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Search Results: 1 - 10 of 14044 matches for " Andrea Soddu "
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Rare K decays in a model of quark and lepton masses
P. Q. Hung,Andrea Soddu
Physics , 2001, DOI: 10.1103/PhysRevD.65.054035
Abstract: An extension of a model of neutrino masses to the quark sector provides an interesting link between these two sectors. A parameter which is important to describe neutrino oscillations and masses is found to be a crucial one appearing in various ``penguin'' operators, in particular the so-called Z penguin. This parameter is severely constrained by the rare decay process $K_{L} \to \mu^{+} \mu^{-}$. This in turn has interesting implications on the decay rates of other rare processes such as $K_{L} \to \mu e$, etc..., as well as on the masses of the neutrinos and the masses of the vector-like quarks and leptons which appear in our model.
Auditory Resting-State Network Connectivity in Tinnitus: A Functional MRI Study
Audrey Maudoux, Philippe Lefebvre, Jean-Evrard Cabay, Athena Demertzi, Audrey Vanhaudenhuyse, Steven Laureys, Andrea Soddu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0036222
Abstract: The underlying functional neuroanatomy of tinnitus remains poorly understood. Few studies have focused on functional cerebral connectivity changes in tinnitus patients. The aim of this study was to test if functional MRI “resting-state” connectivity patterns in auditory network differ between tinnitus patients and normal controls. Thirteen chronic tinnitus subjects and fifteen age-matched healthy controls were studied on a 3 tesla MRI. Connectivity was investigated using independent component analysis and an automated component selection approach taking into account the spatial and temporal properties of each component. Connectivity in extra-auditory regions such as brainstem, basal ganglia/NAc, cerebellum, parahippocampal, right prefrontal, parietal, and sensorimotor areas was found to be increased in tinnitus subjects. The right primary auditory cortex, left prefrontal, left fusiform gyrus, and bilateral occipital regions showed a decreased connectivity in tinnitus. These results show that there is a modification of cortical and subcortical functional connectivity in tinnitus encompassing attentional, mnemonic, and emotional networks. Our data corroborate the hypothesized implication of non-auditory regions in tinnitus physiopathology and suggest that various regions of the brain seem involved in the persistent awareness of the phenomenon as well as in the development of the associated distress leading to disabling chronic tinnitus.
PKC Theta Ablation Improves Healing in a Mouse Model of Muscular Dystrophy
Luca Madaro, Andrea Pelle, Carmine Nicoletti, Annunziata Crupi, Valeria Marrocco, Gianluca Bossi, Silvia Soddu, Marina Bouché
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031515
Abstract: Inflammation is a key pathological characteristic of dystrophic muscle lesion formation, limiting muscle regeneration and resulting in fibrotic and fatty tissue replacement of muscle, which exacerbates the wasting process in dystrophic muscles. Limiting immune response is thus one of the therapeutic options to improve healing, as well as to improve the efficacy of gene- or cell-mediated strategies to restore dystrophin expression. Protein kinase C θ (PKCθ) is a member of the PKCs family highly expressed in both immune cells and skeletal muscle; given its crucial role in adaptive, but also innate, immunity, it is being proposed as a valuable pharmacological target for immune disorders. In our study we asked whether targeting PKCθ could represent a valuable approach to efficiently prevent inflammatory response and disease progression in a mouse model of muscular dystrophy. We generated the bi-genetic mouse model mdx/θ?/?, where PKCθ expression is lacking in mdx mice, the mouse model of Duchenne muscular dystrophy. We found that muscle wasting in mdx/θ?/? mice was greatly prevented, while muscle regeneration, maintenance and performance was significantly improved, as compared to mdx mice. This phenotype was associated to reduction in inflammatory infiltrate, pro-inflammatory gene expression and pro-fibrotic markers activity, as compared to mdx mice. Moreover, BM transplantation experiments demonstrated that the phenotype observed was primarily dependent on lack of PKCθ expression in hematopoietic cells. These results demonstrate a hitherto unrecognized role of immune-cell intrinsic PKCθ activity in the development of DMD. Although the immune cell population(s) involved remain unidentified, our findings reveal that PKCθ can be proposed as a new pharmacological target to counteract the disease, as well as to improve the efficacy of gene- or cell- therapy approaches.
