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BackgroundParkinson's disease (PD) is a neurodegenerative movement disorder affecting 1-5% of the general population for which neither effective cure nor early diagnostic tools are available that could tackle the pathology in the early phase. Here we report a multi-stage procedure to identify candidate genes likely involved in the etiopathogenesis of PD.MethodsThe study includes a discovery stage based on the analysis of whole exome data from 26 dominant late onset PD families, a validation analysis performed on 1542 independent PD patients and 706 controls from different cohorts and the assessment of polygenic variants load in the Italian cohort (394 unrelated patients and 203 controls).ResultsFamily-based approach identified 28 disrupting variants in 26 candidate genes for PD including PARK2, PINK1, DJ-1(PARK7), LRRK2, HTRA2, FBXO7, EIF4G1, DNAJC6, DNAJC13, SNCAIP, AIMP2, CHMP1A, GIPC1, HMOX2, HSPA8, IMMT, KIF21B, KIF24, MAN2C1, RHOT2, SLC25A39, SPTBN1, TMEM175, TOMM22, TVP23A and ZSCAN21. Sixteen of them have not been associated to PD before, were expressed in mesencephalon and were involved in pathways potentially deregulated in PD. Mutation analysis in independent cohorts disclosed a significant excess of highly deleterious variants in cases (p = 0.0001), supporting their role in PD. Moreover, we demonstrated that the co-inheritance of multiple rare variants (≥ 2) in the 26 genes may predict PD occurrence in about 20% of patients, both familial and sporadic cases, with high specificity (> 93%; p = 4.4 × 10- 5). Moreover, our data highlight the fact that the genetic landmarks of late onset PD does not systematically differ between sporadic and familial forms, especially in the case of small nuclear families and underline the importance of rare variants in the genetics of sporadic PD. Furthermore, patients carrying multiple rare variants showed higher risk of manifesting dyskinesia induced by levodopa treatment.ConclusionsBesides confirming the extreme genetic

Establishing specific cell lineages from human induced pluripotent stem cells (hiPSCs) is vital for cell therapy approaches in regenerative medicine, particularly for neurodegenerative disorders. While neural precursors have been induced from hiPSCs, the establishment of hiPSC-derived human neural stem cells (hiNSCs), with characteristics that match foetal hNSCs and abide by cGMP standards, thus allowing clinical applications, has not been described. We generated hiNSCs by a virus-free technique, whose properties recapitulate those of the clinical-grade hNSCs successfully used in an Amyotrophic Lateral Sclerosis (ALS) phase I clinical trial. Ex vivo, hiNSCs critically depend on exogenous mitogens for stable self-renewal and amplification and spontaneously differentiate into astrocytes, oligodendrocytes and neurons upon their removal. In the brain of immunodeficient mice, hiNSCs engraft and differentiate into neurons and glia, without tumour formation. These findings now warrant the establishment of clinical-grade, autologous and continuous hiNSC lines for clinical trials in neurological diseases such as Huntington’s, Parkinson’s and Alzheimer’s, among others.

Establishing specific cell lineages from human induced pluripotent stem cells (hiPSCs) is vital for cell therapy approaches in regenerative medicine, particularly for neurodegenerative disorders. While neural precursors have been induced from hiPSCs, the establishment of hiPSC-derived human neural stem cells (hiNSCs), with characteristics that match foetal hNSCs and abide by cGMP standards, thus allowing clinical applications, has not been described. We generated hiNSCs by a virus-free technique, whose properties recapitulate those of the clinical-grade hNSCs successfully used in an Amyotrophic Lateral Sclerosis (ALS) phase I clinical trial. Ex vivo, hiNSCs critically depend on exogenous mitogens for stable self-renewal and amplification and spontaneously differentiate into astrocytes, oligodendrocytes and neurons upon their removal. In the brain of immunodeficient mice, hiNSCs engraft and differentiate into neurons and glia, without tumour formation. These findings now warrant the establishment of clinical-grade, autologous and continuous hiNSC lines for clinical trials in neurological diseases such as Huntington’s, Parkinson’s and Alzheimer’s, among others.

