Introduction, by H. J. Cargas.--St. Paul and Teilhard de Chardin, by J. H. Adams.--Teilhard and Dante, by M. Gable.--Tennyson and Teilhard, by E. R. August.--Teilhard, neo-Marxism, existentialism, by M. Barthelemy-Madaule.--Whitman, Teilhard, and Jung, by R. Benoit.--C. G. Jung and Teilhard de Chardin, by N. Braybrooke.--Camus and Teilhard, by P. Rosazza.--Bonhoeffer and Teilhard, by C. M. Hegarty.--Voices of convergence: Teilhard, McLuhan, and Brown, by D. J. Leary.
The sporadic nature of Alzheimer's disease argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and the period of their action are unknown. Recent studies in rodents have shown that exposure to lead during brain development predetermined the expression and regulation of the amyloid precursor protein and its amyloidogenic beta-amyloid product in old age. Here, we report that the expression of AD-related genes [APP, BACE1 ] as well as their transcriptional regulator were elevated in aged (...) monkeys exposed to Pb as infants. Furthermore, developmental exposure to Pb altered the levels, characteristics, and intracellular distribution of Abeta staining and amyloid plaques in the frontal association cortex. These latent effects were accompanied by a decrease in DNA methyltransferase activity and higher levels of oxidative damage to DNA, indicating that epigenetic imprinting in early life influenced the expression of AD-related genes and promoted DNA damage and pathogenesis. These data suggest that AD pathogenesis is influenced by early life exposures and argue for both an environmental trigger and a developmental origin of AD. (shrink)
Alzheimer's disease is characterized by plaques of amyloid-beta peptide, cleaved from amyloid-beta protein precursor . Our hypothesis is that lifespan profiles of AD-associated mRNA and protein levels in monkeys would differ from mice and that differential lifespan expression profiles would be useful to understand human AD pathogenesis. We compared profiles of AbetaPP mRNA, AbetaPP protein, and Abeta levels in rodents and primates. We also tracked a transcriptional regulator of the AbetaPP gene, specificity protein 1 , and the beta amyloid precursor (...) cleaving enzyme . In mice, AbetaPP and SP1 mRNA and their protein products were elevated late in life; Abeta levels declined in old age. In monkeys, SP1, AbetaPP, and BACE1 mRNA declined in old age, while protein products and Abeta levels rose. Proteolytic processing in both species did not match production of Abeta. In primates, AbetaPP and SP1 mRNA levels coordinate, but an inverse relationship exists with corresponding protein products as well as Abeta levels. Comparison of human DNA and mRNA sequences to monkey and mouse counterparts revealed structural features that may explain differences in transcriptional and translational processing. These findings are important for selecting appropriate models for AD and other age-related diseases. (shrink)
Alzheimer's disease is characterized by amyloid-beta peptide -loaded plaques in the brain. Abeta is a cleavage fragment of amyloid-beta protein precursor and over production of APP may lead to amyloidogenesis. The regulatory region of the APP gene contains consensus sites recognized by the transcription factor, specificity protein 1 , which has been shown to be required for the regulation of APP and Abeta. To understand the role of SP1 in APP biogenesis, herein we have characterized the relative distribution and localization (...) of SP1, APP, and Abeta in various brain regions of rodent and primate models using immunohistochemistry. We observed that overall distribution and cellular localization of SP1, APP, and Abeta are similar and neuronal in origin. Their distribution is abundant in various layers of neocortex, but restricted to the Purkinje cell layer of the cerebellum, and the pyramidal cell layer of hippocampus. These findings suggest that overproduction of Abeta in vivo may be associated with transcriptional pathways involving SP1 and the APP gene. (shrink)
An enumeration of the emendations and interpretations of these verses would fill the space necessary for a whole article. Consequently, I shall proceed at once to a consideration of what I conceive to be the correct restoration of the passage. The last word of verse 601, νριθμος, is evidently genuine, and is accepted by all scholars. The preceding word, μλων, has been changed to μηνν. Jebb regards this as a certain correction, for ‘in no other way can νριθμος be justified.’ (...) That is true, if the adjective is to be taken with γ ; but, in my opinion, it agrees with χρνος. Cf. νριθμος χρνος , O.C. 617 μριος χρνος, Ai. 712 μγας χρνος. As we shall see, it is added as a reinforcement to παλαις to convey the notion that the months seemed numberless because they were so cheerless. Cf. O. T. 561 μακρ παλαιο τ' ༂ν μετρηθεεν χρνοι. (shrink)
No tragic poet uses the phrase μxs22EFνος πνxs22EFουσαν, except Aeschylus, who employs it in describing the Erinyes, not a Greek maiden. Similarly Homer of his ‘Mut-schnaubende’ heroes and of the savage steeds of Diomed. Hence, in the Sophoclean passage, some scribe may have mistaken the familiar ΜΕΝΟCΠΝΕΟΤCΑΝ for the more unusual ΜΕΝΕΙCΙCΤΝΟΤCΑΝ. Initial C attached itself to the preceding word, and ΤΝΟΤCΑΝ became ΠΝΟΤCΑΝ, which was promptly changed to πνxs22EFουσαν.