Penemuan Vaksin HIV Masih Jauh

LONDON -- Setelah lebih dari duapuluh tahun meneliti, para ilmuwan ternyata tidak semakin dekat untuk menemukan vaksin HIV. ''Ini tantangan besar, sebab untuk mengendalikan HIV dengan imunologi. Komunitas ilmiah harus mengalahkan alam, menghadapi alam, dengan keunggulan empat miliar tahun evolusi. Hal itu ternyata belum bisa dilakukan,'' ujar pakar biologi peraih Hadiah Nobel, Profesor David Baltimore, seperti dilansir BBC.

Baltimore yang juga Presiden Perhimpunan Amerika untuk Kemajuan Sains (AAAS) mengaku kekurangberhasilan tersebut mungkin bisa dipahami. ''Tapi, tidak bisa diterima,'' jelasnya . Saat berbicara dalam pertemuan tahunan AAAS di Boston, Baltimore, ia mengatakan bahwa HIV telah mengembangkan cara untuk melindungi diri dari sistem kekebalan manusia. ''Jadi, kita harus bertindak selangkah lebih jauh daripada alam,'' kilahnya.

Dia mengungkapkan, upaya untuk mengendalikan virus melalui antibodi atau dengan meningkatkan sistem kekebalan tubuh manusia berakhir tanpa hasil. Baltimore juga mengaku kecewa dengan kalangan ilmuwan pengembang vaksin. eye

http://republika.co.id/koran_detail.asp?id=324241&kat_id=359

Proyek 1000 Genom

Amerika, Inggris dan Cina kini bekerja sama dalam Proyek 1000 Genom. Proyek ini bertujuan untuk memetakan genom manusia terbaru dengan data variasi DNA biomedis paling lengkap dan lebih detail menurut Richard Durbin dari Sanger Institute. Proyek ini melibatkan institusi Wellcome Trust Sanger Institute dari Inggris, National Human Genome Research Institute (NHGRI) dari Amerika, dan Beijing Genomics Institute-Shenzhen, Cina.

Proyek 1000 genom ini mungkin untuk dilakukan saat ini karena teknologi pengurutan genetika, bioinformatika dan teknik lainnya makin mengalami kemajuan. Dengan proyek ini upaya untuk menemukan faktor genetika yang terlibat dalam penyakit dan kesehatan manusia daapt dilakukan dengan lebih efektif lagi.

Perbedaan yang ada pada individu merupakan pengaruh dari satu persen DNA, sehingga dengan riset dalam 1000 genom ini, informasi mengenai DNA akan lebih mendetail. Perbedaan satu persen pada DNA sering kali bertanggung jawab atas perbedaan dalam kerentanan terhadap penyakit dan reaksi pengobatan. Ilmuwan telah mendaftarkan puluhan wilayah variasi genom manusia yang spesifik (haplotipe) dan mengasosiasikannya dengan penyakit umum, seperti penyakit jantung koroner, kanker payudara, arthritics, dan penyakit akibat penuaan.

Peta DNA yang berhasil disusun tahun 2000 lalu masih belum terlalu detail, oleh karena itu ilmuwan ingin mengembangkannya lagi agar peta DNA yang ada saat ini menjadi lebih detail dan gambaran genom akan menjadi lebih jelas dalam menemukan faktor genetika suatu penyakit.

Proyek ini akan memetakan DNA dari beragam kelompok etnis yang spesifik, termasuk Yoruba di Ibadan, Nigeria; Chinese di Denver, Colorado; Chinese di Beijing; Toscani di Italia, India Gujarati di Houston, Texas; orang Meksiko di Los Angeles; serta warga keturunan Afrika di barat daya Amerika Serikat.

Dengan memanfaatkan teknologi sequencing dan metode komputasional terbaru, diharapkan dapat memberikan peta genom lengkap bagi ilmuwan biomedis, yang akan memaparkan segala bentuk variasi sampai tingkat satu persen dan ini akan mengubah cara ilmuwan untuk mempelajari penyakit genetis kata Francis Collins, wakil NHGRI.

