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1. Construction and test of the SM1 type Micromegas chambers for the upgrade of the ATLAS forward muon spectrometer

Author

Agarwala, J., Alviggi, M.G., Antonelli, M., Anulli, F., Arcangeletti, C., Auricchio, S., Bagnaia, P., Bariani, S., Baroncelli, A., Bashta, I., Bauce, M., Beretta, M., Bini, C., Calabró, D., Camerlingo, M.T., Canale, V., Capitolo, E., Capponi, M., Capradossi, G., Carducci, G., Caserio, A., Cassese, C., Cerioni, S., Chiarella, V., Ciapetti, G., D’Amico, V., De Cecco, S., De Fazio, B., Del Gaudio, M., Di Donato, C., Di Nardo, R., D’Uffizi, D., Farilla, A., Farina, E., Ferrari, R., Fiore, G., Frattari, G., Freddi, A., Gaudio, G., Gauzzi, P., Giagu, S., Gigli, S., Gnesi, I., Gorini, E., Gravili, F.G., Greco, M., Iaciofano, A., Iengo, P., Innocente, A., Introzzi, G., Iodice, M., Ippolito, V., Kourkoumeli Charalampidi, A., Lacava, F., Lalli, E., Lanza, A., Lauciani, S., Laurelli, P., Luminari, L., Mancini, G., Martinelli, L., Massarotti, P., Miccoli, A., Mirto, A., Negri, A., Orestano, D., Paruzza, G., Pepe, M., Petruccetti, M., Petrucci, F., Pezzotti, L., Pileggi, G., Pirola, M., Piscitelli, C., Polesello, G., Policicchio, A., Pontoriere, G., Ponzio, B., Primavera, M., Rebuzzi, D., Rimoldi, A., Romano, E., Roscilli, L., Rovelli, G., Russo, V., Sansoni, A., Safai Tehrani, F., Scagliotti, C., Schioppa, M., Sekhniaidze, G., Sessa, M., Sottocornola, S., Trattino, P., Tskhadadze, E., Turco, P., Vannicola, D., Vannoli, L., Vassilieva, T., Vecchio, V., Ventura, A., Vercellati, F., Vilucchi, E., Zullo, A., and Zunica, G.

Published
2022
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2. One year of surgical mask testing at the University of Bologna labs: Lessons learned from data analysis

Author

Boi, C., Borsetti, F., Brugo, T.M., Cappelletti, M., De Angelis, M.G., Fedi, S., Di Giacomo, S., Fabiani, T., Foli, G., Garelli, A., Genchi, U., Ghezzi, D., Gualandi, C., Lalli, E., Magnani, M., Maurizzi, A., Mazzi, F., Mehrabi, N., Minelli, M., Montalbano, R., Morelli, L., Nici, S., Onesti, R., Paglianti, A., Papchenko, K., Pappalardo, S., Parisi, N.F., Rapino, S., Reggio, M., Roselli, M., Ruggeri, E., Sabatini, L., Saracino, E., Scarponi, G.E., Serra, L., Signorini, V., Storione, A., Torsello, M., Tugnoli, E., Vargiu, C.M., Vidali, G., and Violante, F.S.

Published
2022
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3. Construction and test of the SM1 type Micromegas chambers for the upgrade of the ATLAS forward muon spectrometer

