يعرض 1 - 10 نتائج من 334 نتيجة بحث عن '"Quero G."', وقت الاستعلام: 0.74s تنقيح النتائج
  1. 1
    دورية أكاديمية

    المساهمون: Ruta, V., Naro, C., Pieraccioli, M., Leccese, A., Archibugi, L., Cesari, E., Panzeri, V., Allgower, C., Arcidiacono, P. G., Falconi, M., Carbone, C., Tortora, G., Borrelli, F., Attili, F., Spada, C., Quero, G., Alfieri, S., Doglioni, C., Kleger, A., Capurso, G., Sette, C.

    مصطلحات موضوعية: alternative splicing, chemoresistance, RNA processing

    الوصف: Pancreatic ductal adenocarcinoma (PDAC) is characterized by extremely poor prognosis. PDAC presents with molecularly distinct subtypes, with the basal-like one being associated with enhanced chemoresistance. Splicing dysregulation contributes to PDAC; however, its involvement in subtype specification remains elusive. Herein, we uncover a subtype-specific splicing signature associated with prognosis in PDAC and the splicing factor Quaking (QKI) as a determinant of the basal-like signature. Single-cell sequencing analyses highlight QKI as a marker of the basal-like phenotype. QKI represses splicing events associated with the classical subtype while promoting basal-like events associated with shorter survival. QKI favors a plastic, quasi-mesenchymal phenotype that supports migration and chemoresistance in PDAC organoids and cell lines, and its expression is elevated in high-grade primary tumors and metastatic lesions. These studies identify a splicing signature that defines PDAC subtypes and indicate that QKI promotes an undifferentiated, plastic phenotype, which renders PDAC cells chemoresistant and adaptable to environmental changes.

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/38325381; info:eu-repo/semantics/altIdentifier/wos/WOS:001200308600001; volume:5; issue:2; numberofpages:23; journal:CELL REPORTS MEDICINE; https://hdl.handle.net/20.500.11768/160081Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85185295199; https://www.sciencedirect.com/science/article/pii/S266637912400034X?via=ihubTest

  2. 2
    دورية أكاديمية

    المساهمون: Brusco, N., Sebastiani, G., Di Giuseppe, G., Licata, G., Grieco, G. E., Fignani, D., Nigi, L., Formichi, C., Aiello, E., Auddino, S., Quero, G., Cefalo, C. M. A., Cinti, F., Mari, A., Ferraro, P. M., Pontecorvi, A., Alfieri, S., Giaccari, A., Dotta, F., Mezza, T.

    الوصف: Aims/hypothesis: Endoplasmic reticulum (ER) stress and beta cell dedifferentiation both play leading roles in impaired insulin secretion in overt type 2 diabetes. Whether and how these factors are related in the natural history of the disease remains, however, unclear. Methods: In this study, we analysed pancreas biopsies from a cohort of metabolically characterised living donors to identify defects in in situ insulin synthesis and intra-islet expression of ER stress and beta cell phenotype markers. Results: We provide evidence that in situ altered insulin processing is closely connected to in vivo worsening of beta cell function. Further, activation of ER stress genes reflects the alteration of insulin processing in situ. Using a combination of 17 different markers, we characterised individual pancreatic islets from normal glucose tolerant, impaired glucose tolerant and type 2 diabetic participants and reconstructed disease progression. Conclusions/interpretation: Our study suggests that increased beta cell workload is accompanied by a progressive increase in ER stress with defects in insulin synthesis and loss of beta cell identity. Graphical abstract: [Figure not available: see fulltext.]

