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University of Cagliari

EducationCagliari, Italy
About: University of Cagliari is a education organization based out in Cagliari, Italy. It is known for research contribution in the topics: Population & Dopamine. The organization has 11029 authors who have published 29046 publications receiving 771023 citations. The organization is also known as: Università degli Studi di Cagliari & Universita degli Studi di Cagliari.


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Journal ArticleDOI
Lindsay M. Morton1, Susan L. Slager2, James R. Cerhan2, Sophia S. Wang3, Claire M. Vajdic4, Christine F. Skibola5, Paige M. Bracci6, Silvia de Sanjosé, Karin E. Smedby7, Brian C.-H. Chiu8, Yawei Zhang9, Sam M. Mbulaiteye1, Alain Monnereau10, Jennifer Turner11, Jacqueline Clavel12, Hans-Olov Adami7, Hans-Olov Adami13, Ellen T. Chang14, Ellen T. Chang15, Bengt Glimelius7, Bengt Glimelius16, Henrik Hjalgrim17, Mads Melbye17, Paolo Crosignani, Simonetta Di Lollo18, Lucia Miligi, Oriana Nanni, Valerio Ramazzotti, Stefania Rodella, Adele Seniori Costantini, Emanuele Stagnaro, Rosario Tumino, Carla Vindigni, Paolo Vineis19, Nikolaus Becker20, Yolanda Benavente, Paolo Boffetta21, Paul Brennan22, Pierluigi Cocco23, Lenka Foretova, Marc Maynadié24, Alexandra Nieters25, Anthony Staines26, Joanne S. Colt1, Wendy Cozen27, Scott Davis28, Scott Davis29, Anneclaire J. De Roos30, Patricia Hartge1, Nathaniel Rothman1, Richard K. Severson31, Elizabeth A. Holly6, Timothy G. Call2, Andrew L. Feldman2, Thomas M. Habermann2, Mark Liebow2, Aaron Blair1, Kenneth P. Cantor1, Eleanor Kane32, Tracy Lightfoot32, Eve Roman32, Alex Smith32, Angela Brooks-Wilson33, Angela Brooks-Wilson34, Joseph M. Connors33, Randy D. Gascoyne33, John J. Spinelli33, Bruce K. Armstrong35, Anne Kricker35, Theodore R. Holford9, Qing Lan1, Tongzhang Zheng9, Laurent Orsi12, Luigino Dal Maso, Silvia Franceschi22, Carlo La Vecchia36, Carlo La Vecchia37, Eva Negri36, Diego Serraino, Leslie Bernstein3, Alexandra M. Levine3, Jonathan W. Friedberg38, Jennifer L. Kelly38, Sonja I. Berndt1, Brenda M. Birmann13, Christina A. Clarke39, Christopher R. Flowers40, James M. Foran2, Marshall E. Kadin41, Marshall E. Kadin42, Ora Paltiel, Dennis D. Weisenburger3, Martha S. Linet1, Joshua N. Sampson1 
TL;DR: Using a novel approach to investigate etiologic heterogeneity among NHL subtypes,risk factors that were common among subtypes as well as risk factors that appeared to be distinct among individual or a few subtypes are identified, suggesting both subtype-specific and shared underlying mechanisms.
Abstract: Non-Hodgkin lymphoma (NHL) is the most common hematologic malignancy and the fifth most common type of cancer in more developed regions of the world (1). Numerous NHL subtypes with distinct combinations of morphologic, immunophenotypic, genetic, and clinical features are currently recognized (2,3). The incidence of NHL subtypes varies substantially by age, sex, and race/ethnicity (4–7). However, the etiological implications of this biological, clinical, and epidemiological diversity are incompletely understood. The importance of investigating etiology by NHL subtype is clearly supported by research on immunosuppression, infections, and autoimmune diseases, which are the strongest and most established risk factors for NHL. Studies of solid organ transplant recipients and individuals infected with HIV demonstrate that risks are markedly increased for several—but not all—NHL subtypes (8–13). Some infections and autoimmune diseases are associated with a single specific subtype [eg, human T-cell lymphotropic virus, type I (HTLV-I) with adult T-cell leukemia/lymphoma (14), celiac disease with enteropathy-type peripheral T-cell lymphoma (PTCL) (15–17)], whereas others [eg, Epstein–Barr virus, hepatitis C virus (HCV), Sjogren’s syndrome (18–21)] have been associated with multiple subtypes. In the last two decades, reports from individual epidemiological studies of NHL have suggested differences in risks among NHL subtypes for a wide range of risk factors, but most studies have lacked the statistical power to assess any differences quantitatively and have not systematically evaluated combinations of subtypes. One study assessed multiple risk factors and found support for both etiologic commonality and heterogeneity for NHL subtypes, with risk factor patterns suggesting that immune dysfunction is of greater etiologic importance for diffuse large B-cell lymphoma (DLBCL) and marginal zone lymphoma than for chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and follicular lymphoma (22). However, that analysis was limited to approximately 1300 NHL cases and considered only the four most common NHL subtypes. Pooling data from multiple studies through the International Lymphoma Epidemiology Consortium (InterLymph) have provided substantial insight into associations between specific risk factors and NHL subtypes, with evidence that family history of hematologic malignancy, autoimmune diseases, atopic conditions, lifestyle factors (smoking, alcohol, anthropometric measures, and hair dye use), and sun exposure are associated with NHL risk (19,21,23–32). However, no previous study has compared patterns of risk for a range of exposures for both common and rarer NHL subtypes. We undertook the InterLymph NHL Subtypes Project, a pooled analysis of 20 case–control studies including 17 471 NHL cases and 23 096 controls, to advance understanding of NHL etiology by investigating NHL subtype-specific risks associated with medical history, family history of hematologic malignancy, lifestyle factors, and occupation. The detailed risk factor profiles for each of 11 NHL subtypes appear in this issue (15–17,33–40). In this report, we assess risk factor heterogeneity among the NHL subtypes and identify subtypes that have similar risk factor profiles.

