Analysis of Pesticide Levels in Honey and Pollen from Irish Honey Bee Colonies Using a Modified Dutch Mini-Luke Method with Gas and Liquid Chromatography-Tandem Mass Spectrometry Detection.

Determining the levels of agrochemicals, such as pesticides, that honey bees are exposed to is critical for understanding what stress factors may be contributing to colony declines. Although several pesticide detection methods are available for honey, limited work has been conducted to adapt these methods for pollen. Here, we address this gap by modifying the Dutch mini-Luke extraction method (NL method) for pesticide analysis in honey and pollen from throughout the island of Ireland. The NL method was modified to enable detection in small-sized samples and validated for both pollen and honey matrices. The modified NL method combined with liquid and gas chromatography-tandem mass spectrometry gave consistent results in terms of accuracy and precision measured by recovery experiments and was successfully applied in the analysis of a range of pesticide residues. The modified NL method developed here provides a key tool for detecting pesticides in honey bee colony resources and the environment more broadly.

Knockdown of interleukin-1 receptor 1 is not neuroprotective in the 6-hydroxydopamine striatal lesion rat model of Parkinson's disease.

It is well established that neuroinflammation is associated with the progression of many neurodegenerative diseases, including Parkinson's disease (PD). Activated microglia and elevated levels of pro-inflammatory cytokines such as interleukin-1ß (IL-1ß) have been found in the brain and cerebrospinal fluid of PD patients, suggesting that IL-1ß may be involved in the pathogenesis of this disease. This study aimed to knock down the expression of the interleukin-1 type 1 receptor (IL-1R1) to evaluate any potential therapeutic effect of limiting the action of IL-1ß in the substantia nigra following a unilateral intrastriatal 6-hydroxydopamine (6-OHDA) lesion in rats. Adult Sprague-Dawley rats received intranigral injections of shRNA specific for IL-1R1, followed 2 weeks later by intrastriatal 6-OHDA. Injection of IL-1R1 shRNA did not prevent 6-OHDA-induced loss of motor function or loss of nigral dopamine neurons. IL-1R1 expression was increased in the midbrain following 6-OHDA injection; this effect was attenuated in 6-OHDA-treated animals that had received IL-1R1 shRNA. These data suggest that while IL-1R1 was increased in 6-OHDA-treated animals and reduced following shRNA injection, the neurodegeneration induced by 6-OHDA was not mediated through IL-1R1.