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Search Results: 1 - 10 of 3474 matches for " Elisa Porcellini "
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Alzheimer's disease gene signature says: beware of brain viral infections
Elisa Porcellini, Ilaria Carbone, Manuela Ianni, Federico Licastro
Immunity & Ageing , 2010, DOI: 10.1186/1742-4933-7-16
Abstract: In this report we suggest that the polymorphism association in 8 of these genes is consistent with a non conventional interpretation of AD etiology.Nectin-2 (NC-2), apolipoprotein E (APOE), glycoprotein carcinoembryonic antigen related cell adhesion molecule- 16 (CEACAM-16), B-cell lymphoma-3 (Bcl-3), translocase of outer mitochondrial membrane 40 homolog (T0MM-40), complement receptor-1 (CR-l), APOJ or clusterin and C-type lectin domain A family-16 member (CLEC-16A) result in a genetic signature that might affect individual brain susceptibility to infection by herpes virus family during aging, leading to neuronal loss, inflammation and amyloid deposition.We hypothesized that such genetic trait may predispose to AD via complex and diverse mechanisms each contributing to an increase of individual susceptibility to brain viral infectionsThe incidence of Alzheimer's disease (AD) is rising sharply and a large fraction of the elderly population will ultimately be affected by the disease. Because of an urgent need for effective preventative and therapeutic measures, extensive research has focused on pathogenetic mechanisms of the disease. However, effective therapy is not already available. AD pathology is characterized by neuronal loss leading to brain atrophy and a decrement of the cerebral metabolism. Major neuropathologic lesions are: (i) synapse and neuron loss; (ii) extracellular amyloid deposits and amyloid plaques, principally composed of amyloid beta (Aβ) peptide; (iii) intraneuronal accumulation of hyperphosphorylated Tau proteins leading to neurofibrillary degeneration; (iv) reactive astrogliosis; (v) brain inflammation. Current views of AD pathogenetic mechanisms describe amyloid deposition and neuritic plaque formation as a central mechanisms leading to neuro-degeneration, cognitive impairment and sporadic AD [1]. Therefore, therapeutic approaches have focused on reducing amyloid load and plaque deposition or clearance of brain amyloid. Other mechanisms may b
Altered glycosylation profile of purified plasma ACT from Alzheimer’s disease
Ianni Manuela,Manerba Marcella,Di Stefano Giuseppina,Porcellini Elisa
Immunity & Ageing , 2010, DOI: 10.1186/1742-4933-7-s1-s6
Abstract: Background Alzheimer’s disease (AD) is one of the most frequent cause of neurodegenerative disorder in the elderly. Inflammation has been implicated in brain degenerative processes and peripheral markers of brain AD related impairment would be useful. Plasma levels of alpha-1-antichymotrypsin (ACT), an acute phase protein and a secondary component of amyloid plaques, are often increased in AD patients and high blood ACT levels correlate with progressive cognitive deterioration. During inflammatory responses changes in the micro-heterogeneity of ACT sugar chains have been described. Methods N-Glycanase digestion from Flavobacterium meningosepticum (PNGase F) was performed on both native and denatured purified ACT condition and resolved to Western blot with the purpose to revealed the ACT de-glycosylation pattern. Further characterization of the ACT glycan profile was obtained by a glycoarray; each lectin group in the assay specifically recognizes one or two glycans/epitopes. Lectin-bound ACT produced a glyco-fingerprint and mayor differences between AD and controls samples were assessed by a specific algorithms. Results Western blot analysis of purified ACT after PNGase F treatment and analysis of sugar composition of ACT showed significantly difference in “glyco-fingerprints” patterns from controls (CTR) and AD; ACT from AD showing significantly reduced levels of sialic acid. A difference in terminal GlcNac residues appeared to be related with progressive cognitive deterioration. Conclusions Low content of terminal GlcNac and sialic acid in peripheral ACT in AD patients suggests that a different pattern of glycosylation might be a marker of brain inflammation. Moreover ACT glycosylation analysis could be used to predict AD clinical progression and used in clinical trials as surrogate marker of clinical efficacy.
