Wednesday, December 31, 2008

The Dark Matter and Dark Energy 96% of the Universe

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Astronomers Aim to Grasp Mysterious Dark Matter
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special To – Mon Dec 29, 9:07 am ET AFP/NASA/File – This August 2008 image taken by the Hubble Space Telescope and Chandra X-ray Observatory show a clear … For the past quarter century, dark matter has been a mystery we've just had to live with. But the time may be getting close when science can finally unveil what this befuddling stuff is that makes up most of the matter in the universe.

Dark matter can't be seen. Nobody even knows what it is. But it must be there, because without it galaxies would fly apart.

Upcoming experiments on Earth such as the Large Hadron Collider (LHC) particle accelerator in Switzerland, and a new spacecraft called Gaia set to launch in 2011, could be the key to closing the case on one of the biggest unsolved mysteries in science.

A disturbing truth is accepted by most astronomers: There is a lot more stuff in the universe than what we can see. Scientists now think visible matter — all the planets, stars, and galaxies that shine down on us — represents only about 4 percent of the mass-energy budget of the universe, while dark matter and its even more esoteric cousin, dark energy, make up the rest.

"There is no consensus actually at all as to what dark matter is," said Gerard Gilmore, an astronomer at the University of Cambridge who wrote a recent essay for the Dec. 5 issue of the journal Science about the search for dark matter.

A leading hypothesis posits that dark matter is composed of some kind of exotic particle, yet to be detected, that doesn't interact with light, so we can't see it. One such theorized class of particles is called WIMPs (Weakly interacting massive particles), which are thought to be neutral in charge and weigh more than 100 times the mass of a proton.

Atom smasher

The newly-opened LHC, a 17-mile-long (27 kilometer-long) underground ring in which sprays of protons speed around and crash into each other, could be the first experiment to detect WIMPS. The particle accelerator officially went online in September 2008, but was halted shortly after due to a fault with its construction — it's due to go back online in the summer of 2009. Since the LHC is the largest and most powerful atom smasher ever built, its collisions could produce the extremely high energies needed to create the elusive particles.

In fact, the LHC will likely create a host of never-before-seen particles, opening up a realm of the universe that physicists have been eager to explore.

"The assumption is, there will be whole families of new types of particles," Gilmore said in a podcast interview with a reporter from Science. "The challenge then is to say, well OK, we now then have a new set of ingredients in our recipe for how nature is put together, but what is the recipe that uses this set of ingredients? I.e., what mix of these particles does nature actually use to create the universe, and how?"

Weighing the universe

That's where Gaia comes in. The European Space Agency satellite is designed to measure positions and speeds of about 1 billion nearby stars with unprecedented precision. Its vision is so sharp it should be able to discern the equivalent of a shirt button on the surface of the moon as seen from Earth, Gilmore said.

By establishing where things are in our galaxy, the spacecraft will help scientists measure the weight and distribution of mass in the Milky Way in much greater detail than ever before. These measurements are vital for models that attempt to describe how the pull of dark matter has shaped our galaxy.

"What Gaia will do is measure the distances of stuff and measure how they're moving in three dimensions around space to much better precision than we've had before, which will allow us to weigh things on all sorts of scales down to the smallest scales we can find," Gilmore said. "They will tell us to exquisite precision how the dark matter is distributed in space, which is the recipe we need to determine its properties."

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Friday, December 26, 2008

Star of Bethlehem: Eclipse of Jupiter or Supernova?

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Star of wonder

By Rebecca Ellis

A comet, an eclipse, a supernova, an alignment of planets - was the Star of Bethlehem, said to have led the wise men to the Baby Jesus, a real astronomical event?

Some 2,000 years ago, wise men saw an incredible star shining over the Holy Land. It was their signal to embark on an epic journey to visit the new Messiah. But what exactly was the Star of Bethlehem?

Modern science is unravelling the mystery behind one of the most famous astronomical stories in history. New developments in technology allow astronomers to map the ancient night skies with extraordinary accuracy.

As they study the movements of the planets and stars, experts are challenging the traditional assumption that it was a blazing comet - instead there are several unusual astronomical events that the wise men could have seen in the skies.

The Bible tells us remarkably little about the star, with only the Gospel of St Matthew mentioning it. He records the wise men asking: "Where is he who has been born King of the Jews? For we have seen his star in the east and have come to worship him."

No date or detailed description is given. Even the identity of the men is obscure. Rather than the kings of popular imagination, the wise men are thought to have been priests from Persia, known as Magi. Keen astrologers who looked to the stars for guidance, the Magi combined science with faith to predict the birth of a new Messiah.

So what prompted them to travel to Bethlehem? Most experts agree Jesus was born in 4BC or earlier, as King Herod, who ruled over Judea at the time, is recorded as dying in 4BC. Now astronomers have identified four celestial events in this period that could have been the Star of Bethlehem.


An ancient clay tablet, now in the British Museum, is a key part of one theory which says the star was a rare series of planetary meetings, known as a triple conjunction.

This happened between Jupiter and Saturn and occurred in the night sky in 7BC, says Dr David Hughes, emeritus professor of astronomy at the University of Sheffield.

Jupiter, the royal star, and Saturn came together three times over several months. Significantly, this happened during the constellation of Pisces, a sign associated with Israel.

There is evidence on the clay tablet that Persian astronomers predicted this. The tablet calculates solar, lunar and planetary activity for that year, and describes the conjunctions.


A 2,000-year-old coin, minted north of Judea, is part of the evidence behind another theory. Dr Mike Molnar of Rutgers University, New Jersey, believes the star could have been an occultation, or eclipse, of the moon with Jupiter on 17 April 6BC.

He argues the Magi saw the star in the constellation of Aries, not Pisces. The coin depicts Aries the ram leaping across the sky and looking back at a star.

According to astrological texts from the time, Aries ruled over Judea, with Jerusalem as the capital of the Near East, making it the sign of the Jews.

Dr Molnar believes the Magi saw this eclipse. Just before sunrise, Jupiter would have risen in the east, just as St Matthew describes their sighting of the Star. Then, as the moon passed directly between Earth and Jupiter, the kingmaker planet was hidden from view.


Some think the star could have been a much bigger celestial event. European Space Agency astronomer Dr Mark Kidger believes it would have taken more than unusual planetary movements to persuade such seasoned astronomical experts to travel to Judea.

The Magi could have seen a star entering its supernova phase, one of the most energetic and explosive events known to astronomers.

He has even identified a candidate - DO Aquilae - which erupted in 1927 and is likely to have erupted several times previously. If it had erupted 2,000 years ago, the Magi would have seen it just above the horizon, in the east.

He hopes radio telescopes in the future will be able to detect a faint bubble of expanding gas around Aquilae and calculate when exactly the bubble started to expand.


One theory has the most surprising twist. The date for celebrating Christmas was only fixed centuries after the event - and is questioned by many - but Texan law professor and astronomer Rick Larson believes Jesus really could have been born on 25 December. But on 25 December 2BC.

Unlike other astronomers, he has looked at later celestial events because he thinks the calculation of King Herod's death is inaccurate. The 4BC date is based on the writings of the historian Josephus, but every Josephus manuscript he has studied dating before 1544 is consistent with Herod having died in 1BC.

In 2BC Jupiter met up with one of the brightest stars in the sky, Regulus, known by the Magi as the "little king". Nine months later, Jupiter met Venus, known as the mother planet. These meetings would have been symbolically significant, as was the timescale involved.

The planets would have seemed so close they would have looked like one bright light in the sky. Professor Larson believes this light was what prompted the Magi to travel to the east. As they made their way, Jupiter continued to move across the sky until it appeared to stand still over Bethlehem.

Below is a selection of your comments.

Could anyone provide a simple text or explanation for young children? At school we have been looking out for the "Christmas Star" in the early evening and morning skies, but as a non-astronomer I don't really know how to explain it.
Catherine Vincer, Taunton, Somerset

Catherine, a lot of planetaria around the country will be running a Christmas Star show at the moment. There's a map of most sites in the UK at
Andy, Newcastle

Surely trying to find a factual explanation for a more than likely fictitious event is impossible. There are just as many interpretations for the story of the birth of Jesus as there are possibilities for notable cosmological events around the same time.
Mike Shawcross, London

Back in 2007 The Archbishop of Canterbury said that the Christmas story of the Three Wise Men was nothing but a 'legend'. Even the heads of this religion don't believe a word of it.
Nigel Martin, High Wycombe

I think some of you need to brush up on your historical facts before making such bold statements. Anyway, if you take the viewpoint that God is real, which you must do in order to give this idea serious consideration rather than a passing thought, then you have to consider that God is all powerful by definition and can bring about events such as this in a manner that he chooses.

From this viewpoint, He created science and can use it or he can "break the rules" and use supernatural methods ie angels etc. This being said, the reason why the star is not such a big issue and is merely mentioned in Matthew is because he is talking about the coming of the Messiah. At Christmas diner I will not spend much time noticing the sprouts but I will definitely relish the turkey.
Dave, High Wycombe

The star of Bethlehem was not any of the astronomical events listed here. It was a metaphor. Light is a common metaphor throughout the Jewish and Christian scriptures, and is almost universal in other religions too. We should not spend time searching for a historical event to explain this star; rather we should be contemplating what it means for a child born 2,000 years to be described as "the light of the world".
David Brown, London

Whatever the explanation for the star (and it's a question scientists could argue about for another 2000 years), the point is that this marked the arrival of God on earth in human form. The creator of the stars, planets and everything that exists had arrived in Bethlehem and He wasn't going to let that go unnoticed.
Julia, Birmingham

I thought that the more scholarly New Testament experts were generally agreed that the Nativity stories were made up out of whole cloth, so as to make ancient prophecies appear to be fulfilled. Moreover, if a star or planet is spotted in the east, it will be in the west a few hours later (unless it is only visible in the east just before dawn); and if the Magi came from the east, how could they have seen the star in the east and over Bethlehem?
Tim Weakley, Dundee

One problem with working out what's meant by the passage in Matthew is the ambiguity of "in the east"; are the Magi in the east, or is the star? Persian Magi would have travelled west to Jerusalem, not east as Prof Larson's theory seems to require. And Aquilae is not (yet) a supernova, but has erupted as a nova (a different sort of event) several times - dating earlier novae is prohibitively difficult, though.
Alex Roberts, London, UK

A very appropriate signal from the Almighty, whatever the explanation.
Cdr David Aldrich, Exford, Somerset, UK

Interesting, but in the story of Jesus this was no ordinary star - it doesn't stay on high, but moves as a guide and comes to rest very near the infant Jesus (Matthew 2.9-10). In the NRSV translation it says "until it stopped".

