Found a way to reopen growth plates (2 Viewers)

[birthdefect]

Yes

birthdefect loik what I tagged Biomaxx in, I tagged yall in the replies

lmk which parts you want me to read ill read it

 

[DoorHandle5]

lmk which parts you want me to read ill read it

I tagged you bro.

 

[DoorHandle5]

Thoughts? You seem smart Biomaxx

birthdefect look what I tagged biomaxx in

 

[birthdefect]

birthdefect look what I tagged biomaxx in

the stem cell niche doesnt remain in humans?
thats what plate fusion is in humans
when all the cartilage is replaced with bone, which estrogen speeds up by increasing how quickly they differentiate both non genomically and genomically
rat plate fusion isnt the same as humans

 

[DoorHandle5]

the stem cell niche doesnt remain in humans?
thats what plate fusion is in humans
when all the cartilage is replaced with bone, which estrogen speeds up by increasing how quickly they differentiate both non genomically and genomically
rat plate fusion isnt the same as humans

What if it did remain, would my theory work?

 

[birthdefect]

What if it did remain, would my theory work?

if it did remain ie was more similar to rat plates AND the concept works in rats then yea it would

 

[DoorHandle5]

if it did remain ie was more similar to rat plates AND the concept works in rats then yea it would

niche =/= structure

 

[birthdefect]

niche =/= structure

?

 

[ysl]

ngl

 

[Syna]

Veridic this is where the mental retardation of this baboon began

 

[Veridic]

Veridic this is where the mental retardation of this baboon began

Trying to find the part that actually reverses epiphyseal fusion in this post...

You can really tell who graduated from the university of looksmax tiktok comment sections

 

[Syna]

Nigga is trying to apply mouse biology to human biology, its stupid af, it's useless if you signal something that is already dead and closed, even more stupid to extrapolate info from animal studies and think that human biology makes a perfect conversion from it, even more to think you can alter the state of solid bone, you cant reverse the cartilage ossification at all, once its ossified there is no way back, also you can't even make this function localized, and also the biggest fallacy of this is the fact that if people grew because of PTH analogs women would grow after using them for osteporosis.

There is no niche or any functional cartilage left for chondrocytes to work on whatsoever, so the PTH proliferation theory is so bs, the studies and theory also only demonstrates plasticity and not the power to reverse the ossification, also what he mentioned of the "PTCH1 knockout" even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors not the controlled longitudinal growth that he is thinking about, also another fallacy, what he mentioned of the "PTHrP/SOX9" only shows that they can help maintain the proliferation and inhibit hypertrophy, and aid the repair of the physeal injuries, but not reopen fused growth plates, no way to revive fused bone, also the insane risk of an osteosarcoma, also no way to organize cell in a 3d controlled way as a columnar structure resting with proliferating columns (prehypertrophic and hypertrophic), polarized stem cells, and with real balanced paracrine gradients (which are the PTHrP from the resting zone vs. Ihh from the hypertrophic zone),again after ossification it's just bone with no real cartilage niche. Also all the clinical trials is just studies performed on animals with open growth plates, all of this is use to treat physeal injuries not reverse it.
PrettyBoyMaxxing

Bone growth comes in a ton of diff ways, not just elongation, this is why all the pharma for increasing bones with this and that is retarded af, you can't control where the growth is gonna occur and certainly not localized.

Basically, 1: growth plates senescence prohibits this as this is a genetic biological process 2: once it's solid bone there is not cartilage matrix left, all bone, 3: even if there is is the cell and cartilage structure is completely disorganized which would not cause any longitudinal organized growth, 4 the gene once methylated is not usable at all, 5: you cant signal it to work again cause its already fused, 6: there needs to be something taking care of the cartilage to create for it not to instantly ossify cause of the highly osteogenic environment (explained in more words: "PTCH1 knockout" even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors not the controlled longitudinal growth that he is thinking about, also another fallacy, what he mentioned of the "PTHrP/SOX9" only shows that they can help maintain the proliferation and inhibit hypertrophy, and aid the repair of the physeal injuries, but not reopen fused growth plates, no way to revive fused bone, also the insane risk of an osteosarcoma, also no way to organize cell in a 3d controlled way as a columnar structure resting with proliferating columns (prehypertrophic and hypertrophic), polarized stem cells, and with real balanced paracrine gradients (which are the PTHrP from the resting zone vs. Ihh from the hypertrophic zone),again after ossification it's just bone with no real cartilage niche).

