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Статті в журналах з теми "MEDICINA MOLECOLARE"
Camporesi, Silvia, and Stefano Giaimo. "Medicina molecolare. Questioni filosofiche." PARADIGMI, no. 1 (April 2011): 29–48. http://dx.doi.org/10.3280/para2011-001003.
Повний текст джерелаSerra, Angelo. "La sperimentazione sull'embrione umano: una nuova esigenza della scienza e della medicina?" Medicina e Morale 42, no. 1 (February 28, 1993): 97–116. http://dx.doi.org/10.4081/mem.1993.1072.
Повний текст джерелаBellavite, P., M. Semizzi, P. Musso, R. Ortolani, and G. Andrioli. "Medicina ufficiale e terapie non convenzionali: dal conflitto all’integrazione?" Medicina e Morale 50, no. 5 (October 31, 2001): 877–904. http://dx.doi.org/10.4081/mem.2001.735.
Повний текст джерелаSantoro, Massimo, Michele Grieco, Rosa Marina Melillo, Alfredo Fusco, and Giancarlo Vecchio. "Molecular defects in thyroid carcinomas: Role of the RET oncogene in thyroid neoplastic transformation." European Journal of Endocrinology 133, no. 5 (November 1995): 513–22. http://dx.doi.org/10.1530/eje.0.1330513.
Повний текст джерелаSalvatore, Domenico, Angela Celetti, Nicole Fabien, Christian Paulin, Maria Luisa Martelli, Caterina Battaglia, Daniela Califano, et al. "Low frequency of p53 mutations in human thyroid tumors; p53 and Ras mutation in two out of fifty-six thyroid tumours." European Journal of Endocrinology 134, no. 2 (February 1996): 177–83. http://dx.doi.org/10.1530/eje.0.1340177.
Повний текст джерелаPalmieri, G., G. Lotrecchiano, G. Ricci, R. Spiezia, G. Lombardi, AR Bianco, and G. Torino. "Gonadal function after multimodality treatment in men with testicular germ cell cancer." European Journal of Endocrinology 134, no. 4 (April 1996): 431–36. http://dx.doi.org/10.1530/eje.0.1340431.
Повний текст джерелаMagistroni, Riccardo. "La ricerca oggi." Giornale di Clinica Nefrologica e Dialisi 25, no. 3 (July 10, 2013): 282–87. http://dx.doi.org/10.33393/gcnd.2013.1056.
Повний текст джерелаMartegani, M. P., A. Gasbarri, A. Bartolazzi, and L. Ruco. "La diagnosi molecolare di sarcoma sinoviale." Pathologica 94, no. 5 (October 1, 2002): 257–62. http://dx.doi.org/10.1007/s102420200042.
Повний текст джерелаPuntoni, Riccardo. "Attività Del Gruppo Dl Epidemiologia Molecolare." Tumori Journal 83, no. 2 (March 1997): VIII. http://dx.doi.org/10.1177/030089169708300235.
Повний текст джерелаBoiocchi, Mauro. "Attività Del Gruppo Dl Oncologia Molecolare Della Sic." Tumori Journal 83, no. 2 (March 1997): X. http://dx.doi.org/10.1177/030089169708300237.
Повний текст джерелаДисертації з теми "MEDICINA MOLECOLARE"
Rihawi, Karim <1984>. "Caratterizzazione molecolare per la medicina personalizzata nel paziente oncologico." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2021. http://amsdottorato.unibo.it/9944/1/TESI%20DOTTORATO%20Karim%20Rihawi_final.pdf.
