Sprinkled in tissues throughout the body, from just below the surface of the skin to deep redoubts like the liver and bone marrow, adult stem cells are not, critics say, the answer to every ill. "For certain diseases, adult cells appear very promising, for hepatic and cardiac diseases in particular," says Ronald McKay, a researcher at the National Institutes of Health. "However, if you're asking for a solution to Parkinson's disease or diabetes, I would say the cells that offer the best way are fetal and embryonic." Still, in the unforgiving crucible of clinical studies, where medical potential meets the fickle realities of the human body, adult stem cells are already being tested, while the initial use of embryonic stem cells in humans is perhaps three to five years away.
While a number of biotech companies have adult stem cell research programs, Osiris has been especially aggressive about taking the cells into human trials. Since 1999, for example, doctors working with the company have been testing the ability of mesenchymal stem cells derived from bone marrow to help patients with cancer more quickly rebuild their blood and immune systems, which can be damaged by chemotherapy. In these studies, the mesenchymal stem cells were intended to enhance traditional bone marrow or umbilical-cord-blood transplants. "What we can say so far," says University of Minnesota professor of pediatrics John E. Wagner, who heads one of the studies, "is that we have seen no negative side effects, and we have the impression that it's faster."Recent animal studies emerging from academic labs have underscored the major take-home lesson about adult stem cells in the past year or so: these cells are much more biologically versatile, and capable of adopting many more cellular fates, than anyone previously thought. Last May, pathologist Neil Theise of New York University and stem cell biologist Diane Krause of Yale University and their colleagues published a report in the journal Cell claiming that an adult stem cell from the bone marrow of mice had the capacity to form multiple tissues-blood, lung, liver, stomach, esophagus, intestines and skin. Theise believes these adult stem cells are as flexible as the embryonic kind, and he refers to them as the "ultimate adult stem cell." And a team led by Freda Miller of McGill University in Montral recently published work showing that adult stem cells plucked out of the skin, an easily accessible site for harvest, can develop into fat, muscle and neural cells.
Another similarly surprising wrinkle in the adult stem cell story has emerged in the last year in research at Stanford University and the National Institutes of Health. The lab of Eva Mezey at the National Institute of Neurological Disorders and Stroke, for example, has shown that, in mice, transplanted bone-marrow-derived stem cells can migrate to the brain and develop into cells with characteristics of neurons and other types of brain cells. It is part of a string of intriguing, but far from definitive, experiments suggesting that the fate of adult stem cells is determined to an enormous degree by the local environment in which they are placed.
Skeptics warn that stem cell experiments in mice don't automatically translate into human biology. Still, all these studies reinforce the notion that the adult body maintains a reserve of stem cells, certainly in the bone marrow and probably in many other tissues as well-although the supplies seem to dwindle with age. "They seem to be part of a natural repair system, so that when you damage a tissue, they come from the marrow in large numbers," says Darwin J. Prockop, director of Tulane University's Center for Gene Therapy in New Orleans, LA. In other words, adult stem cells appear to act as the body's on-call, 24-hour-a-day microscopic medical dispensary for wound repair.
http://www.technologyreview.com/Biotech/12643/page2/A DNA sequence is called "sense" if its sequence is the same as that of a messenger RNA copy that is translated into protein.[17] The sequence on the opposite strand is called the "antisense" sequence. Both sense and antisense sequences can exist on different parts of the same strand of DNA (i.e. both strands contain both sense and antisense sequences). In both prokaryotes and eukaryotes, antisense RNA sequences are produced, but the functions of these RNAs are not entirely clear.[18] One proposal is that antisense RNAs are involved in regulating gene expression through RNA-RNA base pairing.[19]
A few DNA sequences in prokaryotes and eukaryotes, and more in plasmids and viruses, blur the distinction between sense and antisense strands by having overlapping genes.[20] In these cases, some DNA sequences do double duty, encoding one protein when read along one strand, and a second protein when read in the opposite direction along the other strand. In bacteria, this overlap may be involved in the regulation of gene transcription,[21] while in viruses, overlapping genes increase the amount of information that can be encoded within the small viral genome
From the foreword by
David S. Nassar, Founder/CEO, MarketWise Trading School L.L.C.
