That's not a stupid question - it's a very good one. I don't confidently know the answer to that, as I haven't studied embryonic stem cells. My understanding is that it has something to do with the fact that by maturing in the new host, the host is tolerant of them. But I really don't know.
You are exactly right that aging can have a profound effect on stem cells. There is a wealth of data that suggests decrements in function and plasticity with increased age and comorbid conditions such as alcohol use, diabetes, or renal failure in the donor (see Dimmeler in JACC, 2002 and Rauscher in Circulation, 2003 for more details). A Chinese group studied the biological characteristics of human bone-marrow-derived mesenchymal stem cells from donors of different ages and found that the expansion ability and cytokine production of cells was lowest in cells from donors over the age of 40 (sorry, don't have the reference handy). Multiple other groups have also demonstrated decreased proliferation in cells derived from older donors and proliferation capacity appears to be inversely correlated with telomere length. Differentiation capacity of mesenchymal stem cells from older donors has been shown to be decreased in multiple studies, with some reports measuring a decrement as soon as 40 years of age.
A lot of people who would stand to benefit the most from "stem cells" (older, more medical problems) therefore are also disproportionately likely to have fewer cells with less regenerative capacity. One potential solution is to get cells from other people. A key problem with most adult cells (received from other adults) is the risk of immunologic rejection. This is likely to be much less of a problem with embryonic-derived cells, which don't express as many immunologically pertinent proteins. We just don't know what the best cell type will be - yet another reason to study both cell types in parallel.
Another person you might consider is Paul Fedak in Toronto. He has done work in the role of matrix metalloproteinase homeostasis in cardiac physiology. He can be contacted at: paul [dot] fedak [at] utoronto [dot] ca
See also his article (Pubmed ID: 16256799) on the same in tje Journal of Thoracic and Cardiovascular Surgery in November 2005
Sounds like an interesting project. I think that some of the people mentioned in the parent article would be a good place to start (Piero Anversa and Annarosa Leri). Roberto Bolli in Louisville also works in this area. Here are a couple of PubMed abstracts that I thought might be pertinent. I'm sure there are others, but you are likely to get some additional recommendations from either contacting some of these folks, or looking at the reference lists for their articles. Hope this helps!
Kassab GS and Navia JA. Biomechanical considerations in the design of graft: The Homeostasis Hypothesis. Annu Rev Biomed Eng 2006 Apr 19. Dept of Biomedical Engineering, UC-Irvine, gkassab[at]uci[dot]edu, PMID: 16704364
Abstract:Since its inception in the 1960s, coronary artery bypass graft (CABG) evolved as one of the most common, best documented, and most effective of all major surgical treatments for ischemic heart disease. Despite its widespread use, however, the outcome is not completely satisfactory. The objective of this review is to highlight the physical determinants of biomechanical design of CABG so that future procedures would have prolonged patency and better outcome. Our central axiom postulates the existence of a mechanical homeostatic state of the blood vessel, i.e., the variation in vessel wall stresses and strains are relatively small under physiological conditions. Any perturbation of mechanical homeostasis leads to growth and remodeling. In this sense, stenosis and failure of a graft may be viewed as an adaptation process gone awry. We outline the principles of engineering design and discuss the biofluid and biosolid mechanics principles that may have the greatest bearing on mechanical homeostasis and the long-term outcome of CABG. Expected online publication date for the Annual Review of Biomedical Engineering Volume 8 is July 11, 2006. Please see http://www.annualreviews.org.floyd.lib.umn.edu/cat alog/pub_dates.asp for revised estimates.
Anversa P, Leri A, Kajstrura J. Cardiac regeneration. J Am Coll Cardiol 2006 May 2; 47(9):1769-76. Cardiovascular Research Institute, NY Medical College, piero_anversa[at]nymc[dot]edu, PMID: 16682300 (see also 16549650)
Abstract: The role and even the existence of new myocyte formation in the adult heart remain controversial. Documentation of cell cycle regulators, deoxyribonucleic acid synthesis, and mitotic images has only in part modified the view that myocardial growth can be accomplished exclusively from hypertrophy of an irreplaceable population of differentiated myocytes. However, myocyte regeneration and death occur physiologically, and these cellular processes are enhanced in pathologic states. These observations have challenged the view of the heart as a postmitotic organ and have proposed a new paradigm in which parenchymal and non-parenchymal cells are continuously replaced by newly formed younger populations of myocytes as well as by vascular smooth muscle and endothelial cells. Heart homeostasis is regulated by a stem cell compartment characterized by multipotent cardiac stem cells that possess the ability to acquire the distinct cell lineages of the myocardium. Similarly, adult bone marrow cells are able to differentiate into cells beyond their own tissue boundary and create cardiomyocytes and coronary vessels. This process has been termed developmental plasticity or transdifferentiation. Because of these properties, bone marrow cells and cardiac stem cells have been employed experimentally in the reconstitution of dead myocardium after infarction. These cell classes hold promise for the treatment of heart failure in humans.