Author

Agarwala J., Alviggi M. G., Antonelli M., Anulli F., Arcangeletti C., Auricchio S., Bagnaia P., Bariani S., Baroncelli A., Bashta I., Bauce M., Beretta M., Bini C., Calabro D., Camerlingo M. T., Canale V., Capitolo E., Capponi M., Capradossi G., Carducci G., Caserio A., Cassese C., Cerioni S., Chiarella V., Ciapetti G., D'Amico V., De Cecco S., De Fazio B., Del Gaudio M., Di Donato C., Di Nardo R., D'Uffizi D., Farilla A., Farina E., Ferrari R., Fiore G., Frattari G., Freddi A., Gaudio G., Gauzzi P., Giagu S., Gigli S., Gnesi I., Gorini E., Gravili F. G., Greco M., Iaciofano A., Iengo P., Innocente A., Introzzi G., Iodice M., Ippolito V., Kourkoumeli Charalampidi A., Lacava F., Lalli E., Lanza A., Lauciani S., Laurelli P., Luminari L., Mancini G., Martinelli L., Massarotti P., Miccoli A., Mirto A., Negri A., Orestano D., Paruzza G., Pepe M., Petruccetti M., Petrucci F., Pezzotti L., Pileggi G., Pirola M., Piscitelli C., Polesello G., Policicchio A., Pontoriere G., Ponzio B., Primavera M., Rebuzzi D., Rimoldi A., Romano E., Roscilli L., Rovelli G., Russo V., Sansoni A., Safai Tehrani F., Scagliotti C., Schioppa M., Sekhniaidze G., Sessa M., Sottocornola S., Trattino P., Tskhadadze E., Turco P., Vannicola D., Vannoli L., Vassilieva T., Vecchio V., Ventura A., Vercellati F., Vilucchi E., Zullo A., Zunica G., Agarwala, J., Alviggi, M. G., Antonelli, M., Anulli, F., Arcangeletti, C., Auricchio, S., Bagnaia, P., Bariani, S., Baroncelli, A., Bashta, I., Bauce, M., Beretta, M., Bini, C., Calabro, D., Camerlingo, M. T., Canale, V., Capitolo, E., Capponi, M., Capradossi, G., Carducci, G., Caserio, A., Cassese, C., Cerioni, S., Chiarella, V., Ciapetti, G., D'Amico, V., De Cecco, S., De Fazio, B., Del Gaudio, M., Di Donato, C., Di Nardo, R., D'Uffizi, D., Farilla, A., Farina, E., Ferrari, R., Fiore, G., Frattari, G., Freddi, A., Gaudio, G., Gauzzi, P., Giagu, S., Gigli, S., Gnesi, I., Gorini, E., Gravili, F. G., Greco, M., Iaciofano, A., Iengo, P., Innocente, A., Introzzi, G., Iodice, M., Ippolito, V., Kourkoumeli Charalampidi, A., Lacava, F., Lalli, E., Lanza, A., Lauciani, S., Laurelli, P., Luminari, L., Mancini, G., Martinelli, L., Massarotti, P., Miccoli, A., Mirto, A., Negri, A., Orestano, D., Paruzza, G., Pepe, M., Petruccetti, M., Petrucci, F., Pezzotti, L., Pileggi, G., Pirola, M., Piscitelli, C., Polesello, G., Policicchio, A., Pontoriere, G., Ponzio, B., Primavera, M., Rebuzzi, D., Rimoldi, A., Romano, E., Roscilli, L., Rovelli, G., Russo, V., Sansoni, A., Safai Tehrani, F., Scagliotti, C., Schioppa, M., Sekhniaidze, G., Sessa, M., Sottocornola, S., Trattino, P., Tskhadadze, E., Turco, P., Vannicola, D., Vannoli, L., Vassilieva, T., Vecchio, V., Ventura, A., Vercellati, F., Vilucchi, E., Zullo, A., and Zunica, G.

Subjects
Nuclear and High Energy Physics, Muon detector, Micromegas, Instrumentation, LHC, ATLAS, High Energy Physics, Micromegas, Muons
Abstract

Large-size Resistive Micromegas have been chosen for the upgrade of the forward muon spectrometer of the ATLAS experiment, the New Small Wheel project. These chambers, together with small-strip Thin Gap Chambers (sTGC), allow reconstruction of high-momentum muon tracks in a high-radiation environment and provide a robust low-threshold single-muon trigger. A collaboration of seven INFN units built 32 SM1 type chambers, corresponding to one fourth of the total number needed for this upgrade. Each SM1 chamber has a surface of approximately 2 m2 and four sensitive layers. The production was shared among five INFN construction sites and it was completed in fall 2020. The construction methods, as well as the results of the quality tests done on components of the detector and on the assembled chambers, are reported in the present paper.

