An international team of scientists reports that a single 400-milligram daily dose of celecoxib, commonly called Celebrex® and manufactured by Pfizer, significantly reduced recurrence of adenomas, or pre-malignant colon tumors - within three years of previous adenoma removal.
The New England Journal of Medicine today published findings from the Prevention of Spontaneous Adenomatous Polyps (PreSAP) study, involving more than 1,550 participants at 107 sites in 32 countries on six continents. The study was led by Nadir Arber, M.D., chair of the Integrated Cancer Prevention Center and professor of medicine and gastroenterology at the Tel Aviv Sourasky Medical Center and Bernard Levin, M.D., vice president of Cancer Prevention and Population Sciences at The University of Texas M. D. Anderson Cancer Center.
"Celecoxib 400 mg once daily significantly reduced colorectal adenoma occurrence, with a greater effect on advanced adenomas," said Arber.
As excess amounts of the protein cyclooxygenase (COX-2) are associated with adenomas and colon cancer, PreSAP researchers studied celecoxib - a selective COX-2 inhibitor - to prevent the pre-cancerous lesions.
The differences between the placebo and celecoxib groups was substantial.
In the placebo-controlled, double-blind PreSAP trial, study leaders randomly assigned participants to receive either a single 400-mg dose of celecoxib (approximately 930 subjects) or a placebo (nearly 630 subjects). Subjects received colonoscopies after one and three years to detect potential pre-malignant tumors and their sizes, as well the overall adenoma burdens for participants. All polyps were removed and examined by study pathologists.
At the conclusion of the trial, the cumulative adenoma rate for the celecoxib study group was 33.6 percent, while the cumulative rate of adenoma development in the placebo group was 49.3 percent (a 36 percent reduction). Celecoxib administration was associated with a 50 percent reduction in larger, potentially more dangerous adenomas.
"Unlike the recent Adenoma Prevention with Celecoxib (APC) trial, we did not find a statistically significant increase in cardiovascular risk associated with the use of 400 mg of celecoxib once daily," said Levin. "That said, because of the significant cardiac side effects seen in the APC study, further cardiovascular research on the use of all anti-inflammatory drugs, such as Celebrex®, Aleve® and Motrin®, as chemoprevention tools is warranted.
"Low dose aspirin also has been shown to reduce adenoma formation in individuals with a prior history of polyps and has the potential to decrease cardiovascular disease risk," said Levin. "However, its use is associated with an increased risk of upper-gastrointestinal bleeding and stroke."
Drugs have trade-offs. As better methods of detecting risks are developed we'll gain better ways to estimate the risks each of us face. We do not all share the same levels of risk of cancer, stroke, heart disease, and other killers. A person at great risk of colon cancer but low risk of heart disease and stroke would gain far more from celecoxib than someone with the opposite pattern of relative risks.
A couple of other recent papers give a sense of the interest medical researchers have in celecoxib against cancer: Celecoxib and Curcumin Synergistically Inhibit the Growth of Colorectal Cancer Cells and Radiosensitivity Enhancement by Combined Treatment of Celecoxib and Gefitinib on Human Lung Cancer Cells. Celecoxib might also slow the development of prostate cancer. Celecoxib might also be helpful against breast cancer.
Generally, COX-2 works by regulating the production of prostaglandins in cells. In the Mayo study, celecoxib reduced levels of COX-2 protein in mammary tumor cells; the therapy was even more effective in minimizing the amounts of COX-2 dependent prostaglandin E metabolites in mammary tumor cells.
“Celecoxib treatment appears to exert its antiproliferative, antiangiogenic, and pro-apoptotic effects by regulating the prostaglandin pathways,” Mukherjee said. “This leads to the reduction in primary breast tumor mass.”
She noted that in an experiment with a limited number of mice, celecoxib appeared to completely inhibit metastasis of the breast tumor.
A COX-2 inhibitor is not going to cure cancer all by itself. But all the ways that cancer cells differ from regular cells make potential targets for drugs that target those differences. Some cancers will get cured by using multiple drugs to target many differences of cancer cells at once. Celecoxib should be seen as a potential player in multi-drug therapies aimed at hitting cancer cells in many ways at once.
Democratic lawmakers and Gov. Arnold Schwarzenegger on Wednesday struck a deal on legislation to reduce the state's greenhouse gas emissions by 25 percent over the next two decades.
Under the bill, California would take the lead in limiting greenhouse gas by reducing emissions to 1990 levels by the year 2020.
This can only be accomplished by either much higher energy prices or big technological advances. California has a better chance of achieving this goal of the price of oil remains high.
California's economy and population have grown since 1990. So to reach the 1990 level of emissions California will have to cut emissions 25%.
Democrats and top aides to Gov. Arnold Schwarzenegger have spent the last few months negotiating a bill that would put the state on the path to reducing its emissions by an estimated 25 percent by 2020, to the levels of 1990.
But the cut per capita will be higher due to population growth which will occur in the next 15 years. Though the state government could (at least in theory) set fossil fuels energy taxes so high that the population of the state declines.
The bill gives the California Air Resources Board, which enforces the state’s air pollution controls, the lead authority for generally establishing how much industry groups contribute to global warming pollution, for assigning emission targets, and for setting noncompliance penalties. It sets out a two-year time frame, until 2009, to establish how the system will operate and then allows three years, until 2012, for the industries to start their cutbacks.
Will California state, county, and local governments be forced to reduce emissions by 25%? Or will they take the "Do as I say, not as I do" approach.
Also, will most of the requirement for emissions reduction be placed on industry and not on private individuals or governments? If that happens then the percentage decrease in energy for industry will be much higher than 25%.
Will some future California legislature scale back the ambitions of this law? Will exemptions be made or time tables changed? I suspect so.
Rising energy prices in California will drive higher energy using industries to move to other states or abroad. Also, rather than build CO2 emitting coal and natural gas fed electric power plants the state government could let electric prices rise until demand falls enogh to cause a great reduction in CO2 emissions by power plants.
Update: Think about the politics involved in implementing such a large reduction in CO2 emissions. Will fear of the mass of voters prevent the California state government from upping gasoline taxes? If so, the goal becomes hard to meet by energy demand reduction.. Demand for energy will rise greatly by 2020. The size of reduction needed as compared to trend is probably more on the order of 35% or 40%. How to accomplish that without providing a strong disincentive against use of vehicles?
The big recent run-up in oil prices has temporarily almost stopped the growth in US oil demand,. But to actually reverse oil demand growth and by such a large amount is far harder. It can be done with prices or with technological innovations. To do it with prices probably would require an additional gasoline tax of $3 or $4 or $5. Elected representatives of the people aren't going to do that to their voters - not in America anyway.
Biomass might be able to do it. The ratio of hydrocarbons out to hydrocarbons in for farming will improve in the next 15 years. Cellulosic technology and bioengineered plants could make biomass ethanol a viable way to reduce net carbon emissions.
Another possibility comes from breakthroughs in battery technology. A shift to electric cars would make it pretty easy to make a huge cutback in carbon dioxide emissions. Electric power plants burning coal and natural gas could probably sequester carbon for about 2 cents a kilowatt hour. Also, wind power will get cheaper.
I also wonder how much the goal will get met by cheating. How to cheat? Buy electricity from another state. Build electric power generator plants in Nevada and ship the electric power in. Emissions would drop in California.
Heavy energy using industries in California should start developing their exit strategies. Their cheapest way to emit less in Calfornia is to emit more somewhere else.
I also expect a lot of money to pour into lobbying in Sacramento as various industries and groups play a game of political hot potato and try to win exemptions for their groups from emissions reductions requirements.
The costs of achieving the goals of the new legislation are unknown. Traditional coal-fired power plants emit about a ton of carbon dioxide per megawatt-hour generated. State-of-the-art gas-fired power plants emit about half that amount. Currently, credits for voluntary reductions in the U.S. trade for anywhere from $1 a ton to $5 a ton. However, nobody knows what those prices will be under a mandatory, California-only market.
$1 per 1000 kwh would be a tenth of a penny per kwh as compared to a California electric price of about 13 cents per kwh or about 8 cents per kwh nationally. So a tenth of a penny wouldn't impact electric power prices much. But I do not see where a supply of carbon credits would be large enough to supply the entire electric power industry.
The California plan, which won final legislative approval Thursday but which still faces a battle in the courts before it can take effect, calls for a 25 percent cut in emissions of carbon dioxide by 2020. It envisions controls on some of the largest industrial groups including utilities and oil refineries.
Oil can get refined in other states and piped in. Big computer server farms can move out of the state and get accessed over the internet.
What businesses would be affected?
Utility plants, oil and gas refineries, factories and cement kilns, among other major emitters of the gases.
California can not accomplish its goal unless it reduces gasoline consumption. But it might not have the legal authority to cut tailpipe CO2 emissions. If the state government tries to cut everything else more in order to make up for the inability to cut vehicle tailpipe emissions then energy for non-transportation purposes will have to become very expensive.
While environmentalists are hailing the measure, some businesses argue that the only way for oil refineries to meet the tough caps would be to reduce production of transportation fuels by 17%, said Tupper Hull, a spokesman for the Western States Petroleum Association trade group. "This has the potential to be very damaging to the California economy," Hull said. "It will put a lot of strain on the marketplace." Already, Hull said, the state's 14 refineries are operating at capacity, producing 45 million gallons of gasoline and diesel a day. California also imports 3.5 million gallons a day from other regions.
California can't stop that importation. If the state did then the importers could sue in federal court on US constitutional grounds.
Here is why I think that refiners and electric power generators from outside of California will be able to generate carbon emissions and sell their products into California unhindered by the state government's attempt to reduce greenhouse gas emissions.
Section 8. The Congress shall have power to lay and collect taxes, duties, imposts and excises, to pay the debts and provide for the common defense and general welfare of the United States; but all duties, imposts and excises shall be uniform throughout the United States;
To borrow money on the credit of the United States;
To regulate commerce with foreign nations, and among the several states, and with the Indian tribes;
I expect we will see court cases fought over the application of this legislation where interstate commerce is involved. Sellers of electricity, refined oil products, and other products will fight in court for their ability to produce outside of California and sell into California. Oregon, Baja California Mexico and other neighoring regions will produce and sell more energy products into California as a result of this legislation.
GM has announced a new V8 turbo diesel that will fit in cars which currently use the GM small block V8 but will be 25% more fuel efficient. The engine is quiet enough to sound like a conventional gasoline engine and will meet all state and federal diesel engine emissions standards in 2010. The fuel efficient diesel will hit the market in 2010 or 2011.
Details are scanty, because GM is waiting to receive patents on some of the engine's technology, but Freese promised it would meet emissions requirements in all 50 states when it goes on sale. That's a significant accomplishment. The United States will have the most stringent limits on diesel emissions in the world in 2010.
GM is billing this engine as a premium diesel for use in Cadillacs and SUVs where the higher price for the diesel can be more easily justified.
• GM promises the engine will use 25% less fuel than a comparable gasoline V8.
• GM developed the engine to match or beat the world's finest diesels on power, fuel economy, sound and vibration. That makes it what Freese calls a premium diesel, like the ones that power most luxury sedans like the Audi A8, BMW 7-series and Mercedes-Benz S-class in Germany.
Diesels have not reached as wide a market in the US as they do in Europe in large part because diesels cost $1000 to $2000 more and the cheaper fuel in the US reduces the pay back for the more expensive diesel engines. Also, the diesels have been louder and smellier and their emissions have kept them out of cars in some states (most notably California). The higher cost of oil combined with technological innovations that lower noise and emissions might bring about a surge in diesel usage in the United States.
With these changes come a strengthened block and upgraded main bearings. All of these improvements will, however, require the use of new low-sulphur diesel, which is slated to hit fuel stations this fall. The new diesel is key to the particulate filters success, as it only contains 15 parts per million of sulphur, down from the current 550 parts per million. If our current diesel fuel were used, the engine wouldnt last long.
Quiet, low emissions, and high performance diesels for passenger cars will compete against gasoline hybrids as more fuel efficient alternatives to conventional gasoline cars. The most efficient liquid fuel burning car would use both a diesel engine and hybrid technology. But that pairing would combine the higher costs of diesels with the higher costs of hybrids. So I'm not sure we'll ever see hybrid diesel passenger cars in mass production.
Will the cost of hybrids fall far enough that by 2010 even very clean and quiet diesels won't be able to compete? If battery density increases enough then pluggable hybrids (i.e. hybrids that you can plug into an electric cord to recharge their batteries) might outcompete diesels due to the lower cost of electricity as a way to power an automobile.
Another competitive pressure for diesels is ethanol. Ethanol has a lower production cost than diesel fuel. If the production of ethanol scales up high enough then by 2010 ethanol (even adjusted for its lower energy density per gallon) might be so much cheaper than diesel fuel that a hybrid or conventional car powered by ethanol might cost less per mile traveled than a car powered by diesel.
Assuming $3 per gallon gasoline, 15,000 miles driven per year, and applicable hefty tax credits for buying a hybrid an Edmunds study finds that the Toyota Prius and Ford Escape Hybrid are the only hybrids whose higher costs pay off within 3 years.
Edmunds.com's study indicates that the higher purchase price is completely recovered for the Ford Escape Hybrid and Toyota Prius within three years of ownership, while buyers of the Honda Civic Hybrid, Saturn VUE Green Line and Toyota Camry Hybrid reach break-even within six years of ownership, in each case assuming the vehicle is driven 15,000 miles per year.
The Prius does not have an exact non-hybrid equivalent to compare to. The Prius pays off within 2.1 years when compared against the Toyota Camry LE. But when compared against the Toyota Corolla LE it takes 13.6 years to pay off.
The rest of the hybrids take over 5 years to pay off. Some have abysmally long pay-off periods. The Toyota Highlander Hybrid Limited takes 15.5 years to pay off.
Full tax credits are only provided to consumers until shortly after each manufacturer has sold 60,000 hybrids. After that threshold is reached, the tax credit gets cut in half. For Toyota and Lexus buyers, that threshold has been reached — so anyone who buys a Toyota or Lexus hybrid after September 30, 2006 will only qualify for half the tax credit. The credit for these models will drop to 25% in April 2007 and then to zero in October 2007.
"If you're in the market for a hybrid, right now is the best time to buy," said Joanne Helperin, Senior Editor of Edmunds.com's Fuel Economy Guide. "It will take buyers much longer to break-even if their tax credit is halved."
These results do not represent the triumph of the free market. Even the impressive Prius pay-off period is due to a few thousand dollar US federal tax credit. (see this article for a summary table of results)
But beware: The numbers here include the Prius' gigantic $3,150 federal tax credit, which will drop to $1,575 in October, because the number of total Toyota hybrids sold has reached a 60,000-unit-per-manufacturer cap.
Commuters who put an average 25,000 miles on their vehicle will find their break-even times dramatically shortened (see chart below); those who drive significantly less than 15,000 miles per year will find it takes even longer to reach the break-even point.
I'm guessing the big hybrids have longer pay-off periods in part because their tax credits do not scale up as their prices do. So the tax credits end up representing a smaller percentage of total purchase price.
For low yearly mileage drivers (e.g. FuturePundit) hybrids are not worth the money. But if you are stuck driving long miles and can buy one before the tax credits decline the best hybrids can pay off in a few years. They'll pay off even faster if the price of gasoline goes even higher.