I know much less about this, so am sort of speculating, but I know that the scar consists of fibrous tissue, which is created from fibroblasts. There might be some of these present in the heart, but they more likely arrive via blood vessels, leave the vessels (extravasate), and migrate to the damaged area.
These pumps are called LVADs, or Left Ventricular Assist Devices, and they have been widely used for years (and continue to be). Here's one site with some pretty general, readable information on them. There are a few varieties (some provide pulsatile flow, like the HeartMate XVE) and some provide axial, non-pulsatile flow (HeartMate II). I don't work for Thoratec, but those are by far the most commonly used ones at my institution. Here is a link to some videos from Thoratec if you're interested. Hope you find this useful.
Sort of. The news that there are cells in the heart that can impact repair was news - in 2003, as the article mentioned. This story was that they have gotten better at identifying where those cells are. An important step, but not as important as the 2003 step was.
I'm doing some stem cell work in a very similar area and may be able to clarify a few points:
1. They are not talking about embryonic cells. These are often referred to as "cardiac stem cells" and we each have them in our hearts. Thus they would be considered adult stem cells. As mentioned, their existence was established by Anversa's lab (and confirmed by others) a few years ago. That was a huge milestone, because we previously believed that all cells in the heart were "terminally differentiated" or incapable of generating new cells. We now know that there *are* cells in the hear that can do this, but not fast enough to make a difference in most cases. For example, if you have a heart attack, part of the muscle dies. For whatever reason (not enough cells, don't replicate fast enough, etc.), the cardiac stem cells are unable to completely repair the damage. Current trials of stem cells in the heart have focused on delivering cells derived from other sources (bone marrow, muscle cells, etc.), but it would be ideal to understand enough about the cardiac stem cells to be able to just "activate" them or at least improve the efficiency of what they do.
2. You are absolutely right we are talking about adult stem cells and even that those exist in the heart is old news. The only news here is that this is a step towards identifying them more efficiently/effectively (which would help as alluded to in my point #1). It's an important step, but an incremental one and I don't think it merited a Slashdot story - I agree with you that it's not that big of a deal.
What they did was isolate endothelial progenitor cells from a patient and then let those grow to create a new vessel. Thus all the cells in the vessel were grown from a population of cells in the donor and are as much the patient's own cells as any other. I don't think the distinction that you make about being GROWN from the patient's cells as opposed to being the patient's own [cells] is important.
Also, could you elaborate about what you mean that rejection is a possibility with someone's own cells (often referred to as an autograft as opposed to an allograft, which is receiving tissue from someone else)? The cells certainly may die on implant (for various reasons, although it didn't happen in the patients in this study), but there is no reason to expect that they will be rejected, as they are immunologically indistinuishable from the person's own cells.
I think that's unlikely. Increased blood flow to improve athletic performance would be needed at a capillary (very small arteries) level and these are MUCH larger diameter arteries. The most likely uses are for dialysis fistulas and as conduits for bypassing diseased arteries (e.g., femoral-popliteal arterial bypass, coronary artery bypass graft).
IANAJW (I am not a Jehovah's Witness), but I suspect that they would be OK with it. My understanding of their belief is that blood contains part of a person's soul and that by accepting blood (or blood products) from another person, it makes your blood a combination of the 2 people. Then on judgement day it would be impossible to sort out who the righteous person is/was. At least that was how someone explained it to me once. My apologies to any Witnesses out there if I've mangled their beliefs and I'd also be grateful for a more learned clarification.
As this study was a matter of isolating endothelial progenitor cells from a person's OWN blood vessel, growing them into a "vessel" and reimplanting them into the same person, I would guess that there would be no objection.
