Steve Potter of Georgia Institute of Technology has built a hybrid rat neuron robot called a hybrot.
In his experiment, Potter places a droplet of solution containing thousands of rat neuron cells onto a silicon chip that’s embedded with 60 electrodes connected to an amplifier. The electrical signals that the cells fire at one another are picked up by the electrodes which then send the amplified signal into a computer. The computer, in turn, wirelessly relays the data to the robot.
Endless science fiction parallels come to mind. How about the Star Trek original series episode where Spock's brain was stolen in order to use it run a planet? Rolf Pfeifer of the University of Zurich, Switzerland foresees the use of neurons to make self-healing computer systems. Neuronal stem cells could be induced to form new connections to repair damage. Picture hybrot battlebots that would be silicon-biological hybrids that would be extremely difficult to kill.
If human neurons were used to make hybrots then how many neurons would it have to have before we'd hear demands for the recognition of hybrot rights? But if the hybrots were designed to desire to kill a large portion of humanity how could they be granted rights?
Existing computational paradigms do not approach the capabilities of even simple organisms in terms of adaptability and real-time control. There are computational mechanisms and network architectures in living neural systems that are missing from even the most sophisticated artificial computing systems. This project consists of the development of computational systems that incorporate both living neuronal networks and artificial elements, including robotic testbeds and signal-processing circuitry. These hybrid neuronal-robotic systems (‘Hybrots’) will provide a platform for discovering, exploring, and using the computational dynamics of living neuronal networks to perform real-time tasks in the physical world. Cultured networks of molluscan and mammalian neurons will be interfaced to robotic systems via multi-electrode array substrates capable of distributed, spatio-temporal stimulation and recording of neural activity. Unlike brains in animals, in vitro networks are amenable to detailed observation and manipulation of every cell in the network. Both high-speed optical recording, and time-lapse microscopy will be employed. By embodying the networks with actuators and sensors, the dynamical attractor landscape of neuronal networks will be studied under the conditions for which they evolved: continuous real-time feedback for adaptive behavioral contr
"We call it the 'Hybrot' because it is a hybrid of living and robotic components," he said. "We hope to learn how living neural networks may be applied to the artificial computing systems of tomorrow. We also hope that our findings may help cases in which learning, memory, and information processing go awry in humans."
The team uses networks of cultured rodent brain cells as the Hybrot's brain, and has essentially given the cultured neural networks a body in the form of a mobile robot. Potter's group hopes the research will lead to advanced computer systems that could some day assist in situations where humans have lost motor control, memory or information processing abilities. The neural interfacing techniques they are developing could be used with prosthetic limbs directly controlled by the brain. Advances in neural control and information processing theory could have application, for example, in cars that drive themselves or new types of computing architectures.
Inside Potter's lab, a droplet containing a few thousand living neurons from rat cortex is placed on a special glass petri dish instrumented with an array of 60 micro-electrodes. The neurons are kept alive in an incubator for up to two years using a new sealed-dish culture system that Potter developed and patented. The neural activity recorded by the electrodes is transmitted to the robot, the Khepera, made by K-Team S.A, which serves as the body of the cultured networks. It moves under the command of neural activity that is being transmitted to it, and information from the robot's sensors is sent back to the cultured net in the form of electrical stimuli.
Central to the experiments is Potter's belief that over time, the team will be able to establish a living network system that learns like the human brain.
Check out the UCSC Human Genome Browser Gateway. As an example type AA205474 into the position field and then click on Submit. Then click on one of the BRCA1 occurrences on the left side column. This will bring up a page that includes "Links to sequence". Choose the Genome Sequence link and then choose Submit on the next page. That should finally take you to the BRCA1 gene sequence. Some variants of BRCA1 are linked to an increased risk of breast cancer.
The enormous weight of lead-acid batteries and limited range of electric cars illustrate the importance of energy density in energy storage technologies.
Researchers at the US Naval Undersea Warfare Center Division have developed a semi-fuel cell, which is a high energy density source for underwater vehicle applications with energy densities approaching 6 to 7 times that of silver-zinc batteries. The new electrochemical system is based on a magnesium anode, a seawater/catholyte electrolyte and an electrocatalyst of palladium and iridium catalyzed on carbon paper.
To put this in perspective compare some of other battery technologies currently in use:
Long a mainstay for undersea vehicle programs, the lead acid battery has been used because of its low cost, known performance, reliability and reasonable cycle life. Its principal disadvantages are low specific energy (30 Wh/kg) and energy density (65 Wh/litre), loss of capacity at low temperatures and the production of hydrogen gas during charges as well as high rate discharges. Nickel cadmium batteries have a specific energy (30 Wh/kg) and energy density (75 Wh/litre) that are comparable to lead acid. Their cost, performance, reliability and cycle life are also comparable. Unlike lead acid batteries, however, cold temperatures do not degrade their performance significantly. A major limitation of the nickel cadmium battery is memory effect, requiring more stringent battery management.
Until recently, the silver-zinc battery has been the battery of choice for long range missions. Silver-zinc batteries are available off-the-shelf and have a higher specific energy (130 Wh/kg) and density (240 Wh/litre) than most other commonly available secondary batteries. High cost, limited cycle and shelf life, and a long recharging process reduce its overall attraction. While at normal discharge rates, 40 to 50 cycles can be expected from the battery, this reduces to 10 or 15 at high discharge rates. Cycle life is also reduced if the battery is discharged below 80% of rated capacity and thus, a 20% reserve is required at the end of the mission. Silver-zinc batteries have been used extensively in AUVs and their performance is reliable and documented. Their high cost and short life have, however, prompted consideration of alternative technologies.
Note that the high cost and short life-time of the silver-zinc battery has restricted its use to specialty applications such as underwater vehicles. Its not clear what the lifetime would be for the Navy semi-fuel cell. Still, its energy density greatly surpasses than of any type of battery that turned up on some Google searches.
Forbes has a nice write-up on the microfluidic chip designs of Cal Tech biophysicist Stephen R. Quake
He and his group, along with Caltech's Axel Scherer, added a few clever twists. His chips, the size of a half-dollar or smaller, are made with two layers of rubber, relying on a technique similar to injection molding used to make toys. The bottom layer has hundreds or thousands of tiny intersecting liquid-handling channels, each about the width of a human hair (100 microns). The top layer contains hundreds of control channels through which pressurized water is pumped. Valves are formed where the control channels cross over the fluid channels. When pressurized water is fed over such an intersection, the pressure pushes down the thin layer of rubber, separating it from the fluid below, and it clamps shut the fluid channel below, like stepping on a hose. Quake's lab can make the chips with $30 bottles of rubber, an ultraviolet light to create molds and a convection oven to cure the rubber. A grad student can design and make a new chip in less than two days.
Quake predicts that his chips will have 100 times the number of cells and valves in a few years. These chips will be used for handheld instant blood chemistry testers, mini DNA sequences that are orders of magnitude smaller and cheaper than today's models, mini-labs for analysing the state of single cells, for testing large numbers of drugs against large numbers of cells in parallel, and countless other biochemical tasks that can be made orders of magnitude less expensive and less time-consuming.
Quake's chip technology is being commercialized by venture capital start-up Fluidigm. They have a picture of one of the chips on their web site. Fluidigm is developing this technology to lower the cost of polymerase chain reaction (PCR) which is widely used for DNA sequencing.
South San Francisco, CA, September 26, 2002 - Fluidigm Corporation and The California Institute of Technology announced today major advancements in complexity and function of microfluidic device technology. Using its novel fabrication technology, the MSL™(multi-layer soft lithography) process, Fluidigm has demonstrated a fluidic microprocessor that can run 20,000 PCR assays at sub-nanoliter volumes, the smallest documented volume of massively parallel PCR assays. This technology is being developed in the near term to run over 200,000 parallel assays. Fluidigm believes this fluidic architecture will make significant contributions in cancer detection research as well as in large scale genetic association studies.
At the same time, a group led by Dr. Stephen Quake, Associate Professor in the Department of Applied Physics at the California Institute of Technology and co-founder of Fluidigm, published an article in Science today describing a paradigm for large scale integration of microfluidic devices. These devices are capable of addressing and recovering the contents from one among thousands of individual picoliter chambers on the microfluidic chip.
Using new techniques of multiplexed addressing, Quake's group built chips with as many as 6,000 integrated microvalves and up to 1000 individually addressable picoliter chambers. These chips were used to demonstrate microfluidic memories and tools for high throughput screening. Additionally, on a separate device with over 2000 microvalves, they demonstrated the ability to load two different reagents and perform distinct assays in 250 sub-nanoliter reaction chambers and then recover the contents.
"We now have the tools in hand to design complex microfluidic systems and, through switchable isolation, recover contents from a single chamber for further investigation. These next-generation microfluidic devices should enable many new applications, both scientific and commercial," said Dr. Quake.
"Together, these advancements speak to the power of MSL technology to achieve large scale integration and the ability to make a commercial impact in microfluidics," said Gajus Worthington, President and CEO of Fluidigm. "PCR is the cornerstone of genomics applications. Fluidigm's microprocessor, coupled with the ability to recover results from the chip, offers the greatest level of miniaturization and integration of any platform," added Worthington.
Fluidigm hopes to leverage these advancements as it pursues genomics and proteomics applications. Fluidigm has already shipped a prototype product for protein crystallization that transforms decades-old methodologies to a chip-based format, vastly reducing sample input requirements and improving cost and labor by orders of magnitude.
Note as well Fluidigm's development of a prototype to automate protein crystallization which is used for the determination of 3 dimensional structure of proteins. Fluidigm is selling their Topaz prototype protein crystallization kit and they list the following benefits for it:
There are countless uses for smaller cheaper mini chemistry labs. As this technology advances it will accelerate the rate of advance of biological science and biotechnology literally by orders of magnitude. The impact will be greater than the impact of computers to date because it will make possible the cure of diseases, the reversal of aging and the enhancement of human intellectual and physical performance.
Jeanne Kwik and others at the Johns Hopkins Center for Civilian Biodefense Strategies have written a paper examining the threat that terrorists will be able to uses advances in biotechnology to make biological weapons of mass destruction.
December 20, 2002
Researchers Warn Biotech Advances Could Be Misused By Terrorists
Center for Civilian Biodefense Strategies Urges Oversight of Scientific Information
The same scientific advances in biotechnology, genetics, and medicine that are intended to improve life could also be used to develop biological weapons capable of causing mass destruction, according to researchers from the Johns Hopkins Bloomberg School of Public Health’s Center for Civilian Biodefense Strategies. They urge governments and the scientific community to adopt a system of checks and balances to prevent the misappropriation of scientific discoveries and technology. Their analysis is outlined in an article published in the January 2003 edition of the journal Biosecurity and Bioterrorism.
The Hopkins researchers call the potential misapplication of science the “Persephone effect,” named after the Greek myth of an innocent girl who was kidnapped and forced to share her time between Hades and Earth. The myth accounts for the change of the seasons and the annual cycle of growth and decay.
“Biology, medicine, agriculture, and other life sciences were always considered the ‘good’ sciences, but like Persephone they could be used to bring death and destruction in the form of biological weapons,” explained lead author Gigi Kwik, PhD, a fellow with the Johns Hopkins Center for Civilian Biodefense Strategies and assistant scientist in the Department of Health Policy and Management at the Johns Hopkins Bloomberg School of Public Health.
According to Dr. Kwik and her colleagues, recent advances in aerosol technology, microbiology, and genetics are areas of concern. In the article, they noted that the same aerosol technology used to develop inhaled insulin for the treatment of diabetes could also be used to push anthrax or other large molecules past the lung’s immune system and deep into the airways where they can cause disease. Antibiotic-resistant strains of bacteria help scientists determine which antibiotic therapies will be most effective in treating an illness, but former Soviet bioweapons builders are suspected using this technology to develop antibiotic-resistant forms of plague, anthrax, and tularemia. Last year, Australian researchers inadvertently created a lethal form of mousepox by adding a single gene to the virus, and this year scientists in the United States were able to create polio virus from scratch by assembling pieces of DNA. The Hopkins researchers suggest these technologies could make harmless unregulated organisms dangerous and render obsolete current policies to restrict access to dangerous pathogens.
Technology is just a way of doing things. It can be used for good or ill. But we appear to be reaching a stage of technological development where it is becoming easier for relatively small groups to use technology for tremendous ill. One of the characteristics of advanced technology is that it lets us more easily do more complex manipulations of matter. Technology advances to first make a previously impossible task possible to do if one has a great deal of money and highly skilled workers. So, for instance, it look most of the best physicists on the planet and the resources of the richest nation to build the first nuclear bomb. But as technology advances further the difficulty diminishes. It takes less money, fewer people, and less skilled people to accomplish some task because more advanced technologies are available to help do it. We can see the consequence of this for nuclear bomb development where much smaller and poorer nations can build nuclear bombs using less resources and fewer and less able scientists.
One of my greatest worries for the 21st century is that technological advances will shift the battlefield in favor of effectively anonymous attackers (i.e. attackers who attempt to blend into the societies that they attack and who are rarely seen operating as fighters). Such attackers may not even choose to operate as terrorists because death rather than terror may be their main objective. This trend could run so far that civilization will be very difficult or perhaps even impossible to defend.
This threat looks set to grow larger with time. The more that biological science and biotechnology advance the easier it will be to modify pathogens to make them more lethal and to create delivery systems that are more effective at getting pathogens into humans and into agricultural plants and livestock. Technology makes things easier to do. The problem is that the ability to attack may well advance more rapidly than the ability to defend. There have been periods in history when technological advances shifted the balance in favor of the defenders (eg in the modern era machine guns contributed to the trend near the end of the US Civil War when trench warfare began and then in WWI trench warfare reached its widest application) and other periods in history when technological advances shifted the balance back in favor of the attackers (eg the maturation of the tank helped to end the era of trench warfare after WWI).
For most of the modern era even when the state of technology has favored attackers it favored large state attackers. Civilization could still organize itself around the most powerful states. But what happens if we find ourselves in a situation where it becomes incredibly easy for small groups to build devices (eg mini-nukes or bioweapons) that can cause huge amounts of devastation? Defense may become so much harder than attack that large organized polities may become extremely hard to defend. There may be no technological solution to this problem.
Britain's High Court has barred a couple from creating a 'designer baby' to try to save the life of their sick child.
In a first-of-its-kind ruling, the court said the British Human Fertilisation and Embryology Authority (HFEA) has no legal power to authorise such a treatment, the Guardian reported.
The judge found that UK law prohibits selection for particular genetic qualities in babies.
The case focused on a decision by the Human Fertilisation and Embryology Authority (HFEA) to allow Raj and Shahana Hashmi, from Leeds, to select an embryo to provide a life-saving transplant for their son, Zain, who has a rare genetic blood disorder. The Hashmis have been trying for a new baby using the technique since July, but will now have to stop.
