Europe against GMO crops! Please, sign the Avaaz petition! I already did.
It's us who decide, not Monsanto!!!

Saturday, 31 May 2008

A new dimension of stupidity

Just when you think it cannot get any worse, and it does. After the sabotage on the magnets, we see a new attempt to stop LHC from the US side, thought on different ground- that a black hole produced in it will eat the Earth. Now, I won't get into proving it isn't possible, my particle physicist knowledge is on bachelor level. Or ok, actually master. But it's not the point. The point is that this case is ridiculous. No judge can actually decide on this, no matter of the evidences, for the simple reason that the judge should be on the cutting edge of science. Which he or she is not. That kind of decisions are put in the hands of scientists and people that oversee their projects. And if all those brilliant minds didn't see a danger, I find it very unlikely that others are just sooo much smarter. The could be, of course, but if a whole species of scientists are not smart enough to prevent something like this, should such specie exist at all? And the question I am asking is first, why closing only LHC, Tevatron is close enough also. And question number two-until when science will be nothing but a puppet in the hands of public opinion? Why we're spending our lives on learning if our knowledge is always inferior to any fool that claim otherwise and makes more fun for the media than we do. Answers, please...
(the comments in brackets in italic are mine, I appologise if some of them are rude, but it is because I really feel strongly about doomsday anti-scientific propaganda)

Asking a Judge to Save the World, and Maybe a Whole Lot More

Published: March 29, 2008

None of this nor the rest of the grimness on the front page today will matter a bit, though, if two men pursuing a lawsuit in federal court in Hawaii turn out to be right. They think a giant particle accelerator that will begin smashing protons together outside Geneva this summer might produce a black hole or something else that will spell the end of the Earth — and maybe the universe.

Scientists say that is very unlikely — though they have done some checking just to make sure.

The world’s physicists have spent 14 years and $8 billion building the Large Hadron Collider, in which the colliding protons will recreate energies and conditions last seen a trillionth of a second after the Big Bang. Researchers will sift the debris from these primordial recreations for clues to the nature of mass and new forces and symmetries of nature.

But Walter L. Wagner and Luis Sancho contend that scientists at the European Center for Nuclear Research, or CERN, have played down the chances that the collider could produce, among other horrors(what are the other horrors?), a tiny black hole, which, they say, could eat the Earth. Or it could spit out something called a “strangelet” that would convert our planet to a shrunken dense dead lump of something called “strange matter.” (by the mechanism of stranglingess? seriously...) Their suit also says CERN has failed to provide an environmental impact statement as required under the National Environmental Policy Act. (National??? Of which nation, because they are many in EU! And what did exactly USA did under the Kyoto protocol and did Europe prosecute it about it?)

Although it sounds bizarre, the case touches on a serious issue that has bothered scholars and scientists in recent years — namely how to estimate the risk of new groundbreaking experiments and who gets to decide whether or not to go ahead.

The lawsuit, filed March 21 in Federal District Court, in Honolulu, seeks a temporary restraining order prohibiting CERN from proceeding with the accelerator until it has produced a safety report and an environmental assessment. It names the federal Department of Energy, the Fermi National Accelerator Laboratory, the National Science Foundation and CERN as defendants.

According to a spokesman for the Justice Department, which is representing the Department of Energy, a scheduling meeting has been set for June 16.

Why should CERN, an organization of European nations based in Switzerland, even show up in a Hawaiian courtroom?

In an interview, Mr. Wagner said, “I don’t know if they’re going to show up.” CERN would have to voluntarily submit to the court’s jurisdiction, he said, adding that he and Mr. Sancho could have sued in France or Switzerland, but to save expenses (so they try to save the Earth from being eaten by a black hole, but went for the cheaper option???) they had added CERN to the docket here. He claimed that a restraining order on Fermilab and the Energy Department, which helps to supply and maintain the accelerator’s massive superconducting magnets, would shut down the project anyway.

James Gillies, head of communications at CERN, said the laboratory as of yet had no comment on the suit. “It’s hard to see how a district court in Hawaii has jurisdiction over an intergovernmental organization in Europe,” Mr. Gillies said.

“There is nothing new to suggest that the L.H.C. is unsafe,” he said, adding that its safety had been confirmed by two reports, with a third on the way, and would be the subject of a discussion during an open house at the lab on April 6.

But Mr. Wagner is not mollified. “They’ve got a lot of propaganda saying it’s safe,” he said in an interview, “but basically it’s propaganda.” (and what he says and does basically is... what???)

In an e-mail message, Mr. Wagner called the CERN safety review “fundamentally flawed” and said it had been initiated too late. The review process violates the European Commission’s standards for adhering to the “Precautionary Principle,” he wrote, “and has not been done by ‘arms length’ scientists.”

Physicists in and out of CERN say a variety of studies, including an official CERN report in 2003, have concluded there is no problem. But just to be sure, last year the anonymous Safety Assessment Group was set up to do the review again.

This is not the first time around for Mr. Wagner. He filed similar suits in 1999 and 2000 to prevent the Brookhaven National Laboratory from operating the Relativistic Heavy Ion Collider. That suit was dismissed in 2001. The collider, which smashes together gold ions in the hopes of creating what is called a “quark-gluon plasma,” has been operating without incident since 2000. (hmmm, that smells of paranoia)

Mr. Wagner, who lives on the Big Island of Hawaii, studied physics and did cosmic ray research at the University of California, Berkeley, and received a doctorate in law from what is now known as the University of Northern California in Sacramento. He subsequently worked as a radiation safety officer for the Veterans Administration. (as WHAT???)

Mr. Sancho, who describes himself as an author and researcher on time theory, lives in Spain, probably in Barcelona, Mr. Wagner said. (time theory, hmmm, sound like picking his nose to me)

Doomsday fears have a long, if not distinguished, pedigree in the history of physics. At Los Alamos before the first nuclear bomb was tested, Emil Konopinski was given the job of calculating whether or not the explosion would set the atmosphere on fire.

The Large Hadron Collider is designed to fire up protons to energies of seven trillion electron volts before banging them together. Nothing, indeed, will happen in the CERN collider that does not happen 100,000 times a day from cosmic rays in the atmosphere, said Nima Arkani-Hamed, a particle theorist at the Institute for Advanced Study in Princeton.

What is different, physicists admit, is that the fragments from cosmic rays will go shooting harmlessly through the Earth at nearly the speed of light, but anything created when the beams meet head-on in the collider will be born at rest relative to the laboratory and so will stick around and thus could create havoc.

According to a paper by the cosmologist Stephen Hawking in 1974, a tiny black hole would rapidly evaporate in a poof of radiation and elementary particles, and thus pose no threat. No one, though, has seen a black hole evaporate. (we have not seen a black hole as a matter of fact too, and some people believe we won't)

As a result, Mr. Wagner and Mr. Sancho contend in their complaint, black holes could really be stable, and a micro black hole created by the collider could grow, eventually swallowing the Earth.

But William Unruh, of the University of British Columbia, whose paper exploring the limits of Dr. Hawking’s radiation process was referenced on Mr. Wagner’s Web site, said they had missed his point. “Maybe physics really is so weird as to not have black holes evaporate,” he said. “But it would really, really have to be weird.”

Lisa Randall, a Harvard physicist whose work helped fuel the speculation about black holes at the collider, pointed out in a paper last year that black holes would probably not be produced at the collider after all, although other effects of so-called quantum gravity might appear.source

Thursday, 29 May 2008

The mechanism of seeing

Ah, lovely article due to NY Times on the mechanism of seeing and gathering of information by the eyes. I hope you enjoy it as much as I did!

What is the difference between seeing a scene casually and automatically, as in, you’re at the window and you glance outside at the same old streetscape and nothing registers, versus the focused seeing you’d do if you glanced outside and noticed a sign in the window of your favorite restaurant, and oh no, it’s going out of business because, let’s face it, you always have that Typhoid Mary effect on things. In both cases the same sensory information, the same photonic stream from the external world, is falling on the retinal tissue of your eyes, but the information is processed very differently from one eyeful to the next. What is that difference? At what stage in the complex circuitry of sight do attentiveness and awareness arise, and what happens to other objects in the visual field once a particular object has been designated worthy of a further despairing stare?

