#université paris cité

[floweringpear]

november 2024 — visiting the musée d'histoire de la médecine, université paris cité

[bpod-bpod]

Staunch Supporters

Bacterial toxins can compromise blood vessels' leakiness affecting blood pressure. This study reveals that blood vessel lining cells' membranes, under the control of proteins called caveolin-1 and cavin1, stiffen to regulate the leakiness via tunnels called transendothelial cell macroapertures

Read the published the research article here

Video from work by Camille Morel and colleagues

Institut Pasteur, Université Paris Cité, CNRS UMR6047, Inserm U1306, Unité des Toxines Bactériennes, Département de Microbiologie, Paris, France

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in eLife, March 2024

You can also follow BPoD on Instagram, Twitter and Facebook

[thatsonemorbidcorvid]

A healthy immune system defends the body against disease and infection. However, for one in 10 people, mostly women, the immune system malfunctions and attacks its own cells. This causes more than 80 types of autoimmune diseases, such as lupus, multiple sclerosis, and rheumatoid arthritis. The reason women may be more affected, according to a couple of recent studies, may be linked to a faulty mechanism that is supposed to shut down one of a woman’s two X-chromosomes.

One study from Stanford University shows that a molecule called Xist (pronounced ‘exist’), which turns off one copy of the X-chromosome in every cell in the female body, can trigger a rogue immune response. Another study from France, not yet peer-reviewed, shows that when certain genes on the silenced X-chromosome become active again, it can cause lupus-like symptoms in older mice.

Since most autoimmune diseases are diagnosed after puberty, more in girls than in boys, sex hormones were thought to be the primary driver of this difference. For example, four in five patients with autoimmune diseases are women. Ten times more women than men get lupus. And 20 times more women develop Sjögren's syndrome, an illness that mainly causes dry eyes and dry mouth.

“Our study shows that you do not need female sex hormones; you don't even need a second X-chromosome; just this Xist [molecule] could have a major role in developing some autoimmune diseases,” says Howard Chang, a dermatologist and molecular geneticist at Stanford University School of Medicine in California, who led the study.

“There is clear evidence now that the sex bias in autoimmune disease is not only linked to hormones but also to the presence of the number of X chromosomes and to the process of X chromosome inactivation,” says Claire Rougeulle, an epigeneticist who led the second study at the National Centre for Scientific Research (CNRS) in the Université Paris Cité in France.

That so many antibodies exist that target/destroy the molecules required to silence or shut-off the X-chromosome, “was not known at all,” says Jean-Charles Guéry, an immunologist at the Toulouse Institute for Infectious and Inflammatory Diseases (Infinity) in France.

Paradoxically, the increased risk of autoimmune disease in women may even be an evolutionary adaptation to protect the lives of their children. “Women have a better immune system to fight things,” says Johann Gudjonsson, a dermatologist at the University of Michigan, Ann Arbor.

Women tend to produce more antibodies than men, which protects both them and their babies through breastmilk, says Vanessa Kronzer, a Rheumatologist at the Mayo Clinic in Rochester, Minnesota.

Hormones are also involved. Female estrogen hormones boost immunity while male hormones not only suppress immunity but also protect against autoimmunity. These differences in sex hormones were thought to explain why women have more robust immunity, making them also more vulnerable to developing autoimmune diseases than men. But that may not be the only reason.

SILENCING ONE X CHROMOSOME

Each cell in a woman’s body has two X-chromosomes, one from the mother and one from the father. Men have an X-chromosome from their mother and a much smaller Y-chromosome from their father.

The Y-chromosome contains just about a hundred genes, but the X-chromosome contains more than 900.

To make sure the activity of genes located on the X-chromosome is equal in both men and women, one of the two X-chromosomes in every female cell randomly shuts down. This happens early in fetal development when the Xist molecule and its partner proteins coil around one of the X-chromosomes and switch it off. If both X-chromosomes remain equally active, the cell will die.

As a result, the female body contains a mosaic of cells in which either the mother’s or the father’s X-chromosome is silenced. This X-chromosome inactivation is the reason female Calico cats develop a patchwork of orange and brown fur. While some of their hairs express a black color from one active X-chromosome, others develop an orange color from the other.

However, X-chromosome inactivation is far from perfect, and 15 to 23 percent of genes remain active. One such gene that continues to function, when it should not, has been linked to lupus. More evidence comes from boys and men who are born with an extra X chromosome who also have an increased risk of developing autoimmune diseases, suggesting the critical role of the X chromosome.