In his surprise ruling, Mr Justice Maurice Kay said the HFEA had acted beyond its legal powers. Under the 1990 Human Fertilisation and Embryology Act, it could grant licences to clinics "for the purpose of assisting women to carry children" and to ensure embryos were in a suitable condition for that purpose.
Had the Hashmi's succeeded in creating a suitable baby then at birth the stem cells from the baby could have been injected into their existing child Zain.
Neither the couple nor their four other children are bone marrow matches for Zain, who suffers from the rare blood disorder thalassaemia and is expected to die without a transplant. Stem cells taken from the baby's umbilical cord at birth could replace Zain's bone marrow.
By contrast, in the United States this technique is practiced. Recall the story back in 2000 when Jack and Lisa Nash had a daughter Molly who suffered from a genetic disorder called Fanconi anemia. The Nashes elected to have IVF done and an embryo selected that would be free of the disease. Lisa Nash then had an embryo implanted that was free of the Fanconi mutation.
Her parents, Jack and Lisa Nash of Englewood, Colo., wanted more children but were afraid to conceive because both carry a faulty version of the Fanconi gene, meaning each child would have a 25 percent chance of developing the disease.
The Nashes used a process called pre-implantation genetic diagnosis, or PGD: Embryos were created from Lisa Nash's eggs and her husband's sperm. Then the fertilized eggs were analyzed, and when one was found to be disease-free and a tissue match, it was implanted. The couple had to try the procedure several times before she became pregnant.
Lisa then gave birth on August 29,2000 to a healthy baby Adam and used his umbilical stem cells to treat his older sister Molly.
The test tube baby, named Adam, was born in Denver on Aug. 29. Doctors collected cells from his umbilical cord, a painless procedure, and on Sept. 26 infused them into his sister Molly's circulatory system. The girl is recuperating in a Minneapolis hospital, and within about a week doctors should know whether the procedure was successful.
Whether or not the transplant works, doctors and ethicists said, the procedure is both a promising and worrisome harbinger of where scientific advances are taking human reproduction in the near future--at least for those who can afford to take that path.
This treatment worked for Molly Nash.
Six weeks after her brother Adam was born--he was genetically selected and tissue-typed from 15 embryos to match her--his umbilical cord blood was infused into her and she is now reported to be a thriving, healthy little girl.
In the United States there is still relatively little reproductive technology legislation enacted on either the state or federal level (though many bills have been introduced and interest continues to run high).
Although it did enact the Fertility Clinic Success Rate and Certification Act to require reporting of success rates from IVF clinics2, the federal government generally remains reluctant to regulate reproductive technologies. Only a handful of states have enacted reproductive technology legislation and, with the exception of legislation aimed at reproductive cloning (see Table 1)3, most focus solely on record keeping and physician involvement in artificial insemination4. Louisiana, for example, is the only state that explicitly prohibits the sale of human oocytes, whereas Virginia is the only state that explicitly sanctions the sale of human oocytes5.
In the USA the debate over embryonic stem cells is far from resolved. By contrast, in the UK the government is very supportive of embryonic stem cell research. But as the recent UK ruling on pre-implantation genetic diagnosis demonstrates, on the manipulation and selection of fertilized eggs for the purpose of reproduction it is the USA that allows the greater freedom for making individual choices.
The UK's regulatory regime will likely give the UK an edge in developing therapies that utilize embryonic stem cells. But the regulatory regime (or lack thereof) in America currently provides a greater opportunity for the development of techniques for the genetic engineering of offspring.
Prof. Yair Reisner of the Weizmann Institute of Science in Rehovot Israel is the leader of a team that has successfully grown functional kidneys in mice from pig and human stem cells taken from embryos.
Reisner and Ph.D. student Benny Dekel of the Weizmann Institute's Immunology Department, with Prof. Justen Passwell, the head of the pediatric department at the Sheba Medical Center, transplanted human and porcine "kidney precursor cells" (stem cells that are destined to become kidney cells) into mice. Both human and porcine tissues grew into perfect kidneys, the size of the mice's kidneys. The miniature human and pig kidneys were functional, producing urine. In addition, blood supply within the kidney was provided by host blood vessels as opposed to donor blood vessels, greatly lowering the risk of rejection.
The scientists pinpointed the ideal time during embryonic development in which the stem cells have the best chance to form well-functioning kidneys with minimal risk for immune rejection. Their findings suggest that 7-8 week (human) and 4 week (porcine) tissue offers an optimal window of opportunity for transplantation. If taken at earlier time points the tissues will develop disorganized tissue that would include non-kidney structures such as bone, cartilage, and muscle. If taken at later time points the risk for immune rejection is substantial.
Within this optimal time range the tissue doesn't contain certain cells that the body recognizes as foreign (antigen-presenting cells), the scientists found. These cells, which originate in the blood system, reach a developing kidney only after ten weeks.
After growing the human and porcine kidney tissue in mice, the scientists checked how human lymphocytes (fighter cells in the immune system) might react to it. They injected human lymphocytes into immunodeficient mice (that have no immune system and thus do not interfere with the immune response). The findings were encouraging: as long as the kidney precursors were transplanted within the right time range, the lymphocytes did not attack the new pig or human kidneys – despite the fact that lymphocytes and kidney precursors originated from different donors. Immune rejection was also tested in normal mice and was shown to be reduced compared to that induced by precursors from later time points.
There is an obvious problem for the use of this approach in the United States: The precursor stem cell tissue has to be harvested from 7-8 week old human embryos (which were aborted embryos). The idea of allowing an embryo to develop for 2 whole months before harvesting will elicit strong opposition from the opponents of embryonic stem cell use. An attempt to make organs available which are grown by this method (whether from abortions or from embryos grown in a lab) may well lead the US Congress to outlaw the technique.
As an alternative approach there is a chance that pig embryonic stem cells could be coaxed into forming kidneys that would be immunologically compatible with humans and compatible with human metabolic needs for kidney function. That is likely the reason why the Israeli group also used porcine stem cells in this set of experiments. But the use of porcine stem cells to create human-compatible kidneys may be technically harder than the use of human stem cells for the same purpose. In order to make the porcine stem cell approach work it may be necessary to put human versions of some genes into pigs.
Another alternative approach would be to figure out how to instruct cells that are more differentiated to become less differentiated cell types. Then it might be possible to, for instance, tell an adult kidney cell to revert back to the state that its progenitors were in at the 7th or 8th week of embryonic development. It is difficult to say how long it would take to develop a way to do that. By contrast, the ethically and legally more problematic approach of allowing a human embryo to develop thru the series of steps it normally goes thru is technically well understood and doesn't require as much knowledge of how cells differentiate. Therefore what is today the easiest technical approach also happens to be the approach that elicits the greatest political opposition.
Update: Charles Murtaugh corrects my sloppy use of the term "embryonic stem cells" (which you will no longer see above since I fixed it). In these experiments the embryos were sufficiently far along in their development that the cells taken from the embryos had undergone enough differentiation that they were no longer capable of becoming all cell types (i.e. no longer pluripotent). Therefore they were not embryonic stem cells (which are pluripotent and undifferentiated) even though they were stem cells extracted from embryos. So what to call these cells? The widely used term "adult stem cells" hardly seems adequate to describe stem cells that are not pluripotent but which come from an embryo. The word "adult" implies cells rather older than those used in this experiment and stem cells taken from an adult wouldn't have the same qualities. Though some writers use the term "non-embryonic stem cells" it seems to my ear that "non-pluripotent stem cells" would be an even more precise term.
Gina Kolata has an article in the New York Times about the growing popularity of the use of hormones to try to roll back some of the effects of aging. Testosterone and human growth hormone (HGH) are used for men and women. Plus, estrogen and progesterone are used by women. Some use DHEA, thyroid or other hormones as well. This has intensified the debate about whether these hormones provide a net benefit.
Until recently, most scientists considered anti-aging treatments to be little more than snake oil, provided by hucksters. Now, few doubt that growth hormone and testosterone can reshape aging bodies, potentially making them more youthful.
But whether they counteract aging is unknown. And their long-term risks are ill defined. So medical experts ask whether it is right to regard aging as a disease, as fierce as a malignant cancer, to be fought with any and all means, tested or not.
First of all, yes, aging really should be fought by any means that really works. There is nothing beneficial to the individual about physical aging. An older body does not function as well as it did when it was younger. The mind doesn't function as well either. Learning is more difficult, the ability to do complex problem solving is diminished, old memories are harder to recall, and assorted brain disorders such as depression, Alzheimer's Disease, Parkinson's, and dementia are more common, . Various cells can no longer do their jobs at all and in some cases even whole organs can no longer carry out their functions. The body has a reduced ability to handle environmental changes, infections, stresses and trauma. The aged body makes life harder and less pleasureable for the person whose body has aged and for those whose jobs it is to help the aging and for those who care about and give care to aging family members and friends. The body is at greater risk of all manners of illness and death. What reason is there to be complacent in the face of all that if we can possibly do anything about it?
People who are taking testosterone and HGH are doing so because they feel immediate benefits such as better muscle tone, less fat, more stamina, perceived greater ability to concentrate, and other benefits that can be directly experienced in the short term. However, these benefits do not provide any clue as to whether replacement hormones will shorten or lengthen life expectancy. There's reason for skepticism from an evolutionary perspective: it would not have been that hard for evolution to select for an aging body to retain its ability to make hormones at the same level as the body made them in its youth. The fact that it doesn't may be because it was harmful to do so. Some hormones are known to boost the risk of some types of cancers. Also, a metabolism sped up by hormones may be akin to an engine that is operated at higher RPMs. Parts of it may wear out faster if they are being stimulated by higher hormone levels.
Another reason to be skeptical of hormone therapies is that they do cause side-effects in the short term. Most worryingly some people develop insulin resistance while on hormone therapy. The resistance usually goes away once the therapy is stopped and not all people who take hormones to feel rejuvenated suffer this side effect. Still, it is possible that a period of time spent on hormone therapy will increase the chance of developing insulin resistance (aka type II diabetes) later on.
Another reason to be skeptical of the benefits of hormones as an anti-aging therapy is that scientists have tried large numbers of experiments on animals to try to find ways to increase life expectancy. Many combinations of hormones have been tried. The only consistently successful method to increase average and max life expectancy in wild type (ie not special in-bred lab strains) found to date is calorie restriction. Hormones do not increase animal life expectancy and more often than not actually decrease it.
Is the lack of known data on the long term effects of hormone therapies an argument against taking them? The answer depends on your own personal values. Some people (I know one such person) are taking hormones chiefly for the short term benefits. They know they are taking a risk. They want a more vigorous life and a greater feeling of healthiness in their 40s, 50s, and 60s even if there is a chance of decreased life expectancy as a result. For someone such as myself who thinks that people should be able to do with their bodies as they please as long as they do not create costs for others (and someone who dies sooner is probably decreasing their net burden in terms of total government benefits that they receive in retirement) its hard to argue why this choice should not be allowed. As Blondie put it: "Die young, stay pretty, live fast because it won't last."
Having said all this, it is still possible that some combination of hormones could increase life expectancy. The problem is that there are probably many more combinations that are harmful than are beneficial and we just don't have any idea what combination might be beneficial. To know that ideal hormone regimen might well require knowledge of an individual's genetic variations and the condition of the various organs in the individual's body. It is possible that the only way to improve longer term health with hormones would involve the implantation of a genetically engineered or silicon-based hormone dispenser organ that could deliver hormones with a greater precision than what is possible thru the use of pills or shots. Such an implant could take into account the constantly changing internal condition of the body to adjust the levels of hormones to a more optimized level. This sort of capability still lies somewhere in the future. But it seems plausible that some day it will be possible to develop a better endocrine regulatory system than the one that we are all born with naturally.
The problem today is that we lack the knowledge to know whether or how we could tweak the endocrine system of humans to extend life. Even if we knew how to design and build an incredibly sophisticated device for monitoring metabolism in real time to adjust hormone levels of aging people we still wouldn't know what to tell the device to do. Hormone levels change as we age. Why? Here are some possibilities for why hormone levels change as we age:
We do not know which one or combination of these possibilities is correct. Even if we did we wouldn't then immediately know what to do about it. People who are taking replacement hormones are therefore engaging in a massive experiment in hopes that anything that provides an immediate benefit will provide a longer term benefit as well.
Researchers have produced an organic light-emitting diode (LED) that is about 25 times more efficient than the best quantum-dot LEDs to date. The structure contains a single layer of cadmium-selenium quantum dots sandwiched between two organic thin films. Seth Coe and colleagues at the Massachusetts Institute of Technology believe that their approach could be used to fabricate other hybrid organic-inorganic devices (S Coe et al. 2002 Nature 420 800).
In a separate story about the race of many companies to bring organic LED products to market Nobel Laureate Alan Heeger sees organic LEDs revolutionizing light fixture technology.
Heeger, whose discoveries in polymer conductivity earned him and two colleagues a Nobel prize in 2000, said the innovations in lighting could be more dramatic than those in consumer electronics.
OLEDs, coupled with mature inorganic LED technology that already brightens traffic signals and auto taillights, could replace incandescent and fluorescent light bulbs with wallpaper that changes lighting patterns and colors, sheets of radiant film that could be cut to size or light cords that accent walls, handrails or steps, Heeger said.
No need for light bulbs. Though I suppose if some of your wallpaper stopped glowing you might need to re-wallpaper part of a wall to get it glowing again.
A physicist friend who alerted me to this article says this will motivate scientists and companies to accelerate the development of quantum computing.
The semiconductor industry has obeyed Moore's Law for about 40 years and some experts believe that it will be valid for another two decades. However, Laszlo Kish at Texas A&M University believes that thermal noise -- which increases as circuits become smaller -- could put an end to Moore's Law much sooner (LB Kish 2002 Physics Letters A 305 144).
By watching the effects that experimental drugs have on gene expression gene chips allow drugs which cause dangerous side effects to be identified at an earlier stage and at lower cost.
How is Merck using these things? Rosetta President Stephen Friend, who is now an executive vice president at Merck's labs, laid the groundwork. Friend used DNA chips to examine several potential medicines, some of which Merck had axed because animal studies showed risks of side effects. The DNA chips, in combination with Rosetta's software, flagged the duds from the drugs as well as the animal studies, but more quickly and cheaply. This means that medicines that are likely to fail will be less likely to make it into clinical trials.
Kim sees another opportunity down the road. DNA chips can be used to find genetic differences between people who respond to a drug and those who do not, starting in Phase II, or mid-stage, clinical trials. Since many drugs only seem to work for certain people, this would mean companies to target medicines to patients who would be helped--making clinical trials cheaper and easier.
Another way that gene chips (aka DNA chips or gene microarrays) will accelerate drug development is by finding genes and gene products to target for drug development.
