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Articles on the placenta 



Blood money for what? The continuing saga AIMS Journal, 2005, Vol 17 No 4 In the AIMS Journal (Vol 16, No 4), Professor Naomi Pfeffer, a sociologist and historian who researches and writes about human tissue collection and stem cell research and therapy, explained why unregulated private blood banks threaten to exploit pregnant women. George Macridis, Managing Director of Future Health Technologies responded: Blood Money for What? For an insurance policy for the future. George Macridis While Professor Naomi Pfeffer's article on unregulated private cord blood banks contained some interesting points, I feel that I must disagree with her about some of the conclusions she drew. Although stem cell transplants are currently used to treat leukaemias and blood disorders, medical researchers have discovered that stem cells may have an important future role to play in combating heart disease and diabetes. This means that there is every point in storing umbilical cord blood, if a parent chooses to do so, because we do not know what advances are around the corner. Professor Pfeffer is correct when she states that it is not yet known whether stored cells remain viable after a prolonged freezing period. However, there is evidence that they can remain viable after 15 years. It is quite likely that they will last longer. Also, because at Future Health Technologies our facilities are accredited by the Department of Health, if parents feel they no longer need the stored cells then they can be donated to the NHS cord blood bank. For a parent to store blood in a private bank ensures they can gain access to the sample if it is ever needed, something which does not necessarily happen with the NHS bank. I believe that Professor Pfeffer is missing the point when she says that stem cells collected from cord blood will not be useful for the treatment of an individual with a genetically inherited disease, as the stem cells themselves would have the same defect. While this is undoubtedly true, it should also be mentioned that the cord blood is extremely likely to be compatible with siblings and other family members. As a result, stored cord blood from a healthy sibling could potentially be used to treat one with a genetically inherited disorder. Here at Future Health Technologies, we aim to ensure that all our clients are completely informed about stem cells, their use, potential and the procedure in collecting and storing them. There is no such thing as the ultimate health insurance and we have never promised such. We are completely open about the fact that the stored cord blood may never need to be used. In fact we compare banking stem cells to taking out house insurance Ð very few people will ever need to claim but it is always reassuring to have it. We agree that there may have been some over-hyping of the potential of stem cells by the media in the sense that although there are constant developments it may be some years before stem cells are used to treat common diseases. But we believe that parents should be fully informed of the services available and have the freedom to choose whether to take advantage of them. One issue where I would wholeheartedly back Professor Pfeffer is in the lack of regulation of private cord blood banks. It is shocking that we are, to the best of my knowledge, the only such bank that has been fully accredited by the Department of Health. The only way for members of the public to be able to use the private sector with confidence is if all such organisations have to obtain accreditation before being allowed to operate in the UK. This would ensure that, at the very least, all would meet minimum standards. WE INVITED PROFESSOR PFEFFER TO COMMENT ON HIS LETTER AND THIS IS HER REPLY: Professor Naomi Pfeffer Our body, our own stem cell bank I welcome the letter from George Macridis, MD of Future Health Technologies, as it provides me with an opportunity to explain how placing your baby's umbilical cord blood in a private bank has become even more unnecessary than I previously pointed out. Stem cell research is a rapidly moving field. One of the most exciting recent discoveries is that so-called progenitor cells, the cells which are the basic building blocks of all tissue and organs in the human body, are found in adults. These 'adult' progenitor cells can be recovered, expanded and used to repair damage of tissue and organs of the person from whom they are collected. And another recent research finding is that 'adult' cells are much more plastic than had been thought, which means they can be manipulated to form other cells, so that, for example, cells that line the nasal passage might be reprogrammed to repair a damaged spinal cord. These findings sound the death knell of private cord blood banks: there is no need to store a baby's umbilical cord blood 'just in case' she needs stem cell therapy later on in life because progenitor cells can be found in her body. Another great advantage of this discovery is it gets rid of the problem of immunology. A transplant of stem cells from one person to another risks rejection for the same reason as a transplanted organ such as a kidney or a heart is rejected. A transplant recipient, throughout their life, must take drugs to prevent their immune system from rejecting the transplant. George Macridis might claim that stored cord blood from a healthy baby could still be used to treat a sibling with a genetically inherited disorder, but closely related people do not necessarily have a similar immunological identity. The only exception to this rule is identical twins where both siblings will have the same genetically inherited disorder. In using progenitor stem cells collected from the patient's body, the problem of rejection disappears. The technical term for this process is autologous; a stem cell transplant from another person is called allogenic. Therapies using autologous stem cells are recognized as the most promising development in stem cell research. Their value is currently being tested, for example, in the treatment of heart disease, and to see whether it is possible to 'grow' a patient's own skin to treat a drastic burn or wound. Autologus treatments mean that each of us is our own stem cell bank. Autologous treatments with 'adult' progenitor cells mean there is no good reason to pay a private tissue banker to freeze your baby's cord blood.

