Energy Management System

I 2019 utviklet Sindre Laukvik og Vebjørn Randal en EMS-modell som skulle simulere et hybrid fremdriftssystem og skulle gi mulighet for demonstrasjoner, øvinger og kunne brukes til FOU på FHS/SKSK (Randal & Laukvik, 2019). Elektriske fremdriftssystem er i stadig utvikling og antall fartøy som blir hybride øker. For å utnytte den tilgjengelige energien som finnes om bord, er det viktig at samspillet mellom generator og batteri er optimal. Et EMS gjør denne jobben. Før arbeidet begynte bestod modellen av et aggregat, en tralle med sinus inverter, PLS, batteribank, kontaktorer og strømsensorer. Programmet ble hentet ut fra vedlegg. Gjennom arbeidet på modellen er den videreutviklet ved å følge opp utviklernes anbefa linger. Det ble anbefalt å skaffe mer presise sensorer, frigjøre plass på DIN skinne, støyreduserende tiltak på DC-siden, optimalisere software, forbedre brukergrensesnitt og brukervennlighet. PLS er styreenheten som er selve hjernen til hele modellen. Det er tilført en Raspberry Pi LCD skjerm for å gjøre modellen uavhengig av en PC. Et viktig moment ved modellens uavhengighet er at aggregatet er automatisert. Kravet er at aggregatet skal ha automatisk oppstart når batteriet nærmer seg tomt. Her er det tilført en Arduino for å styre en servo som igjen betjener aggregatets choke. Start/stopp-signal til aggregatet og brytersignalet til Arduino styres av PLS. Det har blitt implementert ferrittkjerner på AC og DC side for å redusere støy generelt i modellen. Spesielt er det viktig at forbruker, batteribanken og finelektronikken i anlegget får renest mulig strøm og spenning. Det ble målt strøm og spenning ved hjelp av oscilloskop for å undersøke støynivået med og uten ferritt kjerner. Testene avslørte at ferrittkjernene hadde en positiv innvirkning på både strøm- og spenningskurver. Et EMI-filter kan muligens redusere støynivået ytterlige. Dette kan undersøkes fremover. For å gjøre modellen mer brukervennlig er det blitt laget et deksel pleksiglass for å gjøre den værbestandig og for å sikre brukeren fra eksponerte strømbærende elementer. Det er også kjøpt inn en eksos slange for å kjøre modellen inne og jordingsspyd for å kunne kjøre den ute. Modellen styres gjennom LCD skjerm. Som et hybrid fremdriftssystem Sammendrag v produserer modellen elektrisk energi gjennom et aggregat og kan lagre energi i en batteribank. Modellen prioriterer batteridrift og aggregatet slås inn når ladenivået til batteribanken er lavt. Det er også mulig å drifte modellen i landstøms modus. Modellen kan brukes, men også videreutvikles. Dette kommer frem i konklusjon med anbefalinger (7). Oppgaven har lykkes ved å videreutvikle EMS modellen slik at den er mer autonom, brukervennlig og presis

Overcast on Osiris: 3D radiative-hydrodynamical simulations of a cloudy hot Jupiter using the parametrized, phase-equilibrium cloud formation code EDDYSED (article)

This is the final version. Available from OUP via the DOI in this recordThe dataset associated with this article is available in ORE: https://doi.org/10.24378/exe.1483We present results from 3D radiative-hydrodynamical simulations of HD 209458b with a fully coupled treatment of clouds using the EDDYSED code, critically, including cloud radiative feedback via absorption and scattering. We demonstrate that the thermal and optical structure of the simulated atmosphere is markedly different, for the majority of our simulations, when including cloud radiative effects, suggesting this important mechanism cannot be neglected. Additionally, we further demonstrate that the cloud structure is sensitive to not only the cloud sedimentation efficiency (termed fsed in EDDYSED), but also the temperature–pressure profile of the deeper atmosphere. We briefly discuss the large difference between the resolved cloud structures of this work, adopting a phase-equilibrium and parametrized cloud model, and our previous work incorporating a cloud microphysical model, although a fairer comparison where, for example, the same list of constituent condensates is included in both treatments is reserved for a future work. Our results underline the importance of further study into the potential condensate size distributions and vertical structures, as both strongly influence the radiative impact of clouds on the atmosphere. Finally, we present synthetic observations from our simulations reporting an improved match, over our previous cloud-free simulations, to the observed transmission, HST WFC3 emission, and 4.5 μm Spitzer phase curve of HD 209458b. Additionally, we find all our cloudy simulations have an apparent albedo consistent with observations.Leverhulme TrustScience and Technology Facilities Council (STFC

Change in pulmonary diffusion capacity in a general population sample over 9 years

