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2. Structural and non-coding variants increase the diagnostic yield of clinical whole genome sequencing for rare diseases

Author

Pagnamenta, Alistair T., Camps, Carme, Giacopuzzi, Edoardo, Taylor, John M., Hashim, Mona, Calpena, Eduardo, Kaisaki, Pamela J., Hashimoto, Akiko, Yu, Jing, Sanders, Edward, Schwessinger, Ron, Hughes, Jim R., Lunter, Gerton, Dreau, Helene, Ferla, Matteo, Lange, Lukas, Kesim, Yesim, Ragoussis, Vassilis, Vavoulis, Dimitrios V., Allroggen, Holger, Ansorge, Olaf, Babbs, Christian, Banka, Siddharth, Baños-Piñero, Benito, Beeson, David, Ben-Ami, Tal, Bennett, David L., Bento, Celeste, Blair, Edward, Brasch-Andersen, Charlotte, Bull, Katherine R., Cario, Holger, Cilliers, Deirdre, Conti, Valerio, Davies, E. Graham, Dhalla, Fatima, Dacal, Beatriz Diez, Dong, Yin, Dunford, James E., Guerrini, Renzo, Harris, Adrian L., Hartley, Jane, Hollander, Georg, Javaid, Kassim, Kane, Maureen, Kelly, Deirdre, Kelly, Dominic, Knight, Samantha J. L., Kreins, Alexandra Y., Kvikstad, Erika M., Langman, Craig B., Lester, Tracy, Lines, Kate E., Lord, Simon R., Lu, Xin, Mansour, Sahar, Manzur, Adnan, Maroofian, Reza, Marsden, Brian, Mason, Joanne, McGowan, Simon J., Mei, Davide, Mlcochova, Hana, Murakami, Yoshiko, Németh, Andrea H., Okoli, Steven, Ormondroyd, Elizabeth, Ousager, Lilian Bomme, Palace, Jacqueline, Patel, Smita Y., Pentony, Melissa M., Pugh, Chris, Rad, Aboulfazl, Ramesh, Archana, Riva, Simone G., Roberts, Irene, Roy, Noémi, Salminen, Outi, Schilling, Kyleen D., Scott, Caroline, Sen, Arjune, Smith, Conrad, Stevenson, Mark, Thakker, Rajesh V., Twigg, Stephen R. F., Uhlig, Holm H., van Wijk, Richard, Vona, Barbara, Wall, Steven, Wang, Jing, Watkins, Hugh, Zak, Jaroslav, Schuh, Anna H., Kini, Usha, Wilkie, Andrew O. M., Popitsch, Niko, and Taylor, Jenny C.

Published
2023
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4. Next Generation Sequencing Analysis in Early Onset Dementia Patients.

Author

Bonvicini, Cristian, Scassellati, Catia, Benussi, Luisa, Di Maria, Emilio, Maj, Carlo, Ciani, Miriam, Fostinelli, Silvia, Mega, Anna, Bocchetta, Martina, Lanzi, Gaetana, Giacopuzzi, Edoardo, Ferraboli, Sergio, Pievani, Michela, Fedi, Virginia, Defanti, Carlo Alberto, Giliani, Silvia, Alzheimer’s Disease Neuroimaging Initiative, Frisoni, Giovanni Battista, Ghidoni, Roberta, and Gennarelli, Massimo

Subjects
Alzheimer’s Disease Neuroimaging Initiative, Humans, Dementia, Apolipoproteins E, Risk Assessment, Retrospective Studies, Age of Onset, Alleles, Aged, Middle Aged, Female, Male, Presenilin-2, Genetic Variation, Genetic Association Studies, High-Throughput Nucleotide Sequencing, Prion Proteins, C9orf72 Protein, Alzheimer’s disease, Lewy body dementia, common variants, early onset dementia, frontotemporal dementia, next generation sequencing, rare mutations, Alzheimer's disease, frontotemporal dementia, Clinical Sciences, Cognitive Sciences, Neurosciences, Neurology & Neurosurgery
Abstract