A promising green strategy for the fabrication of fully biobased chitosan adsorbents for wastewater purification is presented. Nanographene oxide (nGO)-type carbon dots were derived from chitosan (nGOCS) or from cellulose (nGOCL) through a two-step process including microwave-assisted hydrothermal carbonization and oxidation. Finally, nGO were evaluated as biobased property enhancers in chitosan hydrogel adsorbents. Macroporous chitosan hydrogels were synthesized by cross-linking with genipin, and the incorporation of nGO into these hydrogels was shown to facilitate the cross-linking reaction leading to more robust 3D cross-linked networks. This was evidenced by the increased storage modulus and by the swelling ratio that decreased from 5.7 for pristine chitosan hydrogel to 2.6 for hydrogel with 5 mg/mL nGOCS and 3.3 for hydrogel with 5 mg/mL nGOCL. As a further proof of the concept the hydrogels were shown to be effective adsorbent for the common anti-inflammatory drug diclofenac sodium (DCF). Here, the addition of nGO promoted the DCF adsorption process leading to 100% removal of DCF after only 5 h. The synergistic effect of electrostatic interactions, hydrogen bonding, and pi-pi stacking could explain the high adsorption of DCF on the hydrogels. The developed biobased CS/nGO hydrogels are thus promising adsorbents with great potential for purification of trace pharmaceuticals from wastewater., QC 20171221

Distinct midbrain dopamine (mDA) neuron subtypes are found in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA), but it is mainly SNc neurons that degenerate in Parkinson's disease. Interest in how mDA neurons develop has been stimulated by the potential use of stem cells in therapy or disease modeling. However, very little is known about how specific dopaminergic subtypes are generated. Here, we show that the expression profiles of the transcription factors Sox6, Otx2, and Nolz1 define subpopulations of mDA neurons already at the neural progenitor cell stage. After cell-cycle exit, Sox6 selectively localizes to SNc neurons, while Otx2 and Nolz1 are expressed in a subset of VTA neurons. Importantly, Sox6 ablation leads to decreased expression of SNc markers and a corresponding increase in VTA markers, while Otx2 ablation has the opposite effect. Moreover, deletion of Sox6 affects striatal innervation and dopamine levels. We also find reduced Sox6 levels in Parkinson's disease patients. These findings identify Sox6 as a determinant of SNc neuron development and should facilitate the engineering of relevant mDA neurons for cell therapy and disease modeling.

Mesencephalic-diencephalic dopaminergic (mdDA) neurons play a relevant role in the control of movement, behavior, and cognition. Indeed loss and/or abnormal functioning of mdDA neurons are responsible for Parkinson's disease as well as for addictive and psychiatric disorders. In the last years a wealth of information has been provided on gene functions controlling identity, fate, and proliferation of mdDA progenitors. This review will focus on the role exerted by Otx genes in early decisions regulating sequential steps required for the neurogenesis of mesencephalic dopaminergic (mesDA) neurons. In this context, the regulatory network involving Otx functional interactions with signaling molecules and transcription factors required to promote or prevent the development of mesDA neurons will be analyzed in detail.

Neurons usually migrate and differentiate in one particular encephalic vesicle. We identified a murine population of diencephalic neurons that colonized the telencephalic amygdaloid complex, migrating along a tangential route that crosses a boundary between developing brain vesicles. The diencephalic transcription factor OTP was necessary for this migratory behavior. © 2010 Nature America, Inc. All rights reserved.

