Here's another reason to be skeptical of claims that obesity doesn't increase mortality risks.
A long-term study of the elderly has revealed that their average rate of weight loss doubles in the year before symptoms of Alzheimer's-type dementia first become detectable. The finding may be useful to researchers seeking ways to detect and treat Alzheimer's before it causes irreversible brain damage.
The study is the first to confirm in precise detail a link between weight loss and dementia tentatively identified a decade ago. Researchers report in the September 2006 Archives of Neurology that one year before study volunteers were diagnosed with very mild dementia, their rate of weight loss doubled from 0.6 pounds per year to 1.2 pounds per year. The analysis used data from the Memory and Aging Project at the Alzheimer's Disease Research Center (ADRC) of Washington University School of Medicine in St. Louis.
Alzheimer's researchers are working hard to find biomarkers, indicators that can be used to detect the presence of Alzheimer's before clinical symptoms become obvious. Studies at the ADRC and elsewhere have strongly suggested that if Alzheimer's treatments will ever prevent lasting cognitive damage, they may have to be given to patients before memory loss and other disruptions caused by the disorder are evident.
When you read claims that being overweight is not correlated with shorter lifespans keep in mind that a number of illnesses cause weight loss before the illnesses are diagnosed. Cancer can cause weight loss. Unexpected weight loss is sometimes the reason people with undiagnosed cancer go to a doctor and end up with a cancer diagnosis. But cancer is not the only major disease common in old age that causes weight loss. As reported above, even Alzheimer's causes weight loss before diagnosis.
Botton line: People who keep their weight down as a conscious choice are mixed in with people who have lost weight due to illness. So reports which show similar risk of death in the overweight and regular weight are misleading unless they are carefully crafted to control for illness as a cause of weight loss.
A couple of recent studies did attempt to control for illness as a cause of weight loss. They used weight of their subjects before the subjects reached old age. This allowed them to reduce the bias caused by weight loss due to undiagnosed illnesses. They found that being overweight really does shorten life expectancy. See my post Two Studies Find Being Overweight Shortens Life Expectancy for the details.
In Milan (or as the Italians say, Milano) Italy some people have a mutation of high density lipoprotein (HDL) cholesterol called Apolipoprotein A-I Milano which is suspected of reducing the risk of heart and cardiovascular disease. In order to investigate whether Apo A-I Milano really does reduce risk of cardiovascular diseases researchers at Cedars-Sinai put human variations of HDL choelsterol into mice and then measured the resulting mice. While normal human HDL cholesterol reduced plaque build-up by 25% the Apo A-I Milano version of the gene reduces plaque build-up by 65%.
LOS ANGELES - Transfer of a gene that produces a mutant form of good cholesterol provides significantly better anti-plaque and anti-inflammation benefits than therapy using the "normal" HDL gene, according to a mouse study conducted by cardiology researchers at Cedars-Sinai Medical Center and reported in the Oct. 3 issue of the Journal of the American College of Cardiology.
Apolipoprotein A-I is a naturally occurring component of normal HDL (high-density lipoprotein), the "good" cholesterol that circulates in the blood stream. Apolipoprotein A-I Milano is a mutant form, which was originally found in a small number of individuals in Italy who appear to be protected from cholesterol-related heart disease. Researchers are studying the possibility of treating vascular inflammation and plaque buildup through the transfer of protective genes.
"There has been uncertainty and controversy about whether apo A-I Milano is a better form of HDL than the "wild type" (regular) apo A-I in terms of protective effect against atherosclerosis and vascular inflammation, which are tied together," said Prediman K. Shah, M.D., director of the Division of Cardiology and the Atherosclerosis Research Center at Cedars-Sinai.
"We used a unique approach to do a head-to-head comparison, which allowed us to conclusively ascertain the differences between the two genes. Our study demonstrated that A-I Milano gene transfer is much more effective in reducing plaque and vascular inflammation than the normal (wild type) form of apo A-I," said Shah, the article's senior author.
Compared to control, wild type apo A-I gene transfer led to about a 25 percent decrease in the amount of plaque buildup in the animals' aortas and other vessels. Apo A-I Milano gene transfer resulted in a 65 percent reduction. The amount of gene product (protein) produced by each gene was identical, measured in the blood and in the plaque.
A gene therapy that converted our livers to make Apo A-I Milano HDL cholesterol would likely reduce both inflammation and the rate of accumulation of damage from oxidation and plaque build-up in the circulatory system. My guess is such a treatment would reduce the amount of free radicals in the blood and therefore also reduce the rate of brain aging.
Drugs that raise the concentration of HDL cholesterol will hit the market many years before a gene therapy that converts our bodies to make Apo A-I Milano HDL. We might also see clinical use of intravenous administration of Apo A-I Milano HDL as a way to get a bigger and quicker benefit, especially for those suffering angina. Also see my post Synthetic HDL Cholesterol Reduces Artery Clogging In 6 Weeks.
The completion of the Allen Institute for Brain Science's inaugural project signals a remarkable leap forward in one of the last frontiers of medical science -- the brain.
The Institute today announced the completion of the groundbreaking Allen Brain Atlas, a Web-based, three-dimensional map of gene expression in the mouse brain. Detailing more than 21,000 genes at the cellular level, the Atlas provides scientists with a level of data previously not available.
Since humans share more than 90 percent of their genes with mice, the Atlas offers profound opportunity to further understanding of human disorders and diseases such as Alzheimer's, Parkinson's, epilepsy, schizophrenia, autism and addiction. About 26 percent of American adults -- close to 58 million people -- suffer from a diagnosable mental disorder in a given year.
Many human brain diseases have mouse equivalents developed using genetic engineering on lab mice. As the cost of measuring gene activity drops a logical next step would be to repeat this work using mice which have a variety of brain disorders.
You can access the Brain Atlas for free online.
"This project is an unprecedented union of neuroscience and genomics," said philanthropist and Microsoft co-founder Paul G. Allen, who provided $100 million in seed money to launch the Allen Institute for Brain Science and its first project, the Allen Brain Atlas, in 2003. "The comprehensive information provided by the Atlas will help lead scientists to new insights and propel the field of neuroscience forward dramatically."
Publicly available at no cost, the map shows which genes are active -- or "expressed" -- within the brain and which regions and cells they are expressed in, thereby linking them to particular brain functions.
The brain uses most of the genome.
The project has already led to several significant new findings about the brain. It reveals that 80 percent of genes are turned on in the brain, much higher than the 60 to 70 percent scientists previously believed.
It indicates that very few genes are turned on in only one region of the brain -- paving the way for additional insight about the benefits and potential side effects of drug treatments. And it shows the location of genes associated with specific functions, providing scientists with valuable information about regional brain activity.
Many brain scientists use the Atlas.
Even before its announced completion, the Atlas was receiving more than 4 million hits monthly and being accessed by approximately 250 scientists on any given work day. Users are not required to provide information about their work, but anecdotal evidence indicates that the Atlas is already assisting research projects.
"I use it around the clock, night and day. My whole lab does," said Stanford University neurobiology professor Ben A. Barres, who is using the Atlas to confirm his team's findings about glial cells, a type of non-neuronal cell within the nervous system.
"It's completely essential. It's saved us years and years of work, maybe decades. We could never have done all this, either financially or in terms of the amount of labor and time. It was just so incredibly generous of Mr. Allen to do this, and I think it's hard to even overstate what the payoff is going to be for research."
Researchers at the Allen Institute created the database using a process known as in-situ hybridization. A mouse brain is sliced into thin layers and then labeled with a DNA "probe" that binds only to a single gene, highlighting the expression pattern for that gene.
In-situ maps were made for every gene in the mouse genome, then loaded into a massive database. To complete the entire database, researchers processed 170 genes per day, and produced some 1,000 gigabytes of data each day. The finished atlas cost about $41 million to produce.
The development of gene array chips and other technologies for measuring many parts of a biological system at once look set to continue to accelerate the rate at which scientists can collect information from cells and organisms. The Brain Atlas couldn't have been developed 10 years ago. 10 years from now we'll have still more orders of magnitude improvement in the ability to measure and collect data on the activites inside cells and organisms.
A map of gene activity in the human brain neocortex is next up for the Allen Institute.
The next project, Jones said, will be to develop a digital, three-dimensional, interactive map of the genes at work in a human brain's neocortex, the outer layer that is the seat of higher thought and emotion, using brains from cadavers as well as tissue removed during brain surgeries.
We are coming to the end of the dark ages of how the human brain works.
Methyl groups (a carbon and 3 hydrogens attached to a larger molecule) get placed on outsides of DNA double helixes in order to control gene expression. A group of scientists has found that embryonic cell type have unqiue patterns of methyl group attachment (methylation) that make them different from other cell types.
