I have decided to send my son for Stem Cell Therapy, i heard there are two diffrent types, one where they extract blood from his bottom and use the fat from there as apparently there are alot of stem cells present in there, and the other one is from the cord blood, which would be the better option?
这个人问到底用屁股上的血呢还是脐带血。
Does your son have CP? I'm not sure if u can use cord blood cells to treat cp....I know u cannot use sibling cord blood, it would have to be their own.....but most commonly they use what they call adult stem cells for cp wich they take from the child's own spinal fluid. We almost went to germany about 2 yrs ago for stem cell treatment, but we decided not too.....it's still risky, there is a possible risk of rumors due to the fact that no one has fully figured out how to control stem cells yet in order to make them do exactly what we want them to do. We decided not to go after consulting a stem cell dr in France and my cousin in Toronto who is a stem cell researcher for sick kids hospital, one of the leading children's hospitals in the world. They said nothing is proven safe or effective yet, it's still early and it's better to save your money for a few yrs and use it when the treatment will likely be more effective. They told me in 10 or so years there will be stem cell treatment approved in Canada for cp, so that was 2 yrs ago, 8 years to go. We decided to wait, the clinic we were going to got shut down after some deaths and other clinics have been shut down too....we researched it pretty thoroughly and we feel it's still very experimental....there is a study at duke university that u should look up online, the doctor running it even says its experimental and maybe in 10 years there will be something, she believes we will cure cp one day soon, but is it today? I personally don't think so. Good luck with your decision.
第三方代孕--可混血--可选男女-可双胞胎。：溦`信：【ivf 2 2 2 2】服务项目：试管婴儿（试管二、三代技术）（可以提供性别筛选）（包成功男、女孩）（精与卵供应不需排队等待）（早期血液性别鉴定）第三方代孕，无身体接触 招聘代妈【有怀孕经验的优先】作者: popo 时间: 2012-9-18 23:06
最近的消息是杜克大学在征集做干细胞的志愿者，条件如下：
Here are the qualifications to be considered:
1) Child must have confirmed diagnosis of CP w/diplegia, hemiplegia or quadriplegia and be between 12 months & 6 yrs old 确诊脑瘫， １２个月～６岁
2) Child must use his or her own cord blood 存有自身的脐带血
3) You must be able to travel to Duke University in North Carolina 能到杜克大学
Scientists Create “Endless Supply” of Myelin-Forming Cells
November 01, 2012
In a new study appearing this month in the Journal of Neuroscience, researchers have unlocked the complex cellular mechanics that instruct specific brain cells to continue to divide. This discovery overcomes a significant technical hurdle to potential human stem cell therapies; ensuring that an abundant supply of cells is available to study and ultimately treat people with diseases.
“One of the major factors that will determine the viability of stem cell therapies is access to a safe and reliable supply of cells,” said University of Rochester Medical Center (URMC) neurologist Steve Goldman, M.D., Ph.D., lead author of the study. “This study demonstrates that – in the case of certain populations of brain cells – we now understand the cell biology and the mechanisms necessary to control cell division and generate an almost endless supply of cells.”
The study focuses on cells called glial progenitor cells (GPCs) that are found in the white matter of the human brain. These stem cells give rise to two cells found in the central nervous system: oligodendrocytes, which produce myelin, the fatty tissue that insulates the connections between cells; and astrocytes, cells that are critical to the health and signaling function of oligodendrocytes as well as neurons.
Damage to myelin lies at the root of a long list of diseases, such as multiple sclerosis, cerebral palsy, and a family of deadly childhood diseases called pediatric leukodystrophies. The scientific community believes that regenerative medicine – in the form of cell transplantation – holds great promise for treating myelin disorders. Goldman and his colleagues, for example, have demonstrated in numerous animal model studies that transplanted GPCs can proliferate in the brain and repair damaged myelin.
However, one of the barriers to moving forward with human treatments for myelin disease has been the difficulty of creating a plentiful supply of necessary cells, in this case GPCs. Scientists have been successful at getting these cells to divide and multiply in the lab, but only for limited periods of time, resulting in the generation of limited numbers of usable cells.
“After a period of time, the cells stop dividing or, more typically, begin to specialize and form astrocytes which are not useful for myelin repair,” said Goldman. “These cells could go either way but they essentially choose the wrong direction.”
Overcoming this problem required that Goldman’s lab master the precise chemical symphony that occurs within stem cells, and which instructs them when to divide and multiply, and when to stop this process and become oligodendrocytes and astrocytes.
One of the key players in cell division is a protein called beta-catenin. Beta-catenin is regulated by another protein in the cell called glycogen synthase kinase 3 beta (GSK3B). GSK3B is responsible for altering beta-catenin by adding an additional phosphate molecule to its structure, essentially giving it a barcode that the cell then uses to sort the protein and send it off to be destroyed. During development, when cell division is necessary, this process is interrupted by another signal that blocks GSK3B. When this occurs, the beta-catenin protein is spared destruction and eventually makes its way to the cell’s nucleus where it starts a chemical chain reaction that ultimately instructs the cell to divide. However, after a period of time this process slows and, instead of replicating, the cells begin to then commit to becoming one type or another. The challenge for scientists was to find another way to essentially trick these cells into continuing to divide, and to do so without risking the uncontrolled growth that could otherwise result in tumor formation.
The new discovery hinges on a receptor called protein tyrosine phosphatase beta/zeta (PTPRZ1). Goldman and his team long suspected that PTPRZ1 played an important role in cell division; the receptor shows up prominently in molecular profiles of GPCs. After a six-year effort to discern the receptor’s function, they found that it works in concert with GSK3B and helps “label” beta-catenin protein for either destruction or nuclear activity. The breakthrough was the identification of a molecule – called pleiotrophin – that essentially blocks the function of the PTPRZ1 receptor. They found that by regulating the levels of pleiotrophin, they were able to essentially “short circuit” PTPRZ1’s normal influence on cell division, allowing the cells to continue dividing.
While the experiments were performed on cells derived from human brain tissue, the authors contend that the same process could also be applied to GPCs derived from embryos or from “reprogrammed” skin cells. This would greatly expand the number of cells potentially derived from single patient samples, whether for transplantation back to those same individuals or for use in other patients.
Additional authors on the paper include its first author, URMC graduate student Crystal McClain, Ph.D., and Fraser Sim, Ph.D., a member of Goldman’s lab and now an assistant professor at the University at Buffalo. The study was supported by the National Institute of Neurological Disorders and Stroke, the Department of Defense, the Adelson Medical Research Foundation, and the National Multiple Sclerosis Society.