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Looking into the Brain with Light

By Michael Chorost

A new noninvasive diagnostic technology could give doctors the single most important sign of brain health: oxygen saturation. Made by an Israeli company called OrNim and slated for trials on patients in U.S. hospitals later this year, the technology, called targeted oximetry, could do what standard pulse oximeters can't.

A standard pulse oximeter is clipped onto a finger or an earlobe to measure oxygen levels under the skin. It works by transmitting a beam of light through blood vessels in order to measure the absorption of light by oxygenated and deoxygenated hemoglobin. The information allows physicians to know immediately if oxygen levels in the patient's blood are rising or falling.

Prior to the development of pulse oximeters, the only way to measure oxygen saturation was to take a blood sample from an artery and analyze it in a lab. By providing an immediate, noninvasive measure of oxygenation, pulse oximeters revolutionized anesthesia and other medical procedures.

While pulse oximeters have become accurate and reliable, they have a key limitation: they can't measure oxygen saturation in specific areas deep inside the body. Because pulse oximeters measure only the blood's overall oxygen levels, they have no way of monitoring oxygen saturation in a specific region. This is especially problematic in the case of brain injuries, since the brain's oxygenation can then differ from the rest of the body's.

Information on oxygenation in specific regions of the brain would be valuable to neurologists monitoring a brain-injured patient, as it could be used to search for localized hematomas and give immediate notice of hemorrhagic strokes. When a stroke occurs, an area of the brain is deprived of blood and thus oxygen, but there is no immediate way to detect the attack's occurrence.

CT and MRI scans give a snapshot of tissue damage, but they can't be used for continuous monitoring. It can also be very difficult to conduct such scans on unconscious patients hooked up to life-support devices.

Wade Smith, a neurologist at the University of California, San Francisco, and an advisor to OrNim, points out that, while cardiologists have devices to monitor hearts in detail, neurologists have no equivalent tool. With brain-injured patients, Smith says, "the state of the art is flying blind."

OrNim's new device uses a technique called ultrasonic light tagging to isolate and monitor an area of tissue the size of a sugar cube located between 1 and 2.5 centimeters under the skin. The probe, which rests on the scalp, contains three laser light sources of different wavelengths, a light detector, and an ultrasonic emitter.

The laser light diffuses through the skull and illuminates the tissue underneath it. The ultrasonic emitter sends highly directional pulses into the tissue. The pulses change the optical properties of the tissue in such a way that they modulate the laser light traveling through the tissue. In effect, the ultrasonic pulses "tag" a specific portion of tissue to be observed by the detector. Since the speed of the ultrasonic pulses is known, a specific depth can be selected for monitoring.

The modulated laser light is picked up by the detector and used to calculate the tissue's color. Since color is directly related to blood oxygen saturation (for example, arterial blood is bright red, while venous blood is dark red), it can be used to deduce the tissue's oxygen saturation. The measurement is absolute rather than relative, because color is an indicator of the spectral absorption of hemoglobin and is unaffected by the scalp.

Deeper areas could be illuminated with stronger laser beams, but light intensity has to be kept at levels that will not injure the skin. Given the technology's current practical depth of 2.5 centimeters, it is best suited for monitoring the upper layers of the brain. Smith suggests that the technology could be used to monitor specific clusters of blood vessels.

While the technology is designed to monitor a specific area, it could also be used to monitor an entire hemisphere of the brain. Measuring any area within the brain could yield better information about whole-brain oxygen saturation than a pulse oximeter elsewhere on the body would. Hilton Kaplan, a researcher at the University of Southern California's Medical Device Development Facility, says, "If this technology allows us to actually measure deep inside, then that's a big improvement over the limitations of decades of cutaneous versions."

Michal Balberg, the CEO and cofounder of OrNim, thinks that it may ultimately be feasible to deploy arrays of probes on the head to get a topographic map of brain oxygenation. In time, brain oxygenation may be considered a critical parameter that should be monitored routinely. Balberg says, "Our development is directed toward establishing a new brain vital sign that will be used to monitor any patient [who's] unconscious or under anesthesia. We believe that this will affect patient management in the coming decade in a manner comparable to pulse oximeters."

Michael Chorost covers medical devices for Technology Review. His book about cochlear implants, Rebuilt: How Becoming Part Computer Made Me More Human, was published in 2005.

From here

Genetic Variant Predicts Heart Disease Risk

By Apoorva Mandavilli

Testing for a genetic variation could predict the likelihood that a patient will respond well to certain statins. But some researchers say it's too soon to use the variation to determine treatment.

Researchers from Celera reported yesterday in the Journal of the American College of Cardiology that a single substitution in the sequence of a gene called KIF6 makes people both more susceptible to heart attacks and more responsive to certain drugs that lower cholesterol. Though there is no known biological explanation linking the variation to heart disease, the study found that it increases the risk of heart attacks and strokes by 55 percent.

Celera, the company best known for sequencing the human genome, examined 35 single-nucleotide polymorphisms (SNPs) in 30,000 patients. Of those, "KIF6 is by far the most significant," says Thomas J. White, chief scientific officer at Celera. In fact, nearly 60 percent of the study population was found to carry the KIF6 variant. (According to the study, these findings take into account other factors, such as smoking, high blood pressure, and cholesterol levels.)

The researchers also found that carriers of the KIF6 variant responded better to the cholesterol-lowering drugs pravastatin (Pravachol) and atorvastatin (Lipitor). For example, among patients with the genetic variation, those who took pravastatin were 37 percent less likely to experience a heart attack than those who took the placebo. Those without the genetic variation who took the drug were only 14 percent less likely to experience a heart attack than those who took the placebo. Statins are big sellers for the pharmaceutical industry. In 2006, Lipitor, the world's best-selling drug, brought in $13 billion in global sales.

"This is one of the first studies to show an interaction with therapy" and genotype, says Marc Sabatine, professor of medicine at Harvard Medical School and a coauthor on one of the papers. "That is very exciting to see."

Surprisingly, the researchers found that KIF6 doesn't appear to work by lowering levels of LDL or "bad" cholesterol, the standard by which drugs used to prevent heart attacks are normally measured. White says that KIF6 may instead act by stabilizing "vulnerable plaques," which are particularly prone to triggering heart attacks.

Celera is developing a diagnostic that would test for the KIF6 variant and expects to launch it in a few months.

But some experts caution that it may be premature to introduce such diagnostic tests before there is further confirmation of KIF6's role in heart disease.

"Even if there are beneficial results, the standard should be that you need to document that knowing the genetic information is clinically useful," says Sekar Kathiresan, director of preventive cardiology at Massachusetts General Hospital.

Coronary heart disease caused one of every five deaths in the United States in 2006, so scientists have for quite some time been on the hunt for genes linked to heart attacks.

Rapid advances in technology have made that task much easier. At the same time, many of the genetic links to heart disease identified so far haven't held up on further analysis. At present, the only credible link is to a variant of the gene 9p21, identified last year by the Icelandic company deCODE Genetics, says Kathiresan. DeCODE offers a $200 diagnostic test for the 9p21 variant. (See "Gene Variant Linked to Heart Disease.")

A second gene, PCSK9, also looks promising, Kathiresan adds. "Nearly everything else is in the realm of 'possible but not definite.'"

It's good that KIF6 has been identified as a potential risk factor in several different studies, Kathiresan says. In each of the studies, he notes, there is less than a one-in-20 probability that the finding is a result of chance, which is generally considered an acceptable threshold for statistical significance.

But because of the high possibility of false positives, the threshold for genome-wide association studies should be much higher, on the order of one in 20 million, Kathiresan says. Both the 9p21 and the PCSK9 pass that test, he says.

"The key issue here is we don't know if these [KIF6 studies] are real results," Kathiresan says. "You need to show that it is clinically useful, and they have not crossed that threshold."

From here

Detecting Asthma Irritants

By Brittany Sauser

Researchers at Georgia Tech Research Institute (GTRI) in Atlanta have developed a portable sensor system to monitor the air quality for people suffering from asthma. The device is a combination of sensors that measure the level of chemicals in the air thought to cause asthma attacks, such as ozone, volatile organic compounds, and formaldehyde. It is lightweight and small enough to fit into a patient's pocket, so exposure levels can be continuously monitored.

The only way that we are going to understand how environmental factors affect asthma is if we can measure a person's exposures on a day-to-day basis, says Charlene Bayer, the leader of the Environmental Exposures and Analysis Group at GTRI and the sensor system's principal investigator. "To do so, we need a device like this that can hold numerous sensors in a small, portable package.".

An estimated 20 million Americans suffer from asthma, according to the National Institutes of Health (NIH), and identifying the triggers of an attack is currently a guessing game. "There are a few devices on the market that measure one or two chemicals, but they are stationary and the size of a desktop computer," says Mark Jones, the chief executive officer of Keehi Technologies and the lead engineer developing the sensor system.

Currently, the only way to control an asthma attack is with medication, or "trigger avoidance." In 2007, the total health-care costs of asthma in the United States were approximately $19.7 billion, according to the NIH.