San Diego, Calif. -- Scientists from the Burnham Institute for Medical Research (BIMR) and Illumina Inc., in collaboration with stem cell researchers around the world, have found that the DNA of human embryonic stem cells is chemically modified in a characteristic, predictable pattern. This pattern distinguishes human embryonic stem cells from normal adult cells and cell lines, including cancer cells. The study, which appears online today in Genome Research, should help researchers understand how epigenetic factors contribute to self-renewal and developmental pluripotence, unique characteristics of human embryonic stem cells that may one day allow them to be used to replace diseased or damaged cells with healthy ones in a process called therapeutic cloning.
Embryonic stem cells are derived from embryos that are undergoing a period of intense cellular activity, including the chemical addition of methyl groups to specific DNA sequences in a process known as DNA methylation. The methylation and demethylation of particular DNA sequences in the genome are known to have profound effects on cellular behavior and differentiation. For example, DNA methylation is one of the critical epigenetic events leading to the inactivation of one X chromosome in female cells. Failure to establish a normal pattern of DNA methylation during embryogenesis can cause immunological deficiencies, mental retardation and other abnormalities such as Rett, Prader-Willi, Angelman and Beckwith-Wiedemann syndromes.
This result is entirely unsurprising. Methylation is an expected way that cells get controlled to act like one cell type rather than other cell types. For example, methyl groups can prevent proteins from binding to a section of DNA and thereby prevent cellular machnery from reading specific genes that have been methylated.
The way more exciting result here is the development of technology for measuring methylation of hundreds of sites on DNA at a time.
Until recently, DNA methylation could only be studied one gene at a time. But a new microarray-based technique developed at Illumina enabled the scientists conducting this new study to simultaneously examine hundreds of potential methylation sites, thereby revealing global patterns. "Analyzing the DNA methylation pattern of hundreds of genes at a time opens a new window for epigenetic research," says Dr. Jian-Bing Fan, director of molecular biology at Illumina. "Exciting insights into development, aging, and cancer should come quickly from understanding global patterns of DNA methylation."
The ability to rapidly read large amounts of epigenetic information is more important than the results from any one set of experiments that collect epigenetic data.
This report provides yet another illustration of how advances in instrumentation for biological systems are accelerating the rate of advance of biological science and technology.
To examine global DNA methylation patterns in human embryonic stem cells, the researchers analyzed 14 human embryonic stem cell lines from diverse ethnic origins, derived in several different labs, and maintained for various times in culture. They tested over 1500 potential methylation sites in the DNA of these cells and in other cell types and found that the embryonic stem cells shared essentially identical methylation patterns in a large number of gene regions. Furthermore, these methylation patterns were distinct from those in adult stem cells, differentiated cells, and cancer cells.
"Our results suggest that therapeutic cloning of patient-specific human embryonic stem cells will be an enormous challenge, as nuclei from adult cells will have to be epigenetically reprogrammed to reflect the specific DNA methylation signature of normal human embryonic stem cells," explains Dr. Jeanne Loring, co-director of the stem cell center at BIMR. "This reinforces the need for basic research directed at understanding the fundamental biology of human embryonic stem cells before therapeutic uses can be considered."
Some day techniques to change methylation patterns on the genome will be found. Those techniques will make it much easier to change cells into any desired cell type for therapeutic purposes. The ability to rapidly read methylation patterns will make it easier to test techniques tin the development of ways to change methylation patterns. So advances in reading methylation patterns will lead to advances for growing replacement organs and for creating stem cell therapies.
Another point: The increase in ability to read methylation patterns sounds like it was of orders of magnitude. Some people argue that anti-aging therapies are a distant prospect because even at Moore's Law (which is a doubling time for computer power of about 18 to 24 months) rates of advance it will take a long time before biotechnology cna reverse full body aging. But the advance reported above for reading methylation patterns sounds like it was much faster than the rate of Moore's Law. But biotechnology can advance more rapidly than computer technology did because biotechnology is in the process of harnessing techniques first developed for the computer industry over a period of decades.
Think of it this way: The move to put biochemical tests and sensors on chips amounts to jumping biotechnology over onto computer semiconductor technology. But that semiconductor technology took decades to develop and now biotechnology is starting to get moved over onto semiconductor devices. This allows biotech to capture in a relatively short period of time the gains of decades of semiconductor technology. So I'm not surprised to read about sudden orders of magnitude increases in the ability to do biological experiments using silicon chips.
A drug that treats type 2 diabetes might work against Alzheimer's.
Providence, RI – Stimulation of a receptor in the brain that controls insulin responses has been shown to halt or diminish the neurodegeneration of Alzheimer's disease, providing evidence that the disease can be treated in its early stages, according to a study by researchers at Rhode Island Hospital and Brown Medical School.
Researchers have found that peroxisome-proliferator activated receptor (PPAR) agonists prevent several components of neurodegeneration and preserve learning and memory in rats with induced Alzheimer's disease (AD). They found that an agonist for PPAR delta, a receptor that is abundant in the brain, had the most overall benefit.
"This raises the possibility that you can treat patients with mild cognitive impairment who have possible or probable Alzheimer's disease. This is really amazing because right now, there's just no treatment that works," says lead author Suzanne M. de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital and a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI.
The study appears in the September issue (Volume 10, Issue 1) of the Journal of Alzheimer's Disease (www.j-alz.com).
Alzheimer's looks to be a type of diabetes that is specific to the brain.
In previous studies, the researchers demonstrated that Alzheimer's is a brain-specific neuroendocrine disorder, or a Type 3 diabetes, distinct from other types of diabetes. They showed that insulin and IGF-I receptors are produced separately in the brain, and begin to disappear early in Alzheimer's and continue to decline as the disease progresses. As insulin signaling breaks down, it leads to increased oxidative stress, impaired metabolism and cell death – all causing neurodegeneration.
Scientists were also previously able to replicate Alzheimer's in rats with Streptozotocin (STZ), a compound that is known to destroy insulin producing cells in the pancreas and cause diabetes. When injected into the brains of rats, the compound mimicked the neurodegeneration of Alzheimer's disease – plaque deposits, neurofibrillary tangles, diminished brain size, impaired cognitive function, cell loss and overall brain deterioration.
Since PPAR gamma is already approved as a treatment for Type 2 (insulin resistant) diabetes in humans it would be pretty easy to try it out in early stage Alzheimer's patients. PPAR alpha and PPAR delta would also be useful against Alzheimer's.
Having created an animal model for Alzheimer's, researchers in this study induced Alzheimer's with STZ and then administered treatment with three classes of PPAR agonists – alpha, gamma and delta. All are found in various tissues and organs in the body, including the brain, and PPAR gamma is already FDA approved as a treatment for Type 2 diabetes, or adult-onset diabetes. The two other classes of PPAR agonists have not yet been approved for clinical use.
Following treatment, many of the abnormalities associated with Alzheimer's were reduced or nearly disappeared. The agonists affected different regions of the brain, with PPAR delta producing the most striking effect in preserving the hypothalamus and temporal lobes, areas of the brain responsible for memory, learning, and behavior. In these brain regions, PPAR alpha and PPAR gamma were effective in reducing amyloid gene expression. PPAR delta had the most benefit for reducing oxidative stress and improving learning and memory.
"That was the most spectacular," de la Monte says, "because everybody wants something for cognitive impairment, and that was the most improved with the PPAR delta agonist."
Researchers were not able to stop the deterioration of insulin and its receptors. However, by administering PPAR, they were able to bypass the defects in insulin signaling and preserve the cells that need insulin to thrive. PPAR molecules go directly to the nucleus of cells and tell DNA to turn on or off genes that are normally regulated by insulin, thus preventing them from dying and allowing them to communicate with each other. The major effects of the PPAR treatments were to increase brain size, preserve insulin and IGF-II receptor bearing neurons, and preserve learning and memory.
"The trigger for dementia is the loss of insulin and IGF producing cells. The cells that need those growth factors subsequently die. This study shows you can block the second phase, which is responsible for dementia. This is great news for patients since you treat early stages of disease," de la Monte says.
Another promising result for Alzheimer's patients is that these drugs could be given in the form of a pill, de la Monte says. In the study, the drugs were injected to control the amounts administered.
"One of the most exciting findings was that peripheral (intraperitoneal) injection of the PPAR agonists either partially or completely rescued the brains from neurodegeneration," the authors write.
Alzheimer's appears to be caused by parallel abnormalities – impaired insulin signaling and oxidative stress, which is regulated by the genes NOS and NOX. The PPAR agonists treatments target both problems. They preserve the cells regulated by insulin and IGF, and they decrease oxidative stress, resulting in fewer lesions in the brain.
"If the diagnosis is suspected or patients are in the early phases of AD, there's a good possibility they could get treatment that will help them. It's possible that in the moderate phase, treatment will also help, but more work needs to be done to show that," de la Monte says.
Treatment is not likely to work in the late stages of the disease, she says, because the cells have already died.
All the reports lately about much earlier stage tests for Alzheimer's will turn out to be very useful because periodic testing as we age might be used to determine when to start treatment for type 3 diabetes.
