Tuesday, 31 July 2007

Bone marrow restores fertility in female mice

Donor-derived egg cells present in ovaries, but all offspring are from marrow recipients' own eggs July 31, 2007

A new study from Massachusetts General Hospital (MGH) researchers confirms that female mice that receive bone marrow transplantation after fertility-destroying chemotherapy can go on to have successful pregnancies throughout their normal reproductive life. The report in the August 1 Journal of Clinical Oncology verifies that donor marrow can restore fertility in female mice through an as-yet unidentified mechanism. While donor-derived egg cells or oocytes were observed in the ovaries of marrow recipients, all pups born were from the recipients’ own eggs. “Consistent with our past work, cells derived from the donor bone marrow are getting into the ovaries and developing into immature oocytes,” says Jonathan Tilly, PhD, director of the Vincent Center for Reproductive Biology (www.vcrb.org) at MGH, the study’s senior author. “Although these oocytes derived from marrow cells don’t appear competent, at least thus far, to make fertilizable eggs, marrow does contribute something that allows a resumption of fertility in female mice sterilized by chemotherapy.” In a 2005 paper published in the journal Cell, Tilly’s group found that the ovaries of female mice that had received bone marrow or blood cell transplants after fertility-destroying doses of chemotherapy appeared normal and contained immature oocytes expressing a marker protein indicating they came from the donor cells. This report followed a 2004 Nature paper, also from Tilly’s team, reporting that female mice continued producing eggs well into adulthood, in contrast to the long-held belief that female mammals are born with a finite supply of eggs that is depleted throughout life. Both those papers have been extremely controversial, and the current study was designed to follow up the 2005 paper and to address criticisms raised by other researchers. In the current study, adult female mice treated with infertility-inducing chemotherapy received bone marrow transplants from non-treated, healthy adult females either one week or two months after chemotherapy. The mice were then housed with healthy adult males and followed for 7 months, a time period in which a group of control females achieved at least five successful pregnancies each. Both the males and the donor females were black in coat color while the recipient females were white-coated. As a result, the coat color of any pups would indicate the source of egg cells used to make the offspring, with tan coats signifying eggs from the recipients and black coats indicating that the eggs had come from marrow donors. Of the 10 females that received bone marrow transplants one week after chemotherapy, all but one achieved several successful pregnancies during the study period. One gave birth to four litters, one gave birth to five litters, and seven gave birth to six litters of pups. All pups were offspring of the recipients. In a comparison group of 13 females that did not receive marrow after chemotherapy, 10 did become pregnant, but none delivered more than three litters. Additional experiments indicated that mice receiving transplants one week after chemotherapy had better fertility outcomes than did those transplanted at eight weeks. Similarly, resuming mating sooner after transplantation also improved fertility rates. When chemotherapy doses were increased to levels expected to cause death in half the mice, those that also received bone marrow transplants had improved rates of both survival and long-term fertility. The coat-color results of the mating trial indicated that the transplanted marrow’s contribution to restoring fertility did not involve cells destined to becoming fertilizable eggs. To further investigate this observation, the MGH-Vincent researchers gave chemotherapy-treated females marrow from transgenic females that express a green fluorescent protein (GFP) marker only on germline cells, which are precursor cells involved in producing oocytes. Two months after the transplant, the researchers observed GFP-marked oocytes in immature follicles within recipient ovaries. However, donor-derived oocytes made up less than 2 percent of the total number of oocytes contained within follicles, and no mature follicles contained GFP-marked cells. Among the published reports raising objections to the previous work of Tilly’s group – none of which actually attempted to duplicate those experiments – one theorized that GFP-marked cells observed in recipient ovaries in the 2005 Cell paper might be donor immune cells rather than oocytes. To address that conjecture, the MGH-Vincent team isolated immune cells from normal mice, from the germline-only GFP strain used in their experiments, and from a strain of mice expressing GFP in all cells. Careful analysis confirmed that no immune cells from the germline-only GFP strain contained the marker protein, making it highly unlikely that GFP-labeled cells in the ovaries of females receiving germline-only-labeled marrow were anything other than oocytes. This was further confirmed by experiments showing that isolated immune cells did not express the oocyte-specific marker genes previously used by Tilly’s group to identify the marrow-derived oocytes. Tilly and his colleague note that, since agents that protect fertility most likely would need to be given before chemotherapy to be effective, whatever the donor marrow contributes probably acts by restoring rather than preserving fertility. “Right now, we really don’t know exactly what it is in marrow that restores recipient oocyte production and rescues long-term fertility. However, we do know without question that immature oocytes can be generated from cells in adult bone marrow, but they are probably not critical to the fertility rescue observed after the transplants.” Since the 2005 Cell paper, Tilly points out, three studies have been published by other groups showing that, similar to his team’s work in females, bone marrow cells from adult male mice or from men can be coaxed to make immature sperm cells, both in lab dishes and after transplantation into the testes. “Clearly, something is going on here regarding the ability of stem cells in bone marrow to produce immature egg and sperm cells, and we need to figure out what it is,” he says. .........


