Méthodologie d'éconconception pour un procédé innovant: la bioélétrosynthèse des déchets organiques

International audienceBulk chemicals and liquid fuels are currently produced almost exclusively from petrochemical feedstock. In the light of emission reduction targets and the dependence on non renewable resources, the production of the same or functionally equivalent chemicals from renewable resources may play an important role [1, 2]. The project BIORARE (Bioelectrosynthesis for the refinery of residual waste) was set up to contribute to this objective. Its purpose is to use microbial electrosynthesis for the direct production of fuels and chemicals from organic waste and CO2 (see figure 1). Ecoconception is used to help to make choices. This is this work which is study.In a first step, we had to determine which parameters of the Bioelectrosynthesis (BES) could be the most impacting ones to define the priorities to be considered to minimize the potential impacts of the entire process. Some flows could be sensitive: the nature and the quantity of outputs, the nature and the quantity of materials, and the amount of energy used. The inventory of these flows had to be the first step. Thanks to databases and literature four have been identified as sensitive: electrodes, membrane, energy and chemicals produced.After determining this, we have to design the model for coupling anaerobic digestion to the BES. This was realized using Life Cycle Assessment approach. The goal of this assessment is to determine the relative influence of various target parameters on the impacts of the process. For example, results will allow assessing if the choice of a material for the electrode could have a significant influence on total impacts. Our methodology illustrates to what extend Life Cycle Assessment could help for the conception of a process, through the evaluation of the contribution of various parameters to the impacts. After, it is possible to integrate them into a model to determine what impacts they could have on the whole production chemicals or fuels from organic waste system.ACV de production de bioéthanol par bioélectrosynthèse de déchets organiques

An Evo-Devo perspective on ever-growing teeth in mammals and dental stem cell maintenance

Peer reviewe

Chromosomal neighbourhoods allow identification of organ specific changes in gene expression

Author summary Development of organs is typically associated with small and hard to detect changes in gene expression. Here we examined how often genes regulating specific organs are neighbours to each other in the genome, and whether this gene neighbourhood helps in the detection of changes in gene expression. We found that genes regulating individual organ development are very rarely close to each other in the mouse and human genomes. We built an algorithm, called DELocal, to detect changes in gene expression that incorporates information about neighbouring genes. Using transcriptomes of developing mouse molar teeth containing gene expression profiles of thousands of genes, we show how genes regulating tooth development are ranked high by DELocal even if their expression level changes are subtle. We propose that developmental biology studies can benefit from gene neighbourhood analyses in the detection of differential expression and identification of organ specific genes. Although most genes share their chromosomal neighbourhood with other genes, distribution of genes has not been explored in the context of individual organ development; the common focus of developmental biology studies. Because developmental processes are often associated with initially subtle changes in gene expression, here we explored whether neighbouring genes are informative in the identification of differentially expressed genes. First, we quantified the chromosomal neighbourhood patterns of genes having related functional roles in the mammalian genome. Although the majority of protein coding genes have at least five neighbours within 1 Mb window around each gene, very few of these neighbours regulate development of the same organ. Analyses of transcriptomes of developing mouse molar teeth revealed that whereas expression of genes regulating tooth development changes, their neighbouring genes show no marked changes, irrespective of their level of expression. Finally, we test whether inclusion of gene neighbourhood in the analyses of differential expression could provide additional benefits. For the analyses, we developed an algorithm, called DELocal that identifies differentially expressed genes by comparing their expression changes to changes in adjacent genes in their chromosomal regions. Our results show that DELocal removes detection bias towards large changes in expression, thereby allowing identification of even subtle changes in development. Future studies, including the detection of differential expression, may benefit from, and further characterize the significance of gene-gene neighbour relationships.Peer reviewe