Serum neutrophil gelatinase-B associated lipocalin (NGAL) levels in Down’s syndrome patients
Dogliotti Giada,Galliera Emanuela,Licastro Federico,Porcellini Elisa
Immunity & Ageing , 2010, DOI: 10.1186/1742-4933-7-s1-s7
Abstract: Neutrophil gelatinase-associated lipocalin (NGAL) is a group of proteins with different functions. NGAL is released by different cell types such as epithelial cell, hepatocytes and renal tubular cells during inflammation and after cell injury. Expression of NGAL is induced under various pathophysiological conditions such as infection, cancer, inflammation, kidney injury, cardiovascular disease, burn injury, and intoxication, which has an important anti-apoptotic and anti-inflammatory role. Subjects with Down’s syndrome (DS) are affected by many pathological age related conditions such as mental retardation, Alzheimer’s disease, immune defects and increased susceptibility to infections. The aim of this study is to evaluate possible use of NGAL as a marker of inflammatory status for allow an early diagnosis of inflammatory disease such as autoimmune disease in DS patients, that are more susceptible to these pathologies, especially in elderly subjects. In this study were recruited 3 groups of DS subjects (children, adults and elderly) and compared them to healthy control group. The molecules of interest was determinated by immuno-enzymatic assay (ELISA). Our results show that NGAL plasmatic level was significantly higher in DS patients compared to healthy controls. Moreover NGAL levels increase in correlation with the age, and showed a significantly correlation between the increase with the severity of disease. DS is characterized by an enhancement of gene production such as GART, SOD-1 and CBS that encode specific protein and enzyme involved in hydrogen peroxide and superoxide production, species highly cytotoxic implicated in inflammation and ageing. NGAL may have the potential application to ameliorate the toxicity induced by oxidative stress conditions such as Alzheimer’s disease, thalassemia, cardiovascular disease, burn injury, transplantation, diabetes, and aging.
Multi factorial interactions in the pathogenesis pathway of Alzheimer’s disease: a new risk charts for prevention of dementia
Licastro Federico,Porcellini Elisa,Forti Paola,Buscema Massimo
Immunity & Ageing , 2010, DOI: 10.1186/1742-4933-7-s1-s4
Abstract: Background The population longitudinal study named “The Conselice Study” has been the focus of the present investigation. 65 years old or older participants of this population study on brain aging were followed up for 5 years: 937 subjects completed the follow-up. Relationships of 46 genetic, phenotypic, clinical and nutritional factors on incident cognitive decline and incident dementia cases were investigated. Results A new statistical approach, called the Auto Contractive Map (AutoCM) was applied to find relationship between variables and a possible hierarchy in the relevance of each variable with incident dementia. This method, based on an artificial adaptive system, was able to define the association strength of each variable with all the others. Moreover, few variables resulted to be aggregation points in the variable connectivity map related to cognitive decline and dementia. Gene variants and cognate phenotypic variables showed differential degrees of relevance to brain aging and dementia. A risk map for age associated cognitive decline and dementia has been constructed and will be presented and discussed. Conclusion This map of variables may be use to identify subjects with increased risk of developing cognitive decline end/or dementia and provide pivotal information for early intervention protocols for prevention of dementia.
