Approaching Laestadianism

The aim of this thematic issue on research on the Laestadian movement is to dwell with and look back on how the research on Laestadius and the Laestadian movement has developed, but at the same time show the latest developments in this research. In order to do so, researchers from the Nordic countries contributed to this thematic issue on research perspectives on the Laestadian movement. ‘Approaching Laestadianism’ presents theoretical articles and research overviews in order to present updates and tendencies in the research about the Laestadian movement

Bears are simply voles writ large: social structure determines the mechanisms of intrinsic population regulation in mammals

The literature reveals opposing views regarding the importance of intrinsic population regulation in mammals. Different models have been proposed; adding importance to contrasting life histories, body sizes and social interactions. Here we evaluate current theory based on results from two Scandinavian projects studying two ecologically different mammal species with contrasting body sizes and life history traits: the root vole Microtus oeconomus and the brown bear Ursus arctos. We emphasize four inter-linked behavioral aspects—territoriality, dispersal, social inhibition of breeding, and infanticide—that together form a density-dependent syndrome with potentially regulatory effects on population growth. We show that the two species are similar in all four behaviors and thus the overall regulatory syndrome. Females form matrilineal assemblages, female natal dispersal is negatively density dependent and breeding is suppressed in philopatric young females. In both species, male turnover due to extrinsic mortality agents cause infanticide with negative effects on population growth. The sex-biased and density-dependent dispersal patterns promote the formation of matrilineal clusters which, in turn, leads to reproductive suppression with potentially regulatory effects. Hence, we show that intrinsic population regulation interacting with extrinsic mortality agents may occur irrespective of taxon, life history and body size. Our review stresses the significance of a mechanistic approach to understanding population ecology. We also show that experimental model populations are useful to elucidate natural populations of other species with similar social systems. In particular, such experiments should be combined with methodical innovations that may unravel the effects of cryptic intrinsic mechanisms such as infanticid

New views on how population-intrinsic and community-extrinsic processes interact during the vole population cycles

Based on evidence from a series of recent studies linking behaviour to demography in experimental vole populations we propose how intrinsic and extrinsic factors interact through the various phases of the multi-annual population cycles of voles and lemmings. We hypothesise that population growth in the increase phase of the cycle is enhanced by a high degree of space sharing (sociality) among reproductive females who share resource patches, especially during winter. These social females enjoy a high reproductive output due to good resource conditions, and facilitation provided by communal thermoregulation, breeding and defence of weanlings towards infanticidal conspecifics. We hypothesise on the other hand that the crash phase is initiated and enhanced by predation of adult males that leads to a series of cascading events involving infanticidal behaviour by immigrant males, increased mortality of adult social females, and inversely density-dependent and/or disturbance-induced dispersal. These events further enhance predation-induced mortality and thus a negative feed-back loop to the rate of the crash. In this framework we may explain how extrinsic factors such as predation and winter resource distribution contribute to transitions between docile and aggressive behaviours, and how this transition is spatially synchronised by inversely density-dependent dispersal that may act to mediate a rapidly spreading wave throughout the population. We propose that innate differences among rodent species in their propensities for different social organizations also determine their propensity for exhibiting multi-annual cycles as well as other cycle-related phenomena such as shape of the population cycles and spatial synchrony. We provide a set of testable predictions for further empirical evaluation

The role of colonization in the dynamics of patchy populations of a cyclic vole species

