Acute kidney injury that occurs during pregnancy or in the post-partum period (PR-AKI) is a serious obstetric complication with risk of significant associated maternal and fetal morbidity and mortality. Recent data indicates that the incidence of PR-AKI is increasing, although accurate calculation is limited by the lack of a uniform diagnostic criteria that is validated in pregnancy. Hypertensive and thrombotic microangiopathic disorders of pregnancy have been identified as major contributors to the burden of PR-AKI. As is now accepted regarding preeclampsia, HELLP syndrome and atypical hemolytic uremic syndrome, it is believed that PR-AKI may have long-term renal, cardiovascular and neurocognitive consequences that persist beyond the post-partum period. Further research regarding PR-AKI could be advanced by the development of a pregnancy-specific validated definition and classification system; and the establishment of refined animal models that would allow researchers to further elucidate the mechanisms and sequelae of the disorder.
Anxiety during pregnancy is associated with adverse outcomes in mothers and infants. Unfortunately, as anxiety is often synonymously mentioned with depression, the studies focusing solely on anxiety during pregnancy are not as robust as those in the field of depression are. In this work, we provide an overview of what is currently known about general anxiety during pregnancy, pregnancy-related anxiety and the potential impacts anxiety could have on post-partum care. An overview of potential risk factors, post-partum maternal outcomes, infant outcome along with pharmacological and nonpharmacological treatments are covered with a specific focus on high-risk pregnancies. Although anxiety during pregnancy is normative; anxiety can become problematic and negatively impact upon behavior, resulting in potential harm to the mother, as well as her developing fetus or child (ren) at home. The clinical diagnosis for anxiety and conditions associated with anxiety often require lengths of time that are not applicable for the pregnant patient, which has led to diagnosis and terms such as pregnancy-related anxiety. Importantly, increasing awareness about the increased potential risk to mothers who may be affected by anxiety during pregnancy or the post-partum period has the potential to improve maternal mental health screening and access to care.
Glutamine (Gln), a preferred fuel source for enterocytes, is critical for intestinal epithelial cell integrity and barrier function. Chronic enteritis inhibits apical Na(+)-Gln cotransport. It is not known whether inflammatory cytokines that are secreted during inflammation inhibit Na(+)-Gln cotransport. Thus, this study aimed to examine whether TNF-α would affect apical Na(+)-Gln cotransport in intestinal epithelial cells. In this study, the presence of Na(+)-Gln cotransport was established by measuring Gln uptake in 10 days postconfluent IEC-6 cells grown on transwell plates. Cation, amino acid specificity, and siRNA transfection studies established that Na(+)-Gln cotransport is mediated via B(0)AT1. Immunoblotting and immunofluorescence studies established the apical membrane localization of B(0)AT1 in IEC-6 cells. Tumour necrosis factor α (TNF-α) inhibited Na(+)-Gln cotransport in a concentration- and time-dependent manner with an inhibitory concentration of 1.53 nmol·L(-1). Quantitative real-time PCR and Western blot analyses indicated that TNF-α did not alter B(0)AT1-specific transcripts or protein expression level. Kinetic studies revealed that TNF-α inhibited Na(+)-Gln cotransport by reducing the affinity of the cotransporters for Gln, and this effect was antagonized by genistein. Thus, we conclude that the TNF-α inhibition of Na(+)-Gln cotransport occurs at the post-translational level, and that the IEC-6 cell line is an excellent system to study the role of cytokines in Na(+)-Gln cotransport.
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