Little is known about the cues controlling the generation of motoneuron populations in the mammalian ventral midbrain. We show that Otx2 provides the crucial anterior-posterior positional information for the generation of red nucleus neurons in the murine midbrain. Moreover, the homeodomain transcription factor Nkx6-1 controls the proper development of the red nucleus and of the oculomotor and trochlear nucleus neurons. Nkx6-1 is expressed in ventral midbrain progenitors and acts as a fate determinant of the Brn3a+ (also known as Pou4f1) red nucleus neurons. These progenitors are partially dorsalized in the absence of Nkx6-1, and a fraction of their postmitotic offspring adopts an alternative cell fate, as revealed by the activation of Dbx1 and Otx2 in these cells. Nkx6-1 is also expressed in postmitotic Isl1+ oculomotor and trochlear neurons. Similar to hindbrain visceral (branchio-) motoneurons, Nkx6-1 controls the proper migration and axon outgrowth of these neurons by regulating the expression of at least three axon guidance/neuronal migration molecules. Based on these findings, we provide additional evidence that the developmental mechanism of the oculomotor and trochlear neurons exhibits more similarity with that of special visceral motoneurons than with that controlling the generation of somatic motoneurons located in the murine caudal hindbrain and spinal cord.

GABAergic and glutamatergic neurons modulate inhibitory and excitatory networks in the CNS, and their impairment may cause neurological and psychiatric disorders. Thus, understanding the molecular mechanisms that control neurotransmitter phenotype and identity of excitatory and inhibitory progenitors has considerable relevance. Here we investigated the consequence of Otx2 (orthodenticle homolog) ablation in glutamatergic progenitors of the dorsal thalamus (referred to as thalamus). We report that Otx2 is cell-autonomously required in these progenitors to repress GABAergic differentiation. Our data indicate that Otx2 may prevent GABAergic fate switch by repressing the basic helix-loop-helix gene Mash1 (mammalian achaete-schute homolog) in progenitors expressing Ngn2 (neurogenin homolog). The lack of Otx2 also resulted in the activation of Pax3 (paired box gene), Pax7, and Lim1 (Lin-11/Isl-1/Mec-3), three genes normally coexpressed with Mash1 and GABAergic markers in the pretectum, thus suggesting that thalamic progenitors lacking Otx2 exhibit marker similarities with those of the pretectum. Furthermore, Otx2 ablation gave rise to a marked increase in proliferating activity of thalamic progenitors and the formation of hyperplastic cell masses. Thus, this study provides evidence for a novel and crucial role of Otx2 in the molecular mechanism by which identity and fate of glutamatergic precursors are established in the thalamus. Our data also support the concept that proper assignment of identity and fate of neuronal precursors occurs through the suppression of alternative differentiation programs.

Midbrain neurons synthesizing the neurotransmitter dopamine play a central role in the modulation of different brain functions and are associated with major neurological and psychiatric disorders. Despite the importance of these cells, the molecular mechanisms controlling their development are still poorly understood. The secreted glycoprotein Wnt1 is expressed in close vicinity to developing midbrain dopaminergic neurons. Here, we show that Wnt1 regulates the genetic network, including Otx2 and Nkx2-2, that is required for the establishment of the midbrain dopaminergic progenitor domain during embryonic development. In addition, Wnt1 is required for the terminal differentiation of midbrain dopaminergic neurons at later stages of embryogenesis. These results identify Wnt1 as a key molecule in the development of midbrain dopaminergic neurons in vivo. They also suggest the Wnt1-controlled signaling pathway as a promising target for new therapeutic strategies in the treatment of Parkinson's disease.

Here, we have investigated the neurological consequences of restricted inactivation of Otx2 in adult En1cre/+; Otx2flox/flox mice. In agreement with the crucial role of Otx2 in midbrain patterning, the mutants had a substantial reduction in tyrosine hydroxylase containing neurons. Although the reduction in the number of DAergic neurons was comparable between the SNc and the VTA, we found an unexpected selectivity in the deinnervation of the terminal fields affecting preferentially the ventral striatum and the olfactory tubercle. Interestingly, the mutants showed no abnormalities in exploratory activity or motor coordination. However, the absence of normal DA tone generated significant alterations in DA D1-receptor signalling as indicated by increased mutant striatal levels of phosphorylated DARPP-32 and by an altered motor response to amphetamine. Therefore, we suggest that the En1cre/+; Otx2flox/flox mutant mouse model represents a genetic tool for investigating molecular and behavioural consequences of developmental neuronal dysfunction in the DAergic system.

