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Take part in our open morning Given the works in the rue de Bruxelles and the renovation of part of the University parking lots, we invite you to use public transport whenever possible (train or bus) to reach Namur. UNamur boasts an ideal location, in the heart of the city just a five-minute walk from the TEC and SNCB train stations.If you're coming by car, take a look at the parking map provided. Look forward to seeing you on Saturday, June 29!

The workshop provides a forum for the discussion of new research directions and applications in Artificial Life, Evolutionary Computation and in related fields, where different disciplines and research areas could effectively meet. It was first held in 2007 in Sampieri (Ragusa), as the incorporation of two separate workshops (WIVA and GSICE).

Initiated in 1969 by Pullmann and Del Re, the congress is an annual meeting to promote collaboration and friendship between Latin-speaking theoretical chemists. In its early years, European researchers were the main contributors. Subsequently, the Latin American community has made a major contribution, with the emergence of teams whose international reputation now extends far beyond our own community.We are delighted to be holding this meeting at the University of Namur, 55 years after the first CHITEL was organised in Paris, France. We are sure that this 2024 edition will once again be an opportunity to take advantage of the good humour and dynamism of Latin to encourage, develop and strengthen scientific exchanges.We look forward to welcoming you at the University of Namur,The CHITEL 2024 Local Organising Committee. Website

COVID-19 is an infectious disease caused by SARS-CoV-2. COVID-19 was quickly declared a pandemic by the World Health Organization (WHO) on March 11, 2020.At the start of the pandemic, healthcare professionals were faced with the marketing of numerous kits designed to measure binding antibodies. The role of neutralizing antibodies as the best correlate of protection against SARS-CoV-2 infection was quickly highlighted. A neutralization assay with the use of pseudovirus was therefore developed by our team and compared with several binding assays.There have been considerable efforts to produce and clinically validate new vaccines against COVID-19. The CRO-VAX HCP study was designed to assess the humoral response in a population of healthcare professionals who had received two doses of COVID-19 BNT162b2 vaccine.Given the decline in vaccine efficacy over time and the emergence of variants likely to evade immunity, a third dose was quickly recommended by the authorities to boost immunity. This was administered to 155 volunteers in the CRO-VAX HCP study.Still facing a decline in vaccine efficacy over time and the emergence of new variants, a second adapted booster was proposed. In September 2022, 54 participants in the CRO-VAX HCP study received this second booster. The humoral response was assessed and neutralizing antibodies against several variants were measured. In addition, we also measured the cellular response using an interferon-gamma release assay. Compared with the humoral response, which declines considerably over time, the cellular response remained fairly stable. This could therefore explain why individuals with low antibody titers can still be protected against a severe form of the disease .

The school will deal with optimizing computations on different types of hardware (CPU, GPU), presenting their respective characteristics, architectures and bottlenecks. It will cover both generic optimization methods applicable to all types of hardware, and the various libraries, technologies and languages available to achieve the best possible performance. Ideally, the machine's peak performance. Hardware considered: CPU, GPU.Languages considered: C++17, C++20, CUDA, Fortran, Rust, PythonLibraries considered: SYCL, Eve, Numpy, cunumerics, legate, Jax, Thrust.Compilers considered: G++, Clang++, nvc++, gfortran, nvfortran, dpc++.Profiling tools: Valgrind, Maqao, Perf, NSight, Malt and NumaProfAll methods will be illustrated on simple examples, such as Hadamard products, reductions, barycenter calculations and matrix products in order to be applied to a single problem: the simulation of a Gray Scott reaction. This problem is simple enough to be understood quickly, yet complex enough to be difficult for compilers to optimize without help. Each method will be broken down into simple versions, using default options, and one or more advanced versions, which will allow their advantages and disadvantages to be discussed and quantified.For more information on its content, please consult the school websiteOn the University of Namur satellite site, you'll enjoy the following benefits: Interaction with official LAPP trainers; Group support and a good working atmosphere; Lunch and a drink at the end of the day on the first day; You choose what you want to follow on site. We encourage you to come on the first day, but you make up your own program on the other days.To register for the UNamur satellite site: https://docs.google.com/forms/d/e/1FAIpQLScxikCQTfsQl9zZfnidm4xLSuDpdJGcgyLKOfJ2wo4VMgrgRw/viewform Read more

