Mechanism of improvement in mitral regurgitation after cardiac resynchronization therapy.
; Lancellotti, Patrizio ; et al
in European Heart Journal (2008), 29(6), 757-65
AIMS: The aim of the current study was to evaluate the relationship between the presence of left ventricular (LV) dyssynchrony at baseline and acute vs. late improvement in mitral regurgitation (MR) after ... [more ▼]
AIMS: The aim of the current study was to evaluate the relationship between the presence of left ventricular (LV) dyssynchrony at baseline and acute vs. late improvement in mitral regurgitation (MR) after cardiac resynchronization therapy (CRT). METHODS AND RESULTS: Sixty eight patients consecutive (LV ejection fraction 23 +/- 8%) with at least moderate MR (>or=grade 2+) were included. Echocardiography was performed at baseline, 1 day after CRT initiation and at 6 months follow-up. Speckle tracking radial strain was used to assess LV dyssynchrony at baseline. The majority of patients improved in MR after CRT, with 43% improving immediately after CRT, and 20% improving late (after 6 months) after CRT. Early and late responders had similar extent of LV dyssynchrony (209 +/- 115 ms vs. 190 +/- 118 ms, P = NS); however, the site of latest activation in early responders was mostly inferior or posterior (adjacent to the posterior papillary muscle), whereas the lateral wall was the latest activated segment in late responders. CONCLUSION: Current data suggest that the presence of baseline LV dyssynchrony is related to improvement in MR after CRT. LV dyssynchrony involving the posterior papillary muscle may lead to an immediate reduction in MR, whereas LV dyssynchrony in the lateral wall resulted in late response to CRT. [less ▲]Detailed reference viewed: 28 (4 ULg)
Mechanism of lipolysis in milk : a modelistic approach using in Langmuir film balance.
Danthine, Sabine ; Blecker, Christophe ; Paquot, Michel et al
Poster (2004, February 11)Detailed reference viewed: 10 (1 ULg)
Mechanism of lipolysis in milk : a modelistic approach using Langmuir film balance.
Danthine, Sabine ; Blecker, Christophe
Poster (2007, October 11)Detailed reference viewed: 14 (2 ULg)
Mechanism of reoxygenation after antiangiogenic therapy using SU5416 and its importance for guiding combined antitumor therapy
; ; et al
in Cancer Research (2006), 66(19), 9698704
Emerging preclinical studies support the concept of a transient "normalization" of tumor vasculature during the early stage of antiangiogenic treatment, with possible beneficial effects on associated ... [more ▼]
Emerging preclinical studies support the concept of a transient "normalization" of tumor vasculature during the early stage of antiangiogenic treatment, with possible beneficial effects on associated radiotherapy or chemotherapy. One key issue in this area of research is to determine whether this feature is common to all antiangiogenic drugs and whether the phenomenon occurs in all types of tumors. In the present study, we characterized the evolution of the tumor oxygenation (in transplantable liver tumor and FSAII tumor models) after administration of SU5416, an antagonist of the vascular endothelial growth factor receptor. SU5416 induced an early increase in tumor oxygenation [measured by electronic paramagnetic resonance (EPR)], which did not correlate with remodeling of the tumor vasculature (assessed by CD31 labeling using immunohistochemistry) or with tumor perfusion (measured by dynamic contrast enhanced-magnetic resonance imaging). Inhibition of mitochondrial respiration (measured by EPR) was responsible for this early reoxygenation. Consistent with these unique findings in the tumor microenvironment, we found that SU5416 potentiated tumor response to radiotherapy but not to chemotherapy. In addition to the fact that the characterization of the tumor oxygenation is essential to enable correct application of combined therapies, our results show that the long-term inhibition of oxygen consumption is a potential novel target in this class of compounds. [less ▲]Detailed reference viewed: 42 (9 ULg)
Mechanism of resistance to anti-angiogenic therapy.
Cimino, Jonathan ; Sounni, Nor Eddine ; Debois, Delphine et al
Poster (2013, May 17)Detailed reference viewed: 9 (1 ULg)
Mechanism of Single-Electron Capture by the Dichlorocarbene Dication.