Completely wrong with the take that animal biology is the same as human biology, it's actually pretty fucking diff on every single level, keep backpeddling with the claims "thats why this is just a theory" but you were affirming this would work, all the lab rat studies you mentioned, the xrays and scans only showed increase of BMD not elongation of the bones or the revival of cells and chondrocytes, when you are conducting a scientific research anomalies need to be mentioned and noted, guess what? none of the studies mentioned showed or noted any of that, this studies are conducted by real scientists not people like you, also the entire growth plate cartilage undergoes programmed senescence, the entire plates is replaced by bone and the left chondrocytes are disorganized and not on any sort of structure that could be re used for longitudinal


bone growth, also PTH analogs promote bone formation that's why they are use to increase BMD, but they don't keep the cartilage alive which is what i needed for it to then ossify, basically because when you have closed growth plates THERE IS NOT CARTILAGE LEFT, also the cartilage niche goes to shit once the plate is already ossified, also there is no way to control the highly osteogenic environment, if we ignore all what i said before and this magically works it would ossify super fast, not the span of time needed for proper cartilage growth and then ossification, all the animal studies conducted also don't show any evidence that could proof this at all whatsoever,

 

[Syna]

Veridic

 

[Syna]

surgerymax tho i must warn you, you might wanna up the cerebro dose cause the neurotoxicity reading this bs will cause is insane.

 

[surgerymax]

surgerymax tho i must warn you, you might wanna up the cerebro dose cause the neurotoxicity reading this bs will cause is insane.

stopped reading after seeing he was using a rodent model with growth plates that don't fucking fuse anyway

 

[Syna]

stopped reading after seeing he was using a rodent model with growth plates that don't fucking fuse anyway

He is so fucking retarded he can't even comprehend that banded sleeping doesn't work cause of how fucking gravity works

 

[certifiedvolcel]

Abaloparatide for 3 weeks daily then hgh + AI

Explanation later in comments

tales

 

[certifiedvolcel]

View attachment 40583
proof that the stem cell niche remains. in all the images, stem cells are stained red, and in the bottom row of images, osteoblasts are stained green. you can see the line of scrimmage



once the osteoblast invasion of the proliferating zone (with the columnar chondrocytes) has come and passed, the stem cells are now subject to the whims of the osteoblasts forever after



fortunately, this new structure is heavily perfused, with plenty of vessels, meaning that systemic peptide administration will see peptide leaking into the stem cell niche



what's fascinating, and indeed, optimism inducing, is that the chondroprogenitors (stem cells that constitute the resting zone of a functional growth plate) develop the ability to self-replenish only postnatally. prior (fetal & neonatal), these cells constitute a reservoir that is otherwise depleted.



in a murine model, it only takes 14 days postnatally for these stem cells to reach peak concentrations in the growth plate



the theory is that you inject the abaloparstide for a few weeks to revive the growth plates, then you stop and start injecting hgh to grow + AI to keep the plates open



in the immature growth plate, angiogenesis only features towards the bottom of the apparatus in conjunction with osteogenic influences, like osteoblasts. obviously, maturation of the growth involves this region encroaching further and further up the plate with the aid of estrogen, crunching the proliferating & prehypertrophic zones until the resting zone becomes adjacent to the line of scrimmage



these blood vessels grapevining about the stem cell niche in our matured growth plates will ensure that systemically-injected abaloparatide will get its opportunity to impart impact



and do not doubt how plastic the growth plate can be; the concept of plasticity is useful, even if misapplied in heightmaxxing communities. a growth plate dissected and reimplanted in rabbit bones quickly re-establishes itself and functions normally. even when the growth plate is implanted in a perpendicular manner, it still operates as it would (albeit adding cells along the width as opposed length of the bone, but that's besides the point).



studies have even shown that "cartilaginous islands," otherwise known as "ectopic" cartilage, can be generated when stem cells are exposed to SOX9 or even hedgehog molecules



this tells me that the growth plate can be resuscitated with affairs are orchestrated correctly

tldr