Institution
University of Fribourg
Education•Fribourg, Freiburg, Switzerland•
About: University of Fribourg is a education organization based out in Fribourg, Freiburg, Switzerland. It is known for research contribution in the topics: Population & Glacier. The organization has 6040 authors who have published 14975 publications receiving 542500 citations. The organization is also known as: UNIFR & Universität Freiburg.
Topics: Population, Glacier, Excited state, Hubbard model, Scattering
Papers published on a yearly basis
Papers
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TL;DR: It is concluded that adverse health effects of diesel exhaust not only emerge from its chemical composition, but also from the interplay between its physical properties, the physiological and cellular properties, and function of the human respiratory tract.
Abstract: Diesel engine emissions are among the most prevalent anthropogenic pollutants worldwide, and with the growing popularity of diesel-fueled engines in the private transportation sector, they are becoming increasingly widespread in densely populated urban regions. However, a large number of toxicological studies clearly show that diesel engine emissions profoundly affect human health. Thus the interest in the molecular and cellular mechanisms underlying these effects is large, especially concerning the nature of the components of diesel exhaust responsible for the effects and how they could be eliminated from the exhaust. This review describes the fundamental properties of diesel exhaust as well as the human respiratory tract and concludes that adverse health effects of diesel exhaust not only emerge from its chemical composition, but also from the interplay between its physical properties, the physiological and cellular properties, and function of the human respiratory tract. Furthermore, the primary molecular and cellular mechanisms triggered by diesel exhaust exposure, as well as the fundamentals of the methods for toxicological testing of diesel exhaust toxicity, are described. The key aspects of adverse effects induced by diesel exhaust exposure described herein will be important for regulators to support or ban certain technologies or to legitimate incentives for the development of promising new technologies such as catalytic diesel particle filters.
197 citations
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TL;DR: The generic impact scoring system (GISS) provides an objective and transparent method to aid prioritization of alien species for management according to their impacts, applicable across taxa and habitats.
Abstract: “One hundred worst” lists of alien species of the greatest concern proved useful for raising awareness of the risks and impacts of biological invasions amongst the general public, politicians and stakeholders. All lists so far have been based on expert opinion and primarily aimed at representativeness of the taxonomic and habitat diversity rather than at quantifying the harm the alien species cause. We used the generic impact scoring system (GISS) to rank 486 alien species established in Europe from a wide range of taxonomic groups to identify those with the highest environmental and socioeconomic impact. GISS assigns 12 categories of impact, each quantified on a scale from 0 (no impact detectable) to 5 (the highest impact possible). We ranked species by their total sum of scores and by the number of the highest impact scores. We also compared the listing based on GISS with other expert-based lists of the “worst” invaders. We propose a list of 149 alien species, comprising 54 plants, 49 invertebrates, 40 vertebrates and 6 fungi. Among the highest ranking species are one bird (Branta canadensis), four mammals (Rattus norvegicus, Ondatra zibethicus, Cervus nippon, Muntiacus reevesi), one crayfish (Procambarus clarkii), one mite (Varroa destructor), and four plants (Acacia dealbata, Lantana camara, Pueraria lobata, Eichhornia crassipes). In contrast to other existing expert-based “worst” lists, the GISS-based list given here highlights some alien species with high impacts that are not represented on any other list. The GISS provides an objective and transparent method to aid prioritization of alien species for management according to their impacts, applicable across taxa and habitats. Our ranking can also be used for justifying inclusion on lists such as the alien species of Union concern of the European Commission, and to fulfill Aichi target 9.
196 citations
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TL;DR: The evidence indicating that such preferential catch-up fat is primarily driven by energy conservation mechanisms operating via suppressed thermogenesis is reviewed, with glucose thus spared from oxidation in skeletal muscle being directed towards de novo lipogenesis and storage in white adipose tissue.