This links onto how the ancients and Jews viewed stars. The ancients believed stars to be animate beings and the Jews identified them with angels (look at Job 38.7). The prominent Greek medieval theologian Theophylact and the New Testament Apocryphal book the Arabic Gospel of the Infancy must be right in identifying the star with an angel, and you can compare this with the angelic guide of the Exodus (Ex 23.20,23, 32.34).

The star was about confirming who Jesus was. Of course it depends on what you believe in as to whether you take this view. Ultimately though looking for a scientific explanation misses Matthew's point.
Mike Lowe, Burton on Trent

Since the story of the wise men is only mentioned in Matthew's gospel, which itself was not written until several decades after the time of Jesus, probably not even by Matthew, then why consider the story of the wise men to be at all reliable?

A lot more needs to be explained than just the nature of the "star" - how they knew to go to Bethlehem, for instance, when Jerusalem would surely have been the more obvious target, and how they precisely located Jesus within that town.

The most probable explanation is surely that this story is not true and was added later by Christian writers to support their case that Jesus was divine - after all, it wouldn't be the first instance where a story in the Bible has been exaggerated.
Peter, London

Another interesting possibility is a metaphysical explanation. When working with the energy system, known as the chakra system, one of the energy centres is known as the Christ centre, and this is felt on the forehead. When meditating on this energy point , a bright star of energy can be perceived and this fills you with joy and bliss.

Reference to this has been around for several thousand years in the Hindu tradition. The wise men of the east followed their intuition or spiritual guidance to find Christ. The Star of the East is a synonym for the Christ energy point, something we all have access to within ourselves.
Cam, Congleton, UK

More likely the "star" was an invention of second century Christians to make their myths more closely follow Old Testament prophecies.
Paul Williams, London

Science cannot answer this. The star was not a naturally occurring heavenly body as the Bible clearly states that the star led the astrologers first to King Herod and then to Jesus, after Herod claimed he too wanted to worship the Christ.

A naturally occurring celestial body would not stop above a specific location to identify the whereabouts of Jesus. The star also put the life of Jesus in jeopardy by its first leading the Magi to Herod who wanted to kill the Messiah who he saw as a threat to his reign.

The result of this chain of events resulted in the murder of all male children in Bethlehem. Logically the origin of the "star" was evil and supernatural. If this was a naturally occurring event God would surely have foreseen it and would not have allowed the life of his son to be endangered by its presence.
Chris, Nottingham, UK

The "great northern star" is the star Sirius that appears to follow the sun (Jesus) at that time of year if you live in that part of the world. The 12 disciples represent the 12 signs of the zodiac and the reference to fishes is a reference to the movement into Pisces which according to the calendar was when the story of Christ came about.

All religion is merely interpretation of astrological events. So the story of Christ did happen but only when you realise it was just the stars. No real man ever existed all historical evidence of the time proves this.

Sam, this is slightly incorrect as there is a wealth of supporting evidence for an individual called Jesus being alive and active at this time. Whether the star was a supernova, conjunction of planets or early alien spaceship it is hard to tell. One must look at the source of the original "story" and decide whether it can be verified at all
Jenny, Southampton

The great north star is not Sirius, but Polaris. Sirius is much brighter than Polaris and is often mistaken for the North Star, as people assume the North Star is the brightest. Which can be quite embarrassing if you're navigating by it as I don't think its ascension/declination ever approach that of Polaris.
David, Highworth

If we start going down the route of "metaphysics" and metaphors (Sun = Jesus?) then why discuss the physical possibilities of the Star at all? You have to accept that there is some historical accuracy in the New Testament otherwise why enter into the debate?

I think the historical accuracy of the New Testament DOES stand up to scrutiny, otherwise all the atheists and other sceptics would have torn it apart by now, but they can't. So, what was the nature of the Star? Well, I think any one of the scientific explanations sounds good to me.
John Baharie, Sunderland

I am a Shia Muslim. I believer Jesus was born on 25th day of 11th month of the lunar calendar. We celebrated his birth last month. I think when you calculate it back, you get the date of Jesus' birth accurately. As to the star, it was Angel Gabriel coming down to Earth.
Ali, Manchester, UK

Story from BBC NEWS:

Published: 2008/12/23 09:27:25 GMT


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Wednesday, November 26, 2008

The Golden Age of Piracy

Global7 the new Millennial Renaissance Vision for the Globe
Features - November 26, 2008

What Would Blackbeard Do? Why Piracy Pays
Q&A with economist Peter Leeson
By John Matson

In the so-called golden age of piracy, spanning the late 17th and early 18th centuries, pirate captains such as Blackbeard and Bartholomew Roberts roamed the seas in search of plunder.

Their fearsome exploits became the stuff of lore, inspiring countless films, books, amusement-park rides and, ahem, more films. But those same exploits also fed a reputation that facilitated their activities—a sort of brand name that was widely known and was instantly recognizable by its logo, the Jolly Roger (a black flag with a skull and crossbones).

In a new paper, "Pirational Choice," and in the forthcoming book The Invisible Hook: The Hidden Economics of Pirates, economist Peter Leeson of George Mason University in Fairfax, Va., examines the inner workings of pirate organizations.

He makes the case that pirates, far from being the unrestrained barbarians of legend, were actually shrewd businessmen who carefully calculated their actions to increase their haul while minimizing risk and expenditure. Leeson spoke to us recently about his research and how modern-day pirates stack up against their golden-age counterparts. An edited transcript follows.

Your central thesis seems to be that pirates are not the roving ruthless barbarians that they've been portrayed as but instead are very conscious and rational money-maximizers.

That's right. Piracy is an employment, and I think that we should think about sailors' decisions to enter piracy as opposed to, say, the legitimate merchant service as an employment decision just like anybody else's. The same features that are driving pirates' behavior drive our behavior when we think about employment options. And they are rational again in the traditional economic sense, which is that they respond to incentives and they consistently act to achieve their goals.

You discuss strategies that pirates employ to brand themselves and to develop the image of barbarians not to be trifled with. And you highlight this by citing the example of the Jolly Roger.

At the time that pirates of the early 18th century were operating in the Caribbean, there were other potential attackers that a merchant crew might confront. The reason that's important is because those other potential attackers were less fearsome than pirates, because they were constrained by the law. Pirates could do whatever they wanted to you if you resisted them, but these guys were, at least in principle, somewhat limited.

So if pirates wanted to take the prey with as little resistance as possible, which they did because they wanted to keep costs down, what they needed to do was to somehow indicate that "I'm a pirate and I will kill you if you resist me," as opposed to one of these legitimate attackers. And in response to that need, which is again a profit-driven purpose, pirates developed the Jolly Roger.

Can you please clarify the term "separating equilibrium" that pops up in your chapter on the Jolly Roger?
A separating equilibrium is to be contrasted with what's called a pooling equilibrium. It's part of signaling theory, the idea that people want to engage in various behaviors to communicate something about themselves that isn't directly observable. What makes for a successful signal is if it's more costly for some types to send than it is for others.

Think about it this way: if the Jolly Roger was so effective at facilitating merchant ship surrender, then why didn't the legitimate belligerents, the other guys attacking merchant ships, also want to hoist the Jolly Roger? Because it could have facilitated easier surrender for them, too. My point is that they did want to.

A pooling equilibrium was threatened but was largely prevented by what is called the single-crossing property in economics—the fact that it's more costly for the one type than for the other. And it was more costly for a privateer ship, which was legitimate, because if they raised the Jolly Roger, all of a sudden their status moves from legitimate ... to criminal—they could be caught and hanged. So that's an added cost for them. But pirates, since they were already outlaws, they had already incurred that cost.

In terms of establishing the pirate brand, you discuss cruelty as a means of achieving that notoriety.

That's exactly right. Again, if we think of piracy as a business, as I think we should, their reputation was just as important as it is for any other business. So in order to institutionalize the brand name that they wanted to cultivate, what they needed to do was first work diligently in creating it. The way that they did that was through ruthlessly adhering to this idea of torturing people if they didn't comply with them once they had boarded their ship.

We normally think about pirates as sort of blood-lusting, that they want to slash somebody to pieces. [It's probably more likely that] a pirate, just like a normal person, would probably rather not have killed someone, but pirates knew that if that person resisted them and they didn't do something about it, their reputation and thus their brand name would be impaired. So you can imagine a pirate rather reluctantly engaging in this behavior as a way of preserving that reputation.

In fact, you point out that to be bloodthirsty would undercut the desired result, because it would signal to potential targets that they might as well resist.
The reason that cruelty was effective is because it constituted a cost of a behavior that pirates wanted to deter. If you're a merchant crew and you know that pirates, no matter what you do, are going to try and slaughter you once they board you, well then of course there's no cost to you resisting them.

You might as well try; you'll probably lose, but you're no worse off than if you had just surrendered to them peacefully in the first place. So it was critical for pirates that they only applied heinous tortures when, in fact, they were using it to penalize behavior.

And this is part of this idea of what I call the "invisible hook." It's analogous, in some ways, to Adam Smith's invisible hand [a hypothesized force by which a free-market economy naturally benefits the greater good] in the sense that, of course, pirate prey are worse off as a result of pirates attacking them, but a profit-motivated pirate crew is likely to behave better toward the people they're attacking than one that in fact was truly sadistic and didn't care about money at all. And this is a case where we can see that.

Is that how you're able to separate cause from correlation? What's to say that these pirates weren't just, say, bands of bloodthirsty marauders that lucked into this strategy?

