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121 results on '"Georges, P"'

2. Screening for cryptococcal antigenemia and meningeal cryptococcosis, genetic characterization of Cryptococcus neoformans in asymptomatic patients with advanced HIV disease in Kinshasa, Democratic Republic of Congo

Author

Zono, Bive Bive, Sacheli, Rosalie, Kasumba, Dacquin Muhandwa, Situakibanza, Hippolyte Nani-Tuma, Mavanga, Alphonse, Anyshayi, Justin Mwambi, Etondo, Mamie, Muwonga, Jérémie, Moutschen, Michel, Mvumbi, Georges Lelo, and Hayette, Marie-Pierre

Published
2024
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12. Mapping the habitat refugia of Isidella elongata under climate change and trawling impacts to preserve Vulnerable Marine Ecosystems in the Mediterranean

Author

Georges, Vincent, Vaz, Sandrine, Carbonara, Pierluigi, Fabri, Marie-Claire, Fanelli, Emanuela, Follesa, Maria Cristina, Garofalo, Germana, Gerovasileiou, Vasilis, Jadaud, Angélique, Maiorano, Porzia, Marin, Pilar, Mytilineou, Chryssi, Orejas, Covadonga, Del Mar Otero, Maria, Smith, Chris J., Thasitis, Ioannis, and Lauria, Valentina

Published
2024
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15. Genomic surveillance of SARS-CoV-2 reveals highest severity and mortality of delta over other variants: evidence from Cameroon

Author

Fokam, Joseph, Essomba, Rene Ghislain, Njouom, Richard, Okomo, Marie-Claire A., Eyangoh, Sara, Godwe, Celestin, Tegomoh, Bryan, Otshudiema, John O., Nwobegahay, Julius, Ndip, Lucy, Akenji, Blaise, Takou, Desire, Moctar, Mohamed M. M., Mbah, Cleophas Kahtita, Ndze, Valantine Ngum, Maidadi-Foudi, Martin, Kouanfack, Charles, Tonmeu, Sandrine, Ngono, Dorine, Nkengasong, John, Ndembi, Nicaise, Bissek, Anne-Cecile Z. K., Mouangue, Christian, Ndongo, Chanceline B., Epée, Emilienne, Mandeng, Nadia, Kamso Belinga, Sandrine, Ayouba, Ahidjo, Fernandez, Nicolas, Tongo, Marcel, Colizzi, Vittorio, Halle-Ekane, Gregory-Edie, Perno, Carlo-Federico, Ndjolo, Alexis, Ndongmo, Clement B., Shang, Judith, Esso, Linda, de-Tulio, Oliviera, Diagne, Moussa Moise, Boum, II, Yap, Mballa, Georges A. E., and Njock, Louis R.

Published
2023
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25. Non-Invasive Photoacoustic Imaging of In Vivo Mice with Erythrocyte Derived Optical Nanoparticles to Detect CAD/MI.

Author

Liu, Yonggang, Hanley, Taylor, Chen, Hao, Long, Steven R, Gambhir, Sanjiv S, Cheng, Zhen, Wu, Joseph C, Fakhri, Georges El, Anvari, Bahman, and Zaman, Raiyan T

Abstract

Coronary artery disease (CAD) causes mortality and morbidity worldwide. We used near-infrared erythrocyte-derived transducers (NETs), a contrast agent, in combination with a photoacoustic imaging system to identify the locations of atherosclerotic lesions and occlusion due to myocardial-infarction (MI). NETs (≈90 nm diameter) were fabricated from hemoglobin-depleted mice erythrocyte-ghosts and doped with Indocyanine Green (ICG). Ten weeks old male C57BL/6 mice (n = 9) underwent left anterior descending (LAD) coronary artery ligation to mimic vulnerable atherosclerotic plaques and their rupture leading to MI. 150 µL of NETs (20 µM ICG,) was IV injected via tail vein 1-hour prior to photoacoustic (PA) and fluorescence in vivo imaging by exciting NETs at 800 nm and 650 nm, respectively. These results were verified with histochemical analysis. We observed ≈256-fold higher PA signal from the accumulated NETs in the coronary artery above the ligation. Fluorescence signals were detected in LAD coronary, thymus, and liver. Similar signals were observed when the chest was cut open. Atherosclerotic lesions exhibited inflammatory cells. Liver demonstrated normal portal tract, with no parenchymal necrosis, inflammation, fibrosis, or other pathologic changes, suggesting biocompatibility of NETs. Non-invasively detecting atherosclerotic plaques and stenosis using NETs may lay a groundwork for future clinical detection and improving CAD risk assessment.

