Wood addition in the hatchery and river environments affects post‐release performance of overwintering brown trout

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Genome-wide CRISPR Screens in T Helper Cells Reveal Pervasive Crosstalk between Activation and Differentiation

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Importance of infection of haemosporidia blood parasites during different life history stages for long‐term reproductive fitness of collared flycatchers

The interaction between birds and haemosporidia blood parasites is a well‐used system in the study of parasite biology. However, where, when and how parasites are transmitted is often unclear and defining parasite transmission dynamics is essential because of how they influence parasite‐mediated costs to the host. In this study, we used cross‐sectional and longitudinal data taken from a collared flycatcher Ficedula albicollis population to investigate the temporal dynamics of haemosporidia parasite infection and parasite‐mediated costs to host fitness. We investigated host–parasite interactions starting at the nestling stage of the bird's life‐cycle and then followed their progress over three breeding attempts to quantify their fitness – measured as the number of offspring they produced that recruited back into the breeding population. We found that the majority of haemosporidia blood parasite infections occurred within the first year of life and that the most common parasite lineages that infected the breeding population also infected juvenile birds in the natal environment. Moreover, our findings suggest that collared flycatcher nestlings in poorer condition could be at a higher risk of haemosporidia blood parasite infection. In this study, only female and not male bird fitness was adversely affected by parasite infection and the cost of infection on female fitness depended on the timing of transmission. In conclusion, our study indicates that in collared flycatchers, early‐life is potentially important for many of the interactions with haemosporidia parasite lineages, and evidence of parasite‐mediated costs to fitness suggest that these parasites may have influenced the host population dynamics.     

Deficiency of the mitochondrial sulfide regulator ETHE1 disturbs cell growth,glutathione level and causes proteome alterations outside mitochondria

The mitochondrial enzyme ETHE1 is a persulfide dioxygenase essential for cellular sulfide detoxification, and its deficiency causes the severe and complex inherited metabolic disorder ethylmalonic encephalopathy (EE). In spite of well-described clinical symptoms of the disease, detailed cellular and molecular characterization is still ambiguous. Cellular redox regulation has been described to be influenced in ETHE1 deficient cells, and to clarify this further we applied image cytometry and detected decreased levels of reduced glutathione (GSH) in cultivated EE patient fibroblast cells. Cell growth initiation of the EE patient cells was impaired, whereas cell cycle regulation was not. Furthermore, Seahorse metabolic analyzes revealed decreased extracellular acidification, i. e. decreased lactate formation from glycolysis, in the EE patient cells. TMT-based large-scale proteomics was subsequently performed to broadly elucidate cellular consequences of the ETHE1 deficiency. More than 130 proteins were differentially regulated, of which the majority were non-mitochondrial. The proteomics data revealed a link between ETHE1-deficiency and down-regulation of several ribosomal proteins and LIM domain proteins important for cellular maintenance, and up-regulation of cell surface glycoproteins. Furthermore, several proteins of endoplasmic reticulum (ER) were perturbed including proteins influencing disulfide bond formation (e.g. protein disulfide isomerases and peroxiredoxin 4) and calcium-regulated proteins. The results indicate that decreased level of reduced GSH and alterations in proteins of ribosomes, ER and of cell adhesion lie behind the disrupted cell growth of the EE patient cells.     

A cell cycle study of human mammary epithelial cells.

The growth regulation of human mammary epithelial cells (HMEC) cultured in a growth factor/hormone-enriched (e.g. EGF, insulin) medium with bovine pituitary extract as the only undefined supplement was studied. The doubling times of the cultures, in which the cells appear in colonies, was 55-72 h, and a considerable intercolonial heterogenecity in proliferative activity could be demonstrated. However, every colony, irrespective of the size of the growth fraction, comprised a sub-population of rapidly growing cells which had a mean generation time of approximately 22 h. When insulin was removed from the culture medium, HMEC proliferation was inhibited. This growth inhibition was shown to be a result of a cell cycle-specific block.     

Leapfrog migration and residents: New migratory habits in Swedish Greylag geese

Knowledge about intraspecific and individual variation in bird migration behavior is important to predict spatiotemporal distribution, patterns of phenology, breeding success, and interactions with the surrounding environment (e.g., human livelihoods). Such variation is key to adaptive, evolutionary responses, i.e., how individuals respond spatiotemporally to the environment to maximize fitness. In this study we used GPS location data from one to three full annual cycles from 76 Greylag geese (Anser anser) to test the hypothesis that geese originating at five latitudinally separated capture sites in Sweden have different migration strategies. We also assessed individual consistency in movement strategy over consecutive annual cycles. We used the scale‐independent net squared displacement modeling framework to quantify variables of autumn and spring migration for geese from each capture site: distance, timing, and duration. Our results demonstrate a positive correlation between migration distance and latitudinal origin. Geese from the northernmost site on average migrated farther south and about 15 times as far as the short‐moving or resident geese from the two southernmost sites. Movement strategies of individual geese varied considerably both within and among capture sites. Individual consistency in movement strategy from one annual cycle to the consecutive was high in geese from the northern sites moving the farthest, whereas the resident or short‐moving geese from the southernmost sites generally showed lower or no individual consistency. These changes have come about during a time span so short (i.e., ca. 35 years or 8–10 generations) that it can unlikely be explained by classical Darwinian between‐generation adaptation. Consequently, and given that young geese follow their parents during their first migration, we presume an important role of within‐family, inter‐generation change as a driver behind the large‐scale changed migration habits in Swedish Greylag geese.     