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Monday, 30 July 2007

Using stem cells to help heart attack victims

Using stem cells to help heart attack victims July 30, 2007 New research at The University of Nottingham is paving the way for techniques that use stem cells to repair the damage caused by heart attacks. The research, funded with a grant of £95,000 the Biotechnology and Biological Sciences Research Council (BBSRC), is looking at the process that turns a stem cell into a cardiomyocyte — the beating cell that makes up the heart. The Nottingham researchers are developing a new system to monitor cardiomyocytes in real time as they differentiate from stem cells into beating heart cells. The system uses electrophysiology to record the electrical properties in a cell and will be the first time it has been used to study cardiomyocyte cells in the UK. The researchers hope that their research could provide more detailed information on the electrical activity of stem cell derived cardiomyocytes. In the longer term, this could facilitate their use in regenerating the damaged hearts of heart attack victims. Dr Chris Denning, of the University’s Wolfson Centre for Stem Cells, Tissue Engineering & Modelling, said: “Human embryonic stem cells promise unrivalled opportunities. However, they are difficult, time-consuming and expensive to grow in the lab. " "Our understanding of how to convert them into cardiomyocytes is poor. At the moment we only know how to produce a few million cardiomyocytes, but to treat just one heart attack patient, we may need one billion that all function in the correct way." To help overcome the many challenges that stem cells bring, Dr Denning and co-investigator Professor Stephen Hill plan to engineer a novel system for real-time analysis of cardiomyocytes during early development so their properties are better understood. The team has already demonstrated that sufficient numbers of stem cell-derived cardiomyocytes can be produced for detailed analysis and they plan to use new 'electrophysiology' systems to record changes in the cells when cultured. Electrophysiology is the study of cells' electrical properties and this is the first time that the method has been used in the UK to study stem cell-cardiomyocyte biology. Dr Denning added: "This research will enable rapid development of stem cell-derived cardiomyocytes as a tool for understanding the heart and its diseases." "But before we can consider using stem cells to treat heart-attack patients there are many problems which will take many years to solve. We don't yet know how to deliver the cells to a patient's heart and prevent them being washed away so that they actually stay in the heart and both survive and function." “It will take many years to overcome these challenges and put stem cell-derived cardiomyocytes into medical usage." The researchers will also be monitoring how the cells respond to different pharmacological agents in order to improve drug-screening processes and reduce the need for animal testing. "A key part of the project is to monitor the effects of different drugs on the cells,” said Dr Denning. “At present, only limited information is available on how they respond to pharmacological or gene modulating agents." "Between 1990 and 2001, 8 different drugs were withdrawn from the market in the USA at an estimated cost of $8billion because they caused unexpected deaths in several hundred patients. Our aim is to reduce such occurrences by having better test methods to test the drugs before they reach the clinic." "By studying the drugs' effects on the heart cells in the lab, this could reduce the need for animals in clinical trials." ......... ZenMaster

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Sunday, 29 July 2007

Would you like a pig’s heart?

