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See detailMechanism of Thiamine Transport in Neuroblastoma Cells. Inhibition of a High Affinity Carrier by Sodium Channel Activators and Dependence of Thiamine Uptake on Membrane Potential and Intracellular Atp
Bettendorff, Lucien ULg; Wins, Pierre

in Journal of Biological Chemistry (1994), 269(20), 14379-14385

Nerve cells are particularly sensitive to thiamine deficiency. We studied thiamine transport in mouse neuroblastoma (Neuro 2a) cells. At low external concentration, [14C]thiamine was taken up through a ... [more ▼]

Nerve cells are particularly sensitive to thiamine deficiency. We studied thiamine transport in mouse neuroblastoma (Neuro 2a) cells. At low external concentration, [14C]thiamine was taken up through a saturable high affinity mechanism (Km = 35 nM). This was blocked by low concentrations of the Na+ channel activators veratridine (IC50 = 7 +/- 4 microM) and batrachotoxin (IC50 = 0.9 microM). These effects were not antagonized by tetrodotoxin and were also observed in cell lines devoid of Na+ channels, suggesting that these channels are not involved in the mechanism of inhibition. At high extracellular concentrations, thiamine uptake proceeds essentially via a low affinity carrier (Km = 0.8 mM), insensitive to veratridine but blocked by divalent cations. In both cases, the uptake was independent on external sodium, partially inhibited (10-35%) by depolarization and sensitive to metabolic inhibitors. A linear relationship between the rate of thiamine transport and intracellular ATP concentration was found. When cells grown in a medium of low thiamine concentration (6 nM) were exposed to 100 nM extracellular thiamine, a 3-fold increase in intracellular thiamine diphosphate was observed after 2 h while the concomitant increase in intracellular free thiamine was barely significant. These data suggest a secondary active transport of thiamine, the main driving force being thiamine phosphorylation rather than the sodium gradient. [less ▲]

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See detailMechanism of Trypanosoma brucei gambiense resistance to human serum.
Uzureau, Pierrick; Uzureau, Sophie; Lecordier, Laurence et al

in Nature (2013), 501(7467), 430-4

The African parasite Trypanosoma brucei gambiense accounts for 97% of human sleeping sickness cases. T. b. gambiense resists the specific human innate immunity acting against several other tsetse-fly ... [more ▼]

The African parasite Trypanosoma brucei gambiense accounts for 97% of human sleeping sickness cases. T. b. gambiense resists the specific human innate immunity acting against several other tsetse-fly-transmitted trypanosome species such as T. b. brucei, the causative agent of nagana disease in cattle. Human immunity to some African trypanosomes is due to two serum complexes designated trypanolytic factors (TLF-1 and -2), which both contain haptoglobin-related protein (HPR) and apolipoprotein LI (APOL1). Whereas HPR association with haemoglobin (Hb) allows TLF-1 binding and uptake via the trypanosome receptor TbHpHbR (ref. 5), TLF-2 enters trypanosomes independently of TbHpHbR (refs 4, 5). APOL1 kills trypanosomes after insertion into endosomal/lysosomal membranes. Here we report that T. b. gambiense resists TLFs via a hydrophobic beta-sheet of the T. b. gambiense-specific glycoprotein (TgsGP), which prevents APOL1 toxicity and induces stiffening of membranes upon interaction with lipids. Two additional features contribute to resistance to TLFs: reduction of sensitivity to APOL1 requiring cysteine protease activity, and TbHpHbR inactivation due to a L210S substitution. According to such a multifactorial defence mechanism, transgenic expression of T. b. brucei TbHpHbR in T. b. gambiense did not cause parasite lysis in normal human serum. However, these transgenic parasites were killed in hypohaptoglobinaemic serum, after high TLF-1 uptake in the absence of haptoglobin (Hp) that competes for Hb and receptor binding. TbHpHbR inactivation preventing high APOL1 loading in hypohaptoglobinaemic serum may have evolved because of the overlapping endemic area of T. b. gambiense infection and malaria, the main cause of haemolysis-induced hypohaptoglobinaemia in western and central Africa. [less ▲]

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See detailMechanisms controlling the air-sea CO2 flux in the North Sea
Prowe, F. A. E.; Thomas, H.; Pätsch, J. et al

in Continental Shelf Research (2009), 29

The mechanisms driving the air–sea exchange of carbon dioxide (CO2) in the North Sea are investigated using the three-dimensional coupled physical–biogeochemical model ECOHAM (ECOlogical model, HAMburg ... [more ▼]

The mechanisms driving the air–sea exchange of carbon dioxide (CO2) in the North Sea are investigated using the three-dimensional coupled physical–biogeochemical model ECOHAM (ECOlogical model, HAMburg). We validate our simulations using field data for the years 2001–2002 and identify the controls of the air–sea CO2 flux for two locations representative for the North Sea’s biogeochemical provinces. In the seasonally stratified northern region, net CO2 uptake is high (2:06molm 2 a 1) due to high net community production (NCP) in the surface water. Overflow production releasing semi labile dissolved organic carbon needs to be considered for a realistic simulation of the low dissolved inorganic carbon (DIC) concentrations observed during summer. This biologically driven carbon drawdown outcompetes the temperature-driven rise in CO2 partial pressure (pCO2) during the productive season. In contrast, the permanently mixed southern region is a weak net CO2 source (0:78molm 2 a 1). NCP is generally low except for the spring bloom because remineralization parallels primary production. Here, the pCO2 appears to be controlled by temperature. [less ▲]