Visual attentiveness is born of limited resources. “The basic problem is that far more information lands on your eyes than you can possibly analyze and still end up with a reasonable sized brain,” Dr. Wolfe said. Hence, the brain has evolved mechanisms for combating data overload, allowing large rivers of data to pass along optical and cortical corridors almost entirely unassimilated, and peeling off selected data for a close, careful view. In deciding what to focus on, the brain essentially shines a spotlight from place to place, a rapid, sweeping search that takes in maybe 30 or 40 objects per second, the survey accompanied by a multitude of body movements of which we are barely aware: the darting of the eyes, the constant tiny twists of the torso and neck. We scan and sweep and perfunctorily police, until something sticks out and brings our bouncing cones to a halt.

The mechanisms that succeed in seizing our sightline fall into two basic classes: bottom up and top down. Bottom-up attentiveness originates with the stimulus, with something in our visual field that is the optical equivalent of a shout: a wildly waving hand, a bright red object against a green field. Bottom-up stimuli seem to head straight for the brainstem and are almost impossible to ignore, said Nancy Kanwisher, a vision researcher at M.I.T., and thus they are popular in Internet ads.

Top-down attentiveness, by comparison, is a volitional act, the decision by the viewer that an item, even in the absence of flapping parts or strobe lights, is nonetheless a sight to behold. When you are looking for a specific object — say, your black suitcase on a moving baggage carousel occupied largely by black suitcases — you apply a top-down approach, the bouncing searchlights configured to specific parameters, like a smallish, scuffed black suitcase with one broken wheel. Volitional attentiveness is much trickier to study than is a simple response to a stimulus, yet scientists have made progress through improved brain-scanning technology and the ability to measure the firing patterns of specific neurons or the synchronized firing of clusters of brain cells.

Recent studies with both macaques and humans indicate that attentiveness crackles through the brain along vast, multifocal, transcortical loops, leaping to life in regions at the back of the brain, in the primary visual cortex that engages with the world, proceeding forward into frontal lobes where higher cognitive analysis occurs, and then doubling back to the primary visual centers. En route, the initial signal is amplified, italicized and annotated, and so persuasively that the boosted signal seems to emanate from the object itself. The enhancer effect explains why, if you’ve ever looked at a crowd photo and had somebody point out the face of, say, a young Franklin Roosevelt or George Clooney in the throng, the celebrity’s image will leap out at you thereafter as though lighted from behind.

Whether lured into attentiveness by a bottom-up or top-down mechanism, scientists said, the results of change blindness studies and other experiments strongly suggest that the visual system can focus on only one or very few objects at a time, and that anything lying outside a given moment’s cone of interest gets short shrift. The brain, it seems, is a master at filling gaps and making do, of compiling a cohesive portrait of reality based on a flickering view.

“Our spotlight of attention is grabbing objects at such a fast rate that introspectively it feels like you’re recognizing many things at once,” Dr. Wolfe said. “But the reality is that you are only accurately representing the state of one or a few objects at any given moment.” As for the rest of our visual experience, he said, it has been aptly called “a grand illusion.” Sit back, relax and enjoy the movie called You. source

Tuesday, 27 May 2008

Newsbits March

In today's issue we have:

  • a new way to predict earthquakes,
  • a giant medicine failure that turns into a new way of treatment of deceases,
  • killer wheat fungus that could cause major problems
  • new insights on our need of sleep, that I rather disagree
  • and last but not least, a new treatment of tinnitus.

Quiet period could hint of impending earthquake

04 March 2008,Kate Ravilious

It is not exactly an early warning system, but earthquakes may indeed hint at their intentions before they rumble. According to a large satellite survey, a few hours before a night-time earthquake there is a significant reduction in the intensity of very low frequency radio waves coming from beneath the ground in the region.

Frantisek Nemec of the University of Orléans in France and colleagues put together two-and-a-half years of electromagnetic wave readings taken by the French satellite DEMETER. They analysed the intensity of these emissions for more than 9000 earthquakes with magnitudes 4.8 or greater, and compared them with background levels.

The team observed a decrease of around 5 decibels in emission intensity up to 4 hours before shallow earthquakes, which occur less than 40 kilometres below the surface. They only found this decrease for earthquakes that happened during the night. (Geophysical Research Letters, DOI: 10.1029/2007GL032517). source

My comment: Why only during the night?

Reprogrammed immune cells could fight disease

  • 16 March 2008,Linda Geddes

TWO years ago, on 13 March 2006, six previously healthy young men were left fighting for their lives after being injected with an experimental drug in a safety trial at Northwick Park Hospital in London. The drug was supposed to damp down cells in the immune system whose unwanted activity leads to autoimmune diseases like rheumatoid arthritis. But things went badly wrong, and the volunteers' immune systems started to run out of control, causing damage that led to multiple organ failure.

Though all six survived, the drug, TGN1412, being developed by TeGenero of Würzburg, Germany, was abandoned. However, the principle on which it was based still holds promise for therapies to prevent rejection of transplanted organs, and treatments for autoimmune disease and cancer (see "Cancer's little helpers"). source
( GVHD occurs when T-cells in the transplanted bone marrow recognise their new
host's cells as foreign, and start attacking them. This is similar to what
happens in autoimmune diseases, in which T-cells react against the body's own
tissues, or in transplant rejection, when they attack the donated tissue. T-regs
can directly suppress these attacks. "Regulatory T-cells are our body's own
mechanism of preventing it from destroying itself," says Fiona Powrie, an
immunologist at the University of Oxford. "We are trying to ramp up the body's
natural control system."

Using T-regs would have several advantages over conventional immunosuppressants.
These drugs, which often have to be taken for life, have a blanket effect that
dampens down the whole immune system. This makes the body more vulnerable to
infection, increases the risk of cancer and suppresses the very immune responses
that might enable the body to control autoimmunity.

"The current approach of using pharmacological immunosuppression doesn't make
any sense at all," says Matthias Edinger at the University Hospital in
Regensburg, Germany. T-regs would have a more specific effect, and it could be
made more specific still by generating T-regs that target only effector T-cells
that react to a particular antigen. This should mean that they only suppress the
immune cells that are co-ordinating an immune attack. Furthermore, experiments
with mice suggest that a single injection of T-regs is enough to shift the
balance of the immune system long-term, perhaps eliminating the need for
lifelong drugs.)
For the whole article click here

My comment: I find the idea very elegant. And I'm absolutely fascinated by the way our body works.

Killer wheat fungus threatens starvation for millions

  • 13 March 2008,Debora MacKenzie

A WHEAT disease that could destroy most of the world's main wheat crops could strike south Asia's vast wheat fields two years earlier than research had suggested, leaving millions to starve. The fungus, called Ug99, has spread from Africa to Iran, and may already be in Pakistan. If so, this is extremely bad news, as Pakistan is not only critically reliant on its wheat crop, it is also the gateway to the Asian breadbasket, including the vital Punjab region.

Scientists met this week in Syria to decide on emergency measures to track Ug99's progress. They hope to slow its spread by spraying fungicide or even stopping farmers from planting wheat in the spores' path. The only real remedy will be new wheat varieties that resist Ug99, and they may not be ready for five years. The fungus has just pulled ahead in the race. source

("The only real remedy will be new wheat varieties that resist the Ug99 fungus and they may not be ready for five years"Ug99, a virulent strain of black stem rust (Puccinia graminis) was identified in Uganda in 1999. Since then it has invaded Kenya and Ethiopia and, last year, Yemen. From previous fungal invasions, scientists expected the prevailing winds to carry Ug99 spores to Egypt, Turkey and Syria, and then east to Iran, a major wheat-grower, buying them some time. But on 8 June 2007, Cyclone Gonu hit the Arabian peninsula, the worst storm there for 30 years.

There could be more unpleasant surprises in store. On mature wheat, the fungus reproduces asexually to release billions of identical spores. If the spores drift onto a barberry bush (Berberis vulgaris), however, they switch to sexual reproduction, and so could swap genes with other stem rusts to produce completely new variants. Iran is a hotspot for barberry.

Scientists have now found out how Ug99 took hold, says Rick Ward of CIMMYT, the wheat breeding institute in Mexico that started the Green Revolution. "It turns out most of Kenya was planted with a wheat variety that contained only one gene for rust resistance, SR24," he told New Scientist.

"We advise at least two resistance genes," says Ward. Wheat with the SR24 gene alone gives any Ug99 strains resistant to SR24 a huge advantage, just as misuse of antibiotics selects for antibiotic-resistant bacteria, says Ward. Farmers then switched to using wheat with other resistance genes and the same thing happened.

Ug99 is now resistant to the three major anti-rust genes used in nearly all the world's wheat. "The real solution is disease resistance that relies on a number of genes," says Ward. Wheat with multigene resistance does not so much destroy the fungus as slow it down. The hope is that with several genes involved it will be much harder for the fungus to become resistant and there will be less selection pressure for it to do so.

The problem is that crop breeding is slow. It usually takes at least five years to cross disease-resistant lines with wheat varieties adapted to local conditions in the world's wheat-growing countries, then grow enough seed to plant fields threatened by Ug99.)
The whole article can be found here.

My comment: Interestingly enough, there is no mention of GMo crops in the article. While googling the issue gave some very weird titles. Anyway, obviously exactly the poor genetic pool is the problem, so I hope there is a decision that won't kill millions.

Do we read too much into our need for sleep?

  • 15 March 2008,Emma Young

IT IS one of the biggest mysteries in biology: why do we, and many other animals, spend a huge proportion of our lives simply sleeping? We cannot eat or mate while asleep, and are vulnerable to attack. Where is the survival advantage in that? Yet, deprive an experimental rat or fruit fly of sleep and the consequences can be fatal. Surely sleep must have evolved to fulfil some crucial biological function, such as refreshing the body or rebooting the brain? That is what sleep researchers have been thinking for some time - although they still cannot agree on what sleep is for. But perhaps they are wrong.

One leading researchers is now proposing a radical rethink. After two decades spent studying the sleeping behaviour of a range of animals, Jerry Siegel from the University of California, Los Angeles, has come to the controversial conclusion that sleep did not evolve for ...source

(Instead of performing some vital biological function Dr Siegel proposes sleep's fundamental purpose is simply to conserve energy and keep an individual out of danger.

He said: "In the wild the best strategy for passing on your genes is to be asleep for as long as you can get away with."
Although many researchers assume an animal is more vulnerable while it is sleeping Dr Siegel believes being awake is riskier - not least because you are more likely to be injured.

He contends there are just too many "inconvenient truths" to make biology the primary explanation for sleep although he does accept that his theory leaves some key questions unanswered.) source/it's not the new scientist article, but similar/

My comment: Sleep is important. I don't know could they say that people deprived from REM are ok. I have been deprived of it-due to massive insomnia and then the use of sleeping pills that pretty much eliminate the REM too, and I know how it feels. You're all right on the outside, but you feel like you're empty on the inside. Like all the colors of the day have been taken away from you. I can't understand how some people claim sleep is not important and then to fall happily asleep in the night. I suggest them to try to not sleep for a week and then to think it over.

New Therapies Fight Phantom Noises of Tinnitus

Published: April 1, 2008

For the 12 million Americans who suffer from severe tinnitus, the phantom tones inside their head are louder than anything else.

The most promising therapies, experts say, are based on discoveries made in the last five years about the brain activity of people with tinnitus. With brain-scanning equipment like functional magnetic resonance imaging, researchers in the United States and Europe have independently discovered that the brain areas responsible for interpreting sound and producing fearful emotions are exceptionally active in people who complain of tinnitus.

“We’ve discovered that tinnitus is not so much ringing in the ears as ringing in the brain,” said Thomas J. Brozoski, a tinnitus researcher at Southern Illinois University School of Medicine in Springfield.

Indeed, tinnitus can be intense in people with hearing loss and even those whose auditory nerves have been completely severed. In the absence of normal auditory stimulation, the brain is like a driver trying to tune in to a radio station that is out of range. It turns up the volume trying but gets only annoying static. Richard Salvi, director of the Center for Hearing and Deafness at the State University of New York at Buffalo, said the static could be “neural noise” — the sound of nerves firing. Or, he said, it could be a leftover sound memory.

Adam Edwards, a 34-year-old co-owner of a wheel repair shop in Dallas, said he developed tinnitus four years ago after target shooting with a pistol.

Mr. Edwards says he has gotten relief from a device developed by an Australian audiologist, which became widely available in the United States last year. Manufactured by Neuromonics Inc. of Bethlehem, Pa., it looks like an MP3 player and delivers sound spanning the full auditory spectrum, digitally embedded in soothing music.

Similar to white noise, the broadband sound, tailored to each patient’s hearing ability, masks the tinnitus. (The music is intended to ease the anxiety that often accompanies the disorder.) Patients wear the $5,000 device, which is usually not covered by health insurance, for a minimum of two hours a day for six months. Since completing the treatment regimen last year, Mr. Edwards said his tinnitus had “become sort of like Muzak at a department store — you hear it if you think about it, but otherwise you don’t really notice.”

Other treatments showing promise include surgically implanted electrodes and noninvasive magnetic stimulation, both intended to disrupt and possibly reset the faulty brain signals responsible for tinnitus. Using functional M.R.I. to guide them, neurosurgeons in Belgium have performed the implant procedure on several patients in the last year and say it has suppressed tinnitus entirely.

But the treatment is controversial. “It’s a radical option and not proven yet,” said Jennifer R. Melcher, an assistant professor of otology and laryngology at Harvard Medical School.

The magnetic therapy, similar to treatments used for depression and chronic pain, involves holding a magnet in the shape of a figure eight over the skull. Clinicians use functional M.R.I. to aim the magnetic pulses so they reach regions of the brain responsible for interpreting sound. Patients receive a pulse every second for about 20 minutes. “It works for some people but not for others,” said Anthony Cacace, professor of communication science and nerve disorders at Wayne State University in Detroit. Since tinnitus has so many causes, Dr. Cacace said, the challenge now is to find out which “subsets of patients benefit from this treatment.” source

Sunday, 25 May 2008

More on how our immune system works in our brain

So so cool! Please read it, I am personally shocked by the intelligence of the Nature. Really! It's unbelievable how our bodies are done by so complicated mechanism, but also the simplest possible.

How the immune system fine-tunes the brain

  • 01 March 2008,Bijal Trivedi

THROUGHOUT most of the body our immune system reigns supreme. Molecular whistle-blowers seek out bacteria, viruses and sickly cells and tag them for destruction. Trigger-happy demolition crews patrol the area killing invaders and infected cells, then efficiently clean up the mess. They are a crack team that takes no prisoners. Even so, there is one place where the immune system is not invited: the brain, or so we've been led to believe.

With 100 billion neurons linked via a quadrillion connections, the brain has always been considered too delicate - and too important - to be subjected to the destructive power of a molecular search-and-destroy team. Even a small mistake could damage or destroy the essential wiring that keeps us alive. Instead, the brain is protected by the blood-brain barrier, a highly selective filtration system which keeps out invaders and the army of patrolling white blood cells.

Now, though, this view is changing. In the past decade key immune molecules have been discovered in the brain. And researchers working out exactly what they are doing there are making some surprising discoveries. The brain has taken potentially destructive molecules and put them to work as architects, fine-tuning networks of neurons and removing any unwanted connections. Now they believe these same molecules, when the system fails, might be involved in conditions as diverse as Alzheimer's, glaucoma, schizophrenia and autism.

