What are stem cells?
Stem cells are the master cells of the human body. What define stem cells from other cells is their ability to self-generate themselves and the ability to differentiate into other cell types.
Stem cells are at the center of a new field of science called regenerative medicine. All stem cells?regardless of their source?have three general properties: they are capable of dividing and renewing themselves for long periods; they are unspecialized; and they can give rise to specialized cell types.
Self-regeneration is the ability of stem cells to divide and produce more stem cells. During early development, the cell division is symmetrical i.e. each cell divides to gives rise to daughter cells each with the same potential. Later in development, the cell divides asymmetrically with one of the daughter cells produced also a stem cell and the other a more differentiated cell (such as brain cell, blood cell, etc.)
When stem cells are being transplanted into the body and arrive (through migration or through direct injection) into the injured part of the brain being targeted for tissue regeneration, the stem cells are coming into contact with growth chemicals in the body. These chemicals program the stem cells to grow into the tissue surrounding it.
Stem cells can typically be broken into four types:
• Embryonic stem cells - Stem cells taken from human embryos
• Fetal stem cells- Stem cells taken from aborted fetal tissue
• Umbilical stem cells - Stem cells take from umbilical cords
• Adult stem cells - Stem cells taken from adult tissue
*Cord blood presents new hope for diabetes patients
Stem cell therapy is getting acceptance everywhere in the world. Now the therapy is gaining its importance, in the treatment of diabetes, especially for the type 1 diabetes (IDDM).
It can be added that as many as three million Americans may be living with type 1 diabetes. Type 1 diabetes is usually diagnosed in children and young adults and was previously known as juvenile diabetes.The disease causes the body to stop producing insulin, a hormone that converts sugar, starches and other food into energy needed for daily life and it can lead to various problems like heart disease, kidney disease, blindness, nerve damage, foot complications and skin problems.
Current therapies for type 1 diabetes involve delivering insulin to the bloodstream. However, the new parents have a choice when their child is born: they can either bank or discard their newborn´´s umbilical cord blood. After a baby is born and the umbilical cord is cut, some blood remains in the blood vessels of the placenta and the portion of the umbilical cord still attached to it. The cord blood contains all of the normal elements of blood: red blood cells, white blood cells, platelets and plasma; however, it is also rich in blood-forming stem cells similar to those found in bone marrow.
Researchers from the University of Florida (UF) in Gainesville, Fla., are the first to experiment with cord blood infusions as a treatment for children with type 1 diabetes. The investigators received the idea in part from a patient´s father who had read scientists elsewhere were able to reverse diabetes in mice by taking bone marrow from an animal and infusing it into its identical sibling without using chemotherapy or radiation. In the lab, scientists were able to coax stem cells from cord blood into making insulin.
For the study, researchers identified children recently diagnosed with type 1 diabetes whose families had banked their cord blood at birth. Most of the participants were still producing a small amount of insulin. The researchers then gave patients intravenous infusions of stem cells isolated from their own cord blood. In the first six months, patients given the infusions required less insulin: on average, 0.45 versus 0.69 units of insulin per kilogram per day.
The experimental treatment is not a cure, but it is a significant step toward a better understanding of the disease. In the future, researchers hope they can intervene and repair early damage during the "honeymoon period" �� the first several months after diagnosis when insulin needs are minimal. They hope the cord blood treatment will eventually become part of a combination therapy approach to treating the disease. The study was funded by the Juvenile Diabetes Research Foundation and the National Institutes of Health.
*Treatment of MSA
Treatment of MSA
MSA is a member of Synuclein disease family. There is a series of symptoms associated with clinical pathological change which includes OPCA (oliva-pons-cerebella atrophy), sporadic degeneration of the nigrostriatal system, accompanied with vegetative nerve functional disturbance: Parkinson´´s symptoms (tremors, rigidity, walking difficulty); vegetative nerve functional damage (it is related to the loss of lateral horn cells and brain stem pigment group cells. The clinical symptoms are orthostatic hypotension, swoon, impotence, adiapneustia, thirst, urinary retention,fecal incontinence. In general, paralysis of the vocal cords is the most important and earliest symptom of vegetative nerve functional disturbance, (patient always experiences hoarseness); cerebella symptoms and pyramidal signs. The symptoms will be different for every patient, so in 1969, Dr. Graham and Dr. Oppenheimer proposed naming this complicated disease MSA. But currently doctors still cannot find an effective solution.