Rationale: Data on the change in diffusion capacity of the lung for carbon monoxide (DL_CO) over time are limited. We aimed to examine change in DL_CO (ΔDL_CO) over a 9-year period and its predictors. Methods: A Norwegian community sample comprising 1,152 subjects aged 18–73 years was examined in 1987 and 1988. Of the 1,109 subjects still alive, 830 (75%) were re-examined in 1996/97. DL_CO was measured with the single breath-holding technique. Covariables recorded at baseline included sex, age, height, weight, smoking status, pack years, occupational exposure, educational level, and spirometry. Generalized estimating equations analyses were performed to examine relations between ΔDL_CO and the covariables. Results: At baseline, mean [standard deviation (SD)] DL_CO was 10.8 (2.4) and 7.8 (1.6) mmol·min−1·kPa−1 in men and women, respectively. Mean (SD) ΔDLCO was −0.24 (1.31) mmol·min^−1·kPa^−1. ΔDL_CO was negatively related to baseline age, DL_CO, current smoking, and pack years, and positively related to forced expiratory volume in 1 second (FEV_1) and weight. Sex, occupational exposure, and educational level were not related to ΔDL_CO. Conclusions: In a community sample, more rapid decline in DL_CO during 9 years of observation time was related to higher age, baseline current smoking, more pack years, larger weight, and lower FEV_1.publishedVersio

The lower airways microbiome and antimicrobial peptides in idiopathic pulmonary fibrosis differ from chronic obstructive pulmonary disease

Background The lower airways microbiome and host immune response in chronic pulmonary diseases are incompletely understood. We aimed to investigate possible microbiome characteristics and key antimicrobial peptides and proteins in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Methods 12 IPF patients, 12 COPD patients and 12 healthy controls were sampled with oral wash (OW), protected bronchoalveolar lavage (PBAL) and right lung protected sterile brushings (rPSB). The antimicrobial peptides and proteins (AMPs), secretory leucocyte protease inhibitor (SLPI) and human beta defensins 1 and 2 (hBD-1 & hBD-2), were measured in PBAL by enzyme linked immunosorbent assay (ELISA). The V3V4 region of the bacterial 16S rDNA gene was sequenced. Bioinformatic analyses were performed with QIIME 2. Results hBD-1 levels in PBAL for IPF were lower compared with COPD. The predominant phyla in IPF were Firmicutes, Bacteroides and Actinobacteria; Proteobacteria were among top three in COPD. Differential abundance analysis at genus level showed significant differences between study groups for less abundant, mostly oropharyngeal, microbes. Alpha diversity was lower in IPF in PBAL compared to COPD (p = 0.03) and controls (p = 0.01), as well as in rPSB compared to COPD (p = 0.02) and controls (p = 0.04). Phylogenetic beta diversity showed significantly more similarity for IPF compared with COPD and controls. There were no significant correlations between alpha diversity and AMPs. Conclusions IPF differed in microbial diversity from COPD and controls, accompanied by differences in antimicrobial peptides. Beta diversity similarity between OW and PBAL in IPF may indicate that microaspiration contributes to changes in its microbiome.publishedVersio

Sputum microbiota and inflammation at stable state and during exacerbations in a cohort of chronic obstructive pulmonary disease (COPD) patients

Background: Exacerbations of chronic obstructive pulmonary disease (COPD) are debilitating events and spur disease progression. Infectious causes are frequent; however, it is unknown to what extent exacerbations are caused by larger shifts in the airways’ microbiota. The aim of the current study was to analyse the changes in microbial composition between stable state and during exacerbations, and the corresponding immune response. Methods: The study sample included 36 COPD patients examined at stable state and exacerbation from the Bergen COPD Cohort and Exacerbations studies, and one patient who delivered sputum on 13 different occasions during the three-year study period. A physician examined the patients at all time points, and sputum induction was performed by stringent protocol. Only induced sputum samples were used in the current study, not spontaneously expectorated sputum. Sputum inflammatory markers (IL-6, IL-8, IL-18, IP-10, MIG, TNF-α) and antimicrobial peptides (AMPs, i.e. LL-37/hCAP-18, SLPI) were measured in supernatants, whereas target gene sequencing (16S rRNA) was performed on corresponding cell pellets. The microbiome bioinformatics platform QIIME2TM and the statistics environment R were applied for bioinformatics analyses. Results: Levels of IP-10, MIG, TNF-α and AMPs were significantly different between the two disease states. Of 36 sample pairs, 24 had significant differences in the 12 most abundant genera between disease states. The diversity was significantly different in several individuals, but not when data was analysed on a group level. The one patient case study showed longitudinal dynamics in microbiota unrelated to disease state. Conclusion: Changes in the sputum microbiota with changing COPD disease states are common, and are accompanied by changes in inflammatory markers. However, the changes are highly individual and heterogeneous events.publishedVersio

Repeated bronchoscopy in health and obstructive lung disease: is the airway microbiome stable?