The brain's connections, the synapses, can potentially link each neuron to thousands of others, forming complex electrical pathways that control the body and behaviour. By far the most important changes to our brain's wiring happens in key stages of development - in the uterus as the brain wires up, in childhood as we grow and learn, and again during puberty as the brain prepares for adulthood. Each of these growth spurts is followed by a period of pruning, where unnecessary connections are cut back. In adulthood this process continues, with the brain constantly updating its connections, adding branches as we learn a skill or make a new memory, and cutting back those that it doesn't need. Without this constant trimming the brain risks becoming confused by competing information and crossed wires.

The first hint that the immune system was involved in this process came in 1998 when Carla Shatz, then at the University of California, Berkeley, stumbled across one of the body's key immune markers - the major histocompatibility complex (MHC) - in the brains of fetal cats. MHC Class 1 (MHC1) is a group of genes that encode proteins found on the surface of almost every cell in the body and flags each cell as "self". Any cell displaying the wrong MHC1 proteins - called human leukocyte antigen (HLA) in humans - is deemed foreign, and is tagged for destruction by specialised groups of white blood cells.

Organ transplants, for example, must have similar MHC markers to the recipient's to prevent rejection. Chunks of brain tissue transplanted into genetically different individuals can survive, however, and since no one had found MHC1 gene expression in the brain, this made perfect sense. After all, without the immune system's circulating sentinels, brain cells would have no need to prove they belonged. Now, though, it seemed that MHC1 had been there all along.

Shatz's discovery came about while she was investigating how the visual system wires up during fetal development and early life. She wanted to know which genes control the organisation of neurons as they grow from the eye to the visual centres of the brain and become organised into distinct zones - one from the right eye and one from the left.

The brain was known to send electrical "test signals" along these new pathways in the uterus, signals that somehow reinforce existing synapses and eliminate those that aren't required. What wasn't clear was which genes control this process. Shatz set about answering this question by stopping electrical signals being sent along the neural pathways in fetal cats, first with drugs to halt electrical activity in the neurons, and later by keeping mice in the dark or closing one eye at birth. She then analysed messenger RNA from human brain tissue to discover which genes were turned on or off compared to the controls. To her surprise, when the visual pathway was blocked, MHC1 was one of the gene families most affected, with expression dropping significantly. "[I thought], this is really nuts," says Shatz. "What is this doing in the brain? It's not even supposed to be there."
“This is really nuts... what's this doing in the brain? It's not even supposed to be there”

In follow-up studies Shatz and her team compared normal mouse brains with those of mice lacking MHC1. They found that without MHC1 the wiring in their visual cortex became unruly, compared to the neatly arranged connections of controls. In recent experiments they have knocked out MHC1's partner molecule in the immune system, a protein called PirB, to similar effect.

Shatz now believes that MHC and PirB work together as a molecular brake to stop the neurons making too many connections. "When you lack these molecules the circuits change way too much. You get excessive synaptic plasticity - too many connections and a lack of balance of inputs," she says.

MHC1 is not the only immune molecule moonlighting in the brain. Ben Barres, a neuroscientist at Stanford University in California, discovered that another, called C1q, was also involved in tweaking connections.

Like Shatz, Barres was intrigued by the formation of the visual system, and keen to understand how some synapses are stabilised to form a permanent part of the adult brain while others are lost. He focused his attention on brain cells called glia - in particular a type of glial cell called an astrocyte. Textbooks dismiss astrocytes as "boring support cells", says Barres, "the glue that holds the neurons together", and credit them with menial tasks like mopping up cell corpses, ions, and spilt neurotransmitters. Barres believed the cells were doing much more. "When you look under the electron microscope, anywhere you see synapses you see glia," he says.

By culturing neurons with and without glial cells, Barres discovered that neurons need astrocytes to build synapses. Without them there was almost no synaptic activity, but when he mixed neurons with astrocytes, or bathed them in liquid where the astrocytes had been, synapse activity exploded 100-fold.

In 2005 Barres reported that astrocytes were secreting a molecule called thrombospondin, which stimulated synapse formation. He later found that the job of pruning fell to C1q, which was secreted by the neurons themselves. The two molecules were working together to make and break connections.

In the rest of the body C1q forms part of the "complement cascade" - a gang of protein molecules that stick to bacteria and other invaders and target them for destruction. In the visual system, though, C1q clustered specifically on synapses. Mice lacking C1q formed too many connections and their visual system failed to develop properly. "We have shown it is required... it is getting rid of the bad synapses," says Barres.

He thinks that this process is analogous to the immune system. In the body C1q tags bacteria to alert white blood cells called macrophages to come in and eat the invaders, like a cellular Pac-Man. In the brain C1q tags synapses for destruction, and they are then engulfed by microglia - the macrophages of the nervous system, Barres believes.

Marc Freeman, a neurobiologist at the University of Massachusetts Medical School in Worchester, says that whether redundant synapses are actually engulfed still needs to be proved, although "it's a good bet". It makes sense that the immune and nervous systems would share some of the same molecules, says Freeman. "C1q is a way to very specifically tag a synapse for removal."

Barres believes that aberrant C1q activity could be involved in neurodegenerative diseases. Working with Simon John, a geneticist at The Jackson Laboratory in Bar Harbor, Maine, Barres is exploring the role of C1q in a mouse model of glaucoma.

In glaucoma, neurons in the retina and the optic nerve - the bundle of nerves carrying images from the retina to the brain - begin to die. In mice C1q levels rise dramatically from almost zero and the molecules cluster on retina early in the disease. As the mouse ages, more and more C1q is produced and more and more synapses are lost. Only late in the disease does this lead to the death of neurons.

In people with glaucoma, says Barres, neurons only die when they have lost most of their synapses. Others such as Eliezer Masliah and Robert Terry, molecular pathologists at the University of California, San Diego, have shown that Alzheimer's also results in massive synapse loss. It is estimated that when a person first visits their neurologist with the earliest detectable form of dementia, they have already lost 60 per cent of their synapses in the parts of their brain involved in memory. "That's interesting because in Alzheimer's C1q goes through the roof," says Barres.

This raises the possibility of blocking the C1q cascade to prevent the death of neurons. It might not cure Alzheimer's or glaucoma, but such a treatment could potentially delay the progression of the disease by reducing the death rate of neurons.

So could errors in the MHC1 system also be responsible for disease? Perhaps. Lisa Boulanger, a neuroscientist at the University of California, San Diego, is investigating a possible link between the chances of developing schizophrenia or autism and stimulation of the immune system during fetal development. In genetically susceptible individuals, the risk of a child developing schizophrenia later in life is significantly increased if the mother develops a viral infection during the second trimester of pregnancy. Boulanger wonders whether the explanation could lie in the impact of the mother's immune response on the developing brain of her baby.

"Our hypothesis is that mom's immune system gets stimulated, she releases factors known as cytokines that change MHC expression - and you don't want to change MHC expression during fetal brain development because it is busy building the fetal brain," she says.

A common symptom of both schizophrenia and autism is sensory overload, where the person affected reports feeling bombarded with an overwhelming mixture of sensory information. Could a lack of pruning, due to underactive MHC1 be behind a confused and over-connected brain? In an effort to find out, Boulanger is now looking for behaviours analogous to autism or schizophrenia in mice whose mothers had challenges to their immune system during pregnancy, and in mice with genetically altered levels of MHC1. Initial tests show that MHC1-deficient mice do indeed exhibit symptoms of sensory overload in a diagnostic test called "prepulse inhibition".

This test is also used in humans as a measure of the brain's ability to filter out overwhelming sensory information. In the test, a loud tone causes people to startle and flinch, but playing a soft tone 50 milliseconds before the loud one reduces the startle response. This is a sign that the brain is filtering out information coming in too fast to process - a normal brain can't handle it so the second tone is filtered out and not heard. But some people with schizophrenia and autism lack the ability to filter, so startle just as much on hearing two tones as one. In Boulanger's tests, mice without MHC1 startle in much the same way as people with schizophrenia and autism. They also have a similar imbalance in the levels of excitatory neurotransmitters.

