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Gill, S.

Publications and source records attributed to Gill, S..

5 recordsLinked to original sources

Pesticide exposure affects flight dynamics and reduces flight endurance in bumblebees

The emergence of agricultural land use change creates a number of challenges that insect pollinators, such as eusocial bees, must overcome. Resultant fragmentation and loss of suitable foraging habitats, combined with pesticide exposure, may increase demands on foraging, specifically the ability to reach resources under such stress. Understanding the effect that pesticides have on flight performance is therefore vital if we are to assess colony success in these changing landscapes. Neonicotinoids are one of the most widely used classes of pesticide across the globe, and exposure to bees has been associated with reduced foraging efficiency and homing ability. One explanation for these effects could be that elements of flight are being affected, but apart from a couple of studies on the honeybee, this has scarcely been tested. Here we used flight mills to investigate how exposure to a field realistic (10ppb) acute dose of imidacloprid affected flight performance of a wild insect pollinator - the bumblebee, Bombus terrestris audax. Intriguingly, intial observations showed exposed workers flew at a significantly higher velocity over the first [3/4] km of flight. This apparent hyperactivity, however, may have a cost as exposed workers showed reduced flight distance and duration to around a third of what control workers were capable of achieving. Given that bumblebees are central place foragers, impairment to flight endurance could translate to a decline in potential forage area, decreasing the abundance, diversity and nutritional quality of available food, whilst potentially diminishing pollination service capabilities.\n\nSummary StatementAcute neonicotinoid exposure impaired flight endurance and affected velocity of Bombus terrestris workers, which may dramatically reduce colony foraging potential and pollination provision in pesticide applied landscapes.

ecology

Multi-laminate Annulus Fibrosus Repair Scaffold with an Interlamellar Matrix Enhances Impact Resistance, Prevents Herniation and Assists in Restoring Spinal Kinematics

Focal defects in the annulus fibrosus (AF) of the intervertebral disc (IVD) from herniation or surgical injury have detrimental impacts on IVD mechanical function. Thus, biomaterial-based repair strategies, which can restore the mechanical integrity of the AF and support long-term tissue regeneration are needed. Accordingly, a collagen-based multi-laminate scaffold with an underlying \"angle-ply\" architecture has been previously reported demonstrating similar mechanical properties to native AF tissue. The objectives of this work were to: 1) enhance the biomaterials impact strength, 2) define its contribution to spinal kinematics, and 3) assess its ability to prevent IVD herniation. First, AFRPs were enriched with a glycosaminoglycan-based (GAG) interlamellar matrix (ILM), and then tested for its radially-directed impact resistance under physiological stresses. Subsequent kinematic testing was conducted using a characterized GAG-enriched AFRP as an AF focal defect closure device. In summary, AFRPs demonstrated 1) incorporation of a GAG-based ILM significantly increased radial impact strength, 2) restoration of axial FSU kinematics and 3) ability to prevent herniation of native IVD tissues. Together, these results suggest that the AFRP demonstrates the mechanical robustness and material properties to restore an IVDs physiological mechanical function through the adequate closure of an AF focal defect.

bioengineering

A pilot investigation of chemonucleolysis-induced intervertebral disc degeneration in the ovine lumbar spine

Intervertebral disc (IVD) degeneration (IVDD) initiates in the nucleus pulposus (NP) and is marked by elevated levels of pro-inflammatory cytokines and matrix-degrading proteases, leading to structural and functional disruption. IVDD therapeutics are currently being investigated; however, such approaches require validation using large animal models that recapitulate clinical, biochemical, and biomechanical hallmarks of the human pathology. Others have previously utilized intradiscal administration of chondroitinase-ABC (C-ABC) to initiate IVDD in the NP of sheep lumbar IVDs. While these studies examined changes in IVD height, hydration, and tissue micro-architecture, changes in biochemical content and mechanical properties were not assessed. Thus, the objective herein was to comprehensively characterize this ovine model IVDD for salient features reported in human degenerate IVDs by evaluating biochemical, biomechanical, and histological changes. Briefly, C-ABC (1U) was administered via intradiscal injection into the L1/2, L2/3, and L3/4 IVDs, and degeneration was assessed at 6- and 10-weeks via longitudinal magnetic resonance (MR) imaging. After 6 weeks, degenerative samples showed significant reductions in IVD heights (p=0.048) and MR imaging index (p=0.048), which worsened at 10 weeks. Post-mortem degenerate and controls IVDs were evaluated for differences in interleukin-1{beta} concentration, axial and torsional functional spinal unit kinematics, and histological microarchitecture. Degenerate IVDs demonstrated significantly elevated concentrations of interleukin-1{beta} (p=0.002). Additionally, degenerative samples showed increased creep displacement (p=0.022) and compressive stiffnesss (p=0.007) concurrent with decreased long-term elastic (p=0.007) and viscous dampening coefficients (p=0.002). Histological analysis of degenerative IVDs showed changes in microarchitecture, including derangement of the nucleus pulposus and annulus fibrosus tissue as well as cartilaginous end-plate irregularities. This pilot study demonstrated that intradiscal injection of 1U C-ABC induces significant and progressive degeneration of sheep lumbar IVDs over the time course investigated. The changes observed in this pilots study small sample size resemble the hallmarks of moderate to severe IVD degeneration observed in humans. Further study is warranted on a larger sample size to further validate these findings.

bioengineering

The crossmodal congruency effect, a tool incorporation metric, suffers from a learning effect with repeated exposures

The incorporation of feedback into a persons body schema is well established. The crossmodal congruency effect (CCE) task is used to objectively quantify incorporation without being susceptible to experimenter biases. This visual-tactile interference task is used to calculate the CCE score as a difference in response time for incongruent and congruent trials. Here we show that this metric is susceptible to a learning effect that causes attenuation of the CCE score due to repeated task exposure sessions. We demonstrate that this learning effect is persistent, even after a 6 month hiatus in testing. Two mitigation strategies are proposed: 1. Only use CCE scores that are taken after learning has stabilized, or 2. Use a modified CCE protocol that decreases the task exposure time. We show that the modified and shortened CCE protocol, which may be required to meet time or logistical constraints in laboratory or clinical settings, reduced the impact of the learning effect on CCE results. Importantly, the CCE scores from the modified protocol were not significantly more variable than results obtained with the original protocol. This study highlights the importance of considering exposure time to the CCE task when designing experiments and suggests two mitigation strategies to improve the utility of this psychophysical assessment.

neuroscience

Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits

Chronic sleep disturbances, associated with cardio-metabolic diseases, psychiatric disorders and all-cause mortality1,2, affect 25-30% of adults worldwide3. While environmental factors contribute importantly to self-reported habitual sleep duration and disruption, these traits are heritable4-9, and gene identification should improve our understanding of sleep function, mechanisms linking sleep to disease, and development of novel therapies. We report single and multi-trait genome-wide association analyses (GWAS) of self-reported sleep duration, insomnia symptoms including difficulty initiating and/or maintaining sleep, and excessive daytime sleepiness in the UK Biobank (n=112,586), with discovery of loci for insomnia symptoms (near MEIS1, TMEM132E, CYCL1, TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR/OPHN1) and a composite sleep trait (near INADL and HCRTR2), as well as replication of a locus for sleep duration (at PAX-8). Genetic correlation was observed between longer sleep duration and schizophrenia (rG=0.29, p=1.90x10-13) and between increased excessive daytime sleepiness and increased adiposity traits (BMI rG=0.20, p=3.12x10-09; waist circumference rG=0.20, p=2.12x10-07).

genetics