Microarray technologies, or DNA chips, provide a high-density, high-throughput platform for measuring and analyzing the expression patterns of thousand of genes in parallel. Comparing expression levels of healthy and diseased tissues will reveal genes with a role in a disease process that can help researchers further accelerate discovery and validation of gene targets.
While gene chips and bioinformatics will accelerate drug development we are approaching the age in which drugs will not be the most important form of medical treatment. The biggest benefits for health and longevity will come from cell therapy and gene therapy. Cell therapy will be a far more powerful therapy because it will allow the replacement of aged, damaged, and dead cells. Gene therapy will be more powerful because the added genes will effectively program cells to become healthy again and even to replicate and again replace other cells that have died. Neither of these therapies are what we've traditionally called drugs. Still, gene chips will also accelerate the development of cell therapies and gene therapies as well.
Update: Here's a nice collection of microarray gene chip links.
Consider the cloak and dagger possibilities for when bacteria will become controllable by radio waves.
Only millionths of a millimetre across, the gold nanoparticle acts as an antenna, harvesting energy from a radio-frequency electromagnetic field. This energy breaks up the enzyme, rendering it useless. When the field is switched off, the parts of the enzyme re-assemble of their own accord.
This is grist for science fiction and spy TV show and movie plots. Imagine someone who could be blackmailed by the threat of activating dormant bacteria in their body. "Mr. Bond, if you do not cooperate with us immediately I will unleash the bubonic plague bacteria in you with a flick of this button." Of course Bond would have a radio cigarette lighter signal jammer that Q gave him. He could have secretly seduced the fiendish bad guy's equally bad girlfriend the night before and unknowingly infected her with the bacteria too. When the bad guy flicks the activation signal she'd collapse on the balcony and they'd both see it happen thru the plate glass window. The bad guy would run at him in a rage and Bond would deftly send him thru the plate glass window and over the balcony to his death.
The scaled up mega-disaster version would involve a dormant bacteria that had infected most of a country's population. Terrorists would threaten to kill them all unless assorted demands were met.
One big challenge in trying to develop nanotechnology is to find ways to control the arrangement of matter at the atomic level. Biological structures such as crystallized protein may provide a way to organize the formation of nanotech structures.
Crystallized proteins also hold great promise as nanostructure templates, said Vicki Colvin, director of Rice University's Center for Biological and Environmental Nanotechnology in Houston. At least 1,000 protein patterns are already known, more than what's available with polymers or other methods, she told the conference.
Many of the crystal structures have high percentages of water in them, an ideal setup for nanotech materials chemistry, Colvin said. Some of them are fragile, however, and would need a chemical "two by four" to do the job, she said.
The Economist reports that the venture capitalists are still not pouring a lot of money into nanotechnology
Lured by such large numbers, and always on the look-out for the next big thing, venture capitalists are fervently courting nanotechnologists. But as one pundit put it, so far there are more meetings on investing in nanotechnology than there are serious opportunities to punt. Investors are finding that business plans are often little more than repackaged research-grant proposals. And many of the top “nanotechnology” companies are actually developing more conventional microsystems.
However, industrial concerns which do a lot of business in chemicals and materials are spending a lot of money on nanotech in order to make better products in their traditional product markets. BASF is spending $100 million per year on Nanotech research and development.
The company is also developing a water-repelling and self-cleaning film that mimics the nanoscale features present on the surface of the lotus flower leaf. Any water on the surface beads up and rolls off because of the water – repelling nature of the material. Instead of sliding off the water, the droplet rolls off, collecting dirt particles on its surface as it does so. The film is based on a combination of nanoscale crystals developed using technical waxes and a polymer such as polyethylene or polypropylene.
BASF is also developing nanomaterials to generate different colors in polymers without the use of dyes. The colors are generated by forming a film of ordered nanoscale crystals set at a specific angle to the light. Different uniform particle sizes generate different colors. The crystalline film is composed of a polystyrene core surrounded by a shell of polybutyl acrylate. The film is sprayed onto a surface in liquid form and dries into ordered crystals. Applications could include packaging films, decorative papers, and cosmetic applications, including nail polish and hairspray, BASF says.
For many companies the best path toward further refinement of their products is to work with increasingly smaller materials and to manipulate materials on a smaller scale. The development of nanotech doesn't need venture capital funding in order to happen. A lack venture capital funding might be a sign that most of the obvious next steps in development are already being undertaken by existing companies.
A survey of the growing use of computer simulation models of disease processes and metabolism includes a report on the success of a couple asthma simulation models named Bill and Allen to predict that an approach for asthma treatment wouldn't work.
Because Bill's asthma didn't seem to reflect real life and Allen didn't respond to the interleukin-5 blockers, Aventis didn't pursue these compounds as potential asthma therapies. The Entelos model seems to have been accurate. Despite promising animal studies, when other companies recently tested interleukin-5 blockers in people, they found that the compounds have much less effect than the researchers had originally expected.
Each simulation of a disease begins by modeling the normal physiology and interaction of the organs involved. "We are striving for a whole-body approach to health and disease," says Jeff Trimmer of Entelos. "We want to use [our models] to understand how a person gets sick." Even when models don't seem to simulate what happens in real life—as in Bill—the findings can help researchers better understand physiological factors that are important in causing diseases, says Trimmer.
Computer simulations will eventually speed the rate of biomedical advance by orders of magnitude.
At this point in time a diagnosis of glioma brain tumor is pretty much a death sentence. But these amazing experiments with genetically engineered neural stem cells may provide a highly precise way to kill glioblastoma cancer cells.
LOS ANGELES -- Researchers at Cedars-Sinai Medical Center's Maxine Dunitz Neurosurgical Institute in Los Angeles have combined a special protein that targets cancer cells with neural stem cells (NSC) to track and attack malignant brain tumor cells. Results of their study appear in the Dec. 15 issue of Cancer Research.
Glioblastoma multiforme, or gliomas, are a particularly deadly type of brain tumor. They are highly invasive with poorly defined borders that intermingle with healthy brain tissue, making them nearly impossible to remove surgically without catastrophic consequences. Furthermore, cells separate from the main tumor and migrate to form satellites that escape treatment and often lead to recurrence.
Cedars-Sinai researchers recently published results of a study showing that neural stem cells have the ability to track glioma cells as they migrate. By engineering neural stem cells to secrete interleukin 12, they were able to elicit a local immune response that attacked cancer cells at the tumor site and in the satellites.
The current study used genetically engineered neural stem cells – cells that have the potential to differentiate into any of several types of cells of the central nervous system – to deliver a protein that is known for its cancer-fighting properties: tumor necrosis factor related apoptosis inducing ligand, or TRAIL. TRAIL has been shown to cause apoptosis, or cell death, in several types of cancers without causing toxicity to normal cells.
In vitro studies demonstrated that unmodified TRAIL cells quickly attacked human glioblastoma cells, with nearly all of the tumor cells being killed within 24 hours. TRAIL-secreting neural stem cells also resulted in significant cancer cell death, and the genetically engineered stem cells maintained their viability, strongly expressing TRAIL for as long as 10 days.
Similar results were found in vivo when human glioblastoma cells in mice were treated with TRAIL-secreting NSC and controls. A week after treatment, strong secretion of TRAIL was visible in the main tumor mass and in disseminating tumor pockets and satellites, indicating that the engineered cells were actively tracking tumor cells. The tumors treated with NSC-TRAIL had also decreased significantly in size, compared with the controls. Furthermore, while the treatment was dramatically effective in killing glioma cells, it was not toxic to normal brain tissue.
Note that the scientists were able to test human neural stem cells in a mouse model of the disease. The ability of human stem cells to live in mice allows the more rapid development of stem cell therapies for humans.
Anorexia and Bulimia Nervosa may be caused by an auto-immune disorder where antibodies attack the hypothalamus or pituitary.
Three-quarters of the anorexic and bulimic women studied by Serguei Fetissov of the Karolinska Institute in Stockholm carry blood antibodies targeted against appetite centres in the brain, he finds. Just 16% of those without eating disorders have such antibodies1.
Another article with additional details.
To test the theory, the investigators withdrew blood serum from 57 women between the ages of 17 and 42 who had anorexia, bulimia or both. Most of the women (74 percent) produced antibodies that, when applied to sections of rat brains and rat pituitary glands, selectively attached to cells that produce three specific neuropeptides: alpha-MSH, ACTH and LHRH.
This is a fascinating result. The targeting of adrenocorticotropic hormone suggests that stress may trigger the auto-immune response. But there may be a genetic predisposition for this inappropriate immune response. It brings up the question of just what other behavioral and endocrine disorders of currently unknown cause might be caused by auto-immune responses.
In order to advance in our understanding of biological systems we need better tools for measuring what goes on in cells and between cells. Tools that let us watch more things at once at a smaller scale, for longer periods of time and with greater sensitivity can greatly speed up the rate at which the functioning of biological systems can be puzzled out. Quantum dots can do all those things as a number of recent reports have shown.
A team at Rockefeller University and the US Naval Research Laboratory have developed a way to use quantum dots to label different kinds of proteins in living cells to fluoresce at different colors so that the internal components of cells can be tracked and imaged for long periods of time.
Quantum dots are nano-sized crystals that exhibit all the colors of the rainbow due to their unique semiconductor qualities. These exquisitely small, human-made beacons have the power to shine their fluorescent light for months, even years. But in the near-decade since they were first readily produced, quantum dots have excluded themselves from the useful purview of biology. Now, for the first time, this flexible tool has been refined, and delivered to the hands of biologists.
Quantum dots are about to usher in a new plateau of comparative embryology, as well as limitless applications in all other areas of biology.
Two laboratories at The Rockefeller University -- the Laboratory of Condensed Matter Physics, headed by Albert Libchaber, Ph.D., and the Laboratory of Molecular Vertebrate Embryology, headed by Ali Brivanlou, Ph.D. -- teamed up to produce the first quantum dots applied to a living organism, a frog embryo. The results include spectacular three-color visualization of a four-cell embryo.
The scientists' results appear in the Nov. 29 issue of Science.
"We always knew this physics/biology collaboration would bear fruit," says co-author Brivanlou, "we just never knew how sweet it would be. Quantum dots in vivo are the most exciting, and beautiful, scientific images I have ever seen."
To exploit quantum dots' unique potential, the Rockefeller scientists needed to make a crucial modification to existing quantum dot technology. Without it, frog embryos and other living organisms would be fallow ground for the physics-based probes.
"Quite simply, we cannot do this kind of cell labeling with organic fluorophores," says Brivanlou. Organic fluorophores (synthetic molecules such as Oregon Green and Texas Red) don't have the longevity of quantum dots. What's more, organic fluorophores and fluorescent proteins (such as green fluorescent protein, a jellyfish protein, and luciferase, a firefly protein) represent a small number of colors, subject to highly specific conditions for effectiveness. Quantum dots can be made in dozens of colors just by slightly varying their size. The application potential in embryology alone is monumental.
Hydrophobic, but not claustrophobic
Benoit Dubertret, Ph.D., a postdoctoral fellow working with Libchaber, toiled for two years with quantum dots' biggest problem: their hydrophobic (water-fearing) outer shell. This condition, a by-product of quantum dots' synthesis, makes them repellent to the watery environment of a cell, or virtually any other biological context.
The ability to do track cells as they differentiate has enormous value for the development of stem cell therapies and the growth of replacement organs.
These scientists have developed the ability to have the cells take up the quantum dots using endocytosis so that injection into a cell is no longer necessary. They have also developed a way to link quantum dots to antibodies that have affinity to specific proteins.
The unique physical properties of quantum dots overcome these obstacles. Simply by altering their size, scientists can manufacture them to produce light in any color of the rainbow, and, additionally, only one wavelength of light is required to illuminate all of the different-colored dots. Thus, spectral overlap no longer limits the number of colors that can be used at once in an experiment. In addition, quantum dots do not stop glowing even after being visualized for very long periods of time: compared to most known fluorescent dyes, they shine for an average of 1,000 times longer.
But while quantum dots solve these problems, they have limitations of their own - the biggest one being their water-fearing or "hydrophobic" nature. For quantum dots to mix with the watery contents of a cell, they have to possess a water-loving, or "hydrophilic" coat. Three years ago, Simon and Jaiswal's colleagues at the U.S. Naval Research Laboratory made their dots biocompatible by enveloping them in a layer of the negatively charged dihydroxylipoic acid (DHLA).
In the same study, the researchers overcame a second major obstacle of making quantum dots biologically useful - building protein-specific dots. By linking antibodies specific for an experimental protein to the DHLA-capped dots, they were able to demonstrate protein-specificity in a test tube.
In the present study, the Rockefeller scientists in collaboration with their U.S. Naval Research Laboratory colleagues have again synthesized protein-specific quantum dots, but this time they have shown their efficacy in living cells - a first for this budding technology. To do this, the researchers employed two different methods of synthesizing the quantum dots, both of which involved linking the negatively charged DHLA-capped dots to positively charged molecules - either avidin or protein G bioengineered to bear a positively charged tail. Because avidin and protein G can be made to readily bind antibodies, the researchers could then attach the dots to their protein-specific antibody of choice.
The critical test was to determine specificity: can quantum dots achieve the same exquisite selectivity that occurs when a protein is synthesized fused to GFP? To answer this question, Simon and colleagues engineered a population of cells growing together in a dish to randomly produce different levels of a membrane protein fused to GFP. When these cells were incubated with quantum dots conjugated to an antibody specific for that membrane protein, the pattern of GFP fluorescence matched the fluorescence of the quantum dots. However, the fluorescence of quantum dots lasted immeasurably longer, and the proteins could now be imaged in a rainbow of colors.
"Researchers should now be able to rapidly create an assortment of quantum dots that specifically bind to several proteins of interest," says Jaiswal.
Uncharted cellular terrainProteins aren't the only subjects the researchers successfully lit up with quantum dots: cells too were labeled and observed in their normal setting for very long periods of time. In the Nature Biotechnology paper, the researchers monitored human tissue culture cells tagged with quantum dots over two weeks with no adverse effects on cells. They also continuously observed slime mold cells labeled with quantum dots through 14 hours of growth and development without detecting any damage. This type of cell-tracking approach would allow researchers to study cell fate either outside the body in culture, or in whole developing organisms.
Quantum Dot Corporation researchers use quantum dots to detect cancer cells.
Hayward, CA, December 2, 2002 - Quantum Dot Corporation (QDC), the leader in Qdot(tm) biotechnology applications and products, announced today the publication of a seminal scientific paper in the prestigious journal Nature Biotechnology. The paper, entitled "Immunofluorescent labeling of cancer marker Her2 and other cellular targets with semiconductor quantum dots", was published in the on-line version of Nature Biotechnology, following collaborative work performed by scientists at Genentech and QDC. The print version will be published in January 2003."The promise of Qdot conjugates to revolutionize biological detection has now become a reality. Our work with Genentech is the first practical application of the Qdot technology in an important biological system - specific detection of breast cancer markers. These results demonstrate the dramatic sensitivity and stability benefits enabled using Qdot detection," said Xingyong Wu, Ph.D., senior staff scientist at QDC, and the lead author of the paper. "We have also demonstrated cancer marker detection in live cancer cells, an extremely difficult task using conventional methods," continued Dr. Wu.