What is the biggest value of the current crop of hybrids? It is not that they save fuel. They are too few in number to have much impact on total fuel demand. It is not that they reduce air pollution. Again, they are too few in number to reduce the total amount of air pollution by all that much. Also it is not that they allow some people to feel morally superior or more better about their effect on the environment. No, none of those things. The biggest value of the current crop of hybrids is that they provide incentives for battery makers and entrepreneurs to create better hybrids.
NEW YORK August 24, 2006 -- Researchers at Columbia University Medical Center have successfully restored normal memory and synaptic function in mice suffering from Alzheimer's disease. The study was published today on the website of the journal Cell.
Scientists at Columbia's Taub Institute for Research on Alzheimer's Disease and the Aging Brain have identified an enzyme that is required for normal cognition but that is impaired in a mouse model of Alzheimer's. They discovered that mice regained the ability to form new memories when the enzyme's function was elevated.
The research suggests that boosting the function of this enzyme, known as ubiquitin C-terminal hydrolase L1 (Uch-L1), may provide a promising strategy for battling Alzheimer's disease, and perhaps reversing its effects.
In the new study, the Columbia researchers discovered that the enzyme Uch-L1 is part of a molecular network that controls a memory molecule called CREB, which is inhibited by amyloid beta proteins in people with Alzheimer's. By increasing Uch-L1 levels in mice that had Alzheimer's, they were able to improve the animals' ability to create new memories.
"Because the amyloid beta proteins that cause Alzheimer's may play a normal, important physiological role in the body, we can't destroy them as a therapy," explained Ottavio Arancio, M.D., Ph.D., Assistant Professor of Pathology at Columbia University Medical Center and co-principal investigator of the study with Michael Shelanski, MD, Ph.D., Chairman of the Department of Pathology at the Columbia University College of Physicians and Surgeons. "What makes this newly discovered enzyme exciting as a potentially effective therapy is that it restores memory without destroying amyloid beta proteins."
We'll have effective cures for Alzheimer's before cancer becomes totally curable. Alzheimer's is an easier problem.
"While amyloid beta is certainly a key player in Alzheimer's disease--and efforts to reduce it remain a worthy goal--our results show that, even in the presence of the plaque, damage to memory can be reversed."
The findings suggest that neurons' protein-ridding machinery, the so-called ubiquitin/proteasomal pathway, may play an important early role in the pathogenesis of Alzheimer's disease, he added.
Ubiquitin is a "tag" that marks proteins for destruction by the cellular "garbage disposal" known as the proteasome, Shelanski explained. Uch-L1 acts as the proteasome's "gatekeeper," he added. Before proteins can be eliminated by the proteasome, Uch-L1 must remove their ubiquitin tag.
Earlier studies found that the brains of Alzheimer's disease patients show an accumulation of ubiquitin-tagged proteins, suggesting some defect of the protein degradation machinery, the researchers noted. Studies of the brains of humans with Alzheimer's after death found evidence that the proteasome remained intact but largely unable to degrade proteins.
Interestingly, Uch-L1--a protein found almost exclusively in nerve cells--was also found at reduced levels in the Alzheimer's brain. Unpublished studies by Shelanski's group found that cells treated with Aß exhibited a rapid drop in Uch-L1, he said.
Uch-L1 doesn't sound like it stops the underlying cause of Alzheimer's. But if boosting it delays Alzheimer's disease progression drugs that boost Uch-L1 will buy Alzheimer's sufferers valuable time while treatments are devised that fix the underlying causes of the disease.
We need gene therapies that will rejuvenate the mechanisms which brain cells use to break down and remove proteins that are no longer needed. The aging of junk removal mechanisms probably leads to accumulation of junk in and around cells. That junk causes damage to cells and interferes with their operations and communications.
Development of treatments to improve intracellular and extracellular junk removal are two of the rejuvenation Strategies for Engineered Negligible Senescence (SENS).
A pair of studies in the New England Journal of Medicine find that contrary to a controversial CDC study (more on it here) released last year being overweight (which is less heavy than being obese) really does shorten life expectancy.
Being overweight during midlife is associated with an increased risk of death, according to a new study conducted by the National Cancer Institute (NCI), part of the National Institutes of Health, in collaboration with AARP, the nation's leading organization for persons 50-Plus. Results of the study appear in the August 24, 2006, issue of the New England Journal of Medicine*.
Previous research had established a link between obesity and increased risk of death, but whether a relationship also existed between being overweight and increased risk of death remained uncertain. In 2004, the Centers for Disease Control and Prevention (CDC) reported that 34.1 percent of the U.S. adult population was overweight, but not obese**. Overweight and obesity are defined using a measurement called body-mass index (BMI), calculated as a person's weight divided by the square of their height. A BMI of 18.5 - 25.0 is considered normal, whereas people who have a BMI of 25.0 - 29.9 are considered overweight, and individuals with a BMI over 30.0 are regarded as obese. (Click to view BMI chart)
The NIH-AARP Diet and Health Study of 527,265 monitored the health status of Americans from 1995 through 2005 via mailed questionnaires and by surveying death records. When the analysis focused on BMI at age 50 among persons who had never smoked, the researchers, led by Kenneth F. Adams, Ph.D., of NCI's Division of Cancer Epidemiology and Genetics, found that the risk of mortality among participants who were overweight increased by 20 to 40 percent. Mortality risk among obese participants increased two to three-fold.
"BMI at age 50 gives a more accurate representation of the amount of excess fatness a person was exposed to over decades," said Michael F. Leitzmann, M.D., NCI, senior author of the study. "On the other hand, body weight reported at age 65, for example, might reflect a recent weight loss due to cancer or other disease. If that person then dies the next year, it would be inaccurate to classify that person in the normal BMI range when their pre-cancer BMI was actually overweight."
I think their focus on BMI before major illneseses develop is the correct approach. As people get older and sicker health problems start influencing body weight and weight becomes as much an effect as a cause of health status..
They also aimed at getting data on non-smokers in order to avoid weight reduction caused by smoking.
Some earlier studies have shown that being overweight was not associated with an increased risk of death. However, smoking and chronic illness are associated with a lower BMI and an increased risk of death, which may distort the relationship between BMI and mortality.
An advantage of the current study was the availability of data on more than 186,000 male and female participants who had never smoked. This allowed the researchers to untangle the complex relationships between body weight, smoking, existing disease, and risk of death. Other possible confounding factors that were accounted for included age, race or ethnic group, level of education, physical activity, and alcohol intake.
This result is not surprising given what we know about blood lipid levels and other aspects of metabolism among the overweight and obese.
While studies have linked being either underweight or overweight to poor health, the effect of being overweight or obese on the risk of dying has been a topic of recent controversy. Researchers have long used the body-mass index (BMI), weight in kilograms divided by the square of height in meters, as a measure of the appropriateness of weight in relation to height. Researchers from Yonsei University, in Seoul, South Korea, and the Johns Hopkins Bloomberg School of Public Health report in one of the largest studies to date (over 1.2 million study participants) that having either a high or low BMI increases risk of death. The researchers found that the effect of BMI on the risk of dying varied among major causes of death and that the risk of death from being overweight or obese was greater in younger people. The study is published in the Aug. 24, 2006, edition of the New England Journal of Medicine.
While higher BMI values was associated with less respiratory causes of death the higher BMI values were associated with higher rates of cancer and heart diease. Note that cancer and heart diseases are the two biggest killers.
The researchers found that the relationship of BMI with risk of dying varied among the major causes of death considered. The risk of death from cancer increased beginning at BMI levels of 26.0-28.0 and rose further at higher levels, according to the researchers. Risk for death from respiratory causes was highest at the lowest BMI values and decreased with higher BMI values, whereas the risk of death from atherosclerotic cardiovascular disease increased progressively with higher BMI values. Information on cardiovascular risk factors showed an increasingly unfavorable profile with increasing BMI values. Study participants younger than 50 years of age had the highest relative risk of death associated with a high BMI. The researchers report no evidence of an increased risk of death for 65-year-old and above, obese individuals.
Dr. Meir Stampfer, chairman of the epidemiology department at the Harvard School of Public Health who was not involved in either study, called both articles fine.
“They show quite convincingly, yet again, that overweight and, in particular, obesity, raise the risk of mortality,’’ Dr. Stampfer said. “It really should be the final word on this issue that’s arisen as to whether overweight is actually bad for you or not.”
For overweight people losing weight and keeping it off is hard. Drugs to suppress appetite will increase life expectancy.
Many types of cancer cells have a surplus of procaspase-3. Procaspase-3 can be converted to caspase-3 which initiates the cell suicide process called apoptosis. However, cancer cells have mutations which prevent the conversion of procaspase-3 to caspase-3. Well, a team of scientists developed a drug called procaspase activating compound one (PAC-1) which converts procaspase-3 to caspase-3 and thereby initiates cell suicide.
CHAMPAIGN, Ill. -- Scientists have found a way to trick cancer cells into committing suicide. The novel technique potentially offers an effective method of providing personalized anti-cancer therapy. Most living cells contain a protein called procaspase-3, which, when activated, changes into the executioner enzyme caspase-3 and initiates programmed cell death, called apoptosis. In cancer cells, however, the signaling pathway to procaspase-3 is broken. As a result, cancer cells escape destruction and grow into tumors.
"We have identified a small, synthetic compound that directly activates procaspase-3 and induces apoptosis," said Paul J. Hergenrother, a professor of chemistry at the University of Illinois at Urbana-Champaign and corresponding author of a paper to be posted online this week ahead of regular publication by the journal Nature Chemical Biology. "By bypassing the broken pathway, we can use the cells' own machinery to destroy themselves."
To find the compound, called procaspase activating compound one (PAC-1), Hergenrother, with colleagues at the U. of I., Seoul National University, and the National Center for Toxicological Research, screened more than 20,000 structurally diverse compounds for the ability to change procaspase-3 into caspase-3.
The treatment works because procaspase-3 is often much more abundant in cancer cells than in healthy cells, says Paul Hergenrother at University of Illinois in Urbana, US, who led the study: “In tissue from 23 colon cancer patients we found that, on average, levels of procaspase-3 are eightfold higher than in healthy cells – sometimes as much as 20-fold higher.”
Healthy cells, such as white blood cells, were found to be significantly less affected by the addition of PAC-1 because they had much lower levels of procaspase-3, so cell-suicide could not be triggered.
When the scientists tested PAC-1 on cancerous and non-cancerous tissue from the same person, the tumour cells were 2,000-fold more sensitive to PAC-1.
"It is now clear that many cancers have elevated concentrations of procaspase-3," wrote Prof Hergenrother in the Nature paper. "Others have heightened or reduced concentrations of procaspase-3 depending on the cancer subtype." He added that a systematic analysis of procaspase-3 concentrations in a variety of cancer types was needed to determine which cancers would be most amenable to treatment with a molecule such as PAC-1.
The continued discovery of differences between cancerous and normal cells will provide more targets for anti-cancer drug development. The continued advance in general understanding of cell metabolism and gene regulation will lead to the discovery of many more enzymes and intra-cellular messengers which will become targets for anti-cancer drug development.
I am very optimistic that most of us will live long enough to witness the total defeat of cancer.
You know some technological trend is arriving when popular sports stars and celebrities embrace it. Human umbilical cord stem cell banking is hitting the mainstream. English football (soccer) players are putting the cord blood stem cells of their babies in a cord stem cell bank.
PREMIERSHIP footballers are storing stem cells from their newborn babies as a potential future treatment for their own career-threatening sports injuries.
They are freezing the cells taken from the umbilical cord blood of their babies as a possible future cure for cartilage and ligament problems. Stem cells can be used to regenerate damaged organs and tissue because they are the earliest form of cells.
The article states that some of the footballers are storing their babies cord blood for the benefit of the babies. But I suspect their own high risk of injuries has made them a lot more aware of the idea of using stem cells to do repairs.
Britain, like America, has multiple umbilical cord stem cell banks. My advice if you want to use one: Make sure its financing ensures it will stick around for a decade or longer.
He is one of five professional footballers who have frozen their children’s stem cells with Liverpool-based CryoGenesis International (CGI), one of about seven commercial stem cell “banks” in Britain.
In the past five years more than 11,000 British parents have paid up to £1,500 to store their babies’ stem cells in the banks in order to grow tissue, should their children become ill.
These athletes may never benefit from the cord stem cells. Cord stem cells can be used for some childhood blood diseases and immune diseases. But the cells aren't yet usable in humans for most of the injuries they are likely to suffer.
Be prepared to spend some money. CGI's standard service of £1275 equals about $2,407.70 USD.
OPTION 1: STANDARD SERVICE - £1275
Send just £125 now for the collection kit and to cover transportation and administration costs.
The balance of £1150 becomes due after the sample has been processed and stored.
But you can save with option 2 by signing up online.
Umbilical cord blood stem cell transplants are less prone to rejection than either bone marrow or peripheral blood stem cells. This is probably because the cells have not yet developed the features that can be recognized and attacked by the recipient's immune system. Also, because umbilical cord blood lacks well-developed immune cells, there is less chance that the transplanted cells will attack the recipient's body, a problem called graft versus host disease.
The umbilical cord stem cells are also younger and probably more vigorous and capable of more rapid and numerous cell division. Plus, the umbilical cord stem cells can probably become more cell types than adult stem cells. Embryonic stem cells are even more flexible than umbilical cord stem cells.
Tampa FL (Jan. 4, 2005) – Stem cells from umbilical cord blood effectively treated heart attacks in an animal study, report cardiologist Robert J. Henning, MD, and colleagues at the University of South Florida and James A. Haley Veterans' Hospital.
When injected into rats' hearts soon after a heart attack, stem cells taken from human umbilical cord blood (HUCB) greatly reduced the size of heart damage and restored pumping function to near normal. This improvement occurred without the need for drugs to prevent the rats' immune system from rejecting the human cells.
Maybe 5 or 10 years from now it'll be routine to inject umbilical cord stem cells into hearts after heart attacks.
Another study from September 2004 found that umbilical cord stem cells reduce the extent of stroke damage in an animal model by delivering neurotrophic factors that helped neurons in the damaged region to survive.
Stem cells taken from umbilical cord blood, then given intravenously along with a drug known to temporarily breach the brain's protective barrier, can dramatically reduce stroke size and damage, Medical College of Georgia and University of South Florida researchers say.
"What we found was interesting, phenomenal really," says Dr. Cesario V. Borlongan, neuroscientist and lead author of the study published in the October issue of the American Heart Association journal, Stroke.
Researchers first gave the drug, mannitol, to provide temporary passage through the blood-brain barrier then transfused human umbilical cord blood cells into a stroke animal model. When used in the first hours and days following a stroke, stroke size decreased by 40 percent and resulting disability was significantly reduced.
The Stroke paper also explored how stem cells provide neuroprotection. The researchers speculated it was by providing the large influx of nourishing neurotrophic factors secreted by the stem cells. To test that theory, they looked at what happened when they used antibodies that negated some of the factors. "When we blocked the neurotrophic factors, it blocked the positive effect," Dr. Borlongan says.
Neurotrophic factors such as Brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and neurotrophin three (NT-3) help neurons stay alive and encourage neural stem cells to divide. Stem cells that deliver these factors could plausibly help prevent neurons from committing suicide when they are damaged from a stroke - or from a trauma experienced on a football field.
