We have known about the research that Dr. Robert Tracy Ballock have been doing for a while now and as for myself, it has been a very long time since I took the time to read over his research papers. Tyler has commented in at least two old posts that Professor Ballock is an ally in finding a solution. Of all the researchers in the world who knows about the molecular signal pathways of the growth plates and endochondral ossifications, he is the person to talk to.
I recently found an article that showed that back in 2000 Ballock was awarded some type of prestigious orthopaedic award for his accomplishment of succeeding in creating in the test tube a type of cartilagenous tissue that has almost the exact same properties as the growth plates we have in our body naturally when we were younger.
What I gathered that was important from the article below is the name of another person doing similar research, a Qian Chen. This is NOT the same Cory Chen that Tyler says would help us with the research. Chen is a common Chinese name and I would guess this Qian Chen is another Chinese Graduate student/visiting scholar turned Professor.
With a quick google search, I managed to find Qian Chen’s Profile on the Brown University’s Database. His current title is the Michael G. Ehrlich, MD Professor of Orthopaedic Research
Orthopaedics.
The thing that we as height increase researchers should focus on are his publications and research. The good thing about academics is that most of them have a copy of their CVs available in PDF to look at HERE. I wanted to see what this orthopaedic surgery professor has been doing research on, and hope that over time I can read over his papers.
Two studies interest me. They are…
- Chen, Q., Lei, W., Wang, Z., Sun, X., Luo, J., and Yang, X. Endochondral bone formation and extracellular matrix, Current Topics in Bone Biology, 145-162, Deng, H., and Liu, Y. (Eds) World Scientific Publishing Co. 2005
- Phornphutkul, C., Wu, K., Yang, X., Chen, Q., and Gruppuso, P. IGF-I Signaling is Modified During Chondrocyte Differentiation, J. Endocrinology, 183: 477-486, 2004
He was given a grant by the National Center for Research Resources back in 2007 which is mentioned HERE.
Here is a list of Qian Chen’s projects that he is either still doing from grant money, or that he has finished. Some of the projects he has been involved in will be critical for us to read over and learn more about.
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Ongoing Research Support PHS RO1 AG17021 Chen (PI) 03/15/06-02/28/11 RO3 AR 052479 (Wei) 04/01/06-03/31/09 1 P20 RR024484-01 Chen (PI) 09/01/07-07/31/12 Completed Research Support Biomedical Research Grant Chen (PI) 01/01/02-12/31/04 PHS K02 AG00811 Chen (PI) 08/01/98-07/31/04 PHS 7RO1 AG17021 Chen (PI) 09/01/98-08/31/05 |
Growth plate, cartilage, ligament research honored – Wednesday, March 15, 2000 – Kappa Delta awards presented today – (From the American Academy of Orthopaedic Surgeons, 2000 Section C, The Annual Meeting Edition of the AAOS Bulletin).
The article is copy and pasted below. i have highlighted the major points about this….
Research into development of a “test tube growth plate,” cartilage cell properties in skeletal diseases and ligament growth will be honored with Kappa Delta awards during the Opening Ceremony in the convention center Auditorium today.
The investigators will present their scientific papers and results of their research projects at the Orthopaedic Research Society meeting which will precede the AAOS meeting.
The Elizabeth Winston-Lanier Award will be presented to R. Tracy Ballock, MD, for developing a “test tube model of the growth plate that reproduces many of the same features of the growth plate in the body.”
Results of these studies with the test tube model demonstrate that thyroid hormone, which is an essential regulator of bone growth in children, works by locally increasing the amount of bone morphogenetic (producing growth) protein in the growth plate and also by modulating the level of proteins associated with the cell division cycle, reported Dr. Ballock.
Dr. Ballock, an assistant professor of orthopaedics and pediatrics at Case Western Reserve University and University Hospitals of Cleveland, Ohio, explained that long bones grow by elongation at either end at the cartilage growth plates. “Somewhat surprisingly,” he noted, “the growth plates at the top and bottom of each bone grow at markedly different rates. In order for a person’s arms or legs to be the same length, there has to be some coordination of the growth at the growth plates by circulating hormones and local growth factors produced by the growth plates themselves.”
Dr. Ballock and associates have focused on identifying the molecular signals that regulate the long bone growth in children. The results from the Ohio study “provide the first glimpse of the molecular pathways used by thyroid hormone to regulate endochondral ossification–the conversion of cartilage to bone–and to establish a new pattern for interpreting the roles of systemic hormones and peptide growth factors in regulating cell growth and differentiation during longitudinal bone growth in children.”
The experiments are clinically relevant because the process of endochondral ossification is “arguably the single most important biological pathway in orthopaedics,” said Dr. Ballock. This essential series of cellular events is responsible for the development of the skeleton in utero, results in the longitudinal growth of the limbs and trunk, and provides for the regeneration of bone tissue during fracture healing.”