One of the things we can do is look at testable implications of the rational-choice theory. If in fact pirates were truly madmen, we would not expect them to only display that madness in particular cases. Especially, it would be a great coincidence if it happened to be those cases in which it stood to make them money. And that's pretty much precisely what we observe.

Notice the sort of piratical paradox, if you will, that we confront. You've got these depraved and feral sea bandits living somehow by a strict pirate's code, holding judicial sessions, and regulating alcohol use and gambling. The two things just don't seem to match up. First of all, that undermines the claim that pirates were simply crazy, because when it was in their interest, they seemed to be able to behave perfectly rationally.

And the rational-choice framework can really allow us to resolve that piratical paradox, in that you can take one basic core assumption about human behavior and explain two things that seemingly are at odds with each other, as opposed to positing ad hoc pirate motives as we go from practice to practice.

One example that you point to in demonstrating the efficiency of pirate behavior is that, according to at least one pirate historian, Blackbeard didn't kill a single man.

That's a perfect illustration of what we're talking about here and another actual prediction that comes out of the rational-choice theory to a certain extent. The actual instances that we have of pirate brutality—and there are a number of them—an economist would characterize as out-of-equilibrium play, not the norm. Those cases are recorded precisely because something really nasty happened.

And the fact that Blackbeard didn't have to actually kill anybody is an indication of what we would call equilibrium play. The reputation that he'd created was so effective that he didn't have to actually ever carry through on the threat that lay behind that image.

One thing that I thought was interesting is the fact that some of these pirate ships had institutionalized a form of worker's compensation.

They did, and I talk about that in-depth in a different paper I wrote. But that's exactly what they had. And one of the things that's marvelous about the system is, first of all, its earliness. That was not a common thing in the 17th- and 18th-century world.

Merchant sailors, for example, didn't have access to something similar through the state until after pirates had already adopted this. But in any event it was a highly detailed scheme, so if you lost your right arm it would be worth x number of pieces of eight, and if you lost your left leg it would be worth y number of pieces of eight in compensation. So it was quite a developed system.

In this paper you focus primarily on the "golden age" of piracy. But what do you make of piracy today, especially with the Somali pirates in the news of late?
Modern-day pirates … are similar to old-school pirates in the sense that they are plundering on the sea and that they are engaged in plunder on the sea where government is weak.

Other than that, when it comes to their institutional organization, for example, overwhelmingly they seem to be just not that interesting. Now—and as far as I know this is the only case we have of this—when the French government took a pirate crew earlier this year, they did find an actual pirate's manual that laid out rules about how they would treat prisoners. It points again to the profit-seeking idea—it's not because they're nice people, it's because the prisoners are valuable as hostages.

But it's still nowhere near as elaborate or as interesting. The constitutions that 18th-century pirates had ... created a true system of social governance on the pirate ship. Seventeenth- and 18th-century pirates were pioneers, in a certain way, of constitutional democracy. They had checks and balances aboard their ship, they had an early form of quasi-judicial review, and they were democratic, which was virtually unheard of in the Western world at that time.

The reason modern pirates don't have that, I think, is because 18th-century pirates spent lots and lots of time together at sea. It could be months on end. And they lived and worked and operated apart from legitimate society for long periods of time, which meant that the pirate ship was a kind of floating society. And that society, like any other one, required rules in order for it to be functional.

If you look at modern pirates, they tend to spend very little time together on their ships. Modern pirate expeditions tend to be in-and-out operations. And since they aren't really together in the same way that 18th-century pirate crews were, they don't really constitute floating societies.

Therefore they don't face the same kinds of social problems, at least to the same extent, that the 18th-century pirates did, and so that's why they don't have elaborate rules. No society, no rules.

They still seem to be turning a pretty nice profit.
Oh, absolutely. They seem to be doing well. I don't think that they're inferior predators. It's just that they're not as interesting predators.

Challenges of decreasing ability to tune out irrelevant information leading to memory loss?

Global7 the new Millennial Renaissance Vision for the Globe

Distractions 'hit old-age memory'

Mental slowing down in old age can be blamed partly on being more easily distracted, research suggests.

The Canadian team asked young and old people to attempt a memory test while in a scanner showing which bits of their brain were working.

The older subjects did worse at the tests, and their brains responded more to the background buzzing and banging from the scanner itself.

The study was published in the Journal of Neuroscience.

Other researchers have suggested that mental decline may be due to a decreasing ability to "tune out" irrelevant information from their senses.

This has been shown for both sound and vision, where older subjects were more likely to focus on the landscape in a picture rather than the figure within it.

The University of Toronto study used a standard face recognition test, placing 12 old and 12 young volunteers within a "functional MRI" scanner, which allows scientists to see which parts of the brains are activated during a particular activity.

Of prime interest was activity in the hippocampus, and area of the brain known to be involved with the laying down of memories.

When both the old and young volunteers failed to remember a face, there was less activity in the hippocampus, as might be expected.

However, when the older subjects failed, there was also increased activity in two other parts of the brain, the auditory cortex and the pre-frontal cortex, which are responsible for processing signals from the external environment.

Unnecessary information

Dale Stevens, who led the study, said that that brains of the older people were processing too much unnecessary information - in this case the normal knocking and rattling sounds that an MRI machine produces.

"The old brains showed increased activation in certain regions that should normally be quieter or turned down."

He said that the poorer performance overall of the older people might be due to an inability to "tune out" this noise while their brains were trying to form new memories of the faces.

Dr Jan de Fockert, a psychologist from the Institute of Cognitive Neuroscience at University College London, said that there were a number of competing theories as to why "selective attention" - the ability to focus on something in spite of distraction - might decline with age.

One suggestion, he said, is that the brain loses the ability to inhibit the processing of distracting signals.

Another suggests that an age-related decline in "working memory" - the information storage needed for the completion of everyday tasks, rather than longer-term storage - made it harder for individuals to pay close attention to one thing.

He said: "This seems like a very interesting paper, although it does not prove that the problems with selective attention are contributing to poor performance in the memory tasks."

Story from BBC NEWS:

Published: 2008/11/26 11:19:15 GMT


Sunday, November 16, 2008

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Our passion is to reach our individual and collective potential via science, creativity and interactive engagement of all 6.6 Billion People

The oldest and most efficient female humanoid pelvis discovered in Ethiopia

Should we reduce the global population or increase the creative potential of every new born that comes to bless the world?

Pelvis Dated To 1.2 Million Years Ago Shows Ancestors May Have Been Born With Big Heads
Science Daily (based on a report provided by Indiana University) | November 15, 2008

A reconstruction of the 1.2 million-year-old pelvis discovered in 2001 in the Gona Study Area at Afar, Ethiopia, that has led researchers to speculate early man was better equipped than first thought to produce larger-brained babies. The actual fossils remain in Ethiopia. (Credit: Scott W. Simpson, Case Western Reserve University)

Sileshi Semaw
Discovery of the most intact female pelvis of Homo erectus may cause scientists to reevaluate how early humans evolved to successfully birth larger-brained babies.
"This is the most complete female Homo erectus pelvis ever found from this time period," said Indiana University Bloomington paleoanthropologist Sileshi Semaw. "This discovery gives us more accurate information about the Homo erectus female pelvic inlet and therefore the size of their newborns."

A reconstruction of the 1.2 million-year-old pelvis discovered in 2001 in the Gona Study Area at Afar, Ethiopia, that has led researchers to speculate early man was better equipped than first thought to produce larger-brained babies. The actual fossils remain in Ethiopia.

The discovery will be published in Science this week (Nov. 14) by Semaw, leader of the Gona Project in Ethiopia, where the fossil pelvis was discovered with a group of six other scientists that includes IU Department of Geosciences graduate student Melanie Everett.

Reconstructing pelvis bone fragments from the 1.2 million-year-old adult female, Semaw and his co-workers determined the early ancestor's birth canal was more than 30 percent larger than earlier estimates based on a 1.5-million-year-old juvenile male pelvis found in Kenya. The new female fragments were discovered in the Gona Study Area in Afar, Ethiopia, in 2001 and excavation was completed in 2003.

Scientists also were intrigued by other unique attributes of the specimen, such as its shorter stature and broader body shape more likely seen in hominids adapted to temperate climates, rather than the tall and narrow body believed to have been efficient for endurance running.

Early humans became taller and narrower over time, scientists believe, partly due to long distance running and to help them maintain a constant body temperature. One consequence, however, is that a narrower pelvis would have been less accommodating to producing larger-brained offspring.

But rather than a tall, narrow hominid with the expected slight pelvic region, Semaw and the Gona researchers found evidence of a hominid ready to produce offspring with a much larger brain size.

"The female Homo erectus pelvic anatomy is basically unknown," Semaw said. "And as far as the fossil pelvis of ancestral hominids goes, all we've had is Lucy (dated at 3.2 million years and also found in Ethiopia), and she is very much farther back in time from modern humans."

Scientists studying early man predominantly find fragments of craniums and dental remains, while fossil bones from the neck down are rarely discovered. Even more difficult to verify are Homo erectus fossil bones that can be identified as those belonging to a female.

Scientists had thought early adult Homo erectus females, because of the assumed small birth canal, would produce offspring with only a limited neonatal brain size. These young would have then experienced rapid brain growth while still developmentally immature, leading researchers to envision a scenario of maternal involvement and child-rearing on par with that of modern humans. But those theories had been based upon extrapolations from the existing male skeleton from Kenya.

"This find will give us far more accurate information," Semaw said. Semaw is also a research scientist at the Stone Age Institute, a research center near Bloomington dedicated to the study of early human evolution and culture. It is affiliated with Indiana University's CRAFT, the Center for Research into the Anthropological Foundations of Technology.

Gona has turned out to be a productive dig site for Semaw. In 1997 Semaw and colleagues reported the oldest known stone tools used by ancestral humans. Then in 2004 he coauthored a paper summarizing Gona's geological properties and the site's cornucopia of hominid fossils spanning several million years. At the time, Science gave the article an "Editor's Choice" recognition. In 2005 he and colleagues published an article in Nature announcing the discovery of Ardipithecus ramidus, one of the earliest ancestral hominids, dating between 4.3 and 4.5 million years ago.

Scott Simpson (Case Western Reserve University School of Medicine and the Cleveland Museum of Natural History), Jay Quade (University of Arizona), Naomi Levin (University of Utah), Robert Butler (University of Portland) and Guillaume Dupont-Nivet (Utrecht University, Netherlands) also contributed to the report. Support for the research was provided by the Leakey Foundation, the National Science Foundation, the National Geographic Society and the Wenner-Gren Foundation.

The authors thank Ethiopia's Authority for Research and Conservation of Cultural Heritage and the National Museum of Ethiopia for research permits and support.

Adapted from materials provided by Indiana University.
Wide-hipped homo changes picture of Homo erectus
By Maggie Fox, Health and Science Editor

WASHINGTON (Reuters) – The fossil of a wide-hipped Homo erectus found in Ethiopia suggests females of the pre-human species swayed their hips as they walked and gave birth to relatively developed babies with big heads, researchers said on Thursday.

The finding transforms thinking about some early human ancestors and evolution and suggests that helpless babies came along relatively late in the human lineage.

"We could look at this pelvis and then, using a series of measurements, we can calculate ... how big the baby's head could be at birth," said Scott Simpson, a paleontologist at Case Western Reserve University who worked on the study.

Writing in the journal Science, Simpson and colleagues said the size and shape of the 1.2 million-year-old pelvis indicates that H. erectus females had hips wider than those of modern human females and their infants were born with heads about 30 percent larger than previously calculated.

"What this means is the offspring were not as helpless as a modern human," he said in a telephone interview.

"It is not coming out walking and talking. But it was probably capable of more advanced behavior at a younger age like grasping, like sitting up ... than we would see in a modern human."

An extended childhood is a particularly human characteristic. Helpless babies require intensive care, not only from the mothers but from an extended group, which may have spurred the development of human society and culture.

Homo erectus, Latin for "upright man," arose in Africa 1.8 to 2 million years ago, migrating to Asia and Europe before becoming extinct about half a million years ago. Experts agree it was likely a direct ancestor of modern humans.

Scientists did not know much about what its body would have looked like until the discovery of "Turkana Boy," an adolescent H. erectus whose bones were discovered in 1984.

His slim-hipped build led researchers to believe that H. erectus gave birth to small-headed babies that would have required a great deal of care in early life, much like modern human infants.

But Simpson said Turkana boy's pelvis was damaged and the restoration of a near-complete female pelvis from Gona, Ethiopia, changes this picture.

"This H. erectus would have even wider hips (than modern women)," Simpson said.

One main difference between human males and females is hip width, which makes women sway as they walk and which allows men to run and walk more efficiently.

"The reason women do have that sway is their hips are a little further apart," Simpson said. "She would have had a good one."

(Editing by Alan Elsner)

Tuesday, November 04, 2008

Global7 the new Millennial Renaissance Vision for the Globe

The benefits of flaxseed
The Benefits of Flaxseed
Is flaxseed the new wonder food?
Preliminary studies show that flaxseed may help fight everything from heart disease and diabetes to even breast cancer.

By Carol Sorgen
Reviewed By Michael Smith, MD
on Monday, March 10, 2003

Flaxseed may be on everyone's lips -- and in everyone's cereal -- but this new darling of the plant world has been around for more than 4,000 years, known even in the days of Hippocrates for its healthful benefits.

Flaxseed has been a part of human and animal diets for thousands of years in Asia, Europe, and Africa, and more recently in North America and Australia, says Kaye Effertz, executive director of AmeriFlax, a trade promotion group representing U.S. flaxseed producers. As flax gained popularity for its industrial uses, however, its popularity as a food product waned, but it never lost its nutritional value. "Today flax is experiencing a renaissance among nutritionists, the health conscious public, food processors, and chefs alike," says Effertz.

The reason for the increasing interest in flaxseed is its apparent benefits for a host of medical conditions, says Roberta Lee, MD, medical director of the Center for Health and Healing at Beth Israel Deaconess Medical Center in New York.

Flaxseed is very high in omega-3 essential fatty acids, Lee explains. It's the omega 3s -- "good" fats -- that researchers are looking at in terms of their possible effects on lowering cholesterol, stabilizing blood sugar, lowering the risk of breast, prostate, and colon cancers, and reducing the inflammation of arthritis, as well as the inflammation that accompanies certain illnesses such as Parkinson's disease and asthma.

In addition to the omega-3s, the remaining two components of flaxseed -- lignans and fiber -- are being studied for their health benefits as well, says Diane Morris, PhD, RD, spokesperson for the Flax Council of Canada. Lignans, for example, act as both phytoestrogens and antioxidants, while the fiber contained in the flaxseed is of both the soluble and insoluble type. "Flax is an interesting mixture of nutrients and other components," says Morris.

Though studies conducted to date have been limited in scope and small in nature, their results are promising, says Morris. In a small Canadian study of 39 women, for example, researchers from the University of Toronto found that flaxseed may boost conventional treatment for breast cancer.

In the study, reported in the American Institute for Cancer Research Newsletter in 1998, postmenopausal women with breast cancer ate either a plain muffin or a muffin containing 25 grams of flaxseed oil every day for approximately five-and-a-half weeks. Of the 29 out of the 39 women who ate both muffins, researchers found reductions in the growth of their tumors.

These results were encouraging, says Morris, but she adds, "It's just one study." The favorable results of that study, however, are leading to others. At the John Wayne Cancer Institute in Santa Monica, Calif., for example, investigators are also looking into the effect of essential fatty acids on breast cancer, says Rachel Beller, MS, RD, director of the Brander Nutritional Oncology Counseling and Research Program. But here, too, says Beller, it's too soon to have any conclusive findings.

In addition to research on breast cancer, Morris says, other studies are looking at heart disease, blood pressure, diabetes, menopause, osteoporosis, and inflammatory bowel disease, to name just a few.

Yet another study has found that omega-3 fatty acids, and by extension, flaxseed, can reduce the risk of macular degeneration -- an eye disease that destroys vision by damaging nerve cells in the eye.

The results of a Harvard study, published in August 2001 in the Archives of Ophthalmology, showed that people with a high intake of omega-6 (vegetable oils) were more likely to develop macular degeneration, while those with a combination of lower omega-6 intake and high omega-3 intake were less likely to have the disease.
"Flaxseed is the best source of omega-3 fatty acids," says Lylas G. Mogk, MD, director of the Henry Ford Visual Rehabilitation and Research Center in Detroit, chairman of the Vision Rehabilitation Committee of the American Academy of Ophthalmology, and co-author of Macular Degeneration: The Complete Guide to Saving and Maximizing Your Sight.

Flaxseed is also good for combating dry eyes, a very common problem, says Mogk, probably because of our poor omega-3 intake. "Dry eyes are usually the result of an insufficient outer oil layer in the tear film, so the water in the tears doesn't have anything to keep it from evaporating," she says. Omega-3 fatty acids help the oil glands produce the proper consistency of oil so it will flow from the oil glands and coat the surface of the eye.

Mogk recommends that her patients take a tablespoon a day of flaxseed oil. "I think all adults should do this," she says, "and most certainly those at high risk for macular degeneration (which includes those between the ages of 65 and 74, those who have a family member with the disease, women, and whites).

Flaxseed is available in supermarkets and health food stores and comes in whole seeds, ground seeds, or oil. Most nutrition experts recommend the ground seeds, which have "all the goodies," says Morris -- the fiber, the lignans, and the essential fatty acids. Whole seeds will pass through your system undigested, she says, while the oil lacks the fiber, which, if nothing else, will help alleviate any problems of constipation. (Some patients with diverticulosis, however, find the ground flaxseed too irritating; for those people, says Lee, the flaxseed oil is a better choice.)

Ninety-six percent of the flaxseed grown in the U.S. is grown in North Dakota because of its cooler climate and wide open spaces, says Kaye Effertz; for those same reasons, Canada is also a top grower of flaxseed. Flaxseed comes in two colors -- reddish brown and golden brown. The color makes no difference when it comes to nutritional value.

Rachel Beller recommends buying ground flaxseed in vacuum-packed bags. Most people refrigerate their flaxseed, but Morris says that's not a necessity (even though she does it herself). Whole seeds will last from 10-12 months, she says, while ground flax has a shelf life of about four months, even out of the refrigerator.

The recommended daily amount of flaxseed is approximately 1-2 tablespoons of ground flaxseed, or 1 teaspoon of flax oil (which is best used cold, perhaps mixed in a vinaigrette salad dressing). Morris' favorite way to get her flaxseed is to mix a tablespoon of the ground seeds with 2 tablespoons of honey, and then spread the mixture on toast. "It has a nutty flavor," she says, "and is a great alternative to buttering your toast."

1. Texas nutritionist Natalie Elliott offers these additional suggestions for adding flax to your diet:
Sprinkle ground flax on cereal, yogurt, or salads.
2. Mix flax into meatloaf or meatballs.
3. Add ground flax to pancake, muffin, or cookie batter, or other baked goods such as pie crust.
4. Coat fish or homemade chicken nuggets in ground flaxseed and oven fry.
5. Toss salads with flax oil and vinegar.
6. Or try one of her favorites, "Nat's Flax Snacks":
7. 1 cup Karo corn syrup
1 cup brown sugar
1 cup smooth peanut butter
1 cup ground flax
1 teaspoon vanilla
6 cups of Rice Krispies

Mix together the first five ingredients in a saucepot over low heat until melted and smooth. Add Rice Krispies to the pot and stir. Pour contents into a buttered 9"x13" pan. Press down to flatten. Stir, cool, and cut into 8 bars.