Is it worth it to bank your baby's umbilical cord stem cells? Hard to say. Umbilical cord stem cells will become useful for a much larger range of illnesses and disorders in the future. But the same will happen with other kinds of stem cells. Umbilical cord stem cells will get more government research funding than embryonic stem cells. So for that reason they have better prospects. But methods will surely be found to make adult stem cells and adult differentiated stem cells more flexible, youthful, and useful. By the time you need stem cell treatments you might have multiple choices. On the other hand, maybe your baby will need a treatment 15 years from now and umbilical cord stem might be their best choice at that time.
One out of six American men will develop prostate cancer at some point in their life, and more than a third of them will experience a recurrence after undergoing treatment, putting them at high risk to die of the disease. New research from the Moores Cancer Center and School of Medicine at University of California, San Diego suggests that diet changes, reinforced by stress management training, may be effective in slowing or halting the spread of the this deadly cancer.
The 6-month study, published in the September issue of Integrative Cancer Therapies, focused on the change in the levels of prostate-specific antigen (PSA), an indicator of the cancer, in response to a plant-based diet and stress reduction. Patients were taught to increase consumption of plant-based foods such as whole grains, cruciferous and leafy green vegetables, beans and legumes, and fruit, and to decrease the intake of meat, dairy products and refined carbohydrates. They were also provided with stress management training, which included meditation, yoga and t’ai chi exercises.
Aside: Does anyone know of reliable research using stress markers such as blood cortisol to compare the effectiveness of various stress management techniques?
The plant-based diet and stress reduction intervention was effective in significantly reducing the PSA rate, indicating a reduction in the rate of progression of the prostate cancer. Ten patients with recurrent, invasive prostate cancer completed the pilot clinical trial. Rates of PSA rise were determined for each patient from the time of disease recurrence following treatment up to the start of the study (pre-study), and from the time immediately preceding the study intervention to the end of the intervention (0-6 months).By the end of the intervention, four of 10 patients experienced an absolute reduction in their PSA levels, and nine of 10 experienced a decrease in the rate of further PSA rise. The median time it took for the men’s PSA levels to double increased from 11.9 months at pre-study to 112.3 months (intervention).
That's a dramatic change for people who already have prostate cancer. I'd like to see this broken down in a more detailed study that just diet changes and stress reduction separately. I'd also like to see various diet changes compared. Would a diet that drastically improved blood lipid profiles provide most of the benefit? Reduce triglycerides and LDL cholesterol and raise HDL cholesterol to lower your PSA?
Massive electic generator plants emit much less pollution per amount of electricity generated as comapred to the much smaller electric generators which institutions have for back-up. During periods of heavy demand for electricity utilities which lack sufficient electric generation capacity incentivize customers to activate their own back-up generators and the result is much higher levels of air pollution.
Power plants built since 1970 are subject to stringent pollution controls. But rules for backup generators are far less strict, and, in most cases, there are no pollution restrictions for diesel generators not used more than 500 hours a year. The Pataki administration proposed new pollution rules several years ago, but they have not been put into effect.
Studies have shown that for each watt of power output, diesel generators produce up to 20 times as much particulate pollution, or soot, as the most advanced, natural gas-fired power plants, and up to 200 times as much nitrogen oxides, precursors to ozone, or smog. They even emit several times as much pollutants per watt of power output as the average power plants that burn oil or coal.
“This is pretty much the dirtiest source of electricity you can find,” said Peter Iwanowicz, director of environmental health for the American Lung Association of New York State.
A given quantity of fossil fuel will produce less pollution when burned if it is burned in a massive electric generator plant. This makes intuitive sense. The electric utilities can afford to hire full-time engineering staffs to make their combustion chambers burn efficiently and to make sure their scrubbers work well. Smaller diesel burning generators aren't as optimized or as regulated.
There's a lesson here: Regional opposition to big new electric power plants leads to the proliferation and usage of smaller fossil fuel burning electric power generators. So the opposition to electric power plants leads to dirtier air, not cleaner air.
Local generation of electric power is appealing if it is done in non-polluting ways. But use of fossil fuels for local electric generation is both much more polluting and more costly.
Micro wind turbines and photovoltaics provide very clean locally generated electricity. But these sources cost much more and also aren't available 24 hours a day and 7 days a week. An acceleration in the development technologies to lower the cost of cleaner energy sources could bring us a cleaner environment and lower costs at the same time.
Biotech company Advanced Cell Technology (ACT) has announced development of a technique that can extract pluripotent human embryonic stem cells from a human embryo without destroying the embryo. In theory this technique provides a way to get human embryonic stem cells without destroying what some religious people think is a human life.
Alameda, CA, August 23, 2006 – Advanced Cell Technology, Inc. (OTC Bulletin Board: ACTC.OB) today reported that company scientists have successfully generated human embryonic stem cells (hES cells) using an approach that does not harm embryos. The technique is reported in an article appearing online (ahead of print) in the journal Nature. The article describes a method for deriving stem cells from human blastomeres with a single-cell biopsy technique called Preimplantation Genetic Diagnosis (PGD). This technique is used in in vitro fertilization (IVF) clinics to assess the genetic health of preimplantation embryos. The cell lines produced using this technique appear to be identical to hES cell lines derived from later stage embryos using techniques that destroy the embryo’s developmental potential. ACT had previously reported the successful use of a similar technique in mice in Nature in October 2005.
“Until now, embryonic stem cell research has been synonymous with the destruction of human embryos,” stated Robert Lanza, M.D., Vice President of Research & Scientific Development at ACT, and the study’s senior author. “We have demonstrated, for the first time, that human embryonic stem cells can be generated without interfering with the embryo’s potential for life. Overnight culture of a single cell obtained through biopsy allows both PGD and the development of stem-cell lines without affecting the subsequent chances of having a child. To date, over 1,500 healthy children have been born following the use of PGD.” Current technology derives hES cells from the inner cell mass of later-stage embryos known as blastocysts, destroying their potential for further development. ACT’s approach generates human embryonic stem cells from a single cell obtained from an 8-cell-stage embryo. The researchers used left-over embryos from fertility clinics which use IVF to create embryos for implantation. To create hES cell lines, the researchers used single cells obtained from unused embryos produced by IVF for clinical purposes. Nineteen stem-cell outgrowths and two stable hES cell lines were obtained. These cell lines were genetically normal and retained their potential to form all of the cells in the human body, including nerve, liver, blood, vascular, and retinal cells that could potentially be used to treat a range of human diseases.
“Until now, embryonic stem cell research has been synonymous with the destruction of human embryos,” stated Robert Lanza, M.D., Vice President of Research & Scientific Development at ACT, and the study’s senior author. “We have demonstrated, for the first time, that human embryonic stem cells can be generated without interfering with the embryo’s potential for life. Overnight culture of a single cell obtained through biopsy allows both PGD and the development of stem-cell lines without affecting the subsequent chances of having a child. To date, over 1,500 healthy children have been born following the use of PGD.”
Current technology derives hES cells from the inner cell mass of later-stage embryos known as blastocysts, destroying their potential for further development. ACT’s approach generates human embryonic stem cells from a single cell obtained from an 8-cell-stage embryo.
The researchers used left-over embryos from fertility clinics which use IVF to create embryos for implantation.
To create hES cell lines, the researchers used single cells obtained from unused embryos produced by IVF for clinical purposes. Nineteen stem-cell outgrowths and two stable hES cell lines were obtained. These cell lines were genetically normal and retained their potential to form all of the cells in the human body, including nerve, liver, blood, vascular, and retinal cells that could potentially be used to treat a range of human diseases.“One of the major ethical objections of those who oppose the generation of human embryonic stems cells is that all techniques, until now, have resulted in the destruction of the embryo,” stated Ronald Green, Ph.D., Director of Dartmouth College’s Ethics Institute and Chairman of ACT’s Ethics Advisory Board. “This technique overcomes this hurdle and has the potential to play a critical role in the advancement of regenerative medicine. It also appears to be a way out of the current political impasse in this country and elsewhere.”
But the new method, reported yesterday by researchers at Advanced Cell Technology on the Web site of the journal Nature, had little immediate effect on longstanding objections of the White House and some Congressional leaders yesterday. It also brought objections from critics who warned of possible risk to the embryo and the in vitro fertilization procedure itself, in which embryos are generated from a couple’s egg and sperm.
Regarding possible risks: Trying to get a pregnancy started the natural way poses large risks to the eggs that get fertilized using old fashioned sexual procreation. Perhaps half of all conceptions spontaneously abort with most never even recognized as pregnancies.
The incidence of spontaneous abortion is estimated to be 50% of all pregnancies, based on the assumption that many pregnancies abort spontaneously with no clinical recognition.
I predict that advances in reproductive biotechnology will eventually lead to the ability to create embryos and start pregnancies that have a far higher chance of going to term than pregnancies started the natural way.
Does in vitro fertilization (IVF ) work better using fresh human eggs as compared to eggs that were frozen and then thawed? Kutluk Oktay MD and colleagues at the Cornell's Center for Reproductive Medicine and Infertility New York City looked at the relative success rates of using freshly donated human eggs versus thawed eggs to start pregnancies that go to term and produce live births. They compared two methods of freezing called slow-freezing (SF) and vitrification (VF) as well as freshly harvested eggs. IVF was done with intracytoplasmic sperm injection (ICSI). Fresh eggs produced almost 3 times the number of live births as eggs using the best freezing method, slow freezing. (ET stands for Embryo Transfer)
Live-birth rates per oocyte thawed were 1.9% and 2.0% for SF and VF, respectively, before June 2005. Live-birth rates per injected oocyte and ET, respectively, were 3.4% and 21.6% for SFM and were 6.6% and 60.4% for IVF with unfrozen oocytes.
Yet the 21.6% success for the better freezing method is high enough to be usable. That's good news because frozen eggs have a few benefits. First, women who are going to undergo medical treatments (e.g. chemotherapy for cancer) might become sterile or suffer sufficient damage to their ovaries that their eggs would be at risk of producing defective babies. Extracting and freezing eggs from a woman before she undergoes a medical treatment opens up the possibility of still being able to have healthy children afterward if the illness can be cured.
Another reason to freeze eggs is to allow a young woman to store some eggs away to use to have children in her late 30s or 40s when fertility declines drastically.
A third possible reason to freeze eggs is that it opens up the possibility of a much larger market of donor eggs. A woman could have eggs harvested and stored for transport to wherever a market demand for her particular eggs exists. Then buyers could have much larger selections to choose from. Egg donation will become more commonplace if women can have eggs harvested while she is young to be sold for decades afterward.
Many countries do not allow the sale of donor eggs. However, in the massive market called the United States of America egg selling is allowed. One center in Texas even will put together donor eggs and sperm and ship already fertilized embryos to IVF clinics for implantation.
The Abraham Center of Life allows people to order custom-made embryos and have them shipped to an IVF clinic for implantation.
The embryos are created with the eggs and sperm of rigorously screened, "qualified" donors who have never met each other. Conception occurs as the embryo bank fills its orders. Customers can even specify the eye and hair colour that they would like their baby to have.
They can't guarantee the hair and eye color just yet. But with advances in genetic testing fertility clinics will eventually be able to offer high probabilities for sex, appearances, intelligence level (high IQ will become very popular), personality type, disease risks, and other characteristics.
Advances in egg freezing and thawing methods combined with advances in DNA testing and IVF will increase the advantages of using donor eggs and therefore increase the demand for egg donors. See my posts High Intelligence Sperm and Egg Donor Prices Rising, The Growing Market For Donor Eggs, and More Single Women Using Sperm Donors. I also predict the development of a larger market for donor eggs and sperm will make humans more genetically determined and less influenced by their environment. See my post Children Of The Future May Be More Genetically Determined.
PHILADELPHIA -- The ability to sort cells or manipulate microscopic particles could soon be in the hands of small laboratories, high schools and amateur scientists, thanks to researchers at the University of Pennsylvania School of Engineering and Applied Science. They have created a device, called "electric tweezers," which can manipulate and move almost any object seen on a simple microscope slide.
The research was led by graduate student Brian Edwards, with the help of his advisor Nader Engheta, professor, and Stephane Evoy, adjunct assistant professor, both of Penn's Electrical and Systems Engineering Department. While devices with similar functionality using lasers exist, they often cost upwards of a quarter-million dollars. Edwards' device performs some of the same tasks as laser tweezers, yet at a price anticipated to be in the same range as a high-end desktop computer.
"The tweezers create an electric field that you can use to manipulate almost any object on a microscopic scale. It has the potential of being a powerful tool for research," said Edwards, a doctoral candidate in Penn's Electrical and Systems Engineering Department. "I would prefer not to put a limit on the type of tasks that can be done with it, but I hope it will find uses in anything from picking an individual cell out of a culture to fabricating circuits."
All it would take to use electric tweezers is a computer and a microscope. The tweezers' action occurs on a common glass microscope slide embedded with five electrodes. These electrodes create an electric field that can be used to push, pull, move and spin a selected object in any direction without actual physical contact. Using software Edwards developed, an operator can select an individual object from a microscope image on a computer screen.
"Different types of particles respond differently to different frequencies in the electric field," Edwards said. "Once you lock onto the object of interest you can move it however you like."
The electric tweezers take advantage of the phenomenon known as dielectrophoresis, where electric fields impart a force upon a neutral particle. In essence, the object that is selected surfs atop the hills and valleys created by subtly changing the electric field. The principle works best on the microscopic scale, which makes it ideal for this application.
Biotechnology is headed down the same path as electronic technology. Computers are accelerating the advance of biotechnology and processes developed to make semiconductors help to push microfluidics technology forward. The general trend is going to be toward smaller, cheaper, and more automated lab instruments.
Altering the makeup of bugs in the gut could be a way of tackling insulin resistance and related problems such as non alcoholic fatty liver disease, according to new research published this week.
The study also has implications for the treatment of associated conditions such as type 2 diabetes, obesity and heart disease.
The research shows that the type of microbes found in the guts of mice with a certain genetic makeup causes them to be pre-disposed to insulin resistance and non-alcoholic fatty liver disease (NAFLD). On a high fat diet, these microbes transform the nutrient choline, found in food and essential for metabolising fat, into methylamines.
Scientists believe that these methylamines, which can only be produced by the microbes in the gut, lead to insulin resistance. In addition, because choline is needed to transport fat out of the liver, altering choline metabolism leads to fat accumulating in the liver and NAFLD.
This is good news. Why? Bacteria can be defeated. Any time I read about how some disease is caused by chronic infection it makes me more optimistic. We can develop drugs and vaccines that'll stop pathogens. Better that chronic diseases of old age be caused by pathogens than by the body simply wearing out. The pathogens are easier to stop than the wearing out of cells.
Here is part of the abstract from the PNAS paper for this report. Bacteria reduce choline availability while also increasing exposure to harmful methylamines.
Multivariate statistical modeling of the spectra shows that the genetic predisposition of the 129S6 mouse to impaired glucose homeostasis and NAFLD is associated with disruptions of choline metabolism, i.e., low circulating levels of plasma phosphatidylcholine and high urinary excretion of methylamines (dimethylamine, trimethylamine, and trimethylamine-N-oxide), coprocessed by symbiotic gut microbiota and mammalian enzyme systems. Conversion of choline into methylamines by microbiota in strain 129S6 on a high-fat diet reduces the bioavailability of choline and mimics the effect of choline-deficient diets, causing NAFLD. These data also indicate that gut microbiota may play an active role in the development of insulin resistance.
The practical question: Can we use this information now? We need answers to some basic questions: Which human stomach bacteria convert choline to methylamines? Do they all do this? Are antibiotics or the consumption of competing bacteria the best way to shift the balance of bacteria in the stomach away from bacteria that convert choline to methylamine?