Patterning of the vertebrate eye appears to be controlled by the mutual regulation and the progressive restriction of the expression domains of a number of genes initially co-expressed within the eye anlage. Previous data suggest that both Otx1 and Otx2 might contribute to the establishment of the different eye territories. Here, we have analysed the ocular phenotype of mice carrying different functional copies of Otx1 and Otx2 and we show that these genes are required in a dose-dependent manner for the normal development of the eye. Thus, all Otx1(-/-); Otx2(+/-) and 30% of Otx1(+/-); Otx2(+/-) genotypes presented consistent and profound ocular malformation, including lens, pigment epithelium, neural retina and optic stalk defects. During embryonic development, optic vesicle infolding was severely altered and the expression of pigment epithelium-specific genes, such as Mitf or tyrosinase, was lost. Lack of pigment epithelium specification was associated with an expansion of the prospective neural retina and optic stalk territories, as determined by the expression of Pax6, Six3 and Pax2. Later in development the presumptive pigment epithelium region acquired features of mature neural retina, including the generation of Islet1-positive neurones. Furthermore, in Otx1(-/-); Otx2(+/-) mice neural retina cell proliferation, cell differentiation and apoptotic cell death were also severely affected. Based on these findings we propose a model in which Otx gene products are required for the determination and differentiation of the pigment epithelium, co-operating with other eye patterning genes in the determination of the specialised tissues that will constitute the mature vertebrate eye.

The mammalian cochlea is sophisticated in its function and highly organized in its structure. Although the anatomy of this sense organ has been well documented, the molecular mechanisms underlying its development have remained elusive. Information generated from mutant and knockout mice in recent years has increased our understanding of cochlear development and physiology. This article discusses factors important for the development of the inner ear and summarizes cochlear phenotypes of mutant and knockout mice, particularly Otx and Otx2. We also present data on gross development of the mouse cochlea.

The mammalian cochlea is sophisticated in its function and highly organized in its structure. Although the anatomy of this sense organ has been well documented, the molecular mechanisms underlying its development have remained elusive. Information generated from mutant and knockout mice in recent years has increased our understanding of cochlear development and physiology. This article discusses factors important for the development of the inner ear and summarizes cochlear phenotypes of mutant and knockout mice, particularly Otx and Otx2. We also present data on gross development of the mouse cochlea.