"Research has shown that if you can reduce the triggering of an asthma attack, you will reduce the impact of the disease," says Mark Millard, the director of the Baylor Martha Foster Lung Care Center at Baylor University Medical Center in Dallas, TX. The new sensor system, he says, is really trying to answer the question, "What are the triggers for people with asthma?"

The device is about the size of a cell phone and contains a total of five sensors that measure different possible asthma triggers: ozone, nitrogen dioxide, formaldehyde, carbon dioxide, and total volatile organic compounds--the brew of chemicals that are emitted as gases from products such as paints, cleaning supplies, and building materials. The device also includes temperature and humidity sensors and a clock, to put a time stamp on the measurements. The researchers used sensors already on the market and kept the device small by outfitting the sensors on a two-sided circuit board.

Establishing a timeline is important for late-phase reactions, says Millard, since reactions to compounds such as formaldehyde may happen four to six hours after a patient is exposed. "Now we can look at the data and know that a patient was exposed to a lot of those compounds and that could be the trigger."

To measure the air quality, a small motor in the device sucks in air through an intake hose. Before the air passes over the sensors, it encounters a small filter that removes particulates, such as dust and pollen. The mass of the filter is measured before and after a sampling period to determine the total amount of particles. The air is then evenly distributed over the sensors.

"It takes about 30 seconds for the air to pass through the device and the data to be stored, and then it goes to sleep for another minute. In one hour it takes approximately 50 or 60 samples," says Jones.

The device can be worn for up to 24 hours before the particle filter needs to be replaced and the memory on the device is full. The data can be downloaded from the sensor system onto a computer.

Millard says the device is unique and innovative, but that he would like to see its capabilities expanded to measure tobacco smoke. He would also like to be able to separate out the particle measurements so they can be measured in real time--an upgrade that Bayer says will be introduced once the device is commercialized. Bayer would also like to get more specific readings on the different volatile organic compounds.

"We would like to get to the point where we can pop certain sensors in and out so a patient can target it towards their particular needs," says Bayer. "Asthma is a very complicated disease and there are a number of different airborne exposures that can exacerbate an asthma attack. This technology will allow us to find the source of exacerbation and understand the health impacts," she says.

The researchers at GTRI are currently in talks with an undisclosed company to commercialize the device, says Bayer. The initial target users will be asthma patients but the device will be open for use by others who want to study environmental exposures.

From here

Sel Penyebab Leukemia Ditemukan

Selasa, 29 Januari 2008 | 13:28 WIB

TEMPO Interaktif, Oxford:
Tim peneliti menemukan bahwa kedua anak kembar tersebut memiliki sel tunas abnormal praleukemia dalam darah mereka. Sel itu bisa "tidur" dalam sumsum tulang atau berkembang menjadi sel tunas leukemia. Hasil ini dikonfirmasi oleh eksperimen yang menggunakan sel tali pusar manusia.

"Penelitian ini berarti kami dapat mengetes apakah penanganan leukemia lymphoblastic akut pada anak bisa dikaitkan dengan menghilangnya dan berkembangnya sel tunas leukemia," kata Profesor Tariq Enver dari Unit Hematologi Molekuler Universitas Oxford, yang memimpin penelitian tersebut. "Mulai saat ini, upaya penyembuhan bisa difokuskan pada upaya membidik sel tunas praleukemia dan sel tunas kanker dengan obat yang ada atau yang akan kita kembangkan."

Upaya penyembuhan yang terfokus, menurut Tariq, bisa menghindari efek samping pengobatan kanker kemoterapi yang menyakitkan dan terkadang justru membahayakan kondisi tubuh pasien. Hal ini sangat penting karena terbukti, Olivia, salah satu anak kembar yang terkena leukemia, mengalami kebutaan di sebelah matanya akibat infeksi yang tidak bisa dilawan tubuhnya saat kemoterapi.

Para ilmuwan telah melacak kemungkinan sel tunas prakanker itu akibat fusi abnormal dari dua gen yang terjadi selama kehamilan ibu. Fusi ini menghasilkan protein hibrida, sebuah "kesalahan" genetik yang terjadi secara acak dan menyebabkan sel menjadi terjangkit leukemia. Gen yang diambil dari si kembar lantas ditransplantasikan ke tikus laboratorium yang mengkonfirmasi adanya hubungan langsung antara malfungsi genetik dari sel tunas tersebut dan leukemia.

Lembaga donor Inggris yang membiayai penelitian itu, Leukemia Research and the Medical Research Council, dan Rumah Sakit Great Ormond Street menyatakan sangat gembira atas penemuan itu dan berharap penelitian dilanjutkan ke upaya mencegah dan mengobati penyakit tersebut.

AMAL IHSAN | SCIENCEDAILY

from here

Next Steps for Stem Cells

By Emily Singer

Searching the brain of an Alzheimer's patient for clues into the origin of the disease is like trying to find the cause of a plane crash in the wrecked aftermath. However, a recent breakthrough in stem-cell research could generate new cellular models that allow scientists to study disease with unprecedented accuracy, from its earliest inception to a cell's final biochemical demise.

Last November, two groups of scientists announced that they had independently achieved one of the stem-cell field's biggest goals: the ability to reprogram adult cells into embryonic-like stem cells without the need for human embryos. (See "Stem Cells without the Embryos.") The findings garnered extensive media attention, largely because the new method obviated the need for human embryos, a major ethical minefield that has stymied research.

But scientists at stem-cell labs around the world are excited for another reason. The technique creates cells that are genetically matched to an individual, meaning that it's now possible to create novel cell models that capture all the genetic quirks of complex diseases. "Being able to have human cells with human disease in a dish accessible for testing is a real boon to technology and to science," says Evan Snyder, director of the Stem Cells and Regeneration Program at the Burnham Institute, in La Jolla, CA.

While animal models exist for many human diseases, they typically only incorporate certain aspects of the disease and can't capture the complexity of human biology. In addition, some disorders known to have a significant genetic component, such as autism, have proved difficult to model in animals.

To reprogram cells, scientists from Wisconsin and Japan independently engineered skin cells to express four different genes known to be expressed in the developing embryo. For reasons not yet clear to scientists, this treatment turns back the developmental clock. The resulting cells are pluripotent, meaning that they can develop into any type of cell in the body, and they can apparently divide indefinitely in their undifferentiated state. The first two published studies on the new technique reprogrammed cells from a skin-cell line, while a third study, published last month, generated stem cells from the skin biopsy of a healthy volunteer.

No one has yet generated cell lines from a patient, although scientists have been talking about doing so for years. Previously, the only way to make such models for complex genetic diseases was through human therapeutic cloning, also known as nuclear transfer, which is fraught with technical and ethical issues and has not yet been achieved. (See "Stem Cells Reborn" and "The Real Stem Cell Hope.") "Assuming that these procedures are as easy to do as it seems, it's definitely more tractable than nuclear transfer," says Snyder. His own lab is trying to generate such models, as is "probably everyone else you could call on your rolodex," he says.

To generate a disease-specific cell model, scientists would take some cells from a patient with a particular disease and revert them to an embryonic state. The cells would then be prodded to develop into the tissue type damaged in that disease, such as dopamine neurons in Parkinson's disease or blood cells in sickle-cell anemia. By comparing the differentiation process in cells derived from healthy and diseased people, scientists could observe how that disease unfolds at a cellular level. They could also use the cells to test drugs that might correct those biochemical abnormalities. "We want to use these cells to ask and answer questions that can't be asked and answered any other way," says M. William Lensch, a research scientist at the Harvard Stem Cell Institute and Children's Hospital Boston.

The relative simplicity of the approach--and the fact that it can be supported by federal funding--means that many more scientists are likely to attempt reprogramming than cloning. (In 2001, President Bush limited federal funding for embryonic stem-cell research to embryonic stem-cell lines already in existence.) According to Story Landis, chair of the Stem Cell Task Force at the National Institutes of Health, in Bethesda, MD, the funding agency has already announced two programs to fund reprogramming research and would welcome applications to derive cell lines from patients.

While no one has yet announced that he or she has derived a disease-specific cell model, George Daley's lab at Harvard may be in the lead. Last month, he and his team published a paper in Nature showing that they can reprogram cells from a skin biopsy from a healthy person, and they are already trying to repeat the feat with tissue from patients. Ultimately, they are interested in developing models of sickle-cell anemia and Fanconi anemia, a hereditary disease in which the bone marrow doesn't produce enough new cells to replenish the blood.

For example, patients with Fanconi anemia often suffer from skeletal problems, and their cells show an impaired ability to repair DNA. "We don't have any idea why kids with DNA repair defect would get a blood disease, and why they sometimes get these bone abnormalities," says Lensch, who works with Daley. But with stem-cell lines developed from a patient, "we could push the cells to develop into bone and blood, and try to learn about the links between the two."

Such models could also help resolve long-held debates about specific diseases, such as Alzheimer's. By differentiating reprogrammed cells from Alzheimer's patients into neurons and comparing them with neurons derived from healthy embryonic stem cells or with cells with mutations that mimic a rare, hereditary form of the disease, scientists will be able to determine how much of Alzheimer's is due to the environment versus genes, as well as how similar the sporadic form of the disease is to the hereditary form. (Most drugs on the market for Alzheimer's were developed using models that mimic the hereditary form of the disease and have shown limited efficacy in patients.) "This is a whole new world of investigation," says Lawrence Goldstein, a neuroscientist at the University of California, San Diego, whose lab is about to begin collecting skin cells from Alzheimer's patients.