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/36280617; info:eu-repo/semantics/altIdentifier/wos/WOS:000871276400001; volume:66; issue:2; firstpage:354; lastpage:366; numberofpages:13; journal:DIABETOLOGIA; https://hdl.handle.net/11573/1675058Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85140460796

  3. 3
    دورية أكاديمية

    المساهمون: J. Lavanchy, A. Vardazaryan, P. Mascagni, D. Mutter, N. Padoy, G.G. Laracca, G. Ludovica, C. Fiorillo, G. Quero, S. Alfieri, L. Baldari, E. Cassinotti, L. Boni, D. Cuccurullo, G. Costamagna, B. Dallemagne

    مصطلحات موضوعية: Settore MED/18 - Chirurgia Generale

    الوصف: Surgical video analysis facilitates education and research. However, video recordings of endoscopic surgeries can contain privacy-sensitive information, especially if the endoscopic camera is moved out of the body of patients and out-of-body scenes are recorded. Therefore, identification of out-of-body scenes in endoscopic videos is of major importance to preserve the privacy of patients and operating room staff. This study developed and validated a deep learning model for the identification of out-of-body images in endoscopic videos. The model was trained and evaluated on an internal dataset of 12 different types of laparoscopic and robotic surgeries and was externally validated on two independent multicentric test datasets of laparoscopic gastric bypass and cholecystectomy surgeries. Model performance was evaluated compared to human ground truth annotations measuring the receiver operating characteristic area under the curve (ROC AUC). The internal dataset consisting of 356,267 images from 48 videos and the two multicentric test datasets consisting of 54,385 and 58,349 images from 10 and 20 videos, respectively, were annotated. The model identified out-of-body images with 99.97% ROC AUC on the internal test dataset. Mean ± standard deviation ROC AUC on the multicentric gastric bypass dataset was 99.94 ± 0.07% and 99.71 ± 0.40% on the multicentric cholecystectomy dataset, respectively. The model can reliably identify out-of-body images in endoscopic videos and is publicly shared. This facilitates privacy preservation in surgical video analysis.

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/37286660; info:eu-repo/semantics/altIdentifier/wos/WOS:001009117000071; volume:13; issue:1; firstpage:1; lastpage:8; numberofpages:8; journal:SCIENTIFIC REPORTS; https://hdl.handle.net/2434/979448Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85161016521

  4. 4
    دورية أكاديمية

    المساهمون: Cintoni, Marco, Grassi, Futura, Palombaro, M., Rinninella, Emanuele, Pulcini, Gabriele, Di Donato, A., Salvatore, Lisa, Quero, Giuseppe, Tortora, Giampaolo, Alfieri, Sergio, Gasbarrini, Antonio, Mele, Maria Cristina

    الوصف: Background: Pancreatic cancer incidence is growing, but the prognosis for survival is still poor. Patients with pancreatic cancer often suffer from malnutrition and sarcopenia, two clinical conditions that negatively impact oncological clinical outcomes. The aim of this systematic review was to analyze the impact of different nutritional interventions on clinical outcomes in patients with pancreatic cancer during chemotherapy. Methods: A systematic review of MedLine, EMBASE, and Web of Science was carried out in December 2022, identifying 5704 articles. Titles and abstracts of all records were screened for eligibility based on inclusion criteria, and nine articles were included. Results: All nine articles included were prospective studies, but a meta-analysis could not be performed due to heterogenicity in nutritional intervention. This Systematic Review shows an improvement in Quality of Life, nutritional status, body composition, oral intake, and Karnofsky Performance Status, following nutritional interventions. Conclusions: This Systematic Review in pancreatic cancer patients during chemotherapies does not allow one to draw firm conclusions. However, nutritional support in pancreatic cancer patients is advisable to ameliorate oncological care. Further well-designed prospective studies are needed to identify nutritional support’s real impact and to establish a reliable way to improve nutritional status of pancreatic cancer patients during chemotherapy.