Innate immunity and inflammation in ageing: a key for understanding age-related diseases
Federico Licastro, Giuseppina Candore, Domenico Lio, Elisa Porcellini, Giuseppina Colonna-Romano, Claudio Franceschi, Calogero Caruso
Immunity & Ageing , 2005, DOI: 10.1186/1742-4933-2-8
Abstract: The first line of immune defence mainly operates by detection of a broad range of molecular patterns foreign to mammalian tissues, called pathogen-associated molecular patterns that induce the activation of the innate immunity and inflammatory response [1]. The constitutive expression of a limited set of pattern recognition receptors by many cell types of the innate immunity does not require clonal expansion of specific cell populations. These germ cell-encoded proteins recognize microbial pathogens or ligands from damaged tissues based on shared molecular structures and induce host responses that localize the spread of infection and enhance systemic resistance to infection. Therefore, the expression of a limited number of highly active genes during the activation of innate immunity is able to induce rapid (minutes to hours) efficient defensive immune responses [2].Several cell types contribute to innate immunity and the mononuclear phagocyte lineage plays a pivotal role in innate immunity. Monocytes, macrophages and their tissue-differentiated derivatives, such as microglia in the nervous system, express pattern recognition receptors, namely various scavenger and Toll-like receptors [3]. These receptors induce transmembrane signals that activate NF-kB and mitogen dependent protein kinase pathways [4]. Toll-like receptor activation also induces the expression of a wide number of genes encoding proteins, such as cytokines, with regulatory functions upon leukocyte activation and tissue inflammation [5]. Therefore, the capacity of each individual organism to regulate the activation of innate immunity and local inflammatory responses is crucial for initiating defensive action against pathogens, limiting tissue damage and enhancing fast recovery and tissue healing.In response to cell injury elicited by trauma or infection the inflammatory response sets in, constituting a complex network of molecular and cellular interactions directed to facilitate a return to physiologic
Infraspinatus scapular retraction test: a reliable and practical method to assess infraspinatus strength in overhead athletes with scapular dyskinesis
Giovanni Merolla,Elisa De Santis,Fabrizio Campi,Paolo Paladini,Giuseppe Porcellini
Journal of Orthopaedics and Traumatology , 2010, DOI: 10.1007/s10195-010-0095-x
Abstract: The good realibility and the easy reproducibility make the ISRT an excellent test to assess patients with infraspinatus weakness due to scapular dyskinesis and address them toward an appropriate program of rehabilitation aimed to restore scapular musculature balance and control.
Regenerative medicine: a review
Porcellini, Adolfo;
Revista Brasileira de Hematologia e Hemoterapia , 2009, DOI: 10.1590/S1516-84842009000800017
Abstract: regenerative medicine is a technique to replace or repair defective or diseased tissue or organs by in vitro design with in vivo usage. it can be considered a relatively new branch of medicine born in 1997 when whithman dh et al. proposed to integrate platelet enriched plasma (prp) in fibrin glue. in 1998 marx et al. demonstrated that prp was able to induce bone regeneration of the jaw. in the same period it was discovered that a fraction of stem cells of bone marrow origin was able to repair several mesenchymal tissues or organs.
Pro-inflammatory genetic profile and familiarity of acute myocardial infarction
Manuela Ianni, Sergio Callegari, Antonio Rizzo, Paolo Pastori, Paolo Moruzzi, Domenico Corradi, Elisa Porcellini, Gianluca Campo, Roberto Ferrari, Marco M Ferrario, Stefania Bitonte, Ilaria Carbone, Federico Licastro
Immunity & Ageing , 2012, DOI: 10.1186/1742-4933-9-14
Abstract: This study showed that a genetic signature consisting of the concomitant presence of the CC genotype of VEGF, the A allele of IL-10 and the A allele of IFN-γ was indeed present in the Offs population. In fact, the above genetic markers were more frequent in unaffected Offs (46.4%) and patients with sporadic AMI (31.8%) than in the CTR (17.3%) and the differences were highly statistically significant (Offs vs CTR: p?=?0.0001, OR?=?4.129; AMI vs CTR: p?=?0.0001, OR?=?2.224). During the 24-year follow-up, Offs with a positive familiarity in spite of a relatively young age showed an increased prevalence of diabetes, ischemic heart disease and stroke. These findings reinforce the notion that subjects with a familial history of AMI are at risk of an accelerated aging of cardiovascular system resulting in cardiovascular events.Our data suggest that selected genes with immune regulatory functions are part of the complex genetic background contributing to familiarity for cardiovascular diseases. This inflammatory genetic profile, along with classical cardiovascular risk factors, may be used for better defining individual risk of AMI in unaffected subjects.
