Plants release large amounts of volatile organic compounds (VOCs) in response to attackers. Several VOCs can serve as volatile signals to elicit defense responses in undamaged tissues and neighboring plants, but many questions about the ecological functions of VOCs remain unanswered. Tea plants are impacted by two harmful invaders, the piercing herbivore Empoasca (Matsumurasca) onukii Matsuda and the pathogen Colletotrichum fructicola. To determine the VOC signals in tea, we confirmed CsOPR3 as a marker gene and set up a rapid screening method based on a 1.51 kb CsOPR3 promoter fused with a β-glucuronidase (GUS) reporter construct (OPR3p::GUS) in Arabidopsis. Using this screening system, a terpenoid volatile (E)-nerolidol was identified as a potent signal that elicits plant defenses. The early responses triggered by (E)-nerolidol included the activation of a mitogen-activated protein kinase and WRKY, an H 2 O 2 burst, and the induction of jasmonic acid and abscisic acid signaling. The induced plants accumulated high levels of defenserelated chemicals, which possessed broad-spectrum anti-herbivore or anti-pathogen properties, and ultimately triggered resistance against Empoasca onukii and Colletotrichum fructicola in tea. We propose that these findings can supply an environmentally friendly management strategy for controlling an insect pest and a disease of tea plants.

BackgroundAlthough serum cystatin C (sCysC), urinary N-acetyl-β-d-glucosaminidase (uNAG), and urinary albumin/creatinine ratio (uACR) are clinically available, their optimal combination for acute kidney injury (AKI) detection and prognosis prediction remains unclear. We aimed to assess the discriminative abilities of these biomarkers and their possible combinations for AKI detection and intensive care unit (ICU) mortality prediction in critically ill adults.MethodsA multicenter, prospective observational study was conducted in mixed medical-surgical ICUs at three tertiary care hospitals. One thousand eighty-four adult critically ill patients admitted to the ICUs were studied. We assessed the use of individual biomarkers (sCysC, uNAG, and uACR) measured at ICU admission and their combinations with regard to AKI detection and prognosis prediction.ResultsAUC-ROCs for sCysC, uNAG, and uACR were calculated for total AKI (0.738, 0.650, and 0.683, respectively), severe AKI (0.839, 0.706, and 0.771, respectively), and ICU mortality (0.727, 0.793, and 0.777, respectively). The panel of sCysC plus uNAG detected total and severe AKI with significantly higher accuracy than either individual biomarkers or the other two panels (uNAG plus uACR or sCysC plus uACR). For detecting total AKI, severe AKI, and ICU mortality at ICU admission, this panel yielded AUC-ROCs of 0.756, 0.863, and 0.811, respectively; positive predictive values of 0.71, 0.31, and 0.17, respectively; and negative predictive values of 0.81, 0.97, and 0.98, respectively. Moreover, this panel significantly contributed to the accuracy of the clinical models for AKI detection and ICU mortality prediction, as measured by the AUC-ROC, continuous net reclassification index, and incremental discrimination improvement index. The comparable performance of this panel was further confirmed with bootstrap internal validation.ConclusionsThe combination of a functional marker (sCysC) and a tubular damage marker (uNAG) revealed significantly superior discriminative performance for AKI detection and yielded additional prognostic information on ICU mortality.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-017-1626-0) contains supplementary material, which is available to authorized users.

BackgroundThe NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been identified as an important mediator of blood–brain-barrier disruption in sepsis-associated encephalopathy (SAE). However, no information is available concerning the critical upstream regulators of SAE.MethodsLipopolysaccharide (LPS) was used to establish an in vitro model of blood–brain barrier (BBB) disruption and an in vivo model of SAE. Disruption of BBB integrity was assessed by measuring the expression levels of tight-junction proteins. NLRP3 inflammasome activation, pro-inflammatory cytokines levels, and neuroapoptosis were measured using biochemical assays. Finally, the FITC-dextran Transwell assay and Evan’s blue dye assay were used to assess the effect of Maf1 on LPS-induced endothelial permeability in vitro and in vivo.ResultsWe found that Maf1 significantly suppressed the brain inflammatory response and neuroapoptosis induced by LPS in vivo and in vitro. Notably, Maf1 downregulated activation of the NF-κB/p65-induced NLRP3 inflammasome and the expression of pro-inflammatory cytokines. In addition, we found that Maf1 and p65 directly bound to the NLRP3 gene promoter region and competitively regulated the function of NLRP3 in inflammations. Moreover, overexpression of NLRP3 reversed the effects of p65 on BBB integrity, apoptosis, and inflammation in response to LPS. Our study revealed novel role for Maf1 in regulating NF-κB-mediated inflammasome formation, which plays a prominent role in SAE.ConclusionsRegulation of Maf1 might be a therapeutic strategy for SAE and other neurodegenerative diseases associated with inflammation.