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3. POS-001 A NOVEL CFHR5 COPY NUMBER VARIATION ASSOCIATED WITH POST-PARTUM ATYPICAL HUS SUPERIMPOSED TO HELLP SYNDROME

Author

Piras, R., primary, Alberti, M., additional, Bresin, E., additional, Baraldi, O., additional, La Manna, G., additional, Breno, M., additional, Liguori, L., additional, Mele, C., additional, Valoti, E., additional, Gastoldi, S., additional, Donadelli, R., additional, Benigni, A., additional, Remuzzi, G., additional, and Noris, M., additional

Published
2022
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5. Methylphenidate Analogues as a New Class of Potential Disease-Modifying Agents for Parkinson's Disease: Evidence from Cell Models and Alpha-Synuclein Transgenic Mice

Author

Casiraghi, A., Longhena, F., Faustini, G., Ribaudo, G., Suigo, L., Camacho-Hernandez, G. A., Bono, F., Brembati, V., Newman, A. H., Gianoncelli, A., Straniero, V., Bellucci, A., and Valoti, E.

Subjects
threo methyl 2-(piperidin-2-yl)-2-(p-tolyl)acetate hydrochloride, α-synuclein/synapsin III complex, motor recovery effect, methylphenidate analogues, Parkinson’s disease
Abstract

Parkinson's disease (PD) is characterized by dopaminergic nigrostriatal neurons degeneration and Lewy body pathology, mainly composed of α-synuclein (αSyn) fibrillary aggregates. We recently described that the neuronal phosphoprotein Synapsin III (Syn III) participates in αSyn pathology in PD brains and is a permissive factor for αSyn aggregation. Moreover, we reported that the gene silencing of Syn III in a human αSyn transgenic (tg) mouse model of PD at a pathological stage, manifesting marked insoluble αSyn deposits and dopaminergic striatal synaptic dysfunction, could reduce αSyn aggregates, restore synaptic functions and motor activities and exert neuroprotective effects. Interestingly, we also described that the monoamine reuptake inhibitor methylphenidate (MPH) can recover the motor activity of human αSyn tg mice through a dopamine (DA) transporter-independent mechanism, which relies on the re-establishment of the functional interaction between Syn III and α-helical αSyn. These findings support that the pathological αSyn/Syn III interaction may constitute a therapeutic target for PD. Here, we studied MPH and some of its analogues as modulators of the pathological αSyn/Syn III interaction. We identified 4-methyl derivative

Published
2022

7. Impact of a complement factor H gene variant on renal dysfunction, cardiovascular events and response to ACE inhibitor therapy in type 2 diabetes

Author

Valoti, E, Noris, M, Perna, A, Rurali, E, Gherardi, G, Breno, M, Parvanova, A, Iliev, I, Bossi, A, Trevisan, R, Dodesini, A, Ferrari, S, Stucchi, N, Benigni, A, Remuzzi, G, Ruggenenti, P, Valoti E., Noris M., Perna A., Rurali E., Gherardi G., Breno M., Parvanova A. I., Iliev I. P., Bossi A., Trevisan R., Dodesini A. R., Ferrari S., Stucchi N., Benigni A., Remuzzi G., Ruggenenti P., Valoti, E, Noris, M, Perna, A, Rurali, E, Gherardi, G, Breno, M, Parvanova, A, Iliev, I, Bossi, A, Trevisan, R, Dodesini, A, Ferrari, S, Stucchi, N, Benigni, A, Remuzzi, G, Ruggenenti, P, Valoti E., Noris M., Perna A., Rurali E., Gherardi G., Breno M., Parvanova A. I., Iliev I. P., Bossi A., Trevisan R., Dodesini A. R., Ferrari S., Stucchi N., Benigni A., Remuzzi G., and Ruggenenti P.

