Paris Descartes University - Sorbonne Paris Cité , also known as "Paris V", is a public research university in Paris, France. It belongs to the leading academic alliance Sorbonne Paris Cité. It was established in order to succeed the medicine department of the world's second oldest academic institution, the University of Paris , shortly before the latter officially ceased to exist on December 31, 1970, as a consequence of the French cultural revolution of 1968, often referred to as "the French May". It is one of the best and the most prestigious French universities, mainly in the areas of medical science, biomedical science, law, computer science, economics and psychology.Headquartered in the historic École de Chirurgie in the 6th arrondissement of Paris, the university strongly focuses on medical science , biomedical science , social science , mathematics, computer science and law .A major pole of research and learning, Paris Descartes - Sorbonne Paris Cité is one of the most prestigious universities in France and the best one in its main domains. On that basis among others, it was rated by the 2013 QS World University Ranking 51-100th in Pharmacy and Pharmacology , 101-150th in Biological science , 100th in Medicine , 151-200th in Psychology , 151-200th in Linguistics , and 151-200th in Law .The University Paris Descartes supports a modern approach of social science on the basis of fieldwork, participant observation and ethnography . The dual master's degree in partnership with other important French academic institutions such as the École Normale Supérieure emphasizes opportunities offered as far as research is concerned.Faculty members have included eminent jurists, doctors and politicians. Wikipedia.
Institute Curie, French National Center for Scientific Research, French Institute of Health, Medical Research, Assistance Publique Hopitaux De Paris and University of Paris Descartes | Date: 2016-07-29
A composition that can be used as a vaccine containing means for targeting at least one antigen to dendritic cells and as adjuvants a granulocyte macrophage colony stimulating factor and a CpG oligodeoxynucleotide and/or a CpG-like oligodeoxynucleotide. This composition can used to treat cancers, infectious diseases caused by bacterial, viral, fungal, parasitic or protozoan infections, allergies and/or autoimmune diseases.
French Institute of Health, Medical Research, French National Center for Scientific Research, Genethon, University of Paris Descartes, École Nationale Supérieure de Chimie de Paris, University of Évry Val d'Essonne and Assistance Publique Hopitaux De Paris | Date: 2016-09-16
The present invention relates to a method for treating a Leber congenital amaurosis in a patient harbouring the mutation c.2991+1655 A>G in the CEP290 gene, comprising the step of administering to said patient at least one antisense oligonucleotide complementary to nucleic acid sequence that is necessary for preventing splicing of the cryptic exon inserted into the mutant c.2291+1655 A>G CEP290 mRNA
French Institute of Health, Medical Research, University of Paris Descartes, Fondation Imagine, Assistance Publique Hopitaux De Paris Aphp, French National Center for Scientific Research, University Grenoble Alpes, French Atomic Energy Commission and University of Burgundy | Date: 2015-02-18
The present invention relates to methods and pharmaceutical compositions for the treatment of diseases mediated by the NRP-1/OBR complex signaling pathway. In particular, the present invention relates to a method for treating a disease selected from the group consisting of cancers, obesity and obesity related diseases, anorexia, autoimmune diseases and infectious diseases in a subject in need thereof comprising administering the subject with a therapeutically effective amount of an antagonist of the NRP-1/OBR signaling pathway.
French Institute of Health, Medical Research, University of Paris Descartes and Assistance Publique Hopitaux De Paris Aphp | Date: 2015-04-29
The present invention relates to methods and pharmaceutical compositions for treating vaso-occlusive crises. In particular, the present invention relates to a method of treating a vaso-occlusive crisis in a subject in need thereof comprising administering to the subject a therapeutically effective amount of agent capable of degrading, destabilizing or depleting the blood-borne extracellular DNA from the blood of the subject.
Institute Pasteur Paris, French National Center for Scientific Research, University of Paris Descartes and Assistance Publique Hopitaux De Paris | Date: 2016-10-12
The present invention relates to polynucleotides enabling the rapid, simple and specific detection of Group B Streptococcus highly-virulent ST-17 clones. The present invention also relates to the polypeptides encoded by said polynucleotides, as well as to antibodies directed or raised against said polypeptides. The present invention also relates to kits and methods for the specific detection of Group B Streptococcus highly-virulent ST-17 clones, using the polynucleotides, the polypeptides or the antibodies according to the invention.
