Mikromobilitet med og uden motor – Evaluering af adfærd og hjelmbrug: Artikel

Mikromobilitet omhandler korte rejser på små køretøjer med relativ lav hastighed. Mikromobilitet er de seneste fem år blevet mere udbredt især i form af små elektriske køretøjer, men også som små manuelle køretøjer. Formålet med nærværende artikel har været at udforske og evaluere adfærden blandt brugere af motoriserede og ikke motoriserede små køretøjer i form af løbehjul med og uden motor, skateboard med og uden motor, selvbalancerende køretøj og rulleskøjter. Artiklen er tredelt med følgende formål:1. Udvikling i adfærd: At evaluere hvordan brugen af el-løbehjul har udviklet sig i Aarhus fra forsøgsordningernes år 1 (2019) til år 3-4 (2021-2022).2. Hjelmkrav: At evaluere effekten af det i 2022 indførte hjelmkrav for el-løbehjul, el-skateboards og selvbalancerende køretøjer for hjelmbrugen på disse køretøjer.3. Ikke motoriseret mikromobilitet: At undersøge adfærden blandt brugere af rulleskøjter og manuelle skateboards og løbehjul i sammenligning med brugere af motoriserede små køretøjer.Projektet er baseret på registrering i trafikken i Aarhus i 2019-2022, hvor fire rådgivere kontinuerligt har registreret informationer om køretøj, adfærd og brugere, som efterfølgende er analyseret i regneark. Der er registreringer fra alle ugedage, fra kl. 5.00-24.00 og for over 200 forskellige lokaliteter i Aarhus. I 2021 er der fx foretaget registrering i trafikken i over 250 timer. Vi har fx i alt registrering af 5.111 små elektriske køretøjer i Aarhus i 2019-2021, og af 650 ikke motoriserede køretøjer i 2021

Spøgelsescyklisme – Udbredelse, kendetegn og risiko: Artikel

En spøgelsescyklist er en cyklist, som ulovligt cykler mod færdselsretningen, dvs. i den forkerte side af vejen på veje med to eller flere kørespor. I dette projekt er spøgelsescyklister inddelt i grønne, gule og røde spøgelsescyklister, som er cyklister, som cykler hhv. kort (under 50 m), mellemlangt (50-500 m) og langt (over 500 m) mod færdselsretningen. Betegnelsen spøgelsescyklist er inspireret af spøgelsesbilist, som er en bilist, der kører mod færdselsretningen. Spøgelsesbilisme har fået stor opmærksomhed i mange år, mens opmærksomheden mod spøgelsescyklisme har været begrænset. I denne artikel har vi derfor rettet opmærksomheden mod netop spøgelsescyklisme.Formålet med projektet har været at udforske spøgelsescyklistfænomen nærmere, og konkret at undersøge 1) hvor mange de er, 2) hvornår de findes, 3) hvor de findes, 4) hvem de er, 5) hvorfor de findes, 6) hvor farlige de er og 7) hvordan antallet kan reduceres. For at undersøge disse delmål har vi foretaget 1) litteraturstudie af danske og udenlandske studier, erfaringer og tiltag, 2) analyse af 21 stræknings- og krydstællinger af cykeltrafik i København og Aarhus, 3) registrering af kendetegn og adfærd for 750 spøgelsescyklister i Aarhus, 4) videooptagelse og -analyse på fem lokaliteter i Aarhus, 5) stopinterview i trafikken af 50 spøgelsescyklister i Aarhus, og 6) landsdækkende web-spørgeundersøgelse blandt 1010 repræsentativt udvalgte danske trafikanter

Bose-Einstein Condensates in Optical Lattices: Band-Gap Structure and Solitons

We analyze the existence and stability of spatially extended (Bloch-type) and localized states of a Bose-Einstein condensate loaded into an optical lattice. In the framework of the Gross-Pitaevskii equation with a periodic potential, we study the band-gap structure of the matter-wave spectrum in both the linear and nonlinear regimes. We demonstrate the existence of families of spatially localized matter-wave gap solitons, and analyze their stability in different band gaps, for both repulsive and attractive atomic interactions

Various correlations in a Heisenberg XXZ spin chain both in thermal equilibrium and under the intrinsic decoherence

In this paper we discuss various correlations measured by the concurrence (C), classical correlation (CC), quantum discord (QD), and geometric measure of discord (GMD) in a two-qubit Heisenberg XXZ spin chain in the presence of external magnetic field and Dzyaloshinskii-Moriya (DM) anisotropic antisymmetric interaction. Based on the analytically derived expressions for the correlations for the cases of thermal equilibrium and the inclusion of intrinsic decoherence, we discuss and compare the effects of various system parameters on the correlations in different cases. The results show that the anisotropy Jz is considerably crucial for the correlations in thermal equilibrium at zero temperature limit but ineffective under the consideration of the intrinsic decoherence, and these quantities decrease as temperature T rises on the whole. Besides, J turned out to be constructive, but B be detrimental in the manipulation and control of various quantities both in thermal equilibrium and under the intrinsic decoherence which can be avoided by tuning other system parameters, while D is constructive in thermal equilibrium, but destructive in the case of intrinsic decoherence in general. In addition, for the initial state $|\Psi_1(0) > = \frac{1}{\sqrt{2}} (|01 > + |10 >)$, all the correlations except the CC, exhibit a damping oscillation to a stable value larger than zero following the time, while for the initial state $|\Psi_2(0) > = \frac{1}{\sqrt{2}} (|00 > + |11 >)$, all the correlations monotonously decrease, but CC still remains maximum. Moreover, there is not a definite ordering of these quantities in thermal equilibrium, whereas there is a descending order of the CC, C, GMD and QD under the intrinsic decoherence with a nonnull B when the initial state is $|\Psi_2(0) >$.Comment: 8 pages, 7 figure