Objective Little is known concerning the stability of the lower airway microbiome. We have compared the microbiota identified by repeated bronchoscopy in healthy subjects and patients with ostructive lung diseaseases (OLD). Methods 21 healthy controls and 41 patients with OLD completed two bronchoscopies. In addition to negative controls (NCS) and oral wash (OW) samples, we gathered protected bronchoalveolar lavage in two fractions (PBAL1 and PBAL2) and protected specimen brushes (PSB). After DNA extraction, we amplified the V3V4 region of the 16S rRNA gene, and performed paired-end sequencing (Illumina MiSeq). Initial bioinformatic processing was carried out in the QIIME-2 pipeline, identifying amplicon sequence variants (ASVs) with the DADA2 algorithm. Potentially contaminating ASVs were identified and removed using the decontam package in R and the sequenced NCS. Results A final table of 551 ASVs consisted of 19 × 106 sequences. Alpha diversity was lower in the second exam for OW samples, and borderline lower for PBAL1, with larger differences in subjects not having received intercurrent antibiotics. Permutational tests of beta diversity indicated that within-individual changes were significantly lower than between-individual changes. A non-parametric trend test showed that differences in composition between the two exams (beta diversity) were largest in the PSBs, and that these differences followed a pattern of PSB > PBAL2 > PBAL1 > OW. Time between procedures was not associated with increased diversity. Conclusion The airways microbiota varied between examinations. However, there is compositional microbiota stability within a person, beyond that of chance, supporting the notion of a transient airways microbiota with a possibly more stable individual core microbiome.publishedVersio

Dynamic differences in dietary polyunsaturated fatty acid metabolism in sputum of COPD patients and controls

Introduction: Disturbances in onset and resolution of inflammation in chronic obstructive pulmonary disease (COPD) are incompletely understood. Dietary polyunsaturated fatty acids (PUFAs) can be converted into lipid mediators here collectively named oxylipins. These include classical eicosanoids, but also pro-resolving mediators. A balanced production of pro-inflammatory and pro-resolving oxylipins is of importance for adequate inflammatory responses and subsequent return to homeostasis. Objectives: Here we investigated if PUFA metabolism is disturbed in COPD patients. Methods: Free PUFA and oxylipin levels were measured in induced sputum samples from the Bergen COPD cohort and COPD exacerbation study using liquid chromatography-mass spectrometry. Additionally, effects of whole cigarette smoke on PUFA metabolism in air-liquid interface cultures of primary bronchial epithelial cells were assessed. Results: Significantly lower levels of free alpha-linolenic acid, linoleic acid and eicosapentaenoic acid (EPA) were detected in sputum from stable COPD patients compared to controls. During acute exacerbation (AE), levels of free arachidonic acid and docosapentaenoic acid were higher than in stable COPD patients. Furthermore, levels of omega-3 EPA- and docosahexaenoic acid-derived oxylipins were lower in sputum from stable COPD patients compared to controls. Cyclooxygenase-2-converted mediators were mostly increased during AE. In vitro studies additionally showed that cigarette smoke exposure may also directly contribute to altered epithelial PUFA metabolism, and indirectly by causing airway epithelial remodelling. Conclusions: Our findings show significant differences in PUFA metabolism in COPD patients compared to controls, further changed during AE. Airway epithelial remodelling may contribute to these changes. These findings provide new insight in impaired inflammatory resolution in COPD.publishedVersio

Factors associated with coronary heart disease in COPD patients and controls

Background: COPD and coronary heart disease (CHD) frequently co-occur, yet which COPD phenotypes are most prone to CHD is poorly understood. The aim of this study was to see whether COPD patients did have a true higher risk for CHD than subjects without COPD, and to examine a range of potential factors associated with CHD in COPD patients and controls. Methods: 347 COPD patients and 428 non-COPD controls, were invited for coronary computed tomography angiography (CCTA) and pulmonary CT. Arterial blood gas, bioelectrical impedance and lung function was measured, and a detailed medical history taken. The CCTA was evaluated for significant coronary stenosis and calcium score (CaSc), and emphysema defined as >10% of total area <-950 Hounsfield units. Results: 12.6% of the COPD patients and 5.7% of the controls had coronary stenosis (p100 compared to 31.6% of the controls (p100 was 1.68 (1.12–2.53) in COPD patients compared with controls. Examining the risk of significant stenosis and CaSc>100 among COPD patients, no variable was associated with significant stenosis, whereas male sex [OR 2.85 (1.56–5.21)], age [OR 3.74 (2.42–5.77)], statin use [OR 2.23 (1.23–4.50)] were associated with CaSc>100, after adjusting for body composition, pack-years, C-reactive protein, use of angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), diabetes, emphysema score, GOLD category, exacerbation frequency, eosinophilia, and hypoxemia. Conclusion: COPD patients were more likely to have CHD, but neither emphysema score, lung function, exacerbation frequency, nor hypoxemia predicted presence of either coronary stenosis or CaSc>100.publishedVersio