I have been thinking about when the embryonic window actually occurs in humans. I have tried to logically reason from the patent and will try to share it with everyone in a simple way. Thoughts and comments are welcomed.
Here are some studies with mice and conclusions taken from the patent. Wound induction in these examples are most likely incisional wounding and not abrasion. No EGFR inhibition in the first four examples.
“Figure 16. No new HF are evident 11 days after wound induction in 21- day-old mice”
“Figure 4. Appearance of hair germs 12 days after wound induction”
“12 days after wound induction, hair germs, with similar morphology to fetal hair germs, were observed in the wound site”
“Figure 17. 14 days after wound induction, new HF have begun to form”
“Figure 11. New hair growth 25 days”
“AG1478 (150 [mu]M in 10 [mu]L volume) was administered as a single injection. 11 days after incisional wounding (1 cm<2>) to the middle of the wound near the skin surface. EGF receptor inhibitor administration led to generation of more and larger hair follicles compared with control mice that were wounded only”
"An area of the backs of 50-day old mice was subjected to depilation and removal of the epidermis using a rotating felt wheel. Fifteen days later, HF placodes, hair germs and other signs of follicle neogenesis were present "
Me again. First by day 12 signs of hair formation is seen in mice wounded by incision. By day 14 the hair follicles have begun to form. One day before any signs of hair follicles can be seen an injection with EGFR inhibitor creates more and larger hair follicles. This must be the “window of oppurtunity” for incisional wounding in mice. When the skin is abraded this seems to occur a bit later, at day 15 signs of har formation is seen, when wounding deep the hair follicles have already begun to form by now. Since the window of opportunity seem to be one day before any signs of hair germs it should be by day 14 when abrading the skin in mice.
Also it is clear, as stated by others before, that waxing the hair before will enhance the hair follicle formation:
“As depicted in Figure 20A- B, the depilated mice exhibited enhanced EDIHN relative to the non-depilated mice depicted in the previous Example by a factor of 11-fold”
I will compare these findings with experiments with human skin:
"To determine whether human skin responded to EDIHN as did mouse skin, human skin was grafted onto SCID (immuno-def[iota]cient) mice and subjected to depilation by plucking and wound induction three days later. Seven days following wound induction, formation of new HF was observed in the human skin "
“adult human skin was grafted onto mice, abraded, and examined at 7 days post-abrasion. New HF were generated in the human skin, which mimicked normal hair follicle formation during fetal development”
“Figure 2 IA. EDIHN in human skin grafted to immunodeficient (scid) mice, seven days after induction of an excisional wound. Arrows indicate new HF”
“Figure 21B. Dermal abrasion of human skin grafts results in EDIHN. Human adult skin (W) was grafted onto mice, abraded, and examined seven days later, by staining for S100A6 (first, second, and fourth rows) or S100A4 (third row). Hair germs (HG) and dermal papilla (DP) are indicated.”
Me again. Human skin apparently form hair follicles faster than mouse skin (yes I am disregarding the fact that the skin was grafted on mice for the moment) and incisional wounding seem to work faster than abrasion. Since the window of oppurtunity seems to be one day before any signs of hair germs I come to the conclusion that this most likely occur by day 6 in humans when abrading the skin. Since we dont know what happens when administering EGFR inhibitors before the window of oppurtunity I would like to see someone try a topical Gefitinib solution applied at day 6 post wounding. I would do it my self but these drugs are way out of my budget. Thoughts?