Leyh, Bernard ;
in Journal of the American Society for Mass Spectrometry (1996), 7
The single-electron capture (SEC) by dichlorocarbene with eight different atomic and molecular target gases, (CCl2)2++G->(CCl2)++G+, has been studied by product ion spectroscopy and ion kinetic energy ... [more ▼]
The single-electron capture (SEC) by dichlorocarbene with eight different atomic and molecular target gases, (CCl2)2++G->(CCl2)++G+, has been studied by product ion spectroscopy and ion kinetic energy spectroscopy. The experimental data have been interpreted in the framework of a theoretical model that describes the charge exchange process. Exothermic charge exchange is handled within the Landau-Zener model, whereas endothermic charge exchange is described by the Demkov model. The calculated data reproduce qualitatively the essential features of the experimental results: (1) the appearance of a reaction window centered at an exothermicity in the 4-4.5 eV range, (2) the lower SEC cross sections for endothermic charge exchange, (3) the wider internal energy distributions obtained for CCl2+ in the endothermic regime than in the exothermic one, which results in larger dissociation yields, (4) the excitation of molecular targets that accompany their ionization in the SEC process, and (5) the kinetic energy released on the CCl++Cl fragments in dissociative SEC. [less ▲]Detailed reference viewed: 8 (0 ULg)
Mechanism of sound production in Oreochromis niloticus
; ; et al
Poster (2007)Detailed reference viewed: 19 (1 ULg)
Mechanism of sound production in Oreochromis niloticus
; ; et al
Poster (2008)Detailed reference viewed: 8 (1 ULg)
Mechanism of the exchanges catalysed by the oxoglutarate translocator of rat heart mitochondria. Kinetics of the exchange reactions between 2-oxoglutarate, malate and malonate.
Sluse, Francis ; ;
in European Journal of Biochemistry (1972), 25Detailed reference viewed: 6 (2 ULg)
Mechanism of the exchanges catalysed by the oxoglutarate translocator of rat-heart mitochondria. Kinetics of the external-product inhibition.
Sluse, Francis ; ;
in Archives Internationales de Physiologie et de Biochimie (1973), 81Detailed reference viewed: 6 (1 ULg)
Mechanism of the medium-duration afterhyperpolarization in rat serotonergic neurons
Alix, Philippe ; ; et al
in European Journal of Neuroscience (2014), 39(2), 186-196
Most serotonergic neurons display a prominent medium-duration afterhyperpolarization (mAHP), which is mediated by small conductance Ca2+-activated K+ (SK) channels. Recent ex vivo and in vivo experiments ... [more ▼]
Most serotonergic neurons display a prominent medium-duration afterhyperpolarization (mAHP), which is mediated by small conductance Ca2+-activated K+ (SK) channels. Recent ex vivo and in vivo experiments have suggested that SK channel blockade increases the firing rate and/or bursting in these neurons. The purpose of this study was therefore to characterize the source of Ca2+ which activates the mAHP channels in serotonergic neurons. In voltage clamp experiments, an outward current was recorded at -60 mV after a depolarizing pulse to + 100 mV. A supra-maximal concentration of the SK channel blockers apamin or (-)- bicuculline methiodide blocked this outward current. This current was also sensitive to the broad Ca2+ channel blocker Co2+ and was partially blocked by both ω-conotoxin and mibefradil, which are blockers of N-type and T-type Ca2+ channels, respectively. Neither blockers of other voltage-gated Ca2+ channels nor DBHQ, an inhibitor of Ca2+-induced Ca2+ release, had any effect on the SK current. [less ▲]Detailed reference viewed: 100 (22 ULg)
Mechanism 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 ;
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 ▲]Detailed reference viewed: 25 (1 ULg)
Mechanism of Trypanosoma brucei gambiense resistance to human serum.
; ; 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 ▲]Detailed reference viewed: 65 (7 ULg)
Mechanisms and factors of the Quaternary drainage system evolution in the Ardennes: new perspectives from 10Be dating of fluvial terraces and knickpoint propagation modelling
Demoulin, Alain ; ; Beckers, Arnaud
Scientific conference (2013, December 03)Detailed reference viewed: 50 (7 ULg)
Mechanisms and Functional Significance of Stroke-Induced Neurogenesis
Marlier, Quentin ; ; Vandenbosch, Renaud et al
in Frontiers in Neuroscience (2015)Detailed reference viewed: 26 (11 ULg)
Mechanisms controlling the air-sea CO2 flux in the North Sea
; ; 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 ▲]Detailed reference viewed: 109 (1 ULg)
Mechanisms controlling the oxygen consumption in experimentally induced hypochloremic alkalosis in calves
Cambier, Carole ; ; Amory, Hélène 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 ▲]Detailed reference viewed: 89 (16 ULg)
Mechanisms for nonrecurrent genomic rearrangements associated with CMT1A or HNPP: rare CNVs as a cause for missing heritability.
; ; 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 ▲]Detailed reference viewed: 105 (2 ULg)