Genome-wide analyses identify a role for SLC17A4 and AADAT in thyroid hormone regulation.

Thyroid dysfunction is an important public health problem, which affects 10% of the general population and increases the risk of cardiovascular morbidity and mortality. Many aspects of thyroid hormone regulation have only partly been elucidated, including its transport, metabolism, and genetic determinants. Here we report a large meta-analysis of genome-wide association studies for thyroid function and dysfunction, testing 8 million genetic variants in up to 72,167 individuals. One-hundred-and-nine independent genetic variants are associated with these traits. A genetic risk score, calculated to assess their combined effects on clinical end points, shows significant associations with increased risk of both overt (Graves' disease) and subclinical thyroid disease, as well as clinical complications. By functional follow-up on selected signals, we identify a novel thyroid hormone transporter (SLC17A4) and a metabolizing enzyme (AADAT). Together, these results provide new knowledge about thyroid hormone physiology and disease, opening new possibilities for therapeutic targets

Geographical and temporal distribution of SARS-CoV-2 clades in the WHO European Region, January to June 2020

We show the distribution of SARS-CoV-2 genetic clades over time and between countries and outline potential genomic surveillance objectives. We applied three available genomic nomenclature systems for SARS-CoV-2 to all sequence data from the WHO European Region available during the COVID-19 pandemic until 10 July 2020. We highlight the importance of real-time sequencing and data dissemination in a pandemic situation. We provide a comparison of the nomenclatures and lay a foundation for future European genomic surveillance of SARS-CoV-2.Peer reviewe

Multiomics analysis of rheumatoid arthritis yields sequence variants that have large effects on risk of the seropositive subset

