University of Palermo

About: University of Palermo is a education organization based out in Palermo, Italy. It is known for research contribution in the topics: Population & Medicine. The organization has 15621 authors who have published 40250 publications receiving 964384 citations. The organization is also known as: Università degli Studi di Palermo & Universita degli Studi di Palermo.

Ecological impacts of global warming and water abstraction on lakes and reservoirs due to changes in water level and related changes in salinity

Abstract: According to the Intergovernmental Panel on Climate Change report released in September 2014, unprecedented changes in temperature and precipitation patterns have been recorded globally in recent decades and further change is predicted to occur in the near future, mainly as the result of human activity. In particular, projections show that the Mediterranean climate zone will be markedly affected with significant implications for lake water levels and salinity. This may be exacerbated by increased demands for irrigation water. Based on long-term data from seven lakes and reservoirs covering a geographical gradient of 52° of latitudes and a literature review, we discuss how changes in water level and salinity related to climate change and water abstraction affect the ecosystem structure, function, biodiversity and ecological state of lakes and reservoirs. We discuss mitigation measures to counteract the negative effects on ecological status that are likely to result from changes in climate and water abstraction practices. Finally, we highlight research required to improve knowledge of the impacts of anthropogenically induced changes on lake water level and consequent changes in salinity.

Role of TGF-β Pathway Polymorphisms in Sporadic Thoracic Aortic Aneurysm: rs900 TGF-β2 Is a Marker of Differential Gender Susceptibility

Abstract: Thoracic aortic aneurysm (TAA) is a progressive disorder involving gradual dilation of ascending and/or descending thoracic aorta with dissection or rupture as complications. It occurs as sporadic or defined syndromes/familial forms.Genetic, molecular and cellular mechanims of sporadic TAA forms are poorly characterized and known. Thus, our interest has been focused on investigating the role of genetic variants of transforming growth factor-β (TGF-β) pathways in TAA risk. On the other hand, no data on the role of genetic variants of TGF-β pathway in sporadic TAA exist until now. In addition, other cytokines, including IL-10, orchestrate TAA pathophysiology. Their balance determines the ultimate fate of the aortic wall as healing atherosclerosis or aneurysm formation. Thus, in this paper it was analyzed the role of ten polymorphisms of genes encoding TGF-β isoforms and receptors, and IL-10 in sporadic TAA. Our study included cases affected by sporadic TAA and two control groups. The most relevant finding obtained allows us to propose that rs900 TGF-β2 SNP is associated with sporadic TAA in women. This might open new perspectives for the analysis of sporadic TAA susceptibility factors and prevention.

β-Amyloid Monomers Are Neuroprotective

Abstract: The 42-aa-long beta-amyloid protein--Abeta(1-42)--is thought to play a central role in the pathogenesis of Alzheimer's disease (AD) (Walsh and Selkoe, 2007). Data from AD brain (Shankar et al., 2008), transgenic APP (amyloid precursor protein)-overexpressing mice (Lesne et al., 2006), and neuronal cultures treated with synthetic Abeta peptides (Lambert et al., 1998) indicate that self-association of Abeta(1-42) monomers into soluble oligomers is required for neurotoxicity. The function of monomeric Abeta(1-42) is unknown. The evidence that Abeta(1-42) is present in the brain and CSF of normal individuals suggests that the peptide is physiologically active (Shoji, 2002). Here we show that synthetic Abeta(1-42) monomers support the survival of developing neurons under conditions of trophic deprivation and protect mature neurons against excitotoxic death, a process that contributes to the overall neurodegeneration associated with AD. The neuroprotective action of Abeta(1-42) monomers was mediated by the activation of the PI-3-K (phosphatidylinositol-3-kinase) pathway, and involved the stimulation of IGF-1 (insulin-like growth factor-1) receptors and/or other receptors of the insulin superfamily. Interestingly, monomers of Abeta(1-42) carrying the Arctic mutation (E22G) associated with familiar AD (Nilsberth et al., 2001) were not neuroprotective. We suggest that pathological aggregation of Abeta(1-42) may also cause neurodegeneration by depriving neurons of the protective activity of Abeta(1-42) monomers. This "loss-of-function" hypothesis of neuronal death should be taken into consideration when designing therapies aimed at reducing Abeta burden.