Blood money for what?

Professor Naomi Pfeffer explains why the unregulated private blood banks threaten to exploit pregnant women

Is ‘banking’ your baby’s umbilical cord-blood really a wise concerning consent and ownership are raised with the collec-

decision? Private cord-blood bankers want expectant

mothers to believe it is. The UK Cord Blood Bank calls it ‘a lifesaving choice’; the company Smart Cells claims it offers families extra peace of mind.

But experts warn it is a complete waste of money; new parents can certainly find better ways of spending a thousand pounds. The picture these companies paint is, at best, a rose- colourd one and, at worst, misleading. Their promotional material exaggerates the likelihood of a child succumbing to a life-threatening disease, twists complex unanswered sci- entific questions into established ‘facts’ and presents false claims as to therapeutic efficacy.

Where did it all start?

Until recently, placentas have been thrown away without a second thought. But because they hold between three- and five-fluid ounces of cord blood, which is rich in stem cells, placentas have now been transformed from a waste product into a potentially valuable resource.

No one knows the true worth of stem cells: many of the claims made about them are highly spec-

ulative. Stem cells are central to normal
human growth and development, and
have two unique properties: the capacity
to renew themselves; and the potential
to differentiate into one of the 200 or so
different types of cells in the body, such
as hair, nerves and blood. Other cells are
unable to replenish themselves and are
renewed from other sources; they are
also differentiated—that is, committed to becoming a partic- ular type of tissue.

Stem cells are found in embryos, fetuses, placental (umbil- ical cord) blood and bone marrow. The stem cells found in early embryos are ‘totipotent’ (unspecialised), and have the capacity to become any other type of cell.

This plasticity diminishes as the embryo develops. Indeed, the stem cells in placental blood are ‘multipotent’—that is, their potential to become other types of tissue is more restrict- ed than it was in the early embryo.

The plasticity of adult stem cells is even more limited but, in time, scientists may be able to de-differentiate them by ‘turning back the clock’ and making them behave like un- specialised cells again.

Totipotent stem cells are considered the most valuable, but they are also the most controversial as they are found in so-called ‘spare’ or ‘leftover’ embryos created in the laborato- ry as part of in-vitro fertilisation (IVF) treatment. Opponents of embryonic stem-cell research also object to the collection of stem cells from aborted fetuses. Some tricky questions

million of taxpayers’ money annually. Any findings from their investment will, it is hoped, be freely available on the NHS.

Christopher Reeve hoped that stem cell research would find a way to repair spinal injuries like the one he suffered when he fell from his horse. Other peo- ple are praying that it will produce treat- ments for the common degenerative dis-

eases that are currently incurable, including Parkinson’s and Alzheimer’s, and also identify ways of encouraging stem cells to develop into cells that could be used in the regeneration of other diseased and damaged tissues. One day, for example, it may be possible to make a relatively small number of stem cells grow into a very large number of pancreatic cells that can produce insulin and cure diabetes.

Transplantation

It is difficult to distinguish hype from reality in stem-cell research. For more than two decades, stem cells have been used to successfully treat some life-threatening diseases of the blood, in particular, leukaemia. In this case, the treatment involves transplanting bone marrow collected from a volun- teer donor, whose tissue type matches as closely as possible that of the recipient. A family member is usually suitable; otherwise, doctors consult a donor registry to find an unre- lated match. The Anthony Nolan Trust, a charity formed in 1974, holds the UK’s largest stem-cell register and helps people anywhere in the world to find a donor.

‘For more than two decades, stem cells have been used to successfully treat some life-threatening diseases of the blood.’

tion of umbilical cord blood that is not the mother’s, but the baby’s.

