Person:
García Lobo, Jimena

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First Name
Jimena
Last Name
García Lobo
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Veterinaria
Department
Farmacología y Toxicología
Area
Toxicología
Identifiers
UCM identifierScopus Author IDDialnet ID

Search Results

Now showing 1 - 10 of 16
  • Item
    Project number: 267
    Aprendizaje colaborativo/competitivo mediante gamificación, a través del uso integrado de un mando wiimote como pizarra digital interactiva, un sistema virtual de respuesta en el aula, y dispositivos móviles con acceso a internet
    (2017) Pino Sans, Javier Del; Anadón Baselga, María José; Frejo Moya, María Teresa; Díaz Plaza, María Jesús; Capo Martí, Miguel Andrés; García Lobo, Jimena; Lobo Alonso, Margarita; Moyano-Cires Ivanoff, Paula Viviana; Zeballos Deza, Gabriela; Flores Calle, Andrea
    Integración de pizarra digital, una aplicación informática propia como sistema de respuesta (clicker) y otras aplicaciones no propias para facilitar la evaluación continua, aumentar la motivación y rendimiento de los estudiantes a un coste muy bajo.
  • Item
    Project number: 160
    Aprendizaje flexible y personalizado para atender la diversidad en el aula, mediante la gamificación, a través del uso integrado de un sistema virtual de respuesta en el aula para dispositivos móviles con acceso a internet y una aplicación de screencasting
    (2018) Pino Sans, Javier Del; Martin Sopeña, Alejandra; López Salas, Alejandra; De Frías González, Mariano; Zeballos Deza, Gabriela; Moyano-Cires Ivanoff, Paula Viviana; García Sánchez, José Manuel; Frejo Moya, María Teresa; Anadón Baselga, María José; Capo Martí, Miguel Andrés; Díaz Plaza, María Jesús; Lobo Alonso, Margarita; García Lobo, Jimena; Pelayo Alarcón, Adela; Blanco Caneda, María Luisa; Peligros Gómez, María Isabel; Menárguez Palanca, Francisco Javier; López Varela, María Del Carmen; Ortega Medina, Luis; Rodríguez Gil, Yolanda; Agra Pujol, Carolina; Fernández Aceñero, María Jesús; Sola Vendrell, Emma
  • Item
    Project number: 15
    Aprendizaje global, flexible y personalizado para atender la diversidad y favorecer la inserción laboral de los estudiantes, mediante el uso del flipped learning (micro-learning/teaching), a través del uso de infografías y herramientas TACs digitales
    (2023) Moyano-Cires Ivanoff, Paula Viviana; Abascal Camacho, María Luisa; Anadón Baselga, María José; Bellón López, Miguel Ángel; Capo Martí, Miguel Andrés; Frias Gonzalez, Mariano de; Frejo Moya, María Teresa; Flores Calle, Andrea; García Lobo, Jimena; García Sánchez, José Manuel; Guerra Menendez, Lucia; Lobo Alonso, Margarita; Naval López, María Victoria; Pelayo Alarcón, Adela; Pino Sans, Javier Del; Pinzón Bayón, Alba; Ruiz Fernández, Matilde; Sanjuán López, Javier; Sola Vendrell, Emma
  • Item
    Cadmium-induced neurotoxic effects on rat basal forebrain cholinergic system through thyroid hormones disruption
    (Environmental Toxicology and Pharmacology, 2021) Sola Vendrell, Emma; Moyano-Cires Ivanoff, Paula Viviana; Flores, Andrea; García Lobo, Jimena; García Sánchez, José Manuel; Anadón Baselga, María José; Frejo Moya, María Teresa; Pelayo Alarcón, Adela; Fernández Fernández, María De La Cabeza; Pino Sans, Javier Del
    Cadmium (Cd) single and repeated exposure produces cognitive dysfunctions. Basal forebrain cholinergic neurons (BFCN) regulate cognitive functions. BFCN loss or cholinergic neurotransmission dysfunction leads to cognitive disabilities. Thyroid hormones (THs) maintain BFCN viability and functions, and Cd disrupts their levels. However, Cd-induced BFCN damages and THs disruption involvement was not studied. To research this we treated male Wistar rats intraperitoneally with Cd once (1 mg/kg) or repetitively for 28 days (0.1 mg/kg) with/without triiodothyronine (T3, 40 µg/kg/day). Cd increased thyroid-stimulating-hormone (TSH) and decreased T3 and tetraiodothyronine (T4). Cd altered cholinergic transmission and induced a more pronounced neurodegeneration on BFCN, mediated partially by THs reduction. Additionally, Cd antagonized muscarinic 1 receptor (M1R), overexpressed acetylcholinesterase S variant (AChE-S), downregulated AChE-R, M2R, M3R and M4R, and reduced AChE and choline acetyltransferase activities through THs disruption. These results may assist to discover cadmium mechanisms that induce cognitive disabilities, revealing a new possible therapeutic tool.
