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49 results on '"Garcia, Fernando"'

1. IFN‐γ stimulates Paneth cell secretion through necroptosis mTORC1 dependent

Author

Encarnacion‐Garcia, Maria R., primary, De la Torre‐Baez, Raúl, additional, Hernandez‐Cueto, María A., additional, Velázquez‐Villegas, Laura A., additional, Candelario‐Martinez, Aurora, additional, Sánchez‐Argáez, Ana Beatriz, additional, Horta‐López, Perla H., additional, Montoya‐García, Armando, additional, Jaimes‐Ortega, Gustavo Alberto, additional, Lopez‐Bailon, Luis, additional, Piedra‐Quintero, Zayda, additional, Carrasco‐Torres, Gabriela, additional, De Ita, Marlon, additional, Figueroa‐Corona, María del Pilar, additional, Muñoz‐Medina, José Esteban, additional, Sánchez‐Uribe, Magdalena, additional, Ortiz‐Fernández, Arturo, additional, Meraz‐Ríos, Marco Antonio, additional, Silva‐Olivares, Angélica, additional, Betanzos, Abigail, additional, Baay‐Guzman, Guillermina Juliana, additional, Navarro‐Garcia, Fernando, additional, Villa‐Treviño, Saúl, additional, Garcia‐Sierra, Francisco, additional, Cisneros, Bulmaro, additional, Schnoor, Michael, additional, Ortíz‐Navarrete, Vianney F., additional, Villegas‐Sepúlveda, Nicolás, additional, Valle‐Rios, Ricardo, additional, Medina‐Contreras, Oscar, additional, Noriega, Lilia G., additional, and Nava, Porfirio, additional

Published
2024
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7. Top 10 public health challenges to track in 2023: Shifting focus beyond a global pandemic

Author

Lucero‐Prisno, Don Eliseo, primary, Shomuyiwa, Deborah Oluwaseun, additional, Kouwenhoven, M. B. N., additional, Dorji, Thinley, additional, Odey, Goodness Ogeyi, additional, Miranda, Adriana Viola, additional, Ogunkola, Isaac Olushola, additional, Adebisi, Yusuff Adebayo, additional, Huang, Junjie, additional, Xu, Lin, additional, Obnial, Joseph Christian, additional, Huda, Aminath, additional, Thepanondh, Sarawut, additional, Dayrit, Manuel Millar, additional, Evardone, Salvador B., additional, Lamawansa, M. D., additional, Solomon Ethiopia, Samrawit, additional, Aziato, Lydia, additional, Adongo, Philip Baba, additional, Samai, Mohamed Hindolo, additional, Garcia, Fernando B., additional, Villaruz, Joselito F., additional, Karunathilake, Indika Mahesh, additional, Li, Hao, additional, Azanza, Patrick Alain, additional, Findlay, Ian, additional, and Wong, Martin C. S., additional

Published
2023
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9. A Molecular Mechanism Underlying Genotype-Specific Intrahepatic Cholestasis Resulting From MYO5B Mutations

Author

Overeem, Arend W., Li, Qinghong, Qiu, Yi-Ling, Cartón-Garcia, Fernando, Leng, Changsen, Klappe, Karin, Dronkers, Just, Hsiao, Nai-Hua, Wang, Jian-She, Arango, Diego, van Ijzendoorn, Sven C. D., Universitat Autònoma de Barcelona, Center for Liver, Digestive and Metabolic Diseases (CLDM), and Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI)

Subjects
0301 basic medicine, Genotype, Endosome, Mutant, Myosin Type V, Cholestasis, Intrahepatic, medicine.disease_cause, Pediatrics, Frameshift mutation, 03 medical and health sciences, 0302 clinical medicine, Tumor Cells, Cultured, medicine, Genetics, Missense mutation, Humans, FAILURE, TRAFFICKING, RAB11A, Mutation, MYO5B protein, Human, Myosin Heavy Chains, Hepatology, Chemistry, MYOSIN VB, Progressive familial intrahepatic cholestasis, MICROVILLUS INCLUSION DISEASE, Cholestasis, Progressive familial intrahepatic, Original Articles, medicine.disease, Protein subcellular localization prediction, TRANSPORT, EXPORT, Cell biology, 030104 developmental biology, Lipid metabolism, Metabolism, 030211 gastroenterology & hepatology, Original Article
Abstract

