Separation of Gas from Liquids in Viscous Systems

Increased knowledge of the degassing process in separation of gas from oil is important in connection with development of subsea separation and boosting units for heavy oil fields. The focus in the thesis is on theory and equipment design for two-phase separation of oil and gas. A review of gravitational separators and compact separation technology with a focus on subsea installations is given first. An extensive literature review related to theory governing the degassing process is further presented. The effectiveness of the degassing process depends on the gas’ ability to migrate out of the oil. Bubble dynamics theory, especially correlations for calculation of a bubbles velocity in a liquid is therefore examined. Bubble size, fluid properties, especially liquid viscosity, and gas volume fraction in the liquid is decisive factors for the bubble velocity. A comparison of several correlations obtained in various literature is made to determine the best available for modeling degassing. Most of the correlations have a limited range of validity in terms of bubble size and Reynolds number. It is verified that they are highly inaccurate outside this range. A correlation developed to be valid for a large range of bubble sizes seems to predict bubble velocities reasonably well. Because of its large range of validity, this is chosen to be used in the development of a separator model. Some experimental work is performed on two liquids with different viscosity. It is verified that separation of gas in viscous liquids requires significantly more retention time for the smallest bubbles reach the liquid surface. Occasional deviations from the examined theory are observed, especially for the more viscous liquid. Based the chosen correlation for bubble velocity a simplified model for horizontal and vertical gravity separators is developed. Separator size, fluid properties, flow rate and distribution of bubbles are input parameters. The model calculates how much of the initial gas volume fraction that remains in the liquid after separation. Consequence of high liquid viscosity and distribution of bubble size and bubble distribution in the liquid are evaluated by use of the model. When the oil becomes very viscous is it important that separator and internals are designed to optimize the conditions for degassing. This implies among others an inlet device which provides an ability to control the bubble distribution and keep the size of bubbles as large as possible. Methods are suggested for increased effectiveness in degassing of heavy oils, by reducing viscosity, increase the coalescence rate and affecting the flow pattern. Separation of other phases and undesirable components is also important and may make it difficult to optimize the design for the degassing process. However, a separator should be efficient in all respects, making knowledge of the degassing process anyhow important. The thesis gives an overview of important parameters in the degassing process. Much work still remains to develop correlations and models which can give a more exact description of real systems. Continuous development in separator components and not at least compact separation technology is important to effectively be able to produce heavy oil, especially in terms of subsea installations

Skulderfunksjon og aktiv bevegelsesdeficit i skulderen hos pasienter med revmatoid artritt

Formål: Å undersøke skulderfunksjon hos pasienter med RA for å finne ut om det var forskjeller mellom de som hadde og de som ikke hadde aktiv bevegelsesdeficit (mindre aktiv enn passiv bevegelighet) med hensyn til demografiske data, sykdomsparametre og funksjon i skulderen; og å undersøke om aktiv bevegelsesdeficit, bevegelighet, muskelstyrke og smerter assosierte med selvrapportert skulderfunksjon i utføring av daglige gjøremål. Teoretisk forankring: RA er en kronisk inflammatorisk sykdom som angriper ledd og periartikulært bløtvev. Smerter, muskelsvakhet, redusert beveglighet og ledd-destruksjon er vanlige følger, og kan føre til problemer med daglige gjøremål. Studier viser at 65-90% av pasienter med RA har skulderproblemer. En studie av pasienter som fikk skulderprotese viste at de fleste hadde mer passiv bevegelighet enn de greide å nyttiggjøre seg aktivt, og manglende aktiv bevegelse relateres til muskelfunksjon. Svekkelse av rotatorcuffens muskler eller rupturer av senene forekommer hyppig ved RA, og kan være en årsak til dysfunksjon . Metode: Studien inkluderte 123 pasienter med RA og skulderproblemer. Demografiske data ble registrert. Sykdomsaktivitet ble målt med 28-Joint Disease Activity Score (DAS28), fysisk funksjon med Modified Health Assessment Questionnaire (MHAQ), smerter med Visuell Analog Skala (VAS), bevegelsesutslag i skulder med goniometer, muskelstyrke med fjærvekt, og aktivitetsbegrensing mht. skulderfunksjon med spørreskjemaet Disability in the Arm, Shoulder and Hand, funksjonsdel (DASH funksjon) Aktiv bevegelsesdeficit ble definert som aktivt bevegelsesutslag ≥20° mindre enn passivt utslag i abduksjon og/eller fleksjon. Resultater: Førtifem pasienter (36.6%) hadde aktiv bevegelsesdeficit. Sammenlignet med de uten deficit hadde disse pasientene høyere sykdomsaktivitet (p=0.009), dårligere fysisk funksjon(MHAQ)(p=0.001) , mer leddsmerter (p=0.009) og skuldersmerter (p=0.002), dårligere muskelstyrke (p=0.03) og mer aktivitetsbegrensing relatert til skulderfunksjonen (DASH funksjon) (p<0.001). Det var ingen forskjell mellom gruppene mht. sykdomsvarighet (p=0.71) eller varighet av skulderplagene (p=0.59). Aktiv bevegelsesdeficit, passiv bevegelighet, muskelstyrke og smerter forklarte 33.7% av variansen i DASH-funksjon score. Konklusjon: Sammenlignet med de andre pasientene var gruppen med aktiv bevegelsesdeficit dårligere av sykdommen og hadde dårligere skulderfunksjon og mer smerter, mens det ikke var forskjell mht. varighet av sykdommen eller skulderplagene. Aktiv bevegelsesdeficit sammen med bevegelighet, muskelstyrke og smerter forklarte mer enn en tredjedel av variansen i DASH-funksjon