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Many, if not most, diseases have their roots in our genes. Genes - through the proteins they encode - determine how efficiently we process foods, how effectively we detoxify poisons, and how vigorously we respond to infections. More than 4,000 diseases are thought to stem from mutated genes inherited from one's mother and/or father. Common disorders such as heart disease and most cancers arise from a complex interplay among multiple genes and between genes and factors in the environment.
When a gene contains a mutation, the protein encoded by that gene will be abnormal. Some protein changes are insignificant, others are disabling.
http://www.accessexcellence.org/AE/AEPC/NIH/gene05.php
Each type of base on one strand forms a bond with just one type of base on the other strand. This is called complementary base pairing. Here, purines form hydrogen bonds to pyrimidines, with A bonding only to T, and C bonding only to G. This arrangement of two nucleotides binding together across the double helix is called a base pair. The double helix is also stabilized by the hydrophobic effect and pi stacking, which are not influenced by the sequence of the DNA.[12] As hydrogen bonds are not covalent, they can be broken and rejoined relatively easily. The two strands of DNA in a double helix can therefore be pulled apart like a zipper, either by a mechanical force or high temperature.[13] As a result of this complementarity, all the information in the double-stranded sequence of a DNA helix is duplicated on each strand, which is vital in DNA replication. Indeed, this reversible and specific interaction between complementary base pairs is critical for all the functions of DNA in living organisms.[1]
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Martin, a sandy-haired, good-humored senior researcher at Baltimore-based Osiris Therapeutics, has been paying weekly visits to this room for six months. It is a cardiac ward of sorts: all of the pigs in the room have suffered heart attacks. Some of them, however, have subsequently received a highly unusual form of treatment, an injection of stem cells-specifically, an adult form of these versatile progenitor cells isolated from bone marrow. It is Martin's hope that these special cells, known to biologists as adult mesenchymal stem cells, have grown and transformed themselves within the pigs' hearts to form new, healthy tissue right at the site of injury.
Indeed, it is the uncanny ability to zero in on areas of physiological damage and then to organize the process of healing and repair that makes these and other kinds of stem cells so laden with medical possibility. Most of the cells in the body are specialized to perform specific functions in specific tissues, but stem cells-found both in embryos and in various locations in the adult body-can form a number of different tissues and so could in theory be used to treat a vast array of diseases. Rebuilding hearts after heart attacks, regenerating livers ravaged by cirrhosis or viral disease, reconstructing damaged joints, seeding the brain with fresh neurons to reverse the effects of Parkinson's disease and Lou Gehrig's disease-those are just some of the fantastic medical promissory notes that doctors predict these remarkably potent cells will ultimately redeem.
Still, a professional rivalry has emerged between researchers who think stem cells derived from embryos have the greatest medical promise and those who are instead betting on cells derived from adult tissues. Embryonic stem cells are able to form more than 200 separate and distinct tissues, while adult stem cells are "multipotent," able to form just a limited number of tissues; the Osiris cells, for example, have only six possible fates. But because of their controversial origins in embryos left over from in vitro fertilization, embryonic stem cells have met fierce public opposition from religious and political conservatives that has slowed funding and research opportunities. And while President George W. Bush's August decision to allow limited federal funding for embryonic stem cell research could help open the field, its political future remains murky.
While this public drama has been playing out, embryonic stem cells' supposedly less potent and seemingly less glamorous biological cousins, the adult stem cells, have quietly been writing a fascinating story of their own-a story that in many ways is more advanced, clinically and commercially, than the embryonic stem cell story. While federal funding bans and policy debates have relegated human embryonic stem cell research to labs at a handful of companies, in the parallel universe of adult stem cell research has come great progress, with both companies and academic scientists publishing one striking finding after another. On the strength of those studies, a number of human trials using adult stem cells have been launched in the past two years, with several more high-profile experimental treatments scheduled to begin human testing within the next year.
http://www.technologyreview.com/Biotech/12643/The DNA sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health, depending on where they occur and whether they alter the function of essential proteins. The types of mutations include:
This type of mutation is a change in one DNA base pair that results in the substitution of one amino acid for another in the protein made by a gene.
