS and spinal fractures including date of death and treatment were prepared and analysed for epidemiological purposes. RESULTS: 17297 individual patients with AS were admitted to treatment facilities in Sweden between 1987 and 2011. 990 patients with AS (age 66±14 years) had 1131 spinal fractures, of which 534 affected cervical, 352 thoracic, and 245 lumbar vertebrae. 13% had multiple levels of injuries during the observed period. Surgically treated patients had a greater survival than those treated non-surgically (HR = 0.79, p = 0.029). Spinal cord injury was the major factor contributing to mortality in this cohort (HR = 1.55, p<0.001). The proportion of surgically treated spinal fractures increased linearly during the last decades (r = 0.92, p<0.001) and was 64% throughout the observed years. CONCLUSIONS: Spinal cord injury threatened the survival of patients with spinal fractures related to AS. Even though surgical treatment is associated with a considerable complication rate, it improved the survival of spinal fractures related to AS

Thrombospondin-1: An Islet Endothelial Cell Signal of Importance for β-Cell Function

OBJECTIVE: Loss of thrombospondin (TSP)-1 in pancreatic islets has been shown to cause islet hyperplasia. This study tested the hypothesis that endothelial-derived TSP-1 is important for β-cell function. RESEARCH DESIGN AND METHODS: Islet function was evaluated both in vivo and in vitro. Messenger RNA and protein expression were measured by real-time PCR and Western blot, respectively. The role of endothelial-derived TSP-1 for β-cell function was determined using a transplantation design in which recipient blood vessels either were allowed to grow or not into the transplanted islets. RESULTS: TSP-1–deficient mice were glucose intolerant, despite having an increased β-cell mass. Moreover, their islets had decreased glucose-stimulated insulin release, (pro)insulin biosynthesis, and glucose oxidation rate, as well as increased expression of uncoupling protein-2 and lactate dehydrogenase-A when compared with control islets. Almost all TSP-1 in normal islets were found to be derived from the endothelium. Transplantation of free and encapsulated neonatal wild-type and TSP-1–deficient islets was performed in order to selectively reconstitute with TSP-1–positive or –negative blood vessels in the islets and supported that the β-cell defects occurring in TSP-1–deficient islets reflected postnatal loss of the glycoprotein in the islet endothelial cells. Treatment of neonatal TSP-1–deficient mice with the transforming growth factor (TGF)β-1–activating sequence of TSP-1 showed that reconstitution of TGFβ-1 activation prevented the development of decreased glucose tolerance in these mice. Thus, endothelial-derived TSP-1 activates islet TGFβ-1 of importance for β-cells. CONCLUSIONS: Our study indicates a novel role for endothelial cells as functional paracrine support for pancreatic β-cells

Angiopoetin-2 signals do not mediate the hypervascularization of islets in type 2 diabetes

Aims Changes in the islet vasculature have been implicated in the regulation of β-cell survival and function during the progression to type 2 diabetes (T2D). Failure of the β-cell to compensate for the increased insulin demand in obesity eventually leads to diabetes; as a result of the complex interplay of genetic and environmental factors (e.g. ongoing inflammation within the islets) and impaired vascular function. The Angiopoietin/Tie (Ang/Tie) angiogenic system maintains vasculature and is closely related to organ inflammation and angiogenesis. In this study we aimed to identify whether the vessel area within the islets changes in diabetes and whether such changes would be triggered by the Tie-antagonist Ang-2. Methods Immunohistochemical and qPCR analyses to follow islet vascularization and Ang/Tie levels were performed in human pancreatic autopsies and isolated human and mouse islets. The effect of Ang-2 was assessed in β-cell-specific Ang-2 overexpressing mice during high fat diet (HFD) feeding. Results Islet vessel area was increased in autopsy pancreases from patients with T2D. The vessel markers Tie-1, Tie-2 and CD31 were upregulated in mouse islets upon HFD feeding from 8 to 24 weeks. Ang-2 was transiently upregulated in mouse islets at 8 weeks of HFD and under glucolipotoxic conditions (22.2 mM glucose/ 0.5 mM palmitate) in vitro in human and mouse islets, in contrast to its downregulation by cytokines (IL-1β, IFN- and TNF-α). Ang-1 on the other hand was oppositely regulated, with a significant loss under glucolipotoxic condition, a trend to reduce in islets from patients with T2D and an upregulation by cytokines. Modulation of such changes in Ang-2 by its overexpression or the inhibition of its receptor Tie-2 impaired β-cell function at basal conditions but protected islets from cytokine induced apoptosis. In vivo, β-cell-specific Ang-2 overexpression in mice induced hypervascularization under normal diet but contrastingly led to hypovascularized islets in response to HFD together with increased apoptosis and reduced β-cell mass. Conclusions Islet hypervascularization occurs in T2D. A balanced expression of the Ang1/Ang2 system is important for islet physiology. Ang-2 prevents β-cell mass and islet vascular adaptation in response to HFD feeding with no major influence on glucose homeostasis