Ancien possesseur : Massa, Alfred de (1837-1913). Ancien possesseur, Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi]. Arr. pour quatuor à cordes, Tragedia per musica en 3 actes arrangée pour quatuor à cordes. - Les récitatifs n'ont pas été repris. - Livret d'Antonio Simeone Sografi. - 1re représentation : Venise, Théâtre La Fenice, 26 décembre 1796. - Vl 2, vla, vlc. - Rel. maroquin rouge estampée à chaud, Présentation musicale : [Partition], Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Quatuors à cordes -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi. Acte 1, scène 3. Quelle pupille tenere], Identifié d'après la partition complète F-Pn / D. 2135. - Mention à la p. de t. : "Teatro di Milano". - Livret d'Antonio Simeone Sografi. - 1re représentation : Venise, Théâtre La Fenice, 26 décembre 1796. - Rôle : [Curiazio] (Sol 2). - Vl 2, vla, ob 2, fag 2, cor 2, tr 2, b. - Papier bleuté, Présentation musicale : [Partition], Incipit : Queste pupille tenere (aria), Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Airs d'opéra -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Cimador, Giambattista (1761-1805). Compositeur. [Pimmalione], P. de t. dans un encadr. gr. représentant un décor de théâtre. - Scène dramatique en 2 parties. - Livret d'Antonio Simeone Sografi d'après Jean-Jacques Rousseau. - 1re représentation : Venise, Théâtre San Samuele, 26 janvier 1790. - Rôles : Pimmalione (Ut 4), Galatea (Ut 1). - Vl 2, vla, ob 2, fag, cor 2, bc. - 1re éd. : Padoue : Penada, 1790, Présentation musicale : [Partition], Incipit : Ah ! che spirto né vita più darvi non poss'io, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Livret d'Antonio Simeone Sografi. - 1re représentation : Venise, Théâtre La Fenice, carnaval 1797. - Rôles : Augure [sommo] (Fa 4), Sabina (Ut 1), Curiazio (Ut 1), Licinio (Ut 1), P[ublio] Orazio (Ut 4), M[arco] Orazio (Ut 4), Orazia (Ut 1). - Choeur : Ut 4 (2), Fa 4. - Vl 2, vla, fl, ob 2, cl 2 (en si bémol, do), fag 2, cor 2 (en mi bémol, do), tr 2, bc. - Différences par rapport à F-Pn / L. 4661 et D. 2135-36. - L'aria "Munge il nembo", le récitatif "Vieni, ah mia dolce" et l'aria "Calma la pensa" ne figurent pas dans les autres exemplaires. - Papier bleuté pour les f. 160-182 du 1er vol. et au début du 3me vol.. - Partie de cors 1 et 2 du choeur final reliée à la fin du vol. 2. - Nombreuses annotations au crayon et crayon rouge, collettes et ratures. - Pagination ajoutée a posteriori pour les vol. 1 et 3. - Au contreplat supérieur de chaque vol., papillon du papetier : "Fortin M.d papetier. Rue Helvétius, N° 48, entre celles neuve des petits champs et Chabanois", Présentation musicale : [Partition], Incipit : Odi o ciel i nostri lai, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Livret d'Antonio Simeone Sografi. - Sig. du copiste à la p. de t. et au f. 185 du 2e vol.. - 1re représentation : Venise, Théâtre La Fenice, carnaval 1797. - Rôles : Augure [sommo] (Fa 4), Sabina (Ut 1), Curiazio (Ut 1), Licinio (Ut 1), P[ublio] Orazio (Ut 4), M[arco] Orazio (Ut 4), Orazia (Ut 1). - Choeur : Ut 4 (2), Fa 4. - Vl 2, vla, fl, ob 2, cl 2 (en si bémol, do), fag 2, cor 2 (en mi bémol, do), tr 2, bc. - Différences par rapport aux partitions F-Pn / L. 4658 et L. 4661 : les arias "Serbate eterni" (acte 1, scène 4), "Quel denza notte" (acte 2), "Ah mia cara" et "Presta in pace" (acte 3, scène 2), le récitatif "tutti nel cireo" (acte 3, scène 1), les choeurs "Si adorni" et "Ah crudel" ne figurent pas dans L. 4658 et L. 4661 ; le récitatif "Ed a un tal patto" (acte 1, scène 5) est beaucoup plus long. - Fin de la scène 12 différente à partir du récitatif "Al campo all'armi". - Fin de la marche (acte 1, scène 6) différente par rapport à F-Pn / L. 4661. - Le récitatif "Dov'è lo sposo" est copié 2 fois à la suite. - L'aria "Dolce fiamma di gloria" (acte 2, scène 10) mq.. - Foliotation ajoutée. - Rel. demi parchemin vert, Présentation musicale : [Partition], Incipit : Odi oh ciel i nostri affani, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Livret d'Antonio Simeone Sografi. - 1re représentation : Venise, Théâtre La Fenice, carnaval 1797. - Rôles : Augure [sommo] (Fa 4), Sabina (Ut 1), Curiazio (Ut 1), Licinio (Ut 1), P[ublio] Orazio (Ut 4), M[arco] Orazio (Ut 4), Orazia (Ut 1). - Choeur : Ut 4 (2), Fa 4. - Vl 2, vla, fl, ob 2, cl 2 (en si bémol, do), fag 2, cor 2 (en mi bémol, do), tr 2, bc. - Différences par rapport à F-Pn / L. 4661 et D. 2135-36. - L'aria "Munge il nembo", le récitatif "Vieni, ah mia dolce" et l'aria "Calma la pensa" ne figurent pas dans les autres exemplaires. - Papier bleuté pour les f. 160-182 du 1er vol. et au début du 3me vol.. - Partie de cors 1 et 2 du choeur final reliée à la fin du vol. 2. - Nombreuses annotations au crayon et crayon rouge, collettes et ratures. - Pagination ajoutée a posteriori pour les vol. 1 et 3. - Au contreplat supérieur de chaque vol., papillon du papetier : "Fortin M.d papetier. Rue Helvétius, N° 48, entre celles neuve des petits champs et Chabanois", Présentation musicale : [Partition], Incipit : Odi o ciel i nostri lai, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras -- +* 1700......- 1799......+:18e siècle