She admits that so far "all of these things are just correlated in a very interesting way" and more experiments are required to discover whether there really are changes in the MHC in the brains of people who develop schizophrenia. To do this she is using tissue samples from brain banks and is collaborating with local physicians to test whether levels of secreted MHC might be altered in the blood or urine. That could potentially pave the way for a diagnostic test for autism or schizophrenia. "It's a long shot," she admits. Schizophrenia symptoms may not manifest themselves until 20 years after an initial insult, perhaps during gestation.

MHC1 may also shed light on the causes of cognitive deficits and diseases of normal ageing. MHC1 is expressed in the brain throughout life, says Shatz. If the relative amount of MHC1 increases, then this imbalance could lead to overpruning. In the elderly, a relative increase in MHC1 in the hippocampus might be responsible for loss of memory and spatial awareness. "If you could get rid of MHC1 you might be able to facilitate recovery of learning and memory," adds Shatz.

Potential treatments are a long way off, but the idea that the brain is an immune-free zone is beginning to change. "These are very unexpected results and they go against the dogma in the field," says Shatz. "The fields of immunology and neuroscience are so separated that if you talk to immunologists about these ideas, they are likely to say that the neuroscientists are crazy, which is great...This is a wonderful moment in science."


My comment: I found this here. It was very hard to find it, although I don't understand why one author writing on another should be paid . At least they should give the links to the scientific articles and then people that are willing to be able to read it in the raw way. Science should be free! Which means not underpaid or running on charity, but that it should be free for distribution.

Single MicroRNA Fine-tunes Innate Immune Response

ScienceDaily (Feb. 24, 2008) — Over the last few years scientists have discovered hundreds of microRNAs--tiny RNAs that regulate the expression of protein-coding genes. However, the functions of these novel molecules in mammals are largely unknown.

Now, scientists in the lab of Whitehead Fellow Fernando Camargo have discovered the first microRNA shown to play a key role in the immune system's early warning system--the innate immune response. The research reveals that microRNA-223 controls the production and activation of granulocytes, white blood cells essential for host defense against invading pathogens. The findings may have implications for the treatment of inflammatory conditions as well as leukemia.

"MicroRNA-223 is unique because its expression is entirely restricted to a specific branch of the immune system," says Camargo. "We found that microRNA-223 is crucial for the development and function of the innate branch of the immune system. Our work suggests that microRNA-223 physiologically fine-tunes both the generation and function of granulocytic cells, delimiting their production and dampening their activation."

The study indicated that microRNA-223 targets Mefc2, a transcription factor that promotes the expansion of granulocyte cell progenitors. (Transcription factors are proteins that regulate gene expression.) By knocking out Mefc2, the authors found that some of the effects caused by microRNA-223 were eliminated.

The researchers demonstrated that mice modified to lack microRNA-223 expression had up to three times as many granulocytes in their bone marrow and blood. Moreover, the granulocytes matured more rapidly and then reacted more aggressively to stimuli. This increased activity caused tissue inflammation and damage within the lungs with age or, in an acute inflammation model, within the liver, muscle and kidneys.

"If you have an infection in the lungs, granulocytes will migrate to the site of the infection and attack," says Jonathan Johnnidis, first author of the paper and a former technician in the Camargo lab, and now a graduate student in molecular biology at the University of Pennsylvania. "Once the infection is cleared granulocytes usually migrate away and settle down. However, in this case they didn't stand down after they were done fighting. Instead they continued an inflammatory response that did more damage."

"Like a hand grenade once you pop the trigger out, these granulocytes are going to explode, regardless of whether they are surrounded by healthy tissue or harmful bacteria," adds Camargo. "Lack of microRNA-223 makes it much easier to activate the grenade."

Camargo plans to further investigate the effect of this microRNA on disease. "Our work suggests that microRNA-223 physiologically fine-tunes both the generation and function of granulocytic cells, delimiting their production and preventing excessive activation," he says. "Also, since many forms of leukemia express diminished levels of microRNA-223, we are investigating how silencing of this microRNA may contribute to the development of that disease."

Journal reference: Jonathan B. Johnnidis, Marian H.Harris, Robert T. Wheeler, Sandra Stehling-Sun, Michael H. Lam, Oktay Kirak, Thijn Brummelkamp, Mark D. Fleming and Fernando D. Camargo. "Regulation of progenitor cell proliferation and granulocyte function by microRNA-223" Nature, Volume 451, Number 781

Adapted from materials provided by Whitehead Institute for Biomedical Research. source

Thursday, 22 May 2008

Corruption in science part 2-the White house

After the If you were interested in my last post on corruption in science, please, check the comment I made that develop further the story with tobacco industry financing Universities and particularly one contract (Virginia Commonwealth's University and Philip Morris) that states the company should approve any research that is being published on the issue and the University shouldn't discuss the contract even if asked. Very independent, huh?
Not moving on.
In today's news you can see how the White House understands the idea of independent science. Interesting, right? Not for a first time, the White House ignores an advice from the experts for no good reason. Or ok, a mistake, for obviously good enough reason, just not very clear one.
So what is corruption and are we ready to fight it? Corruption for me is the opposite of rationality. Rationality offers the best set of decisions for everyone. Corruption provides the best solutions but only to the few in suitable position. All the rest are suffering. Even those in positions will ultimately suffer, because Earth is so deeply interconnected. But because corruption isn't rational, they won't know it before a whole new wave of events has set off and problems get harder to solve. But that's not a problem because the damage is usually indirect and those few people on top never know where it's coming from.
Should we just watch and pick our noses? I don't think so.

White House ignored air quality advice

For many researchers, the Bush administration will be best remembered for the way it has manipulated scientific advice for political ends. The latest evidence of this tactic is a controversial proposal to change the way US air-quality standards are set, according to the Union of Concerned Scientists (UCS) in Washington DC.

When the Environmental Protection Agency said last week that it would beef up air-quality controls by cutting ground-level ozone limits from 80 parts per billion to 75 ppb, it seemed like good news. Ozone can trigger respiratory problems and heart attacks. The new rules should save lives and, by cutting pressure on hospitals, might create financial benefits that outweigh the cost of implementing the changes.

However, around a year ago the EPA's own scientific advisers told the agency that there was "overwhelming" evidence that an even tighter limit of 70 ppb would save thousands more lives. The decision to ignore that advice has angered public-health groups.

Now worse may be to come. The administration wants to reform the process for setting air-quality standards and may allow political appointees to help draft the advisory reports, a job that is currently in the hands of researchers. The UCS fears this will allow the White House to suppress this kind of independent scientific advice in future.

"The interference in science has been a consistent theme of this administration for many years now," says Tim Donaghy of the UCS. "The administration has changed the rules along the way so that, when the next administration gets into office, the role science plays in setting regulations will be greatly diminished." source

Monday, 19 May 2008

Corruption in science or how cigarette company pays for lung-cancer research

Ever wondered what is making a contract with the Devil? Read below and you might find out.

I'm not so critical toward taking "dirty" money for science, science is science and it needs money. And if you're going to save the humanity, who cares where those money are coming from.

But sometimes there is a contradiction-you take money, to write "against" the source of those money, or be objective toward that source. Can you do that? Probably. Will you do it? Probably not. Because what's the motivation behind that financing? Humanity? I doubt it. If a cigarette company pays you to research lung cancers and you happen to find out cigarettes don't cause lung cancers so often, something is definitely smelly. Even if it's not. The least you can do is to inform people who's financing you. To make them aware.

Because as a scientist, you have a responsibility to the society. You can't bear the responsibility for every discovery and its use, but if you consciously put out something wrong and harmful-that's bad. And you have absolutely no excuse.

Cigarette Company Paid for Lung Cancer Study

In October 2006, Dr. Claudia Henschke of Weill Cornell Medical College jolted the cancer world with a study saying that 80 percent of lung cancer deaths could be prevented through widespread use of CT scans.

