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Internaf-News May 1999 Page 3 Back to Index
Washington Post Staff Writer Sunday, May 23, 1999; Page A1 A presidentially appointed ethics panel has decided to recommend that the federal government begin funding some research on human embryos, saying the moral cost of destroying embryos in research is outweighed by the social good that could come from the work. Citing recent evidence that some human embryo cells have the potential to grow into replacement tissues to treat a wide variety of chronic diseases, the National Bioethics Advisory Commission has concluded that it is essentially unfair to millions of patients for Congress to continue its broad, four-year-old funding ban on human embryo research. Instead, federal rules should be written that ensure an appropriate measure of protection and respect for human embryos, according to a draft version of the report and interviews with commissioners and others. Those rules would allow federally financed researchers to conduct studies on leftover embryos from fertility clinics if the embryos were no longer wanted by the parents who made them. "These are very difficult judgments to make, but it's a balancing act," said Harold T. Shapiro, chairman of the bioethics commission and president of Princeton University. "We have moral obligations to the future health and welfare of people, and we need to balance these with, at the very least, the symbolic moral obligation we have to the embryo." The recommendations go further than those recently proposed by the National Institutes of Health. Those call for federally funded research on laboratory-grown human embryo cells, but not on human embryos themselves. The more conservative NIH recommendations already have drawn fire from some members of Congress. Observers said the bioethics commission's report is likely to escalate the long-standing political tussle over the moral status of embryos and the wrenching national debate over abortion. "I have a sense that this is going to be one of the liveliest debates on the Senate and the House floors this session," said Sen. Arlen Specter (R-Pa.), who last fall held a hearing on stem-cell research. Contentious as the issue is, there are signs that public opinion may be moving toward support of at least limited embryo research. "Patients and their families faced with life-threatening and chronically disabling diseases want science to move as quickly as possible," said Daniel Perry, executive director of the Alliance for Aging Research and chief of a new coalition of patient groups advocating research on human embryonic stem cells, the embryo-derived cells that have generated so much recent excitement. The new group, Patients' Coalition for Urgent Research, or CURe, includes more than two dozen national organizations, such as the American Cancer Society and the Christopher Reeve Paralysis Foundation. At an inaugural event last week, the group released poll results indicating that 74 percent of Americans support human embryonic stem-cell research. "We're not naive and we know there's not going to be a cure tomorrow," Perry said. "But it's a good thing for federal funding to be there because it means the research will be done more quickly and it will be more accountable to the public." The commission's report, due to be released next month, is the second federal ethics analysis in less than five years to conclude that certain kinds of research on human embryos warrant federal support. The previous one, by a panel convened by the NIH, was partially approved by President Clinton in 1994 but then rejected by Congress, which passed an appropriations rider blocking all such funding and has renewed that ban annually ever since. The 17-member bioethics commission calls for a more limited range of embryo experiments than did the 1994 panel. It does not support the use of federal funds to create new human embryos just for research, for example the single provision that Clinton rejected in 1994 and it offers specific policy guidelines to keep studies within narrow scientific and ethical bounds. But the biggest difference between 1994 and 1999, experts said, is that the benefits of embryo research are now far less theoretical. If the morality of human embryo research is pegged in part to the benefits that are likely to accrue to sick and dying people, as many ethicists, religious leaders and others believe, then the tipping point of acceptability appears to have been reached, the report concludes. "This research is allied with a noble cause," the draft report states, "and any taint that