Publications by authors named "Nicole Banko"

Adverse birth outcomes are common in HIV-positive pregnant women receiving combination antiretroviral therapy (cART), especially when cART is initiated in early pregnancy. The mechanisms remain poorly understood. Using a mouse model we demonstrate that protease inhibitor based-cART exposure beginning on day 1 of pregnancy was associated with a pro-angiogenic/pro-branching shift in the placenta driven by lower Flt-1 levels and higher Gcm-1 expression.

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Background: It has been reported that pregnant women receiving protease inhibitor (PI)-based combination antiretroviral therapy (cART) have lower levels of progesterone, which put them at risk of adverse birth outcomes, such as low birth weight. We sought to understand the mechanisms involved in this decline in progesterone level.

Methods: We assessed plasma levels of progesterone, prolactin, and lipids and placental expression of genes involved in progesterone metabolism in 42 human immunodeficiency virus (HIV)-infected and 31 HIV-uninfected pregnant women.

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Article Synopsis
  • - The study investigates the role of glycogen synthase kinase (GSK)-3α and GSK-3β in atherosclerosis using LDLR(-/-) mice and examines the effects of deleting these genes in liver and myeloid cells while on a high-fat diet.
  • - Results showed that deleting GSK3α in myeloid cells reduced atherosclerotic lesion size and complexity, while deletion of GSK3β had no significant impact.
  • - The findings indicate that GSK3α promotes M1 macrophage polarization associated with inflammation; its loss leads to a shift towards an M2 macrophage phenotype, which is less inflammatory and may slow atherosclerosis progression.
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Studies have implicated signaling through glycogen synthase kinase (GSK) 3α/β in the activation of pro-atherogenic pathways and the accelerated development of atherosclerosis. By using a mouse model, we examined the role of GSK3α in the development and progression of accelerated atherosclerosis. We crossed Gsk3a/GSK3α-knockout mice with low-density lipoprotein receptor (Ldlr) knockout mice.

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Atherosclerosis is a disease of the large arteries and a major underlying cause of myocardial infarction and stroke. Several different mouse models have been developed to facilitate the study of the molecular and cellular pathophysiology of this disease. In this manuscript we describe specific techniques for the quantification and characterization of atherosclerotic lesions in the murine aortic sinus and ascending aorta.

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