Lysosomal abnormalities in hereditary spastic paraplegia types SPG15 and SPG11

Objective Hereditary spastic paraplegias (HSPs) are among the most genetically diverse inherited neurological disorders, with over 70 disease loci identified (SPG1-71) to date. SPG15 and SPG11 are clinically similar, autosomal recessive disorders characterized by progressive spastic paraplegia along with thin corpus callosum, white matter abnormalities, cognitive impairment, and ophthalmologic abnormalities. Furthermore, both have been linked to early-onset parkinsonism. Methods We describe two new cases of SPG15 and investigate cellular changes in SPG15 and SPG11 patient-derived fibroblasts, seeking to identify shared pathogenic themes. Cells were evaluated for any abnormalities in cell division, DNA repair, endoplasmic reticulum, endosomes, and lysosomes. Results Fibroblasts prepared from patients with SPG15 have selective enlargement of LAMP1-positive structures, and they consistently exhibited abnormal lysosomal storage by electron microscopy. A similar enlargement of LAMP1-positive structures was also observed in cells from multiple SPG11 patients, though prominent abnormal lysosomal storage was not evident. The stabilities of the SPG15 protein spastizin/ZFYVE26 and the SPG11 protein spatacsin were interdependent. Interpretation Emerging studies implicating these two proteins in interactions with the late endosomal/lysosomal adaptor protein complex AP-5 are consistent with shared abnormalities in lysosomes, supporting a converging mechanism for these two disorders. Recent work withZfyve26−/− mice revealed a similar phenotype to human SPG15, and cells in these mice had endolysosomal abnormalities. SPG15 and SPG11 are particularly notable among HSPs because they can also present with juvenile parkinsonism, and this lysosomal trafficking or storage defect may be relevant for other forms of parkinsonism associated with lysosomal dysfunction

Rickettsia felis–associated Uneruptive Fever, Senegal

During November 2008–July 2009, we investigated the origin of unknown fever in Senegalese patients with a negative malaria test result, focusing on potential rickettsial infection. Using molecular tools, we found evidence for Rickettsia felis–associated illness in the initial days of infection in febrile Senegalese patients without malaria

THE CHANGING PACE OF INSULAR LIFE : 5000 YEARS OF MICROEVOLUTION IN THE ORKNEY VOLE (MICROTUS ARVALIS ORCADENSIS)

Peer reviewe

A new glucocerebrosidase-deficient neuronal cell model provides a tool to probe pathophysiology and therapeutics for Gaucher disease

Glucocerebrosidase is a lysosomal hydrolase involved in the breakdown of glucosylceramide. Gaucher disease, a recessive lysosomal storage disorder, is caused by mutations in the gene GBA1. Dysfunctional glucocerebrosidase leads to accumulation of glucosylceramide and glycosylsphingosine in various cell types and organs. Mutations in GBA1 are also a common genetic risk factor for Parkinson disease and related synucleinopathies. In recent years, research on the pathophysiology of Gaucher disease, the molecular link between Gaucher and Parkinson disease, and novel therapeutics, have accelerated the need for relevant cell models with GBA1 mutations. Although induced pluripotent stem cells, primary rodent neurons, and transfected neuroblastoma cell lines have been used to study the effect of glucocerebrosidase deficiency on neuronal function, these models have limitations because of challenges in culturing and propagating the cells, low yield, and the introduction of exogenous mutant GBA1. To address some of these difficulties, we established a high yield, easy-to-culture mouse neuronal cell model with nearly complete glucocerebrosidase deficiency representative of Gaucher disease. We successfully immortalized cortical neurons from embryonic null allele gba(-/-) mice and the control littermate (gba(+/+)) by infecting differentiated primary cortical neurons in culture with an EF1 alpha-SV40T lentivirus. Immortalized gba(-/-) neurons lack glucocerebrosidase protein and enzyme activity, and exhibit a dramatic increase in glucosylceramide and glucosylsphingosine accumulation, enlarged lysosomes, and an impaired ATP-dependent calcium-influx response; these phenotypical characteristics were absent in gba(+/+) neurons. This null allele gba(-/-) mouse neuronal model provides a much-needed tool to study the pathophysiology of Gaucher disease and to evaluate new therapies