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Titlebook: Immunology of Pregnancy; Gil Mor Book 20061st edition Springer-Verlag New York 2006 T cell.apoptosis.complications.cytokine.embryo.fetus.h

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發(fā)表于 2025-3-25 15:10:03 | 只看該作者
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發(fā)表于 2025-3-25 19:44:22 | 只看該作者
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發(fā)表于 2025-3-25 21:07:45 | 只看該作者
Evolution of the Mammalian Reproductive Tract and Placentation,rvation of primitive genitourinary genes. The products include the renin-angiotensin system and the innate immune system. This explains what might otherwise be considered an ectopic presence of these systems in the mammalian reproductive tract and the interaction of the allograft embryo and maternal
24#
發(fā)表于 2025-3-26 00:35:15 | 只看該作者
Toll-Like Receptors and Pregnancy,ense against a diverse array of possible pathogens. Clinical studies have shown a strong association between certain pregnancy complications and intrauterine infections. Therefore, innate immune responses to microorganisms at the maternal-fetal interface may have a significant impact on the success
25#
發(fā)表于 2025-3-26 06:32:40 | 只看該作者
26#
發(fā)表于 2025-3-26 10:06:18 | 只看該作者
Th1/Th2 Balance of the Implantation Site in Humans,ocyst stage and the endometrium must be in a receptive phase. Wilcox et al. have estimated that 65% of conceptions end in unrecognized losses. These failures can be divided into failure to implant (20%), initial apposition but no adhesion or invasion (28%), and failure to develop immediately after i
27#
發(fā)表于 2025-3-26 16:09:34 | 只看該作者
The Regulation of Human Trophoblast Apoptosis and Survival during Pregnancy,rimester. In pregnancies complicated by preeclampsia or intrauterine growth restriction (IUGR), a greater incidence of villous and extravillous trophoblast apoptosis has been observed, suggesting that the deregulation of trophoblast apoptosis may contribute to pathological conditions. Apoptosis may
28#
發(fā)表于 2025-3-26 18:17:25 | 只看該作者
29#
發(fā)表于 2025-3-27 00:23:31 | 只看該作者
Potential Role of Glucocorticoids in the Pathophysiology of Intrauterine Growth Restriction (IUGR),t” to poor utero-placental perfusion due to defective trophoblast invasion that ultimately compromises fetal well-being..–. The resultant hypoxia curtails the remodeling of uterine vessels by invasive cytotrophoblasts in the second trimester..,. Our results suggest that mediators of fetal stress [i.
30#
發(fā)表于 2025-3-27 02:19:59 | 只看該作者
NK Cells and Pregnancy,rived trophoblasts can have a profound impact on pregnancy. Altered NK cell numbers and activity have been associated with a variety of clinical conditions such as endometriosis, recurrent pregnancy loss, and preeclampsia. Uterine NK cells have a unique phenotype compared to blood NK cells and this
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