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See detailMechanisms for tolerance to diatomaceous earth between strains of Tribolium castaneum
Rigaux, Marylin; Haubruge, Eric ULg; Fields, Paul

in Entomologia Experimentalis et Applicata (2001), 101

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See detailMechanisms involved in exogenous C2- and C6-ceramide-induced cancer cell toxicity.
Fillet, Marianne ULg; Bentires-Alj, Mohamed; Deregowski, Valérie et al

in Biochemical Pharmacology (2003), 65(10), 1633-42

Ceramides are important intracellular second messengers that play a role in the regulation of cell growth, differentiation, and programmed cell death. To determine whether ceramides can mediate the ... [more ▼]

Ceramides are important intracellular second messengers that play a role in the regulation of cell growth, differentiation, and programmed cell death. To determine whether ceramides can mediate the apoptosis of HCT116 and OVCAR-3 cancer cells, exogenous C2-, C6-, and C16-ceramides were used to mimic the endogenous lipid increase that follows a large variety of stresses. C2- and C6-ceramides (cell-permeable ceramide analogs), but not C16-ceramide, induced nuclear factor-kappaB (NF-kappaB) DNA-binding, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and mitochondrial cytochrome c release, indicating that apoptosis occurs through the caspase cascade and the mitochondrial pathway. No difference in survival was observed between control cells and cells expressing mutated IkappaBalpha and treated with the permeable ceramides. This suggests that, at least in these cell lines, stable NF-kappaB inhibition did not modify the ceramide-induced cytotoxicity pathway. C6-ceramide also induced a double block in G1 and G2, thus emptying the S phase. [less ▲]

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See detailMechanisms of Actions of Inhaled Anesthetics
Seutin, Vincent ULg

in New England Journal of Medicine [=NEJM] (2003), 349(9), 909-910

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See detailMechanisms of active folding of the landscape (Southern Tianshan, China)
Hubert, Aurelia ULg; Suppe, J.; Gonzales-Mieres, R.

in Journal of Geophysical Research (2007), 112(10.1029/2006JB004362),

We explore the kinematic mechanisms of active large-scale folding, based on analysis of two adjacent major anticlines in Tian Shan (central Asia) that share an acceleration of shortening rate leading to ... [more ▼]

We explore the kinematic mechanisms of active large-scale folding, based on analysis of two adjacent major anticlines in Tian Shan (central Asia) that share an acceleration of shortening rate leading to topographic emergence and folded geomorphic surfaces. Their folding mechanisms are fundamentally different. Yakeng anticline is a gentle pure shear detachment fold with 1200 m of shortening and a well-constrained history of growth beginning at 5.5 Ma with an order-of-magnitude increase in shortening rate from 0.16 to 1.2–1.6 mm/yr at 0.16–0.21 Ma. The shape of the deformed topographic surface and of subsurface horizons deposited during deformation is a linearly proportional image at reduced amplitude of the deeper structure, which shows that instantaneous uplift rates have been pointwise linearly proportional to the current finite fold amplitude. In contrast, Quilitak anticline is a complex fault bend fold with uplift rates proportional to the sine of the fault dip, showing discontinuities in uplift rate across active axial surfaces. The 10- to 20-km-wide anticline is topographically emergent only in a central 5- to 7-km-wide mountainous uplift, the abrupt southern edge of which is marked by 600- to 700-m-high triangular facets that result from active folding of a pediment across an active axial surface. The giant facets are shown to form by kink band migration and record postemergence deformation since an order-of-magnitude acceleration in shortening rate from 0.6 t 4–5 mm/yr, apparently contemporaneous with Yakeng. Sections logged across the active 115-m-wide hinge zone show that recent strata provide a bed- by-bed record of fold scarp growth, which is quantitatively deciphered by fitting bed shapes to a finite width kink band migration model. [less ▲]

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See detailMechanisms of ATM regulation by TGF-beta
Paupert, Jenny ULg; Barcellos-Hoff, Mary-Helen

Poster (2007)