Is it right to clone animals for human transplants? July 29, 2007 Several research groups, and companies, are trying to make transgenic and cloned pigs to alleviate the organ donor shortage. Opponents have said that it raises serious ethical issues over the use of animals and poses a major safety question for humans. Do you think this marks a scientific breakthrough in cloning and availability of organs for transplants? Or does it raise concerns over the methods being used in cloning technology? Could you think of receiving a pig organ or tissue yourself, if needed? Pigs are very suitable for many reasons, they haven’t been chosen without thought: they are about the same size (body weight) as we are, they have a very similar internal anatomy as we, they grown fast (full size within a year) and are genetically well characterised. Several research groups, and now companies, are trying to make transgenic pigs for many years now, which would lack one of the major immunological obstacles to this xenotransplantation (transplanting organs between different animals and humans). It’s a simple sugar molecule on the surface of pig cells that now has been removed in these new breeds, and before was known to be the major immunological reactant in humans transplanted with pig tissues. The animals lack the gene responsible for "alpha-1,3-galactosyltransferase" (GT) — an enzyme normally present in the pig vascular system. Humans have natural, preformed antibodies to GT, resulting in immediate (acute) rejection of any pig-to-human transplant. The fact that these genetically engineered "GT-knockout" pigs lack GT removes one obstacle to cross-species transplantation, or xenotransplantation, between pigs and humans. Apart from the possible transplantation of organs such as the kidney or heart, pigs are also viewed as a potentially invaluable source of islet cells — the insulin-producing cells of the pancreas — for use in transplantation as a treatment for type-1 diabetes. Preliminary studies have reported encouraging results with transplantation of organs from GT-KO pigs into nonhuman primates. Hearts transplanted from GT-KO pigs into baboons have survived for several months, without the need for intensive drug treatment to suppress the recipient animal's immune system. However, many obstacles remain to be overcome before exploratory studies of xenotransplantation from GT-KO pigs to humans can begin. The transplanted hearts do not show the pattern of acute, overwhelming rejection typical of cross-species transplantation. However, there is evidence of another type of rejection, characterized by blood clots developing in the small blood vessels. This suggests a possible "coagulation dysregulation" between pigs and primates. New approaches will be needed to address the problem: either improved approaches to immunosuppressant drug therapy or further genetic manipulation of the donor animals. A lot is also known about pig’s physiology during medical procedure’s which make them suitable for this kind of treatment. Do you know that live sedated pigs are used for many training purposes for catastrophe medicine (surgeons who need training on complex wounds) and military doctors (shot gun and shell wounds)! Some argue these issues can be very emotional and scary for many people. True, but that’s exactly why they need to be discussed, to take away the scary part. It is usually when you don’t know, or don’t talk about something straight out, it becomes more and more scary. When you get to know the details and ventilating your anxiety it usually becomes easier to live with. Some people ask “Why spend so much money and effort on this?” This kind of work to develop donor organs from pigs, is not particular expensive compared to other things our societies put money on. And in the long run there will be a lot of savings instead, when people can live a healthy life instead. And they are definitely not impractical experiments. If you think so, you have not understood the slightest of what can be done to help people. ......... ZenMaster

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Scientists devise 'dimmer switch' to regulate gene expression