Small print at the end of the study, published in The New England Journal of Medicine, noted that it had been financed in part by a little-known charity called the Foundation for Lung Cancer: Early Detection, Prevention & Treatment. A review of tax records by The New York Times shows that the foundation was underwritten almost entirely by $3.6 million in grants from the parent company of the Liggett Group, maker of Liggett Select, Eve, Grand Prix, Quest and Pyramid cigarette brands.

The foundation got four grants from the Vector Group, Liggett’s parent, from 2000 to 2003.

Dr. Jeffrey M. Drazen, editor in chief of the medical journal, said he was surprised. “In the seven years that I’ve been here, we have never knowingly published anything supported by” a cigarette maker, Dr. Drazen said.

An increasing number of universities do not accept grants from cigarette makers, and a growing awareness of the influence that companies can have over research outcomes, even when donations are at arm’s length, has led nearly all medical journals and associations to demand that researchers accurately disclose financing sources.

Vector issued a press release on Dec. 4, 2000, saying that it intended to give $2.4 million to Weill Cornell to finance Dr. Henschke’s research. Articles in Business Week and USA Today mentioned the gift. No mention was made of the foundation, begun so hastily that its 2000 tax return stated “not yet organized.”

Paul Caminiti, a Vector spokesman, confirmed that the company donated $3.6 million to the foundation over three years. The company “had no control or influence over the research,” he said.

Prominent cancer researchers and journal editors, told of the foundation by The Times, said they were stunned to learn of Dr. Henschke’s association with Liggett. Cigarette makers are so reviled among cancer advocates and researchers that any association with the industry can taint researchers and bar their work from being published.

“If you’re using blood money, you need to tell people you’re using blood money,” said Dr. Otis Brawley, chief medical officer of the American Cancer Society. The society gave Dr. Henschke more than $100,000 in grants from 2004 to 2007, money it would not have provided had it known of Liggett’s grants, Dr. Brawley said.

In an e-mail message, Drs. Henschke and Yankelevitz wrote, “It seems clear that you are trying to suggest that Cornell was trying to conceal this gift, which is entirely false.”

In the Vector press release, Dr. Henschke was quoted as saying that, thanks to the Vector grants, “we have raised the initial funding needed to support this important research and data collection on the effectiveness of spiral CT screening.”

Dr. Henschke’s work, while controversial among cancer researchers, has been embraced by many lung-cancer advocacy organizations, which have pushed for legislation in California, New York and Massachusetts to create trust funds to pay for lung cancer screening — often with language tailored to benefit Dr. Henschke’s group.

In New York, a bill would create a $10 million fund “to carry out lung cancer early detection research using computer tomography (CT) scanning” at a place “that was established by the multi-institutional, multi-disciplinary research program that began at 22 sites in the state in the year 1991,” a description that could only fit Dr. Henschke’s group.

But the disclosure that Dr. Henschke’s work was in part underwritten by grants from a cigarette maker will undercut those efforts, prominent cancer researchers said.

Corporate financing can have subtle effects on research and lead to unconscious bias. Studies have shown that sponsored research tends to reach conclusions that favor the sponsor, which is why disclosure is encouraged. The tobacco industry has a long history of underwriting research — sometimes through independent-sounding foundations — to make cigarettes seem less dangerous.

Since 1999, Dr. Henschke has asserted that annual CT scans of smokers and former smokers would detect lung cancer when tumors are small enough to be cured, preventing as many as 80 percent of the 160,000 deaths a year from lung cancer, by far the biggest cause of cancer deaths in the United States.

Her 2006 study said that, after screening 31,567 people from seven countries, CT scans uncovered 484 lung cancers, 412 of them at a very early stage. Three years later, most of those patients were still alive, and she projected that 80 percent would be alive after 10 years and assumed that they would have died without the screens.

Critics question both her survival projections and her assumption that all would have died without screening. Indeed, most in the cancer establishment say that Dr. Henschke has yet to prove her case. CT scans have radiation risks and sometimes detect cancers that would not have progressed, leading to risky procedures like biopsies and lung surgery when not needed.


Saturday, 17 May 2008

The massacre of bats

Bats Perish, and No One Knows Why

Published: March 25, 2008

It was broad daylight in the middle of winter, and bats flew out of the mine about one a minute. Some had fallen to the ground where they flailed around on the snow like tiny wind-broken umbrellas, using the thumbs at the top joint of their wings to gain their balance.

All would be dead by nightfall. Mr. Hicks, a mammal specialist with the state’s Environmental Conservation Department, said: “Bats don’t fly in the daytime, and bats don’t fly in the winter. Every bat you see out here is a ‘dead bat flying,’ so to speak.”

In what is one of the worst calamities to hit bat populations in the United States, on average 90 percent of the hibernating bats in four caves and mines in New York have died since last winter.

Wildlife biologists fear a significant die-off in about 15 caves and mines in New York, as well as at sites in Massachusetts and Vermont. Whatever is killing the bats leaves them unusually thin and, in some cases, dotted with a white fungus. Bat experts fear that what they call White Nose Syndrome may spell doom for several species that keep insect pests under control.

Researchers have yet to determine whether the bats are being killed by a virus, bacteria, toxin, environmental hazard, metabolic disorder or fungus. Some have been found with pneumonia, but that and the fungus are believed to be secondary symptoms.

Merlin Tuttle, the president of Bat Conservation International, an education and research group in Austin, Tex., said: “So far as we can tell at this point, this may be the most serious threat to North American bats we’ve experienced in recorded history. “

This month, Mr. Hicks took a team from the Environmental Conservation Department into the hibernaculum that has sheltered 200,000 bats in past years, mostly little brown bats (Myotis lucifugus) and federally endangered Indiana bats (Myotis sodalis), with the world’s second largest concentration of small-footed bats (Myotis leibii).

In a dank galley of the mine, Mr. Hicks asked everyone to count how many out of 100 bats had white noses. About half the bats in one galley did. They would be dead by April, he said.

In January 2007, a cave explorer reported an unusual number of bats flying near the entrance of a cavern near Albany. In March and April, thousands of dead bats were found in three other mines and caves. In one case, half the dead or living bats had the fungus.

One cave had 15,584 bats in 2005, 6,735 in 2007 and an estimated 1,500 this winter. Another went from 1,329 bats in 2006 to 38 this winter. Some biologists fear that 250,000 bats could die this year.

Since September, when hibernation began, dead or dying bats have been found at 15 sites in New York. Most of them had been visited by people who had been at the original four sites last winter, leading researchers to suspect that humans could transmit the problem.

In Vermont, Scott Darling, a wildlife biologist with the Fish and Wildlife Department, said: “The last tally that I have is approximately 20 sites in New York, 4 in Vermont and 2 in Massachusetts. We only have estimates of the numbers of bats in the affected sites — more or less 500,000. It is impossible for us to count the dead bats, as many have flown away from the caves and died — we have over 90 reports from citizens across Vermont — as well as many are still dying.”

People are not believed to be susceptible to the affliction. But New Jersey, New York and Vermont have advised everyone to stay out of all caverns that might have bats. Visitors to affected caves and mines are asked to decontaminate all clothing, boots, ropes and other gear, as well as the car trunks that transport them.

It’s very scary and a little overwhelming from a biologist’s perspective,” Ms. von Oettingen said. “If we can’t contain it, we’re going to see extinctions of listed species, and some of species that are not even listed.”

Biologists are concerned that if the bats are being killed by something contagious either in the caves or elsewhere, it could spread rapidly, because bats can migrate hundreds of miles in any direction to their summer homes, known as maternity roosts. At those sites, females usually give birth to one pup a year, an added challenge for dropping populations.

Nursing females can eat up to half their weight in insects a day, Mr. Hicks said.

Other researchers want to know whether recently introduced pesticides, including those released to stop West Nile virus, may be contributing to the problem, either through a toxin or by greatly reducing the bat’s food source.

The die-offs are big enough that they may have economic effects. A study of Brazilian free-tailed bats in southwestern Texas found that their presence saved cotton farmers a sixth to an eighth of the cash value of their crops by consuming insect pests.source

My comment:Weird, huh? Reminds you of the movie "The happening"? I know it's not on air yet, but the story goes in similar lines. Anyway, I think that any massive die-off of living things should be investigated thoroughly. We simply have to know what's going on. Because we could be the next.