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See detailMechanisms of ATM regulation by TGF-beta
Paupert, Jenny ULg; Barcellos-Hoff, Mary-Helen

Poster (2008)

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See detailMechanisms of ATM regulation by TGF-beta
Paupert, Jenny ULg; Barcellos-Hoff, Mary-Helen

Poster (2008)

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See detailMechanisms of breathing and gas exchanges in healthy cattle: effect of somatic growth
Lekeux, Pierre ULg

in Archives Internationales de Physiologie et de Biochimie (1987), 95(2), 5

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See detailMechanisms of cancer-related anemia and rationale for erythropoietin treatment
Beguin, Yves ULg

in Cancer Biotherapy (1997), 1

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See detailMechanisms of cell death in the injured auditory system: Otoprotective strategies
Lefèbvre, Philippe ULg; Malgrange, Brigitte ULg; Lallemend, François et al

in Audiology & Neuro-otology (2002), 7(3, May-Jun), 165-170

Oxidative stress insults such as neurotrophin withdrawal, sound trauma, hypoxia/ischemia, ototoxic antibiotics, and chemotherapeutic agents have been shown to induce apoptosis of both auditory hair cells ... [more ▼]

Oxidative stress insults such as neurotrophin withdrawal, sound trauma, hypoxia/ischemia, ototoxic antibiotics, and chemotherapeutic agents have been shown to induce apoptosis of both auditory hair cells and neurons. In this paper, we review some components of the apoptotic pathways leading to the death of hair cells and auditory induced by growth factor withdrawal or cisplatin intoxication: (1) reactive oxygen species and free radicals are formed as by-products of several metabolic pathways and these molecules can themselves cause cell damage by reacting with cellular proteins; (2) activation of caspases, and (3) activation of calpain. These mechanisms have several different points at which inhibitors could be targeted to protect cells from programmed cell death, including the prevention of oxidative stress-induced apoptosis and the activation of caspases and calpains. Copyright (C) 2002 S. Karger AG, Basel. [less ▲]

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See detailMechanisms of cell entry by human papillomaviruses: an overview.
Horvath, Caroline Aj; Boulet, Gaelle Av; Renoux, Virginie ULg et al

in Virology Journal (2010), 7

ABSTRACT: As the primary etiological agents of cervical cancer, human papillomaviruses (HPVs) must deliver their genetic material into the nucleus of the target cell. The viral capsid has evolved to ... [more ▼]

ABSTRACT: As the primary etiological agents of cervical cancer, human papillomaviruses (HPVs) must deliver their genetic material into the nucleus of the target cell. The viral capsid has evolved to fulfil various roles that are critical to establish viral infection. The particle interacts with the cell surface via interaction of the major capsid protein, L1, with heparan sulfate proteoglycans. Moreover, accumulating evidence suggests the involvement of a secondary receptor and a possible role for the minor capsid protein, L2, in cell surface interactions.The entry of HPV in vitro is initiated by binding to a cell surface receptor in contrast to the in vivo situation where the basement membrane has recently been identified as the primary site of virus binding. Binding of HPV triggers conformational changes, which affect both capsid proteins L1 and L2, and such changes are a prerequisite for interaction with the elusive uptake receptor. Most HPV types that have been examined, appear to enter the cell via a clathrin-dependent endocytic mechanism, although many data are inconclusive and inconsistent. Furthermore, the productive entry of HPV is a process that occurs slowly and asynchronously and it is characterised by an unusually extended residence on the cell surface.Despite the significant advances and the emergence of a general picture of the infectious HPV entry pathway, many details remain to be clarified. The impressive technological progress in HPV virion analysis achieved over the past decade, in addition to the improvements in general methodologies for studying viral infections, provide reasons to be optimistic about further advancement of this field.This mini review is intended to provide a concise overview of the literature in HPV virion/host cell interactions and the consequences for endocytosis. [less ▲]

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See detailMechanisms of cell migration in the adult brain: modelling subventricular neurogenesis.
Van Schepdael, An ULg; Ashbourn, J. M. A.; Beard, R. et al

in Computer Methods in Biomechanics & Biomedical Engineering (2013)