XIST TRIGGERS AUTOANTIBODIES

Chang has been studying the Xist molecule for many years and in 2015 he discovered that many proteins working together with Xist were involved in autoimmune disorders and were attacked by rogue antibodies, called autoantibodies. Instead of fighting foreign invaders, such as germs, autoantibodies mistakenly target an individual’s own cells.

To test whether faulty X-chromosome inactivation was the reason more women suffer from autoimmune diseases than men, Chang’s team engineered male mice that produce the Xist molecule, which is usually only present in female cells.

However, Xist molecule alone did not cause the autoimmune disease in the engineered male mice.

Only when researchers injected an irritant into these genetically modified male mice did the levels of autoantibody rise and trigger a lupus-like disease. With the addition of the irritant, the autoantibody levels in Xist-producing males matched those in females and were higher than in normal males without Xist. These engineered mice also showed more extensive tissue damage and signs of heightened inflammation when exposed to the irritant.

That suggests that even with Xist, either a genetic susceptibility or an environmental trigger is needed to cause the female-biased autoimmune disease. The study hints that only when cells get damaged, either by an environmental trigger or due to genetic susceptibility, Xist molecules and its protein partners leak outside of the cell and cause the immune system to produce autoantibodies against the Xist-protein complex, which then initiates an autoimmune disease.

“So that's one major reason why, of course, most women do not get autoimmune disease,” says Chang. “Even though every woman is expressing Xist throughout their body.”

X-CHROMOSOME TIES TO LUPUS

Rougeulle collaborated with Céline Morey, a fellow epigeneticist in Paris, to understand what happens when the X-chromosome is not completely turned off.

They engineered female mice to display imperfect X-chromosome inactivation—in which most, but not all, the genes on the second X-chromosome were shut off. The researchers resorted to incomplete inactivation because blocking all Xist activity would keep both X-chromosomes fully functional and kill the mice. While French scientists weren’t expecting their mice to develop an autoimmune disease, they were surprised when engineered female mice showed symptoms of a lupus-like condition.

“You don't see the symptoms of autoimmune disease in these mice right away, but you begin to see it as they get older,” says Morey.

This supports Guéry’s 2018 study that showed that when a gene that promotes inflammation escapes inactivation in immune cells, it increases risk of developing lupus.

The common theme between the Stanford and French study is that both link the X-chromosome, and the process of X-chromosome inactivation, to autoimmunity, says Rougeulle.

Mechanisms linked with X-chromosome inactivation do seem to explain the sex differences in some autoimmune diseases such as lupus and Sjögren's, says Guéry. “[But] you cannot have a single mechanism for all autoimmune diseases.”

PREDICTING WHO MIGHT DEVELOP AN AUTOIMMUNE DISEASE

The Stanford study discovered that autoantibodies against many proteins associated with Xist are found in the blood of patients suffering from auto-immune diseases, such as lupus, scleroderma, or dermatomyositis.

While some autoantibodies were specific to certain autoimmune diseases, others were common among several. So, it might be possible to develop a panel of autoantibodies that could be used to distinguish between different disorders.

Rougeulle warns, however, that the current studies do not show whether the autoantibody levels rise significantly preceding the diseases, so more studies are needed before a diagnostic tool can be developed.

[scottsbifh]

Evening view of Paris.

Photo taken from above the Left Bank (possibly/probably from the Tour Zamansky of the Sorbonne Université). The bridge that is lit up in the center of the photo is the Pont Saint-Louis, which is a pedestrian bridge linking the Île de la Cité with the Île Saint Louis. Behind you can see the Hôtel de Ville and of course, the Basilique du Sacré-Cœur in the upper right corner.

posted to FB group World Beautiful Places & City's

[sante-enfants-environnement]

Pesticides et risques sanitaires pour les enfants, avec Xavier Coumoul (Inserm, Univ. Paris Cité)

Bonjour à tous, Voici une nouvelle vidéo publiée sur la Chaîne YouTube Santé des enfants et environnement, intitulée “Pesticides et risques sanitaires pour les enfants, avec Xavier Coumoul (Inserm, Univ. Paris Cité)”, ainsi que le podcast associé et quelques points clés de l’échange, selon moi.       Présentation de Xavier Coumoul (Inserm, Université Paris Cité) – échange sur risques sanitaires…

[theculturedmarxist]

Several years after the emergence of SARS-CoV-2, the virus that causes COVID-19, researchers still face plenty of unanswered questions. For example, we know COVID is associated with a variety of neurological symptoms, both short- and long-term, but it still isn’t entirely clear whether these cognitive issues are the result of the virus directly infecting brain cells or simply due to a broader systemic inflammatory response.