Published March 10, 2003.
1. SOURCES: Kaye Effertz, executive director, AmeriFlax, Mandan, N.D. Roberta Lee, MD, medical director, Center for Health and Healing, Beth Israel Deaconess Medical Center, New York.
2. Diane Morris, PhD, RD, spokesperson for Flax Council of Canada, Toronto. Rachel Beller, MS, RD, director, Brander Nutritional Oncology Counseling and Research Program,
3. John Wayne Cancer Institute, Santa Monica, Calif. Archives of Ophthalmology, August 2001. "Research Update: Flaxseed Shows Promise Against Breast Cancer," American Institute for Cancer Research Newsletter 59, Winter 1998.
4. Natalie Elliott, co-owner, Brain Waves Music and Wellness Center, Austin, Texas.
© 2003 WebMD Inc. All rights reserved.

Friday, October 31, 2008

Global7 the new Millennial Renaissance Vision for the Globe

Our Passion is to reach our individual and collective potential-Always!

Scientific American Magazine - October 28, 2008

25 Years Later: Can HIV Be Cured?
Eliminating HIV from the body would require flushing the virus out of its hiding places and preventing those reservoirs from being refilled. A tall order but perhaps not impossible

By Mario Stevenson

In contrast to the failed attempts at developing a vaccine against HIV, efforts to provide drug therapies stand as a great success. More than 25 agents have been approved thus far, and the right combinations can suppress replication of the virus, often keeping blood levels so low as to be undetectable by standard tests.

These powerful drug cocktails, collectively termed highly active antiretroviral therapy, or HAART, have prolonged life and health in countless infected individuals. Yet vexingly, today’s treatments cannot actually cure the infection. If for any reason therapy is interrupted, the virus rapidly rebounds.

Figuring out how HIV manages to hang around in the company of these potent drugs is one of the most important tasks currently facing researchers. Over the past decade investigators have gleaned key insights into this mystery. The answers, we hope, will ultimately reveal whether complete eradication of the virus in a patient is feasible.

Understanding the nature of HIV’s hiding places, or reservoirs, and what it will take to eradicate them requires some insight into how HIV typically behaves in the body. Like all viruses, HIV needs to get into the body’s cells to replicate.

There the invader exploits the cells’ machinery to make copies of its own genome and to translate viral genes into proteins. It thus generates new viral copies, called virions, which spread to other cells. But unlike most human viruses, HIV actually inserts its genome into that of the cell.

Every time the cell reproduces, the viral genes get copied and passed down to the daughter cells, thereby ensuring that the virus persists for as long as the cell and its progeny survive in the body.

The immune system typically manages to eliminate viruses by knocking out infected cells. It identifies such cells readily by the bits of viral proteins, or antigens, they display on their surface to flag the presence of interlopers within.

In the case of HIV, the immune system has a hard time eradicating infected cells on its own in part because the virus attacks components of the immune system itself. The body does manage for a while to counterattack, generating healthy new immune cells able to recognize the virus and other infectious agents. In untreated individuals, however, the virus gains the upper hand over time, leading to AIDS.

Today’s powerful drug combinations protect the immune system because they suppress HIV replication and limit the spread of virus to new cells. In theory, these treatments should permit the still healthy parts of the immune system to clear out any remaining infected cells and cure the disease. So why is the drug-protected immune system failing to do that job?

Keeping a Low Profile

A big component of the answer appears to be the persistence of cells that are genetically able to make new virions but that do not produce any and thus do not inform the immune system of their presence.

As David I. Watkins notes in “The Vaccine Search Goes On,” starting on page 69, HIV preferentially infects immune cells called helper T lymphocytes, which mostly reside in the lymph nodes and connective tissue of the gastrointestinal tract but also occupy other lymph nodes and circulate in the blood.

In the course of fighting most kinds of viral infections, the bulk of helper T cells involved in the fight die off when they are no longer needed. A subset, however, survives as long-lived memory T cells, ready to multiply and call in the reserves when they encounter signs of reinfection.

It is these memory T cells that appear to produce the most virus in HIV-infected patients. As they prepare to divide to fight remembered pathogens, they both duplicate their own DNA and proteins and churn out new HIV virions. Most of the infected memory cells die from the virus itself or the immune attack against them, but some return to a dormant state.

At that point, HIV exists only as viral DNA sitting quietly in the cells’ genome. This viral DNA does not get copied and does not give rise to viral proteins, so no protein bits get displayed on the surface. Consequently, anti-HIV drugs have no effect on the cells, and the immune system remains blind to them.

This understanding has been informed by studies published in 1997. Teams led independently by Robert F. Siliciano of Johns Hopkins University, Anthony S. Fauci of the National Institutes of Health and Douglas D. Richman of the University of California, San Diego, found that inactive T lymphocytes isolated from HIV-infected individuals do not manufacture HIV.

When those cells were roused, however, the previously dormant virus began replicating anew. HIV is not the only virus to exhibit such latency. An array of viruses can enter into similarly quiet states. In fact, some, such as the herpesviruses, make proteins that actually encourage the virus to become latent.

Estimates based on the life span of memory T cells suggest it would take in excess of five decades for the reservoir of cells infected with latent HIV to naturally die out.

Researchers are also beginning to comprehend that it is not only latent helper T cells that bring HIV back after therapy stops. It seems that despite the absence of virus in the blood, some helper T cells and other cells keep on making new virus at a low level even when therapy seems to be working beautifully.

This activity falls under the radar of tests, because the virus either hides successfully in the cells or, when released, stays trapped in tissues and does not find its way into the blood.

In the past year, for instance, research has revealed that helper T lymphocytes in the gut get depleted within weeks of the individual contracting HIV and even before the virus is detected in the blood.

It is therefore possible that during treatment the virus can continue to replicate in tissues such as those of the gut—activity that could go unnoticed for quite some time until the virus spills over into the blood.

Another Unwitting Accomplice

Most AIDS research has focused on helper T cells because they circulate in the blood, which can easily be drawn for study. Recently, however, investigators have come to realize that other immune cells infected by HIV—macrophages and dendritic cells—may also contribute to resurgence of the virus after HIV therapy is halted or after the virus becomes resistant to it.

Less is known about macrophages and den­dritic cells because they are located strictly in tissues, but recent findings suggest that drug therapy may not totally stop HIV reproduction in these cells. The level may be too low to result in the virus reaching the blood in detectable amounts.

It may, however, be high enough to reach nearby T lymphocytes and to continually restock the reservoir of dormant infected memory T cells. Also, some infected macrophages seem to evade being killed by the virus inside them or by other components of the immune system. Macrophages, then, may sit ready to pump up replication when drug therapy stops.

In 2001, for instance, Malcolm A. Martin of the NIH and his colleagues reported that although monkeys infected with simian immunodeficiency virus (SIV)—a close relative of HIV—lost most of their helper T lymphocytes within a few weeks of being infected, copious quantities of virus were still being produced.

Mac­rophages, it turned out, were generating the virus. Subsequent treatment of the monkeys with a drug that inhibits viral replication—and thus prevents infection of new cells—failed to significantly lower the amount of virus in the animals’ blood. This finding meant that the macrophages were not dying in the process of spewing out new copies of the virus.

HIV also seems to replicate somewhat differently in macrophages as compared with T cells—in a way that may be additionally advantageous to the virus. Whereas in T cells the virus components assemble close to, and subsequently detach from, the cell surface, in macrophages some viral particles appear to be deposited into compartments within the cells called vacuoles.

Eventually the vacuoles may migrate up to the cell surface to release the stored virus particles. The packing of the virus into walled-off compartments might help HIV dodge immune detection by preventing the display of antigens on the cell surface that tip the immune system off to the presence of an intruder.

Finally, studies suggest that higher drug concentrations are needed to suppress viral replication in macrophages than in T cells. Exactly why this should be the case is uncertain. Yet we do know that some cellular proteins whose normal function is to excrete biological substances from the cell can interfere with drug therapy by hindering the uptake and retention of drugs.

Perhaps, then, in macrophages these cellular proteins are particularly active and so prevent the drugs from being efficiently retained inside the cells. The same thing may occur in dendritic cells, although so far very little is known about how these cells respond to HIV.

Anatomical Refuges
It is not only the inherent properties of helper T cells and macrophages that allow HIV to persist in the face of intensive therapy. Certain of these cells also sit in anatomical compartments that may shelter them from various drugs or immune defenses, or both. Ridding the body of HIV would necessitate reaching it in those places.

The central nervous system (CNS) is one such compartment. Researchers have long known that the CNS is susceptible to HIV infection. The neurological problems that arise in late-stage AIDS stem largely from the production of neurotoxins released from infected macrophages in the brain.

To enter the brain, any molecule or cell must cross the blood-brain barrier, essentially a selectively permeable membrane that regulates the traffic of cells and other substances from the blood to the CNS. Macrophages that become infected with HIV in the tissues outside the CNS can apparently cross the blood-brain barrier and settle down in the CNS, where the virus may go on to infect specialized mac­rophages known as microglia, which reside permanently within the CNS.

Evidence suggests that infection of cells in the CNS would afford the virus some degree of protection from drugs because certain of them—notably protease inhibitors important to the proper processing of new viral proteins—do not efficiently cross the blood-brain barrier.

Further, most other circulating immune cells stay out of the brain. No one knows whether infected cells in the brain can send HIV out to other parts of the body, but if the virus-infected macrophages can cross the blood-brain barrier into the CNS, they can probably filter back out as well.

Other sites that seem difficult for some drugs to penetrate include the walls of the gastrointestinal tract and the genital tract. Semen often contains HIV RNA even in people whose blood seems to be clear of the virus.

New Plans of Attack

At a minimum, thoroughly clearing HIV from an infected individual would require removal of all latently infected T cells.

One way that researchers are currently exploring to address the latent reservoirs is treating patients with compounds that stimulate dormant infected T lymphocytes to divide, in the hopes that the cells will make virus and thus become vulnerable to antiretroviral therapy.

A couple of limited human trials have tested this approach using drugs previously approved to treat other conditions. They have yielded mixed results, however.

The ideal agents would tickle the T cells enough to rekindle the production of the viral proteins that get displayed on the cell surface but not so much as to trigger the cells to make new copies of the virus.

To that end, researchers are currently exploring the potential of drugs that would induce the synthesis of HIV proteins by altering the organization of chromatin (complexes of DNA and protein that compose chromosomes) in dormant infected T cells. Yet even these so-called chromatin remodelers would be of limited use if they worked only in T cells and the virus were also present in macrophages.

A second prong of attack for clearing HIV from the body would involve blocking all viral replication, so that HIV disappears not only from the blood but from all tissues and from all cell types that harbor it.

Drugs currently in use typically interfere with one of two enzymes: reverse transcriptase, which converts the virus’s genetic material from RNA to DNA for insertion into the cellular genome, or protease, which helps nascent viral particles to mature. Within weeks after a person starts standard therapy, the level of virus in the individual’s blood drops to undetectable levels.

The slope of decay is fairly consistent from patient to patient, which researchers have taken to mean that the therapies thoroughly forestall viral replication. Yet recent studies have shown that intensifying existing drug regimens with raltegravir, a new drug that targets a viral enzyme not hit by earlier agents (the viral integrase enzyme, which stitches HIV DNA into the cells’ own DNA), actually accelerates the viral decay.

This success suggests that infected cells can probably be hit faster and more effectively than is now the case. If that surmise is correct, the work also implies that intensifying HIV therapy even further might limit the size of the original latent reservoir, block its later restocking and—dare we hope—lower replication so much that the immune system really can wipe out any virus-making reservoirs left over when latent infected memory cells are eliminated.

In the past year several new drugs that interfere with previously untargeted steps in viral replication have entered into clinical trials. In addition to the integrase inhibitor, another drug blocks infection by interfering with the ability of the virus to attach to a molecular receptor known as CCR5 that sits on the cell surface.

Research also suggests that certain cellular proteins may be good therapeutic targets. Whereas HIV commandeers some of these proteins to aid its replication (CCR5, for example), it is now apparent that other cellular proteins—or cellular restrictions, as they are termed—actually antagonize viral replication.

Six years ago Michael H. Malim of King’s College London and his research group identified the first of these cellular restrictions, called A3G. This protein is abundant in macrophages and in lymphocytes.

Unfortunately, the virus has evolved a countermeasure to A3G: it makes a protein called Vif that induces the degradation of A3G. The good news is that both A3G and the viral Vif protein represent promising targets for therapy. Drugs that inhibit Vif or otherwise protect A3G from degradation would theoretically render human cells resistant to HIV infection.

Just this year Paul D. Bieniasz of the Aaron Diamond AIDS Research Center in New York City and John C. Guatelli of U.C.S.D. and their teams independently identified a second cellular restriction, named tetherin, that prevents the release of new copies of the virus from infected cells.

The virus has evolved a defense against tetherin, too—in this case, the viral Vpu protein. Drugs that stymie Vpu could prevent HIV from spreading to new cells.

Basic research will probably continue to reveal novel therapeutic targets, which could lead to the development of new antiviral agents that hit HIV in multiple ways. If we can design drugs that complement and intensify the effects of existing therapies, we may finally be able to deplete the all-important latent reservoir and eradicate the virus.

To that end, larger studies exploring the impact of long-term therapy in­tensification on the virus are currently under way, with results expected within the next two years. Those findings should tell us whether the eradication of HIV from an infected in­dividual is a realistic goal. We wait with great anticipation.

Note: This article was originally printed with the title, "Can HIV Be Cured?".

Further Reading
25 Years Later: The AIDS Vaccine Search Goes On
Hope and the Fight against HIV
Special Report: HIV--25 Years Later
Science of Snacks: Thinking Makes You Hungry

On the Web
Updates: Whatever Happened to LED Lightbulbs?
Medical Mystery: Only One Person Has Survived Rabies without Vaccine--But How?
Deadly by the Dozen: 12 Diseases Climate Change May Worsen

Reseach confirms wearing red boosts attraction to men

Global7 the new Millennial Renaissance Vision for the Globe

Our Passion is to reach our individual and collective potential-always!

Dear Patriotic global scientists:

Re: the majic is with the colour red! says recent reseaarch

It is interesting our choices are influenced by our vision and color, especially when it relates to men.

Vison and colour has been a very important part of our emotional characteristics for centuries. For the first time, research is shown men like women who dress red at their dates.

What colour is attractive to women? Do women pay more attention to sound rather than colour? What is common for both sexes, colour, sound and shapes, touch and temperature?

More reserach is needed to complement these initial findings. Here is the BBC story for us to think through.

Dr B Jesus (Globalbelai)
~*~*~*~*~*~*~*~*~*~*~*~*~*~Listen up, ladies: If you're looking to score, break out that red dress.

Men were more eager to bed women wearing red than those decked out in other colors, according to five studies involving 149 men and 32 women published today in the Journal of Personality and Social Psychology. The men also judged those women as more attractive than those sans red duds.

"I'm not going to let my 16-year-old daughter wear red, let's put it that way," says study author Andrew Elliot, a professor of psychology at the University of Rochester. "I do think a female who's interested in a male and going on a date ought to pull that red shirt out of the closet, because most likely it will make her more attractive to him."

There are two explanations for the phenomenon, says Elliot, a visiting professor at the University of Munich this semester. Society's emphasis on red on Valentine's Day as well as in sexy red lingerie may have taught men to link the color with romance, he says. There may also be an evolutionary explanation, based on humans' close genetic relationship with primates: Male primates tend to be especially attracted to female primates who show their red hindquarters, made rosy by increased blood flow when they're most fertile.

The men in the study were asked to rate their level of sexual interest on a scale of one to nine (one signifying zero interest and nine representing the strongest) in the women in photos they were shown. They were also asked to grade the women's attractiveness using the same scale. The desirability score was about 1.5 points higher and their attractiveness rating 1.2 points higher for women in red than for those in gray, green or blue.

Women surveyed didn’t rate their red-clad sisters as being any more attractive than those sporting garb in other hues, and neither they nor the guys found the ladies in red to appear any more likable, nicer or smarter than those in other colors. That suggests that red has a very specific color association with sexual behavior, Elliot says.

Women are likely to show a similar level of increased attraction to men in red in follow-up research he’s doing now, Elliot adds.

"The hypothesis is that you're going to see the same thing for females rating males, but through a different process," he says. "Females are more attracted to dominant, higher-status males. Red is a dominant cue in the wild when it's shown on a male. So human females who see red on a male will view him as more dominant, and that will lead her to be more attracted to him."

One caveat: The findings may be colored by certain situations. Elliot's previous research found that people who literally saw red immediately before a writing task performed worse—possibly because of our negative association with teachers' red pens used to point out errors.

(Image by iStockphoto)


Wearing red 'boosts attraction'
Women who don a little red dress before going out with a man may find their date more attentive and generous, according to scientists.

The University of Rochester study, published in a psychology journal, supports other evidence linking the colour to attractiveness.

Men said they would spend more money on a woman pictured in red, compared with the same woman wearing a blue shirt.

Experts say that red signals ovulation or attractiveness in other species.

It's fascinating to find that something as ubiquitous as colour can be having an effect on our behaviour without our awareness
Professor Andrew Elliot
University of Rochester

The colour has traditionally been linked with romantic and sexual matters, from red hearts on Valentine's Day, to red-light districts.

The researchers say that their study is clear evidence that the colour red makes men feel more amorous - even if this is only on a subconscious level.

Their volunteers were told they had $100, shown the picture of their "date", then asked how much of that money they were prepared to spend.

On average, wearing red meant a more expensive night out, and in general, a higher rating of attractiveness.

When the pictures were shown to other women, there were no wardrobe-dependent differences in attractiveness ratings.

Monkey business

Professor Andrew Elliot, who led the research, published in the Journal of Personality and Social Psychology, said: "It's fascinating to find that something as ubiquitous as colour can be having an effect on our behaviour without our awareness."

Dr Jo Setchell, an anthropologist from Durham University, said that, as the colour of blood, red was the easiest signal for an animal to produce externally, and had become a handy method of advertising fertility.

"For example, a lot of female monkeys have bright red sexual swellings, which show that they are around the time of ovulation.

"There has been controversy over whether, in female humans, ovulation is advertised or not, although there is some evidence that behaviour, such as going out, changes around that time.

"But wearing red could give you an advantage."

Story from BBC NEWS:

Published: 2008/10/28 08:19:06 GMT


Sunday, October 12, 2008

Noble Laurates vision about hiv pandemics

Global7 the new Millennial Renaissance Vision for the Glob
News - October 6, 2008

AIDS in 1988

In their first collaborative article 20 years ago, 2008 Nobel Prize winner Luc Montagnier, along with Robert Gallo, co-investigators who discovered HIV, introduced a Scientific American single-topic issue on AIDS. They recounted the breakthrough and offered prospects for vaccine, for therapy and for the epidemic
By Robert C. Gallo ad Luc Montagnier

Editor's Note: Luc Montagnier shared the 2008 Nobel Prize in Medicine or Physiology, awarded on October 6. The new Nobel laureate co-authored this article, originally published in the October 1988 issue of Scientific American. We are making it available here due to its historical significance.

As recently as a decade ago it was widely believed that infectious disease was no longer much of a threat in the developed world. The remaining challenges to public health there, it was thought, stemmed from noninfectious conditions such as cancer, heart disease and degenerative diseases. That confidence was shattered in the early 1980's by the advent of AIDS.

Here was a devastating disease caused by a class of infectious agents--retroviruses--that had first been found in human beings only a few years before. In spite of the startling nature of the epidemic, science responded quickly. In the two years from mid-1982 to mid-1984 the outlines of the epidemic were clarified, a new virus-the human immunodeficiency virus (HN)-was isolated and shown to cause the disease, a blood test was formulated and the virus's targets in the body were established.

Following that initial burst, progress has been steady, albeit slower. Yet in some respects the virus has outpaced science. No cure or vaccine is yet available, and the epidemic continues to spread; disease-causing retroviruses will be among the human population for a long time.

In view of that prospect, it is essential to ask where we stand in relation to AIDS in 1988. How was HN discovered and linked to AIDS? How does the virus cause its devastation? What are the chances that AIDS will spread rapidly outside the known high-risk groups? What are the prospects for a vaccine? For therapy? How can the epidemic most effectively be fought? Those are some of the questions this article and this issue of Scientific American have set out to answer.