Calcium : A Crucial Potentiator for Efficient Enzyme Digestion of the Human Pancreas

Background: Effective digestive enzymes are crucial for successful islet isolation. Supplemental proteases are essential because they synergize with collagenase for effective pancreatic digestion. The activity of these enzymes is critically dependent on the presence of Ca2+ ions at a concentration of 5-10 mM. The present study aimed to determine the Ca2+ concentration during human islet isolation and to ascertain whether the addition of supplementary Ca2+ is required to maintain an optimal Ca2+ concentration during the various phases of the islet isolation process. Methods: Human islets were isolated according to standard methods and isolation parameters. Islet quality control and the number of isolations fulfilling standard transplantation criteria were evaluated. Ca2+ was determined by using standard clinical chemistry routines. Islet isolation was performed with or without addition of supplementary Ca2+ to reach a Ca2+ of 5 mM. Results: Ca2+ concentration was markedly reduced in bicarbonate-based buffers, especially if additional bicarbonate was used to adjust the pH as recommended by the Clinical Islet Transplantation Consortium. A major reduction in Ca2+ concentration was also observed during pancreatic enzyme perfusion, digestion, and harvest. Additional Ca2+ supplementation of media used for dissolving the enzymes and during digestion, perfusion, and harvest was necessary in order to obtain the concentration recommended for optimal enzyme activity and efficient liberation of a large number of islets from the human pancreas. Conclusions: Ca2+ is to a large extent consumed during clinical islet isolation, and in the absence of supplementation, the concentration fell below that recommended for optimal enzyme activity. Ca2+ supplementation of the media used during human pancreas digestion is necessary to maintain the concentration recommended for optimal enzyme activity. Addition of Ca2+ to the enzyme blend has been implemented in the standard isolation protocols in the Nordic Network for Clinical Islet Transplantation.Peer reviewe

En empirisk analyse av det kjønnsdelte arbeidsmarkedet i Norge : med fokus på kvinners deltidsarbeid i perioden 2003 til 2011

Denne masteroppgaven benytter empiriske metoder for å analysere omfanget av deltidsarbeid blant kvinner i Norge. Flere faktorer er inkludert for å identifisere hvilke kvinner som arbeider deltid, og hvordan dette eventuelt har endret seg over tid. Vi vil se på både endogen og eksogen påvirkning. Datamaterialet bygger på forløpsdatabasen FD-trygd. Det inneholder blant annet variabler som; bakgrunn, familiesituasjon, utdanning, næring, yrke m.m. Vi har hovedsakelig sett på perioden 2003 til 2011. Spesielt har vi vært interessert i effekten av Arbeidsmiljølovendringen per 1. januar 2006, der deltidsansatte fikk rett til å få utvidet sin stilling før arbeidsgiver ansetter nye arbeidstakere. Vi finner at endringsloven har hatt en positiv effekt på gjennomsnittlig arbeidstid for kvinner. Vi mener derfor vi kan antyde at deltid ikke kun handler om preferanser. Ellers finner vi at kvinner fortsatt arbeider mindre enn menn og at mange kvinner jobber i kvinnedominerte yrker som salg- og service, men at vi har en utvikling der kvinner i større grad går inn i mannsdominerte yrker hvor kjønnsforskjellene i arbeidstid minimeres. Vi finner også at barn vil påvirke kvinners arbeidstid mer enn menns. Vi finner større kjønnsforskjeller mellom kvinner og menn med grunnskole-/eller videregående skolenivå enn mellom kvinner og menn med høyere utdannelse

Role of Thrombospondin-1 in Endogenous and Transplanted Pancreatic Islets

Type 1 diabetes mellitus is a severe life-long disease with a pronounced risk of developing secondary complications. One way to avoid the latter is to restore the fine tuning of blood glucose homeostasis by transplantation of pancreatic islets. However, isolated islets need to be properly engrafted and to re-establish a vascular network in order to regain function. Earlier studies have shown that pancreatic islets experimentally transplanted to e.g. the liver or the kidney become poorly revascularized. In the present thesis, mice deficient of the angiostatic factor thrombospondin-1 (TSP-1) were found to have an impaired beta-cell function. Development of this beta-cell dysfunction was prevented by treatment of TSP-1 deficient mice from birth with the TGFbeta-1 activating sequence of TSP-1. TSP-1 in islets was predominantly expressed in the endothelial cells. Isolated islet endothelial cells was observed to have a low proliferatory and migratory capacity towards angiogenic stimuli, but this could be reversed by neutralizing antibodies to the angiostatic factors alpha1-antitrypsin, endostatin or TSP-1. Transient downregulation of TSP-1 expression in mouse islet cells prior to transplantation improved graft revascularization, blood perfusion, oxygenation and function when evaluated one-month post-transplantation. The same result was achieved when islets or recipients of islets were pre-treated with the hormone prolactin one-month post-transplantation. The present study illustrates the importance of the angiostatic factor TSP-1 for islet beta-cell function and engraftment of islets following transplantation. Interference with TSP-1 can possibly be used to improve the results of clinical islet transplantation