Despite the excitement, Lensch and others caution against abandoning other embryonic stem-cell research, especially therapeutic cloning. "We're in the early stages of this research, where we're excited about the possibilities but still need to show it's both useful and representative of the disease," says Snyder. In addition, he says, embryonic stem cells and perhaps cloned stem cells will be needed as controls for future studies.

Scientists also say that it's too soon to tell how easy it will be to generate stem-cell lines from patients: the genetic variations that lead to the disease could also impact the reprogramming process. "With some genetic disease, I think it will be really difficult," says Lensch.

from here

Gene Therapy for Chronic Pain

By Jocelyn Rice

A new kind of gene therapy could bring relief to patients suffering from chronic pain while bypassing many of the debilitating side effects associated with traditional painkillers.

Researchers at Mount Sinai School of Medicine injected a virus carrying the gene for an endogenous opioid--a chemical naturally produced by the body that has the same effect as opiate painkillers such as morphine--directly into the spinal fluid of rats. The injections were targeted to regions of the spinal cord called the dorsal root ganglia, which act as a "pain gate" by intercepting pain signals from the body on their way to the brain. "You can stop pain transmission at the spinal level so that pain impulses never reach the brain," says project leader Andreas Beutler, an assistant professor of hematology and medical oncology at Mount Sinai.

The injection technique is equivalent to a spinal tap, a routine procedure that can be performed quickly at a patient's bedside without general anesthesia.

Because it targets the spinal cord directly, this technique limits the opiate-like substance, and hence any side effects, to a contained area. Normally, when opiate drugs are administered orally or by injection, their effects are spread throughout the body and brain, where they cause unwanted side effects such as constipation, nausea, sedation, and decreased mental acuity.

Side effects are a major hurdle in treating chronic pain, which costs the United States around $100 billion annually in treatment and lost wages. While opiate drugs can be very effective, the doses required to successfully control pain are often too high for the patient to tolerate.

"The side effects can be as bad as the pain," says Doris Cope, director of the University of Pittsburgh Medical Center's Pain Medicine Program. Achieving the benefits of opiate treatment without their accompanying side effects, Cope says, would be a "huge step forward."

Beutler hopes to do just that. "Our strategy was to harness the strength of opioids but target it to the pain gate, and thereby create pain relief without the side effects that you always get when you have systemic distribution of opioids," he says.

Several groups have previously attempted to administer gene therapy for pain through spinal injections, but they failed to achieve powerful, long-lasting pain relief. The new technique produced results that lasted as long as three months from a single injection, and unpublished follow-up studies suggest that the effect could persist for a year or more.

Beutler credits his team's success to the development of an improved virus for delivering the gene. The team uses a specially adapted version of adeno-associated virus, or AAV--a tiny virus whose genome is an unpaired strand of DNA. All the virus's own genes are removed, and the human endogenous opioid gene is inserted in their place. Beutler's team also mixed and matched components from various naturally occurring AAV strains and modified the genome into a double-stranded form. These tweaks likely allow the virus to infect nerve cells more easily and stick around longer.

Once the virus is injected into the spinal fluid and makes its way into the nerve cells of the pain gate, it uses the host cells' machinery to churn out the opioid protein--which then goes to work blocking pain signals on their way to the brain. Normally, the gene is rarely activated. But the version used for therapy has no such limitations because the gene carried by the AAV has been modified to continuously produce the opioid chemical.

Cope says that using endogenous opioids is inherently superior to injecting synthetic opiate drugs directly into the spinal fluid, an approach that requires the installation of a pump in order to deliver the drugs over a long time period. "It's kind of a holy grail," she says. "If the body's own system for pain control were activated by genetic expression, that would be superior to an artificial medication."

In Beutler's study, which was published this week in PNAS, rats were surgically modified to have a stronger than usual response to pressure on their paws, mimicking the effects of so-called neuropathic pain. The gene-therapy treatment effectively restored the rats to a normal level of pain sensitivity. The team also tested a nonopioid gene, which produced comparable pain relief through an entirely different mechanism. But while the opioid gene's effects will likely extend to humans, who respond to opiates the same way rats do, the nonopioid's effects may be rat specific.

The Stockholm-based company Diamyd Medical has been developing a different approach to gene therapy for chronic pain that also bypasses the side effects of standard pain treatment. The approach uses a deactivated version of herpes simplex virus (HSV). HSV can be administered straight through the skin as it naturally finds and infects peripheral nerves and travels to the spinal cord on its own. Darren Wolfe of Diamyd says that this method is superior to spinal injection because it's safer and easier, and it can be administered repeatedly.

Because of these considerations, the HSV method may be preferable for treating localized pain. However, when chronic pain involves multiple areas of the body--as it often does with, for example, metastasized cancers--going straight to the pain gate could work more efficiently.

While both of these methods have proved effective in animal models of pain, their efficacy in human patients remains to be shown. Diamyd recently applied to the FDA to begin phase I clinical trials, and Beutler estimates that his approach could be tested on humans in as few as three years.

From here

Gadis Australia Pasien Pertama Dunia yang Berubah Golongan Darah

Canberra (ANTARA News) - Seorang gadis remaja Australia --Demi-Lee Brennan-- menjadi pasien pertama yang mengubah golongan darahnya dan menerima sistem kekebalan dari donor organnya.

Brennan yang kini berusia 15 tahun menerima transplantasi organ hati pada saat usianya 9 tahun karena organ harinya tidak berfungsi.

"Hal itu adalah kesempatan kedua saya untuk dapat bertahan hidup," kata Brennan kepada media massa setempat ketika menceriterakan bagaimana tubuhnya berhasil menerima dan beradaptasi bedah transplantasi yang dapat dikatakan "Mukjizat" yang datang dari Tuhan. "Sungguh sulit dipercaya."

Golongan darah Brennan mengalami perubahan dari "O" negatif menjadi "O" positif pada saat ia sakit dan diberikan pengobatan untuk menghindari penolakan terhadap organ hati donor oleh sistem kekebalan tubuhnya.

Sel batang pembuluh darah hatinya yang baru memasuki sumsum tulang belakangnya yang mengubah seluruh sistem kekebalan tubuhnya, berarti si remaja Brennan tak lagi memerlukan obat-obatan anti penolakan tubuh.

Para dokter dari Rumah Sakit Anak Westmead di Sydney mengatakan mereka belum dapat memberikan keterangan kasus Brennan yang mengalami kesembuhan, seperti yang mereka sampaikan dalam majalah kedokteran, The New England Journal of Medicine.

"Terus terang kami belum menemukan penjelasan untuk hal itu," kata Michel Stormon seorang ahli hepatologi pediatri seperti dikutip Reuters.

Sturat Dorrney, mantan kepala bagian unit transplantasi di rumah sakit itu mengatakan, kasus Brennan dapat membuka jalan bagi terapi transplantasi organ, karena biasanya sistem kekebalan tubuh pasien penerima menyerang transplantasi jaringan di donor.

"Kini kami harus kembali mengkaji ulang semua tahapan yang terjadi pada Demi-Lee dan melihat mengapa hal itu dapat terjadi dan kalau-kalau dapat melakukan pengulangan kembali," kata Dorney.

"Kami berpikir hal itu mungkin karena kami menggunakan organ hati dari seseorang yang usianya masih muda dan Demi-Lee memiliki sel darah putih dalam jumlah rendah mungkin karena dua faktor itulahyang menjadi alasan," katanya kepada harian Daily Telegraph.

Penolakan tubuh umumnya ditangani dengan kombinasi obat-obatan walaupun penolakan kronik tidak terjadi dua arah (bolak-balik).

Hanya tujuh dalam 10 operasi transplantasi di Australia yang berhasil setelah lima tahun berselang yang dikarenakan oleh penolakan tubuh di pasien. (*)

from here

Pil KB Cegah Kanker Indung Telur

Beijing (ANTARA News) - Pil KB dapat berbuat lebih dari sekedar mencegah kehamilan, pil tersebut juga dapat melindungi perempuan dari kanker indung telur selama lebih dari 30 tahun atau lebih setelah mereka mengkonsumsinya, demikian hasil penelitian di Inggris yang disiarkan pekan ini.

Makin lama perempuan mengkonsumsi pil itu, makin rendah resiko mereka terserang penyakit itu, yang lebih umum menyerang setelah perempuan berusia 50 tahun, tulis para peneliti tersebut di jurnal "Lancet".

Perempuan yang mengkonsumsi pil itu selama 15 tahun mengurangi resiko mereka terserang penyakit tersebut separuhnya, kata para peneliti itu.

Di seluruh dunia, pil tersebut sudah membantu 200.000 perempuan dari serangan kanker indung telur dan telah mencegah 100.000 kematian akibat penyakit itu, kata Valerie Beral dari University of Oxford dan rekannya dalam laporan mereka.

