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https://riquim.fq.edu.uy/files/original/8c67c67df990c572136fc39f61dd5726.PNG
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https://riquim.fq.edu.uy/files/original/b44972c16a6c994860ebf9db3e7db815.pdf
c845c1000b6329c094a98acfecd6b7ea
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Bibliografía Nacional Química
Description
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Contiene la producción científica nacional de los profesionales químicos e investigadores, durante el período 1929 hasta la fecha.
Contributor
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Departamento de Documentación y Biblioteca
RIQUIM
Document
A resource containing textual data. Note that facsimiles or images of texts are still of the genre text.
Original Format
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PDF
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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<strong>Untargeted metabolomics of 3xTg-AD neurotoxic astrocytes</strong>
Subject
The topic of the resource
SISTEMA NERVIOSO
FLAVONOIDES
FENOTIPO
ENFERMEDADES NEUROMUSCULARES
ASTROCITOS
NEURODEGENERACION
TRANSCRIPTOMICA
METABOLOMICA
ENFERMEDAD DE ALZHEIMER
RATONES 3x-Tg-AD
DEMENCIA
BIBLIOGRAFIA NACIONAL QUIMICA
2025
Abstract
A summary of the resource.
Alzheimer’s disease (AD) is the most common form of dementia, affecting approximately 47 M people worldwide. Histological features and genetic risk factors, among other evidence, supported the amyloid hypothesis of the disease. This neuronocentric paradigm is currently undergoing a shift, considering evidence of the role of other cell types, such as microglia and astrocytes, in disease progression. Previously, we described a particular astrocyte subtype obtained from the 3xTg-AD murine model that displays neurotoxic properties in vitro. We continue here our exploratory analysis through the lens of metabolomics to identify potentially altered metabolites and biological pathways. Cell extracts from neurotoxic and control astrocytes were compared using high-resolution mass spectrometrybased metabolomics. Around 12 % of metabolic features demonstrated significant differences between neurotoxic and control astrocytes, including alterations in the key metabolite glutamate. Consistent with our previous transcriptomic study, the present results illustrate many homeostatic and regulatory functions of metabolites, suggesting that neurotoxic 3xTg-AD astrocytes exhibit alterations in the Krebs cycle as well as the prostaglandin pathway.This is the first metabolomic study performed in 3xTg-AD neurotoxic astrocytes. These results provide insight into metabolic alterations potentially associated with neurotoxicity and pathology progression in the 3xTg-AD mouse model and strengthen the therapeutic potential of astrocytes in AD. Biological significance: Our study is the first high-resolution metabolomic characterization of the novel neurotoxic 3xTg-AD astrocytes. We propose key metabolites and pathway alterations, as well as possible associations with gene expression alterations in the model. Our results are in line with recent hypotheses beyond the amyloid cascade, considering the involvement of several stress response cascades during the development of Alzheimer’s disease. This work could inspire other researchers to initiate similar studies in related models. Furthermore, this work illustrates a powerful workflow for metabolite annotation and selection that can be implemented in other studies.
Creator
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<strong>Carvalho, Diego</strong>
<strong>Díaz Amarilla, Pablo</strong>
<strong>Smith, Mathew R.</strong>
<strong>Santi, María Daniela</strong>
<strong>Martinez-Busi, Marcela</strong>
<strong>Go, Young-Mi</strong>
<strong>Jones, Dean P.</strong>
<strong>Duarte, Pablo</strong>
<strong>Savio, Eduardo</strong>
<strong>Abin-Carriquiry, Juan A.</strong>
<strong>Arredondo Unanua, María Florencia</strong>
Source
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Journal of Proteomics, v.310, 2025. -- e105336
Publisher
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Elsevier
Date
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2025
Rights
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<div class="element-text">
<p><strong>Información sobre Derechos de Autor</strong></p>
<p>(Por favor lea este aviso antes de abrir los documentos u objetos)</p>
<p><strong>La legislación uruguaya protege el derecho</strong> de autor sobre toda creación literaria, científica o artística, tanto en lo que tiene que ver con sus derechos morales, como en lo referente a los derechos patrimoniales con sujeción a lo establecido por el derecho común y las siguientes leyes (LEY 9.739 DE 17 DE DICIEMBRE DE 1937 SOBRE PROPIEDAD LITERARIA Y ARTISTICA CON LAS MODIFICACIONES INTRODUCIDAS POR LA LEY DE DERECHO DE AUTOR Y DERECHOS CONEXOS No. 17.616 DE 10 DE ENERO DE 2003, LEY 17.805 DE 26 DE AGOSTO DE 2004, LEY 18.046 DE 24 DE OCTUBRE DE 2006 LEY 18.046 DE 24 DE OCTUBRE DE 2006)</p>
<p><strong>ADVERTENCIA -</strong> La consulta de este documento queda condicionada a la aceptación de las siguientes condiciones de uso: Este documento es únicamente para usos privados enmarcados en actividades de investigación y docencia. No se autoriza su reproducción con fines de lucro. Esta reserva de derechos afecta tanto los datos del documento como a sus contenidos. En la utilización o cita de partes debe indicarse el nombre de la persona autora.</p>
</div>
Format
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PDF
Extent
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11 p.