Published
2022

4. Complexity and versatility of the transcriptional response to cAMP

Author

Delmas, V., Molina, C. A., Lalli, E., de Groot, R., Foulkes, N. S., Masquilier, D., Sassone-Corsi, P., Blaustein, M. P., editor, Grunicke, H., editor, Habermann, E., editor, Pette, D., editor, Reuter, H., editor, Sakmann, B., editor, Schweiger, M., editor, Weibel, E. R., editor, and Wright, E. M., editor

Published
1994
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12. Reduction of Fmr1 mRNA Levels Rescues Pathological Features in Cortical Neurons in a Model of FXTAS

Author

Drozd, M. (Malgorzata), Delhaye, S. (Sébastien), Maurin, T. (Thomas), Castagnola, S. (Sara), Grossi, M. (Mauro), Brau, F. (Frédéric), Jarjat, M. (Marielle), Willemsen, R. (Rob), Capovilla, M. (Maria), Hukema, R.K. (Renate), Lalli, E. (Enzo), Bardoni, B. (Barbara), Drozd, M. (Malgorzata), Delhaye, S. (Sébastien), Maurin, T. (Thomas), Castagnola, S. (Sara), Grossi, M. (Mauro), Brau, F. (Frédéric), Jarjat, M. (Marielle), Willemsen, R. (Rob), Capovilla, M. (Maria), Hukema, R.K. (Renate), Lalli, E. (Enzo), and Bardoni, B. (Barbara)

Abstract

Fragile X-associated tremor ataxia syndrome (FXTAS) is a rare disorder associated to the presence of the fragile X premutation, a 55–200 CGG repeat expansion in the 5′ UTR of the FMR1 gene. Two main neurological phenotypes have been described in carriers of the CGG premutation: (1) neurodevelopmental disorders characterized by anxiety, attention deficit hyperactivity disorder (ADHD), social deficits, or autism spectrum disorder (ASD); and (2) after 50 years old, the FXTAS phenotype. This neurodegenerative disorder is characterized by ataxia and a form of parkinsonism. The molecular pathology of this disorder is characterized by the presence of elevated levels of Fragile X Mental Retardation 1 (FMR1) mRNA, presence of a repeat-associated non-AUG (RAN) translated peptide, and FMR1 mRNA-containing nuclear inclusions. Whereas in the past FXTAS was mainly considered as a late-onset disorder, some phenotypes of patients and altered learning and memory behavior of a mouse model of FXTAS suggested that this disorder involves neurodevelopment. To better understand the physiopathological role of the increased levels of Fmr1 mRNA during neuronal differentiation, we used a small interfering RNA (siRNA) app

Published
2019
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15. Contribution de la signalisation du récepteur α à l’acide rétinoïque dans la morphologie et la zonation fonctionnelle du cortex surrénalien

Author

El Zein, R.M., primary, Rickard, A., additional, Golib Dzib, J.F., additional, Fernandes-Rosa, F.L., additional, Samson-Couterie, B., additional, Rocha, A., additional, Poglitsch, M., additional, Lefebvre, H., additional, Gomez-Sanchez, C.E., additional, Amar, L., additional, Ghyselinck, N.B., additional, Benecke, A., additional, Lalli, E., additional, Zennaro, M.C., additional, and Boulkroun, S., additional

Published
2018
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20. FRAXE-associated mental retardation protein (FMR2) is an RNA-binding protein with high affinity for G-quartet RNA forming structure

Author

Bensaid M, Melko M, Bechara EG, Davidovic L, Berretta A, Catania MV, Gecz J, Lalli E, and Bardoni B.