A nonsense mutation is also a change in one DNA base pair. Instead of substituting one amino acid for another, however, the altered DNA sequence prematurely signals the cell to stop building a protein. This type of mutation results in a shortened protein that may function improperly or not at all.
An insertion changes the number of DNA bases in a gene by adding a piece of DNA. As a result, the protein made by the gene may not function properly.
A deletion changes the number of DNA bases by removing a piece of DNA. Small deletions may remove one or a few base pairs within a gene, while larger deletions can remove an entire gene or several neighboring genes. The deleted DNA may alter the function of the resulting protein(s).
A duplication consists of a piece of DNA that is abnormally copied one or more times. This type of mutation may alter the function of the resulting protein.
This type of mutation occurs when the addition or loss of DNA bases changes a gene’s reading frame. A reading frame consists of groups of 3 bases that each code for one amino acid. A frameshift mutation shifts the grouping of these bases and changes the code for amino acids. The resulting protein is usually nonfunctional. Insertions, deletions, and duplications can all be frameshift mutations.
Nucleotide repeats are short DNA sequences that are repeated a number of times in a row. For example, a trinucleotide repeat is made up of 3-base-pair sequences, and a tetranucleotide repeat is made up of 4-base-pair sequences. A repeat expansion is a mutation that increases the number of times that the short DNA sequence is repeated. This type of mutation can cause the resulting protein to function improperly.
Although each cell contains a full complement of DNA, cells use genes selectively. Some genes enable cells to make proteins needed for basic functions; dubbed housekeeping genes, they are active in many types of cells. Other genes, however, are inactive most of the time. Some genes play a role in early development of the embryo and are then shut down forever. Many genes encode proteins that are unique to a particular kind of cell and that give the cell its character - making a brain cell, say, different from a bone cell. A normal cell activates just the genes it needs at the moment and actively suppresses the rest.
Nucleases are enzymes that cut DNA strands by catalyzing the hydrolysis of the phosphodiester bonds. Nucleases that hydrolyse nucleotides from the ends of DNA strands are called exonucleases, while endonucleases cut within strands. The most frequently-used nucleases in molecular biology are the restriction endonucleases, which cut DNA at specific sequences. For instance, the EcoRV enzyme shown to the left recognizes the 6-base sequence 5′-GAT|ATC-3′ and makes a cut at the vertical line. In nature, these enzymes protect bacteria against phage infection by digesting the phage DNA when it enters the bacterial cell, acting as part of the restriction modification system.[78] In technology, these sequence-specific nucleases are used in molecular cloning and DNA fingerprinting.
Enzymes called DNA ligases can rejoin cut or broken DNA strands.[79] Ligases are particularly important in lagging strand DNA replication, as they join together the short segments of DNA produced at the replication fork into a complete copy of the DNA template. They are also used in DNA repair and genetic recombination.
In late 2003, researchers at Advanced Cell Technology, a small biotech startup in Worcester, MA, thought they were about to do something remarkable. They had painstakingly generated cloned human embryos from adult cells and were trying to keep them alive long enough to harvest their inner cell masses, precious balls of cells that give rise to stem cells.
It was one of the most sought-after prizes of biomedical research: a way to grow embryonic stem cells directly from, say, a skin cell taken from a specific patient. It was also one of biomedicine's most speculative projects; indeed, the scientists at Advanced Cell Technology (ACT) were the only team in the United States actively pursuing it. But Robert Lanza (see "Stem Cell Hope"), who headed the group, says he believes that his team at ACT was on the verge of success. If he's right, and if the work had continued, the company would almost certainly have had in its hands the key to a revolutionary new set of biomedical tools -- and possibly to new treatments for a host of different diseases.
But in February 2004, the ACT scientists' hopes were dashed. A South Korean stem cell scientist named Hwang Woo Suk of Seoul National University and his colleagues announced in the journal Science that they had created patient-specific stem cells. The achievement vaulted Hwang to scientific stardom. His country named him its "supreme scientist" and honored him with a postage stamp depicting a paralyzed man able to walk again. Patients clamored to be part of his work. Hwang embraced his role as an international stem cell celebrity, announcing plans to create something called the World Stem Cell Hub, where members of his lab would clone and culture stem cell lines for scientists around the globe.