Brain Connectivity in Pathological and Pharmacological Coma
Quentin Noirhomme,Andrea Soddu,Rémy Lehembre,Audrey Vanhaudenhuyse,Pierre Boveroux,Mélanie Boly,Steven Laureys
Frontiers in Systems Neuroscience , 2010, DOI: 10.3389/fnsys.2010.00160
Abstract: Recent studies in patients with disorders of consciousness (DOC) tend to support the view that awareness is not related to activity in a single brain region but to thalamo-cortical connectivity in the frontoparietal network. Functional neuroimaging studies have shown preserved albeit disconnected low-level cortical activation in response to external stimulation in patients in a “vegetative state” or unresponsive wakefulness syndrome. While activation of these “primary” sensory cortices does not necessarily reflect conscious awareness, activation in higher-order associative cortices in minimally conscious state patients seems to herald some residual perceptual awareness. PET studies have identified a metabolic dysfunction in a widespread frontoparietal “global neuronal workspace” in DOC patients including the midline default mode network (“intrinsic” system) and the lateral frontoparietal cortices or “extrinsic system.” Recent studies have investigated the relation of awareness to the functional connectivity within intrinsic and extrinsic networks, and with the thalami in both pathological and pharmacological coma. In brain damaged patients, connectivity in all default network areas was found to be non-linearly correlated with the degree of clinical consciousness impairment, ranging from healthy controls and locked-in syndrome to minimally conscious, vegetative, coma, and brain dead patients. Anesthesia-induced loss of consciousness was also shown to correlate with a global decrease in cortico-cortical and thalamo-cortical connectivity in both intrinsic and extrinsic networks, but not in auditory, or visual networks. In anesthesia, unconsciousness was also associated with a loss of cross-modal interactions between networks. These results suggest that conscious awareness critically depends on the functional integrity of thalamo-cortical and cortico-cortical frontoparietal connectivity within and between “intrinsic” and “extrinsic” brain networks.
Changes in Effective Connectivity by Propofol Sedation
Francisco Gómez, Christophe Phillips, Andrea Soddu, Melanie Boly, Pierre Boveroux, Audrey Vanhaudenhuyse, Marie-Aurélie Bruno, Olivia Gosseries, Vincent Bonhomme, Steven Laureys, Quentin Noirhomme
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071370
Abstract: Mechanisms of propofol-induced loss of consciousness remain poorly understood. Recent fMRI studies have shown decreases in functional connectivity during unconsciousness induced by this anesthetic agent. Functional connectivity does not provide information of directional changes in the dynamics observed during unconsciousness. The aim of the present study was to investigate, in healthy humans during an auditory task, the changes in effective connectivity resulting from propofol induced loss of consciousness. We used Dynamic Causal Modeling for fMRI (fMRI-DCM) to assess how causal connectivity is influenced by the anesthetic agent in the auditory system. Our results suggest that the dynamic observed in the auditory system during unconsciousness induced by propofol, can result in a mixture of two effects: a local inhibitory connectivity increase and a decrease in the effective connectivity in sensory cortices.
Cerebral functional connectivity periodically (de)synchronizes with anatomical constraints
Rapha?l Liégeois,Erik Ziegler,Pierre Geurts,Francisco Gomez,Mohamed Ali Bahri,Christophe Phillips,Andrea Soddu,Audrey Vanhaudenhuyse,Steven Laureys,Rodolphe Sepulchre
Quantitative Biology , 2014,
Abstract: This paper studies the link between resting-state functional connectivity (FC), measured by the correlations of the fMRI BOLD time courses, and structural connectivity (SC), estimated through fiber tractography. Instead of a static analysis based on the correlation between SC and the FC averaged over the entire fMRI time series, we propose a dynamic analysis, based on the time evolution of the correlation between SC and a suitably windowed FC. Assessing the statistical significance of the time series against random phase permutations, our data show a pronounced peak of significance for time window widths around 20-30 TR (40-60 sec). Using the appropriate window width, we show that FC patterns oscillate between phases of high modularity, primarily shaped by anatomy, and phases of low modularity, primarily shaped by inter-network connectivity. Building upon recent results in dynamic FC, this emphasizes the potential role of SC as a transitory architecture between different highly connected resting state FC patterns. Finally, we show that networks implied in consciousness-related processes, such as the default mode network (DMN), contribute more to these brain-level fluctuations compared to other networks, such as the motor or somatosensory networks. This suggests that the fluctuations between FC and SC are capturing mind-wandering effects.
