Natural Height Growth - Cancer, Stem Cells, Regenerative Tissue Engineering, Transdifferentiation

Time 2020-12-11 16:04:21

Web Name: Natural Height Growth - Cancer, Stem Cells, Regenerative Tissue Engineering, Transdifferentiation

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Cancer,Stem,Growth,

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Whole bone mechanics and mechanical testing Lateral impact loading of a long bone causes bending. The fracture starts at the tension side (away from the site of impact) and progresses across the bone up to the middle. When it reaches the compressive side, it ‘runs’ along the direction of maximal shear (at 45 to the transverse), creating a butterfly fragment. -See Figure 9 of the paper for the image I can t copy and paste it.But the above image is basically what happens with the arrow being the point of impact.  3 point bending is another method in the above study that doesn t really occur physiologically and may be worth tryingBut the whole reason behind LSJL in the first place was that the epiphysis is more easily deformable than the diaphysis which is why Yokota developed the joint loading modality. when a long bone is impact-loaded in a direction perpendicular to its long axis it bends, such that the side contacted by the impact is loaded in compression, while the opposite side is loaded in tension. As a result, failure will begin on the opposite side to the impact (the tensile side) since it will reach its ultimate strength sooner than the side loaded in compression. As the advancing crack will reach the middle of the bone, it will reach compressed tissue, and due to bone’s higher resistance to this type of load, it will advance in a path nearer to the bone’s longitudinal direction, along the directions of maximal shear stress. In this way it will form a fracture with a so-called ‘butterfly’ fragment, commonly seen in practice Lateral impact loading of the spine is kind of studied here:Impact Loading of the Lumbar Spine During Football BlockingBut I couldn t really find any interesting insights.Lateral impact loading in general is generally studied on cartilage because it does not occur really often physiologically. The effects of lateral impact loading where studied mainly terms of fracture but the forces should be about the same.  Instead of loading in the middle we re putting the impact near the longitudinal ends of the bones but still on the diaphysis.  The impact causes compressive and tensile strain in the bone which drives fluid forces(intramedullary pressure, interstitial fluid flow, blood perfusion).Fluid forces degrade bone and provide the microenvironment for longitudinal bone growth without needing to be in the plastic deformation range. I was reviewing old LSJL papers and I found this nugget from Diaphyseal bone formation in murine tibiae in response to knee loading  conceivable hypothesis underlying these observations of bone formation with the knee-loading modality is that mechanical loads applied to the epiphysis induce the osteogenic signal towards the diaphysis through fluid flow in the lacunocanalicular network (1st model) or through alteration in blood circulation (2nd model) Potential contributors to enhance bone formation in the tibia with knee loading. This schematic illustration includes muscle contraction, alteration in intramedullary pressure, load-driven interstitial fluid flow, and activation of blood perfusion. So these are all the methods to stimulate the bone.  We want to find the method that stimulates interstitial fluid flow, blood perfusion, and intramedullary pressure the best to increase height.  I believe that lateral impact loading is the best except it does not involve muscle contraction.  The simple solution is to contract your muscle while performing lateral impact loading.  The two most common methods of stimulating these forces muscular loading and axial impact are not enough to stimulate these forces above the threshold needed to increase height.Here s some more information about the fluid flow and intramedullary pressure.Blood bone perfusion can be measured(Noninvasive methods of measuring bone blood perfusion) so it would be nice if we could test several different methods to see what generates the highest force.FLUID MOVEMENT IN BONE: THEORETICAL AND EMPIRICAL Evidence from the literature and from our laboratory demonstrates a pronounced and rapid flow of fluids and associated solutes through the extravascular spaces in bone. Minutes after injection, large molecules such as ferritin and horseradish peroxidase (HRP) have been localized throughout the osteocytic lacunae and canaliculi of cortical bone in the chick, rat and dog. Patterns of marker movement preclude diffusion as the mechanism for solute movement and suggest a centrifugal bulk flow of fluids. We have developed a computer model of bone fluid flow that has led to the conclusion that the pattern and rate of fluid movement is governed by the pressure differential across the bone, the vascular architecture, and the porosity of the mineralized matrix. The validity of simulations in which a substance is injected and monitored over time has been tested by comparisons with actual injections of markers in the rat. Evidence is presented for a relationship between blood flow and bone dynamics in growth, repair and pathology of bone. We employed the tail suspension model of weightlessness in the rat to test the effect of posture on the perfusion of cortical bone using injections of HRP. Data indicated that perfusion of the femur was reduced by this treatment. We propose a rheostat mechanism, which suggests that bone perfusion may set limits for bone growth and remodeling. Therefore, bone mass reflects the ability of the vasculature to supply oxygen and nutrients to the cells on and within the mineralized matrix. The blood supply to the long bones comes from three sources: the nutrient arteries. the periosteal arteries. and the metaphyseal-epiphyseal arteries The studies can go on and on.  