Publications

The basic mechanics of the fiber push-out process are studied by measuring the stress distributions along c-axis sapphire fibers in γ-TiAl matrices. The stress measurements were made in situ during fiber push-out tests using a piezo-spectroscopy method. By focussing an optical microprobe into a sapphire fiber, the frequency shift distribution of the characteristics R lines of Cr3+, and hence the stress distribution along the fiber were determined at each increment of applied load. By comparing the measured stress distributions with ones calculated using finite element method, key mechanical parameters including residual stress before composite slicing, debond length at each load, debond energy and the frictional stress along the interface in both debonding and sliding phases were determined. Two coating systems (Mo/Al2O3 and CVD-C/Al2O3) were studied. The results also show that while the debond energies differ by an order of magnitude, the frictional stresses are very similar in magnitude, suggesting that the interface morphology is of greater importance than the nature of the coating.

Magnetische Levitation (MagLev) ist eine einfache Trennmethode für Kristallpolymorphe mit Dichteunterschieden (Δρ) von nur 0.001 g cm−3. Für vier organische Verbindungen wurden dichtebasierte Trennungen verschiedener kristalliner Formen gezeigt: 5-Methyl-2-[(2-nitrophenyl)amino]-3-thiophencarbonitril, Sulfathiazol, Carbamazepin und trans-Zimtsäure.

Abstract For Abstract see ChemInform Abstract in Full Text.

Early pubertal onset in females is associated with increased risk for adult obesity and cardiovascular disease, but whether this relationship is independent of preceding childhood growth events is unclear. Furthermore, the association between male puberty and adult disease remains unknown. To clarify the link between puberty and adult health, we evaluated the relationship between pubertal timing and risk factors for type 2 diabetes and cardiovascular disease in both males and females from a large, prospective, and randomly ascertained birth cohort from Northern Finland.Pubertal timing was estimated based on pubertal height growth in 5,058 subjects (2,417 males and 2,641 females), and the relationship between puberty and body weight, glucose and lipid homeostasis, and blood pressure at age 31 years was evaluated with linear regression modeling.Earlier pubertal timing associated with higher adult BMI, fasting insulin, diastolic blood pressure, and decreased HDL cholesterol in both sexes (P < 0.002) and with higher total serum cholesterol, LDL cholesterol, and triglycerides in males. The association with BMI and diastolic blood pressure remained statistically significant in both sexes, as did the association with insulin levels and HDL cholesterol concentrations in males after adjusting for covariates reflecting both fetal and childhood growth including childhood BMI.We demonstrate independent association between earlier pubertal timing and adult metabolic syndrome-related derangements both in males and females. The connection emphasizes that the mechanisms advancing puberty may also contribute to adult metabolic disorders.

Longer sleep duration was associated with an increased risk of developing colorectal cancer among individuals who were overweight or snored regularly. This observation raises the possibility that sleep apnea and its attendant intermittent hypoxemia may contribute to cancer risk.

OBJECTIVE Both stressful intrauterine milieus and genetic susceptibility have been linked to later-life diabetes risk. The current study aims to examine the interaction between low birth weight, a surrogate measure of stressful intrauterine milieus, and genetic susceptibility in relation to risk of type 2 diabetes in adulthood. RESEARCH DESIGN AND METHODS The analysis included two independent, nested case-control studies of 2,591 type 2 diabetic case subjects and 3,052 healthy control subjects. We developed two genotype scores: an obesity genotype score based on 32 BMI-predisposing variants and a diabetes genotype score based on 35 diabetes-predisposing variants. RESULTS Obesity genotype scores showed a stronger association with type 2 diabetes risk in individuals with low birth weight. In low–birth weight individuals, the multivariable-adjusted odds ratio (OR) was 2.55 (95% CI 1.34–4.84) by comparing extreme quartiles of the obesity genotype score, while the OR was 1.27 (1.04–1.55) among individuals with birth weight &amp;gt;2.5 kg (P for interaction = 0.017). We did not observe significant interaction between diabetes genotype scores and birth weight with regard to risk of type 2 diabetes. In a comparison of extreme quartiles of the diabetes gene score, the multivariable-adjusted OR was 3.80 (1.76–8.24) among individuals with low birth weight and 2.27 (1.82–2.83) among those with high birth weight (P for interaction = 0.16). CONCLUSIONS Our data suggest that low birth weight and genetic susceptibility to obesity may synergistically affect adulthood risk of type 2 diabetes.

Leukocyte telomere length (LTL) is a heritable biomarker of genomic aging. In this study, we perform a genome-wide meta-analysis of LTL by pooling densely genotyped and imputed association results across large-scale European-descent studies including up to 78,592 individuals. We identify 49 genomic regions at a false dicovery rate (FDR) < 0.05 threshold and prioritize genes at 31, with five highlighting nucleotide metabolism as an important regulator of LTL. We report six genome-wide significant loci in or near SENP7, MOB1B, CARMIL1, PRRC2A, TERF2, and RFWD3, and our results support recently identified PARP1, POT1, ATM, and MPHOSPH6 loci. Phenome-wide analyses in >350,000 UK Biobank participants suggest that genetically shorter telomere length increases the risk of hypothyroidism and decreases the risk of thyroid cancer, lymphoma, and a range of proliferative conditions. Our results replicate previously reported associations with increased risk of coronary artery disease and lower risk for multiple cancer types. Our findings substantially expand current knowledge on genes that regulate LTL and their impact on human health and disease.