This is the postprint version of the article. The published article can be located at www.springerlink.comThe crash phase of vole populations with cyclic dynamics regularly leads to vast areas of uninhabited habitats. Yet although the capacity for cyclic voles to re-colonize such empty space is likely to be large and predicted to have become evolved as a distinct life history trait, the processes of colonization and its effect on the spatio-temporal dynamics have been little studied. Here we report from an experiment with root voles (Microtus oeconomus) specifically targeted at quantifying the process of colonization of empty patches from distant source patches and its resultant effect on local vole deme size variation in a patchy landscape. Three experimental factors: habitat quality (1), predation risk (2) and inter-patch distance (3) were employed among 24 habitat patches in a 100x300 m experimental area. The first born cohort in the spring efficiently colonized almost all empty patches irrespective of the degree of patch isolation and predation risk, but dependent on habitat quality. Just after the initial colonization wave the deme sizes in patches of the same quality were underdispersed relative to Poission variance, indicating regulated (density-dependent) settlement. Towards the end of the breeding season local demographic processes acted to smooth out the initial post colonization differences among source and colonization patches, and among patches of initially different quality. However, at this time demographic stochasticity had also given rise to a large (overdispersed) variation in deme sizes that may have contributed to overshadow the effect of other factors. The results of this experiment confirmed our expectation that the space-filling capacity of voles is large. The costs associated with transience appeared to be so low, at least at the spatial scale considered in this experiment, that such costs is not likely to substantially constrain habitat selection and colonization in the increase phase of cyclic patchy populations.2014-09-3

Why Do the Boreal Forest Ecosystems of Northwestern Europe Differ from Those of Western North America?

The boreal forest is one of the largest terrestrial biomes on Earth. Conifers normally dominate the tree layer across the biome, but other aspects of ecosystem structure and dynamics vary geographically. The cause of the conspicuous differences in the understory vegetation and the herbivore–predator cycles between northwestern Europe and western North America presents an enigma. Ericaceous dwarf shrubs and 3– to 4-year vole–mustelid cycles characterize the European boreal forests, whereas tall deciduous shrubs and 10-year snowshoe hare–lynx cycles characterize the North American ones. We discuss plausible explanations for this difference and conclude that it is bottom-up: Winter climate is the key determinant of the dominant understory vegetation that then determines the herbivore–predator food-web interactions. The crucial unknown for the twenty-first century is how climate change and increasing instability will affect these forests, both with respect to the dynamics of individual plant and animal species and to their community interactions

Comparison of organic and conventional food and food production. Part II: Animal health and welfare in Norway

publishedVersio

Extended Coagulation Profiling in Isolated Traumatic Brain Injury:A CENTER-TBI Analysis

Background: Trauma-induced coagulopathy in traumatic brain injury (TBI) remains associated with high rates of complications, unfavorable outcomes, and mortality. The underlying mechanisms are largely unknown. Embedded in the prospective multinational Collaborative European Neurotrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study, coagulation profiles beyond standard conventional coagulation assays were assessed in patients with isolated TBI within the very early hours of injury. Methods: Results from blood samples (citrate/EDTA) obtained on hospital admission were matched with clinical and routine laboratory data of patients with TBI captured in the CENTER-TBI central database. To minimize confounding factors, patients with strictly isolated TBI (iTBI) (n = 88) were selected and stratified for coagulopathy by routine international normalized ratio (INR): (1) INR &lt; 1.2 and (2) INR ≥ 1.2. An INR &gt; 1.2 has been well adopted over time as a threshold to define trauma-related coagulopathy in general trauma populations. The following parameters were evaluated: quick’s value, activated partial thromboplastin time, fibrinogen, thrombin time, antithrombin, coagulation factor activity of factors V, VIII, IX, and XIII, protein C and S, plasminogen, D-dimer, fibrinolysis-regulating parameters (thrombin activatable fibrinolysis inhibitor, plasminogen activator inhibitor 1, antiplasmin), thrombin generation, and fibrin monomers. Results: Patients with iTBI with INR ≥ 1.2 (n = 16) had a high incidence of progressive intracranial hemorrhage associated with increased mortality and unfavorable outcome compared with patients with INR &lt; 1.2 (n = 72). Activity of coagulation factors V, VIII, IX, and XIII dropped on average by 15–20% between the groups whereas protein C and S levels dropped by 20%. With an elevated INR, thrombin generation decreased, as reflected by lower peak height and endogenous thrombin potential (ETP), whereas the amount of fibrin monomers increased. Plasminogen activity significantly decreased from 89% in patients with INR &lt; 1.2 to 76% in patients with INR ≥ 1.2. Moreover, D-dimer levels significantly increased from a mean of 943 mg/L in patients with INR &lt; 1.2 to 1,301 mg/L in patients with INR ≥ 1.2. Conclusions: This more in-depth analysis beyond routine conventional coagulation assays suggests a counterbalanced regulation of coagulation and fibrinolysis in patients with iTBI with hemostatic abnormalities. We observed distinct patterns involving key pathways of the highly complex and dynamic coagulation system that offer windows of opportunity for further research. Whether the changes observed on factor levels may be relevant and explain the worse outcome or the more severe brain injuries by themselves remains speculative.</p