Повний текст джерелаCirculating tumor cells (CTCs) represent a subset of cells found in the blood of patients with solid tumors, which are mainly involved in the process of metastatization. CTCs preserve primary tumor heterogeneity and mimic tumor properties, and may be considered as clinical biomarker, preclinical model, and therapeutic target. As such, CTCs can play a pivotal role as being a component of liquid biopsy which has potential in analyzing the genomic landscape of patients with cancer, supervising treatment responses, monitoring minimal residual disease, and managing non-invasive therapy resistance. Compared with traditional tissue biopsy, liquid biopsy is noninvasive and real-time. Therefore, CTCs can be used to tailor treatment in oncology patients. The aim of this work is to obtain through the detection of CTCs a multi-level molecular characterization using different tumor samples from the same patient or the same sample but taken throughout different stages of the disease. In our study 190 patients were enrolled; among them, 19 had a CTC count > 4. We report the results of these patients highlighting the strengths and the pitfalls of the techniques utilized as well as the clinical implications of the genetic analyses which followed the identification and isolation of CTCs.
LIBERATOSCIOLI, LAURA. "Biologia molecolare della paraoxonasi." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/548.
Повний текст джерелаDe, Rocco Daniela, and Rocco Daniela De. "STUDIO CLINICO E MOLECOLARE DELLA SINDROME DI BERNARD-SOULIER." Doctoral thesis, Università degli studi di Trieste, 2015. http://hdl.handle.net/10077/10848.
Повний текст джерела2013/2014
La sindrome di Bernard-Soulier (BSS) è una rara piastrinopenia ereditaria causata da alterazioni a livello del complesso glicoproteico GPIb-IX-V, presente sulla membrana piastrinica e responsabile della adesione delle piastrine in seguito a danno vascolare. La BSS si trasmette come malattia autosomica recessiva (BBSA1) e i pazienti affetti presentano piastrine giganti e severi episodi di sanguinamento. Tuttavia in tempi recenti sono state descritte delle famiglie con una forma dominante nota come BSSA2. In questi pazienti la piastrinopenia è moderata e le piastrine presentano un volume leggermente aumentato. Finora sono state individuate solo 5 varianti in eterozigosi nel BSSA2:, 4 nel gene GP1BA e 1 in GP1BB. Fatta eccezione per p.Ala172Val del gene GP1BA che è relativamente frequente nella la popolazione Italiana, le altre 4 sono state descritte in singole famiglie. I pochi casi di cui disponiamo, soprattutto per la forma recessiva non ci permettono di avere informazioni sui meccanismi patogenetici e sulla sua evoluzione nel tempo. Per questo motivo è stato istituito un Consorzio Internazionale per lo studio della BSS grazie al quale è stato possibile raccogliere i dati clinici e molecolari di 132 famiglie. Tutte le informazioni sono state inserite in un database (BSS Consortium database) attualmente gestito dal nostro laboratorio e consultabile dai gruppi di studio che hanno aderito al Consorzio. Inoltre per aumentare le informazioni sulle varianti identificate nel BSSA1 abbiamo incrementato i dati molecolari delle famiglie del Consorzio con i dati di altre 79 famiglie descritte in letteratura, raggiungendo un totale di 211 famiglie. Tutte le mutazioni identificate in queste famiglie sono state poi inserite in un database pubblico disponibile in rete (LOVD: Leiden Open Variation Database). La raccolta e l’elaborazione dei dati ci ha permesso di chiarire alcuni aspetti clinici e molecolari della malattia. Tuttavia data l’eterogeneità genetica e l’elevata espressione fenotipica gli studi genotipo-fenotipo si sono rivelati difficili da eseguire. Nonostante le molte informazioni acquisite, il database risulta ancora incompleto e limitato; per questo motivo è necessario raccogliere nuovi casi e inserire assieme alle varianti anche i relativi studi funzionali che si rivelano indispensabili per poter definire l’effetto delle varianti sul complesso GPIb-IX-V. Nell’ambito invece dello studio e caratterizzazione della forma meno grave di BSS (BSSA2) sono stati selezionati 120 pazienti piastrinopenici senza diagnosi caratterizzati da piastrine grandi. In questi pazienti sono stati analizzati i geni GP1BA, GP1BB e GP9 e sono state identificate 11 diverse varianti: 1 nonsense, 2 mutazioni di framshift, 1 mutazione nel codone di inizio e 5 varianti missense. Gli studi funzionali eseguiti sulle varianti missense per stabilire il loro ruolo patogenetico sono ancora in corso. Tuttavia se gli studi dovessero confermare la loro patogenicità 11 pazienti su 120 risulterebbero BSSA2 e questa forma dovrebbe essere considerata una tra le piastrinopenie ereditarie più frequenti in Italia. In conclusione grazie a questo studio è stato possibile raccogliere la più ampia casistica di pazienti affetti da BSSA1 fin’ora descritta e ottenere numerose informazioni sia sulla clinica che sulle mutazioni coinvolte. Il BSS Consortium database permetterà ai clinici che hanno partecipato allo studio di osservare nel tempo l’andamento della malattia nei pazienti e di ottenere informazioni utili per stabilire un corretto protocollo per la presa in carico dei pazienti. Infine la caratterizzazione di nuove forme di BSSA2 rappresenta il punto di partenza per descrivere al meglio la malattia BSSA2 sia dal punto di vista clinico che molecolare. In futuro sarà quindi indispensabile estendere il BSS Consortium database anche alla forma BSSA2.