"What had been a terribly risky field that many scientists were loath to venture into now became a possibility," says Evan Snyder, director of the Stem Cells and Regeneration Program at the Burnham Institute for Medical Research in La Jolla, CA. Many U.S. researchers who had been unable or unwilling to start cloning work themselves began planning collaborations with the Korean scientists. "We knew [cloning] would take a lot of time and money, and the Korean government was willing to throw so much at this one problem," says Snyder. "When that seemed to have been accomplished, many of us said, Well, that's a relief. Now we can do the real science experiments."
However, Lanza and his colleagues, who had been so close to cloning stem cells, watched dejectedly. "It was embarrassing," says Lanza. "This obscure group announced they had done it." ACT was already on shaky financial ground, but Hwang's achievement made its situation even more precarious. The company also abruptly lost its supply of human eggs -- a crucial ingredient in cloning research -- because clinics that ran donor programs felt no further need to participate in research whose central goal had been achieved. As a result, the scientists literally had to put their work on ice. "We had to freeze down lots of our cells. It shut down that research, and there has been no active research since," says Lanza. There was, plainly, no glory -- or profits -- in coming in second.
http://www.technologyreview.com/Biotech/16813/
To function correctly, each cell depends on thousands of proteins to do their jobs in the right places at the right times. Sometimes, gene mutations prevent one or more of these proteins from working properly. By changing a gene’s instructions for making a protein, a mutation can cause the protein to malfunction or to be missing entirely. When a mutation alters a protein that plays a critical role in the body, it can disrupt normal development or cause a medical condition. A condition caused by mutations in one or more genes is called a genetic disorder.
In some cases, gene mutations are so severe that they prevent an embryo from surviving until birth. These changes occur in genes that are essential for development, and often disrupt the development of an embryo in its earliest stages. Because these mutations have very serious effects, they are incompatible with life.
It is important to note that genes themselves do not cause disease—genetic disorders are caused by mutations that make a gene function improperly. For example, when people say that someone has “the cystic fibrosis gene,” they are usually referring to a mutated version of the CFTR gene, which causes the disease. All people, including those without cystic fibrosis, have a version of the CFTR gene.
http://ghr.nlm.nih.gov/handbook/mutationsanddisorders/mutationscausedisease
Genes are working subunits of DNA. DNA is a vast chemical information database that carries the complete set of instructions for making all the proteins a cell will ever need. Each gene contains a particular set of instructions, usually coding for a particular protein.
DNA exists as two long, paired strands spiraled into the famous double helix. Each strand is made up of millions of chemical building blocks called bases. While there are only four different chemical bases in DNA (adenine, thymine, cytosine, and guanine), the order in which the bases occur determines the information available, much as specific letters of the alphabet combine to form words and sentences.
DNA resides in the core, or nucleus, of each of the body's trillions of cells. Every human cell (with the exception of mature red blood cells, which have no nucleus) contains the same DNA. Each cell has 46 molecules of double-stranded DNA. Each molecule is made up of 50 to 250 million bases housed in a chromosome.
The DNA in each chromosome constitutes many genes (as well as vast stretches of noncoding DNA, the function of which is unknown). A gene is any given segment along the DNA that encodes instructions that allow a cell to produce a specific product - typically, a protein such as an enzyme - that initiates one specific action. There are between 50,000 and 100,000 genes, and every gene is made up of thousands, even hundreds of thousands, of chemical bases.
Human cells contain two sets of chromosomes, one set inherited from the mother and one from the father. (Mature sperm and egg cells carry a single set of chromosomes.) Each set has 23 single chromosomes - 22 autosomes and an X or Y sex chromosome. (Females inherit an X from each parent, while males get an X from the mother and a Y from the father.)
For a cell to make protein, the information from a gene is copied, base by base, from DNA into new strands of messenger RNA (mRNA). Then mRNA travels out of the nucleus into the cytoplasm, to cell organelles called ribosomes. There, mRNA directs the assembly of amino acids that fold into completed protein molecule.