Institute Curie and University of Paris Descartes | Date: 2015-04-21
An in vitro method for determining whether a patient has, or is at risk of having or developing an autoimmune disease or for assessing the severity or predicting the outcome of an autoimmune disease, comprising a step of detecting or quantifying in a biological sample obtained from said patient an immune anti-IL2 response, peptides specifically recognised by anti-IL2 antibodies or IL-2-specific T cells of T1D, systemic lupus erythematosus, rheumatoid arthritis, Sjgrens syndrome and autoimmune polymyositis patients, and pharmaceutical compositions.
Institute Pasteur Paris and University of Paris Descartes | Date: 2017-01-11
The application relates to Listerin monocytogenes, more particularly to the determination of the clone to which a L. monocytogenes isolate belongs. The means of the application involve primers and/or probes, more particularly multiplex primers. The means of the application are notably useful to assess the invasivity that said L. monocytogenes isolate might show in a human being.
News Article | May 3, 2017
A new genetic fingerprinting technique is the first to show the huge diversity of the malaria parasite, one of nature’s most persistent and successful human pathogens. The technique validates a previously untestable “strain hypothesis” that was proposed more than 20 years ago and opens up new ways of thinking about how to tackle this cunning killer. Key to that understanding is changing the way we think about malaria—that it is not so much like the measles and more like the flu. As reported in the Proceedings of the National Academy of Sciences, researchers collected blood samples from 641 children, aged 1 to 12 years from Bakoumba, a village in Gabon, West Africa and the genetic fingerprints of parasites from 200 infected children. Remarkably, every child was infected with malaria parasites that had a different fingerprint from the parasites in every other child. In 1994, Professors Sunetra Gupta and Karen Day, both then working at Imperial College London and later the University of Oxford, proposed that the malaria transmission system may be organized into a set of strains based on diversity of the genes that code for the surface coat of the parasite. If true, this strain diversity could explain why people can be re-infected with malaria many times over. It has taken until now for Day and colleagues to develop and optimize the mathematical and laboratory techniques to finally address the hypothesis. The malaria parasite is a single-celled microorganism (known as a Plasmodium) that infects red blood cells and is transferred from human to human via mosquitoes. It has been infecting people for tens of thousands of years, and, according to the World Health Organization, in 2015, nearly half of the world’s population remained at risk of malaria. Over the past 20 years, Day’s team has developed a way to genetically fingerprint malaria parasites from small amounts of blood based on what are called var genes. Every parasite has approximately 60 of these var genes but only uses one at a time and can switch between the one it uses. The genes encode proteins that coat the surface of the red blood cells that the parasite infects. The var genes are significant because they determine the ability of the parasite to disguise itself from the human immune system, and contribute to the virulence of the disease. If the genes that encode the surface coat overlap between two parasites, such as you would expect in siblings that would share a maximum of 50 percent of their genes, then when someone is re-infected, the immune system will recognize these malaria parasites and quickly purge them if they have seen the parent infections. But if there is little or no overlap in these genes, then the immune system won’t recognize the malaria parasite as readily, leading to chronic infection. The study shows that “the parasite has evolved this enormous diversity with limited overlap between the sets of var genes likely so it can keep re-infecting the same humans,” says Day, now a professor of population science and dean of science at the University of Melbourne. Coauthor Mercedes Pascual, an ecologist and professor at the University of Chicago, describes this as “the parasites forming niches by diversifying. They compete with each other for hosts, and distance themselves from each other to invade the same population of humans, a limited resource.” Current malaria control programs don’t target the diversity of the parasite, Day says. “With malaria, we attack something that is conserved between all strains, but the problem is if you don’t get rid of all of the malaria parasites with current strategies, you have this enormous diversity that can allow the system to bounce back quickly to pre-control levels. The resilience of the system is coming from the diversity, so you’ve got to monitor how approaches to control attack diversity and not just the parasite per se.” Interestingly, the theory of malaria control is based on malaria having no diversity and being like