XXVII Ciclo
XXVII Ciclo
1979
LAZZARETTI, CLARA. "Azione Molecolare E Cellulare Degli Ormoni Della Riproduzione." Doctoral thesis, Università degli studi di Modena e Reggio Emilia, 2022. http://hdl.handle.net/11380/1278344.
Повний текст джерелаClassically, follicle-stimulating hormone receptor (FSHR) and luteinizing hormone (LH) receptor (LHCGR) -driven cAMP-mediated signaling boosts human ovarian follicle growth and oocyte maturation. However, contradicting in vitro data suggest a different view on physiological significance of FSHR-mediated cAMP signalling, showing at the same time the activation of steroidogenic and pro-apoptotic events. These signals can be impaired by estrogens inducing anti-apoptotic events via nuclear receptors and non-genomic action of a G protein-coupled estrogen receptor (GPER). The aim of the project is to better understand the role of estrogens/gonadotropins and their membrane receptors in regulating ovarian physiology and the selection of the dominant follicle. In this study it was demonstrated that GPER heteromerizes both with FSHR and LHCGR at the cell surface of HEK293 cells overexpressing the two receptors as well as human primary granulosa lutein cells (hGLC). FSHR/GPER heteromers reprogram cAMP/death signals into proliferative stimuli fundamental for sustaining oocyte survival. In human granulosa cells, survival signals are missing at high FSHR:GPER ratio, which negatively impacts follicle maturation and strongly correlates with preferential Gαs protein/cAMP-pathway coupling and FSH responsiveness of patients undergoing controlled ovarian stimulation. In contrast, FSHR/GPER heteromers triggered anti-apoptotic/proliferative FSH signaling delivered via the Gβγ dimer, whereas impairment of heteromer formation or GPER knockdown enhanced the FSH-dependent cell death and steroidogenesis. On the other hand, GPER/LHCGR complex does not affect the LH and hCG-induced cAMP production and do not compromise the activation of the cAMP/PKA pathway, as it is indicated by similar CREB and ERK1/2 phosphorylation and same progesterone production in hGLC treated with siRNA against GPER, and the mock-treated one. Interestingly, GPER displace the LHCGR/Gαq coupling and consequently impedes the intracellular Ca2+ release and IP1 accumulation in LHCGR-GPER co-expressing HEK293 cells upon LH and hCG treatment compared to LHCGR-expressing cells. Also, it was demonstrated that in presence of GPER the kinetic of FSHR internalization through early and late endosomes is reduced, suggesting its ability to blockade FSHR at the intracellular level and reduce FSHR recycling on cell membrane. Indeed, FSHR internalization is necessary for GPER to inhibit FSH-induced cAMP response. According to our results, estrogens are selectively involved in the regulation of pro- and anti-apoptotic signals and receptor internalization through FSHR/GPER complexes and in modulation of LHCGR-mediated signaling cascade. Our findings indicate how oocyte maturation depends on the capability of GPER to shape FSHR and LHCGR selective signals, indicating hormone receptor heteromers may be a marker of cell proliferation.
