How Wireless instrumentation is achieved in thermal power plant?
Monthly Archives: July 2010
Main Steam Pressure Calculation in Boiler
how pressure of main steam is decided for any thermal power plant?
Example.
For 250MW , main steam pressure is around 140 bar. how it is calculated? is there any calculation for deciding pressure?
Love of Logic [Science Tattoo] | The Loom
Melissa writes,
I have a mathematical tattoo on my left forearm. It’s in Frege’s notation (from “Grundgesetze der Arithmetik”), which was one of the first modern logical notations. If it were written on a flat surface, it would start with the short vertical line, which is the assertion sign. What it asserts is: If {Cantor’s theorem} then {heart}.
Cantor’s Theorem says that the power set of any set is strictly larger than the set itself. (The power set of a set is the set of all its subsets.) For finite sets, this is pretty obvious; for example, the power set of {1,2} is {{}, {1}, {2}, {1,2}}. In general, if a finite set has n members, its power set has 2^n. But Cantor’s Theorem is also true for *infinite* sets, which is kind of unexpected. After all, the set of all even numbers is the same size as the set of all numbers — why does the power set of the set of all numbers have to be bigger?
That’s why the proof of the theorem is so cool. It proves it for finite sets and infinite sets, no matter how huge, at the same time. You start by assuming that some arbitrary set S has the same number of members as its power set P(S). That is, assume there’s a one-one function f which maps the members of S to the members of P(S). Now consider the set D, which consists of all and only the members of S that don’t get mapped to a set of which they’re a member. (So, for instance, if 7 is a member of S, and f(7) = {4, 5, 12}, then 7 is in D because it’s not a member of f(7).) D is a subset of S, so it’s a member of P(S). That means that f maps some member of S, call it d, to D. But: is d in D or not? If it is, then it’s a member of f(d), so by the definition of D, it’s not in D. If it’s not in D, then it’s not a member of f(d), so, again by the definition of D, it’s in D. Either way leads to a contradiction, and there’s only one way out: it’s not possible to have a one-one function from any set to its power set. QED! (Of course, you also have to prove that P(S) can’t be *smaller* than S, but that’s easy.)
When I saw how short and simple (and beautiful!) the proof of such a powerful theorem was, I knew I could spend the rest of my life doing set theory and logic. So last year, when I got my bachelor’s degree in philosophy and went on to grad school, I celebrated by getting the theorem tattooed on my arm. As for the tattoo itself, it’s easiest to read from the bottom. The stuff on the right-hand side of the ‘=’ means: for all a, if a is in r, then a is in u. (In other words, r is a subset of u.) The whole bottom line means: for all r, r is in v if and only if it’s a subset of u. (So v is the power set of u.) The bottom line and the one above it together mean: if v is the power set of u, then v is strictly bigger than u. So those two lines state Cantor’s Theorem, and the whole tattoo means: if Cantor’s Theorem, then {heart}. (Incidentally, I got that heart symbol from an illustration in “Alice in Wonderland”. It’s the top of the King of Hearts’s crown.)
Click here to go to the full Science Tattoo Emporium.
From the Vault: Clint Is Dead, Long Live Clint! | The Loom
[A post from 2005 I'm fond of]
Clint, the chimpanzee in this picture, died several months ago at a relatively young age of 24. But part of him lives on. Scientists chose him–or rather, his DNA–as the subject of their first attempt to sequence a complete chimpanzee genome. In the new issue of Nature, they’ve unveiled their first complete draft, and already Clint’s legacy has offered some awesome insights into our own evolution.
The editors of Nature have dedicated a sprawling space in the journal to this scientific milestone. The main paper is 18 pages long, not to mention the supplementary information kept on Nature’s web site. In addition, the journal has published three other papers that take a closer look at particularly interesting (and thorny) aspects of the chimpanzee genome, such as what it says about the different fates of the Y chromosome (the male sex chromosome) in chimpanzees and humans. Other scientists offer a series of commentaries on topics ranging from brain evolution to chimpanzee culture. The journal Science has also gotten in on the action, with a paper comparing the expression of chimp and human genes as well as comments on the importance of chimpanzee conservation and research. (Thankfully, some of this material is going to be made available online for free.)
