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Institution

University of Bologna

EducationBologna, Emilia-Romagna, Italy
About: University of Bologna is a education organization based out in Bologna, Emilia-Romagna, Italy. It is known for research contribution in the topics: Population & Galaxy. The organization has 38387 authors who have published 115176 publications receiving 3460869 citations. The organization is also known as: Università di Bologna & UNIBO.


Papers
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Journal ArticleDOI
TL;DR: In this paper, the projected spectroscopic temperature of clusters obtained from X-ray observations is always lower than the emission-weighed temperature, which is related to the fact that the emissionweighted temperature does not reflect the actual spectral properties of the observed source.
Abstract: Theoretical studies of the physical processes in clusters of galaxies are mainly based on the results of numerical simulations, which in turn are often directly compared to X-ray observations. Although trivial in principle, these comparisons are not always simple. We show that the projected spectroscopic temperature of clusters obtained from X-ray observations is always lower than the emission-weighed temperature. This bias is related to the fact that the emission-weighted temperature does not reflect the actual spectral properties of the observed source. This has implications for the study of thermal structures in clusters, especially when strong temperature gradients, like shock fronts, are present. In real observations shock fronts appear much weaker than what is predicted by emission-weighted temperature maps. We propose a new formula, the spectroscopic-like temperature function that better approximates the spectroscopic temperature, making simulations more directly comparable to observations

382 citations

Journal ArticleDOI
TL;DR: The data provide strong genetic implication that aberrant activation of PI3K/Akt pathway plays an extensive role in thyroid tumorigenesis, particularly in FTC and ATC, and promotes progression of BTA to FTC and to ATC as the genetic alterations of this pathway accumulate.
Abstract: Purpose: To investigate the overall occurrence and relationship of genetic alterations in the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in thyroid tumors and explore the scope of this pathway as a therapeutic target for thyroid cancer. Experimental Design: We examined collectively the major genetic alterations and their relationship in this pathway, including PIK3CA copy number gain and mutation, Ras mutation, and PTEN mutation, in a large series of primary thyroid tumors. Results: Occurrence of any of these genetic alterations was found in 25 of 81 (31%) benign thyroid adenoma (BTA), 47 of 86 (55%) follicular thyroid cancer (FTC), 21 of 86 (24%) papillary thyroid cancer (PTC), and 29 of 50 (58%) anaplastic thyroid cancer (ATC), with FTC and ATC most frequently harboring these genetic alterations. PIK3CA copy gain was associated with increased PIK3CA protein expression. A mutual exclusivity among these genetic alterations was seen in BTA, FTC, and PTC, suggesting an independent role of each of them through the PI3K/Akt pathway in the tumorigenesis of the differentiated thyroid tumors. However, coexistence of these genetic alterations was increasingly seen with progression from differentiated tumor to undifferentiated ATC. Their coexistence with BRAF mutation was also frequent in PTC and ATC. Conclusions: The data provide strong genetic implication that aberrant activation of PI3K/Akt pathway plays an extensive role in thyroid tumorigenesis, particularly in FTC and ATC, and promotes progression of BTA to FTC and to ATC as the genetic alterations of this pathway accumulate. Progression of PTC to ATC may be facilitated by coexistence of PI3K/Akt pathway–related genetic alterations and BRAF mutation. The PI3K/Akt pathway may thus be a major therapeutic target in thyroid cancers.

382 citations

Journal ArticleDOI
TL;DR: In heterogeneous networks, TCP connections that incorporate a terrestrial or satellite radio link are greatly disadvantaged with respect to entirely wired connections, because of their longer round trip times (RTTs), so a new TCP proposal, the TCP Hybla, is presented and discussed in the paper.
Abstract: SUMMARY In heterogeneous networks, TCP connections that incorporate a terrestrial or satellite radio link are greatly disadvantaged with respect to entirely wired connections, because of their longer round trip times (RTTs). To cope with this problem, a new TCP proposal, the TCP Hybla, is presented and discussed in the paper. It stems from an analytical evaluation of the congestion window dynamics in the TCP standard versions (Tahoe, Reno, NewReno), which suggests the necessary modifications to remove the performance dependence on RTT. TCP Hybla performance is firstly evaluated in the case of an ideal channel, with good correlation between analytical and simulation data. Then, more realistic situations, which require the adoption of a benchmark network topology and a careful ns-2 simulation set-up, are examined. In particular, TCP Hybla performance is compared with that achievable by TCP standard in the presence of congestion and link losses, either separately or jointly considered. In all the examined cases, the superiority of TCP Hybla is evident, as it greatly reduces the severe penalization suffered by wireless, and especially satellite, TCP connections. Finally, it is worth noting that TCP Hybla does not infringe the end to end semantics of TCP and is compatible with other promising enhancements. Copyright # 2004 John Wiley & Sons, Ltd.

382 citations

Journal ArticleDOI
TL;DR: In vitro findings suggest that tactics to regulate mTOR and c-Met by elevating levels of miR-199a-3p may have therapeutic benefits in highly lethal cancers such as HCC.
Abstract: MicroRNAs (miRNA) have rapidly emerged as modulators of gene expression in cancer in which they may have great diagnostic and therapeutic import. MicroRNA-199a-3p (miR-199a-3p) is downregulated in several human malignancies including hepatocellular carcinoma (HCC). Here, we show that miR-199a-3p targets mammalian target of rapamycin (mTOR) and c-Met in HCC cells. Restoring attenuated levels of miR-199a-3p in HCC cells led to G 1 -phase cell cycle arrest, reduced invasive capability, enhanced susceptibility to hypoxia, and increased sensitivity to doxorubicin-induced apoptosis. These in vitro findings were confirmed by an analysis of human HCC tissues, which revealed an inverse correlation linking miR-199a-3p and mTOR as well as a shorter time to recurrence after HCC resection in patients with lower miR-199a-3p expression. These results suggest that tactics to regulate mTOR and c-Met by elevating levels of miR-199a-3p may have therapeutic benefits in highly lethal cancers such as HCC. Cancer Res; 70(12); 5184–93. ©2010 AACR.

382 citations

Journal ArticleDOI
TL;DR: Comparison of inhibition titrations in combination with the analysis of the primary structures has enabled us to identify amino acid residues in cytochrome b that may be involved in the binding of the inhibitors and, by extrapolation, quinone/quinol.

382 citations


Authors

Showing all 39076 results

NameH-indexPapersCitations
Anil K. Jain1831016192151
H. S. Chen1792401178529
Stefan Schreiber1781233138528
Alvio Renzini16290895452
David H. Adams1551613117783
Roberto Romero1511516108321
Thomas E. Starzl150162591704
Paolo Boffetta148145593876
Kypros H. Nicolaides147130287091
J. Fraser Stoddart147123996083
Fabio Finelli147542111128
Jack Hirsh14673486332
Kjell Fuxe142147989846
Andrew Ivanov142181297390
Peter Lang140113698592
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023398
20221,031
20217,486
20207,099
20196,390
20185,737