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Summary: In this open population-based study from Northern Norway, there was no increase in hip fracture incidence in women and men from 1994 to 2008. Age-adjusted hip fracture rates was lower compared to reported rates from the Norwegian capital Oslo, indicating regional differences within the country. Introduction: The aim of the present population-based study was to describe age- and sex-specific incidence of hip fractures in a Northern Norwegian city, compare rates with the Norwegian capital Oslo, describe time trends in hip fracture incidence, place of injury, seasonal variation and compare mortality after hip fracture between women and men. Methods: Data on hip fractures from 1994 to 2008 in women and men aged 50 years and above were obtained from the Harstad Injury Registry. Results: There were altogether 603 hip fractures in Harstad between 1994 and 2008. The annual incidenc rose exponentially from 5.8 to 349.2 per 10,000 in men, and from 8.7 to 582.2 per 10,000 in women from the age group 50-54 to 90+ years. The age-adjusted incidence rates were 101.0 and 37.4 in women and men, respectively, compared to 118.0 in women ( p = 0.005) and 44.0 in men ( p = 0.09) in Oslo. The age-adjusted incidence rates did not increase between 1994-1996 and 2006-2008. The majority of hip fractures occurred indoors and seasonal variation was significant in fractures occurring outdoors only. After adjusting for age at hip fracture, mortality after fracture was higher in men than in women 3, 6 and 12 months ( p ≤ 0.002) after fracture. Conclusions: There are regional differences in hip fracture incidence that cannot be explained by a north-south gradient in Norway. Preventive strategies must be targeted to indoor areas throughout the year and to outdoor areas in winter. [ABSTRACT FROM AUTHOR]

Based on grain-size analysis of sediment samples from a delta at Altermarka, it has previously been suggested that two tills were deposited on the delta surface as a glacier planed off the delta topsets and created its adverse surface slope. In this reinvestigation of the delta, there was no evidence that a glacier overrode the surface: the topset beds remain intact and no appreciable till was found. Sediments resembling the ‘till’ samples were located, but soil processes and other sedimentary processes easily account for the wide grain-size distributions of these sediments. As a result, this study cautions against using grain-size analysis, on its own, to interpret the genesis of sediments. Other processes potentially responsible for the adverse surface slope include differential isostatic rebound, recent differential slip along ancient thrust faults, and failure of the delta surface to reach sea level. Based on the sedimentology of the topset beds and the local relative sea level history (indicating the delta (9495±70 14 C yr BP) formed about the time of the local marine limit (9560–9375 14 C yr BP) 17 m higher than the delta surface), the feature is determined to have built up below sea level with an adverse surface slope. [ABSTRACT FROM AUTHOR]

South of Svartisen Ice Cap, the relative age of ice-flow indicators shows that as the Fennoscandian Ice Sheet declined in the area glacial ice was diverted from a westward to a southward flow direction toward Ranafjord. Eventually, an active ice cap with an accumulation center over the Svartisen highlands was isolated in front of the inland ice sheet and extended all the way to Ranafjord. The maximum limit of the southern portion of the Svartisen ice mass is determined by the location of ice-marginal deposits and the limit of young southeastward striations at high elevations that cross-cut the westward ice-flow indicators formed by the ice sheet. Radiocarbon ages of mollusk shells in glaciomarine sediments within the margin of this ice cap show that Svartisen was at its maximum extent around 9500 BP, retreated from its maximum position shortly before about 9300 BP, and receded halfway to the present position of Svartisen by about 9000 BP. [ABSTRACT FROM AUTHOR]

Background: Reindeer herding in Norway is based on traditional Sámi pastoralism with the animals free ranging throughout the year. The animals move over large areas in varying terrain and often in challenging weather conditions. Winter crises, such as difficult grazing conditions caused by icing or large amounts of snow, are survival bottlenecks for reindeer. Calves are especially vulnerable, and many may die from starvation during winter crises. Predation and starvation are the predominant narratives to explain losses, however, carcasses are difficult to find and often little remains after scavenging and decay. Documentation of the causes of death is therefore scarce., Results: In this study, we investigated the cause of reindeer mortality in Troms and Finnmark, Nordland and Trøndelag during 2017-2019. Necropsies (n = 125) and organ investigation (n = 13) were performed to document cause of death. Body condition was evaluated using visual fat score and bone marrow fat index. A wide range of causes of death was detected. The diagnoses were categorized into the following main categories: predation (n = 40), emaciation (n = 35), infectious disease (n = 20), trauma (n = 11), feeding related disease (n = 5), neoplasia (n = 4), others (n = 6) and unknown (n = 17). Co-morbidities were seen in a number of diagnoses (n = 16). Reindeer herders are entitled to economic compensation for reindeer killed by endangered predators, but a lack of documentation leads to a gap between the amount of compensation requested and what is awarded. An important finding of our study was that predators, during winter, killed animals in good as well as poor body condition. Emaciation was also shown to be associated with infectious diseases, and not only attributable to winter grazing conditions., Conclusions: This study highlights the importance of examining dead reindeer to gain knowledge about why they die on winter pasture. The work presented herein also shows the feasibility and value of increased documentation of reindeer losses during winter., (© 2023. The Author(s).)

Background: Protein encoding genes have long been the major targets for research in schizophrenia genetics. However, with the identification of regulatory microRNAs (miRNAs) as important in brain development and function, miRNAs genes have emerged as candidates for schizophrenia-associated genetic factors. Indeed, the growing understanding of the regulatory properties and pleiotropic effects that miRNA have on molecular and cellular mechanisms, suggests that alterations in the interactions between miRNAs and their mRNA targets may contribute to phenotypic variation., Methodology/principal Findings: We have studied the association between schizophrenia and genetic variants of miRNA genes associated with brain-expression using a case-control study design on three Scandinavian samples. Eighteen known SNPs within or near brain-expressed miRNAs in three samples (Danish, Swedish and Norwegian: 420/163/257 schizophrenia patients and 1006/177/293 control subjects), were analyzed. Subsequently, joint analysis of the three samples was performed on SNPs showing marginal association. Two SNPs rs17578796 and rs1700 in hsa-mir-206 (mir-206) and hsa-mit-198 (mir-198) showed nominal significant allelic association to schizophrenia in the Danish and Norwegian sample respectively (P = 0.0021 & p = 0.038), of which only rs17578796 was significant in the joint sample. In-silico analysis revealed that 8 of the 15 genes predicted to be regulated by both mir-206 and mir-198, are transcriptional targets or interaction partners of the JUN, ATF2 and TAF1 connected in a tight network. JUN and two of the miRNA targets (CCND2 and PTPN1) in the network have previously been associated with schizophrenia., Conclusions/significance: We found nominal association between brain-expressed miRNAs and schizophrenia for rs17578796 and rs1700 located in mir-206 and mir-198 respectively. These two miRNAs have a surprising large number (15) of targets in common, eight of which are also connected by the same transcription factors.