Why all the attention to the chimpanzee genome? One important reason is that it can tell us what parts of the human genome make us uniquely human–in other words, which parts that were produced by natural selection and other evolutionary processes over the past six million years or so, since our hominid ancestors diverged from the ancestors of our closest living relatives, chimpanzees. (Bonobos, sometimes known as pygmy chimpanzees, are also our first cousins, having split off from chimpanzees 2-5 million years ago.) Until now, scientists could only compare the human genome to the genomes of more distantly related species, such as mice, chickens, and fruit flies. They learned a lot from those comparisons, but it was impossible for them to say whether the differences between humans and the other species were unique to humans, or unique to apes, or to primates, or to some broader group. Now they can pin down the evolutinary sequence much more precisely. Until scientists rebuild the Neanderthal genome–if they ever do–this is going to be the best point of comparison we will ever get. (For more of the background on all this, please check out my new book on human evolution, which will be out in November.)
The analysis that’s being published today is pretty rudimentary. It’s akin to what you’d expect from a reporter who got to spend an hour flipping through 10,000 pages of declassified government documents. But it’s still fascinating, and I’d wager that it serves as a flight plan for research on the evolution of the human genome for the next decade.
First off, scientists can get a more precise figure of how different human and chimpanzee DNA is. In places where you can line up stretches of DNA precisely, there are 35 million spots where a single “letter” of the code (a nucleotide) is different. That comes to about 1.2% of all the DNA. The scientists also found millions of other spots in the genomes where a stretch of DNA had been accidentally deleted, or copied and inserted elsewhere. This accounts for about a 3% difference. Finally, the scientists found many genes that had been duplicated after the split between humans and chimps, corresponding to 2.7% of the genome.
By studying the human genome, scientists have also gotten a better picture of the history of the genomic parasites that we carry with us. About half of the human genome consists of DNA that does not produce proteins that are useful to our well-being. All they do is make copies of themselves and reinsert those copies at other spots in the genome. Other animals have these virus-like pieces of DNA, including chimpanzees. Some of the genomic parasites we carry are also carried by chimpanzees, which means that we inherited them from our common ancestor. Many of these parasites have suffered mutations that make them unable to copy themselves any longer. But in some cases, these parasites have been replicating (and evolving) much faster in one lineage than the other. One kind of parasite, called SINES, have spread three times faster in humans than in chimps. Some 7,000 genomic parasites known as Alu repeats exist in the human genome, compared to 2,300 in the chimp genome. While a lot of these parasites have no important effect on our genome, others have. They’ve helped delete 612 genes in humans, and they’ve combined pieces of some 200 other genes, producing new ones.
In some cases, the interesting evolution has occurred in the chimpanzee lineage, not in our own ancestry. Scientists have noted for a long time that the Y chromosome has been shrinking for hundreds of millions of years. Its decline has to do with how it is copied each generation. Out of the 23 pairs of our chromosomes, 22 have the same structure, and as a result they swap some genes as they are put into sperm or egg cells. Y chromosomes do not, because their counterpart, the X, is almost completely incompatible. My Y chromosome is thus a nearly perfect clone of my father’s. Mutations can spread faster when genes are cloned than when they get mixed together during recombination. As a result, many pieces of the Y chromosome have disappeared over time, and many Y genes that once worked no longer do.
Scientists have discovered that Clint and his fellow chimpanzee males have taken a bigger hit on the Y than humans have. In the human lineage, males with mutations to the Y chromosome have tended to produce less offspring than those without them. (This is a process known as purifying selection, because it strips out variations.) But the scientists found several broken versions of these genes on the chimpanzee Y chromosome.
Why are chimpanzees suffering more genetic damage? The authors of the study suggest that it has to do with their sex life. A chimpanzee female may mate with several males when she is in oestrus, and so mutations that give one male’s sperm an edge over other males are ben strongly favored by selection. If there are harmful mutations elsewhere on that male’s Y chromosome, they may hitchhike along. We humans are not so promiscuous, and the evidence is in our Y chromosome.
As for the mutations that make us uniquely human, the researchers point out some suspects but make no arrests. The researchers found that a vast number of the differences between the genomes are inconsquential. In other words, these mutations didn’t have any appreciable effect on the structure of proteins or on the general workings of the human cell. But the scientists did identify a number of regions of the genome, and even some individual genes, where natural selection seems to have had a major impact on our own lineage. A number of these candidates support earlier studies on smaller parts of the genome that I’ve blogged about here. Some of these genes appear to have helped in our own sexual arms race; others created defenses against malaria and other diseases.
When scientists first lobbied for the money (some twenty to thirty million dollars) for the chimp genome project, they argued that the effort would yield a lot of insight into human diseases. The early signs seem to be bearing them out. In their report on the draft sequence, they show some important genetic differences between humans and chimpanzees that might have bearing on important questions such as why we get Alzheimer’s disease and chimps don’t and why chimpanzees are more vulnerable to sleeping sickness than we are, and so on.
There is also a lot of variation within our own species when it comes to disease-related genes, and here too the chimpanzee genome project can shed light. The researchers show how some versions of these genes found in humans are the ancestral form also shared by chimpanzees. New mutations have arisen in humans and spread in the recent past, possibly favored by natural selection. The ancestral form of one gene called PRSS1, for example, causes pancreatitis, while the newer form does not.
But our genetic defenses and weaknesses to diseases aren’t really what we’d like to think make us truly, uniquely human. The most profound difference between the bodies of humans and chimpanzees is the brain. Much of the evolution that’s been going on in genes expressed in the brain has been purifying. There are a lot of ways to screw up a brain, in other words. But some genes appear to have undergone strong positive selection–in other words, new mutation sequences have been favored over others. It’s possible that relatively few genes played essential roles in producing the human brain.
You can feel the excitement of discovery thrumming through these papers, but it comes with a certain sadness as well. It doesn’t come just from the fact the chimpanzee whose DNA made this all possible died before he became famous. Lots of chimpanzees are dying–so many, in fact, that conservationists worry that they may become extinct from hunting, disease, and habitat destruction. And once a species is gone, it takes a vast amount of information about evolutionary history with it.
I was reminded of this fact when I read another chimpanzee paper that appears in the same issue of Nature, reporting on the first fossil of a chimpanzee ever discovered. It may be hard to believe that no one had found a chimp fossil before. A big part of the problem, scientists thought, was that chimpanzees were restricted to rain forests and other places where fossils don’t have good odds of surviving. The fossils that have now been discovered don’t amount to much–just a few teeth–and they raise far more questions than they answer. They date back about 500,000 years, to an open woodlands in Kenya where paleoanthropologists have also found fossils of tall, big-brained hominids that may have been the direct ancestors of Homo sapiens. So apparently chimpanzees once coexisted with hominids in the open woodlands that were once thought to be off-limits to them. More chimpanzee fossils will help address this puzzle, but they may never fully resolve it.
The chimpanzees of Kenya became extinct long ago, and now other populations teeter on the brink. To make sense of Clint’s genome, scientists need to document the variations both within and between chimpanzee populations–not just genetic variations, but variations in how they eat, how they organize their societies, how they use tools, and all the other aspects of the lives. If they don’t get that chance, the chimpanzee genome may become yet another puzzling fossil.
Vector Group
Sir
We are going to install 3 No of Alternators each of 7540 KVA and 6.3 KV.
Our project is that we have to sync. alternator on a 6.3 KV bus then used STEP Up by transformers ( 6 NO each 4000 KVA paralle connected ) to 11 KV bus.
Our problem is that what will be the Vector Group of Tr
Good Information on Smart Positioners?
I have been taxed with writing a short course covering digital valves and general smart field instrumentation. Could anyone guide me to some good information on smart positioners?
Much appreciated.
What is Transformer Grouping
What is transformer vector grouping and thier types
The Case for Late-Life Interventions in Aging
A position paper by Aubrey de Grey, a number of other important biogerontologists, and folk from the LifeStar Institute: "The social and medical costs of the biological aging process are high and will rise rapidly in coming decades, creating an enormous challenge to societies worldwide. In recent decades, researchers have expanded their understanding of the underlying deleterious structural and physiological changes (aging damage) that underlie the progressive functional impairments, declining health, and rising mortality of aging humans and other organisms and have been able to intervene in the process in model organisms, even late in life. To preempt a global aging crisis, we advocate an ambitious global initiative to translate these findings into interventions for aging humans, using three complementary approaches to retard, arrest, and even reverse aging damage, extending and even restoring the period of youthful health and functionality of older people." This more or less reflects the LifeStar Institute position, complementary with that of the SENS Foundation, but with more of an organizational focus.
View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20630854
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Brain Size Correlates With Species Longevity
Via ScienceDaily: "Mammals with larger brains in relation to body size tend to live longer. This is the conclusion reached by researchers [after] having analysed almost 500 mammal species and obtaining new data on the relation between brain size and lifespan. ... The brain size of some mammals is larger than expected for their body size. This is the case of large primates, such as chimpanzees and gorilla, and of whales, dolphins and elephants. Scientists have spent years investigating why sometimes nature favours the development of large brains given that they require much more time to reach functional maturity and use up so much energy. ... the size of the brain affects lifespan regardless of the size of the body. Hyenas, for example, have a larger brain than giraffes in proportion to body size and on average live longer, although they are smaller than these herbivores. ... it is possible that a longer life works in favour of a delay in reproductive cycles and this would in turn allow progenitors to invest more resources and time in caring for their offspring. This also leads to the formation of stable social groups whose members, according to the Social Intelligence Hypothesis (SIH), must deal with more cognitive demands than animals living alone, and this would be the reason for larger brains."
View the Article Under Discussion: http://www.sciencedaily.com/releases/2010/07/100715110001.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
A Conservative View of Longevity Science
This opinion piece is an example of the sort of viewpoint held by those who believe that metabolic manipulation to modestly slow aging is the only viable way forward in longevity science: "When I tell people that anti-aging drugs are no longer a distant prospect, they often assume I'm talking about the quest for immortality. That's not surprising, given the buzz generated in recent years by visionaries who speculate about re-engineering the human body to last thousands of years. But actually I don't find that far-out prospect very interesting - it bears the same relationship to serious aging science that warp-drive spaceships do to aeronautical engineering. What really grabs me are experimental advances that may impinge on the lives of people I know, maybe even mine. ... the only practical, near-term way to substantially increase healthy life span today is to simultaneously lower the risk of all diseases of aging. The way we now mainly buy time - administering therapies for one progressive, old-age disease at a time when it's too late to do much good - can't do that. Anti-aging drugs could, and at the same time they would go a long way toward ending the ruinously costly game of diminishing returns we're playing in geriatric medicine, as we eke out incremental gains with ever pricier palliatives. In effect, they would be preventive medicines of unprecedented scope and efficacy, drastically lowering the risk of everything from Alzheimer's to osteoporosis to wrinkles in the way that hypertension drugs now cut heart-attack risk."
View the Article Under Discussion: http://www.huffingtonpost.com/david-stipp/why-anti-aging-science-re_b_644308.html
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Urging a Global Collaboration Against Aging
From the LifeStar Institute: "Leaders in the biology and polices of aging research at the first LifeStar Institute Global Aging Science Summit conclude the time has come to launch an ambitious global effort to keep aging generations youthful, productive, and engaged to unprecedented ages. In laboratories all over the world, using genome sciences, diets including calorie restriction, and techniques of cell science and regenerative medicine, scientists are now keeping living organisms alive and healthy for increasing lengths of time never before thought possible. The obvious question: When will medical science do the same for us? ... The scientific panel proposes that the United States and nations across the world create a global collaboration and launch an Apollo-like Project with the following goal: translate laboratory knowledge about the degenerative changes of aging into new kinds of medicines for humans that can prevent and repair those changes. The panel urges governments and the biomedical industry to fund three key initiatives: (1) Use public health agencies to inform citizens on how they can improve their lifestyles. (2) Develop the first genuine anti-aging medicines that are able to boost the body's ability to maintain health (3) Develop and apply regenerative methods that can remove, replace, repair, and neutralize the cellular and molecular damage that accumulate in aging bodies and restore youthful structure and function."