Anyone know the answers to these questions?
Pull up to most service stations in this country of 185 million people and you will find fuel pumps offering three choices: ethanol, gasoline or premium gasoline. The labels are slightly misleading: The gasoline varieties are blends that contain at least 20 percent ethanol. The ethanol is usually significantly cheaper -- 53 cents per liter (about $2 per gallon), compared with about 99 cents per liter for gasoline ($3.74 per gallon) in Sao Paulo this past week.
Note that ethanol contains less energy per liter or gallon. So you need a third or a half more ethanol to drive the same distance as you can with pure gasoline. But the Brazilian gasoline has already been diluted with ethanol and therefore already takes you a shorter distance than pure gasoline. So the 53 cents per liter price for pure ethanol is much cheaper per mile or kilometer driven than the 99 cents per liter gasoline/ethanol blend. Mind you, in the United States, ethanol is much more expensive and costs more than gasoline per mile travelled.
Ethanol from sugar cane has replaced 40% of gasoline in Brazil. (but see the post update at the bottom for why this is less impressive than it sounds - in a word "diesel").
Ethanol is not solely responsible for Brazil's newfound energy independence -- domestic oil exploration has exploded in recent years -- but it has replaced about 40 percent of the country's gasoline consumption, according to Caio Carvalhal, an analyst with Cambridge Energy Research Associates in Rio de Janeiro.
The Brazilian sugar cane industry funded development of cheaper ways to convert sugar cane into ethanol. The government eliminated subsidies for ethanol back in the 1980s.
Through it all, the Center for Sugarcane Technology in Sao Paulo state -- a research facility created in the early 1970s and funded by the sugar industry -- continued working to improve efficiency in ethanol production by tinkering with almost everything from the genetic structure of sugar cane varieties to the industrial components of extraction. By the time oil prices began to steadily rise in the early years of this decade, ethanol producers had reduced production costs of a liter of ethanol from about 60 cents to about 20 cents.
By contrast, the US sugar cane industry funds lobbyists to keep the US government blocking Brazilian sugar from the US market. They argue this saves US jobs. But lots (all?) of the field hands are brought in from Caribbean islands. Money provides plenty of incentive for people to deceive and use government for their benefit and the expense of others. But I digress.
You might be thinking "Hey, why not just import Brazilian ethanol and lower our cost of vehicle fuel while at the same time reducing net carbon release into the atmosphere?" Hah! When large sums of money are involved lobbyists Archer Daniels Midland and the corn farmers have got you beat. A large tariff on Brazilian ethanol makes it much more expensive in the United States.
President Bush suggested earlier this year eliminating a tariff of 54 cents per gallon of Brazilian ethanol, but corn growers and their congressional allies have stymied that idea.
I feel compelled to digress again into trade politics but only because I have a really great idea for Brazil. My advice to the Brazilians: Stop letting any of your models come to the US and pose in Victoria's Secret catalogs until the US government agrees to let in Brazilian sugar and sugar cane ethanol. American citizens might tolerate having to pay more for Breyers than Dreyers in order to get sugar rather than corn syrup as ice cream flavoring. But American men will only find the backbone they need to stand up to the corn farmers and ADM when they find out that the farmers are preventing them from looking at Gisele Bündchen, Michelle Alves, Shirley Mallmann, Isabeli Fontana, Fernanda Tavares, and Ana Beatriz Barros.
Brazilian sugarcane ethanol is about 20% cheaper than US corn ethanol to manufacture. I'm surprised that the difference in price is so small.
The U.S. Department of Agriculture released a report last month that concluded sugar is not economically feasible for a domestic ethanol industry under current conditions.
The cost of producing a gallon of ethanol from sugarcane would be $2.40 while Brazil makes it for 81 cents, the report said. U.S. corn-based ethanol costs about $1.03 per gallon to make, it said.
The price quoted for Brazilian ethanol is in gallons. The 81 cents for a gallon is lower than the about $2 per gallon quoted in the first article above. But part of that difference is due to the cost of distribution and retail sales. Perhaps there's a tax on it as well.
Considering that in the past three months the price of ethanol has jumped 54 percent to $3.67 a gallon -- more than double what it costs to manufacture -- companies that produce ethanol are enjoying an enormous profit, at the expense of the American consumer and taxpayer. Archer Daniels Midland, the Illinois-based conglomerate that controls nearly one-fourth of the ethanol market, will earn an estimated $1.3 billion from ethanol alone during the current fiscal year. No wonder ethanol companies are hot investments on Wall Street.
Does pure ethanol really cost that much at wholesale? If so, even with a tariff Brazilian sugar cane ethanol should be cheaper than the market price for US corn ethanol. Does anyone know what is going on behind these figures?
So I'll save money if I use ethanol?
Actually, no. Ethanol contains less energy than gasoline, which means mileage is lower. In city driving, for example, the base model Chevy Silverado pickup truck gets 16 miles per gallon of gasoline, but just 12 miles per gallon of ethanol.
Here is a nice web page explaining how to compare ethanol to gasoline when looking at prices. Ethanol has another cost though: You have to stop and get gasoline more often. Time is money. Ethanol costs you more in time.
US farmers face one big problem competing with Brazilian ethanol: Brazil gets more sunshine than the United States. On the other hand, Brazil's sugar cane ethanol cost advantage is not that large. The development of cellulosic technologies to extract all the energy out of the cellulose portion of plants would cut US ethanol costs substantially. However, it would do the same to sugar cane.
Question: Is the currently unusable cellulose fraction of a corn plant larger than the currently unusable fraction of a sugar cane? If so, then cellulosic technology will reduce Brazil's ethanol manufacturing cost advantage.
Another question: How much rain forest will get cut down as Brazil expands ethanol production?
In 2005 the United States used 9.125 million barrels of gasoline per day At 42 gallons per barrel that is 383.25 million gallons per day and times 365.25 days per year that is 139.982 billion gallons per year. To replace that with biomass energy would require perhaps 210 billion gallons of ethanol. Let us put that into perspective. The optimistic view is for ethanol production to expand to meet the demand for about 7% of the gasoline vehicle liquid fuel market.
If oil prices remain high, then U.S. fuel consumption of ethanol could at least double from the 2005 level of four billion gallons. But industry executives like Archer Daniels Chief Executive Patricia Woertz have set their sights even higher. Last week, in announcing the company's record earnings for its June 2006 fiscal year, Woertz said ethanol demand could triple.
"It looks like it has room to grow to 14 billion or 15 billion [gallons per year]," she said, "which is a full 10% blend in the gasoline pool in the United States." Unfortunately, before ethanol refiners can reach that goal, they might reach the limits of the country's corn supply. America's entire corn crop would satisfy just 12% of gasoline consumption, leaving no corn to feed livestock and humans. So there just won't be enough corn for corn ethanol to grow from a fuel additive into a large-scale substitute for fossil fuel. Crop years vary, too.
There are 101 ethanol production plants in the nation, producing 5 billion gallons of ethanol per year, Siekman said.
Thirty-three plants to produce another 2 billion gallons are in the works in various areas throughout the country, Siekman said.
The 5 billion gallons represents about 2 and a half percent of the energy used to propel gasoline-burning vehicles (as distinct from diesel powered vehicles). We need cellulosic technologies to allow ethanol to displace most gasoline from the market. I'm guessing we'll see cellulosic technologies move into ethanol production in the next 10 years. Oil prices are so high that lots of groups have plenty of incentives to solve the problems for how to release the energy in cellulose.
High oil prices are going to continue to drive a shift to alternatives. For transportation ethanol looks to be the alternative that can ramp up most quickly. As better battery technologies come out hybrids will grow as well. Eventually when batteries improve enough pluggable hybrids will set the stage where ethanol will compete with wall socket electricity to power vehicles. Therefore the use of gasoline looks set to peak before oil production peaks.
The U.S. is producing slightly more ethanol than Brazil, however gasoline demand in Brazil is only 4.28 billion gallons compared to the U.S. where gasoline demand is 140 billion gallons (23 times that in Brazil). The U.S. can't build an ethanol market based on sugarcane. Nor can the U.S. ramp up corn-based ethanol in the same way Brazil increased ethanol use with sugarcane. Brazil energy independence is due to increased crude oil production - not ethanol.
How did Brazil achieve energy independence? Not with ethanol but by increasing crude oil production. Brazil’s increase in crude oil production over the 2004 to 2005 period was 9 times larger than its increase in ethanol production over the same time period, and was 4 times larger over the 2000 to 2005 period. Clearly, it has been Brazil’s increased crude production, particularly over the 2004 to 2005 time frame, which has been the dominant factor in pushing Brazil towards energy independence.
On the production side, in 2005 Brazil produced 627 million barrels of oil, for an annual per capita oil production of 3.4 barrels per person. The U.S. produced 2.5 billion barrels of oil in 2005, for an annual per capita oil production of 8.4 barrels per person. The annual shortfall between oil consumption and oil production in Brazil was 0.2 barrels per person in 2005. In the U.S., the shortfall between consumption and production was much larger at 16.9 barrels per person.
The question then arises: “Just how much did widespread use of ethanol in Brazil contribute toward their energy independence?” The answer is: “Not much”. In 2005, Brazil produced 4.8 billion gallons of ethanol, or 114 million barrels. However, a barrel of ethanol contains approximately 3.5 million BTUs, and a barrel of oil contains approximately 6 million BTUs. Therefore, 114 million barrels of ethanol only displaced 67 million barrels of oil, around 10% of Brazil’s oil consumption. In other words, Brazil’s energy independence miracle was 10% ethanol and 90% domestic crude oil production. Brazil did not farm their way to energy independence.
According to a March 2006 presentation by the Brazilian Ministry of Mines and Energy, the actual breakdown of vehicle fuels in Brazil at the present time (by volume) is 53.9% diesel, 26.2% gasoline, 17% ethanol and 2.9% natural gas.
17% is a lot less than 40%. Also, that is 17% of a small total amount of fuel and a small per capita use of fuel as compared to the United States.
Thanks to The Ergosphere's Engineer-Poet for alerting me to the relatively large role that diesel plays in Brazil for vehicle fuel.
Update II: Engineer-Poet makes an argument on why ethanol from biomass is a bad idea. I happen to agree that biomass energy has big downsides. But my guess is that coming advances in cellulosic technology will so lower the cost of biomass ethanol that ethanol usage will increase greatly in the next 10 years. I do not treat that as a happy prospect. Large scale biomass energy production will cause humanity to compete (too successfully) with nature and take habitat away from other species. Since I'm fond of other species I'm not happy about that. I'd much prefer we use nuclear, solar, and other energy sources that use much smaller ecological footprints.
A cup of coffee may cause a heart attack in some people within an hour of drinking it, according to a study reported in the journal Epidemiology (“Transient Exposure to Coffee as a Trigger of a First Nonfatal Myocardial Infarction,” (Volume 17, Issue 5, September 2006.) The risk was highest among people with light or occasional coffee intake, and those with a sedentary lifestyle or other risk factors for coronary heart disease.
Studying 503 cases of non-fatal myocardial infarction in Costa Rica, Ana Baylin of Brown University and her colleagues of Harvard School of Public Health surveyed participants about their coffee consumption in the hours and days before their heart attack. They also studied the participants’ socio-demographic characteristics, lifestyle, and medical history. They theorized that caffeine causes short-term increases in blood pressure and sympathetic nervous activity that could affect a vulnerable atherosclerotic plaque, and trigger a heart attack.
The researchers found that the moderate coffee drinkers, by having a cup of coffee, increased their risk of having a heart attack by 60%. There was little effect among heavy coffee drinkers, but light coffee drinkers increased their risk of heart attack by more than four times. This may be because lighter drinkers are less acclimated to the effects of caffeine. Baylin and her team also found that patients with three or more risk factors for coronary heart disease more than doubled their risk.
“People at high risk for a heart attack who are occasional or regular coffee drinkers might consider quitting coffee altogether,” comments Baylin, adding that for these individuals, a cup of coffee could be “the straw that broke the camel’s back.”
Also see my quite useful post Scientists Demonstrate Best Way To Use Caffeine.
Update: A New York Times survey of the health effects of coffee finds it has anti-inflammatory effects and studies have found that coffee reduces the risk of diabetes, liver cirrhosis, heart disease, and other disorders. The heart health benefit of coffee comes only in a sub-range of coffee consumption.
Some studies show that cardiovascular risk also decreases with coffee consumption. Using data on more than 27,000 women ages 55 to 69 in the Iowa Women’s Health Study who were followed for 15 years, Norwegian researchers found that women who drank one to three cups a day reduced their risk of cardiovascular disease by 24 percent compared with those drinking no coffee at all.
But as the quantity increased, the benefit decreased. At more than six cups a day, the risk was not significantly reduced.
The identification of the beneficial and harmful compounds in coffee and other foods will eventually lead to the development of foods which contain optimal concentrations of beneficial compounds and much less of the harmful compounds. Genetic engineering, breeding, and food processing methods will all be used to optimize the health benefits of foods based on increasing amounts of scientific knowledge..
St. Paul, MN -- With projected costs of ischemic stroke in the United States expected to top $2.2 trillion dollars by 2050, the American Academy of Neurology (AAN) is urging Congress to further increase funding for the National Institutes of Health (NIH).
This estimate is probably a big overestimate because of the advances in biomedical technology that will occur between now and 2050. Stem cells therapies will start doing artery repairs certainly by 2025 and probably sooner. Also, drugs will come on the market that raise cardiovascular health improving HDL cholesterol and will work synergistically with drugs that lower the harmful types of cholesterol. Also, drugs that target different ways to lower general cholesterol will come on the market as well. Plus, gene therapies and drugs that improve vein and artery health by rejuvenating stem cells and other vascular cells will also make it onto the market by the 2020s.
Having said all that, this report in Neurology still serves the useful purpose of pointing out just how expensive each of the major diseases are in a single affluent country. The international costs are of course much higher. The size of these costs argue for greater efforts to develop treatments that will prevent stroke as well as other diseases. Each disease case avoided amounts to a large economic cost avoided as well as an increase in life expectancy and health.
A study published August 16, 2006 in the online edition of Neurology, the scientific journal of the AAN, found the total cost of stroke from 2005-2050, in 2005 dollars, is projected to be $1.52 trillion for non-Hispanic whites, $379 billion for African Americans and $313 billion for Hispanics.
"With the cost of stroke reaching $2.2 trillion, it is essential the NIH have the resources to halt this impending epidemic," said Catherine M. Rydell, CEO and Executive Director of the AAN. "The NIH has the ability to perform the research that can save countless lives and billions of dollars in health care costs if Congress would adequately fund its mission. The AAN will continue to work with our partners at the American Stroke Association, a division of the American Heart Association, and others to stress to Congress the importance of funding NIH."
The AAN is strongly supporting a budget increase of five percent, or $1.4 billion, to bring overall funding for the NIH FY-07 budget appropriation to $30 billion.
The researchers claim that rising rates of obesity and diabetes might cause an increase in the rate of stroke. This argument is plausible in the short to medium term.
"Doing the right thing now ultimately could be cost-saving in the future, but we have a long way to go before all Americans receive adequate stroke prevention and emergency stroke care," she says. "If our society is not going to do it for the right reasons, perhaps we can do it because it's going to be obscenely expensive."