Tempo Interaktif

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

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

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

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

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.

from here

Killing Skin-Cancer Stem Cells

Harvard Medical School researchers have identified a class of cells that initiates skin-cancer melanomas; they are also developing a therapy that specifically targets these cells. In a major study, the researchers characterized these cells and linked them to disease progression in humans. They also demonstrated that an antibody targeting these cells slows tumor growth in mice. The work may lead to new treatments for resistant melanoma. It also has broader implications for cancer biology.

There is a growing consensus amongst cancer biologists that not all cancer cells are equal. There is a hierarchy of cells inside a tumor, and only a few cells, called cancer stem cells, are capable of generating new tumors. Such tumor-initiating cells have been identified in many cancers, including those of the colon, brain, and breast. These cells are also thought to play an important role in chemotherapy resistance and cancer recurrence.

Previously, researchers had connected the presence of cancer stem cells with breast-cancer patient outcomes. Now the Harvard team has demonstrated a second important connection between cancer stem cells and clinical impacts, linking the presence of such cells with the speed at which the disease progresses in humans.

"We've defined for the first time a direct link between cancer stem cells and cancer progression," says Markus Frank, an assistant professor at Harvard Medical School, who led the melanoma research.

This research grew out of Frank's study of a protein made by some melanomas that confers resistance to chemotherapy. In a paper published today in the journal Nature, Frank and his colleagues at Harvard Medical School and Brigham and Women's Hospital, in Boston, report that human melanoma cells that make this protein can be characterized as cancer stem cells because they generate tumors when implanted in mice. Examining melanoma biopsies, they found that tumors expressing this protein were more aggressive.

Frank's group also demonstrated that an antibody specifically targeting the melanoma stem-cell protein slowed tumor growth in mice. Many other researchers are working on therapies that attack cancer stem cells, but Frank believes that his group is the first to develop such an antibody.

"Most current therapies target the bulk cells of the tumor," he says. "Resistant stem cells are left behind," allowing the tumor to come back after therapy seems to be progressing. Frank and other researchers hope that therapies that specifically target cancer stem cells can completely eradicate tumors.

Robert Weinberg, a founding member of the Whitehead Institute for Biomedical Research, in Cambridge, MA, and director of the Ludwig Center for Molecular Oncology at MIT, agrees that the Harvard work adds to the growing evidence of cancer stem cells' importance. "We don't really understand how tumors renew themselves, or how to treat many tumors," he says. Some researchers remain unconvinced, Weinberg says, but he and many others think that cancer stem cells may hold the answers to these questions. Cancer stem cells are "going to be very important," he predicts. Slowly but surely, he believes, the evidence is building.

Frank says that much remains to be learned about the newly identified melanoma stem cells. It's not clear, for example, whether the protein that the Harvard researchers have been focusing on causes the cells to act as cancer stem cells, or whether this protein is simply a marker for these cells. Further studies of their gene-expression patterns will tell the researchers more about what makes them different from normal melanoma cells. In the meantime, the Harvard researchers will continue to develop their antibody in hopes of taking it to human trials.

From Here

Autis Lebih Disebabkan 'Kecelakaan' Genetis

BOSTON -- Faktor genetis secara dramatis jarang meningkatkan kemungkinan munculnya autis pada anak-anak. Ini berdasarkan hasil penelitian di Boston, Amerika Serikat (AS). Penelitian baru ini berpotensi menjadi pintu gerbang yang lebih baik untuk menyembuhkan autis yang selama ini lebih dikenal disebabkan faktor genetis.

Penelitian dalam kasus autis selama ini memang terfokus pada faktor genetis karena sejauh ini sekitar 10 persen kasus autis diketahui disebabkan faktor tersebut. Namun, para peneliti di Boston memperkirakan faktor gen terindentifikasi hanya menyumbang sekitar satu persen penyakit autis.