Scientists devise 'dimmer switch' to regulate gene expression in mammal cells July 29, 2007 Three Boston University biomedical engineers have created a genetic dimmer switch that can be used to turn on, shut off, or partially activate a gene’s function. Professor James Collins, Professor Charles Cantor and doctoral candidate Tara Deans invented the switch, which can be tuned to produce large or small quantities of protein, or none at all. The research detailing their new switch, “A Tunable Genetic Switch Based on RNAi and Repressor Proteins for Regulating Gene Expression in Mammalian Cells,” appears in the July 27 issue of Cell. This switch helps advance the field of synthetic biology, which rests on the premise that complex biological systems can be built by arranging components or standard parts, as an electrician would to build an electric light switch. Much work in the field to date uses bacteria or yeast, but the Boston University team used more complex mammalian cells, from hamsters and mice. The switch has several new design features that extend possible applications into areas from basic research to gene therapy. “There are a number of technologies available to regulate gene expression, but they each come with limitations,” said Collins. “One of the central problems is you can’t get a really tight ‘off’ state.” Even when genetic switches are turned off, a trickle of the protein that is meant to be repressed still gets made. Some genetic switches get around this by entirely snipping out a gene to stop production of a specific protein, but this approach is irreversible. To overcome these challenges, “Tara came up with a design that really combined two different technologies to repress or shut down gene expression,” Collins added. “We said, okay, we’ve got these two technologies, both that give a pretty good ‘off,’ why not try to combine them together to get a really clear and strong ‘off,’” said Collins. The first strategy, a repressor protein, sits on DNA like a roadblock, preventing any gene product -messenger RNA (mRNA) - from being made. If any mRNA gets past this repressor, the second technique, interfering RNA (RNAi) attaches to the functional mRNA, rendering it useless. The cell cannot turn it into protein. “I was delighted to see that when the two systems are coupled, it is possible to completely turn a gene’s function off,” said Deans. This switch is also reversible and tunable. By adding a chemical - Isopropyl-alfa-thiogalactopyranoside - the repressor components are blocked and the gene turns on again. The gene’s activity can be tuned up or down by adjusting the amount of this chemical. The researchers demonstrated the strength of their “off” switch by hooking it up to the gene for diphtheria toxin, then inserting it into cells. One molecule of diphtheria toxin can kill a cell, but with the genetic switch turned off, the cells survived for weeks. When the researchers flipped the switch, toxin production was triggered and the cell died. They also showcased the switch’s capability for delicately tuning gene expression, by installing it alongside a gene that leads to apoptosis, programmed cell death, once a certain threshold concentration of the gene’s product is reached. They gradually increased the gene’s activity until they met and passed this threshold. This tuning feature is important, said Deans, because “many diseases are not a result of missing a gene, but rather a result of too much or too little expression. With the ability to tune the level of gene expression in our switch, we could explore threshold responses and how these result in disease phenotypes.” The switch may also hold promise for therapeutic applications. “It gives a really nice regulator scheme for cell and gene therapy,” said Collins. “I think in the coming decades we’ll increasingly see these therapies being introduced as part of routine medical practice.” ......... ZenMaster

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Thursday, 26 July 2007

Protein Distinguishes Fetal and Adult Stem Cells

Protein Distinguishes Fetal and Adult Stem Cells July 26, 2007 In a discovery that fills a critical gap in the understanding of stem cells, researchers have discovered a protein that fetal, but not adult, blood-forming stem cells need to replenish themselves. Finding regulatory pathways specific to fetal blood-forming cells could help scientists understand childhood leukemias and generate blood-forming cells for bone marrow transplants. Research published in the July 26, 2007, issue of Cell. Sean J. Morrison, Ph.D., HHMI investigator University of Michigan Medical School For the full story, go to: http://www.hhmi.org//news/morrison20070727.html ......... ZenMaster

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Tuesday, 24 July 2007

Most egg cells in a female body die naturally

Most egg cells in a female body die naturally by programmed cell death July 24, 2007 Some facts: A 20-week-old human female foetus has around 7 million potential egg cells, or oocytes, in her developing ovaries. By birth this number has dropped to 1 million, and by puberty it is only some 300,000 cells left. Programmed cell death - apoptosis - takes the oocytes out. 'Death by neglect' is one possible explanation for this regulated drop in numbers. 'Death by defect' is another possibility. Distinct ‘killer molecules’ is involved in this form of apoptosis. The body puts in a quality control check, which cannot be overridden, to screen out bad eggs. For example, oocytes that are stalled during cell division will in this way be removed. Furthermore, in each menstrual cycle around 15 oocytes start to mature. Usually only one of these is chosen for release and possible fertilisation and the rest die off. The healthiest egg – ‘the one that gets ahead of the pack’ - may out-compete the rest to ensure the best end result – a healthy offspring. When a woman's supply of oocytes runs out she will enter the menopause. During the entire lifespan, only a few egg cells will become a healthy baby (0 to at the most 15 or 20 still in some cultures). The question:

What is so special with egg cells, so that they can’t be used for research or cure? Most, sometimes all will die anyway!

See also: Human Ovulation Caught on Camera CellNEWS - Wednesday, 18 June 2008 Most egg cells in a female body die naturally by programmed cell death CellNEWS - Tuesday, 24 July 2007 How much is a human egg worth? CellNEWS - Wednesday, 21 February 2007 Back to the question: How much is a human egg worth? CellNEWS - Tuesday, 09 October 2007 ........ ZenMaster

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Sunday, 22 July 2007

Does a clone have a ‘soul’?