Oxidative Stress Posttranslationally Regulates the Expression of Ha-Ras and Ki-Ras in Cultured Astrocytes
Samantha Messina,Luigi Frati,Antonio Porcellini
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/792705
Abstract: Addition of hydrogen peroxide to cultured astrocytes induced a rapid and transient increase in the expression of Ha-Ras and Ki-Ras. Pull-down experiments with the GTP-Ras-binding domain of Raf-1 showed that oxidative stress substantially increased the activation of Ha-Ras, whereas a putative farnesylated activated form of Ki-Ras was only slightly increased. The increase in both Ha-Ras and Ki-Ras was insensitive to the protein synthesis inhibitor, cycloheximide, and was occluded by the proteasomal inhibitor, MG-132. In addition, exposure to hydrogen peroxide reduced the levels of ubiquitinated Ras protein, indicating that oxidative stress leads to a reduced degradation of both isoforms through the ubiquitin/proteasome pathway. Indeed, the late reduction in Ha-Ras and Ki-Ras was due to a recovery of proteasomal degradation because it was sensitive to MG-132. The late reduction of Ha-Ras levels was abrogated by compound PD98059, which inhibits the MAP kinase pathway, whereas the late reduction of Ki-Ras was unaffected by PD98059. We conclude that oxidative stress differentially regulates the expression of Ha-Ras and Ki-Ras in cultured astrocytes, and that activation of the MAP kinase pathway by oxidative stress itself or by additional factors may act as a fail-safe mechanism limiting a sustained expression of the potentially detrimental Ha-Ras.
Oxidative Stress Posttranslationally Regulates the Expression of Ha-Ras and Ki-Ras in Cultured Astrocytes
Samantha Messina,Luigi Frati,Antonio Porcellini
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/792705
Abstract: Addition of hydrogen peroxide to cultured astrocytes induced a rapid and transient increase in the expression of Ha-Ras and Ki-Ras. Pull-down experiments with the GTP-Ras-binding domain of Raf-1 showed that oxidative stress substantially increased the activation of Ha-Ras, whereas a putative farnesylated activated form of Ki-Ras was only slightly increased. The increase in both Ha-Ras and Ki-Ras was insensitive to the protein synthesis inhibitor, cycloheximide, and was occluded by the proteasomal inhibitor, MG-132. In addition, exposure to hydrogen peroxide reduced the levels of ubiquitinated Ras protein, indicating that oxidative stress leads to a reduced degradation of both isoforms through the ubiquitin/proteasome pathway. Indeed, the late reduction in Ha-Ras and Ki-Ras was due to a recovery of proteasomal degradation because it was sensitive to MG-132. The late reduction of Ha-Ras levels was abrogated by compound PD98059, which inhibits the MAP kinase pathway, whereas the late reduction of Ki-Ras was unaffected by PD98059. We conclude that oxidative stress differentially regulates the expression of Ha-Ras and Ki-Ras in cultured astrocytes, and that activation of the MAP kinase pathway by oxidative stress itself or by additional factors may act as a fail-safe mechanism limiting a sustained expression of the potentially detrimental Ha-Ras. 1. Introduction An increased formation of reactive oxygen species (ROS) has been implicated in the pathogenesis of several CNS disorders including Alzheimer’s disease, Parkinson’s disease, acute and chronic cerebrovascular disorders, and brain ageing. In particular, oxidative stress in the CNS occurs after ischemic, traumatic, or excitotoxic insults when the excessive generation of ROS overwhelms the intracellular antioxidant capacity [1]. Neurons are highly sensitive to oxidative damage, whereas astrocytes exert a protective function acting as cell scavengers and producing neurotrophic factors in response to ROS [2–6]. Astrocytes respond to ROS with the activation of MAP kinases (MAPKs), including the extracellular signal-regulated kinases ERK1/2, JUN kinases (JNKs), and p38 MAPKs [7, 8]. The monomeric GTP-binding protein, Ras, has an established role in activating these pathways and has been implicated in the cellular response to oxidative stress [9, 10]. Mammalian cells contain three ubiquitously expressed Ras isoforms, Ha-, Ki-, and N-Ras that share a high degree of structural homology [11]. Ha- and Ki-Ras generate opposing effects on the redox state of cells in heterologous expression systems. Ki-Ras exerts an
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