Like other viruses, retroviruses cannot replicate- without taking over the biosynthetic apparatus of a cell and exploiting it for their own ends. What is unique about retroviruses is their capacity to reverse the ordinary flow of genetic information--from DNA to RNA to proteins (which are the cell's structural and functional molecules).

The genetic material of a retrovirus is RNA In addition, the retrovirus carries an enzyme called reverse transcriptase, which can use the viral RNA as a template for making DNA The viral DNA can integrate itself into the genome (the complement of genetic information) of the host. Having made itself at home among the host's genes, the viral DNA remains latent until it is activated to make new virus particles. The latent DNA can also initiate the process that leads to tumor formation.

Retroviruses and their cancer causing potential are not new to science. At the beginning of this century several investigators identified transmissible agents in animals that were capable of causing leukemias (cancers of blood cells) as well as solid-tissue tumors. In the succeeding decades retroviruses were identified in many animal species. Yet the life cycle of retroviruses remained obscure until 1970, when Howard M. Temin of the University of Wisconsin at Madison and (independently) David Baltimore of the Massachusetts Institute of Technology discovered reverse transcriptase, confirming Temin's hypothesis that the retroviral life cycle includes an intermediate DNA form, which Temin had called the provirus. The details of viral replication quickly fell into place.

In spite of such discoveries, by the mid-1970's no infectious retroviruses had been found in human beings, and many investigators firmly believed no human retrovirus would ever be found. Their skepticism had several grounds. Many excellent scientists had tried and failed to find such a virus.

Moreover, most animal retroviruses had been fairly easy to find, because they replicated in large quantities, and the new virus particles were readily observed in the electron microscope; no such phenomenon had been found in human beings. In spite of this skepticism, by 1980 a prolonged team effort led by one of us (Gallo) paid off in the isolation of the first human retrovirus: human T-lymphotropic virus type I (HTLV-I).

HTLV-I infects T lymphocytes, white blood cells that have a central role in the immune response. The virus causes a rare, highly malignant cancer called adult T-cell leukemia (ATL) that is endemic in parts of Japan, Africa and the Caribbean but is spreading to other regions as well.

Two years after the discovery of HlLV-I the same group isolated its close relative, HTLVII. HTLV-II probably causes some cases of a disease called hairy-cell leukemia as well as T-cell leukemias and lymphomas of a more chronic type than those linked to HTLV-I. The two viruses. however. share some crucial features. They are spread by blood. by sexual intercourse and from mother to child. Both cause disease after a long latency. and both infect T lymphocytes. When AIDS was first recognized. these properties took on great additional significance.

The first AIDS cases were diagnosed in 1981 among young homosexual men in the U.S. Although the syndrome was puzzling. it soon became clear that all its victims suffered from a depletion of a specific subset of T cells- T4 cells and that as a result they fell prey to pathogens that would easily be controlled by a healthy immune system. A variety of hypotheses were advanced to explain AIDS. including breakdown of the victims' immune systems following repeated exposure to foreign proteins or even to sperm-during homosexual intercourse. It seemed more plausible. however. to explain a new syndrome by the appearance of a new infectious agent.

To one of us (Gallo) the likeliest agent was a retrovirus. It had already been shown that the AIDS pathogen. like HTLV-I. could be transmitted by sexual intercourse and by blood. Furthermore. Max Essex of the Harvard School of Public Health had shown that a retrovirus of cats called feline leukemia virus (FeLV) could cause either cancer or immune suppression.

Since in most species the infectious retroviruses are closely related. it seemed plausible that the same was true in human beings. Hence the initial hypothesis was that the cause of AIDS was a close relative of HTLV-I. That hypothesis. as it turned out. was wrong. Nonetheless, it was fruitful because it stimulated the search that led to the correct solution.

The retrovirus hypothesis for the origin of AIDS reached the other one of us in France in the following way. Almost as soon as AIDS was first diagnosed. a working group on the syndrome had been formed by a circle of young clinicians and researchers in France. One member of the group.

Jacques Leibowitch of the Raymond Poincare Hospital in Paris. had had some contact with Gallo's team and carried the HTLV hypothesis back to France. The members of the French group wanted to test that hypothesis. and they had the biological materials to do so because the group included clinicians with patients afflicted by AIDS or pre-AIDS. What they lacked, however, was the collaboration of virologists experienced in work with retroviruses.

The French author of this article and his colleagues Francoise Barre-Sinoussi and Jean-Claude Chermann at the Pasteur Institute fitted that description. They were engaged in several lines of work on cancer and interferon including attempts to find retroviruses in patients with cancer particularly in cultures of lymphocytes.

A member of the working group, Willy Rozenbaum of the Salpetriere Hospital, asked whether they were interested in analyzing tissues from a patient with lymphadenopathy. or swollen glands. (Lymphadenopathy can be an early sign of the process that culminates in AIDS.

Such a patient was chosen because finding a virus early in the disease seemed more meaningful than finding one later. when AIDS patients were infected with many opportunistic agents.) The answer was yes, and in January, 1983, a specimen from the swollen lymph node of a young homosexual arrived at Montagnier's laboratory.

The specimen was minced. put into tissue culture and analyzed for reverse transcriptase. After two weeks of culture. reverse-transcriptase activity was detected in the culture medium. A retrovirus was present. But which one? The first possibility that had to be tested was whether the virus was one of the known HTLVs. or perhaps a close relative of them.

That possibility was tested using specific HTLV-I reagents supplied by Gallo. The virus did not react significantly with the HTLV-I reagents; a similar result was later obtained with HTLV-Il reagents. A strenuous effort was begun to characterize the new agent.

Among the first results of that effort was the finding that the new virus (which was named lymphadenopathy associated virus. or LAV) grew in T4 cells but not in related cells called T8; that finding was made by David Klatzmann and Jean-Claude Gluckman of the Salpetriere Hospital in collaboration with the Pasteur group.

It was shown that the virus could kill T4 cells or inhibit their growth. Electron micrographs of the new virus were different from those of HTLV-I and resembled those of a retrovirus of horses. A viral protein called P25 (or P24) that is not present in HTLV-I was identified. In collaboration with virologists from the Claude Bernard Hospital a blood test for lAY antibodies was formulated.

Several examples of lAY or lAV-like viruses were isolated from homosexual men, hemophiliacs and central Africans. Early results of applying the blood test were suggestive but not fully conclusive. lAV antibodies were found in a large fraction of lymphadenopathy patients but in only a minority of AIDS patients. Yet the proportion increased as the sensitivity of the test improved. By October, 1983, it had reached 40 percent. At that point one of us (Montagnier) was convinced lAV was the best candidate for the cause of AIDS.

To the other one of us the evidence did not seem so clear. For one thing, results had been obtained (by Gallo and Essex) indicating that some AIDS patients are infected with HTLV-I or a variant of that virus. It is now known that those results stemmed partly from the fact that among people infected with HIV are some who are also infected with the HTLV's. Moreover, only a minority albeit a substantial one-of AIDS patients had shown serological evidence of lAY infection.

In addition, when it was first isolated, lAY could not be grown in large amounts in continuous cell lines. Without large quantities of virus it was difficult to prepare specific lAY reagents that could be used to show that all people with AIDS or pre-AIDS were infected by the same type of virus.

Therefore on the American side much effort was concentrated on growing the pathogen from the blood of AIDS patients in mass, continuous culture. By the end of 1983 that task had been accomplished by the Gallo team: several cell lines had been identified that could support the growth of the new agent.

The first reagents for specifically typing this virus were rapidly made. Employing those reagents, it was shown that 48 isolates obtained beginning in early 1983 from AIDS patients and people in risk groups were all the same type of virus, which was called HTLV-III on the American side.

A blood test was formulated and used to show that HTLV-III was present in almost all people with AIDS, in a variable proportion of people at risk of the disease (including people who had received blood contaminated by the virus but had no other risk factors) and in no healthy heterosexuals. The cause of AIDS had been conclusively established.

These results confirmed and extended the ones from France. lAV and HTLV-III were soon shown to be the same virus. Before long an international commission had changed its name to HIV, to eliminate confusion caused by two names for the same entity and to acknowledge that the virus does indeed cause AIDS. Thus contributions from our laboratories in roughly equal proportions-had demonstrated that the cause of AIDS is a new human retrovirus.

That HIV is the cause of AIDS is by now firmly established. The evidence for causation includes the fact that HIV is a new pathogen, fulfilling the original postulate of "new disease, new agent." In addition, although the original tests found evidence of HIV infection in only a fraction of people with AIDS, newer and more sensitive methods make it possible to find such evidence in almost every individual with AIDS or pre-AIDS.

Studies of blood-transfusion recipients indicate that people exposed to HIV who have no other risk factors develop AIDS. The epidemiological evidence shows that in every country studied so far AIDS has appeared only after HIV. What is more, HIV infects and kills the very T4 cells that are depleted in AIDS. Although the causative role of HIV in AIDS has been questioned, to us it seems clear that the cause of AIDS is as well established as that of any other human disease.

Soon after the causation was established, a series of findings began to fill in the scientific picture of HIV. In a remarkably short time the genetic material of the virus was cloned and sequenced (in our laboratories and several others).

The genetic complexity of HIV began to emerge when a gene called TAT was discovered by William A Haseltine of the Dana-Farber Cancer Institute, Flossie Wong-Staal of the National Cancer Institute and their collaborators. Such complexity is significant because it underlies the capacity of HIV to remain latent for a long period, . then undergo a burst of replication, a pattern that may hold the key to the pathology of AIDS.

There were other significant early findings. One of us (Gallo), with his colleagues Mikulas Popovic and Suzanne Gartner, showed that HIV could infect not only the T4 cell but also another type of white blood cell, the macrophage. The same one of us, working with his colleagues Beatrice H. Hahn, George M. Shaw and Wong-Staal, found HIV in brain tissues. It seems possible that the macrophage, which can cross the blood-brain barrier, may bring virus into the brain, explaining the central-nervous-system pathology seen in many AIDS patients.

