In the face of widespread pollinator decline, research has increasingly focused on ways that pesticides could be harming bees. Fungicides are pesticides that are used in greater volumes than insecticides, yet significantly fewer studies have investigated the effects of these agrochemicals. The fungicide Pristine® is commonly used on bee-pollinated crops and has been shown to be detrimental to physiological processes that are key to honey bee foraging, such as digestion and learning. This study seeks to investigate how Pristine® exposure affects the amount of water, nectar, and pollen that honey bees collect. Colonies were fed either plain pollen patties or pollen patties containing 23 ppm Pristine®. Exposure to fungicide had no significant effect on corbicular pollen mass, the crop volumes of nectar or water foragers, or the proportions of foragers collecting different substances. There was a significantly higher sugar concentration in the crop of Pristine®-exposed nectar foragers (43.6%, 95% CI [38.8, 48.4]) compared to control nectar foragers (36.3%, 95% CI [31.9, 40.6]). The higher sugar concentration in the nectar of Pristine®-treated bees could indicate that the agrochemical decreases sucrose responsiveness or nutritional status in bees. Alternatively, fungicide exposure may increase the amount of sugar that bees need to make it back to the hive. Based on these results, it would appear that fungicides like Pristine® do not strongly affect the amounts of substances that honey bees collect, but it is still highly plausible that treated bees forage more slowly or with lower return rates.
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First, a spatially collapsed model is used to develop voltage gated ion channels to study the excitability of the model neuron. Changing the channel densities reproduces different in situ observed firing patterns and induces a switch from resonator to integrator properties. Second, morphologically realistic multicompartment models are studied to investigate the passive properties of MN5. The passive electrical parameters fall in a range that is commonly observed in neurons, MN5 is spatially not compact, but for the single subtrees synaptic efficacy is location independent. Further, different subtrees are electrically independent from each other. Third, a continuum approach is used to formulate a new cable theoretic model to study the output in a dendritic cable with many subtrees, both analytically and computationally. The model is validated, by comparing it to a corresponding model with discrete branches. Further, the approach is demonstrated using MN5 and used to investigate spatially distributions of voltage gated ion channels.
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Assessment of DNA methylation was performed on human skeletal muscle and blood using reduced representation bisulfite sequencing (RRBS) for high-throughput identification and pyrosequencing for site-specific confirmation. Sorbin and SH3 homology domain 3 (SORBS3) was identified in skeletal muscle to be increased in methylation (+5.0 to +24.4 %) in the promoter and 5’untranslated region (UTR) in the obese participants (n= 10) compared to lean (n=12), and this finding corresponded with a decrease in gene expression (fold change: -1.9, P=0.0001). Furthermore, SORBS3 was demonstrated in a separate cohort of morbidly obese participants (n=7) undergoing weight-loss induced by surgery, to decrease in methylation (-5.6 to -24.2%) and increase in gene expression (fold change: +1.7; P=0.05) post-surgery. Moreover, SORBS3 promoter methylation was demonstrated in vitro to inhibit transcriptional activity (P=0.000003). The methylation and transcriptional changes for SORBS3 were significantly (P≤0.05) correlated with obesity measures and fasting insulin levels. SORBS3 was not identified in the blood methylation analysis of lean (n=10) and obese (n=10) participants suggesting that it is a muscle specific marker. However, solute carrier family 19 member 1 (SLC19A1) was identified in blood and skeletal muscle to have decreased 5’UTR methylation in obese participants, and this was significantly (P≤0.05) predicted by insulin sensitivity.
These findings suggest SLC19A1 as a potential blood-based biomarker for obese, insulin resistant states. The collective findings of SORBS3 DNA methylation and gene expression present an exciting novel target in skeletal muscle for further understanding obesity and its underlying insulin resistance. Moreover, the dynamic changes to SORBS3 in response to metabolic improvements and weight-loss induced by surgery.