Efficiency tests of a twenty horse-power Avery Traction Engine no. 2116

Citation: Carnahan, August Belmont, Barnard, Asa William, and Thompson, Roger S. Efficiency tests of a twenty horse-power Avery Traction Engine no. 2116. Senior thesis, Kansas State Agricultural College, 1905.Morse Department of Special CollectionsIntroduction: Purpose: The purpose of the following is to set forth the mechanical efficiency of the Avery traction engine No. 2116, running as a stationary engine and as a traction engine; to determine the evaporative power of the boiler under a reasonable load While being fired with Lansing coal from the Kansas Penitentiary; and to determine the draft per ton of haul over dirt and macadamized roads with an ordinary four inch wagon. The instruments used for the tests for mechanical efficiency were: Two Crosby indicators, each closely connected A Crosby disk revolution counter/ A Prony brake/ A platform scale and/ An indicator reducing motion/ To make a reliable test of an engine requires a correct application of instruments and a skillful manipulation of the same. The error of every instrument should be determined before and after the test and necessary corrections made for the same. No instrument of doubtful reading should be used under any circumstances. Ease of manipulation adds much to the accuracy with *high a reading may be made. All readings ought to be made simultaneously in order that they may harmonize. The Indicators: Of the sources of error accompanying the use of indicators we found that two above all should be sought out

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Abstract: Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies