121 research outputs found
Electronic Dictionaries for Information Retrieval, Automatic Textual Analysis and Semantic-Based Data Mining Software
No full textToday Lexicon-Grammar (LG) remains one of the most consistent
Natural Language Processing (NLP) approaches, especially for
Semantic-Based Data Mining (SBDM) and Semantic Web. Its main goal
is to describe all mechanisms of word combinations closely related to the
concrete use of lexical units and to sentence creation. Also, it gives an
exhaustive description of lexical and syntactic structures of several
languages. LG was set up by the French linguist Maurice Gross during
the ‘60s, and subsequently developed for and applied to Italian by
Annibale Elia, Emilio D’Agostino and Maurizio Martinelli. Its
theoretical approach is prevalently based on Zelig Sabbettai Harris’
Operator-Argument Grammar, which assumes that each human language
is a self-organizing system, and that the syntactic and semantic properties
of a given word may be calculated on the basis of the relationships this
word has with all other co-occurring words inside given sentence
contexts. Simple sentences2 are the minimal linguistic meaning structures
upon which LG founds its studies on natural language syntactic features.
In the last twenty years, LG has also reached important results in the
domain of automatic textual analysis and parsing with NLP-oriented
software such as INTEX3, UNITEX4, and more recently NOOJ5.
1 Alberto Postiglione is author of paragraph 4.1. Mario Monteleone is author of
paragraphs 3.1 and 4. Federica Marano is author of paragraphs 3.2 and 4.3. Johanna
Monti is author of sections 1 and 2. Antonella Napoli is author of paragraph 4.2.
2 In LG, a simple sentence is formed by a unique predicative element (a verb, but
also a name or an adjective) plus all the necessary arguments it selects to achieve
acceptability and grammaticality. The study of simple sentences is completed analyzing
the rules of co-occurrence and selection restriction, which are distributional and
transformational rules based on predicate syntactic-semantic properties.
3 For more on INTEX, see http://intex.univ-fcomte.fr/.
4 For more on UNITEX, see http://www-igm.univ-mlv.fr/~unitex/.
5 For more on NooJ, see http://www.nooj4nlp.net/pages/nooj.html.
ALBERTO POSTIGLIONE - MARIO MONTELEONE -
FEDERICA MARANO - JOHANNA MONTI - ANTONELLA NAPOLI1
Università degli Studi di Salerno
ELECTRONIC DICTIONARIES FOR INFORMATION RETRIEVAL,
AUTOMATIC TEXTUAL ANALYSIS AND SEMANTIC-BASED
DATA MINING SOFTWARE
1. Theoretical and analytical framework: Lexicon-Gramma
The Unexpected Role of Aβ1-42 Monomers in the Pathogenesis of Alzheimer's Disease.
No full textAmyloid- (A) has been proposed as a biomarker and a drug target for the therapy of Alzheimer’s disease (AD).
The neurotoxic entity and relevance of each conformational form of A to AD pathology is still under debate; A oligomers
are considered the major killer form of the peptide whereas monomers have been proposed to be involved in physiological
process. Here we reviewed some different effects mediated by monomers and oligomers on mechanisms involved in AD
pathogenesis such as autophagy and tau aggregation. Data reported in this review demonstrate that A monomers could
have a major role in sustaining the pathogenesis of AD and that AD therapy should be focused not only in the removal of
oligomers but also of monomers
Amyloid-β42 activates the expression of BACE1 through the JNK pathway
No full textThe sequential endoproteolytic cleavages operated by the γ-secretase and the β-secretase (BACE1) on the amyloid-β protein precursor (AβPP) result in the production of the amyloid-β (Aβ) species, with two C-terminal variants, at residue 40 or at residue 42. Accumulation in brain tissue of small, soluble aggregates of Aβ42 is the major pathogenic event of Alzheimer's disease (AD). However, the physiologic activity of Aβ peptides is still elusive. Here, we show that expression of BACE1 is regulated by Aβ42, which augments BACE1 gene transcription through the JNK/c-jun signaling pathway. Of note, Aβ40 has much less effect on BACE1 expression. These findings unveil a positive feedback loop in which γ-secretase cleavage of AβPP releases a functionally-active peptide, Aβ42, that promotes BACE1 transcription. Thus, gene expression induced by Aβ42 may have implications in the neuronal dysfunction and degeneration that occurs in AD
Baldomero Fernández Moreno: Ciudad, deriva de la urbe
