Browsing Faculty of Medicine, Dentistry and Life Sciences by Publisher "Oxford Academic"
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The effect of rainfall upon the behaviour and use of under-road culverts in four amphibian speciesHabitat fragmentation and road mortalities are major contributors towards declines in amphibian populations. This has seen the introduction of culverts, passages that run under roads and provide safe passage for amphibians. Research investigating the effects of rainfall upon amphibian culvert use is limited. This study, conducted at Frankfield Loch in Glasgow, assesses how time elapsed since rainfall influences migration behaviour and the use of culverts across four different species; common toads (Bufo bufo), common frogs (Rana temporaria and newts, a group composed of smooth newts (Lissotriton vulgaris) and palmate newts (Lissotriton helveticus). Analysis of images taken by a custom made, time lapse camera found that significantly fewer common toads (r = 0.148, n = 468, p = 0.001) and common frogs (r = −0.175, n = 106, p = 0.037) used the culvert as time since rainfall increased. This may have been caused by the culvert not maintaining wet enough conditions for amphi- bians. The study also found that more newts (r = 0.272, n = 92, p = 0.004) and common toads (r = 0.531, n = 19, p = 0.010) were using the culvert to move away from Frankfield Loch as time since rainfall increased. An increase in juvenile newts was also observed as time since rainfall increased (r = 0.214, n = 92, p = 0.020). This may have been caused by a decrease in baro- metric pressure, which follows a decrease in rainfall, acting as a cue for migration and juvenile dispersal. The study recom- mends careful consideration of the design of each culvert, incorporating species-specific preferences and the requirements of juveniles. The study also suggests that where possible the culvert should be designed to hold water for longer.
Lamin A/C dysregulation contributes to cardiac pathology in a mouse model of severe spinal muscular atrophyCardiac pathology is emerging as a prominent systemic feature of spinal muscular atrophy (SMA), but little is known about the underlying molecular pathways. Using quantitative proteomics analysis, we demonstrate widespread molecular defects in heart tissue from the Taiwanese mouse model of severe SMA. We identify increased levels of lamin A/C as a robust molecular phenotype in the heart of SMA mice and show that lamin A/C dysregulation is also apparent in SMA patient fibroblast cells and other tissues from SMA mice. Lamin A/C expression was regulated in vitro by knockdown of the E1 ubiquitination factor ubiquitin-like modifier activating enzyme 1, a key downstream mediator of SMN-dependent disease pathways, converging on β-catenin signaling. Increased levels of lamin A are known to increase the rigidity of nuclei, inevitably disrupting contractile activity in cardiomyocytes. The increased lamin A/C levels in the hearts of SMA mice therefore provide a likely mechanism explaining morphological and functional cardiac defects, leading to blood pooling. Therapeutic strategies directed at lamin A/C may therefore offer a new approach to target cardiac pathology in SMA.