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interesting article i stumbled over

#1

interesting article:

http://hplusmagazine.com/2014/05/08/tota...in-decade/

[Editor’s note: recent medical developments such as growing a vagina in a laboratory, advances in gender prosthetics,  creating sperm from skin cells, etc. suggest this article is worthy of re-read and a place in the very Best of H+.]
Recently I made a bet with a member of the Institute for Ethical and Emerging Technologies.  That bet sounded to him like I was being wildly optimistic, and he jumped at it, thinking it was a sure bet that I would lose.
That bet was that by the end of this decade, medical technology would be able to change the gender of anyone to the opposite gender, with full reproductive abilities of the new gender.
That probably sounds wildly optimistic to most of you as well, but not to me.  To be honest, I think the deck is stacked in my favor.  Why?  Because we are a lot closer to realizing this achievement than most of you probably realize.
To illustrate, take a look at this recent Wired article, which describes the current ability to use stem cells mixed with the fat from a patient’s own body to grow additional breast mass in women or to regrow breasts damaged by cancer.  But that’s really very unimportant, because the real breakthrough is that this can be done for nearly every kind of tissue.  It’s still at a primitive stage, but scientists already learned how to “program” the stem cells to become different types of tissue.  They’ve made progress in making heart repairs , functional liver tissue, blood, teeth, bone, muscle, and they have even made progress on discovering how to manipulate stem cells to enable them to divide continuously.  This is a small sampling of the various breakthroughs made in just the last few years in hundreds of labs all over the world.  If you understand the implications of all those various articles, it is easy to see that we are learning how to program stem cells to do nearly anything that our body programs them to do.  Each step of learning how to program stem cells leads to greater knowledge of how to control them more precisely.
But stem cells alone are not the only medical advances that are being made.  Another major breakthrough going on in the medical field is in the improving abilities we are gaining in 3D printing.  Not only have we discovered that stem cells can be programmed to repair already existing tissue, we are using modified inkjet printers to lay down layer after layer of them in a pattern, and to basically “print” biological tissue that will “grow” together into a complete organ.
Another technique being researched is the creation of “Biological Legos” in which stem cells are embedded in a block of “glue” which holds the cells together while they form natural intercellular bonds.  Yet another technique is to use an already existing “scaffold” and fill the spaces with stem cells, growing a precisely shaped piece of tissue.
So not only are we learning to tell stem cells what to become, but we are learning how to dictate the shape of the tissues as well.  The implications for plastic surgery should be obvious.  Stem cells seem to offer us the promise that we will soon be able to restore the human body to the exact same state it was in prior to injury, enable us to regrow lost limbs, grow replacement organs on demand, and even reconstruct missing or lost tissue for reconstructive surgery.  Soon, a mastectomy might routinely remove the cancer, and rebuild a healthy breast identical to the one removed.  A heart attack might lead to a regenerated heart healthier after the attack than it was before, and even such routine needs like blood transfusions might be made by pulling your own stem cells to create a personalized supply.
But even this is pretty tame once you combine stem cells with the increasing complexity of automation, because a da Vinci surgeon robot is not going to remain under human control for very long.  So think about those articles above, about how we are learning to guide stem cells to become nearly any tissue.  Think about the day we can tell stem cells precisely what to become, and to grow in precise shapes.  Then think about an autosurgeon connected to a sensor system allowing it to make a complete map of a human body in real time, as it is fed a body map for a desired shape.  A decade from now, a plastic surgeon is likely to use body modeling software developed by MMOs and VR to enable you to decide precisely how you want to look, and then supervise the da Vinci autosurgeon as it uses your own body fat and skin cells to produce a stock of programmable stem cells, and then performs hundreds or even thousands of minimally invasive microsurgeries to place those programmed cells throughout your body, where they will become extra muscle mass, larger breasts, repair damaged internal organs, etc., allowing your future self the option of “resculpting” your personal appearance.
“But wait,” you say, “wasn’t this article about changing sex?  So you’re saying that changing sex could be done this way too?”
Yes.  However, just being able to control stem cells to the point that we can dictate what kind of cell they become, and what shape they will have at maturity isn’t all that’s involved.  There are additional differences that have to be addressed in changing sex, such as hormones, biological function and reproductive function.  But researchers have already discovered how to tell ovaries to become testes.  While this is not as easy to reverse as you might think, because according to this study the ovaries apparently have to “fight” to stay ovaries, we are making great strides in understanding these various chemical and genetic “triggers”, including such seemingly unimportant ones as the triggers that promote the growth of blood vessels to various types of tissue.  We’re also making progress at creating “artificial” ovaries, and stem cells have been successfully used to give rabbits larger penises.
This means that as we learn to control what a stem cell becomes, we will more than likely learn how to tell them to become male or female specific organ structures as well as more generic organs.  With the abilities of cell printers to be able to make internal organs, an ability that I expect to replace organ transplants by mid to late decade, the ability to “print” sex organs seems assured.  It’s rabbit penises now, but can you really believe that men won’t pay to get bigger sex organs even more than women pay to have bigger breasts?  Especially when it becomes a matter of a single visit to a surgeon’s office that will heal faster than a vasectomy?
So, in a decade, I think it is quite likely that the patient seeking to alter their gender would start by seeing their surgeon, who would take a complete scan of the person.  This scan would then be entered in to a program that would allow the patient and the surgeon to transform the patient’s body into the precise appearance desired.  Once the body shape has been defined, the program would determine what changes would be needed, the amounts and types of stem cell stocks needed, the minimal surgery needed to reroute the urinary tract, nerves, etc. and then would proceed to extract the samples needed to create stem cell stocks.  The creation of the proper organs would then begin, using a 3d printer to create the needed tissues.  Once sufficient stocks were cultured the patient would be placed into the autodoc and, as the doctor supervised, be transformed.
It’s possible that even such steps as printing the organs might be unneeded as the autosurgeon might be able to construct the needed organs in situ.
This ability to control stem cells is why I think I’m stacking the deck.  We already know quite a bit about how to do so, and the rate at which that we are making progress, as well as the potential uses for controllable stem cells, makes this a medical technology that will be developed much further over the next few years.  Regenerative medicine not only promises to help cure such issues as heart disease and spinal cord injuries, but to grow replacement organs, replace missing and damaged tissue, and even to potentially allow such abilities as replacing missing limbs.  It’s a vitally important area of research, and as Wired points out, with such “frivolous” uses as breast enhancement, and the eventual penile enhancement so close to market, it’s going to be the biggest medical money-maker of the next decade.  It’s just one small part of the numerous advances that will be made in the next decade, but it’s one that is likely to make an enormous change to our social dynamics.  Unlike silicone, there is no “unnaturalness” to a stem cell breast enhancement, and I’m certain that the ability to make any size breasts will likely emerge before mid-decade.  Combine that with the ability to make bigger penises, which I also expect to come along mid-decade, and plastic surgery is likely to become as acceptable as getting a new hairstyle.  As we continue to make progress, and gain further abilities to use stem cells to heal, regrow, or reshape the body, more people are likely to use them to make themselves look more attractive, enhance their bodies, or even to rejuvenate and repair the effects of aging.  The potential uses for stem cells are enormous and, relatively speaking, changing someone’s sex is just one small possibility in thousands.
But it’s still something I consider to be a pretty safe bet.

article about lab-grown vagina:
http://www.nydailynews.com/life-style/he...-1.1761999

ovaries to testes article:
https://sciblogs.co.nz/code-for-life/201...t-mammals/

ou’d think that in adult mammals ovaries are ovaries, and that’s it. They’re committed to being what they are.
[Image: rb2_large_gray.png]
Or as geneticists would say, they’re terminally differentiated: they’ve reached the end of their differentiation pathway.
Well, it seems you’d think wrong. (This writer, too!)
In a stunning paper Henriette Uhlenhaut and 14 others show that if adult mice lose a Foxl2 gene, ovaries become testes.
These researchers raised mice in which they could delete the Foxl2 gene by treatment of tamoxifen, a compound that competes to block the estrogen receptor. (They used an inducible cre-recombinase system that responds to estrogen antagonist, tamoxifen. I’m summarising very lightly here for a general reader; biologists should start with the summary article.)
The surprising and unexpected result was that when adult mice were induced to lose their Foxl2 gene, their ovaries changed into testes! (I emphasis ‘adult’, as while embryos are still developing, adults are not.)
One up-shot is that this tells us that the ovary ’fights’ to maintain it’s status as an ovary throughout life. It’s not permanently committed. It is not a pathway that comes on ’by default’, either. Lose the Foxl2 gene and it changes.
Slightly more formally, this research shows that the ovary has to maintain constant suppression of the key testis development gene Sox9 by Foxl2; if not ovarian granulosa and theca cells change to become testicular Sertoli and Leydig cells, respectively.
Uhlenhaut and colleagues observe that the full set of genes associated with testis development becomes active and these XX (genetically female) mice produce similar amounts of the male sex hormone testosterone as XY (genetically male) mice.
My initial thoughts were that this work might be related to the well-known sex-reversal seen in some species of fish. The Australian scientists writing the summary article share this view (but coming from much more knowledge of the background than I have). They say it may also explain the female to male sex reversal of goats in polled intersex syndrome, where a region of their genome containing the Foxl2 gene has been lost. These workers also point to their own work, where ’knockdown’ of another gene, Dmrt1, required for testis development in chickens (and probably all other birds), results in feminization of the birds.
Taken together, it seems the view of the permanence of the status of the ovary in adult females in many species, not just mice, is under review.
It’s possible that this gene control pathway is also involved in human patients with premature ovarian failure or other disorders of sex development. I’m sure that these patients and their families will follow this emerging story closely.

sooo, if you induce the addition of Foxl2 gene, could the testis become ovaries????? interesting thought. 
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#2

More interesting articles

http://scienceblogs.com/notrocketscience...to-testes/

One gene stops ovaries from turning into testes



In science, we don’t often get to talk about male repression, but a new discovery gives us just such a chance. It turns out that ovaries can only remain ovaries by constantly suppressing their ability to become male. Silence a single gene, and adult ovaries turn into testes. That adult tissues can be transformed in this way would be surprising enough, but doing so by changing a single gene is truly astonishing.
[Image: i-cdd4a4a416a1c551fe14d11cd030d438-Ovary.jpg]As embryos, our gonads aren’t specific to either gender. Their default course is a female one, but they can be diverted through the action of a gene called SRY that sits on the Y chromosome. SRY activates another gene called Sox9, which sets off a chain reaction of flicked genetic switches. The result is that premature gonads develop into testes. Without SRY or Sox9, you get ovaries instead.
But Henriette Uhlenhaut from the European Molecular Biology Laboratory has found that this story is woefully incomplete. Maleness isn’t just forced onto developing gonads by the actions of SRY – it’s permanently kept at bay by another gene called FOXL2.

