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Institution

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.


Papers
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Journal ArticleDOI
TL;DR: This survey is directed to those who want to approach this complex discipline and contribute to its development, and finds that still major issues shall be faced by the research community.

12,539 citations

Journal ArticleDOI
TL;DR: The effect of various drugs on the extracellular concentration of dopamine in two terminal dopaminergic areas, the nucleus accumbens septi (a limbic area) and the dorsal caudate nucleus (a subcortical motor area), was studied in freely moving rats by using brain dialysis as mentioned in this paper.
Abstract: The effect of various drugs on the extracellular concentration of dopamine in two terminal dopaminergic areas, the nucleus accumbens septi (a limbic area) and the dorsal caudate nucleus (a subcortical motor area), was studied in freely moving rats by using brain dialysis. Drugs abused by humans (e.g., opiates, ethanol, nicotine, amphetamine, and cocaine) increased extracellular dopamine concentrations in both areas, but especially in the accumbens, and elicited hypermotility at low doses. On the other hand, drugs with aversive properties (e.g., agonists of kappa opioid receptors, U-50,488, tifluadom, and bremazocine) reduced dopamine release in the accumbens and in the caudate and elicited hypomotility. Haloperidol, a neuroleptic drug, increased extracellular dopamine concentrations, but this effect was not preferential for the accumbens and was associated with hypomotility and sedation. Drugs not abused by humans [e.g., imipramine (an antidepressant), atropine (an antimuscarinic drug), and diphenhydramine (an antihistamine)] failed to modify synaptic dopamine concentrations. These results provide biochemical evidence for the hypothesis that stimulation of dopamine transmission in the limbic system might be a fundamental property of drugs that are abused.

4,610 citations

Journal ArticleDOI
Alan E. Renton1, Elisa Majounie1, Adrian James Waite2, Javier Simón-Sánchez3, Javier Simón-Sánchez4, Sara Rollinson5, J. Raphael Gibbs1, J. Raphael Gibbs6, Jennifer C. Schymick1, Hannu Laaksovirta7, John C. van Swieten4, John C. van Swieten3, Liisa Myllykangas7, Hannu Kalimo7, Anders Paetau7, Yevgeniya Abramzon1, Anne M. Remes8, Alice Kaganovich1, Sonja W. Scholz9, Sonja W. Scholz1, Sonja W. Scholz10, Jamie Duckworth1, Jinhui Ding1, Daniel W. Harmer11, Dena G. Hernandez6, Dena G. Hernandez1, Janel O. Johnson6, Janel O. Johnson1, Kin Y. Mok6, Mina Ryten6, Danyah Trabzuni6, Rita Guerreiro6, Richard W. Orrell6, James Neal2, Alexandra Murray12, J. P. Pearson2, Iris E. Jansen3, David Sondervan3, Harro Seelaar4, Derek J. Blake2, Kate Young5, Nicola Halliwell5, Janis Bennion Callister5, Greg Toulson5, Anna Richardson5, Alexander Gerhard5, Julie S. Snowden5, David M. A. Mann5, David Neary5, Mike A. Nalls1, Terhi Peuralinna7, Lilja Jansson7, Veli-Matti Isoviita7, Anna-Lotta Kaivorinne8, Maarit Hölttä-Vuori7, Elina Ikonen7, Raimo Sulkava13, Michael Benatar14, Joanne Wuu14, Adriano Chiò15, Gabriella Restagno, Giuseppe Borghero16, Mario Sabatelli17, David Heckerman18, Ekaterina Rogaeva19, Lorne Zinman19, Jeffrey D. Rothstein9, Michael Sendtner20, Carsten Drepper20, Evan E. Eichler21, Can Alkan21, Ziedulla Abdullaev1, Svetlana Pack1, Amalia Dutra1, Evgenia Pak1, John Hardy6, Andrew B. Singleton1, Nigel Williams2, Peter Heutink3, Stuart Pickering-Brown5, Huw R. Morris12, Huw R. Morris2, Huw R. Morris22, Pentti J. Tienari7, Bryan J. Traynor9, Bryan J. Traynor1 
20 Oct 2011-Neuron
TL;DR: The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases, and a large hexanucleotide repeat expansion in the first intron of C9ORF72 is shown.

3,784 citations

Journal ArticleDOI
TL;DR: In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.
Abstract: Eleven susceptibility loci for late-onset Alzheimer's disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this disease remains unexplained. We conducted a large, two-stage meta-analysis of genome-wide association studies (GWAS) in individuals of European ancestry. In stage 1, we used genotyped and imputed data (7,055,881 SNPs) to perform meta-analysis on 4 previously published GWAS data sets consisting of 17,008 Alzheimer's disease cases and 37,154 controls. In stage 2, 11,632 SNPs were genotyped and tested for association in an independent set of 8,572 Alzheimer's disease cases and 11,312 controls. In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.

3,726 citations

Journal ArticleDOI
TL;DR: A framework exists on a framework for the definition and classification of cancer cachexia, a multifactorial syndrome defined by an ongoing loss of skeletal muscle mass that cannot be fully reversed by conventional nutritional support and leads to progressive functional impairment.
Abstract: Summary To develop a framework for the definition and classification of cancer cachexia a panel of experts participated in a formal consensus process, including focus groups and two Delphi rounds. Cancer cachexia was defined as a multifactorial syndrome defined by an ongoing loss of skeletal muscle mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutritional support and leads to progressive functional impairment. Its pathophysiology is characterised by a negative protein and energy balance driven by a variable combination of reduced food intake and abnormal metabolism. The agreed diagnostic criterion for cachexia was weight loss greater than 5%, or weight loss greater than 2% in individuals already showing depletion according to current bodyweight and height (body-mass index [BMI] 2 ) or skeletal muscle mass (sarcopenia). An agreement was made that the cachexia syndrome can develop progressively through various stages—precachexia to cachexia to refractory cachexia. Severity can be classified according to degree of depletion of energy stores and body protein (BMI) in combination with degree of ongoing weight loss. Assessment for classification and clinical management should include the following domains: anorexia or reduced food intake, catabolic drive, muscle mass and strength, functional and psychosocial impairment. Consensus exists on a framework for the definition and classification of cancer cachexia. After validation, this should aid clinical trial design, development of practice guidelines, and, eventually, routine clinical management.

3,548 citations


Authors

Showing all 11160 results

NameH-indexPapersCitations
Carmine M. Pariante9654833794
Jinlong Yang9576535981
Francesco Dettori95102641313
A. A. Affolder9466338067
Xavier Vilasis-Cardona94103539289
Bruno Dallapiccola9493543208
Zhiguo Yuan9363328645
Guido Busca9153832109
Raphael Noel Tieulent8941724926
Alexander J. Blake89113335746
Eugenio Coronado8974033461
Yuet Wai Kan8829325485
Ezio Ghigo8869332383
Biagio Saitta8895135436
Pietro Cortese8741724794
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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