Brown and her colleagues say their $2.2 trillion estimate is extremely conservative, because it is based on current rates of the conditions that put people at higher risk of stroke -- such as diabetes, cardiovascular disease and obesity. Such conditions are projected to become even more common in the future.
The $2.2 trillion estimate includes the cost of everything from ambulances and hospital stays to medications, nursing home care, at-home care and doctor's visits. They also include lost earnings for stroke survivors under age 65, based on current median salaries for each ethnic group. Earnings of those over 65 weren't included.
The aging of Western populations will force raises in retirement ages. Earnings losses from stroke therefore are probably underestimated by their assumption of only counting people under 65 as workers.
What can Americans do to decrease this looming bill? No matter what their age or ethnicity, individuals can cut their own risk of a future stroke by quitting smoking, losing weight, eating healthily, exercising, and keeping their blood pressure, cholesterol levels and any heart-rhythm problems under control, says Brown.
Meanwhile, doctors and hospitals can do a better job of providing preventive care and screening to patients with high blood pressure, clogged arteries and heart-rhythm problems. And, they can improve their use of a post-stroke drug called tPA.
We should strive to eat healthy diets. But we should also press for acceleration of the development of stem cell therapies, gene therapies, microfluidics, and other avenues of research that will lead to enormously more powerful therapies. We need rejuvenation therapies based on Strategies for Engineered Negligible Senescence (SENS). SENS therapies will make stroke and heart attacks extremely rare.
Many scientists would like to take human embryonic stem cells (hESC) and find ways to instruct the cells to become whatever cell type that is needed. But restrictions on funding hESC work has slowed that avenue of investigation. Well, scientists at the University of Florida may have found a way to avoid the need for hESC to create neurons or neural progenitor cells for therapeutic purposes.
GAINESVILLE, Fla. -- University of Florida researchers have shown ordinary human brain cells may share the prized qualities of self-renewal and adaptability normally associated with stem cells.
Writing online today (Aug. 16) in Development, scientists from UF's McKnight Brain Institute describe how they used mature human brain cells taken from epilepsy patients to generate new brain tissue in mice.
Furthermore, they can coax these pedestrian human cells to produce large amounts of new brain cells in culture, with one cell theoretically able to begin a cycle of cell division that does not stop until the cells number about 10 to the 16th power.
They can grow large numbers of neurons. But how hard will it be to instruct those neurons to go into the brain and take up positions that replace lost neurons? For example, people with Parkinson's Disease have lost a lot of dopaminergic neurons. But neurons grown in culture aren't helpful unless they can be made to take up residence in those regions of the brain that have lost neurons and then once there the neurons would need to form appropriate connections with other neurons. Still, this is a hopeful result.
"We can theoretically take a single brain cell out of a human being and - with just this one cell - generate enough brain cells to replace every cell of the donor's brain and conceivably those of 50 million other people," said Dennis Steindler, Ph.D., executive director of UF's McKnight Brain Institute. "This is a completely new source of human brain cells that can potentially be used to fight Parkinson's disease, Alzheimer's disease, stroke and a host of other brain disorders. It would probably only take months to get enough material for a human transplant operation."
The findings document for the first time the ability of common human brain cells to morph into different cell types, a previously unknown characteristic, and are the result of the research team's long-term investigations of adult human stem cells and rodent embryonic stem cells.
Every sperm is sacred,
Every sperm is great,
If a sperm is wasted,
God gets quite irate.
Let the heathen spill theirs,
On the dusty ground,
God shall make them pay for,
Each sperm that can't be found.
Every sperm is wanted,
Every sperm is good,
Every sperm is needed,
In your neighbourhood.
Every neuron is sacred? Does every neuron contain part of a soul? If you torture a human neuron in lab culture are you torturing a human?
Well, whether or not human neurons are sacred they can grow in mouse brains. They also can grow in culture. Once sperm can be created from regular cells and grown in large numbers in culture dishes will those spem be sacred too?
Human neurons in the brain of a mouse or rat will not make that animal think human thoughts. Their skulls are far too small to provide enough space for enough human neurons to form links that make higher level thought possible.
LA JOLLA, CA - Like most neurodegenerative diseases, Alzheimer's disease usually appears late in life, raising the question of whether it is a disastrous consequence of aging or if the toxic protein aggregates that cause the disease simply take a long time to form.
Now, a collaboration between researchers at the Salk Institute for Biological Studies and the Scripps Research Institute shows that aging is what's critical. Harmful beta amyloid aggregates accumulate when aging impedes two molecular clean-up crews from getting rid of these toxic species.
This finding opens the door for development of drugs preventing build-up of toxic protein aggregates in the brain. The study appears in the Aug. 10 issue of Science Express, the advanced online edition of the journal Science.
Biogerontologist Aubrey de Grey has repeatedly made the argument that biomedical science could do more to reduce death from assorted diseases of old age by reversing aging than by researching treatments for each disease. This paper provides evidence for his assertion. If brain cells could be rejuvenated they'd once more break down toxic proteins as well as they did when they were younger. Then the incidence of Alzheimer's diease would plummet.
The clearing out of beta amyloid protein fragments becomes less efficient as we age.
Throughout life, brain cells produce aggregation-prone beta-amyloid fragments that must be cleared. "This process is very efficient when we are young but as we get older it gets progressively less efficient," says Cohen. As the affected individual reaches the seventh decade of life the clearance machineries fail to degrade the continually forming toxic aggregates and the disease emerges. In individuals who carry early onset Alzheimer's-linked mutation, an increased "aggregation challenge" leads to clearance failure and the emergence of Alzheimer's much earlier – usually during their fifth decade.
Drugs that block steps in the formation of beta amyloid protein fragments might help. But we'd be better if we could get brain cells to once again effectively taking out the trash. We need Strategies for Engineered Negligible Senescence.
Men who have a low testosterone level after age 40 may have a higher risk of death over a four-year period than those with normal levels of the hormone, according to a report in the August 14/28 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Unlike women undergoing menopause, middle-aged men generally do not experience a dramatic decrease in the production of sex hormones, according to background information in the article. Testosterone levels gradually decline as a man ages, decreasing approximately 1.5 percent per year after age 30. The effects of low testosterone levels include decreased muscle mass and bone density, insulin resistance, decreased sex drive, less energy, irritability and feelings of depression.
Molly M. Shores, M.D., and colleagues at the VA Puget Sound Health Care System and University of Washington, Seattle, studied the relationship between hormone levels and death in a total of 858 male veterans older than age 40 years. All participants received care in the VA Puget Sound Health Care System and had their testosterone levels checked at least twice between 1994 and 1999, with at least one week and no more than two years elapsing between tests. The men were followed for an average of 4.3 years and a maximum of eight years, through 2002.
About 19 percent (166) of the men had a low testosterone level; 28 percent (240) had an equivocal testosterone level, meaning that their tests revealed an equal number of low and normal levels; and 53 percent (452) had normal testosterone levels. One-fifth (20.1 percent) of the men with normal testosterone levels died during the course of the study, compared with 24.6 percent of men with equivocal levels and 34.9 percent of those with low levels. Men with low testosterone levels had an 88 percent increase in risk of death compared with those who had normal levels. When the researchers considered other variables that may influence risk of death, such as age, other illnesses and body mass index, the association between low testosterone levels and death persisted.
Is the lower testosterone a cause of earlier death? Or is it just another symptom of the same underlying cause? If testosterone is a cause then will testosterone supplementation increase longevity among those whose testosterone is especially low?
Natural selection did not create human male and female sexual desires that are mutually compatible. Men in long term relationships sound sexually frustrated.
The researchers from Hamburg-Eppendorf University interviewed 530 men and women about their relationships.
They found 60% of 30-year-old women wanted sex "often" at the beginning of a relationship, but within four years of the relationship this figure fell to under 50%, and after 20 years it dropped to about 20%.
In contrast, they found the proportion of men wanting regular sex remained at between 60-80%, regardless of how long they had been in a relationship.
The Germans found, however, that living apart slows the decline in female libido, confirming the maxim “absence makes the heart grow fonder”.
Women whose husbands or boyfriends have higher educational qualifications than their own also maintain their sex drive. This, speculates Klusmann, is because such men are regarded as a “valuable mate of choice” by other women.
Some people think nature is great. Nature is all about conflict and competition. Natural selection has produced males and females who have instincts which give desires and drives that make them come up well less than perfectly compatible. If men and women ever become more compatible it will be due to genetic engineering and other biotechnologies that adjust us to make us have more mutually satisfying desires.
When sexual desires and drive become far more manipulable with neurobiotechnology will men and women in long term relationships more often increase the woman's sex drive or decrease the man's? I suspect the decision will be made at least partially based on available time. People will turn down their sex drives when working long hours and raising kids but turn up their sexual desire when they have more time. Taking a vacation? Turn up your libido. Cialis, Levitra, and Viagra are already a step in this direction. But they turn up sexual desire in men whereas what's more needed are down switches in men and up switches in women.
To the extent that genetic variations will turn out to predict sex drives in long term relationships I'm expecting some people to genetically evaluate potential spouses based on the expected difference in their sex drives. I also expect them to genetically evaluate for how likely their mate is to cheat on them. I fully expect human geneticists to find genetic variations that increase promiscuity.
Previous studies have suggested a potential link between AMD and lutein and zeaxanthin, plant pigments known as carotenoids and found in leafy green vegetables, corn, egg yolks, squash, broccoli and peas. These compounds may reduce the risk of AMD by absorbing blue light that could damage the macula, by preventing free radicals from damaging eye cells and by strengthening eye cell membranes. Suzen M. Moeller, Ph.D., University of Wisconsin, Madison, and colleagues with the Carotenoids in Age-Related Eye Disease Study (CAREDS) Research Study Group, assessed the effects of dietary lutein plus zeaxanthin in 1,787 women ages 50 to 79 years in Iowa, Wisconsin and Oregon. The women with the highest and lowest dietary intakes of lutein and zeaxanthin in the Women's Health Initiative, a large study of postmenopausal women that began between 1994 and 1998, were recruited to participate in CAREDS. At the beginning of the study, participants filled out a questionnaire to evaluate what their diets were like 15 years before the beginning of the study. Blood samples were taken to assess levels of carotenoids and color photographs of the retina were used to determine the presence and progression of AMD. A higher intake of lutein plus zeaxanthin was associated with a lower risk of intermediate-stage AMD in women younger than age 75 years who had a stable intake of the carotenoids over the 15-year period and did not have previous AMD or a chronic disease, such as cardiovascular disease, diabetes or hypertension, that might alter their dietary habits. However, no significant difference was observed in the overall group of women or when comparing lutein and zeaxanthin levels in the blood to AMD occurrence. There was a weak association between dietary lutein plus zeaxanthin and advanced-stage AMD in all the women and in women younger than age 75 years.
Eat more kale. Per half cup kale is highest with 10 mg lutein and then collard greens with 7.7 mg and spinach with 3.3 mg.
A carotenoid, lutein is found in green vegetables, especially spinach, as well as kale and broccoli. But egg yolks, although they contain significantly less lutein than spinach, are a much more bioavailable source whose consumption increases lutein concentrations in the blood many-fold higher than spinach.
Eat eggs for your eyes.
Martha Clare Morris, Sc.D., associated professor at the Institute for Healthy Aging at Rush University Medical Center, and her colleagues assessed the connection between dietary fat and dietary copper intake in 3,718 Chicago residents age 65 years and older. Participants underwent cognitive testing at the beginning of the study, after three years and after six years. An average of one year after the study began, they filled out a questionnaire about their diets. The dietary recommended allowance of copper for adults is .9 milligrams per day. Organ meats, such as liver, and shellfish are the foods with the highest copper levels, followed by nuts, seeds, legumes, whole grains, potatoes, chocolate and some fruits. Copper pipes may also add trace amounts of the metal to drinking water.
Cognitive abilities declined in all participants as they aged. Overall, copper intake was not associated with the rate of this decline. However, among the 604 individuals (16.2 percent of the study group) who consumed the most saturated and trans fats, cognitive function deteriorated more rapidly with the more copper they had in their diets. “The increase in rate for the high-fat consumers whose total copper intake was in the top 20 percent (greater than or equal to 1.6 milligrams per day) was equivalent to 19 more years of age,” the authors write.
This sounds like a stronger argument for reducing saturated and trans fats than for reducing copper in the diet. We already have plenty of reasons to avoid saturated and trans fats. Here's another one.
The Scottish Council on Human Bioethics has released a report entitled Embryonic, Fetal and Post-natal Animal-Human Mixtures: An Ethical Discussion where they discuss what scientists are doing with mixing human and animal cells and the ethical issues arising from this work.
Genetic Human-Mouse Chimeric Fetuses
Recently Scientists at Stanford University injected human neuronal stem cells into mouse fetuses, creating mice whose brains were about 1% human. By dissecting the mice at various stages, the researchers were able to see how the added brain cells moved about as they multiplied and made connections with mouse cells . The same scientists now want to add human brain stem cells that have the defects that cause Parkinson's disease, Lou Gehrig's disease and other brain ailments and study how those cells make connections. Indeed, scientists suspect that these diseases, though they manifest themselves in adulthood, begin when something goes wrong in early development.
Because of this, the Stanford team is also thinking about making chimeric mice whose brains are 100% human. However, they suggest that if the brains look as if it is taking on a distinctly human architecture - a development that could suggest a specific amount of 'humanness' - they could be killed. On the other hand, if they look as if they are organising themselves in a mouse brain architecture, they could be used for research [92,93].
In January 2005, an informal ethics committee at Stanford University endorsed the proposal to create mice with brains made nearly completely of human brain cells. The chairperson of this committee indicated, in this respect, that the board was satisfied that the size and shape of the mouse brain would prevent the human cells from creating any traits of humanity. But just in case, the committee recommended closely monitoring the mice's behaviour and immediately killing any that display human-like behaviour .
They go on to briefly describe experiments that have been done with chimeric fetuses of human cells with sheep, monkey, and pig cells. In each case human stem cells were injected into locations in animal fetuses. They also discuss the potential to introduce human stem cells at a much earlier stage in development where the injected cells can be expected to become a larger percentage of the resulting animal's total cell count.
In 2003, Scientist at the South Korean firm Maria Biotech, were reported to have injected human embryonic stem cells labelled with a fluorescent protein into 11 mouse blastocysts which later developed. The embryos were then carried by foster mice, whereby five offspring were born with fluorescence in tissues including the heart, bones, kidney, and liver. However, the scientists terminated the project after having to address "severe protests" from the public .
They take a hard line against any tinkering that results in a creature that has human neurons sharing a brain with animal neurons.
This is an interesting position. They draw the line against mixing human neurons with non-human neurons. Perhaps they see human neurons as somehow sacred.
Okay, what is the appeal of this position? First off, it avoids the really difficult problem of defining what is a rights-possessing entity. Make sure nothing that is a mix of human and non-human mind comes into existence. Then we never have to face that question. Well, that's the hope anyway. But the hope is wrong. We will end up having to face that question anyway when someone tinkers with another species and just changes its DNA to make it smarter without using human DNA to create the smarter result. We will face the question when people start creating human offspring that have modifications of genes that govern cognitive ability. We will face that question when artificial intelligences are created.
The need to create a scientific definition of humans will be forced upon us by technological advances. That definition (or, rather, definitions since consensus will not be possible) will threaten religious definitions, ideological definitions, and other definitions based upon fantasies of what we wish to believe is nature.