BackgroundEarly onset dementias (EOD) are rare neurodegenerative dementias that present before 65 years. Genetic factors have a substantially higher pathogenetic contribution in EOD patients than in late onset dementia.ObjectiveTo identify known and/or novel rare variants in major candidate genes associated to EOD by high-throughput sequencing. Common-risk variants of apolipoprotein E (APOE) and prion protein (PRNP) genes were also assessed.MethodsWe studied 22 EOD patients recruited in Memory Clinics, in the context of studies investigating genetic forms of dementia. Two methodological approaches were applied for the target-Next Generation Sequencing (NGS) analysis of these patients. In addition, we performed progranulin plasma dosage, C9Orf72 hexanucleotide repeat expansion analysis, and APOE genotyping.ResultsWe detected three rare known pathogenic mutations in the GRN and PSEN2 genes and eleven unknown-impact mutations in the GRN, VCP, MAPT, FUS, TREM2, and NOTCH3 genes. Six patients were carriers of only common risk variants (APOE and PRNP), and one did not show any risk mutation/variant. Overall, 69% (n = 9) of our early onset Alzheimer's disease (EAOD) patients, compared with 34% (n = 13) of sporadic late onset Alzheimer's disease (LOAD) patients and 27% (n = 73) of non-affected controls (ADNI, whole genome data), were carriers of at least two rare/common risk variants in the analyzed candidate genes panel, excluding the full penetrant mutations.ConclusionThis study suggests that EOD patients without full penetrant mutations are characterized by higher probability to carry polygenic risk alleles that patients with LOAD forms. This finding is in line with recently reported evidence, thus suggesting that the genetic risk factors identified in LOAD might modulate the risk also in EOAD.

Published
2019

6. Clinical validation of a combinatorial PharmAcogeNomic approach in major Depressive disorder: an Observational prospective RAndomized, participant and rater-blinded, controlled trial (PANDORA trial)

Author

Minelli, Alessandra, Barlati, Stefano, Vitali, Erika, Bignotti, Stefano, Dattilo, Vincenzo, Tura, Giovanni Battista, Maffioletti, Elisabetta, Giacopuzzi, Edoardo, Santoro, Vincenza, Perusi, Giulia, Cobelli, Chiara, Magri, Chiara, Bonizzato, Silvia, Bocchio-Chiavetto, Luisella, Spina, Edoardo, Vita, Antonio, and Gennarelli, Massimo

Published
2021
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10. CHARR efficiently estimates contamination from DNA sequencing data

Author

Lu, Wenhan, primary, Gauthier, Laura D., additional, Poterba, Timothy, additional, Giacopuzzi, Edoardo, additional, Goodrich, Julia K., additional, Stevens, Christine R., additional, King, Daniel, additional, Daly, Mark J., additional, Neale, Benjamin M., additional, and Karczewski, Konrad J., additional

Published
2023
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12. Bi-allelic genetic variants in the translational GTPases GTPBP1 and GTPBP2 cause a distinct identical neurodevelopmental syndrome