Stem cell research in the US

Actor Christopher Reeve, who played Superman in the 1978 movie, backed a campaign before his untimely death to over- turn US President George W. Bush’s refusal to allow federal or publicly funded research to use human embryonic stem cells. The publicity surrounding the campaign conveyed the impression that all stem cell research is outlawed in the US but, in fact, it can and does proceed with funding from other, private sources. However, where research is driven by the profit motive, valuable findings are immediately made com- mercial and, often, any resultant product may become too expensive for most people to benefit from.

In contrast, research using stem cells from every or any source is permitted in the UK, although embryonic stem-cell researchers must obtain a licence from the Human Fertilisa- tion and Embryology Authority (HFEA), which is backed by the Medical Research Council (MRC) to the tune of £4.

Aging of the placenta
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  1. Harold Fox

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It is widely believed that during the relatively short duration of a normal pregnancy the placenta progressively ages and is, at term, on the verge of a decline into morphological and physiological senescence.1-3 This belief is based on the apparent convergence of clinical, structural, and functional data, all of which have been taken, rather uncritically, as supporting this concept of the placenta as an aging organ with, all too often, no distinction being made between time related changes and true aging changes. I will review some of these concepts and consider whether the placenta truly undergoes an aging process. For the purposes of this review an aging change is considered to be one which is intrinsic, detrimental, and progressive and which results in an irreversible loss of functional capacity, an impaired ability to maintain homeostasis, and decreased ability to repair damage.

Morphological changes

The placenta is unusual in so far as its basic histological structure undergoes a considerable change throughout its lifespan. For some time it has been customary to describe the appearances of the placental villi in terms of their changing appearance as pregnancy progresses, comparing, for instance, typical first trimester villi with those in third trimester placentas. It has often been implied that this changing appearance is an aging process, but it is now recognised that this temporal variability in villous appearances reflects the continual development and branching of the villous tree (fig 1) In recent years the relation between the growth of the villous tree and the villous histological appearances has been formally codified5-8with identification of five types of villi (fig 2).

Figure 1

Diagrammatic representation of a peripheral villous tree, showing a large central stem villus: the lateral branches from this are the mature intermediate villi from which the terminal villi protrude.

Figure 2

Representation of the peripheral branches of a mature villous tree together with typical cross sections of the five villous types. The figures are reproduced from Haines & Taylor. Textbook of Obstetrical and Gynaecological Pathology. 4th Edn. 1995, by kind permission of Churchill Livingstone and Professor P Kaufmann.

1 Mesenchymal villi 

These represent a transient stage in placental development and they can differentiate into either mature or immature intermediate villi. They comprise the first generation of newly formed villi and are derived from trophoblastic sprouts by mesenchymal invasion and vascularisation. They are found mainly in the early stages of pregnancy but a few may still be found at term They have complete trophoblastic mantles with many cytotrophoblastic cells and regularly dispersed nuclei in the syncytiotrophoblast: their loose, immature-type stroma is abundant and contains a few Hobauer cells, together with poorly developed fetal capillaries.

 

2 Immature intermediate villi

These are peripheral extensions of the stem villi and are the predominant form seen in immature placentas. These villi have a well preserved trophoblastic mantle in which cytotrophoblastic cells are numerous; the syncytial nuclei are evenly dispersed and there are no syncytial knots or vasculo-syncytial membranes. They have an abundant loose stroma that contains many Hofbauer cells: capillaries, arterioles, and venules are present.

3 Stem villi 

These comprise the primary stems which connect the villous tree to the chorionic plate, up to four generations of short thick branches and further generations of dichotomous branches. Their principal role is to serve as a scaffolding for the peripheral villous tree, and up to one third of the total volume of the villous tissue of the mature placenta is made up of this villous type, the proportion of such villi being highest in the central subchorial portion of the villous tree. Histologically, the stem villi have a compact stroma and contain either arteries and veins or arterioles and venules; superficially located capillaries may also be present.

4  Mature intermediate villi

These are the peripheral ramifications of the villous stems from which most terminal villi directly arise. They are large (60–150 μm in diameter) and contain capillaries admixed with small arterioles and venules, the vessels being set in a very loose stroma which occupies more than half of the villous volume. The syncytiotrophoblast has a uniform structure, no knots or vasculo-syncytial membranes being present. Up to a quarter of the villi in a mature placenta are of this type.