Mereka menemukan segmen kromoson yang berhubungan dengan gen dalam perkembangan otak hilang atau terduplikat lebih sering pada orang yang terkena autis dan juga pada orang yang menderita keterbelakangan mental. Ini terjadi dalam beberapa kasus, namun secara acak lebih banyak berasal dari 'kecelakaan' genetis. Hasil dari studi Autism Consortium, yang dimuat di New England Journal of Medicine, mengonfirmasikan bahwa penelitian di AS dan Kanada di tahun sebelumnya, memilah dan menemukan faktor selain faktor genetik itu dalam pengecekan dua DNA lain dalam database. ''Ini sungguh jelas,'' ujar Dr Andrew Zimmerman, direktur Kennedy Krieger Institute'Center for Autism & Related Disorders di Baltimore.

Zimmerman memprediksi, anak-anak dengan diagnosis terbaru autis atau yang mengalami keterbelakangan mental saat ini bisa diketahui melalui kerusakan di kromoson 16. Atau, dengan mempelajari lebih banyak contoh DNA yang mungkin berhubungan dengan autis dari variasi gen lain.

Penelian ini diharapkan menjadi awal untuk digunakan dan diberikan kepada beberapa orang tua yang sering menanyakan, apakah penyebab kasus autis yang menimpa anak mereka. Dan, bagaimana sebaiknya anak-anak di masa depan yang terkena autis segera diketahui pihak keluarga. ''Kami menyediakan banyak petunjuk secara biologi mengenai autis,'' ujar ketua peneliti Mark J Daly.

Ketika sisi biologi digunakan, ujar juru bicara ahli autis Geraldine Dawson, para ilmuwan lain dapat mencoba mendesain obat-obatan sebagai target untuk menyembuhkan autis yang menyerang di otak. ''Saya pikir kromoson 16 akan menjadi isu hangat bagi peneltian autis,'' ujar Thomas Lehner, kepala peneliti genomik di National Institute of Mental Health.

Autis merupakan penyakit yang sangat kompleks dan sulit dipahami, dengan karakteristik si penderita dapat terlihat dari kelakuan yang sulit berinteraksi secara sosial dan sulit berkomunikasi. Peneliti umumnya menemukan bahwa ini merupakan kasus genetik. Adapula yang menduga ini disebabkan adanya merkuri pada vaksin yang diberikan ke bayi.

Perbandingan jumlah anak yang terkena autis di AS adalah satu anak di antara 150 anak normal. Dari studi ini, kelompok peneliti mempelajari keseluruhan 46 kromoson dari DNA dengan sampel 1.441 anak yang terkena autis atau sejenis. Mereka juga mengamati DNA dari sebagian besar orang tua mereka dan 2.800 orang lainnya, yang ternyata diketahui tak memiliki autis.

Peneliti menemukan 25 segmen gen kromoson 16 yang hilang di lima anak yang terkena autis, tapi orang tuanya tidak autis. Ini memperlihatkan di beberapa kasus genetik tidak berhubungan dengan orang tua. Namun, autis tak jarang muncul dari sel telur atau sperma yang mengalami kecelakaan saat dibentuk. Tujuh anak lainnya dengan autis memiliki duplikasi kromoson 16, namun dari semua hanya satu orang tua yang memiliki duplikasi yang sama.

from here

A New Treatment for Alzheimer's?

By Anna Davison

A drug commonly used to treat arthritis caused a dramatic and rapid improvement in patients with Alzheimer's disease, according to physicians in California. However, scientists and others not involved in the work worry that the report, which was based on trials in a few patients and hasn't been independently confirmed, may offer little more than false hope for Alzheimer's sufferers and their families.

Alzheimer's patients injected with the anti-inflammatory drug etanercept--marketed as Enbrel--showed dramatic improvements in their functioning within minutes, according to Edward Tobinick, director of the Institute for Neurological Research, a private medical facility in Los Angeles where the patients were treated, and an assistant clinical professor of medicine at the University of California, Los Angeles.

