Publications by authors named "Armando Burgos"

Article Synopsis
  • Rhesus macaques naturally develop colorectal cancers (CRC) that closely resemble human CRC in terms of histology, progression, and genetic characteristics, making them valuable for studying cancer immunotherapy.
  • Detailed analyses, including advanced imaging and molecular techniques like DNA sequencing and transcriptomics, confirmed similarities in mutation patterns and functional behaviors between macaque and human CRCs, particularly highlighting MLH1 loss and microsatellite instability.
  • The research also indicated a significant presence of DNA hypermethylation, particularly affecting MLH1, contributing to alterations in DNA topology that may impact transcription factor binding, showcasing the complex molecular landscape of CRC in these primates.
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The four dengue virus serotypes co-circulate globally and cause significant human disease. Dengue vaccine development is challenging because some virus-specific antibodies are protective, while others are implicated in enhanced viral replication and more severe disease. Current dengue tetravalent vaccines contain four live attenuated serotypes formulated to theoretically induce balanced protective immunity.

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The link between CD4 T and B cells during immune responses to DENV and ZIKV and their roles in cross-protection during heterologous infection is an active area of research. Here we used CD4 lymphocyte depletions to dissect the impact of cellular immunity on humoral responses during a tertiary flavivirus infection in macaques. We show that CD4 depletion in DENV/ZIKV-primed animals followed by DENV resulted in dysregulated adaptive immune responses.

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Due to their phylogenetic proximity to humans, nonhuman primates (NHPs) are considered an adequate choice for a basic and preclinical model of sepsis. Gram-negative bacteria are the primary causative of sepsis. During infection, bacteria continuously release the potent toxin lipopolysaccharide (LPS) into the bloodstream, which triggers an uncontrolled systemic inflammatory response leading to death.

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Objective: We hypothesized that autophagy-related genes will be differentially expressed in periodontitis, suggesting an impaired gingival autophagic response associated with disease.

Background: Autophagy is a cellular physiologic mechanism to maintain tissue homeostasis, while deficient autophagic responses increase inflammation and susceptibility to infection.

Methods: Rhesus monkeys [<3 years to 23 years of age (n = 34)] were examined for periodontal health and naturally occurring periodontitis.

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Background: Neuropeptides (NPs) are innate pivotal regulators of the immunoinflammatory response. Nevertheless, their role in the pathogenesis of periodontal disease remains unknown. Changes in gene expression of 10 NPs and 16 NP receptors (NPRs) coincident with the initiation, progression, and resolution of periodontitis were determined.

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Aim: Variations in the expression of cytokines during the progression of periodontitis remain ill-defined. We evaluated the expression of 19 cytokine genes related to T-cell phenotype/function during initiation, progression and resolution of periodontitis, and related these to the expression of soft and bone tissue destruction genes (TDGs).

Materials And Methods: A ligature-induced periodontitis model was used in rhesus monkeys (M.

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