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Zwischen 1843 und 1888 veröffentlichte Fanny Lewald 24 teils mehrbändige Romane, 27 Bände Novellen und Erzählungen, eine sechsbändige Autobiographie, fünf Reisetagebücher, zahlreiche Feuilletons, Erinnerungen an bekannte Persönlichkeiten, frauenemanzipatorische Schriften und soziale Appelle in Zeitungen und Zeitschriften - ein umfangreiches Werk. Über den Zeitraum von annähernd einem halben Jahrhundert spiegeln ihre Schriften die wechselvolle deutsche Geschichte wider - Vormärz, Märzrevolution 1848, Restauration, Reichseinigung, Kaiserreich - ebenso wie die Geschichte der deutschen Literatur von jungdeutscher Tendenz- und Reflexionsliteratur bis hin zum poetischen Realismus und Naturalismus. Denn mit zahlreichen romantheoretischen Äußerungen, die sich sowohl in ihren Prosawerken wie in Briefen und anderen nichtfiktiven Schriften finden lassen, macht Fanny Lewald wie wenige andere Autorinnen des Vormärz ihren poetologischen Standpunkt deutlich. Früh- und Spätwerk der Autorin sind, bezogen auf ihr erzählerisches Konzept und die Gestaltungsweise, sehr unterschiedlich. Doch in einem Punkt bleibt sich Fanny Lewald treu - ihre Prosa bleibt lebensnah, zeitlebens favorisiert sie den sozialen und psychologischen Roman.
[Rezension zu:] Vanessa van Ornam: Fanny Lewald And Nineteenth-Century Constructions of Feminity
(2004)
Rezension zu: Vanessa van Ornam: Fanny Lewald And Nineteenth-Century Constructions of Feminity. New York, Washington, D.C./Baltimore, Bern, Frankfurt am Main, Berlin, Brüssel, Wien, Oxford: Peter Lang, 2002 (North American Studies in Nineteenth-Century German Literature, hrsg. v. Jeffrey L. Sammons, Bd. 29).
Ophthalmo-acromelic syndrome (OAS), also known as Waardenburg Anophthalmia syndrome, is defined by the combination of eye malformations, most commonly bilateral anophthalmia, with post-axial oligosyndactyly. Homozygosity mapping and subsequent targeted mutation analysis of a locus on 14q24.2 identified homozygous mutations in SMOC1 (SPARC-related modular calcium binding 1) in eight unrelated families. Four of these mutations are nonsense, two frame-shift, and two missense. The missense mutations are both in the second Thyroglobulin Type-1 (Tg1) domain of the protein. The orthologous gene in the mouse, Smoc1, shows site- and stage-specific expression during eye, limb, craniofacial, and somite development. We also report a targeted pre-conditional gene-trap mutation of Smoc1 (Smoc1tm1a) that reduces mRNA to ~10% of wild-type levels. This gene-trap results in highly penetrant hindlimb post-axial oligosyndactyly in homozygous mutant animals (Smoc1tm1a/tm1a). Eye malformations, most commonly coloboma, and cleft palate occur in a significant proportion of Smoc1tm1a/tm1a embryos and pups. Thus partial loss of Smoc-1 results in a convincing phenocopy of the human disease. SMOC-1 is one of the two mammalian paralogs of Drosophila Pentagone, an inhibitor of decapentaplegic. The orthologous gene in Xenopus laevis, Smoc-1, also functions as a Bone Morphogenic Protein (BMP) antagonist in early embryogenesis. Loss of BMP antagonism during mammalian development provides a plausible explanation for both the limb and eye phenotype in humans and mice.
The Transition Radiation Detector (TRD) was designed and built to enhance the capabilities of the ALICE detector at the Large Hadron Collider (LHC). While aimed at providing electron identification and triggering, the TRD also contributes significantly to the track reconstruction and calibration in the central barrel of ALICE. In this paper the design, construction, operation, and performance of this detector are discussed. A pion rejection factor of up to 410 is achieved at a momentum of 1 GeV/c in p–Pb collisions and the resolution at high transverse momentum improves by about 40% when including the TRD information in track reconstruction. The triggering capability is demonstrated both for jet, light nuclei, and electron selection.