"Ketika anda berusia 60 tahun, ada manfaatnya jika anda mengkonsumsinya lima tahun atau 10 tahun saat anda berusia 20-an tahun," kata Beral dalam suatu wawancara telefon. "Makin lama anda mengkonsumsinya, makin baik bagi anda tatkala resiko kanker indung telur tinggi."

Sebanyak 300 juta perempuan telah menggunakan pil KB sejak pil itu diperkenalkan pada awal 1060-an. Ratusan kajian telah meneliti keamanannya, sebagian menunjukkan manfaat dan yang lain memperlihatkan peningkatan resiko kanker payudara dan kanker leher rahim.

Beral dan rekannya mengatakan penelitian mereka, yang menganalisis 45 kajian kanker indung telur di 21 negara, memperlihatkan bahwa manfaat pil tersebut lebih besar dari resikonya. Kanker

Kanker indung telur sangat mematikan karena perempuan seringkali mengalami gejala ringan atau tak menghadapi gejala sama sekali hingga penyakit itu telah berkembang.

Resiko kanker payudara, yang juga mengakibatkan stroke dan pembekuan darah, jauh lebih kecil dan hanya ada saat perempuan mengkonsumsi pil tersebut dan tak lama setelah mereka berhenti, kata Beral seperti dikutip Xinhuanet.

Mengkonsumsi pil itu selama 10 tahun mengurangi resiko kanker indung telur sebelum usia 75 tahun dari 12 per 1.000 perempuan jadi 8 per 1.000. Pil tersebut juga mengurangi resiko kematian akibat penyakit itu dari 7 per 1.000 perempuan jadi 5 per 1.000 sebelum usia 75 tahun, demikian temuan studi tersebut.

Lebih dari 100 juta perempuan sekarang mengkonsumsi pil tersebut, jadi akhirnya itu akan mencegah lebih dari 30.000 kasus kanker indung telur setiap tahun selama beberapa dasawarsa ke depan, tulis para peneliti tersebut. (*)

Copyright © 2008 ANTARA

Pengobatan Kanker Juga Bantu Obati Osteoporosis

Washington (ANTARA News) - Obat yang digunakan untuk mengobati kanker tulang sumsum juga dapat membantu mengobati osteoporosis dengan merangsang sel-sel tungkai, kata beberapa peneliti AS, Jumat.

Mereka mendapati bahwa Velcade, yang dibuat oleh Millenium Pharmaceuticals Inc (MLNM.O) untuk mengobati tumor ganda di sumsum tulang, mengaktifkan sel-sel tungkai yang berubah menjadi tulang.

Ujicoba terhadap tikus memperlihatkan membantu mengaktifkan jaringan tulang dan mungkin merupakan pengobatan yang berpotensi bagi osteoporosis, kata satu tim di Massachusetts General Hospital dan Harvard Stem Cell Institute di "Journal of Clinical Investigation".

Ahli sel tungkai di Harvard Dr. David Scadden mengatakan, para ilmuwan telah berharap menemukan cara untuk menggunakan obat guna merangsang sel-sel tungkai, yang merupakan sel pengendali tubuh.

"Terapi sel tungkai seringkali dikira sebagai tindakan memasukkan sel baru ke dalam tubuh, tapi studi ini menunjukkan bahwa pengobatan dapat mengubah sel-sel tungkai yang ada yang terdapat di jaringan tubuh dan bertindak sebagai obat pengaktifan untuk meningkatkan mekanisme perbaikan sendiri tubuh," kata Scadden dalam suatu pernyataan.

"Obat yang mengarahkan sel-sel tak matang untuk menjadi sejenis sel khusus, seperti dalam studi ini, dapat berpotensi sangat bermanfaat," katanya seperti dikutip Reuters.

Velcade, yang secara generika dikenal sebagai "bortezamib", merangsang sel-sel tungkai "mesenchymal", demikian temuan para peneliti tersebut. Sel-sel itu berkembang menjadi zat pembangun-tulang "osteoblast" dan beberapa jenis sel lain termasuk "cartilage", lemak, kulit dan otot.

Ujicoba pada tikus memperlihatkan obat tersebut meningkatkan kegiatan "osteoblast", dan ketika digunakan pada tikus yang menderita osteoporosis, obat itu secara mencolok meningkatkan kepadatan dan susunan tulang.

"Jika paradigma yang terlihat dalam studi ini terbukti benar bagi jaringan lain, kita mungkin memiliki pilihan untuk memperbaiki dan mengaktifkan kembali berbagai tempat yang terpengaruh oleh cedera atau penyakit dengan menggunakan obat --itu akan sangat menggairahkan," kata Scadden. (*)

Copyright © 2008 ANTARA

Mixing Up the Immune System

By Anna Davison

By performing bone-marrow transplants along with kidney transplants, doctors in Boston were better able to trick recipients' immune systems into accepting the new organs as if they were their own.

Even though the patients received donor kidneys that weren't a good match, most of them were successfully weaned off of immune-suppressing drugs about a year after their transplants. Normally, patients have to take the drugs, which can have serious side effects, for the rest of their lives.

"It's groundbreaking work," says John C. Magee, director of the Kidney Transplant Program at the University of Michigan, who was not involved in the study. "They've shown that you can reeducate the immune system."

The technique could be applied to other kinds of transplants and used in the treatment of autoimmune diseases, says Megan Sykes, one of many researchers who carried out the work at Massachusetts General Hospital. Sykes is the associate director of the hospital's Transplantation Biology Research Center.

The team has been working for about 20 years to outsmart the immune system by inducing tolerance to a donor organ. In this study, reported in this week's issue of the New England Journal of Medicine, the scientists transplanted bone marrow along with a mismatched kidney, giving patients a kind of hybrid immune system that blended elements of both the donor and the recipient.

Four out of five patients who received bone-marrow transplants in conjunction with kidney transplants didn't need long-term treatment with immune-suppressing drugs. The technique was not successful for the fifth patient, however: his body rejected the donor kidney. He was given a second--and successful--transplant according to conventional protocol.

Doctors try to match people with similar versions of the genes that play a crucial role in immune reactions to foreign tissue. This genetic region is known as the human leucocyte antigen (HLA) complex. But finding a good match isn't always possible, so doctors often use a mismatched kidney and put the patient on immunosuppressive drugs to reduce the risk of rejection. The patients in the study, whose ages ranged from 22 to 46, were all suffering from advanced kidney disease and were unable to find living donors who were a very good tissue match. They received kidneys from family members who were HLA mismatched.

Before the surgery, the transplant team gave the patients drugs to deplete their bone marrow and suppress their immune response. After receiving new kidneys and then an intravenous infusion of bone marrow from their donors, the patients were kept in a relatively sterile environment to reduce their chance of infection, and to allow the bone marrow to regenerate and produce new immune cells that wouldn't attack the donor kidney.

In the months after their transplants, the patients in the study were treated with immunosuppressive drugs, but four out of five of them were able to discontinue those drugs between 9 and 14 months after surgery, and their new kidneys have been functioning well in the years since.

"I think it's quite exciting," Magee says. "It shows what's possible."

The researchers' approach could make transplants more feasible for people whose immune systems are already compromised by conditions like HIV, according to Yasir Qazi, medical director of the kidney and pancreas transplant program at the University of Southern California. (Qazi was not involved in the work.) Sykes says that the approach could potentially be used to treat autoimmune diseases such as type 1 diabetes. "It could have huge benefits," she says.

Although immunosuppressive drugs have revolutionized transplant medicine, they can increase the risk of cancer and heart disease. "Immunosuppression is great, because it makes kidneys work, but it's bad because it has lots of side effects," Magee says. "Some people say that in many ways, you're trading one disease for another. You still have to take lots of medicine and see a doctor."

The protocol developed by Sykes and her colleagues initially requires heavier drug treatment than that required with the standard kidney-transplant procedure, to allow the recipient's body to accept donated bone marrow as well as a donated kidney. But, she points out, the patient is only on the drugs for a limited time.

From here

Synthesizing a Genome from Scratch

By Emily Singer

In a technical tour de force, scientists at the J. Craig Venter Institute, in Rockville, MD, have synthesized the genome of the bacterium Mycoplasma genitalium entirely from scratch. The feat is a stepping stone in creating precisely engineered microbial machines capable of generating biofuels and performing other useful functions.

"It really is groundbreaking that you can synthetically build a genome for a bacterium," says Chris Voigt, a synthetic biologist at the University of California, San Francisco, who was not involved in the project. "It's bigger by orders of magnitude than what's been done before."

Biologists creating genetically engineered organisms now routinely order pieces of DNA that are 10,000 to 20,000 base pairs long--big enough to incorporate the genes for a single metabolic pathway. That allows researchers to engineer microbes that can perform specific tasks, but the ability to synthesize entire genomes could grant a whole new level of control over biological design. (See "Tumor-KillingBacteria.")

In the new study, scientists ordered 101 DNA fragments, encompassing the entire Mycoplasma genome, from commercial DNA synthesis companies. These fragments were designed so that each overlapped its neighboring sequence by a small amount; these overlapping stretches stick together, thanks to the chemical properties of DNA. Researchers then bound the fragments piece by piece, eventually generating the full 582,970 base pair Mycoplasma sequence. The findings were published Thursday in the online edition of Science.