Author

Hannah, Michael G., Bugiardini, Enrico, Bertini, Enrico, Kriouile, Yamna, El-Khorassani, Mohamed, Aguennouz, Mhammed, Groppa, Stanislav, Karashova, Blagovesta M., Goraya, Jatinder S., Sultan, Tipu, Avdjieva, Daniela, Kathom, Hadil, Tincheva, Radka, Banu, Selina, Veggiotti, Pierangelo, Verrotti, Alberto, Lanari, Marcello, Savasta, Salvatore, Macaya, Alfons, Garavaglia, Barbara, Borgione, Eugenia, Papacostas, Savvas, Vikelis, Michail, Chelban, Viorica, Kaiyrzhanov, Rauan, Cortese, Andrea, Sullivan, Roisin, Papanicolaou, Eleni Z., Dardiotis, Efthymios, Maqbool, Shazia, Ibrahim, Shahnaz, Kirmani, Salman, Rana, Nuzhat N., Atawneh, Osama, Lim, Shen-Yang, Zuccotti, Gian V., Marseglia, Gian L., Esposito, Susanna, Shaikh, Farooq, Cogo, Paola, Corsello, Giovanni, Mangano, Salvatore, Nardello, Rosaria, Mangano, Donato, Scardamaglia, Annarita, Koutsis, George, Scuderi, Carmela, Ferrara, Pietro, Morello, Giovanna, Zollo, Massimo, Berni-Canani, Roberto, Terracciano, Luigi M., Sisto, Antonio, Di Fabio, Sandra, Strano, Federica, Scorrano, Giovanna, Di Bella, Saverio, Di Francesco, Ludovica, Manizha, Ganieva, Isrofilov, Maksud, Guliyeva, Ulviyya, Salayev, Kamran, Khachatryan, Samson, Xiromerisiou, Georgia, Spanaki, Cleanthe, Fiorillo, Chiara, Iacomino, Michele, Gaudio, Eugenio, Munell, Francina, Gagliano, Antonella, Jan, Farida, Chimenz, Roberto, Gitto, Eloisa, Iughetti, Lorenzo, Di Rosa, Gabriella, Maghnie, Mohamad, Pettoello-Mantovani, Massimo, Gupta, Neerja, Kabra, Madhulika, Benrhouma, Hanene, Tazir, Meriem, Bottone, Gabriella, Farello, Giovanni, Delvecchio, Maurizio, Di-Donato, Giulio, Obeid, Makram, Bakhtadze, Sophia, Saadi, Nebal W., Miraglia-Del-Giudice, Michele, Maccarone, Rita, Zaki, Maha S., Triki, Chahnez C., Kara, Majdi, Karimiani, Ehsan G., Salih, Ahmed M., Ramenghi, Luca A., Seri, Marco, Di-Falco, Giovanna, Mandarà, Luana, Barrano, Giuseppe, Elisa, Maurizio, Cherubini, Enrico, Operto, Francesca F., Valenzise, Mariella, Cattaneo, Antonino, Zazzeroni, Francesca, Alesse, Edoardo, Matricardi, Sara, Zafar, Faisal, Ullah, Ehsan, Afzal, Erum, Rahman, Fatima, Ahmed, Muhammad M., Parisi, Pasquale, Spalice, Alberto, De Filippo, Maria, Licari, Amelia, Trebbi, Edoardo, Romano, Ferdinando, Heimer, Gali, Al-Khawaja, Issam, Al-Mutairi, Fuad, Alkuraya, Fowzan S., Rizig, Mie, Shashkin, Chingiz, Zharkynbekova, Nazira, Koneyev, Kairgali, Salpietro, Vincenzo, Maroofian, Reza, Wangen, Jamie, Ciolfi, Andrea, Barresi, Sabina, Efthymiou, Stephanie, Lamaze, Angelique, Aughey, Gabriel N., Al Mutairi, Fuad, Rad, Aboulfazl, Rocca, Clarissa, Calì, Elisa, Accogli, Andrea, Zara, Federico, Striano, Pasquale, Mojarrad, Majid, Tariq, Huma, Giacopuzzi, Edoardo, Taylor, Jenny C., Oprea, Gabriela, Skrahina, Volha, Rehman, Khalil Ur, Abd Elmaksoud, Marwa, Bassiony, Mahmoud, El Said, Huda G., Abdel-Hamid, Mohamed S., Al Shalan, Maha, Seo, Gohun, Kim, Sohyun, Lee, Hane, Khang, Rin, Issa, Mahmoud Y., Elbendary, Hasnaa M., Rafat, Karima, Marinakis, Nikolaos M., Traeger-Synodinos, Joanne, Ververi, Athina, Sourmpi, Mara, Eslahi, Atieh, Khadivi Zand, Farhad, Beiraghi Toosi, Mehran, Babaei, Meisam, Jackson, Adam, Bertoli-Avella, Aida, Pagnamenta, Alistair T., Niceta, Marcello, Battini, Roberta, Corsello, Antonio, Leoni, Chiara, Chiarelli, Francesco, Dallapiccola, Bruno, Faqeih, Eissa Ali, Tallur, Krishnaraya K., Alfadhel, Majid, Alobeid, Eman, Maddirevula, Sateesh, Mankad, Kshitij, Banka, Siddharth, Ghayoor-Karimiani, Ehsan, Tartaglia, Marco, Chung, Wendy K., Green, Rachel, Jepson, James E.C., and Houlden, Henry

Published
2024
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17. Genome-wide association studies on Northern Italy isolated populations provide further support concerning genetic susceptibility for major depressive disorder.

Author

Dattilo, Vincenzo, primary, Ulivi, Sheila, additional, Minelli, Alessandra, additional, La Bianca, Martina, additional, Giacopuzzi, Edoardo, additional, Bortolomasi, Marco, additional, Bignotti, Stefano, additional, Gennarelli, Massimo, additional, Gasparini, Paolo, additional, and Concas, Maria Pina, additional

Published
2022
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19. Genome-wide association studies on Northern Italy isolated populations provide further support concerning genetic susceptibility for major depressive disorder.