"The patients improve literally before your eyes," says Tobinick, who began using etanercept in Alzheimer's patients three years ago. He uses an unconventional method to administer the drug; he injects it near patients' spines. In 2006, he reported success with weekly treatments given to 15 people over the course of six months. In a case study in the latest issue of the Journal of Neuroinflammation, Tobinick and Hyman Gross, who practices in Santa Monica, describe how a patient improved within 10 minutes of treatment, and how cognitive tests performed two hours after the treatment showed a marked improvement over tests given before the injection. Tobinick says that the rapid improvement is typical in patients he has injected with etanercept. He treats them weekly, or, in some cases, less often.

"In each case, the person was more alert, calm, attentive, and they stayed on track," says Sue Griffin, director of research at the Donald W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences, who watched Tobinick treat several patients. Griffin says that she was skeptical when she first heard about Tobinick's approach, but having witnessed the effect firsthand, she says, "It was just completely amazing, like nothing I'd ever seen for an Alzheimer's person."

Minutes before the treatment, the patient in the case study couldn't recall the year or which state he was in. Ten minutes after the injection, he answered these questions correctly. As part of a cognitive assessment performed the day before the treatment, the patient was asked to draw a clock face showing a certain time. He sketched a square. Two hours after the injection, he drew a round face with two hands in approximately the correct positions.

The case report on this patient's rapid improvement is "interesting," says William Thies, vice president of medical and scientific relations for the Alzheimer's Association, but he adds that "we're going to need more information before it's something that people should get wildly excited about."

"There are some kernels of good science here," says David Standaert, director of the Center for Neurodegeneration and Experimental Therapeutics at the University of Alabama at Birmingham, but he cautions that "this is not enough evidence that we would start treating people outside of a trial." Standaert was not involved in the work.

Etanercept has been used since 1998, primarily to treat rheumatoid arthritis. It's usually injected into the thigh, stomach, or upper arm, but Tobinick says that by injecting it into the neck, near the spine, the drug can reach the brain. It's a method that requires considerable skill. "It would be incorrect for anyone to think that they could just take Enbrel if they have Alzheimer's, and they'll get better," he says.

For decades, scientists have been trying to figure out how Alzheimer's disease does its damage so that they can determine how it might be treated. A hallmark of the disease is the globs of protein that form in the brain. There's mounting evidence that "part of what damages the brain is the body's own immune responses to these abnormal proteins," Standaert says. Various anti-inflammatory drugs have been trialed in Alzheimer's patients, but with disappointing results.

Etanercept reduces inflammation by blocking a protein called tumor necrosis factor (TNF), which plays an important role in immune responses. TNF occurs naturally in the brain, but studies have found elevated levels in people suffering from Alzheimer's disease.

Recent evidence suggests that TNF regulates the activity of synapses, which connect brain cells and enable electrical signals to travel around the brain. In Alzheimer's patients, an excess of TNF may wreck havoc on those connections, Tobinick says. "Even though the neurons may be working, the connections between the neurons and between the different lobes of the brain may not be working properly."

By using etanercept to reduce levels of TNF in the brains of Alzheimer's patients, Tobinick thinks he may have normalized those connections, leading to an immediate improvement in cognitive functioning. He says that he's working with academic partners to design larger-scale trials of the treatment. However, Sonia Fiorenza, a spokeswoman for Amgen, which markets Enbrel, says that the company won't be sponsoring trials because it doesn't believe there's enough evidence that it may be useful in Alzheimer's disease.

Some researchers want to see independent studies carried out, in part because Tobinick has disclosed that he has stock in Amgen and holds patents on the use of the drug and other anti-TNF agents to treat Alzheimer's disease.

It's not unusual for researchers to have a financial interest in something they're studying, Thies says, and "it doesn't stop them from doing good science." However, "you're going to have to have some independent confirmation in the hands of others."

"You have to do these [studies] double blind, placebo controlled, by people who don't have a financial interest," says J. Wesson Ashford, a senior research scientist at the Stanford University/VA Aging Clinical Research Center. (He was not involved in Tobinick's work.) "I'd really like to believe it, but I've seen it so many times, when people say something and it doesn't turn out to be anything."

"This is something that's got to be looked at," Griffin says. "I hope that scientists will pay attention to this, and the funding agencies will pay attention to this."

