Proteomic and Properties Analysis of Botanical Insecticide Rhodojaponin III-Induced Response of the Diamondback Moth, <i>Plutella xyllostella</i> (L.)

<div><p>Background</p><p>Rhodojaponin III, as a botanical insecticide, affects a wide variety of biological processes in insects, including reduction of feeding, suspension of development, and oviposition deterring of adults in a dose-dependent manner. However, the mode of these actions remains obscure.</p><p>Principal Findings</p><p>In this study, a comparative proteomic approach was adopted to examine the effect of rhodojaponin III on the <i>Plutella xyllostella</i> (L.). Following treating 48 hours, newly emergence moths were collected and protein samples were prepared. The proteins were separated by 2-DE, and total 31 proteins were significantly affected by rhodojaponin III compared to the control identified by MALDI-TOF/TOF-MS/MS. These differentially expressed proteins act in the nervous transduction, odorant degradation and metabolic change pathways. Further, gene expression patterns in treated and untreated moths were confirmed by qRT-PCR and western blot analysis. RNAi of the chemosensory protein (PxCSP) gene resulted in oviposition significantly increased on cabbage plants treated with rhodojaponin III.</p><p>Conclusions</p><p>These rhodojaponin III-induced proteins and gene properties analysis would be essential for a better understanding of the potential molecular mechanism of the response to rhodojaponin III from moths of <i>P. xylostella</i>.</p></div

Two-dimensional electrophoresis map of proteins in <i>p. xylostella</i>. untreated (control), treated (exposed to rhodojaponin III).

<p>Two-dimensional electrophoresis map of proteins in <i>p. xylostella</i>. untreated (control), treated (exposed to rhodojaponin III).</p

Identification of Differentially Expressed protein spots.

a<p>Spot No. is the unique number of the position where the spot display in the master gel;</p>b<p>The number of peaks that match the trypsin peptides;</p>c<p>The number of peaks that do not match the trypsin peptides;</p>d<p>Protein score based on combined mass/mass spectrums;</p>e<p>Each spot corresponding to a certain protein had at least one of the shown peptides identified.</p

RNAi-mediated knockdown of <i>PxCSP-2</i> gene confused oviposition behavior (twenty-five pairs were analyzed per group).

<p>(A) Rhodojaponin III untreated; (B) Rhodojaponin III treated. The data represent the mean values ± S.E.M of three replicates. ‘*’ means statistically significant difference in number of eggs on the cabbage leaves compared to DEPC water (<i>t</i>-test, p<0.05).</p

Image_2_25(OH)D-but not 1,25(OH)2D–Is an independent risk factor predicting graft loss in stable kidney transplant recipients.pdf

BackgroundVitamin D deficiency (VDD) or vitamin D insufficiency is common in kidney transplant recipients (KTRs). The impact of VDD on clinical outcomes in KTRs remain poorly defined and the most suitable marker for assessing vitamin D nutritional status in KTRs is unknown so far.MethodsWe conducted a prospective study including 600 stable KTRs (367 men, 233 women) and a meta-analysis to pool existing evidence to determine whether 25(OH)D or 1,25(OH)2D predicted graft failure and all-cause mortality in stable KTRs.ResultsCompared with a higher 25(OH)D concentration, a low concentration of 25(OH)D was a risk factor for graft failure (HR 0.946, 95% CI 0.912−0.981, p = 0.003), whereas 1,25 (OH)2D was not associated with the study end-point graft loss (HR 0.993, 95% CI 0.977−1.009, p = 0.402). No association was found between either 25(OH)D or 1,25 (OH)2D and all-cause mortality. We furthermore conducted a meta-analysis including 8 studies regarding the association between 25(OH)D or 1,25(OH)2D and graft failure or mortality, including our study. The meta-analysis results were consistent with our study in finding that lower 25(OH)D levels were significantly associated with the risk of graft failure (OR = 1.04, 95% CI: 1.01−1.07), but not associated with mortality (OR = 1.00, 95% CI: 0.98−1.03). Lower 1,25(OH)2D levels were not associated with the risk of graft failure (OR = 1.01, 95% CI: 0.99−1.02) and mortality (OR = 1.01, 95% CI: 0.99−1.02).ConclusionBaseline 25(OH)D concentrations but not 1,25(OH)2D concentrations were independently and inversely associated with graft loss in adult KTRs.</p

