Institution
University of Palermo
Education•Palermo, Italy•
About: University of Palermo is a education organization based out in Palermo, Italy. It is known for research contribution in the topics: Population & Cancer. 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.
Topics: Population, Cancer, Catalysis, Diabetes mellitus, Volcano
Papers published on a yearly basis
Papers
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TL;DR: The capacity of betalains to protect endothelium from cytokine‐induced redox state alteration, through ICAM‐1 inhibition, is shown in an in vitro model of endothelial cells.
Abstract: It has been suggested that some pigments would have antioxidant properties and that their presence in dietary constituents would contribute to reduce the risk of oxidative stress-correlated diseases. Among others, inflammatory response depends on redox status and may implicate oxidative stress. Vascular endothelial cells are a direct target of oxidative stress in inflammation. We have tested the impact of the free radical scavenger and antioxidant properties of betalains from the prickle pear in an in vitro model of endothelial cells. Here we show the capacity of betalains to protect endothelium from cytokine-induced redox state alteration, through ICAM-1 inhibition.
156 citations
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TL;DR: Modulation of apoptosis-related proteins by TH1 and TH2 cytokines controls thyrocyte survival in thyroid autoimmunity.
Abstract: After autoimmune inflammation, interactions between CD95 and its ligand (CD95L) mediate thyrocyte destruction in Hashimoto's thyroiditis (HT). Conversely, thyroid autoimmune processes that lead to Graves' disease (GD) result in autoantibody-mediated thyrotropin receptor stimulation without thyrocyte depletion. We found that GD thyrocytes expressed CD95 and CD95L in a similar manner to HT thyrocytes, but did not undergo CD95-induced apoptosis either in vivo or in vitro. This pattern was due to the differential production of TH1 and TH2 cytokines. Interferon gamma promoted caspase up-regulation and CD95-induced apoptosis in HT thyrocytes, whereas interleukin 4 and interleukin 10 protected GD thyrocytes by potent up-regulation of cFLIP and Bcl-xL, which prevented CD95-induced apoptosis in sensitized thyrocytes. Thus, modulation of apoptosis-related proteins by TH1 and TH2 cytokines controls thyrocyte survival in thyroid autoimmunity.
156 citations
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TL;DR: The review is divided in three chapters describing in succession the mechanisms of RB1 inactivation in cancer cells, the alterations of pRb pathway in tumorigenesis and the RB protein and E2F family in cancer.
Abstract: Loss of RB1 gene is considered either a causal or an accelerating event in retinoblastoma. A variety of mechanisms inactivates RB1 gene, including intragenic mutations, loss of expression by methylation and chromosomal deletions, with effects which are species-and cell type-specific. RB1 deletion can even lead to aneuploidy thus greatly increasing cancer risk. The RB1gene is part of a larger gene family that includes RBL1 and RBL2, each of the three encoding structurally related proteins indicated as pRb, p107, and p130, respectively. The great interest in these genes and proteins springs from their ability to slow down neoplastic growth. pRb can associate with various proteins by which it can regulate a great number of cellular activities. In particular, its association with the E2F transcription factor family allows the control of the main pRb functions, while the loss of these interactions greatly enhances cancer development. As RB1 gene, also pRb can be functionally inactivated through disparate mechanisms which are often tissue specific and dependent on the scenario of the involved tumor suppressors and oncogenes. The critical role of the context is complicated by the different functions played by the RB proteins and the E2F family members. In this review, we want to emphasize the importance of the mechanisms of RB1/pRb inactivation in inducing cancer cell development. The review is divided in three chapters describing in succession the mechanisms of RB1 inactivation in cancer cells, the alterations of pRb pathway in tumorigenesis and the RB protein and E2F family in cancer.
156 citations
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TL;DR: This approach is not targeted at replacing a dynamic simulation model, but it represents a simple decision support tool for the preliminary assessment of the energy demand related to any building and any weather condition.
156 citations
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TL;DR: Sarcopenia recognises insulin resistance and obesity as risk factors, and is frequently associated with cardiometabolic disorders, including non‐alcoholic fatty liver disease (NAFLD).
Abstract: SummaryBackground
Sarcopenia recognises insulin resistance and obesity as risk factors, and is frequently associated with cardiometabolic disorders, including non-alcoholic fatty liver disease (NAFLD).
Aim
To test the prevalence of sarcopenia and its relation with the severity of fibrosis (main outcome) and the entire spectrum of liver histology in patients with NAFLD.
Methods
We considered 225 consecutive patients with histological diagnosis of NAFLD (Kleiner score). The skeletal muscle index (%) (total appendicular skeletal muscle mass (kg)/weight (kg) × 100), a validated measure of sarcopenia, was assessed by bioelectrical impedance analysis. Sarcopenia was defined as a skeletal muscle mass index ≤37 in males and ≤28 in females.
Results
The prevalence of sarcopenia showed a linear increase with the severity of fibrosis, and severe fibrosis (F3–F4) was more than doubled in sarcopenia (48.3% vs. 20.4% in fibrosis ≤F2, P 50 (OR 6.53, CI 2.95–14.4, P < 0.001), IFG/Diabetes (OR 2.14, CI 1.05–4.35, P = 0.03) and NASH (OR 13.3, CI 1.64–108.1, P = 0.01). Similarly, a significant association was found between sarcopenia and NASH (P = 0.01), steatosis severity (P = 0.006), and ballooning (P = 0.01), but only the association with severe steatosis was maintained (OR 2.02, CI 1.06–3.83, P = 0.03) after adjusting for confounders.
Conclusions
In Western patients with NAFLD, with high prevalence of metabolic disorders and advanced liver disease, sarcopenia was associated with the severity of fibrosis and steatosis, independently of hepatic and metabolic risk factors. Studies are needed to assess the impact of interventions to reduce sarcopenia on NAFLD progression.
156 citations
Authors
Showing all 15895 results
Name | H-index | Papers | Citations |
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Robin M. Murray | 171 | 1539 | 116362 |
Frede Blaabjerg | 147 | 2161 | 112017 |
Jean Bousquet | 145 | 1288 | 96769 |
Zhanhu Guo | 128 | 886 | 53378 |
Jean Ballet | 115 | 263 | 46301 |
Antonio Facchetti | 111 | 602 | 51885 |
Michele Pagano | 97 | 306 | 42211 |
Frank Z. Stanczyk | 93 | 620 | 30244 |
Eleonora Troja | 91 | 271 | 30873 |
Francesco Sciortino | 90 | 536 | 28956 |
Zev Rosenwaks | 89 | 772 | 32039 |
Antonio Russo | 88 | 934 | 34563 |
Carlo Salvarani | 88 | 730 | 31699 |
Giuseppe Basso | 87 | 643 | 33320 |
Antonio Craxì | 86 | 659 | 39463 |