"We consider this a second and significant step in a three-step process of our attempt to create the first synthetic organism," says Craig Venter, president of the Venter Institute. Venter and his colleagues ultimately want to create a minimal genome--one with the least number of genes needed to sustain life. Pinpointing the minimal genome will both shed light on key cellular processes and provide a base for designing sophisticated synthetic organisms. "We ultimately want to design cells that could function in a robust fashion to make unique biofuels," says Venter.

The researchers' next step will be to show that the synthetic genome functions as it should. "We have the whole genome assembled in a tube, but we need to transplant it into the cell of a different species to show that it can reboot the cell," says Hamilton Smith, a Nobel laureate who oversaw the project at the Venter Institute. Last year, Smith's group transplanted the genome of one species of Mycoplasma into another, demonstrating that this type of transplant is possible. (See "Transplanting a Genome.")

While the synthesis of a genome might be impressive from a scientific perspective, it is not yet a practical way to engineer microbes to make biofuels. Instead, several companies, including Synthetic Genomics, a biotech company founded by Venter to engineer microbes for energy, are using more traditional metabolic engineering techniques to generate fuel-producing bacteria. (See "Building Better Biofuels.") "What we're doing with synthetic chromosomes will be the design process for the future," says Venter.

Others in the field are excited about that prospect. "Being able to synthesize genomes opens up a new world," says Voigt. "You can build things on the scale of the genome." For example, he says, scientists are now engineering bacteria to perform different steps in the conversion of biomass into ethanol--one strain to break down the biomass, another to make ethanol. But ideally, scientists could put those processes together to create one organism that could eat biomass and spit out fuel. (See "The Price of Biofuels.") "That would require genome-scale design," Voigt says.

He likens the current project, which required multiple steps to glue the fragments together, to the last computers designed before automated manufacturing and microfabrication techniques were introduced. Similar advances are needed for more ambitious genome-synthesis projects. "We still need to develop 'one step' genome construction methods in order to reduce the costs and turn time of genome construction," says Drew Endy, a synthetic biologist at MIT.

From Here

Growth Hormone: Fountain of Youth or Early Killer?

Growth hormone holds a conflicted status in the world of life extension. Some believe it turns back the clock, with evidence from humans suggesting that hormone treatment reduces fat and boosts muscle. But animal studies show the opposite: mice without growth hormone live significantly longer and are protected against cancer, one of the most deadly diseases of aging.

Valter Longo, a scientist at the University of Southern California, in Los Angeles, hopes to untangle this conundrum by studying an unusual group of people in Ecuador: those with a genetic mutation that renders them insensitive to growth hormone. "They are the largest population in the world that is growth-hormone deficient," says Longo. Studies of the group could provide a valuable window into whether growth-hormone depletion could, in fact, be used to extend longevity. The study could also shed light on how to develop drugs against the diseases of aging without introducing unintended side effects.

Growth hormone is a crucial protein produced by the pituitary that directs growth and cell division. People who lack the hormone or the ability to respond to it are extremely short, while those whose hormone levels dip in middle age, such as after damage to the pituitary, have an increased risk of cardiovascular disease. In mice, however, deficiency of the hormone seems to be beneficial. "In the mouse, the effect is major and striking," says Andrzej Bartke, a biologist at Southern Illinois University in Springfield, who is not involved in the project. "They seem protected from cancer and appear to have delayed aging by various measures. But there is almost no evidence that growth-hormone deficiency would extend life in humans."

The group Longo plans to study lives in the rural Loja province in the southern portion of Ecuador. These isolated mountain communities have a high rate of an otherwise rare condition known as Laron dwarfism. People with the condition lack a functioning version of the receptor that binds to growth hormone.They are small and obese, but little data exists on their longevity.

Children with the condition seem more susceptible to pneumonia and diarrhea, common scourges of poor rural communities, and they die at twice the rate of their unaffected siblings. Those who survive to adulthood typically have high cholesterol and triglycerides, risk factors for heart disease. Some die of heart disease, an uncommon occurrence in rural Ecuador, but preliminary reports suggest that Laron dwarves are protected from artherosclerosis, arterial hardening that can lead to heart attack. Adding to the puzzle is anecdotal evidence suggesting that they don't get cancer or type 2 diabetes. "It's a balance: if you turn down risk of cancer, you might turn up risk of heart disease," says Steven N. Austad, a biologist at the University of Texas Health Sciences Center, in San Antonio, who is not involved in the project.

To try to determine how the hormone impacts diseases of aging, Longo plans to compare rates of cancer, heart disease, and diabetes, as well as longevity data, in those with one or two copies of the gene and their unaffected relatives. Those who carry one functioning copy of the growth-hormone receptor appear normal; if they are protected against cancer and do not suffer from obesity and heart disease, they may represent a happy medium of growth-hormone exposure. So far, the scientist has genotyped about 300 people--100 with two copies of the mutation, and 200 relatives and controls.

"If blocking growth hormone is associated with an improvement or decreased incidence of cancer, there are tools that we have as physicians to address that," says Pinchas Cohen, a pediatric endocrinologist at the University of California, Los Angeles, who has treated children with Laron dwarfism. Drugs that inhibit secretion of the hormone or block its action already exist. And drug companies are now testing blockers of a molecule that acts downstream of growth hormone, called IGF-1, as a treatment for cancer. If IGF-1 works, it's not yet clear if the most effective intervention will be as a preventative measure, perhaps targeting families with a history of cancer, or if growth-hormone or IGF-1 depletion could be used as a cancer treatment.

Not everyone is optimistic that limiting growth hormone in people will have the same effects it does in mice. "Growth hormone in humans is different than that of most mammals," says Austad. It has a broader mechanism of action and appears to have evolved rapidly since we diverged from other mammalian ancestors. "No one knows why," says Austad, "but something has happened to make growth hormone very different in humans."

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Treating Muscular Dystrophy with Stem Cells

Researchers at the University of Texas Southwestern Medical Center (UT Southwestern) have used embryonic stem cells from mice to grow muscle cells. These same cells, injected into mice with a mild form of muscular dystrophy, formed healthy, functional muscle fibers at the site of deteriorating tissue. Scientists say that the research, while still in its early stages, could eventually lead to a cell-based therapy for patients with muscular dystrophy and other muscle-related diseases. The research was recently published in the online edition of Nature Medicine.

According to the Muscular Dystrophy Association, about 250,000 people in the United States have some form of the disease. The most well known, Duchenne muscular dystrophy, is caused by a genetic mutation that disrupts the formation of dystrophin, an important protein involved in the formation of muscle cells. In the absence of dystrophin, muscles are unable to regenerate, and they gradually weaken and waste away. Eventually, the deteriorated area is taken over by fat and connective tissue.

Rita Perlingeiro, assistant professor of developmental biology at UT Southwestern, says that embryonic stem cells may be the key to reversing muscular dystrophy's debilitating effects. The advantage lies in the cells' pluripotency--the ability to transform into any mature cell, be it bone, muscle, or cartilage. However, many researchers have found it difficult to direct every stem cell in a culture to form a specific type of cell. In lab experiments, scientists often end up with a mixture of cells that, when injected into an animal, form large clusters resembling a tumor.

So Perlingeiro and her team set two main goals: to find the right set of cues to convert embryonic stem cells into muscle cells, and to look for ways to isolate muscle cells from the rest of the culture medium, in order to inject a dose of pure muscle cells into a mouse model.

In normal embryologic development, stem cells turn into various tissue and bone, depending on a combination of molecular and genetic signals. In the case of muscle cells, past research has shown that the gene Pax-3 is essential in pointing stem cells down the path of muscle formation. With this knowledge, Perlingeiro and her team grew mouse-derived embryonic stem cells in a culture dish, then genetically manipulated the solution to overexpress Pax-3. They found that, compared with mixtures without Pax-3, a significant number of stem cells exposed to the activated gene formed muscle cells.

However, not all of the cells turned into muscle, and when the team injected the solution into a mouse with a mild form of muscular dystrophy, the mixture caused tumors to form. The team then focused on developing an identification process that would make muscle cells stand out from the rest of the solution. Once again, Perlingeiro looked to basic developmental research and found that, during normal muscle formation in the embryo, stem cells that become very early versions of muscle cells display certain surface molecules, or markers. The team repeated the first phase of its experiment, exposing embryonic stem cells to Pax-3, and looked for the telltale markers indicating muscle cells. The researchers then isolated these cells, creating a solution that consisted solely of muscle cells.

In preparation for injecting the new solution into a mouse model, the team first injected cardiotoxin into the mouse's leg. The effect inhibited the production of dystrophin, causing a weakening of the muscle--a condition resembling muscular dystrophy. Perlingeiro and her colleagues then injected the mouse with the muscle-cell solution. The team then took muscle biopsies and, after immuno-staining, found that, compared with mice that did not receive the solution, treated mice exhibited more dystrophin, indicating healthy muscle regeneration.

To confirm their results, the researchers ran both groups of mice on a treadmill; they found that the mice that received the solution outlasted the group that did not. Perlingeiro went a step further: after sacrificing both animal groups, she and her colleagues extracted every leg muscle, treated or untreated. They then placed each muscle in a bath and tested its strength by exposing it to an electrical impulse. The team found that the stronger contractions came from the muscles treated with the stem-cell-derived solution.

