Abstract:The ant assemblage of Radoboj (Croatia) described by Heer (1849, 1867) is considered the richest known Miocene assemblage of Europe. However, Heer's data can no longer be used for analysis of the palaeontological history of ants, because they are strongly outdated and require a revision. Such a revision was the purpose of our study. We found in collections of three museums of Austria (Universalmuseum Joanneum in Graz, Geologische Bundesanstalt, and Naturhistoricshes Museum in Wien) a total of 537 compression fossils of ants from Radoboj, 459 of which were identified earlier by Heer. We designated the holotypes, lectotypes and neotypes for 54 of the 62 species described by Heer, and subsequently compared the other specimens to these types. As a result, we have identified 350 specimens to subfamily and 309 specimens to species. We re-described 23 species originally described by Heer (1849, 1867) and two species described by Mayr (1867). One genus and eight species are described as new; 27 species and varieties described by Heer are synonymized. The taxonomic placement of eight species described by Heer remains unclear. As a result of our revision, the known assemblage of Radoboj includes 33 species of 15 genera and five subfamilies. The assemblage of Radoboj is especially similar at the subfamily level to the assemblage of Bembridge, UK (Late Eocene) and Stavropol, RF (Middle Miocene).

The nature of the selection factors underlying the evolution of aging remains controversial [1-3]. Many specialists in evolutionary gerontology support a set of ideas called the "evolutionary theory of aging" [1, 2]. This theory is based on the idea that the selection efficiency decreases with age. It is also assumed that vitality and fertility are high in youth at the cost of reduced fitness at later ages [4, 5]. An alternative view is that programmed aging and death may be favored by some kind of selection [3, 6-16]. A subsequent theoretical experiment called the "Fable about Fox and Hares" was suggested by one of the authors of this paper (VPS) [17]. Two young hares differing "intellectually" have equal chances to escape from a fox since both of hares are running faster than a www.aging-us.com

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This review discusses genetic and molecular pathways that link circadian timing with metabolism, resulting in the emergence of positive and negative regulatory feedback loops. The Nrf2 pathway is believed to be a component of the anti-aging program responsible for the healthspan and longevity. Nrf2 enables stress adaptation by activating cell antioxidant defense and other metabolic processes via control of expression of over 200 target genes in response to various types of stress. The GSK3 system represents a “regulating valve” that controls fine oscillations in the Nrf2 level, unlike Keap1, which prevents significant changes in the Nrf2 content in the absence of oxidative stress and which is inactivated by the oxidative stress. Furthermore, GSK3 modifies core circadian clock proteins (Bmal1, Clock, Per, Cry, and Rev-erbα). Phosphorylation by GSK3 leads to the inactivation and degradation of circadian rhythm-activating proteins (Bmal1 and Clock) and vice versa to the activation and nuclear translocation of proteins suppressing circadian rhythms (Per and Rev-erbα) with the exception of Cry protein, which is likely to be implicated in the fine tuning of biological clock. Functionally, GSK3 appears to be one of the hubs in the cross-regulation of circadian rhythms and antioxidant defense. Here, we present the data on the crosstalk between the most powerful cell antioxidant mechanism, the Nrf2 system, and the biorhythm-regulating system in mammals, including the impact of GSK3 overexpression and knockout on the Nrf2 signaling. Understanding the interactions between the regulatory cascades linking homeostasis maintenance and cell response to oxidative stress will help in elucidating molecular mechanisms that underlie aging and longevity.