Ancien possesseur : Bricqueville, Eugène H. de (1854-1933). Ancien possesseur, Ancien possesseur : Prunières, Henry (1886-1942). Ancien possesseur, Ancien possesseur : Thibault, Geneviève (1902-1975). Ancien possesseur, Titre uniforme : Andreozzi, Gaetano (1755-1826). Compositeur. [Giovanna d'Arco. No quest'anime non sanno], Aria extraite de "Giovanna d'Arco", opera seria en 4 actes. - Livret de Simeone Antonio Sografi. - 1re représentation : Vicenza, Théâtre Nuovo, 27 juin 1789. - Voix : Ut 4. - Vl 2, vla 2, cl 2 (en mi la fa), ob 2, cor 2 (en mi la fa), fag, b. - Le début du récitatif ("Riccardo") est biffé et corrigé dans "O figlio", Présentation musicale : [Partition], Incipit : Riccardo che fai (récitatif), Incipit : No quest'anime non sanno (aria), Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : Chambure1, Appartient à l’ensemble documentaire : RISMMss, Airs d'opéra -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Guglielmi, Pietro Carlo (1772-1817). Compositeur. Compositeur. [Le convenienze teatrali], Titre pris à la garde volante. - Opera buffa en un acte. - Librettiste non identifié (Giuseppe Palomba ?), livret d'après la pièce éponyme de Simeone Antonio Sografi. - 1re représentation : Palerme, Théâtre di Santa Cecilia, 30 mai 1801 (en deux actes). - Rôles : Giuseppina (Ut 1), Impresario (Fa 4), Conte (Fa 4), Luisa (Ut 1), Gerardo (Fa 4), Daria (Ut 1), Gennaro (Fa 4), Guglielmo (Ut 4). - Vl 2, vla, b, fl, ob, fag, cl (en ut, si bémol), clno (en si bémol), a-trb (en ut), cor (en ut, ré, mi bémol, fa, sol, si bémol). - Plusieurs copistes. - Collettes et traces de collettes postérieures. - Nombreux passages biffés. - Au dos, deux étiquettes anciennes d'origine : en bas, inscription manuscrite "380" ; en haut, étiquette gravée comportant une partition, des instruments de musique, deux masques et, au centre, l'inscription manuscrite "Guglielmi // Convenienze Teatrali // Atto unico". - Mention "NJ" en haut à gauche de la p. 1, Présentation musicale : [Partition], Incipit : Eccellentissimo dello scenario, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras -- +* 1800......- 1899......+:19e siècle

