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Your search keyword '"Conconi, M.T."' showing total 25 results
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25 results on '"Conconi, M.T."'

9. Poly-ɛ-caprolactone composite scaffolds for bone repair

Author

DI LIDDO, R., primary, PAGANIN, P., additional, LORA, S., additional, DALZOPPO, D., additional, GIRAUDO, C., additional, MIOTTO, D., additional, TASSO, A., additional, BARBON, S., additional, ARTICO, M., additional, BIANCHI, E., additional, PARNIGOTTO, P.P., additional, CONCONI, M.T., additional, and GRANDI, C., additional

Published
2014
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12. T-52 The role of immunity and gender during acute liver injury

Author

Di Liddo, R., primary, Amodio, V., additional, Cappon, A., additional, Arcidiacono, D., additional, Bizzaro, D., additional, Tasso, A., additional, Conconi, M.T., additional, Parnigotto, P., additional, Sturniolo, G.C., additional, Burra, P., additional, and Russo, F.P., additional

Published
2013
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14. OC-5 Systemic administration of a novel human umbilical cord mesenchymal stem cells population accelerates the resolution of acute liver injury

Author

Arcidiacono, D., primary, Bizzaro, D., additional, Chioato, T., additional, Di Liddo, R., additional, Banerjee, A., additional, Cappon, A., additional, Bo, P., additional, Conconi, M.T., additional, Parnigotto, P.P., additional, Mirandola, S., additional, Gringeri, E., additional, Carraro, A., additional, Cillo, U., additional, Russo, F.P., additional, and Burra, P., additional

Published
2012
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15. 1070 IMMUNE RESPONSE AND GENDER DISPARITY INFLUENCE LIVER REGENERATION AFTER ACUTE HEPATIC INJURY

Author

Arcidiacono, D., primary, Cappon, A., additional, Bizzaro, D., additional, Di Liddo, R., additional, Mescoli, C., additional, Cardin, R., additional, Piciocchi, M., additional, Chioato, T., additional, Conconi, M.T., additional, Parnigotto, P.P., additional, Rugge, M., additional, Sturniolo, G.C., additional, Burra, P., additional, and Russo, F.P., additional

Published
2011
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22. Experimental abdominal wall defect repaired with acellular matrix.

Author

Gamba, P.G., Conconi, M.T., Lo Piccolo, R., Zara, G., Spinazzi, R., and Parnigotto, P.P.

Subjects
ABDOMINAL wall, ABDOMINAL muscles, RESPIRATORY organs, EXTRACELLULAR matrix proteins, NEOVASCULARIZATION, BLOOD-vessel development
Abstract

In the surgical repair of congenital abdominal-wall defects (AWD), the ready availability of a non-immunogenic and non-prosthetic biomaterial that could guide the regeneration of normal tissue is a fascinating possibility. Biomaterials are already in use, but in our experience, an acellular matrix (ACM) can stimulate exact regeneration of the absent tissue. We explored the possibility of using an ACM to repair a muscular AWD in an animal model. Male New Zealand white rabbits (3–4 kg, n = 18) were anesthetized and the abdominal wall was shaved and scrubbed; a vertical incision was made in the left lower quadrant and a large patch of external-oblique muscle was resected (3 × 3 cm). The animals underwent reconstruction with homologous diaphragm acellular matrix (HDAM) grafts that were previously prepared using a detergent enzymatic method. The patches were evaluated histologically at 9 (n = 6), 40 (n = 6), and 90 (n = 6) days post-surgery in each group; moreover, 90 days post-surgery an electromyogram (EMG) (n = 6) of the implanted matrix was recorded. Histologic analysis demonstrated that the HDAM supported fibroblast migration, deposition of newly-formed collagen, and neovascularization. No signs of necrosis, or evidence of skeletal-muscle-cell ingrowth were detected. The EMG revealed minimum muscular electrophysiologic activity, probably due to muscle underlying the patch. The HDAM we employed was thus not able to produce reconstruction of the skeletal muscle, and was progressively remodeled into fibrous tissue. Since the ultimate reason for failure of muscle regeneration is a lack of myogenesis, future studies will use ACMs preconditioned by various regulators of myoblast proliferation and differentiation. [ABSTRACT FROM AUTHOR]