Author

Dattilo, Vincenzo, Ulivi, Sheila, Minelli, Alessandra, La Bianca, Martina, Giacopuzzi, Edoardo, Bortolomasi, Marco, Bignotti, Stefano, Gennarelli, Massimo, Gasparini, Paolo, and Concas, Maria Pina

Subjects
GENOME-wide association studies, DISEASE risk factors, GENETIC variation, MONOGENIC & polygenic inheritance (Genetics), MENTAL illness, PHENOTYPES
Abstract

Major depressive disorder (MDD) is a psychiatric disorder with pathogenesis influenced by both genetic and environmental factors. To date, the molecular-level understanding of its aetiology remains unclear. Thus, we aimed to identify genetic variants and susceptibility genes for MDD with a genome-wide association study (GWAS) approach. We performed a meta-analysis of GWASs and a gene-based analysis on two Northern Italy isolated populations (cases/controls n = 166/472 and 33/320), followed by replication and polygenic risk score (PRS) analyses in Italian independent samples (cases n = 464, controls n = 339). We identified two novel MDD-associated genes, KCNQ5 (lead SNP rs867262, p = 3.82 × 10−9) and CTNNA2 (rs6729523, p = 1.25 × 10−8). The gene-based analysis revealed another six genes (p < 2.703 × 10−6): GRM7, CTNT4, SNRK, SRGAP3, TRAPPC9, and FHIT. No replication of the genome-wide significant SNPs was found in the independent cohort, even if 14 SNPs around CTNNA2 showed association with MDD and related phenotypes at the nominal level of p (<0.05). Furthermore, the PRS model developed in the discovery cohort discriminated cases and controls in the replication cohort. Our work suggests new possible genes associated with MDD, and the PRS analysis confirms the polygenic nature of this disorder. Future studies are required to better understand the role of these findings in MDD. [ABSTRACT FROM AUTHOR]

Published
2023
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23. Characterization of three sialidases from Danio rerio

Author

Forcella, Matilde, primary, Manzoni, Marta, additional, Benaglia, Giuliana, additional, Bonanomi, Marcella, additional, Giacopuzzi, Edoardo, additional, Papini, Nadia, additional, Bresciani, Roberto, additional, Fusi, Paola, additional, Borsani, Giuseppe, additional, and Monti, Eugenio, additional

Published
2021
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26. Additional file 1 of Clinical validation of a combinatorial PharmAcogeNomic approach in major Depressive disorder: an Observational prospective RAndomized, participant and rater-blinded, controlled trial (PANDORA trial)

Author

Minelli, Alessandra, Barlati, Stefano, Vitali, Erika, Bignotti, Stefano, Dattilo, Vincenzo, Tura, Giovanni Battista, Maffioletti, Elisabetta, Giacopuzzi, Edoardo, Santoro, Vincenza, Perusi, Giulia, Cobelli, Chiara, Magri, Chiara, Bonizzato, Silvia, Bocchio-Chiavetto, Luisella, Spina, Edoardo, Vita, Antonio, and Gennarelli, Massimo

Abstract

Additional file 1. SPIRIT 2013 Checklist: Recommended items to address in a clinical trial protocol and related documents*.

Published
2021
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27. Whole Blood Transcriptome Characterization of 3xTg-AD Mouse and Its Modulation by Transcranial Direct Current Stimulation (tDCS)

Author

Magri, Chiara, Vitali, Erika, Cocco, Sara, Giacopuzzi, Edoardo, Rinaudo, Marco, Martini, Paolo, Barbon, Alessandro, Grassi, Claudio, Gennarelli, Massimo, Rinaudo, Marco (ORCID:0000-0002-6130-7335), Grassi, Claudio (ORCID:0000-0001-7253-1685), Magri, Chiara, Vitali, Erika, Cocco, Sara, Giacopuzzi, Edoardo, Rinaudo, Marco, Martini, Paolo, Barbon, Alessandro, Grassi, Claudio, Gennarelli, Massimo, Rinaudo, Marco (ORCID:0000-0002-6130-7335), and Grassi, Claudio (ORCID:0000-0001-7253-1685)

Abstract

The 3xTg-AD mouse is a widely used model in the study of Alzheimer’s Disease (AD). It has been extensively characterized from both the anatomical and behavioral point of view, but poorly studied at the transcriptomic level. For the first time, we characterize the whole blood transcriptome of the 3xTg-AD mouse at three and six months of age and evaluate how its gene expression is modulated by transcranial direct current stimulation (tDCS). RNA-seq analysis revealed 183 differentially expressed genes (DEGs) that represent a direct signature of the genetic background of the mouse. Moreover, in the 6-month-old 3xTg-AD mice, we observed a high number of DEGs that could represent good peripheral biomarkers of AD symptomatology onset. Finally, tDCS was associated with gene expression changes in the 3xTg-AD, but not in the control mice. In conclusion, this study provides an in-depth molecular characterization of the 3xTg-AD mouse and suggests that blood gene expression can be used to identify new biomarkers of AD progression and treatment effects.