might attach from the source of the stem cells diminishes in proportion to the potential good which the research may yield." The commission's report is still undergoing revisions. But interviews with commissioners and others involved in its crafting indicate that a clear consensus exists for some basic recommendations. For now, the report will say, federal funding should be made available only for research on embryos made by in vitro fertilization for infertile couples. A single cycle of IVF can result in the creation of a dozen or more embryos, of which three or four typically are transferred to the womb. The rest are frozen for later efforts. Under the report's recommendation, if any are left over when the couple stops trying to get pregnant, the couple could donate them for federal research (or have them destroyed or keep them frozen indefinitely). Federally funded scientists would be allowed to ask parents for permission to conduct studies on their embryos only after the parents had independently decided to abandon them. And if any compensation were to be allowed, it would be very limited. With protections such as these in place, the commission concludes, parents and not the federal government would be "morally responsible" for the embryos' demise. Most commissioners also favor creation of a national oversight board that would be responsible for ensuring that only those embryo experiments deemed most worthy get federal support. The commission concedes that it cannot settle the debate over embryos' intrinsic moral value. But for the purposes of making public policy, it seeks to find an ethical middle ground by balancing the potential harm to embryos against the potential benefits to patients. The commission notes, for example, that even many conservatives support abortion under certain circumstances. "Conservatives who accept that killing a fetus is permissible where it is necessary to save the life of the mother should agree with liberals that it is also permissible to destroy embryos where it is necessary to save people." The new analysis comes at a time of growing public clamor for full-bore pursuit of research into human embryonic and fetal stem cells cell types discovered just last year that have the potential to grow into many kinds of tissues. Researchers envision cultivating the cells into replacement neurons for patients with Parkinson's disease, insulin-secreting cells for diabetics, and heart muscle cells for victims of heart attacks, among other uses. But it wasn't only advances in science that led the commission to decide it is time to invite federal investment in embryo research, said Eric Meslin, the commission's executive director. Since the 1994 NIH report, Meslin said, people have been reconsidering their feelings about embryo research. A growing number seem to have found room within their personal belief systems to justify limited amounts of such research including many religious leaders who testified to the commission. "The community has been coming to the view that these sources of cells are ethically acceptable with a number of protections put in place," Meslin said. Many also favor a federal presence in the stem-cell field so research priorities will be selected on the basis of what is best for the nation's health and welfare, instead of on the basis of maximum profitability for the companies now pursuing the technology with private money. The American Society for Reproductive Medicine, the professional organization that oversees fertility clinics, where most of the nation's uncounted thousands of spare embryos are stored in freezers, expressed support for the commission's conclusions. "We would certainly welcome federal funding and oversight for research involving human embryos and human embryonic stem cells, and we would hope that Congress would act on the commission's recommendation," said Sean Tipton, a spokesman for the organization in Washington. But others, including antiabortion activist John Cavanaugh-O'Keefe of the Laytonsville, Md.-based Eugenics Watch, vowed to fight the move. And congressional support is hardly assured. Rep. Jay Dickey (R-Ark.), a co-author of the rider that has banned embryo research since 1995, said through a spokesman that he strongly opposes the commission's views. "Any NIH action to initiate funding of such research would violate both the letter and spirit of the federal law banning federal support for research in which human embryos are harmed or destroyed," Dickey wrote in a recent letter to Health and Human Services Secretary Donna E. Shalala. © Copyright 1999 The Washington Post Company
