Among patients with acute myocardial infarction and cardiogenic shock, the risk of death or renal-replacement therapy at 30 days was lower with culprit-lesion-only PCI than with immediate multivessel PCI, and mortality did not differ significantly between the two groups at 1 year of follow-up. (Funded by the European Union Seventh Framework Program and others; CULPRIT-SHOCK ClinicalTrials.gov number, NCT01927549 .).

bBacteria emit volatile organic compounds with a wide range of effects on bacteria, fungi, plants, and animals. The antifungal potential of bacterial volatiles has been investigated with a broad span of phytopathogenic organisms, yet the reaction of oomycetes to these volatile signals is largely unknown. For instance, the response of the late blight-causing agent and most devastating oomycete pathogen worldwide, Phytophthora infestans, to bacterial volatiles has not been assessed so far. In this work, we analyzed this response and compared it to that of selected fungal and bacterial potato pathogens, using newly isolated, potato-associated bacterial strains as volatile emitters. P. infestans was highly susceptible to bacterial volatiles, while fungal and bacterial pathogens were less sensitive. Cyanogenic Pseudomonas strains were the most active, leading to complete growth inhibition, yet noncyanogenic ones also produced antioomycete volatiles. Headspace analysis of the emitted volatiles revealed 1-undecene as a compound produced by strains inducing volatile-mediated P. infestans growth inhibition. Supplying pure 1-undecene to P. infestans significantly reduced mycelial growth, sporangium formation, germination, and zoospore release in a dose-dependent manner. This work demonstrates the high sensitivity of P. infestans to bacterial volatiles and opens new perspectives for sustainable control of this devastating pathogen. During the last decade, it has become evident that bacteria communicate with other organisms through the emission of volatile compounds. Highly significant volatile-mediated effects of bacteria have been reported for various target organisms, including bacteria themselves (1-5), plants (5-9), and fungi (10-12). The research carried out to understand the nature of this volatile-mediated interaction of bacteria with plants and with other bacteria has focused so far on model organisms (e.g., Arabidopsis thaliana and Escherichia coli) and has enabled identification of some of the active compounds involved in the respective interactions, such as indole, 2,3-butanediol, dimethyl disulfide, hydrogen sulfide, and ammonia. The research on model organisms has also contributed to understanding of the mechanisms underlying the observed phenotypic changes of increased (13-15) or decreased (16, 17) plant biomass and increased antibiotic resistance in bacteria (2-4, 18).As far as fungi are concerned, most studies investigating their response to bacterial volatiles have focused on potential application and have thus largely neglected deeper investigation of the chemical nature of the active compounds and/or of the mode of action of these molecules. In addition to the inorganic volatiles hydrogen cyanide (19) and ammonia (20), few volatile organic compounds, such as sulfur compounds and long-chain ketones, have been unequivocally shown to inhibit the growth of phytopathogenic fungi when applied at biologically relevant concentrations (12). With the ultimate prospect of using the antifungal potential of bacterial...

AIMS The Academic Research Consortium for High Bleeding Risk (ARC-HBR) defined consensusbased criteria for patients at high bleeding risk (HBR) undergoing percutaneous coronary intervention (PCI). We aimed to validate the ARC-HBR criteria for the bleeding outcomes using a large cohort of patients undergoing PCI. METHODS AND RESULTS Between 2009 and 2016, patients undergoing PCI were prospectively included in the Bern PCI Registry. Patients were considered to be at HBR if at least one major criterion or two minor criteria were met. The primary endpoint was Bleeding Academic Research Consortium (BARC) 3 or 5 bleeding at one year; ischaemic outcomes were assessed using the device-oriented composite endpoints (DOCE) of cardiac death, target vessel myocardial infarction, and target lesion revascularisation. Among 12,121 patients, those at HBR (n=4,781, 39.4%) had an increased risk of BARC 3 or 5 bleeding (6.4% vs 1.9%; p<0.001) and DOCE (12.5% vs 6.1%; p<0.001) compared with those without HBR. The degree of risk and prognostic value were related to the risk factors composing the criteria. The ARC-HBR criteria had higher sensitivity than the PRECISE-DAPT score and the PARIS bleeding risk score (63.8%, 53.1%, 31.9%), but lower specificity (62.7%, 71.3%, 86.5%) for BARC 3 or 5 bleeding. CONCLUSIONS Patients at HBR defined by the ARC-HBR criteria had a higher risk of BARC 3 or 5 bleeding as well as DOCE. The bleeding risk was related to its individual components. The ARC-HBR criteria were more sensitive for identifying patients with future bleedings than other contemporary risk scores at the cost of specificity. ClinicalTrials.gov Identifier: NCT02241291 Visual summary. According to the ARC-HBR criteria, 40% of patients undergoing PCI were at HBR. Compared with patients without HBR, those at HBR had an increased risk of BARC 3 or 5 bleeding (6.4% vs 1.9%, p<0.001). There was a gradual risk increase for BARC 3 or 5 bleeding and DOCE as a function of the ARC-HBR score. BARC: Bleeding Academic Research Consortium; DOCE: device-oriented composite endpoints; HBR: high bleeding risk.

