1,721,976 research outputs found
The RAS oncogene in brain tumors and the involvement of let-7 microRNA
Full text linkRAS oncogenes are master regulator genes in many cancers. In general, RAS-driven cancers have an oncogenic RAS mutation that promotes disease progression (colon, lung, pancreas). In contrast, brain tumors are not necessarily RAS-driven cancers because RAS mutations are rarely observed. In particular, glioblastomas (the most lethal brain tumor) do not appear to have dominant genetic mutations that are suitable for targeted therapy. Standard treatment for most brain tumors continues to focus on maximal surgical resection, radiotherapy and chemotherapy. Yet the convergence of genomic aberrations such as EGFR, PDGFR and NF1 (some of which are clinically effective) with activation of the RAS/MAPK cascade is still considered a key point in gliomagenesis, and KRAS is undoubtedly a driving gene in gliomagenesis in mice. In cancer, microRNAs (miRNA) are small, non-coding RNAs that regulate carcinogenesis. However, the functional consequences of aberrant miRNA expression in cancer are still poorly understood. let-7 encodes an intergenic miRNA that is classified as a tumour suppressor, at least in lung cancer. Let-7 suppresses a plethora of oncogenes such as RAS, HMGA, c-Myc, cyclin-D and thus suppresses cancer development, differentiation and progression. let-7 family members are direct regulators of certain RAS family genes by binding to the sequences in their 3'untranslated region (3'UTR). let-7 miRNA is involved in the malignant behaviour in vitro-proliferation, migration and invasion-of gliomas and stem-like glioma cells as well as in vivo models of glioblastoma multiforme (GBM) via KRAS inhibition. It also increases resistance to certain chemotherapeutic agents and radiotherapy in GBM. Although let-7 therapy is not yet established, this review updates the current state of knowledge on the contribution of miRNA let-7 in interaction with KRAS to the oncogenesis of brain tumours
Giuseppe Messina, S. J. — L’aramaico antiquo. Indagine sull’aramaico del vecchio Testamento. Rome, Institut biblique, 1934
No full textMouterde Paul. Giuseppe Messina, S. J. — L’aramaico antiquo. Indagine sull’aramaico del vecchio Testamento. Rome, Institut biblique, 1934. In: Mélanges de l'Université Saint-Joseph, tome 18, 1934. pp. 210-211
Pratiche di assessment: un questionario per sviluppare la literacy dei docenti = Assessment’ practices: a tool to frame teachers’ literacy
Full text linkIl contributo presenta il processo di validazione di uno strumento
di mappatura delle pratiche di assessment dei docenti.
In vista della validazione sono state portate a termine le seguenti
fasi: costruzione del questionario; test per la validazione
statistica; validazione di contenuto grazie alla collaborazione
di esperti; re-test finale per la validazione di costrutto. Si è scelto
di impostare lo strumento a partire da una revisione del costrutto
di assessment literacy per comprendere le pratiche di
assessment as learning (Hadji, 2017).The paper presents the validation process of a mapping tool
for teachers’ assessment practices. For validation, the following
phases were completed: construction of the questionnaire;
tests for statistical validation; content validation, with the collaboration
of experts; final re-test for validation of the construct.
We decided to set up the tool starting from a revision
of the assessment literacy construct, in order to understand the
practices inspired by assessment as learning
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Attachment and Emotional Development: What can we Learn From Children’s Descriptions of Well-being and Distress?
No full text
Decoding the role of the lncRNA HOTAIRM1 in human motor neurons
Full text linkThe mammalian genome produces thousands of long non-coding RNAs (lncRNAs), which have been demonstrated to be fundamental in the control of many biological processes. These molecules play a crucial role in the multilayered regulation of physiological and disease-related gene expression programs, having significant implications in shaping central nervous system (CNS) complexity.
Neuronal differentiation is a timely and spatially regulated process, relying on precisely orchestrated gene expression control. The coordinated activity of transcription factors and non-coding RNAs (ncRNAs), organized in intricate regulatory networks, drives cell fate specification ensuring correct and specific neuronal functions. We previously described,1 at both the molecular and functional level, the lncRNA nHOTAIRM1 as a neuronal-enriched transcript, which is upregulated during in vitro neuronal differentiation and highly expressed in post-mitotic motor neurons (MNs). We demonstrated that the nuclear nHOTAIRM1, even if much less abundant than its cytoplasmic counterpart, it is involved in the achievement of correct neuronal differentiation timing as an epigenetic regulator of NEUROG2 expression.1 Remarkably, among all human brain tissues, nHOTAIRM1 is specifically expressed in the spinal cord. Consistently, we found that nHOTAIRM1 accumulates in MN-enriched ventral spinal cord lineages differentiated from human induced pluripotent stem cells (iPSCs).1 All this evidence prompted us to further investigate the role of the highly expressed nHOTAIRM1 specifically on MN generation and/or function, to ultimately determine whether its deregulation affects MN differentiation and activity. To experimentally address these questions, here we applied a genome editing-based loss-of-function approach to a model system that efficiently recapitulates spinal MN differentiation, and we identified key nHOTAIRM1 target genes implicated in MN maturation, morphology and activity. Our findings allowed us to conclude that nHOTAIRM1 directs multiple crucial aspects of MN physiology, from their development to the acquisition of appropriate morphological features and motor function
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