Development and Validation of the Body Size Scale for Assessing Body Weight Perception in African Populations

Background

The social valorisation of overweight in African populations could promote high-risk eating behaviours and therefore become a risk factor of obesity. However, existing scales to assess body image are usually not accurate enough to allow comparative studies of body weight perception in different African populations. This study aimed to develop and validate the Body Size Scale (BSS) to estimate African body weight perception.

Methods

Anthropometric measures of 80 Cameroonians and 81 Senegalese were used to evaluate three criteria of adiposity: body mass index (BMI), overall percentage of fat, and endomorphy (fat component of the somatotype). To develop the BSS, the participants were photographed in full face and profile positions. Models were selected for their representativeness of the wide variability in adiposity with a progressive increase along the scale. Then, for the validation protocol, participants self-administered the BSS to assess self-perceived current body size (CBS), desired body size (DBS) and provide a “body self-satisfaction index.” This protocol included construct validity, test-retest reliability and convergent validity and was carried out with three independent samples of respectively 201, 103 and 1115 Cameroonians.

Results

The BSS comprises two sex-specific scales of photos of 9 models each, and ordered by increasing adiposity. Most participants were able to correctly order the BSS by increasing adiposity, using three different words to define body size. Test-retest reliability was consistent in estimating CBS, DBS and the “body self-satisfaction index.” The CBS was highly correlated to the objective BMI, and two different indexes assessed with the BSS were consistent with declarations obtained in interviews.

Conclusion

The BSS is the first scale with photos of real African models taken in both full face and profile and representing a wide and representative variability in adiposity. The validation protocol proved its reliability for estimating body weight perception in Africans.     

Reaction of wild-type and Glu243Asp variant yeast cytochrome c oxidase with O2

We have studied internal electron transfer during the reaction of Saccharomyces cerevisiae mitochondrial cytochrome c oxidase with dioxygen. Similar absorbance changes were observed with this yeast oxidase as with the previously studied Rhodobacter sphaeroides and bovine mitochondrial oxidases, which suggests that the reaction proceeds along the same trajectory. However, notable differences were observed in rates and electron-transfer equilibrium constants of specific reaction steps, for example the ferryl (F) to oxidized (O) reaction was faster with the yeast (0.4 ms) than with the bovine oxidase (~ 1 ms) and a larger fraction Cu_A was oxidized with the yeast than with the bovine oxidase in the peroxy (P_R) to F reaction. Furthermore, upon replacement of Glu243, located at the end of the so-called D proton pathway, by Asp the P_R → F and F → O reactions were slowed by factors of ~ 3 and ~ 10, respectively, and electron transfer from Cu_A to heme a during the P_R → F reaction was not observed. These data indicate that during reduction of dioxygen protons are transferred through the D pathway, via Glu243, to the catalytic site in the yeast mitochondrial oxidase. This article is part of a Special Issue entitled: 18th European Bioenergetic Conference.     

NAD(P)H Quinone-Oxydoreductase 1 Protects Eukaryotic Translation Initiation Factor 4GI from Degradation by the Proteasome