View the Article Under Discussion: http://www.lifestarinstitute.org/index.php?pagename=aging_science_meeting_paper
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Using Stem Cells to Build Test Platforms
Here is an example of the other use for stem cells: to grow tissue that can be used to test and understand specific diseases. "Researchers are applying new stem cell technology to use skin samples to grow the brain cells thought to be responsible for the onset of Parkinson's disease ... [the] team will be gathering data from over 1,000 patients with early stage Parkinson's disease and taking small samples of skin tissue to grow special stem cells - induced pluripotent stem cells (iPS cells). iPS cells can be generated from accessible tissue such as the skin and then used to generate specific types of cell. The researchers will use the iPS cells to grow dopamine neurons - the brain cells responsible for the production of dopamine, as it is these cells which die in patients with Parkinson's, leading to the onset of the disease. ... iPS cells provide new and exciting opportunities to grow and study dopamine neurons from patients for the first time. This technology will prove to be extremely important in diseases which affect the brain because of its relative inaccessibility - it's far easier to get a skin sample than a brain biopsy. Once we have neurons from patients we can compare the functioning of cells taken from patients with the disease and those without to better understand why dopamine neurons die in patients with Parkinson's."
View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-07/babs-scc_1071210.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
LEF Funds Granulocyte Cancer Therapy
A press release: "In a discovery that made headline news around the world, Dr. Zheng Cui, of the Wake Forest University School of Medicine, developed a colony of mice with super-charged granulocytes that successfully fight off many forms of virulent cancer. ... In a surprising turn of events Dr. Cui also found that a similar cancer-killing activity is present in the granulocytes of some healthy humans. ... When the Life Extension Foundation learned that this potential cancer cure was not being funded, it immediately made a $200,000 grant to fund the study at the South Florida Bone Marrow/Stem Cell Transplant Institute ... This new clinical trial will test this approach in humans with advanced cancer, including metastases, who have not been helped by conventional cancer therapies. The trial has received an IND (investigational new drug) status from the Food and Drug Administration (FDA) and Institutional Review Board approval. ... In January of this year, Dr. Maharaj notified the Life Extension Foundation that progress was being slowed because expected funding sources had dried up. Life Extension responded with another grant of $600,000 to further advance what could be a cure for cancer."
View the Article Under Discussion: http://www.prweb.com/releases/2010/07/prweb4239704.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
The Genetics of Hormesis-Induced Longevity
Hormesis is the process whereby suffering a little biochemical damage switches metabolism into a high-repair, damage-resistant mode, thereby extending life. Here, researchers examine changes in gene expression associated with hormesis: "Ionizing radiation generates oxidative stress, which is thought to be a major cause of aging. Although living organisms are constantly exposed to low levels of radiation, most studies examining the effect of radiation have focused on accelerated aging and diminished life span that result from high-dose radiation. On the other hand, several studies have suggested that low-dose radiation enhances the longevity of Drosophila melanogaster. Therefore, investigation of the biological effects of low-dose radiation could contribute to a more comprehensive understanding of the aging process. In this study, microarray and quantitative real time-PCR were used to measure genome-wide changes in transcript levels in low-dose irradiated fruit flies that showed enhanced longevity. In response to radiation, approximately 13% of the genome exhibited changes in gene expression, and a number of aging-related genes were significantly regulated. These data were compared with quantitative trait loci affecting life-span to identify candidate genes involved in enhanced longevity induced by low-dose radiation. This genome-wide survey revealed novel information about changes in transcript levels in low-dose irradiated flies and identified 39 new candidate genes for molecular markers of extended longevity induced by ionizing radiation. In addition, this study also suggests a mechanism by which low-dose radiation extends longevity."
