Publications by authors named "Julia Mota"

Article Synopsis
  • Anastomotic pseudoaneurysms of interposition vein grafts are rare but serious complications in vascular surgery, particularly concerning the carotid arteries, requiring urgent intervention to avoid critical issues like rupture and thromboembolism.
  • A case report details a 49-year-old male who developed a false aneurysm after a carotid surgery complication and successfully underwent open surgical repair involving the removal of the affected graft and reconstruction using a vein graft from the subclavian artery.
  • The conclusion emphasizes that while endovascular techniques exist, open surgical repair remains the standard treatment for these pseudoaneurysms due to its ability to effectively address infection and ensure better long-term outcomes, suggesting that further research should continue to refine surgical strategies.
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Chagas disease, the parasitic infection caused by , afflicts about 6 million people in Latin America. Here, we investigated the hypothesis that may fuel heart parasitism by activating B1R, a G protein-coupled (brady) kinin receptor whose expression is upregulated in inflamed tissues. Studies in WT and B1R mice showed that DNA levels (15 days post infection-dpi) were sharply reduced in the transgenic heart.

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IFN-γ-producing γδ T cells have been suggested to play an important role in protection against infection with Trypanosoma cruzi. However, little is known about the mechanisms leading to functional differentiation of this T cell subset in this model. In the current work, we investigated the possibility that the IL-18/MyD88 pathway is central for the generation of effector γδ T cells, playing a role for resistance against infection.

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Article Synopsis
  • TCTs from Chagas disease can trigger inflammation and microvascular leakage through the activation of innate immune cells via TLR2 and subsequent immune pathways.
  • The study reveals that mast cells (MCs) play a crucial role in this inflammatory response, particularly through the activation of the kallikrein-kinin system (KKS), leading to increased bradykinin levels.
  • In experiments with mice, it was found that MCs are essential for controlling the parasite load in the heart, suggesting that MC interactions with the KKS are vital for regulating inflammation during Chagas disease.
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