Studies looking at human brain tissue have yielded contradictory results. Some have found direct traces of SARS-CoV-2, while others report only inflammatory damage. Animal models certainly demonstrate it is possible for the virus to infect the brain, but human tissue samples are obviously taken after a patient dies, meaning researchers can only hypothesize what happens during an acute infection.

In a new study, led by scientists from Institut Pasteur and Université Paris Cité, an animal model was used to investigate several questions yet to be resolved. How could the SARS-CoV-2 virus enter the brain through the olfactory system? Are different SARS-CoV-2 variants more or less likely to enter the brain? And is losing one’s sense of smell directly linked to the virus entering the brain?

Using a hamster model, the research compared infection with the original SARS-CoV-2 virus from 2020 to several subsequent variants including Gamma, Delta and Omicron/BA.1 variants. Interestingly, the findings confirmed epidemiological observations showing acute disease severity is reduced in Omicron infections, however, all variants demonstrated similar neuroinvasive capabilities. And most strikingly, all variants infected the brain’s olfactory regions regardless of whether symptoms of anosmia (loss of sense of smell) were present or not.

"This suggests that anosmia and neuronal infection are two unrelated phenomena," says first author Guilherme Dias de Melo. "If we follow this line of reasoning, it is quite possible that even an asymptomatic – and therefore clinically benign – infection is characterized by the spread of the virus in the nervous system."

To study exactly how SARS-CoV-2 could infect brain cells the researchers utilized a modeling system called microfluidic cell culture. This allowed a close-up look at how the virus could move from neuron to neuron. The findings revealed the virus was able to travel between neurons via tiny projections between the cells called axons.

"The virus seems to effectively exploit the physiological mechanisms of the neuron to move in both directions,” explained Dias de Melo. “The SARS-CoV-2 variants we studied – the ancestral Wuhan variant, Gamma, Delta and Omicron/BA.1 – infect neurons in vitro and are capable of moving along axons."

The researchers conclude this suggests all SARS-CoV-2 variants have the capacity to infect the brain, via the olfactory pathway, regardless of clinical disease presentations. This means it is possible even mild infections can lead to the virus infiltrating the brain.

Hervé Bourhy, another author on the study, says future work will need to explore the relationship between acute SARS-CoV-2 brain infections and persistent symptoms seen in long COVID.

"The next step will be to understand, from the animal model, whether the virus is able to persist in the brain beyond the acute phase of infection, and whether the presence of the virus can induce persistent inflammation and the symptoms described in cases of long COVID, such as anxiety, depression and brain fog,” said Bourhy.

The new study was published in Nature Communications.

[lago-morpha]

Visual artist, May Murad was born in 1984 in Gaza, Palestine, She currently lives and works in Paris. After studying Fine Arts at Al-Aqsa University in Gaza, she graduated there in 2006. In December 2018, she arrived in France as a refugee and embarked on an artistic journey that began with a residence of several months at the Cité internationale des arts, with the support of the Welfare association. This first residency allowed her to pursue her work in France for a year with the Dufraine Foundation, owned by the Académie des Beaux-arts à Chars , from 2019 to 2020. In 2021, she returned to the Cité internationale des arts thanks to the support of the City of Paris for the preparation of her “Virtual Reality” exhibition. May Murad is also a member of the association "Artists in Exile". She is currently preparing a master's degree at the Sorbonne Nouvelle Université in geopolitics of art and culture, where she deals with contemporary Palestinian art in times of crisis. May carried on her artistic work paying special attention to the development of drawing and painting techniques. The aesthetic vision she has is inspired by her personal experiences as an artist who had lived in Gaza and today is settled in France; in exile. Her artistic experiences take her through the elaboration of various projects. We are witnessing a personal account about life in exile, an artist’s life experiencing an unfamiliar world and land of refuge that needs henceforth to be adapted to feel home. This artistic project is perfectly aligned with May’s vision that seeks to incorporate art in reality and ordinary life, it also has its fully coherent place in a continuum that reflects the creative research field the artist has been working on for a few years now and whom she entitled “Virtual Reality”.