Altres ajuts: Supported by grants from the Nederlandse vereniging voor Gastroenterologie (to S. I. J.) and the Natural Science Foundation of China, Nos. 81873543 and 81570468 (to J. S. W.). Progressive familial intrahepatic cholestasis (PFIC) 6 has been associated with missense but not biallelic nonsense or frameshift mutations in MYO5B, encoding the motor protein myosin Vb (myoVb). This genotype-phenotype correlation and the mechanism through which MYO5B mutations give rise to PFIC are not understood. The aim of this study was to determine whether the loss of myoVb or expression of patient-specific myoVb mutants can be causally related to defects in canalicular protein localization and, if so, through which mechanism. We demonstrate that the cholestasis-associated substitution of the proline at amino acid position 600 in the myoVb protein to a leucine (P660L) caused the intracellular accumulation of bile canalicular proteins in vesicular compartments. Remarkably, the knockout of MYO5B in vitro and in vivo produced no canalicular localization defects. In contrast, the expression of myoVb mutants consisting of only the tail domain phenocopied the effects of the Myo5b-P660L mutation. Using additional myoVb and rab11a mutants, we demonstrate that motor domain-deficient myoVb inhibited the formation of specialized apical recycling endosomes and that its disrupting effect on the localization of canalicular proteins was dependent on its interaction with active rab11a and occurred at the trans -Golgi Network/recycling endosome interface. Our results reveal a mechanism through which MYO5B motor domain mutations can cause the mislocalization of canalicular proteins in hepatocytes which, unexpectedly, does not involve myoVb loss-of-function but, as we propose, a rab11a-mediated gain-of-toxic function. The results explain why biallelic MYO5B mutations that affect the motor domain but not those that eliminate myoVb expression are associated with PFIC6.

Published
2020

11. Assessment of nitrogen diagnosis methods in sunflower

Author

Tovar Hernandez, Sergio, primary, Diovisalvi, Natalia, additional, Carciochi, Walter Daniel, additional, Izquierdo, Natalia, additional, Sainz Rozas, Hernán, additional, Garcia, Fernando, additional, and Reussi Calvo, Nahuel I., additional

Published
2021
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13. Predicting soil test phosphorus decrease in non‐P‐fertilized conditions

Author

Appelhans, Stefania C., primary, Carciochi, Walter D., additional, Correndo, Adrian, additional, Gutierrez Boem, Flavio H., additional, Salvagiotti, Fernando, additional, Garcia, Fernando O., additional, Melchiori, Ricardo J.M., additional, Barbagelata, Pedro A., additional, Ventimiglia, Luis A., additional, Ferraris, Gustavo N., additional, Vivas, Hugo S., additional, Caviglia, Octavio P., additional, and Ciampitti, Ignacio A., additional

Published
2020
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16. Normal and pathological neuronal distribution of the human mesencephalic locomotor region

Author

Sébille, Sophie B., primary, Rolland, Anne‐Sophie, additional, Faillot, Matthieu, additional, Perez‐Garcia, Fernando, additional, Colomb‐Clerc, Antoine, additional, Lau, Brian, additional, Dumas, Sylvie, additional, Vidal, Sara Fernandez, additional, Welter, Marie‐Laure, additional, Francois, Chantal, additional, Bardinet, Eric, additional, and Karachi, Carine, additional

Published
2018
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19. Eradication of common mynasAcridotheres tristisfrom Denis Island, Seychelles

Author

Feare, Chris J, primary, van der Woude, Jildou, additional, Greenwell, Phill, additional, Edwards, Hannah A, additional, Taylor, Jenni A, additional, Larose, Christine S, additional, Ahlen, Per-Arne, additional, West, Jack, additional, Chadwick, Will, additional, Pandey, Smita, additional, Raines, Katherine, additional, Garcia, Fernando, additional, Komdeur, Jan, additional, and de Groene, Arjan, additional