These results remind me of other studies on brain aging. As we age glucose concentrations drop more rapidly and rise more slowly when we do mental work. Basically, our brains can not get enough glucose for sustained concentration. Is the brain glucose shortage seen in normal aging just a milder manifestation of the Type 3 diabetes that these reseachers claim is the cause of Alzheimer's? As we age would we be better able to maintain sustained concentration by taking drugs developed to stimulate insulin receptors in the brain?
Also, is Alzheimer's caused by a glucose shortage that robs the neurons of enough energy to remove the junk (e.g. beta amyloid plaque) that accumulates? Or does the lack of stimulation of the insulin receptors reduce the signalling that tells intracellular machinery to break down the accumulated junk?
Thanks to Lou Pagnucco for the heads up.
Embryonic stem cells can serve as a renewable source of replacement tissue to rescue visual function in rats with degenerative eye disease similar to age-related macular degeneration, a leading cause of blindness in humans, according to a report to be published in the Fall 2006 (Volume 8, Number 3) issue of Cloning and Stem Cells, a peer-reviewed journal published by Mary Ann Liebert, Inc. The paper is available online ahead of print at www.liebertpub.com/clo
Robert Lanza, M.D. and Irina Klimanskaya, Ph.D. at Advanced Cell Technology (Worcester, MA), and Raymond Lund, Ph.D. and colleagues at the University of Utah Health Science Center (Salt Lake City) generated retinal pigment epithelium (RPE)--the cells that support photoreceptor function in the eye--from human embryonic stem cell lines grown in culture in the laboratory. They transplanted the engineered tissue into the eyes of rats that had a defect in their RPE. This defect results in the loss of photoreceptors and visual function.
The authors reported 100% improvement in visual performance (spatial acuity) in treated animals compared to an untreated control group, and the transplanted RPE cells did not cause any pathology. In the treated rats, spatial acuity, or the ability to see fine detail, was approximately 70% that of normal rats (that had no RPE defect).
"These observations are very exciting as they show that one day it will be possible to treat diseases of human eyes with cells," says Ian Wilmut, Ph.D., Editor-In-Chief of Cloning and Stem Cells and director of the Centre for Regenerative Medicine, in Edinburgh, Scotland. "They also emphasize the great potential benefit of research with human embryo stem cells, in this case for cell therapy."
Macular degeneration is the leading cause of blindness in persons over age 60 in the United States and affects more than 30 million people worldwide. Embryonic stem cells would offer a readily available, safe, and reproducible source of replacement tissue to restore photoreceptors damaged or destroyed by disease and to restore a range of visual functions.
All 18 hESC lines they worked with could produce retinal cells.
"One important advantage offered by hES-derived cells over other cells developed to mimic or replace lost retinal pigment epithelium is that they more closely resemble primary human RPEs," stated Raymond D. Lund, Ph.D., Professor at the Moran Eye Center, University of Utah Health Science Center, Salt Lake City and the study's lead author. "Another significant advantage of using these cells is that a range of lines can be derived allowing the opportunity to 'tissue match' donor cells with recipient, a real advantage given that RPE cells are highly immunogenic and susceptible to rejection without some form of immunosuppression."
"Embryonic stem cells promise to provide a well-characterized and reproducible source of replacement cells for clinical studies," stated Robert Lanza, M.D., Vice President of Research & Scientific Development at ACTC and senior author of the paper. "All 18 human embryonic stem cell lines we studied reliably produced retinal cells that could potentially be used to treat retinal degenerative diseases, such as macular degeneration. We showed that these cells have the capacity to rescue visual function in animals that otherwise would have gone blind. Importantly, the cells did not appear to cause any unwanted pathological responses in the animals following transplantation."
Once useful human therapies are available which have been created using hESC the people making ethical arguments against the use of hESC are going to face much more opposition than they do today. The hypothetical future promise of hESC doesn't today motivate people to support hESC research as much as the availability of real treatments will.
The opponents of the use of hESC really ought to push harder to increase funding to develop other methods to create flexible and youthful stem cells. If they fail to do that they will find they are fighitng for a losing cause.
In a move that might provide a away around ethical objections to other ways to create human embryonic stem cells scientists were able to extract human embryonic stem cells from embryos that had ceased to grow
The journal STEM CELLS(R) today announced that scientists were able, for the first time, to derive pluripotent human embryonic stem cells (hESCs) from non-viable early human embryos.
The team, led by Professor Miodrag Stojkovic, derived hESCs using surplus and donated embryos that had stopped their cleavage. The scientists demonstrated that these non-viable embryos could be used under suitable laboratory conditions for derivation of hESCs and for study of early human development.
This progress, published in STEM CELLS(R), encourages other scientists to perform hESC research using both viable and non-viable pre-implantation embryos in their attempt to understand and fight debilitating diseases.
'This should get round opposition to stem cell science because live embryos will no longer need to be used in all experiments,' said Professor Miodrag Stojkovic, the researcher who carried out the experiments at the Centre for Stem Cell Biology at Newcastle University last year.
The embryos used were from attempts at in vitro fertilization where the embryos stopped growing even before implantation.
Stojkovic's experiments were carried out while he was working at the Centre for Stem Cell Biology at Newcastle last year. In a paper, published last week online on the website of the journal Stem Cells, Stojkovic reveals he and his colleagues took 13 embryos, created by IVF. All 13 had stopped developing a few days after conception. 'They were in a very early stage of development,' said Stojkovic, now head of Sintocell, the Serbian medical research centre.
The team then waited 24 hours to check that the embryos were no longer dividing before beginning their experiments.
Some ethicists still see problems with this approach.
But other stem cell scientists and ethicists quickly raised a host of reasons that the advance may have little practical impact on the stormy research field. Among them are concerns that cells from dead embryos may be genetically abnormal, and the lack of a definitive test for proving that an embryo has no lingering potential for life.
How to get around the genetic abormality problem? In theory doctors could take embryos from pregnant women who die from trauma such as from car accidents. The removal of cells from embryos to use for therapy development would be analogous to using organs. But I'm guessing that the early stage pregnancies where the embryos still have pluripotent (highly flexible) stem cells aren't going to be recognized either by the mother or by emergency room workers.
It could turn out that some of the IVF embryos stop dividing for epigenetic (chemical state around the genes rather than the genes themselves) reasons. If that turns out to be the case then some stem cells extracted using this technique might turn out to be in good genetic shape.
The full paper is available with free access.Here's the abstract excerpted from the paper (PDF format).
Human embryonic stem cells (hESC) hold huge promise in modern regenerative medicine, drug discovery, and as a model for studying early human development. However, usage of embryos and derivation of hESC for research and potential medical application has resulted in polarised ethical debates since the process involves destruction of viable developing human embryos. Here we describe that not only developing embryos (morulae and blastocysts) of both good and poor quality but also arrested embryos could be used for the derivation of hESC. Analysis of arrested embryos demonstrated that these embryos express pluripotency marker genes such OCT4, NANOG and REX1. Derived hESC lines also expressed specific pluripotency markers (TRA-1-60, TRA-1-81, SSEA4, alkaline phosphatase, OCT4, NANOG, TERT and REX1) and differentiated under in vitro and in vivo conditions into derivates of all three germ layers. All the new lines including line derived from late arrested embryo have normal karyotype. These results demonstrate that arrested embryos are additional valuable resources to surplus and donated developing embryos and should be used to study early human development or derive pluripotent hESC.
Washington, D.C.— Plug-in hybrid vehicles could contribute greatly to reducing automobile oil consumption and emissions, but reaching those goals requires major progress in key areas. According to a report released today by the American Council for an Energy-Efficient Economy, the environmental and economic appeal of plug-in hybrid vehicles will depend heavily upon cleaner power sources and further battery advances. The report, Plug-In Hybrids: An Environmental and Economic Outlook, examines the benefits of plug-ins relative to today’s hybrids. It finds that greenhouse gas emissions reductions associated with a plug-in powered by today’s electric grid would be about 15% on average across the nation, ranging from 32% using California electricity to zero using Upper Midwest electricity.
Note the lack of mention of particulates or mercury from coal burning electric plants.
Plug-ins’ oil savings could be quite large. Battery size and cost rise steeply with the amount of fuel savings, however, suggesting that plug-ins with modest electric-only range will appear first. According to report co-author James Kliesch, the “electric-then-gasoline” depiction of plug-in operation is not realistic and has contributed to overstatements of the fuel savings potential of plug-ins in the popular media. “Achieving adequate battery lifetimes and minimizing battery costs will require a vehicle control logic that turns on the internal combustion engine when extra power is needed, even within the ‘electric-only’ range of the vehicle,” said Kliesch. The ACEEE report estimates fuel savings relative to today’s hybrids of 30% for a plug-in with a 20-mile electric-only range and 50% for a 40-mile range.
We need better battery technology to make plug-ins cost effective.
Where the electricity comes from determines whether plug-ins deliver a net environmental benefit.
For a plug-in owner in California, where most electricity on the grid is generated by low-pollution facilities, driving a PHEV might cut emissions of carbon dioxide by one-third compared with driving a regular hybrid.
