12 research outputs found
Effects of lubricant viscosity and surface texturing on ring-pack performance in internal combustion engines
Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2006.Includes bibliographical references (p. 117-120).The piston ring-pack contributes approximately 25% of the mechanical losses in an internal combustion engine. Both lubricant viscosity and surface texturing were investigated in an effort to reduce this ring-pack friction and increase engine efficiency. While both optimizing viscosity and surface texturing are predicted to cause a reduction in ring/liner friction individually, a combined approach may cause an even greater friction reduction while mitigating unwanted side-effects such as oil consumption and wear. Existing MIT models, with some modifications and supplementary programs to allow investigation of the parameters of interest, were used to conduct this research. A ring-pack model based on average flow-factor Reynolds analysis was used for both studies, with a modified form of this program, along with a supplementary deterministic model for surface analysis, used for the study of surface texturing. Although these advanced models are applicable in a wide range of cases, the surface textures studied in this research are very different than a typical cylinder liner surface, and can be represented only approximately by the averaged Reynolds analysis upon which the ring simulation is based.(cont.) For this reason, the analysis of surface features has focused on a parametric study, whose goal is to analyze trends relating ring/liner friction to surface parameters, and to make a general evaluation of the potential of surface texturing to reduce ring-pack losses. Study of lubricant viscosity effects throughout the engine cycle indicated that conditions in the mid-stroke region have the main influence (compared to the end-strokes) on friction power losses, and that reducing viscosity here could lead to a reduction in ring-pack FMEP of -7%. Changes in cylinder liner surface texturing, also, can lead to significant friction reductions. Patterns of both grooves and round dimples were shown to reduce ring/liner friction by increasing hydrodynamic pressure in the lubricant, thus increasing oil film thickness and reducing both asperity contact and hydrodynamic friction. Also, because the effect of reducing viscosity is to decrease oil film thickness, and that of the surface texturing considered is to increase it, these two parameters can be optimized together, and balanced so that oil film thickness remains constant. Then, negative side-effects such as wear (due to decrease in film thickness) and oil consumption (resulting from an increase in film thickness) can be negated, even as friction is reduced even further than is possible using viscosity or surface effects alone.by Rosalind Takata.S.M
Adverse Drug Reactions in Children—A Systematic Review
Adverse drug reactions in children are an important public health problem. We have undertaken a systematic review of observational studies in children in three settings: causing admission to hospital, occurring during hospital stay and occurring in the community. We were particularly interested in understanding how ADRs might be better detected, assessed and avoided
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Low-Engine-Friction Technology for Advanced Natural-Gas Reciprocating Engines
This program aims at improving the efficiency of advanced natural-gas reciprocating engines (ANGRE) by reducing piston and piston ring assembly friction without major adverse effects on engine performance, such as increased oil consumption and wear. An iterative process of simulation, experimentation and analysis is being followed towards achieving the goal of demonstrating a complete optimized low-friction engine system. To date, a detailed set of piston and piston-ring dynamic and friction models have been developed and applied that illustrate the fundamental relationships between design parameters and friction losses. Low friction ring designs have already been recommended in a previous phase, with full-scale engine validation partially completed. Current accomplishments include the addition of several additional power cylinder design areas to the overall system analysis. These include analyses of lubricant and cylinder surface finish and a parametric study of piston design. The Waukesha engine was found to be already well optimized in the areas of lubricant, surface skewness and honing cross-hatch angle, where friction reductions of 12% for lubricant, and 5% for surface characteristics, are projected. For the piston, a friction reduction of up to 50% may be possible by controlling waviness alone, while additional friction reductions are expected when other parameters are optimized. A total power cylinder friction reduction of 30-50% is expected, translating to an engine efficiency increase of two percentage points from its current baseline towards the goal of 50% efficiency. Key elements of the continuing work include further analysis and optimization of the engine piston design, in-engine testing of recommended lubricant and surface designs, design iteration and optimization of previously recommended technologies, and full-engine testing of a complete, optimized, low-friction power cylinder system
