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Author Correction: A cell-free platform for the prenylation of natural products and application to cannabinoid production.
In the original version of this Article, the genotype of the M30 mutant presented in Fig. 3b was given incorrectly as Y288V/A232S, and the M31 mutant was given incorrectly as M1/A232S. The correct genotype of the M30 mutant is Y288A/A232S and for M31 it is Y288V/A232S. In addition, to keep consistency in genotype formatting, the genotype of the M27 mutant should be Y288V/G286S. The errors have been corrected in both the PDF and HTML versions of the Article
Differential Susceptibility of Japanese Beetle, Oriental Beetle, and European Chafer (Coleoptera: Scarabaeidae) Larvae to Five Soil Insecticides
Efficacy of bendiocarb, chlorpyrifos, diazinon, ethoprop, and isofenphos was evaluated against last-instar larvae of European chafer, Rhizotrogus majalis (Razoumowsky), Japanese beetle, Popillia japonica Newman, and Oriental beetle, Anomala orientalis Waterhouse, by incorporating insecticides into soil at one-half New York State recommended rates in a laboratory bioassay. Mortality was assessed at 1, 2, 3, 4, and 5 wk. The experiment was repeated three times with white grubs collected at different times and from different locations in New York. White grub species differed significantly in their response to some of the insecticides; European chafer was generally least susceptible. Diazinon provided high mortality of Oriental beetle and European chafer grubs but very low mortality of Japanese beetles. Isofenphos provided generally low mortality of all three grub species, although the levels of mortality varied among species. Ethoprop provided uniform mortality of all three grub species. Results of these studies indicate the need to develop species-specific insecticide recommendations for the white grub complex
Invasive alien species in the food chain : advancing risk assessment models to address climate change, economics and uncertainty
Economic globalization depends on the movement of people and goods between countries. As these exchanges increase, so does the potential for translocation of harmful pests, weeds, and pathogens capable of impacting our crops, livestock and natural resources (Hulme 2009), with concomitant impacts on global food security (Cook et al. 2011)
Human epicardial adipose tissue expresses a pathogenic profile of adipocytokines in patients with cardiovascular disease
Introduction: Inflammation contributes to cardiovascular disease and is exacerbated with
increased adiposity, particularly omental adiposity; however, the role of epicardial fat is poorly
understood.
Methods: For these studies the expression of inflammatory markers was assessed in epicardial fat
biopsies from coronary artery bypass grafting (CABG) patients using quantitative RT-PCR. Further,
the effects of chronic medications, including statins, as well as peri-operative glucose, insulin and
potassium infusion, on gene expression were also assessed. Circulating resistin, CRP, adiponectin
and leptin levels were determined to assess inflammation.
Results: The expression of adiponectin, resistin and other adipocytokine mRNAs were
comparable to that in omental fat. Epicardial CD45 expression was significantly higher than control
depots (p < 0.01) indicating significant infiltration of macrophages. Statin treated patients showed
significantly lower epicardial expression of IL-6 mRNA, in comparison with the control abdominal
depots (p < 0.001). The serum profile of CABG patients showed significantly higher levels of both
CRP (control: 1.28 ± 1.57 μg/mL vs CABG: 9.11 ± 15.7 μg/mL; p < 0.001) and resistin (control:
10.53 ± 0.81 ng/mL vs CABG: 16.8 ± 1.69 ng/mL; p < 0.01) and significantly lower levels of
adiponectin (control: 29.1 ± 14.8 μg/mL vs CABG: 11.9 ± 6.0 μg/mL; p < 0.05) when compared to
BMI matched controls.
Conclusion: Epicardial and omental fat exhibit a broadly comparable pathogenic mRNA profile,
this may arise in part from macrophage infiltration into the epicardial fat. This study highlights that
chronic inflammation occurs locally as well as systemically potentially contributing further to the
pathogenesis of coronary artery disease
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