Journal of Neurology (1989) 236: 120-122 By H.M. Meinck, P.W. Schonle, and B. Conrad Summary. The chronic motor handicaps of a 30-year-old multiple sclerosis patient acutely improved while he smoked a marihuana cigarette. This effect was quantitatively assessed by means of clinical rating, electromyographic investigation of the leg flexor reflexes and electromagnetic recording of the hand action tremor. It is concluded that cannabinoids may have powerful beneficial effects on both spasticity and ataxia that warrant further evaluation. Key words: Multiple sclerosis---Spasticity---Ataxia---Cannabinoids---Flexor reflex Introduction This study was prompted by a young man with multiple sclerosis (MS) who used marihuana as a remedy for his various motor, micturition and sexual handicaps. After smoking a marihuana cigarette on the ward, he clinically improved. He agreed to the beneficial effects of marihuana being investigated by means of quantitative clinical and electrophysiological assessment. Case Report This male patient, born in 1955, had had MS since 1983. At the time of our experiments he was bound to a wheelchair because of severe limb and gait ataxia and spastic tetraparesis. After micturition, his residual urine volume was 100-150 ml. He complained of impotence, with erections lasting less than 5 min and lacking ejaculation. He tried a marihuana cigarette in about 1984 and noted an instantaneous improvement of his motor and sexual functions lasting for several days. Since then, he regularly took some marihuana biscuits each week, which enabled him to climb stairs, to walk on even ground, and to have erections for more than 30 min. allowing him a quite satisfactory sexual life. Methods From 12 October 1985 the patient abstained from all drugs, including marihuana. He was hospitalized between 17 October and 25 October. On 22 October, one "experimental" marihuana cigarette was allowed, and various electrophysiological experiments were performed as described below. Clinical rating was performed daily by the same neurologist and on 22 October before and after the "experimental" cigarette. Rating comprised motor functions relevant to the electrophysiological tests described below (see Fig. 1). The flexor reflex was elicited by a painful electrical shock to the foot sole and recorded from the quadriceps (Q), posterior biceps (PB), gastrocnemius (G) and tibialis anterior (TA) muscles. The EMG was full-wave rectified, and eight consecutive reflexes were summated. Five control series of eight consecutive reflexes were run at intervals of about 5 min. The patient was then asked to take one whiff of his "experimental" cigarette, and further series of reflexes were run in the manner described above (for details see [12]). Finger movements were recorded in a standardized pointing task performed before and after both the "experimental" cigarette and the flexor reflex experiment. Basically, the recording device consisted of a three-coil-transmitter system generating non-homogeneous magnetic fields, and a miniaturized receiver coil attached to the finger tip. When the finger moved through the magnetic fields a signal was induced in the receiver coil, allowing the computation of the two-dimensional movement trajectory (for details see [15]). Ten trials were performed before and after marihuana smoking, each consisting of a pointing movement of the right index finger over a 10-cm distance. The forearm rested on a stable support, but the finger and hand could not reach the target. Results Clinical rating showed a moderate deterioration of motor functions between 17 October and 22 October (Fig. 1) On 22 October, before the "experimental" cigarette, he was incapable of walking a few steps even with support: his muscle force in the legs did not exceed MRC grade 3. Muscle tone ranged between slightly and moderately increased, and the leg deep tendon reflexes were exaggerated or clonic with sustained ankle and knee clonus. The receptive field of the Babinski sign covered the whole foot and the shin. Ataxia in the arms was severe and could not be tested in the legs because of distinct hip flexor paresis. About 145 min after the marihuana cigarette, muscle force was somewhat increased in the knee extensors and ankle flexors (but not in the hip flexors), and muscle tone was reduced. The leg deep tendon reflexes showed normalization, too, corresponding to a clear shortening of the periods of clonus. The receptive field of the Babinski sign was confined to the lateral foot sole margin. Ataxia in finger-nose testing was moderate. After the flexor reflex experiment, the