Published
2021

28. Bartter-Gitelman Spectrum: 50-Year Follow-up With Revision of Diagnosis After Whole-Genome Sequencing.

Author

Stevenson, Mark, Pagnamenta, Alistair T, Mack, Heather G, Savige, Judith, Giacopuzzi, Edoardo, Lines, Kate E, Taylor, Jenny C, and Thakker, Rajesh V

Subjects
NUCLEOTIDE sequencing, DIAGNOSIS, CHRONIC kidney failure, GENETIC disorder diagnosis, RENAL tubular transport disorders, HYPERALDOSTERONISM, MUSCLE cramps
Abstract

Bartter syndrome (BS) and Gitelman syndrome (GS) are renal tubular disorders affecting sodium, potassium, and chloride reabsorption. Clinical features include muscle cramps and weakness, in association with hypokalemia, hypochloremic metabolic alkalosis, and hyperreninemic hyperaldosteronism. Hypomagnesemia and hypocalciuria are typical of GS, while juxtaglomerular hyperplasia is characteristic of BS. GS is due to SLC12A3 variants, whereas BS is due to variants in SLC12A1 , KCNJ1 , CLCNKA , CLCNKB , BSND , MAGED2 , or CASR. We had the opportunity to follow up one of the first reported cases of a salt-wasting tubulopathy, who based on clinical features was diagnosed with GS. The patient had presented at age 10 years with tetany precipitated by vomiting or diarrhea. She had hypokalemia, a hypochloremic metabolic alkalosis, hyponatremia, mild hypercalcemia, and normomagnesemia, and subsequently developed hypocalciuria and hypomagnesemia. A renal biopsy showed no evidence for juxtaglomerular hyperplasia. She developed chronic kidney failure at age 55 years, and ocular sclerochoroidal calcification, associated with BS and GS, at older than 65 years. Our aim was therefore to establish the genetic diagnosis in this patient using whole-genome sequencing (WGS). Leukocyte DNA was used for WGS analysis, and this revealed a homozygous c.226C > T (p.Arg76Ter) nonsense CLCNKB mutation, thereby establishing a diagnosis of BS type-3. WGS also identified 2 greater than 5-Mb regions of homozygosity that suggested likely mutational heterozygosity in her parents, who originated from a Greek island with fewer than 1500 inhabitants and may therefore have shared a common ancestor. Our results demonstrate the utility of WGS in establishing the correct diagnosis in renal tubular disorders with overlapping phenotypes. [ABSTRACT FROM AUTHOR]

Published
2022
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39. Genome-wide analysis of consistently RNA edited sites in human blood reveals interactions with mRNA processing genes and suggests correlations with cell types and biological variables

Author

Giacopuzzi, E, Gennarelli, M, Sacco, C, Filippini, A, Mingardi, J, Magri, C, Barbon, A, Giacopuzzi, Edoardo, Gennarelli, Massimo, Sacco, Chiara, Filippini, Alice, Mingardi, Jessica, Magri, Chiara, Barbon, Alessandro, Giacopuzzi, E, Gennarelli, M, Sacco, C, Filippini, A, Mingardi, J, Magri, C, Barbon, A, Giacopuzzi, Edoardo, Gennarelli, Massimo, Sacco, Chiara, Filippini, Alice, Mingardi, Jessica, Magri, Chiara, and Barbon, Alessandro