Abstract: The analyses of large epidemiological databases have suggested that infants and children who show catch-up growth, or adiposity rebound at a younger age, are predisposed to the development of obesity, type 2 diabetes and cardiovascular diseases later in life. The pathophysiological mechanisms by which these growth trajectories confer increased risks for these diseases are obscure, but there is compelling evidence that the dynamic process of catch-up growth per se, which often overlaps with adiposity rebound at a younger age, is characterized by hyperinsulinemia and by a disproportionately higher rate in the recovery of body fat than lean tissue (i.e. preferential 'catch-up fat'). This paper first focuses upon the almost ubiquitous nature of this preferential 'catch-up fat' phenotype across the life cycle as a risk factor for obesity and insulin-related complications - not only in infants and children who experienced catch-up growth after earlier fetal or neonatal growth retardation, or after preterm birth, but also in adults who show weight recovery after substantial weight loss owing to famine, disease-cachexia or periodic dieting. It subsequently reviews the evidence indicating that such preferential catch-up fat is primarily driven by energy conservation (thrifty) mechanisms operating via suppressed thermogenesis, with glucose thus spared from oxidation in skeletal muscle being directed towards de novo lipogenesis and storage in white adipose tissue. A molecular-physiological framework is presented which integrates emerging insights into the mechanisms by which this thrifty 'catch-up fat' phenotype crosslinks with early development of insulin and leptin resistance. In the complex interactions between genetic constitution of the individual, programming earlier in life, and a subsequent lifestyle of energy dense foods and low physical activity, this thrifty 'catch-up fat' phenotype--which probably evolved to increase survival capacity in a hunter-gatherer lifestyle of periodic food shortages--is a central event in growth trajectories to obesity and to diseases that cluster into the insulin resistance (metabolic) syndrome.
196 citations
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TL;DR: This work finds that the bilayer phospholipid composition and surface tension are key parameters of LD budding, and reveals the importance of altering ER physical chemistry for controlled cellular LD formation.
196 citations
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TL;DR: The relevant regulatory mechanisms of eNOS enzymatic activity that are emerging to play a role in endothelial dysfunction in atherosclerosis are focused on.
Abstract: Over the last two decades, it has become evident that decreased bioavailability of endothelial nitric oxide (NO) produced from endothelial NO synthase (eNOS), referred to as endothelial dysfunction, plays a crucial role in the development and progression of atherosclerosis. Much progress has been made in understanding the mechanisms of decreased endothelial NO bioavailability at the levels of regulation of eNOS gene expression, eNOS enzymatic activity and NO inactivation. Initial studies suggest that increasing eNOS gene expression would improve endothelial NO release in the hope of inhibiting the progression of atherosclerosis. Recent experimental studies, however, do not always support this therapeutic concept and show some evidence that overexpression of eNOS in atherosclerosis may be even harmful for the disease progression.Thus, recent research to improve endothelial function in atherosclerosis has focused on regulation of eNOS enzymatic activity and prevention of NO inactivation by oxidative stress. Since the role of oxidative stress in endothelial NO bioavailability has been reviewed in a large number of comprehensive articles, this article focuses on the relevant regulatory mechanisms of eNOS enzymatic activity that are emerging to play a role in endothelial dysfunction in atherosclerosis.
196 citations
Authors
Showing all 6204 results
Name | H-index | Papers | Citations |
---|---|---|---|
Jens Nielsen | 149 | 1752 | 104005 |
Sw. Banerjee | 146 | 1906 | 124364 |
Hans Peter Beck | 143 | 1134 | 91858 |
Patrice Nordmann | 127 | 790 | 67031 |
Abraham Z. Snyder | 125 | 329 | 91997 |
Csaba Szabó | 123 | 958 | 61791 |
Robert Edwards | 121 | 775 | 74552 |
Laurent Poirel | 117 | 621 | 53680 |
Thomas Münzel | 116 | 1055 | 57716 |
David G. Amaral | 112 | 302 | 49094 |
F. Blanc | 107 | 1514 | 58418 |
Markus Stoffel | 102 | 620 | 50796 |
Vincenzo Balzani | 101 | 476 | 45722 |
Enrico Bertini | 99 | 865 | 38167 |
Sandeep Kumar | 94 | 1563 | 38652 |