Modelling of natural organic matter affinity for mackinawite, FeS, based on FTIR spectra by partial least squares regression (PLSR)

Marine sediments represent the most important sink for natural organic matter (NOM) across geological time spans, in which carbon-containing molecules are sequestered away and can escape remineralization to CO2 by microbial degradation. Strong associations between iron oxide minerals and organic matter reaching the seafloor play a fundamental role in this preservation and have been known for some decades. Despite the importance of this protective mechanism in the balances of the global carbon budget, very little is known about the affinity of NOM for reduced iron species such as mackinawite (FeS) in the anoxic layers of sediment. In this study, equilibrium partition coefficients (Kd) for three types of NOM (soil leachate, corn leaf and plankton lysate) on FeS were determined through batch sorption experiments. Attenuated Total Reflectance Fourier Transform Infrared spectra (ATR-FTIR) of the organic matter was then used as model inputs to train a partial least squares regression model (PLSR) to quantitatively predict Kd values based on the FTIR spectra of NOM. The final model fit the training data with an R2 of 0.97 (n = 17) and the validation data with a Q2 of 0.98 (n = 5) and a RMSEP of 0.036. Inspection of the PLSR regression coefficients indicate that functional groups characteristic of polysaccharides are the greatest positive predictors of NOM sorption onto FeS at sediment pore water pH. To our knowledge, this research presents a novel machine-learning approach to the quantitative modelling of NOM sorption to minerals found in marine environments

Sex differences in research funding, productivity and impact: An analysis of Québec university professors

Abstract Using the entire population of professors at universities in the province of Quebec (Canada), this paper analyzes the relationship between sex and research funding, publication rates, and scientific impact. Since age is an important factor in research and the population pyramids of men and women are different, the role of age is also analyzed. The paper shows that, after they have passed the age of about 38, women receive, on average, less funding for research than men, are generally less productive in terms of publications, and are at a slight disadvantage in terms of the scientific impact (measured by citations) of their publications. Various explanations for these differences are suggested, such as the more restricted collaboration networks of women, motherhood and the accompanying division of labour, women's rank within the hierarchy of the scientific community and access to resources as well as their choice of research topics and level of specialization

Loss of hepatic DEPTOR alters the metabolic transition to fasting

Objective The mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that functions into distinct protein complexes (mTORC1 and mTORC2) that regulates growth and metabolism. DEP-domain containing mTOR-interacting protein (DEPTOR) is part of these complexes and is known to reduce their activity. Whether DEPTOR loss affects metabolism and organismal growth in vivo has never been tested. Methods We have generated a conditional transgenic mouse allowing the tissue-specific deletion of DEPTOR. This model was crossed with CMV-cre mice or Albumin-cre mice to generate either whole-body or liver-specific DEPTOR knockout (KO) mice. Results Whole-body DEPTOR KO mice are viable, fertile, normal in size, and do not display any gross physical and metabolic abnormalities. To circumvent possible compensatory mechanisms linked to the early and systemic loss of DEPTOR, we have deleted DEPTOR specifically in the liver, a tissue in which DEPTOR protein is expressed and affected in response to mTOR activation. Liver-specific DEPTOR null mice showed a reduction in circulating glucose upon fasting versus control mice. This effect was not associated with change in hepatic gluconeogenesis potential but was linked to a sustained reduction in circulating glucose during insulin tolerance tests. In addition to the reduction in glycemia, liver-specific DEPTOR KO mice had reduced hepatic glycogen content when fasted. We showed that loss of DEPTOR cell-autonomously increased oxidative metabolism in hepatocytes, an effect associated with increased cytochrome c expression but independent of changes in mitochondrial content or in the expression of genes controlling oxidative metabolism. We found that liver-specific DEPTOR KO mice showed sustained mTORC1 activation upon fasting, and that acute treatment with rapamycin was sufficient to normalize glycemia in these mice. Conclusion We propose a model in which hepatic DEPTOR accelerates the inhibition of mTORC1 during the transition to fasting to adjust metabolism to the nutritional status. Keywords: DEPTOR; mTOR; Liver; Glucose; Fastin

Le FORUM, Vol. 34 No. 3

https://digitalcommons.library.umaine.edu/francoamericain_forum/1027/thumbnail.jp

Le FORUM, Vol. 36 No. 4

https://digitalcommons.library.umaine.edu/francoamericain_forum/1035/thumbnail.jp

Le FORUM, Vol. 37 No. 1

https://digitalcommons.library.umaine.edu/francoamericain_forum/1036/thumbnail.jp

Le FORUM, Vol. 34 No. 2

https://digitalcommons.library.umaine.edu/francoamericain_forum/1026/thumbnail.jp

The Hepatokine TSK does not affect brown fat thermogenic capacity, body weight gain, and glucose homeostasis

Objectives Hepatokines are proteins secreted by the liver that impact the functions of the liver and various tissues through autocrine, paracrine, and endocrine signaling. Recently, Tsukushi (TSK) was identified as a new hepatokine that is induced by obesity and cold exposure. It was proposed that TSK controls sympathetic innervation and thermogenesis in brown adipose tissue (BAT) and that loss of TSK protects against diet-induced obesity and improves glucose homeostasis. Here we report the impact of deleting and/or overexpressing TSK on BAT thermogenic capacity, body weight regulation, and glucose homeostasis. Methods We measured the expression of thermogenic genes and markers of BAT innervation and activation in TSK-null and TSK-overexpressing mice. Body weight, body temperature, and parameters of glucose homeostasis were also assessed in the context of TSK loss and overexpression. Results The loss of TSK did not affect the thermogenic activation of BAT. We found that TSK-null mice were not protected against the development of obesity and did not show improvement in glucose tolerance. The overexpression of TSK also failed to modulate thermogenesis, body weight gain, and glucose homeostasis in mice