patient was able to walk a few metres between the couch and his wheelchair with support. Some of these improvements lasted beyond 23 October and even 24 October (Fig 1). The flexor reflex showed the desynchronized and prolonged reflex pattern typical of spastic paresis (Fig. 2a: cf [13]). As soon as 2 min after the whiff of the marihuana cigarette, a clear attenuation of the reflex activity was noted. Attenuation was about equal in all four muscles (20%-30% of the last three control recordings) and progressed until 17 min after the whiff. A second whiff (18 min after the first one) did not induce further reflex attenuation. Single sweep recordings showed that the reflex attenuation after marihuana was not due to enhanced habituation;: after marihuana even the first of the eight consecutive reflex responses was attenuated. Electromagnetic recording of action tremor revealed a coarse 3 Hz hand and finger tremor with an amplitude between 1 and 3 cm, persisting throughout nearly the whole movement. Hours after the "experimental" cigarette, action tremor was almost completely abolished, although the movements were made at about the same speed (Fig. 2b). Discussion Our findings clearly show that there are indeed motor actions of marihuana which were (a) reproducible in a laboratory situation most exhaustive to the patient. (b) quantitatively assessable by means of electrophysiological testing, and (c) in line with the results of clinical rating. Our findings further correspond with earlier anecdotal clinical reports [4, 6, 11, 14]. Little is known about the neurophysiological background of the antispastic and antiataxic actions of marihuana seen in our patient. However, some findings in experimental animals seem relevant to our observations. Cannabinoids in higher dosages attenuate the monosynaptic reflex [1,2,17,18] principally corresponding to the attenuation of both deep tendon reflexes and clonus in our patient (Fig. 1). Polysynaptic reflexes were also attenuated after tetrahydrocannabinol derivatives in experimental animals [1, 7, 20], fitting in well with the narrowing of the receptive field of the Babinski sign (Fig. 1) and with the results of our flexor reflex experiment. As cannabinoids have analgesic properties [16,20], attenuation of the pathological flexor reflex in the present case could represent analgesic rather than antispastic effects of the drug. However, analgesic effects are also attributed to several antispastic drugs [10,21] and, on the other hand, classical analgesics such as opioids may improve spastic symptoms [19]. One might, therefore, indeed wonder whether both the antispastic and analgesic actions of such drugs are in fact at least to a substantial degree based on common neuronal mechanisms such as an increase of presynaptic inhibition or a decrease of postsynaptic excitation of multireceptive interneurones at various levels of the neuraxis. Whatever the mechanism, the antispastic actions of marihuana in both clinical rating and electrophysiological testing are similar to those seen in spastic patients after either 0.3 mg tizanidine [13], 150 mcg clonidine, or 10 mg diazepam (unpublished observations). The important difference is that marihuana apparently also has antiataxic actions (Fig. 2b: see also [4] not ascribed to any antispastic drug. The biochemical basis of the motor effects of marihuana is obscure. Available data, although somewhat controversial, suggest that cannabinoids release brain serotonin from its storage sites and block its re-uptake [8], inhibit the synthesis of prostaglandins within the CNS [9] and-- in large doses -- elevate brain acetylcholine and reduce its utilization [5]. The relationship of these neurotransmitters to spasticity and ataxia is unknown: none of the well-established antispastic drugs is thought to interfere with them; they are only scarcely, if at all, found within the cerebellum [3]. Acknowledgement. We thank our patient for his kind cooperation throughout this study. References 1. Boyd ES, Merritt DA (1965) Effects of a tetrahydrocannabinol derivative on some motor systems in the cat. Arch Int Pharmacodyn Ther 153: 1-12 2. Capek R, Esplin B (1976) Effects of delta-9-tetrahydrocannabinol on the homosynaptic depression in the spinal monosynaptic pathway: implications for transmitter dynamics in the primary afferents. In: Nahas GG, Paton WDM, Idaanpaan-Heikkila JE (eds) Marihuana -- chemistry, biochemistry, and cellular effects. Springer, New York Berlin Heidelberg. pp 385-395 3. Chan-Palay V (1984) Purkinje cells of the cerebellum: localization and function of multiple neuroactive