8 results on '"de la Garza, R. G."'
Search Results
2. Erratum to: Intrauterine Growth Retardation (IUGR) as a Novel Condition of Insulin-Like Growth Factor-1 (IGF-1) Deficiency
- Author
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Martín-Estal, I., primary, de la Garza, R. G., additional, and Castilla-Cortázar, I., additional
- Published
- 2016
- Full Text
- View/download PDF
3. Intrauterine Growth Retardation (IUGR) as a Novel Condition of Insulin-Like Growth Factor-1 (IGF-1) Deficiency
- Author
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Martín-Estal, I., primary, de la Garza, R. G., additional, and Castilla-Cortázar, I., additional
- Published
- 2015
- Full Text
- View/download PDF
4. Liver status and outcomes in patients without previous known liver disease receiving anticoagulant therapy for venous thromboembolism
- Author
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Martinez-Urbistondo D., de la Garza R. G., Villares-Fernandez P., Font C., Schellong S., Lopez-Nunez J. J., Gil-Diaz A., del Carmen Diaz-Pedroche M., Hirmerova J., Monreal M., Adarraga M., Aibar J., Alonso J., Amado C., Arcelus J., Asuero A., Ballaz A., Barba R., Barbagelata C., Barron M., Barron-Andres B., Blanco-Molina A., Beddar Chaib F., Botella E., Castro J., Chasco L., Criado J., de Ancos C., del Toro J., Demelo-Rodriguez P., Diaz-Brasero A., Diaz-Pedroche M., Diaz-Peromingo J., Di Campli M., Dubois-Silva A., Escribano J., Esposito F., Farfan-Sedano A., Fernandez-Capitan C., Fernandez-Reyes J., Fidalgo M., Flores K., Font L., Francisco I., Gabara C., Galeano-Valle F., Garcia M., Garcia-Bragado F., Garcia de Herreros M., de la Garza R., Garcia-Diaz C., Gomez-Cuervo C., Grau E., Guirado L., Gutierrez J., Hernandez-Blasco L., Jara-Palomares L., Jaras M., Jimenez D., Jimenez R., Jimenez-Alfaro C., Joya M., Lainez-Justo S., Lalueza A., Latorre A., Lima J., Lobo J., Lopez-Jimenez L., Lopez-Miguel P., Lopez-Nunez J., Lopez-Reyes R., Lopez-Saez J., Lorenzo A., Madridano O., Maestre A., Marchena P., Martin del Pozo M., Martin-Martos F., Mella C., Mercado M., Moises J., Munoz-Blanco A., Nieto J., Nofuentes-Perez E., Nunez-Fernandez M., Olid-Velilla M., Olivares M., Osorio J., Otalora S., Otero R., Paredes D., Pedrajas J., Porras J., Portillo J., Redondo I., Rodriguez-Matute C., Rosa V., Ruiz-Artacho P., Ruiz-Ruiz J., Salgueiro G., Sanchez-Martinez R., Sanchez-Munoz-Torrero J., Sancho T., Soler S., Suarez-Rodriguez B., Surinach J., Torres M., Torres-Sanchez A., Tolosa C., Trujillo-Santos J., Uresandi F., Valero B., Valle R., Varona J., Vela L., Vela J., Vidal G., Villalobos A., Villares P., Zamora C., Ay C., Nopp S., Pabinger I., Engelen M., Vanassche T., Verhamme P., Maly R., Accassat S., Ait Abdallah N., Bertoletti L., Bura-Riviere A., Catella J., Couturaud F., Crichi B., Debourdeau P., Espitia O., Farge-Bancel D., Grange C., Helfer H., Lacut K., Le Mao R., Mahe I., Morange P., Moustafa F., Poenou G., Sarlon-Bartoli G., Suchon P., Quere I., Braester A., Brenner B., Kenet G., Tzoran I., Basaglia M., Bilora F., Bortoluzzi C., Brandolin B., Ciammaichella M., De Angelis A., Di Micco P., Imbalzano E., Merla S., Pesavento R., Prandoni P., Siniscalchi C., Tufano A., Visona A., Vo Hong N., Zalunardo B., Nishimoto Y., Sato Y., Make K., Skride A., Strautmane S., Fonseca S., Martins F., Meireles J., Bosevski M., Bounameaux H., Mazzolai L., Caprini J., Bui H., Martinez-Urbistondo, D., de la Garza, R. G., Villares-Fernandez, P., Font, C., Schellong, S., Lopez-Nunez, J. J., Gil-Diaz, A., del Carmen Diaz-Pedroche, M., Hirmerova, J., Monreal, M., Adarraga, M., Aibar, J., Alonso, J., Amado, C., Arcelus, J., Asuero, A., Ballaz, A., Barba, R., Barbagelata, C., Barron, M., Barron-Andres, B., Blanco-Molina, A., Beddar Chaib, F., Botella, E., Castro, J., Chasco, L., Criado, J., de Ancos, C., del Toro, J., Demelo-Rodriguez, P., Diaz-Brasero, A., Diaz-Pedroche, M., Diaz-Peromingo, J., Di