The point is that there is a threshold of forces:blood perfusionIntramedullary pressureInterstitial fluid flowMuscular contractionSuch that you can grow taller.  I believe that the primary force is intramedullary pressure.  LSJL(Knee loading) is primary deformations of the epiphysis which I don t believe to be the best way to increase intramedullary pressure as it is indirect.  The best way to increase intramedullary pressure is directly on the region itself.  Thus lateral impact loading directly on the diaphysis.Bodybuilders should already have high blood perfusion and muscular contraction so it is unlikely that those two forces can make you taller.  Unless that threshold is really, really high.Interstitial fluid flow unless it degrades bone is mostly about delivering nutrients to bone which in and of itself will not make you taller(unless you have open plates).Unless these forces increase intramedullary pressure, which all these forces have been shown to increase intramedullary pressure(Exercise training augments regional bone and marrow blood flow during exercise), they are probably not going to make you taller.  The problem is these forces do not increase intramedullary pressure enough.  Muscular contraction is indirect loading and limited by muscle size and speed by which you contract the muscles.  Imagine the bone is a balloon.  The muscle is the pump.  The air is going out and you have to pump it faster than it s going in.  Whether the balloon gets pumped(high enough intramedullary pressure) depends on the strength(size of muscle) and speed of the pumps(speed of contraction).  Axial loading does not really drive fluid flow as well as lateral loading.Maybe electrical muscular stimulation can make for above normal muscular stimulation but if the contractions are very rapid they re unlikely to be able to be very strong.The goal of impact loading is to bypass the limitations of muscular contraction and directly increase intramedullary pressure.   The goal of lateral loading is that it is more effective than axial loading in driving flow.Femoral venous ligation has been shown to increase bone length in (growing 8 week old) rats.  Veins take blood towards the heart so they decrease intramedullary pressure.  In that study Intramedullary Pressure was only increased by 50%.  Imagine if the pressure was higher.I believe that the key to growing taller involves passing an intramedullary pressure threshold and that lateral impact loading may be the key to passing that threshold. Trying the new lateral impact loading method, I tried looking at activities that people are already doing that generate lateral impact loading.  Muay Thai shin conditioning seemed to only be surface level conditioning, gymnastics and punching generate axial impact loading(punching may occasionally generate lateral impact on the metacarpals but really you want to punch with the knuckles), and tennis may occasionally generate lateral impact but the force is entirely dependent on the speed on which you receive the ball.But it looks like running may generate lateral impact in the metatarsals.  I originally thought that most of the impact in running is axial and absorbed in the heel but when doing up stairs I do have lateral impact on my metatarsals.   So where the impact is on the foot depends on the style and type of running and jumping.  And it looks like the forces in running are sufficient to induce microfracture in the metatarsals.Now stress fractures in the metatarsals do seem to occur mostly in people with bone disorders but if the lateral impact is sufficient to induce a stress fracture even in a bone weakened state then it is probably sufficient to induce longitudinal bone growth.  This isn t perfectly true as the frequency will be different.  The stress fracture could not necessarily be a result of lateral impact loading it could be repetitive torsional forces for instance.The question is whether is there any evidence that the repetitive impact loading on the metatarsals induced by running and jumping induces longitudinal bone growth?  The answer is maybe.  In pregnancy and running, the increase in shoe size is thought to be a decrease in arch size.Look at the metatarsals, if the metatarsals got longer then the arch size would be reduced because the metatarsals are closer to the ground then the other bones thus reducing the arch angle.  So longer feet via metatarsal growth would be the cause of the flatter arches rather than flatter arches being the cause of feet growth.Let s look at the paper Dimensional changes of the feet during pregancy. Women commonly report that the feet become larger during pregnancy. These changes could be due to the ac- cumulation of fluid or fat, or both, or to changes in ligaments caused by the extra weight that is carried during pregnancy or by hormonally induced alterations of the connective tissue in the ligaments.   