6 research outputs found
Sans titres: Anthologie collective Français 335 (automne 2011)
http://deepblue.lib.umich.edu/bitstream/2027.42/89432/1/sans_titres.pd
Dissolution and biodurability of mineral fibres
Dissolution rates of mineral fibres in several environments are obtained as proxies for
their biodurability in body fluids. This chapter provides a description of the experimental
methods, the parameters and characteristics to be fixed during the design of dissolution
experiments in closed (batch reactors) and open systems (flow-through cells), as well as
details of the dissolution media. The dissolution of mineral fibres in buffered inorganic
solutions is the key to understanding their behaviour during weathering processes
because it contributes not only to their chemical transformation, but also to the
breakdown of the fibres that may be dispersed in the environment. On the other hand,
preparation of fluids representing different interstitial conditions in the lung is described,
with particular attention to artificial lysosomal fluid (ALF) employed to mimic the
environment that inhaled particles would encounter after phagocytosis by alveolar and
interstitial macrophages. Moreover, the use of a neutral fluid such as Gamble’s solution
(GS) simulates the interstitial lung fluid and airway lining fluid. Finally, the results of
studies of mineral fibre dissolution in inorganic and body fluids, found in the literature,
are discussed.
Methodologies for assessing the biodurability of fibres are illustrated, starting from
dissolution rate data and focus on in vitro studies. Rate constants are used to assess fibre
lifetimes utilizing a fibre-shrinking model equation. Finally, literature studies show
differences in biopersistence between serpentine and amphibole asbestos, due to their
different crystal structures and dissolution conditions of pH and solution composition
Comparative metabolomic profiling reveals that dysregulated glycolysis stemming from lack of salvage NAD⁺ biosynthesis impairs reproductive development in Caenorhabditis elegans
Temporal developmental progression is highly coordinated in Caenorhabditis elegans. However, loss of nicotinamidase PNC-1 activity slows reproductive development, uncoupling it from its typical progression relative to the soma. Using LC/MS we demonstrate that pnc-1 mutants do not salvage the nicotinamide released by NAD(+) consumers to resynthesize NAD(+), resulting in a reduction in global NAD(+) bioavailability. We manipulate NAD(+) levels to demonstrate that a minor deficit in NAD(+) availability is incompatible with a normal pace of gonad development. The NAD(+) deficit compromises NAD(+) consumer activity, but we surprisingly found no functional link between consumer activity and reproductive development. As a result we turned to a comparative metabolomics approach to identify the cause of the developmental phenotype. We reveal widespread metabolic perturbations, and using complementary pharmacological and genetic approaches, we demonstrate that a glycolytic block accounts for the slow pace of reproductive development. Interestingly, mitochondria are protected from both the deficiency in NAD(+) biosynthesis and the effects of reduced glycolytic output. We suggest that compensatory metabolic processes that maintain mitochondrial activity in the absence of efficient glycolysis are incompatible with the requirements for reproductive development, which requires high levels of cell division. In addition to demonstrating metabolic requirements for reproductive development, this work also has implications for understanding the mechanisms behind therapeutic interventions that target NAD(+) salvage biosynthesis for the purposes of inhibiting tumor growth