Sjømakt i en moderne kontekst: Er sjøkontroll fortsatt relevant?

Denne oppgaven handler om sjøkontroll, et av sjømaktens kjernebegreper. Gjennom bruk av en abduktiv og induktiv kvalitativ metode søkes det å besvare hvorvidt sjøkontroll er relevant i dagens moderne kontekst. Oppgaven har en teoretisk redegjørelse av sjømaktens rolle, målsetting og virkemidler. Sjøkontroll har gjennom årtider vært det viktigste målsettingen i sjøstriden, hvor man søker å oppnå en tilstand som gir handlefrihet i det maritime domenet og samtidig, om nødvendig, hindrer en motstander det samme. Oppgaven gjør en grundig beskrivelse av begrepets betydning, innhold og forutsetninger. Sjøkontroll er ikke absolutt og kan modereres gjennom faktorene tid og rom, grad og risikovilje. Ut over sjøkontroll er sjønektelse og maritim maktprojeksjon de viktigste begrepene i sjøstriden. Den moderne kontekst defineres i oppgaven til å bestå av det moderne operasjonsmiljø, det moderne trusselbildet og den sikkerhetspolitiske og strategiske dimensjon. Dagens operasjonsmiljø er langt mer kompleks enn det var for bare noen tiår siden, og elementene i operasjonsmiljøet sameksisterer i tid og rom, påvirker hverandre. Det moderne trusselbildet pregers av langtrekkende presisjonsild, autonome sensorer og hybride trusler. Dagens sikkerhetspolitiske og strategiske dimensjon preges av større alvor og uforutsigbarhet, og de endrede strategiske forutsetningene påvirker også den moderne sjømakten. Sjøkontroll analyseres gjennom faktorene tid og rom, grad og risiko opp mot faktorer i den moderne kontekst. Analysen peker på at det er flere elementer som vil gjøre det utfordrende å etablere og opprettholde sjøkontroll, nå og i fremtiden

HOW PRODUCT SERVICE SYSTEMS FACILITATE ECO-INNOVATION BEHAVIOR

Increasingly firms develop technology-based sharing approaches where users rent, lease and share products, instead of purchasing them. Particularly, the product service system (PSS) concept has recently caught attention by scholars from different disciplines, although surprisingly little from the innovation research community. The writings from our colleagues however lead us to suspect that PSS developing firms might pursue an innovation behavior that is much more in line with recent societal demands for reducing environmental externalities. Recent examples show that adopting the PSS approach could be a way even for profit-driven firms towards a more sustainable economy, actually without too much governmental intervention. However, to our knowledge this argument has yet been hardly discussed in detail. Drawing on concepts from the innovation management literature as well as from environmental management research, we contribute a model that explains why the PSS approach can shift firm innovation behavior towards generating fewer environmental externalities. This model links firm innovation behavior to three antecedents, including two product related characteristics (ownership, product purpose) and the specifics of the PSS related profit function. We argue that these antecedents differ whether firms develop products or PSSs. In the latter case the antecedent specifications impact firms’ R&D objectives in a way that creates incentives to follow innovation trajectories that lead to a reduction of environmental externalities (i.e., ecoinnovation behavior)

The impact of comorbidities on interleukin-17 inhibitor therapy in psoriatic arthritis: a Danish population-based cohort study

Objective To investigate the influence of comorbidities on treatment response, disease activity and persistence with first-line IL-17 inhibitor (IL-17i) treatment in patients with PsA. Methods Patients were divided into three groups depending on the presence and/or severity of comorbidities using the Charlson Comorbidity Index (CCI). Groups were CCI 0: no comorbidities, CCI 1: one comorbidity and CCI ≥2: two or more comorbidities or one or more severe comorbidities. Outcomes in the groups were compared for treatment persistence, treatment response and disease activity. Results A higher CCI score was associated to an elevation in baseline CRP, swollen joint count and frequency of depression and/or anxiety. The median drug persistence in the groups were CCI 0: 1.8 years, CCI 1: 1.9 years and CCI ≥2: 1.5 years, but was not statistically significant to the CCI score. There were no significant differences in clinical response rates between the groups. Conclusion The presence of comorbidities was associated with increased baseline disease activity and frequency of depression and/or anxiety, but was not associated with shorter treatment persistence or lower clinical response rates in a cohort of 155 Danish patients with PsA treated with first-line IL-17i

Comparisons between MHD model calculations and observations of Cassini flybys of Titan

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94689/1/jgra18227.pd

Genome-wide association and HLA fine-mapping studies identify risk loci and genetic pathways underlying allergic rhinitis

Allergic rhinitis is the most common clinical presentation of allergy, affecting 400 million people worldwide, with increasing incidence in westernized countries1,2. To elucidate the genetic architecture and understand the underlying disease mechanisms, we carried out a meta-analysis of allergic rhinitis in 59,762 cases and 152,358 controls of European ancestry and identified a total of 41 risk loci for allergic rhinitis, including 20 loci not previously associated with allergic rhinitis, which were confirmed in a replication phase of 60,720 cases and 618,527 controls. Functional annotation implicated genes involved in various immune pathways, and fine mapping of the HLA region suggested amino acid variants important for antigen binding. We further performed genome-wide association study (GWAS) analyses of allergic sensitization against inhalant allergens and nonallergic rhinitis, which suggested shared genetic mechanisms across rhinitis-related traits. Future studies of the identified loci and genes might identify novel targets for treatment and prevention of allergic rhinitis

Optimizing Staining Protocols for Laser Microdissection of Specific Cell Types from the Testis Including Carcinoma In Situ