May Murad - Je ne suis pas un robot, 2021

[linguistlist-blog]

Calls: SLE Workshop 2025: Isomorphism and Optionality in Language

SLE Workshop 2025: Isomorphism and Optionality in Language Convenors: Benoît Leclercq (Université de Lille) - benoit.leclercq@univ-lille.fr Cameron Morin (Université Paris Cité) - cameron.morin@u-paris.fr FULL WORKSHOP DESCRIPTION HERE: https://societaslinguistica.eu/sle2025/wp-content/uploads/sites/8/2024/12/Isomorphism-and-optionality-in-language_updated.pdf FULL DETAILS FOR ABSTRACT SUBMISSION: https://societaslinguistica.eu/sle2025/third-call-for-papers/ - deadline for abstract http://dlvr.it/THFdGK

[jobrxiv]

2 postdoc positions on Extracellular-Vesicle (EV) -Mitochondria (EM) uptake INSERM, Université Paris Cité See the full job description on jobRxiv: https://jobrxiv.org/job/inserm-universite-paris-cite-27778-2-postdoc-positions-on-extracelullar-vesicle-ev-mitochndria-em-in-par/?feed_id=90322 #ScienceJobs #hiring #research

[global-indian]

Exploring Université de Paris: A Hub for Academic Excellence

Université de Paris Ranking: A Global Leader in Education

Université de Paris, with its long-standing history of excellence, has earned a strong reputation in international rankings. The university consistently ranks among the top universities globally for its research, innovation, and academic programs. In recent years, Université Paris Cité has gained significant recognition, especially in areas such as medicine, science, and humanities, solidifying its position as one of Europe’s premier educational institutions.

According to Université de Paris Ranking, the university is not only highly regarded in France but also maintains a prominent spot in global university rankings. Its focus on interdisciplinary learning and cutting-edge research ensures that students graduate with a comprehensive and forward-thinking education.

Université Paris Cité Bachelor Programs: Shaping Future Leaders

For students looking to begin their academic journey, Université Paris Cité Bachelor programs offer a unique and enriching experience. With a variety of bachelor’s degrees available, students can choose from fields such as science, humanities, social sciences, and more. The university’s commitment to international collaboration, student exchange, and innovative teaching methods ensures that each student receives a well-rounded education, preparing them for the global workforce.

Whether pursuing a career in healthcare, business, or the arts, the Université Paris Cité Bachelor programs are designed to provide a solid academic foundation, research opportunities, and practical experience to ensure student success.

[shesaidwithirony]

Capitalocène plutôt qu'Anthropocène

📸 Yann Toma, Herbarum. Les rêves perdus de l’Arcadie.

On ne peut attribuer la crise environnementale actuelle à toute l'humanité considérée comme un seul bloc. Cela revient à naturaliser, « dés-historiciser » et dépolitiser un mode de production spécifique à un contexte socio-historique :

« Tenir pour responsable l'humanité toute entière du changement climatique c'est laisser le capitalisme s'en tirer à bon compte. (…) S'il est certain que tous les humains vont subir les conséquences du dérèglement climatique et de l’effondrement de la biodiversité (dans des proportions très différentes cependant), il est impossible au regard de l’histoire d’affirmer que tous les membres de l’humanité partagent le même degré de responsabilité dans ce désastre. Un Nord-Américain ne peut pas être aussi responsable des bouleversements du système Terre qu’un Kényan qui consomme en moyenne 30 fois moins de matières premières et d’énergie que lui. Il est difficile d'étudier les causes de la transition géologique sans prendre en compte la dimension politique de ce phénomène. À la différence de l'Anthropocène, la notion de Capitalocène pourrait permettre d'intégrer cette dimension politique dans l'analyse du dérèglement climatique. »

Victor Court — enseignant-chercheur en économie à l'IFP School, IFP Énergies nouvelles ; membre de la chaire « Énergie & Prospérité » et chercheur associé au Laboratoire Interdisciplinaire des Énergies de Demain (LIED, Université Paris Cité)

[actu-juridique]