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/36771433; info:eu-repo/semantics/altIdentifier/wos/WOS:000930980000001; volume:15; issue:3; firstpage:727; lastpage:N/A; issueyear:2023; journal:NUTRIENTS; https://hdl.handle.net/10807/231999Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85147692195

  5. 5
    دورية أكاديمية
  6. 6
    دورية أكاديمية
  7. 7
    دورية أكاديمية

    المساهمون: Jimeenez-Seanchez, C., Sinturel, F., Mezza, Teresa, Loizides-Mangold, U., Montoya, J. P., Li, L., Di Giuseppe, Gianfranco, Quero, Giuseppe, Guessous, I., Jornayvaz, F., Schrauwen, P., Stenvers, D. J., Alfieri, Sergio, Giaccari, Andrea, Berishvili, E., Compagnon, P., Bosco, D., Riezman, H., Dibner, C., Maechler, P.

    مصطلحات موضوعية: diabetes, Settore MED/13 - ENDOCRINOLOGIA

    الوصف: In this study, we identified new lipid species associated with the loss of pancreatic β-cells triggering diabetes. We performed lipidomics measurements on serum from prediabetic mice lacking β-cell prohibitin-2 (a model of monogenic diabetes) patients without previous history of diabetes but scheduled for pancreaticoduodenectomy resulting in the acute reduction of their β-cell mass (~50%), and patients with type 2 diabetes (T2D). We found lysophosphatidylinositols (lysoPIs) were the main circulating lipid species altered in prediabetic mice. The changes were confirmed in the patients with acute reduction of their β-cell mass and in those with T2D. Increased lysoPIs significantly correlated with HbA1c (reflecting glycemic control), fasting glycemia, and disposition index, and did not correlate with insulin resistance or obesity in human patients with T2D. INS-1E β-cells as well as pancreatic islets isolated from nondiabetic mice and human donors exposed to exogenous lysoPIs showed potentiated glucose-stimulated and basal insulin secretion. Finally, addition of exogenous lysoPIs partially rescued impaired glucose-stimulated insulin secretion in islets from mice and humans in the diabetic state. Overall, lysoPIs appear to be lipid species upregulated in the prediabetic stage associated with the loss of β-cells and that support the secretory function of the remaining β-cells.

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/37862465; volume:73; issue:1; firstpage:93; lastpage:107; numberofpages:15; issueyear:2024; journal:DIABETES; https://hdl.handle.net/10807/262626Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85180714495

  8. 8
    دورية أكاديمية

    المساهمون: Brusco, N., Sebastiani, G., Di Giuseppe, G., Licata, G., Grieco, G. E., Fignani, D., Nigi, L., Formichi, C., Aiello, E., Auddino, S., Quero, Giuseppe, Cefalo, Chiara Maria Assunta, Cinti, Francesca, Mari, A., Ferraro, Pietro Manuel, Pontecorvi, Alfredo, Alfieri, Sergio, Giaccari, Andrea, Dotta, F., Mezza, Teresa

    الوصف: Aims/hypothesis: Endoplasmic reticulum (ER) stress and beta cell dedifferentiation both play leading roles in impaired insulin secretion in overt type 2 diabetes. Whether and how these factors are related in the natural history of the disease remains, however, unclear. Methods: In this study, we analysed pancreas biopsies from a cohort of metabolically characterised living donors to identify defects in in situ insulin synthesis and intra-islet expression of ER stress and beta cell phenotype markers. Results: We provide evidence that in situ altered insulin processing is closely connected to in vivo worsening of beta cell function. Further, activation of ER stress genes reflects the alteration of insulin processing in situ. Using a combination of 17 different markers, we characterised individual pancreatic islets from normal glucose tolerant, impaired glucose tolerant and type 2 diabetic participants and reconstructed disease progression. Conclusions/interpretation: Our study suggests that increased beta cell workload is accompanied by a progressive increase in ER stress with defects in insulin synthesis and loss of beta cell identity. Graphical abstract: [Figure not available: see fulltext.]

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/36280617; info:eu-repo/semantics/altIdentifier/wos/WOS:000871276400001; issue:N/A; firstpage:N/A; lastpage:N/A; issueyear:2022; journal:DIABETOLOGIA; https://hdl.handle.net/10807/219430Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85140460796

  9. 9
    دورية أكاديمية
  10. 10
    دورية أكاديمية