Sex-biased dispersal in a northern ungulate population

In most mammals dispersal is male-biased and in many polygynous ungulates female philopatry and matrilineal grouping involve small-scale genetic structure. We have through sex-related differences in microsatellite allele distribution addressed sex-biased dispersal in a spatially expanding northern ungulate population. The Norwegian red deer population (Cervus elaphus atlanticus) has the last hundred years grown substantially and expanded spatially after a major decline from 300 to 100 years ago. Previous Bayesian analyses suggest a present division of genetic variation into five geographically separated subpopulations. Among these subpopulations the overall Fst values were 0.067 (SE=0.014) for males and 0.094 (SE=0.017) for females. Pairwise Fst values were significantly higher for females than males, demonstrating a stronger genetic structure among females, and that dispersal has been lower in females than males. Accordingly, a higher number of male than female first generation dispersers were identified among the five subpopulations using Bayesian assignment with prior population information, but significantly so only with relaxed stringency levels of assignment. The identified male-biased dispersal distances varied from 30 to 300 kilometers suggesting male biased dispersal on a large scale in red deer

Geochronology of sediment cores from the Vefsnfjord, Norway

The sedimentary environment is a repository and carrier for a variety of pollutants, and sediment transport from land to coastal areas is an important environmental process. In the present study, we use 210Pb/226Ra and 137Cs in sediment cores to assess sediment supply rates at four sites within the Vefsnfjord in Nordland county, Norway. This area was highly affected by fallout from the Chernobyl accident in 1986 and inventories of 137Cs in the fjord are much higher than in many other Norwegian fjords. Sedimentation rates between 0.042 and 0.25 g cm−2 y−1 (0.060 and 0.38 cm y−1) were determined using a combination of the Constant Rate of Supply (CRS) and Constant Flux:Constant Sedimentation rate (CF:CS) models. Well-defined 137Cs concentration peaks were used as a supplementary tool to the 210Pb dating methods.publishedVersio

Xenobiotic Exposure and Migraine-Associated Signaling:A Multimethod Experimental Study Exploring Cellular Assays in Combination with Ex Vivo and In Vivo Mouse Models

BACKGROUND: Mechanisms for how environmental chemicals might influence pain has received little attention. Epidemiological studies suggest that environmental factors such as pollutants might play a role in migraine prevalence. Potential targets for pollutants are the transient receptor potential (TRP) channels ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1), which on activation release pain-inducing neuropeptide calcitonin gene-related peptide (CGRP). OBJECTIVE: In this study, we aimed to examine the hypothesis that environmental pollutants via TRP channel signaling and subsequent CGRP release trigger migraine signaling and pain. METHODS: A calcium imaging-based screen of environmental chemicals was used to investigate activation of migraine pain-associated TRP channels TRPA1 and TRPV1. Based on this screen, whole-cell patch clamp and in silico docking were performed for the pesticide pentachlorophenol (PCP) as proof of concept. Subsequently, PCP-mediated release of CGRP and vasodilatory responses of cerebral arteries were investigated. Finally, we tested whether PCP could induce a TRPA1-dependent induction of cutaneous hypersensitivity in vivo in mice as a model of migraine-like pain. RESULTS: A total of 16 out of the 52 screened environmental chemicals activated TRPA1 at 10 or formula presented . None of the investigated compounds activated TRPV1. Using PCP as a model of chemical interaction with TRPA1, in silico molecular modeling suggested that PCP is stabilized in a lipid-binding pocket of TRPA1 in comparison with TRPV1. In vitro, ex vivo, and in vivo experiments showed that PCP induced calcium influx in neurons and resulted in a TRPA1-dependent CGRP release from the brainstem and dilation of cerebral arteries. In a mouse model of migraine-like pain, PCP induced a TRPA1-dependent increased pain response (formula presented ). DISCUSSION: Here we show that multiple environmental pollutants interact with the TRPA1-CGRP migraine pain pathway. The data provide valuable insights into how environmental chemicals can interact with neurobiology and provide a potential mechanism for putative increases in migraine prevalence over the last decades. https://doi.org/10.1289/EHP12413.</p

Absence of P2Y2 receptor does not prevent bone destruction in a murine model of muscle paralysis-induced bone loss

Increased incidence of bone fractures in the elderly is associated with gradual sarcopenia. Similar deterioration of bone quality is seen with prolonged bed rest, spinal cord injuries or in astronauts exposed to microgravity and, preceded by loss of muscle mass. Signaling mechanisms involving uridine-5′-triphosphate (UTP) regulate bone homeostasis via P2Y2 receptors on osteoblasts and osteoclasts, whilst dictating the bone cells’ response to mechanical loading. We hypothesized that muscle paralysis-induced loss of bone quality would be prevented in P2Y2 receptor knockout (KO) mice. Female mice injected with botulinum toxin (BTX) in the hind limb developed muscle paralysis and femoral DXA analysis showed reduction in bone mineral density (<10%), bone mineral content (<16%) and bone area (<6%) in wildtype (WT) compared to KO littermates (with <13%, <21%, <9% respectively). The femoral metaphyseal strength was reduced equally in both WT and KO (<37%) and <11% in diaphysis region of KO, compared to the saline injected controls. Tibial micro-CT showed reduced cortical thickness (12% in WT vs. 9% in KO), trabecular bone volume (38% in both WT and KO), trabecular thickness (22% in WT vs. 27% in KO) and increased SMI (26% in WT vs. 19% in KO) after BTX. Tibial histomorphometry showed reduced formation in KO (16%) but unchanged resorption in both WT and KO. Furthermore, analyses of DXA and bone strength after regaining the muscle function showed partial bone recovery in the KO but no difference in the bone recovery in WT mice. Primary osteoblasts from KO mice displayed increased viability and alkaline phosphatase activity but, impaired bone nodule formation. Significantly more TRAP-positive osteoclasts were generated from KO mice but displayed reduced resorptive function. Our data showed that hind limb paralysis with a single dose of BTX caused profound bone loss after 3 weeks, and an incomplete reversal of bone loss by week 19. Our findings indicate no role of the P2Y2 receptor in the bone loss after a period of skeletal unloading in mice or, in the bone recovery after restoration of muscle function