A new experimental set-up for the study of the formation and dissociation of methane hydrate in sediments

methane hydrates ; sediments ; kinetics ; modelling ; heat transfer ; mass transfer ;International audienceIn this paper, we give a short presentation of the project ForDiMHyS which consists of experimental studies and model establishment (or development) of the kinetics of FORmation and Dissociation of Methane Hydrates in Sediments. We focus on the details of the experimental set-up which is newly, specially designed for this study in the preliminary step of the project. The four French academic teams and two PhD thesis are involved in the ForDiMHyS project on the period 2000-2004. The financial support is given by the five French Partners. The project consists of two-step programs; firstly the data acquisition from the laboratory experimental set-up and secondly simulation of methane production from methane hydrate fields

MARCH1 protects the lipid raft and tetraspanin web from MHCII proteotoxicity in dendritic cells

Dendritic cells (DCs) produce major histocompatibility complex II (MHCII) in large amounts to function as professional antigen presenting cells. Paradoxically, DCs also ubiquitinate and degrade MHCII in a constitutive manner. Mice deficient in the MHCII-ubiquitinating enzyme membrane-anchored RING-CH1, or the ubiquitin-acceptor lysine of MHCII, exhibit a substantial reduction in the number of regulatory T (Treg) cells, but the underlying mechanism was unclear. Here we report that ubiquitin-dependent MHCII turnover is critical to maintain homeostasis of lipid rafts and the tetraspanin web in DCs. Lack of MHCII ubiquitination results in the accumulation of excessive quantities of MHCII in the plasma membrane, and the resulting disruption to lipid rafts and the tetraspanin web leads to significant impairment in the ability of DCs to engage and activate thymocytes for Treg cell differentiation. Thus, ubiquitin-dependent MHCII turnover represents a novel quality-control mechanism by which DCs maintain homeostasis of membrane domains that support DC's Treg cell-selecting function

Metabolism within the tumor microenvironment and its implication on cancer progression: an ongoing therapeutic target

Since reprogramming energy metabolism is considered a new hallmark of cancer, tumor metabolism is again in the spotlight of cancer research. Many studies have been carried out and many possible therapies have been developed in the last years. However, tumor cells are not alone. A series of extracellular components and stromal cells, such as endothelial cells, cancer-associated fibroblasts, tumor-associated macrophages and tumor-infiltrating T cells, surround tumor cells in the so-called tumor microenvironment. Metabolic features of these cells are being studied in deep in order to find relationships between metabolism within the tumor microenvironment and tumor progression. Moreover, it cannot be forgotten that tumor growth is able to modulate host metabolism and homeostasis, so that tumor microenvironment is not the whole story. Importantly, the metabolic switch in cancer is just a consequence of the flexibility and adaptability of metabolism and should not be surprising. Treatments of cancer patients with combined therapies including anti-tumor agents with those targeting stromal cell metabolism, anti-angiogenic drugs and/or immunotherapy are being developed as promising therapeutics.Mª Carmen Ocaña is recipient of a predoctoral FPU grant from the Spanish Ministry of Education, Culture and Sport. Supported by grants BIO2014-56092-R (MINECO and FEDER), P12-CTS-1507 (Andalusian Government and FEDER) and funds from group BIO-267 (Andalusian Government). The "CIBER de Enfermedades Raras" is an initiative from the ISCIII (Spain). The funders had no role in the study design, data collection and analysis, decision to publish or preparation of the manuscript

Type II NKT Cells Stimulate Diet-Induced Obesity by Mediating Adipose Tissue Inflammation, Steatohepatitis and Insulin Resistance

The progression of obesity is accompanied by a chronic inflammatory process that involves both innate and acquired immunity. Natural killer T (NKT) cells recognize lipid antigens and are also distributed in adipose tissue. To examine the involvement of NKT cells in the development of obesity, C57BL/6 mice (wild type; WT), and two NKT-cell-deficient strains, Jα18−/− mice that lack the type I subset and CD1d−/− mice that lack both the type I and II subsets, were fed a high fat diet (HFD). CD1d−/− mice gained the least body weight with the least weight in perigonadal and brown adipose tissue as well as in the liver, compared to WT or Jα18−/− mice fed an HFD. Histologically, CD1d−/− mice had significantly smaller adipocytes and developed significantly milder hepatosteatosis than WT or Jα18−/− mice. The number of NK1.1+TCRβ+ cells in adipose tissue increased when WT mice were fed an HFD and were mostly invariant Vα14Jα18-negative. CD11b+ macrophages (Mφ) were another major subset of cells in adipose tissue infiltrates, and they were divided into F4/80high and F4/80low cells. The F4/80low-Mφ subset in adipose tissue was increased in CD1d−/− mice, and this population likely played an anti-inflammatory role. Glucose intolerance and insulin resistance in CD1d−/− mice were not aggravated as in WT or Jα18−/− mice fed an HFD, likely due to a lower grade of inflammation and adiposity. Collectively, our findings provide evidence that type II NKT cells initiate inflammation in the liver and adipose tissue and exacerbate the course of obesity that leads to insulin resistance

An Empirical Study of Geographic and Seasonal Variations in Diurnal Temperature Range

The diurnal temperature range (DTR) of surface air over land varies geographically and seasonally. The authors have investigated these variations using generalized additive models (GAMs), a nonlinear regression methodology. With DTR as the response variable, meteorological and land surface parameters were treated as explanatory variables. Regression curves related the deviation of DTR from its mean value to values of the meteorological and land surface variables. Cloud cover, soil moisture, distance inland, solar radiation, and elevation were combined as explanatory variables in an ensemble of 84 GAM models that used data grouped into seven vegetation types and 12 months. The ensemble explained 80% of the geographical and seasonal variation in DTR. Vegetation type and cloud cover exhibited the strongest relationships with DTR. Shortwave radiation, distance inland, and elevation were positively correlated with DTR, whereas cloud cover and soil moisture were negatively correlated. A separate analysis of the surface energy budget showed that changes in net longwave radiation represented the effects of solar and hydrological variation on DTR. It is found that vegetation and its associated climate is important for DTR variation in addition to the climatic influence of cloud cover, soil moisture, and solar radiation. It is also found that surface net longwave radiation is a powerful diagnostic of DTR variation, explaining over 95% of the seasonal variation of DTR in tropical regions