273 citations

Journal ArticleDOI
TL;DR: The observations support use of RHC to confirm the presence of precapillary PH suspected by noninvasive testing and identified patients at high risk who should be carefully monitored.
Abstract: Objective. To measure the prevalence of different types of pulmonary hypertension (PH) and to identify patients with systemic sclerosis (SSc) at highest risk in a multicenter European sample, with a metaanalysis of relevant studies. Methods. Consecutive patients with SSc recruited at 11 French and Italian centers underwent detailed evaluations, including Doppler echocardiography, chest computed tomography, pulmonary function tests, and right-heart catheterization (RHC), to detect the presence and causes of PH. A metaanalysis was performed, including data from 4 other studies. Results. Among 206 patients in whom it was suspected, PH was confirmed by RHC in 83 patients (7%). Precapillary PH was found in 64 patients (5%), of whom 42 had pulmonary arterial hypertension (PAH) and 22 had PH secondary to interstitial lung disease (ILD). RHC identified 17 patients (1%) with postcapillary PH secondary to left-heart disease. Patients with DLCO/alveolar volume < 70% were more likely to have precapillary PH (87.5% vs 42%; p < 0.0001). Precapillary and postcapillary PH were associated with advanced age (68 ± 14 vs 59 ± 12 yrs, p < 0.0001, and 74 ± 16 vs 61.5 ± 10 yrs, p < 0.0001, respectively). The metaanalysis of 3818 patients showed a prevalence of precapillary PH of 9% (95% CI 6%–12%) and identified advanced age, longer disease duration, and limited cutaneous disease subset as risk factors for this condition. Conclusion. The prevalence of precapillary PH in our multicenter study of SSc was 5%, and in the metaanalysis 9%. Our observations support use of RHC to confirm the presence of precapillary PH suspected by noninvasive testing. We also identified patients at high risk who should be carefully monitored.