Does a clone have a ‘soul’? July 22, 2007 Sometimes people ask if a cloned human being would have a ‘soul’. If we as humans would go about to clone another human being, we don’t need to ‘give’ or create a ‘soul’ for that cloned individual. What you call a ‘soul’, is only the manifestation of the chemical reactions taking place in and between our brain cells (and possibly in some other cells in the body too). For this to happen there is no need for a God or any God or other ‘higher powers’ of the universe, for that matter. It works by itself. Therefore, a cloned individual will have as much ‘soul’ as you or me, or anybody else have. We are only what we make ourselves to. ......... ZenMaster

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Thursday, 19 July 2007

Precision in Early Embryo Development

Fruit fly research may 'clean up' conventional impressions of biology July 19, 2007 The metamorphosis of biology into a science offering numerically precise descriptions of nature has taken a leap forward with a Princeton team's elucidation of a key step in the development of fruit fly embryos — discoveries that could change how scientists think not just about flies, but about life in general. While biologists have long known that the structure of adult animals follows a blueprint laid out in the early stages of embryonic development, classical biological experiments have provided only isolated "snapshots" of the development process, denying scientists a complete "movie" of it unfolding. Now, by combining experimental methods from physics and molecular biology, the team has replaced these snapshots with the movie, allowing them to see the first steps of blueprint formation in the fly embryo literally live and in colour. The first of two papers in the July 13 issue of the scientific journal Cell describes the sophisticated techniques required to make these movies, techniques that could help scientists investigate a wide variety of biological systems. In the second paper, the group poses a new question, never before asked by scientists studying embryos: “How precisely can cells in the embryo read the blueprint?” So precisely, the paper suggests, that a precious few molecules signalling a change can make a decisive difference. "I think the prevailing view has been that cells accomplish all their functions using a complicated combination of mechanisms, each one of which is rather sloppy or noisy," said team member William Bialek, the John Archibald Wheeler/Battelle Professor in Physics. "This research, however, indicates that in the initial hours of a fly embryo's development, cells make decisions to become one part of the body or another by a process so precise that they must be close to counting every available signalling molecule they receive from the mother.” Three hours into a fly embryo's development, it remains a single large cell with an unusual characteristic. Unlike other cells, which have a single nucleus, the embryo has thousands, each of which awaits a signal from the mother to form itself into a specialized cell. This signal arrives in the form of a droplet of protein called Bicoid that enters the embryo at one end and, like food colouring in water, diffuses out molecule by molecule through the nuclei. The concentration decreases with distance and forms the first blueprint that defines which part of the embryo will become the head and which the backside of the fly. The team's findings indicate that two neighbouring nuclei can determine their different places and functions within the embryo accurately if the concentration of Bicoid between them varies by only about 10 percent — a quantity that on the scale of the tiny embryo amounts to only a few molecules of Bicoid. "This signalling requires a sensitivity approaching the limits set by basic physical principles," Bialek said. "Perhaps more important than the answers we have found so far, this work has led us to sharpen the kinds of questions we ask about living cells as we try to understand them with the same kind of mathematical precision that we understand the rest of the physical world." References: Stability and Nuclear Dynamics of the Bicoid Morphogen Gradient Cell, Vol. 130, 141-152, 13 July 2007 Probing the Limits to Positional Information Cell, Vol. 130, 153-164, 13 July 2007 ......... ZenMaster

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Wednesday, 18 July 2007

Combined Drug and Stem Cell Treatment Hope for Alzheimer’s cure

Hope for Alzheimer’s cure July 17, 2007 Swedish and American researchers say they may be close to finding a cure for Alzheimer’s disease, the most common form of dementia. A research group from the Karolinska Institute in Stockholm and the University of Central Florida in the US say they have found ways to form new nerve cells which could replace those lost in large numbers by sufferers of the disease. The researchers have discovered that new nerve cells are formed when a stem cell transplant is combined with a course of treatment using the new drug Fenserin. The drug is yet to be formally approved but it’s already being used for clinical trials in a study at the Karolinska Institute in which some Alzheimer patients are participating. Even though the drug can stop Alzheimer’s, a transplant of stem cells is necessary in order to cure the disease. But stem cell transplants in the brain are a complicated operation, so scientsits believe this method of treatment will mainly be offered for younger patients, in the early stages of the disease. It is believed that these findings can not only stop the disease’s progress, but also reverse the effects of it. ......... ZenMaster