Small Times has an article that provides an overview of some of these recent results with quantum dots.
A third team of researchers reported their solution to the biocompatibility problem in Science. They sheathed the dots in phospholipid membranes and hooked them to DNA to produce clear images in growing embryos, where the nanocrystals appeared stable and nontoxic.
"These three papers combined indicate that bioconjugate nanocrystals will have major applications in biology and medicine," said Shuming Nie, director of nanotechnology at Emory University's Winship Cancer Institute.
Emory University biomedical engineer Shuming Nie argues that nanotechnology will provide benefits for biomedical applications many years before nanotech becomes beneficial in electronics applications.
Biomedical engineer Shuming Nie is testing the use of nanoparticles called quantum dots to improve clinical diagnostic tests for the early detection of cancer. The tiny particles glow and act as markers on cells and genes, potentially giving scientists the ability to rapidly analyze biopsy tissue from cancer patients so that doctors can provide the most effective therapy available.
Nie, a chemist by training, is an associate professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University and director of cancer nanotechnology at Emory's Winship Cancer Institute.
His research focuses on the field of nanotechnolgy, in which scientists build devices and materials one atom or molecule at a time, creating structures that take on new properties by virtue of their miniature size. The basic building block of nanotechnology is a nanoparticle, and a nanometer is one-billionth of a meter, or about 100,000 times smaller than the width of a human hair.
Nanoparticles take on special properties because of their small size. For example, if you break a piece of candy into two pieces, each piece will still be sweet, but if you continue to break the candy until you reach the nanometer scale, the smaller pieces will taste completely different and have different properties.
Until recently, nanotechnology was primarily based in electronics, manufacturing, supercomputers and data storage. However, Nie predicted several years ago in a paper published in Science that the first major breakthroughs in the field would be in biomedical applications, such as early disease detection, imaging and drug delivery.
"Electronics may be the field most likely to derive the greatest economic benefit from nanotechnology," Nie said. "However, much of the benefit is unlikely to occur for another 10 to 20 years, whereas the biomedical applications of nanotechnology are very close to being realized."
By producing mice that have only one copy of the gene that codes for insulin-like growth factor type 1 (IGF-1) researchers produced mice that lived on average 26% longer.
When the researchers looked at the effects of deleting one copy of the gene in male and female mice, they found that the impact was different for the sexes. Males with one copy of the IGF-1 receptor lived 16% longer than normal male mice, while their female counterparts lived 33% longer than normal females.
The same effect might turn out to be achieveable either by blocking the production of IGF-1 or by creating a drug that bocks the IGF-1 receptor or by creating a drug that suppresses the production of IGF-1. But what is important here is that it demonstrates how the ability to genetically engineer mice allows scientists to test hypotheses and theories about the processes that cause aging and to test intervention strategies to slow it down or reverse it. The sequencing of the mouse genome provides scientists with the locations of many more genes to manipulate to conduct these types of studies.
Update: The researchers were building on work done in invertebrates that suggested a link between IGF-1 levels and longevity.
"These results show that a general decrease in IGF-1 receptor levels can increase lifespan in a mammalian species. Thus, the genetic link between insulin-like signaling and longevity, originally discovered in non-vertebrates, also seems to exist in higher vertebrates", conclude the authors.
Mice that do not have the gastrin-releasing peptide (GRP) gene show enhanced learning of fear.
The researchers next explored whether eliminating GRP's activity could affect the ability to learn fear by studying a strain of knockout mice that lacked the receptor for GRP in the brain.
In behavioral experiments, they first trained both the knockout mice and normal mice to associate an initially neutral tone with a subsequent unpleasant electric shock. As a result of the training, the mouse learns that the neutral tone now predicts danger. After the training, the researchers compared the degree to which the two strains of mice showed fear when exposed to the same tone alone — by measuring the duration of a characteristic freezing response that the animals exhibit when fearful.
"When we compared the mouse strains, we saw a powerful enhancement of learned fear in the knockout mice," said Kandel. Also, he said, the knockout mice showed an enhancement in the learning-related cellular process known as long-term potentiation.
"It is interesting that we saw no other disturbances in these mice," he said. "They showed no increased pain sensitivity; nor did they exhibit increased instinctive fear in other behavioral studies. So, their defect seemed to be quite specific for the learned aspect of fear," he said. Tests of instinctive fear included comparing how both normal and knockout mice behaved in mazes that exposed them to anxiety-provoking environments such as open or lighted areas.
"These findings reveal a biological basis for what had only been previously inferred from psychological studies — that instinctive fear, chronic anxiety, is different from acquired fear," said Kandel.
In additional behavioral studies, the researchers found that the normal and knockout mice did not differ in spatial learning abilities involving the hippocampus, but not the amygdala, thus genetically demonstrating that these two anatomical structures are different in their function.
The regulation of the expression of a large variety of genes in the brain varies from person to person because there are genetic variations in genes and regulatory areas that govern how much each gene makes its resulting protein product(s). Personality types will eventually be shown to have genetic causes. This will of course lead to a desire on the part of prospective parents to exercise some control over which personality-related genetic variations their offspring will get. Genetic engineering of personality will become a hotly debated topic when it becomes clear to the general public that this will be technically possible.
The cost per drug brought to market is $880 million. The ability of computers to analysis greater quantities of information will cut costs and cut development time.
Paradoxically, the biggest gains are to be made from failures. Three-quarters of the cost of developing a successful drug goes to paying for all the failed hypotheses and blind alleys pursued along the way. If drug makers can kill an unpromising approach sooner, they can significantly improve their returns. Simple mathematics shows that reducing the number of failures by 5% cuts the cost of discovery by nearly a fifth. By enabling researchers to find out sooner that their hoped-for compound is not working out, bioinformatics can steer them towards more promising candidates. Boston Consulting believes bioinformatics can cut $150m from the cost of developing a new drug and a year off the time taken to bring it to market.
China has banned reproductive cloning but allows therapeutic cloning. Fear of European opposition to the purchase of foods made from genetically modified crops has caused the government to slow the introduction of genetically modified crops even as it continues to fund the development of many new genetically modified crops.
Bt cotton is one of four crops—along with late-ripening tomatoes, virus-resistant sweet peppers and colour-altered petunias—to have been approved for commercial cultivation in China. There are various GM animals and another 60 GM plants at various stages of development, including virus-resistant wheat, moth-resistant poplars and high-tech tomatoes producing hepatitis-B vaccine.
While the figure for the next 5 or 6 years (hard to tell if they mean 2000 thru 2005 inclusiveworks out to around $100 per years is not much by US standards keep in mind that the salaries of scientists in China are a small fraction of what they are in the USA. So that money could go much further if its doled out wisely. But that brings up another question: how are research grants awarded in China? The article doesn't say and I haven't seen it discussed anywhere.
So, between 1996 and 2000, the central government invested over 1.5 billion yuan ($180m) in biotechnology, as part of its main programme to kickstart the sector. Between 2000 and 2005, it plans to invest another 5 billion yuan. As a result, reckons the Boston Consulting Group, biotechnology is flowering in 300 publicly funded laboratories and around 50 start-up companies, mainly in and around Beijing, Shanghai and Shenzhen.
China's significant and growing efforts in biotech are going to add to the general rate of advance of biotech in the world as a whole.
Stanford has accepted a $12 million dollar anonymous donation to form an institute to study stem cells and cancer cells. Some of that money will be used to clone a human embryo to use as a source of embryonic stem cells.
Stanford University announced Tuesday its intention to clone human embryos, becoming the first U.S. university to publicly embrace the politically charged procedure. The intent of the project is to produce stem cells for medical research.
This private donation demonstrates that nothing short of an outright ban on cloning and on ESC work will stop this kind of work from going forward. Enough governments are either outright supporting this kind of work (eg the UK) or legalizing it while not providing much public funding (eg the USA) that the work is going to go forward.
Cloning is done by taking the nucleus of an adult human cell (typically a skin fibroblast cell) and transferring it into an unfertilized human egg. The success rate for doing this is low enough that it is likely that several attempts will be required before a viable embryonic stem cell line can be made.
The big mystery in cloning is just what happens when the adult nucleus is placed in an unfertilized egg. There must be chemicals and proteins in the cytoplasm of an unfertilized egg that cause a nucleus to revert to an earlier stage of development. If that process of reversion (called de-differentiation) could be better understood then eventually it should become possible to transfer adult differentiated cells into adult stem cells and into other cell types.
"Stanford University is not cloning human embryos," the university declared in a statement Tuesday night, after some confusion arose earlier in the day about its intentions for the new institute.
Stem cells are the precursors of the various cell types that make up all the organs of the body, and, like cancer cells, are marked by a seemingly limitless capacity to proliferate. Controversy arises because the embryos must be destroyed to produce a new line of stem cells.
They want to do it if they think they won't be stopped by political pressure.
Later the university put out a second news release - which one faculty member called ambiguous - and held a press conference to clarify its position. Two faculty members, speaking on condition of anonymity, said they believed the university was hoping to avoid controversy, but probably did not wish to completely foreclose the option of expanding into cloning research.
“We’re not cloning embryos, and we’re not going to clone embryos,” said Stanford spokeswoman Ruthann Richter.
However, at a news conference at Stanford later in the evening, scientists acknowledged that embryos maybe produced by cloning at some time.
“The state of California has said nuclear transfer [the scientific term for cloning] is an acceptable and legal technology and in fact will be supported and funded by the state,” said Paul Berg, a Stanford Nobel laureate. “Cloning is not a nasty word.”
By "Cloning embryos" Richter means that they are not going to do reproductive cloning to create babies that are genetically identical to the DNA donors. But, yes, they really do intend to do cloning to create human embryonic stem cell lines (hESC) for research to develop medical therapies. This is often called therapeutic cloning (at least its called that by the people who are in favor of it). Some religious people see therapeutic cloning as even more morally objectionable than reproductive cloning because the therapeutic clone could in theory become a full human but is prevented from doing so because its never implanted into a womb. Instead its cells are used to do experiments or to grow organs or to inject into a person to replenish cells in the same way that adult stem cells do. To some (though by no means all) religious folks this is seen as murder.
The political battle over this issue will continue to limit the amount of funding available in the USA for doing hESC research. I do not expect to see any increase in federal hESC research funding for years to come. Its also not inconceiveable that additional legislative restrictions could be enacted in the USA. Therefore we can only hope that the scientists who are working with adult stem cells and on general problems of how cells differentiate will find other ways to create therapies that will do the same things that hESC researchers are trying to accomplish.
I am still very optimistic about the future use of stem cells to grow replacement organs, to send in cells to reseed stem cell reservoirs (which will eventually be a widely used aging reversal therapy), and for other therapeutic purposes. A lot of hESC research is being done in other countries, some hESC research is being done in the USA with private money, and also non-human ESC research will still be done in the USA. Much of how ESC operate and differentiate can be worked out in mice and so various important questions in developmental biology will still be worked out. Plus, adult stem cell research does not face the political obstacles that hESC faces.
If ways can be found to de-differentiate adult stem cells and also even to de-differentiate fully differentiated cells (which is what cloning does - but we don't understand exactly how cloning does it) then there will no longer be a need to use human eggs for cloning or use embryo cells left over from IVF. Given that the political climate is not going to improve any time soon it seems to me that scientists should lobby for a very big increase in funding on research into de-differentiation. Lets figure out how to "program around" the problem by learning how to signal the genome in an adult differentiated nucleus to become a relatively less differentiated cell. This is what cloning does, albeit in a hit-or-miss way that is somewhat of a black box mystery at this point. There are compounds in an unfertilized egg's cytoplasm that have the effect on an implanted adult nucleus of making it become less differentiated. We need to discover what those compounds are and how to manipulate their delivery into cells.
Of course, if how to do de-differentiation becomes well enough understood that it becomes possible to make an adult differentiated cell to turn into an embryo cell then religious folks will raise objections to the creation of such cells just as they object to the creation of embryonic cell lines by other means. But lets get legalistic here: if we achieve enough control over the de-differentiation process to be able to stop one step short of creating true embryonic cells we will have cells that are sufficiently undifferentiated as a starting point for therapeutic purposes. Yet strictly speaking we will not have cells that are embryonic.
Working in collaboration with StemCells founders Drs. Fred Gage (The Salk Institute) and Irving Weissman (Stanford Medical Center), the team at StemCells, Inc. led by Dr. Nobuko Uchida, has succeeded for the first time in finding markers for human brain stem cells. Using these markers and state of the art cell sorting, we have been able to purify stem cells away from the other cells in the brain tissue. The purified stem cells have been expanded using proprietary cell culture systems and transplanted back into host mouse brains.
The transplanted stem cells engrafted and differentiated into human neurons and glia that intermingled with host brain counterparts. Remarkably, after seven months, the transplanted human cells survived and migrated to specific functional domains of the host brain, with no sign of tumor formation or adverse effects on the recipients.
In the experiments, started about 1 1/2 years ago by Weissman, Fred Gage of the Salk Institute of La Jolla and colleagues at Palo Alto-based StemCells, neural stem cells from 10-week-old human fetuses survived when injected into a mouse brain. Stem cells are the cells from which all others evolve.
Many of the cells continue to thrive in the brain, 14 months later.
Even more remarkably, the stem cells traveled to various regions of the mouse brain, made themselves at home there and then matured into the type of adult human cell characteristic of that region of the brain. This suggests that they respond to chemical signals in the mouse brain, instructing them how to grow up.
``Every part of the brain was populated with human cells,'' Weissman said.
It is possible to inject stem cells at a much earlier stage of development and that will result in a much wider spread of the stem cells. Recently Dr. Ali H. Brivanlou of Rockefeller University organized a meeting of a small group of American and Canadian biologists co-sponsored by the New York Academy of Sciences and Rockefeller University to debate whether to do an experiment that would create a mouse-human hybrid.
In one test that they discussed, human embryonic stem cells would be injected into an early mouse embryo when it was still a small ball of cells called the blastocyst. Scientists would then see whether the human stem cells showed up in all the mouse's tissues. That ability, known as pluripotentiality, is the hallmark of a true embryonic stem cell.
Injection into another mouse's blastocyst is the standard test for mouse embryonic stem cells. Those cells, like human embryonic stem cells, come from a small pool of all-purpose cells a few days after the fertilized egg has started to divide.
Note that this proposed experiment will elicit greater opposition because it is proposed that embryonic stem cells be used and at that the stem cells be introduced at a much earlier stage where the cells would be able to become a much larger portion of the resulting organism.