273 citations

Journal ArticleDOI
30 Apr 2020-Gut
TL;DR: Active IBD, old age and comorbidities were associated with a negative COVID-19 outcome, whereas IBD treatments were not, and Preventing acute IBD flares may avoid fatal CO VID-19 in patients with IBD.
Abstract: Objectives COVID-19 has rapidly become a major health emergency worldwide. Patients with IBD are at increased risk of infection, especially when they have active disease and are taking immunosuppressive therapy. The characteristics and outcomes of COVID-19 in patients with IBD remain unclear. Design This Italian prospective observational cohort study enrolled consecutive patients with an established IBD diagnosis and confirmed COVID-19. Data regarding age, sex, IBD (type, treatments and clinical activity), other comorbidities (Charlson Comorbidity Index (CCI)), signs and symptoms of COVID-19 and therapies were compared with COVID-19 outcomes (pneumonia, hospitalisation, respiratory therapy and death). Results Between 11 and 29 March 2020, 79 patients with IBD with COVID-19 were enrolled at 24 IBD referral units. Thirty-six patients had COVID-19-related pneumonia (46%), 22 (28%) were hospitalised, 7 (9%) required non-mechanical ventilation, 9 (11%) required continuous positive airway pressure therapy, 2 (3%) had endotracheal intubation and 6 (8%) died. Four patients (6%) were diagnosed with COVID-19 while they were being hospitalised for a severe flare of IBD. Age over 65 years (p=0.03), UC diagnosis (p=0.03), IBD activity (p=0.003) and a CCI score >1 (p=0.04) were significantly associated with COVID-19 pneumonia, whereas concomitant IBD treatments were not. Age over 65 years (p=0.002), active IBD (p=0.02) and higher CCI score were significantly associated with COVID-19-related death. Conclusions Active IBD, old age and comorbidities were associated with a negative COVID-19 outcome, whereas IBD treatments were not. Preventing acute IBD flares may avoid fatal COVID-19 in patients with IBD. Further research is needed.

272 citations

Journal ArticleDOI
TL;DR: The DCS method proposed is based on the concepts of “classifier’s local accuracy” (CLA) and MCB and exploits the concept of MCB for DCS purposes, while the BKS method is aimed at classifier combination.

271 citations

Journal ArticleDOI
TL;DR: It was inferred that most, if not all Delta ccr5 alleles originate from a single mutation event, and that this mutation event probably took place a few thousand years ago in Northeastern Europe.
Abstract: The chemokine receptor CCR5 is encoded by the CMKBR5 gene located on the p21.3 region of human chromosome 3, and constitutes the major co-receptor for the macrophage-tropic strains of HIV-1. A mutant allele of the CCR5 gene, Delta ccr5 , was shown to provide to homozygotes with a strong resistance against infection by HIV. The frequency of the Delta ccr5 allele was investigated in 18 European populations. A North to South gradient was found, with the highest allele frequencies in Finnish and Mordvinian populations (16%), and the lowest in Sardinia (4%). Highly polymorphic microsatellites (IRI3.1, D3S4579 and IRI3.2, D3S4580 ) located respectively 11 kb upstream and 68 kb downstream of the CCR5 gene deletion were used to determine the haplotype of the chromosomes carrying the Delta ccr5 variant. A strong linkage disequilibrium was found between Delta ccr5 and specific alleles of the IRI3.1 and IRI3.2 microsatellites: >95% of the Delta ccr5 chromosomes carried the IRI3.1-0 allele, while 88% carried the IRI3.2-0 allele. These alleles were found respectively in only 2 or 1.5% of the chromosomes carrying a wild-type CCR5 gene. From these data, it was inferred that most, if not all Delta ccr5 alleles originate from a single mutation event, and that this mutation event probably took place a few thousand years ago in Northeastern Europe. The high frequency of the Delta ccr5 allele in Caucasian populations cannot be explained easily by random genetic drift, suggesting that a selection advantage is or has been associated with homo- or heterozygous carriers of the Delta ccr5 allele.

270 citations


Authors

Showing all 11160 results

NameH-indexPapersCitations
Herbert W. Marsh15264689512
Michele Parrinello13363794674
Dafna D. Gladman129103675273
Peter J. Anderson12096663635
Alessandro Vespignani11841963824
C. Patrignani1171754110008
Hermine Katharina Wöhri11662955540
Francesco Muntoni11596352629
Giancarlo Comi10996154270
Giorgio Parisi10894160746
Luca Benini101145347862
Alessandro Cardini101128853804
Nicola Serra100104246640
Jurg Keller9938935628
Giulio Usai9751739392
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202374
2022230
20211,898
20201,903
20191,636
20181,600