Normalization of ground reaction forces

The appropriateness of normalizing data, as one method to reduce the effects of a covariate on a dependent variable, should be evaluated. Using ratio, 0.67-nonlinear, and fitted normalizations, the aim of this study was to investigate the relationship between ground reaction force variables and body mass (BM). Ground reaction forces were recorded for 40 female subjects running at 3.7 +/- 0.18 m x s(-1) (mass = 58 +/- 6 kg). The explained variance for mass to forces (peak-impact-vertical = 70%; propulsive-vertical = 27%; braking = 40%) was reduced to <0.1% for mass to ratio normalized forces (i.e., forces/BM1) with statistically significantly different power exponents (p < 0.05). The smaller covariate effect of mass on loading rate variables of 2-16% was better removed through fitted normalization (e.g., vertical-instantaneous-loading rate/ BM(0.69+/-0.93); +/-95% CI) with nonlinear power exponents ranging from 0.51 to 1.13. Generally, these were similar to 0.67 as predicted through dimensionality theory, but, owing to the large confidence intervals, these power exponents were not statistically significantly different from absolute or ratio normalized data (p > 0.05). Further work is warranted to identify the appropriate method to normalize loading rates either to mass or to another covariate. Ratio normalization of forces to mass, as predicted through Newtonian mechanics, is recommended for comparing subjects of different masses.     

Frontal plane moments do not accurately reflect ankle dynamics during running

The ankle joint has typically been treated as a universal joint with moments calculated about orthogonal axes and the frontal plane moment generally used to represent the net muscle action about the subtalar joint. However, this joint acts about an oblique axis. The purpose of this study was to examine the differences between joint moments calculated about the orthogonal frontal plane axis and an estimated subtalar joint axis. Three-dimensional data were collected on 10 participants running at 3.6 m/s. Joint moments, power, and work were calculated about the orthogonal frontal plane axis of the foot and about an oblique axis representing the subtalar joint. Selected parameters were compared with a paired t-test (alpha = 0.05). The results indicated that the joint moments calculated about the two axes were characteristically different. A moment calculated about an orthogonal frontal plane axis of the foot resulted in a joint moment that was invertor in nature during the first half of stance, but evertor during the second half of stance. The subtalar joint axis moment, however, was invertor during most of the stance. These two patterns may result in qualitatively different interpretations of the muscular contributions at the ankle during the stance phase of running.     

A novel liver specific isoform of the rat LAR transcript is expressed as a truncated isoform encoded from a 5'UTR located within intron 11

Background  

The leukocyte common antigen related receptor (LAR) protein has been shown to modulate the signal transduction of a number of different growth factors, including insulin and insulin-like growth factor 1. Splice variants exhibit differing roles and are expressed according to tissue type and developmental stage.     

哈尔滨西郊赤狐冬季巢区的初步研究

本文利用雪地跟踪方法对哈尔滨西郊5只赤狐在1985-1986年冬季的巢区做了观察。结果表明,5只狐对巢区内各部分使用的强度是不等的,对巢区中部的某些地块使用强度要高于对外围的使用,并具有明显的方向性。5个巢区的平均活动半径为320±68米至557±82米,面积为1.44-4.O9平方公里,线性指数为1.079至2。5只狐相邻距离约1000米。     

Mendelian randomization supports causality between maternal hyperglycemia and epigenetic regulation of leptin gene in newborns

Leptin is an adipokine that acts in the central nervous system and regulates energy balance. Animal models and human observational studies have suggested that leptin surge in the perinatal period has a critical role in programming long-term risk of obesity. In utero exposure to maternal hyperglycemia has been associated with increased risk of obesity later in life. Epigenetic mechanisms are suspected to be involved in fetal programming of long term metabolic diseases. We investigated whether DNA methylation levels near LEP locus mediate the relation between maternal glycemia and neonatal leptin levels using the 2-step epigenetic Mendelian randomization approach. We used data and samples from up to 485 mother-child dyads from Gen3G, a large prospective population-based cohort. First, we built a genetic risk score to capture maternal glycemia based on 10 known glycemic genetic variants (GRS₁₀) and showed it was an adequate instrumental variable (β = 0.046 mmol/L of maternal fasting glucose per additional risk allele; SE = 0.007; P = 7.8 × 10⁻¹¹; N = 467). A higher GRS₁₀ was associated with lower methylation levels at cg12083122 located near LEP (β = −0.072 unit per additional risk allele; SE = 0.04; P = 0.05; N = 166). Direction and effect size of association between the instrumental variable GRS₁₀ and methylation at cg12083122 were consistent with the negative association we observed using measured maternal glycemia. Lower DNA methylation levels at cg12083122 were associated with higher cord blood leptin levels (β = −0.17 log of cord blood leptin per unit; SE = 0.07; P = 0.01; N = 170). Our study supports that maternal glycemia is part of causal pathways influencing offspring leptin epigenetic regulation.     

The receptor for branch-site docking within a group II intron active site

The distinguishing feature of group II introns, and the property that links them with spliceosomal catalysis, is their ability to undergo splicing through branching. In this reaction, the 2'-hydroxyl group of a specific adenosine within intron domain 6 serves as the nucleophile for attack on the 5' splice site. We know less about branching than any other feature of group II intron catalysis, largely because the receptor structure for activating the branch site is unknown. Here, we identify the intronic region that binds the branch site of a group IIB intron. Located in domain 1, close to receptors for intron domain 5 and both splice sites, we demonstrate that the branch-site receptor is a functional element required for transesterification. Furthermore, we show that crosslinked branch sites can carry out both steps of splicing, suggesting that the conformational state of the intron core is set early and that it persists throughout the entire splicing process.     

Properties of the human erythrocyte glucose transport protein are determined by cellular context

Human erythrocyte hexose transfer is mediated by the glucose transport protein GLUT1 and is characterized by a complexity that is unexplained by available hypotheses for carrier-mediated sugar transport [Cloherty, E. K., Heard, K. S., and Carruthers, A. (1996) Biochemistry 35, 10411-10421]. The study presented here examines the possibility that the operational properties of GLUT1 are determined by host cell environment. A glucose transport-null strain of Saccharomyces cerevisiae (RE700A) was transfected with the p426 GPD yeast expression vector containing DNA encoding the wild-type human glucose transport protein (GLUT1), mutant GLUT1 (GLUT1(338)(-)(A3)), or carboxy-terminal hemagglutinin-polyHis-tagged GLUT1 (GLUT1-HA-H6). GLUT1 and GLUT1-HA-H6 are expressed at the yeast cell membrane and restore 2-deoxy-d-glucose, 3-O-methylglucose, and d-glucose transport capacity to RE700A. GLUT1-HA-H6 confers GLUT1-specific sugar transport characteristics to transfected RE700A, including inhibition by cytochalasin B and high-affinity transport of the nonmetabolized sugar 3-O-methylglucose. GLUT1(338)(-)(A3), a catalytically inactive GLUT1 mutant, is expressed but fails to restore RE700A sugar uptake capacity or growth on glucose. In contrast to transport in human red cells, K(m(app)) for 2-deoxy-d-glucose uptake equals K(i(app)) for 2-deoxy-d-glucose inhibition of 3-O-methylglucose uptake. Unlike transport in human red cells or transport in human embryonic kidney cells transfected with GLUT1-HA-H6, unidirectional sugar uptake in RE700A-GLUT1-HA-H6 is not inhibited by reductant and is not stimulated by intracellular sugar. Net uptake of subsaturating 3-O-methylglucose by RE700A-GLUT1-HA-H6 is a simple, first-order process. These findings support the hypothesis that red cell sugar transport complexity is host cell-specific.