Thursday, 15 May 2008

TB crisis in South Africa

TB Patients Chafe Under Lockdown in South Africa

Published: March 25, 2008

PORT ELIZABETH, South Africa — The Jose Pearson TB Hospital here is like a prison for the sick. It is encircled by three fences topped with coils of razor wire to keep patients infected with lethal strains of tuberculosis from escaping.

But at Christmastime and again around Easter, dozens of them cut holes in the fences, slipped through electrified wires or pushed through the gates in a desperate bid to spend the holidays with their families. Patients have been tracked down and forced to return; the hospital has quadrupled the number of guards. Many patients fear they will get out of here only in a coffin.

“We’re being held here like prisoners, but we didn’t commit a crime,” Siyasanga Lukas, 20, who has been here since 2006, said before escaping last week. “I’ve seen people die and die and die. The only discharge you get from this place is to the mortuary.”

Struggling to contain a dangerous epidemic of extensively drug-resistant tuberculosis, known as XDR-TB, the South African government’s policy is to hospitalize those unlucky enough to have the disease until they are no longer infectious. Hospitals in two of the three provinces with the most cases — here in the Eastern Cape, as well as in the Western Cape — have sought court orders to compel the return of runaways.

The public health threat is grave. The disease spreads through the air when patients cough and sneeze. It is resistant to the most effective drugs. And in South Africa, where these resistant strains of tuberculosis have reached every province and prey on those whose immune systems are weakened by AIDS, it will kill many, if not most, of those who contract it.

As extensively drug-resistant TB rapidly emerges as a global threat to public health — one found in 45 countries — South Africa is grappling with a sticky ethical problem: how to balance the liberty of individual patients against the need to protect society.

It is a quandary that has recurred over the past century, not least in New York City, where uncooperative TB patients were confined to North Brother Island in the East River in the early 1900s and to Rikers Island in the 1950s.

In the early 1990s, when New York faced its own outbreak of drug-resistant TB, the city treated people as outpatients and locked them up in hospitals only as a last resort.

Most other countries are now treating drug-resistant TB on a voluntary basis, public health experts say. But health officials here contend that the best way to protect society is to isolate patients in TB hospitals. Infected people cannot be relied on to avoid public places, they say. And treating people in their homes has serious risks: Patients from rural areas often live in windowless shacks where families sleep jammed in a single room — ideal conditions for spreading the disease.

“XDR is like biological warfare,” said Dr. Bongani Lujabe, the chief medical officer at Jose Pearson hospital. “If you let it loose, you decimate a population, especially in poor communities with a high prevalence of H.I.V./AIDS.”

But other public health experts say overcrowded, poorly ventilated hospitals have themselves been a driving force in spreading the disease in South Africa. The public would be safer if patients were treated at home, they say, with regular monitoring by health workers and contagion-control measures for the family. Locking up the sick until death will also discourage those with undiagnosed cases from coming forward, most likely driving the epidemic underground.

Some 563 people were confirmed with extensively drug-resistant TB last year in South Africa and started on treatment, compared with only 20 cases in the United States from 2000 through 2006. A third of those patients in South Africa died in 2007; more than 300 remained in hospitals.

Further complicating matters, South Africa’s provinces have taken different approaches to deciding how long to hospitalize people with XDR-TB. In KwaZulu-Natal, the other province with the most cases, the main hospital is discharging patients after six months of treatment, even if they remain infectious, to make room for new patients who have a better chance of being cured. The province is rapidly adding beds, part of a national expansion of hospital capacity for XDR-TB.

When news of South Africa’s outbreak of extensively drug-resistant TB was announced in Toronto in 2006 at an international AIDS meeting, it sent shudders through the ranks of infectious-disease specialists. These virulent strains had rapidly killed 52 of 53 patients.

Drug resistance emerges in large part because health care systems too often have failed to ensure that patients successfully complete treatments with first- and second-line drugs, according to international health officials.

The medicines for ordinary TB here cost about $36 and take six to eight months to cure the patient. The drugs for XDR-TB cost about $7,000, and treatment lasts two years. At the start, patients endure four to six months of painful daily injections in the buttocks or thigh, a morning ritual at Jose Pearson that leaves faces scrunched up in agony. A 10-year-old boy whose mother recently died here of the disease rubbed cream into his backside to relieve the ache. He now lives on the XDR-TB ward as its solitary child, with no family around.

My comment: I know it sounds cruel, but I do think this is the best way for everybody. And I think it presents interesting problem to think over. Is it better to lock the diseased for the safety of the healthy, ignoring their rights or is it better to protect their rights and just deal with the situation. I'm sure everyone will opt for the first option. That is until he or she isn't infected.
For me, there should be a third option. Like keeping the infected in isolated rooms or at least putting them in rooms according to the degree of the infection. I don't know, it's hard to say what is best, but this treatment is preventing infected people from curing. Which surely breaks few fundamental human rights.
Not to mention that this facilities should be use to study the resistance of TB and the blood of both surviving and death. Just watching them die is useless. You have to take the best out of it. And the is what science is for-to take the best out of the worst and prevent it happening ever again.

Saturday, 10 May 2008


Virtual massage' can relieve amputees' phantom limb pain

Amputees who experience phantom limb pain could find relief in a surprisingly simple way - by paying more attention to the people around them.

Phantom limbs occur when an amputee feels the often painful sensation of touch arising from a limb that is no longer present. Working with combat veterans, Vilayanur Ramachandran, of the Center for Brain and Cognition at the University of California, San Diego, has now discovered a potential cure.

His treatment makes use of the newly discovered properties of mirror neurons. Mirror neurons fire when a person performs an intentional action - such as waving - and also when they observe someone else performing the same action. They are thought to help us predict the intentions of others by creating a "virtual reality" simulation of the action in our minds.

"You also find cells like this for touch," says Ramachandran. "They fire when you touch yourself and when you watch someone else being touched in the same location."

Massaging the skin helps relieve a painful sensation by restoring blood flow and activating sensory fibres, which inhibit pain messages to the brain. By watching another person rubbing their hand, these amputees are apparently tapping into this latter mechanism, says Ramachandran. source

Why men should pair off with younger women

Mick Jagger, Rupert Murdoch and Michael Douglas all have the right idea, evolutionarily speaking. Statistics show that monogamous men have the most children if they marry women younger than themselves. How much younger is the key question.

Last year, a study of Swedish census information suggested a 4 to 6-year age gap is best, but new research has found that in some circumstances a surprisingly large gap – 15 years – is the optimum.

Martin Fieder at the University of Vienna and Susanne Huber of the University of Veterinary Medicine, also in Vienna, Austria, studied the Swedish data and found that a simple equation related the age difference of the parents to the number of offspring. For people who had maintained monogamous relationships throughout adulthood, the most children were found in couples where the man was 4.0 to 5.9 years older than the woman.

The probable reasons behind this state of affairs are not controversial: "Men want women younger than themselves because they are physically attractive," says Fieder, while women tend to prioritise a partner who can provide security and stability, and so tend to opt for older men. source

Anti-ecstasy antibodies

In recent years, crystal meth (methamphetamine) and ecstasy (MDMA) have become some of America's top problem drugs. Meth can cause severe problems in the cardiovascular and central nervous systems. Furthermore, because there is no way to remove the drug from the body, therapies tend to focus on treating its side-effects.

But antibodies that bind to methamphetamines and methamphetamine-like compounds to effectively remove them from the bloodstream could change that. Michael Owens, director of the Center for Alcohol and Drug Abuse at the University of Arkansas, US, and colleagues claim to have developed a way to generate them.

The team have not yet tested the antibodies in humans, only in rats, but they say that a single injection can reduce the level of drug within the bloodstream for several days. By binding to drug molecules, the antibodies prevent them from reaching tissues like the heart and brain, and mark the compounds for clean up by the body.

