Who would have thought that the nucleus isn't random? Hmm...

In 2002, Paul Koehler, a physicist at Oak Ridge National Laboratory (ORNL) in Tennesse, and others were measuring neutron resonances in four types of platinum isotopes. These resonance patterns - which are the energies at which the nucleus of a platinum isotope absorbs neutrons - are affected by the motion of the protons and neutrons inside the nucleus. These motions are thought to be chaotic, at least according to random matrix theory, which is used to determine the behavior of large nuclei. However, in a recent study, Koehler and his colleagues found that the protons and neutrons seem to move in a collective way that can't be explained by any known model of nuclear structure.

“The new results suggest that the roughly 200 nucleons inside the platinum nuclei studied act in unison to exhibit regular rather than chaotic properties,” according to a news article from ORNL's website. “Given the relatively high energy and large number of nucleons involved, such collective behavior is totally unexpected and unexplained.”

The researchers say that their results reject the random matrix theory for this data with a 99.997% probability. But to confirm their claim, the scientists need to perform further experiments on the nuclei of other elements besides platinum, which could verify that the discovery is not simply due to an unusual property of platinum nuclei.

However, the problem is that ORELA has been closed due to budget cuts, and is not scheduled to reopen any time soon. The US Department of Energy has said that other research projects are a higher priority for the field of nuclear science. According to Koehler, there is one other place in the world where similar measurements could be made, which is the Geel Electron Linear Accelerator (GELINA) in Geel, Belgium. Here, the physicists could also repeat early experiments regarding random matrix theory performed in the 1970s at Columbia University, and see if the results hold up to modern instruments and analysis methods.

This indeed  gladdens the heart of Thingumbob in a most predictable manner. Rage no more, ye false gods of pseudoscience!

Here is where the "mental disorder" evinces itself abundantly

Here is an extraordinary title for a recent paper published by Neuron: Neuroeconomic Approaches to Mental Disorders. I am simply thunderstruck by the level of post modern absurdity: " This review surveys the recent and productive application of game-theoretic probes (economic games) to mental disorders" 


Wow...judging a mental disorder by the metric of what any sane person properly views as a mental disorder. Well I guess such turgid gobbledygook pawned off as science is to be expected with an ever increasing frequency so long as Doctor Tarr and Professor Fether are running the asylum.

"Information" as Deus Ex Machina

Wednesday, August 25, 2010

Quantum Entanglement Can Be A Measure Of Free Will, Say Physicists

The same experiments that reveal the nature of entanglement can also be interpreted as a measure of free will, say researchers

The nature of quantum mechanics has forced researchers to reconsider their own role in the process of science. Gone is the Victorian idea that measurement is objective and absolute. Today, we know that in the quantum world, it is impossible to separate the measured from the measurer. But exactly what role measurement plays in the universe, we have yet to fathom.

One intriguing idea is that certain kinds of experiments can tease apart the nature of measurement. And one particularly important class of experiment involves quantum entanglement, the hugely puzzling phenomenon in which widely separated objects share the same existence (or in scientific terms, are described by the same wave function).

Imagine two particles that are entangled in this way. Before any measurement takes place, these particles are in a superposition of states. Then a measurement on one immediately influences the other, somehow determining the outcome of a measurement on it.

Many experiments have shown that this "influence" happens as close to instantaneously as it is possible to measure and certainly cannot be mediated by any lightspeed signal. The same experiments also rule out any hidden correlation between the particles in which the outcome of any measurement is agreed upon in advance. Imagine, for example, some unseen hand that forces experimenters to unknowingly carry out measurements that always make it look as if this spooky action at a distance was taking place.

Today, Jonathan Barrett from the University of Bristol and Nicolas Gisin from the University of Geneva provide us with an interesting new take on this problem. They assume that entanglement does occur as quantum mechanics proscribes and then ask how much free will an experimenter must have to rule out the possibility of hidden interference.

The answer is curious. Barret and Gisin prove that if there is any information shared by the experimenters and the particles they are to measure, then entanglement can be explained by some kind of hidden process that is deterministic.