Subjects
FRAXE, immunofluorescence, mental retardation
Abstract

FRAXE is a form of mild to moderate mental retardation due to the silencing of the FMR2 gene. The cellular function of FMR2 protein is presently unknown. By analogy with its homologue AF4, FMR2 was supposed to have a role in transcriptional regulation, but robust evidences supporting this hypothesis are lacking. We observed that FMR2 co-localizes with the splicing factor SC35 in nuclear speckles, the nuclear regions where splicing factors are concentrated, assembled and modified. Similarly to what was reported for splicing factors, blocking splicing or transcription leads to the accumulation of FMR2 in enlarged, rounded speckles. FMR2 is also localized in the nucleolus when splicing is blocked. We show here that FMR2 is able to specifically bind the G-quartet-forming RNA structure with high affinity. Remarkably, in vivo, in the presence of FMR2, the ESE action of the G-quartet situated in mRNA of an alternatively spliced exon of a minigene or of the putative target FMR1 appears reduced. Interestingly, FMR1 is silenced in the fragile X syndrome, another form of mental retardation. All together, our findings strongly suggest that FMR2 is an RNA-binding protein, which might be involved in alternative splicing regulation through an interaction with G-quartet RNA structure.

Published
2009

21. Genome-Wide Paternal Uniparental Disomy as a Cause of Beckwith-Wiedemann Syndrome Associated with Recurrent Virilizing Adrenocortical Tumors

Author

Bertoin, F., additional, Letouzé, E., additional, Grignani, P., additional, Patey, M., additional, Rossignol, S., additional, Libé, R., additional, Pasqual, C., additional, Lardière-Deguelte, S., additional, Hoeffel-Fornes, C., additional, Gaillard, D., additional, Previderè, C., additional, Delemer, B., additional, and Lalli, E., additional

Published
2014
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24. Genomic Analysis of Sexual Dimorphism of Gene Expression in the Mouse Adrenal Gland

Author

El Wakil, Abeer, Mari, B., Barhanin, J., Lalli, E., El Wakil, Abeer, Mari, B., Barhanin, J., and Lalli, E.

Abstract

A relevant gender difference exists in adrenal physiology and propensity to disease. In mice, a remarkable sexual dimorphism is present in several components of the hypothalamic-pituitary-adrenal axis, with females displaying higher adrenal weight, plasma ACTH, corticosterone, and aldosterone levels than males. The molecular bases of this sexual dimorphism are little known. We have compared global gene expression profiles in males vs. female mouse adrenal glands and also studied the effect that testosterone treatment and castration have on adrenal gene expression in female vs. male mice, respectively. Our study evidenced a set of 71 genes that are coordinately modulated according to sex and hormonal treatments and represent the core sexually dimorphic expression program in the mouse adrenal gland. Moreover, we show that some genes involved in steroid metabolism have a remarkable sexual dimorphic expression and identify new potential markers for the adrenal X-zone, a transitory cellular layer in the inner adrenal cortex, which spontaneously regresses at puberty in males and during the first pregnancy in females and has an uncertain physiological role. Finally, sexually dimorphic expression of the transcriptional regulators Nr5a1 and Nr0b1 may explain at least in part the differences in adrenal steroidogenesis between sexes.

Published
2013
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25. SNP array profiling of childhood adrenocortical tumors reveals distinct pathways of tumorigenesis and highlights candidate driver genes

Author

Letouzé, E. (Eric), Rosati, R. (Roberto), Komechen, H. (Heloisa), Doghman, M. (Mabrouka), Marisa, L. (Laetitia), Flück, C. (Christa), Krijger, R.R. (Ronald) de, Noesel, M.M. (Max) van, Mas, J.-C. (Jean-Christophe), Pianovski, M.A.D. (Mara A.), Zambetti, G.P. (Gerard), Figueiredo, E.G. (Eberval), Lalli, E. (Enzo), Letouzé, E. (Eric), Rosati, R. (Roberto), Komechen, H. (Heloisa), Doghman, M. (Mabrouka), Marisa, L. (Laetitia), Flück, C. (Christa), Krijger, R.R. (Ronald) de, Noesel, M.M. (Max) van, Mas, J.-C. (Jean-Christophe), Pianovski, M.A.D. (Mara A.), Zambetti, G.P. (Gerard), Figueiredo, E.G. (Eberval), and Lalli, E. (Enzo)