Abstract

Complement activation has been increasingly implicated in the pathogenesis of type 2 diabetes and its chronic complications. It is unknown whether complement factor H (CFH) genetic variants, which have been previously associated with complement-mediated organ damage likely due to inefficient complement modulation, influence the risk of renal and cardiovascular events and response to therapy with angiotensin-converting enzyme inhibitors (ACEi) in type 2 diabetic patients. Here, we have analyzed the c.2808G> T, (p.Glu936Asp) CFH polymorphism, which tags the H3 CFH haplotype associated to low plasma factor H levels and predisposing to atypical hemolytic uremic syndrome, in 1,158 type 2 diabetics prospectively followed in the Bergamo nephrologic complications of type 2 diabetes randomized, controlled clinical trial (BENEDICT) that evaluated the effect of the ACEi trandolapril on new onset microalbuminuria. At multivariable Cox analysis, the p.Glu936Asp polymorphism (Asp/Asp homozygotes, recessive model) was associated with increased risk of microalbuminuria [adjusted hazard ratio (HR) 3.25 (95% CI 1.46-7.24), P = 0.0038] and cardiovascular events [adjusted HR 2.68 (95% CI 1.23-5.87), P = 0.013]. The p.Glu936Asp genotype significantly interacted with ACEi therapy in predicting microalbuminuria. ACEi therapy was not nephroprotective in Asp/Asp homozygotes [adjusted HR 1.54 (0.18-13.07), P = 0.691 vs. non-ACEi-treated Asp/Asp patients], whereas it significantly reduced microalbuminuria events in Glu/Asp or Glu/Glu patients [adjusted HR 0.38 (0.24-0.60), P < 0.0001 vs. non-ACEi-treated Glu/Asp or Glu/Glu patients]. Among ACEi-treated patients, the risk of developing cardiovascular events was higher in Asp/Asp homozygotes than in Glu/Asp or Glu/Glu patients [adjusted HR 3.26 (1.29-8.28), P = 0.013]. Our results indicate that type 2 diabetic patients Asp/Asp homozygotes in the p.Glu936Asp CFH polymorphism are at increased risk of microalbuminuria and cardiovascular comp

Published
2019

12. Cluster analysis identifies distinct pathogenetic patterns in c3 glomerulopathies/immune complex–Mediated membranoproliferative GN