Published
2016
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22. Evaluation of the interaction between sodium hypochlorite and several formulations containing chlorhexidine and its effect on the radicular dentin-SEM and push-out bond strength analysis

Author

Graziele Magro, Miriam, primary, Carlos Kuga, Milton, additional, Regina Victorino, Keli, additional, Antonio Vázquez-Garcia, Fernando, additional, Javier Aranda-Garcia, Arturo, additional, Batista Faria-Junior, Norberto, additional, Faria, Gisele, additional, and Luis Shinohara, André, additional

Published
2013
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46. Activation of rat synovium by iron

Author

Sousa, Maria De, primary, Dynesius-Trentham, Roselynn, additional, Mota-Garcia, Fernando, additional, Silva, Manuel Teixeira Da, additional, and Trentham, David E., additional

Published
1988
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48. Invasive breast carcinomas with ATM gene variants of uncertain significance share distinct histopathologic features.

Author

Abdulrahman AA, Heintzelman RC, Corbman M, and Garcia FU

Subjects
Adult, Aged, Breast Neoplasms, Male genetics, Breast Neoplasms, Male pathology, Female, Genetic Variation, Humans, Lymphocytes, Tumor-Infiltrating pathology, Male, Middle Aged, Ataxia Telangiectasia Mutated Proteins genetics, Breast Neoplasms genetics, Breast Neoplasms pathology
Abstract

The increasing availability of next-generation sequencing for clinical research dramatically improved our understanding of breast cancer genetics and resulted in detection of new mutation variants. Cancer risk data relating to some of these variants are insufficient, prompting the designation of variants of uncertain significance (VUS). The histopathologic characteristics of these variants have not been previously described. We propose to depict these characteristics and determine if invasive carcinomas with similar VUS genes share similar histomorphologic features. In total, 28 invasive breast cancers with VUS were retrospectively identified. Tumor sections were reviewed and a predefined set of histopathologic characteristics were documented and compared. Nine of the 28 cases were variants in the ATM gene and were found to share similar histologic characteristics; all had tumor cells with low nuclear grade, absent tumor infiltrating lymphocytes, as well as a marked desmoplastic response. A subset of the above findings were identified in variants of other genes but none had all findings collectively. Furthermore, variants of ATM gene had smaller tumor size, lower pathologic T stage at presentation, and more favorable surrogate molecular subtype compared to variants of other genes. These findings could potentially be used to reclassify VUS and predict which patients may harbor ATM mutations, and hence could have implications in triaging toward ATM variant identification for potential future targeted therapy., (© 2017 Wiley Periodicals, Inc.)

Published
2018
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49. Nodular myofibroblastic stromal hyperplasia of the mammary gland as an accurate name for pseudoangiomatous stromal hyperplasia of the mammary gland.

Author

Leon ME, Leon MA, Ahuja J, and Garcia FU

Subjects
Adolescent, Diagnosis, Differential, Female, Humans, Hyperplasia, Middle Aged, Terminology as Topic, Breast cytology, Breast Diseases classification, Breast Diseases pathology, Hemangiosarcoma pathology, Neoplasms, Muscle Tissue pathology, Stromal Cells pathology
Abstract

Pseudoangiomatous stromal hyperplasia (PASH) of the mammary gland is a well-known benign localized form of stromal overgrowth with probable hormonal etiology. We describe the histologic findings and immunohistochemistry of two cases. Two women, 16 and 58 years old, presented with a breast mass and underwent surgical excision. Grossly, they consisted of a well-circumscribed, rubbery tissue with a solid white-tan homogeneous cut surface. One of the cases showed focal cystic areas. Histologically the lesion showed a proliferation of the collagenous stroma with varying degrees of density, and hyalinization with many pseudovascular slit-like anastomosing spaces lined by spindle cells with scant cytoplasm and bland chromatin. The spindle cells lining the spaces were strongly reactive for vimentin and weakly reactive for CD34, actin, and desmin. They were negative for factor VIII, S-100, and pankeratin. In PASH, the "pseudoangiomatous" term describes a recognizable pattern but does not describe the tumor's histologic nature. We propose the name nodular myofibroblastic hyperplasia of the mammary stroma as a more accurate name.

Published
2002
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