Jakimovska, Frosina. "Characterization of the interaction between nucleophosmin (NPM) and highmobility group a (HMGA) proteins." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2760.
Повний текст джерелаABSTRACT HMGA proteins are members of the high mobility group (HMG) non-histone, architectural chromosomal proteins. The HMGA family consists of: A1a, A1b and A2, the first two being isoforms produced by alternative splicing. These are small proteins, about 100aa residues long, characterized by three basic stretches of AT-hooks which bind to the AT-rich sequences on the DNA minor groove. They are normally present in rapidly proliferating cells (embryo) whereas upon differentiation the levels of these proteins decrease until they are nearly absent from adult cells. Overexpression of these proteins has been correlated with various types of neoplastic transformations. The interaction network of HMGA has been an object of study for years in our laboratory and one of the most intriguing protein-protein interactions studied is the one between HMGA and nucleophosmin. Nucleophosmin (NPM, B23, numatrin or NO38) is one of the most abundant phosphoproteins, mainly localized in the nucleoli but it also shuttles between the nucleus and the cytoplasm. This versatile protein has been proven to be involved in various cellular functions and related to both proliferative and growth-suppressive roles in the cell. The first evidence of the interaction HMGA2-NPM in our lab has been obtained by in vitro assays (affinity chromatography). The step ahead was to see if this interaction occurs in vivo and if it does, to try to find ts functional significance. Thus,immunoprecipitation (IP) experiments were performed.The first one gave the proof thet interaction between HMGA2 protein and NPM (transfected and endogenous) occurs. The second IP gave the evidence that interaction occurs between HMGA1a and NPM too. This in vivo protein-protein interaction was to be given a functional significance. We tested by siRNA HMGA1a treatment if downregulation of HMGA1a expression influences the expression of the SOD2 gene (regulated by NPM). The effect of the HMGA1a silencing has proven to be very slight on the SOD2 gene (a 14% of expression reduction). EMSA experiments have been performed in order to test the effect of NPM on the DNA binding properties of the HMGA2 protein with the DNA probes E3 and HCRII. In both cases it has been observed that NPM increases the DNA binding affinity of the HMGA2 protein.
1979
Vignini, Arianna. "Sindrome metabolica e rischio cardiovascolare: un nuovo approccio allo studio degli effetti a livello molecolare." Doctoral thesis, Università Politecnica delle Marche, 2007. http://hdl.handle.net/11566/242476.
Повний текст джерелаDotti, Isabella. "Towards molecular medicine:optimization of the methods for gene expression analysis in clinical samples." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2626.
Повний текст джерелаThe advent of molecular “-omics” technologies enabled an unprecedented view into the inner molecular mechanisms of cancer and enhanced optimism towards a patient-tailored vision of medicine. The successful application of these molecular approaches in the discovery of candidate biomarker has accelerated the shift towards personalization of medicine. Indeed, biomarkers hold great promise for refining our ability to establish early diagnosis and prognosis, and to predict response to therapy. The develoment of clinically useful biomarkers would be impossible without access to human biological specimens and associated patient data, since they complete the molecular information gained from laboratory research. Furthermore, with the advances of sensitive molecular technologies, human bio-specimens can be now successfully used for wide analysis at all molecular levels (DNA, RNA and proteins), in addition to conventional cytologic and histologic investigations. However, despite the hundreds of reports on tumor markers, only a few markers have proven clinically useful. The insufficient experience in clinical application of molecular methods combined with the high complexity of clinical material represent the major obstacles for the development of clinically useful biomarkers. Thanks to the possibility to have access to the fresh and archival samples from the hospital, our laboratory can investigate the potential of technological innovations and the current technical pitfalls directly on clinical material. The work in my thesis is strictly correlated to this activity. In particular, the first part is focused on the technical optimization of molecular methods for gene expression analysis in biological fluids and especially in urine samples. In this context we validated a new experimental kit for total RNA extraction from urine samples and tested the potential of a colorimetric approach for PCR product detection. The major part of the study is focused on the technical optimization of molecular methods for gene expression analysis in archival material. This activity is in step with one of the main objectives of the European project called “Archive tissues: improving molecular medicine research and clinical practice-IMPACTS”, in which my laboratory and other 20 European centres are directly involved. In this phase the comparison of the experiences between laboratories and their active collaboration are essential for a more rapid validation of protocols dedicated to RNA (but also DNA and protein) analysis. In particular, we investigated some molecular aspects involved in the pre-analytical phase (tissue fixation procedures) and analytical phase (RNA extraction, RNA quantification and integrity assessment, qRT-PCR) of tissue processing. The final objective of this activity will be the definition of common technical guidelines for a reliable quantification of molecular biomarkers for diagnosis, prognosis and therapy directly in human archival samples. Finally, my thesis includes the clinical application of molecular methods for the quantification of candidate biomarkers in two archival case studies (a breast cancer and an adrenal gland cancer case study). In the breast cancer case study we showed that a panel of seven genes (involved in different cell pathways) is associated to patients’ survival. The adrenal gland tumor case study is part of a preliminary study about the angiogenetic process in rare human cancers.