Tomato leaf mold disease is caused by the biotrophic fungus Cladosporium fulvum. During infection, C. fulvum produces extracellular small secreted protein (SSP) effectors that function to promote colonization of the leaf apoplast. Resistance to the disease is governed by Cf immune receptor genes that encode receptor-like proteins (RLPs). These RLPs recognize specific SSP effectors to initiate a hypersensitive response (HR) that renders the pathogen avirulent. C. fulvum strains capable of overcoming one or more of all cloned Cf genes have now emerged. To combat these strains, new Cf genes are required. An effectoromics approach was employed to identify wild tomato accessions carrying new Cf genes. Proteomics and transcriptome sequencing were first used to identify 70 apoplastic in planta-induced C. fulvum SSPs. Based on sequence homology, 61 of these SSPs were novel or lacked known functional domains. Seven, however, had predicted structural homology to antimicrobial proteins, suggesting a possible role in mediating antagonistic microbe-microbe interactions in planta. Wild tomato accessions were then screened for HR-associated recognition of 41 SSPs, using the Potato virus X-based transient expression system. Nine SSPs were recognized by one or more accessions, suggesting that these plants carry new Cf genes available for incorporation into cultivated tomato.Leaf mold disease of tomato (Solanum lycopersicum) is caused by the biotrophic Dothideomycete fungal pathogen Cladosporium fulvum (syn. Passalora fulva and Fulvia fulva) (Thomma et al. 2005). The fungus likely originated in South America, the center of origin for tomato (Jenkins 1948), with Nucleotide sequence data is available in the GenBank database under the following accession numbers: Ecp6, KX943112; Ecp7, KX943113; Ecp8, KX943038; Ecp9-1, KX943041; Ecp9-2, KX943114; Ecp9-3, KX943115; Ecp9-4, KX943116; Ecp9-5, KX943117; Ecp9-6, KX943118; Ecp9-7, KX943119; Ecp9-8, KX943120; Ecp9-9, KX943081; Ecp10-1, KX943046; Ecp10-2, KX943063; Ecp10-3, KX943121; Ecp11-1, KX943050; Ecp12, KX943058; Ecp13, KX943065; Ecp14-1, KX943087; Ecp14-2, KX943122; Ecp15, KX943091; Ecp16, KX943080; Ecp17, KX943051; Ecp18, KX943035; Ecp19-1, KX943036; Ecp19-2, KX943048; Ecp20-1, KX943037; Ecp20-2, KX943057; Ecp20-3, KX943096; Ecp21-1, KX943039; Ecp22, KX943040; Ecp23, KX943044; Ecp24-1, KX943045; Ecp24-2, KX943094; Ecp25, KX943047; Ecp26, KX943052; Ecp27, KX943054; Ecp28-1, KX943056; Ecp28-2, KX943088; Ecp28-3, KX943090; Ecp29, KX943103; Ecp30, KX943076; Ecp31, KX943059; Ecp32-1, KX943062; Ecp32-2, KX943101; Ecp33, KX943066; Ecp34, KX943067; Ecp35, KX943068; Ecp36-1, KX943069; Ecp37, KX943072; Ecp38, KX943073; Ecp39, KX943074; Ecp40, KX943079; Ecp41, KX943082; Ecp42, KX943083; Ecp43-1, KX943089; Ecp44, KX943092; Ecp45, KX943093; Ecp46, KX943095; Ecp47, KX943097; Ecp48, KX943098; Ecp49-1, KX943099; Ecp50-1, KX943100; Ecp51, KX943102; Ecp52, KX943104; Ecp53-1, KX943105; Ecp54-1, KX943107; Ecp55, KX943108; Ecp56, KX943110; Ecp57-1,