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Your search keyword '"Capatina, Nadejda"' showing total 3 results
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3 results on '"Capatina, Nadejda"'

1. Meta-analyses in cholestatic pregnancy: The outstanding clinical questions.

Author

Capatina, Nadejda and Ovadia, Caroline

Subjects
*PREMATURE infants, *BILE acids, *DISEASE management, *META-analysis, *PERINATAL death, *SEVERITY of illness index, *PREGNANCY complications, *CHOLESTASIS
Abstract

Reports of adverse pregnancy outcomes associated with maternal pruritus and liver impairment have circulated since the 1800s, yet the precise diagnosis and management of intrahepatic cholestasis of pregnancy have varied markedly. Recent evidence, including that from individual participant data meta-analyses, has provided an evidence that brings us closer to standardised, and optimal, management of the condition. Based upon increased adverse perinatal outcomes with higher bile acid concentrations, disease management should be according to severity (defined by peak bile acid concentration) in order to recommend appropriate gestation of birth. Similarly, the reduced spontaneous preterm birth rate for patients receiving ursodeoxycholic acid treatment suggests potential benefit for the treatment of patients with moderate-severe disease. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Elevated homocysteine activates unfolded protein responses and causes aberrant trophoblast differentiation and mouse blastocyst development

Author

Capatina, Nadejda, Burton, Graham J, Yung, Hong Wa, Yung, Hong Wa [0000-0002-0869-7426], and Apollo - University of Cambridge Repository

Subjects
placenta, Physiology, Vitamins, unfolded protein response, Trophoblasts, Mice, Blastocyst, Folic Acid, Physiology (medical), endoplasmic reticulum stress, Animals, Humans, Female, pregnancy, trophoblast stem cells, ORIGINAL ARTICLES, hyperhomocysteinemia, Homocysteine, ORIGINAL ARTICLE
Abstract

Funder: Centre for Trophoblast Research PhD studentship, Hyperhomocysteinemia may arise from folate/vitamin B12 deficiency, genetic polymorphisms, kidney disease, or hypothyroidism. It is associated with an increased risk of early pregnancy loss and placenta-related complications of pregnancy, including pre-eclampsia and fetal growth restriction. While the majority of studies of hyperhomocysteinemia focus on epigenetic changes secondary to metabolic disruption, the effects of homocysteine toxicity on placental development remain unexplored. Here, we investigated the influence of hyperhomocysteinemia on early blastocyst development and trophoblast differentiation. Exposure of cultured blastocysts to high homocysteine levels reduces cell number in the trophectoderm layer, most likely through increased apoptosis. Homocysteine also promotes differentiation of a trophoblast stem cell line. Both effects diminish the stem cell pool, and are mediated in an endoplasmic reticulum (ER) unfolded protein response (UPRER )-dependent manner. Targeted alleviation of UPRER may therefore provide a new therapeutic intervention to improve pregnancy outcome in women with hyperhomocysteinemia.

Published
2022
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