The t->cH decay width in the standard model
B. Mele,S. Petrarca,Soddu
Physics , 1999,
Abstract: The t->cH decay width has been computed in the standard model with a light Higgs boson. The corresponding branching fraction has been found to be in the range B(t->cH) ~ 10^{-13} - 10^{-14} for M_Z < m_H < 2 M_W. Our results correct the numerical evaluation usually quoted in the literature.
Reduction in Inter-Hemispheric Connectivity in Disorders of Consciousness
Smadar Ovadia-Caro, Yuval Nir, Andrea Soddu, Michal Ramot, Guido Hesselmann, Audrey Vanhaudenhuyse, Ilan Dinstein, Jean-Flory L. Tshibanda, Melanie Boly, Michal Harel, Steven Laureys, Rafael Malach
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037238
Abstract: Clinical diagnosis of disorders of consciousness (DOC) caused by brain injury poses great challenges since patients are often behaviorally unresponsive. A promising new approach towards objective DOC diagnosis may be offered by the analysis of ultra-slow (<0.1 Hz) spontaneous brain activity fluctuations measured with functional magnetic resonance imaging (fMRI) during the resting-state. Previous work has shown reduced functional connectivity within the “default network”, a subset of regions known to be deactivated during engaging tasks, which correlated with the degree of consciousness impairment. However, it remains unclear whether the breakdown of connectivity is restricted to the “default network”, and to what degree changes in functional connectivity can be observed at the single subject level. Here, we analyzed resting-state inter-hemispheric connectivity in three homotopic regions of interest, which could reliably be identified based on distinct anatomical landmarks, and were part of the “Extrinsic” (externally oriented, task positive) network (pre- and postcentral gyrus, and intraparietal sulcus). Resting-state fMRI data were acquired for a group of 11 healthy subjects and 8 DOC patients. At the group level, our results indicate decreased inter-hemispheric functional connectivity in subjects with impaired awareness as compared to subjects with intact awareness. Individual connectivity scores significantly correlated with the degree of consciousness. Furthermore, a single-case statistic indicated a significant deviation from the healthy sample in 5/8 patients. Importantly, of the three patients whose connectivity indices were comparable to the healthy sample, one was diagnosed as locked-in. Taken together, our results further highlight the clinical potential of resting-state connectivity analysis and might guide the way towards a connectivity measure complementing existing DOC diagnosis.
Updates on HIPK2: a resourceful oncosuppressor for clearing cancer
D’Orazi Gabriella,Rinaldo Cinzia,Soddu Silvia
Journal of Experimental & Clinical Cancer Research , 2012, DOI: 10.1186/1756-9966-31-63
Abstract: Homeodomain-interacting protein kinase 2 (HIPK2) is a multitalented protein that exploits its kinase activity to modulate key molecular pathways in cancer to restrain tumor growth and induce response to therapies. HIPK2 phosphorylates oncosuppressor p53 for apoptotic activation. In addition, also p53-independent apoptotic pathways are regulated by HIPK2 and can be exploited for anticancer purpose too. Therefore, HIPK2 activity is considered a central switch in targeting tumor cells toward apoptosis upon genotoxic damage and the preservation and/or restoration of HIPK2 function is crucial for an efficient tumor response to therapies. As a proof of principle, HIPK2 knockdown impairs p53 function, induces chemoresistance, angiogenesis, and tumor growth in vivo, on the contrary, HIPK2 overexpression activates apoptotic pathways, counteracts hypoxia, inhibits angiogenesis, and induces chemosensitivity both in p53-dependent and -independent ways. The role of HIPK2 in restraining tumor development was also confirmed by studies with HIPK2 knockout mice. Recent findings demonstrated that HIPK2 inhibitions do exist in tumors and depend by several mechanisms including HIPK2 cytoplasmic localization, protein degradation, and loss of heterozygosity (LOH), recapitulating the biological outcome obtained by RNA interference studies in tumor cells, such as p53 inactivation, resistance to therapies, apoptosis inhibition, and tumor progression. These findings may lead to new diagnostic and therapeutic approaches for treating cancer patients. This review will focus on the last updates about HIPK2 contribution in tumorigenesis and cancer treatment.
A new evaluation of the t->cH decay width in the standard model
B. Mele,S. Petrarca,A. Soddu
Physics , 1998, DOI: 10.1016/S0370-2693(98)00822-3
Abstract: We present a new calculation of the t->cH decay rate in the standard model. We find that the corresponding branching fraction is B(t->cH) \sim 10^{-13} - 10^{-14} for M_Z < m_H < 2 M_W, that is about 6 orders of magnitude less than previously evaluated, and usually quoted in the literature.
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