In practical terms, this means that there can be no shared information between the random number generators that determine the parameters of the experiments to be made, and the particles to be measured.

But the same also holds true for the experimenters themselves. It means there can be no information shared between them and the particles to be measured either. In other words, they must have completely free will.

In fact, if an experimenter lacks even a single bit of free will then quantum mechanics can be explained in terms of hidden variables. Conversely, if we accept the veracity of quantum mechanics, then we are able to place a bound on the nature of free will.

That's an interesting way of stating the problem of entanglement and suggests a number of promising, related conundrums: what of systems that are partially entangled and others in which more than two particle become entangled.

Free will never looked so fascinating.

Ref: arxiv.org/abs/1008.3612: How Much Free Will Is Needed To Demonstrate Nonlocality?

This is so very silly...It's amazing that such folrerol isn't the subject of ridicule due to its prima facie absurdity. This seems more like a schoolboy prank than anything else.

Hawking the Misanthrope and Pseudoscience

This is what the media has lately trumpeted as the wisdom of Steven Hawking:

"If we are the only intelligent beings in the galaxy, we should make sure we survive and continue. But we are entering an increasingly dangerous period of our history. Our population and our use of the finite resources of planet Earth are growing exponentially, along with our technical ability to change the environment for good or ill. But our genetic code still carries the selfish and aggressive instincts that were of survival advantage in the past. It will be difficult enough to avoid disaster in the next hundred years, let alone the next thousand or million. Our only chance of long-term survival is not to remain inward-looking on planet Earth, but to spread out into space. We have made remarkable progress in the last hundred years, but if we want to continue beyond the next hundred years, our future is in space. That is why I'm in favor of manned, or should I say, 'personed' spaceflight."

In my book, this type of thinking is the reason that students loathe science classes. The rank solipsism and pessimism is all too palpable. And it points toward the fact that the entire edifice of what passes for modern philosophy of science is a rotting carcass. The truth is that the future of humanity is in colonizing space for the reason that we are continuing thereby to do the unselfish act of perpetuating ongoing and never ending process of perfecting creation. Which is our unique noetic character.

Elenore Prochaska and Beethoven

Elenore, disguised as a man, joined the volunteer Lutzow Free Corps to fight to free Prussia from Napoleon Bonaparte. She died from wounds in the battle of the Gohrde in 1813. Johann Friederich Duncker wrote a play in her honor for which Ludwig van Beethoven composed incidental music.

Let Them Eat Lobster

The simple truth is Barack Obama is a narcissistic flim flam man, in the hip pocket of elite financiers like George Soros. The President, like Nero, is fiddling while his country burns. He couldn't care less about the plight of the unwashed masses. In fact, unlike so many of his democratic cronies, he's even incapable of crocodile tears. It comes as no surprise that his wife acts out the same derangement in character. They are two peas in a pod.

Imagination's Tempest

Heavenly muse, what were those songs sung by your illustrious son Leonardo Da Vinci? His lyre first gained him renown before his brush overshadowed all. The silver lyre he fashioned, where lies it now? The notes unrecorded, unread. How must they have delighted and surprised? He, himself was dismayed by the ephemeral in his music. What would humanity gain to bring back these lost triumphs of Da Vinci now. Perhaps as mankind emerges from the earth on pinions fashioned by plasma, we can bring back his genius in song. Thankfully we do have still his instrumental designs to rebuild.

Leonardo's Harpsichord Viola

Leonardo's Portrait of a Musician

Shimon Perez Almost Hits the Nail on the Head

"Fury as Israel president claims English are 'anti-semitic'

Israel's president has accused the English of being anti-semitic and claimed that MPs pander to Muslim voters."

 It would be more accurate of Mr. Perez to point out that the British establishment has had a long standing policy of hosting radical Muslim groups especially associated with Saudi wahhabism. (Which is the cauldron that created Al Qaida.) This is in keeping with their official cover up of the Saudi British Al Yamamah BAE scandal. Perez missed an opportunity to out the British continuation of the "Great Game."