Image_1_25(OH)D-but not 1,25(OH)2D–Is an independent risk factor predicting graft loss in stable kidney transplant recipients.pdf

BackgroundVitamin D deficiency (VDD) or vitamin D insufficiency is common in kidney transplant recipients (KTRs). The impact of VDD on clinical outcomes in KTRs remain poorly defined and the most suitable marker for assessing vitamin D nutritional status in KTRs is unknown so far.MethodsWe conducted a prospective study including 600 stable KTRs (367 men, 233 women) and a meta-analysis to pool existing evidence to determine whether 25(OH)D or 1,25(OH)2D predicted graft failure and all-cause mortality in stable KTRs.ResultsCompared with a higher 25(OH)D concentration, a low concentration of 25(OH)D was a risk factor for graft failure (HR 0.946, 95% CI 0.912−0.981, p = 0.003), whereas 1,25 (OH)2D was not associated with the study end-point graft loss (HR 0.993, 95% CI 0.977−1.009, p = 0.402). No association was found between either 25(OH)D or 1,25 (OH)2D and all-cause mortality. We furthermore conducted a meta-analysis including 8 studies regarding the association between 25(OH)D or 1,25(OH)2D and graft failure or mortality, including our study. The meta-analysis results were consistent with our study in finding that lower 25(OH)D levels were significantly associated with the risk of graft failure (OR = 1.04, 95% CI: 1.01−1.07), but not associated with mortality (OR = 1.00, 95% CI: 0.98−1.03). Lower 1,25(OH)2D levels were not associated with the risk of graft failure (OR = 1.01, 95% CI: 0.99−1.02) and mortality (OR = 1.01, 95% CI: 0.99−1.02).ConclusionBaseline 25(OH)D concentrations but not 1,25(OH)2D concentrations were independently and inversely associated with graft loss in adult KTRs.</p

Noncanonical autophagy is a new strategy to inhibit HSV-1 through STING1 activation

STING1 (stimulator of interferon response cGAMP interactor 1) plays an essential role in immune responses for virus inhibition via inducing the production of type I interferon, inflammatory factors and macroautophagy/autophagy. In this study, we found that STING1 activation could induce not only canonical autophagy but also non-canonical autophagy (NCA) which is independent of the ULK1 or BECN1 complexes to form MAP1LC3/LC3-positive structures. Whether STING1-induced NCA has similar characters and physiological functions to canonical autophagy is totally unknown. Different from canonical autophagy, NCA could increase single-membrane structures and failed to degrade long-lived proteins, and could be strongly suppressed by interrupting vacuolar-type H+-translocating ATPase (V-ATPase) activity. Importantly, STING1-induced NCA could effectively inhibit DNA virus HSV-1 in cell model. Moreover, STING1[1-340], a STING1 mutant lacking immunity and inflammatory response due to deletion of the tail end of STING1, could degrade virus through NCA alone, suggesting that the antiviral effect of activated STING1 could be separately mediated by inherent immunity, canonical autophagy, and NCA. In addition, the translocation and dimerization of STING1 do not rely on its immunity function and autophagy pathway. Similar to canonical autophagy, LC3-positive structures of NCA induced by STING1 could finally fuse with lysosomes, and the degradation of HSV-1 could be reverted by inhibition of lysosome function, suggesting that the elimination of DNA virus via NCA still requires the lysosome pathway. Collectively, we proved that besides its classical immunity function and canonical autophagy pathway, STING1-induced NCA is also an efficient antiviral pathway for the host cell.</p

Supplementary document for Low threshold AlGaN-based deep ultraviolet laser enabled by nanoporous cladding layer - 6799781.pdf

supplemental materia

Rates and hazard ratios for all-cause and cardiovascular mortality according to categories of serum potassium.

<p>Abbreviations: pys, patient-years; HR, hazard ratio, and other abbreviations and definitions as listed in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086750#pone-0086750-t001" target="_blank">Table 1</a>.</p>a<p>Age- and gender-standardized Mortality rate.</p>b<p>Adjusted for age, gender, BMI, diabetic status, CCI, hemoglobin, serum albumin, hs-CRP, and PDV/BSA.</p

Distribution of baseline serum potassium levels and corresponding mortality rates.

<p>Gender- and age- standardized all-cause and cardiovascular mortality rates (per 100 patient-years) with 95% confidence intervals according to serum potassium categories at baseline.</p