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See detailMechanisms controlling the oxygen consumption in experimentally induced hypochloremic alkalosis in calves
Cambier, Carole ULg; Clerbaux, Thierry; Amory, Hélène ULg et al

in Veterinary Research (2002), 33

The study was carried out on healthy Friesian calves (n = 10) aged between 10 and 30 days. Hypochloremia and alkalosis were induced by intravenous administration of furosemide and isotonic sodium ... [more ▼]

The study was carried out on healthy Friesian calves (n = 10) aged between 10 and 30 days. Hypochloremia and alkalosis were induced by intravenous administration of furosemide and isotonic sodium bicarbonate. The venous and arterial blood samples were collected repeatedly. 2,3-diphosphoglycerate (2,3-DPG), hemoglobin and plasmatic chloride concentrations were determined. The red blood cell chloride concentration was also calculated. pH, PCO2 and PO2 were measured in arterial and mixed venous blood. The oxygen equilibrium curve (OEC) was measured in standard conditions. The correspondence of the OEC to the arterial and mixed venous compartments was calculated, taking blood temperature, pH and PCO2 values into account. The oxygen exchange fraction (OEF%), corresponding to the degree of blood desaturation between the arterial and mixed venous compartments and the amount of oxygen released at the tissue level by 100 mL of blood (OEF Vol%) were calculated from the arterial and mixed venous OEC, combined with PO2 and hemoglobin concentration. Oxygen delivery (DO2) was calculated using the arterial oxygen content, the cardiac output measured by thermodilution, and the body weight of the animal. The oxygen consumption (VO2) was derived from the cardiac output, OEF Vol% and body weight values. Despite the plasma hypochloremia, the erythrocyte chloride concentration was not influenced by furosemide and sodium bicarbonate infusion. Due to the alkalosis-induced increase in the 2,3-DPG, the standard OEC was shifted to the right, allowing oxygen to dissociate from hemoglobin more rapidly. These changes opposed the increased affinity of hemoglobin for oxygen induced by alkalosis. Moreover, respiratory acidosis, hemoconcentration, and the slight decrease in the partial oxygen pressure in mixed venous blood (Pvo(2)) tended to improve the OEF Vol% and maintain the oxygen consumption in a physiological range while the cardiac output, and the oxygen delivery were significantly decreased. It may be concluded that, despite reduced oxygen delivery, oxygen consumption is maintained during experimentally induced hypochloremic alkalosis in healthy 10-30 day old calves [less ▲]

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See detailMechanisms for nonrecurrent genomic rearrangements associated with CMT1A or HNPP: rare CNVs as a cause for missing heritability.
Zhang, Feng; Seeman, Pavel; Liu, Pengfei et al

in American Journal of Human Genetics (2010), 86(6), 892-903

Genomic rearrangements involving the peripheral myelin protein gene (PMP22) in human chromosome 17p12 are associated with neuropathy: duplications cause Charcot-Marie-Tooth disease type 1A (CMT1A ... [more ▼]

Genomic rearrangements involving the peripheral myelin protein gene (PMP22) in human chromosome 17p12 are associated with neuropathy: duplications cause Charcot-Marie-Tooth disease type 1A (CMT1A), whereas deletions lead to hereditary neuropathy with liability to pressure palsies (HNPP). Our previous studies showed that >99% of these rearrangements are recurrent and mediated by nonallelic homologous recombination (NAHR). Rare copy number variations (CNVs) generated by nonrecurrent rearrangements also exist in 17p12, but their underlying mechanisms are not well understood. We investigated 21 subjects with rare CNVs associated with CMT1A or HNPP by oligonucleotide-based comparative genomic hybridization microarrays and breakpoint sequence analyses, and we identified 17 unique CNVs, including two genomic deletions, ten genomic duplications, two complex rearrangements, and three small exonic deletions. Each of these CNVs includes either the entire PMP22 gene, or exon(s) only, or ultraconserved potential regulatory sequences upstream of PMP22, further supporting the contention that PMP22 is the critical gene mediating the neuropathy phenotypes associated with 17p12 rearrangements. Breakpoint sequence analysis reveals that, different from the predominant NAHR mechanism in recurrent rearrangement, various molecular mechanisms, including nonhomologous end joining, Alu-Alu-mediated recombination, and replication-based mechanisms (e.g., FoSTeS and/or MMBIR), can generate nonrecurrent 17p12 rearrangements associated with neuropathy. We document a multitude of ways in which gene function can be altered by CNVs. Given the characteristics, including small size, structural complexity, and location outside of coding regions, of selected rare CNVs, their identification remains a challenge for genome analysis. Rare CNVs may potentially represent an important portion of "missing heritability" for human diseases. [less ▲]

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See detailThe mechanisms for plant growth promotion by PGPRs
Mariutto, Martin ULg

Scientific conference (2009, April 02)

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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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