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Thomas Geeraerts

Publications and source records attributed to Thomas Geeraerts.

9 recordsLinked to original sources
PubMed2006

Effects of SDF-1alpha and gp120IIIB on apoptotic pathways in SK-N-SH neuroblastoma cells.

CXCR4, a chemokine receptor constitutively expressed in the brain, binds both ligands, the chemokine SDF-1alpha and the HIV envelope glycoprotein gp120(IIIB). There seem to be intracellular differences between the neuronal apoptosis induced by SDF-1alpha and that induced by gp120(IIIB), but the apoptotic pathways involved have not been compared in human neuronal cells. In this study, we characterized the apoptotic intracellular pathways activated by neurotoxic concentrations of SDF-1alpha and gp120(IIIB) in human neuroblastoma cells SK-N-SH. SDF-1alpha (10 nM) and gp120(IIIB) (2 nM) induced similar levels of apoptosis after 24 h of incubation (49 +/- 4% and 48 +/- 3%, respectively, of the neurons were apoptotic). SDF1alpha-induced apoptosis was completely abolished by the inhibition of Src phosphorylation by PP2. Exposure to SDF-1alpha (10 nM) triggered an increase in Src phosphorylation, with a maximum after 20 min of incubation (1.80 +/- 0.24 times higher than control, P = 0.01). NMDA calcium flux was enhanced only if cells were incubated with SDF-1alpha for 20 min before applying NMDA. By contrast, gp120(IIIB)-induced apoptosis was not affected by the inhibition of Src phosphorylation. Moreover, gp120(IIIB) enhanced NMDA calcium flux immediately, without modifying Src phosphorylation status. Finally, levels of phospho-JNK increased following exposure to gp120(IIIB) (by a factor of 1.46 +/- 0.4 at 120 min, P = 0.03), but not after exposure to SDF-1alpha. Thus, SDF-1alpha and gp120(IIIB) induced a similar level of neuronal apoptosis, but by activating different intracellular pathways. SDF-1alpha enhanced NMDA activity indirectly via Src phosphorylation, whereas gp120(IIIB) probably activated the NMDA receptor directly and phosphorylated JNK.

Apoptosis↗
PubMed2006

Cardiac output measurement during infrarenal aortic surgery: echo-esophageal Doppler versus thermodilution catheter.

OBJECTIVE: Aortic surgery is associated with various hemodynamic and cardiac output modifications. These disorders may be partly caused by blood flow redistribution between supra-aortic and descending aorta regions during clamping and unclamping. A new echo-esophageal Doppler (Hemosonic 100; Arrow, Reading, PA) calculates cardiac output from a simultaneous measurement of blood flow velocity and diameter of the descending aorta. This calculation may be affected by blood redistribution during aortic clamping. The aim of this study was to compare cardiac output measured by echo-esophageal Doppler and by bolus thermodilution catheter during infrarenal aortic surgery. DESIGN: Prospective, observational study. SETTING: University hospital, single institution. PARTICIPANTS: Twenty-two adult patients. INTERVENTIONS: Infrarenal aortic surgery. MEASUREMENTS AND MAIN RESULTS: Cardiac outputs monitored by both devices were highly correlated during the whole surgical procedure (r2 ranging from 0.54 to 0.76). Bland and Altman analysis showed absence of significant bias before and after clamping (ranging from 0.1 +/- 0.73 L/min to 0.18 +/- 1 L/min, p > 0.05) and a significant bias of 0.5 +/- 1.05 L/min (p < 0.05) during aortic clamping. Limits of agreement did not differ significantly during the whole surgical procedure (ranging from -1.36/2.19 to -2.23/2.49). During clamping and unclamping, changes in cardiac output obtained by both methods were positively correlated (r2 = 0.7). CONCLUSIONS: Bias between both methods was clinically acceptable, and limits of agreement were not significantly modified by aortic clamping. However, larger studies including homogenous aortic pathologies are necessary to validate this method during infrarenal aortic surgery.

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PubMed2006

Changes in cerebral energy metabolites induced by impact-acceleration brain trauma and hypoxic-hypotensive injury in rats.