By understanding the molecular signals that control this growth process, scientists will be able to devise more rational and specific medical and surgical therapies for abnormal long bone growth and dwarfism that affect children.
Next the researchers will pursue the hypothesis that dietary factors in obese children may interfere with the normal thyroid hormone signals to cause a growth plate disorder known as slipped capital femoral epiphysis (SCFE). In this condition, the ball of the hip joint slips off its attachment to the thighbone. Some children with SCFE can develop a severe crippling form of hip disease for which there is no effective treatment.
Qian Chen, PhD, will receive the Young Investigator Award for his outstanding research on cartilage cell properties in skeletal diseases, including arthritis. Dr. Chen and his associates at Penn State have “identified several molecular markers of cartilage cell (chondrocyte) differentiation and demonstrated that these markers are expressed during skeletal development in the young and during osteoarthritis in older people.
“For a long time, it was very difficult to predict, prevent, or treat osteoarthritis because the mechanism of the disease was not known,” he said. “This difficulty stems from the lack of molecular markers of the disease and the lack of characterization of the step-by-step development of the disease.” Dr. Chen’s Musculoskeletal Research Laboratory at the Pennsylvania State University College of Medicine in Hershey has conducted numerous cell culture experiments and animal studies and “is currently focusing on the regulation of the expression of proteins. If the researchers could determine how to inhibit the synthesis of these markers, they could potentially regulate or even prevent osteoarthritis which affects millions of Americans,” he said.
During the study of molecular regulation of chondrocyte differentiation, Dr. Chen and associates discovered that the “two key transitional points during the pathway, from proliferation to maturation, and from maturation to hypertrophy, are subject to regulation by mechanical stress and hormonal molecules.” An earlier study identified molecular markers that are express during chondrocyte differentiation-proliferation, maturation, and hypertrophy. They also identified “molecular properties of extracellular matrix proteins that are expressed specifically in these stages, including cartilage matrix protein, collagen type X, and type II.”
Supported by the National Institute on Aging of NIH and the Arthritis Foundation, the genetic engineering and cell culture studies have provided a significant amount of new information on the chondrocyte differentiation pathway. Their discoveries have revealed underlying mechanisms regulating chondrocyte differentiation” and may contribute to the development of drug therapy that would regulate cellular proliferation and prevent chondrocyte hypertrophy in osteoarthritis.”
Ultimately, the research findings may lead to profound implications for future analysis of cartilage health and maintenance, tissue engineering, and prevention and treatment of osteoarthritis.”
The Ann Doner Vaughn Award will be presented to Laurence E. Dahners, MD, and Gayle E. Lester, PhD, for laboratory research confirming that ligaments grow and contract throughout the structure of the ligament and not just at the growth plates. This finding opens the way for researchers to devise ways to induce ligament growth in structures that are too tight (contracted) or to tighten tissues that are too lax, said Dr. Dahners, professor of orthopaedic surgery at the University of North Carolina at Chapel Hill. Another possible therapeutic value would be to prevent a joint from getting stiff after an injury or to prevent a joint from becoming too lax after a sprain.
For their study, Dr. Dahners and Dr. Lester, associate professor of orthopaedic surgery and pharmacology, placed markers along the deltoid ligaments of seven five-week-old rabbits and then compared the amount of ligament growth between each set of markers in each rabbit’s deltoid ligament. This work “demonstrated that longitudinal ligament growth occurs interstitially rather than at a ‘growth plate’ or growth region,” said Dr. Dahners. In other studies involving rabbits, the researchers concluded “ligament growth is influenced by the application of constant longitudinal mechanical tension to the growing ligament. Mechanical stress seems to play an important rule in modulating growth. As well, the absence of stress has major importance in the development of contracture.
Dr. Dahners explained that ligaments which control joint motion and tendons which connect muscle to bone are made of a fiber called collagen and are in many ways like a rope. There is glue to hold the fibers together in the rope. The rope can shrink or stretch when the fibers slide past each other.
An abundance of evidence supports the hypothesis that changes in ligament length occur through the sliding of discontinuous fibrils past one another, reported Dr. Dahners. “During contracture, the contractile actin cytoskeleton of the fibroblasts is active and presumably provides the motive force in sliding the fibrils past one another while the ligament is shortening, he reported.”
Scientists will continue to research the nature of the “interfibrillar bonds” which bind one fibril to another to prevent sliding. As researchers identify ways to change the interfibrillar bonding, they then may be able to develop mechanisms to lengthen or shorten ligaments to treat patients’ medical conditions.
In their studies, systemic hormonal factors appeared to influence the growth of ligamentous tissue. However, it was locally mediated by mechanical tension, or lack of tension, which caused an increase or decrease in growth throughout the length of the ligament, reported Dr. Dahners.