118 research outputs found
Differential effects of chronic restraint stress on two active avoidance tasks in rats
No full textPreregistrations, data and scripts related to López-Moraga, A., De Ceuninck, M., Van der Heyden, Y., Vercammen, L., Palme, R., Vervliet, B., Beckers, T., & Luyten, L. (2026). Differential effects of chronic restraint stress on two active avoidance tasks in rats. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 144, 111586. https://doi.org/10.1016/j.pnpbp.2025.11158
Array Formatting of the Heat-Transfer Method (HTM) for the Detection of Small Organic Molecules by Molecularly Imprinted Polymers
No full textIn this work we present the first steps towards a molecularly imprinted polymer (MIP)-based biomimetic sensor array for the detection of small organic molecules via the heat-transfer method (HTM). HTM relies on the change in thermal resistance upon binding of the target molecule to the MIP-type receptor. A flow-through sensor cell was developed, which is segmented into four quadrants with a volume of 2.5 μL each, allowing four measurements to be done simultaneously on a single substrate. Verification measurements were conducted, in which all quadrants received a uniform treatment and all four channels exhibited a similar response. Subsequently, measurements were performed in quadrants, which were functionalized with different MIP particles. Each of these quadrants was exposed to the same buffer solution, spiked with different molecules, according to the MIP under analysis. With the flow cell design we could discriminate between similar small organic molecules and observed no significant cross-selectivity. Therefore, the MIP array sensor platform with HTM as a readout technique, has the potential to become a low-cost analysis tool for bioanalytical applications
Optimized selection of materials for IGBT module packaging
No full textThis work is (partially) supported by the energy transition funds project "BREGILAB" organized by the FPS economy, S.M.E.s, Self-employed and Energy (Met de steun van het Energietransitiefonds)
Physics of potential-induced degradation in bifacial p-PERC solar cells
No full textThe combination of increasing operational voltages beyond 1000 V in photovoltaic (PV) installations and the emergence of new PV technologies requires a critical assessment of the susceptibility to potential-induced degradation (PID). Since this failure mode can trigger significant and rapid power losses, it is considered among the most critical failure modes with a high financial impact. Insights in the physical mechanism of the performance loss and its driving factors are critical to develop adapted characterization methods and mitigation solutions. PID in p-type solar cells is triggered by sodium (Na) that diffuses into stacking faults of the silicon lattice, causing shunt paths through the pn-junction. In addition, it is hypothesised that for bifacial p-PERC solar cells positive charges, such as Na+, accumulate in/on the negatively charged AlOx rear passivation layer due to the potential difference between the glass and the rear cell surface. This significantly increases surface recombination. However, the degradation behaviour observed in bifacial monocrystalline p-PERC solar cells under PID stress from both sides (bifacial PID stress) does not match with just one of the degradation mechanisms. A comprehensive test matrix was carried out to understand the physical origin of PID in front emitter bifacial p-PERC solar cells in a glass/glass packaging. The results show that bifacial p-PERC solar cells under bifacial PID stress suffer from both shunting of the pn-junction and increased surface recombination at their rear side. Hereby, we prove that the glass/glass packaging in combination with bifacial solar cells can significantly increase the severity of PID
Factors relacionats amb el manteniment de la inflamació i l'oclusió vascular. Implicacions en l'evolució dels pacients amb arteritis de cèl·lules gegants.
No full text[cat] L'arteritis de cèl·lules gegants (ACG) és una vasculitis sistèmica de caràcter granulomatós que afecta vasos de calibre mitjà i gran. Per aprofundir en els mecanismes que intervenen en el desenvolupament de la hiperplasia intimal i la inflamació en l'ACG, vam dissenyar un nou mètode d'obtenció de cèl·lules miointimals (HTAMC) a partir de biòpsies d'artèries temporals dels pacients. Vam analitzar l'efecte de PDGF-AB, FGF-2, VEGF, EGF, TGFβ, CCL2, IL-6 i IL-1β sobre la proliferació i migració de les HTAMC. El PDGF va ser el principal agent mitogènic, seguit pel FGF-2. Respecte a la migració, només el PDGF i l'EGF van demostrar una acció quimiotàctica. Probablement el comportament d'aquestes cèl·lules in vivo és el resultat d'un balanç de diferents estímuls, per tant, caldrà plantejar-se el disseny de teràpies dirigides i combinades.Donat que el PDGF va ésser el factor que més influencia el comportament de les HTAMC, vam estudiar els efectes de l'imatinib mesylate (Gleevec®), un inhibidor del receptor del PDGF. Vam demostrar que l'imatinib bloqueja les vies de senyalització del PDGF, i conseqüentment, inhibeix la proliferació i la migració de les HTAMC estimulades amb PDGF. També vam estudiar altres funcions del PDGF i vam observar que incrementa l'expressió dels col·làgens tipus I i III i també augmenta la producció de fibronectina en les HTAMC. L'imatinib va inhibir l'estimulació en la producció d'aquestes proteïnes de matriu extracel·lular. D'altra banda, vam demostrar que el PDGF estimulava la secreció de CCL2 i d'angiogenina en les HTAMC i que l'imatinib contrarestava també aquests efectes. Donat que no es disposa d'un model animal de la malaltia, el cultiu de seccions d'artèria temporal sobre Matrigel® és un mètode que ens permet analitzar tota la complexitat d'aquest sistema, ja que conté tots els tipus cel·lulars de l'artèria més l'infiltrat inflamatori. Als set dies, s'inicia el creixement de les HTAMC fins a formar un cultiu