substances. Exp Brain Res [Suppl] 9: 129-144 4. Clifford DB (1983) Tetrahydrocannabinol for tremor in multiple sclerosis. Ann Neurol 13: 669-671 5. Domino EF (1976) Effects of delta-9-tetrahydrocannabinol and cannabinol on rat brain acetylcholine. In: Nahas GG, Paton WDM, Idaanpaan-Heikkila JE (eds) Marihuana -- chemistry, biochemistry and cellular effects. Springer, New York Berlin Heidelberg. pp. 407-413 6. Dunn M. Davis R (1974) The perceived effects of marijuana on spinal cord injured males. Paraplegia 12: 175 7.Gilbert PE (1981) A comparison of THC, nantradol, nabilone, and morphine in the chronic spinal dog. J Clin Pharmacol 21: 311-319 8. Ho BT, Johnson KM (1976) Sites of neurochemical action of delta-9-tetrahydrocannabinol: interaction with reserpine. In: Nahas GG, Paton WDM, Idaanpaan-Heikkila JE (eds) Marihuana -- chenistry, biochemistry, and cellular effects. Springer, New York Berlin Heidelberg, pp. 367-381 9. Howes JF, Osgood PF (1976) Cannabinoids and the inhibition of prostaglandin synthesis. In: Nahas GG, Paton WDM, Idaanpaan-Heikkila JE (eds) Marihuana -- chemistry, biochemistry, and cellular effects. Springer, New York Berlin Heidelberg. pp 415-424 10. Jurna J (1984) Depression of nociceptive sensory activity in the rat spinal cord due to the intrathecal administration of drugs: effects of diazepam. Neurosurgery 15: 917-920 11. Malec J, Harvey RF, Cayner JJ (1982) Cannabis effect on spasticity in spinal cord injury. Arch Phys Med Rehabil: 116-118 12. Meinck H-M, Conrad B (1986) Neuropharmacological investigations in the stiff-man syndrome. J Neurol 233: 340-347 13. Meinck H-M, Benecke R. Conrad B (1985) Cutaneo-muscular control in health and disease: possible implications on spasticity. In: Struppler A, Weindl A (eds) Electromyography and evoked potentials, theories and applications. Advances in applied neurological sciences, vol 1. Springer, New York Berlin Heidelberg, pp 75-83 14. Petro DJ, Ellenberger C (1981) Treatment of human spasticity with delta-9-tetrahydrocannabinol. J Clin Pharmacol 21: 413-416 15. Schonle PW, Grabe K, Wenig P, Hohne J, SchraderJ, Conrad B (1987) Electromagnetic articulography -- use of alternating magnetic fields for tracking movements of multiple points inside and outside the vocal tract. Brain Lang 31: 26-35 16. Segal M (1986) Cannabinoids and analgesia. In: Mechoulam R (ed) Cannabinoids as therapeutic agents. CRC Press Boca Raton, Fla, pp 105-120 17.Tramposch A, Sangdee C, Franz DN, Karler R, Turkanis SA (1981) Cannabinoid-induced enhancement and depresion of cat monosynaptic reflexes. Neuropharmacology 20: 617-621 18. Turkanis SA, Karler R (1983) Effects of delta-9-tetrahydrocannabinol on cat spinal motoneurons. Brain Res 288: 283-287 19. Will JC, Bussel B (1980) Evidence for a direct spinal mechanism in morphine-induced inhibition of nociceptive reflexes in humans. Brain Res 187: 212-215 20. Yaksh TL (1981) The antinociceptive effects of intrathecally administered levonantradol and desacetyllevonantradol in the rat. J Clin Pharmacol 21: 334-340 21. Yaksh TL, Reddy SVR (1981) Studies in the primate on the analgetic effects associated with intrathecal actions of opiates, a-adrenergic agonists and baclofen. Anesthesiology 54: 451-467 Received November 30, 1987/ Received in revised form October 6, 1988/ Accepted November 6, 1988
May 16 1999 INNOVATION Doctors bridge gap to fix severed nerves BRITISH surgeons are hoping to reverse paralysis with the first technique that encourages nerves to regrow effectively. Nerve-transplant trials are to begin this summer with up to 100 patients who will have suffered recent nerve damage in accidents. The technique could revolutionise treatment for thousands of people who suffer damage ranging from loss of sensation caused by a severed nerve in a hand injury to extensive paralysis. Getting nerves to grow or rejoin has been a key goal for tissue engineers for years, but as yet no viable method has been found. A nerve is like a telephone cable with multi-strands of fibres all taking sensory and other messages to the brain and the central nervous system. Nerves connect organs with each other and with the brain, and good connections are crucial to the proper functioning of the body. When a nerve is severed, usually through trauma, small fibres grow out from the severed end nearest to the brain or spinal column in an attempt to bridge the gap. If the gap is small enough the nerve may grow across it and link up with the severed section - which then acts as a conduit along which the new nerve can grow. But such connections do not always work because the right links are not made. In