Surgical stabilisation improves survival of spinal fractures related to ankylosing spondylitis

STUDY DESIGN: National registry cohort studyObjective. To investigate the effect of surgical stabilisation on survival of spinal fractures related to ankylosing spondylitis (AS). SUMMARY OF BACKGROUND DATA: Spinal fractures related to AS are associated with considerable morbidity and mortality. Multiple studies suggest a beneficial effect of surgical stabilisation in these patients. METHODS: In the Swedish patient registry all patients treated in an inpatient facility are registered with diagnosis and treatment codes. The Swedish mortality registry collects date and cause of death for all fatalities. Registry extracts of all patients with AS and spinal fractures including date of death and treatment were prepared and analysed for epidemiological purposes. RESULTS: 17297 individual patients with AS were admitted to treatment facilities in Sweden between 1987 and 2011. 990 patients with AS (age 66±14 years) had 1131 spinal fractures, of which 534 affected cervical, 352 thoracic, and 245 lumbar vertebrae. 13% had multiple levels of injuries during the observed period. Surgically treated patients had a greater survival than those treated non-surgically (HR = 0.79, p = 0.029). Spinal cord injury was the major factor contributing to mortality in this cohort (HR = 1.55, p<0.001). The proportion of surgically treated spinal fractures increased linearly during the last decades (r = 0.92, p<0.001) and was 64% throughout the observed years. CONCLUSIONS: Spinal cord injury threatened the survival of patients with spinal fractures related to AS. Even though surgical treatment is associated with a considerable complication rate, it improved the survival of spinal fractures related to AS

Do biological disease-modifying antirheumatic drugs reduce the spinal fracture risk related to ankylosing spondylitis? : A longitudinal multiregistry matched cohort study

Objectives: Ankylosing spondylitis (AS) is associated with an increased spinal fracture risk due to the loss of elasticity in spinal motion segments. With the introduction of biological disease-modifying antirheumatic drug (bDMARD) treatment for AS, the individual course of the disease has been ameliorated. This study aims to examine the association of bDMARD treatment and risk of spinal fracture. Design: Longitudinal population-based multiregistry observational matched cohort study. Setting: Swedish Patient Registry 1987–2014 and Swedish Prescribed Drugs Registry 2005–2014. Participants: Included were patients ≥18 years of age receiving treatment at a healthcare facility for the primary diagnosis of AS. About 1352 patients received more than one prescription of bDMARD from 2005 to 2014. An untreated control group was created by propensity score matching for age, sex, comorbidity, antirheumatic prescriptions and years with AS (n=1352). Main outcome measures: Spinal fracture-free survival. Results: No bDMARD treatment-related effect on spinal fracture-free survival was observed in the matched cohorts. Male gender (HR=2.54, 95% CI 1.48 to 4.36) and Charlson Comorbidity Index score (HR=3.02, 95% CI 1.59 to 5.75) contributed significantly to spinal fracture risk. Conclusion: bDMARD had no medium-term effect on the spinal fracture-free survival in patients with AS. Trial registration number: NCT0284069

Sustained Beta-Cell Dysfunction but Normalized Islet Mass in Aged Thrombospondin-1 Deficient Mice

Pancreatic islet endothelial cells have in recent years been shown to support beta-cell mass and function by paracrine interactions. Recently, we identified an islets endothelial-specific glycoprotein, thrombospondin-1 (TSP-1), that showed to be of importance for islet angiogenesis and beta-cell function in young mice. The present study aimed to investigate long-term consequences for islet morphology and beta-cell function of TSP-1 deficiency. Islet and beta-cell mass were observed increased at 10-12 weeks of age in TSP-1 deficient mice, but were normalized before 16 weeks of age when compared to wild-type controls. Islet vascularity was normal in 10-12 and 16-week-old TSP-1 deficient animals, whereas islets of one-year-old animals lacking TSP-1 were hypervascular. Beta-cell dysfunction in TSP-1 deficient animals was present at similar magnitudes between 10-12 and 52 weeks of age, as evaluated by glucose tolerance tests. The insulin secretion capacity in vivo of islets in one-year-old TSP-1 deficient animals was only similar to 15% of that in wild-type animals. Using a transplantation model, we reconstituted TSP-1 in adult TSP-deficient islets. In contrast to neonatal TSP-1 deficient islets that we previously reported to regain function after TSP-1 reconstitution, adult islets failed to recover. We conclude that TSP-1 deficiency in islets causes changing vascular and endocrine morphological alterations postnatally, but is coupled to a chronic beta-cell dysfunction. The beta-cell dysfunction induced by TSP-1 deficiency is irreversible if not substituted early in life