MSA is a kind of neurodegenerative disorder, through the causal mechanisms research performed on the molecular level; we can see that the amyloidal change of the CNS lead by the aggregation and aggradation of malconstructed protein is the most important mechanism. That means in the affected neurons, and in the spongiocyte cells, those high soluble proteins can turn into insoluble fibrous polymers, which can transfer into fibrous amyloid deposits which will deposit in the endochylema, cell nucleus and the spatium of extracellulars. These degenerated proteins/ polymers have great neurotoxicity, and they can lead to the damage and death of neurons.
According to recent research, neural stem cells can improve the patient´´s vegetative nerve, cerebellar extrapyramidal symptoms and movement disturbances effectively. On the one side, these stem cells (neural stem cells and bone marrow mesenchymal stem cells) have a complicated and elaborate self controlling system; they can prevent the protein´´s malconstruction and aggregation: molecular chaperone can help the proper protein folding, and prevent the accumulation of non-natural proteins. We can use medication to accelerate the degradation of these malconstructed proteins and endocytose through the ubiquitin-protease bodies system. It can block the development of the disease effectively. On another side, these stem cells can locate in the damaged area of the neural system, repair the damage and help the patient regain more neural functioning.
For these cases, we have a comprehensive treatment for the patient:
1. Improve the internal microenvironment.
2. Stem cells implantation and treatment to help these stem cells locate in the damaged area.
3. Rebuild the neural system; improve the patient´´s neural functioning.
After the 3 steps of treatment were completed, the patient´´s condition had obvious improvements. In general, the MSA patient will still have nonreversible neurodegeneration, while the treatment results showed that neural stem cells implantation treatment can be effective for MSA patients. Now we still need further observation and randomized controlled research to verify our findings.
*Human stem cells promote healing of diabetic ulcers
Human stem cells promote healing of diabetic ulcers
ScienceDaily (Apr 20, 2009)
http://www.sciencedaily.com/releases/2009/04/090420182208.htm
New research at the Salk Institute for Biological Studies casts the role of a neuronal growth factor receptor-long suspected to facilitate the toxic effects of beta amyloid in Alzheimer´´s disease-in a new light, suggesting the molecule actually protects the neuron in the periphery from beta amyloid-induced damage.
The receptor molecule in question, a protein better known as p75, regulates neuronal growth, survival, and degeneration, and guides nerve fibers in growing embryos to their final destinations. Some studies have suggested that it also exacerbates the neurotoxicity associated with beta amyloid deposits, which litter the brains of Alzheimer´´s patients, giving the molecule its questionable reputation.
Yet a team of scientists in the laboratory of Kuo-Fen Lee, Ph.D., a professor in the Clayton Foundation Laboratories for Peptide Biology, found that p75 instead has a neuroprotective effect on the sympathetic nervous system in mice that were genetically engineered to develop Alzheimer´´s disease.
Their findings, published in this week´´s early online edition of the Proceedings of the National Academy of Sciences, challenge the prevailing view of p75´´s harmful role in the condition and could lead to new insights and, ultimately, new protocols for managing the secondary deficits that accompany dementia and memory loss in Alzheimer´´s.
Scientific interest in the peripheral nervous system has been growing as investigators studying neurodegenerative diseases seek new insights into disease progression. "How a disease damages the peripheral nervous system could add a great deal to our understanding of its process, possibly leading to applications down the line that impact patient management and quality of life issues," says Lee, who led the study.
