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排序方式: 共有196条查询结果,搜索用时 15 毫秒
51.
Jiménez Adriana Organista-Juárez Diana Torres-Castro Areli Guzmán-Ruíz Mara A. Estudillo Enrique Guevara-Guzmán Rosalinda 《Neurochemical research》2020,45(8):1781-1790
Neurochemical Research - Type 2 diabetes (T2D) is associated with cognitive decline and dementia. Both neurodegenerative conditions are characterized by olfactory dysfunction (OD) which is also... 相似文献
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Coronary (CAD) and peripheral (PAD) artery diseases are major causes of morbidity and mortality, and millions of CAD and PAD patients are treated by various medications, bypass surgery or angioplasty around the world. Such patients might benefit from novel stem cells and tissue engineering strategies aimed at accelerating natural processes of postnatal collateral vessel formation and repairing damaged tissues. By combining three fundamental “tools”, namely stem cells, biomaterials and growth factors (GFs), such strategies may enhance the efficacy of cell therapy in several ways: (a) by supplying exogenous stem cells or GFs that stimulate resident cardiac stem cell (CSC) migration, engraftment and commitment to cardiomyocytes, and that induce and modulate arterial response to ischemia; (b) by supporting the maintenance of GFs and transplanted stem cells in the damaged tissues through the use of biocompatible and biodegradable polymers for a period of time sufficient to allow histological and anatomical restoration of the damaged tissue. This review will discuss the potential of combining stem cells and new delivery systems for growth factors, such as vehicle-based delivery strategies or cell-based gene therapy, to facilitate regeneration of ischemic tissues. These approaches would promote the ability of resident CSCs or of exogenous multipotent stem cells such as adipose tissue-derived mesenchymal stem cells (AT-MSCs) to induce the healing of damaged tissue, by recruiting and directing these cells into the damage area and by improving angiogenesis and reperfusion of ischemic tissues. 相似文献
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Thomas DL Doty R Tosic V Liu J Kranz DM McFadden G Macneill AL Roy EJ 《Cancer immunology, immunotherapy : CII》2011,60(10):1461-1472
Adoptive transfer of tumor-specific T cells has shown some success for treating metastatic melanoma. We evaluated a novel
strategy to improve adoptive therapy by administering both T cells and oncolytic myxoma virus to mice with syngeneic B16.SIY
melanoma brain tumors. Adoptive transfer of activated CD8+ 2C T cells that recognize SIY peptide doubled survival time, but SIY-negative tumors recurred. Myxoma virus killed B16.SIY
cells in vitro, and intratumoral injection of virus led to selective and transient infection of the tumor. Virus treatment
recruited innate immune cells to the tumor and induced IFNβ production in the brain, resulting in limited oncolytic effects
in vivo. To counter this, we evaluated the safety and efficacy of co-administering 2C T cells, myxoma virus, and either rapamycin
or neutralizing antibodies against IFNβ. Mice that received either triple combination therapy survived significantly longer
with no apparent side effects, but eventually relapsed. Importantly, rapamycin treatment did not impair T cell-mediated tumor
destruction, supporting the feasibility of combining adoptive immunotherapy and rapamycin-enhanced virotherapy. Myxoma virus
may be a useful vector for transient delivery of therapeutic genes to a tumor to enhance T cell responses. 相似文献
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Silvana Morello Rosalinda Sorrentino Amalia Porta Giovanni Forte Ada Popolo Antonello Petrella Aldo Pinto 《Journal of cellular physiology》2009,221(2):378-386
Apoptosis is an endogenous process that can be a useful anti-cancer tool. This study aimed to investigate the effect of Cl-IB-MECA, adenosine receptor A3 agonist, on TRAIL-induced apoptosis of thyroid carcinoma cells. Cl-IB-MECA enhanced TRAIL-mediated apoptosis in FRO but not in ARO cells. This effect was correlated to higher expression levels of DR5 on FRO than ARO cells, that instead presented higher levels of decoy receptors, DcR1 and DcR2. To understand the cross-talk between the effect of Cl-IB-MECA and TRAIL, we evaluated the nuclear translocation of p65 and c-Rel. Since the dependency by NF-κB, TRAIL promoted the nuclear translocation of both p65 and c-Rel subunits. However, the addition of Cl-IB-MECA led to the predominant translocation of c-Rel after TRAIL addition. Furthermore, Bcl-2, cFLIP and pAkt were lower induced than caspase-3 and -9 in FRO cells. To discriminate a specific effect of TRAIL, we used tumour necrosis factor-alpha (TNF-α) with Cl-IB-MECA. In this case, no synergism was observed. In addition, the effect of Cl-IB-MECA was not A3 receptor-dependent since its antagonists, MRS1191 and FA385, failed to block Cl-IB-MECA activity on TRAIL-treated FRO cells. In conclusion, Cl-IB-MECA enhanced TRAIL-mediated apoptosis via NF-κB/c-Rel activation and DR5-dependent manner. This study may shed light on a potential drug cocktail that may prove useful as anti-cancer in an in vivo animal model. J. Cell. Physiol. 221: 378–386, 2009. © 2009 Wiley-Liss, Inc. 相似文献
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Amelia Escolano Sara Martínez‐Martínez Arántzazu Alfranca Katia Urso Helena M Izquierdo Mario Delgado Francisco Martín Guadalupe Sabio David Sancho Pablo Gómez‐del Arco Juan Miguel Redondo 《The EMBO journal》2014,33(10):1117-1133
Macrophages contribute to tissue homeostasis and influence inflammatory responses by modulating their phenotype in response to the local environment. Understanding the molecular mechanisms governing this plasticity would open new avenues for the treatment for inflammatory disorders. We show that deletion of calcineurin (CN) or its inhibition with LxVP peptide in macrophages induces an anti‐inflammatory population that confers resistance to arthritis and contact hypersensitivity. Transfer of CN‐targeted macrophages or direct injection of LxVP‐encoding lentivirus has anti‐inflammatory effects in these models. Specific CN targeting in macrophages induces p38 MAPK activity by downregulating MKP‐1 expression. However, pharmacological CN inhibition with cyclosporin A (CsA) or FK506 did not reproduce these effects and failed to induce p38 activity. The CN‐inhibitory peptide VIVIT also failed to reproduce the effects of LxVP. p38 inhibition prevented the anti‐inflammatory phenotype of CN‐targeted macrophages, and mice with defective p38‐activation were resistant to the anti‐inflammatory effect of LxVP. Our results identify a key role for CN and p38 in the modulation of macrophage phenotype and suggest an alternative treatment for inflammation based on redirecting macrophages toward an anti‐inflammatory status. 相似文献
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Teresa Villarreal-Molina Carlos Posadas-Romero Sandra Romero-Hidalgo Erika Antúnez-Argüelles Araceli Bautista-Grande Gilberto Vargas-Alarcón Eric Kimura-Hayama Samuel Canizales-Quinteros Juan Gabriel Juárez-Rojas Rosalinda Posadas-Sánchez Guillermo Cardoso-Salda?a Aída Medina-Urrutia María del Carmen González-Salazar Rocío Martínez-Alvarado Esteban Jorge-Galarza Alessandra Carnevale 《PloS one》2012,7(11)