The science is advancing to the point that the ethical debates are ceasing to be just theoretical. Researchers want to do experiments that would build their confidence that various cell types derived from embryonic stem cells will be viable as therapeutic agents. Stem cells are so flexible that they can even live in other species. This also increases the chance that organs can be grown in one species using stem cells from another species in order to then be able to do xenotransplantation back to the species from which the stem cells were taken.
Jeremy Rifkin, President of The Foundation on Economic Trends, is hoping to prevent the creation of hybrid animals that contain human cells by getting a patent on the idea.
But the Foundation filed a patent application for a "human-non-human hybrid" in 1997. According to Rifkin, its aim was to draw attention to the negative potential for just such inter-species hybrids inherent in the biotech race to cure human diseases. The patent application was filed jointly with Stuart Newman, a professor of cell biology and anatomy at New York Medical College in Valhalla, and remains under review at the US Patent Office, Rifkin told The Scientist.
But it sounds like Rifkin originally filed this patent in order to challenge the idea of patenting living materials.
The "Humouse" Human/Animal Chimera Patent challenge was filed with the U.S.Patent and Trademark Office (PTO) on December 18, 1997. The patent application is designed to challenge the current PTO policy of conferring patents on living materials, including genes, cells and tissue. On August 16, 2000, the PTO issued its third response to our application and in a stunning reversal, acknowledged, for the first time, that neither the government nor the courts have addressed the question of whether patents can be extended to human beings. The PTO previously had argued, in its review responses to our application, that both the courts and Congress intended to exclude human beings, including human embryonic cells, from patents.
Rifkin's gambit probably won't do anything to block the creation of human-animal hybrids. Whether it will cause any changes in US PTO policy remains to be seen.
There is a proposal in Missouri to extend its DNA sample storage for felons from violent offenders to all offenders. It sounds like the biggest source of reluctance is monetary. Therefore this DNA will be available to test for genes that predispose for criminal behavior.
Like every state in the nation, Missouri currently keeps genetic records for violent offenders.
“Many states are expanding this policy to collect DNA evidence from all convicted felons and I believe it is time for Missouri to take the lead in this and also expand our policy to include all convicted felons,” said District 45 Rep. Cathy Jolly.
First of all, when SNP (Single Nucleotide Polymorphism single DNA letter variations) testing becomes cheap these sample collections will become valued for use in trying to run down the genetic factors that predispose for criminal behavior. Scientists will want access to these stores of DNA samples to look for genetic variations that influence behavior.
Then when more genetic variations which are linked to criminality become identified the US states will have another reason to use these stores of DNA samples: for each convict to get a better idea of just how strong of a tendency there is for further criminal behavior. Expect to see some states move to analyse the genes of felons in order to use the results in parole hearings and even in sentencing hearings.
Johns Hopkins has released a survey on public attitudes toward cloning, genetic engineering of offspring, and other uses of biotechnology related to reproduction.
Washington, DC, December 9, 2002 -- Americans are both hopeful and fearful about the rapidly advancing power of scientists to manipulate human reproduction, according to a new survey released today by the Genetics and Public Policy Center, a Johns Hopkins effort funded by The Pew Charitable Trusts.
The survey explored the knowledge and attitudes of 1,211 respondents about reproductive cloning, genetic testing, and genetic modification and preferences about government regulation. "These technologies give us the power to manipulate the most personal and profound of human activities --beginning a new human life," said Kathy Hudson, director of the Center.
Highlights of the survey:
- Most Americans oppose (76 percent) scientists working on ways to clone humans. Of those who support human cloning research, men outnumber women by more than two to one (26 percent; 11 percent).
- Twenty-two percent of respondents believe a human has already been cloned, with young men most likely to believe it (31 percent).
- The public draws clear distinctions between health and non-health related applications of these technologies. Two thirds of respondents approve of using reproductive genetic testing to help parents have a baby free of a serious genetic disease. An even larger number, over 70 percent, disapprove of trying to use these technologies to identify or select traits such as strength or intelligence.
- Overall, men were twice as likely as women to be highly supportive of reproductive genetic technologies (25 percent; 12 percent).
- Most respondents think the government should regulate the quality and safety of reproductive genetic technologies and limit human reproductive cloning. Notably, the majority of Republicans, Democrats and Independents support government regulation of these technologies.
- Fifty-four percent think about these technologies primarily in terms of health and safety while 33 percent view them in religious or moral terms. Of the variables explored in the survey, this viewpoint is most strongly correlated with approval or disapproval of reproductive genetic technologies. Those who view these technologies in terms of religion and morality are more likely to disapprove of reproductive genetic technologies
- The biggest fears are that using these technologies is too much like "playing God," (34 percent) or that they can be easily used for the wrong purposes (35 percent). The greatest benefits are being able "to wipe out certain genetic diseases forever" (41 percent) and improving parent's chances their baby will be healthy (27 percent).
- The public's knowledge about these technologies is not keeping pace with the steep growth in genetic science. Only 18 percent of respondents were able to correctly answer 6 or more of the 8 knowledge questions.
Most people answering this survey disapproved of the use of genetic techniques to select for higher IQ in offspring. But it seems unlikely that once it becomes possible to influence progeny IQ that the level of resistance will remain as high. A lot of technologies are easy to oppose when their use is still hypothetical. But imagine what happens once selection of offspring traits becomes possible. When a pair of prospective parents can be handed a report of their DNA sequences that shows them all the possible combinations of their DNA can create a viable child and when the IQ and personality types of each possible combination can be spelled out in advance there is going to be a strong desire on the part of many people in that position to choose the combinations that will result in offspring characteristics that they feel are most appealing.
Note that it will be possible to boost offspring intelligence without introducing genetic combinations that neither parent possesses. Each person has two copies of every chromosome. In many cases one chromosome will have better genetic variations for intelligence than the other chromosome. By controlling which of each pair of chromosomes one passes along to one's offspring many (probably most) people will be able to have smarter children. A step beyond that will be the ability to take a genetic variant from one of a pair of chromosomes and put it on the other member of the pair. Again, this still restricts the choices to those genetic variations that each person has but it allows the creation of combinations of genetic characteristics in offspring that would be unlikely to happen in practice. Essentially, genetic technology will allow people to load the dice and produce offspring that have the best combinations of characteristics of their parents but the parents will be much more satisfied with the results.
I believe that the ability to produce better outcomes using just the DNA sequences of a couple will go a long way toward reducing popular opposition to genetic engineering of offspring. The other factor that will reduce public opposition will be the identification of large numbers of harmful mutations. Given the option of not passing along harmful mutations most will opt to edit out those mutations from the DNA that they pass alog to their children. This ability to make smaller steps to control offspring genetic endowment will seem less unnatural to most people and the benefits will seem great enough to overcome their fears. Therefore in spite of these latest results I still expect offspring genetic engineering to become commonplace once it becomes possible.
Wind now supplies 28 million Europeans with electricity.
Europe's wind-driven energy has been growing at 40 percent a year. With a capacity of more than 20,000 megawatts installed on land, it now represents three-fourths of the world's total wind-power output. Europe hopes to raise this to 60,000 megawatts in the next six years. Much of that growth is expected to come from sea-based turbines.
Unfortunately, while the article is rather short on cost information (why didn't the NY Times editors demand the writer put this info in the article?) it doesn't sound like wind power is really cost competitive with other energy sources:
Then there is the issue of price. Industry spokesmen contend that, strictly speaking, the price of wind-driven energy is close to being competitive with other sources. They argue that traditional fossil fuels and nuclear energy get enormous hidden or indirect subsidies, to the tune of billions of dollars a year. For example, in some European countries, governments pay for the insurance of nuclear power plants.
The nuclear insurance costs are a poor example of a power subsidy because nuclear power is not the lowest cost method of producing electricity in the first place. Fossil fuels (I'm guessing natural gas in particular) are the lowest cost energy sources for generating electricity. What subsidies exist for them are mostly in the form of not forcing producers to pay all external costs generated by the pollution from burning the fuels. Such costs are hard to estimate.
I get annoyed by articles like this New York Times article. What it needed (and what the NY Times surely could have gotten from industry sources fairly easily) was a graph of historical cost trends in fossil fuel and wind power generation costs for new fossil fuel and new wind power generation facilities. If we want to project foward about the prospects for wind power it would be useful to know how rapidly it is closing the gap in costs as compared to other power sources.
Over on the Gene Expression blog Razib has responded to my previous post On Religious Belief And Germ Line Engineering. I'd like to flesh out in more detail some of my ideas about genetic engineering and religious belief and experience.
First of all, when it comes to the God stuff there are beliefs, experiences, and behaviors. It will probably be possible to genetic engineering on minds to vary any one of those categories separately or to link them to happen together in various combinations.
Religious beliefs could be genetically engineered to be more likely. It might be possible to genetically engineer a mind to be more or less prone to believe in a God and a supernatural. This could probably be done without programming the mind to feel the presence of a supernatural being as a special experience. It might just be necessary to program in an uncritical sense of wonder and awe at life in such a way that a mind would be more prone to interpret their sense of awe as evidence of a supernatural existence outside of our own existence. Of couse, the more direct and heavy-handed approach would be to reinforce religious beliefs by programming a mind to feel periodic heavy doses of feeling like one is in a divine presence.
Experiences and behaviors could be genetically engineered to go together. Imagine a genetically engineered mind that feels a great deal of pleasure from carrying out some repetitive worshipful action. Imagine, for instance, genetically engineering a mind to respond repetitive bowing by feeling a strong sense of an intense presence. That feeling of a presence could be made to be pleasureable. This would encourage the bowing behavior.
Depending on the needs of the particular religion, the bowing could trigger other emotions along with the pleasure. The pleasure would be what is used to encourage the bowing. But the other emotions that accompanied it could be used to encourage types of desired resulting behaviors. For instance, anger or solidarity or other feelings might accompany the feelings of pleasure. One could even design a mind that would use the previous mental state that existed before the bowing activity as an input into some logic (all subconscious) to choose a new emotional state to experience. So, for instance, if a person came to worship with a group and that person felt some emotion that is akin to a feeling of injustice then the bowing could trigger pleasure and anger at the same time.
Or picture a mind that was genetically engineered to periodically have a strong desire to be with groups of people and also to want to bow. Minds could be genetically engineered to prefer a particular style of worship.
How about forgiveness and love? Hey, why not program them to happen? One could make a bowed head, closed eyes, and hands folded together in front of one in combination with some mental state all together cause someone to feel a strong sense of forgiveness. There are enough different aspects to a prayer ritual that it might be possible to combine the elements of the ritual and process them in a genetically engineered mind to trigger a feeling of forgiveness and of dissolving anger.
Depending on the needs of the particular religion the feeling of anger or the feeling of love could be triggered by ritualistic practices. But herein lies the political problem for humanty as a whole. Religious belief systems can conflict. If different groups genetically engineer their offspring with different God programming (different rituals or environmental stimuli as triggers for different emotional states and behaviors then the gaps between how different groups see each other could grow larger. Conflicts could become more intractable. and the resulting conflicts
As I've previously argued, one of the greatest threats from genetic engineering will come from mind engineering. Most discussions of genetic engineering of the mind that I come across are about whether and when it will be possible to raise intelligence. Certainly that will become possible to do and the impact of doing so will be profound. But the biggest threat to humanity from genetic engineering of progeny comes from genetic engineering that makes different groups of humans incompatible with other groups as a result of incompatible personalities. Differences in religious belief will lead to differences in choices of how to engineer the minds of offspring. This will become on of several reasons why humanity may break up into separate and viciously competing groups of mental types.
A research group at Xerox has developed a material called polythiophene which can be used to make spray-on organic transistors. These organic transistors can be used to make incredibly low cost flat panel displays.
A research fellow from the Xerox Research Centre of Canada has described the design and synthesis of semiconducting organic polymers that allow the printing of electronic patterns on a plastic substrate, paving the way for the printing of integrated circuits on plastic sheets instead of etching them on silicon wafers. Beng Ong made his presentation Tuesday (Dec. 3) at the Materials Research Society's fall conference in Boston.
The manufacturing equipment for making organic polymer transistor displays does not cost very much.
"The reason the cost is lower is that we don't need the same capital-intensive process as the one used with silicon," Ong said. "In our process, we can make the material into ink and ink-jet print it to create a circuit."
"I'm aware of six or eight companies trying to make these transistors," said Dr. Michael D. McCreary, vice president for research and development at E Ink, a display manufacturer in Cambridge, Mass. He said that his company planned to commercialize its first display next year and that it had created a prototype plastic display in partnership with Lucent Technologies.
What we need are displays that are about the thickness of a heavy duty file folder. Then integrate a radio modem into the display and one ought to be able to hold in one's hands a rather lightweight touch sensitive display that can call up the entire internet as well as files stored on the local server. Throw in a headset that allows one to talk commands to the computer.
The passage by the Australian Senate makes the final approval of a law defining Australian law regarding embryonic stem cell research (ESC) a certainty. The Australian House Of Representatives has to agree to the minor changes that the Senate made to the version of the bill that the Australian House already passed (and by a very wide 3-to-1 margin). While the Australian law is not as lax as that in the UK the researchers and investors in Australian will be able to work on embryonic stem cells with far less legal doubt and uncertainty than equivalent researchers face in the US.
After months of delay and often bitter public debate, Australia's Senate yesterday (December 5) passed legislation regulating embryonic stem (ES) cell research 45 votes to 26, along with a separate bill to ban human cloning. The legislation allows scientists to work with existing ES cell lines and to create new lines from surplus in vitro fertilization embryos created before April 5, 2002. It also signals an end to a patchwork of state and territory rules.
The bill must yet gain final sign-off from the House of Representatives on 13 amendments passed by the Senate. Prime Minister John Howard said he expected them to pass when the bill returns to the house next week.
The amendments include more parliamentary scrutiny of research licences and a review of whether a national stemcell bank is required to keep stemcell lines in public hands.
In the US there is enough doubt about the continued legality of even privately funded embryonic stem cell research that it discourages private investment in ESC work.
A debate over the issue went nowhere in the U.S. Senate earlier this year. President George W. Bush and some members of Congress want to ban the research, while others, including some anti-abortion conservatives such as Utah Republican Orrin Hatch, would like to see it continue while banning the use of the technique to create a cloned human baby.
"It's been tied inappropriately to abortion politics, and as long as it remains tied to that issue, the hopes are dismal," Haseltine said.
Current U.S. policy strictly limits the amount of publicly funded research that can be done on embryonic stem cells. Private companies can do as they please but legislation being pushed by Kansas Republican Senator Sam Brownback and others would put an end to that, too.
In the US much of the legal action has shifted to the state level. While many states have been enacting laws that make cloning and ESC work illegal there is now a contra-trend in other states to explicitly allow ESC work.
Following California's lead, lawmakers in at least three other states will take up proposals next year to encourage research on stem cells taken from human embryos. The measures also would permit scientists to use cloning to produce human embryos for stem cell experiments.
More on the move of the fight to the state level.
Similar motives prompted California lawmakers to pass a measure this year supporting embryonic stem cell research, and Gov. Gray Davis signed the bill in September. The Biotechnology Industry Association, a trade group, sent the California law to its affiliates in 35 states and suggested they try to pass similar measures.
Stem cell researcher Dr. Evan Snyder has left Harvard for the Burnham Institute in La Jolla and one of the reasons he cited for the move is the California state law that supports ESC research.
California Gov. Gray Davis, meanwhile, signed a new law Sept. 22 that affirms the state's support of embryonic stem-cell research. That is another reason Snyder was encouraged to move to San Diego.
"I think the new law may go a long way toward making California a place that almost becomes a magnet for stem-cell biologists," he said.
Larry Goldstein, a professor of pharmacology at the University of California San Diego Department of Cellular and Molecular Medicine who lobbied for the state law, said the welcoming political climate could also bring research funding.
"If you're trying to attract private investment, it's more likely to come to a state where (stem-cell research) is legal than in a state where there's uncertainty," Goldstein said.
Christopher Reeve has been lobbying the New Jersey state legislature to pass a bill that authorizes embyronic stem cell research. The bill has made it out of a Senate committee and will now be considered by the full New Jersey Senate.
Although the bill does not provide for government funding, Reeve said it does give key assurances to pharmaceutical companies that might foot the bill.
"Pharmaceutical companies are not interested in going out on a limb with research money if they are afraid the work will be banned," Reeve said.
The Senate Health, Human Services and Senior Citizens Committee approved the bill Monday. It now heads to the full Senate.
A bill has been introduced into the Massachusetts legislature to explicitly legalize ESC research in Massachusetts.
If enacted, the bill would explicitly authorize the controversial research and allow the donation of embryos from fertility treatments for stem cell research.
The bill would also set up a government-administered fund to support stem cell research, to be headed by the state commissioner of public health.
If Congress moves to outlaw ESC work and cloning work then the battleground could move to the courts as it becomes a constitutional question of whether the federal law can trump state laws. It would be interesting to know what legal bloggers such as Eugene Volokh and Glenn Reynolds think would happen in the courts. Even if the states eventually won that battle while the battle was going on US industry would shy away from investing in ESC research. Though adult stem cell research would still proceed and ESC research in other species will also still get done.
Athletes are not allowed to drink coffee or other caffeinated beverages? That seems excessive. Also, cannabis is far more likely to impair than it enhance performance ("Oh, wow, like I totally spaced and forgot I was supposed to be competing in the finals today"). At least the list is going to be fixed.
Insulin is one of a number of drugs that should be removed from the list of banned substances as part of a more scientific approach to the anti-doping battle, a member of the IOC's medical commission said Thursday.
Dr Harm Kuipers told a conference in Madrid that only substances that could be shown both to enhance performance and to produce adverse effects in athletes' health should be prohibited.
He said that caffeine, narcotics such as heroin and morphine, glucocorticoids, pseudo ephedrine and cannabis were all likely to be removed when the World Anti-Doping Agency produces a revised list of banned substances next year.
Orbital Recovery Corporation is proposing that their Geosynch Spacecraft Life Extension System (SLES)TM "space tug" be used to save the stranded Astra 1K Telecommunications Satellite.
ORBITAL RECOVERY CORPORATION OFFERS SPACE RESCUE FOR STRANDED ASTRA 1K TELECOMMUNICATIONS SATELLITE
Washington, D.C., Luxembourg, December 5, 2002 - Orbital Recovery Corporation has proposed an ambitious rescue plan for ASTRA 1K -- one of the world's largest telecommunications satellites -- that was stranded in low Earth orbit last week after its launch vehicle malfunctioned.
The salvage mission would use Orbital Recovery Corp.'s new "space tug" -- called the Geosynch Spacecraft Life Extension System (SLESTM) -- to boost ASTRA 1K from its current 290-km. circular orbit to the desired 35,000-km. operational altitude for telecom satellites.
Orbital Recovery Corp. has been in significant discussions with the stakeholders concerned with the future of the Astra 1K spacecraft, who have indicated a significant interest in the company's proposed solution to recover this massive satellite for normal operation.
The SLES would be launched in approximately 20 months for a rendezvous and docking with ASTRA 1K. Once firmly attached to the stranded telecommunications satellite, the space tug will use its own propulsion system to raise ASTRA 1K's altitude and reduce its inclination to the Clarke Belt orbital plane -- allowing the spacecraft to function for up to its original 13-year expected mission lifetime in geostationary orbit.
"Our SLES is perfectly tailored for the rescue of ASTRA 1K, which is an extremely expensive asset that unfortunately is useless in its wrong orbit," said Orbital Recovery Corp. Chief Executive Officer Walt Anderson. "We have run simulations of the rescue mission that validate its feasibility, and we are ready to work with SES ASTRA in Luxembourg and with the insurance sector to make the flight a reality."
Definition work on the SLES has been completed by Orbital Recovery Corp., which is now creating its industrial team by seeking competitive bids for spacecraft hardware and systems from international suppliers. Earlier this month, the company announced its selection of the DLR German Aerospace Center's robotic technology for the SLES docking and linkup with telecom satellites in orbit. In October, Aon Space joined the Orbital Recovery Corp. team to provide insurance brokering and risk management services.
The SLES is a modular spacecraft that can be adapted to operate with a full range of three-axis telecommunications satellites -- from the small relay platforms to massive 5-metric ton spacecraft such as ASTRA 1K. Proven, off-the-shelf hardware will be used in production of the SLES to keep costs down and ensure high reliability. It will be built around a main bus that contains the spacecraft control/management systems and the primary ion propulsion system.
In addition to the rescue of stranded satellites, the SLES is designed to extend the operating lifetimes of telecommunications satellites in geostationary orbit that routinely are junked when their on-board fuel supply runs out. Orbital Recovery Corp. has identified more than 40 spacecraft currently in orbit that are candidates for life extension using the SLES.
The first SLES mission is targeted for 2004 on the ASTRA 1K rescue flight, with two more deployments the following year and three annually beginning in 2006.
Orbital Recovery Corp. has offices in Washington, D.C. and Los Angeles, and will add an Asia-Pacific presence in early 2003. More information on Orbital Recovery Corp. is available on the company's Web site: www.orbitalrecovery.com.
Images of the SLES can be found here.
Telecommunications satellites typically cost $250 million - and they are designed for an average useful on-orbit life of 10-15 years. Once their on-board propellant load is depleted, the satellites are boosted into a disposal orbit and decommissioned, even though their revenue-generating communications relay payloads continue to function.
Orbital Recovery Corporation's Geosynch Spacecraft Life Extension System (SLES)TM is a novel concept that will significantly prolong the operating lifetimes of these valuable telecommunications satellites.
The SLES will operate as an orbital "tugboat," supplying the propulsion, navigation and guidance to keep a telecom satellite in its proper orbital slot for many years. Another application of the SLES is the rescue of spacecraft that have been placed in a wrong orbit by their launch vehicles, or which have become stranded in an incorrect orbital location during positioning maneuvers.
The SLES is designed to easily mate with all telecommunications satellites now in space or on the drawing boards. After launch, the SLES will rendezvous with the telecommunications satellite, approaching it from below for docking. The SLES will link up using a proprietary docking device that connects to the telecommunication satellite's apogee kick motor.
Apogee kick motors are used by nearly every telecommunications satellite for orbital boost and station-keeping, and they provide a strong, easily accessible interface point for the SLES' linkup that is always within the satellite's center of gravity.
Orbital Recovery Corporation has identified 43 telecommunications satellites currently in orbit that are candidates for life extension using the SLES. The system also will be offered for use on new satellites, allowing manufacturers and operators to conceive such spacecraft for much longer operating periods than currently possible.
The company is targeting the first SLES mission for 2004, with two more deployments the following year and three annually after 2005.
Note how advanced technology cuts costs, reduces waste, and reduces space pollution. So what's the next step? It seems easy to imagine satellites designed to so that they can be refueled by periodic visits of refueling tugs. After all, why launch and attach a complete new set of manuevering engines and controls for each satellite when the satellite's original equipment could continued to be reused if its propellant tanks could be refilled?
Update: The SLES will not be coming to the rescue. The Astra 1K has been crashed into the Pacific Ocean.
Its official, the mouse genome has been sequenced and this is a very good thing. You can read official announcement on the NIH site (which has the best copy for the click-thru to supporting docs), on Eurekalert, and on ScienceDaily. From the announcement:
The sequence shows the order of the DNA chemical bases A, T, C, and G along the 20 chromosomes of a female mouse of the "Black 6" strain - the most commonly used mouse in biomedical research. It includes more than 96 percent of the mouse genome with long, continuous stretches of DNA sequence and represents a seven-fold coverage of the genome. This means that the location of every base, or DNA letter, in the mouse genome was determined an average of seven times, a frequency that ensures a high degree of accuracy.
Earlier this year, the mouse consortium announced that it had assembled the draft sequence of the mouse and deposited it into public databases. The consortium's paper this week reports the initial description and analysis of this text and the first global look at the similarities and the differences in the genomic landscapes of the human and mouse. The analysis was led by the Mouse Genome Analysis Group. Below are some of the highlights.
- Human Sequence: It's Bigger, But Is It Better? The mouse genome is 2.5 billion DNA letters long, about 14 percent shorter than the human genome, which is 2.9 billion letters long. But bigger doesn't always mean better, say scientists. The human genome is bigger because it is filled with more repeat sequences than the mouse genome. Repeat sequences are short stretches of DNA that have been hopping around the genome by copying and inserting themselves into new regions. They are not thought to have functional significance. The mouse genome, it seems, is more fastidious with its housecleaning than the human. Although it is actually accumulating repeat sequence at a greater rate than humans, it is losing them at an even greater rate.
- Shuffling the Chapters of an Ancestral Book. The mouse and human genomes descended from a common ancestor some 75 million years ago. Since then there has been considerable shuffling of the DNA order both within and between chromosomes. Nonetheless, when scientists compared the human and mouse genomes, they discovered that more than 90 percent of the mouse genome could be lined up with a region on the human genome. That is because the gene order in the two genomes is often preserved over large stretches, called conserved synteny. In fact, the mouse genome could be parsed into some 350 segments, or chapters for which there is a corresponding chapter in the human genome. For example, chromosome 3 of the mouse has chapters from human chromosomes 1, 3, 4, 8 and 13, and chromosome 16 of the mouse has chapters from human chromosome 3, 21, 22 and 16.
- Heavy Editing at the Level of Sentences. Although virtually all of the human and mouse sequence can be aligned at the level of large chapters, only 40 percent of the mouse and the human sequences can be lined up at the level of sentences and words. Even within this 40 percent, there has been considerable editing, as evolution relentlessly tinkers with the genome. The change is so great in most places that only with very sensitive tools can scientists discern the relationships.
- Preserving the Gems. Despite the heavy editing, about 5 percent of the genome contains groups of DNA letters that are conserved between human and mouse. Because these DNA sequences have been preserved by evolution over tens of millions of years, scientists infer that they are functionally important and under some evolutionary selection. Interestingly, the proportion of the genome comprised by these functionally important parts is considerably higher than what scientists had expected. In particular, it is about three times as much as can be explained by protein-coding genes alone. This implies that the genome must contain many additional features (such as untranslated regions, regulatory elements, non-protein coding genes, and chromosomal structural elements) that are under selection for biological function. Discovering their meaning will be a major goal for biomedical research in the coming years.
- The Gene Number. When the human genome consortium concluded last year that the human sequence contains only 30,000 to 40,000 protein-coding genes, the news elicited a collective international gasp. Humans, it seems, have only about twice as many genes as the worm or the fly, and fewer genes than rice. Many wondered how human complexity could be explained by such a paucity of genes. The prediction has since been the subject of debate with some researchers suggesting much higher gene counts. The human-mouse comparison will likely put the yearlong speculation to rest, indicating that if anything, the gene numbers may be at the low end of the range. Today's paper suggests that the mouse and the human genomes each seem to contain in the neighborhood of 30,000 protein coding genes.
- Sex, Smell and Infectious Disease. Although the mouse and the human contain virtually the same set of genes, it seems that some families of genes have undergone expansion - or multiplied - in the mouse lineage. These involve genes related to reproduction, immunity and olfaction, suggesting that these physiological systems have been the focus of extensive innovation in rodents. It seems that sex, smell, and pathogens are most on the mouse's evolutionary mind. Scientists do not yet know the reasons for this, but they speculate that a shorter generation time, changes in living environment, lack of verbal and visual cues, and differences in reproduction may account for this.
- Uneven Landscape of the Genomes. Since the two species diverged, the ancestral text has changed considerably, with substitutions occurring in both species. Twice as many of these substitutions have occurred in the mouse compared with the human lineage. A great surprise is that mutation rates seem to vary across the genome in ways that cannot be explained by any of the usual features of DNA.
- Empowering Mouse as a Disease Model. The laboratory mouse has long been used to study human diseases. There are more than a hundred mouse models of Mendelian disorders, where a mutation in mouse counterparts of human disease genes results in a constellation of symptoms highly reminiscent of the human disorder. But there are many more such models to be found, and the availability of the mouse genome sequence will make their discovery only a few "mouse" clicks away. Furthermore, hundreds of additional mouse models of non-Mendelian diseases such as epilepsy, asthma, obesity, colon cancer, hypertension, and diabetes, which have been more difficult to pin down, will now be much more accessible to the tools of the molecular geneticist.
- Understanding the Mouse. The mouse genome sequence will also open new paths of scientific endeavor aimed at understanding how the mouse genome directs the biology of this mammal. Scientists will no longer be working on genes in isolation, but will view individual genes in the context of all other related genes and in the context of a whole organism. They will be able to study many, even all, genes simultaneously, speeding the understanding of the mouse in molecular terms. Scientists say such molecular understanding of the mouse will be essential to realize the full benefits of the human genome sequence.
The sequence information from the mouse consortium has been immediately and freely released to the world, without restrictions on its use or redistribution. The information is scanned daily by scientists in academia and industry, as well as by commercial database companies, providing key information services to biotechnologists.
The work reported in this paper will serve as a basis for research and discovery in the coming decades. Such research will have profound long-term consequences for medicine. It will help elucidate the underlying molecular mechanisms of disease. This in turn will allow researchers to design better drugs and therapies for many illnesses.
"The mouse genome is a great resource for basic and applied medical research, meaning that much of what was done in a lab can now be done through the Web. Researchers can access this information through www.ensembl.org, where all the information is provided with no restriction," says Ewan Birney, Ph.D., Ensembl coordinator at the European Bioinformatics Institute.