Friction Reduction by Piston Ring Pack Modifications of a Lean-Burn Four-Stroke Natural Gas Engine: Experimental Results
The contribution of rare variation to prostate cancer heritability
We report targeted sequencing of 63 known prostate cancer risk regions in a multi-ancestry study of 9,237 men and use the data to explore the contribution of low-frequency variation to disease risk. We show that SNPs with minor allele frequencies (MAFs) of 0.1-1% explain a substantial fraction of prostate cancer risk in men of African ancestry. We estimate that these SNPs account for 0.12 (standard error (s.e.) = 0.05) of variance in risk (∼42% of the variance contributed by SNPs with MAF of 0.1-50%). This contribution is much larger than the fraction of neutral variation due to SNPs in this class, implying that natural selection has driven down the frequency of many prostate cancer risk alleles; we estimate the coupling between selection and allelic effects at 0.48 (95% confidence interval [0.19, 0.78]) under the Eyre-Walker model. Our results indicate that rare variants make a disproportionate contribution to genetic risk for prostate cancer and suggest the possibility that rare variants may also have an outsize effect on other common traits
Genome-wide association study identifies new prostate cancer susceptibility loci
Prostate cancer (PrCa) is the most common non-skin cancer diagnosed among males in developed countries and the second leading cause of cancer mortality, yet little is known regarding its etiology and factors that influence clinical outcome. Genome-wide association studies (GWAS) of PrCa have identified at least 30 distinct loci associated with small differences in risk. We conducted a GWAS in 2782 advanced PrCa cases (Gleason grade ≥ 8 or tumor stage C/D) and 4458 controls with 571 243 single nucleotide polymorphisms (SNPs). Based on in silico replication of 4679 SNPs (Stage 1, P < 0.02) in two published GWAS with 7358 PrCa cases and 6732 controls, we identified a new susceptibility locus associated with overall PrCa risk at 2q37.3 (rs2292884, P = 4.3 × 10 -8). We also confirmed a locus suggested by an earlier GWAS at 12q13 (rs902774, P = 8.6 × 10 -9). The estimated per-allele odds ratios for these loci (1.14 for rs2292884 and 1.17 for rs902774) did not differ between advanced and non-advanced PrCa (case-only test for heterogeneity P 5 0.72 and P 5 0.61, respectively). Further studies will be needed to assess whether these or other loci are differentially associated with PrCa subtypes. © The Author 2011. Published by Oxford University Press. All rights reserved
Two Novel Susceptibility Loci for Prostate Cancer in Men of African Ancestry
Prostate cancer incidence is 1.6-fold higher in African Americans than in other populations. The risk factors that drive this disparity are unknown and potentially consist of social, environmental, and genetic influences. To investigate the genetic basis of prostate cancer in men of African ancestry, we performed a genome-wide association meta-analysis using two-sided statistical tests in 10 202 case subjects and 10 810 control subjects. We identified novel signals on chromosomes 13q34 and 22q12, with the risk-associated alleles found only in men of African ancestry (13q34: rs75823044, risk allele frequency = 2.2%, odds ratio [OR] = 1.55, 95% confidence interval [CI] = 1.37 to 1.76, P = 6.10 × 10−12; 22q12.1: rs78554043, risk allele frequency = 1.5%, OR = 1.62, 95% CI = 1.39 to 1.89, P = 7.50 × 10−10). At 13q34, the signal is located 5’ of the gene IRS2 and 3’ of a long noncoding RNA, while at 22q12 the candidate functional allele is a missense variant in the CHEK2 gene. These findings provide further support for the role of ancestry-specific germline variation in contributing to population differences in prostate cancer risk
Association analyses of more than 140,000 men identify 63 new prostate cancer susceptibility loci.
Genome-wide association studies (GWAS) and fine-mapping efforts to date have identified more than 100 prostate cancer (PrCa)-susceptibility loci. We meta-analyzed genotype data from a custom high-density array of 46,939 PrCa cases and 27,910 controls of European ancestry with previously genotyped data of 32,255 PrCa cases and 33,202 controls of European ancestry. Our analysis identified 62 novel loci associated (P C, p.Pro1054Arg) in ATM and rs2066827 (OR = 1.06; P = 2.3 × 10-9; T>G, p.Val109Gly) in CDKN1B. The combination of all loci captured 28.4% of the PrCa familial relative risk, and a polygenic risk score conferred an elevated PrCa risk for men in the ninetieth to ninety-ninth percentiles (relative risk = 2.69; 95% confidence interval (CI): 2.55-2.82) and first percentile (relative risk = 5.71; 95% CI: 5.04-6.48) risk stratum compared with the population average. These findings improve risk prediction, enhance fine-mapping, and provide insight into the underlying biology of PrCa1