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Background: Fighter aircraft pilots are regularly exposed to physiological challenges from high acceleration (G z ) forces, as well as increased breathing pressure and oxygen supply in the support systems. We studied whether effects on the lung and systemic oxidative stress were detectable after real training flights comprising of a wide variety of exposure conditions, and their combinations., Methods: Thirty-five pilots of the German Air Force performed 145 flights with the Eurofighter Typhoon. Prior to and after flight lung diffusing capacity for carbon monoxide (DL CO ) and nitric oxide (DL NO ), alveolar volume (V A ), and diffusing capacities per volume (K CO , K NO ) were assessed. In addition, the fractional concentration of exhaled nitric oxide (FeNO) was determined, and urine samples for the analysis of molecular species related to 8-hydroxy-2'-deoxyguanosine (8-OHdG) were taken. For statistical analysis, mixed ANOVA models were used., Results: DL NO , DL CO , K NO , K CO and V A were reduced (p < 0.001) after flights, mean ± SD changes being 2.9 ± 5.0, 3.2 ± 5.2, 1.5 ± 3.7, 1.9 ± 3.7 and 1.4 ± 3.1%, respectively, while FeNO decreased by 11.1% and the ratio of 8-OHdG to creatinine increased by 15.7 ± 37.8%. The reductions of DL NO (DL CO ) were smaller (p < 0.001) than those of K NO (K CO ). In repeated flights on different days, baseline values were restored. Amongst various flight parameters comprising G z -forces and/or being indicative of positive pressure breathing and oxygenation support, the combination of long flight duration and high altitude appeared to be linked to greater changes in DL NO and DL CO ., Conclusions: The pattern of reductions in diffusing capacities suggests effects arising from atelectasis and increased diffusion barrier, without changes in capillary blood volume. The decrease in exhaled endogenous NO suggests bronchial mucosal irritation and/or local oxidative stress, and the increase in urinary oxidized guanosine species suggests systemic oxidative stress. Although changes were small and not clinically relevant, their presence demonstrated physiological effects of real training flights in a modern 4th generation fighter jet., (© 2024. The Author(s).)

Key Message: Molecular markers including a potential resistance gene co-segregating with the LpPg1 stem rust resistance locus in perennial ryegrass were identified by massive analysis of cDNA ends (MACE) transcriptome profiling. Stem rust caused by Puccinia graminis subsp. graminicola is a severe fungal disease in the forage crop perennial ryegrass and other grasses. The previously identified LpPg1 locus confers efficient resistance against the pathogen. The aim of this study was to identify candidate genes involved in rust resistance and to use them as a resource for the development of molecular markers for LpPg1. To identify such candidates, bulked segregant analysis was combined with NGS-based massive analysis of cDNA ends (MACE) transcriptome profiling. Total RNA was isolated from bulks of infected and non-infected leaf segments from susceptible and resistant genotypes of a full-sibling mapping population and their respective parental lines and MACE was performed. Bioinformatic analysis detected 330 resistance-specific SNPs in 178 transcripts and 341 transcripts that were exclusively expressed in the resistant bulk. The sequences of many of these transcripts were homologous to genes in distinct regions of chromosomes one and four of the model grass Brachypodium distachyon. Of these, 30 were genetically mapped to a 50.8 cM spanning region surrounding the LpPg1 locus. One candidate NBS-LRR gene co-segregated with the resistance locus. Quantitative analysis of gene expression suggests that LpPg1 mediates an efficient resistance mechanism characterized by early recognition of the pathogen, fast defense signaling and rapid induction of antifungal proteins. We demonstrate here that MACE is a cost-efficient, fast and reliable tool that detects polymorphisms for genetic mapping of candidate resistance genes and simultaneously reveals deep insight into the molecular and genetic base of resistance.

Sensory screening of a series of naturally occurring N-cinnamoyl derivatives of substituted phenethylamines revealed that rubemamine (9, from Chenopodium album) and rubescenamine (10, from Zanthoxylum rubsecens) elicit strong intrinsic umami taste in water at 50 and 10 ppm, respectively. Sensory tests in glutamate- and nucleotide-containing bases showed that the compounds influence the whole flavor profile of savory formulations. Both rubemamine (9) and rubescenamine (10) at 10-100 ppm dose-dependently positively modulated the umami taste of MSG (0.17-0.22%) up to threefold. Among the investigated amides, only rubemamine (9) and rubescenamine (10) are able to directly activate the TAS1R1-TAS1R3 umami taste receptor. Moreover, both compounds also synergistically modulated the activation of TAS1R1-TAS1R3 by MSG. Most remarkably, rubemamine (9) was able to further positively modulate the IMP-enhanced TAS1R1-TAS1R3 response to MSG ∼ 1.8-fold. Finally, armatamide (11), zanthosinamide (13), and dioxamine (14), which lack intrinsic umami taste in vivo and direct receptor response in vitro, also positively modulated receptor activation by MSG about twofold and the IMP-enhanced MSG-induced TAS1R1-TAS1R3 responses approximately by 50%. In sensory experiments, dioxamine (14) at 25 ppm in combination with 0.17% MSG exhibited a sensory equivalent to 0.37% MSG.