Published
2020

26. Temporal structure in spiking patterns of ganglion cells defines perceptual thresholds in rodents with subretinal prosthesis.

Author

Ho, Elton, Lorach, Henri, Goetz, Georges, Laszlo, Florian, Lei, Xin, Kamins, Theodore, Mariani, Jean-Charles, Sher, Alexander, and Palanker, Daniel

Subjects
Retinal Ganglion Cells, Animals, Rats, Electric Stimulation, Sensory Thresholds, Visual Perception, Contrast Sensitivity
Abstract

Subretinal prostheses are designed to restore sight in patients blinded by retinal degeneration using electrical stimulation of the inner retinal neurons. To relate retinal output to perception, we studied behavioral thresholds in blind rats with photovoltaic subretinal prostheses stimulated by full-field pulsed illumination at 20 Hz, and measured retinal ganglion cell (RGC) responses to similar stimuli ex-vivo. Behaviorally, rats exhibited startling response to changes in brightness, with an average contrast threshold of 12%, which could not be explained by changes in the average RGC spiking rate. However, RGCs exhibited millisecond-scale variations in spike timing, even when the average rate did not change significantly. At 12% temporal contrast, changes in firing patterns of prosthetic response were as significant as with 2.3% contrast steps in visible light stimulation of healthy retinas. This suggests that millisecond-scale changes in spiking patterns define perceptual thresholds of prosthetic vision. Response to the last pulse in the stimulation burst lasted longer than the steady-state response during the burst. This may be interpreted as an excitatory OFF response to prosthetic stimulation, and can explain behavioral response to decrease in illumination. Contrast enhancement of images prior to delivery to subretinal prosthesis can partially compensate for reduced contrast sensitivity of prosthetic vision.

Published
2018

43. Endothelial Hey2 deletion reduces endothelial-to-mesenchymal transition and mitigates radiation proctitis in mice.

Author

Mintet, Elodie, Lavigne, Jérémy, Paget, Vincent, Tarlet, Georges, Buard, Valérie, Guipaud, Olivier, Sabourin, Jean-Christophe, Iruela-Arispe, Maria-Luisa, Milliat, Fabien, and François, Agnès

Subjects
Cells, Cultured, Animals, Humans, Mice, Proctitis, Radiation Injuries, Repressor Proteins, Fluorescent Antibody Technique, Immunohistochemistry, Gene Deletion, Phenotype, Basic Helix-Loop-Helix Transcription Factors, Epithelial-Mesenchymal Transition, Human Umbilical Vein Endothelial Cells, Transcriptome, Biomarkers, Stem Cell Research, Prevention, Digestive Diseases, 2.1 Biological and endogenous factors, Biochemistry and Cell Biology, Other Physical Sciences
Abstract

The current study evaluated the role of Hey2 transcription factor in radiation-induced endothelial-to-mesenchymal transition (EndoMT) and its impact on radiation-induced tissue damage in mice. Phenotypic modifications of irradiated, Hey2 siRNA- and Hey2 vector plasmid-transfected human umbilical vein endothelial cells (HUVECs) resembling EndoMT were monitored by qPCR, immunocytochemistry and western blots. Subsequently, in mice, a Cre-LoxP strategy for inactivation of Hey2 specifically in the endothelium was used to study the biological consequences. Total body irradiation and radiation proctitis were monitored to investigate the impact of conditional Hey2 deletion on intestinal stem cells and microvascular compartment radiosensitivity, EndoMT and rectal damage severity. We found that EndoMT occurs in irradiated HUVECs with concomitant Hey2 mRNA and protein increase. While Hey2 silencing has no effect on radiation-induced EndoMT in vitro, Hey2 overexpression is sufficient to induce phenotypic conversion of endothelial cells. In mice, the conditional deletion of Hey2 reduces EndoMT frequency and the severity of rectal tissue damage. Our data indicate that the reduction in mucosal damage occurs through decline in stem/clonogenic epithelial cell loss mediated by microvascular protection. EndoMT is involved in radiation proctitis and this study demonstrates that a strategy based on the reduction of EndoMT mitigates intestinal tissue damage.