NIDDM (Non-insulin dependent diabetes mellitus, as opposed to IDDM or insulin-dependent diabetes mellitus) is not the new term for type 2 diabetes. In fact, it is considered the old and improper way to refer to type 2 diabetes. NIDDM and IDDM are incorrect and misleading, as it is entirely possible for someone with type 2 diabetes to need insulin to control it. Type 1 and 2 refer to the underlying pathology that causes the problem of high blood sugar. NIDDM and IDDM is basically naming the disease based on how it's treated, not on what causes it. Type 1 is caused by destruction or absence of islet cells to make insulin and type 2 is caused by relative insulin insufficiency and/or resistance.
The trials that I have heard of will be small pilot trials. One of the main components of these 'tolerance' trials is that there is a concerted effort to try to prospectively identify biomarkers that may be predictive of when people may no longer need immunosuppressives (or immunotherapeutics as not all medications used in transplantation are truly 'suppressive'). Only if the pilot trials suggest that there may be something will it be moved to larger, more definitive trials. Also, the trials will probably initially take place in islet transplantation for several reasons.
Probably the most important is that it would be ethical to try withdrawing immunosuppression in this population (in contrast to say, heart transplant recipients, who would die if their organ were rejected). In islet transplants, the worst case scenario is that you are back on insulin. It's also possible that you could become sensitized to additional antigens during the rejection process, which may make it harder if you need a kidney down the road.
It is certainly possible that some organs will end up being rejected, but if information can be gleaned from the process that improves the safety and efficacy of transplant regimens, I think it's a reasonable trade-off. Obviously, however, the informed consent process needs to be very carefully thought out and meticulously executed in a tolerance/drug withdrawal trial. The Immune Tolerance Network is a good resource.
The Canadians weren't the first either. From Dr. Shapiro's article (NEJM 2000):
"Islet transplantation has been investigated as a treatment for type 1 diabetes mellitus in selected patients with inadequate glucose control despite insulin therapy....Of the 267 allografts transplanted since 1990..."
The first human islet transplant was done at the University of Minnesota in the mid 1970's (Najarian JS et al, Transplant Proc 1977;9(1):233-236).
You have hit the nail on the head - this has been one of the key problems in islet transplantation over the past 30 years and. Autoimmunity (the body attacking itself) is one of the main reasons that it has been so difficult to prevent eventual rejection of islet transplants and why these transplants have taken so long to even approach the success rate of kidney or whole organ pancreas transplants. Regimens currently available, however (see Shapiro AM et al in NEJM 2000, Hering BJ et al in AJT 2004 and JAMA 2005 for examples) seem to be more successful in both preventing the body from destruction by the immune system (of the foreign tissue AND recurrence of the autoimmunity that caused type 1 diabetes in the first place).
I am also a physician, and there actually are quite a few cases in the literature of people who have stopped taking their immunosuppressives and not rejected their organs. It's not well-understood and there is no way to predict who can do this successfully, but it has happened. Also, the NIH sponspored Immune Tolerance Network has several clinical trials in the pipeline to prospectively test withdrawal of immunosuppressants (very possibly in islet transplant recipients, as it would not be a disaster if they rejected their organ as it would be with a heart, lung, etc.).
The first islet transplants were actually performed at the University of Minnesota in the 1970's. Unfortunately, they were historically not very successful, as the immunosuppressants available at the time had a number of side effects that precluded consistent success. It has also taken quite a while for the technical challenges of extracting the islets from the pancreas without destroying them to be overcome (although this is still an ongoing area of active research).
I look at it like this - the odds are you'll never use it. But if something comes up (child has a sibling with leukemia and needs a transplant or scientists eventually figure out how to do amazing things with these cells), you'd be willing to pay any price to go back in time to get the cells. Go for it!
With regard to "lung plaque" - Everyone is aspirating oral bacteria into their lungs on a daily basis. People with a normal immune system don't have a problem with it. I don't think that your fancy electric toothbrush had anything to do with the material that you were expectorating.
The pain you describe could be cardiac and absence of evidence of a PE is reassuring. Anxiety can also cause those symptoms. Unlikely to be pericarditis - usually is positional and has EKG changes. Would recommend that you raise concern of your heart and possibly anxiety with your doctor.
Good luck.
Let's not pat google on the back quite yet. It is *far* from clear that actinomyces is the 'proper' diagnosis. I agree that seeing an ID specialist may be of benefit, but nothing in his post suggests that he is going to die between now and Friday.
