LCA mainstreaming conditions in Latin America—based on learnings from 2005 to 2014

Purpose

Based on the 2005–2014 developments in the Latin American and the Caribbean region (LAC), this paper aims to understand the conditions’ levels for mainstreaming life cycle assessment/life cycle management (LCA/LCM) and map key next actions.

Methods

Along the paper, four mainstreaming conditions are analyzed: expansion of LCM/LCA training activities, availability of LCA studies, national LCA database operating, and existence and activity of national life cycle network(s). Assuming that countries with better conditions are in a better position to develop national LCA based regulations, policies are also researched to complement this study.

Results and discussion

With nine life cycle (LC) networks in 2014, the LAC region has positively developed its networking capacities since 2005 but not the databases area (only one LCA database, Mexicaniuh, is fully operational). It was found that countries with no networks, lack all LCA trainings, studies, and databases.Local capacities are limited which in best case, Chile, does not exceed 18 practitioners per 10 million inhabitants. Based on the total score on mainstreaming conditions, Mexico and Brazil are the most advanced countries, but their markets for LCA professionals are still small (Valdivia et al. 2015), which suggests that tailored made strategies are needed for stronger uptake of LCA by industrial sectors.Argentina, Peru, Chile, and Colombia are in the second tier but still lack a critical mass of business cases and the political will to improve their mainstreaming conditions.

Conclusions

LCA development in the LAC region since 2005 is overall positive but still insufficient to serve the growth of prosperous LCA markets. Well-functioning LC networks are essential to leapfrog LCA. In 2014, about 27 % of LAC countries counted on a LC network. A common language in the region (except for Portuguese in Brazil) has been instrumental for expanding LCA through regional cooperation. LCA-based policies are boosted when local capacities and databases are available following the cases of Mexico, Chile, and Brazil. More data and research are needed to understand the women role in advancing LCA and the causalities and motivations of LAC companies to decide for LCA implementation. The application of the methodology was possible thanks to good quality data available and delivered key findings to develop national road maps for advancing LCA. No indicator used is specific for the LAC region and similar exercises are encouraged in other regions such as Africa and Asia.

     

Evidence of transmission ratio distortion of DLG5 R30Q variant in general and implication of an association with Crohn disease in men

Recently, we described the association of genetic variation in the discs large homolog 5 (DLG5) gene with inflammatory bowel disease (IBD) in a large European study sample (Stoll et al. in Nat Genet 36:476–480, 2004). Here, we report that the R30Q variant constitutes a susceptibility factor for Crohn disease (CD) in men [odds ratio (OR)=2.49, 95% confidence interval (CI) 1.53–4.06, P<0.001] but not women (OR=1.01, 95% CI=0.70–1.45, P=0.979) using multivariate logistic regression analyses in a unified study sample from Germany, Italy and Quebec. R30Q is a significant predictor for CD in men even when accounting for CARD15 and IBD5 risk variants (adjusted OR=2.41, 95% CI=1.41–4.12, P=0.001). The observed association is driven by a gender-dependent transmission ratio distortion (TRD) among healthy controls (frequency of Q allele: men 5.2%, women 11.3%), an effect that is offset in CD patients (frequency of Q allele: men 10.1%, women 10.9%). This finding is further substantiated by two non-IBD study samples, one of which consists of a newborn screening sample (newborn males 7.1%; newborn females 11%, P=0.036). Further investigation of the observed TRD may contribute towards enlightening the role of DLG5 in physiological processes influencing transmission of chromosomes to the surviving offspring, which, in turn, may help in understanding its implication in the development of CD among men.Frauke Friedrichs and Sonia Brescianini equally contributed to the work.     

Heparan sulfate proteoglycans and their binding proteins in embryo implantation and placentation

Complex interactions occur among embryonic, placental and maternal tissues during embryo implantation. Many of these interactions are controlled by growth factors, extracellular matrix and cell surface components that share the ability to bind heparan sulfate (HS) polysaccharides. HS is carried by several classes of cell surface and secreted proteins called HS proteoglycan that are expressed in restricted patterns during implantation and placentation. This review will discuss the expression of HS proteoglycans and various HS binding growth factors as well as extracellular matrix components and HS-modifying enzymes that can release HS-bound proteins in the context of implantation and placentation.     

Menthol Inhibits Detrusor Contractility Independently of TRPM8 Activation

Agonists such as icilin and menthol can activate the cool temperature-sensitive ion channel TRPM8. However, biological responses to menthol may occur independently of TRPM8 activation. In the rodent urinary bladder, menthol facilitates the micturition reflex but inhibits muscarinic contractions of the detrusor smooth muscle. The site(s) of TRPM8 expression in the bladder are controversial. In this study we investigated the regulation of bladder contractility in vitro by menthol. Bladder strips from wild type and TRPM8 knockout male mice (25–30 g) were dissected free and mounted in organ baths. Isometric contractions to carbachol (1 nM–30 µM), CaCl₂ (1 µM to 100 mM) and electrical field stimulation (EFS; 8, 16, 32 Hz) were measured. Strips from both groups contracted similarly in response to both carbachol and EFS. Menthol (300 µM) or nifedipine (1 µM) inhibited carbachol and EFS-induced contractions in both wild type and TRPM8 knockout bladder strips. Incubation with the sodium channel blocker tetrodotoxin (1 µM), replacement of extracellular sodium with the impermeant cation N-Methyl-D-Glucamine, incubation with a cocktail of potassium channel inhibitors (100 nM charybdotoxin, 1 µM apamin, 10 µM glibenclamide and 1 µM tetraethylammonium) or removal of the urothelium did not affect the inhibitory actions of menthol. Contraction to CaCl₂ was markedly inhibited by either menthol or nifedipine. In cultured bladder smooth muscle cells, menthol or nifedipine abrogated the carbachol or KCl-induced increases in [Ca²⁺]_i. Intravesical administration of menthol increased voiding frequency while decreasing peak voiding pressure. We conclude that menthol inhibits muscarinic bladder contractions through blockade of L-type calcium channels, independently of TRPM8 activation.