some cases the nerve will simply not grow and, if the gap is too wide, the nerve is unable to repair itself. At University College Hospital, London, Professor Gus McGrouther, professor of plastic and reconstructive surgery, and his tissue-engineering team have now pioneered a new approach using a scaffold tube implanted in the body. The tube links the two severed nerve ends, encouraging the nerve to grow along it and match up in exactly the right places. He says: "When the nerve grows naturally after it is cut, the branches can get lost and not reach anywhere at all. What we have been able to do is put a scaffold in between the cut ends that directs the nerve fibres towards the other end of the nerve." A key to the team's success is the material it has used for the scaffold. It is made from a blood protein extracted from the patient's own blood. Because it is a cell-attachment protein, cells, including growing nerve cells, stick to it. The protein is dried under pressure and moulded into the shape needed to match the gap. It can be used flat or shaped into a tube for the nerve to grow along. "We have a guidance system with the matrix, a growth factor to promote growth, and a cell-attachment protein, which means that the cells stick to it and encourage growth," says McGrouther. "We are the first to identify a way of tissue engineering a nerve using the patient's own blood protein." The team is now planning the first clinical trials, which are likely to start this summer. It may involve centres in the Netherlands and Sweden and is likely to involve between 50 and 100 patients. The object of the trial is to get the nerves to grow to restore sensation to those parts of the patients' bodies that are either paralysed or numb. All the cases will need to be recent injuries because after a month or so the severed end of a nerve loses its ability to regenerate. In the trial, the patients will have a pint of blood taken two weeks before the operation from which the protein will be extracted to form the scaffold. They will then have the matrix implanted and be monitored for both nerve growth and the return of any sensation. "This sort of approach to nerve injury will revolutionise nerve repair over the next 10 to 15 years," McGrouther believes. "It will provide a better physical link and join combined with better chemical stimulation for nerve growth."
by Teresa Brady, Ph.D. Fatigue is common in chronic illness. Managing fatigue is an important component of learning to live with a chronic illness. Fatigue can lead to depression, anger, a loss of physical and cognitive skills and a lack of motivation. Sleep can also be a problem. Work implification and energy conservation help reduce fatigue. There are five strategies to help manage fatigue by conserving energy and using it wisely -planning, positioning, pacing, prioritizing and adaptive equipment.
Maintain good posture to take the strain off joints. Use a wheeled cart around the house and sit while working to conserve energy. Arrange work and storage areas to be more efficient.
Look for short cuts. Use convenience foods like cake mixes and adapted equipment like jar openers to make the job easier. Changing habits for energy conservation seems awkward at first but becomes easier over time. It is also possible to reduce fatigue by building energy resources and addressing psychological factors.
Continually striving for perfection and being harsh and demanding of oneself also leads to fatigue. Those who set unreasonably high and rigid standards for themselves become depressed and fatigued when they cant meet the standards. They are never satisfied. They can exhaust themselves struggling to meet unreasonably high expectations. When feeling frantic, take a break and rest for a few moments and think the situation through. Things will go better and will be less fatiguing. Examine expectations and try to determine whose they are - yours or someone elses. Dont wear yourself out meeting expectations that are unreasonable or are not important to you. Take what limited energy you have and learn to use it wisely. Try to accommodate fatigue since it will be difficult to conquer. Try not to be so independent, and dont be afraid to ask for help. Build your energy resources through exercise and make changes to help deal with the psychological component of low energy - a better quality of life will be the result. (Dr. Brady is a licensed psychologist and an occupational therapist who has worked extensively with connective tissue diseases in a variety of settings. She is Executive Director of the Minnesota Arthritis Institute.)