  • Item
    Project number: 170
    Aprendizaje personalizado para facilitar la inserción en el mercado laboral, mediante la gamificación, a través del uso integrado de mundos y sistemas virtuales de respuesta en el aula para dispositivos móviles con acceso a internet
    (2019) Pino Sans, Javier Del; Moyano-Cires Ivanoff, Paula Viviana; Anadón Baselga, María José; Capo Martí, Miguel Andrés; Pelayo Alarcón, Adela; Sola Vendrell, Emma; De Frías González, Mariano; García Sánchez, José Manuel; Sanjuán López, Javier; Mourin Moral, Francisco Javier; Blanco Caneda, María Luisa; Díaz Plaza, María Jesús; Rojas López, Francisco Javier; Frejo Moya, María Teresa; Lobo Alonso, Margarita; García Lobo, Jimena; Ruiz Fernández, Matilde
    Integración de una aplicación informática propia como sistema de respuesta (clicker) y una aplicación de entorno simulado para facilitar la evaluación continúa de forma personalizada, aumentar la motivación y rendimiento a bajo coste.
  • Item
    Project number: 95
    Aprendizaje global, flexible y personalizado para atender la diversidad en el aula, mediante el uso de Flipped Learning, a través del uso integrado de un sistema virtual de respuesta en el aula, y otras herramientas TACs digitales
    (2021) Pino Sans, Javier Del; Moyano-Cires Ivanoff, Paula Viviana; Frejo Moya, María Teresa; Anadón Baselga, María José; Lobo Alonso, Margarita; Pelayo Alarcón, Adela; Capo Martí, Miguel Andrés; Sola Vendrell, Emma; Sanjuán López, Javier; García Sánchez, José Manuel; Ruiz Fernández, Matilde; Mourin Moral, Francisco Javier; Frias González, Mariano De; Naval López, María Victoria; Guerra Menéndez, Lucia; García Lobo, Jimena
  • Item
    Cadmium alters heat shock protein pathways in SN56 cholinergic neurons, leading to AB and phosphorylated Tau protein generation and cell death
    (Food and Chemical Toxicology, 2018) Moyano-Cires Ivanoff, Paula Viviana; García Sánchez, José Manuel; Lobo Alonso, Margarita; Anadón Baselga, María José; Sola Vendrell, Emma; Pelayo Alarcón, Adela; García Lobo, Jimena; Frejo Moya, María Teresa; Pino Sans, Javier Del
    Cadmium, a neurotoxic environmental compound, produces cognitive disorders, although the mechanism remains unknown. Cadmium induces a more pronounced cell death on cholinergic neurons from basal forebrain (BF), mediated, in part, by increase in Aβ and total and phosphorylated Tau protein levels, which may explain cadmium effects on learning and memory processes. Cadmium downregulates the expression of heat shock proteins (HSPs) HSP 90, HSP70 and HSP27, and of HSF1, the master regulator of the HSP pathway. HSPs proteins reduce the production of Aβ and phosphorylated Tau proteins and avoid cell death pathways induction. Thus, we hypothesized that cadmium induced the production of Aβ and Tau proteins by HSP pathway disruption through HSF1 expression alteration, leading to BF cholinergic neurons cell death. Our results show that cadmium downregulates HSF1, leading to HSP90, HSP70 and HSP27 gene expression downregulation in BF SN56 cholinergic neurons. In addition, cadmium induced Aβ and total and phosphorylated Tau proteins generation, mediated partially by HSP90, HSP70 and HSP27 disruption, leading to cell death. These results provide new understanding of the mechanisms contributing to cadmium harmful effects on cholinergic neurons.