All very solid nominations. Carmack and Miyamoto are truly giants of the gaming community. The other person that that immediately comes to mind is Sid Meier - Civilization is the gold standard and had an incredible impact on the industry, perhaps more than Sonic, IMHO.
There are 2 types of diabetes (called type 1 and type 2 - clever, huh?). Cutting down on sugar intake has nothing to do with the development of type 1 diabetes - this is caused when someone's immune system attacks the cells in their pancreas that make insulin. In type 2 diabetes, cutting down on sugar would be beneficial only if it reduces your caloric intake and you don't get overweight. Maintaining a healthy body weight and moderate physical activity are probably the best ways to reduce your risk of developing type 2 diabetes. Once you *have* it, eating a consistent amount of carbohydrates (such as sugar) will make it easier to control your disease.
If you have type 1 diabetes, you can eat as much sugar as you want - BUT then you need to use more insulin. Many people find that it is easier to not gorge on candy bars and then have to chase it with extra shots, but there is no physiologic reason that either group needs to avoid sugar or that doing so in the first place has any impact on the development of the disease.
The same argument could have been made many years ago about any transplant (kidney, heart, liver, etc.) - procedures that are now routine, safe, effective, and cost-effective. We have to start somewhere...
You raise some good points. However, the same arguments could have been made years ago about any transplants, or severe burn victims, or any of a number of problems that were once considered incurable or prohibitively expensive and time-consuming to treat. It is primarily through such pioneering work that that advances can be made routine, safe, and affordable.
Slashdot Mirror
That's not a stupid question - it's a very good one. I don't confidently know the answer to that, as I haven't studied embryonic stem cells. My understanding is that it has something to do with the fact that by maturing in the new host, the host is tolerant of them. But I really don't know.
A lot of people who would stand to benefit the most from "stem cells" (older, more medical problems) therefore are also disproportionately likely to have fewer cells with less regenerative capacity. One potential solution is to get cells from other people. A key problem with most adult cells (received from other adults) is the risk of immunologic rejection. This is likely to be much less of a problem with embryonic-derived cells, which don't express as many immunologically pertinent proteins. We just don't know what the best cell type will be - yet another reason to study both cell types in parallel.
See also his article (Pubmed ID: 16256799) on the same in tje Journal of Thoracic and Cardiovascular Surgery in November 2005
Hope this helps.
Kassab GS and Navia JA. Biomechanical considerations in the design of graft: The Homeostasis Hypothesis. Annu Rev Biomed Eng 2006 Apr 19. Dept of Biomedical Engineering, UC-Irvine, gkassab[at]uci[dot]edu, PMID: 16704364
Abstract:Since its inception in the 1960s, coronary artery bypass graft (CABG) evolved as one of the most common, best documented, and most effective of all major surgical treatments for ischemic heart disease. Despite its widespread use, however, the outcome is not completely satisfactory. The objective of this review is to highlight the physical determinants of biomechanical design of CABG so that future procedures would have prolonged patency and better outcome. Our central axiom postulates the existence of a mechanical homeostatic state of the blood vessel, i.e., the variation in vessel wall stresses and strains are relatively small under physiological conditions. Any perturbation of mechanical homeostasis leads to growth and remodeling. In this sense, stenosis and failure of a graft may be viewed as an adaptation process gone awry. We outline the principles of engineering design and discuss the biofluid and biosolid mechanics principles that may have the greatest bearing on mechanical homeostasis and the long-term outcome of CABG. Expected online publication date for the Annual Review of Biomedical Engineering Volume 8 is July 11, 2006. Please see http://www.annualreviews.org.floyd.lib.umn.edu/cat alog/pub_dates.asp for revised estimates.
