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White P. Lewis Alanio Alexandre Cruciani Mario Gorton Rebecca Millon Laurence Rickerts Volker Barnes Rosemary A. Donnelly J. Peter Loeffler Juergen 《Current fungal infection reports》2020,14(1):76-88
Current Fungal Infection Reports - This review has incorporated the knowledge and experience of the leads of each of the laboratory working parties of the fungal PCR initiative in order to provide... 相似文献
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Laurence Cousseau Martijn Hammers Dries Van de Loock Beate Apfelbeck Mwangi Githiru Erik Matthysen Luc Lens 《Proceedings. Biological sciences / The Royal Society》2020,287(1941)
It remains poorly understood how effects of anthropogenic activity, such as large-scale habitat fragmentation, impact sociality in animals. In cooperatively breeding species, groups are mostly formed through delayed offspring dispersal, and habitat fragmentation can affect this process in two opposite directions. Increased habitat isolation may increase dispersal costs, promoting delayed dispersal. Alternatively, reduced patch size and quality may decrease benefits of philopatry, promoting dispersal. Here, we test both predictions in a cooperatively breeding bird (placid greenbul, Phyllastrephus placidus) from an Afrotropical cloud forest archipelago. Males born in fragmented forest dispersed about 1 year earlier than those born in continuous forest. Contrary to females, males also started to reproduce earlier and mostly settled within their natal patch. Females only rarely delayed their dispersal for more than 1 year, both in fragmented and continuous forests. Our results suggest that early male dispersal and reproduction is jointly driven by a decrease in the value of the natal territory and an increase in local breeding opportunities in fragmented forest. While plasticity in dispersal strategies of cooperative breeders in response to anthropogenic change is believed to optimize reproduction-survival trade-offs, to what extent it shapes the ability of species to respond to rapid environmental change remains to be studied. 相似文献
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Sylvie Pochet Laurence Dugué Monica Sala Valérie Pézo Simon Wain-Hobson 《Nucleosides, nucleotides & nucleic acids》2013,32(7-9):1749-1752
Abstract The use of 5′-triphosphate of 1-(2-deoxy-β-D-ribofuranosyl)imidazole-4-carboxamide (dYTP) in DNA amplification reaction in place of dATP or dGTP yielded mutations frequencies of 3–4×10?2 per base per amplification. A reasonable proportion of transversions (11–15%) was observed in the absence of deletions and insertions. 相似文献
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France Bruck Ludovic Belle Chantal Lechanteur Laurence de Leval Muriel Hannon Sophie Dubois Emilie Castermans Stephanie Humblet-Baron Souad Rahmouni Yves Beguin Alexandra Briquet Frédéric Baron 《Cytotherapy》2013,15(3):267-279
Background aimsGraft-versus-host disease (GVHD) is a life-threatening complication of allogeneic hematopoietic cell transplantation caused by donor T cells reacting against host tissues. Previous studies have suggested that mesenchymal stromal cells (MSCs) could exert potent immunosuppressive effects.MethodsThe ability of human bone marrow derived MSCs to prevent xenogeneic GVHD in non-obese diabetic/severe combined immunodeficient (NOD/SCID) mice and in NOD/SCID/interleukin-2Rγ(null) (NSG) mice transplanted with human peripheral blood mononuclear cells (PBMCs) was assessed.ResultsInjection of 200 × 106 human PBMCs intraperitoneally (IP) into sub-lethally (3.0 Gy) irradiated NOD/SCID mice also given anti-asialo GM1 antibodies IP 1 day prior and 8 days after transplantation induced lethal xenogeneic GVHD in all tested mice. Co-injection of 2 × 106 MSCs IP on day 0 did not prevent lethal xenogeneic GVHD induced by injection of human PBMCs. Similarly, injection of 30 × 106 human PBMCs IP into sub-lethally (2.5 Gy) irradiated NSG mice induced a lethal xenogeneic GVHD in all tested mice. Injection of 3 × 106 MSCs IP on days 0, 7, 14 and 21 did not prevent lethal xenogeneic GVHD induced by injection of human PBMCs.ConclusionsInjection of MSCs did not prevent xenogeneic GVHD in these two humanized mice models. 相似文献
