Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-one placentae from type I (insulin-dependent) pregnant diabetic patients, treated with continuous subcutaneous insulin infusion (CSII), were studied morphologically. Despite a near-optimal blood glucose control the placental changes were identical to those previously reported in diabetic pregnancy. The most frequently observed lesion was that of relative placental immaturity; this, when extensive, was related to antenatal fetal asphyxia. These data indicate that near normoglycaemia, achieved with CSII, does not modify the morphological expression of the disease in the placenta. Furthermore, it highlights the importance of placental development in the context of diabetic pregnancy.
Placenta
PMID:Morphological findings in placentae of insulin-dependent diabetic patients treated with continuous subcutaneous insulin infusion (CSII). 361 74

Unexplained intra-uterine fetal death is still a problem in diabetic pregnancies, especially in those with an LGA-infant. We hypothesized that in these pregnancies impaired placental function, in terms of abnormal placental weight and/or abnormal placental histology, may account for this phenomenon. To test this hypothesis, we assessed the relative placental weight and scored several histological abnormalities in 34 AGA- and 24 LGA-placentae of type 1 diabetic women and in 22 AGA- and 16 LGA-placentae of control women. Relative placental weight was comparable in the LGA-diabetic cases and in the control groups, but was significantly higher in the AGA-diabetic subgroup. Histological abnormalities such as the presence of nucleated fetal red blood cells, fibrinoid necrosis, villous immaturity and chorangiosis were observed more often in the diabetic placentae compared with the control placentae. These differences in histology were particularly observed when we compared both AGA-groups. LGA-control placentae showed a high incidence of histological abnormalities, almost comparable to the diabetic placentae. Only fibrinoid necrosis was significantly more common in the LGA-diabetic placentae. Three of the four cases of perinatal death/asphyxia in the diabetic group concerned an LGA-infant with a relative low placental weight. In conclusion, placentae of women with type 1 diabetes showed several abnormalities that can be associated with impaired functioning. The difference between AGA- and LGA-diabetic placentae was related to relative placental weight and our data suggest that an increase in relative weight may protect the fetus from asphyxia. Placentae from LGA-non-diabetic women showed several similarities to those of women with diabetes.
Placenta
PMID:Placental pathology in women with type 1 diabetes and in a control group with normal and large-for-gestational-age infants. 1312 78

Chromosome number abnormalities are remarkably common in human reproduction. Most are caused by chromosomal non-disjunction and premature chromatid separation in oocyte meiosis I. Pooled data from previous studies showed that one in five oocytes that failed to fertilize after in vitro insemination was abnormal when analysed by conventional cytogenetics. Preconception genetic diagnosis, carried out on the first and second polar bodies by FISH, using 5 chromosome-specific probes (13, 16, 18, 21 and 22), showed that the rate of aneuploidy is higher in women aged 35 or over (52.1 per cent). Oocyte dysmorphy seems to have little effect on the rate of aneuploidy except for giant oocytes, which are usually diploid and may cause triploidy after fertilization. Intra- and extrafollicular influences (perifollicular microvasculature, oxygenation, the presence of residues from cigarette smoke) may disturb maturation, leading to immaturity and aneuploidy. Thus, oocyte meiosis is very sensitive to endogenous and exogenous factors that may cause the production of oocytes with chromosomal abnormalities and therefore, of abnormal zygotes.
Placenta 2003 Oct
PMID:Genetic analysis of the oocyte--a review. 1455 33

To investigate the reasons for fetal losses after somatic cell nuclear transfer, an immunohistochemical and ultrastructural analysis of cloned placentae was performed. The main features observed were a marked reduction of villous vascularization, hypoplasia of trophoblastic epithelium, lack of binucleate cells, immaturity of placental vessels and reduced vasculogenesis. By means of transmission electron microscopy (TEM), a diffuse thickening and lamination of subtrophoblastic basement membrane (SBM) were noted in cloned placentae. These results led us to hypothesize, through an autoamplification model, that the abnormal vascularization, the ischaemia and the low development of an high specialized trophoblastic epithelium were the primary causes of the fetal loss occurring after somatic cells nuclear transfer.
Placenta
PMID:Placental abnormalities in ovine somatic cell clones at term: a light and electron microscopic investigation. 1705 8