"This is not a cure," she adds, but if there's a person who can't dress or feed himself, is arrogant, mean, and up all night, "and you can take them to the point where they can feed themselves, they're calmer, attentive, conversational--in other words, you can stand them--that's great."

From here

Smoking Simulation

Please Stop Smoking If You Don't Want your lung like these.



Udah berhenti donk merokoknya, kasian kan paru-paru kamu.

Alat yang dipergunakan dalam simulasi ini hanya menggunakan alat-alat sederhana yang ada di sekitar kita sehari-hari.

This video showing the effect of smoking to our lung. So stop smoke.!!!!!!!

from metacafe

What is heart disease?

Patsy Westcott

One of the commonest diseases to affect the heart is coronary heart disease (CHD). It's usually caused by atherosclerosis, a build up of fatty materials within the walls of the arteries.

What is CHD?

In CHD, the arteries that supply the heart with oxygen and nutrients become narrowed by atherosclerosis. This restricts the supply of blood and oxygen to the heart, particularly during exertion when there are more demands on the heart muscle.

What are the symptoms of CHD?

The main symptom is angina, caused by insufficient oxygen reaching the heart muscle because of reduced blood flow.

Angina is a feeling of heaviness, tightness or pain in the middle of your chest that may extend to, or just affect, your arms (especially the left), neck, jaw, face, back or abdomen.

It's most often experienced during exertion - if you run for a bus, for example, or climb stairs. It may occur in cold weather, after a heavy meal, or when you're feeling stressed. It can subside once you stop what you're doing and rest, or take medication.

Other CHD symptoms

The following symptoms are by no means always owing to CHD, and could be harmless or caused by other medical conditions. However, if you experience any of them it's a good idea to make an appointment to see your doctor:

• Unusual breathlessness when doing light activity or at rest, or breathlessness that comes on suddenly.
• Palpitations - awareness of your heart beat or a feeling of having a rapid and unusually forceful heart beat, especially if they last for several hours or recur over several days and/or cause chest pain, breathlessness or dizziness.
• Fainting - although not always a serious symptom, fainting is due to insufficient oxygen reaching the brain, so you should report it to your doctor.
• Fluid retention or puffiness (the medical term is oedema) is an abnormal accumulation of fluid in the tissues of the ankles, legs, lungs or abdomen, for example. Although a mild degree of ankle oedema may be quite normal - for example, on a hot day - it can be a sign that the heart isn’t pumping as well as it should (this is known as heart failure). Fluid retention in the lungs, or pulmonary oedema, can cause intense shortness of breath, and may be life-threatening.
• Bluish-tinged fingernails or lips (known medically as cyanosis) can be the result of too little oxygen in the blood.
• Fatigue is a common symptom of heart disease, but has numerous causes, including depression. It's always worth seeing your doctor if you feel unusually tired, especially if this is combined with symptoms that can’t be explained.
  

Heart attack?

Unfortunately, for many people the first indication that something’s wrong is a heart attack.

This happens when the blood supply to a part of the heart muscle is completely interrupted or stops, usually when a blood clot forms in a diseased coronary artery that's already become narrowed by atherosclerosis.

The pain of a heart attack is often severe, and is frequently described as a central, crushing type of pain - like a tight band around the chest. Unlike angina, the pain doesn't subside when you rest.

Sometimes it can be mild, and is mistaken for indigestion. Some people have a heart attack without experiencing pain.

Other heart attack symptoms include sweating, light-headedness, nausea or breathlessness which, again, aren’t alleviated by rest.

If you suspect you, or someone else, is having a heart attack, seek medical help immediately by calling 999. Modern treatments can restore the blood supply to the heart muscle. The sooner treatment is given, the less permanent damage there will be.

What causes CHD?

The most common cause is atherosclerosis. This is a build up of fatty materials within the walls of the arteries throughout the body, most importantly in the arteries to the tissues of the heart - the coronary arteries.

During this process, the inner lining of the arteries becomes furred with a thick, porridge-like sludge (atheroma), consisting of fatty deposits of cholesterol, cell waste and other substances.