ABCB5 belongs to the ABC transporter superfamily composed of 48 members. These transporters have been extensively studied for their role in cancer multidrug resistance and, more recently, in tumorigenesis. ABCB5 has been identified as a marker of skin progenitor cells, melanoma stem cells, and limbal stem cells. Its expression has also been reported, among others, in melanoma, colorectal cancer, hepatocellular carcinoma and several hematological malignancies. The unique feature of ABCB5 is that it exists as both a full transporter (ABCB5FL) and a half-transporter (ABCB5β). Several studies have shown that the ABCB5β homodimer, in contrast to ABCB5FL, cannot confer multidrug resistance. Since these studies focused on a limited number of drugs, we cannot exclude the possibility that this homodimer may be involved in drug resistance or biological functions that have yet to be elucidated. However, it is also reasonable to hypothesize that ABCB5β could dimerize with other half transporters of the ABCB family to become functional. Using three complementary techniques: (1) nanoluciferase-based bioluminescence resonance energy transfer, (2) coimmunoprecipitation, and (3) proximity ligation assay, we identified two novel heterodimers in two melanoma cell lines: ABCB5β/B6 and ABCB5β/B9. Both heterodimers could be expressed in High-Five insect cells when both interacting partners were fused using the linker region of ABCB1, resulting in chimeric heterodimers. ATPase assays revealed that all chimeric heterodimers have a basal ATPase activity and that both functional nucleotide-binding domains in each dimer are required for their basal ATPase activity. Also, we obtained preliminary data suggesting that ABCB5β traffics from the endoplasmic reticulum to melanosomes independently of its dimerization, suggesting that its heterodimers might be located in similar organelles. However, several limitations were encountered when attempting to confirm their intracellular localization. Finally, since several anti-ABCB5 antibodies in the literature have shown a lack of specificity, we generated a mouse monoclonal anti-ABCB5 antibody in collaboration with Atlas Antibodies. The specificity of this antibody was demonstrated by immunofluorescence, making this antibody an important tool in the characterization of ABCB5β and ABCB5FL. Although further studies are needed to elucidate the physiological relevance of ABCB5β heterodimers, preliminary data support the hypothesis that ABCB5β is involved in melanogenesis. Taken together, these results represent an important step towards elucidating the functional role of ABCB5β in melanocytes and melanoma.

The morning will be marked by a lecture by Julien Berthaud, a specialist in the social integration of students, who will share his insights on how this integration becomes a genuine vector for success.Then, scientific papers and experience sharing will enrich our knowledge and spark constructive debate. Lunch will be an opportunity to discover innovative student projects, highlighted in an inspiring exhibition.The afternoon promises to be just as stimulating with a round table moderated by Sabine Henry, where experts will discuss service learning, educational entrepreneurship and spirituality. This dynamic dialogue will be followed by a closing activity: the fresco of engagement, a collective brainstorming session that will lay the foundations for an innovative educational game.Join us for this day of exchange and reflection, and help shape the future of education where student engagement and knowledge vivacity will be the cornerstones of a new educational paradigm.

Discover the program

With its deep skies that hypnotize and subjugate, space exerts an unrivalled fascination on the human species. As the Anthropocene crisis shakes our balances (environmental, technological, democratic), the 'Land of Night' is by turns the last frontier to be colonized, a resource to be exploited, a tourist destination, an observatory for remote surveillance, a dumping ground for orbiting debris, and forever the infinite constellation of our original interrogations as well as our (meta)physical reveries.From the atomic fragment to the great universal whole, the Stellar Scape exhibition brings together some two dozen international artists, researchers and engineers around the imaginaries of astronomy and the revival of space adventures. Through art installations, immersive environments, scientific innovations, speculative projects, we experience this expanding starry landscape, mirroring the cosmic link that connects us in a single space to all those things that appear there not only as they are, but also as they could be. More information on the exhibition