The fetal endometrium becomes responsive to steroid hormones around the fourth month of pregnancy starting with an oestrogenic phase, which is followed late in pregnancy by a secretory phase. Based on post-mortem studies, the endometrium at birth is secretory in only one-third of neonates and proliferative in the remaining cases. Decidual or menstrual changes are rare in fetal endometrium despite high circulating steroid hormone levels, which drop rapidly after birth. Hence, acquisition of progesterone responsiveness appears to be dependent on endometrial maturation and relative immaturity may persist in a majority of girls until the menarche and early adolescence. Two major reproductive disorders have been linked with either advanced or delayed endometrial maturation. First, early-onset endometriosis may be caused by menstruation-like bleeding in the neonate, leading to tubal reflux and ectopic implantation of endometrial stem/progenitor cells. Second, persistence of partial progesterone resistance in adolescent girls may compromise deep placentation and account for the increased risk of major obstetrical syndromes, including preeclampsia, fetal growth retardation and preterm birth. The concept of neonatal origins of common reproductive disorders poses important research challenges but also subsumes potential new preventative strategies.
Placenta 2015 Apr
PMID:The perinatal origins of major reproductive disorders in the adolescent: Research avenues. 2563 11

Nowadays, the continuous rise of maternal obesity is followed by increased gestational diabetes mellitus incidence. GDM is associated with adverse fetal and neonatal outcome that often presents with macrosomia, birth trauma, neonatal hypoglycemia, and respiratory distress syndrome. Inclusion of GDM into 'the great obstetrical syndromes' emphasizes the role of the placenta in interactions of the maternal and fetal unit. The placenta acts as a natural selective barrier between maternal and fetal blood circulations. Placenta is sensitive to the hyperglycemic milieu and responses with adaptive changes of the structure and function. Alteration of the placental development and subsequent vascular dysfunction are presented in 6 out of 7 women with all ranges of diabetic severity. Most placentas from GDM pregnancies present typical histological findings such as villous immaturity, villous fibrinoid necrosis, chorangiosis, and increased angiogenesis. The type of dysfunction depends on how early in pregnancy glycaemia disorders occurred. Generally, if impaired glucose metabolism is diagnosed in the early pregnancy, mainly structural dysfunctions are observed. GDM that is detected in late gestation affects placental function to a greater extent. Moreover many studies suggest that diabetic placental changes are associated with inflammation and oxidative stress that can lead to the chronic fetal hypoxia. This article aims to review particular changes of the development, anatomy and function of the placenta in the environment of abnormal glucose metabolism which can establish the maternal-placental-fetal interface dysfunction as a potential source of adverse pregnancy outcomes. A detailed sequence of events that leads from hyperglycemia to placental dysfunction and subsequent pregnancy complications may become an important issue for further studies.
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PMID:Placental pathologic changes in gestational diabetes mellitus. 2607 74

Placental stem cells are of growing interest for a variety of clinical applications due to their multipotency and ready availability from otherwise frequently discarded biomaterial. Stem cells derived from the placenta have been investigated in a number of disease processes, including wound healing, ischemic heart disease, autoimmune disorders, and chronic lung or liver injury. Fetal intervention for structural congenital defects, such as spina bifida, has rapidly progressed as a field due to advances in maternal-fetal medicine and improving surgical techniques. In utero treatment of structural, as well as non-structural, congenital disorders with cell-based therapies is of particular interest given the immunologic immaturity and immunotolerant environment of the developing fetus. A comprehensive literature review was performed to assess the potential utilization of placenta-derived stem cells for in utero treatment of congenital disorders. Most studies are still in the preclinical phase, utilizing animal models of common congenital disorders. Future research endeavors may include autologous transplantation, gene transfers, induced pluripotent stem cells, or cell-free therapies derived from the stem cell secretome. Though much work still needs to be done, placental stem cells are a promising therapeutic agent for fetal intervention for congenital disease.
Placenta 2017 Nov
PMID:Potential clinical applications of placental stem cells for use in fetal therapy of birth defects. 2865