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<title>IDIBAPS: Institut d'investigacions Biomèdiques August Pi i Sunyer</title>
<link>https://hdl.handle.net/2072/478858</link>
<description/>
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<rdf:li rdf:resource="https://hdl.handle.net/2445/228915"/>
<rdf:li rdf:resource="https://hdl.handle.net/2445/228894"/>
<rdf:li rdf:resource="https://hdl.handle.net/2445/228913"/>
<rdf:li rdf:resource="https://hdl.handle.net/2445/228876"/>
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<dc:date>2026-04-15T21:14:51Z</dc:date>
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<item rdf:about="https://hdl.handle.net/2445/228915">
<title>Venetoclax as a possible chemopreventive agent in adenomatous polyposis: A case report</title>
<link>https://hdl.handle.net/2445/228915</link>
<description>Venetoclax as a possible chemopreventive agent in adenomatous polyposis: A case report; Venetoclax como posible agente quimiopreventivo en la poliposis adenomatosa: a propósito de un caso
Maimouni, Cautar el; Daca Alvarez, Maria de los Angeles; Delgado, Julio (Delgado González); Pellisé Urquiza, Maria; Balaguer Prunés, Francesc
Familial adenomatous polyposis (FAP) is a hereditary colorectal cancer (CRC) syndrome caused by a germline pathogenic variant in the Adenomatous Polyposis Coli (APC) gene. However, a pathogenic mutation in this gene is not identified in 20% of patients.
</description>
<dc:date>2026-04-14T18:13:47Z</dc:date>
</item>
<item rdf:about="https://hdl.handle.net/2445/228894">
<title>Antibody and Cellular Immune Responses in Old α1,3-Galactosyltransferase-Knockout Mice Implanted with Bioprosthetic Heart Valve Tissues</title>
<link>https://hdl.handle.net/2445/228894</link>
<description>Antibody and Cellular Immune Responses in Old α1,3-Galactosyltransferase-Knockout Mice Implanted with Bioprosthetic Heart Valve Tissues
Casós, Kelly; Llatjós, Roger; Blasco Lucas, Arnau; Kuguel, Sebastián G.; Sbraga, Fabrizio; Galli, Cesare; Padler-Karavani, Vered; Le Tourneau, Thierry; Vadori, Marta; Roussel, Jean-Christian; Bottio, Tomaso; Cozzi, Emanuele; Soulillou, Jean Paul; Galiñanes, Manuel; Mañez, Rafael; Costa, Cristina
Structural valve deterioration (SVD) remains a key limitation in bioprosthetic heart valve (BHV) usage influenced by patient age. A deeper understanding of SVD pathogenesis, particularly of the immune-mediated processes altering current BHV materials, is therefore critical. To this end, commercially available BHV tissues of bovine, porcine, and equine origin were investigated following subcutaneous implantation into alpha 1,3-galactosyltransferase-knockout (Gal KO) mice. We compared the immune responses between adult and aged animals via histological assessments of explants and measurement of serum anti-galactose alpha 1,3-galactose (Gal) and anti-non-Gal antibodies at 2 months post-implantation. In contrast to adult mice, old Gal KO mice did not show increased levels of serum anti-Gal or -non-Gal antibodies after receiving specific BHV tissue (i.e., Freedom-Solo). Instead, a significant decrease in serum anti-Gal IgM was found in old recipients of Freedom-Solo. Furthermore, the overall cellular immune response was attenuated in explants from old mice compared with adults (i.e., ATS 3f and Crown). Nevertheless, the Freedom-Solo (bovine) and the Hancock-II (porcine) tissues still elicited strong cellular immune infiltration in the old cohorts. Therefore, the Gal KO mouse model offers a valuable platform to investigate age-related differences regarding cellular and humoral immune responses to various BHV tissues, contributing to our understanding of SVD.
</description>
<dc:date>2026-04-14T10:21:14Z</dc:date>
</item>
<item rdf:about="https://hdl.handle.net/2445/228913">
<title>Trusting the forces of our cell lines</title>
<link>https://hdl.handle.net/2445/228913</link>
<description>Trusting the forces of our cell lines
Moro López, Marina; Farré Ventura, Ramon; Otero Diaz, Jorge; Sunyer Borrell, Raimon
Cells isolated from their native tissues and cultured in vitro face different selection pressures than those cultured in vivo. These pressures induce a profound transformation that reshapes the cell, alters its genome, and transforms the way it senses and generates forces. In this perspective, we focus on the evidence that cells cultured on conventional polystyrene substrates display a fundamentally different mechanobiology than their in vivo counterparts. We explore the role of adhesion reinforcement in this transformation and to what extent it is reversible. We argue that this mechanoadaptation is often understood as a mechanical memory. We propose some strategies to mitigate the effects of on-plastic culture on mechanobiology, such as organoid-inspired protocols or mechanical priming. While isolating cells from their native tissues and culturing them on artificial substrates has revolutionized biomedical research, it has also transformed cellular forces. Only by understanding and controlling them, we can improve their truthfulness and validity.
</description>
<dc:date>2026-04-14T17:16:56Z</dc:date>
</item>
<item rdf:about="https://hdl.handle.net/2445/228876">
<title>Bladder EpiCheck clinical utility to predict BCG response in non-muscle-invasive bladder cancer</title>
<link>https://hdl.handle.net/2445/228876</link>
<description>Bladder EpiCheck clinical utility to predict BCG response in non-muscle-invasive bladder cancer
Roldán, Fiorella L.; Ingelmo-Torres, Mercedes; Mercader Barrull, Clàudia; Figueras Torras, Marcel; Padullés, Bernat; Durán González, María Angeles; Carrasco Jordan, Josep Lluís; Ribal, María José; Franco de Castro, Agustín; Izquierdo Reyes, Laura; Alcaraz Asensio, Antonio; Mengual Brichs, Lourdes
Objective: To evaluate the performance of Bladder Epicheck® (BE; Nucleix Ltd., Rehovot, Israel) in predicting tumour recurrence and bacillus Calmette-Guérin (BCG) failure during the first year after induction treatment.

Patients and methods: Prospective study including 65 patients with non-muscle-invasive bladder cancer treated with BCG between 2018 and 2021. Urine samples analysed with BE were collected before and after BCG induction. Logistic binary regression was used to assess the association between clinical and pathological variables and BE results with tumour recurrence and BCG failure during the first year after induction treatment.

Results: During follow-up, 16 (24.6%) patients experienced a bladder cancer event, 11 (68.8%) of which were BCG failure (high-grade recurrence) and five (31.2%) were low-grade recurrences. The median (range) time to overall recurrence was 7.3 (3.8-17.4) months. A significant association was found between the risk of tumour recurrence/BCG failure and post-BCG cystoscopy (odds ratio [OR] 10.0; P &lt; 0.001 and OR 13.1; P &lt; 0.001, respectively), post-BCG BE result (OR 16.9; P &lt; 0.001 and OR 33.1; P &lt; 0.001, respectively) and pre/post-BCG EpiScore value variation (OR 14.4; P = 0.001 and OR 7.1; P = 0.018, respectively). A nomogram including these three variables outperformed the Club Urológico Español de Tratamiento Oncológico (CUETO) risk tables to predict any bladder cancer event after BCG induction (area under the curve 95.1% vs 67.1%). Result validation in a larger and independent series is needed.

Conclusions: The BE post-BCG status and variations in EpiScore values can help us identify patients at higher risk of any bladder cancer event and BCG failure promptly. These data can have an impact on disease management.
</description>
<dc:date>2026-04-13T17:44:46Z</dc:date>
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