They couldn t find a statistically significant difference in foot length due to pregnancy.  Since most foot increase is due to occasional anecdotal evidence it s likely that most scientific studies haven t had the sample size to find the needle in the haystack of women who had the right force to increase foot length.Ideally, we d find a sport or culture where people walk and run like this then we can be pretty confident that all the load is going to to the metatarsal.If there are anecdotal cases of pregnancy and running increasing foot length then that is some evidence which could possibly occur via the metatarsals then that is some evidence that lateral impact loading can increase bone length.  But there does not seem to be sufficient studies of the effect of running on metatarsal length.  You d have to run in a certain style to induce lateral impact on the metatarsals and the frequency and stimulus would have to be sufficient to induce longitudinal bone growth.  This would be hard to capture in a study.  And what d you expect to see is occasional anecdotal evidence.Apparently, some runners actually get shorter feet from running.  This is speculated due to be to tighter ligaments.  You d expect the ligaments due to get tighter due to the being over stimulated.  Like how muscles shorten due to being constantly overstretched.  This is actually support that certain types of running may lengthen the metatarsals through lateral impact as constant stretching is not consistent with lengthening it is usually consistent with tightening up.We need to look more through anecdotal evidence and try to find patterns.  We should also look at ligament laxity and see if running foot size can really be explained by it. This paper provides some support that mechanical loading stimulates the fluid contents of the bone(angiogenesis is the formation of new blood vesses).  Lateral impact loading is the what I view as the most direct and effective method to move the fluid contents within the bone.This paper is also by both Yokota and Zhang.  Papers such as those below strongly support the use of lateral impact loading for bone tissue stimuli.  That lateral impact loading will increase height requires additional leaps.Before that paper here s some information about Type H blood vessels.Motivating role of type H vessels in bone regeneration Coupling between angiogenesis and osteogenesis has an important role in both normal bone injury repair and successful application of tissue‐engineered bone for bone defect repair. Type H blood vessels are specialized microvascular components that are closely related to the speed of bone healing. Interactions between type H endothelial cells and osteoblasts, and high expression of CD31 and EMCN render the environment surrounding these blood vessels rich in factors conducive to osteogenesis and promote the coupling of angiogenesis and osteogenesis. Type H vessels are mainly distributed in the metaphysis of bone and densely surrounded by Runx2+ and Osterix+ osteoprogenitors{Hence why we may want to tap the metaphysis}. Several other factors, including hypoxia‐inducible factor‐1α, Notch, platelet‐derived growth factor type BB, and slit guidance ligand 3 are involved in the coupling of type H vessel formation and osteogenesis. In this review, we summarize the identification and distribution of type H vessels and describe the mechanism for type H vessel‐mediated modulation of osteogenesis. Type H vessels provide new insights for detection of the molecular and cellular mechanisms that underlie the crosstalk between angiogenesis and osteogenesis. As a result, more feasible therapeutic approaches for treatment of bone defects by targeting type H vessels may be applied in the future.  use of the immunosuppressive drug rapamycin, which has anti‐angiogenic properties, inhibited neovascularization in the fracture callus and delayed fracture healing. Vessels can not only maintain the high metabolic demand for nutrients and oxygen in the callus, but also provide pathways for cells such as inflammatory cells, fibroblasts and osteoblast/osteoclast precursors to enter the defect area. There are two subtypes of vessels, type H vessels and type L vessels, in the capillaries of the metaphysis and bone marrow cavity. These vessels are classified according to their specialized ECs that have specific molecular and morphological properties. Type H vessels are mainly distributed in the metaphyseal region and sub‐periosteum and show strong positive staining with antibodies against two kinds of EC proteins (CD31 and EMCN), while type L vessels are mainly distributed in the diaphyseal region and show weak positive staining for CD31 or EMCN. Type H vessels are interconnected by distal vessel loops or arches and resemble straight columns, while type L vessels mainly located in the diaphysis display a highly branched pattern characteristic of the sinusoidal vasculature of the bone marrow. These two types of vessels are closely connected at the epiphysis‐diaphysis junction and form a complete vascular bed in the bone marrow cavity Although type H ECs only account for 1.77% of all bone ECs and 0.015% of