The eukaryotic translation initiation factor 4GI (eIF4GI) serves as a central adapter in cap-binding complex assembly. Although eIF4GI has been shown to be sensitive to proteasomal degradation, how the eIF4GI steady-state level is controlled remains unknown. Here, we show that eIF4GI exists in a complex with NAD(P)H quinone-oxydoreductase 1 (NQO1) in cell extracts. Treatment of cells with dicumarol (dicoumarol), a pharmacological inhibitor of NQO1 known to preclude NQO1 binding to its protein partners, provokes eIF4GI degradation by the proteasome. Consistently, the eIF4GI steady-state level also diminishes upon the silencing of NQO1 (by transfection with small interfering RNA), while eIF4GI accumulates upon the overexpression of NQO1 (by transfection with cDNA). We further reveal that treatment of cells with dicumarol frees eIF4GI from mRNA translation initiation complexes due to strong activation of its natural competitor, the translational repressor 4E-BP1. As a consequence of cap-binding complex dissociation and eIF4GI degradation, protein synthesis is dramatically inhibited. Finally, we show that the regulation of eIF4GI stability by the proteasome may be prominent under oxidative stress. Our findings assign NQO1 an original role in the regulation of mRNA translation via the control of eIF4GI stability by the proteasome.In eukaryotes, eukaryotic translation initiation factor 4G (eIF4G) plays a central role in the recruitment of ribosomes to the mRNA 5′ end and is therefore critical for the regulation of protein synthesis (14). Two homologues of eIF4G, eIF4GI and eIF4GII, have been cloned (15). Although they differ in various respects, both homologues clearly function in translation initiation. The most thoroughly studied of these is eIF4GI, which serves as a scaffolding protein for the assembly of eIF4F, a protein complex composed of eIF4E (the mRNA cap-binding factor) and eIF4A (an ATP-dependent RNA helicase). Thus, via its association with the mRNA cap-binding protein eIF4E and with another translation initiation factor (eIF3) which is bound to the 40S ribosomal subunit, eIF4GI creates a physical link between the mRNA cap structure and the ribosome, thus facilitating cap-dependent translation initiation (25). eIF4GI functions also in cap-independent, internal ribosome entry site (IRES)-mediated translation initiation. For instance, upon picornavirus infection, eIF4G is rapidly attacked by viral proteases. The resulting eIF4GI cleavage products serve to reprogram the cell''s translational machinery, as the N-terminal cleavage product inhibits cap-dependent translation of host cell mRNAs by sequestering eIF4E while the C-terminal cleavage product stimulates IRES-mediated translation of viral mRNAs (23). Similarly, apoptotic caspases cleave eIF4G into an N-terminal fragment that blocks cap-dependent translation and a C-terminal fragment that is utilized for IRES-mediated translation of mRNAs encoding proapoptotic proteins (22).The regulation of eIF4GI cleavage by viral proteases or apoptotic caspases has been extensively studied. Little is known, however, about the regulation of eIF4GI steady-state levels. Yet the eIF4GI amount that exists at a given moment results from the sum of the effects of de novo synthesis and ongoing degradation. Many cellular proteins are physiologically degraded by the proteasome. This has been shown to be true for eIF4GI, as the factor can be degraded by the proteasome in vitro (5) and in living cells (6). However, how eIF4GI targeting for or protection from destruction by the proteasome is regulated remains unknown.There are two major routes to degradation by the proteasome. In the more conventional route, polyubiquitinated proteins are targeted to the 26S proteasome. Alternatively, a few proteins can be degraded by the 20S proteasome (and sometimes by the 26S proteasome) in a ubiquitin-independent manner (16). Interestingly, it has been shown recently that a few of these proteins (1, 2, 13) can be protected from degradation by the 20S proteasome by binding to the NAD(P)H quinone-oxydoreductase 1 (NQO1). It has been proposed that NQO1 may interact with the 20S proteasome and may consequently block access of target proteins to the 20S degradation core. Because eIF4GI can be degraded in vitro by the 20S proteasome (5) and since it appears that proteasomes can degrade eIF4GI in living cells independently of ubiquitination (6), we asked whether NQO1 could protect eIF4GI from degradation by the proteasome.     

FES kinase participates in KIT-ligand induced chemotaxis

FES is a cytoplasmic tyrosine kinase activated by several membrane receptors, originally identified as a viral oncogene product. We have recently identified FES as a crucial effector of oncogenic KIT mutant receptor. However, FES implication in wild-type KIT receptor function was not addressed. We report here that FES interacts with KIT and is phosphorylated following activation by its ligand SCF. Unlike in the context of oncogenic KIT mutant, FES is not involved in wild-type KIT proliferation signal, or in cell adhesion. Instead, FES is required for SCF-induced chemotaxis. In conclusion, FES kinase is a mediator of wild-type KIT signalling implicated in cell migration.     

Earthworm effects on plant growth do not necessarily decrease with soil fertility

Earthworms are known to generally increase plant growth. However, because plant-earthworm interactions are potentially mediated by soil characteristics the response of plants to earthworms should depend on the soil type. In a greenhouse microcosm experiment, the responsiveness of plants (Veronica persica, Trifolium dubium and Poa annua) to two earthworm species (in combination or not) belonging to different functional groups (Aporrectodea. caliginosa an endogeic species, Lumbricus terrestris an anecic species) was measured in term of biomass accumulation. This responsiveness was compared in two soils (nutrient rich and nutrient poor) and two mineral fertilization treatments (with and without). The main significant effects on plant growth were due to the anecic earthworm species. L. terrestris increased the shoot biomass and the total biomass of T. dubium only in the rich soil. It increased also the total biomass of P. annua without mineral fertilization but had the opposite effect with fertilization. Mineral fertilization, in the presence of L. terrestris, also reduced the total biomass of V. persica. L. terrestris did not only affect plant growth. In P. annua and V. persica A. caliginosa and L. terrestris also affected the shoot/root ratio and this effect depended on soil type. Finally, few significant interactions were found between the anecic and the endogeic earthworms and these interactions did not depend on the soil type. A general idea would be that earthworms mostly increase plant growth through the enhancement of mineralization and that earthworm effects should decrease in nutrient-rich soils or with mineral fertilization. However, our results show that this view does not hold and that other mechanisms are influential.     