Anversa P, Leri A, Kajstrura J. Cardiac regeneration. J Am Coll Cardiol 2006 May 2; 47(9):1769-76. Cardiovascular Research Institute, NY Medical College, piero_anversa[at]nymc[dot]edu, PMID: 16682300 (see also 16549650)
Abstract: The role and even the existence of new myocyte formation in the adult heart remain controversial. Documentation of cell cycle regulators, deoxyribonucleic acid synthesis, and mitotic images has only in part modified the view that myocardial growth can be accomplished exclusively from hypertrophy of an irreplaceable population of differentiated myocytes. However, myocyte regeneration and death occur physiologically, and these cellular processes are enhanced in pathologic states. These observations have challenged the view of the heart as a postmitotic organ and have proposed a new paradigm in which parenchymal and non-parenchymal cells are continuously replaced by newly formed younger populations of myocytes as well as by vascular smooth muscle and endothelial cells. Heart homeostasis is regulated by a stem cell compartment characterized by multipotent cardiac stem cells that possess the ability to acquire the distinct cell lineages of the myocardium. Similarly, adult bone marrow cells are able to differentiate into cells beyond their own tissue boundary and create cardiomyocytes and coronary vessels. This process has been termed developmental plasticity or transdifferentiation. Because of these properties, bone marrow cells and cardiac stem cells have been employed experimentally in the reconstitution of dead myocardium after infarction. These cell classes hold promise for the treatment of heart failure in humans.
I know much less about this, so am sort of speculating, but I know that the scar consists of fibrous tissue, which is created from fibroblasts. There might be some of these present in the heart, but they more likely arrive via blood vessels, leave the vessels (extravasate), and migrate to the damaged area.
These pumps are called LVADs, or Left Ventricular Assist Devices, and they have been widely used for years (and continue to be). Here's one site with some pretty general, readable information on them. There are a few varieties (some provide pulsatile flow, like the HeartMate XVE) and some provide axial, non-pulsatile flow (HeartMate II). I don't work for Thoratec, but those are by far the most commonly used ones at my institution. Here is a link to some videos from Thoratec if you're interested. Hope you find this useful.
Sort of. The news that there are cells in the heart that can impact repair was news - in 2003, as the article mentioned. This story was that they have gotten better at identifying where those cells are. An important step, but not as important as the 2003 step was.
I'm doing some stem cell work in a very similar area and may be able to clarify a few points:
1. They are not talking about embryonic cells. These are often referred to as "cardiac stem cells" and we each have them in our hearts. Thus they would be considered adult stem cells. As mentioned, their existence was established by Anversa's lab (and confirmed by others) a few years ago. That was a huge milestone, because we previously believed that all cells in the heart were "terminally differentiated" or incapable of generating new cells. We now know that there *are* cells in the hear that can do this, but not fast enough to make a difference in most cases. For example, if you have a heart attack, part of the muscle dies. For whatever reason (not enough cells, don't replicate fast enough, etc.), the cardiac stem cells are unable to completely repair the damage. Current trials of stem cells in the heart have focused on delivering cells derived from other sources (bone marrow, muscle cells, etc.), but it would be ideal to understand enough about the cardiac stem cells to be able to just "activate" them or at least improve the efficiency of what they do.
2. You are absolutely right we are talking about adult stem cells and even that those exist in the heart is old news. The only news here is that this is a step towards identifying them more efficiently/effectively (which would help as alluded to in my point #1). It's an important step, but an incremental one and I don't think it merited a Slashdot story - I agree with you that it's not that big of a deal.
Also, could you elaborate about what you mean that rejection is a possibility with someone's own cells (often referred to as an autograft as opposed to an allograft, which is receiving tissue from someone else)? The cells certainly may die on implant (for various reasons, although it didn't happen in the patients in this study), but there is no reason to expect that they will be rejected, as they are immunologically indistinuishable from the person's own cells.
I think that's unlikely. Increased blood flow to improve athletic performance would be needed at a capillary (very small arteries) level and these are MUCH larger diameter arteries. The most likely uses are for dialysis fistulas and as conduits for bypassing diseased arteries (e.g., femoral-popliteal arterial bypass, coronary artery bypass graft).
As this study was a matter of isolating endothelial progenitor cells from a person's OWN blood vessel, growing them into a "vessel" and reimplanting them into the same person, I would guess that there would be no objection.
Hope this helps clarify.
Cheers!
Probably the most important is that it would be ethical to try withdrawing immunosuppression in this population (in contrast to say, heart transplant recipients, who would die if their organ were rejected). In islet transplants, the worst case scenario is that you are back on insulin. It's also possible that you could become sensitized to additional antigens during the rejection process, which may make it harder if you need a kidney down the road.
It is certainly possible that some organs will end up being rejected, but if information can be gleaned from the process that improves the safety and efficacy of transplant regimens, I think it's a reasonable trade-off. Obviously, however, the informed consent process needs to be very carefully thought out and meticulously executed in a tolerance/drug withdrawal trial. The Immune Tolerance Network is a good resource.