New Ataxia/Epilepsy Gene LOS ANGELES -- Five spinocerebellar ataxia (SCA) genes had been previously identified by various research groups, including SCA2, which, like SCA10, was found by the Cedars-Sinai team of Stefan-M. Pulst, M.D. Like SCA2, SCA 10 shows anticipation, a phenomenon whereby onset of the disease is earlier and earlier with each successive generation. The presence of anticipation may provide an important clue for the isolation of the gene, since it may indicate that the genetic defect is caused by unstable DNA repeats. In contrast to other inherited ataxias, however, 20 percent of members of the family affected by the ataxia suffered seizures. "This connection makes isolation of the genetic defect so exciting", says Dr. Pulst, "because it will likely shed light on the much more common epilepsies." It was approximately a year ago that the Pulst team identified the Mexican-American family exhibiting the rare form of ataxia. They have now been able to localize the SCA10 gene on the long arm of chromosome 22 by conducting a search that included some 300 genetic markers covering the entire human genome. It was the 40th of these that suggested the researchers were in the right region. Interestingly, the new gene is not close either to other ataxia genes, or to any for epilepsy. Whereas it took the team 5 years to identify the prior ataxia gene, they expect to identify SCA10 as soon as two years from now, thanks to advances in the Human Genome Project. Dr. Pulst is director of the Cedars-Sinai Division of Neurology since 1993 and became holder of the Carmen and Louis Warschaw Chair in Neurology in 1991. He is also director of the Cedars-Sinai Neurogenetics Laboratory, scientific director of the Parkinson's Disease Research and Treatment Center at the Medical Center, and a professor of medicine at UCLA. Key contributors include first author Lan Zu, PhD, a fellow, and Karla Figueroa, a research associate, in the Rose Moss Laboratory for Parkinson's and Neurodegenerative Diseases of the Burns & Allen Research Institute at Cedars-Sinai Medical Center, and Raji Grewal, MD, a member of the Department of Neurology at the USC School of Medicine. The study was supported by grants from the National Institute of Neurological Diseases and Stroke, the Joseph Drown Foundation, and the Carmen and Louis Warschaw Endowment for Neurology.
TORONTO (AP) _ A controversial surgery which implants fetal cells into an adults brain have helped many Parkinsons patients improve brain function and move better, researchers said Wednesday. The researchers studied 38 American and two Canadian patients who underwent such surgery, the latest effort in the use of cells from aborted fetuses to stimulate brain activity. The patients were randomly chosen to either receive a fetal cell implant or a placebo surgery, said Dr. Curt Freed of the University of Colorado, who led the study and presented the results at a meeting in Toronto of the American Academy of Neurology. Parkinsons, characterized by stiffness and tremors, destroys the brain cells that produce dopamine, a chemical that influences many parts of the brain. The fetal cells are used to replace them. "We simply put in new cells where others have died," said Freed, adding it was the first surgical study of its kind. Over the year following the operation, more than half the patients who received fetal cells had a significant increase in levels of dopamine. But how long the improvements will continue is still under investigation. More than one million Americans suffer from Parkinsons, a degenerative brain disease most often found in people over 50. But younger people can also develop it. Actor Michael J. Fox announced earlier this year that he has Parkinsons. Most of the benefits of the operation, including better motor control, were in patients under 60, said Dr. Stanley Fahn, Freeds partner from New Yorks Columbia Presbyterian Hospital. Researchers believe its because the aging brain is less resilient. Many patients were also able to reduce or stop taking medication. Toronto-area residents Judy Hazlett and Lynda McKenzie, who took part in the trials, said they struggled before volunteering for the surgery. "I debated a long time before I decided to have the fetal tissue," said Hazlett, who was 29 when she was diagnosed with Parkinsons 20 years ago. "But you have to realize its recycled tissue; the woman has already decided to abort the child." Hazlett said the surgery has resulted in "little but amazing changes." She can now sleep through the night, carry a spoon without dropping it, and hold her head up. She is also taking less medication. Its been 10 years since surgeons first experimented with fetal cells implanted in human brains. Since then, more than 100 surgeries have been performed worldwide. The U.S. trials, which lasted nearly five years, were funded by $4.5 million from the National Institutes of Health. They were the first to receive federal research grants in 1993, when President Clinton lifted a Reagan Administration ban on fetal-tissue funding.
The Financial Times Thursday 1st April, 1999 : Genes put pain under controlResearchers in the US have shown for the first time that gene therapy can be used to control pain in animals. The development could lead to new treatments for chronic pain associated with conditions such as cancer, arthritis and angina. The researchers at the University of Pittsburgh and the University of South Carolina treated mice with a herpes virus containing a gene that triggers production of a pain-blocking protein. The gene appeared to act on C-type neurons, which are thought responsible for slow, burning pain. The researchers hope within a few years to devise a treatment that is effective and non-addictive. The study is published in the March issue of the Proceedings of the National Academy of Sciences. University of Pittsburgh: US, tel 0014126242607; http:// www.pitt.edu/rsup/phgt
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