Abstract

Background: A-to-I RNA editing is a co-/post-transcriptional modification catalyzed by ADAR enzymes, that deaminates Adenosines (A) into Inosines (I). Most of known editing events are located within inverted ALU repeats, but they also occur in coding sequences and may alter the function of encoded proteins. RNA editing contributes to generate transcriptomic diversity and it is found altered in cancer, autoimmune and neurological disorders. Emerging evidences indicate that editing process could be influenced by genetic variations, biological and environmental variables. Results: We analyzed RNA editing levels in human blood using RNA-seq data from 459 healthy individuals and identified 2079 sites consistently edited in this tissue. As expected, analysis of gene expression revealed that ADAR is the major contributor to editing on these sites, explaining ~ 13% of observed variability. After removing ADAR effect, we found significant associations for 1122 genes, mainly involved in RNA processing. These genes were significantly enriched in genes encoding proteins interacting with ADARs, including 276 potential ADARs interactors and 9 ADARs direct partners. In addition, our analysis revealed several factors potentially influencing RNA editing in blood, including cell composition, age, Body Mass Index, smoke and alcohol consumption. Finally, we identified genetic loci associated with editing levels, including known ADAR eQTLs and a small region on chromosome 7, containing LOC730338, a lincRNA gene that appears to modulate ADARs mRNA expression. Conclusions: Our data provides a detailed picture of the most relevant RNA editing events and their variability in human blood, giving interesting insights on potential mechanisms behind this post-transcriptional modification and its regulation in this tissue.

Published
2018

47. Exome sequencing of schizophrenia patients with high level of homozygosity identifies a homozygous novel mutation that reduces the glutamate acid decarboxylase 67 (GAD67) activity

Author

MAGRI, Chiara, GIACOPUZZI, Edoardo, BARBON, Alessandro, LA VIA, Luca, Mingardi, J, CONGIU, Chiara, ORIZIO, FLAVIA, BRESCIANI, Roberto, SACCHETTI, Emilio, GENNARELLI, Massimo, Magri, C, Giacopuzzi, E, Barbon, A, LA VIA, L, Mingardi, J, Congiu, C, Orizio, F, Bresciani, R, Sacchetti, E, and Gennarelli, M

Subjects
GAD67
Abstract

An increased load of runs of homozygosity (ROHs) is considered a risk factor for schizophrenia (SZ), suggesting a potential role of recessive genotypes in the pathogenesis of SZ. The whole exome sequencing of SZ patients with high level of ROHs allowed us to identify some rare homozygous mutations with a high probability of being related to SZ, since mapping in neurodevelopment and GABA/glutamatergic synaptic transmission genes. Among these mutations, there was a novel missense substitution (c.391A>G; p.Thr131Ala) in the glutamate acid decarboxylase 1 (GAD1) gene (NM_000817) that encodes for the enzyme (GAD67) catalyzing the production of gamma-aminobutyric acid (GABA) from L-glutamic acid. Since the GAD1 mRNA downregulation as well as reduced levels of GAD67 have been reported in post-mortem brains of SZ patients and since polymorphisms in the GAD1 promoter have been reported as risk factors for SZ, we assessed the biological effect of this mutation to corroborate its potential role in SZ. Confocal immunofluorescence analysis of transfected cells revealed that both the exogenous wild type (WT) and the mutated protein exhibit the same localization: mainly in the Golgi apparatus and in cytosolic vesicles. Biochemical assays showed that the amount of GABA produced by transfected cells expressing the mutated isoform was 30% lower than the amount produced by the cells expressing the WT isoform. These results corroborate the hypothesis that this mutation may impact on the SZ phenotype and supports the hypothesis that also rare recessive mutations are involved in the etiopathogenesis of SZ.

Published
2016

48. Exome sequencing in schizophrenic patients with high levels of homozygosity identifies novel and extremely rare mutations in the GABA/glutamatergic pathways

Author

Giacopuzzi, Edoardo, primary, Gennarelli, Massimo, additional, Minelli, Alessandra, additional, Gardella, Rita, additional, Valsecchi, Paolo, additional, Traversa, Michele, additional, Bonvicini, Cristian, additional, Vita, Antonio, additional, Sacchetti, Emilio, additional, and Magri, Chiara, additional

Published
2017
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50. Mesenchymal stromal cells (MSCs) induce ex vivo proliferation and erythroid commitment of cord blood haematopoietic stem cells (CB-CD34+ cells)

Author

Perucca, Simone, primary, Di Palma, Andrea, additional, Piccaluga, Pier Paolo, additional, Gemelli, Claudia, additional, Zoratti, Elisa, additional, Bassi, Giulio, additional, Giacopuzzi, Edoardo, additional, Lojacono, Andrea, additional, Borsani, Giuseppe, additional, Tagliafico, Enrico, additional, Scupoli, Maria Teresa, additional, Bernardi, Simona, additional, Zanaglio, Camilla, additional, Cattina, Federica, additional, Cancelli, Valeria, additional, Malagola, Michele, additional, Krampera, Mauro, additional, Marini, Mirella, additional, Almici, Camillo, additional, Ferrari, Sergio, additional, and Russo, Domenico, additional

Published
2017
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