Uhlenhaut developed a strain of genetically engineered mice, whose copies of FOXL2 could be deleted with the drug tamoxifen. When she did this, she found that the females’ ovaries turned into testes within just three weeks. The change was a thorough one; the altered organs were testes right down to the structure of their cells and their portfolio of active genes. They developed testosterone-secreting Leydig cells, which pumped out as much of the hormone as their counterparts in XY mice. They only fell short of actually producing sperm.
Uhlenhaut found that FOXL2 and SOX9 are mutually exclusive – when one is active, the other is silent and vice versa. The two genes are at opposite ends of a tug-of-war, with sex as the prize. FOXL2 sticks to a stretch of DNA called TESCO, which controls the activity of Sox9. By sticking to TESCO, FOXL2 keeps Sox9 turned off in the adult ovary. Without its repressive hand, Sox9 switches on and sets about its gender-bending antics.
FOXL2 also has a partner-in-repression – the oestrogen receptor, a docking molecule for the hormone oestrogen. The two proteins interact with one another and they cooperate to block Sox9.
The same genes may help to explain the frequent acts of gender-swapping among, fish, reptiles and birds (no, Steve Connor, “one of the great dogmas of biology” is not that “gender is fixed from birth”). In these animals, oestrogens often cause males to change sex into females, and falling levels of oestrogen can trigger the reverse transformation. FOXL2 may also be involved.  
The fact that oestrogen helps to maintain the gender of mice is surprising. Unlike other back-boned animals, mammals are thought to be largely insensitive to levels of sex hormones outside of development. However, Uhlenhaut suggests that oestrogen’s role in keeping ovaries and ovaries may explain why women sometimes appear slightly more masculine after the menopause, a time characterised by falling oestrogen levels.
There have been hints from many species that FOXL2 plays an important role in determining sex. People who inherit faulty copies of the gene can develop a rare disease called BPES that often leads to infertility because of failing ovaries. Goats whose FOXL2 isn’t controlled properly develop a condition called polled intersex syndrome (PIS), where they become males despite carrying two X chromosomes. Females that lack the gene altogether fail to develop proper ovaries at all.
Understanding how gender is set and maintained is vital, for it is such a basic and pervasive element of our lives. Uhlenhaut’s work isn’t just of academic interest. It could also help to treat disorders of sexual development. It could also change how gender reassignment therapies are done, paving the way for gene therapies rather than multiple painful surgeries.
Reference: Uhlenhaut, N., Jakob, S., Anlag, K., Eisenberger, T., Sekido, R., Kress, J., Treier, A., Klugmann, C., Klasen, C., & Holter, N. (2009). Somatic Sex Reprogramming of Adult Ovaries to Testes by FOXL2 Ablation Cell, 139 (6), 1130-1142 DOI: 10.1016/j.cell.2009.11.021
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#3

interesting: FoxL2 is expressed in adrenal glands as well(in mice):

http://www.bioone.org/doi/10.1095/biolre...prevSearch=
Synergistic Activation of the [i]Mc2r[/i] Promoter by FOXL2 and NR5A1 in Mice[url=http://www.bioone.org/doi/10.1095/biolreprod.110.085621?prevSearch=#n104][/url]

Forkhead box protein L2 (FOXL2) is the earliest ovarian marker and plays an important role in the regulation of cholesterol and steroid metabolism, inflammation, apoptosis, and ovarian development and function. Mutations and deficiencies of the human [i]FOXL2[/i] gene have been shown to cause blepharophimosis-ptosis-epicanthus inversus syndrome as well as premature ovarian failure. Although Foxl2 interacts with steroidogenic factor 1 (Nr5a1) and up-regulates [i]cyp19a1a[/i] gene transcription in fish, FOXL2 represses the transcriptional activity of the gene that codes for steroidogenic acute regulatory protein ([i]Star[/i]) in mice. Most of the recent studies have heavily focused on the FOXL2 target genes ([i]Star[/i] and [i]Cyp19a1[/i]) in the ovaries. Hence, it is of importance to search for other downstream targets of FOXL2 and for the possibility of FOXL2 expression in nonovarian tissues. Herein, we demonstrate that the interplay between FOXL2 and NR5A1 regulates [i]Star[/i] and melanocortin 2 receptor ([i]Mc2r[/i]) gene expression in mammalian systems. Both FOXL2 and NR5A1 are expressed in ovarian and adrenal gland tissues. As expected, FOXL2 represses and NR5A1 enhances the promoter activity of [i]Star[/i]. Notably, the promoter activity of [i]Mc2r[/i] is activated by FOXL2 in a dose-dependent manner. Surprisingly, we found that FOXL2 and NR5A1 synergistically up-regulate the transcriptional activity of [i]Mc2r[/i]. By mapping the [i]Mc2r[/i] promoter, we provide evidence that distal NR5A1 response elements (−1410 and −975) are required for synergistic activation by FOXL2 and NR5A1. These results suggest that the interplay between FOXL2 and NR5A1 on the [i]Mc2r[/i] promoter functions as a novel mechanism for regulating MC2R-mediated cell signaling as well as steroidogenesis in adrenal glands.
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