Author

Iatropoulos, P, Daina, E, Curreri, M, Piras, R, Valoti, E, Mele, C, Bresin, E, Gamba, S, Alberti, M, Breno, M, Perna, A, Bettoni, S, Sabadini, E, Murer, L, Vivarelli, M, Noris, M, Remuzzi, G, Bottanelli, L, Donadelli, R, Cuccarolo, P, Abbate, M, Carrara, C, Cannata, A, Ferrari, S, Gaspari, F, Stucchi, N, Bassani, C, Lena, M, Omati, G, Taruscia, D, Bellantuono, R, Giordano, M, Messina, G, Caruso, M, Gotti, E, Mescia, F, Perticucci, E, Schieppati, A, Verdoni, L, Berto, M, Baraldi, O, Montini, G, Pasini, A, Passler, W, Degasperi, T, Gaggiotti, M, Gregorini, G, Miglietti, N, Guarnieri, A, Cirami, L, Roperto, R, Di Giorgio, G, Barbano, G, Innocenti, M, Ghiggeri, G, Magnasco, A, Rolla, D, Casartelli, D, Lambertini, D, Maggio, M, Cosci, P, Conti, G, Amar, K, Ardissino, G, Marinosci, A, Sinico, R, Montoli, A, Bonucchi, D, Facchini, F, Furci, L, Ferretti, A, Nuzzi, F, Pecoraro, C, Visciano, B, Canavese, C, Radin, E, Stratta, P, Nordio, M, Benetti, E, Parolin, M, Alberici, F, Manenti, L, Brugnano, R, Manenti, F, Capitanini, A, Emma, F, Massella, L, Rosa, M, Mazzon, M, Basso, E, Besso, L, Lavacca, A, Mella, A, Bertero, M, Coppo, R, Peruzzi, L, Porcellini, M, Piccoli, G, Clari, R, Pasi, A, Gangemi, C, Alfandary, H, Dagan, A, Conceiçao, M, Sameiro, F, Croze, L, Malvezzi, P, Tsygin, A, Zelan, B, Nastasi, N, Iatropoulos, Paraskevas, Daina, Erica, Curreri, Manuela, Piras, Rossella, Valoti, Elisabetta, Mele, Caterina, Bresin, Elena, Gamba, Sara, Alberti, Marta, Breno, Matteo, Perna, Annalisa, Bettoni, Serena, Sabadini, Ettore, Murer, Luisa, Vivarelli, Marina, Noris, Marina, Remuzzi, Giuseppe, Bottanelli, L., Donadelli, R., Cuccarolo, P., Abbate, M., Carrara, C., Cannata, A., Ferrari, S., Gaspari, F., Stucchi, N., Bassani, C., Lena, M., Omati, G., Taruscia, D., Bellantuono, R., Giordano, M., Messina, G., Caruso, M., Gotti, E., Mescia, F., Perticucci, E., Schieppati, A., Verdoni, L., Berto, M., Baraldi, O., Montini, G., Pasini, A., Passler, W., Degasperi, T., Gaggiotti, M., Gregorini, G., Miglietti, N., Guarnieri, A., Cirami, L., Roperto, R. M., Di Giorgio, G., Barbano, G., Innocenti, M. L. D., Ghiggeri, G. M., Magnasco, A., Rolla, D., Casartelli, D., Lambertini, D., Maggio, M., Cosci, P. M., Conti, G., Amar, K., Ardissino, G., Marinosci, A., Sinico, R. A., Montoli, A., Bonucchi, D., Facchini, F., Furci, L., Ferretti, A., Nuzzi, F., Pecoraro, C., Visciano, B., Canavese, C., Radin, E., Stratta, P., Nordio, M., Benetti, E., Parolin, M., Alberici, F., Manenti, L., Brugnano, R., Manenti, F., Capitanini, A., Emma, F., Massella, L., Rosa, M., Mazzon, M., Basso, E., Besso, L., Lavacca, A., Mella, A., Bertero, M., Coppo, R., Peruzzi, L., Porcellini, M. G., Piccoli, G. B., Clari, R., Pasi, A., Gangemi, C., Alfandary, H., Dagan, A., Conceiçao, M., Sameiro, F. M., Croze, L., Malvezzi, P., Tsygin, A., Zelan, B., Nastasi, null, Iatropoulos, P, Daina, E, Curreri, M, Piras, R, Valoti, E, Mele, C, Bresin, E, Gamba, S, Alberti, M, Breno, M, Perna, A, Bettoni, S, Sabadini, E, Murer, L, Vivarelli, M, Noris, M, Remuzzi, G, Bottanelli, L, Donadelli, R, Cuccarolo, P, Abbate, M, Carrara, C, Cannata, A, Ferrari, S, Gaspari, F, Stucchi, N, Bassani, C, Lena, M, Omati, G, Taruscia, D, Bellantuono, R, Giordano, M, Messina, G, Caruso, M, Gotti, E, Mescia, F, Perticucci, E, Schieppati, A, Verdoni, L, Berto, M, Baraldi, O, Montini, G, Pasini, A, Passler, W, Degasperi, T, Gaggiotti, M, Gregorini, G, Miglietti, N, Guarnieri, A, Cirami, L, Roperto, R, Di Giorgio, G, Barbano, G, Innocenti, M, Ghiggeri, G, Magnasco, A, Rolla, D, Casartelli, D, Lambertini, D, Maggio, M, Cosci, P, Conti, G, Amar, K, Ardissino, G, Marinosci, A, Sinico, R, Montoli, A, Bonucchi, D, Facchini, F, Furci, L, Ferretti, A, Nuzzi, F, Pecoraro, C, Visciano, B, Canavese, C, Radin, E, Stratta, P, Nordio, M, Benetti, E, Parolin, M, Alberici, F, Manenti, L, Brugnano, R, Manenti, F, Capitanini, A, Emma, F, Massella, L, Rosa, M, Mazzon, M, Basso, E, Besso, L, Lavacca, A, Mella, A, Bertero, M, Coppo, R, Peruzzi, L, Porcellini, M, Piccoli, G, Clari, R, Pasi, A, Gangemi, C, Alfandary, H, Dagan, A, Conceiçao, M, Sameiro, F, Croze, L, Malvezzi, P, Tsygin, A, Zelan, B, Nastasi, N, Iatropoulos, Paraskevas, Daina, Erica, Curreri, Manuela, Piras, Rossella, Valoti, Elisabetta, Mele, Caterina, Bresin, Elena, Gamba, Sara, Alberti, Marta, Breno, Matteo, Perna, Annalisa, Bettoni, Serena, Sabadini, Ettore, Murer, Luisa, Vivarelli, Marina, Noris, Marina, Remuzzi, Giuseppe, Bottanelli, L., Donadelli, R., Cuccarolo, P., Abbate, M., Carrara, C., Cannata, A., Ferrari, S., Gaspari, F., Stucchi, N., Bassani, C., Lena, M., Omati, G., Taruscia, D., Bellantuono, R., Giordano, M., Messina, G., Caruso, M., Gotti, E., Mescia, F., Perticucci, E., Schieppati, A., Verdoni, L., Berto, M., Baraldi, O., Montini, G., Pasini, A., Passler, W., Degasperi, T., Gaggiotti, M., Gregorini, G., Miglietti, N., Guarnieri, A., Cirami, L., Roperto, R. M., Di Giorgio, G., Barbano, G., Innocenti, M. L. D., Ghiggeri, G. M., Magnasco, A., Rolla, D., Casartelli, D., Lambertini, D., Maggio, M., Cosci, P. M., Conti, G., Amar, K., Ardissino, G., Marinosci, A., Sinico, R. A., Montoli, A., Bonucchi, D., Facchini, F., Furci, L., Ferretti, A., Nuzzi, F., Pecoraro, C., Visciano, B., Canavese, C., Radin, E., Stratta, P., Nordio, M., Benetti, E., Parolin, M., Alberici, F., Manenti, L., Brugnano, R., Manenti, F., Capitanini, A., Emma, F., Massella, L., Rosa, M., Mazzon, M., Basso, E., Besso, L., Lavacca, A., Mella, A., Bertero, M., Coppo, R., Peruzzi, L., Porcellini, M. G., Piccoli, G. B., Clari, R., Pasi, A., Gangemi, C., Alfandary, H., Dagan, A., Conceiçao, M., Sameiro, F. M., Croze, L., Malvezzi, P., Tsygin, A., Zelan, B., and Nastasi, null