confluent. L'imatinib inhibeix el creixement de les HTAMC a partir de l'artèria. Aquests resultats in vitro i ex vivo són encoratjadors demostrant que l'imatinib podria ser terapèuticament útil per contrarestar el procés inflamatori i el desenvolupament de la hiperplàsia intimal que es produeix en les artèries en l'ACG, però només un assaig clínic podria comprovar la utilitat de l'imatinib in vivo.En el segon estudi ens vam plantejar esbrinar quin és el paper de l'endotelina (ET) en l'ACG. Primerament, vam quantificar els nivells d'ET en el plasma dels pacients i van concloure que els pacients que patien fenòmens isquèmics tenien significativament més ET circulant que els que no tenien aquestes complicacions. A les biòpsies d'artèria temporal, els pacients van presentar nivells més alts de totes les proteïnes del sistema (ET-1, ECE-1 i ambdós receptors A i B). Mentre que a nivell d'expressió d'ARNm, els pacients tenien nivells més baixos de tots els components. Davant d'aquesta regulació negativa de tot el sistema, ens vam plantejar l'existència d'un mecanisme de retroalimentació negativa degut a l'excés d'ET. Els experiments in vitro amb cèl·lules endotelials i miointimals van demostrar que l'ET no regula negativament la seva pròpia expressió. En canvi, el PDGF i l'IL1β van regular negativament l'expressió de l'ARNm de l'ET en HTAMC.Als pacients tractats durant 8 dies de mitjana amb glucocorticoides, el tractament d'elecció de l'ACG, va disminuir l'ECE-1 i ETAR però no van disminuir els nivells d'ET-1, que és la molècula amb activitat funcional vasoconstrictora. Les nostres dades experimentals indiquen que el PDGF i l'endotelina poden estar implicats en la progressió de les lesions arterials dels pacients amb ACG i pensem que aquests resultats poden ser útils pel disseny d'assaigs clínics de teràpies més dirigides.[eng] Giant Cell Arteritis (GCA) is a chronic inflammatory disease involving large and medium-sized vessels. Vascular remodeling in response to inflammation leads to intimal hyperplasia resulting in lumen occlusion and ischemia of supplied tissues. To gain a better understanding of the mechanisms leading to vascular occlusion in GCA, we developed a system to obtain and culture myointimal cells from temporal arteries (HTAMC) in order to assess the effects of various mediators on proliferation, migration and extracellular matrix production. Among the factors tested, PDGF exhibited the strongest activity in our system. Given that imatinib mesylate is an inhibitor of the PDGF receptor, we tested the effect of this compound in our model. We found that imatinib inhibited HTAMC biologic responses related to the development of intimal hyperplasia. Our findings suggest that imatinib might be a therapeutic option to limit occlusive vasculopathy in large-vessel vasculitis.Fifteen to 20% of our patients develop vascular occlusive events often preceded by transient ischemia. The aims of the second study were to investigate the expression of the endothelin (ET) system in GCA lesions, to assess its relationship with the development of ischemic complications, and to analyze the effects of glucocorticoid treatment on this system.Plasma ET was significantly elevated in GCA patients with ischemic complications. ET-1, endothelin converting enzyme (ECE-1) and both ET receptors (ETAR and ETBR) were increased in temporal arteries from GCA patients compared to controls. Intriguingly, mRNA expression of ET-1, ECE-1 and both receptors was significantly reduced in GCA patients. In order to investigate mechanisms underlying these results, we performed in vitro studies with endothelial cells and HTAMC. ET did not downregulate its own expression. In contrast, PDGF and IL-1β decreased ET expression by HTAMC. Glucocorticoid treatment for 8 days did not efficiently result in decreased ET concentration in tissue. In conclusion, the expression of the ET system components is increased at the protein level in GCA lesions creating a microenvironment prone to development of vasoconstrictive occlusive events which may contribute to ischemic complications. Recovery induced by glucocorticoids is not complete, indicating persistent exposure to the effects of ET during initial treatment
Single-Shot Detection of Neurotransmitters in Whole-Blood Samples by Means of the Heat-Transfer Method in Combination with Synthetic Receptors
No full textSerotonin is an important neurotransmitter that plays a major role in the pathogenesis of a variety of conditions, including psychiatric disorders. The detection of serotonin typically relies on high-performance liquid chromatography (HPLC), an expensive technique that requires sophisticated equipment and trained personnel, and is not suitable for point-of-care applications. In this contribution, we introduce a novel sensor platform that can measure spiked neurotransmitter concentrations in whole blood samples in a fast and low-cost manner by combining synthetic receptors with a thermal readout technique—the heat-transfer method. In addition, the design of a miniaturized version of the sensing platform is presented that aims to bridge the gap between measurements in a laboratory setting and point-of-care measurements. This fully automated and integrated, user-friendly design features a capillary pumping unit that is compatible with point-of-care sampling techniques such as a blood lancet device (sample volume—between 50 µL and 300 µL). Sample pre-treatment is limited to the addition of an anti-coagulant. With this fully integrated setup, it is possible to successfully discriminate serotonin from a competitor neurotransmitter (histamine) in whole blood samples. This is the first demonstration of a point-of-care ready device based on synthetic receptors for the screening of neurotransmitters in complex matrices, illustrating the sensor’s potential application in clinical research and diagnosis of e.g., early stage depression
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