A human placental lactogen B human chorionic thyrotropin C relaxin D inhibin. A dilation stage B expulsion stage C placental stage D gastrula stage. A phagocytosis by the trophoblast cells B proteolytic enzymes produced by the trophoblast cells C settling of the blastocyst onto the prepared uterine lining D adherence of the trophoblast cells to the endometrium.
A cell division by mitosis with little or no growth between successive divisions B the fusion of gametes C splitting the cell into two separate cells D meiosis. A nutrients and respiratory gases only B hormones, blood cells, and nutrients C nutrients, respiratory gases, wastes, and alcohol D respiratory gases, hormones, nutrients, and blood cells. A aspirin B wine C thalidomide D German measles.
A serosae of the ventral body cavity B epithelium of the reproductive tract C epithelium of the pineal and pituitary glands D connective tissues. A all nervous tissue B endothelium of blood and lymph vessels C glandular derivatives of the digestive tract D epithelium of the digestive tract.
A epithelium of the respiratory tract B synovial membranes of the joints C blood, bone marrow, and lymphoid tissue D organs of the urogenital system. A sex readily detected from the genitals B the cardiovascular system becoming fully functional C head larger than body D fetal position assumed. A The corpus luteum is maintained until the placenta takes over its hormone-producing functions. B The corpus luteum degenerates and becomes the corpus albicans. C The ovarian cycle begins.
D Increased levels of FSH will be produced. A The distal parts of the umbilical arteries form the superior vesical arteries. B The fossa ovalis becomes the foramen ovale. C The umbilical vein becomes the ligamentum teres. D The hepatic portal vein forms from the umbilical artery. A The two pronuclei divide. B The head of the sperm forms the male pronucleus.
C The secondary oocyte completes the second meiotic division. D Proteases and acrosin proteinases of the sperm disperse the cells of the corona radiata of the oocyte. A destined to remain in the uterus after the birth of the infant B located between the developing embryo and the myometrium C not a maternal contribution to the placenta D the tissue that surrounds the uterine cavity face of the implanted embryo.
By 72 hours after fertilization, the egg has divided into more than cells and is called the morula. The body systems of the developing embryo are present in at least rudimentary form at eight weeks. A pregnant woman urinates more often than usual because the uterus compresses the bladder, and she must also dispose of fetal metabolic wastes.
In fetal circulation, one way in which blood bypasses the nonaerated lungs is by way of the foramen ovale. Surfactant production in premature infants is rarely a factor in providing normal respiratory activity. Sign in. Implantation is shown by the solid vertical line in lower panels. The day of PdG waning is shown by a dashed vertical line in the upper panels, and the day of hCG falter is shown by a broken vertical line in the lower panels. Both show waning of PdG before hCG falter.
Panel A shows no evidence of suboptimal hCG levels, and B exhibits a suboptimal increase in hCG during the first few days after implantation. C and D Early losses that show no rise in postimplantation PdG. Panel C shows no evidence of suboptimal hCG.
Panel D exhibits rapid hCG increase at time of implantation, but after 3 days hCG becomes suboptimal. E and F Early losses that exhibit an hCG falter before or close to the time of the day of PdG waning; in both cases the hCG pattern suggests problems with the conceptus with no apparent dysfunction of the CL. In the remaining three early losses, in which implantation occurred by Day 9 and PdG waned early, the hCG profiles appear to be suboptimal, suggesting that the conceptus may have contributed to loss.
For example, in one of these women Fig. However, after a 4- to 5-day delay, the hCG rose rapidly and continued to rise through menses before it too declined. The lack of a rapid early hCG rise may have contributed to this loss. The seven early losses after implantation on Luteal Day 10 showed a slight shift to later days of waning PdG than expected, based on nonconception cycles Fig. In both of these, the hCG rise appeared suboptimal. We also examined losses in the no-rise category for evidence of inadequate CL rescue.
Four of the nine conceptions in this group showed waning PdG before hCG falter. The clearest case of CL failure among these four is shown in Figure 7C. The conceptus implanted on Luteal Day 10, and the CL appeared to respond to the conceptus with prolonged production of progesterone.