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Jérémy Ferrier Mathilde Bayet-Robert Bruno Pereira Laurence Daulhac Alain Eschalier Denis Pezet Jacques-Philippe Moulinoux David Balayssac 《PloS one》2013,8(10)
Background
Oxaliplatin is an anticancer drug used for the treatment of advanced colorectal cancer, but it can also cause painful peripheral neuropathies. The pathophysiology of these neuropathies has not been yet fully elucidated, but may involve spinal N-methyl-D-aspartate (NMDA) receptors, particularly the NR2B subunit. As polyamines are positive modulators of NMDA-NR2B receptors and mainly originate from dietary intake, the modulation of polyamines intake could represent an interesting way to prevent/modulate neuropathic pain symptoms by opposing glutamate neurotransmission.Methods
The effect of a polyamine deficient diet was investigated in an animal model of oxaliplatin-induced acute pain hypersensitivity using behavioral tests (mechanical and cold hypersensitivity). The involvement of spinal glutamate neurotransmission was monitored by using a proton nuclear magnetic resonance spectroscopy based metabolomic approach and by assessing the expression and phosphorylation of the NR2B subunit of the NMDA receptor.Results
A 7-day polyamine deficient diet totally prevented oxaliplatin-induced acute cold hypersensitivity and mechanical allodynia. Oxaliplatin-induced pain hypersensitivity was not associated with an increase in NR2B subunit expression or phosphorylation, but with an increase of glutamate level in the spinal dorsal horn which was completely prevented by a polyamine deficient diet. As a validation that the oxaliplatin-induced hypersensitivity could be due to an increased activity of the spinal glutamate system, an intrathecal administration of the specific NR2B antagonist, ifenprodil, totally reversed oxaliplatin-induced mechanical and cold hypersensitivity.Conclusion
A polyamine deficient diet could represent a promising and valuable nutritional therapy to prevent oxaliplatin-induced acute pain hypersensitivity. 相似文献99.
Agathe Hess Lianchun Yu Isabelle Klein Marine De Mazancourt Gilles Jebrak Hervé Mal Olivier Brugière Michel Fournier Maurice Courbage Gaelle Dauriat Elisabeth Schouman-Clayes Christine Clerici Laurence Mangin 《PloS one》2013,8(10)
Breathing is maintained and controlled by a network of automatic neurons in the brainstem that generate respiratory rhythm and receive regulatory inputs. Breathing complexity therefore arises from respiratory central pattern generators modulated by peripheral and supra-spinal inputs. Very little is known on the brainstem neural substrates underlying breathing complexity in humans. We used both experimental and theoretical approaches to decipher these mechanisms in healthy humans and patients with chronic obstructive pulmonary disease (COPD). COPD is the most frequent chronic lung disease in the general population mainly due to tobacco smoke. In patients, airflow obstruction associated with hyperinflation and respiratory muscles weakness are key factors contributing to load-capacity imbalance and hence increased respiratory drive. Unexpectedly, we found that the patients breathed with a higher level of complexity during inspiration and expiration than controls. Using functional magnetic resonance imaging (fMRI), we scanned the brain of the participants to analyze the activity of two small regions involved in respiratory rhythmogenesis, the rostral ventro-lateral (VL) medulla (pre-Bötzinger complex) and the caudal VL pons (parafacial group). fMRI revealed in controls higher activity of the VL medulla suggesting active inspiration, while in patients higher activity of the VL pons suggesting active expiration. COPD patients reactivate the parafacial to sustain ventilation. These findings may be involved in the onset of respiratory failure when the neural network becomes overwhelmed by respiratory overload We show that central neural activity correlates with airflow complexity in healthy subjects and COPD patients, at rest and during inspiratory loading. We finally used a theoretical approach of respiratory rhythmogenesis that reproduces the kernel activity of neurons involved in the automatic breathing. The model reveals how a chaotic activity in neurons can contribute to chaos in airflow and reproduces key experimental fMRI findings. 相似文献
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