total bone marrow ECs, a large number of bone progenitor cells, which can differentiate into osteoblasts and osteocytes, are distributed around these vessels, suggesting that type H vessels may be a potent promoter of bone regeneration. The dense distribution of Runx2+ osteoprogenitors and osteoblasts around these CD31+ vessels in the metaphysis and endosteum confirms their role as a potent promoter of bone regeneration. In contrast, type L vessels have almost no surrounding bone progenitor cells. The two types of ECs were isolated and purified from bone tissue and evaluated for their levels of mRNA expression for secreted growth factors that promote the survival and proliferation of bone progenitor cells. The transcript levels for Pdgfa, Pdgfb, Tgbf1, Tgfb3 and Fgf1 in type H ECs were significantly higher than those in type L ECs. These secretory growth factors are closely related to the proliferation and survival of bone progenitor cells Thus, the findings further confirm a key role for type H vessels in bone regeneration. Type H vessels can transit to type L vessels, suggesting that type H ECs may be the upstream ECs in bone. -this may suggest that tapping the epiphysis would be more effective to gaining height as it transmits the bone progenitor cells from the epiphysis to diaphysis.  But I did not gain any height for years by tapping the epiphysis.  The only period where I showed potential height was where I tried tapping the diaphysis.  I believe this may be due to fused growth plates blocking effective movement between the epiphysis and diaphysis.  This blockage is somewhat shown by the fact that while the epiphysis houses red bone marrow the diaphysis the yellow bone marrow which you wouldn t expect unless there was some sort of bloackage.  However, the metaphysis holds these type H vessels which I recommend tapping there. The proliferation ability of type H vascular ECs in young individuals was significantly stronger than that in adult individuals, while the proliferation ability of type L vascular ECs did not differ significantly between young and old individuals. Notch signalling in type H vascular ECs plays a key role in mediating vascular formation and osteogenic coupling. Cell proliferation and high expression of Noggin protein occur in type H vascular ECs under the action of Notch signalling. Noggin protein can promote proliferation and differentiation of osteoblastic progenitor cells as well as maturation and hypertrophy of chondrocytes. Mature and hypertrophic chondrocytes can guide vascular budding through high secretion of VEGF and promote the generation of new blood vessels. Through the combination of Notch signalling by ECs, Noggin and VEGF, the processes of osteogenesis and angiogenesis are linked together. After blockade of Notch signalling in ECs, vessel disorganization, cartilage defects, reduced bone trabeculae and many other low osteogenesis manifestations were found in bone marrow. These results indicate that type H vessels play important roles in mediating growth of blood vessels, maintaining number of perivascular bone progenitor cells and coupling of osteogenesis and angiogenesis MMP‐9 released from type H ECs, not osteoclasts, are essential for resorbing cartilage to lead longitudinal bone growth When the expression level of PDGF‐BB was knocked down in adult mice, the number of type H vessels was significantly decreased, accompanied by reductions in trabecular bone and cortical bone mass. When a bone defect occurs, monocyte/macrophage lineage cells such as tartrate‐resistant acid phosphatase‐positive (TRAP+) mononuclear cells and osteoblastic cells move to the bone defect area and secrete PDGF‐BB to recruit PDCs for osteogenesis. low‐intensity pulsed ultrasound (LIPUS) can promote blood flow and angiogenesis in the fracture healing process. LIPUS induced substantial increases in osteoblast proliferation and type H vessel number in a rat spinal fusion model. The matrix modification properties of matrix metalloproteinases (MMPs) can also affect angiogenesis and bone formation.MMP‐2 promoted a marked increase in the vessel number in bone, while type H ECs released MMP‐9 with a key role in resorption of articular cartilage during growth of long bones -I believe Lateral Impact Loading will strongly beat LIPUS in stimulating fluid flow just by basis of the word low-intensity.Here s the Yokota paper:Mechanical loading stimulates bone angiogenesis through enhancing type H vessel formation and downregulating exosomal miR‐214‐3p from bone marrow‐derived mesenchymal stem cells Exosomes are important transporters of miRNAs, which play varying roles in the healing of the bone fracture. Angiogenesis is one of such critical events in bone healing, and we previously reported the stimulatory effect of mechanical loading in vessel remodeling. Focusing on type H vessels and exosomal miR‐214‐3p, this study examined the mechanism of loading‐driven angiogenesis. MiRNA sequencing and qRT‐PCR revealed that miR‐214‐3p was increased in the exosomes of the bone‐losing ovariectomized (OVX) mice, while it was significantly decreased by knee loading. Furthermore, compared to the OVX group, exosomes, derived from the loading group, promoted the angiogenesis of endothelial cells. In contrast, exosomes, which were transfected with miR‐214‐3p, decreased the angiogenic