Institution
University of Cagliari
Education•Cagliari, 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.
Topics: Population, Dopamine, Dopaminergic, Context (language use), Medicine
Papers published on a yearly basis
Papers
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TL;DR: It is demonstrated that, in differentiating skeletal muscle cells, p300 physically interacts with the myogenic basic helix–loop–helix (bHLH) regulatory protein MyoD at its DNA binding sites, and p300 potentiates MyOD‐ and myogenin‐dependent activation of transcription from E‐box‐containing reporter genes.
Abstract: The nuclear phosphoprotein p300 is a new member of a family of 'co-activators' (which also includes the CREB binding protein CBP), that directly modulate transcription by interacting with components of the basal transcriptional machinery. Both p300 and CBP are targeted by the adenovirus E1A protein, and binding to p300 is required for E1A to inhibit terminal differentiation in both keratinocytes and myoblasts. Here we demonstrate that, in differentiating skeletal muscle cells, p300 physically interacts with the myogenic basic helix-loop-helix (bHLH) regulatory protein MyoD at its DNA binding sites. During muscle differentiation, MyoD plays a dual role: besides activating muscle-specific transcription, it induces permanent cell cycle arrest by up-regulating the cyclin-dependent kinase inhibitor p21. We show that p300 is involved in both these activities. Indeed, E1A mutants lacking the ability to bind p300 are greatly impaired in the repression of E-box-driven transcription, and p300 overexpression rescues the wild-type E1A-mediated repression. Moreover, p300 potentiates MyoD- and myogenin-dependent activation of transcription from E-box-containing reporter genes. We also provide evidence, obtained by microinjection of anti-p300 antibodies, that p300 is required for MyoD-dependent cell cycle arrest in either myogenic cells induced to differentiate or in MyoD-converted C3H10T1/2 fibroblasts, but is dispensable for maintenance of the postmitotic state of myotubes.
289 citations
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TL;DR: The results highlighted that all the benzo[d]isothiazole derivatives inhibited the growth of leukaemia cell lines, whereas only one of the above mentioned compounds showed antiproliferative activity against two solid tumor-derived cell lines.
287 citations
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TL;DR: A review of recent ethnopharmacological field studies in order to highlight achievements and future needs for improving the quality of such studies and minimal conceptual and methodological requirements for use in future projects.
287 citations
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TL;DR: Key evidence supporting the role of fungal exposure, sensitisation and infection in asthmatics is set out, what is understood about pathogenesis and natural history is understood and the numerous areas for research studies are identified.
Abstract: Sensitization to fungi and long term or uncontrolled fungal infection are associated with poor control of asthma, the likelihood of more severe disease and complications such as bronchiectasis and chronic pulmonary aspergillosis. Modelling suggests that >6.5 million people have severe asthma with fungal sensitizations (SAFS), up to 50% of adult asthmatics attending secondary care have fungal sensitization, and an estimated 4.8 million adults have allergic bronchopulmonary aspergillosis (ABPA). There is much uncertainty about which fungi and fungal allergens are relevant to asthma, the natural history of sensitisation to fungi, if there is an exposure response relationship for fungal allergy, and the pathogenesis and frequency of exacerbations and complications. Genetic associations have been described but only weakly linked to phenotypes. The evidence base for most management strategies in ABPA, SAFS and related conditions is weak. Yet straightforward clinical practice guidelines for management are required. The role of environmental monitoring and optimal means of controlling disease to prevent disability and complications are not yet clear. In this paper we set out the key evidence supporting the role of fungal exposure, sensitisation and infection in asthmatics, what is understood about pathogenesis and natural history and identify the numerous areas for research studies.
286 citations
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TL;DR: There appears to be a therapeutic window for fluoxetine, and the pharmacokinetics of this drug are not affected by either obesity or renal impairment, which makes this drug particularly suitable for use in elderly patients with depression.
Abstract: Fluoxetine is well absorbed after oral intake, is highly protein bound, and has a large volume of distribution. The elimination half-life of fluoxetine is about 1 to 4 days, while that of its metabolite norfluoxetine ranges from 7 to 15 days. Fluoxetine has a nonlinear pharmacokinetic profile. Therefore, the drug should be used with caution in patients with a reduced metabolic capability (i.e. hepatic dysfunction). In contrast with its effect on the pharmacokinetics of other antidepressants, age does not affect fluoxetine pharmacokinetics. This finding together with the better tolerability profile of fluoxetine (compared with tricyclic antidepressants) makes this drug particularly suitable for use in elderly patients with depression. Furthermore, the pharmacokinetics of fluoxetine are not affected by either obesity or renal impairment. On the basis of results of plasma concentration-clinical response relationship studies, there appears to be a therapeutic window for fluoxetine. Concentrations of fluoxetine plus norfluoxetine above 500 µg/L appear to be associated with a poorer clinical response than lower concentrations. Fluoxetine interacts with some other drugs. Concomitant administration of fluoxetine increased the blood concentrations of antipsychotics or antidepressants. The interactions between fluoxetine and lithium, tryptophan and monoamine oxidase inhibitors, in particular, are potentially serious, and can lead to the ‘serotonergic syndrome’. This is because of synergistic pharmacodynamic effects and the influence of fluoxetine on the bioavailability of these compounds.
284 citations
Authors
Showing all 11160 results
Name | H-index | Papers | Citations |
---|---|---|---|
Herbert W. Marsh | 152 | 646 | 89512 |
Michele Parrinello | 133 | 637 | 94674 |
Dafna D. Gladman | 129 | 1036 | 75273 |
Peter J. Anderson | 120 | 966 | 63635 |
Alessandro Vespignani | 118 | 419 | 63824 |
C. Patrignani | 117 | 1754 | 110008 |
Hermine Katharina Wöhri | 116 | 629 | 55540 |
Francesco Muntoni | 115 | 963 | 52629 |
Giancarlo Comi | 109 | 961 | 54270 |
Giorgio Parisi | 108 | 941 | 60746 |
Luca Benini | 101 | 1453 | 47862 |
Alessandro Cardini | 101 | 1288 | 53804 |
Nicola Serra | 100 | 1042 | 46640 |
Jurg Keller | 99 | 389 | 35628 |
Giulio Usai | 97 | 517 | 39392 |