Microarray and RT-PCR based methods are important tools for analysis of gene expression; however, in tissues containing many different cells types, such as the testis, characterization of gene expression in specific cell types can be severely hampered by noise from other cells. The laser microdissection technology allows for enrichment of specific cell types. However, when the cells are not morphologically distinguishable, it is necessary to use a specific staining method for the target cells. In this study we have tested different fixatives, storage conditions for frozen sections and staining protocols, and present two staining protocols for frozen sections, one for fast and specific staining of fetal germ cells, testicular carcinoma in situ cells, and other cells with embryonic stem cell-like properties that express the alkaline phosphatase, and one for specific staining of lipid droplet-containing cells, which is useful for isolation of the androgen-producing Leydig cells. Both protocols retain a morphology that is compatible with laser microdissection and yield RNA of a quality suitable for PCR and microarray analysis

Genome-wide association study of febrile seizures implicates fever response and neuronal excitability genes

Febrile seizures represent the most common type of pathological brain activity in young children and are influenced by genetic, environmental and developmental factors. In a minority of cases, febrile seizures precede later development of epilepsy. We conducted a genome-wide association study of febrile seizures in 7635 cases and 83 966 controls identifying and replicating seven new loci, all with P < 5 x 10(-10). Variants at two loci were functionally related to altered expression of the fever response genes PTGER3 and IL10, and four other loci harboured genes (BSN, ERC2, GABRG2, HERC1) influencing neuronal excitability by regulating neurotransmitter release and binding, vesicular transport or membrane trafficking at the synapse. Four previously reported loci (SCN1A, SCN2A, ANO3 and 12q21.33) were all confirmed. Collectively, the seven novel and four previously reported loci explained 2.8% of the variance in liability to febrile seizures, and the single nucleotide polymorphism heritability based on all common autosomal single nucleotide polymorphisms was 10.8%. GABRG2, SCN1A and SCN2A are well-established epilepsy genes and, overall, we found positive genetic correlations with epilepsies (r(g) = 0.39, P = 1.68 x 10(-4)). Further, we found that higher polygenic risk scores for febrile seizures were associated with epilepsy and with history of hospital admission for febrile seizures. Finally, we found that polygenic risk of febrile seizures was lower in febrile seizure patients with neuropsychiatric disease compared to febrile seizure patients in a general population sample. In conclusion, this largest genetic investigation of febrile seizures to date implicates central fever response genes as well as genes affecting neuronal excitability, including several known epilepsy genes. Further functional and genetic studies based on these findings will provide important insights into the complex pathophysiological processes of seizures with and without fever.Peer reviewe

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

Antimicrobial resistance among migrants in Europe: a systematic review and meta-analysis

BACKGROUND: Rates of antimicrobial resistance (AMR) are rising globally and there is concern that increased migration is contributing to the burden of antibiotic resistance in Europe. However, the effect of migration on the burden of AMR in Europe has not yet been comprehensively examined. Therefore, we did a systematic review and meta-analysis to identify and synthesise data for AMR carriage or infection in migrants to Europe to examine differences in patterns of AMR across migrant groups and in different settings. METHODS: For this systematic review and meta-analysis, we searched MEDLINE, Embase, PubMed, and Scopus with no language restrictions from Jan 1, 2000, to Jan 18, 2017, for primary data from observational studies reporting antibacterial resistance in common bacterial pathogens among migrants to 21 European Union-15 and European Economic Area countries. To be eligible for inclusion, studies had to report data on carriage or infection with laboratory-confirmed antibiotic-resistant organisms in migrant populations. We extracted data from eligible studies and assessed quality using piloted, standardised forms. We did not examine drug resistance in tuberculosis and excluded articles solely reporting on this parameter. We also excluded articles in which migrant status was determined by ethnicity, country of birth of participants' parents, or was not defined, and articles in which data were not disaggregated by migrant status. Outcomes were carriage of or infection with antibiotic-resistant organisms. We used random-effects models to calculate the pooled prevalence of each outcome. The study protocol is registered with PROSPERO, number CRD42016043681. FINDINGS: We identified 2274 articles, of which 23 observational studies reporting on antibiotic resistance in 2319 migrants were included. The pooled prevalence of any AMR carriage or AMR infection in migrants was 25·4% (95% CI 19·1-31·8; I2 =98%), including meticillin-resistant Staphylococcus aureus (7·8%, 4·8-10·7; I2 =92%) and antibiotic-resistant Gram-negative bacteria (27·2%, 17·6-36·8; I2 =94%). The pooled prevalence of any AMR carriage or infection was higher in refugees and asylum seekers (33·0%, 18·3-47·6; I2 =98%) than in other migrant groups (6·6%, 1·8-11·3; I2 =92%). The pooled prevalence of antibiotic-resistant organisms was slightly higher in high-migrant community settings (33·1%, 11·1-55·1; I2 =96%) than in migrants in hospitals (24·3%, 16·1-32·6; I2 =98%). We did not find evidence of high rates of transmission of AMR from migrant to host populations. INTERPRETATION: Migrants are exposed to conditions favouring the emergence of drug resistance during transit and in host countries in Europe. Increased antibiotic resistance among refugees and asylum seekers and in high-migrant community settings (such as refugee camps and detention facilities) highlights the need for improved living conditions, access to health care, and initiatives to facilitate detection of and appropriate high-quality treatment for antibiotic-resistant infections during transit and in host countries. Protocols for the prevention and control of infection and for antibiotic surveillance need to be integrated in all aspects of health care, which should be accessible for all migrant groups, and should target determinants of AMR before, during, and after migration. FUNDING: UK National Institute for Health Research Imperial Biomedical Research Centre, Imperial College Healthcare Charity, the Wellcome Trust, and UK National Institute for Health Research Health Protection Research Unit in Healthcare-associated Infections and Antimictobial Resistance at Imperial College London