5 Terminal villi

These are the final ramifications of the villous tree and are grape-like outgrowths from mature intermediate villi. They contain capillaries, many of which are sinusoidally dilated to occupy most of the cross sectional diameter of the villus. The syncytiotrophoblast is thin and the syncytial nuclei are irregularly dispersed. Syncytial knots may be present and vasculo-syncytial membranes are commonly seen. These terminal villi begin to appear at about the 27th week of gestation and account for 30–40 per cent of the villous volume, 50 per cent of the villous surface area, and 60 per cent of villi seen in cross section at term.

The pattern of development of the villous tree is therefore as follows: During the early weeks of pregnancy all the villi are of the mesenchymal type. Between the 7th and 8th weeks mesenchymal villi begin to transform into immature intermediate villi and these subsequently transform into stem villi. Development of additional immature intermediate villi from mesenchymal villi gradually ceases at the end of the second trimester, but these immature intermediate villi continue to mature into stem villi and only a few persist to term as growth zones in the centres of the lobules. At the beginning of the third trimester mesenchymal villi stop transforming into immature intermediate villi and start transforming into mature intermediate villi. The latter serve as a framework for the terminal villi which begin to appear shortly afterwards and predominate at term.

This progressive elaboration of the villous tree results in a predominance of terminal villi in the mature placenta. Such villi have been conventionally classed as “third trimester villi” and a comparison of their structure with the predominant type of villi in the first trimester— immature intermediate villi—has led many to suggest that as pregnancy progresses the villous trophoblast becomes irregularly thinned and the cytotrophoblast regresses, changes interpreted as being of an aging nature. The villous cytotrophoblast, which is a stem cell for the trophoblast, does not in reality regress, because the absolute number of these cells in the placenta is not decreased at term and in fact continues to increase throughout pregnancy. The apparent sparsity of these cells is due to their wider dispersion within a greatly increased total placental mass.9 10 The focal thinning of the villous syncytiotrophoblast apparent in many terminal villi has often been cited as evidence of syncytial senescence. These thinned areas are, in reality, the “vasculo-syncytial membranes”11 which, although formed in part by mechanical stretching of the trophoblast by ballooning capillary loops,12 never the less differ enzymatically and ultrastructurally from the non-membranous areas of the syncytium and are areas of the syncytiotrophoblast specifically differentiated for the facilitation of gas transfer.13These membranes are therefore a manifestation of topographic functional differentiation within the trophoblast.

The interlinked, but separate, processes of maturation of the villous tree and functional differentiation of the trophoblast result in a predominant villous form that is optimally adapted for materno-fetal transfer diffusion mechanisms: the morphological changes substantially increase trophoblastic surface area14 and a significantly reduce the harmonic mean of the diffusion distance between maternal and fetal blood,15 with a resulting increase in the conductance of oxygen diffusion.16

It is not mere pedantry to distinguish between maturation, which results in increased functional efficiency, and aging, which results in decreased functional efficiency. In this respect it is worth noting that a proportion of placentas from women with severe pre-eclampsia look unusually mature for the length of the period of gestation: this is usually classed as “premature aging” but it would be more accurate to regard the changes as being due to accelerated maturation, this being a compensatory mechanism to increase the transfer capacity of the placenta in the face of an adverse maternal environment.

It has to be admitted that the control mechanisms of placental maturation are unknown. There are many agents thought to be of importance in the control of placental growth, including cytokines, growth factors, oncogenes, prostaglandins and leucotrienes,17-20 but it far from clear as to whether control of growth can be equated with control of maturation. However, villous development, certainly in the later stages of pregnancy, does seem to be driven principally by proliferation of endothelial cells and capillary growth.21 Vascular endothelial growth factors are present in placental tissue22 and the suggestion that hypoxia may stimulate angiogenesis,23 and thus have a significant role in placental development, would corroborate the accelerated placental maturation seen in some cases of maternal pre-eclampsia.