But before we start modifying human nature or creating other intelligent lifeforms we already increasingly face another threat to how we view ourselves: Genetic and neurobiological advances will gradually undermine many beliefs about the nature of humans. Worse, the challenge of what should be considered human will (I predict) be challenged when looking just at genetic variations which exist in humans.
For example, more genetic variations that contribute to violence and criminality will be found. Probably some genetic variations will be found that contribute to psychopathy. Should we consider amoral totally unempathetic minds as humans? We'd be unwise to grant rights to an artificial intelligence with those qualities. Should our standard for rights possession be lower for humans than for AIs or animals uplifted by genetic engineering that raises their intelligence?
Delaying the day we have to face the question of whether chimeras possess human rights or human souls might make sense even if creation of chimeras is eventually allowed some day. The longer we delay the better will be our scientific understanding of human nature and of the cognitive qualities needed to maintain a rights-based society.
A second reason for keeping humans unmixed with other species is that doing so preserves the ability of many humans to feel that humans are special and apart from the rest of life. Many people see humans as special due to having souls which other species do not have. But if a human-chimp chimera could be created the question arises: Would it have a soul? Suppose that a creature looked perfectly human but somehow had 10% of its brain cells from another species. Would it have a soul? It'd have more human brain cells than, say, an Alzheimer's patient. So would it have a soul?
A third reason to oppose creation of human-animal chimeras is to avoid suffering in the resulting creatures. But suppose scientists include a small enough percentage of human cells that the resulting animal thinks and acts like an animal of its type. Or suppose the human cells were genetically modified to be more compatible with, say, neurons in a mouse's brain and that the mouse brain was kept as small as a normal mouse's brain. Potentially that'd avoid the problem of creatures which are not shaped in a way that causes them suffering. Also, the mouse would not possess any higher level of awareness than a normal mouse has.
It seems to me that the biggest benefit of totally banning the creation of human-animal chimeras is that it avoids our feeling confused about how we should treat the results. But we are going to have to wrestle with all the ethical questions that chimeric creatures present us with whether or not we create chimeric creatures. Also, even if the creation of such creatures is banned inevitably people will create them illegally. So we'll still have to decide at some point what criteria to use when weighing what rights to grant them or whether to destroy them upon discovery.
Before taking the line that we should just ban anything that seems yucky or weird consider the potential benefits from letting scientists create chimeras. For example, scientists can study human diseases by putting human cells with human genetic disease into animals. Also, use of animals to grow organs for transplant might work if the organs were grown from the fetal stage using human stem cells injected into the fetus.
Writing for the Christian Science Monitor Amy Green reports on the rapidly growing trend toward purchasing back-up electric power generators for homes.
LONGWOOD, FLA. – The first power outage lasted five days. So did the second one. And the third. The hurricanes that racked Florida in 2004 were a miserable experience for Andre Biewend and his family - including his 3-year-old twins at the time. They were left in a stinking, sweltering home as Mr. Biewend argued with local store owners for dry ice for the fridge.
Not anymore. Biewend, a real estate developer in this suburb of Orlando, invested $15,000 more than a year ago in a standby power generator that keeps his 5,200-square- foot home running through any outage. He likens the generator to an insurance policy - he hopes he never uses it, but now with a baby at home, too, it gives him a sense of security.
The growth in sales has been huge.
The standby generator industry grew five-fold between 2000 and 2005 to a more than $500 million industry, according to Generac Power Systems, the nation's largest generator manufacturer.
I see an important implication of this trend: There's a big demand for non-grid electricity. That electricity costs far more than grid electricty. Therefore electricity from solar photovoltaics does not have to become as cheap as big power plant electricity in order to compete. A substantial portion of the population will buy photovoltaics and batteries for their homes once the price allows them some feeling of environmental satisfaction or increased security against natural disasters. Some will also buy rooftop wind microturbines to generate home electricity from the wind.
As living standards rise for the upper middle class and upper class they find they have money to buy things they never bought before. So more people buy second homes, private jet flights, and other luxury goods. While some people buy big $50,000 SUVs others spend far less on a Toyota Prius in order to feel they are doing something for the environment and in order to signal that they are acting on their political beliefs by putting their money where their mouths are.
The combination of rising affluence and eventually falling prices for photovoltaic installations will drive installation of photovoltaics well in advance of when photovoltaics make sense purely from the price standpoint as compared to local utility electricity. Some will be driven by the desire to make a statement. Others will see photovoltaics as utilitarian luxuries that assure they'll never be without electric power. The desires for status, independence, and security will all push photovoltaics along faster than a simple economic analysis would lead one to expect.
In order for photovoltaics to work as a more secure form of electricity in hurricane zones photovoltaics will need to become integrated into roof tiles and siding so that it will stay anchored to roofs under hurricane force winds. Also, home electric battery arrays will need to become cheaper and longer lasting. But the batteries, photovoltaics, and microturbines will make big in-roads in the home electricity market before their prices fall all the way down to the price of grid power.
Update: The willingness to spend money on convenience rises as incomes rise. Once people have satisfied basic needs they tend more toward satisfying desires. One desire is to never be inconvenienced. Loss of electric power for 5 minutes, 5 hours, or 5 days is an inconvenience and people will spend increasing amounts of money to reduce the risk of that inconvenience the more affluent they become.
Pluggable hybrid vehicles and batteries with higher energy density also increase convenience. First off, one can reduce the frequency of trips to get gasoline. Second, the batteries in a car can run a house in event of a power outage. People will spend to save time. People will also spend to reduce the risk of life disruption from natural events or human technological failures. The desire for greater convenience is going to drive the development of better energy technologies.
In their latest finding on the brain's role in controlling appetite and weight, researchers at the Albert Einstein College of Medicine have shown that reducing levels of fatty acids in the hypothalamus causes rats to overeat and become obese. Their results suggest that restoring fatty-acid levels in the brain may be a promising way to treat obesity. The study, published in the January 15th on-line edition of Nature Neuroscience, was led by Dr. Luciano Rossetti, director of the Diabetes Research Center at Einstein. (The paper will appear in print in the February issue.)
Consumption of fats causes a boost in malonyl CoA in the hypothalamus. Reduction in malonyl CoA boosts appetite.
The study focused on malonyl CoA, a molecule suspected of being one of the critical nutrients influencing hypothalamic regulation of eating behavior. Previous studies had shown that hypothalamic levels of malonyl CoA increase markedly after meals and are suppressed by fasting.
The Einstein researchers wanted to know whether sustained suppression of this nutrient within the hypothalamus could result in obesity. To find out, they piggybacked an enzyme known to degrade malonyl CoA onto an adeno-associated virus and injected the virus into the hypothalamus of rats. The injections caused a chronic decrease in malonyl CoA levels, which dramatically increased the rats' food intake and led to obesity that was maintained for at least four months.
"We showed in this study that disrupting malonyl-CoA levels in this region of the brain impairs the nutrient-sensing mechanism by which the hypothalamus modulates food intake to maintain normal weight," says Dr. Rossetti, who is also the Judy R. and Alfred A. Rosenberg Professor of Diabetes Research at Einstein. "Figuring out a way to re-adjust malonyl-CoA levels in the human hypothalamus could lead to innovative therapies not only to treat obesity but to help prevent diabetes and other consequences of being overweight."
If drugs can be found that either boost malonyl CoA levels in the hypothalamus such drugs might decrease appetite. Alternatively, malonyl CoA binds somewhere to cause the appetite suppression effect. Another option is to look for where it binds and develop drugs that bind at the same place. A malonyl CoA substitute migh also suppress appetite.
Another possibility: Would slow consumption of small amounts of a fat all day reduce total calories consumed? If so, would all fats work equally well for this purpose? Or do particular fats do a better job of suppressing appetite? If so, which fats best suppress appetite?
Old hippies who haven't toked for decades might come back to the stoner life. Marijuana active ingredient tetrahydrocannabinol blocks the formation of beta amyloid plaques which are suspected as a cause of Alzheimers disease.
LA JOLLA, CA, August 9, 2006 - Scientists at The Scripps Research Institute have found that the active ingredient in marijuana, tetrahydrocannabinol or THC, inhibits the formation of amyloid plaque, the primary pathological marker for Alzheimer's disease. In fact, the study said, THC is "a considerably superior inhibitor of [amyloid plaque] aggregation" to several currently approved drugs for treating the disease.
The study was published online August 9 in the journal Molecular Pharmaceutics, a publication of the American Chemical Society.
According to the new Scripps Research study, which used both computer modeling and biochemical assays, THC inhibits the enzyme acetylcholinesterase (AChE), which acts as a "molecular chaperone" to accelerate the formation of amyloid plaque in the brains of Alzheimer victims. Although experts disagree on whether the presence of beta-amyloid plaques in those areas critical to memory and cognition is a symptom or cause, it remains a significant hallmark of the disease. With its strong inhibitory abilities, the study said, THC "may provide an improved therapeutic for Alzheimer's disease" that would treat "both the symptoms and progression" of the disease.
The development of better tests for amyloid plaque formation probably will provide the ability to predict the development of Alzheimer's many years in advance of obvious symptoms. For people who face the threat of losing their memory 10 years hence if THC can prevent or delay that outcome use of THC might be worth it. Though quite a few people won't want to go through every day of their lives high on THC.
THC works better than commercial drugs currently on the market.
"When we investigated the power of THC to inhibit the aggregation of beta-amyloid," Janda said, "we found that THC was a very effective inhibitor of acetylcholinesterase. In addition to propidium, we also found that THC was considerably more effective than two of the approved drugs for Alzheimer's disease treatment, donepezil (Aricept ®) and tacrine (Cognex ®), which reduced amyloid aggregation by only 22 percent and 7 percent, respectively, at twice the concentration used in our studies. Our results are conclusive enough to warrant further investigation."
Alzheimer's is a terrible disease. It gradually robs you of your identity. People who face the prospect of losing their memories should be allowed a great deal of latitutde in terms of what they can do to protect themselves from that fate. I expect drugs, antibodies, and vaccines will all come to market in the next 10 years that stop and reverse beta amyloid plaque formation. Use of THC for this purpose will be transitory at best. But will any government even allow clinical trials of its effectiveness against Alzheimer's?
Rochester, Minn. -- Researchers from Mayo Clinic have discovered that allergic rhinitis is associated with the development of Parkinson's disease later in life. Findings will be published in the Aug. 8 issue of the journal Neurology.
"The association with Parkinson's disease is increased to almost three times that of someone who does not have allergic rhinitis," says James Bower, M.D., Mayo Clinic neurologist and lead study investigator. "That's actually a pretty high elevation."
Previous studies had shown that people who regularly take nonsteroidal anti-inflammatory drugs, such as ibuprofen, are less likely to develop Parkinson's disease. These results prompted the Mayo Clinic investigators to look further into the links between diseases characterized by inflammation and Parkinson's. They studied 196 people who developed Parkinson's disease, matched with people of similar age and gender who did not develop Parkinson's. The study was conducted in Olmsted County, Minn., home of Mayo Clinic, over a 20-year period.
The researchers examined these groups to determine if those who developed Parkinson's disease had more inflammatory diseases. They found that those with allergic rhinitis were 2.9 times more likely to develop Parkinson's. They did not find a similar association between inflammatory diseases such as lupus, rheumatoid arthritis, pernicious anemia or vitiligo and Parkinson's disease. The researchers hypothesize that they may not have found significant links between these diseases and Parkinson's disease due to the relatively small number of those in the population who have these diseases, and thus the small number with these diseases in their population sample study. They also did not find the same association with Parkinson's disease in patients with asthma that they discovered in those with allergic rhinitis.
Would fairly regular use of Flonase (nasal anti-allergy spray) reduce the risk of Parkinson's? Or would antihistamines reduce the risk?
Researchers from the Erasmus Medical Center in the Netherlands studied around 5,300 participants over the age of 55, and found that those who had the highest intake of vitamin B6 had up to a 50 percent reduction in Parkinson's disease risk.
The researchers suspect that B6 exerts a protective effect by lowering blood homocysteine. If that is the mechanism then other nutrients that lower homocysteine (most notably folic acid) might also reduce the risk of Parkinson's.
With the introduction of just four factors, researchers have successfully induced differentiated cells taken from mouse embryos or adult mice to behave like embryonic stem cells. The researchers reported their findings in an immediate early publication of the journal Cell.
The cells--which the researchers designate "induced pluripotent stem cells" (iPS)--exhibit the physical, growth, and genetic characteristics typical of embryonic stem cells, they reported. "Pluripotent" refers to the ability to differentiate into most other cell types.
"Human embryonic stem cells might be used to treat a host of diseases, such as Parkinson's disease, spinal cord injury, and diabetes," said Shinya Yamanaka of Kyoto University in Japan. "However, there are ethical difficulties regarding the use of human embryos, as well as the problem of tissue rejection following transplantation into patients."
Those problems could be circumvented if pluripotent cells could be obtained directly from the patients' own cells.
"We have demonstrated that pluripotent stem cells can be directly generated from fibroblast cultures by the addition of only a few defined factors," Yamanaka said. Fibroblasts make up structural fibers found in connective tissue.
Pluripotent stem cells can become any type of cell in the body. Adult stem cells are not as flexible. But currently the only way to get pluripotent stem cells is from embryonic cells. That raises ethical opposition in some quarters. Pluripotent stem cells created from adult cells would avoid most of the political resistance and at the same time be more immunologically compatible.
If this approach works for humans as well then some day we'll be able to have pluripotent stem cells made from our own cells. Then those cells could be used to grow replacement parts such as internal organs or injected into joints to supply joint material to those suffering from arthritis.
The researchers chose factors to introduce into adult cells by looking at which genes are turned on in embryonic stem cells. Note that advances in biotechnology in recent years have made it a lot easier to measure the levels of activity of many genes at once.
The researchers selected 24 genes--all previously found to play a role in early embryos and embryonic stem cell identity--as candidate factors that might give body cells the ability to become other cell types.The researchers found that four of those factors, known as Oct3/4, Sox2, c-Myc, and Klf4, could lend differentiated fibroblast cells taken from embryonic or adult mice the pluripotency normally reserved for embryonic stem cells.
They further reported that transplantation of the iPS cells under the skin of mice resulted in tumors containing a variety of tissues representing the three primary types found in mammalian embryos. Those primary "germ layers" in embryos eventually give rise to all an animal's tissues and organs.
The researchers still need to repeat this experiment with human cells to find out if this method will work for human cells as well. If they succeed then this discovery could open the gates for much higher levels of research funding for pluripotent stem cells.
Those who have never married have a 58% higher risk of an earlier death, compared with a married reference group, found Robert Kaplan, Ph.D., of the University of California at Los Angeles and Richard Kronick, Ph.D., of UC San Diego.
Strikingly, the 58% never-married penalty was also higher than the 27% combined death rates for those who were separated or divorced and the 39% rate for widowed persons. they reported in the August issue of the Journal of Epidemiology and Community Health.
So if you are hesitating to enter some marriage since you think it has a high chance of failure maybe you ought to plunge in knowing that you are reducing your odds of death. On the other hand, I have a long time married friend who thinks being married makes the passage of time harder to bear.
I bet the never marrieds are less attractive than those who get married on average. Yes, there are some beautiful never-marrieds. But, again, I'm talking on average. Well, good looks are partly a measure of health.
"Having never been married may be associated with more severe isolation because it is associated with greater isolation from children and other family."
Alternatively, it might be that people who have underlying illnesses that threaten their health and shorten their life expectancy are deemed less suitable as marriage material.