Vascular Endothelial Growth Factor (VEGF) and Platelet (PF-4) Factor 4 Inputs Modulate Human Microvascular Endothelial Signaling in a Three-Dimensional Matrix Migration Context

The process of angiogenesis is under complex regulation in adult organisms, particularly as it often occurs in an inflammatory post-wound environment. As such, there are many impacting factors that will regulate the generation of new blood vessels which include not only pro-angiogenic growth factors such as vascular endothelial growth factor, but also angiostatic factors. During initial postwound hemostasis, a large initial bolus of platelet factor 4 is released into localized areas of damage before progression of wound healing toward tissue homeostasis. Because of its early presence and high concentration, the angiostatic chemokine platelet factor 4, which can induce endothelial anoikis, can strongly affect angiogenesis. In our work, we explored signaling crosstalk interactions between vascular endothelial growth factor and platelet factor 4 using phosphotyrosine-enriched mass spectrometry methods on human dermal microvascular endothelial cells cultured under conditions facilitating migratory sprouting into collagen gel matrices. We developed new methods to enable mass spectrometry-based phosphorylation analysis of primary cells cultured on collagen gels, and quantified signaling pathways over the first 48 h of treatment with vascular endothelial growth factor in the presence or absence of platelet factor 4. By observing early and late signaling dynamics in tandem with correlation network modeling, we found that platelet factor 4 has significant crosstalk with vascular endothelial growth factor by modulating cell migration and polarization pathways, centered around P38α MAPK, Src family kinases Fyn and Lyn, along with FAK. Interestingly, we found EphA2 correlational topology to strongly involve key migration-related signaling nodes after introduction of platelet factor 4, indicating an influence of the angiostatic factor on this ambiguous but generally angiogenic signal in this complex environment.National Science Foundation (U.S.) (NSF EFRI grant 735997)National Institutes of Health (U.S.) (NIH Cell Migration Consortium grant GM06346)National Institutes of Health (U.S.) (NIH Cell Decision Processes Center grant GM68762)National Institutes of Health (U.S.) (NIH grant GM69668)National Institutes of Health (U.S.) (NIH grant GM81336

A Case of Hypereosinophilic Syndrome Presenting With Multiorgan Infarctions Associated With Disseminated Intravascular Coagulation

Thromboembolism is one of the most critical complications of hypereosinophilic syndrome (HES). We report here a case of multi-organ infarctions related to HES. A 23-year-old woman was referred to our hospital with hemoptysis. Not only pulmonary, but also renal and splenic infarctions were detected on computed tomography images. Blood tests showed profound peripheral eosinophilia. She was diagnosed with HES with disseminated intravascular coagulation (DIC). We initiated infusion of corticosteroids, which effectively suppressed peripheral eosinophilia. However, consumptive coagulopathy did not improve and intracerebral hemorrhage related to thrombosis then developed. Addition of interferon-alpha resulted in the correction of the DIC associated with HES

The Soluble Tumor Necrosis Factor-Alpha Receptor Suppresses Airway Inflammation in a Murine Model of Acute Asthma

Asthma is a T helper 2 (Th2)-mediated inflammatory airway disease, characterized by airway hyperresponsiveness (AHR), chronic eosinophilic inflammation, episode of reversible bronchoconstriction, and mucus hypersecretion. In these responsies, several cytokines are considered to take part in a pivotal role. Although Th2 cytokines, including interleukin (IL)-4, IL-5 and IL-13, are important in asthma,1 tumor necrosis factor (TNF)-α has been implicated in the inflammatory response, seen in asthma.2 TNF-α is a multifunctional proinflammatory cytokine, and a chemoattractant for neutrophils and eosinophils.3 It increases the cytotoxic effect of eosinophils on endothelial cells,4 epithelial expression of adhesion molecules, such as intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1),6 and the contractile function of smooth muscles,7 and is involved in the activation of T cells.5 Howarth et al.8 reported that TNF-α concentration in bronchoalveolar lavage fluid (BALF) and TNF-α protein and messenger RNA (mRNA) expression in bronchial biopsy specimens were increased in patients with severe asthma compared those with mild disease

MARTX Toxin in the Zoonotic Serovar of Vibrio vulnificus Triggers an Early Cytokine Storm in Mice

Vibrio vulnificus biotype 2-serovar E is a zoonotic clonal complex that can cause death by sepsis in humans and fish. Unlike other biotypes, Bt2 produces a unique type of MARTXVv (Multifunctional-Autoprocessive-Repeats-in-Toxin; RtxA13), which is encoded by a gene duplicated in the pVvBt2 plasmid and chromosome II. In this work, we analyzed the activity of this toxin and its role in human sepsis by performing in vitro, ex vivo, and in vivo assays. First, we demonstrated that the ACD domain, present exclusively in this toxin variant, effectively has an actin-cross-linking activity. Second, we determined that the whole toxin caused death of human endotheliocytes and monocytes by lysis and apoptosis, respectively. Finally, we tested the hypothesis that RtxA13 contributes to human death caused by this zoonotic serovar by triggering an early cytokine storm in blood. To this end, we used a Bt2-SerE strain (R99) together with its rtxA13 deficient mutant, and a Bt1 strain (YJ016) producing RtxA11 (the most studied MARTXVv) together with its rtxA11 deficient mutant, as controls. Our results showed that RtxA13 was essential for virulence, as R99ΔΔrtxA13 was completely avirulent in our murine model of infection, and that R99, but not strain YJ016, induced an early, strong and dysregulated immune response involving the up-regulation of a high number of genes. This dysregulated immune response was directly linked to RtxA13. Based on these results and those obtained ex vivo (human blood), we propose a model of infection for the zoonotic serovar of V. vulnificus, in which RtxA13 would act as a sepsis-inducing toxin