The relationship between maximal repetition performance and muscle fiber type as estimated by noninvasive technique in the quadriceps of untrained women

The purpose of this investigation was to establish a relationship between the number of repetitions an individual can complete at a predetermined load and their percentage of type II muscle fibers in their quadriceps. Subjects included 22 untrained women between the ages of 18 and 35. Day 1 consisted of noninvasive anthropologic testing, 1 repetition maximum (1RM) testing, and recording repetition performance at 70% 1RM. Day 2 consisted of isokinetic dynamometry to determine muscle fiber composition. Results were obtained and analyzed using the Pearson product correlation coefficient (r). The results demonstrated a fair-to-moderate relationship (Pearson r = -0.48, p = 0.02) that individuals with greater percentages of type II muscle fibers performed fewer repetitions at 70% 1RM. The results of this study demonstrate that muscle fiber type composition is an important variable to consider when designing training or rehabilitation programs.     

Exploiting pathogenic Escherichia coli to model transmembrane receptor signalling

Many microbial pathogens manipulate the actin cytoskeleton of eukaryotic target cells to promote their internalization, intracellular motility and dissemination. Enteropathogenic and enterohaemorrhagic Escherichia coli, which both cause severe diarrhoeal disease, can adhere to mammalian intestinal cells and induce reorganization of the actin cytoskeleton into 'pedestal-like' pseudopods beneath the extracellular bacteria. As pedestal assembly is triggered by E. coli virulence factors that mimic several host cell-signalling components, such as transmembrane receptors, their cognate ligands and cytoplasmic adaptor proteins, it can serve as a powerful model system to study eukaryotic transmembrane signalling. Here, we consider the impact of recent data on our understanding of both E. coli pathogenesis and cell biology, and the rich prospects for exploiting these bacterial factors as versatile tools to probe cellular signalling pathways.     

Evaluation of aldose reductase inhibition and docking studies of some secondary metabolites, isolated from Origanum vulgare L. ssp. hirtum

Five polar constituents of Origanum vulgare L. ssp. hirtum were investigated for their ability to inhibit aldose reductase (ALR2), the first enzyme of the polyol pathway implicated in the secondary complications of diabetes. The most active compound was found to be lithospermic acid B. Caffeic acid was inactive as it showed no inhibitory activity against the enzyme. The order of the inhibitory activity of the remaining compounds was: rosmarinic acid >12-hydroxyjasmonic acid 12-O-beta-glucopyranoside > p-menth-3-ene-1,2-diol 1-O-beta-glucopyranoside. Docking studies have been undertaken to gain insight into the binding mode of the investigated compounds at the active site of ALR2. The predicted hydrogen bonding and hydrophobic interactions may explain the observed inhibitory activity.     

LDL receptor deficiency or apoE mutations prevent remnant clearance and induce hypertriglyceridemia in mice

We have used adenovirus-mediated gene transfer and bolus injection of purified apolipoprotein E (apoE) in mice to determine the contribution of LDL receptor family members in the clearance of apoE-containing lipoproteins in vivo and the factors that trigger hypertriglyceridemia. A low dose [5 x 10(8) plaque-forming units (pfu)] of an adenovirus expressing apoE4 did not normalize plasma cholesterol levels of apolipoprotein E-deficient (apoE(-/-)) x low density lipoprotein receptor-deficient (LDLr(-/-)) mice and induced hypertriglyceridemia. A similar phenotype of combined dyslipidemia was induced in apoE(-/-) or apoE(-/-) x LDLr(-/-) mice after infection with a low dose (4 x 10(8) pfu) of an adenovirus expressing the apoE4[R142V/R145V] mutant previously shown to be defective in receptor binding. In contrast, a low dose of 5 x 10(8) pfu of the apoE4-expressing adenovirus corrected hypercholesterolemia in apoE(-/-) mice and did not trigger hypertriglyceridemia. Bolus injection of purified apoE in apoE(-/-) x LDLr(-/-) mice did not clear plasma cholesterol levels and induced mild hypertriglyceridemia. In contrast, similar injection of apoE in apoE(-/-) mice cleared plasma cholesterol and caused transiently mild hypertriglyceridemia. These findings suggest that a) the LDL receptor alone can account for the clearance of apoE-containing lipoproteins in mice, and the contribution of other receptors is minimal, and b) defects in either the LDL receptor or in apoE that affect its interactions with the LDL receptor, increase the sensitivity to apoE-induced hypertriglyceridemia in mice.     

ATX expression and LPA signalling are vital for the development of the nervous system

Autotaxin (ATX) is a secreted glycoprotein widely present in biological fluids, originally isolated from the supernatant of melanoma cells as an autocrine motility stimulation factor. Its enzymatic product, lysophosphatidic acid (LPA), is a phospholipid mediator that evokes growth-factor-like responses in almost all cell types through G-protein coupled receptors. To assess the role of ATX and LPA signalling in pathophysiology, a conditional knockout mouse was created. Ubiquitous, obligatory deletion resulted to embryonic lethality most likely due to aberrant vascular branching morphogenesis and chorio-allantoic fusion. Moreover, the observed phenotype was shown to be entirely depended on embryonic, but not extraembryonic or maternal ATX expression. In addition, E9.5 ATX null mutants exhibited a failure of neural tube closure, most likely independent of the circulatory failure, which correlated with decreased cell proliferation and increased cell death. More importantly, neurite outgrowth in embryo explants was severely compromised in mutant embryos but could be rescued upon the addition of LPA, thus confirming a role for ATX and LPA signalling in the development of the nervous system. Finally, expression profiling of mutant embryos revealed attenuated embryonic expression of HIF-1a in the absence of ATX, suggesting a novel effector pathway of ATX/LPA.     

Energy use in the global food system

The global food system is a major energy user and a relevant contributor to climate change. To date, the literature on the energy profile of food systems addresses individual countries and/or food products, and therefore a comparable assessment across regions is still missing. This paper uses a global multi‐regional environmentally extended input–output database in combination with newly constructed net energy‐use accounts to provide a production and consumption‐based stock‐take of energy use in the food system across different world regions for the period 2000–2015. Overall, the ratio between energy use in the food system and the economy is slowly decreasing. Likewise, the absolute values point toward a relative decoupling between energy use and food production, as well as to relevant differences in energy types, users, and consumption patterns across world regions. The use of (inefficient) traditional biomass for cooking substantially reduces the expected gap between per capita figures in high‐ and low‐income countries. The variety of energy profiles and the higher exposure to energy security issues compared to the total economy in some regions suggests that interventions in the system should consider the geographical context. Reducing energy use and decarbonizing the supply chains of food products will require a combination of technological measures and behavioral changes in consumption patterns. Interventions should consider the effects beyond the direct effects on energy use, because changing production and consumption patterns in the food system can lead to positive spillovers in the social and environmental dimensions outlined in the Sustainable Development Goals.     

Pyrrolylbenzothiazole Derivatives as Aldose Reductase Inhibitors

Abstract

2,2-Dimethyl-4-hydroxy-4-androstene-3,17-dione (4) has been synthesized and has been shown to be a powerful competitive inhibitor of aromatase (K_i = 11.4nM). However, compound 4 does not cause time-dependent loss of enzyme activity, in contrast to the unmethylated parent compound, 4-OHA.