Also, many of the never married men in the study died from infectious disease, most likely HIV, note the authors.
I bet a difference in average lifetime stress between the married and non-married is the biggest cause of the difference in life expectancy. Stress accelerates the aging process. Marriage could reduce stress in a number of ways. For example, I wonder if having two incomes reduces the stress of feared potential and actual unemployment.
I wonder how much of this result is due to IQ. Higher intelligence correlates with longer life expectancy and this relationship holds up even up into the genius range of IQ. Why is this relevant to marriage? Half Sigma has used the General Social Survey Wordsum test as a rough proxy for intelligence and found that the dumbest men have the lowest rates of marriage. Though the rate of never married climbs at the highest Wordsum score levels among men.
Some of the benefit from being married (at least for some married people) probably comes from having someone to pester you to see a doctor or eat better or just to assure you that you are not alone and unwanted.
An article in the Christian Science Monitor claims that ethanol cost less than half the price of gasoline to produce.
The economics make sense. Middle East tensions and other factors have pushed the oil price higher: In June it averaged $65 a barrel. At that price, it cost $2.20 to produce a gallon of gasoline - about $1.56 for the oil itself and 64 cents for refining costs, according to the federal Energy Information Administration.
By contrast, it costs just under $1 to produce a gallon of ethanol at current corn prices of about $2 a bushel, Professor Gallagher estimates. That means ethanol would continue to be profitable even if oil prices drop dramatically and corn prices increase, he says.
But a straight across dollars per gallon comparison between gasoline and ethanol is not a simple apples to apples comparison because ethanol has about two thirds the BTUs of energy per gallon of gasoline. Ethanol at $1 per gallon is therefore about equal to $1.50 per gallon gasoline. This makes it less convenient since it produces lower miles per gallon. Still, $1.50 per gallon is still less than $2.20 per gallon. But this suggests that as corn demand rises and corn prices rise the price gap may narrow - unless oil prices go higher still.
Getting back to the original article, corn ethanol does not scale.
But ethanol made from corn faces a supply problem. Even if the entire US corn crop were devoted to producing E85 (a blend of 85 percent ethanol and 15 percent gasoline), it would supply only about 12 percent of US needs, studies say.
More land can (and probably will) get put into production to grow corn. But the land currently in production can produce higher yields at lower cost than the additional land available for growing corn. Plus, we will pay in higher costs for corn and meat for food.
Biodiesel from soy and animal fats similarly hits scaling problems. The use of plant cellulose to create ethanol will eventually boost ethanol per acre of crops. Maybe that'll be able to scale far enough to replace most gasoline. But better batteries to enable fully electric cars looks much more attractive to me:
Using electricity to power vehicles is so efficient and cheap that, even if the juice flows from a mix of power plants including coal-fired boilers, it would still pollute less on a national basis than using gasoline, say Greene and others who have studied the issue.
Driving 20 to 40 miles a day on electricity stored in a modern lithium ion battery would be like driving on gasoline costing just 75 cents per gallon, Luft says.
We won't all have to walk to work in the future.
The H-System combined cycle generator from General Electric is 60% efficient in turning natural gas into electricity (Combined cycle is where the natural gas is burned to generate electricity and then the waste heat is used to create steam that powers a second generator). Natural gas recovery is 97.5% efficient, processing is also 97.5% efficient and then transmission efficiency over the electric grid is 92% on average. This gives us a well-to-electric-outlet efficiency of 97.5% x 97.5% x 60% x 92% = 52.5%.
Despite a body shape, tires and gearing aimed at high performance rather than peak efficiency, the Roadster requires 0.4 MJ per kilometer or, stated another way, will travel 2.53 km per mega-joule of electricity. The full cycle charge and discharge efficiency of the Tesla Roadster is 86%, which means that for every 100 MJ of electricity used to charge the battery, about 86 MJ reaches the motor.
Bringing the math together, we get the final figure of merit of 2.53 km/MJ x 86% x 52.5% = 1.14 km/MJ. Now let's now compare that to the Prius and a few other options normally considered energy efficient.
The fully considered well-to-wheel efficiency of a gasoline-powered car is equal to the energy content of gasoline (34.3 MJ/liter) plus the refinement & transportation losses (18.3%), multiplied by the miles per gallon or km per liter. The Prius at an EPA rated 55 mpg therefore has an energy efficiency of 0.56 km/MJ. This is actually an excellent number compared with a "normal" car like the Toyota Camry at 0.28 km/MJ.
The Tesla Roadster is not an apples-to-apples comparison to the Prius or Camry for passenger space, trunk space, or general comfort. On the other hand, it accelerates like a bat out of hell. But even if a fully electric full sized car had half of the efficiency of the Roadster it'd still
The Tesla Roadster weights 1140 kg (2508 lb). By contrast, the Toyota Prius weights 1325 kg (2921 lb). That is only 16% more. Though the Prius loses some efficiency as compared to the Roadster due to more wind drag. Still, when much lighter batteries become available if a pure electric Prius-like vehicle can get built with the same weight as the existing Prius then the effective fuel efficiency (using Musk's calculations above) could easily exceed the Prius's by 50% or more. Rumours about a 94 mpg Prius with lithium batteries by 2008 suggest that pure electric cars will have to compete against much tougher hybrid competition. High efficiency hybrids will be more convenient than pure electric cars, especially for road trips where long recharge time would slow travel.
Cellulosic technology will drive down the cost of biomass liquid fuels. Battery advances will both make hybrids more efficient and eventually enable the manufacture of high energy efficiency mass market electric vehicles. Pure electric vehicles will allow coal, nuclear, solar, wind, geothermal, and wave electricity to all compete to power vehicles. Given the increased competition and higher energy efficiency from these coming developments I expect the fuel cost per mile travelled to drop in coming years. Even if the price of oil continues to climb the price of oil will matter less for ground transportation.
While existing antidepressants such as Zoloft, Prozac, and Paxil take weeks to begin working ketamine starts lifting mood within 2 hours.
People with treatment-resistant depression experienced symptom relief in as little as two hours with a single intravenous dose of ketamine, a medication usually used in higher doses as an anesthetic in humans and animals, in a preliminary study. Current antidepressants routinely take eight weeks or more to exert their effect in treatment-resistant patients and four to six weeks in more responsive patients — a major drawback of these medications. Some participants in this study, who previously had tried an average of six medications without relief, continued to show benefits over the next seven days after just a single dose of the experimental treatment, according to researchers conducting the study at the National Institutes of Health's National Institute of Mental Health.
This is among the first studies of humans to examine the effects of ketamine on depression, a debilitating illness that affects 14.8 million people in any given year. Used in very low doses, the medication is important for research, but is unlikely to become a widely used clinical treatment for depression because of potential side effects, including hallucinations and euphoria, at higher doses. However, scientists say this research could point the way toward development of a new class of faster- and -longer-acting medications. None of the patients in this study, all of whom received a low dose, had serious side effects. Study results were published in the August issue of the Archives of General Psychiatry.
Imagine living in perpetual depression. What a hell. Though some readers do not have to imagine. You have my sympathy.
The effect is quick and dramatic.
For this study 18 treatment-resistant, depressed patients were randomly assigned to receive either a single intravenous dose of ketamine or a placebo (inactive compound). Depression improved within one day in 71 percent of all those who received ketamine, and 29 percent of these patients became nearly symptom-free within one day. Thirty-five percent of patients who received ketamine still showed benefits seven days later. Participants receiving a placebo infusion showed no improvement. One week later, participants were given the opposite treatment, unless the beneficial effects of the first treatment were still evident. This "crossover" study design strengthens the validity of the results.
"To my knowledge, this is the first report of any medication or other treatment that results in such a pronounced, rapid, prolonged response with a single dose. These were very treatment-resistant patients," said NIMH Director Thomas R. Insel, M.D.
Receptors for the neurotransmitter glutamate are blocked by ketamine and glutamate regulation appears to play an key role in causing depression.
Ketamine blocks a brain protein called the N-methyl-D-aspartic acid (NMDA) receptor. Previous studies have shown that agents that block the NMDA receptor reduce depression-like behaviors in animals.
NMDA receptors are critical for receiving the signals of glutamate, a brain chemical that enhances the electrical flow among brain cells that is required for normal function. Studies indicate that dysregulation in glutamate could be among the culprits in depression. Using ketamine to block glutamate's actions on the NMDA receptor appears to improve function of another brain receptor — the AMPA receptor — that also helps regulate brain cells' electrical flow.
This result is another clue. Eventually depression will become completely curable and preventable.
Other anti-depressants probably take longer because they act at the beginning of a long chain of causation.
Scientists think the reason current antidepressant medications take weeks to work is that they act on targets close to the beginning of a series of biochemical reactions that regulate mood. The medications' effects then have to trickle down through the rest of the reactions, which takes time. Scientists theorize that ketamine skips much of this route because its target, the NMDA receptor, is closer to the end of the series of reactions in question.
Given that ketamine acts way downstream closer to the final effect of depression it or similarly acting compounds (preferably with fewer side effects) could lift depression while the longer acting compounds build up their effects. For people with severe depression hospitalization or administration of ketamine in clinics might be worth it.
Ravers in settings where people use ecstasy and looking for a new kind of kick have labelled ketamine "Special K" and used it in higher doses. But ketamine has very different effects including paralysis.
At low doses the user may feel euphoric, experience waves of energy, and possibly synaesthesia - sensations such as seeing sounds or hearing colours.
At higher doses the user might become paralysed, experience hallucinations and alternate realities, and a feeling of disassociation giving an 'out of body' experience known as the "K-hole".
Not for casual use.
If you are curious check out the Wikipedia entry on ketamine.
Update: Note that ketamine works for people who fail to get benefit from currently approved anti-depressants. Those who aren't helped by existing anti-depressants probably have tried Selective Serotonin Update Inhibitors (SSRIs) such as Prozac and Zoloft. Well, this result suggests that there are points in the chain of causation where depression can get initiated that are downstream of serotonin receptors and yet upstream of the glutamate receptors. SSRIs won't work with people whose depression gets initiated downstream of serotonin receptors.
Intervention with ketamine might make sense for those people who get no benefit from SSRIs. But ketamine is probably not ideal for them. In most cases the best treatment should act at the earliest stage in the series of events that cause a person to get depressed. Depression has multiple causes. The earliest stage will be different for each different cause.
The mind is a terrible thing to waste. The big risk factors for dementia are the same as the big risk factors for heart disease.
A method to predict a middle-aged person's chance of developing dementia has been devised by scientists.
The test calculates risk by assessing factors such as blood pressure level, body mass index and cholesterol levels, along with age and education.
Having any one of these risk factors doubles a person's chance of developing dementia, and having all three increases their chances by six times, said Dr. Miia Kivipelto, an associate professor at the Aging Research Centre in Stockholm, Sweden, and the study's lead author.
By assessing factors such as blood pressure, body fat and cholesterol levels in 1,400 middle-aged Finns in the 1970s and 1980s, scientists were able to predict, with a 70% accuracy rate, the onset of dementia 20 years later.
If you have high blood pressure then take blood pressure loweriing medicine. If you have high cholesterol then take a statin drug (e.g. Crestor or Lipitor). Also get more exercise and eat better food.
The Actuarial Profession today announced its adoption of new mortality tables (see Note 1). The tables were produced by the Continuous Mortality Investigation (CMI) (see Note 2.), a research organisation of the Actuarial Profession. The tables were published in draft form in 2005 (see Note 3.) and minor adjustments were incorporated in the final version to reflect feedback received from actuaries.
Previous sets of tables have incorporated projections of future mortality, but this has not been done with the latest tables because of the uncertainty surrounding future improvements. The CMI has been undertaking significant research into possible methods of projecting mortality. This research is continuing, but it is not currently expected that this work will lead to adoption of a specific projection basis by the Actuarial Profession. Instead the profession is saying that actuaries – and other professionals using mortality projections – should consider a range of scenarios.
There are important financial implications of any improvement in mortality. For pensioners, improved mortality rates (see Note 4.) mean spending longer in retirement and the latest tables show why many commentators have been calling for retirement ages to increase.
Nick Dumbreck, President of the Institute of Actuaries, commented: “Actuaries have always been expected to satisfy themselves that using a mortality table published by the profession is appropriate for the particular purpose to which it is put and this is no different with the latest tables. However the absence of mortality projections in these tables emphasises the need for actuaries to consider the uncertainty surrounding future mortality experience and to explain the financial repercussions of this uncertainty to their employers and clients.”
Pension funds that provide guaranteed benefits until death are in worse financial shape than they know. As the rate of increase in life expectancies starts to accelerate will governments eventually step in with legal changes to relieve the pension funds of some of their liabilties?
The actuaries show a table of dramatic improvements in the odds of dying at ages 65, 75, and 85. The series "92" represents measured death rates in 1991-1994 and the later series "00" represents death rates during 1999-2002.
The following information is repeated from the Press Release of September 2005. Mortality rates are the probability of dying at a given age. Specimen mortality rates (per 1,000) from the new tables (the "00" Series) and the previous tables (the "92" Series) and the implied improvements are shown in the table below:
Males Females Age "00" series "92" series Improvement "00" Series "92 Series" Improvement 65 12.85 18.12 29% 7.41 10.98 33% 75 40.82 54.20 25% 26.42 34.61 24% 85 111.52 131.07 15% 82.48 91.88 10%
The figures quoted are for pensioners insured under life office pension schemes (ie, not individual annuity-type arrangements) who retire at or after normal retirement dates (ie, excluding early retirements, who may be retiring due to ill-health).
Stem cell therapies for heart disease, drugs to stop Alzheimer's plaque build-up, immunotherapies against cancer, and many other coming treatments are going to cause big surges in longevity. Actuaries have no way of knowing when these treatments will come. But they are already seeing big enough changes in longevity to doubt their abilities to predict future life expectancies. The rate of advance for biomedical science and biotechnology is accelerating.
Aubrey de Grey has coined the term ‘actuarial escape velocity’ (AEV) which is the point at which life expectancy goes up faster than 1 year per year. Once we reach AEV your odds of dying in a given year will become less than your odds of dying in the previous year. Aubrey thinks AEV is within reach within a few decades.
The escape velocity cusp is closer than you might guess. Since we are already so long lived, even a 30% increase in healthy life span will give the first beneficiaries of rejuvenation therapies another 20 years—an eternity in science—to benefit from second-generation therapies that would give another 30%, and so on ad infinitum. Thus, if first-generation rejuvenation therapies were universally available and this progress in developing rejuvenation therapy could be indefinitely maintained, these advances would put us beyond AEV.
I share his optimism because I see advances in biotechnology of sorts that mirror the kinds of advances that occur in electronics. Microfluidics devices built using processes similar to those used to build semiconductor computer chips in particular promise to make laboratory science orders of magnitude faster and cheaper. Therefore many biomedical problems will become easily solvable. These advances in biotechnology will enable us to develop the full range of Strategies for Engineered Negligible Senescence (SENS) and eventually to reverse the aging process.
Animal research from the University of Massachusetts Lowell (UML) indicates that apple juice consumption may actually increase the production in the brain of the essential neurotransmitter acetylcholine, resulting in improved memory.
Neurotransmitters such as acetylcholine are chemicals released from nerve cells that transmit messages to other nerve cells. Such communication between nerve cells is vital for good health, not just in the brain, but throughout the body.
“We anticipate that the day may come when foods like apples, apple juice and other apple products are recommended along with the most popular Alzheimer’s medications,” says Thomas Shea, Ph.D., director of the UML Center for Cellular Neurobiology and Neurodegeneration Research.
