Part of the book: The Human Embryo
Human embryo implantation is mainly regulated by the endocrine system. Since the ovary, fallopian tube, and fundus can directly communicate through the mesosalpinx and ovarian ligament, the local concentration of progesterone in the pathway of the developing embryo is considered to be higher than in systemic blood circulation. The immune system promotes embryo implantation by stimulating progesterone production of the ovary and by inducing endometrial differentiation. The recognition of the developing embryo in the fallopian tube by the immune system is achieved through the para-aortic lymph nodes. On the basis of the above evidence, the autologous immune cells activated in vitro were demonstrated to improve clinical pregnancy rates in patients with repeated implantation failures. In addition, the autonomic nerve system that innervates the fundus, the ovary, and the fallopian tube from the para-aortic region is proposed to regulate the environment of the pathway of the developing embryo. From these findings, we suppose that a unique unilateral functional unit to promote human embryo implantation exists in the pathway of the developing embryo including the para-aortic regions and propose naming this novel functional unit the Fundus-Ovary-Salpinx-Para-aorta Implantation Promoting unit (FOSPa-IP unit).
Part of the book: New Discoveries in Embryology
Currently, dieting and breakfast skipping is increasing among young women in Japan. We found that breakfast skipping among female students was accompanied by menstrual disorders, while students who had dieted in the past experienced deterioration in menstrual pains, warning that abnormal eating in young women may induce obstetric and gynecological disorders in the future. We named this concept “adolescent dietary habit-induced obstetric and gynecologic disease (ADHOGD)”. A questionnaire survey showed that pregnant women who had menstrual pain in their youth were at high risk of hypertensive disorders during pregnancy. In rodents, ovulation was suppressed in young female rats whose feeding was limited to the non-active (light) phase. In female mice, feeding stimulation directly regulated the uterine clock gene rhythm. Furthermore, in conditional knockout mice of uterine Bmal1, the fetuses died before delivery, indicating that abnormal uterine clock function cannot maintain fetal development. These findings suggest a mechanism of ADHOGD, in which hunger stress due to inappropriate eating habits during adolescence and young adulthood affects uterine function via clock gene abnormalities, causing placental dysfunction and fetal growth failure during pregnancy. Thus, valid and appropriate rodent experiments are effective to analyze ADHOGD, especially from the aspect of circadian rhythms.
Part of the book: Rodents and Their Role in Ecology, Medicine and Agriculture