1979
Agostini, Stefania. "Il sistema [MV(N)(PNP)]2+ (M=Tc-99m, Re-188) nella scintigrafia miocardica e in medicina nucleare molecolare." Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425059.
Повний текст джерелаSinigaglia, Milena. "Dissection of the effects induced by VEGF165, VEGF121 and Semaphorin 3A in endothelial cells." Doctoral thesis, Università degli studi di Trieste, 2009. http://hdl.handle.net/10077/3258.
Повний текст джерелаThe development of new blood vessels is a complex and highly regulated process that requires the coordinated action of different growth factors. Vascular Endothelial Growth Factor (VEGF) is a powerful inducer of angiogenesis, acting through the metabolic activation, proliferation and migration of endothelial cells. The major angiogenic member of the VEGF family is VEGF-A, a gene which is transcribed to give rise to at least 4 major splicing variants, of 206, 189, 165 and 121 amino acids in humans. The angiogenic effect of the most abundant isoform (VEGF165) is basically mediated by its interaction with VEGFR2 (KDR) and VEGFR1 (Flt-1) as well as with the co-receptor Neuropilin-1 (NP-1). The shortest isoform (VEGF121) binds VEGFR1 and VEGFR2 only, but not NP-1. NP-1, together with PlexinA1, also acts as a receptor of Semaphorin 3A (Sema3A), a factor also involved in vascular patterning, besides its very well known role in axonal guidance. The aim of this project has been the detailed analysis of the peculiarity/specificity of the effect of VEGF165, VEGF121 and Sema3A in endothelial cells. We first exploited an Adeno Associated Virus (AAV)-based gene delivery to unravel the in vivo effect of these cytokines. In particular, we observed that the prolonged expression of the main isoform of VEGF, VEGF165, acted as a powerful inducer of angiogenesis, stimulating the development of both a larger capillary network and the formation of an impressive new set of arterioles. Most surprisingly, an unexpected effect of VEGF165 was also the recruitment to the sites of its expression, of a vast set of mononuclear cells. These cells derived from the bone marrow and expressed a broad set of monocytic markers (CD45+, CD11b+); their presence correlated with the formation of arterioles and the maturation of the VEGF-induced vasculature. Strikingly, VEGF121 (the shorter form unable to bind NP-1) was, on the contrary, unable to induce maturation of the newly formed capillaries to mature arteries and to recruit cells, an observation that suggested that these monocytes might be essential in blood vessel maturation. We found that cell recruitment both in vitro and in vivo strictly depends on NP-1 and that Sema3A, a NP-1 activator, acts as a powerful recruiter of these cells. The expression of VEGF and Sema3A receptors by CD11b+ cells together with the VEGFR2 interaction with NP-1, indicate that these cells could be target of a peculiar VEGF and/or Sema3A induced signalling pathway. Taken together, these results prompted us to develop an in vitro model to unravel the signalling features elicited by the VEGF165, VEGF121 and Sema3A on endothelial cells. In particular, we wanted to dissect these pathways through a proteomic approach involving the detection of the phosphoproteome of endothelial cells expressing specific receptor after treatment with the various ligands of interest. Due to the large amount of growth factors required for this kind of experimentation, we first established a Baculovirus-based system to generate the recombinant factors. For this purpose, we engineered suitable plasmids encoding VEGF165, VEGF121 and Sema3A endowed of a cleavable histidine tag at the N-terminus. Once the