[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

Innate production of T[H]2 cytokines by adipose tissue-associated c-Kit[+]Sca-1[+] lymphoid cells

Intrauterine growth restriction (IUGR) is found in 1-10% of all pregnancies, and among women with risk factors even twice often. It is connected to worse obstetric results, and its complications can arise long time after delivery. In the paper we described etiology, diagnostics and monitoring of IUGR and its consequences for the child and for the course of neonatal periode.

Intrauterine growth restriction

Interferons and Proinflammatory Cytokines in Pregnancy and Fetal Development.

During pregnancy, several tightly coordinated and regulated processes take place to enable proper fetal development and gestational success. The formation and development of the placenta is one of these critical pregnancy events. This organ plays essential roles during gestation, including fetal nourishment, support and protection, gas exchange and production of several hormones and other mediators. Placental hormones are mainly secreted by the syncytiotrophoblast, in a highly and tightly regulated way. These hormones are important for pregnancy establishment and maintenance, exerting autocrine and paracrine effects that regulate decidualization, placental development, angiogenesis, endometrial receptivity, embryo implantation, immunotolerance and fetal development. In addition, because they are released into maternal circulation, the profile of their blood levels throughout pregnancy has been the target of intense research towards finding potential robust and reliable biomarkers to predict and diagnose pregnancy-associated complications. In fact, altered levels of these hormones have been associated with some pathologies, such as chromosomal anomalies or pre-eclampsia. This review proposes to revise and update the main pregnancy-related hormones, addressing their major characteristics, molecular targets, function throughout pregnancy, regulators of their expression and their potential clinical interest.

The endocrine function of human placenta: an overview.

Fetal growth restriction (FGR) is a condition that affects 5–10% of pregnancies and is the second most common cause of perinatal mortality. This review presents the most recent knowledge on FGR and focuses on the etiology, classification, prediction, diagnosis, and management of the condition, as well as on its neurological complications. The Pubmed, SCOPUS, and Embase databases were searched using the term “fetal growth restriction”. Fetal growth restriction (FGR) may be classified as early or late depending on the time of diagnosis. Early FGR (<32 weeks) is associated with substantial alterations in placental implantation with elevated hypoxia, which requires cardiovascular adaptation. Perinatal morbidity and mortality rates are high. Late FGR (≥32 weeks) presents with slight deficiencies in placentation, which leads to mild hypoxia and requires little cardiovascular adaptation. Perinatal morbidity and mortality rates are lower. The diagnosis of FGR may be clinical; however, an arterial and venous Doppler ultrasound examination is essential for diagnosis and follow-up. There are currently no treatments to control FGR; the time at which pregnancy is interrupted is of vital importance for protecting both the mother and fetus. Early diagnosis of FGR is very important, because it enables the identification of the etiology of the condition and adequate monitoring of the fetal status, thereby minimizing risks of premature birth and intrauterine hypoxia.

Fetal growth restriction: current knowledge.

Resistin concentration and gestational diabetes: a systematic review of the literature

Problem Maternal obesity is frequently associated with gestational diabetes mellitus (GDM), and immunological mechanisms seem to be involved in the physiopathology of these conditions. The aim of this study was to characterize the profile of immune cells in peripheral blood of overweight women with GDM. Method of study This case-control study included 27 glucose-tolerant (controls) and 31 GDM overweight pregnant women. Flow cytometry was used to assess the number of regulatory T cells (Treg) and natural killer (NK) cells in the peripheral blood. In addition, the expression of IL-10, TGF-B, and TNF-A in Treg and expression of IFN-G, TNF-A, granzyme, and perforin in NK cells were analyzed. Results GDM patients had significantly lower frequency of TCD4+ CD25bright and TCD4+ CD25+ FOXP3high cells, higher production of TNF-A by Treg cells and higher percentage of NKCD16+ 56dim cells than the controls. Conclusion The association between obesity and GDM is a condition where it is observed impaired Treg and NK cells profile, findings that seem to be related with the development of IR and inflammation.

Impaired Treg and NK cells profile in overweight women with gestational diabetes mellitus

Monocyte profile in peripheral blood of gestational diabetes mellitus patients.

The study of adipokines in overweight women with early-onset (diagnosed before 20 weeks) gestational diabetes mellitus (GDM) could help to understand the ethiopathological mechanisms of this disorder. Our aim was to assess adipokine levels in overweight pregnant women with early-onset GDM compared to patients with standard-onset (diagnosed at 24–28 weeks) GDM and to glucose-tolerant women at the same gestational ages. This nested case–control study included 133 overweight pregnant women: 33 with early-onset (diagnosed < 20 weeks) GDM; 40 with standard-onset (diagnosed ≥ 24 weeks) GDM and 60 glucose-tolerant (normal oral glucose tolerance tests < 20 and ≥ 24 weeks). Adiponectin, leptin, resistin, visfatin and ghrelin serum levels were measured by ELISA. Adiponectin serum levels were significantly lower in early-onset GDM women than in standard-onset GDM patients or controls matched for gestational age. Leptin serum levels were significantly higher in women with early-onset GDM than in controls. Women with early-onset GDM had lower adiponectin/leptin ratio than those with standard-onset GDM. There were no significant differences in resistin, ghrelin and visfatin serum levels among the participants. Our results suggest that, compared to overweight glucose-tolerant women and patients with standard-onset GDM, overweight women with early-onset GDM have unbalanced adipokine levels, suggesting that they have a more inflammatory profile.

Thalita Frutuoso Lobo

Papers

Fetal growth restriction: current knowledge.

Resistin concentration and gestational diabetes: a systematic review of the literature

Impaired Treg and NK cells profile in overweight women with gestational diabetes mellitus

Monocyte profile in peripheral blood of gestational diabetes mellitus patients.

Adipokine levels in overweight women with early-onset gestational diabetes mellitus