Three very good pieces of biological research

The first is important for space flight and radiation because there may be a way to engineer a biological protection against leukemia by inhibiting a gene called Puma that allows stem cell cancer mutations survival. 

Public release date: 31-Jul-2010
[ Print | E-mail |  Share ] [ Close Window ]

Contact: Penny Fannin
fannin@wehi.edu.au
61-393-452-345
Walter and Eliza Hall Institute

Missing Puma reveals cancer conundrum

		IMAGE: Professor Andreas Strasser from the Walter and Eliza Hall Institute in Melbourne, Australia, has made a discovery that has upended scientists’ understanding of programmed cell death and its role in... Click here for more information.

Walter and Eliza Hall Institute researchers in Melbourne, Australia, have made a discovery that has upended scientists' understanding of programmed cell death and its role in tumour formation.

Programmed cell death, also called apoptosis, is an important process in human biology as it removes unwanted and damaged cells from our bodies. This process protects us against cancer development and autoimmune disease.

The research team's discovery, led by Professor Andreas Strasser from the institute's Molecular Genetics of Cancer Division, has implications for the understanding of how cancers develop and will inform the ongoing development of a new class of anti-cancer drugs called BH3 mimetics.

"Until now everybody believed that a failure of damaged cells to undergo suicide allowed mutated cells to proliferate, which contributes to tumour development," Professor Strasser said. "That's certainly still true but we discovered that, in certain settings, the opposite holds: the body's natural cell-suicide program can fuel tumour development."

The research team's experiments revealed that repeated cycles of cellular depletion and tissue regeneration, by activating stem cells, could promote tumour development.

In situations where the DNA in many cells is damaged, such as when the body is repeatedly exposed to low doses of radiation, there are repeated cycles of cell death in the body's tissues. "Attempts by the body's stem cells to repopulate the depleted tissue can then actually drive the tumour development," Professor Strasser said. "That's because the radiation, while killing many cells within a tissue, will create mutations in some of the surviving stem cells. When such abnormal (mutated) stem cells repopulate the tissue, they will divide many times and this can promote the development of tumours."

The research, done in collaboration with Dr Ewa Michalak, Dr Cassandra Vandenberg, Mr Alex Delbridge, Dr Li Wu, Dr Clare Scott and Professor Jerry Adams, is published in today's issue of the international journal Genes and Development.

Crucial to the team's research was an understanding of what happens to mice exposed to radiation when a gene called Puma is missing. "If normal mice (which have the Puma gene) are given a low dose of radiation it destroys around 80 per cent of the white blood cells," Professor Strasser said. "That does not kill the mouse but it does mean the stem cells in the bone marrow have to work extra hard to replenish the blood system. This can lead to the formation of tumours of white blood cells, called leukaemias, if the stem cells doing the repopulating have cancer-causing mutations.

"The surprise was that mice that don't carry the Puma gene are protected from this type of tumour development. Puma is essential for the death of cells that have damaged DNA. If mice don't have the Puma gene when they receive low doses of radiation the white blood cells are not destroyed, so you don't force mutated stem cells to become activated (and divide) to replenish the blood system."

Professor Strasser said the research suggested that the risk of cancer was increased in people who experienced cycles of tissue destruction followed by tissue re-population by stem cells. "Such cycles may account for the liver cancers frequently associated with viral (hepatitis C) infection or alcohol-related liver damage." The research also helps explain the so-called secondary cancers that sometimes arise in patients who were cured of their primary cancer by chemotherapeutic drugs that cause DNA damage."

The findings will also inform the ongoing development of a new class of anti-cancer drugs called BH3 mimetics. These drugs are designed to kill cancer cells. "Chronic exposure to such drugs could lead to the death of large numbers of normal cells that would then need to be replaced," Professor Strasser said. "In certain circumstances this could promote the development of secondary cancers, particularly if patients are receiving treatments such as chemotherapy or gamma-radiation that can lead to cancer-causing mutations in stem cells."