The Washington Post write-up emphasises the importance of the discovery of more conserved sequence sections than expected.
The big surprise in the research, however, was that about 5 percent of the genetic material of mice and people is highly conserved, and matching genes alone can account for only about 2 percent of it. That means as much as 3 percent of the genetic material is playing a critical but mysterious role--one so important nature has kept that genetic information largely intact for 75 million years.
It's only speculation now, but most scientists think those stretches of DNA will prove to be regulatory regions--instructional segments that somehow govern the behavior of genes. More and more, to cite one example, it looks as though mice and people will turn out to have very different brains not because the genes encoding their brain cells are so different, but because the instructions that regulate how many times those cells reproduce during development are different--producing a far bigger brain in a human than in a mouse.
The discovery of the larger-than-expected conserved areas is the important thing to come out of the mouse DNA sequencing so far. Another interesting discovery is 300 genes that are unique to mice:
But the comparison has also revealed genetic differences too. Mice have around 300 genes humans do not and vice versa. The biggest disparities are linked to sex, smell, immunity and detoxification.
All are genes which help animals adapt to new environments, infections and threats. "All the fast things that happen in evolution are down to life-or-death conflicts, either with other organisms, or within species for mate selection," says Chris Ponting, head of a team at the MRC Functional Genetics Unit in Oxford, UK.
I will be very curious to see whether some scientists eventually track some of those genes to viruses. It is quite possible that viral infections left genes behind at some point and that those genes turned out to do useful things for mice.
These results suggest a much bigger role for RNA that does not code for peptides. Large amounts of the DNA that was unexpectedly found to conserved (not changed by accumulation of random mutations) in humans and mice which does not code for proteins may instead code for regulatory RNA molecules.
RNA, a more ancient chemical version of DNA, performs many basic tasks in a cell, one of which is to form a copy or transcript of a gene and direct the synthesis of the gene's protein. Recently, some of these RNA transcripts have been found to have executive roles all their own, without making any protein. An RNA gene is responsible for the vital task of shutting all the genes on one of the two X chromosomes in each female cell, ensuring that women get the same dose of X-based genes as men, who have just one X chromosome.
The mouse genome sequencing results have provided an immediate benefit for understanding the human genome by helping to identify an additional 1200 human genes that had gone unrecognized.
More than 2,000 of the shared regions identified in this study (out of 3,500) do not contain genes. What precisely these non-gene regions, sometimes called 'junk DNA', are doing in the genome is not yet known.
The consortium researchers discovered about 9,000 previously unknown mouse genes and about 1,200 previously unknown human genes. The mouse genome is 14 percent smaller than the human genome and contains about 2.5 billion letters of DNA.
The genetic differences between humans and mice turn out to be greater than expected:
In the Dec. 5 issue of the journal Nature, Pevzner and other scientists in the 31-institution Mouse Genome Sequencing Consortium published a near-final genetic blueprint of a mouse, together with the first comparative analysis of the mouse and human genomes. (Read NIH news release at http://www.genome.gov/page.cfm?pageID=10005831.) In a companion paper published in today's Genome Research journal, Pevzner and Tesler (in collaboration with Michael Kamal and Eric Lander at the Whitehead/MIT Center for Genome Research) analyze human-mouse genome rearrangements for insights about the evolution of mammals, and outline their development of a new algorithm to differentiate macro- and micro-level genome rearrangements.
Their conclusion: although the mouse and human genomes are very similar, genome rearrangements occurred more commonly than previously believed, accounting for the evolutionary distance between human and mouse from a common ancestor 75 million years ago. "The human and mouse genome sequences can be viewed as two decks of cards obtained by re-shuffling from a master deck--an ancestral mammalian genome," said Pevzner. "And in addition to the major rearrangements that shuffle large chunks of the gene pool, our research confirmed another process that shuffles only small chunks." "We now estimate over 245 major rearrangements that represent dramatic evolutionary events," added Tesler. “In addition, many of those segments reveal multiple micro-rearrangements, over 3,000 within these major blocks—a much higher figure than previously thought (even though some of them may be caused by inaccuracies in the draft sequences)."
To go along with the announcement of the mouse genome sequencing Nature has a collection of articles on the importance of mice in biomedical research. I don't like the funky page design where each choice on that page brings up a pop-up where then one can click to get various articles. But some of the articles are quite interesting. For instance, in this article various scientists describe how the mouse genome sequence data speeds up their work.
While Jenkins and Copeland look back fondly on those early days, the mouse genome sequence (see page 520) is accelerating their research in ways that make their past achievements seem pedestrian. Back in the 1980s, if Jenkins and Copeland were interested in investigating a spontaneous mutation presented at the Jackson Lab's weekly 'Mutant Mouse Circus', it was a laborious process. Identifying the gene involved meant crossing about 1,000 mice to map it to a stretch of chromosome bearing about 20 candidate genes. From there, a postdoc would have to sequence all of them in both normal and mutant mice to find out which was mutated.
"It used to be one postdoc project per mutation...," says Jenkins, "...and it was like looking for a needle in a haystack," adds Copeland. But since the mouse genome sequence became available in May (at http://www.ensembl.org/Mus_musculus), researchers can simply go to the database after the initial breeding experiments and look up all the genes in the relevant chromosomal region. By knowing from their sequences what types of proteins most of them encode, they can choose one or two that look most promising to search for the mutation.
"It took us 15 years to get 10 possible cancer genes before we had the sequence," says Copeland. "And it took us a few months to get 130 genes once we had the sequence." What's more, Jenkins points out, going back and forth between the mouse and human genomes will help to target related human genes that could be candidates for drug development.
This Nature article is especially interesting because it gives a sense of the sheer size of the job of some figuring out how mouse cells function and what methods may help to make the problem more tractable.
One experimental approach in which thousands of genes can be analysed in parallel is to isolate messenger RNA and to display the gene-expression profile on a chip. When this technique is applied to tissues, data are lost because aspects of the three-dimensional structures of multiple cell types are destroyed in the biochemical extraction. Data from in situ analyses contain more detailed information about each gene, but the generation of these data is serial and significantly slower.
Gene expression is being systematically examined at the transcriptional level by several groups, for instance in the 9.5-day-old mouse embryo and in adult tissues (see Box). Two other papers in this issue3, 4 report large-scale analyses of gene expression in embryonic and adult stages, but so far have examined just 0.5% of the genes in the genome, the homologues of the genes on chromosome 21. Transcription studies in situ have relatively limited resolution, and the tissues constituting a multicellular organism are complex mixtures of different cell types. Unless each cell is individually visualized for gene expression in combination with histological criteria, important information relating to biological function is lost, for instance the subcellular compartment(s) occupied by a protein.
The Sanger Institute's Atlas project is being established to systematically examine the expression pattern of every gene product at tissue-, cellular- and subcellular-level resolution, to provide a permanent, definitive and accessible record of the molecular architecture of normal tissues and cells. The ultimate goal is to define protein expression patterns for all 30,000 mouse genes in hundreds of different tissues, all gathered in archival data sets to support research projects worldwide. Data will be collected electronically and archived with a vocabulary allowing complex queries.
A recent report that is quite independent of the mouse genome sequencing effort demonstrates how mice are viewed as such a useful tool that scientists will transfer human genes into mice in order to be able to study the genes more easily.
Philadelphia, PA –Researchers at the University of Pennsylvania School of Medicine have bred a mouse to model human L1 retrotransposons, the so-called "jumping genes." Retrotransposons are small stretches of DNA that are copied from one location in the genome and inserted elsewhere, typically during the genesis of sperm and egg cells. The L1 variety of retrotransposons, in particular, are responsible for about one third of the human genome.
The mouse model of L1 retrotransposition is expected to increase our understanding of the nature of jumping genes and their implication in disease. According to the Penn researchers, the mouse model may also prove to be a useful tool for studying how a gene functions by knocking it out through L1 insertion. Their report is in the December issue of Nature Genetics and currently available online (see below for URL).
"There are about a half million L1 sequences in the human genome, of which 80 to 100 remain an active source of mutation," said Haig H. Kazazian, Jr., MD, Chair of Penn's Department of Genetics and senior author in the study. "This animal model will help us better understand how this happens, as well as provide a useful tool for discovering the function of known genes."
In humans, retrotransposons cause mutations in germ line cells, such as sperm, which continually divide and multiply. Like an errant bit of computer code that gets reproduced and spread online, retrotransposons are adept at being copied from one location and placed elsewhere in the chromosomes. When retrotransposons are inserted into important genes, they can cause disease, such as hemophilia and muscular dystrophy. On the other hand, retrotransposons have been around for 500 to 600 million years, and have contributed a lot to evolutionary change.
Its worth noting about this latest report that according to the mouse and human DNA sequencing project scientsts humans have more junk DNA than mice do and that mice may actually have just as much functional DNA as humans even though the human genome is bigger in total size. The human transposons mentioned in this report may have something to do with this state of affairs. Humans may have been under less selective pressure to keep down the amount of genetic waste that builds up (really probably parasitic DNA) or the human transposons might serve a more useful purpose than mouse transposons do. It will also be interesting to see how the work in this area progresses.
The availability of the mouse genome sequence is already accelerating efforts to understand the human genome more quickly. Also, the sequence data is going to be very helpful for scientists who are using mice to understand general phenomena in mammalian metabolism and cellular genetic regulation. Efforts to create genetically engineered mouse equivalents of human illnesses will be greatly helped by the identification of mouse equivalents of genes in humans. Still, most of the hard work is still to be done. It is much easier to figure out the primary sequence of a genome than it is to figure out how the expression of all genes is controlled or how all proteins function and interact with each other. Many more advances are needed in laboratory techniques, instrumentation, and in computer modelling in order to be able to fully understand how a single cell functions in all its complexity.
Yesterday's release also continues a pattern of humbling genetic revelations. Earlier research showed that humans had scarcely more genes than the lowly roundworm. Now there's proof that people are closely related to tiny, furry rodents.
''We even have the genes that could make a tail,'' said Dr. Jane Rogers, of the Wellcome Trust Sanger Institute in Cambridge, England.
Think could be used to discover the political sympathies of a suspected traitor or terrorist.
In the study, Decety and doctoral student Thierry Chaminade used positron emission tomography (PET) scans to explore what brain systems were activated while people watched videos of actors telling stories that were either sad or neutral in tone. The neutral stories were based on everyday activities such as cooking and shopping. The sad stories described events that could have happened to anyone, such as a drowning accident or the illness of a close relative. The actors were videotaped telling the stories, which lasted one to two minutes, with three different expressions – neutral, happy or sad.
Decety and Chaminade found that, as people watched the videos, different brain regions were activated depending on whether an actor's expressions matched the emotional content of the story.
When the story content and expression were congruent, neural activity increased in emotional processing areas of the brain – the amygdala and the adjacent orbitofrontal cortex and the insula. In addition, increased activation also was noted in what neuroscientists call the "shared representational" network which includes the right inferior parietal cortex and premotor cortex. This network refers to brain areas that are activated when a person has a mental image of performing an action, actually performs that action or observes someone else performing it.
However, these emotional processing areas were suppressed when the story content and expression were mismatched, such as by having a person smile while telling about his mother's death. Instead, activation was centered in the ventromedial prefrontal cortex and superior frontal gyrus, regions that deal with social conflict.
After watching each video clip, the 12 subjects in the study also were asked to rate the storyteller's mood and likability. Not surprisingly the subjects found the storytellers more likable and felt more sympathetic toward them when their emotional expression matched a story's content than when it did not.
"Sympathy is a very basic way in which we are connected to other people," said Decety. "We feel more sympathy if the person we are interacting with is more like us. When people act in strange ways, you feel that person is not like you.
"It is important to note that the emotional processing network of the brain was not activated when the subjects in our study watched what we would consider to be inappropriate social behavior. Knowing how the brain typically functions in people when they are sympathetic will lead to a better understanding of why some individuals lack sympathy."
Imagine a future where people can be genetically engineered to lack sympathy. I think the technical ability to eventually do this is a matter of when, not if. PET Scans might be used to detect the equivalent of Blade Runner replicants.
If SD-6 started using this technique to look for sympathy then Sydney Bristow of Alias could be in a whole world of trouble. Still, it would be hard to word the questions to trip her up since she is supposed to believe that by working for SD-6 she's already working for the CIA.
While their manufacturing process uses fewer silicon wafers they neglect to say how much that will reduce the manufacturing cost of their cells.
A joint venture between the Australian National University and Origin Energy has developed a new type of solar cell with the potential to revolutionise the global solar power industry.
Director of the ANU Centre for Sustainable Energy Systems, Professor Andrew Blakers today unveiled the Sliver CellTM, which uses just one tenth of the costly silicon used in conventional solar panels while matching power, performance and efficiency.
Professor Blakers said, "A solar panel using Sliver CellTM technology needs the equivalent of two silicon wafers to convert sunlight to 140 watts of power. By comparison, a conventional solar panel needs about 60 silicon wafers to achieve this performance.
"By dramatically reducing the amount of expensive pure silicon, the largest cost in solar panels today, this new technology represents a major advance in solar power technology."
Origin Energy's Executive General Manager, Generation, Andrew Stock said, "Origin Energy has worked with ANU's Centre for Sustainable Energy Systems for several years, investing more than $6 million in research to discover a way to harness the sun's power at much lower cost.
"Due to the economy and flexibility of Sliver CellsTM, we believe this technology will play an important role in the future wide-spread adoption of solar power. Sliver CellTM technology is an excellent example of the way Australian researchers can work with Australian industry to innovate a product that leads the world".
ANU Vice-Chancellor, Professor Ian Chubb welcomed the research breakthrough. "Origin Energy is to be congratulated for its foresight and persistence in supporting the ANU team in this project. The company has made a substantial contribution since establishing the research partnership with ANU," Professor Chubb said.
The most expensive part of traditional solar power panels is the silicon from which the individual cells are made. The Sliver CellTM is a radically different concept in photovoltaics. Sliver CellsTM are produced using special micro-machining techniques, then assembled into solar panels using similar methods to those used to make conventional solar panels.
The new technology reduces costs in two main ways – by using much less expensive silicon for similar efficiency and power output, and needing less capital to build a solar panel plant of similar capacity.
The unique attributes of Sliver CellTM technology could open many new Sliver CellTM applications, in addition to conventional rooftop and off-grid uses, including:
- Transparent Sliver CellTM panes to replace building windows and cladding
- Flexible, roll-up solar panels
- High-voltage solar panels, and
- Solar powered aircraft, satellite and surveillance systems
Ray Kurzweil reviews the talks given by participants of the Fifth Annual Alcor Conference on Extreme Life Extension.