Titre uniforme : Guglielmi, Pietro Alessandro (1728-1804). Compositeur. [Gionata Maccabeo], Oratorio en 2 parties. - Livret de Simeone Antonio Sografi. - 1re représentation : Naples : Théâtre San Carlo, 28 février 1798. - Rôles : Egla (Ut 1), Abra (Ut 1), Gionata (Ut 1), Simone (Ut 4), Trifone (Ut 4), Arsace (Fa 4). - Chœur : Ut 1, Ut 3, Ut 4, Fa 4. - Vl 2, vla 2, b, fl 2, ob 2, cl 2 (en si bémol), cor 2 (en do, ré, mi bémol, fa, la, si bémol), fag, tr 2 (en do, ré), arp. - Titre dans un encadrement gravé. - Rel. en veau brun au chiffre de "M. L. B.", Présentation musicale : [Partition], Incipit : Il duol che l'agita (choeur), Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Oratorios -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Gazzaniga, Giuseppe (1743-1818). Compositeur. [Gli Argonauti in Colco. Alma dea che in sen mi vedi (Récitatif et aria)], Mention ajoutée d'une autre main en haut de la p. de titre : "N° 1er". - Scène extraite de "Gli Argonauti in colco", opera seria en 3 actes. - Livret de S. A. Sografi. - 1re représentation : Venise, Théâtre San Samuele, carnaval 1790. - Soliste : Ut 1. - Vl 2, vla 2, fl 2 (dont une fl solo), cor 2 (en ré, la), b.. - Rel. du Conservatoire de la période napoléonienne, dos cuir. - Fait partie d'un recueil factice contenant 10 airs de Giuseppe Gazzaniga. - Pagination continue du recueil à l'encre. - Scène identifiée grâce à Internet Culturale (http://www.internetculturale.it, 2008-01-10), Présentation musicale : [Partition], Incipit : Misera ! ove trascorro per celare il mio duol ! (récitatif), Incipit : Alma dea che in sen mi vedi (aria), Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Airs d'opéra -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Opéras -- +* 1700......- 1799......+:18e siècle

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Livret d'Antonio Simeone Sografi. - 1re représentation : Venise, Théâtre La Fenice, 26 décembre 1796. - Rôles : Augure [sommo] (Fa 4), Sabina (Ut 1), Curiazio (Ut 1), Licinio (Ut 1), P[ublio] Orazio (Ut 4), M[arco] Orazio (Ut 4), Orazia (Ut 1). - Choeur : Ut 4 (2), Fa 4. - Vl 2, vla, fl, ob 2, cl 2 (en si bémol, do), fag 2, cor 2 (en mi bémol, do), tr 2, bc. - La partition L. 4661 présente quelques différences par rapport aux exemplaires F-Pn / L. 4658 et D. 2135-36 : le début de l'acte 3 est dans un ordre différent des autres exemplaires ; la fin de la marche (acte 1, scène 6) est différente de F-Pn / D. 2135-36. - Mq. le choeur "Scopransi" qui suit la marche. - Acte 2, scène 2, mq. le début des paroles du récitatif "Dunque". - P. de t. à la p. 201 du vol. 2, sur laquelle on peut lire : "Sotteranco del sigr Cimarosa" ; suit l'aria "Fra queste tenebre". - Pagination ajoutée. - Papier bleuté. - Rel. demi parchemin, Présentation musicale : [Partition], Incipit : Odi o ciel i nostri affani, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Livret d'Antonio Simeone Sografi. - 1re représentation : Venise, Théâtre La Fenice, 26 décembre 1796. - Rôles : Augure [sommo] (Fa 4), Sabina (Ut 1), Curiazio (Ut 1), Licinio (Ut 1), P[ublio] Orazio (Ut 4), M[arco] Orazio (Ut 4), Orazia (Ut 1). - Choeur : Ut 4 (2), Fa 4. - Vl 2, vla, fl, ob 2, cl 2 (en si bémol, do), fag 2, cor 2 (en mi bémol, do), tr 2, bc. - La partition L. 4661 présente quelques différences par rapport aux exemplaires F-Pn / L. 4658 et D. 2135-36 : le début de l'acte 3 est dans un ordre différent des autres exemplaires ; la fin de la marche (acte 1, scène 6) est différente de F-Pn / D. 2135-36. - Mq. le choeur "Scopransi" qui suit la marche. - Acte 2, scène 2, mq. le début des paroles du récitatif "Dunque". - P. de t. à la p. 201 du vol. 2, sur laquelle on peut lire : "Sotteranco del sigr Cimarosa" ; suit l'aria "Fra queste tenebre". - Pagination ajoutée. - Papier bleuté. - Rel. demi parchemin, Présentation musicale : [Partition], Incipit : Odi o ciel i nostri affani, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras

Titre uniforme : Cimarosa, Domenico (1749-1801). Compositeur. [Gli Orazi ed i Curiazi], Livret d'Antonio Simeone Sografi. - 1re représentation : Venise, Théâtre La Fenice, 26 décembre 1796. - Rôles : Augure [sommo] (Fa 4), Sabina (Ut 1), Curiazio (Ut 1), Licinio (Ut 1), P[ublio] Orazio (Ut 4), M[arco] Orazio (Ut 4), Orazia (Ut 1). - Choeur : Ut 4 (2), Fa 4. - Vl 2, vla, fl, ob 2, cl 2 (en si bémol, do), fag 2, cor 2 (en mi bémol, do), tr 2, bc. - La partition L. 4661 présente quelques différences par rapport aux exemplaires F-Pn / L. 4658 et D. 2135-36 : le début de l'acte 3 est dans un ordre différent des autres exemplaires ; la fin de la marche (acte 1, scène 6) est différente de F-Pn / D. 2135-36. - Mq. le choeur "Scopransi" qui suit la marche. - Acte 2, scène 2, mq. le début des paroles du récitatif "Dunque". - P. de t. à la p. 201 du vol. 2, sur laquelle on peut lire : "Sotteranco del sigr Cimarosa" ; suit l'aria "Fra queste tenebre". - Pagination ajoutée. - Papier bleuté. - Rel. demi parchemin, Présentation musicale : [Partition], Incipit : Odi o ciel i nostri affani, Appartient à l’ensemble documentaire : RISM2, Appartient à l’ensemble documentaire : RISMMss, Opéras

Titre uniforme : Donizetti, Gaetano (1797-1848). Compositeur. [Il Pigmalione], Titre propre non autogr. pris à la couverture. - Mention autogr. à la fin : "Cominciata li 25 7bre // Finita adi // 1 8bre // 1816 // ore quasi due // antimeridiane // giorno di martedi // Ingresso del Legato // nuovo". - Opéra en 1 acte, composé à Bologne en 1816 et représenté pour la première fois au Théâtre Donizetti de Bergame le 13 octobre 1960. - Livret d'Antonio Simone Sografi. - Rôles : Pigmalione (Ut 4), Galatea (Ut 1). - Vl 2, vla, fl 2, ob2, cl 2, cor 2, fag, vlc, b. - Voir Catal. Malherbe, appendice, n° 68, Présentation musicale : [Partition], Opéras -- +* 1800......- 1899......+:19e siècle

En la portada hay una etiqueta del editor Sieber tapando el pie de imprenta original del editor Imbault.- Etiqueta de Sieber: "Chez SIEBER, (Gendre de Le Duc, ) au Magasin de Musique et d'Instruments, Rue de la Loi (ci-devant Richelieu, ) vis-a-vis la Fontaine Traversière, Nº 28. A la Flute enchantée. A PARIS.".- Pie de imprenta tapado por la etiqueta pegada encima: "Chez IMBAULT, Md. de Musique au Mont d'Or, Rue Honoré Nº 200 entre la Rue des Poulies et la Maison d'Aligre ET PÉRISTILE DU THÉATRE DE L'OPERA COMIQUE RUE FAVART Nº 461", En las cuatro páginas siguientes a la portada figura el "Catalogue de musique vocale et instrumentale mise au jour par Imbault", RISM, A/I, Catálogo de impresos musicales del siglo XVIII en la Biblioteca Nacional, 1989, Fecha de publicación basada en Dictionnaire des éditeurs de musique français, volume I, des origines à environ 1820, 1979, Impresión calcográfica de la notación musical