The aim of this study was to describe, in rats, brain energy metabolites changes after different levels of head trauma (T) complicated by hypoxia-hypotension (HH). Male Sprague Dawley rats (n = 7 per groups) were subjected to T by impact-acceleration with 450-g weight drop from 1.50 or 1.80 m (T 1.50 or T 1.80), or to a 15-min period of HH (controlled hemorrhage to mean arterial pressure [MAP] of 40 mm Hg, and mechanical ventilation with N(2) 90%/O(2) 10%), or to their association (T followed by HH). Invasive MAP, intraparenchymental intracranial pressure (ICP), and cerebral blood flow (CBF using Laser Doppler flowmetry) were recorded during the 5 post-traumatic hours. Cerebral microdialysis was used to measure each hour interstitial brain glucose, lactate, pyruvate, and glutamate. For the entire period, the levels of cerebral glucose, pyruvate, and glutamate were not statistically different between groups. In addition, there were no differences associated with the lactate-glucose ratio. Lactate was significantly higher overtime only in T 1.80 + HH group (p < 0.001 vs. every other groups). The lactate-pyruvate ratio increased with trauma level, and was significantly different vs. sham for the entire study period in T 1.50 + HH, in T 1.80, and in T 1.80 + HH. There was no correlation between CBF variations and the lactate-pyruvate ratio (r(2) = 0.00001). The cerebral perfusion pressure was greater than 70 mm Hg in all groups. The prolonged post-traumatic impairment in brain energy metabolism may be related to traumatic brain injury (TBI) severity. It became worse when T was complicated by HH, but was not related to changes in CBF.

Animals↗
PubMed2004

Decrease in left ventricular ejection time on digital arterial waveform during simulated hypovolemia in normal humans.

BACKGROUND: Left ventricular ejection time (LVET) measured in central arteries is modified during hypovolemia. We compared modifications of the pulse wave in a central artery (carotid) and in a peripheral artery (digital) during central hypovolemia induced by lower body negative pressure (LBNP) in conscious volunteers. METHODS: Hypovolemia was simulated with progressive LBNP (baseline, -10, -20, and -30 mm Hg) in nine young healthy volunteers. The carotid arterial pressure waveform was recorded using a Millar tonometric method. The digital pulse wave was measured with a volume-clamp method (Finapres) and the stroke volume with a thoracic impedance method (Biomed). RESULTS: Mean arterial pressure did not change during LBNP. Compared with baseline values, heart rate increased significantly at the -30 mm Hg level (68 +/- 13 beats/min vs. 59 +/- 11 beats/min), and stroke volume decreased as soon as -10 mm Hg was achieved (113 +/- 41 mL vs. 127 +/- 35 mL). Both carotid and digital LVET decreased significantly at the -10 mm Hg level (337 +/- 26 and 339 +/- 24 ms vs. 360 +/- 35 and 361 +/- 24 ms, respectively). CONCLUSION: Peripheral LVET could reflect variation of central LVET during LBNP and be a reliable noninvasive parameter for monitoring hypovolemia.

Adult↗
PubMed2004

Fractalkine reduces N-methyl-d-aspartate-induced calcium flux and apoptosis in human neurons through extracellular signal-regulated kinase activation.

Our purpose was to investigate in human neurons the neuroprotective pathways induced by Fractalkine (FKN) against glutamate receptor-induced excitotoxicity. CX(3)CR1 and FKN are expressed constitutively in the tested human embryonic primary neurons and SK-N-SH, a human neuroblastoma cell line. Microfluorometry assay demonstrated that CX(3)CR1 was functional in 44% of primary neurons and in 70% of SK-N-SH. Fractalkine induced ERK1/2 phosphorylation within 1 min and Akt phosphorylation after 10 min, and both phosphorylation decreased after 20 min. No p38 and SAPK/JNK activation was observed after FKN treatment. Application of FKN triggered a 53% reduction of the NMDA-induced neuronal calcium influx, which was insensitive to pertussis toxin and LY294002 an inhibitor of Akt pathway, but abolished by PD98059, an ERK1/2 pathway inhibitor. Moreover, FKN significantly reduced neuronal NMDA-induced apoptosis, which was pertussis toxin insensitive and abolished in presence of PD98059 and LY294002. In conclusion, FKN protected human neurons from NMDA-mediated excitotoxicity in at least two ways with different kinetics: (i) an early ERK1/2 activation which reduced NMDA-mediated calcium flux; and (ii), a late Akt activation associated with the previously induced ERK1/2 activation.

Apoptosis↗
PubMed2004

Aspirin withdrawal and acute lower limb ischemia.

Aspirin is used mainly to prevent arterial events in patients with arteriopathy. Myocardial infarction and cerebrovascular events have been described after recent aspirin withdrawal. Experimental data suggest rebound platelet activity after aspirin discontinuation. Among a retrospective cohort of 181 patients admitted for acute lower limb ischemia for 4 yr, we studied 11 patients who had recently stopped taking aspirin. Aspirin was administered for vascular event prevention. The median duration of aspirin treatment without vascular events was 12 mo (range, 6-60 mo). The median time between aspirin withdrawal and lower limb ischemia was 23 days (range, 7-60 days). Four of the 11 patients stopped aspirin before a surgical procedure, without any substitution. In five patients, a recent diagnosis of neoplasia was observed. This study should alert clinicians to the risk of discontinuing chronic aspirin therapy in patients with severe peripheral vascular disease.

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