These form raised patches on the artery wall - known as 'plaques' - that narrow the arteries, reducing the space through which blood can flow. At the same time, the blood becomes more prone to clotting.

These growing plaques may block the delivery of nutrients to the artery walls, causing the arteries throughout the circulation to lose their elasticity. In turn, this can lead to high blood pressure, which also increases the risk of CHD.

A heart attack occurs when one of the coronary arteries blocks completely. This final step usually happens when a plaque splits open for some reason, causing a blood clot to form on its surface that obstructs the flow of blood. It’s not yet understood why plaques split open, but inflammation seems to play a part.

When the supply of oxygen and nutrients is completely blocked, the heart muscle and tissue supplied by that artery dies.

Some people are particularly predisposed towards developing atherosclerosis, due to inherited genetic factors. They may have a family history of people dying at a young age from CHD.

An unhealthy diet, lack of exercise, diabetes, high blood pressure and smoking all increase the risk.

Other heart diseases

Other diseases that commonly affect the heart include:

• Infection: bacterial infections are much rarer these days thanks to antibiotics, but can damage the valves of the heart as well as other tissues. Viral infections can damage the heart muscle leading to heart failure, or cause abnormal heart rhythms.
• Congenital heart disease: there's a range of structural abnormalities that can develop in the heart as a baby grows in the womb. These may cause abnormal flow through the heart (for example, through a septal defect or 'hole in the heart') or through the rest of the circulation, and put excessive strain on the infant's heart after it's born.
• Cardiomyopathy: this is disease of the heart muscle and may occur for many different reasons, including CHD, high blood pressure, viral infection, high alcohol intake and thyroid disease.

For many people with heart disease, there are a combination of factors that can cause problems. For example, CHD (most adults have some degree of atherosclerosis, especially if they smoke) and high blood pressure are often found together.

Who's at risk?

Scientists have yet to unravel all of the causes of heart disease. However, certain risk factors can increase your likelihood of developing it. You can’t do much about some of them, such as your age, gender or ethnic group, but risk factors you do have some control over include what you eat, whether you smoke, and the amount of exercise you take.

Key risk factors include:

Your age

It’s recognised that the risk of developing CHD increases with age. Atherosclerosis takes a long time to develop, and arteries naturally become less elastic as we age, often leading to a greater risk of high blood pressure.

Your gender

Many people think of CHD as a male problem. In fact, it accounts for the death of more women than any other disease.

The female sex hormone oestrogen protects against CHD during a woman’s reproductive years by creating a more favourable balance of blood fats and contributing to the elasticity and health of arteries.

After the menopause - or following a total hysterectomy in which the ovaries and uterus are removed - this natural protection can disappear.

The contraceptive pill increases a woman’s risk of clotting problems, such as thrombosis or a heart attack. Although the risk is still small, it’s considerably greater if you smoke. You should consult your doctor before taking the pill.

Your genes

If you’ve a family history of CHD or factors predisposing to it, such as high cholesterol (familial hyperlipidaemia) or blood pressure, you're more at risk.

Your ethnic background

If you’re black or Asian you’re more at risk of heart disease, although different underlying risk factors are at play for each group. If you’re Asian, you’ve a higher risk of developing diabetes, which is a risk factor. If you’re black, you’re more at risk of high blood pressure.

Diabetes

If you have diabetes you’re three times more likely to develop CHD. You’re also more likely to have silent ischaemia (painless angina or a heart attack), because diabetes can affect the nerves which send pain messages. This is especially dangerous because as the person doesn’t receive any warning that they have problems, they don’t seek help which may prevent further damage.

Your weight

Even being moderately overweight increases your risk of CHD. This may be because you're more likely to develop diabetes, have raised blood cholesterol levels and high blood pressure. It's also more difficult to be physically active if you are carrying excess pounds.

Your shape

Apple-shaped people who carry fat around their waist are more at risk of CHD than pear-shaped people who carry excess weight around their hips. The tendency to a particular shape is largely inherited, so if one or both your parents are 'apples', it's worth taking particular care over diet and exercise to lose excess fat.