PdG was maintained at midluteal levels for 5 days after implantation but then declined despite continual increase in the hCG. The other three conceptions showed some disruption in hCG increase example in Fig. For the remaining 33 early losses, the majority of conceptuses implanted after the optimal implantation interval or hCG faltered before or nearly simultaneously with the day of waning PdG examples in Fig.
The level of progesterone required to maintain early pregnancy in humans is not known [ 32 ]. The presence in multiple species of a progesteron surge at the time of implantation suggests that the increase may have functional significance. In this study, we measured urinary progesterone metabolite levels to evaluate the progesterone response to implantation.
Progesterone inhibits uterine contractions and modulates immune function [ 33 — 35 ], but whether an early pregnancy surge in progesterone is needed to optimize these functions is not known.
Delineating the functional importance of an abrupt progesterone rise at time of implantation may provide new insights for promoting successful implantation in assisted reproduction.
The variation in progesterone response to implantation may reflect the quality of the CL, uterine factors, or variation in the strength of the signal coming from the conceptus. To explore these possibilities, we examined markers of CL quality prior to implantation and characteristics of the daily urinary hCG profiles. We hypothesized that pregnancies with delayed or absent PdG rises show evidence of lower CL quality or weaker hCG signaling. Neither of the two markers of CL quality peak estrogen metabolite levels, reflecting follicle development, and preimplantation PdG levels, reflecting luteinization was related to the PdG profile.
However, early hCG levels were important predictors. We also examined in detail the early losses to see when progesterone declined in relation to the timing of hCG falter. Evidence for CL failure was rarely found. Thus, our data suggest that the variability in progesterone response is more strongly associated with signals from the conceptus than with factors inherent to the CL.
However, because hCG concentrations reflect both what the conceptus produces and what reaches the maternal circulation, a weak hCG signal could be caused by uterine problems as well as problems with the conceptus.
Lenton and Woodward [ 18 ] also examined determinants of CL response, although only 18 pregnancies were included in the analyses. They also reported a relationship between the strength of the hCG signal and progesterone response.
Our findings do not support those of Lenton and Woodward that cycles with low preimplantation production of progesterone have a weaker progesterone response to pregnancy.
We also hypothesized that pregnancies implanting late would be associated with a weaker progesterone response because experimental data have shown a weak CL response when hCG is administered late in the luteal phase. Our data did show that late implantations were strongly associated with PdG decline but not with late rise or no rise.
The pregnancies implanting early Luteal Day 8 were less likely to have an early rise than those implanting on Luteal Days 9 or 10, a pattern also observed by Lenton and Woodward [ 18 ]. These authors interpreted this finding as evidence that the CL is unresponsive to hCG until later in the luteal phase. Thus, it is unlikely that the CL is unresponsive. Perhaps the conceptus, although producing hCG, is not mature enough to produce other signals important for stimulating a progesterone rise.
Other data also support the notion that hCG may not be the only important signal maintaining CL function during very early pregnancy. Other factors known to stimulate progesterone production by the CL in experimental studies include prostaglandins E 2 , D 2 , and I 2 [ 38 ]. These prostaglandins might be produced during trophoblast invasion of the uterus. The antibody is no longer available, so its cross-reactivity to newly identifiable forms of hCG such as glycosylated hCG is unknown.
The CL increases production of substances other than progesterone during very early pregnancy, including estrogen, inhibin, and relaxin [ 44 ]. However, these hormones do not all increase at the same time. In primate species such as humans that have a prolonged gestational interval dependent on CL support, intact hCG may be the first of several signals to the CL.
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Epidemiology ; 6 : — Chronological aspects of ultrasonic, hormonal, and other indirect indices of ovulation. Br J Obstet Gynaecol ; : — C aspirin and similar drugs. B Millions of sperm cells are destroyed by the vagina's acidic environment. C the trophoblast forms two distinct layers. C the primitive streak. D The ductus arteriosus constricts and is converted to the ligamentum arteriosum. B reverse peristalsis of the uterus and uterine tubes. A phagocytosis by the trophoblast cells. A cell division by mitosis with little or no growth between successive divisions.
C nutrients, respiratory gases, wastes, and alcohol. C epithelium of the pineal and pituitary glands. B endothelium of blood and lymph vessels.
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