But if the same PHEV were charged in the Midwest, where coal-fired power plants supply the electricity, reduction of CO2 emissions would be nil. Nitrous-oxide emissions (which form smog) would fall slightly, but sulfur-dioxide emissions (which contribute to acid rain) would quadruple.
Still, environmental gains are possible.
Plug-ins would chop CO2 emissions by 15 percent on a national average, compared with conventional hybrid cars, the ACEEE report found. At the same time, the plug-in would emit 157 percent more sulfur-dioxide pollution. The need, plug-in proponents say, is for policies that would clean up the electricity grid so that PHEV technology supplies cleaner skies along with energy independence.
This report overstates the environmental benefits of plug-in hybrids. Anyone see the reason why? Hint: large scale use of plug-ins would require construction of new power plants. What about those plants would make things worse?
Answer: New electric power plants will be more heavily weighted toward coal burners than the existing fleet. Natural gas has become too expensive. Hydro power is all tapped out with limited potential for expansion and environmentalists want to see some existing dams dismantled. Nuclear power has fallen out of fashion. Coal looks set to become a larger percentage of total electric generating capacity. Not only would the coal put out more sulfur but also particulates, mercury and other bad stuff.
In California coal faces big regulatory obstacles and the politicians are forcing a big push into renewables. So a shift toward plug-ins here would probably improve air quality. But the cost in electricity will be higher. In the last year nationally electric power costs rose on average from 9.08 cents to 10.15 cents per kilowatt-hour (kwh) or 11.8%. But in California the cost rose from 11.82 cents to 13.84 cents for a 17% increase. New electric power capacity in California (e.g. wind mills) is much more expensive than existing capacity. So the demand for electric power to run cars will drive up average electric prices for all uses.
We could have regulations that require cleaner coal generators nationally. But that too would raise average electric prices. Plus, as demand grows the percentage of total electric power that comes from cheaper hydro-electric dams will decline and the average cost will rise for that reason as well.
If new electric power capacity came from nuclear plants then shifting to plug-in hybrids would deliver a clear and quite substantial environmental benefit. The same will hold some day when photovoltaics become much cheaper. But right now higher electric power demand translates into higher coal burning electric plant construction in most parts of the United States and in other parts it translates into higher electric power prices.
A new study out in the Journal of the American Medical Association provides more reason to eat fatty fish. Vitamin D and/or omega 3 fatty acids are probably involved in the protective effect of eating fatty fish.
Preliminary research suggests that higher consumption of fatty fish in women is linked with a lower risk of renal cell carcinoma, a common form of kidney cancer, according to a study in the September 20 issue of JAMA.
Renal cell carcinoma (RCC) involving the renal parenchyma (the functional tissue of the kidney) accounts for more than 80 percent of all kidney cancers. Renal cell carcinoma incidence rates in the United States had been increasing in 1970-1990s, especially among black women and men; more recent data suggest a leveling off in this trend for most racial groups. The evidence that fish consumption, especially fatty fish, may be associated with lower risk of several cancers has not been consistent, according to background information in the article.
By differentiating between consumption of fish with differing levels of omega 3 fatty acids the researchers were able to discover a stronger relationship between fish consumption and reduced cancer risk.
Previous studies have analyzed total fish consumption and have not taken into account that there are large differences between fatty fish and lean fish in the content of omega-3 fatty acids and vitamin D. Marine omega-3 polyunsaturated fatty acids, eicosapentaenoic acid and docosahexaneoic acid, which are present in significant amounts in fatty cold-water fish (up to 20-30 times higher content than in lean fish), have been reported to slow the development of cancer. Fatty fish has 3 to 5 times higher content of vitamin D than lean fish, and lower serum vitamin D levels have been associated with development and progression of RCC.
Alicja Wolk, D.M.Sc., of the Karolinska Institutet, Stockholm, Sweden and colleagues investigated the association between fatty fish and lean fish consumption and the risk for development of RCC in a population with a relatively high consumption of fatty fish. The participants, from the Swedish Mammography Cohort, included 61,433 women age 40 to 76 years without previous diagnosis of cancer at baseline (March 1987 to December 1990). Participants filled in a food frequency questionnaire at baseline and in September 1997. The researchers considered fatty fish to include salmon, herring, sardines, and mackerel; lean fish included cod, tuna, and sweet water fish; and other seafood included shrimp, lobster, and crayfish.
During an average of 15.3 years of follow-up between 1987 and 2004, 150 RCC cases were diagnosed. After adjustment for potential confounders, an inverse association of fatty fish consumption with the risk of RCC was found, while no association was found with the consumption of lean fish or other seafood.
Want to cut your kidney cancer risk by about 3/4ths?
“In this large population-based cohort with data on long-term diet, we found that women who consumed one or more servings of fatty fish per week had a statistically significant 44 percent decreased risk of RCC compared with women who did not consume any fish. Women who reported consistent long-term consumption of fatty fish at baseline and 10 years later had a statistically significant 74 percent lower risk,” the authors write.
“Our results support the hypothesis that frequent consumption of fatty fish may lower the risk of RCC possibly due to increased intake of fish oil rich in eicosapentaenoic acid and docosahexaneoic acid as well as vitamin D,” they write. “Our results, however, require confirmation because this is the first epidemiological study addressing this issue.” (JAMA. 2006;296:1371-1376)
The reducting in kidney cancer risk is probably also being accompanied by a reduction in risk of other types of cancer. The vitamin D in the fish has already been linked to reduction of risk for other cancers. See my posts Vitamin D Could Decrease Overall Cancer Risk 30%, Vitamin D Reduces Risk Of Pancreatic Cancer, and Vitamin D Reduces Breast Cancer Risk. Also, omega 3 fatty acids as contributors to reduced kidney cancer risk seem quite plausible. See my post Omega 3 Fatty Acids Cut Rat Prostate Cancer.
I'm having salmon for dinner.
Chronic inflammation is now widely seen as a contributing factor to many diseases of old age. Any dietary or lifestyle choices that increase the amount of inflammation in your body is probably going to accelerate your aging and make you more prone to not just infections but chronic degenerative illnesses such as heart disease and arthritis. With that thought in mind consider that skimping on sleep increases the amount of inflammation in the body.
Researchers at UCLA are the first to show how sleep loss affects the immune system's inflammatory response and suggest sleep interventions as a possible way to address problems associated with inflammation and autoimmune disorders.
Reporting in the Sept. 6 edition of the peer-reviewed journal Archives of Internal Medicine, the research team finds that even modest sleep loss triggers cellular and genetic processes involved in the immune system's inflammatory response to disease and injury.
The findings increase understanding of sleep's role in altering immune cell physiology and suggest sleep interventions as a possible way to address inflammation associated with risk of cardiovascular disease, arthritis, diabetes and other autoimmune disorders.
"This study shows that even a modest loss of sleep for a single night increases inflammation, which is a key factor in the onset of cardiovascular disease and autoimmune disorders such as rheumatoid arthritis." said Dr. Michael Irwin, professor and director of the Cousins Center for Psychoneuroimmunology at the Semel Institute for Neuroscience and Human Behavior at UCLA.
About one-third of the people in the United States have trouble getting a good night's sleep. The problem is more prevalent among people with chronic inflammatory disorders, including heart disease. Epidemiology studies link poor sleep with risk of chronic disease in some people.
Inflammation, with its accompanying redness and swelling, occurs when the immune system floods a diseased or damaged portion of the body with infection-fighting white blood cells that promote healing. However, a variety of immune system disorders can cause the body to turn on itself, sometimes causing inflammation that can damage healthy organs and tissues.
The UCLA research team conducted blood and DNA analyses of 30 healthy adults drawn during the day across three baseline periods and after partial night sleep deprivation. The results show white blood cells called monocytes produce significantly greater amounts of two disease-fighting proteins after a night of sleep loss, compared with amounts found after a night of uninterrupted sleep.
So the dog who insisted I let him out at 4 AM this morning helped accelerate aging. I explained this to him and he was complelely indifferent.
If you can see small changes you can make to your life to up the amount of sleep you get to an adequate amount then make those changes. You'll be better off in the long run.
Update: Does anyone know of scientific research into factors that increase or decrease your need for sleep? For example, if you are doing a lot of mental work and learning during the day does that increase the need for sleep because the mind needs to spend more time processing to form lasting memories of what it learned that day? Or do high fat diets increase the need for sleep as compared to low fat diets? Or does a diet high in vegetables decrease the need for sleep?
Nicotinamide (aka niacinamide as distinct from niacin) is the form of vitamin B3 that does not cause flushing in your skin. Nicotinamide injected into mice provided protection to nerve cells from a mouse disease that is very similar to multiple sclerosis.
A team led by Shinjiro Kaneko, MD, a research fellow at Children's, and senior investigator Zhigang He, PhD, also from Children's, worked with mice that had an MS-like disease called experimental autoimmune encephalitis (EAE). Through careful experiments, they showed that nicotinamide protected the animals' axons from degeneration - not only preventing axon inflammation and myelin loss, but also protecting axons that had already lost their myelin from further degradation.