Summary: Impact of the UPR pathway on the establishment of the UVB-induced senescent phenotype Skin aging, influenced by a combination of intrinsic and extrinsic factors, leads to damage capable of altering skin functions. Among extrinsic factors, ultraviolet (UV) radiation is responsible for skin photoaging. In particular, these elements lead to an accumulation of senescent cells capable of contributing to the development of age-related pathologies such as skin cancers. Indeed, senescence is accompanied by profound morphological and molecular changes within the cell. This includes a modification of its secretome, which becomes enriched with pro-inflammatory cytokines, growth factors and extracellular matrix remodeling enzymes, altering the characteristics of tissues as they age. Nevertheless, the precise mechanisms leading to the senescent phenotype induced by UVB remain largely unknown. In this context, the main objective of this work was to identify molecular mechanisms underlying the establishment of UVB-induced senescence in normal human dermal fibroblasts (NHDFs), mechanisms that could contribute to skin aging. In vitro, we confirmed that repeated UVB exposures induce premature senescence in NHDFs and that this state is associated with activation of the three branches of the UPR (Unfolded Protein Response) pathway responsible for maintaining homeostasis of the endoplasmic reticulum (ER), the primary secretory compartment. These observations were supported by transcriptomic analysis, revealing regulatory elements linked to major senescence pathways and ER functions in UVB-exposed NHDFs. Subsequently, we showed that the ATF6α branch plays a central role in the occurrence of biomarkers of the UVB-induced senescent phenotype. Indeed, ATF6α invalidation not only protects against UVB-induced morphological changes, but reduces the percentage of SA-βgalactosidase (SA-βgal)-positive cells, prevents persistent DNA damage, and alters the expression of major factors of the senescence-associated secretory phenotype (SASP). As SASP exerts, among other things, a pro-tumoral action, we sought to assess whether the conditioned medium (CM) of UVB-exposed fibroblasts invalidated for ATF6α could impact the migration and invasion potential of melanoma-derived cells. However, we did not observe any ATF6α-dependent pro-migratory or pro-invasive effects.To highlight a potential role for ATF6α in another biological process, we exploited our transcriptomic and secretomic analyses and identified a possible effect of ATF6α on the paracrine control of the skin environment. To explore this, we focused on SASP factors (cytokines and metalloproteases) regulated by ATF6α and whose impact on the tissue environment was known. Next, we treated a reconstructed human epidermis (RHE) model with MC derived from NHDFs exposed to UVB or not, and invalidated or not for ATF6α. Surprisingly, we observed that MC from UVB-exposed NHDFs increased RHE thickness and basal keratinocyte proliferation, via an ATF6α-dependent mechanism. Finally, we identified IL8 as a major paracrine factor involved in this process, since IL-8 blockade by neutralizing antibodies prevents excessive keratinocyte proliferation. In conclusion, we report the role of ATF6α in UVB-induced senescence as well as its impact on the preservation of skin homeostasis under stress conditions notably through the regulation of the expression of SASP components. This suggests that ATF6α and its effectors could be promising targets controlling the effects of skin aging.Abstract: Impact of the UPR pathway on the establishment of the senescent phenotype induced by UVBSkin aging, influenced by a combination of intrinsic and extrinsic factors, can result in damage that has the potential to alter skin functions. Among extrinsic factors, ultraviolet (UV) radiation is responsible for skin photoaging. These factors notably contribute to the accumulation of senescent cells which in turn can contribute to the development of age-related pathologies, including skin cancers. Indeed, senescence is characterized by profound morphological and molecular changes within the cell. This includes a modification of its secretome, which becomes enriched in pro-inflammatory cytokines, growth factors, and matrix-remodeling enzymes, altering tissue characteristics during aging. However, the exact mechanisms driving the senescent phenotype induced by UVB remain largely unknown. In this context, the main objective of this work was to identify the underlying molecular mechanisms responsible for the establishment of UVB-induced senescence in normal human dermal fibroblasts (NHDFs), mechanisms that may play a role in skin aging. In vitro, we confirmed that repeated exposures to UVB induce premature senescence of NHDFs and that this state is associated with the activation of the three branches of the Unfolded Protein Response (UPR), which are responsible for maintaining endoplasmic reticulum (ER) homeostasis, the primary cellular secretion compartment. These observations were supported by transcriptomic analysis, revealing regulatory elements related to major senescence pathways and ER functions in UVB-exposed NHDFs. Subsequently, we demonstrated that the ATF6α branch plays a central role in the development of the UVB-induced senescent phenotype. Indeed, the silencing of ATF6α not only protects against morphological changes induced by UVB, but also reduces the percentage of senescence-associated β-galactosidase (SA-βgal) positive cells, prevents the persistence of DNA damage, and alters the expression of major factors associated with the senescence-associated secretory phenotype (SASP).The SASP, exerting a pro-tumoral action, led us to assess whether the conditioned medium (CM) from UVB-exposed fibroblasts invalidated for ATF6α could impact the migration and invasion potential of melanoma cells. However, we did not observe any ATF6α-dependent pro-migratory or pro-invasive effects. To highlight a potential role of ATF6α in another biological process, we further analyzed our transcriptomic and secretomic analyses and identified a possible effect of ATF6α on the paracrine control of the skin environment. To explore this, we focused on SASP factors (cytokines and metalloproteinases) regulated by ATF6α and whose impact on tissue environment was known. Subsequently, we treated a reconstructed human epidermis (RHE) model with CM from NHDFs exposed or not to UVB and invalidated or not for ATF6α. Surprisingly, we observed that the CM from UVB-exposed NHDFs increased the thickness of the RHE as well as the proliferation of basal keratinocytes, via an ATF6α-dependent mechanism. Finally, we identified IL8 as a major paracrine factor involved in this process, as blocking IL-8 with neutralizing antibodies prevented excessive proliferation of keratinocytes. In conclusion, we report the role of ATF6α in UVB-induced senescence and its impact on the preservation of skin homeostasis under stress conditions, particularly through the regulation of the expression of SASP components. This suggests that ATF6α and its effectors could be promising targets for controlling the effects of skin aging. Jury Prof. Yves POUMAY (Department of Medicine, UNamur), chairmanProf. Florence CHAINIAUX (Department of Biology, UNamur), promoter and secretaryProf. Olivier PLUQUET (Canther, University of Lille), co-promoterProf. Isabelle PETROPULOS (Adaptation Biologique et Vieillissement, Sorbonne Université)Prof. Jérôme LAMARTINE (Laboratoire de Biologie Tissulaire et d'Ingénierie thérapeutique, Université Claude Bernard Lyon 1)Prof. Fabienne FOUFELLE (Maladies métaboliques, diabète et comorbidités, Sorbonne Université)

What is "care"? What is health? This opening conference will be an opportunity to explore the contemporary challenges linked to health, care and the transformations needed for a sustainable, inclusive future.Speakers:Barbara Stiegler, philosopher at Bordeaux-Montaigne UniversityGaël Giraud sj, economist and theologian, researcher at CNRS and Doctor Honoris Causa of UNamurFree conference as part of the partnershipRegistration required. Please make sure you select the February 20 conference. I reserve my place Find out more about the Chair's conferences