Perlingeiro says that the study's results are encouraging, as she envisions one day providing stem-cell-based therapy for people with muscular dystrophy and other muscle-related diseases. However, there will have to be more follow-up studies before the technique can be applied to humans.

"I have a long to-do list," says Perlingeiro. "We'd like to use the same technique on human embryonic stem cells."

Recently, researchers were able to turn human skin cells into embryonic stem cells, a technique that bypasses the thorny issues currently surrounding use of embryonic stem cells. Perlingeiro says that combining this technique with her muscle-deriving method may one day yield effective, efficient treatment of diseases such as muscular dystrophy.

"If we can reprogram skin cells to become pluripotent, and use Pax-3 to make muscle, then we would be able to make cells from the patient, and we wouldn't face ethical issues or problems of rejection," says Perlingeiro.

Paul Muhlrad, a research program coordinator for the Muscular Dystrophy Association, says that the study's results are a promising step toward effective treatment for muscle-related diseases. "These researchers present a nice proof of principle that embryonic stem cells can be turned into muscle-producing cells in the laboratory and used to deliver healthy muscle to people with Duchenne muscular dystrophy," says Muhlrad. "Of course, these experiments were done with mice. We've yet to see whether they will work in humans, but this study offers us much hope."

from here

Mixing Mammals

By outfitting mice with a chunk of DNA that directs wing development in bats, scientists have created rodents with abnormally long forelimbs, mimicking one of the steps in the evolution of the bat wing. Their work gives weight to the idea that variations in how genes are controlled, and not just mutations in the coding regions of genes, are a driving force in evolution.

The slightly longer forelimbs of the transgenic mice "make them more batlike," says Nipam Patel, a professor of molecular and cell biology and integrative biology at the University of California, Berkeley, who was not involved in the work. "It seems like a subtle difference, but evolution works by these subtle differences."

The researchers focused on a gene, Prx1, that plays a part in the elongation of limb bones in mammals. The gene's expression is regulated by another sequence of DNA, called a Prx1 enhancer. To investigate how the enhancer shapes limb development, Richard Behringer, a professor of molecular genetics at the University of Texas MD Anderson Cancer Center, and his colleagues around the country put the bat version of the Prx1 enhancer into mice so that it controlled the mouse Prx1 gene. These transgenic animals developed forelimbs that were on average 6 percent longer than normal by the time they were born. It was a significant difference, although "the mice look like mice," Behringer says. "They're not going to fly out of the cage." The researchers report their work in the latest issue of Genes and Development.

To have any chance of flying, mice would have to develop very different forelimbs, like those of bats, which are longer and have membranes stretched between the bones. Behringer says that he'd like to try replacing the limb enhancers in mice with those from other animals, such as whales or wallabies.

Charles Darwin contemplated the evolution of different kinds of limbs in On the Origin of Species. Starting with a basic limb pattern, "successive slight modifications," he wrote, eventually produce the various mammal limbs we see today: human hands, bat wings, whale fins.

"We think what we've done is made one of those slight modifications," Behringer says. "Maybe during evolution you'd have a lot of those and the limb would get a lot longer, and maybe some of the tissue would be retained between digits, ultimately leading to the structures that would allow a bat to fly."

"It's a very nice demonstration of something that people have been suspecting now for some time: that regulatory sequences rather than changes in protein sequences sort of drive evolution," says Susan Mackem, who heads the Developmental Biology Unit at the National Cancer Institute's Center for Cancer Research. Mackem was not involved in Behringer's research.

Behringer's team also found something unexpected. When the researchers created mutant mice that lacked the mouse Prx1 enhancer, the animals developed forelegs of a normal length. That suggests that more than one enhancer controls the expression of the Prx-1 gene in mice, ensuring what Behringer calls a "regulatory redundancy."

"As long as there is one copy to do the work, the other copy can be creative," says Ann Burke, an associate professor of biology at Wesleyan University.

from here

Virus TUMV Sudah Menyebar di Indonesia

Jakarta (ANTARA News) - Penelitian Institut Pertanian Bogor (IPB) menemukan bahwa virus Turnip Mosaic (TUMV) yang menyerang tananam sawi dan oleh Departemen Pertanian dinyatakan belum ada di Indonesia, ternyata sudah menyebar di sejumlah wilayah di dalam negeri.

Pakar virus tanaman dari Departemen Proteksi Tanaman Fakultas Pertanian IPB, Sri Hendrastuti Hidayat PhD, pada Senin mengatakan, berdasarkan Kepmentan No.38 tahun 2006, TUMV digolongkan dalam organisme pengganggu tanaman karantina (OPTK) golongan A1 yang berarti belum pernah dilaporkan keberadaannya di Indonesia.

"Namun dari hasil survey yang kami lakukan, inveksi virus Turnip Mosaic terjadi di beberapa daerah pertanian sayuran di Indonesia," katanya.

Virus tersebut ditemukan pada tanaman ciaisim dan pakchoi, sejenis tanaman sawi di beberapa wilayah seperti di Lampung, Bengkulu, Pontianak, Balikpapan, Samarinda, Poso dan Donggala dengan persentase infeksi hingga 83 persen.

Sebelumnya, virus yang mengakibatkan kerusakan daun dan mengganggu pertumbuhan tanaman tersebut juga ditemukan telah menyebar di wilayah Jawa Barat, Jawa Tengah, Jawa Timur dan Bali pada sekitar 2004.

Oleh karena itu, tambahnya, Departemen Pertanian seharusnya melakukan revisi terhadap Kepmentan no 38/2006 dan tidak lagi memasukkan TuMV dalam OPTK golongan A1 namun diturunkan menjadi A2 atau dikeluarkan dari daftar OPTK karena sudah ditemukan menyebar di hampir seluruh wilayah Indonesia.

Sementara itu Wakil Sekjen Asosiasi Perbenihan Indonesia (Asbenindo), Afrizal Gindow menyatakan, kebijakan Deptan yang memasukkan virus Turnip Mosaic dalam golongan OPTK A1 berdampak pada terhentinya impor benih caisim, sejenis sawi, sejak 2006.

"Proses pemasukan benih golongan kubis-kubisan (Brasica) dari luar negeri untuk kebutuhan benih di Indonesia saat ini menemui kendala terkait status OPTK TUMV," katanya.

Selama ini untuk kebutuhan benih sawi jenis caisim di dalam negeri yang mencapai 100 ton per tahun masih mengandalkan impor karena komoditas tersebut tidak bisa diproduksi di Indonesia yang beriklim tropis.

Afrizal yang juga Direktur Penjualan dan Pemasaran PT East West Seed Indonesia itu mengatakan, terhentinya impor benih sawi tidak hanya merugikan produsen namun juga berdampak pada petani.

Jika setiap hektar pertanaman sawi caisim memerlukan benih sekitar 0,5 kilogram, lanjutnya, maka sedikitnya 200 ribu pembudidaya tanaman tersebut tidak bisa lagi mengembangkan usahanya kalau setiap petani mengusahakan 1 hektar.

"Dengan dikeluarkannya virus TUMV dari golongan OPTK A1 pemasukan benih sawi dari luar tidak lagi terkendala," katanya sembari menambahkan pasar benih sawi di Indonesia mencapai Rp30 miliar per tahun.

Menurut dia, impor benih golongan kubis-kubisan termasuk sawi caisim dari Jepang, China dan Selandia Baru yang merupakan negara produsen benih tanaman tersebut.

Namun semenjak ditemukan serangan TUMV setelah negara-negara tersebut dinyatakan tidak aman oleh Deptan maka impor hanya bisa dilakukan dari negara bagian Idaho Amerika Serikat.

Afrizal menyatakan, jika impor hanya dari AS tidak akan mampu memenuhi kebutuhan dalam negeri karena produksi di negara tersebut juga terbatas.(*)

Copyright © 2008 ANTARA

How Important Is the Latest Cloning Feat?

Scientists at Stemagen, a small biotechnology company in La Jolla, CA, reported yesterday that they have for the first time generated cloned human blastocysts--early-stage embryos--from adult skin cells. This is the first step in generating stem cell lines matched to individuals, which are crucial for creating new cellular models of disease and potentially important for future tissue replacement therapies. (See "Next Steps for Stem Cells" and "The Real Stem Cell Hope".) The new findings also confirm that access to fresh eggs from healthy young donors is a key part of successful cloning. Lack of access to human eggs has been the major barrier in the field. (See "Human Therapeutic Cloning at a Standstill".)

Cloned blastocysts have been generated before, but from embryonic stem cells rather than from adult cells. Scientists theorize that embryonic stem cells are easier to turn into blastocysts because of their earlier developmental stage.

Experts in the field have had a mixed reaction to the new work. "It's a nice achievement, but in my view, they haven't crossed the bar," says Evan Snyder, director of the Stem Cells and Regenerative Medicine Program at the Burnham Institute in La Jolla. "The real test will be, can you generate cell lines that are stable and self-renewing and normal?" Others applaud the confirmation of the feasibility of human cloning. "The fact that it can be done is important," says Jeanne Loring, a stem cell scientist at the Scripps Research Institute in La Jolla. "It wipes away that blot on our scientific integrity," she says, referring to a massive fraud unveiled in 2005 in which South Korean scientist Woo Suk Hwang claimed to have generated stem cell lines from cloned human embryos. (See "Stem Cells Reborn".)