Placental growth

It has long been maintained that placental growth and DNA synthesis cease at about the 36th week of gestation and that any subsequent increase in placental size is due to an increase in cell size rather than to an increase in the number of cells.24Simple histological examination of the term placenta will, however, serve to refute this view, because immature intermediate villi are often present in the centres of lobules and these clearly represent a persistent growth zone. Furthermore, total placental DNA content continues to increase in an almost linear manner until and beyond the 42nd week of gestation.25 This finding agrees with autoradiographic and flow cytometric studies that have shown continuing DNA synthesis in the term organ,26-28 and with morphometric investigations that have shown persistent villous growth, continuing expansion of the villous surface area, and progressive branching of the villous tree up to and beyond term.14 29

Placental growth certainly slows, but clearly does not cease, during the last few weeks of gestation, although this decline in growth rate is neither invariable nor irreversible, because the placenta can continue to increase in size if faced with an unfavourable maternal environment, such as pregnancy at high altitude, or severe maternal anaemia, while the potential for a recrudescence of growth is shown by the proliferative response to ischaemic syncytial damage. Those who contend that a decreased placental growth rate during late pregnancy is evidence of senescence often seem be comparing the placenta with an organ such as the gut, in which continuing viability depends on a constantly replicating stem cell layer producing short-lived postmitotic cells. A more apt comparison would be with an organ such as the liver, which is formed principally of long-lived postmitotic cells and which, once an optimal size has been attained to meet the metabolic demands placed on it, shows little evidence of cell proliferation while retaining a latent capacity for growth activity. There seems no good reason why the placenta, once it has reached a size sufficient to adequately meet its transfer function, should continue to grow, and the term placenta, with its considerable functional reserve capacity, has more than met this aim.

Functional activity

There have been few vertical studies of placental function throughout pregnancy, but there is no evidence that any of the major indices of placental function decline—namely, proliferative, transfer, and secretory capacities.30 As already remarked, the diffusion conductance of the organ is increased, largely as a result of morphological changes, but there is considerable evidence that specific placental carrier mediated transfer systems are also augmented.20 The placental production of hormones continues unabated until term: the synthesis of human chorionic gonadotrophin declines towards the end of the first trimester but this is clearly due to a gene switch which results in progressively increasing secretion of human placental lactogen.

The placenta also retains its full proliferative capacity until term as shown by its ability to repair and replace, as a result of proliferation in the villous cytotrophoblastic cells, of a villous syncytiotrophoblast that has been ischaemically damaged in women with severe pre-eclampsia.13

Clinical factors

The single most important factor leading to a belief in placental senescence has been the apparently increased fetal morbidity and mortality associated with prolonged pregnancy, this traditionally being attributed to “placental insufficiency” consequent on senescence of the organ.1 31 In the past it was thought that about 11% of pregnancies extended to or beyond the 42nd week of gestation32 33 : the introduction of a routine ultrasound examination in early pregnancy reduced the incidence of prolonged pregnancies to about 6%34 and it has even been claimed that with very accurate dating studies the incidence of truly prolonged gestations does not exceed 1%.35 This casts some doubt on the validity of a great deal of the historical information about the risks and ill effects of prolonged pregnancy, but it is never the less widely accepted that perinatal mortality increases after the 42nd week of gestation.36

Any increase in perinatal mortality after the 42nd week of gestation is due, in part, to the high incidence of fetal macrosomia: 10% of infants from prolonged pregnancies weigh over 4000 g and 1% over 4500 g and these fetuses are at particular risk of complications such as shoulder dystocia. The presence of this large number of macrosomic fetuses is a clear indication that, in this subset at least, the placenta continues to function well beyond the 40th week of gestation and remains capable of sustaining untrammelled fetal growth.

The classic clinical syndrome of the “postmature” infant1 31 is not commonly seen today but seems to be clearly related to the development of oligohydramnios. There is no doubt that amniotic fluid volume tends to decrease in a proportion of prolonged pregnancies39 and that oligohydramnios is associated with a high incidence of fetal heart rate decelerations.36 This has been attributed by some to cord compression,40 41 but one study, while confirming that cord compression is common in prolonged pregnancies, was unable to correlate such compression with fetal acidosis.42 It is often assumed, and indeed commonly stated, that the decline in amniotic fluid volume in these cases is an indication of “placental insufficiency” but, in reality, there is no evidence that in late pregnancy the placenta plays any part in the production of amniotic fluid or in the control of amniotic fluid volume.43

The two most potent causes of increased morbidity in prolonged pregnancy are therefore clearly unrelated to any change in placental functional capacity. Examination of placentas from prolonged pregnancies shows no evidence of any increased incidence of gross placental abnormalities, such as infarcts, calcification, or massive perivillous fibrin deposition. The most characteristic histological abnormality, found in a proportion of cases but certainly not in all, is decreased fetal perfusion of the placental villi.13 The fetal villous vessels are normal in placentas from prolonged pregnancies44 and Doppler flow velocimetry studies have, in general but not unanimously, indicated that there is no increased fetal vascular resistance in such placentas.45-47The decreased fetal perfusion is therefore probably a consequence of oligohydramnios, because umbilical vein flow studies have shown that fetal blood flow to the placenta is often reduced in cases of oligohydramnios.48

It has to be admitted that the pathophysiology of prolonged pregnancy has not been fully elucidated. It seems, however, quite clear that any ill effects which may befall the fetus in prolonged gestations can not be attributed to placental insufficiency or senescence.