Intriguingly, mice with EAE who received daily nicotinamide injections under their skin had a delayed onset of neurologic disability, and the severity of their deficits was reduced for at least eight weeks after treatment. The greater the dose of nicotinamide, the greater the protective effect.
This is great news because nicotinamide has very low toxicity, is cheap, and is easy to administer. Just taking large doses in pills might be enough to greatly slow the progress of MS.
The highest nicotinamide doses provided the biggest benefit.
On a scale of 1 to 5 (1 indicating mild weakness only in the tail, 4 indicating paralysis involving all four limbs, and 5, death from the disease), mice receiving the highest doses of nicotinamide had neurologic scores between 1 and 2, while control mice had scores between 3 and 4. All differences between treated groups and controls were statistically significant.
Mice with the greatest neurologic deficits had the lowest levels of NAD in their spinal cord, and those with the mildest deficits had the highest NAD levels. Mice that had higher levels of an enzyme that converts nicotinamide to NAD (known as Wlds mice) responded best to treatment.
Moreover, nicotinamide significantly reduced neurologic deficits even when treatment was delayed until 10 days after the induction of EAE, raising hope that it will also be effective in the later stages of MS. 'The earlier therapy was started, the better the effect, but we hope nicotinamide can help patients who are already in the chronic stage,' says Kaneko.
In other experiments, the researchers demonstrated that nicotinamide works by increasing levels of NAD in the spinal cord and that NAD levels decrease when axons degenerate. Finally, they showed that giving NAD directly also prevented axon degeneration.
NAD is used extensively by cells to produce energy through the breakdown of carbohydrates.
Perhaps nicotinamide works by boosting energy output so that damaged nerve cells can repair themselves faster and thereby avoid too much accumulated damage.
As much as I like high technology I even more like low tech solutions that can be put into practice immediately.
If you are wondering about dosing: The doses were 125 mg per kg and 500 mg per kg. A kilogram is 2.2 pounds. I have no idea whether the human doses would need to scale by those ratios.
Cholesterol lowering statin drugs also reduce the damage caused by MS.
CHAPEL HILL - Scientists from the University of North Carolina at Chapel Hill have established how statins -- cholesterol-lowering drugs -- inhibit inflammation and nerve cell damage caused by multiple sclerosis.
Preliminary research has shown that multiple sclerosis (MS) patients taking statins with their standard drug regimen develop less nerve cell damage over time than MS patients on standard therapy. Understanding the precise mechanisms by which statins fight multiple sclerosis is an important step toward approving the commonly used drugs for MS treatment, said Dr. Silva Markovic-Plese, associate professor of neurology, immunology and microbiology in the UNC School of Medicine.
In tests performed on blood samples from people with relapse-remitting MS, statins shut down several inflammatory processes. The statins inhibited the formation of immune-system cells called lymphocytes and monocytes, which cause inflammation by attacking the body's nerve cells.
"When we compared the effects of statins to well-understood MS therapies such as interferon, an anti-inflammatory, statins were equal if not stronger in some aspects," Markovic-Plese said. The researchers also examined blood samples from healthy people.
People suffering from MS ought to consider taking one of the statin drugs such as Crestor (Rosuvastatin), Lipitor (Atorvastatin), Zocor (Simvastatin), Mevacor (Lovastatin), Pravachol (Pravastatin), or Lescol (Fluvastatin).
An article in MIT's Technology Review reports on the potential of thin film batteries to replace lithium ion batteries and to make electric cars feasible.
These new batteries replace the liquid or gel electrolyte with thin layers of solid glass-like or polymer materials, which are more stable. "Nothing can leak, nothing can freeze, nothing can boil, rupture, or explode," says Tim Bradow, vice president of business development at Infinite Power Solutions of Golden, CO, a leading developer of thin-film batteries.
All those recent exploding and burning laptop battery stories do not mean we've hit a technological limit in battery development. Thin film batteries will lower costs, increase safety, and increase capacity all at the same time.
MIT battery researcher Donald Sadoway says the use of solid electrolytes allows the use of pure lithium in the battery anode and this maximizes the amount of electricity that can be stored. Plus, this approach is amenable to use of a much lower cost manufacturing process.
In contrast to the glass-like electrolyte used by Infinite Power Solutions and others, Sadoway has developed a solid-polymer electrolyte (today's lithium-ion polymer batteries use a gel) for use in thin-film batteries. This electrolyte, he says, could be processed in rolls like newspaper, or some other high-throughput process. Such a process for thin-film batteries, although not now being developed by industry, could bring down costs, he says, while innovative ways of packaging electrodes could reduce size. "We've made batteries in the laboratory that are 300 watt-hours per kilogram," he says. "That's two times the best lithium-ion [battery] on the market today."
Low cost and high capacity could open the door to electric cars. Electric cars could end our dependence on liquid fuels for ground transportation. This would allow nuclear, coal, solar, and wind to compete directly oil, gasoline, and diesel fuel.
Note that battery energy storage capacity does not have to equal the energy content of gasoline or even of ethanol in order to make electric cars that will go as far on a charge as a car can go on a tank of gasoline. A shift to pure electric vehicles would allow the elimination of a heavy engine and a heavy transmission. Some of the weight budget currently allocated to the drivetrain could instead go to batteries. Then the car could be powered by electric motors located in each wheel.No need for a transmission and axle to turn the wheels.
“It is getting harder and harder for American farmers to say they feed the world,” said Ken Cook, president of the Environmental Working Group, an environmental research group based in Washington. “Instead, they feed S.U.V.’s.”
The decline of wheat and the broad relandscaping of America’s farmland have come about for several reasons. Better seed technology has given corn and soybeans a widening edge over wheat, and more favorable subsidies have encouraged farmers to abandon wheat. Changing consumer tastes and food packaging advancements have slowed American wheat demand.
But the growing biofuels industry is creating the strongest drag on wheat lately, as corn and soybeans are increasingly favored for their use in ethanol and biodiesel.
Fears of genetically engineered foods in major export markets have kept US farmers from shifting to genetically engineered wheat. So seed suppliers invest less in genetic engineering of new wheat strains. Whereas corn is used more for animal feed and so consumer fears of genetically modified food crops do not have as much impact. Therefore the gap between corn and wheat production costs gradually shifts in favor of corn.
Corn needs more energy and water inputs.
Corn yields are rising faster than wheat yields.
American corn yields rose by 30 percent from 1995 to 2005, while wheat yields grew by only 17 percent. In recent years corn has pulled further ahead, with an annual growth rate in yield that is four times that of wheat.
Lester Brown, president of the Earth Policy Institute, argues that the increasing demand for biomass to make ethanol and biodiesel will bring the demand for energy into competition with the demand for food.
With so many distilleries being built, livestock producers fear there may not be enough corn to feed animals, possibly leading to shortages in milk, eggs, beef, pork and poultry. And because the United States supplies 70 percent of world corn exports, importing countries — such as Egypt, Japan and Mexico — should be worried, too.
In agricultural terms, our appetite for automotive fuel is insatiable: The grain required to fill a 25-gallon SUV gas tank with ethanol would feed one person for a full year. If the United States converted its entire grain harvest into ethanol, it would satisfy less than 16 percent of its auto fuel needs.
Since I see the growth of demand for biomass ethanol and biodiesel as inevitable I tend toward favoring even more rapid development of biomass energy technologies. Sufficient advances in genetic engineering and chemical plant engineering to make ethanol and biodiesel might reduce the amount of land diverted to produce biomass energy.
Though I'd much rather see a bigger push to accelerate the development of photovoltaics and nuclear power as alternatives to turning huge amounts of land into energy production farms. Photovoltaics and nuclear power would use much less land to produce the same amount of usable energy.
A new process promises to cut the cost of producing ethanol from corn.
A Purdue University team led by professor Li-fu Chen and research assistant Qin Xu, both from the Purdue food science department, discovered a new method to create ethanol from corn. The method also produces biodegradable byproducts that could be safely eaten.
Existing methods of corn-to-ethanol conversion produce as much as 2.6 gallons of ethanol per bushel. The new Chen-Xu method produces 2.85 gallons for a 9.6% improvement. But this method also reduces energy use in the conversion process and produces less waste.
The Chen-Xu Method produces about 2.85 gallons of ethanol for every bushel of corn processed. That output is slightly higher than current methods, but the same process that creates the ethanol also creates other marketable products. Chen said the method also meets federal Clean Air Act standards, eliminating costs that other methods incur in meeting environmental regulations.
"One of the common methods of manufacturing ethanol, called dry milling, is often the cause of air pollutants by drying and storage of DDG, a byproduct of the process," Chen said. "Another method - wet milling - produces an odor because it requires the input of sulfur dioxide. The Chen-Xu Method eliminates both issues, and the only odor comes from the smell of the corn and yeast fermentation."