VEGF receptor 2/‐3 heterodimers detected in situ by proximity ligation on angiogenic sprouts

The vascular endothelial growth factors VEGFA and VEGFC are crucial regulators of vascular development. They exert their effects by dimerization and activation of the cognate receptors VEGFR2 and VEGFR3. Here, we have used in situ proximity ligation to detect receptor complexes in intact endothelial cells. We show that both VEGFA and VEGFC potently induce formation of VEGFR2/‐3 heterodimers. Receptor heterodimers were found in both developing blood vessels and immature lymphatic structures in embryoid bodies. We present evidence that heterodimers frequently localize to tip cell filopodia. Interestingly, in the presence of VEGFC, heterodimers were enriched in the leading tip cells as compared with trailing stalk cells of growing sprouts. Neutralization of VEGFR3 to prevent heterodimer formation in response to VEGFA decreased the extent of angiogenic sprouting. We conclude that VEGFR2/‐3 heterodimers on angiogenic sprouts induced by VEGFA or VEGFC may serve to positively regulate angiogenic sprouting.     

Relative importance of habitat connectivity in shaping the genetic profiles of two southern African elephant‐shrews

Aim When interpreting genetic patterns across a landscape it is surprisingly difficult to disentangle the effects of landscape connectivity from those of species biology. Here, the spatial distributions of genetic variation of two sympatric elephant‐shrew species, the western rock elephant‐shrew (Elephantulus rupestris) and the round‐eared elephant‐shrew (Macroscelides proboscideus), are determined and compared. We selected these species because they have similar biologies but differ markedly in habitat use, the rationale being that differences in their genetic structure should be a result largely of landscape variables directly or indirectly affecting dispersal rather than of the biology of the species. Location South Africa and Namibia. Methods Mitochondrial sequence data (control region and cytochrome b) were used to describe the phylogeographic structure of these elephant‐shrew species across their distribution. To determine whether genetic variation is significantly structured, spatial analyses of molecular variation were performed. Isolation‐by‐distance versus alternative patterns of genetic structure was investigated using a Mantel test. Results Our analyses indicated an overall structured genetic profile for E. rupestris, a species closely associated with rocky outcrops. This was in contrast to a pattern mostly of isolation‐by‐distance across the distribution of M. proboscideus, a species found on gravel plains. Main conclusions Specific landscape features will differentially affect gene flow (both historical and current), and therefore also the spatial genetic structure, of species with markedly different habitat requirements. The genetic profiles for the two species included here support predictions based on the connectivity of their respective occupied habitats. The results also support the more general prediction that species with a naturally clustered distribution (such as E. rupestris) should have a more structured genetic pattern than those having a more continuous distribution (M. proboscideus).     

Social class in childhood and general health in adulthood: questionnaire study of contribution of psychological attributes

ObjectiveTo determine the contribution of psychological attributes (personality characteristics and coping styles) to the association between social class in childhood and adult health among men and women.DesignPartly retrospective, partly cross sectional study conducted in the framework of the Dutch GLOBE study.SubjectsSample of general population from south east Netherlands consisting of 2174 men and women aged 25-74 years. Baseline self reported data from 1991 provided information on childhood and adult social class, psychological attributes, and general health.ResultsIndependent of adult social class, low childhood social class was related to self rated poor health (odds ratio 1.67 (95% confidence interval 1.02 to 2.75) for subjects whose fathers were unskilled manual workers versus subjects whose fathers were higher grade professionals). Subjects whose fathers were manual workers generally had more unfavourable personality profiles and more negative coping styles. External locus of control, neuroticism, and the absence of active problem focused coping explained about half of the association between childhood social class and self rated poor health. The findings were independent of adult social class and height.ConclusionsA higher prevalence of negative personality profiles and adverse coping styles in subjects who grew up in lower social classes explains part of the association between social class in childhood and adult health. This finding underlines the importance of psychological mechanisms in the examination of the negative effects of adverse socioeconomic conditions in childhood.

Key messages

• Regardless of adult social class, low social class in childhood is related to poor general health in adulthood
• Adverse personality profiles and negative coping styles are more common in people who grew up in lower social classes
• Psychological attributes, such as low perceived control, explain a substantial part of the direct association between childhood social class and adult health
• Psychological mechanisms may explain adverse health outcomes in adults who have a low socioeconomic background

     

IFN-γ production in response to <Emphasis Type="Italic">in vitro</Emphasis> stimulation with collagen type II in rheumatoid arthritis is associated with HLA-DRB1<Superscript>*</Superscript>0401 and HLA-DQ8

Introduction

Despite much work over past decades, whether antigen-specific immune reactions occur in rheumatoid arthritis (RA) and to what extent such reactions are directed towards joint-specific autoantigens is still questionable. One strong indicator for antigenic involvement in RA is the fact that certain major histocompatibility complex (MHC) class II genotypes [human leucocyte antigen (HLA)-DR4 and HLA-DR1] predispose for the development of the disease [1]. In the present report, collagen type II (CII) was studied as a putative autoantigen on the basis of both clinical and experimental data that show an increased frequency of antibodies to CII in RA patients [2,3,4] and that show that CII can induce experimental arthritis [5].It is evident from the literature that RA peripheral blood mononuclear cells (PBMCs) respond poorly to antigenic stimulation [6,7,8], and in particular evidence for a partial tolerization to CII has been presented [9]. The strategy of the present work has accordingly been to reinvestigate T-cell reactivity to CII in RA patients, to relate it to the response to commonly used recall antigens and to analyze IFN-γ responses as an alternative to proliferative responses.