Connectivity in the network macrostructure of Tursiops truncatus in the Pelagos Sanctuary (NW Mediterranean Sea): does landscape matter?

The bottlenose dolphin (Tursiops truncatus Montagu, 1821) is a regularly observed species in the Mediterranean Sea, but its network organization has never been investigated on a large scale. We described the network macrostructure of the bottlenose dolphin (meta)population inhabiting the Pelagos Sanctuary (a wide protected area located in the north-western portion of the Mediterranean basin) and we analysed its connectivity in relation to the landscape traits. We pooled effort and sighting data collected by 13 different research institutions operating within the Pelagos Sanctuary from 1994 to 2011 to examine the distribution of bottlenose dolphins in the Pelagos study area and then we applied a social network analysis, investigating the association patterns of the photo-identified dolphins (806 individuals in 605 sightings). The bottlenose dolphin (meta)population inhabiting the Pelagos Sanctuary is clustered in discrete units whose borders coincide with habitat breakages. This complex structure seems to be shaped by the geo-morphological and ecological features of the landscape, through a mechanism of local specialization of the resident dolphins. Five distinct clusters were identified in the (meta)population and two of them were solid enough to be further investigated and compared. Significant differences were found in the network parameters, suggesting a different social organization of the clusters, possibly as a consequence of the different local specialization.     

Accelerated bio‐cognitive aging in Down syndrome: State of the art and possible deceleration strategies

Down syndrome (DS) has been proposed by George Martin as a segmental progeroid syndrome since 1978. In fact, DS persons suffer from several age‐associated disorders much earlier than euploid persons. Furthermore, a series of recent studies have found that DS persons display elevated levels of age biomarkers, thus supporting the notion that DS is a progeroid trait. Nowadays, due to the progressive advancements in social inclusion processes and medical assistance, DS persons live much longer than in the past; therefore, the early‐onset health problems of these persons are becoming an urgent and largely unmet social and medical burden. In particular, the most important ailment of DS persons is the accelerated cognitive decline that starts when they reach about 40 years of age. This decline can be at least in part counteracted by multi‐systemic approaches including early‐onset cognitive training, physical activity, and psychosocial assistance. However, no pharmacological treatment is approved to counteract this decline. According to the most advanced conceptualization of Geroscience, tackling the molecular mechanisms underpinning the aging process should be a smart/feasible strategy to combat and/or delay the great majority of age‐related diseases, including cognitive decline. We think that a debate is needed urgently on if (and how) this strategy could be integrated in protocols to face DS‐associated dementia and overall unhealthy aging. In particular we propose that, on the basis of data obtained in different clinical settings, metformin is a promising candidate that could be exploited to counteract cognitive decline in DS.     

Algal Remodeling in a Ubiquitous Planktonic Photosymbiosis

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Precise Gene Editing Preserves Hematopoietic Stem Cell Function following Transient p53-Mediated DNA Damage Response

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PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties

Th1 cytokines promote monocyte differentiation into proatherogenic M1 macrophages, while Th2 cytokines lead to an "alternative" anti-inflammatory M2 macrophage phenotype. Here we show that in human atherosclerotic lesions, the expression of M2 markers and PPARgamma, a nuclear receptor controlling macrophage inflammation, correlate positively. Moreover, PPARgamma activation primes primary human monocytes into M2 differentiation, resulting in a more pronounced anti-inflammatory activity in M1 macrophages. However, PPARgamma activation does not influence M2 marker expression in resting or M1 macrophages, nor does PPARgamma agonist treatment influence the expression of M2 markers in atherosclerotic lesions, indicating that only native monocytes can be primed by PPARgamma activation to an enhanced M2 phenotype. Furthermore, PPARgamma activation significantly increases expression of the M2 marker MR in circulating peripheral blood mononuclear cells. These data demonstrate that PPARgamma activation skews human monocytes toward an anti-inflammatory M2 phenotype.     

The Barnes Maze Task Reveals Specific Impairment of Spatial Learning Strategy in the Intrahippocampal Kainic Acid Model for Temporal Lobe Epilepsy

Neurochemical Research - Temporal lobe epilepsy (TLE) is an acquired form of focal epilepsy, in which patients not only suffer from unprovoked, devastating seizures, but also from severe...