Abstract

Membranoproliferative GN (MPGN) was recently reclassified as alternative pathway complement–mediated C3 glomerulopathy (C3G) and immune complex–mediated membranoproliferative GN (IC-MPGN). However, genetic and acquired alternative pathway abnormalities are also observed in IC-MPGN. Here, we explored the presence of distinct disease entities characterized by specific pathophysiologic mechanisms. We performed unsupervised hierarchical clustering, a data-driven statistical approach, on histologic, genetic, and clinical data and data regarding serum/plasma complement parameters from 173 patients with C3G/IC-MPGN. This approach divided patients into four clusters, indicating the existence of four different pathogenetic patterns. Specifically, this analysis separated patients with fluid-phase complement activation (clusters 1–3) who had low serum C3 levels and a high prevalence of genetic and acquired alternative pathway abnormalities from patients with solid-phase complement activation (cluster 4) who had normal or mildly altered serum C3, late disease onset, and poor renal survival. In patients with fluid-phase complement activation, those in clusters 1 and 2 had massive activation of the alternative pathway, including activation of the terminal pathway, and the highest prevalence of subendothelial deposits, but those in cluster 2 had additional activation of the classic pathway and the highest prevalence of nephrotic syndrome at disease onset. Patients in cluster 3 had prevalent activation of C3 convertase and highly electron-dense intramembranous deposits. In addition, we provide a simple algorithm to assign patients with C3G/IC-MPGN to specific clusters. These distinct clusters may facilitate clarification of disease etiology, improve risk assessment for ESRD, and pave the way for personalized treatment.

Published
2018

13. 6-Methoxy7-benzofuranoxy and 6-methoxy-7-indolyloxy analogues of WB4101: discovery of a potent and selective a1D-adrenoceptor antagonist

Author

Fumagalli L., Pallavicini M., Bolchi C., Chiodini G., Gobbi M., Laurino P., Straniero V., Valoti E., BUDRIESI, ROBERTA, CHIARINI, ALBERTO, MICUCCI, MATTEO, Fumagalli L., Pallavicini M., Budriesi R., Bolchi C., Chiarini A., Chiodini G., Gobbi M., Laurino P., Micucci M., Straniero V., and Valoti E.

Subjects
invers agonism, α1D-AR antagonist, in vitro characterzation
Abstract

Previous results have shown that replacement of one of the two o-methoxy groups at the phenoxy residue of the potent, but not subtype-selective, α1-AR antagonist (S)-WB4101 [(S)-1] by phenyl, or by ortho,meta-fused cyclohexane, or especially by ortho,meta-fused benzene preferentially elicits α1D-AR antagonist affinity. Such observations inspired the design of four new analogues of 1 bearing, in lieu of the 2,6-dimethoxyphenoxy residue, a 6-methoxy-substituted 7-benzofuranoxy or 7-indolyloxy group or, alternatively, their corresponding 2,3-dihydro form. Of these new compounds, which maintain, rigidified, the characteristic ortho heterodisubstituted phenoxy substructure of 1, the S enantiomer of the dihydrobenzofuranoxy derivative exhibited the highest α1D-AR antagonist affinity (pA2 9.58) with significant α1D/α1A and α1D/α1B selectivity. In addition, compared both to α1D-AR antagonists structurally related to 1 and to the well-known α1D-AR antagonist BMY7378, this derivative had modest 5-HT1A affinity and neutral α1-AR antagonist behavior.