View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20617381
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
The Cost of Obesity
A good example of what obesity does to your long term health: "Men who enter adult life obese face a life-long doubling of the risk of dying prematurely, new research has found. In a study presented today (Tuesday) at the International Congress on Obesity in Stockholm, researchers tracked more than 5,000 military conscripts starting at the age of 20 until up to the age of 80. They found that at any given age, an obese man was twice as likely to die as a man who was not obese and that obesity at age 20 years had a constant effect on death up to 60 years later. They also found that the chance of dying early increased by 10% for each BMI point above the threshold for a healthy weight and that this persisted throughout life, with the obese dying about eight years earlier than the non-obese. ... Body mass index (BMI) was measured at the average ages of 20, 35 and 46 years, and the researchers investigated that in relation to death in the next follow-up period. A total of 1,191 men had died during the follow-up period of up to 60 years. The results were adjusted to eliminate any influence on the findings from year of birth, education and smoking. ... At age 70 years, 70% of the men in the comparison group and 50% of those in the obese group were still alive and we estimated that from middle age, the obese were likely to die eight years earlier than those in the comparison group."
View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-07/iaft-sfl071210.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
On Calorie Restriction
Christopher Westphal of Sirtris is writing a series of guest columns in the Boston Globe: "Last week, I wrote that the best way to live healthier longer was to eat less and exercise more. Meticulous readers asked which of these two approaches, precisely, had more scientific support. Such questions may reflect wishful thinking: Those who exercise a lot might wonder if they can eat the equivalent of steak and fries every night. And for those who don't want too much exercise, might they focus instead on eating less? Unfortunately for those who, like me, have modest will power at the table, the data are clear. The most robust way to increase healthy lifespan in a broad variety of organisms is in fact calorie restriction. In other words, it behooves us to cut our calorie intake markedly, while still maintaining a balanced diet that includes essential vitamins and minerals. Whether we can bring ourselves to do so is another question entirely. ... Who among us, you might ask, would have the fortitude to emulate the calorie restriction studies conducted on animals? It turns out that there are at least hundreds of Americans, and many more individuals worldwide, who are severely restricting their calorie intake in the hopes of extending their healthy lifespans. Studies have indeed found that key cardiovascular measurements, such as blood pressure and heart rate, are much improved in individuals who significantly restrict their calorie intake."
View the Article Under Discussion: http://www.boston.com/bostonglobe/editorial_opinion/oped/articles/2010/07/12/eat_a_lot_less_live_a_lot_longer/
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
PTEN and Nerve Regeneration
Via EurekAlert!: "Scientists have discovered a way to enhance nerve regeneration in the peripheral nervous system. This important discovery could lead to new treatments for nerve damage caused by diabetes or traumatic injuries. Peripheral nerves connect the brain and spinal cord to the body, and without them, there is no movement or sensation. Peripheral nerve damage is common and often irreversible. ... [Researchers] used a rat model to examine a pathway that helps nerves to grow and survive. Within this pathway is a molecular brake, called PTEN, that helps to prevent excessive cell growth under normal conditions. In addition to discovering for the first time that PTEN is found in the peripheral nervous system, [the team] demonstrated that following nerve injury, PTEN prevents peripheral nerves from regenerating. The team was able to block PTEN, an approach that dramatically increased nerve outgrowth. ... We were amazed to see such a dramatic effect over such a short time period. No one knew that nerves in the peripheral system could regenerate in this way, nerves that can be damaged if someone has diabetes for example. This finding could eventually help people who have lost feeling or motor skills recover and live with less pain."