No full textThe article raises a rereading of Baldomero Fernández Moreno as author of one of the first truly modern books of Argentine poetry. It gives particular attention to the publication of nine urban poems in 1915 and, fundamentally, in his book of 1917, Ciudad. The poet’s revaluation leads Monteleone to affirm that Baldomero opened a triple path in Argentine poetry: “the projection of an own personality on the face and the gaze of others between the tension of the individual and the collective, centered on space urban; the recognition of objects, as a way of situating the materiality of the world; the leeway as poetic discourse and social self-consciousness”.El artículo plantea una relectura de Baldomero Fernández Moreno como autor de uno de los primeros libros verdaderamente modernos de la poesía argentina. Se detiene en la publicación de nueve poemas urbanos en 1915 y, fundamentalmente, en su poemario de 1917, Ciudad. La revaloración del poeta lleva a Monteleone a afirmar que Baldomero abrió un triple camino en la poesía argentina: “la proyección de un rostro propio en la cara y la mirada de los otros en la tensión de lo individual y lo colectivo, centrada en el espacio urbano; el reconocimiento de los objetos, como un modo de situar la materialidad del mundo; la deriva como discurso poética y autoconsciencia social.
Baldomero Fernández Moreno: Ciudad, deriva de la urbe
No full textThe article raises a rereading of Baldomero Fernández Moreno as author of one of the first truly modern books of Argentine poetry. It gives particular attention to the publication of nine urban poems in 1915 and, fundamentally, in his book of 1917, Ciudad. The poet’s revaluation leads Monteleone to affirm that Baldomero opened a triple path in Argentine poetry: “the projection of an own personality on the face and the gaze of others between the tension of the individual and the collective, centered on space urban; the recognition of objects, as a way of situating the materiality of the world; the leeway as poetic discourse and social self-consciousness”.El artículo plantea una relectura de Baldomero Fernández Moreno como autor de uno de los primeros libros verdaderamente modernos de la poesía argentina. Se detiene en la publicación de nueve poemas urbanos en 1915 y, fundamentalmente, en su poemario de 1917, Ciudad. La revaloración del poeta lleva a Monteleone a afirmar que Baldomero abrió un triple camino en la poesía argentina: “la proyección de un rostro propio en la cara y la mirada de los otros en la tensión de lo individual y lo colectivo, centrada en el espacio urbano; el reconocimiento de los objetos, como un modo de situar la materialidad del mundo; la deriva como discurso poética y autoconsciencia social.
Dual Mechanism of Toxicity for Extracellular Injection of Tau Oligomers versus Monomers in Human Tau Mice
No full textThe mechanism of tau toxicity is still unclear. Here we report that recombinant tau oligomers and monomers, intraventricularly injected in mice with a pure human tau background, foster tau pathology through different mechanisms. Oligomeric forms of tau alter the conformation of tau in a paired helical filament-like manner. This effect occurs without tau hyperphosphorylation as well as activation of specific kinases, suggesting that oligomers of tau induce tau assembly through a nucleation effect. Monomers, in turn, induce neurodegeneration through a calpain-mediated tau cleavage that leads to accumulation of a 17kDa neurotoxic peptide and induction of apoptotic cell death
The Decrease of Uch-L1 Activity Is a Common Mechanism Responsible for Aβ 42 Accumulation in Alzheimer’s and Vascular Disease
No full textAlzheimer's disease (AD) is a multifactorial pathology causing common brain spectrum disorders in affected patients. These mixed neurological disorders not only include structural AD brain changes but also cerebrovascular lesions. The main aim of the present issue is to find the factors shared by the two pathologies. The decrease of ubiquitin C-terminal hydrolase L1 (Uch-L1), a major neuronal enzyme involved in the elimination of misfolded proteins, was observed in ischemic injury as well as in AD, but its role in the pathogenesis of AD is far to be clear. In this study we demonstrated that Uch-L1 inhibition induces BACE1 up-regulation and increases neuronal and apoptotic cell death in control as well as in transgenic AD mouse model subjected to Bengal Rose, a light-sensitive dye inducing that induces a cortical infarction through photo-activation. Under the same conditions we also found a significant activation of NF-κB. Thus, the restoration of Uch-L1 was able to completely prevent both the increase in BACE1 protein levels and the amount of cell death. Our data suggest that the Uch-L1-mediated BACE1 up-regulation could be an important mechanism responsible for Aβ peptides accumulation in vascular injury and indicate that the modulation of the activity of this enzyme could provide new therapeutic strategies in AD
