in summary, gore3000's "big change" points #1-#2 represent *minor* modifications of systems which are *already* present in egg-laying species, #3-#4 represent *no* change -- it's hardly an oversimplification to say that the only major steps necessary to convert from an egg-layer to a placental animal is to a) lose the shell, and b) slap the existing chorioallantoic membrane against the uterine wall:
While your detailing of live birth in sharks and other species is very interesting, for the sake of brevity, I shall not discuss it here since not even evolutionists would claim that mammals descended from sharks. You will also note that I will not have any need to insult you since the facts speak for themselves.
According to you all that is needed for a change from egg laying is to get rid of the egg shell and attach the baby to the uterus and there you are! A complete change in mode of reproduction. Problem is that science tells us it is not that easy.
IMPLANTATION:
When considering the fact that in any given menstrual cycle, healthy couples who have intercourse regularly without the use of contraception only have a 25 to 30 percent chance of beginning a pregnancy [1], that only 70 to 75 percent of blastocysts created are able to implant and that only 58 percent of the blastocysts that implant survive past the second week of gestation [2], one comes to understand the miracle of reproduction.
From: Fetal Death
About 6 days after fertilization, the embryo is shaped like a sphere. The surface of the sphere is made up of a layer of specialized cells called the trophoblast. At this phase of development, the embryo is called the blastocyst. The trophoblast later gives rise to the cells that will form the fetus\x{2019} part of the placenta. (The placenta is made up of both maternal and fetal tissues.) The trophoblast is coated with a protein known as L-selectin. The wall of the uterus is coated with carbohydrate molecules. The researchers believe that as the blastocyst travels along the uterine wall, L-selectin on its surface binds to the carbohydrates on the uterine wall, until the blastocyst gradually slows to a complete stop. After this happens, the cells that later become the fetus\x{2019} contribution to the placenta develop. The placental tissue from the fetus then invades the uterine wall by sending finger-like extensions into it. These projections make contact with the maternal blood supply, becoming the pipeline through which the fetus derives nutrients and oxygen, and rids itself of carbon dioxide and wastes.
...
The researchers found that the amount of carbohydrate on the uterine wall was greatest at the time when uterine receptivity to the blastocyst was greatest.
From: Researchers Discover How The Embryo Attaches to the Uterus
Implantation is regulated by a complex interplay between trophoblasts and endometrium. On the one hand trophoblasts have a potent invasive capacity and if allowed to invade unchecked, would spread throughout the uterus. The endometrium, on the other hand, controls trophoblast invasion by secreting locally acting factors (cytokines and protease inhibitors), which modulate trophoblast invasion. Ultimately, normal implantation and placentation is a balance between regulatory gradients created by both the trophoblasts and endometrium (Figure 4).
Figure 4. Regulation of trophoblast invasion by an hCG gradient. Within the placenta the syncytiotrophoblasts generate high levels of hCG which shifts cytotrophoblast differentiation towards a non-invasive hormone secreting villous-type trophoblast. The closer the trophoblasts are to the endometrium the less hCG is made, allowing the trophoblasts to differentiate into anchoring type cells which make the placental glue protein trophouteronectin. Trophoblasts that leave the placenta and migrate within the endo and myometrium are induced to make proteases and protease inhibitors, presumably to facilitate trophoblast invasion into the maternal tissues.
From: Implantation
Without the above happening - with the cooperation of both the baby and the mother, there will be no pregnancy and no reproduction.
THE PLACENTA
Eggs of course do not have a placenta. Without it though, mammalian reproduction would be impossible. There is a quite a bit necessary for a placenta to do its job:
The placenta is the link between a fetus and its mother about the exchange of substances and the thermoregulation. At the childbirth it will be replaced by digestive system, lungs and kidneys of the newborn, for the exchange of substances.
The thermoregulation will be driven by the central nervous system through the control of the blood circulation and of the metabolism.
Other placental functions:
* Production of hormones
* Transmission of chemical messages
* Regulation of the resistances of the fetal circulation
* Regulation of oxygenation of the fetal blood.
How and how much these functions are achieved is still mainly unknown.
The proper perfusion of the placental vessels is a prerequisite for the complete growth of the fetus.
From: Physiology of Fetoplacental Circulation
Does not seem like something you can just say 'abracadabra' and arise by random chance!
At birth there has to be a complete change from blood circulation through the mother to circulation through the baby, this includes a complete switch in the lung function of the baby from its being a consumer of oxygen to an acquirer of oxygen:
In the fetus, the systemic, pulmonary and umbilical circulations have several links. The umbilical and placental circulations are a temporary system for the life and the growth of the fetus, that is abandoned at the childbirth, when drastic changes take place transferring the function of gas exchange from the placenta to the lungs.
Above right - Fetal Circulation in Sheep, Above left - Changes in the Circulation from the fetus to the newborn and adult
From: Fetal Circulation
Does not seem like it could have happened with a single mutation does it?
The transfer of blood requires a very complex system:
we can classify the placental vessels as follows:
+ chorionic vessels;
+ vessels of the cotyledons;
+ capillary vessels in the villi;
+ paravascular capillary network.
The villi can be classified in 5 main groups: stem villi, mature and immature intermediate villi, terminal villi and to mesenchimal villi [20].
From: Anatomy of the Fetal Side
Amazing what can be done with a single mutation eh!