View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-07/uoc-ndi070910.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/
Brown rice and other whole grains can prevent type 2 diabetes
Natural health advocates have long advocated nutrient-dense whole grains over the bleached and processed kinds, like white rice and white bread. Brown rice, for example, is loaded with fiber, B vitamins, phytochemicals and other nutrients. Scientists are now documenting that it has specific disease-fighting properties, too. For example, NaturalNews recently reported on Temple University research that found a compound in brown rice which lowers blood pressure and may prevent heart attacks (http://www.dreddyclinic.com/diet/alcaline/alk_diet.php). Now Harvard School of Public Health (HSPH) investigators have discovered eating two or more servings of brown rice per week slashes the risk of type 2 diabetes.
"Rice consumption in the U.S. has dramatically increased in recent decades. We believe replacing white rice and other refined grains with whole grains, including brown rice, would help lower the risk of type 2 diabetes," Qi Sun, who headed the research while at HSPH and is now an instructor of medicine at Brigham and Women's Hospital in Boston, said in a statement to the media. Read more...
Sikora & al-Megrahi
The Guardian are reporting today that the British Government regards the release of the Lockerbie bomber, Abdelbaset al-Megrahi, as a ‘mistake’, but a matter for the Scottish Government. This is consistent with their views in opposition. Hilary Clinton is also reported as looking into claims by Democrat senators that BP lobbied Libya. This is politics, the US is rapidly expanding its business ties with Libya and it is incoherent to criticise the release of a terrorist while doing business with the government under whose instruction he acted. But that is not my interest. The Guardian state that:
New York Democrat senators Frank Lautenberg, Kirsten Gillibrand and Charles Schumer and New Jersey Democrat senator Robert Menendez called for an inquiry, after reports that a cancer expert, who backed the three-month prognosis, now believed Megrahi could live for 10 or 20 years.
But yesterday, professor Karol Sikora, medical director of CancerPartners UK, said his words were taken out of context, and that the chances of Megrahi surviving for a decade were “less than 1%”.
He said: “There was a greater than 50% chance, in my opinion, that he would die within the first three months then gradually as you go along the chances get less and less.
“So the chances of living 10 years is less than 1%, something like that.”
Sikora was one of the doctors who originally examined Megrahi and claimed last year that his 3 month estimate was made on the request of the Libyans. This was not the first time Sikora has found himself in trouble. Imperial College sought legal advice to prevent Sikora from erroneously claiming he was an honorary professor at the instituition. He was also Dean of the Faculty of Integrated Medicine until it has its contract terminated by the University of Buckingham, where Sikora is also Dean of the Medical School. Sikora was also involved with the Prince’s Foundation for Integrated Health, Prince Charles’ pro-quackery charity until it collapsed due to financial fraud.
With respect to the claims above about the chances of living 10 years as being less than 1%, according to Cancer Research UK (CRUK), in England & Wales (Scotland is similar) 10 year survival rates are approximately 70%. The one year survival rates are close to 90%. Sikora’s claims appear to be inconsistent with this.
It remains a mystery to me why figures such as Sikora are employed by governments and universities.
*Update*
A commentator has pointed out that al-Megrahi had metastatic prostate cancer with a Gleason score of 9 so the figures I quoted above do not apply. This is quite correct. Men with metastatic prostate cancer at the time of diagnosis and with a Gleason score of 9 have a 20% chance of surviving for 10 years for someone of Megrahi’s age. Sikora is still out by a factor of 20 and my criticism stands.
Just another point, I do not intend to let the comments descend into conspiracy theories and will delete those that persist in posting them. My focus here is on the public credibility of Sikora, not the wider detail surrounding the Lockerbie bombing or the politics behind the extradition of al-Megrahi.
Contact lenses change color when blood glucose increases in diabetics
In the future, diabetics may be able to wear contact lenses that continuously alert them to variations in their glucose levels by changing colors - potentially replacing the need to routinely draw blood throughout the day.
The non-invasive technology, developed by Chemical and Biochemical Engineering professor Jin Zhang at The University of Western Ontario, uses extremely small nanoparticles embedded into the hydrogel lenses. These engineered nanoparticles react with glucose molecules found in tears, causing a chemical reaction that changes their color.
References:
Nanocomposites could change diabetes treatment. The University of Western Ontario, 2010.
Image source: OpenClipArt.org.
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