potential. Notably, knee loading{knee loading is traditional LSJL} significantly improved the microvascular volume{volume of the smallest blood vessels}, type H vessel formation, and bone mineral density and contents, as well as BV/TV, Tb.Th, Tb.N, and Tb.Sp. In cell cultures, the overexpression of miR‐214‐3p in endothelial cells reduced the tube formation and cell migration. Collectively, this study demonstrates that knee loading promotes angiogenesis by enhancing the formation of type H vessels and downregulating exosomal miR‐214‐3p. In blood flow, shear stress and strain in the vessels are the major biomechanical parameters. Mechanical forces play a crucial role in vascular injury and repair, which can directly activate the mechanosensing molecules. We have developed joint loading modalities, in which dynamic lateral loads are applied to synovial joints such as the elbow, knee, and ankle. mechanical loading induces dynamic deformation in the epiphysis that drives the alteration in intramedullary pressure in the medullary cavity and interstitial fluid flow in the lacunocanalicular network. -I found from experience that due to the rats not having fused growth plates this may be different than humans.  The fused growth plate may reduce the the ability of the fluids from the epiphysis to reach the intermedullary cavity.  It may happen somewhat but not to the extent as with open growth plates.  Thus instead of targeting the epiphysis we target the metaphyseal region which is below the epiphyseal line.  Also there have been studies by Yokota that have shown a limit to the bone deformation that can be achieved by lateral loading. knee loading stimulated wound healing in the femoral neck and tibia, prevented cartilage degeneration, and promoted vessel remodeling and bone healing in osteoporosis of the femoral head. As nanometer‐scale particles, exosomes are one form of extracellular vesicles (EVs) together with microvesicles and apoptotic bodies. Exosomes are small vesicles of endocytic origin and are suggested to act as an essential mediator in intercellular communications. For instance, bone marrow‐derived mesenchymal stem cells (BMMSCs) play a vital role in osteoblastic differentiation via a paracrine pathway, and several studies have demonstrated the role of BMMSC‐derived EVs in vessel remodeling and bone healing. In vivo experiments revealed that exosomes markedly stimulated bone regeneration and angiogenesis in critical‐sized calvarial defects in ovariectomized rats In the current study, loads with 1 N and 5 Hz were given for 6 min/day for 14 consecutive days. compared to the sham control, OVX treatment decreased cell migration and knee loading enhanced it The image isn t big enough for me to see if there s any abnormalities. Mechanical forces such as shear stress and cyclic strain can regulate the adhesion, proliferation, migration, and differentiation of stem cells via serious signaling pathways. The enrichment and differentiation of stem cells play an important role in the angiogenesis and maintenance of vascular homeostasis. There s no smoking gun in these studies that show that an increase in the movement of the various fluids can lead to creation of longitudinal bone growth.  But it shows that the epiphysis and metaphysis get the good type h vessels but the diaphysis gets the type L vessels.  Thus just contracting muscles and building heart rate to increase blood flow will not cut it.  You ll need a stronger force such as lateral impact loading near the metaphysis.  To grow taller we d need a mechanism such as enhanced osteoclast activity degrading cortical bone to allow for interstitial longitudinal bone growth or we d need fluid movement in the bone directly degrading the cortical bone.  Lateral impact should provide the strongest fluid forces needed to stimulate this.Lateral synovial joint loading should provide some benefit but epiphyseal deformation seems to have a limit and the limit of fluid forces to reach the medullary cavity may be limited by the epiphyseal line. Here s the new LSJL method I m trying,Here s the thread where I share my progress and my thoughts.The method isn t quite lateral synovial joint loading but it is based on the same science.  I remember watching a Hiroki Yokota where he explains that he got the idea for lateral loading the synovial joints because of a water bottle.  Axial loading does not drive a lot of fluid through the bottle but lateral loading does.This is the lecture where he made that point but I can t seem to access it.The problem with lateral loading of the epiphysis is that there seemed to be a limit to be bone deformation of the epiphysis.  Also, the epiphyseal line may reduce the ability for the fluid forces to be transmitted through the rest of the bone.  Also, there was problems with slippage of the clamp.Most fluid forces generated in the bone are generated via muscular contractions and axial loading/impact.  There is a threshold that has to be generated in terms of fluid forces(Hydrostatic pressure, fluid flow, etc.) that needs to be surpassed to potentially induce longitudinal bone growth i.e. degradation of cortical bone, a chondrogenic microenviroenvironment, mesenchymal condensation, etc.Lateral impact doesn t really occur physiologically,  I looked at muay thai shin condition and it seemed to be mostly surface level not really affecting deep within the bone.  