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The study starts from two analogous works, a book and a pamphlet, produced in the 16th century, which portray Nicolas Durand de Villegagnon as the Cyclops Polyphemus, a figure established by classical texts such as the Odyssey by Homer and Cyclops by Euripides. Through this unusual comparison between a mythological monster and the Knight of Malta, both the poem and the etching represent Villegagnon and vilify him through certain discursive strategies. Such an invective project is grounded in religious, political, and economic quarrels which have taken place in the context of the enterprise known as ‘France Antarctique’ in Guanabara Bay. The Frenchman Durand is transformed into a barbarian and uncivilized figure, becoming as threatening as the Brazilian cannibal tribes. [ABSTRACT FROM AUTHOR]

Introduction: Mitochondrial defects have been implicated in Parkinson's disease (PD) since complex I poisons were found to cause accelerated parkinsonism in young people in the early 1980s. More evidence of mitochondrial involvement arose when many of the genes whose mutations caused inherited PD were discovered to be subcellularly localized to mitochondria or have mitochondrial functions. However, the details of how mitochondrial dysfunction might impact or cause PD remain unclear. The aim of our study was to better understand mitochondrial dysfunction in PD by evaluating mitochondrial respiratory complex mutations in a Drosophila melanogaster (fruit fly) model of PD. Methods: We have conducted a targeted heterozygous enhancer/suppressor screen using Drosophila mutations within mitochondrial electron transport chain (ETC) genes against a null PD mutation in parkin. The interactions were assessed by climbing assays at 2–5 days as an indicator of motor function. A strong enhancer mutation in COX5A was examined further for L-dopa rescue, oxygen consumption, mitochondrial content, and reactive oxygen species. A later timepoint of 16–20 days was also investigated for both COX5A and a suppressor mutation in cyclope. Generalized Linear Models and similar statistical tests were used to verify significance of the findings. Results: We have discovered that mutations in individual genes for subunits within the mitochondrial respiratory complexes have interactions with parkin, while others do not, irrespective of complex. One intriguing mutation in a complex IV subunit (cyclope) shows a suppressor rescue effect at early time points, improving the gross motor defects caused by the PD mutation, providing a strong candidate for drug discovery. Most mutations, however, show varying degrees of enhancement or slight suppression of the PD phenotypes. Thus, individual mitochondrial mutations within different oxidative phosphorylation complexes have different interactions with PD with regard to degree and direction. Upon further investigation of the strongest enhancer (COX5A), the mechanism by which these interactions occur initially does not appear to be based on defects in ATP production, but rather may be related to increased levels of reactive oxygen species. Conclusions: Our work highlights some key subunits potentially involved in mechanisms underlying PD pathogenesis, implicating ETC complexes other than complex I in PD.

El síndrome cyclops es una entidad patológica que involucra la presencia de un nódulo fibrótico adyacente a la plástica de LCA que genera un déficit de extensión progresiva. Se han postulado diversos factores de riesgo que predisponen a la generación de esta lesión, entre las cuales se incluye un surco intercondíleo estrecho, el uso de injertos cuadricipitales de doble banda, la perdida de extensión activa en el postoperatorio y la contractura de isquiotibiales. El síndrome cyclops puede ser diagnosticado erróneamente cuando la presentación clínica es atípica, tardía, o incluso cuando se encuentran lesiones asociadas en las evaluaciones imagenológicas. El objetivo del siguiente estudio es reportar una serie de casos de síndrome cyclops de presentación tardía, con restitución integra del rango de movilidad y funcionales luego de la exéresis artroscópica de la lesión.

Mitochondrial defects have been implicated in Parkinson's disease (PD) since complex I poisons were found to cause accelerated parkinsonism in young people in the early 1980s. More evidence of mitochondrial involvement arose when many of the genes whose mutations caused inherited PD were discovered to be subcellularly localized to mitochondria or have mitochondrial functions. However, the details of how mitochondrial dysfunction might impact or cause PD remain unclear. The aim of our study was to better understand mitochondrial dysfunction in PD by evaluating mitochondrial respiratory complex mutations in a Drosophila melanogaster (fruit fly) model of PD. We have conducted a targeted heterozygous enhancer/suppressor screen using Drosophila mutations within mitochondrial electron transport chain (ETC) genes against a null PD mutation in parkin. The interactions were assessed by climbing assays at 2–5 days as an indicator of motor function. A strong enhancer mutation in COX5A was examined further for L-dopa rescue, oxygen consumption, mitochondrial content, and reactive oxygen species. A later timepoint of 16–20 days was also investigated for both COX5A and a suppressor mutation in cyclope. Generalized Linear Models and similar statistical tests were used to verify significance of the findings. We have discovered that mutations in individual genes for subunits within the mitochondrial respiratory complexes have interactions with parkin , while others do not, irrespective of complex. One intriguing mutation in a complex IV subunit (cyclope) shows a suppressor rescue effect at early time points, improving the gross motor defects caused by the PD mutation, providing a strong candidate for drug discovery. Most mutations, however, show varying degrees of enhancement or slight suppression of the PD phenotypes. Thus, individual mitochondrial mutations within different oxidative phosphorylation complexes have different interactions with PD with regard to degree and direction. Upon further investigation of the strongest enhancer (COX5A), the mechanism by which these interactions occur initially does not appear to be based on defects in ATP production, but rather may be related to increased levels of reactive oxygen species. Our work highlights some key subunits potentially involved in mechanisms underlying PD pathogenesis, implicating ETC complexes other than complex I in PD. • Mitochondrial electron transport chain mutations interact with parkin PD phenotypes. • Specific fly mutations in complexes I, II, III, and IV enhance or suppress parkin. • A cyclope complex IV subunit mutation suppresses parkin early gross motor defects. • Specific ETC subunit roles could be vital in PD and should be investigated further. [ABSTRACT FROM AUTHOR]

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