Each human cell contains 23 pairs of chromosomes, which can be distinguished by size and by unique banding patterns. This set is from a male, since it contains a Y chromosome. Females have two X chromosomes.
Different genes are activated in different cells, creating the specific proteins that give a particular cell type its character.
http://www.accessexcellence.org/AE/AEPC/NIH/gene03.php
All the functions of DNA depend on interactions with proteins. These protein interactions can be non-specific, or the protein can bind specifically to a single DNA sequence. Enzymes can also bind to DNA and of these, the polymerases that copy the DNA base sequence in transcription and DNA replication are particularly important.
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Structural proteins that bind DNA are well-understood examples of non-specific DNA-protein interactions. Within chromosomes, DNA is held in complexes with structural proteins. These proteins organize the DNA into a compact structure called chromatin. In eukaryotes this structure involves DNA binding to a complex of small basic proteins called histones, while in prokaryotes multiple types of proteins are involved.[64][65] The histones form a disk-shaped complex called a nucleosome, which contains two complete turns of double-stranded DNA wrapped around its surface. These non-specific interactions are formed through basic residues in the histones making ionic bonds to the acidic sugar-phosphate backbone of the DNA, and are therefore largely independent of the base sequence.[66] Chemical modifications of these basic amino acid residues include methylation, phosphorylation and acetylation.[67] These chemical changes alter the strength of the interaction between the DNA and the histones, making the DNA more or less accessible to transcription factors and changing the rate of transcription.[68] Other non-specific DNA-binding proteins found in chromatin include the high-mobility group proteins, which bind preferentially to bent or distorted DNA.[69] These proteins are important in bending arrays of nucleosomes and arranging them into more complex chromatin structures.[70]
A distinct group of DNA-binding proteins are the single-stranded-DNA-binding proteins that specifically bind single-stranded DNA. In humans, replication protein A is the best-characterised member of this family and is essential for most processes where the double helix is separated, including DNA replication, recombination and DNA repair.[71] These binding proteins seem to stabilize single-stranded DNA and protect it from forming stem-loops or being degraded by nucleases.
In contrast, other proteins have evolved to specifically bind particular DNA sequences. The most intensively studied of these are the various classes of transcription factors, which are proteins that regulate transcription. Each one of these proteins bind to one particular set of DNA sequences and thereby activates or inhibits the transcription of genes with these sequences close to their promoters. The transcription factors do this in two ways. Firstly, they can bind the RNA polymerase responsible for transcription, either directly or through other mediator proteins; this locates the polymerase at the promoter and allows it to begin transcription.[73] Alternatively, transcription factors can bind enzymes that modify the histones at the promoter; this will change the accessibility of the DNA template to the polymerase.[74]
As these DNA targets can occur throughout an organism's genome, changes in the activity of one type of transcription factor can affect thousands of genes.[75] Consequently, these proteins are often the targets of the signal transduction processes that mediate responses to environmental changes or cellular differentiation and development. The specificity of these transcription factors' interactions with DNA come from the proteins making multiple contacts to the edges of the DNA bases, allowing them to "read" the DNA sequence. Most of these base-interactions are made in the major groove, where the bases are most accessible.[76]
http://en.wikipedia.org/wiki/DNA
| Type of Camera | Compact digital camera |
| Effective Pixels | 10.0 million |
| Image Size (Pixels) | 3648 x 2736 (High: 3648 / Normal: 3648), 2592 x 1944 (Normal: 2592), 2048 x 1536 (Normal: 2048), 1024 x 768 (PC: 1024), 640 x 480 (TV: 640), 1920 x 1080 (16:9) |
| Lens | 5x Zoom-Nikkor; f/3.5-5.6 |
| Vibration Reduction | Electronic VR |
| Digital Zoom | Up to 4x |
| Focus Range | Normal mode: 35cm, Macro mode: 10 cm |
| LCD Monitor | 2.5"; 230,000-dot, wide viewing angle TFT LCD with anti-reflection coating |
| Storage Media | SD memory cards and internal memory (approx. 50MB) |
