An Approach Study for Reducing the Early Embryonic Loss in Egyptian Buffalo-cows

SummaryThe endothelial protein C receptor (EPCR) is expressed by trophoblast cells. Mid-gestation pregnancy loss is described in animals with a haemochorial placenta lacking EPCR. The A6936G allele of the EPCR gene (PROCR) may be associated with lower EPCR densities on trophoblasts, but data are lacking for its effect on the risk of pregnancy loss in humans. A 1:2 case-control study on unexplained pregnancy loss was nested in the NOHA First cohort: 3,218 case couples and 6,436 control couples were studied for PROCR A6936G, coagulation factor V gene (F5) G1691A and coagulation factor II gene (F2) G20210A polymorphisms. Ethnicity and time of pregnancy loss defined through biometry-based gestational ages (embryonic loss < 10th week ≥ foetal loss) were analysed. The PROCR A6936G allele, in mothers and fathers, was associated only with foetal loss in both Europeans and non-Europeans. Increasing probability levels of carrying a homozygous child were increasingly associated with the risk of foetal demise. The F5 G1691A and F2 G20210A alleles, only in mothers, were only and independently associated with foetal loss in Europeans. In our population, the PROCR A6936G allele describes women, but also men and thus couples, at risk for first unexplained foetal loss. This risk is independent of the foetal loss risk conferred to our local Mediterranean European women by the F5 G1691A and F2 G20210A alleles. Data confirm that the relationship between thrombophilias and pregnancy loss varies according to ethnicity and loss type.

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Single gene mutations in early embryonic loss

Journal of Assisted Reproduction and Genetics ◽

10.1007/bf01204244 ◽

1992 ◽

Vol 9 (6) ◽

pp. 504-505 ◽

Cited By ~ 2

Author(s):

Yury Verlinsky

Keyword(s):

Single Gene ◽

Gene Mutations ◽

Embryonic Loss

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Fatty acid composition of fat globule membrane neutral lipids from Egyptian buffalo, goat and cow's milk

Food Chemistry ◽

10.1016/0308-8146(87)90079-3 ◽

1987 ◽

Vol 24 (1) ◽

pp. 11-19 ◽

Cited By ~ 4

Author(s):

Y Shahin

Keyword(s):

Fatty Acid Composition ◽

Fatty Acid ◽

Acid Composition ◽

Neutral Lipids ◽

Cow’S Milk ◽

Cow's Milk ◽

Fat Globule ◽

Egyptian Buffalo

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Neonatally Induced Mild Diabetes in Rats and Its Effect on Maternal, Placental, and Fetal Parameters

Experimental Diabetes Research ◽

10.1155/2012/108163 ◽

2012 ◽

Vol 2012 ◽

pp. 1-7 ◽

Cited By ~ 21

Author(s):

Yuri Karen Sinzato ◽

Gustavo Tadeu Volpato ◽

Isabela Lovizutto Iessi ◽

Aline Bueno ◽

Iracema de Mattos Paranhos Calderon ◽

...

Keyword(s):

Fetal Development ◽

Diabetic Rats ◽

Female Rats ◽

Corpora Lutea ◽

Reproductive Outcomes ◽

Glucose Levels ◽

Blood Glucose Levels ◽

Insulin Tolerance ◽

Mild Diabetes ◽

Embryonic Loss

The aim of this study was to assess placental changes and reproductive outcomes in neonatally induced mild diabetic dams and fetal development in their offspring. At birth, female rats were assigned either to control or diabetic group (100 mg of streptozotocin/Kg, subcutaneously). At adulthood, the female rats were mated. During pregnancy, the blood glucose levels and glucose and insulin tolerance tests were performed. At term, maternal reproductive outcomes, fetal and placental weight, and placental morphology were analyzed. Diabetic rats had smaller number of living fetuses, implantations and corpora lutea, and increased rate of embryonic loss. Placenta showed morphometric alterations in decidua area. Our results showed that mild diabetes was sufficient to trigger alterations in maternal organism leading to impaired decidua development contributing to failure in embryonic implantation and early embryonic losses. Regardless placental decidua alteration, the labyrinth, which is responsible for the maternal-fetal exchanges, showed no morphometric changes contributing to an appropriate fetal development, which was able to maintain normal fetal weight at term in mild diabetic rats. Thus, this experimental model of diabetes induction at the day of birth was more effective to reproduce the reproductive alterations of diabetic women.

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