Automatic waterline registration of a ship model in waves

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Development of an upwind sailing ergometer

Purpose: To develop a sailing ergometer that accurately simulates upwind sailing exercise. Methods: A sailing ergometer that measures roll moment accompanied by a biofeedback system that allows imposing a certain quasi-isometric upwind sailing protocol (ie, 18 bouts of 90-s hiking at constantly varying hiking intensity interspersed with 10 s to tack) was developed. Ten male high-level Laser sailors performed an incremental cycling test (ICT; ie, step protocol at 80W + 40 W/3 min) and an upwind sailing test (UST). During both, heart rate (HR), oxygen uptake (VO2), ventilation (V-E), respiratory-exchange ratio, and rating of perceived exertion were measured. During UST, also the difference between the required and produced hiking moment (HM) was calculated as error score (ES). HR, VO2, and V-E were calculated relative to their peak values determined during ICT. After UST, the subjects were questioned about their opinion on the resemblance between this UST and real-time upwind sailing. Results: An average HM of 89.0% +/- 2.2% HMmax and an average ES of 4.1% +/- 1.8% HMmax were found. Mean HR, VO2, and V-E were, respectively, 80% +/- 4% HRpeak, 39.5% +/- 4.5% VO2peak, and 30.3% +/- 3.7% V-Epeak. Both HM and cardiorespiratory values appear to be largely comparable to literature reports during on-water upwind sailing. Moreover, the subjects gave the upwind sailing ergometer a positive resemblance score. Conclusions: Results suggest that this ergometer accurately simulates on-water upwind sailing exercise. As such, this ergometer could be a great help in performance diagnostics and training follow-up

Shortening of membrane lipid acyl chains compensates for phosphatidylcholine deficiency in choline-auxotroph yeast

Phosphatidylcholine (PC) is an abundant membrane lipid component in most eukaryotes, including yeast, and has been assigned multiple functions in addition to acting as building block of the lipid bilayer. Here, by isolating S. cerevisiae suppressor mutants that exhibit robust growth in the absence of PC, we show that PC essentiality is subject to cellular evolvability in yeast. The requirement for PC is suppressed by monosomy of chromosome XV or by a point mutation in the ACC1 gene encoding acetyl-CoA carboxylase. Although these two genetic adaptations rewire lipid biosynthesis in different ways, both decrease Acc1 activity, thereby reducing average acyl chain length. Consistently, soraphen A, a specific inhibitor of Acc1, rescues a yeast mutant with deficient PC synthesis. In the aneuploid suppressor, feedback inhibition of Acc1 through acyl-CoA produced by fatty acid synthase (FAS) results from upregulation of lipid synthesis. The results show that budding yeast regulates acyl chain length by fine-tuning the activities of Acc1 and FAS and indicate that PC evolved by benefitting the maintenance of membrane fluidity

A Comparison of the Sensitivity and Fecal Egg Counts of the McMaster Egg Counting and Kato-Katz Thick Smear Methods for Soil-Transmitted Helminths

Currently, in public health, the reduction in the number of eggs excreted in stools after drug administration is used to monitor the efficacy of drugs against parasitic worms. Yet, studies comparing diagnostic methods for the enumeration of eggs in stool are few. We compared the Kato-Katz thick smear (Kato-Katz) and McMaster egg counting (McMaster) methods, which are commonly used diagnostic methods in public and animal health, respectively, for the diagnosis and enumeration of eggs of roundworms, whipworms and hookworms in 1,536 stool samples from children in five trials across Africa, Asia and South America. The Kato-Katz method was the most sensitive for the detection of roundworms, but there was no significant difference in sensitivity between the methods for hookworms and whipworms. The sensitivity of the methods differed across the trials and magnitude of egg counts. The Kato-Katz method resulted in significantly higher egg counts, but these were subject to lack of accuracy caused by intrinsic properties of this method. McMaster provided more reliable estimates of drug efficacies. We conclude that the McMaster is an alternative method for monitoring large-scale treatment programs. It allows accurate monitoring of drug efficacy and can be easily performed under field conditions

Identification of a Shared Genetic Susceptibility Locus for Coronary Heart Disease and Periodontitis

Recent studies indicate a mutual epidemiological relationship between coronary heart disease (CHD) and periodontitis. Both diseases are associated with similar risk factors and are characterized by a chronic inflammatory process. In a candidate-gene association study, we identify an association of a genetic susceptibility locus shared by both diseases. We confirm the known association of two neighboring linkage disequilibrium regions on human chromosome 9p21.3 with CHD and show the additional strong association of these loci with the risk of aggressive periodontitis. For the lead SNP of the main associated linkage disequilibrium region, rs1333048, the odds ratio of the autosomal-recessive mode of inheritance is 1.99 (95% confidence interval 1.33–2.94; P = 6.9×10−4) for generalized aggressive periodontitis, and 1.72 (1.06–2.76; P = 2.6×10−2) for localized aggressive periodontitis. The two associated linkage disequilibrium regions map to the sequence of the large antisense noncoding RNA ANRIL, which partly overlaps regulatory and coding sequences of CDKN2A/CDKN2B. A closely located diabetes-associated variant was independent of the CHD and periodontitis risk haplotypes. Our study demonstrates that CHD and periodontitis are genetically related by at least one susceptibility locus, which is possibly involved in ANRIL activity and independent of diabetes associated risk variants within this region. Elucidation of the interplay of ANRIL transcript variants and their involvement in increased susceptibility to the interactive diseases CHD and periodontitis promises new insight into the underlying shared pathogenic mechanisms of these complex common diseases