Resistência de genótipos de palma de óleo (Elaeis guineensis Jacq.) ao ataque de Opsiphanes invirae Hübner, 1808 (lepidoptera: nymphalidae) no Estado do Pará

Pós-graduação em Agronomia (Entomologia Agrícola) - FCAV

Cem anos do direito internacional público (1913) de Jos�� mendes (1861-1918) – olhar reflexivo sobre o direito internacional nas arcadas (1911-1918)

Ensino do Direito internacional nas arcadas – Jos�� Mendes foi professor ordinário da disciplina (1911-1918) – sua obra Direito internacional público – preleções (1913) completa cem anos de publicação.

Scott Joplin: Treemonisha

Scott Joplin’s (1867–1917) opera Treemonisha is the only opera in existence about the Reconstruction era African-American experience written by a black man who actually lived through it. This fact alone makes the opera a work of tremendous significance. Further, Joplin’s music is profoundly expressive and as stylistically unique as anything ever created in America. Through his score and libretto, Joplin vividly documented a culture that has left us few other artifacts: The echoes of the “field hollers,” spirituals, fiddle tunes, revival hymns, and ancient African dances of his rural childhood are all heard, along with the dialects of his people rising up from slavery. Yet for all of its obvious significance, Treemonisha has been a deeply misunderstood work. The opera was complex and virtually unprecedented, two reasons why 1910s America could not embrace it. And tragically, Joplin's original 1911 materials for the opera were almost entirely destroyed in the early 1960s. In the early 1970s several attempts were made to reconstruct it, but for the most part these were not concerned with the opera’s cultural origins or historic authenticity. But now, on the centennial of this extraordinary creation, comes this new recording of a completely authentic reconstruction of Treemonisha by Rick Benjamin, based on eighteen years of research.

Party Size and Constituency Representation: Evidence from the 19th-Century U.S. House of Representatives

Research on congressional parties assumes, but has not directly shown, that party size affects individual members' calculations. Drawing on a key case from the nineteenth-century House the secession-driven Republican hegemony of 1861 this article explores the hypothesis that party voting not only declines but also becomes more strongly linked to constituency factors as relative party size increases. The analysis reveals that the jump in party size coincides with (1) a decrease in party voting among individual continuing members, (2) a strengthening association between some constituency factors and party voting, and (3) patterns of decline in individual party voting that are explained in part by constituency measures.

Unilateral focal polymicrogyria in a patient with classical Aarskog-Scott syndrome due to a novel missense mutation in an evolutionary conserved RhoGEF domain of the faciogenital dysplasia gene FGD1

Faciogenital dysplasia or Aarskog-Scott syndrome (AAS) is an X-linked disorder characterized by craniofacial, skeletal, and urogenital malformations and short stature. Mutations in the only known causative gene FGD1 are found in about one-fifth of the cases with the clinical diagnosis of AAS. FGD1 is a guanine nucleotide exchange factor (GEF) that specifically activates the Rho GTPase Cdc42 via its RhoGEF domain. The Cdc42 pathway is involved in skeletal formation and multiple aspects of neuronal development. We describe a boy with typical AAS and, in addition, unilateral focal polymicrogyria (PMG), a feature hitherto unreported in AAS. Sequencing of the FGD1 gene in the index case and his mother revealed the presence of a novel mutation (1396A>G; M466V), located in the evolutionary conserved alpha-helix 4 of the RhoGEF domain. M466V was not found in healthy family members, in >300 healthy controls and AAS patients, and has not been reported in the literature or mutation databases to date, indicating that this novel missense mutation causes AAS, and possibly PMG. Brain cortex malformations such as PMG could be initiated by mutations in the evolutionary conserved RhoGEF domain of FGD1, by perturbing the signaling via Rho GTPases such as Cdc42 known to cause brain malformation.