Using a machine originally designed to make plastics, the Chen-Xu Method grinds corn kernels and liquefies starch with high temperatures. The water input required by wet milling is reduced by 90 percent, Chen said. Wastewater output is cut by 95 percent, and electricity use is reduced by 47 percent.
"The total operating cost of a Chen-Xu Method ethanol plant should be much less than that of a wet-milling plant, and total equipment investment is less than half," Chen said. "And with proper planning and management, total equipment investment should be less than that of a dry-milling plant."
Lower capital costs, lower operating costs, more ethanol output for with less corn, less electricity, less waste. What's not to like?
Biomass energy technologies are going to keep dropping in cost and increasing in net energy efficiency. Gasoline currently costs more to make than ethanol even after adjusting for the lower energy content of a gallon of ethanol as compared to a gallon of gasoline. The price of oil may drop further. But the cost of converting biomass to ethanol will continue to drop in the coming years.
Good news. Big money is starting to support research to conquer aging and make us young again.
Peter A. Thiel, co-founder and former CEO of online payments system PayPal, and Founder and Managing Member of Clarium Capital Management, a San Francisco-based hedge fund, today announced his pledge of $3.5 Million to support scientific research into the alleviation and eventual reversal of the debilities caused by aging, to be conducted under the auspices of the Methuselah Foundation, a charity co-founded and Chaired by Dr. Aubrey de Grey.
Mr. Thiel commented, "Rapid advances in biological science foretell of a treasure trove of discoveries this century, including dramatically improved health and longevity for all. I'm backing Dr. de Grey, because I believe that his revolutionary approach to aging research will accelerate this process, allowing many people alive today to enjoy radically longer and healthier lives for themselves and their loved ones."
Mr. Thiel will donate a total of $500,000 over the next three years to fund pilot research projects intended to deliver early stage validation of the "SENS" approach to combating the debilitation caused by aging.
Additionally, from now until the end of 2009, Mr. Thiel promises to match every Dollar donated to the Methuselah Foundation for SENS research with a 50 cent matching contribution from himself, up to a maximum of $3 Million of matching funds.
Dr. de Grey said, "I am extremely grateful to Peter for his bold and visionary initiative. I have been working with leading biologists and biochemists around the world in identifying promising research projects, and with this generous donation we will go to work straightaway."
SENS (Strategies for Engineered Negligible Senescence) is a set of approaches to repair the body and reverse the aging process to make bodies fully young again. Click through on one of the SENS links and read all about it if the term is new to you.
I expect Thiel's donations to be the first of many very large donations aimed at reversing the aging process. The large number of multi-millionaires are very sharp people who know they really can't take their money with them when they die. So why not use a piece of their wealth to take a stab at making their bodies young again?
The full reversal of the aging process is an achievable goal. We will develop the biotechnologies to grow replacement parts, to do gene therapy, to send in stem cells to do repairs, and to remove the junk that accumulates in cells and between cells as we age. Daily announcements from biological resesarch labs demonstrate progress toward many of the technologies needed to reverse the aging process. Some people who are alive today will live to see the conquest of aging and the end of death from old age.
Semiconductor technology advances are mostly funded by sales of computer processors, memory, and other digital computer parts. Those advances have created capabilities to manipulate small scale devices for a variety of other purposes including microfluidic devices that function as biological and chemical labs on a chip. Another application being pursued at MIT is the development of extremely small gas turbines for generation of electricity. MIT researchers expect their miniature gas turbine to eventually compete with very large natural gas burning electric generator plants in efficiency.
MIT researchers are putting a tiny gas-turbine engine inside a silicon chip about the size of a quarter. The resulting device could run 10 times longer than a battery of the same weight can, powering laptops, cell phones, radios and other electronic devices.
It could also dramatically lighten the load for people who can't connect to a power grid, including soldiers who now must carry many pounds of batteries for a three-day mission -- all at a reasonable price.
The researchers say that in the long term, mass-production could bring the per-unit cost of power from microengines close to that for power from today's large gas-turbine power plants.
Making things tiny is all the rage. The field -- called microelectromechanical systems, or MEMS -- grew out of the computer industry's stunning success in developing and using micro technologies. "Forty years ago, a computer filled up a whole building," said Professor Alan Epstein of the Department of Aeronautics and Astronautics. "Now we all have microcomputers on our desks and inside our thermostats and our watches."
Cheap mass manufactured miniature electric generators could eliminate the need to connect to the electric grid, thereby reducing vulnerability from central system failures. Distributed generation would also cut transmission line losses of electricity due to resistance in cables.. However, large electric generator plants have one really big advantage: Their emissions can be rmonitored, regulated, and controlled.
A pair of reports make the potential losses from a killer bird H5N1 flu pandemic look a lot smaller. First off, at the US military's Uniformed Services University of the Health Sciences some researchers have discovered that plasma taken from recovered flu victims in 1918 reduced the fatality rate of others infected by the killer 1918 flu.
USU faculty have discovered that a treatment for the Spanish Influenza pandemic may also be effective for current Avian Influenza patients. Navy Capt. Edward Kilbane, Army Col. Jeffrey Jackson and Navy Lt. Cmdr. Thomas Luke, are all alumni and faculty of the Uniformed Services University of the Health Sciences (USU). They, along with retired Navy physician, Capt. Stephen Hoffman, published their research Tuesday, Aug. 29, in the online edition of the Annals of Internal Medicine.
The four researchers analyzed medical literature reported during the Spanish Flu pandemic of 1918 to 1920. They found that transfusions with blood products from Spanish Flu survivors may have reduced the risk of death in seriously ill Spanish Flu patients.
The meta-analysis of these data show that treatment of patients in 1918 with convalescent whole blood, plasma or serum obtained from humans who had recovered from Spanish Influenza resulted in a reduced mortality of seriously ill patients by 50 percent.
If antibodies extracted from patients who recover from H5N1 avian flu would work against H5N1 in other people then each infected person who recovers could produce enough antibodies each week to help several people.
Another report argues that by switching to use of cell cultures to grow pandemic flu vaccine enough vaccine could be produced in the United States to treat the entire population of the US in a few months.
In a study led by University of Michigan professor of chemical and biomedical engineering Henry Wang and doctoral student Lyle Lash, researchers examined the economics of producing egg versus cell culture vaccines in the event of a flu pandemic. They found that training personnel to make cell culture vaccines in existing facilities is the only way to make enough doses to cover the United States in a short time without requiring huge capital investments to build new dedicated flu vaccine cell culture facilities.
...
The reasons to shift from egg to cell culture production are time and capacity, both of which are critical factors in responding to a pandemic, researchers said. It takes much longer to compile millions of hen eggs than it would to grow up existing cell lines from frozen vials, Lash said. While cell culture has a lower yield than egg culture, there is more existing capacity for cell culture than for inoculating and processing eggs.
"Based on existing dosages, we'd have enough doses in about 3 to 4 months to cover the U.S. with the system we propose," Lash said. Currently, it would take six months to make 250 to 300 million doses of pandemic flu vaccine for the United States. "What we're proposing could make 600 million doses in four months."
If you could manage to isolate yourself and your family for a few months starting at the very beginning of a pandemic then you could come out after those few months and get vaccinated. Also, plasma treatments would become available.
This all reminds me that I've yet to stockpile N95 and N100 face masks. They'd be helpful for occasional trips to the store. Otherwise I'll totally isolate myself if a killer pandemic hits.
Every time a piece of safety equipment becomes fairly cheap the United States government and governments of other highly industrialized nations have moved to require the use of that equipment. When automated operation of cars by embedded computers becomes safer than human driving will governments move to require installation of such artificially intelligent (AI) computer systems in all new cars? Will governments eventually go even further and some day even ban the operation of cars and trucks by humans?
The US government is going to mandate computer-controlled features to help maintain vehicle control. Electronic anti-lock brakes (ABS) and other computer-controlled means to keep tire traction on the road will become mandatory in the United States for all new cars.
The National Highway Traffic Safety Administration is set to announce a preliminary regulation requiring electronic stability control technology on all new vehicles.
I predict the US government will require all new cars be constructed to support fully automated operation within 20 to 30 years.
Auto companies think automated systems for avoiding loss of driving control are more important than air bags for reducing accidents, injuries, and deaths.
The Insurance Institute for Highway Safety estimated in a report in June that as many as 10,000 deaths a year could be prevented if all vehicles were equipped with the feature. Auto companies have said the systems are more critical in preventing deaths than air bags, which are credited with saving 1,200 lives per year.
Many computer-assisted driving technologies are hitting the market. All these technologies will become more advanced and lower in cost in coming decades. Toyota is moving from radar to optical (i.e. light-based) sensors to detect and automatically try to avoid crashes into road obstacles such as pedestrians.
Toyota Motor Corp. and Denso Corp. collaborated with NEC to implement the chip in autos. It was adopted as an image-processing unit for a pre-crash safety system for Toyota's Lexus LS460 to be introduced in the fall. Toyota already offered a pre-crash safety system that employs milliwave radar.
The Lexus road obstacle avoidance will work by automatically activating the brake.