Neurogenesis has been the subject of active research in recent years. Although the majority of neurons form during the embryonic period, neurogenesis continues in restricted regions of the mammalian brain ... [more ▼]

Neurogenesis has been the subject of active research in recent years. Although the majority of neurons form during the embryonic period, neurogenesis continues in restricted regions of the mammalian brain well into adulthood. In rodent brains, neuronal migration is present in the rostral migratory stream (RMS), connecting the subventricular zone to the olfactory bulb (OB). The migration in the RMS is characterised by a lack of dispersion of neuroblasts into the surrounding tissues and a highly directed motion towards the OB. This study uses a simple mathematical model to investigate several theories of migration of neuroblasts through the RMS proposed in the literature, including chemo-attraction, chemorepulsion, general inhibition and the presence of a migration-inducing protein. Apart from the general inhibition model, all the models were able to provide results in good qualitative correspondence with the experimental observations. [less ▲]

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See detailThe mechanisms of chronic ischemic mitral regurgitation
RADERMECKER, Marc ULg; LANCELLOTTI, Patrizio ULg

in Annals of Thoracic Surgery (2007), 83(5), 1919-20

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See detailMechanisms of cohort suppression and population fluctuation in tiger salamanders
Whiteman, Howard; Wissinger, Scott; Denoël, Mathieu ULg

Conference (2006)

The mechanisms underlying population fluctuation have been well studied in mammals and insects but less research has focused on amphibians. Yet, the current global decline of amphibians equires that we ... [more ▼]

The mechanisms underlying population fluctuation have been well studied in mammals and insects but less research has focused on amphibians. Yet, the current global decline of amphibians equires that we understand these mechanisms, and be able to distinguish between anthropogenically induced declines and natural population fluctuations. We have followed a marked population of the Arizona tiger salamander, Ambystoma tigrinum nebulosum, for over 16 years during which time the population has completed two “boom and bust” cycles, generated by a dominant cohort that appears to suppress larval recruitment until it senesces. We tested two hypotheses for this suppression, cannibalism and resource depression, using a series of meso- and microcosm experiments. We found significant lethal and sublethal (behavior, diet, growth rates) effects of cannibalism by large larvae and paedomorphic adults on hatchling and 1st-year larvae, suggesting that both cannibalism and the threat of cannibalism are important in cohort suppression. Resource depression experiments revealed that paedomorphic adults did not affect larval survival, diet, or growth, despite reduced prey densities, because paedomorphs mainly reduced large bodied prey, whereas hatchlings fed primarily on smaller benthic and zooplanktonic invertebrates. Future experiments will determine how hatchlings are impacted by boom cohorts that are more similar in size and diet. Our results lend insight into the mechanisms underlying fluctuations in this population, and suggest that a better understanding of natural population fluctuations will aid amphibian conservation efforts. [less ▲]

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See detailMechanisms of dexamethasone-induced insulin resistance in healthy humans.
Tappy, L.; Randin, D.; Vollenweider, P. et al

in Journal of Clinical Endocrinology and Metabolism (1994), 79(4), 1063-9

Insulin resistance may result from decreased muscle blood flow, impaired cellular glucose transport, or intracellular deficits of glucose metabolism. The mechanisms responsible for dexamethasone-induced ... [more ▼]