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Monday, 16 July 2007

EU Ethics group adopts opinion on hESCs use

Ethics group adopts opinion on human embryonic stem cell use July 16, 2007 The European Group on Ethics (EGE) in Science and New Technologies has issued an opinion setting out guidelines for use during the ethics review of EU-funded research projects involving human embryonic stem cells (hESC). The report was drawn up following a request in November 2006 from European Commission President José Manuel Barroso. ......... ZenMaster

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Friday, 13 July 2007

Cells take risks with their identities

Cells take risks with their identities July 12, 2007 Contrary to textbook models, many genes that should be 'off' in embryonic stem cells and specialized adult cells remain primed to produce master regulatory proteins, leaving those cells vulnerable to identity changes. Biologists have long thought that a simple on/off switch controls most genes in human cells. Flip the switch and a cell starts or stops producing a particular protein. But new evidence suggests that this model is too simple and that our genes are more ready for action than previously thought. Scientists in the lab of Whitehead Member Richard Young have discovered that many human genes hover between “on” and “off” in any given cell. According to the study these genes begin making RNA templates for proteins — a process termed transcription — but fail to finish. The templates never materialize, and the proteins never appear. “Surprisingly, about one-third of our genes, including all the regulators of cell identity, fall into this new class,” says Young, who is also an MIT professor of biology. “It seems awfully risky for an adult cell to leave genes primed that could change its identity.” The human body comprises more than 200 types of cells. Each cell contains the same complete set of genes, but expresses only a unique fraction of them, churning out proteins that make it a nerve or skin or white blood cell. Scientists have known for years that a cell hides the genes it doesn’t need by coiling the dormant DNA tightly around protein spools called histones. The new study, however, suggests that DNA packaging stays loose at the beginning of many inactive genes, contrary to textbook models. Whitehead postdoctoral researchers Matthew Guenther and Stuart Levine screened the entire human genome for a chemical signature — a landmark — that corresponds with this looser DNA packaging configuration and thus with transcription initiation. They worked with embryonic stem cells, liver cells and white blood cells. “We expected to find the landmark on 30 to 40 percent of the genes because that’s how many are active in each cell,” Guenther says. “We were shocked when it showed up on more than 75 percent of the genes in both unspecialized embryonic stem cells and specialized adult cells.” Further experiments confirmed that the majority of inactive genes undergo “transcriptional tryouts.” They begin making RNA, but never complete the job. Apparently, most of an inactive gene remains tightly coiled around histones, which prevent the RNA transcriptional machinery from progressing along the DNA. “These genes are like cars revving their engines before the beginning of a race,” Guenther explains. “They’re not parked in a garage with their engines off. They’re at the starting gate, waiting for a flag that says ‘go.’” These overzealous “cars” include all the genes responsible for directing cells along particular developmental paths — master regulators that should have no reason for gearing up in healthy specialized cells. Activating such genes might cause a cell to assume new properties. This vulnerability to metamorphosis could help to explain why some cells acquire new, unhealthy states in cancer, autoimmune diseases, diabetes and other illnesses. It could also explain why researchers — including Whitehead Member Rudolf Jaenisch, who is also an author on the latest study — were recently able to convert mouse adult skin cells to embryonic stem cells by simply introducing four key genes. Given the right signals, inactive developmental regulators primed for transcription could roar to life. “This is a new model for regulation of the developmental regulators,” Young maintains. “It could bring us a step closer to reprogramming cells in a controlled fashion, which has important applications for regenerative medicine.” ......... ZenMaster

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Monday, 9 July 2007

Who should ‘own’ genetic information?