Campli, M., Dubois-Silva, A., Escribano, J., Esposito, F., Farfan-Sedano, A., Fernandez-Capitan, C., Fernandez-Reyes, J., Fidalgo, M., Flores, K., Font, L., Francisco, I., Gabara, C., Galeano-Valle, F., Garcia, M., Garcia-Bragado, F., Garcia de Herreros, M., de la Garza, R., Garcia-Diaz, C., Gomez-Cuervo, C., Grau, E., Guirado, L., Gutierrez, J., Hernandez-Blasco, L., Jara-Palomares, L., Jaras, M., Jimenez, D., Jimenez, R., Jimenez-Alfaro, C., Joya, M., Lainez-Justo, S., Lalueza, A., Latorre, A., Lima, J., Lobo, J., Lopez-Jimenez, L., Lopez-Miguel, P., Lopez-Nunez, J., Lopez-Reyes, R., Lopez-Saez, J., Lorenzo, A., Madridano, O., Maestre, A., Marchena, P., Martin del Pozo, M., Martin-Martos, F., Mella, C., Mercado, M., Moises, J., Munoz-Blanco, A., Nieto, J., Nofuentes-Perez, E., Nunez-Fernandez, M., Olid-Velilla, M., Olivares, M., Osorio, J., Otalora, S., Otero, R., Paredes, D., Pedrajas, J., Porras, J., Portillo, J., Redondo, I., Rodriguez-Matute, C., Rosa, V., Ruiz-Artacho, P., Ruiz-Ruiz, J., Salgueiro, G., Sanchez-Martinez, R., Sanchez-Munoz-Torrero, J., Sancho, T., Soler, S., Suarez-Rodriguez, B., Surinach, J., Torres, M., Torres-Sanchez, A., Tolosa, C., Trujillo-Santos, J., Uresandi, F., Valero, B., Valle, R., Varona, J., Vela, L., Vela, J., Vidal, G., Villalobos, A., Villares, P., Zamora, C., Ay, C., Nopp, S., Pabinger, I., Engelen, M., Vanassche, T., Verhamme, P., Maly, R., Accassat, S., Ait Abdallah, N., Bertoletti, L., Bura-Riviere, A., Catella, J., Couturaud, F., Crichi, B., Debourdeau, P., Espitia, O., Farge-Bancel, D., Grange, C., Helfer, H., Lacut, K., Le Mao, R., Mahe, I., Morange, P., Moustafa, F., Poenou, G., Sarlon-Bartoli, G., Suchon, P., Quere, I., Braester, A., Brenner, B., Kenet, G., Tzoran, I., Basaglia, M., Bilora, F., Bortoluzzi, C., Brandolin, B., Ciammaichella, M., De Angelis, A., Di Micco, P., Imbalzano, E., Merla, S., Pesavento, R., Prandoni, P., Siniscalchi, C., Tufano, A., Visona, A., Vo Hong, N., Zalunardo, B., Nishimoto, Y., Sato, Y., Make, K., Skride, A., Strautmane, S., Fonseca, S., Martins, F., Meireles, J., Bosevski, M., Bounameaux, H., Mazzolai, L., Caprini, J., and Bui, H.
- Subjects
medicine.medical_specialty ,VTE risk assessment ,Healthy individual ,Elevated liver enzymes ,Hemorrhage ,Gastroenterology ,Liver disease ,Recurrence ,Fibrosis ,Internal medicine ,Internal Medicine ,medicine ,Anticoagulation adverse event ,Humans ,In patient ,Registries ,Clinical VTE ,business.industry ,Liver Diseases ,Anticoagulants ,Venous Thromboembolism ,medicine.disease ,Im - Original ,Non-invasive liver assessment ,Healthy individuals ,Increased risk ,Anticoagulant therapy ,Emergency Medicine ,Anticoagulation adverse events ,business ,Venous thromboembolism ,Major bleeding - Abstract
The association between elevated liver enzymes or FIB-4 (fibrosis index 4) and outcome in patients with venous thromboembolism (VTE) has not been evaluated. Data from patients in RIETE (Registro Informatizado Enfermedad TromboEmbólica) were used to assess the association between elevated liver enzymes or FIB-4 levels and the rates of major bleeding or death in apparent liver disease-free patients with acute VTE under anticoagulation therapy. A total of 6206 patients with acute VTE and without liver disease were included. Of them, 92 patients had major bleeding and 168 died under anticoagulation therapy. On multivariable analysis, patients with elevated liver enzymes were at increased mortality risk (HR: 1.58; 95% CI: 1.10–2.28), while those with FIB-4 levels > 2.67 points were at increased risk for major bleeding (HR: 1.69; 95% CI: 1.04–2.74). Evaluation of liver enzymes and FIB-4 index at baseline in liver disease-free patients with VTE may provide additional information on the risk for major bleeding or death during anticoagulation. Supplementary Information The online version contains supplementary material available at 10.1007/s11739-021-02858-x.