recombinant protein expression conditions were set up, we moved to optimize protein purification by affinity chromatography, together with the removal of the tag. The functionality of baculovirus-expressed VEGF165 and VEGF121 was ascertained by the analysis of VEGF receptor phosphorylation, as well as proliferation assays on endothelial cells; a cell contraction assay confirmed that the recombinant Sema3A produced was as active as protein expressed in mammalian cells. To dissect the differential signalling induced by each of the recombinant factors, we explored their transduction pathways in endothelial cell lines expressing the main receptors (KDR and NP1). We set up the lysis conditions and bi-dimensional SDS-PAGE, together with the optimal phospho-proteome staining. The findings obtained, together with phospho-enrichment approaches, strongly supported that peculiar signalling pathways exist in endothelial cells, selectively triggered by VEGF165, VEGF121 and Sema3A, as demonstrated by the differential pattern of phosphorylated proteins induced by the recombinant proteins. Furthermore, we first demonstrated a close similarity in the phospho-tyrosine proteome induced by VEGF165 and Sema3A, at least in the cellular system examined.
1980
Biondi, Roberta <1989>. "Evidenziazione sierologica e molecolare di Chlamydia pneumoniae e Simkania negevensis in pazienti affetti da patologia aterosclerotica carotidea." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amsdottorato.unibo.it/8499/1/Tesi%20PhD%20Roberta%20Biondi.pdf.
Повний текст джерелаAtherosclerosis is a multifactorial and complex pathology. Some studies show a possible involvement of microorganisms, but the results are contradictory. The aim of this study is to evaluate the presence of anti- Chlamydia pneumoniae and anti-Simkania negevensis antibodies in sera of patients waiting for carotid endarterectomy (CEA) surgery. In addition, after the surgery it was possible to search DNA of microorganisms into the removed pathological tissue. For the serological evaluation it was used a home-made immunoenzymatic technique, for the molecular evaluation a nested PCR. For this study, 50 patients were enrolled. The obtained results pointed out a positivity of the 28% for IgG anti-Simkania negevensis and of the 10% for IgA; for C. pneumoniae the percentages were of 20% of IgG and 8% for IgA. Molecular data of the PCR obtained were: 34% of positivity for S. negevensis and 26% for C. pneumoniae. The results of this study support the hypothesis that these microorganisms can develop a quiescent or persistent status of the infection, in which it is possible to observe, through technique of PCR, DNA of them into the pathological tissue.
Книги з теми "MEDICINA MOLECOLARE"
Antonino, Annetta, ed. Il progresso terapeutico: Dalla tavoletta sumera alla medicina molecolare. Sansepolcro (Arezzo): Aboca museum, 2008.
Знайти повний текст джерелаCorbellini, Gilberto. Le grammatiche del vivente: Storia della biologia e della medicina molecolare. Roma: GLF, Editori Laterza, 1999.
Знайти повний текст джерелаBuoninconti, Raffaello. I recettori dell’angiotensina: Dalla biologia molecolare alla terapia con gli antagonisti recettoriali. Milano: Springer-Verlag Italia, 2007.
Знайти повний текст джерелаAzzone, G. F. Biologia e medicina tra molecole, informazione e storia: Logica delle spiegazioni e struttura del pensiero. Roma: Laterza, 1991.
Знайти повний текст джерелаIntroduzione alla Medicina Molecolare. Milan: Springer-Verlag, 2005. http://dx.doi.org/10.1007/88-470-0381-4.
Повний текст джерелаRoss, Dennis W. Introduzione alla Medicina Molecolare. Springer, 2005.
Знайти повний текст джерела