To clone an embryo, a process also called nuclear transfer, scientists first strip an egg of its genetic material. Then they insert DNA from an adult cell, such as a skin cell, into the egg. Through an unknown process, the egg turns back the clock on the adult DNA and begins to develop as a normally fertilized egg would. From the embryo, researchers could theoretically collect a specialized ball of cells that can be coaxed to turn into stem cells. So far, however, no one has successfully performed this feat.

Stemagen, a relatively unknown player in the field, probably owes its success to access to human eggs through a close association with a local fertility clinic. (The company was founded by a fertility specialist at the Reproductive Sciences Center in La Jolla.) "We were able to get access to high-quality oocytes and have them in the incubator within one to two hours," says Andrew French, Stemagen's chief scientific officer.

Egg donors and the intended parents gave eggs in excess of those needed for in vitro fertilization to the Stemagen scientists for research. Regulations in many states prohibit compensation for donated eggs for ethical reasons, a requirement that has slowed other cloning efforts.

Starting with 25 fresh oocytes, French and colleagues generated five blastocysts--five- to six-day-old embryos consisting of 30 to 70 cells. Rather than attempting to generate stem cell lines from the embryos, the researchers sent them to an independent company for genetic confirmation of their results. "They showed we had completely removed the DNA from the egg donor and replaced it with DNA from the skin-cell donor," says French. One blastocyst was confirmed as a clone via two DNA-fingerprinting methods, while genetic analysis of two others indicated the likelihood that they were clones.

The next crucial step will be generating stem cell lines from cloned embryos, which many stem cell scientists speculate will be the most challenging step. "That's likely where Hwang failed," says Synder.

French and colleagues are planning such experiments, with results potentially in the next eight to twelve months. "The quality of our blastocysts improved with each experiment," says French. Based on the success rate of previous attempts to make stem cells from regular embryos, he estimates that Stemagen will be able to generate a stem cell line from between five and ten cloned embryos and report the results in the next year. The company aims to sell or license the lines to pharmaceutical companies and others who would use them to test new drugs or develop new therapies.

While human therapeutic cloning has always been an ethically contentious area of research--partly because it requires the creation and destruction of human embryos--it has recently come under greater fire. After the announcement of new techniques for reprogramming adult cells so that they turn into stem cells without first forming embryos, some opponents called for a halt on embryonic-stem-cell research. (See "Stem Cells without the Embryos".)

However, researchers in the field emphasize the need to pursue all reprogramming techniques. "Even though there are other techniques to reprogram a cell that have gotten a lot of press, we still don't know how those compare with the reprogramming you actually see with nuclear transfer," says Snyder. "My feeling is, if we understand nuclear transfer better, we will be able to do the other kind of reprogramming more efficiently."

From here

Magnetic Cell Therapy

Stents are expandable stainless-steel scaffolds commonly used to prop open clogged arteries. But inserting a stent can damage an artery's inner lining, and stented arteries may reclose after several months, causing blood clots and possibly heart attacks. Now researchers at the Children's Hospital of Philadelphia have devised a way to use tiny iron-bearing nanoparticles and a magnetic field to direct cells with therapeutic properties to the sites of steel stents. The cells could help repair arterial damage and prevent clotting, among other things.

"Stents have been known to induce severe trauma," says Robert Levy, chair of pediatric cardiology at the Children's Hospital of Philadelphia. "Repairing blood vessels with cell therapy is a very important concept that can be realized with magnetic targeting."

Levy and his colleagues engineered nanoparticles, or tiny spheres, of polylactic acid, a biodegradable polymer used in sutures and other medical applications. The team then loaded each nanoparticle with a small dose of magnetically responsive iron oxide and inserted it into a bovine endothelial cell--a cell found in a blood vessel's inner lining. The bovine cells were genetically altered to express a fluorescent marker, making them easily detectable.

Next, the researchers surgically implanted small metal stents in the carotid arteries of live rats. They injected the rats with a solution of treated endothelial cells and created a steady magnetic field around each rat using two large, external electromagnetic coils. Levy says that the magnetic field he and his colleagues applied was less than a tenth of the strength of the fields generated by conventional MRI machines. After 48 hours, the team created images of the rat using bioluminescence imaging.

The researchers found that the magnetic field caused the cells to migrate to the metal stents under two scenarios: when cells were injected directly into the carotid artery, near the stent location, and when they were injected farther away, in the aortic arch, whence they could have branched out to all areas of the body. In tests that didn't use a magnetic field, the cells migrated throughout the body with little direction.

Magnetically directing cells, particularly endothelial cells, to the sites of metal stents may have a significant therapeutic effect, says Levy. During surgical implantation, stents tend to scrape off endothelial cells, whose normal functions include helping prevent blood clotting. Endothelial cells are also barriers to inflammatory cells. While inflammatory cells normally flock to an injury to help repair it, in the absence of endothelial cells, they build up excessively, creating arterial blockage. In recent years, stents have been engineered to release anticlotting drugs to prevent arteries from reclosing. But such drug-releasing stents have problems of their own, including preventing endothelial cells from regenerating.

"Two years ago, clinicians noticed that patients in significant numbers were having problems with these stents, probably because the endothelium wasn't properly healed," says Levy. "Clotting, myocardial infarctions, and sudden deaths occurred, and this has caused a big uproar over stent usage."

Levy hopes that magnetically directing new endothelial cells to blood vessels may solve many of the problems that stents currently face. His team plans to continue experimenting on rats, using endothelial cells derived from rats instead of cows, to minimize risk of rejection. Now that he has found a way to direct cells to metal stents, Levy is also looking at other potential therapies, including nitric oxide, which is known to relax and dilate blood vessels. He is currently engineering cells to genetically express enzymes that produce nitric oxide, and he will eventually load them with iron-oxide nanoparticles that will drive them to the sites of stents, further opening arteries.

Levy adds that the magnetic-based technique has applications outside of cardiovascular therapy. For example, in treating lung cancer, clinicians often use metal stents to keep airways open. However, a patient's tumor may continue to grow, eventually obstructing the passage despite the stenting. Magnetically targeted therapies could help deliver specific drugs to stent sites to treat tumors, in addition to keeping airways open.

"Metallic implants are also widely used in other areas, like orthopedics, for complex fractures, and correcting spinal curvature, where cell therapies could also be helpful," says Levy. "Steel implants are widely used in medicine, and there are all sorts of situations where applications could be used."

What's more, Levy envisions that such therapies can be applied using conventional MRI machines. The magnetic field generated by MRI cores is an order of magnitude more powerful than the ones Levy used in his experiments, so fewer iron-oxide nanoparticles could produce the same effect.

Robert Langer, Institute Professor at MIT, believes that Levy's technique is a promising step toward directed cell therapies. "They were able to localize more drugs into the targeted areas," he says. "I think it's a neat idea that has a lot of potential."

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Kedelai Plus LIPI Dapat Tingkatkan Produktivitas

Cibinong, Bogor (ANTARA News) - Pusat Penelitian (Puslit) Bioteknologi Lembaga Ilmu Pengetahuan Indonesia (LIPI) selama ini mengembangkan kedelai plus, benih yang telah diproses sehingga mampu melipatgandakan produktivitas dua kali dari rata-rata nasional 1,2 ton per hektare (ha) menjadi 2,6 ton hingga 3,6 ton per ha.

"Sudah terbukti ditanam di tempat yang sulit untuk kedelai seperti di Musirawas, Sumsel dan beberapa tempat lain di Jawa sejak 2004," kata Peneliti Puslit Bioteknologi LIPI, Harmastini Sukiman M.Agr, di Cibinong Science Center, Bogor, Kamis.

Meningkatnya produktivitas, ujarnya, karena benih telah mengandung mikroba rhizobium yang diinjeksi ke dalamnya dengan teknologi vakumisasi sehingga ketika ditanam, kandungan nitrogen di dalam tanahnya meningkat 20 persen dan menjadi subur bagi kedelai.

Karakter bakteri rhizobium, ujarnya, bersimbiose dengan tanaman kacang-kacangan dan dapat membantu penyerapan Nitrogen dari udara serta mengubahnya menjadi unsur yang tersedia bagi tanaman.

Cara kerjanya, benih kedelai dari varietas apapun diinsersi oleh bakteri rhizobium BTCC-B64 hasil riset LIPI dengan media pertumbuhan YEM-broth lalu dicampurkan oleh alat pencampur dengan teknologi vakum sehingga dihasilkan kedelai Plus.

Keuntungan Kedelai Plus, urainya, selain produksi biji yang meningkat, juga mudah ditanam oleh petani, dan kebutuhan pupuk berkurang hingga 60 persen.

Sementara itu, Deputi bidang Ilmu Pengetahuan Hayati LIPI, Prof Dr Endang Sukara, mengatakan bahwa sebenarnya pada masa Presiden Megawati, kedelai plus ini telah diperkenalkan, namun entah mengapa hasil riset ini hingga kini tidak dipakai secara massal.