CHANGES IN THE MOTHER:
Human placental lactogen (hPL) is a potent glycoprotein made throughout gestation, increasing progressively until the 36th week, where it can be found in the maternal serum at a concentration of 5-15 µg/ml, the highest concentration of any known protein hormone. The major source of hPL appears to be the villous syncytiotrophoblasts, where it is made at a constant level throughout gestation. In addition to the villous syncytiotrophoblast, hPL has been identified in invasive trophoblasts during the first trimester. hPL appears to regulate the lipid and carbohydrate metabolism of the mother (Figure 14). Placental researchers have also demonstrated by immunohistochemical studies that villous syncytiotrophoblasts contain prolactin, relaxin and chorionic adrenocorticotropin, an ACTH-like protein. The physiological role of placental ACTH is unclear, but as with other placental hormones, all of these hormones may represent a shift from maternal to placental control.
From: Formation of the early Placneta
Amazing what little is needed to change from egg laying to live bearing - just a complete change in the mother!
IMMUNOLOGICAL REJECTION PROBLEMS:
In spite of the fact that the placenta and fetus are foreign to the mother, most pregnancies show no evidence of immunologic rejection. When immunologic reactions do occur, they can be against any of the components of the gestation (placenta and fetus). These reactions can occur at all stages of pregnancy, and can occur repeatedly, pregnancy after pregnancy.
...
In approximately 1-2% of all gestations, mononuclear cells can be seen infiltrating into the chorionic villi of the placenta. Until the work of Redline and Patterson, however, the origin of these cells had been controversial, some arguing for a fetal origin, some for a maternal origin. Since immunochemistry alone could not answer this question they utilized in situ hybridization for Y and X markers in male gestations to demonstrate that the lymphocytes present in cases of chronic villitis are maternally derived, allowing us to focus on the causes of this apparent maternal immunologic reaction against trophoblast and/or villous antigens. Immunohistochemistry of such cases has shown that the cells within the villous core are T-cells and macrophages.
Occasionally placentas manifest an intervillous space that is filled with mononuclear cells. When immunohistochemically stained, these cells are revealed to be monocytic/macrophage in origin. This monocytic intervillositis has been associated with IUGR, preeclampsia, recurrent pregnancy loss and intrauterine fetal demise.
From: Immunological Rejection
Of course the above problem had to be solved before a single baby was born since immunological rejection causes loss of pregnancy.
THE AMNIOTIC SAC
One of the purposes of the amniotic sac is to prevent immunological problems with the mother:
since the bag of waters prevents bacteria from entering the uterus by acting as a barrier, membranes aren't usually ruptured until delivery is imminent.
From: Amniotomy
The amniotic fluid plays an important part in the baby's development:
What is amniotic fluid?
Amniotic fluid is the stuff that surrounds your baby as he grows in the amniotic sac in your uterus during pregnancy, and it serves some important purposes. It cushions your baby against trauma (if you fall down, for example) and keeps the umbilical cord from being compressed (which can reduce your baby's oxygen supply). It protects both the baby and the uterus from infection, provides a zero gravity environment for the baby to move around in, and helps the baby's digestive, musculoskeletal, and breathing systems develop properly.
Where does it come from?
During the first 16 weeks of gestation, the placenta, the amniotic membranes, the umbilical cord, and the baby's skin all produce fluid to fill the amniotic sac as the fetus grows. After that, the fetus starts to swallow the fluid, pass it through his kidneys, and excrete it back out as urine, which he then swallows, recycling the full volume of fluid every few hours. (Yes, that means most of the fluid is eventually urine.) He also excretes some fluid from his lungs. And small amounts are either absorbed by the amniotic sac and diffused into the mother's body or sent back to the mother through the blood in the umbilical cord. Thus, the fetus plays an important role in keeping just the right amount of fluid in the amniotic sac. When there's too little it's called oligohydramnios; when there's too much, it's called hydramnios or polyhydramnios.
From: Pregnancy complications
Seems the amniotic sac is a pretty essential part of the baby's excretory system.
THE UMBILICAL CORD
The umbilical cord is of course essential in this whole process. It is not as simple as one would think:
The umbilical cord normally contains two umbilical arteries and one umbilical vein. These are embedded within a loose, proteoglycan rich matrix known as Wharton's jelly (Figure 5). This jelly has physical properties much like a polyurethane pillow, which if you have ever tried twisting such a pillow you know is resistent to twisting and compression. This property serves to protect the critical vascular lifeline between the placenta and fetus (Figure 6).
Less commonly, but with potentially devastating consequences,the umbilical cord can become knotted (Figure 8). If the knot is loose, fetal circulation is maintained. However, if the knot is tightened, for example at the time of fetal descent through the birth canal, the tightening knot can occlude the circulation between the placenta and fetus, resulting in an intrauterine demise. The Wharton's jelly surrounding the fetal vessels is capable of withstanding significant torsional and compressional forces, as shown in Figure 9. Occasionally, however, Wharton's jelly does not develop in all portions of the cord. When this occurs, the fetal vessels are no longer protected from torsional forces and they can become occluded if twisted sufficiently (Figure 10), again leading to an intrauterine demise.
From: The Umbilical Cord
Seems that the jelly around the umbilical cord is quite necessary. Even with the strong service Wharton's jelly provides in preventing knotting, babies die because of the cutting off of the blood supply.
CONCLUSIONS:
Seems we need quite a lot to happen for this transformation! Even the individual processes within the system which are necessary to accomplish the change over are quite complex and could not have arisen as a result of a single mutation. Further, all the processes are interrelated. The separation of the umbilical cord has to signal a changeover to breathing by lungs and blood circulation wholly within the baby. The joining of the baby to the uterine wall starts the signaling of changes in the mother. In fact, the whole process can be seen as a very careful interaction between the baby and the mother.
As a result of all the above, I think it should be pretty clear to those who have an open mind that at no point is there a possibility that the changes necessary to achieve a transformation of the reproductive system from egg laying to mammalian live birth can be achieved in a single generation. There are way too many changes needed to make a claim that all these changes could have occurred in any sort of gradual manner and that they are far too many to have occurred suddenly in a stochastic manner.