Proteins, like people, are often judged by the company they keep. For instance, p75 belongs to the same family as tumor necrosis factor and was widely thought to mediate cell death in some context. Various in vitro studies have examined p75 in combination with beta amyloid, seeking evidence that it helps induce nerve cell death in Alzheimer´´s disease.
To gather evidence about P75 and the sympathetic nervous system, Lee´´s team crossed a mouse model for Alzheimer´´s disease with a line of mice genetically modified to lack the gene for p75. Without p75, they theorized, the neurotoxic effects of beta amyloid would be reduced, and the mice would show fewer Alzheimer´´s symptoms.
"The role of p75 had been controversial for some time, but based on the evidence at the time, we expected to see indications that it mediates beta amyloid neurotoxicity," says co-first author Tasha Bengoechea, Ph.D., a former graduate student in Lee´´s lab. "We thought removing p75 while overexpressing amyloid would have a positive effect on neuron viability. The opposite was true."
Along with profound motor problems, the p75-deficient mice exhibited severe defects in the wiring of nerves to multiple organs, and the majority died within just three weeks. (Mice normally live up to two years.)When the researchers scaled down the production of toxic beta amyloid by deleting one copy of BACE1, which encodes the molecular shears that make the first cut in the production of beta amyloid fragments, the nerves in the sympathetic nervous system of p75-deficient mice were substantially restored.
"This is the first time the interplay between p75 and beta amyloid in the peripheral sympathetic system, a system that has not been paid much attention before, has been demonstrated," adds postdoctoral researcher and co-first author Zhijiang Chen, Ph.D. "Our findings will ultimately help to design novel strategies to treat the symptoms of the Alzheimer´´s disease and improve the quality of life for Alzheimer´´s disease patients."
The study was funded by a grant from the National Institutes of Health. Researchers who also contributed to the work included postdoctoral researcher Deborah O´´Leary, Ph.D., of the Salk Institute´´s Clayton Foundation Peptide Biology Laboratory, and Eliezer Masliah, Ph.D, a professor in the Department of Neurosciences at the University of California, San Diego.
*Stem cell treatment for Parkinson's disease
Stem cell treatment for Parkinson´´s disease
Parkinson´´s disease is a brain disorder that occurs when certain nerve cells in the brain die or become damaged. The normal function of these nerve cells is the production of Dopamine, a vital chemical which is responsible of our body´´s smooth and well coordinated movements. The lack of Dopamine as a result of damaged nerve cells can cause the Parkinson´´s symptoms of shaking (tremors), stiffness of the muscles, freeze ups, balance difficulties and slowness of movement.
To treat Parkinson´´s disease we apply a unique procedure, specifically designed for Parkinson´´s patients, in which we implant adult stem cells extracted from the human retina, called "Human Retinal Pigment Epithelial cells"(HRPE) by injection. These special cells have the quality of producing Dopamine, which the lack of this chemical, causes the symptoms of Parkinson´´s disease.
Another important advantage of these cells is that they have no immunosuppressive reactions and therefore patients do not need to take additional drugs during the treatment.
The treatment includes the implantation of HRPE cells, along with a daily cocktail of medications that "fertilize"the damaged area, helping the cells to survive and to keep on renewing themselves.
While the treatment cannot completely remove all symptoms of the disease, it can greatly reduce the tremors, decrease muscle tension, improve continuity of movement and balance, increase muscle strength, decrease freeze ups, etc.
In June 2006 we performed the first published successful stem cell treatment for Parkinson´´s worldwide, of an American patient who came to our hospital at a very advanced stage of Parkinson´´s disease.
So far, more than 50 Parkinson´´s patients have been treated with HRPE stem cells from Peking University´´s Stem Cells Research Center ("Beida") and various other cooperating hospitals. All of the patients showed increasing dopamine metabolism, and the conditions of all the patients improved after the transplantation (usually the improvement occurred one week after the injection). The first clinical trial was performed in 2004, but long term follow-up is still under investigation (at least 1-3 years of follow-up), so the treatment is still under careful control, especially in the selection of suitable patients.
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