"Ini masalah kebijakan, masalah tata niaga yang lebih mengutamakan impor dalam bentuk kedelai jadi, daripada mengembangkan pertanian kedelai," katanya.

Padahal, ia mengingatkan, kedelai yang diimpor itu adalah kedelai hasil rekayasa genetik sementara kedelai plus dalam negeri ini asli hayati. (*)

antara

Gene Therapy for Alcoholics

Researchers in Chile have succeeded in keeping the drinking habits of alcoholic rats in check using gene therapy. The treatment mimics a natural mutation common in East Asian people, which lowers their tolerance to alcohol, making them less likely to become alcoholics.

According to the National Institutes of Health, 17.6 million people abuse alcohol or are alcohol dependent in the United States alone. If the gene-therapy technique could be applied to humans, scientists say that it may be a valuable addition to the drugs and behavioral approaches currently used to treat alcoholism.

The gene therapy works in a similar way to a drug currently used to treat alcoholics, which is effective but unpopular with patients, many of whom stop taking it.

"It's great when innovative approaches are being used for treatment, because we need them," says George Koob, codirector of the Pearson Center for Alcoholism and Addiction Research, at the Scripps Research Institute. He was not involved in the work in Chile.

The gene therapy, described in the latest issue of the journal Alcohol: Clinical and Experimental Research, curbed the activity in the liver of an enzyme--aldehyde dehydrogenase--that plays a major role in metabolizing alcohol. Nearly a third of East Asians have a natural genetic mutation that has the same effect, so when they drink, their faces turn red, their hearts pound, and they feel sick--all good incentives to go easy on alcohol.

The gene therapy tested by Yedy Israel, a professor of pharmacological and toxicological chemistry at the University of Chile, and his colleagues triggers the same unpleasant response to alcohol in rats.

"It's a new way of doing an old thing," Koob says. "I think it's very clever and very interesting."

The researchers in Chile started with rats bred for their alcoholic tendencies and offered them unlimited quantities of diluted ethanol--the equivalent of higher-alcohol premium beer--for two months to make them even more dependent. The researchers then cut off the animals' access to alcohol and injected some of them with a virus containing a gene that inhibits aldehyde dehydrogenase.

Three days later, the researchers implemented a month of daily "happy hours," letting the rats drink as much as they wanted. In an hour, each of the animals put away the equivalent, in human terms, of about seven premium beers--10 times more alcohol than what was put away by alcoholic animals that hadn't been through the two-month dependency regimen.

During the first happy hour, rats that were given gene therapy "didn't realize they were going to feel bad, and they drank a tremendous amount," Israel says. Afterward, "the animals clearly didn't look comfortable." Those rats then markedly reduced their alcohol consumption on subsequent days. Over the course of the happy hours, they drank half as much, on average, as the untreated animals. The effect lasted throughout the monthlong study.

Israel and his colleagues are now working on ways of delivering gene therapies that last for years or even a lifetime, in the hope of developing long-lasting treatments for alcoholism. Most of the medications available now need to be taken at least once a day, and many alcoholics don't comply with the routine. A longer-lasting drug is likely to be more successful, Israel says.

Two of the three existing drug treatments approved for alcoholism by the Food and Drug Administration--naltrexone and acamprosate--limit the craving for alcohol. The other treatment--disulfiram--works in a similar way to Israel's gene therapy: by making patients sick if they drink. The trace of alcohol in mouthwash is enough to trigger a reaction, and most alcoholics "really dislike this medication," says Carolyn Drazinic, an assistant professor in the Department of Psychiatry and the Department of Genetics and Developmental Biology at the University of Connecticut. She was not involved in the gene-therapy research.

"All of these drugs," Israel says, "really require patients' compliance with their medication, which is rare."

Drazinic says, though, that a lifelong treatment that makes someone sick after a whisper of alcohol might not have too many takers. "There may be a lot of patients who would refuse something like this, if they've ever experienced a disulfiram reaction," she says. Drazinic believes that a more popular option might be a treatment that doesn't last a lifetime, but long enough not to be a daily hassle.

That, Koob says, would be better than "someone sitting there with a baseball bat telling you to take your Antabuse [the trade name for disulfiram] with your Wheaties."

Robert Swift, a professor of psychiatry and human behavior and the associate director of

Brown University's Center for Alcohol and Addiction Studies, says that the gene-therapy approach "is a very interesting technique, but it's not ready for prime time."

"There are a lot of medications that reduce drinking in animals but may not be as effective in humans," he says. "The question is, can you really make enough difference in the enzymes that humans will reduce their drinking?"

Gene therapy is risky, and if it's ever used to treat alcoholism in humans, it should be a last-ditch option for hardcore alcoholics, Swift says. However, those patients are often suffering from liver damage, and "if someone's got damaged liver cells, you've got a greater risk of complications from genetic treatment."

Israel's gene-therapy approach is "perfectly logical," says Raymond White, director of the University of California, San Francisco's Ernest Gallo Clinic and Research Center, where scientists study the biological basis of alcohol and substance abuse. But White adds that he'd be quite surprised "if this became a real therapy."

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DNA Deletion Linked to Autism

A specific structural variation on chromosome 16 dramatically boosts the risk of autism, according to a study published today in the New England Journal of Medicine. The finding--one of the most significant to date--permits the development of new diagnostic tests to identify children at risk, and could ultimately point to specific biochemical pathways to target in drug development.

"This is one of the single largest [influences] and most frequent genetic causes for autism identified so far," says Bai-Lin Wu,director of the Genetics Diagnostic Laboratory at Children's Hospital Boston and one of the senior authors on the study.

Autism spectrum disorder--or autism, as it is commonly called--refers to a group of developmental disabilities with wide-ranging language, social, and behavioral symptoms. The disorder is known to have a strong genetic influence, with up to 90 percent of cases thought to have a genetic component. However, because the disorder is linked to a combination of genetic variations, each playing a minor role, identifying specific genetic triggers has been difficult. Now new microarray technologies, which allow scientists to screen a million or more genetic variations in thousands of patients, are enabling the much larger studies needed to pinpoint these triggers.

In the new paper, scientists say that they used microarrays to scour the DNA of more than 2,000 individuals with autism. They found that deletion or duplication of approximately 500 of the same DNA letters on chromosome 16 was strongly linked to autism, accounting for about one percent of cases. "While that doesn't sound like a huge number, the fact that these people carry the identical spontaneous deletion or duplication would be incredibly unlikely to happen by chance," says Mark Daly, a geneticist at Massachusetts General Hospital's (MGH) Center for Human Genetic Research, in Boston, and at the Whitehead Institute, in Cambridge, and one of the study's senior authors.

The results were independently identified by three different groups--at MGH; Children's Hospital Boston; and deCODE Genetics, in Iceland--that are studying three different populations, giving added weight to the work.

The findings build on previous reports that autism is linked to genetic deletions or duplications that arise spontaneously, rather than being passed down through generations. In almost all cases, parents of the affected people did not carry the chromosome 16 variation.

One of the most immediate clinical benefits of the research will be the development of inexpensive diagnostic tests. "Because the variation occurs so frequently, you could directly test for the presence or absence of a duplication or deletion as part of standardized genetic testing for autism," says James Gusella, a neurogeneticist at Harvard Medical School, in Boston, who participated in the research. For example, children who show developmental delays but are too young to undergo clinical autism testing could be screened for this variation, allowing parents and doctors to prescribe intervention for those who test positive. "We will be able to find at-risk children early on so that language and behavior problems can be treated much earlier," says Yiping Shen, director of research and development at Children's Hospital's Genetics Diagnostic Laboratory, who was also involved in the work.

Such testing could also predict if parents with one autistic child are at greater risk of having another; if their child's autism is linked to a spontaneous variation, they are at no greater risk than the general population. Researchers at Children's Hospital, which provides genetic testing to families, are already developing a clinical diagnostic test.

Scientists are also trying to pinpoint the specific gene or genes within this section of DNA that underlie the increased risk. Daly and his collaborators plan to sequence this region of the genome in another group of people with autism, in search of single-letter mutations that might disrupt the function of specific genes. "Genetics provides us with the only opportunity to gain insight into the biological mechanisms that underlie autism," says Daly. "We can look at individual gene discovery as a small first step in the overall path to develop treatments."

Previous studies have identified autism risk genes. However, these studies have focused on people with genetic disorders that often co-occur with autism, such as Fragile-X syndrome, complicating the role those genes play in the disorder. "Up until now, we haven't had the capacity to look at a single gene that is associated with pure autism," says Gusella.

The findings could point to additional spots in the human genome to search for autism risk genes. The variation on chromosome 16 lies within a genetic "hot spot," an area that is predisposed to undergoing structural duplications due to the architecture of the DNA, says Evan Eichler, a geneticist at the University of Washington in Seattle, who wrote an editorial accompanying the paper. "Every time we produce gametes, there's a finite probability of this region to duplicate," he says. In addition, the region has a high concentration of genes that are rapidly evolving in humans. While the significance of that finding is not yet clear, it may explain autism's status as a relatively young disease.

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