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Introduction: The reported gross and histopathologic changes in the placenta associated with SARS-CoV-2 infection are heterogeneous. We sought to summarize placental histopathologic findings from pregnancies affected by SARS-CoV-2 infection according to timing of infection and symptom severity.

Methods: We conducted a retrospective cohort study of patients with SARS-CoV-2 infection during pregnancy who had deliveries at Mayo Clinic, Rochester, Minnesota, from April 2020 through June 2021.

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Backgrounds: Many pregnant women suffer from more than one pregnancy complication. However, whether those women experienced a higher risk of adverse birth outcomes is unclear. This study aims to assess the association between the comorbidity of gestational diabetes mellitus (GDM) and hypertension disorders of pregnancy (HDP) and adverse birth outcomes.

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Individuals who are at risk of not achieving a full milk supply are often overlooked in scientific literature. There is available guidance to help establish an adequate milk supply for healthy individuals experiencing a physiologic labor and birth, and there are robust recommendations for the lactating parents of small, sick, and preterm newborns to ensure that these newborns can receive human milk. Missing from the literature are clinical practice guidelines that address the preexisting health, pregnancy, birth, or newborn-related risk factors for suboptimal lactation.

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Placental trophoblasts constitute the interface between the fetal and maternal environments and physically prevent maternal-fetal viral transmission. However, congenital human cytomegalovirus (HCMV) infection in the early stages of pregnancy results in severe symptoms in the fetus. HCMV is the most common causative agent of intrauterine infection.

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use multiple mechanisms to disseminate from the intestinal lamina propria to the mesenteric lymph nodes.

Microbiol Spectr

December 2024

Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky, USA.

Unlabelled: are facultative intracellular bacterial pathogens that cause foodborne disease in humans. The bacteria can use the surface protein InlA to invade intestinal epithelial cells or transcytose across M cells in the gut, but it is not well understood how the bacteria traffic from the underlying lamina propria to the draining mesenteric lymph nodes (MLN). Previous studies indicated that associated with both monocytes and dendritic cells in the intestinal lamina propria.

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