- Published
- 2021
5. Insulin-like growth factor-1 deficiency and metabolic syndrome
- Author
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Aguirre, G. A., primary, De Ita, J. Rodríguez, additional, de la Garza, R. G., additional, and Castilla-Cortazar, I., additional
- Published
- 2016
- Full Text
- View/download PDF
6. Intrauterine Growth Retardation (IUGR) as a Novel Condition of Insulin-Like Growth Factor-1 (IGF-1) Deficiency.
- Author
-
MartÃ-n-Estal, I., de la Garza, R. G., and Castilla-CortÃczar, I.
- Published
- 2016
- Full Text
- View/download PDF
7. Erratum to: Intrauterine Growth Retardation (IUGR) as a Novel Condition of Insulin-Like Growth Factor-1 (IGF-1) Deficiency.
- Author
-
MartÃ-n-Estal, I., de la Garza, R. G., and Castilla-CortÃczar, I.
- Published
- 2016
- Full Text
- View/download PDF
8. IGF-1 modulates gene expression of proteins involved in inflammation, cytoskeleton, and liver architecture.
- Author
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Lara-Diaz VJ, Castilla-Cortazar I, Martín-Estal I, García-Magariño M, Aguirre GA, Puche JE, de la Garza RG, Morales LA, and Muñoz U
- Subjects
- Acute-Phase Proteins genetics, Animals, Cadherins genetics, Cadherins metabolism, Crosses, Genetic, Cytoskeletal Proteins genetics, Cytoskeletal Proteins metabolism, Desmosomes immunology, Desmosomes metabolism, Desmosomes pathology, Extracellular Matrix Proteins genetics, Extracellular Matrix Proteins metabolism, Gene Expression Profiling, Hepatitis immunology, Hepatitis pathology, Hepatitis prevention & control, Injections, Subcutaneous, Insulin-Like Growth Factor I administration & dosage, Insulin-Like Growth Factor I genetics, Insulin-Like Growth Factor I therapeutic use, Lipid Peroxidation, Liver immunology, Liver pathology, Male, Mice, Mice, Transgenic, Oxidative Stress, Receptors, Somatomedin genetics, Tight Junction Proteins genetics, Tight Junction Proteins metabolism, Acute-Phase Proteins metabolism, Gene Expression Regulation, Hepatitis metabolism, Inflammation Mediators metabolism, Insulin-Like Growth Factor I metabolism, Liver metabolism, Receptors, Somatomedin metabolism
- Abstract
Even though the liver synthesizes most of circulating IGF-1, it lacks its receptor under physiological conditions. However, according to previous studies, a damaged liver expresses the receptor. For this reason, herein, we examine hepatic histology and expression of genes encoding proteins of the cytoskeleton, extracellular matrix, and cell-cell molecules and inflammation-related proteins. A partial IGF-1 deficiency murine model was used to investigate IGF-1's effects on liver by comparing wild-type controls, heterozygous igf1
+/- , and heterozygous mice treated with IGF-1 for 10 days. Histology, microarray for mRNA gene expression, RT-qPCR, and lipid peroxidation were assessed. Microarray analyses revealed significant underexpression of igf1 in heterozygous mice compared to control mice, restoring normal liver expression after treatment, which then normalized its circulating levels. IGF-1 receptor mRNA was overexpressed in Hz mice liver, while treated mice displayed a similar expression to that of the controls. Heterozygous mice showed overexpression of several genes encoding proteins related to inflammatory and acute-phase proteins and underexpression or overexpression of genes which coded for extracellular matrix, cytoskeleton, and cell junction components. Histology revealed an altered hepatic architecture. In addition, liver oxidative damage was found increased in the heterozygous group. The mere IGF-1 partial deficiency is associated with relevant alterations of the hepatic architecture and expression of genes involved in cytoskeleton, hepatocyte polarity, cell junctions, and extracellular matrix proteins. Moreover, it induces hepatic expression of the IGF-1 receptor and elevated acute-phase and inflammation mediators, which all resulted in liver oxidative damage.- Published
- 2017
- Full Text
- View/download PDF
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