Who should ‘own’ genetic information? July 8, 2007 We all share our genetic make up with relatives, but should we also share ownership of the results of DNA analysis or should this knowledge be considered private? Two experts give their views in this week’s BMJ. Dr Anneke Lucassen, a clinical geneticist at the University of Southampton, believes that if anyone is to own genetic information, it has to be all those who have inherited it and, more importantly, it must be available to all those who might be at risk. The question, she says, is how to balance a right to privacy with disclosing risks to others. Patient confidentiality is of course one of the most important cornerstones of medical practice, she writes. Nevertheless, confidentiality is rarely seen as absolute, and there are both statutory and professional guidelines on exceptions to the duty of confidentiality. The Human Genetics Commission’s 2002 report suggested that ‘genetic solidarity’ and altruism should be promoted, while UK guidelines state that where there is a serious preventable harm, confidentiality may be breached. Methods for sharing information need to be sensitive and relevant, she says, but today’s increasingly individualistic modern medicine must find ways of facilitating this. It should not be denied because of a narrow view of information ownership, she concludes. But Professor Angus Clarke at the Institute of Medical Genetics in Cardiff argues that genetic information should be regarded as private and personal. To treat it as if it were owned in common by a body as vague and ill defined as ‘the family’ is flawed, he says. He concedes that there are occasions when genetic information does belong intrinsically to the family. For example, in a genetic linkage study looking at the pattern of sharing of DNA sequences. While he does not deny that family members should be prepared to share important medical information with their relatives, two particular problems arise, he says. The first occurs when an individual fails to pass potentially important information to their relatives. He argues that genetic disorders are not sufficiently similar to infectious diseases such as gonorrhoea, syphilis and HIV, that doctors have a duty to enforce disclosure by patients or clients to other members of their family. The harm done by a failure to disclose will usually not entail an immediate and grave form of damage, he writes. The second problem is when an individual forbids health professionals to release or to use genetic test results to provide more accurate or relevant medical advice to their relatives. Once family members know that a relative has been diagnosed with a particular genetic condition, Professor Clarke argues that the more detailed, technical information (such as the precise mutation causing the disease in the family) belongs to the laboratory or the health service that generated it and not to either the individual or the family. ......... ZenMaster

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Thursday, 5 July 2007

Engineered blood vessels function like native tissue

Engineered blood vessels function like native tissue July 5, 2007 Blood vessels that have been tissue-engineered from bone marrow adult stem cells may in the future serve as a patient's own source of new blood vessels following a coronary bypass or other procedures that require vessel replacement, according to new research from the University at Buffalo Department of Chemical and Biological Engineering. “Our results show that bone marrow is an excellent source of adult stem cells containing smooth muscle and endothelial cells, and that these stem cells can be used in regenerative medicine for cardiovascular applications,” said Stelios T. Andreadis, Ph.D., associate professor in the UB Department of Chemical and Biological Engineering in the School of Engineering and Applied Sciences. The UB researchers developed a novel method for isolating functional smooth muscle cells from bone marrow by using a fluorescent marker protein and a tissue-specific promoter for alpha-actin, a protein found in muscles that is responsible for their ability to contract and relax. Although not yet strong enough for coronary applications, the UB group’s tissue-engineered vessels (TEVs) performed similarly to native tissue in critical ways, including their morphology, their expression of several smooth muscle cell proteins, the ability to proliferate and the ability to contract in response to vasoconstrictors, one of the most important properties of blood vessels. The TEVs also produced both collagen and elastin, which give connective tissue their strength and elasticity and are critical to the functioning of artificial blood vessels. “These are the first tissue-engineered vessels to demonstrate the ability to make elastin in vivo,” said Andreadis. In addition, the smooth muscle cells isolated from the bone marrow are mesenchymal cells, that is, stem cells that can differentiate into several cell types. Several studies have shown that mesenchymal stem cells may be immunoprivileged, which means they will not trigger an immune reaction when transplanted into another individual, Andreadis said. “If true, this means that you may be able to develop a universal cell source for smooth muscle cells, so that you could potentially make these vessels into an ‘off-the-shelf’ product, available to any patient,” Andreadis said. The TEVs were implanted into sheep and functioned normally for five weeks. Andreadis’ group now is working on ways to make the TEVs stronger. It also is studying the differences between stem cells taken from older versus younger individuals. ......... ZenMaster

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