Conclusions

A review of the available evidence indicates that the placenta does not undergo a true aging change during pregnancy. There is, in fact, no logical reason for believing that the placenta, which is a fetal organ, should age while the other fetal organs do not: the situation in which an individual organ ages within an organism that is not aged is one which does not occur in any biological system. The persisting belief in placental aging has been based on a confusion between morphological maturation and differentiation and aging, a failure to appreciate the functional resources of the organ, and an uncritical acceptance of the overly facile concept of “placental insufficiency” as a cause of increased perinatal mortality.

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Blood money for what? The continuing saga

In the AIMS Journal (Vol 16, No 4), Professor Naomi Pfeffer, a sociologist and historian who researches and writes about human tissue collection and stem cell research and therapy, explained why unregulated private blood banks threaten to exploit pregnant women. George Macridis, Managing Director of Future Health Technologies responded:

Letters

Blood Money for What? For an insurance policy for the future.
While Professor Naomi Pfeffer’s article on unregulated private cord blood banks contained some interesting points, I feel that I must disagree with her about some of the conclusions she drew.

Although stem cell transplants are currently used to treat leukaemias and blood disorders, medical researchers have discovered that stem cells may have an important future role to play in combating heart disease and diabetes.

This means that there is every point in storing umbilical cord blood, if a parent chooses to do so, because we do not know what advances are around the corner.

Professor Pfeffer is correct when she states that it is not yet known whether stored cells remain viable after a prolonged freezing period. However, there is evidence that they can remain viable after 15 years. It is quite likely that they will last longer.

Also, because at Future Health Technologies our facilities are accredited by the Department of Health, if parents feel they no longer need the stored cells then they can be donated to the NHS cord blood bank. For a parent to store blood in a private bank ensures they can gain access to the sample if it is ever needed, something which does not necessarily happen with the NHS bank.

I believe that Professor Pfeffer is missing the point when she says that stem cells collected from cord blood will not be useful for the treatment of an individual with a genetically inherited disease, as the stem cells themselves would have the same defect. While this is undoubtedly true, it should also be mentioned that the cord blood is extremely likely to be compatible with siblings and other family members. As a result, stored cord blood from a healthy sibling could potentially be used to treat one with a genetically inherited disorder.

Here at Future Health Technologies, we aim to ensure that all our clients are completely informed about stem cells, their use, potential and the procedure in collecting and storing them. There is no such thing as the ultimate health insurance and we have never promised such.

We are completely open about the fact that the stored cord

blood may never need to be used. In fact we compare banking stem cells to taking out house insurance – very few people will ever need to claim but it is always reassuring to have it.

We agree that there may have been some over-hyping of the potential of stem cells by the media in the sense that although there are constant developments it may be some years before stem cells are used to treat common diseases. But we believe that parents should be fully informed of the services available and have the freedom to choose whether to take advantage of them.

One issue where I would wholeheartedly back Professor Pfeffer is in the lack of regulation of private cord blood banks. It is shocking that we are, to the best of my knowledge, the only such bank that has been fully accredited by the Department of Health.

The only way for members of the public to be able to use the private sector with confidence is if all such organisations have to obtain accreditation before being allowed to operate in the UK. This would ensure that, at the very least, all would meet minimum standards.

WE INVITED PROFESSOR PFEFFER TO COMMENT ON HIS LETTER AND THIS IS HER REPLY:
Our body, our own stem cell bank
I welcome the letter from George Macridis, MD of Future Health Technologies, as it provides me with an opportunity to explain how placing your baby's umbilical cord blood in a private bank has become even more unnecessary than I previously pointed out.