Le droit parlementaire financier : état des lieux et pistes d’évolution

https://justifiable.fr/?p=2103 https://justifiable.fr/?p=2103 #des #dévolution #droit #État #financier #lieux #parlementaire #pistes Programme   Jeudi 5 Décembre   14h00 : Discours d’ouverture 14h20 : Introduction – Existe-t-il un droit parlementaire financier ?Mathieu Carpentier (Université Toulouse Capitole)   1. Sources historiques et juridiques du droit parlementaire financier Présidence : Fabrice Bin, Institut d’études politiques de Toulouse 14h30 : Histoire et évolution du droit parlementaire financier : aux sources de l’article 40Jerôme Henning, Université Toulouse Capitole 14h50 : Eugène Pierre et les finances publiquesXavier Cabannes, Université Paris Cité 15h10 : Les normes du droit parlementaire financierVincent Dussart, Université Toulouse Capitole 15h30 : Discussion 15h50 : Pause   2. Les acteurs Présidence : Fabrice Bin, Institut d’études politiques de Toulouse 16h00 : Les pouvoirs du gouvernement sont-ils trop importants ?Stéphane Mouton, Université Toulouse Capitole 16h20 : Les commissions des finances et des affaires sociales disposent-elles de prérogatives suffisantes ?Gilles Toulemonde, Université de Lille 16h40 : L’équilibre des forces au sein des commissions des finances et des affaires socialesJean-Pierre Camby, Université Versailles Saint-Quentin 17h00 : Les commissions des finances et la régulation budgétaireChristophe Pierucci, Université de Strasbourg 17h20 : L’information du Parlement, les annexes budgétaires et le principe de sincéritéJean-Luc Albert, Université Aix-Marseille 17h40 : Discussion 18h00 : Fin de la 1ère journée   Vendredi 6 Décembre   3. La procédure Présidence : Michel Lascombe, Institut d’études politiques de Lille 9h00 : Conventions, pratiques, précédentsAlain Laquièze, Université Paris Cité 9h20 : De l’Assemblée au Sénat, des pratiques différentes ?Audrey de Montis, Université de Rennes 9h40 : A quoi sert encore la commission mixte paritaire en matière financière ?Alain Pariente, Université de Bordeaux 10h00 : Le calendrier et les délaisBasile Ridard, Université de Poitiers 10h20 : Discussion 10h40 : Pause 11h00 : Prévenir l’obstruction en matière budgétaire et socialeChloë Geynet-Dussauze, Sciences Po Lille 11h20 : Litanie, liturgie, léthargie : le vote des créditsValentin Dalias, Université Toulouse Capitole 11h40 : Débat : Faut-il réformer l’article 40 ?Mathieu Carpentier, Université Toulouse CapitoleAurélien Baudu, Université de Lille 12h20 : Discussion   12h40 : Déjeuner   4. Le contrôle Présidence : Aurore Gaillet, Université Toulouse Capitole 14h30 : La clarté et la sincérité du débat parlementaire budgétaireValérie Palma-Amalric, Institut national universitaire Champollion 14h50 : La jurisprudence sur les cavaliers budgétaires et sociaux est-elle cohérente ?Aurélie Dort, Université de Lorraine 15h10 : Les rapports parlementaires en matière financière, doctrine de l’administration parlementaire ?Gérald Sutter, administrateur des services de l’Assemblée nationale 15h30 : Discussion 15h50 : Pause 16h10 : SynthèseMatthieu Conan, Université Paris 1 Panthéon-Sorbonne 16h30 : Fin des travaux     Contact : soumaya.abdouli@ut-capitole.fr Inscription en bas de page : https://imh.ut-capitole.fr/accueil/activites-de-recherche/colloques/le-droit-parlementaire-financier-etat-des-lieux-et-pistes-devolution Colloque organisé par l’IMH, Université Toulouse Capitole avec la SSFP sous la direction scientifique de Mathieu Carpentier et Vincent Dussart Source link JUSTIFIABLE s’enrichit avec une nouvelle catégorie dédiée à l’Histoire du droit, alimentée par le flux RSS de univ-droit.fr. Cette section propose des articles approfondis et régulièrement mis à jour sur l’évolution des systèmes juridiques, les grandes doctrines, et les événements marquants qui ont façonné le droit contemporain. Ce nouvel espace est pensé pour les professionnels, les étudiants, et les passionnés d’histoire juridique, en quête de ressources fiables et structurées pour mieux comprendre les fondements et l’évolution des normes juridiques. Plongez dès maintenant dans cette catégorie pour explorer le passé et enrichir vos connaissances juridiques.

[bpod-bpod]

Early Communication

Transfer of soluble factors and organelles from cell to cell via open-ended tunnelling nanotubes��demonstrated in living zebrafish embryos

Read the published research article here

Video from work by Olga Korenkova and Shiyu Liu, and colleagues

Institut Pasteur, Université Paris Cité, CNRS UMR 3691, Membrane Traffic and Pathogenesis, Paris, France

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Developmental Cell, November 2024

You can also follow BPoD on Instagram, Twitter and Facebook

[sante-enfants-environnement]

Risques liés aux Micro- et Nano-Plastiques (MNP), avec Francelyne Marano (Université Paris Cité)

Bonjour à tous, Voici une nouvelle vidéo publiée sur la Chaîne YouTube Santé des enfants et environnement, intitulée “Risques liés aux Micro- et Nano-Plastiques (MNP), avec Francelyne Marano (Université Paris Cité)”, ainsi que le podcast associé et quelques points clés de l’échange, selon moi.       Présentation de Francelyne Marano, professeur émérite à l’Université Paris Cité Bonjour les…