Owens says that his team's antibodies bind to many drugs from the same chemical "family". Cocaine and nicotine are single, specific compounds but methamphetamines share a basic chemical skeleton with many other drugs. So-called "designer drugs" are made by modifying this skeleton to create specific effects. The team say their therapy works for meth, amphetamines and ecstasy.

Read the full ecstasy antibody patent application. source

Genome is a snip at $60,000

WHEN the cost of sequencing a human genome gets down to the price of a family car, then the era of personalised genomics will truly be upon us. This was the prediction from James Watson, co-discoverer of the structure of DNA, in an interview with New Scientist (20 October 2007, p 58) last year.

Well, it's getting close. Last week, Applied Biosystems of Foster City, California, announced that it had sequenced the genome of a Nigerian man at a cost of less than $60,000, excluding labour. "We are committed to pushing the limits of this technology," says Shaf Yousaf of Applied Biosystems. "These prices will come down further in the next year or two."

Several companies are already offering partial personal-genome scans, based on single-letter changes in parts of the genome, for about $1000. Cheap full-genome sequencing would help us to understand why people differ from others, and could help determine whether someone was at risk of a particular disease. source

Carbon monoxide could fight disease

CARBON monoxide, that notorious killer, could also be a life-saver. A small quantity of the gas given to people with a potentially fatal lung disease led to signs of improvement in their condition. It is also showing promise for treating other chronic and acute inflammatory conditions.

At high concentrations, carbon monoxide (CO) displaces oxygen from red blood cells, and in effect kills by asphyxiation. Its healing effects have emerged in ongoing experiments in animals, which show that low levels of CO can reduce inflammation and oxidative damage to tissue.

In fact CO is produced as a normal part of a reaction that generates antioxidants in the blood when tissues are inflamed. It was once dismissed as a worthless by-product of this reaction, but now it seems that the gas itself has the ability to calm inflammation in humans too. source

More on that study:here

Mic based on fly ear can pinpoint sounds

IT MAY be inspired by a humble fly, but a sensor just a couple of centimetres in diameter could turn out to be the best microphone yet for pinpointing the source of a sound. The device could be added to hearing aids or mounted on autonomous robotic vehicles to locate cries for help during disaster relief efforts.

Humans detect slight differences in the timing of sound waves as they arrive at each eardrum and use this to reconstruct where a sound is coming from. However, the differences are only noticeable because our eardrums are at least a few centimetres apart. In contrast, despite the small distance between its two eardrums, the parasitic fly Ormia ochracea can pinpoint a sound source far more accurately than humans.

Its secret is a chitin bridge that links the fly's eardrums. source

Wednesday, 7 May 2008

Fighting meningitis and aging!

The End of Aging? Inside the New Hunt for a Cure to Growing Old

By Glenn Harlan Reynolds
Popular Mechanics

We’ve long regarded aging as something almost mystical or supernatural, and it’s easy to see why. Unlike, say, smallpox, aging doesn’t come on suddenly or spread from person to person. You also don’t recover from it, as you do from most infectious diseases. It happens gradually, and it’s pretty much unrelenting. Eyesight dims, joints get stiff and achy, teeth go bad and, in general, things just keep getting worse until death arrives.

But research demonstrates that aging isn’t a supernatural process; it’s a physical one that gradually occurs as systems wear out beyond the body’s ability to repair them. Cells fill up with metabolic debris called lipofuscin that they can’t digest, accompanied by decreasing functionality. They also undergo glycation, gumming up and caramelizing with sugars that have bonded to proteins. Mitochondrial DNA can suffer mutations, and the body slowly loses stem cells, which weakens healing and repair.

Aging is breakdown, but broken things can be fixed.

Biogerontologists like Aubrey de Grey, author of Ending Aging, believe that living longer is a fairly straightforward engineering problem: Find out what breaks and fix it. De Grey promotes an approach he calls Strategies for Engineered Negligible Senescence, or SENS. It identifies seven specific breakdowns and attempts to attack each of them in turn. He and others are researching longevity with support from nonprofits and an X Prize approach aimed at extending the life span of mice. (Researchers call it the Mprize, a reference to their quest to engineer the “Methuselah mouse.”). De Grey says that it will probably be 20 or 30 years before we see effective antiaging drugs on the market.

Scientists have already identified more modest life extenders. It’s pretty thoroughly established that red wine’s resveratrol activates the SIRT-1 gene, which seems to clean out intracellular gunk. (The gene is also triggered by calorie restriction.) Studies show that rats dosed with resveratrol—or given low-calorie diets—seem to live longer and remain far more vital than ordinary rats. Sirtris Pharmaceuticals is currently conducting human testing of a drug called SRT501 as a treatment for diabetes, but it may also hold promise for retarding the aging process and alleviating a number of inflammatory diseases that go with getting older.

At Stanford, researchers have reversed the aging of skin in mice, making it look and act like young skin, which contains cells that reproduce rapidly. This treatment isn’t ready for humans, but it suggests an approach. And given the popularity of cosmetics that merely address the appearance of aging, it seems likely a product that actually produces new skin would sell like hot cakes.

Meanwhile, commercial res­veratrol supplements are available, and people are taking them, including some scientists in the field. As part of the research for this column, I started taking one. To find out if it’s working, click here for a follow-up on my experience.

On the flip side, people often see extended longevity as dubious, envisioning extra years in the nursing home. As Jay Leno says, “People tell you to eat right and exercise, but that only gives you more years in your 80s. Who needs that? What I really want are more years in my 20s.” New treatments for aging would give us just that—or at least healthier years in our 60s and 70s. The goal isn’t just more years in your life, but more life in your years.

On a societal level, the extension of peoples’ productive working lives could pay huge dividends. If people stay youthful longer, we’ll see less pressure on the stressed-out social security systems of most industrialized countries. If 65-year-olds were as vigorous as 35-year-olds, or even 45-year-olds, there would be no reason to fund their retirement. Pushing the retirement age back a decade or two could save trillions. And, of course, if you can actually reverse aging, the whole notion of retirement becomes obsolete. source

My comment: Does it need a comment at all? I'm grabbing the red wine and hoping for the best!:) Ok on a serious note, I often meet a fear in people what will happen if we increase our life with another 20 or 50 years. I like the last paragraph of the article in that sense. A century ago, the life expectancy were 30 years lower. Are we now more miserable than then because we live longer? I doubt it!

Uganda: Vaccine Program Vanquishes a Dangerous Type of Childhood Meningitis

Published: March 11, 2008

A dangerous type of childhood meningitis has been virtually eliminated in Uganda in just five years after a vaccine was introduced, according to a study released this week.

That should save the lives of 5,000 children a year, the authors estimated.

“This is the first time we’ve seen this kind of impact, a 100 percent drop,” said Dr. Julian Lob-Levyt, executive secretary of the GAVI Alliance, which paid for the vaccines. “We hope this can be repeated in other countries.”

The study, released by the World Health Organization, monitored cases from 2001 to 2006.

The vaccine, known as Hib, protects against haemophilus influenzae type B, a bacterium that can inflame the lining of the brain or cause pneumonia. Each year, it kills 386,000 children globally. Three million more have severe side effects like deafness, paralysis or retardation.

The vaccine has existed since 1991 but was rare in the third world until the creation of the alliance — originally the Global Alliance for Vaccines and Immunization — in 2000. Even at prices offered to poor countries, it had cost $7 , seven times as much as other vaccines.

The alliance joins United Nations health agencies, the World Bank, vaccine companies, universities and the Bill & Melinda Gates Foundation, and receives money from $1 billion in bonds issued by the International Finance Facility for Immunization.

By guaranteeing large orders, the alliance tries to drive down the price of vaccines. It estimates that it has helped prevent 2.3 million early deaths since 2000.

In wealthy countries, Hib vaccine is typically given at the age of 8 weeks. source

My comment: Unfortunately we here don't have that vaccine, but because meningitis is one of my greatest fears, I think it's great to see that vaccine working. I'm just waiting to see if it's going to have some side effects before I praise it.