The study will be published in the August issue of the international Journal of Alzheimer’s Disease. The abstract is now available online at http://www.j-alz.com/issues/9/vol9-3.html.
I'd like to see experiments like this one repeated with a wider range of fruits and vegetables at a range of doses to identify the foods that deliver the most benefit the least amount of calories consumed. Also, use of quercetin, other flavonoids, and other antioxidants by themselves would help tease out which compounds are delivering the benefits.
In this novel animal study at UML, adult (9-12 months) and old (2-2.5 years) mice, some specially bred to develop Alzheimer’s-like symptoms, were fed three different diets (a standard diet, a nutrient-deficient diet, and a nutrient-deficient diet supplemented with apple components (in this case, apple juice concentrate was added to their drinking water).
Among those fed the apple juice-supplemented diet, the mice showed an increased production of acetylcholine in their brains. Also, after multiple assessments of memory and learning using traditional Y maze tests, researchers found that the mice who consumed the apple juice-supplemented diets performed significantly better on the maze tests.
Diet optimization for aging brains could provide great personal and economic benefits for hundreds of millions of people.
In fact, the normal adults had the same acetylcholine levels regardless of diet.
However, the genetically engineered mice on the nutrient-poor diet had lower acetylcholine levels. But this drop was prevented in those given apple juice.
In the aged mice on a normal diet, acetylcholine levels were lower than in the normal adult mice; and their levels were even lower if placed on the nutrient-poor diet. But, again, this decline was prevented by the addition of apple juice to drink.
Eat apple sauce with your salmon dinner.
Update: Elderly people in Singapore who occasionally consume curry score higher on a standard test of cognitive function. The turmeric in curry and, in particular, the curcumin in the turmeric might be behind this effect. Those who benefitted did not even have to eat it once a month. Just occasional consumption is enough to produce a measurable benefit.
This result opens up all sorts of possibilities. Dr Viren Swami of University College London and Dr Martin Tovée of Newcastle University found that before they eat dinner men find heavier set and less curvy women more attractive.
How full a man's stomach is can dictate the type of woman he will fancy, UK research suggests.
A study of 61 male university students found those who were hungry were attracted to heavier women than those who were satiated.
The hungry men also paid much less attention to a woman's body shape and regarded less curvy figures as more attractive.
The molecular mechanism by which this works might be manipulable some day. Could a drug target brain locations which govern attraction without affecting whether a person feels hungry? If so, a guy could (knowingly or not) take a drug that makes his skinny or fatty mate look more attractive all the time.
I've long thought that a drug which increased the range of men or women which a person finds attractive would allow a person to be a lot more satisfied when pursuing the opposite sex. Also, a drug or other treatment that allowed a mind to find a single person the most attractive (say stare at that person while getting the treatment to imprint that shape as ideal) would allow everyone to think their mate is most attractive.
Biotechnological manipulation of feelings of attraction might not cause natural selection problems. In the future people will genetically engineer their offspring anyway. So hooking up with a person who is less attractive due to genetic problems doesn't have to lead to genetically less fit offspring. That will be able to get fixed with genetic engineering at the time of conception.
Male students entering and exiting a school dining hall were shown pictures and women and asked to rate them.
They recruited male university students as they entered or exited a campus dining hall during dinner time.
They asked the men to rate how hungry they were on a scale of one to seven. Using these responses, the researchers selected 30 hungry and 31 satiated men to take part in the study.
The men were then asked to rate the attractiveness of 50 women of varying weights, all within a healthy range, who had been photographed wearing tight grey leotards and leggings.
Skinny women should want to go out to dinner with men since the men will find them more attractive as dinner progresses. Heavier set women might want to go bicycling with a guy to build up his appetite in more ways than one.
Gainesville, Fla. -- Nearly 6 percent of morbidly obese children and adults have a genetic defect that keeps them feeling like their stomach is running on empty, no matter how much they have eaten.
The press release refers to genetic defects. The term "defect" implies an error or mistake. But a type of mutation that occurs in 6% of the population (correction: oops, 6% of the morbidly obese - gotta read more carefully) surely occurs at too high a frequency to be a mistake. The ancestors of the carriers of these mutations gained selective advantage and left more surviving offspring due to the mutations that made them more hungry.
The problem humans face today is that in industrialized countries mutations which increase the desire for food are now more a burden than a benefit. But the mutations are only defects if you use modern conditions as a reference to come up with standards for how humans should function.
Once you cross the bridge of defining modern civilization as the standard by which to decide which genetic variations are defects you've crossed a much larger bridge than most people appreciate. Consider the fight-or-flight reflex where someone feels adrenaline flowing and feels the urge to either run or attack. Since this reflex gets triggered totally inappropriately in arguments in office building meetings (few will start beating up co-workers or running for their lives down aisles of cubicles) it is hard to see the fight-or-flight reflex as adaptive at this point. If anything, the stress from adrenaline rush probably accelerates your aging.
If the fight-or-flight response and other counter-productive responses we have in modern situations are defects because they are counter-productive in modern conditions then all humans are full of defects and humanity is in need of a genetic redesign. I happen to think that, yes, we are in need of a massive redesign to adapt us to the technological and urban environments which we live in and to make it easier for us to live longer. But that will not become the majority view until we develop a far more detailed understanding of many genetic variations and how they govern the way we function.
These University of Florida scientists identified 11 mutations that make a receptor involved in hunger regulation to behave in ways that they consider to be abnormal.
Mutations of the melanocortin-4 receptor, a gene found in brain cells that play a role in regulating hunger, are the most common cause of genetic obesity. Now University of Florida researchers have determined how some of these mutations cause the receptor to miss signals from molecules that tell the body when to eat and when to put down the fork, placing scientists one step closer to finding a way to correct these defects.
In a side-by-side comparison of 40 genetic mutations, UF medicinal chemists found that 11 caused the receptor to behave abnormally, according to findings recently published in the online edition of the journal Biochemistry.
The goal is to discover the molecular glitch that causes the receptor to malfunction so chemists can make drugs to treat it, said Carrie Haskell-Luevano, Ph.D., a UF associate professor of medicinal chemistry and the study's lead author. UF researchers have already found a molecule that seems to correct one of the mutations, keeping the hunger-signaling pathway running smoothly, Haskell-Luevano said.
The collection of melanocortin-4 receptor gene mutations for obesity has been building up for years. See these papers from 1999 and 2004 for examples of earlier work on obesity and the melanocortin-4 receptor.
The discovery of more genetic variations that influence some behavior or metabolic processs opens up targets for drug development and also makes it easy to study the causes of differences in behaviors and metabolic processes.
Dallas -- July 31, 2006 -- Giving up your regular late-night snack may be hard, and not just because it's a routine. The habit may genetically change an area of the brain to expect the food at that time, researchers at UT Southwestern Medical Center have discovered.
By training mice to eat at a time when they normally wouldn't, the researchers found that food turns on body-clock genes in a particular area of the brain. Even when the food stopped coming, the genes continued to activate at the expected mealtime.
"This might be an entrance to the whole mysterious arena of how metabolic conditions in an animal can synchronize themselves with a body clock," said Dr. Masashi Yanagisawa, professor of molecular genetics and senior author of the study.
Maybe when people get older their brains get programmed to be hungry at more times of the day?
Hackettstown, NJ – July 31, 2006 -- Flavanol-rich cocoa could offer powerful cardiovascular benefits for the nearly 78 million baby boomers in the United States today, suggests a new study published in the August issue of the Journal of Hypertension.
Researchers at Harvard Medical School and the Brigham and Women's Hospital in Boston found that drinking a standardized flavanol-rich cocoa beverage improved several measures of blood vessel function, especially among older study participants. Flavanols are the natural compounds in cocoa that are increasingly being linked to promising circulatory benefits – including improved blood flow and a reduced tendency to form damaging clots.
In the current study, 15 healthy young adults under age 50, and 19 healthy adults over age 50 drank the specially-made flavanol rich cocoa beverage daily for four to six days. The researchers tracked changes in the function of their peripheral arteries using several measures, including peripheral arterial tonometry a standard method for evaluating the health of an individual's blood vessels. At the study's completion, significant improvements in vessel function following the consumption of flavanol rich cocoa were seen in both young and older adults. While aging has previously been shown to lead to a deterioration of blood vessel function, this study is the first to demonstrate that the consumption of flavanol-rich cocoa can improve this age-related loss of vessel function in older adults. In agreement with previous studies using this same cocoa, these improvements in both young and older adults appear to be linked to the ability of cocoa flavanols to influence the body's production of nitric oxide, a key regulator of blood vessel tone.
Compared to the younger subjects, the vessel responses of the older men and women were significantly more pronounced after drinking the flavanol-rich cocoa beverage -- suggesting that the consumption of this flavanol rich cocoa offers a dietary approach for maintaining endothelial vessel function, and indicates the possibility that this cocoa could be useful for improving endothelial function in our aging population.
We have to eat foods to get various nutrients. But then there are the foods with a variety of non-nutrient compounds that have medicinal value: decreased cancer risk, decreased heart risk, and other benefits. It is hard to figure out how to make optimal choices.
A lot of chocolates have low levels of flavonols. Mars has seen to it that Dark Dove chocolate is higher in flavonols than other chocolates. But it still contains plenty of sugar and cocoa fat of course. So its net benefit is far from clear - at least to me. Lower calorie foods that have healthy compounds seem better choices. But if you are going to eat chocolate make it as dark and low sugar as possible.
A small but informative clinical trial by Johns Hopkins investigators shows that a pill combining chemicals found in turmeric, a spice used in curries, and onions reduces both the size and number of precancerous lesions in the human intestinal tract.
In the study, published in the August issue of Clinical Gastroenterology and Hepatology, five patients with an inherited form of precancerous polyps in the lower bowel known as familial adenomatous polyposis (FAP) were treated with regular doses of curcumin (the chemical found in turmeric) and quercetin, an antioxidant in onions, over an average of six months. The average number of polyps dropped 60.4 percent, and the average size dropped by 50.9 percent, according to a team led by Francis M. Giardiello, M.D., at the Division of Gastroenterology, The Johns Hopkins University School of Medicine, and Marcia Cruz-Correa, M.D., Ph.D., at Johns Hopkins and the University of Puerto Rico School of Medicine.
"We believe this is the first proof of principle that these substances have significant effects in patients with FAP," says Giardiello.
Dietary ways to delay the development of cancer might save your life. Various cancers will become curable some time in the next 20 years. It would be so totally unfun to die the year before a cure to your future cancer. Dietary changes that reduce your cancer risks, even if they just delay the development of cancer, could save your life.
The curcumin dose used is much larger than that found in turmeric in Indian food.
Previous observational studies in populations that consume large amounts of curry, as well as laboratory research on rodents have strongly suggested that curcumin -- a relatively innocuous yellow pigment extracted from turmeric, the powdered root of the herb curcuma longa and one of the main ingredients in Asian curries -- might be effective in preventing and/or treating cancer in the lower intestine, according to Cruz-Correa. She said curcumin has been given to cancer patients, and previous studies have demonstrated that is well tolerated at high doses.
Similarly, quercetin -- a member of a group of plant-derived polyphenolic anti-oxidant substances known as flavanoids (found in a variety of foods including onions, green tea and red wine) -- has been shown to inhibit growth of colon cancer cell lines in humans and abnormal colorectal cells in rodents.
Although these substances were administered together, due to relative dose levels it is Giardiello's belief that curcumin is the key agent.
"The amount of quercetin we administered was similar to what many people consume daily; however, the amount of curcumin is many times what a person might ingest in a typical diet, since turmeric only contains on average 3 percent to 5 percent curcumin by weight," says Giardiello. Because of this, he cautions that simply consuming curry and onions may not have the same effect as was produced in this study.
Curcumin capsules would be easier than eating turmeric on everything.
For the most quercetin, eat red and yellow onions; white onions have very little. Coming soon: super-potent onions. At the University of Wisconsin and the University of Texas M.D. Anderson Cancer Center, researchers are developing onions extra-high in quercetin and other disease-fighting phytochemicals. Red wine, broccoli and tea are also rich in quercetin.
Apples have it too. "An apple a day...". Eventually we'll get foods genetically engineered to contain all the best cancer risk reducers. In the meantime, if you want to boost topical absorption of quercetin 1000 times ultrasound with quercetin will dramatically boost quercetin absorption.
Scientists used a special mouse model for hormone-sensitive prostate cancer that closely mirrors the disease in humans. Researchers fed one group of mice a diet comprised of 20 percent fat with a healthy one-to-one ratio of omega-6 to omega-3 fatty acids. A second group of mice were fed the same diet but with the fat derived from mostly omega-6 fatty acids.
The study showed that tumor cell growth rates decreased by 22 percent and PSA levels were 77 percent lower in the group receiving a healthier balance of fatty acids compared with the group that received predominantly omega-6 fatty acids.
The most likely mechanism for the tumor reductions, according to researchers, was due to an increase of the prostate tumor omega-3 fatty acids DHA and EPA and a lowering of the omega-6 acid known as arachidonic acid. These three fatty acids compete to be converted by cyclooxgenase enzymes (COX-1 and COX-2) into prostaglandins, which can become either pro-inflammatory and increase tumor growth, or anti-inflammatory and reduce growth.
Researchers found that pro-inflammatory prostaglandin (PGE-2) levels were 83 percent lower in tumors in the omega-3 group than in mice on the predominantly omega-6 fatty acid diet, demonstrating that higher levels of DHA and EPA may lead to development of more anti-inflammatory prostaglandins.
"This is one of the first studies showing changes in diet can impact the inflammatory response that may play a role in prostate cancer tumor growth," Aronson said. "We may be able to use EPA and DHA supplements while also reducing omega-6 fatty acids in the diet as a cancer prevention tool or possibly to reduce progression in men with prostate cancer."
The fish in the oceans are getting exhausted and fish costs more than cheaper land-based meat sources. We need genetically engineered crops that make more omega 3 fatty acids.
Monsanto has grown high-yielding, Omega-3-enriched soybeans, extracted the oil and shown that it has a pleasant taste and no fish odor that might turn off food companies and consumers, said Robb Fraley, chief technology officer. If the oil proves to be stable enough for use in processed foods, which must sit on store shelves without spoiling, and gains regulatory approval, he sees it appearing some time after 2010 in salad dressings, soy milks, margarines, yogurts and other foods.
"We have a lot of excitement about this," he said. "We now can open the door to a whole new way of delivering Omega-3s in the diet through food" rather than supplements in pill form.
Vistive Omega-3 is another modification in the pipeline, due to become available around 2011-2012. According to the company, the “enhanced oils represent an environmentally sustainable, economical source of Omega-3s, providing consumers with new options for omega-rich foods.”
DuPont, one of the major movers and shakers in this area, revealed last week that it has developed a transgenic soybean with a long-chain omega-3 content of 40 per cent, and is heading for field testing of the crop.
DuPont's focus has been on maximising both EPA and DHA, and scientists based at the DuPont Experimental Station in Delaware, have expanded the standard procedure of desaturating and elongating the shorter chain fatty acids by using co-expression of an additional enzyme, omega-3 microsomal desaturase from the fungus Saprolegnia diclina, to convert the omega-6 very long chain polyunsaturated fatty acids (VLC-PUFAs) to omega-3s.
The previous article says BASF is also putting a big effort into development of high omega 3 crops.