###

The research was supported by the National Health and Medical Research Council, the Leukemia and Lymphoma Society, the National Institutes of Health (US), the Juvenile Diabetes Research Foundation, Cancer Council Victoria and the Victorian Government.

The second and third regard regulatory functions that protect genomic integrity. This class of research coming increasingly to the forefront as science uncovers a remarkable network of a sort of metagenome that regulates genetic replication from the "outside." This involves a whole host of molecules, especially small fragments of regulatory RNA as evidenced below.

[ Print | E-mail |  Share ] [ Close Window ]

Contact: John Ascenzi
Ascenzi@email.chop.edu
267-426-6055
Children's Hospital of Philadelphia 

Red blood cells have a tiny but effective protector -- microRNA

Genetic molecules resist chemical stress, may have wider roles

Pediatric researchers have discovered a new biological pathway in which small segments of RNA, called microRNA, help protect red blood cells from injury caused by chemicals called free radicals. The microRNA seems to have only a modest role when red blood cells experience normal conditions, but steps into action when the cells are threatened by oxidant stress.

Led by hematologist Mitchell Weiss, M.D., Ph.D., of The Children's Hospital of Philadelphia, the current study describes how a particular microRNA fine-tunes gene activity by acting on an unexpected signaling pathway.

The study appears in the August 1 issue of the journal Genes & Development, simultaneously with a similar study of microRNAs and red blood cells by a University of Texas team led by Eric Olson, Ph.D. The two studies reinforce each other, said Weiss.

MicroRNAs are single-stranded molecules of ribonucleic acid (RNA) averaging only 22 nucleotides long. Scientists estimate that 500 to 1000 microRNAs exist in the human genome. First characterized in the early 1990s, they received their current name in 2001. Over the past decade, scientists have increasingly recognized that microRNAs play a crucial role in regulating genes, most typically by attaching to a piece of messenger RNA and blocking it from being translated into a protein, but many details remain to be discovered.

"Although microRNAs affect the formation and function of most or all tissues, for most microRNAs, we don't know their precise mechanisms of action," said Weiss. "In this case we already knew this microRNA, called miR-451, regulates red blood cells in zebrafish and mice, and because it is highly conserved in evolution, we presume it operates in humans as well. But its functional roles were poorly understood."

By investigating how microRNAs influence red blood cell development, Weiss and colleagues aimed to understand how such development goes wrong in hemolytic anemia, in which red blood cells are destroyed in large numbers, or in disorders of abnormal blood cell production. The current study used knockout mice—bioengineered animals in which the miR-451 gene was removed and could not function.

They found that preventing the activity of miR-451 produced only modest effects—mild anemia in the mice—but when the team subjected mice to oxidant stress by dosing them with a drug that produces free radicals, the mice had profound anemia. The oxygen radicals attacked hemoglobin, the iron-carrying molecule in red blood cells.

"This is a common theme in microRNAs—frequently, they don't play a central role during tissue formation or normal conditions, but they have a strong protective effect when an organism is stressed," said Weiss. "Over evolutionary time, red blood cells have evolved ways to protect themselves; one of those ways is the action of microRNA."

Weiss's team found that miR-451, acting through intermediate steps on a signaling pathway, affects a key protein, FoxO3. As a transcription factor, FoxO3 regulates hundreds of genes; in this case, FoxO3 stimulates specific genes that protect red blood cells from oxidant stress. The knockout mice in this study, having lost miR-451's function, showed impaired FoxO3 activity, and less ability to protect their red blood cells.

The regulatory pathway seen here, Weiss added, may have medical implications beyond blood cell development. "This finding does not have immediate clinical application for patients with blood diseases, but it sheds light on how microRNAs fine tune physiological functions in different contexts," said Weiss. FoxO3 regulates anti-oxidant functions in heart cells and also acts as a tumor suppressor, so miR-451 may have an important role in heart protection and in fighting cancers. "Further studies may broaden our knowledge of how this microRNA may defend the body against disease," he added.