Insulin resistance may result from decreased muscle blood flow, impaired cellular glucose transport, or intracellular deficits of glucose metabolism. The mechanisms responsible for dexamethasone-induced insulin resistance were investigated in healthy human subjects. During a 2-h hyperinsulinemic clamp, dexamethasone decreased glucose uptake, oxidation, and nonoxidative glucose disposal during the first hour. During the second hour, glucose uptake was normalized by means of hyperglycemia; glucose oxidation, however, remained suppressed by dexamethasone. Dexamethasone also abolished the insulin-mediated increase in calf blood flow. When acipimox was administered during the clamps to correct glucocorticoid-induced inhibition of glucose oxidation, dexamethasone decreased whole body glucose uptake and nonoxidative glucose disposal in the same proportion as when no acipimox was administered. However, glucose oxidation and insulin-mediated calf blood flow were normalized after acipimox. During the second hour, exogenous glucose infusion was matched to that used in the control clamp and normalized whole body glucose uptake. However, hyperglycemia developed, indicating insulin resistance. It is concluded that dexamethasone 1) decreases glucose oxidation independently of glucose transport; this inhibition is reversed by acipimox; and 2) decreases whole body glucose uptake independently of increased lipolysis, decreased glucose oxidation, or an altered muscle blood flow. [less ▲]

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See detailMechanisms of ectopic bone formation by human osteoprogenitor cells on CaP biomaterial carriers.
Chai, Y. C.; Roberts, S. J.; Desmet, E. et al

in Biomaterials (2012)

Stem cell-based strategies for bone regeneration, which use calcium phosphate (CaP)-based biomaterials in combination with developmentally relevant progenitor populations, have significant potential for ... [more ▼]

Stem cell-based strategies for bone regeneration, which use calcium phosphate (CaP)-based biomaterials in combination with developmentally relevant progenitor populations, have significant potential for clinical repair of skeletal defects. However, the exact mechanism of action and the stem cell-host-material interactions are still poorly understood. We studied if pre-conditioning of human periosteum-derived cells (hPDCs) in vitro could enhance, in combination with a CaP-based biomaterial carrier, ectopic bone formation in vivo. By culturing hPDCs in a biomimetic calcium (Ca(2+)) and phosphate (P(i)) enriched culture conditions, we observed an enhanced cell proliferation, decreased expression of mesenchymal stem cell (MSC) markers and upregulation of osteogenic genes including osterix, Runx2, osteocalcin, osteopontin, and BMP-2. However, the in vitro pre-conditioning protocols were non-predictive for in vivo ectopic bone formation. Surprisingly, culturing in the presence of Ca(2+) and P(i) supplements resulted in partial or complete abrogation of in vivo ectopic bone formation. Through histological, immunohistochemical and microfocus X-ray computed tomography (muCT) analysis of the explants, we found that in situ proliferation, collagen matrix deposition and the mediation of osteoclastic activity by hPDCs are associated to their ectopic bone forming capacity. These data were validated by the multivariate analysis and partial least square regression modelling confirming the non-predictability of in vitro parameters on in vivo ectopic bone formation. Our series of experiments provided further insights on the stem cell-host-material interactions that govern in vivo ectopic bone induction driven by hPDCs on CaP-based biomaterials. [less ▲]

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See detailMechanisms of Hand Motor Recovery After Stroke: An Electrophysiologic Study of Central Motor Pathways
Bastings, Eric; Rapisarda, Giuseppe; Pennisi, Giovanni et al

in Journal of Neurologic Rehabilitation (1997), 11(2), 97-108

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See detailMechanisms of HTLV-1 persistence and transformation.
Boxus, Mathieu ULg; Willems, Luc ULg

in British Journal of Cancer (2009), 101(9), 1497-501

Adult T-cell leukaemia (ATL) is caused by the human T-cell lymphotropic virus type 1 (HTLV-1). HTLV-1 has elaborated strategies to persist and replicate in the presence of a strong immune response. In ... [more ▼]

Adult T-cell leukaemia (ATL) is caused by the human T-cell lymphotropic virus type 1 (HTLV-1). HTLV-1 has elaborated strategies to persist and replicate in the presence of a strong immune response. In this review, we summarise these mechanisms and their contribution to T-cell transformation and ATL development. [less ▲]

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See detailMechanisms of inflammation in equine airways
Lekeux, Pierre ULg; Bureau, Fabrice ULg; Art, Tatiana ULg et al

in Proceedings : 3er Congreso Iberoamericano de Veterinarios Especializados en Equinos, Montevideo (2001)

Detailed reference viewed: 12 (1 ULg)