"Islet transplantation has been investigated as a treatment for type 1 diabetes mellitus in selected patients with inadequate glucose control despite insulin therapy....Of the 267 allografts transplanted since 1990..."
The first human islet transplant was done at the University of Minnesota in the mid 1970's (Najarian JS et al, Transplant Proc 1977;9(1):233-236).
See also the International Islet Transplant Registry for additional historical details on islet transplantation.
You have hit the nail on the head - this has been one of the key problems in islet transplantation over the past 30 years and. Autoimmunity (the body attacking itself) is one of the main reasons that it has been so difficult to prevent eventual rejection of islet transplants and why these transplants have taken so long to even approach the success rate of kidney or whole organ pancreas transplants. Regimens currently available, however (see Shapiro AM et al in NEJM 2000, Hering BJ et al in AJT 2004 and JAMA 2005 for examples) seem to be more successful in both preventing the body from destruction by the immune system (of the foreign tissue AND recurrence of the autoimmunity that caused type 1 diabetes in the first place).
I am also a physician, and there actually are quite a few cases in the literature of people who have stopped taking their immunosuppressives and not rejected their organs. It's not well-understood and there is no way to predict who can do this successfully, but it has happened. Also, the NIH sponspored Immune Tolerance Network has several clinical trials in the pipeline to prospectively test withdrawal of immunosuppressants (very possibly in islet transplant recipients, as it would not be a disaster if they rejected their organ as it would be with a heart, lung, etc.).
The first islet transplants were actually performed at the University of Minnesota in the 1970's. Unfortunately, they were historically not very successful, as the immunosuppressants available at the time had a number of side effects that precluded consistent success. It has also taken quite a while for the technical challenges of extracting the islets from the pancreas without destroying them to be overcome (although this is still an ongoing area of active research).
I look at it like this - the odds are you'll never use it. But if something comes up (child has a sibling with leukemia and needs a transplant or scientists eventually figure out how to do amazing things with these cells), you'd be willing to pay any price to go back in time to get the cells. Go for it!
With regard to "lung plaque" - Everyone is aspirating oral bacteria into their lungs on a daily basis. People with a normal immune system don't have a problem with it. I don't think that your fancy electric toothbrush had anything to do with the material that you were expectorating. The pain you describe could be cardiac and absence of evidence of a PE is reassuring. Anxiety can also cause those symptoms. Unlikely to be pericarditis - usually is positional and has EKG changes. Would recommend that you raise concern of your heart and possibly anxiety with your doctor. Good luck.
Let's not pat google on the back quite yet. It is *far* from clear that actinomyces is the 'proper' diagnosis. I agree that seeing an ID specialist may be of benefit, but nothing in his post suggests that he is going to die between now and Friday.
All very solid nominations. Carmack and Miyamoto are truly giants of the gaming community. The other person that that immediately comes to mind is Sid Meier - Civilization is the gold standard and had an incredible impact on the industry, perhaps more than Sonic, IMHO.
There are 2 types of diabetes (called type 1 and type 2 - clever, huh?). Cutting down on sugar intake has nothing to do with the development of type 1 diabetes - this is caused when someone's immune system attacks the cells in their pancreas that make insulin. In type 2 diabetes, cutting down on sugar would be beneficial only if it reduces your caloric intake and you don't get overweight. Maintaining a healthy body weight and moderate physical activity are probably the best ways to reduce your risk of developing type 2 diabetes. Once you *have* it, eating a consistent amount of carbohydrates (such as sugar) will make it easier to control your disease.
If you have type 1 diabetes, you can eat as much sugar as you want - BUT then you need to use more insulin. Many people find that it is easier to not gorge on candy bars and then have to chase it with extra shots, but there is no physiologic reason that either group needs to avoid sugar or that doing so in the first place has any impact on the development of the disease.
I hate Micro$oft as much as anyone, but does this really surprise anyone here?
The same argument could have been made many years ago about any transplant (kidney, heart, liver, etc.) - procedures that are now routine, safe, effective, and cost-effective. We have to start somewhere...
You raise some good points. However, the same arguments could have been made years ago about any transplants, or severe burn victims, or any of a number of problems that were once considered incurable or prohibitively expensive and time-consuming to treat. It is primarily through such pioneering work that that advances can be made routine, safe, and affordable.