| File Format | Compressed JPEG, motion JPEG AVI, mono/wav file |
| Shooting Modes | Auto, Smile, Scene modes, High sensitivity, movie modes |
| Scene Modes | Portrait, Landscape, Sports, Night portrait, Party/indoor, Beach/snow, Sunset, Dusk/dawn, Night landscape, Close-up, Panorama assist, Museum, Fireworks show, Copy, Backlight |
| Capture Modes | Single, Continuous (approx. 1.3 fps), BSS (Best Shot Selector), Multi-shot 16 (16 frames in a single burst), Interval timer shooting |
| Video Recording | Yes (with sound) |
| Exposure Metering System | Matrix, Center-weighted, Spot |
| Sensitivity | Auto gain (ISO 64-800), High-sensitivity shooting mode (ISO 64-1600), Manual ISO 64, 100, 200, 400, 800, 1600, 2000 |
| White Balance | Auto, Preset manual, Daylight, Incandescent, Fluorescent, Cloudy, Flash |
| Self-Timer | 2 and 10 sec. duration |
| Flash Sync Modes | Auto, Auto with red-eye reduction, Off, Fill flash, Slow sync |
| Supported Languages | Total of 24 languages |
| Power Requirements | Rechargeable Li-ion Battery EN-EL11 (supplied), AC Adapter EH-62E (optional) |
| Battery Life (on a fully charged battery) | Approx. 200 shots with EN-EL11 battery (based on CIPA standard) |
| Dimensions | Approx. 90 x 53.5 x 22 mm excluding projections |
| Supplied Accessories (may differ by country or area) | Rechargeable Li-ion Battery EN-EL11, Battery Charger MH-64, AV/USB Cable UC-E12, Strap AN-CP14, Software Suite CD-ROM |
| Weight (without batteries and memory card) | Approx. 120 g |
PrimeGen, a small biotech company based in Irvine, CA, says that it has solved one of the major hurdles in using reprogrammed stem cells for human therapies. Last year, scientists announced that they had successfully created embryonic-like stem cells from adult cells, circumventing the ethical and technical hurdles associated with embryonic stem cells. But the method used viruses to deliver genes, raising concerns over cancer risk.
According to an article in Forbes,
PrimeGen claimed Tuesday it had circumvented this problem. Instead of genes, it uses unspecified carbon-based "delivery particles" to insert four proteins into cells to stimulate the reprogramming process. This caused some of the cells to revert to being much like embryonic stem cells, PrimeGen said. PrimeGen said it has done the experiment with retinal, skin and testicular cells.
"Our goals are ambitious--we believe with this therapy, we can be in clinic in 2010," said PrimeGen president John Sundsmo in an interview. He said he couldn't release details on what the delivery particles are until the company finalizes an agreement with a corporate partner.
However, some scientists are skeptical. Rather than being published in a peer-reviewed scientific journal, the findings were released during a brief presentation at a stem-cell industry conference in New York.
According to Forbes,
Many outside scientists said they weren't familiar with the work and weren't quite sure what to think. "Until the work goes through [peer-review], it would be difficult to evaluate," says James Thomson, the researcher at University of Wisconsin, Madison, who created the first embryonic stem cells in 1998. George Daley, of Harvard University, said he was "pretty suspicious of publication by press release."
Nonetheless, "if this is real it really is a significant step," says Arnold Kriegstein, director of the Institute for Regenerative Medicine at U.C.-San Francisco. "They could be on to something."
A gene mutation is a permanent change in the DNA sequence that makes up a gene. Mutations range in size from a single DNA building block (DNA base) to a large segment of a chromosome.
Gene mutations occur in two ways: they can be inherited from a parent or acquired during a person’s lifetime. Mutations that are passed from parent to child are called hereditary mutations or germline mutations (because they are present in the egg and sperm cells, which are also called germ cells). This type of mutation is present throughout a person’s life in virtually every cell in the body.
Mutations that occur only in an egg or sperm cell, or those that occur just after fertilization, are called new (de novo) mutations. De novo mutations may explain genetic disorders in which an affected child has a mutation in every cell, but has no family history of the disorder.
Acquired (or somatic) mutations occur in the DNA of individual cells at some time during a person’s life. These changes can be caused by environmental factors such as ultraviolet radiation from the sun, or can occur if a mistake is made as DNA copies itself during cell division. Acquired mutations in somatic cells (cells other than sperm and egg cells) cannot be passed on to the next generation.