Impaired glucose metabolism in bipolar patients and response to mood stabilizer treatments
No full textBackground: Metabolic dysfunctions in patients with bipolar disorder (BD) are critical factors that interfere with outcome, but only one study evaluated the influence of glucose dysmetabolism on the response to treatment with lithium. We aimed to investigate the potential impact of glucose metabolic status on clinical characteristics of BD patients and their response to treatment with different mood stabilizers in monotherapy or in combination. Methods: 45 BD patients with insulin resistance (IR) or type 2 diabetes mellitus (DM2) and 46 patients with normal glucose metabolism, treated with mood stabilizers for at least one year were assessed by diagnostic and rating instruments. Their clinical characteristics were compared and an ordinal logistic regression model was adopted to identify possible predictors of response to mood stabilizer treatments. Results: Compared to patients with normal glucose metabolism, BD patients with impaired glucose metabolism showed a worse clinical presentation of their psychiatric illness and a worse response to mood stabilizers. Ordinal logistic regression analysis evidenced that impaired glucose metabolism was the only predictor of poor response to mood stabilizers (OR 4.3; 95% CI: 1.7–11.1; p < 0.002). Limitations: Cross-sectional design and the relatively small sample size, are the main limitations of our study. Conclusions: Our findings expand literature data suggesting that BD patients with impaired glucose metabolism are at a greater risk of not responding to lithium as well as to different mood stabilizer treatments
Stroke and Amyloid-beta Downregulate TREM-2 and Uch-L1 Expression that Synergistically Promote the Inflammatory Response
No full textNeuroinflammation is involved in the pathogenesis of Alzheimer's disease, and the transcription factor NF-kappa B is a player in this event. We found here that the ischemic damage alone or in association with A beta(1-42) activates the NF-kappa B pathway, induces an increase of BACE1 and a parallel inhibition of Uch-L1 and TREM2, both in vitro and in vivo, in Tg 5XFAD and in human brains of sporadic AD. This mechanism creates a synergistic loop that fosters inflammation. We also demonstrated a significant protection exerted by the restoration of Uch-L1 activity. The rescue of the enzyme is able to abolish the decrease of TREM2 and the parameters of neuroinflammation.BM
Aβ1-42-mediated down-regulation of Uch-L1 is dependent on NF-κB activation and impaired BACE1 lysosomal degradation
No full textAmyloid-β 1-42 accumulation is the major pathogenetic event in Alzheimer's disease (AD), believed to be responsible for synaptic dysfunction and neuronal cell death. However, the physiologic activity of Aβ peptides remains elusive: Aβ might not only play a toxic role, but also act as a functional signaling intermediate. We recently reported that Aβ1-42 promotes BACE1 transcription through the activation of the JNK-c-jun pathway. Here, we show that the Aβ1-42-mediated increase in BACE1 expression is accompanied by a decrease in ubiquitin C-terminal hydrolase L1 (Uch-L1) expression and activity in different cellular models such as neuroblastoma SH-SY5Y as well as NT(2) neuronal cells. We also found that the increase in BACE1 and the decrease in Uch-L1 are related events and depend on NF-κB pathway; thus, Aβ1-42 is able to activate NF-κB pathway and the pretreatment with a pharmacological inhibitor, able to block the nuclear translocation of the transactivating unit p65, almost completely prevents both the decrease in Uch-L1 and the increase in BACE1 expression. In addition, the decrease in Uch-L1 activity interferes with the lysosomal degradation of BACE1, as demonstrated by the decrease in Cathepsin D activity and the partial accumulation of BACE1 in lysosomes after Aβ1-42 treatment as well after Uch-L1 inhibition. In support of the in vitro data, we observed low protein levels of Uch-L1 associated with high protein levels of BACE1 in sporadic AD brains. Our data suggest that Uch-L1 could be an attractive target for the development of new therapeutic approaches for AD
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