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101.
Kathleen E. Sullivan Hamid Bassiri Ahmed A. Bousfiha Beatriz T. Costa-Carvalho Alexandra F. Freeman David Hagin Yu L. Lau Michail S. Lionakis Ileana Moreira Jorge A. Pinto M. Isabel de Moraes-Pinto Amit Rawat Shereen M. Reda Saul Oswaldo Lugo Reyes Mikko Seppänen Mimi L. K. Tang 《Journal of clinical immunology》2017,37(7):693-694
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Beatriz Febrero Antonio Ríos Jose Manuel Rodríguez Belén Ferri Luis Polo Pascual Parrilla 《Endocrine pathology》2012,23(4):260-263
Crohn??s disease is one of the causes of secondary amyloidosis, which can lead to amyloid infiltration of the thyroid gland. It is essential to follow strict controls to prevent the appearance of a large amyloid goiter. Two patients with amyloid goiter secondary to Crohn??s disease, with a large adipose tissue component and who required surgical treatment, were studied. Both surgical interventions were difficult because of the fragility of the thyroid tissue. A patient with Crohn??s disease and secondary amyloidosis could begin to develop amyloid goiter. This is usually fast growing and commonly causes compressive symptoms, although in some cases it only grows in the neck with no evidence of these symptoms. When surgery is indicated, patients should be remitted to hospitals with experienced endocrine surgeons, given that there is a high risk of developing complications. 相似文献
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Aniel J. L. Brambila-Tapia Jorge I. G��mez-Nava Laura Gonz��lez-L��pez Lucila Sandoval-Ram��rez Julio Med��na-D��az Montserrat Maldonado Sergio R. Gutierrez-Ure?a Gloria Mart��nez-Bonilla Beatriz T. Mart��n-M��rquez M��nica V��zquez del Mercado Arnulfo Nava-Zavala Jos�� F. Mu?oz-Valle Mario Salazar-P��ramo Ingrid P. D��valos-Rodr��guez 《Rheumatology international》2011,31(8):1065-1068
The objective of this study is to establish whether there is an association between the presence of FCGR3A V(176) polymorphism with SLE or its manifestations. We included 94 patients according to the 1982 ACR criteria as well as 98 controls matched by age and gender. The 11 ACR diagnostic criteria were analyzed on the clinical files. The polymorphism FCGR3A V(176) was determined by direct sequencing. There was not an association between the polymorphism FCGR3A V(176) with SLE or its main manifestations. The allelic frequency for F(176) was: 0.80 and 0.72 in cases and controls, respectively (P?=?0.09, IC95%: 0.42?C1.07); and the genotypic frequency in the group of cases was: 0.65 for homozygotes F(176)/F(176), 0.30 for heterozygotes and 0.05 for the homozygotes V(176)/V(176), while for the control group it was 0.53, 0.39 and 0.08, respectively. The polymorphism FCGR3A V(176) is not associated with SLE or any of its manifestations in patients with SLE from the West of Mexico. 相似文献
105.
Melatonin enhances neural stem cell differentiation and engraftment by increasing mitochondrial function
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Miguel Mendivil‐Perez Viviana Soto‐Mercado Ana Guerra‐Librero Beatriz I. Fernandez‐Gil Javier Florido Ying‐Qiang Shen Miguel A. Tejada Vivian Capilla‐Gonzalez Iryna Rusanova José M. Garcia‐Verdugo Darío Acuña‐Castroviejo Luis Carlos López Carlos Velez‐Pardo Marlene Jimenez‐Del‐Rio José M. Ferrer Germaine Escames 《Journal of pineal research》2017,63(2)
Neural stem cells (NSCs) are regarded as a promising therapeutic approach to protecting and restoring damaged neurons in neurodegenerative diseases (NDs) such as Parkinson's disease and Alzheimer's disease (PD and AD, respectively). However, new research suggests that NSC differentiation is required to make this strategy effective. Several studies have demonstrated that melatonin increases mature neuronal markers, which reflects NSC differentiation into neurons. Nevertheless, the possible involvement of mitochondria in the effects of melatonin during NSC differentiation has not yet been fully established. We therefore tested the impact of melatonin on NSC proliferation and differentiation in an attempt to determine whether these actions depend on modulating mitochondrial activity. We measured proliferation and differentiation markers, mitochondrial structural and functional parameters as well as oxidative stress indicators and also evaluated cell transplant engraftment. This enabled us to show that melatonin (25 μM) induces NSC differentiation into oligodendrocytes and neurons. These effects depend on increased mitochondrial mass/DNA/complexes, mitochondrial respiration, and membrane potential as well as ATP synthesis in NSCs. It is also interesting to note that melatonin prevented oxidative stress caused by high levels of mitochondrial activity. Finally, we found that melatonin enriches NSC engraftment in the ND mouse model following transplantation. We concluded that a combined therapy involving transplantation of NSCs pretreated with pharmacological doses of melatonin could efficiently restore neuronal cell populations in PD and AD mouse models depending on mitochondrial activity promotion. 相似文献
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Laura Pérez-Egido María Antonia García-Casillas Isabel Simal María Fanjul Agustin Cañizo Julio A. Cerdá Beatriz Fernandez Manuel de la Torre Javier Ordoñez Juan Carlos de Agustin 《Journal of pediatric surgery》2019,54(4):693-695