Mutations may also occur in a single cell within an early embryo. As all the cells divide during growth and development, the individual will have some cells with the mutation and some cells without the genetic change. This situation is called mosaicism.
Some genetic changes are very rare; others are common in the population. Genetic changes that occur in more than 1 percent of the population are called polymorphisms. They are common enough to be considered a normal variation in the DNA. Polymorphisms are responsible for many of the normal differences between people such as eye color, hair color, and blood type. Although many polymorphisms have no negative effects on a person’s health, some of these variations may influence the risk of developing certain disorders.
http://ghr.nlm.nih.gov/handbook/mutationsanddisorders/genemutation
| Type of Camera | Compact digital camera |
| Effective Pixels | 10.0 million |
| Image Size (Pixels) | 3648 x 2736 (High: 3648/Normal: 3648), 3072 x 2304 (Normal: 3072), 2592 x 1944 (Normal: 2592), 2048 x 1536 (Normal: 2048), 1024 x 768 (PC: 1024), 640 x 480 (TV: 640) |
| Lens | 4x Zoom-Nikkor; f/2.7-5.8 |
| Vibration Reduction | Optical lens shift VR |
| Digital Zoom | Up to 4x |
| Focus Range | Normal mode: 50cm, Macro mode: 3 cm |
| LCD Monitor | 2.7"; 230,000-dot, wide viewing angle TFT LCD with anti-reflection coating |
| Storage Media | SD memory cards and internal memory (approx. 45MB) |
| File Format | Compressed JPEG, AVI, mono/wav file |
| Shooting Modes | Auto, scene modes, high-sensitivity shooting mode, BSS (best shot selector), Color options, Date imprint |
| Scene Modes | Portrait, Landscape, Sports, Night portrait, Party/indoor, Beach/snow, Sunset, Dusk/dawn, Night landscape, Close-up, Museum, Copy, Back light, Active child |
| Capture Modes | Single, Continuous (approx.1.0fps) |
| Video Recording | Yes (with sound) |
| Exposure Metering System | Matrix metering, Center-weighted metering |
| Sensitivity | Auto (auto gain ISO 100-800), Manual selection: ISO 100, 200, 400, 800, 1600, 3200, High-Sensitivity mode (ISO 100-2000) |
| White Balance | Auto, Preset manual, Daylight, Incandescent, Fluorescent, Cloudy, Flash |
| Self-Timer | 2 and 10 sec. duration |
| Flash Sync Modes | Auto, Auto with red-eye reduction, Off, Fill flash, Slow sync |
| Supported Languages | Total of 23 languages |
| Power Requirements | Rechargeable Li-ion Battery EN-EL10 (supplied), AC Adapter EH-62D (optional) |
| Battery Life (on a fully charged battery) | Approx. 190 shots with EN-EL10 battery (based on CIPA standard) |
| Dimensions | Approx. 88.5 x 53 x 22.5 mm excluding projections |
| Supplied Accessories (may differ by country or area) | Rechargeable Li-ion Battery EN-EL10, Battery Charger MH-63, USB Cable UC-E6, Audio Video Cable EG-CP14, Strap AN-CP14, AC power cord PW-EH30, Software Suite CD-ROM |
| Weight (without batteries and memory card) http://www.nikon.com.sg/productitem.php?pid=1227-6a0929c8d3 | Approx. 130 g |
 |
| Commodity genomics: The Polonator, at top, is an inexpensive sequencing machine developed by George Church’s lab at Harvard Medical School and by Danaher Motion, an instrument company in Salem, NH. At bottom are genetic markers with fluorescent tags that glow red, green, yellow, and blue. Each marker is bound to a single base on a fragment of DNA. During a sequencing run, the Polonator captures and analyzes 5.7 million such images to generate the sequence of each fragment. Credit: Danaher Motion-Dover |
An inexpensive new gene-sequencing machine is due to hit the market next month, and its creators hope that it will make sequencing more common, ultimately giving a boost to personalized medicine. The machine is the brainchild of George Church, a genomics pioneer who developed the first direct sequencing technology as a graduate student in the 1980s and helped initiate the Human Genome Project soon after.