The new Lexus LS460 with the image processors will automatically slam on the brakes a split second before hitting a pedestrian or vehicle and prevent a collision or reduce impact.
Systems that monitor driver wakefulness and attention are also starting to hit the market. Cameras aimed at drivers try to alert drivers when they are not paying attention and an obstacle looms.
And if all the coddling means your attention wanders, there is a camera checking the driver's eyes are on the road.
Lexus' Pedro Pacheco says: "In the event that there is an obstacle in front of the car and the driver is at the same time looking at the side of the road, the system will sound a warning to alert the driver.
I've also read proposals to have cars automatically detect whether a person has been drinking alcohol and is too drunk to operate a car.
Driver monitoring systems can detect a driver falling asleep behind the wheel.
Dr. Grace, a former Carnegie Mellon University professor, is CEO of Attention Technologies Inc., which just started marketing a Driver Fatigue Monitor -- a dashboard-mounted camera that measures how often a sleepy driver's eyes close at night and then sets off a warning alarm.
Attention Technologies is one of two local companies that have developed anti-drowsiness monitors.
The other is AssistWare Technology Inc., another Carnegie Mellon spinoff that is selling a forward-mounted camera that sets off an alarm when a vehicle veers out of its lane or wanders erratically within the lane.
Volvo is one of many car companies developing driver monitoring systems.
GÖTEBORG, Sweden (November 30, 2005) – Volvo Car Corporation is taking a decisive new step toward helping drivers avoid vehicle collisions with its new Volvo Driver Alert system, technology designed to monitor a vehicle's progress on the road and alert the driver if it detects signs of fatigue or distraction. The system helps drivers make the right decision, rather than taking control of the vehicle.
The company intends to patent the Driver Alert technology and plans to make the system available in Volvo vehicles within two years.
Driver fatigue is a major traffic safety problem around the world. According to the U.S. National Highway Traffic Safety Administration (NHTSA), approximately 100,000 collisions are caused every year on American highways by drivers who fall asleep. Fifteen hundred of the collisions result in fatalities and a further 71,000 lead to physical injuries. In Europe, the situation is very similar: the German Insurance Association – GDV (Gesamtverband der Deutschen Versicherungswirtschaft e.V.) – estimates that 25 per cent of all fatal collisions on German roads are caused by fatigue.
BMW is also working on warning systems to alert drivers when they are drifting out of their lanes.
Safe motoring in style means maintaining maximum attention also on long distances. And this is precisely why BMW Group engineers have developed an assistance system helping the driver to avoid situations where they begin to lose their attention and awareness. Lane Departure Warning therefore informs the driver in good time of any unattended deviation from the car’s proper course, telling the driver through clear signals to countersteer and move back in the desired direction. This serves to avoid driving errors resulting from lack of concentration on traffic conditions.
Adaptive Cruise Control is a new technology that automatically adjusts vehicle speed to maintain a driver-selected distance from the vehicle ahead in the same lane. This next generation of cruise control uses forward-looking radar, installed behind the grill of a vehicle, to detect the speed and distance of the vehicle ahead of it, and then automatically adjusts your speed accordingly.
How does it work? The radar headway sensor sends information to a digital signal processor, which in turn translates the speed and distance information for a longitudinal controller. The result? If the lead vehicle slows down, or if another object is detected, the system sends a signal to the engine or braking system to decelerate. Then, when the road is clear, the system will re-accelerate the vehicle back to the set speed.
The fancy driving automation systems are coming out first on the more expensive models.
BMW AG, DaimlerChrysler AG and Toyota Motor Corp. are among the makers of premium models that are starting to market cars that automate many parts of the driving experience: self-parking cars (with the driver inside or out); parking guidance systems (for the less-lazy driver); enhanced cruise-control systems that work in stop-and-go-traffic and maintain a safe distance between cars; and warning systems that tell you when you've strayed from your lane.
Brakes and gas pedals are not the only parts of cars which are coming under partial computer car. Automotive engineers are also targetting control of the steering wheel. Mercedes has just introduced a radar-based parking assistance technology as an option in their CL-class cars.
First, the parking guidance system automatically uses side mounted radar sensors to monitor whether the space on either the driver or passenger side is adequate to park the vehicle. If it is, the dashboard displays a "P" icon, alerting the driver to the fact a suitable space is available.
Once the driver stops the vehicle and changes to reverse gear, the instrument cluster then displays a bird's eye view of the parking situation along with guide lines showing how best to park. Red lines indicate the current steering angle, while yellow lines show the steering angle needed. As the driver turns the steering wheel and the two lines coincide, they then combine to form green lines, alerting the driver that he is now in the appropriate angle to reverse.
Finally, as the driver is reversing, an audible signal gives notice when it's time to countersteer, perfectly situating them and their new coupe in that ordinarily too-tight-to-fit-in parking space.
You can see where all this is going. As optical and radar sensors and computers drop in price and become more powerful and as software algorithms become more sophisticated computers are going to gradually take over more driving tasks from truck and car drivers. Computers will become better than drivers and computer-operated cars will become safer than human-operated cars.
Biogerontologist Aubrey de Grey foresees a human future where biotechnologies allow us to live in eternal youth and never grow old. Once we reach that future accidents, murder, and suicide will become the major causes of death. Aubrey expects political movements will successfuly bring about a ban on cars in order to reduce death from accidents. I do not think most governments and polities will go down that path. More likely computers will make car operation so incredibly safe and accidents so rare that cars will not have much impact on average longevity.
Update: Skepticism about the feasibility of computer-operated vehicles became harder to maintain when the Defense Advanced Research Project Agency's Grand Challenge periodic contest for autonomous driverless vehicles finally produced winners in October 2005.
A robotic Volkswagen called “Stanley”, developed by a team from Stanford University in Palo Alto, California, won a $2 million prize on Sunday for winning a tough desert race of driverless vehicles.
And in a stunning improvement on 2004’s Grand Challenge, when no car completed more than 5% of the course, four other vehicles also finished. The 212-kilometre race across the Nevada desert is set by the US Defense Advanced Research Projects Agency (DARPA).
It says something about the rate of advance of the underlying technologies that so many contestants could all suddenly achieve the needed capability in the same year.
On May 1, 2006 DARPA announced a more difficult next phase Grand Challenge for autonomous vehicles to navigate an urban terrain. (PDF format)
The Defense Advanced Research Projects Agency (DARPA) today announced plans to hold its third Grand Challenge competition on November 3, 2007.
The DARPA Urban Challenge will feature autonomous ground vehicles executing simulated military supply missions safely and effectively in a mock urban area. Safe operation in traffic is essential to U.S. military plans to use autonomous ground vehicles to conduct important missions.
DARPA will award prizes for the top three autonomous ground vehicles that compete in a final event where they must safely complete a 60-mile urban area course in fewer than six hours. First prize is $2 million, second prize is $500,000 and third prize is $250,000. To succeed, vehicles must autonomously obey traffic laws while merging into moving traffic, navigating traffic circles, negotiating busy intersections and avoiding obstacles.
Does anyone doubt this challenge will be conquered within 5 years?
If the findings of a British researcher are correct then obsessive compulsive mobile cell phone users have a substance abuse problem where the substance is a cell phone.
Psychologist Dr David Sheffield asked to group of students to fill in a survey based on one used to diagnose gambling addiction.
The volunteers, who were aged between 18 and 25, were asked questions such as whether relatives had ever asked them to cut down on their mobile use and if they became bad tempered when denied access to their phone.
Analysis of the results showed one in seven became restless and irritable when they couldn't make phone calls and had no qualms about would lying to cover up the amount of time they spent on their handset.
Ninety per cent said they took their mobiles wherever they went and third used phone calls to lift their mood. Seven per cent even said they would rather lose a job or relationship than give up their mobile.
They have to have their mobile cell phone fixes.
People who gave up mobile phones experienced a drop in blood pressure.
People are becoming addicted to mobile phones, causing them to become stressed and irritable, work suggests.
Dr David Sheffield, of the University of Staffordshire, found problem behaviour linked to using a mobile in 16% of 106 users who were studied.
In a separate study, to be presented at a conference in Essex later, he found blood pressure was lower in those who had given up using mobile phones.
I know people who excessively use their cell phones. So this report rings true. Humans are not evolved to live in the technological societies we've created. They are not adapted to use the technologies they encounter in their environments.
(Philadelphia, PA) - Building on previous work, researchers at the University of Pennsylvania School of Medicine have found that deleting an inflammation enzyme in a mouse model of heart disease slowed the development of atherosclerosis. What's more, the composition of the animals' blood vessels showed that the disease process had not only slowed, but also stabilized. This study points to the possibility of a new class of nonsteroidal anti-inflammatory drugs (NSAIDs) that steer clear of heart-disease risk and work to reduce it.
Drugs that block the same gene (or its protein product) that was knocked out in these mice might also stop the development of arterial plaque that clogs up our circulatory systems. Mouse knock-out experiments once again deliver the goods.