Your activity levels

Watching too much television and taking the car instead of walking both increase your risk of obesity and, consequently, your risk of CHD. Lack of activity also decreases your body's ability to extract oxygen from your blood, weakens your bones (leading to a risk of osteoporosis) and your muscles, and encourages high cholesterol levels.

Blood pressure

Blood pressure is the force of blood in your arteries and is determined by how hard your heart works and the health of your blood vessels.

High blood pressure (or hypertension) is when the pressure is persistently higher than it should be (above 140/90 in healthy individuals), causing increased strain on your arteries. Over time, the force of the blood flowing through the arteries causes the smooth lining to roughen and the walls to become thicker. This causes the arteries to narrow and become less elastic.

Because high blood pressure often has no symptoms it's important to have your blood pressure checked regularly, so you can take steps to reduce it if it's raised, before it leads to heart disease or a stroke.

Your cholesterol

Cholesterol is a waxy, fatty substance made by your liver. It's also present in some foods such as animal fats, eggs and shellfish. Your body needs some cholesterol to produce hormones and to produce the bile needed to digest fat. It's also the main ingredient of cell membranes.

Cholesterol travels around your bloodstream in special proteins called lipoproteins. There are two types: low-density lipoproteins or LDL (also known as 'bad cholesterol'), which carries cholesterol to your body's cells, and high-density lipoproteins or HDL (also known as 'good cholesterol'), which helps clear excess cholesterol from your arteries and carries it back to your liver to be destroyed.

If you have high levels of LDL and low levels of HDL you're more at risk of heart disease.

Factors predisposing towards unhealthy cholesterol levels include eating a diet high in saturated (animal) fats and/or transfats found in processed foods, being overweight, drinking too much alcohol and not doing enough exercise.

Cholesterol and atherosclerosis

Atherosclerosis, a build up of fatty materials within the walls of arteries, is set off when LDL cholesterol undergoes a chemical reaction called oxidation - the same reaction that causes butter to go rancid.

Oxidation is caused by free radicals - harmful molecules produced as a result of the normal metabolism that occurs within the body.

Free radicals also come from ionising radiation from the sun's rays, ozone and nitrous oxide from car exhausts and cigarette smoke. These free radicals contribute to atherosclerosis that results in heart disease.

Smoking

Smoking increases your risk of having a heart attack two-fold or three-fold. In fact, if you're under 50 and smoke, you're five times more likely to die of CHD than a non-smoker.

There are several reasons for this. Nicotine triggers the release of the stress hormone adrenalin, which raises your heart rate and blood pressure, increasing your heart's need for oxygen.

Carbon monoxide, found in tobacco smoke, displaces oxygen from your blood cells, depriving your heart of oxygen. Other chemicals in cigarette smoke trigger the release of free radicals, the harmful molecules involved in the development of atherosclerosis.

Smoking also decreases the level of ‘good fats’ in the body, such as HDL, and may increase blood pressure and make the blood more likely to form clots. Smoking is particularly dangerous when other risk factors such as diabetes or high blood pressure are also present.

Raised homocysteine levels

Some people with CHD have raised levels of a substance called homocysteine, an amino acid (one of the building blocks that make up protein) that your body uses to build tissues.

Raised homocysteine levels are thought to damage the lining of arteries, a crucial step in the development of atherosclerosis. They've been found to be a factor in the oxidation of cholesterol and also appear to increase blood clotting.

Smoking and inactivity lead to raised homocysteine levels, and low levels of folic acid and vitamins B6 and B12, in particular, have also been linked to this.

However, recent studies have failed to show convincingly that high homocysteine levels are associated with an increased risk of CHD, and there's no proof that efforts to lower homocysteine (such as taking folic acid supplements) can protect from atherosclerosis.

Because the evidence remains uncertain, experts are reluctant to designate a raised homocysteine level as a risk factor for CHD until further research provides a clearer answer.

This article was last medically reviewed by Dr Trisha Macnair in March 2007.
First published in June 2001.

From bbc