Robert Freitas is a Research Scientist at Zyvex, a nanotechnology company, and in my view the world's leading pioneer in nanomedicine. He is the author of a book by the same name and the inventor of a number of brilliant conceptual designs for medical nanorobots. In his first major presentation of his pioneering conceptual designs, Freitas began his lecture by lamenting that "natural death is the greatest human catastrophe." The tragedy of medically preventable natural deaths "imposes terrible costs on humanity, including the destruction of vast quantities of human knowledge and human capital." He predicted that "future medical technologies, especially nanomedicine, may permit us first to arrest, and later to reverse, the biological effects of aging and most of the current causes of natural death."
Freitas presented his design for "respirocytes," nanoengineered replacements for red blood cells. Although much smaller than biological red blood cells, an analysis of their functionality demonstrates that augmenting one's blood supply with these high pressure devices would enable a person to sit at the bottom of a pool for four hours, or to perform an Olympic sprint for 12 minutes, without taking a breath. Freitas presented a more complex blueprint for robotic "microbivores," white blood cell replacements that would be hundreds of times faster than normal white blood cells.
Freitas has the full text of his conference lecture entitled "Death Is An Outrage" on his web site.
The end result of all these nanomedical advances will be to enable a process I call “dechronification” – or, “rolling back the clock.” I see no serious ethical problems with this. According to the volitional normative model of disease that is most appropriate for nanomedicine, if you’re physiologically old and don’t want to be, then for you, oldness and aging are a disease, and you deserve to be cured. After all, what’s the use of living many extra hundreds of years in a body that lacks the youthful appearance and vigor that you desire? Dechronification will first arrest biological aging, then reduce your biological age by performing three kinds of procedures on each one of the 4 trillion tissue cells in your body.
* First, a respirocyte- or microbivore-class device will be sent to enter every tissue cell, to remove accumulating metabolic toxins and undegradable material. Afterwards, these toxins will continue to slowly re-accumulate as they have all your life, so you’ll probably need a whole-body cleanout to prevent further aging, maybe once a year.
* Second, chromosome replacement therapy can be used to correct accumulated genetic damage and mutations in every one of your cells. This might also be repeated annually.
* Third, persistent cellular structural damage that the cell cannot repair by itself such as enlarged or disabled mitochondria can be reversed as required, on a cell by cell basis, using cellular repair devices.
We’re still a long way from having complete theoretical designs for many of these machines, but they all appear possible in theory, so eventually we will have good designs for them.
Freitas links to another article of his that further expounds on the coming ability of nanobots to repair bodies and reverse aging:
Artificial "biobots" could be in our bodies within five to 10 years. Advances in genetic engineering are likely to allow us to construct an artificial microbe - a basic cellular chassis - to perform certain functions. These biobots could be designed to produce vitamins, hormones, enzymes or cytokines in which the host body was deficient, or they could be programmed to selectively absorb and break down poisons and toxins. A new company called engeneOS, Inc., founded in late 2000, has already announced plans to develop artificial Engineered Genomic Operating Systems using the techniques of molecular biology. These systems will comprise a library of component device modules and proprietary modular components. This will allow the engineering and construction of programmable biobots with novel form and function.
Unfortunately, Kurzweil says little about Aubrey de Grey's presentation at the conference and yet de Grey is proposing the development of some fairly specific rejuvenation techniques that show a lot of promise. What is important about the techniques that Aubrey advocates is that they can be made to work many years before nanomedicine becomes possible. In fact, Aubrey argues (and I agree), that we know enough now about the molecular mechanisms of aging and that we already have sufficently advanced biochemical tools and techniques to start developing some forms of aging-reversal intervention. The candidate methods of intervention and aging reversal could be tested using the tools that biochemists and molecular biologists already possess and the results of the tests would show how much various interventions may help.
Aubrey also holds the radical view (and is having success in convincing a number of noted biologists on this) that it will be faster to the develop aging reversal therapies to avoid the diseases of old age than it will be to continue to try to develop treatments for those diseases to deal with the disorders of old age once they appear. His argument is that it is the processes of aging that are increasing the incidence of the many disorders of old age and so if we make our bodies younger we will avoid many of the diseases that inflict people as they grow older.
Aubrey has co-authored a paper with a prominent list of biologists (Aubrey D. N. J. de Grey, Bruce N. Ames, Julie K. Andersen, Andrzej Bartke, Judith Campisi, Christopher B. Heward, Roger J. M. McCarter and Gregory Stock) which describes some of the techniques that could be used to reverse aging. The paper is entitled Time to Talk SENS: Critiquing the Immutability of Human Aging.
Aging is a three-stage process: metabolism, damage and pathology. The biochemical processes that sustain life generate toxins as an intrinsic side-effect. These toxins cause damage, of which a small proportion cannot be removed by any endogenous repair process and thus accumulates. This accumulating damage ultimately drives age-related degeneration. Interventions can be designed at all three stages. However, intervention in metabolism can only modestly postpone pathology, because production of toxins is so intrinsic a property of metabolic processes that greatly reducing that production would entail fundamental redesign of those processes. Similarly, intervention in pathology is a "losing battle" if the damage that drives it is accumulating unabated. By contrast, intervention to remove the accumulating damage would sever the link between metabolism and pathology, so has the potential to postpone aging indefinitely. We survey the major categories of such damage and the ways in which, with current or foreseeable biotechnology, they could be reversed. Such ways exist in all cases, implying that indefinite postponement of aging – which we term "engineered negligible senescence" – may be within sight. Given the major demographic consequences if it came about, this possibility merits urgent debate.
The term "negligible senescence" was coined1 to denote the absence of a statistically detectable increase with organismal age in a species’ mortality rate. It is accepted as the best operational definition of the absence of aging, since aging is itself best defined as an increase with time in the organism’s susceptibility to life-threatening challenges. It has been compellingly shown to exist only in one metazoan, Hydra;2 certain cold-blooded vertebrates may exhibit negligible senescence but limitations of sample size leave the question open;1 and it has not been suggested that any warm-blooded animal (homeotherm) does so. Indeed, humans are among the slowest-aging homeotherms.
Since Gilgamesh, civilization has sought to emulate Hydra – to achieve a perpetually youthful physiological state – by intervention to combat the aging process. Such efforts may appropriately be termed "strategies for engineered negligible senescence" (SENS). This phrase makes explicit the inevitable exposure to extrinsic, age-independent causes of death (which is blurred by more populist terms such as "immortality" or "eternal youth"), while also stressing the goal-driven, clinical nature of the task (in contrast to the basic-science tenor of, for example, "interventive biogerontology"). Here we discuss the feasibility, within about a decade, of substantive progress towards that goal.
Click thru and read the full paper. If you don't have college level training in biology it might be a bit hard to follow on some points. But most of it can be understood by the interested layman.
A press release from Argonne National Laboratory reports on an attempt to make an embeddable replacement artificial retina.
LOS ANGELES, Nov. 26, 2002 – Secretary of Energy Spencer Abraham toured the University of Southern California's ophthalmology laboratories at the Doheny Eye Institute and heard from the national research team that hopes to restore vision to millions of people with blindness caused by retinal disorders. As a result of recent breakthroughs in science and engineering technology, Abraham announced that DOE will commit $9 million over three years to augment artificial retina research, including support for a laboratory within the Doheny Eye Institute on the USC campus.
The DOE national labs, partnering with the University of Southern California and North Carolina State University, are designing a micro-electronic device that would be implanted in the eye on the surface of the retina. A microelectrode array would perform the function of normal photoreceptive cells.
You can find more about this recent announcement in this UPI article.
Optobionics cofounders Vincent Chow and Dr. Alan Chow have invented and already surgically implanted their Artificial Silicon Retina in some human test subjects. The seeing abilty it provides is still pretty crude. But its impressive there are actually people walking around using their device. From an ABC News report in May 2002 the results for some test subjects are described:
Two years ago, Chow put an artificial retina into Bennett's right eye. Before surgery she couldn't see a thing, but when the bandages came off, she was shocked.
She can now see light and shadow, which means she can slowly find her way around. Bennett still cannot see shapes. But is it better than what she had before?
"Oh Lord, yes, yes," Bennett said.
John Crocker, another of Chow's patients, was blind for more than 50 years. But right after his operation, he got a huge surprise.
"I was walking through the house," Crocker said. "And I stopped and I looked and I could see the lights on our Christmas tree, which is the first time that's ever happened for a long time."
However, the Optobionics implant is providing more benefit than expected because its providing a source of stimulation that is somehow improving the functioning of the real retina:
How the Optobionics ASR works:
What Dr. Chow found is that the chips also seem to be stimulating remaining healthy cells.
"We're pretty excited. We initially expected only some light perception where the implant was. What seems to be improvement outside the areas was unexpected," he said.
He said the device is having a "rescue effect" on the retina, restoring cells located near the implant site.
"What we think is happening is the implant is stimulating other cells around the retina. We're finding vision is improving not just where the implant is but also in areas near the implant," he said.
The ASR™ microchip is a silicon chip 2mm in diameter and 25 microns thick, less than the thickness of a human hair. It contains approximately 5,000 microscopic solar cells called “microphotodiodes,” each with its own stimulating electrode. These microphotodiodes are designed to convert the light energy from images into electricalchemical impulses that stimulate the remaining functional cells of the retina in patients with AMD and RP types of conditions.
The ASR microchip is powered solely by incident light and does not require the use of external wires or batteries. When surgically implanted under the retina—in a location known as the “subretinal space”—the ASR chip is designed to produce visual signals similar to those produced by the photoreceptor layer. From their subretinal location, these artificial “photoelectric” signals from the ASR microchip are in a position to induce biological visual signals in the remaining functional retinal cells which may be processed and sent via the optic nerve to the brain.
Click thru to the previous link to see a picture of the ASR on a penny. Its quite small.
The Blindness Foundation is supporting a number of other groups which are also working on artificial retina development:
Several other research groups are working to develop an artificial retina. The Foundation currently supports two groups: Dr. Eugene de Juan and Mark Humayun of The Foundation’s Research Center at Johns Hopkins University, and Drs. Joseph Rizzo and John Wyatt, of Harvard Medical School and Massachusetts Institute of Technology, respectively. The Foundation also supports Dr. Richard Normann at the University of Utah, who is developing a silicon chip to be implanted in the visual cortex of the brain.
Obviously the first users for this sort of technology will be blind people. It will be a wonderful boon that will restore eyesight for millions of people. But what comes next? Once the resolution of an artificial retina can exceed that of a human eye (and that is a matter of when, not if) and it becomes possible to combine it with an artificial iris that has zoom capablity then suddenly artificial eye implants will become attractive for people with perfectly healthy eyes. If the future artificial retinas can be made from thin films that can shift their molecular configurations on-the-fly then it ought to be possible to even reconfigure (perhaps by straining eye muscles in some trained pattern) the retinas to look at different parts of the light spectrum as well. Imagine, for instance, soldiers or police shifting their eyesight into the infrared when on a dangerous nighttime operation. Or imagine just any person wanting to up their light sensitivity when outside at night or in a room with little available light.
Sufficiently advanced technologies developed to treat disease conditions will inevitably morph into technologies that will enhance function. Research on artificial implants for blindness is laying the groundwork for the eventual development of vastly superior artificially enhanced eyesight.
Update: Here are some details on the role that Lawrence Livermore National Laboratory plays in the DOE artificial retina projectp
Lawrence Livermore National Laboratory engineers are developing a microelectrode array for a multi-laboratory DOE project to construct an artificial retina or "epiretinal prosthesis."
LLNL's polymer-based microelectrode array.
The three-year DOE project brings together national labs, universities and a private company, with Oak Ridge serving as the lead laboratory.
An epiretinal prosthesis could restore vision to millions of people suffering from eye diseases such as retinitis pigmentosa, macular degeneration or those who are legally blind due to the loss of photoreceptor function. In many cases, the neural cells to which the photoreceptors are connected remain functional.
Project leader Dr. Mark Humayun, of the University of Southern California, has shown that electrical stimulation of the viable retinal cells can result in visual perception. These findings have sparked a worldwide effort to develop a retinal prosthesis device.
Expertise in biomedical microsystems at Lawrence Livermore's Center for Microtechnology is being tapped to develop a "flexible microelectrode array," able to conform to the curved shape of the retina, without damaging the delicate retinal tissue, and to integrate electronics developed by North Carolina State University. The device will serve as the interface between an electronic imaging system and the human eye, directly stimulating neurons via thin film conducting traces and electroplated electrodes.
"We're very excited to be a part of this collaboration," said Peter Krulevitch of the Lab's Center for Microtechnology and leader of the team developing the flexible microelectrode array. Other LLNL team members include LLNL employee and UC Davis graduate student Mariam Maghribi, fabrication technician Julie Hamilton, participating guest Dennis Polla, undergraduate summer student Armando Tovar from Trinity University, MIT graduate student Christina Park, engineer Courtney Davidson and scientist Tom Wilson.
Lab engineers have pioneered the use of poly(dimethylsiloxane), a form of silicone rubber simply called PDMS, in fabricating hybrid integrated microsystems for biomedical applications. In particular, the Lab has worked on "metalization" -- applying metals for electronics and electrodes to PDMS for implant devices.
"It's our important contribution to this project," Krulevitch said. "We've developed a technique for fabricating metal lines that can be stretched. This is really critical for a flexible device designed to conform to the shape of the retina."
The electronic array must be robust enough to withstand damage from the implant procedure and be biocompatible -- able to withstand the physiological conditions in the eye. Another reason for using PDMS is that silicone rubber is not only flexible, but is a promising material from a biocompatibility standpoint.
Humayun's group implanted three first-generation LLNL devices in a dog's eye to identify needed design and fabrication improvements. Livermore engineers are now working on a second-generation microelectrode array with smaller electrodes in greater numbers, and developing techniques to integrate the electrodes with electronics chips. The array's perimeter -- 4 mm across -- has been reinforced with micromolded ribs to facilitate handling and prevent curling or folding. The current version of the array is longer for short-term implant experiments. But the final device for implant will measure 4 mm by 4 mm.
Applications for the flexible electrode array go beyond the retinal prosthesis, according to Krulevitch, who says it has the potential to allow development of next-generation medical implant devices such as the "cochlear implant" for hearing. The technology could one day be used for "deep brain stimulation devices" for treating such diseases as Parkinson's, and spinal cord stimulation devices for treatment of chronic pain.###
Partners in the project include Oak Ridge, Argonne, Sandia, Los Alamos, USC Doheny Eye Institute and North Carolina State University.
For more information on the overall DOE Artificial Retina project, check the Web at: http://www.energy.gov/HQPress/releases02/novpr/pr02248.htm
Founded in 1952, Lawrence Livermore National Laboratory has a mission to ensure national security and to apply science and technology to the important issues of our time. Lawrence Livermore National Laboratory is managed by the University of California for the U.S. Department of Energy's National Nuclear Security Administration.
Laboratory news releases and photos are also available electronically on the World Wide Web of the Internet at URL http://www.llnl.gov/PAO and on UC Newswire.