measles. You contract measles once and have lifelong immunity, whereas you can get malaria or the flu many times because there are multiple strains circulating. “Malaria is like flu, but our fingerprinting results show that it is way more complicated,” Day says. By analyzing the var genes, researchers came up with a unique identifier, or fingerprint, for each malaria strain that they call a var code. “Looking down the microscope you would have said all of the infections look the same, but when we did the fingerprinting genetically with this variant antigen gene system, we could see that every child had a different parasite fingerprint, and importantly, each fingerprint was highly unrelated to all other fingerprints,” Day says. This unrelatedness was a surprise, Day says. “Malaria has sex as part of its lifecycle, every time it goes through a mosquito. And so, because the malaria parasite mates you would expect to find related parasites that we might call parents, siblings, cousins, and aunts and uncles in the population.” “Even with very high levels of sex between parasites, their competition for available hosts can be so intense, that really only very unrelated parasites would be fit enough to survive and here we have a structure where highly related parasites were not detected,” says Yael Artzy-Randrup, a theoretical ecologist from the University of Amsterdam, and a coauthor of the study. “Malaria is similar to flu in that humans can be infected multiple times by different malaria parasite variants. However, in contrast to the flu, the situation with malaria is much more complex. With malaria, at any given point of time there is a high diversity of variants coexisting even in very small human populations, while in flu, variants usually replace each other, and people will only be infected by one variant at a time.” After waiting 20 years to get their results, the researchers suffered a setback in 2012 when Hurricane Sandy cut the power to Day’s laboratory at New York University, destroying samples that represented months of work. The team was eventually able to recover and continue its work. Once the team had assembled all the data, they had to assure their scientific peers—many of whom were skeptical of the strain hypothesis—that the pattern of diversity and unrelatedness they were seeing was not just through random chance. Researchers tested the results using statistical and computational techniques inspired by the analysis of complex systems in ecology, such as communities of species in ecosystems. They found that the system was non-random, and the relatives were absent from the population. The project is connected to a central question in ecology: what is the structure of diversity? “We are asking this question for the ensemble of parasites within a population of Plasmodium falciparum, but it can also be asked for the ensemble of tree species in a rainforest,” Pascual says. “It is an exciting time for bringing together quantitative analyses and deep sampling of biological systems in the field. “Our findings indicate that the enormous diversity of the parasite is structured and that we need to consider the implications of this structure for intervention, and possibly develop a different way to model transmission in malaria altogether.” Additional researchers from the University of Melbourne, the University of Chicago, New York University, the University of Michigan, the University of Amsterdam, the University of Montpellier, and the University of Paris Descartes are coauthors of the study.
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: SC1-PM-04-2016 | Award Amount: 9.99M | Year: 2017
Sudden cardiac arrest (SCA) causes ~20% of all deaths in Europe. SCA is lethal within minutes if left untreated and survival rates are presently only 5-20%. Therefore, there is a large medical need to improve SCA prevention and treatment. Designing effective individualized prevention and treatment strategies requires knowledge on genetic and environmental risk factors. So far, these efforts have been hampered by the lack of sufficiently large study cohorts of SCA patients with detailed information. Obtaining SCA patient samples is challenging as the condition happens suddenly and unexpectedly. In this project, leading European scientific teams which have created large relevant population cohorts, mostly dedicated to SCA research, join forces to fully exploit available data towards improving SCA management. This will be done by: - Building an unique and growing database of >100.000 (DNA) samples including >20.000 SCA patient samples, by combining existing European databases and infrastructures. - Identifying risk factors (inherited, acquired, environmental) and first-response treatment strategies that may explain the differences in SCA occurrence and survival between European countries - Collaborating with professional networks, such as the European Heart Rhythm Association, and European Resuscitation Council, to translate the outcomes into changes in clinical practice and influencing European health policies on SCA management.