Published
2002
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25. Adrenomedullin Expression Characterizes Leukemia Stem Cells and Associates With an Inflammatory Signature in Acute Myeloid Leukemia

Author

Giorgia Simonetti, Davide Angeli, Elisabetta Petracci, Eugenio Fonzi, Susanna Vedovato, Alessandra Sperotto, Antonella Padella, Martina Ghetti, Anna Ferrari, Valentina Robustelli, Rosa Di Liddo, Maria Teresa Conconi, Cristina Papayannidis, Claudio Cerchione, Michela Rondoni, Annalisa Astolfi, Emanuela Ottaviani, Giovanni Martinelli, Michele Gottardi, Simonetti G., Angeli D., Petracci E., Fonzi E., Vedovato S., Sperotto A., Padella A., Ghetti M., Ferrari A., Robustelli V., Di Liddo R., Conconi M.T., Papayannidis C., Cerchione C., Rondoni M., Astolfi A., Ottaviani E., Martinelli G., and Gottardi M.

Subjects
Cancer Research, CD34, Biology, acute myeloid leukemia, Immune tolerance, hemic and lymphatic diseases, medicine, adrenomedullin, hematopoiesis, inflammation, leukemia stem cells, Progenitor cell, RC254-282, Original Research, Myeloid leukemia, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, Haematopoiesis, Leukemia, medicine.anatomical_structure, Oncology, hematopoiesi, Cancer research, Bone marrow, Stem cell
Abstract

Adrenomedullin (ADM) is a hypotensive and vasodilator peptide belonging to the calcitonin gene-related peptide family. It is secreted in vitro by endothelial cells and vascular smooth muscle cells, and is significantly upregulated by a number of stimuli. Moreover, ADM participates in the regulation of hematopoietic compartment, solid tumors and leukemias, such as acute myeloid leukemia (AML). To better characterize ADM involvement in AML pathogenesis, we investigated its expression during human hematopoiesis and in leukemic subsets, based on a morphological, cytogenetic and molecular characterization and in T cells from AML patients. In hematopoietic stem/progenitor cells and T lymphocytes from healthy subjects, ADM transcript was barely detectable. It was expressed at low levels by megakaryocytes and erythroblasts, while higher levels were measured in neutrophils, monocytes and plasma cells. Moreover, cells populating the hematopoietic niche, including mesenchymal stem cells, showed to express ADM. ADM was overexpressed in AML cells versus normal CD34+ cells and in the subset of leukemia compared with hematopoietic stem cells. In parallel, we detected a significant variation of ADM expression among cytogenetic subgroups, measuring the highest levels in inv(16)/t(16;16) or complex karyotype AML. According to the mutational status of AML-related genes, the analysis showed a lower expression of ADM in FLT3-ITD, NPM1-mutated AML and FLT3-ITD/NPM1-mutated cases compared with wild-type ones. Moreover, ADM expression had a negative impact on overall survival within the favorable risk class, while showing a potential positive impact within the subgroup receiving a not-intensive treatment. The expression of 135 genes involved in leukemogenesis, regulation of cell proliferation, ferroptosis, protection from apoptosis, HIF-1α signaling, JAK-STAT pathway, immune and inflammatory responses was correlated with ADM levels in the bone marrow cells of at least two AML cohorts. Moreover, ADM was upregulated in CD4+ T and CD8+ T cells from AML patients compared with healthy controls and some ADM co-expressed genes participate in a signature of immune tolerance that characterizes CD4+ T cells from leukemic patients. Overall, our study shows that ADM expression in AML associates with a stem cell phenotype, inflammatory signatures and genes related to immunosuppression, all factors that contribute to therapy resistance and disease relapse.

Published
2021

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