Funding Information: Funding The study was funded by NORDFORSK (grant agreement no. 90825, project NORA), the Swedish Research Council (2018-02803), the Swedish innovation Agency (Vinnova), Innovationsfonden and The Research Council of Norway, Region Stockholm-Karolinska Institutet and Region Västerbotten (ALF), the Danish Rheumatism Association (R194-A6956), the Swedish Brain Foundation, Nils and Bibbi Jensens Foundation, the Knut and Alice Wallenberg Foundation, Margaretha af Ugglas Foundation, the South-Eastern Heath Region of Norway, the Health Research Fund of Central Denmark Region, Region of Southern Denmark, the A.P. Moller Foundation for the Advancement of Medical Science, the Colitis-Crohn Foreningen, the Novo Nordisk Foundation (NNF15OC0016932), Aase og Ejnar Danielsens Fond, Beckett-Fonden, Augustinus Fonden, Knud and Edith Eriksens Mindefond, Laege Sofus Carl Emil Friis and Hustru Olga Doris Friis’ Legat, the Psoriasis Forskningsfonden, the University of Aarhus, the Danish Rheumatism Association (R194-A6956, A1923, A3037 and A3570 – www. gigtforeningen.dk), Region of Southern Denmark’s PhD Fund, 12/7725 (www.regionsyddanmark.dk) and the Department of Rheumatology, Frederiksberg Hospital (www.frederiksberghospital. dk). MoBa Genetics has been funded by the Research Council of Norway (#229624, #223273), South East and Western Norway Health Authorities, ERC AdG project SELECTionPREDISPOSED, Stiftelsen Kristian Gerhard Jebsen, Trond Mohn Foundation, the Novo Nordisk Foundation and the University of Bergen. KB and SB acknowledge the Novo Nordisk Foundation (grant NNF14CC0001). Funding Information: competing financial interests as employees. OAA is a consultant to HealthLytix. The following coauthors report the following but unrelated to the current report: Karolinska Institutet, with JA as principal investigator, has entered into agreements with the following entities, mainly but not exclusively for safety monitoring of rheumatology immunomodulators: Abbvie, BMS, Eli Lilly, Janssen, MSD, Pfizer, Roche, Samsung Bioepis and Sanofi, unrelated to the present study. SB has ownerships in Intomics A/S, Hoba Therapeutics Aps, Novo Nordisk A/S, Lundbeck A/S and managing board memberships in Proscion A/S and Intomics A/S. BG has received research grants from AbbVie, Bristol Myers-Squibb and Pfizer; OH has received research grants from AbbVie, Novartis and Pfizer, DVJ has received speaker and consultation fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB, AGL has received speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB; and CT has received consulting fees from Roche, speaker fees from Abbvie, Bristol Myers-Squibb, Nordic Drugs, Pfizer and Roche, and an unrestricted grant from Bristol Myers-Squibb. Publisher Copyright: © Funding Information: Funding The study was funded by NORDFORSK (grant agreement no. 90825, project NORA), the Swedish Research Council (2018-02803), the Swedish innovation Agency (Vinnova), Innovationsfonden and The Research Council of Norway, Region Stockholm-Karolinska Institutet and Region Västerbotten (ALF), the Danish Rheumatism Association (R194-A6956), the Swedish Brain Foundation, Nils and Bibbi Jensens Foundation, the Knut and Alice Wallenberg Foundation, Margaretha af Ugglas Foundation, the South-Eastern Heath Region of Norway, the Health Research Fund of Central Denmark Region, Region of Southern Denmark, the A.P. Moller Foundation for the Advancement of Medical Science, the Colitis-Crohn Foreningen, the Novo Nordisk Foundation (NNF15OC0016932), Aase og Ejnar Danielsens Fond, Beckett-Fonden, Augustinus Fonden, Knud and Edith Eriksens Mindefond, Laege Sofus Carl Emil Friis and Hustru Olga Doris Friis’ Legat, the Psoriasis Forskningsfonden, the University of Aarhus, the Danish Rheumatism Association (R194-A6956, A1923, A3037 and A3570 – www. gigtforeningen.dk), Region of Southern Denmark’s PhD Fund, 12/7725 (www.regionsyddanmark.dk) and the Department of Rheumatology, Frederiksberg Hospital (www.frederiksberghospital. dk). MoBa Genetics has been funded by the Research Council of Norway (#229624, #223273), South East and Western Norway Health Authorities, ERC AdG project SELECTionPREDISPOSED, Stiftelsen Kristian Gerhard Jebsen, Trond Mohn Foundation, the Novo Nordisk Foundation and the University of Bergen. KB and SB acknowledge the Novo Nordisk Foundation (grant NNF14CC0001). Funding Information: competing financial interests as employees. OAA is a consultant to HealthLytix. The following coauthors report the following but unrelated to the current report: Karolinska Institutet, with JA as principal investigator, has entered into agreements with the following entities, mainly but not exclusively for safety monitoring of rheumatology immunomodulators: Abbvie, BMS, Eli Lilly, Janssen, MSD, Pfizer, Roche, Samsung Bioepis and Sanofi, unrelated to the present study. SB has ownerships in Intomics A/S, Hoba Therapeutics Aps, Novo Nordisk A/S, Lundbeck A/S and managing board memberships in Proscion A/S and Intomics A/S. BG has received research grants from AbbVie, Bristol Myers-Squibb and Pfizer; OH has received research grants from AbbVie, Novartis and Pfizer, DVJ has received speaker and consultation fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB, AGL has received speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB; and CT has received consulting fees from Roche, speaker fees from Abbvie, Bristol Myers-Squibb, Nordic Drugs, Pfizer and Roche, and an unrestricted grant from Bristol Myers-Squibb. Publisher Copyright: ©Objectives To find causal genes for rheumatoid arthritis (RA) and its seropositive (RF and/or ACPA positive) and seronegative subsets. Methods We performed a genome-wide association study (GWAS) of 31 313 RA cases (68% seropositive) and ∼1 million controls from Northwestern Europe. We searched for causal genes outside the HLA-locus through effect on coding, mRNA expression in several tissues and/or levels of plasma proteins (SomaScan) and did network analysis (Qiagen). Results We found 25 sequence variants for RA overall, 33 for seropositive and 2 for seronegative RA, altogether 37 sequence variants at 34 non-HLA loci, of which 15 are novel. Genomic, transcriptomic and proteomic analysis of these yielded 25 causal genes in seropositive RA and additional two overall. Most encode proteins in the network of interferon-Alpha/beta and IL-12/23 that signal through the JAK/STAT-pathway. Highlighting those with largest effect on seropositive RA, a rare missense variant in STAT4 (rs140675301-A) that is independent of reported non-coding STAT4-variants, increases the risk of seropositive RA 2.27-fold (p=2.1×10-9), more than the rs2476601-A missense variant in PTPN22 (OR=1.59, p=1.3×10-160). STAT4 rs140675301-A replaces hydrophilic glutamic acid with hydrophobic valine (Glu128Val) in a conserved, surface-exposed loop. A stop-mutation (rs76428106-C) in FLT3 increases seropositive RA risk (OR=1.35, p=6.6×10-11). Independent missense variants in TYK2 (rs34536443-C, rs12720356-C, rs35018800-A, latter two novel) associate with decreased risk of seropositive RA (ORs=0.63-0.87, p=10-9-10-27) and decreased plasma levels of interferon-Alpha/beta receptor 1 that signals through TYK2/JAK1/STAT4. Conclusion Sequence variants pointing to causal genes in the JAK/STAT pathway have largest effect on seropositive RA, while associations with seronegative RA remain scarce.Peer reviewe