Characterisation of age and polarity at onset in bipolar disorder

Background Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools. Aims To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics. Method Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts. Results Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO. Conclusions AAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.publishedVersio

GWAS of Suicide Attempt in Psychiatric Disorders and Association With Major Depression Polygenic Risk Scores

Objective: More than 90% of people who attempt suicide have a psychiatric diagnosis;however, twin and family studies suggest that the genetic etiology of suicide attempt is partially distinct from that of the psychiatric disorders themselves. The authors present the largest genome-wide association study (GWAS) on suicide attempt, using cohorts of individuals with major depressive disorder, bipolar disorder, and schizophrenia from the Psychiatric Genomics Consortium. Methods: The samples comprised 1,622 suicide attempters and 8,786 nonattempters with major depressive disorder;3,264 attempters and 5,500 nonattempters with bipolar disorder;and 1,683 attempters and 2,946 nonattempters with schizophrenia. A GWAS on suicide attempt was performed by comparing attempters to nonattempters with each disorder, followed by a meta-analysis across disorders. Polygenic risk scoring was used to investigate the genetic relationship between suicide attempt and the psychiatric disorders. Results: Three genome-wide significant loci for suicide attempt were found: one associated with suicide attempt in major depressive disorder, one associated with suicide attempt in bipolar disorder, and one in the meta-analysis of suicide attempt in mood disorders. These associations were not replicated in independent mood disorder cohorts from the UK Biobank and iPSYCH. No significant associations were found in the meta-analysis of all three disorders. Polygenic risk scores for major depression were significantly associated with suicide attempt in major depressive disorder (R-2=0.25%), bipolar disorder (R-2=0.24%), and schizophrenia (R-2=0.40%). Conclusions: This study provides new information on genetic associations and demonstrates that genetic liability for major depression increases risk for suicide attempt across psychiatric disorders. Further collaborative efforts to increase sample size may help to robustly identify genetic associations and provide biological insights into the etiology of suicide attempt

GWAS of Suicide Attempt in Psychiatric Disorders Identifies Association With Major Depression Polygenic Risk Scores

Objective: Over 90% of suicide attempters have a psychiatric diagnosis, however twin and family studies suggest that the genetic etiology of suicide attempt (SA) is partially distinct from that of the psychiatric disorders themselves. Here, we present the largest genome-wide association study (GWAS) on suicide attempt using major depressive disorder (MDD), bipolar disorder (BIP) and schizophrenia (SCZ) cohorts from the Psychiatric Genomics Consortium. Method: Samples comprise 1622 suicide attempters and 8786 non-attempters with MDD, 3264 attempters and 5500 non-attempters with BIP and 1683 attempters and 2946 non-attempters with SCZ. SA GWAS were performed by comparing attempters to non-attempters in each disorder followed by meta-analyses across disorders. Polygenic risk scoring was used to investigate the genetic relationship between SA and the psychiatric disorders. Results: Three genome-wide significant loci for SA were found: one associated with SA in MDD, one in BIP, and one in the meta-analysis of SA in mood disorders. These associations were not replicated in independent mood disorder cohorts from the UK Biobank and iPSYCH. No significant associations were found in the meta-analysis of all three disorders. Polygenic risk scores for major depression were significantly associated with SA in MDD (R2=0.25%, P=0.0006), BIP (R2=0.24%, P=0.0002) and SCZ (R2=0.40%, P=0.0006). Conclusions: This study provides new information on genetic associations and demonstrates that genetic liability for major depression increases risk for suicide attempt across psychiatric disorders. Further collaborative efforts to increase sample size hold potential to robustly identify genetic associations and gain biological insights into the etiology of suicide attempt