Stem cell research is a rapidly moving field. One of the most exciting recent discoveries is that so-called progenitor cells, the cells which are the basic building blocks of all tissue and organs in the human body, are found in adults. These 'adult' progenitor cells can be recovered, expanded and used to repair damage of tissue and organs of the person from whom they are collected. And another recent research finding is that 'adult' cells are much more plastic than had been thought, which means they can be manipulated to form other cells, so that, for example, cells that line the nasal passage might be reprogrammed to repair a damaged spinal cord. These findings sound the death knell of private cord blood banks: there is no need to store a baby's

AIMS JOURNAL vol 17 no4 2005 25

page2image3690192

Letters

umbilical cord blood 'just in case' she needs stem cell therapy later on in life because progenitor cells can be found in her body.

Another great advantage of this discovery is it gets rid of the problem of immunology. A transplant of stem cells from one person to another risks rejection for the same reason as a transplanted organ such as a kidney or a heart is rejected. A transplant recipient, throughout their life, must take drugs to prevent their immune system from rejecting the transplant. George Macridis might claim that stored cord blood from a healthy baby could still be used to treat a sibling with a genetically inherited disorder, but closely related people do not necessarily have a similar immunological identity. The only exception to this rule is identical twins where both siblings will have the same genetically inherited disorder.

In using progenitor stem cells collected from the patient's body, the problem of rejection disappears. The technical term for this process is autologous; a stem cell transplant from another person is called allogenic. Therapies using autologous stem cells are recognized as the most promising development in stem cell research. Their value is currently being tested, for example, in the treatment of heart disease, and to see whether it is possible to 'grow' a patient's own skin to treat a drastic burn or wound. Autologus treatments mean that each of us is our own stem cell bank. Autologous treatments with 'adult' progenitor cells mean there is no good reason to pay a private tissue banker to freeze your baby's cord blood.

Professor Naomi Pfeffer

page2image3690608

Book Reviews

The following review was first published in the AIMS Journal, Vol 17, No 1, 2005 and is reprinted here in view of its relevance to this particular journal.

Informed Choice in Maternity Care,

By Mavis Kirkham. Palgrave, 2004

This is a jewel of a book and it has come out at just the right time, when "choice" for pregnant and birthing women is actually official policy. . It summarises much of the useful research on the barriers to women knowing about, and choosing from the care available, and how inadequate the range of options is.("Would you like oral or subcutaneous vitamin K for your baby?" No mention that you could refuse it altogether) Here the authors draw lessons from the research which help us to see things at a much deeper level, and we come away feeling not just better informed, but wiser.. I have seldom wanted to re-read chunks of a book as soon as I had finished it, but this one I re-started the next day, particularly the rich first chapter by Nadine Edwards, and the closing chapter by the Editor. Then I dipped into bits of the middle as well.

How naive we all were when we fell on the well-written, detailed informed choice leaflets from MIDIRS with such relief when they appeared. . At last women would be empowered. We should have foreseen that obstetricians would ban from their units the ones they disapproved of, midwives would be choosy over who got what, and everyone would feel threatened at the possibility of women knowing too much. The researchers described what happened as they watched. Julia Simpson’s description of doctor’s behaviour is even more enlightening. If that is how they talk when they know a researcher is watching,

what must it be like the rest of the time? "As obstetricians we need to learn to start being very manipulative with the women, because they are being very manipulative with us."

A book you can’t afford to miss - Jean Robinson

Pregnancy and birth - a guide for deaf women

By Sabina Iqbal

Published by Royal National Institute for the Deaf (RNID) in association with the National Childbirth Trust
ISBN 1 904296 03 3

This book is clearly written in plain English, well laid out and includes lots of photographs, and covers all you would expect in a book for women about the childbearing year. The author is a deaf social worker, and the advisory panel includes NCT antenatal teaching tutors and obstetricians, though no midwives. I enjoyed the focus on the real stories of deaf women and their partners. These illustrate the difficulties often faced in obtaining effective communication support when accessing maternity services and make suggestions for facilitating this. There is a very good chapter of information for health professionals; up to date advice on nutrition and antenatal screening; a thorough glossary and list of organisations for further information. If I had to nitpick I would say that, as ever, advice directs you to a GP rather than a midwife when you are first pregnant; it rather glosses over breech presentation (when the baby is coming bottom first); and while there is a photograph of good positioning for breastfeeding, it is showing poor attachment with the baby on the nipple only.

I would recommend this book to deaf women - Penny Davidson, Student Midwife

26 AIMS JOURNAL vol 17 no4 2005