Abstract

Context: Childhood adrenocortical tumors (ACT) are rare malignancies, except in southern Brazil, where a higher incidence rate is associated to a high frequency of the founder R337H TP53 mutation. To date, copy number alterations in these tumors have only been analyzed by low-resolution comparative genomic hybridization. Objective: We analyzed an international series of 25 childhood ACT using high-resolution single nucleotide polymorphism arrays to: 1) detect focal copynumberalterations highlighting candidate driver genes; and 2) compare genetic alterations between Brazilian patients carrying the R337H TP53 mutation and non-Brazilian patients. Results: We identified 16 significantly recurrent chromosomal alterations (q-value < 0.05), the mostfrequent being -4q34, +9q33-q34, +19p, loss of heterozygosity (LOH) ofchromosome17and 11p15. Focal amplifications and homozygous deletions comprising well-known oncogenes (MYC, MDM2, PDGFRA, KIT, MCL1, BCL2L1) and tumor suppressors (TP53, RB1, RPH3AL) were identified. In addition, eight focal deletions were detected at 4q34, defining a sharp peak region around the noncodingRNALINC00290 gene. Although non-Brazilian tumors with a mutated TP53 were similar to Brazilian tumors, those with a wild-type TP53 displayed distinct genomic profiles, with significantly fewer rearrangements (P = 0.019). In particular, three alterations (LOH of chromosome 17, +9q33-q34, and -4q34) were significantly more frequent in TP53-mutated samples. Finally, two of four TP53 wild-type tumors displayed as sole rearrangement a copy-neutral LOH of the imprinted region at 11p15, supporting a major role for this region in ACT development. Conclusions: Our findings highlight potential driver genes and cellular pathways implicated in childhood ACT and demonstrate the existence of different oncogenic routes in this pathology. Copyright

Published
2012
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32. Genome-Wide Paternal Uniparental Disomy as a Cause of Beckwith-Wiedemann Syndrome Associated with Recurrent Virilizing Adrenocortical Tumors.

Author

Bertoin, F., Letouzé, E., Grignani, P., Patey, M., Rossignol, S., Libé, R., Pasqual, C., Lardière-Deguelte, S., Hoeffel-Fornes, C., Gaillard, D., Previderè, C., Delemer, B., and Lalli, E.

Subjects
BECKWITH-Wiedemann syndrome, TUMOR surgery, FIBROADENOMAS, LOSS of heterozygosity, DISEASE relapse, HUMAN genome, NEPHROBLASTOMA
Abstract

Beckwith-Wiedemann syndrome (BWS) is an overgrowth syndrome characterized by fetal macrosomia, macroglossia, and abdominal wall defects. BWS patients are at risk to develop Wilms tumor, neuroblastoma, hepatoblastoma, and adrenal tumors. A young woman with BWS features, but with inconclusive genetic evidence for the disease, came to clinical observation for signs of virilization at the age of 16 years. An adrenocortical tumor was diagnosed and surgically resected. The tumor underwent 2 local relapses that were also surgically treated. The patient was also operated to remove a breast fibroadenoma. SNP arrays were used to analyze chromosome abnormalities in normal and tumor samples from the patient and her parents. The patient presented genome-wide mosaic paternal uniparental disomy (patUPD) both in the adrenocortical and the breast tumors, with different degrees of loss of heterozygosity (LOH). The more recent relapses of the adrenocortical tumor showed a loss of part of chromosome 17p that was absent in the first tumor. Analysis of a skin biopsy sample also showed mosaic patUPD with partial LOH, while no LOH was detected in leukocyte DNA. This case shows that virilizing adrenocortical tumors may be a clinical feature of patients with BWS. The SNP array technology is useful to diagnose genome-wide patUPD mosaicism in BWS patients with an inconclusive molecular diagnosis and underlines the tumorigenic potential of the absence of the maternal genome combined with an excess of the paternal genome. [ABSTRACT FROM AUTHOR]

Published
2015
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