Tennis may cause a little bit of lateral impact within the bone.  But it s dependent on the force of the ball in the racket transmitting into the arm.  It s not easily reproducible.  So lateral impact on the bone is not really something that occurs physiologically.In distraction osteogenesis, one of the key steps is a hematomma allowing for bone regeneration to occur.  This establishes that the bone marrow is a very powerful stimulating force on the bone.The goal is to try to mimic this mechanical stimuli without actually breaking the bone and the method is to try to generate as much fluid pressure on the bone as possible.We could combine lateral impact, with epiphyseal clamping, and muscular contraction to try to increase the fluid forces of the bone to be higher.  We want the tapping to be on the cortical bone of diaphysis so it stimulates the marrow cavity.   That the marrow cavity turns to fat yellow bone marrow should be a big clue.  If something changes from development it it something we likely want to try to revert to get to an early developmental stage.Now how to prove that this occurs?Method 1:  Self testing.Method 2:  Look inside the bone to see how it responds to fluid forces(it s been done with hydrostatic pressure and interstitial fluid flow  but mostly at a cellular level).  We d ideally want to see degradation of cortical bone(can measure via certain osteoclast markers), chondrogenic differentiation, and mesenchymal condensation.  This would take possibly years in the lab.But there have been numerous studies showing the power of fluid forces in bone.  Lateral impact generates the most fluid forces in bone.  Fluid forces that have been shown to induce chondrogenic differentiation and powerful regeneration.To contradict this theory, provide evidence that:Lateral impact on the bone does not generate the most fluid forces in the bonelateral impact already occurs physiologically in an activity or sportNo amount of lateral impact could pass the pressure/other thresholds to stimulate longitudinal bone growth.Crispr is an exciting technology because of the DIY possibilities facilitated by website like The ODIN.  as far as I know there have been no instances of genetic doping.  Crispr on live adult humans is in exact.  You can only edit one gene at a time and the number of cells that are actually edited may be low.  There are still a number of potential targets:1) general anabolic target like HGH,IGF1,IGF2.  This would make it easier to see gains in slow height increase.  Some bones like the jaw do have potential to grow naturally in adulthood.  As seen in people with acromegaly.  An anabolic target would allow us to see a height increase method that may take a year to yield results get results in a much shorter time frame.  Something like HGH also increases bone turnover since cortical bone may impede height increase this would be useful for height seekers.2)  inject specifically in the articular cartilage.  since these cells are an isolated population pretty much this is a possible target.  Even if crispr only alters one cell if it results in massive ECM production that could lead to height increase due to ECM you could also increase chondrocyte proliferation   this would have to be tested on animal models first as you would want to know what kind of effects this is going to have If your knee is overproducing ECM that could result in loss of knee function. if you have open growth plates injecting there is a possibility too but again we d want to know what happens in animal models first as you could really mess up your growth plate.3)  target the osteoclasts.  You could weaken the bone enough to allow growth.  Cortical bone inhibits bone from growing interstitially(from within) so if you degrade it you could allow for bone to now grow interstitially.  But this could really mess up your bone and Hgh already increases bone turnover.  .  And it would be hard to inject into the bone itself.4) weaken ligaments and periosteum which may constrain growth again would have to be tested on animals first as you would have the potential to mess up your body.5) target the marrow cavity.  You could potentially induce differentiation of stem cells within the marrow cavity.  This could create neo-growth plates.  It would be exceptionally hard to do this as a lot depends on the microenvironment of the cell.There s not a lot of potential for self test for CRISPR.  At most you could target one gene in contrast to a mechanical method which can alter many genes.  The best bet is a general anabolic as making a bone length increase faster would be a huge aid in testing.  However, there are likely already people trying to do this and I haven t seen amazing results with myostatin(which does help for bone too).The best bet for DIY CRISPR testing is on animals.  Experiments would have to be designed carefully to not go over budget.  Ideally though a ton of genes and methods would be targeted to see what sticks.Here s a paper on musculoskeletal applications of CRISPR technology.  mouse RAW264 cells deleted for Zscan10 and differentiated into osteoclasts by RANKL With orthopaedic tissues, the extracellular matrix also presents a significant barrier to deliverystimulation were found to have increased osteoclast activity.

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