Language
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Inglés
Type
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Artículo
Identifier
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10.1016/j.jprot.2024.105336
Astrocitos
Demencia
Enfermedad de Alzheimer
Enfermedades neuromusculares
Fenotipo
Flavonoides
Metabolómica
Neurodegeneracion
Ratones 3x-Tg-AD
Sistema nervioso
Transcriptomica
-
https://riquim.fq.edu.uy/files/original/4d03b7a53da138ef48c1026dec5a3c16.pdf
0ebebc2e46cd599f97051dd7aefd7031
https://riquim.fq.edu.uy/files/original/43f926b84142e890bc9e0a6dc76fea03.png
85def0ee6f08aad6775fdf97a1b95c52
Omeka Image File
The metadata element set that was included in the `files_images` table in previous versions of Omeka. These elements are common to all image files.
Bit Depth
8
Height
257
Width
196
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Bibliografía Nacional Química
Description
An account of the resource
Contiene la producción científica nacional de los profesionales químicos e investigadores, durante el período 1929 hasta la fecha.
Contributor
An entity responsible for making contributions to the resource
Departamento de Documentación y Biblioteca
RIQUIM
Document
A resource containing textual data. Note that facsimiles or images of texts are still of the genre text.
Original Format
If the image is of an object, state the type of object, such as painting, sculpture, paper, photo, and additional data
PDF
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
<strong>Aggressive mutation in a familial adenomatous polyposis syndrome family : when phenotype guides clinical surveillance</strong>
Subject
The topic of the resource
FENOTIPO
POLIPOSIS ADENOMATOSA FAMILIAR
BIBLIOGRAFIA NACIONAL QUIMICA
2018
Abstract
A summary of the resource.
Familial adenomatous polyposis (FAP) is an autosomal dominant genetic condition, caused by mutations in the adenomatous polyposis coli (APC) tumor suppressor gene. Desmoid tumors (DTs) are seen in 15% to 20% of FAP patients. Specific location of mutation serves as a guide to predict colonic and extra colonic manifestations and their aggressiveness. A severe FAP-phenotypic family was registered in a genetic counselling high-risk Uruguayan hereditary cancer clinic. Proband’s DNA was analysed by NGS, detecting a pathogenic mutation in APC gene. All willing family members were counselled and encouraged to be tested. Here we report a kindred formed by 16 individuals with a very severe FAP phenotype. A two-base deletion mutation: c.4393_4394delAG in APC gene and a consequent premature stop codon was detected. DTs were diagnosed in 6 individuals, ranging from 2 to 25 years of age. The causes of death were diverse: gastric cancer, rectal cancer and desmoid tumor. The already described genotype-phenotype correlation has proved its worth in this family, as clinical features reflect the mutation location at 3’ end of APC gene. The inheritable and lethal nature of the disease needs a tailored follow up approach in order to reduce mortality, optimize local tumor control, and preserve patients’ quality of life.
Creator
An entity primarily responsible for making the resource
<strong>Neffa, Florencia</strong>
<strong>García, Lucía</strong>
<strong>Della Valle, Adriana</strong>
<strong>Carusso, Florencia</strong>
<strong>Vergara, Carolina</strong>
<strong>Sanchez, Daniel</strong>
<strong>Sapone, Marta</strong>
<strong>Sylveira, Noelia</strong>
<strong>Revello, Ana Laura</strong>
<a title="Curriculum Vitae" href="http://buscadores.anii.org.uy/buscador_sni/exportador/ExportarPdf?hash=8b87e8e50f3fa6cbb61ecc6edf70e6f8" target="_self"><strong>Esperón, Patricia</strong></a>
Source
A related resource from which the described resource is derived
Journal of Gastrointestinal Oncology v.8, no. 9, 2018. -- p. 553-559
Publisher
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AME
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
Rights
Information about rights held in and over the resource
<p><strong>Información sobre Derechos de Autor</strong></p>
<p>(Por favor lea este aviso antes de abrir los documentos u objetos)</p>
<p><strong> La legislación uruguaya protege el derecho</strong> de autor sobre toda creación literaria, científica o artística, tanto en lo que tiene que ver con sus derechos morales, como en lo referente a los derechos patrimoniales con sujeción a lo establecido por el derecho común y las siguientes leyes (LEY 9.739 DE 17 DE DICIEMBRE DE 1937 SOBRE PROPIEDAD LITERARIA Y ARTISTICA CON LAS MODIFICACIONES INTRODUCIDAS POR LA LEY DE DERECHO DE AUTOR Y DERECHOS CONEXOS No. 17.616 DE 10 DE ENERO DE 2003, LEY 17.805 DE 26 DE AGOSTO DE 2004, LEY 18.046 DE 24 DE OCTUBRE DE 2006)</p>
<p><strong> ADVERTENCIA -</strong> La consulta de este documento queda condicionada a la aceptación de las siguientes condiciones de uso: Este documento es únicamente para usos privados enmarcados en actividades de investigación y docencia. No se autoriza su reproducción con fines de lucro. Esta reserva de derechos afecta tanto los datos del documento como a sus contenidos. En la utilización o cita de partes debe indicarse el nombre de la persona autora.</p>
Format
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PDF
Language
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Inglés
Type
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Artículo
Identifier
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DOI:: 10.21037/jgo.2018.06.10
Fenotipo
Poliposis adematosa