Church sees greater access to sequencing as a vital component in the drive toward personalized medicine, in which treatments and preventative medicine are tailored to an individual's genetic makeup. The new machine, which was developed with an "open source" philosophy, was commercialized by Danaher Motion, based in Salem, NH, with the specific intent of keeping costs low. "It seems like the biomedical-instrument field in general tries not to commoditize," says Church, who heads the Center for Computational Genetics at Harvard Medical School, in Boston. "It tries to keep profit margins high and slow the inevitable decrease in cost." The Danaher device will cost roughly $150,000, a third to a tenth of the cost of systems currently on the market.
The technology will become an integral part of Church's other brainchild, the Personal Genome Project, an effort to enable personalized medicine by providing a test bed for new genomics technologies and analytic tools. Church and his collaborators are using the new device to sequence the genomes of the project's first 10 volunteers, who will share their genome sequences, medical records, and other personal information with both scientists and the public. Church hopes that, ultimately, thousands of people or more will have their genomes sequenced as part of the project, and that the result will be a huge compendium of data that is useful to both the volunteers themselves and to the research community. "Part of the goal of this project is as a bridge between the research market, which is small, and the consumer market," says Church.
Church's group has spent the past several years developing prototypes of the sequencing device--known as the Polonator--from off-the-shelf components. Church originally planned to create an instruction manual for building a Polonator from scratch and post it on the Internet, but he ultimately decided that it would be more effective to develop a commercial device. His team partnered with Danaher Motion, a precision-instrument maker that built movable microscope stages for earlier versions of the technology. Over the past year, Danaher has worked with Church to develop the cheapest and most robust system possible.
The device is a commercial version of the polony sequencing approach developed in Church's lab over the past 10 years. Millions of beads coated with small fragments of the DNA to be sequenced are spread on a glass slide. Next, a series of fluorescently labeled DNA bases bind to the fragments. Finally, a standard fluorescence microscope reveals which base is at each position on a fragment. (The commercial version of the technology can accommodate a billion beads and has a more sophisticated imaging instrument.)
While the scientists don't yet have the final figures on the Polonator's accuracy and throughput, they expect that it will sequence 10 billion base pairs in a single 80-hour run, a capacity equal to or greater than that of currently available technologies. Harvard and MIT's jointly run Broad Institute for genomic medicine, in Cambridge, MA, and the Max Planck Institute, in Germany, have already purchased devices at the $150,000 sticker price, and the machines should be delivered within the next week or two. General availability is expected by mid- to late May.
Despite almost no marketing, the Polonator has already created a buzz in the research community. McCarthy brought a prototype to a sequencing conference in Florida earlier this year and says that people were lined up to see it until the early hours of the morning. Last week, scientists at a genome-sequencing conference in San Diego, where McCarthy gave his first public presentation on the technology, found the concept intriguing. One of those in attendance was Vladimir Benes, head of the genomics core facility at the European Molecular Biology Laboratory, in Heidelberg, Germany. "It's definitely in the spirit of George Church to make technology as accessible as possible and let the community do what they like," Benes said at the time.
Patrice Milos, chief scientific officer at Helicos BioSciences, a company based in Cambridge, MA, that has just released its own sequencing machine, had a more muted reaction. "As with any technology, it's seeing what they can deliver that matters," Milos said.
The Polonator embodies an open-source philosophy. It was designed so that users can tinker with it in any way they wish. All the parts can be swapped out, and scientists can use enzymes and chemicals other than those sold by Danaher for the sequencing process. Church and others are already working on alternative chemical processes that could make the instrument more efficient. "The fact that it's open source is great," says Andrew Barry, supervisor of process development at the Broad Institute. "It's going to be a community-driven instrument."
Church believes that sequencing will ultimately be a more effective personalized-medicine tool than the microarray technologies currently on the market. (Several companies now offer chips studded with small pieces of DNA that can be used to detect specific genetic variations linked to disease.) By looking at the entire genome, sequencing is able to identify mutations that microarrays cannot. "Sequencing is turning out to be as cost effective at most things as chips are now," Church says. "And you can do things with sequencing you can't do with chips."
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