Assessing freshwater ecotoxicity of agricultural products in life cycle assessment (LCA): a case study of wheat using French agricultural practices databases and USEtox model

Purpose  

A life cycle assessment (LCA) was conducted on winter wheat, based on real agricultural practices databases, on a sample divided into four production scenarios. The main objectives of this study are (1) to assess the environmental impact of winter wheat, using an LCA covering field practices, and the transport and storage of grain until it is sold to a miller; (2) to use the USEtox model (Rosenbaum et al. in Int J Life Cycle Assess 13:532–546, 2008) to assess the part of the total freshwater ecotoxicity impact due to pesticide use, its variability among plots, and to identify the active ingredients with the strongest impact; (3) and with the help of fungicide, insecticide, herbicide experts, to identify active ingredients to replace these high-impact pesticides and estimate the effect of such a substitution on total freshwater ecotoxicity.     

Renin inhibitors for the treatment of hypertension: design and optimization of a novel series of tertiary alcohol-bearing piperidines

The design and optimization of a novel series of renin inhibitor is described herein. Strategically, by committing the necessary resources to the development of synthetic sequences and scaffolds that were most amenable for late stage structural diversification, even as the focus of the SAR campaign moved from one end of the molecule to another, highly potent renin inhibitors could be rapidly identified and profiled.     

Clonal Growth Strategies Along Flooding and Grazing Gradients in Atlantic Coastal Meadows

Specific composition and species clonal traits were characterized along combined flooding and grazing gradients to answer two questions. i) To what extent does the interaction of flooding and grazing influence the clonal characteristics of the vegetation? ii) Are the effects of both environmental factors independent or interactive? This study was carried out in a wet meadow along the Atlantic coast (France). Three plant communities (hygrophilous, meso-hygrophilous and mesophilous) were distinguished along a flooding gradient and five levels of grazing pressure were controlled through an experimental design (from no grazing to heavy grazing). We monitored species composition and retrieved, for each species, the type of clonal growth organs (CGOs) and clonal traits from the CLO-PLA3 database. We identified two syndromes of clonal traits: ??above-ground splitters?? and ??below-ground integrators??. Clonal traits played a key role in plant assembly in the studied meadows. The interaction of both environmental factors selected for particular syndromes of clonal traits; however, flooding had a stronger filtering effect than grazing. The hygrophilous community was dominated by above-ground splitters, whereas the meso-hygrophilous vegetation was dominated by below-ground integrators. In the mesophilous community, clonal composition was the most diverse and shared clonal traits with the vegetation of both the hygrophilous and meso-hygrophilous communities. Grazing impact on CGOs and clonal traits differed between plant communities, i.e., the effect of grazing was modulated by the flooding regime. This study confirmed that vegetation responses to grazing might depend on the pool of traits, primarily filtered by environmental factors such as flooding.     

Characterization of the axon initial segment (AIS) of motor neurons and identification of a para-AIS and a juxtapara-AIS, organized by protein 4.1B

Background

The axon initial segment (AIS) plays a crucial role: it is the site where neurons initiate their electrical outputs. Its composition in terms of voltage-gated sodium (Nav) and voltage-gated potassium (Kv) channels, as well as its length and localization determine the neuron's spiking properties. Some neurons are able to modulate their AIS length or distance from the soma in order to adapt their excitability properties to their activity level. It is therefore crucial to characterize all these parameters and determine where the myelin sheath begins in order to assess a neuron's excitability properties and ability to display such plasticity mechanisms. If the myelin sheath starts immediately after the AIS, another question then arises as to how would the axon be organized at its first myelin attachment site; since AISs are different from nodes of Ranvier, would this particular axonal region resemble a hemi-node of Ranvier?

Results

We have characterized the AIS of mouse somatic motor neurons. In addition to constant determinants of excitability properties, we found heterogeneities, in terms of AIS localization and Nav composition. We also identified in all α motor neurons a hemi-node-type organization, with a contactin-associated protein (Caspr)⁺ paranode-type, as well as a Caspr2⁺ and Kv1⁺ juxtaparanode-type compartment, referred to as a para-AIS and a juxtapara (JXP)-AIS, adjacent to the AIS, where the myelin sheath begins. We found that Kv1 channels appear in the AIS, para-AIS and JXP-AIS concomitantly with myelination and are progressively excluded from the para-AIS. Their expression in the AIS and JXP-AIS is independent from transient axonal glycoprotein-1 (TAG-1)/Caspr2, in contrast to juxtaparanodes, and independent from PSD-93. Data from mice lacking the cytoskeletal linker protein 4.1B show that this protein is necessary to form the Caspr⁺ para-AIS barrier, ensuring the compartmentalization of Kv1 channels and the segregation of the AIS, para-AIS and JXP-AIS.

Conclusions

α Motor neurons have heterogeneous AISs, which underlie different spiking properties. However, they all have a para-AIS and a JXP-AIS contiguous to their AIS, where the myelin sheath begins, which might limit some AIS plasticity. Protein 4.1B plays a key role in ensuring the proper molecular compartmentalization of this hemi-node-type region.