Senior author Garret FitzGerald, MD, Director of the Institute for Translational Medicine and Therapeutics at Penn, and colleagues report their findings this week in the online edition of the Proceedings of the National Academy of Sciences.
NSAIDs like ibuprofen (Advil) and naproxen (Naprosyn) relieve pain and inflammation by blocking the cyclooxygenases, or COX enzymes (COX-1 and COX-2). These enzymes help make fats called prostaglandins. COX-2 is the most important source of the two prostaglandins - PGE2 and prostacyclin - that mediate pain and inflammation. However, COX-2-derived PGE2 and prostacyclin may also protect the heart, and loss of this function - particularly suppression of prostacyclin - explains the risk of heart attacks from NSAIDs that inhibit COX-2, such as rofecoxib (Vioxx), valdecoxib (Bextra), and celecoxib (Celebrex).
The problems with COX-2 inhibitors have prompted the search for alternative drug targets that suppress pain and inflammation yet are safe for the cardiovascular system. One possibility is an enzyme called mPGES-1, which converts PGH2 (a chemical product of COX-2) into PGE2. Previous studies at other institutions in mice lacking mPGES-1 suggest that inhibitors of this enzyme might retain much of the effectiveness of NSAIDs in combating pain and inflammation. However, unlike COX-2 inhibition or deletion, the Penn researchers had found that mPGES-1 deletion did not elevate blood pressure or predispose the mice to thrombosis. This work began to raise the possibility that mPGES-1 inhibitors might even benefit the heart.
In the PNAS study, the researchers studied the impact of deleting the mPGES-1 gene in mice predisposed to hardening of the arteries. Removing the enzyme had a dramatic effect on the development of the disease. "Both male and female mice slowed their development of atherosclerosis," explains first author Miao Wang, PhD, a postdoctoral fellow in the Penn Institute.
The composition of the blood vessels of the transgenic mice suggested that the disease process had not only slowed, but also stabilized. Collaborators Ellen Pure and Alicia Zukas at the Wistar Institute examined the detailed structure of the diseased arteries. Deleting mPGES-1 resulted in a dramatic change in the cellular constituents of the atherosclerotic plaques seen in the transgenic mice. In the absence of the enzyme, the diseased vessels were depleted of immune cells called macrophages, which led to the predominance of vascular smooth muscle cells in blood vessel walls. In turn, this led to a switch in the form of collagen - a fibrous structure that contributes to the fabric of plaques - to a more stable and benign form.
"It seems that it is the complete reverse of the mechanism that creates problems for COX-2 inhibitors," says FitzGerald. Mice lacking mPGES-1 boost their production of prostacyclin, the major heart-protecting fat produced by COX-2. They do this by redirecting prostacylcin to vascular smooth muscle cells. The same mechanism explains the group's earlier findings on blood pressure and thrombosis.
"It remains to be determined whether specific inhibitors of mPGES-1 can replicate the consequences of removing the gene" explains FitzGerald, "And if so, whether these results will translate from mice to humans."
In the meantime, these results, say the investigators, will fuel interest in the possibility of a new class of "super NSAIDs," which may not just avoid the risk of heart disease, but also actually work to diminish it.
The build-up of artery plaque is going to become totally preventable and in short order. Diet alone already can reduce the risk enormously. Eat the ape diet if you want to lower your risk of heart disease, stroke and other diseases..
University of California, Davis researchers have shown that statins not only improve cholesterol levels, but also dramatically reduce disease-causing inflammation in patients with metabolic syndrome -- a condition defined by symptoms that include abdominal obesity and high blood pressure.
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The UC Davis team conducted a double-blind, randomized, placebo-controlled study in which they gave a standard daily dose of a statin (Simvastatin or placebo) to 50 patients with metabolic syndrome. After eight weeks, they measured cholesterol levels, as well as biomarkers of inflammation in the circulation, but more importantly, in cells pivotal in all stages of plaque formation, the monocytes. They found, as expected, that statin lowered low-density-lipoprotein- cholesterol and non-high-density-lipoprotein-cholesterol levels, both of which the American Heart Association guidelines target for treatment of metabolic syndrome.
Jialal and his colleagues also found marked reductions in two pivotal biomarkers of inflammation: C-reactive protein (CRP) and interleukin-6. While these markers are typically elevated in insulin resistance, a condition that precedes the development of diabetes, statin therapy reduced these levels by 36 percent and 44 percent, respectively.
Chronic inflammation is harmful and widespread.
As for people who have a need to take one of the existing NSAIDs, a recent pair of papers in the Journal of the American Medical Association found that Celebrex does not pose as large of a heart risk as Vioxx.
In one paper, three researchers at Harvard examined 114 clinical trials of Vioxx and other drugs and found that Vioxx was linked to substantially higher rates of increased blood pressure than was Celebrex, a similar painkiller, which is still sold.
In the other paper, two Australian researchers found that Vioxx appeared more dangerous than Celebrex or several older painkillers in observational studies, which examine the safety and effectiveness of drugs in real-world settings after they are approved.
David Graham of the FDA, writing as a private citizen, argues in JAMA that naproxen appears safest out of all the NSAIDs and probably is neutral in terms of risk of heart attack (MI or myocardial infarction).
Some people spend their whole lives in search of happiness and escape from a feeling of hopelessness and ennui. They lack the technology that would grant them immediate satisfaction. Knock out a gene and be happy.
A new breed of permanently 'cheerful' mouse is providing hope of a new treatment for clinical depression. TREK-1 is a gene that can affect transmission of serotonin in the brain. Serotonin is known to play an important role in mood, sleep and sexuality. By breeding mice with an absence of TREK-1, researchers were able create a depression-resistant strain. The details of this research, which involved an international collaboration with scientists from the University of Nice, France, are published in Nature Neuroscience this week.
"Depression is a devastating illness, which affects around 10 percent of people at some point in their life," says Dr. Guy Debonnel an MUHC psychiatrist, professor in the Department of Psychiatry at McGill University, and principal author of the new research. "Current medications for clinical depression are ineffective for a third of patients, which is why the development of alternate treatments is so important."
Mice without the TREK-1 gene ("knock-out" mice) were created and bred in collaboration with Dr. Michel Lazdunski, co-author of the research, in his laboratory at the University of Nice, France. "These 'knock-out' mice were then tested using separate behavioral, electrophysiological and biochemical measures known to gauge 'depression' in animals," says Dr. Debonnel. "The results really surprised us; our 'knock-out' mice acted as if they had been treated with antidepressants for at least three weeks."
One of the reasons I watch for mouse gene knock-out studies is that they are a glimpse into the choices prospective parents (and domineering governments) will face when it becomes possible to tinker with the DNA of eggs, sperm, and embryos. In the future some people will opt for offspring genetic engineering to make their kids congenitally happy uncurable optimists. Other people will genetically engineer their kids to be highly objective analytical realists. Not a few of the latter will want to come up with ways to infect the obnoxiously optimistic with viruses that will reprogram them for more realism and less optimism.
Other future parents will opt for drugs instead of genetic engineering to make their kids happy, calm, content, and confident. Make Johnny and Jill grow up as joyful kids but then tell them at age 18 they just have to stop taking the pills and they'll be able to suffer all the doubts, depression, and sadness that the older generations experienced.
Gene knock-out studies also provide glimpses into just how little free will we have (if we even have any at all).
The discoveries from gene knock-out studies will become a torrent when efforts to create mice with gene knock-outs for each mouse gene achieve their goals.
Adults in Japan who consumed higher amounts of green tea had a lower risk of death due to all causes and due to cardiovascular disease, according to a study in the September 13 issue of JAMA. But there was no link between green tea consumption and a reduced risk of death due to cancer.
Tea is the most consumed beverage in the world aside from water. Three billion kilograms of tea are produced each year worldwide, according to background information in the article. Because of the high rates of tea consumption in the global population, even small effects in humans could have large implications for public health. Among teas, green tea polyphenols have been extensively studied as cardiovascular disease (CVD) and cancer chemopreventive agents. Although substantial evidence from in vitro and animal studies indicates that green tea preparations may impede CVD and carcinogenic processes, the possible protective role of green tea consumption against these diseases in humans remains unclear.
Shinichi Kuriyama, M.D., Ph.D., of the Tohoku University School of Public Policy, Sendai, Japan, and colleagues examined the association between green tea consumption and mortality (death rate) due to all causes, CVD, and cancer within a large population. The study, initiated in 1994, included 40,530 adults (age 40 to 79 years) in northeastern Japan, where green tea is widely consumed. Within this region, 80 percent of the population drinks green tea and more than half of them consume 3 or more cups and day. The participants, who had no history of stroke, coronary heart disease, or cancer at baseline, were followed for up to 11 years (1995-2005) for all-cause death and for up to 7 years (1995-2001) for cause-specific death.
Over 11 years of follow-up, 4,209 participants died, and over 7 years of follow-up, 892 participants died of cardiovascular disease and 1,134 participants died of cancer. The researchers found that green tea consump