Published
2017

44. Ancient DNA reveals selection acting on genes associated with hypoxia response in pre-Columbian Peruvian Highlanders in the last 8500 years.

Author

Fehren-Schmitz, Lars and Georges, Lea

Subjects
Humans, Acclimatization, Evolution, Molecular, Genetic Drift, Genotype, Archaeology, Peru, Nitric Oxide Synthase Type III, Selection, Genetic, Hypoxia-Inducible Factor-Proline Dioxygenases, Hypoxia, DNA, Ancient, Evolution, Molecular, Selection, Genetic, DNA, Ancient, Genetics, Biochemistry and Cell Biology, Other Physical Sciences
Abstract

Archaeological evidence shows that humans began living in the high altitude Andes approximately 12,000 years ago. Andean highlanders are known to have developed the most complex societies of pre-Columbian South America despite challenges to their health and reproductive success resulting from chronic exposure to hypoxia. While the physiological adaptations to this environmental stressor are well studied in contemporary Andean highlanders, the molecular evolutionary processes associated with such adaptations remain unclear. We aim to better understand how humans managed to demographically establish in this harsh environment by addressing a central question: did exposure to hypoxia drive adaptation via natural selection within Andean populations or did an existing phenotype--characterized by reduced susceptibility to hypoxic stress--enable human settlement of the Andes? We genotyped three variable loci within the NOS3 and EGLN1 genes previously associated with adaptation to high altitude in 150 ancient human DNA samples from Peruvian high altitude and coastal low altitude sites in a time frame between ~8500-560 BP. We compare the data of 109 successful samples to forward simulations of genetic drift with natural selection and find that selection, rather than drift, explains the gradual frequency changes observed in the highland populations for two of the three SNPs.

Published
2016

45. In vivo evidence for an endothelium-dependent mechanism in radiation-induced normal tissue injury.

Author

Rannou, Emilie, François, Agnès, Toullec, Aurore, Guipaud, Olivier, Buard, Valérie, Tarlet, Georges, Mintet, Elodie, Jaillet, Cyprien, Iruela-Arispe, Maria Luisa, Benderitter, Marc, Sabourin, Jean-Christophe, and Milliat, Fabien

Subjects
Intestines, Intestinal Mucosa, Endothelium, Animals, Mice, Knockout, Mice, Radiation Injuries, Experimental, Cell Survival, Gene Expression Regulation, Gamma Rays, Serpin E2
Abstract

The pathophysiological mechanism involved in side effects of radiation therapy, and especially the role of the endothelium remains unclear. Previous results showed that plasminogen activator inhibitor-type 1 (PAI-1) contributes to radiation-induced intestinal injury and suggested that this role could be driven by an endothelium-dependent mechanism. We investigated whether endothelial-specific PAI-1 deletion could affect radiation-induced intestinal injury. We created a mouse model with a specific deletion of PAI-1 in the endothelium (PAI-1KO(endo)) by a Cre-LoxP system. In a model of radiation enteropathy, survival and intestinal radiation injury were followed as well as intestinal gene transcriptional profile and inflammatory cells intestinal infiltration. Irradiated PAI-1KO(endo) mice exhibited increased survival, reduced acute enteritis severity and attenuated late fibrosis compared with irradiated PAI-1(flx/flx) mice. Double E-cadherin/TUNEL labeling confirmed a reduced epithelial cell apoptosis in irradiated PAI-1KO(endo). High-throughput gene expression combined with bioinformatic analyses revealed a putative involvement of macrophages. We observed a decrease in CD68(+)cells in irradiated intestinal tissues from PAI-1KO(endo) mice as well as modifications associated with M1/M2 polarization. This work shows that PAI-1 plays a role in radiation-induced intestinal injury by an endothelium-dependent mechanism and demonstrates in vivo that the endothelium is directly involved in the progression of radiation-induced enteritis.

Published
2015

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