Sketches of Kafir Life

https://commons.und.edu/settler-literature/1180/thumbnail.jp

Formula for the Absorption Coefficient for Multi-Wall Nanotubes

We present a formalism for calculating the absorption coefficient of a pair of coaxial tubules. A spatially nonlocal, dynamical self-consistent field theory is obtained by calculating the electrostatic potential produced by the charge density fluctuations as well as the external electric field. There are peaks in the absorption spectrum arising from plasma excitations corresponding either to plasmon or particle-hole modes. In this paper, we numerically calculate the plasmon contribution to the absorption spectrum when an external electric field is applied. The number of peaks depends on the radius of the inner as well as outer tubule. The height of each peak is determined by the plasmon wavelength and energy. For a chosen wave number, the most energetic plasmon has the highest peak corresponding to the largest oscillator strength of the excited modes. Some of the low-frequency plasmon modes have such weak coupling to an external electric field that they are not seen on the same scale as the modes with larger energy of excitation. We plot the peak positions of the plasmon excitations for a pair of coaxial tubules. The coupled modes on the two tubules are split by the Coulomb interaction. The energies of the two highest plasmon branches increase with the radius of the outer tubule. On the contrary, the lowest modes decrease in energy as this radius is increased. No effects due to inter-tubule hopping are included in these calculations

Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms

Clonal proliferation in myeloproliferative neoplasms (MPN) is driven by somatic mutations in JAK2, CALR or MPL, but the contribution of inherited factors is poorly characterized. Using a three-stage genome-wide association study of 3,437 MPN cases and 10,083 controls, we identify two SNPs with genome-wide significance in JAK2V617F-negative MPN: rs12339666 (JAK2; meta-analysis P=1.27 × 10−10) and rs2201862 (MECOM; meta-analysis P=1.96 × 10−9). Two additional SNPs, rs2736100 (TERT) and rs9376092 (HBS1L/MYB), achieve genome-wide significance when including JAK2V617F-positive cases. rs9376092 has a stronger effect in JAK2V617F-negative cases with CALR and/or MPL mutations (Breslow–Day P=4.5 × 10−7), whereas in JAK2V617F-positive cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia vera (allelic χ2 P=7.3 × 10−7). Reduced MYB expression, previously linked to development of an ET-like disease in model systems, associates with rs9376092 in normal myeloid cells. These findings demonstrate that multiple germline variants predispose to MPN and link constitutional differences in MYB expression to disease phenotype

Can We Modify the Intrauterine Environment to Halt the Intergenerational Cycle of Obesity?

Child obesity is a global epidemic whose development is rooted in complex and multi-factorial interactions. Once established, obesity is difficult to reverse and epidemiological, animal model, and experimental studies have provided strong evidence implicating the intrauterine environment in downstream obesity. This review focuses on the interplay between maternal obesity, gestational weight gain and lifestyle behaviours, which may act independently or in combination, to perpetuate the intergenerational cycle of obesity. The gestational period, is a crucial time of growth, development and physiological change in mother and child. This provides a window of opportunity for intervention via maternal nutrition and/or physical activity that may induce beneficial physiological alternations in the fetus that are mediated through favourable adaptations to in utero environmental stimuli. Evidence in the emerging field of epigenetics suggests that chronic, sub-clinical perturbations during pregnancy may affect fetal phenotype and long-term human data from ongoing randomized controlled trials will further aid in establishing the science behind ones predisposition to positive energy balance

Early influences on cardiovascular and renal development

The hypothesis that a developmental component plays a role in subsequent disease initially arose from epidemiological studies relating birth size to both risk factors for cardiovascular disease and actual cardiovascular disease prevalence in later life. The findings that small size at birth is associated with an increased risk of cardiovascular disease have led to concerns about the effect size and the causality of the associations. However, recent studies have overcome most methodological flaws and suggested small effect sizes for these associations for the individual, but an potential important effect size on a population level. Various mechanisms underlying these associations have been hypothesized, including fetal undernutrition, genetic susceptibility and postnatal accelerated growth. The specific adverse exposures in fetal and early postnatal life leading to cardiovascular disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life may underlie the complex associations of fetal growth retardation and low birth weight with cardiovascular disease in later life. To estimate the population effect size and to identify the underlying mechanisms, well-designed epidemiological studies are needed. This review is focused on specific adverse fetal exposures, cardiovascular adaptations and perspectives for new studies. Copyrigh

Cut-off points for anthropometric indices of adiposity: differential classification in a large population of young women

Anthropometric indices of adiposity include BMI, waist circumference and waist:height ratio. In the recruitment phase of a prospective cohort study carried out between 1998 and 2002 we studied a population sample of 11 786 white Caucasian non-pregnant women in Southampton, UK aged 20-34 years, and explored the extent to which proposed cut-off points for the three indices identified the same or different women and how these indices related to adiposity. Height, weight and waist circumference were measured and fat mass was estimated from skinfold thicknesses; fat mass index was calculated as fat mass/height1.65. Of the subjects, 4869 (42 %) women were overweight (BMI >/= 25 kg/m2) and 1849 (16 %) were obese (BMI >/= 30 kg/m2). A total of 890 (8 %) subjects were not overweight but had a waist circumference >/= 80 cm and 748 (6 %) subjects were overweight but had a waist circumference /= 0.5. Of the variation in fat mass index, 85 % was explained by BMI, 76 % by waist circumference and 75 % by waist:height ratio. Our findings demonstrate that many women are differentially classified depending on which index of adiposity is used. As each index captures different aspects of size in terms of adiposity, there is the need to determine how the three indices relate to function and how they can be of use in defining risk of ill health in women