Published
2013

34. GAMMOPATIA MONOCLONALE DI SIGNIFICATO INDETERMINATO (MGUS) IN UN LAVORATORE ESPOSTO A PESTICIDI: CONSIDERAZIONI EZIOPATOGENETICHE, SORVEGLIANZA SANITARIA E MISURE PREVENTIVE.

Author

Taino, G., Brevi, M., Valoti, E., and Imbriani, M.

Abstract

Copyright of Giornale Italiano di Medicina del Lavoro ed Ergonomia is the property of Giornale Italiano di Medicina del Lavoro ed Ergonomia Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2011

40. [A case of occupational pulmonary siderosis: the pathogenetic and prognostic considerations]

Author

Vitulo P, Valoti E, Eloisa Arbustini, Rossi A, and Catenacci G

Subjects
Diagnosis, Differential, Male, Siderosis, Chronic Disease, Humans, Middle Aged, Prognosis, Bronchoalveolar Lavage Fluid, Respiratory Function Tests
Abstract

Pulmonary siderosis is a disease which can be considered with the pneumoconioses of the so-called inert dust (either by deposit or by accumulation) and, from the earliest nosographic descriptions dating back to the thirties and forties, it has been substantially considered a benign form because of the scarce sclerogenic evolution and the preservation of discrete respiratory function. We present a case of pulmonary siderosis characterized on one hand by the importance and clarity of the cytopathological picture and on the other by the presence of changes, although modest, in lung function which confirm the most recent hypotheses in the literature on the potential evolution of pneumosiderotic diseases and their relatively less benign prognosis. From a preventive point of view the case draws attention to the need for greater control of environmental hygiene conditions in small factories. From an insurance and medico-legal point of view siderosis has recently been explicitly added to the occupational diseases which can be declared to the Italian state department dealing with occupational disease and disability payments (I.N.A.I.L.) (DPR of the 13.04.1994, section 47).

50. EFFETTUAZIONE IN SEQUENZA DELL'AUDIOMETRIA TONALE E DELLE OTOEMISSIONI ACUSTICHE (D.P.O.A.E.) COME TECNICA DI APPROFONDIMENTO NELLO STUDIO DEL DANNO UDITIVO RICONDUCIBILE A TRAUMA ACUSTICO CRONICO IN UN'INDUSTRIA PETROLCHIMICA.

Author

Valoti, E., Lunati, M. P., De Zotti, P., Taino, G., and Imbriani, M.

Abstract

Nell'ambito delle otoemissioni acustiche, i prodotti di distorsione (DPOAE), grazie alle loro caratteristiche di multifrequenzialità e di non-necessità di collaborazione da parte dei soggetti esaminati, costituiscono un "valore aggiunto" alle tradizionali tecniche di indagine (soprattutto all'audiometria tonale) nella diagnosi dei danni uditivi neurosensoriali correlati all'esposizione cronica a rumore industriale. L'indagine in oggetto, realizzata nel corso del 2010, ha coinvolto 583 dipendenti di sesso maschile di un'importante azienda petrolchimica, esposti a rumorosità ambiental-lavorativa di livello medio. In un primo tempo i 583 lavoratori sono stati sottoposti ad audiometria tonale in cabina silente, collocata nell'Infermeria aziendale; dal totale degli esaminati sono stati quindi selezionati 97 casi audiograficamente compatibili, in tutto o in parte, con danno neurosensoriale da trauma acustico cronico. In un secondo tempo i suddetti 97 casi sono stati sottoposti a nuova audiometria tonale (in cabina silente, con adeguato riposo acustico, presso Studio Audiologico) e subito dopo, in sequenza, a registrazione delle DPOAE. Al termine dell'indagine, solamente su 21 dipendenti (cioè il 3,6% del totale degli esaminati ed il 21,6% dei soggetti con profilo audiografico compatibile) è stato possibile formulare una diagnosi certa di ipoacusia neurosensoriale da trauma acustico cronico. In conclusione, l'indagine ha evidenziato che la registrazione delle DPOAE è inscindibile dall'esecuzione dell'audiometria tonale liminare (quest'ultima effettuata secondo le corrette procedure individuate dalla SIMLII) e che solo la valutazione dei risultati dei due esami effettuati in sequenza permette la miglior affidabilità e precisione diagnostica. [ABSTRACT FROM AUTHOR]

Published
2011

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