###

The National Institutes of Health, the Roche Foundation for Anemia Research and the March of Dimes Foundation provided grant support for this study. Weiss's co-authors included Barry H. Paw, M.D., Ph.D., of Brigham and Women's Hospital and Harvard Medical School; Duonan Yu, Camila O. dos Santos, and several other colleagues from The Children's Hospital of Philadelphia; and collaborators from Northwestern University, Chicago; Mount Sinai School of Medicine, New York City; and the Amnis Corporation, Seattle.

"miR-451 protects against erythroid oxidant stress by repressing 14-3-3zeta," Genes and Development, published online July 31, 2010, in print issue on Aug. 1, 2010. doi: 10.1101/gad.1942110.

About The Children's Hospital of Philadelphia: The Children's Hospital of Philadelphia was founded in 1855 as the nation's first pediatric hospital. Through its long-standing commitment to providing exceptional patient care, training new generations of pediatric healthcare professionals and pioneering major research initiatives, Children's Hospital has fostered many discoveries that have benefited children worldwide. Its pediatric research program is among the largest in the country, ranking third in National Institutes of Health funding. In addition, its unique family-centered care and public service programs have brought the 460-bed hospital recognition as a leading advocate for children and adolescents. For more information, visithttp://www.chop.edu.

---

[ Print | E-mail |  Share ] [ Close Window ]

ublic release date: 1-Aug-2010
[ Print | E-mail |  Share ] [ Close Window ]

Contact: Blaine Friedlander
bpf2@cornell.edu
607-254-8093
Cornell University

'Guardian of the genome': Protein helps prevent damaged DNA in yeast

ITHACA, N.Y. — Like a scout that runs ahead to spot signs of damage or danger, a protein in yeast safeguards the yeast cells' genome during replication -- a process vulnerable to errors when DNA is copied -- according to new Cornell research.

Researchers from Cornell University's Weill Institute for Cell and Molecular Biology have discovered how a protein called Mec1 plays the role of "guardian of the genome," explained Marcus Smolka, assistant professor of molecular biology and genetics. The findings "DNA Damage Signaling Recruits the Rtt107-Slx4 Scaffolds via Dpb11 to Mediate Replication Stress Response," are detailed in the journal Molecular Cell (July 30, 2010).

Previous studies have shown that cells lacking Mec1 accumulate damaged DNA and become more sensitive to agents that interfere with replication. The researchers report that the Mec1 protein monitors and repairs the machinery responsible for replicating the DNA. At times, when DNA becomes damaged, the replication machinery can actually detach from the DNA -- like a train coming off a track -- but Mec1 coordinates the repair of the machinery and the DNA itself, allowing it to restart and continue replicating.

"Mec1 organizes the cell's response against things that jeopardize the integrity of the genome," Smolka said.

During the replication process, Mec1 accumulates at trouble spots such as lesions in the DNA or other blocks to replication. Mec1 is known as a kinase, a type of enzyme that modifies other proteins by adding a phosphate group to them (a process called phosphorylation), which then leads to a functional change in the protein. The researchers report that Mec1 adds a phosphate group to a protein known as Slx4, which then triggers Slx4 to anchor to the replication machinery. Slx4 then can employ a variety of tools to repair DNA and the replication machinery.

The findings are important because researchers have discovered counterparts (called orthologues) to Mec1, other related proteins with similar biological pathways in humans. Also, mutations to the human genes that produce Mec1 and related proteins can lead to cancer predisposition and neurological disorders. At the same time, cancer cells employ their own similar replication repair system, so understanding the process may help researchers design interventions that interrupt replication of cancer DNA.

Recently, other researchers discovered that the human version of Mec1, called ATR, phosphorylates a protein that is the human counterpart to Slx4. The next step, Smolka said, will be to see if after phosphorylation the human Slx4 also anchors to the replication machinery to repair any damaged machinery or DNA.

###

Co-authors include Patrice Ohouo, a graduate student in biochemistry, molecular and cell biology; Francisco M. Bastos de Oliveira, a postdoctoral researcher; and Beatriz Almeida, a research support specialist; all members of Smolka's lab.

---

[ Print | E-mail |  Share ] [ Close Window ]