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    Insulin Signaling Disruption and INF-γ Upregulation Induce Aβ1–42 and Hyperphosphorylated-Tau Proteins Synthesis and Cell Death after Paraquat Treatment of Primary Hippocampal Cells
    (Chemical Research in Toxicology, 2022) Abascal, Maria Luisa; Sanjuan, Javier; Moyano-Cires Ivanoff, Paula Viviana; Sola Vendrell, Emma; Flores, Andrea; García Sánchez, José Manuel; García Lobo, Jimena; Frejo Moya, María Teresa; Pino Sans, Javier Del
    Acute and long-term paraquat (PQ) exposure produces hippocampal neurodegeneration and cognition decline. Although some mechanisms involved in these effects were found, the rest are unknown. PQ treatment, for 1 and 14 days, upregulated interferon-gamma signaling, which reduced insulin levels and downregulated the insulin pathway through phosphorylated-c-Jun N-terminal-kinase upregulation, increasing glucose levels and the production of Aβ1–42 and phosphorylated-tau, by beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) overexpression and phosphorylated-GSK3β (p-GSK3β; ser9) level reduction, respectively, which induced primary hippocampal neuronal loss. This novel information on the PQ mechanisms leading to hippocampal neurodegeneration could help reveal the PQ actions that lead to cognition dysfunction.
  • Item
    Project number: 14
    Aprendizaje flexible y personalizado para atender la diversidad en el aula, mediante el uso del flipped learning (aprendizaje invertido), a través del uso integrado de un sistema virtual de respuesta en el aula, y otras herramientas TACs
    (2020) Pino Sans, Javier Del; Moyano-Cires Ivanoff, Paula Viviana; Frejo Moya, María Teresa; Lobo Alonso, Margarita; García Lobo, Jimena; Anadón Baselga, María José; Capo Martí, Miguel Andrés; Frias González, Mariano De; Rojas López, Francisco Javier; Ruiz Fernández, Matilde; Sola Vendrell, Emma; Mourin Moral, Francisco Javier; Sanjuán López, Javier; García Sánchez, José Manuel
    Integración de una aplicación informática propia como sistema de respuesta (clicker) y diferentes herramientas TCs para facilitar la evaluación continua de forma personalizada, aumentar la motivación y rendimiento de los estudiantes a bajo coste.
  • Item
    Manganese induced ROS and AChE variants alteration leads to SN56 basal forebrain cholinergic neuronal loss after acute and long-term treatment
    (Food and Chemical Toxicology, 2019) Moyano-Cires Ivanoff, Paula Viviana; García Sánchez, José Manuel; Anadón Baselga, María José; Lobo Alonso, Margarita; García Lobo, Jimena; Frejo Moya, María Teresa; Sola Vendrell, Emma; Pelayo Alarcón, Adela; Pino Sans, Javier Del
    Manganese (Mn) induces cognitive disorders and basal forebrain (BF) cholinergic neuronal loss, involved on learning and memory regulation, which could be the cause of such cognitive disorders. However, the mechanisms through which it induces these effects are unknown. We hypothesized that Mn could induce BF cholinergic neuronal loss through oxidative stress generation, cholinergic transmission and AChE variants alteration that could explain Mn cognitive disorders. This study shows that Mn impaired cholinergic transmission in SN56 cholinergic neurons from BF through alteration of AChE and ChAT activity and CHT expression. Moreover, Mn induces, after acute and long-term exposure, AChE variants alteration and oxidative stress generation that leaded to lipid peroxidation and protein oxidation. Finally, Mn induces cell death on SN56 cholinergic neurons and this effect is independent of cholinergic transmission alteration, but was mediated partially by oxidative stress generation and AChE variants alteration. Our results provide new understanding of the mechanisms contributing to the harmful effects of Mn on cholinergic neurons and their possible involvement in cognitive disorders induced by Mn.