How the virus infects both T4 cells and macro phages became clear when Robin A Weiss of the Chester Beatty Laboratories and, independently, Klatzmann and the Pasteur group showed that HN enters its target cells by interacting with the molecule called CD4. CD4 has a significant role in the immune function of T4 lymphocytes and also serves as a marker for that group of cells. The early work by the British and French teams showed that HN infects cells by binding to CD4. Hence only cells bearing that marker can be infected. (Although CD4 is the marker for the T4 cells, it is also found in smaller numbers on some macrophages, allowing them to be infected.)

Several additional findings rounded out the early discoveries. The potential of the epidemic to spread beyond the original risk groups was shown when Robert R. Redfield and one of us (Gallo) demonstrated that HIV can be transmitted during heterosexual intercourse. Members of the Gallo team also showed that the genetic makeup of the virus is highly variable from strain to strain, a fact that may complicate the attempt to formulate an AIDS vaccine.

After the rapid initial advance the pace slowed somewhat and began to approximate that of a more mature area of research. Yet the continuing work was not without surprises. In October, 1985, one of us (Montagnier) was engaged in analyzing blood samples brought to his laboratory by a visiting investigator from Portugal. Many of the samples were from people who had lived in Guinea-Bissau, a former Portuguese colony in West Africa. Among them were some people who had been diagnosed by Portuguese clinicians and investigators as having AIDS in spite of the fact that their blood showed no sign of HN infection.

One sample, in fact, was negative for HN using the most sophisticated techniques available at the time. Yet workers in the laboratory were able to isolate a virus from the patient's blood. DNA "probes" (short pieces of DNA from the HIV genome) were then prepared. If the new virus were closely related to the original AIDS agent, those probes would bind to its genetic material. As it turned out, there was little binding, and it became clear that the new isolate was not simply a strain of the original AIDS virus but a new virus designated HN-2. Soon a second example was isolated by workers at the Claude Bernard Hospital; many others followed.

In evolutionary terms HIV-2 is clearly related to HIV-1, the virus responsible for the main AIDS epidemic. The two viruses are similar in their overall structure and both can cause AIDS, although the pathogenic potential of HN-2 is not as well established as that of the first AIDS virus. HN-2 is found mainly in West Africa, whereas HN-1 is concentrated in central Africa and other regions of the world. The finding of HIV-2 suggests that other undiscovered HIVs may exist, filling out a spectrum of related pathogens.

The isolation of HN-2 immediately raises the question of the evolutionary origins of these viruses. Although the answer to that question has not been found, some hints have been provided by the discovery in other primate species of related viruses called simian immunodeficiency viruses (SN's). The first such virus, found in the macaque monkey, is designated SN macaque. Isolated and characterized by Ronald C. Desrosiers and his co-workers at the New England Regional Primate Research Center in collaboration with Essex and his colleague Phyllis Kanki, SN macaque has been shown to be closely related to HIV-2, raising the possibility that HIV-2 may have come into human beings relatively recently from another primate species.

No such close simian relative has been found for HN-1 (although the right group of primates may not yet have been studied in sufficient detail). Hence the origin of HN-1 remains more mysterious than the origin of its relative HN-2. It is likely, however, that HN-1 has been in human beings for some time. One of us (Gallo), with Temin, has used the divergence among HN strains and the virus's probable rate of mutation to estimate how long the virus has infected people. It was tentatively concluded that HN has infected human beings for more than 20 years but less than 100, an estimate compatible with those by other workers and with our knowledge of the epidemic.

Where was HN hiding all those years, and why are we only now experiencing an epidemic? Both of us think the answer is that the virus has been present in small, isolated groups in central Africa or elsewhere for many years. In such groups the spread of HN might have been quite limited and the groups themselves may have had little contact with the outside world. As a result the virus could have been contained for decades.

That pattern may have been altered when the way of life in central Africa began to change. People migrating from remote areas to urban centers no doubt brought HN with them. Sexual mores in the city were different from what they had been in the village, and blood transfusions were commoner. Consequently HN may have spread freely. Once a pool of infected people had been established, transport networks and the generalized exchange of blood products would have carried it to every corner of the world. What had been remote and rare became global and common.

What weapons are available against this scourge? Perhaps the best weapon is knowledge. One key form of knowledge is a deeper understanding of HN, its life cycle and the mechanisms by which it causes disease. Although HN kills T4 cells directly, it has become clear that the direct killing of those cells is not sufficient to explain the depletion seen in AIDS. Indirect mechanisms must also be at work. What are they?

Many possibilities have been suggested. Infection by HIV can cause infected and uninfected cells to fuse into giant cells called syncytia, which are not functional. Autoimmune responses, in which the immune system attacks the body's own tissues, may also be at work. What is more, HIV infected cells may send out protein signals that weaken or destroy other cells of the immune system. In addition HN is fragile, and as the virus particle leaves its host cell, a molecule called gp120 frequently falls off the virus's outer coat. As Dani P. Bolognesi of the Duke University Medical Center and his co-workers have shown, gp120 can bind to the CD4 molecules of uninfected cells. When that complex is recognized by the immune system, cells thus marked may be destroyed.

That list does not exhaust the possibilities. One of us (Montagnier) is exploring the possibility that the binding of the virus to its target cells triggers the release of enzymes called proteases. Proteases digest proteins, and if they were released in abnormal quantities, they might weaken white blood cells and shorten their lives. The various proposed mechanisms are not exclusive, and several may operate at once. Yet one is probably central, and some of the most significant work on AIDS is that of distinguishing the central mechanism from the peripheral ones that accompany it.

Although it is clear that a large enough dose of the right strain of HN can cause AIDS on its own, cofactors can clearly influence the progression of the disease. People whose immune systems are weakened before HN infection may progress toward AIDS more quickly than others; stimulation of the immune system in response to later infections may also hasten disease progression.

Interaction with other pathogens may also increase the likelihood that AIDS will develop. Specifically, a herpes virus called human B-cell lymphotropic virus (HBLV) or human herpes virus 6 (HHV-6) that was discovered in the laboratory of one of us (Gallo) can interact with HN in a way that may increase the severity of HN infection. Ordinarily HHV-6 is easily controlled by the immune system. In a person whose immune system is impaired by HN, however, HHV-6 may replicate more freely, becoming a threat to health. In addition, although one of the main hosts of HHV-6 is a white blood cell called the B cell, the virus , can also infect T4 lymphocytes. If the T cell is simultaneously infected by HN, HHV-6 can activate the latent AIDS virus, further impairing the immune system and worsening the cycle.

Clearly, in spite of rapid progress there are many gaps in our understanding of HN and AIDS. Should we panic? The answer is no, for several reasons. The most obvious is that panic does no good. The second reason is that it now seems unlikely HIV infection will spread as rapidly outside the original high-risk groups in the industrial countries as it has within them. A third reason is that this disease is not beyond the curative power of science. Although current knowledge is imperfect, it is sufficient to provide confidence that effective therapies and a vaccine will be developed.

The possibilities for therapy are particularly impressive. In the first phase of the search for AIDS therapies it was necessary to exploit any drug that seemed to provide even a remote chance of combating HIV infection. A variety of compounds formulated for other purposes were taken off the shelf and tested. Most were of little value, but one (AZT), originally formulated as an anticancer drug, turned out to be the first effective anti-AIDS agent. More recently, an experimental regimen in which AZT is alternated with the related compound known as dideoxycytidine offers even greater promise.

Bringing AZT into clinical use was a significant accomplishment, because it gave hope that AIDS would not remain incurable forever. As a form of therapy, however, AZT is not perfect and will probably be supplanted by less toxic agents formulated on the basis of what is known about the HIV life cycle. One promising agent is CD4, the molecule that serves as the viral receptor. Early tests show that soluble CD4 can bind to the virus and prevent it from infecting new cells. Many other drugs are in trials; one of them, perhaps combined with compounds that bolster the immune system, may provide therapy for HIV infection.

In assessing the progress that has been made toward achieving fully effective AIDS therapy, it must be kept in mind that this work has two facets. In addition to combating a complex and evasive pathogen, it must pioneer entirely new areas of medicine.

The reason is that there are few effective treatments for viral diseases-and almost none for retroviruses. There are various reasons for this, among them the fact that viruses (unlike bacteria, for which effective therapies exist) always appropriate the biosynthetic apparatus of the host cell. As a result drugs effective against viruses tend to damage mammalian cells. Yet we are confident that the dual goals of pioneering science and clinical effectiveness will be met.

What is true of therapy is also true of vaccines: an AIDS vaccine will be a pioneering scientific achievement. Since the HIV genome has the capacity to integrate into the chromosomes of the host cell, little serious consideration has been given to using preparations containing the whole virus as a vaccine. An AIDS vaccine must consist of subunits, or parts, of the virus in the right combination. Yet experience with subunit vaccines is slight. Indeed, so far only a few subunit vaccines have proved practical. Much work is under way to find the combination of HIV subunits that will yield the greatest protective response. As in the case of therapy, we believe there will be a practical vaccine against HIV.

Perhaps an even more persuasive reason for hope is that even without a vaccine or a cure, what is already known could bring the epidemic under control. The blood supply has already been largely secured by the presence of a blood test. Moreover, the modes of transmission of HIV-blood, sexual intercourse and from mother to child-are firmly established. Hence any individual can drastically reduce his or her risk of infection. If such knowledge were applied everywhere, there would be a sharp leveling off in the spread of HIV infection, as there has been in some groups in the developed world. The lesson here is that there is a need for education about HIV infection--in clear, explicit language and as early as possible.

Yet there are parts of the epidemic where education alone is not sufficient, and it is in those areas that humanity will be tested. Users of intra· venous drugs, for example, are notoriously resistant to educational campaigns alone. It seems clear that the effort to control AIDS must be aimed in part at eradicating the conditions that give rise to drug addiction. Those conditions are in turn linked to social and economic patterns. Eliminating the disease may entail eliminating some of the social differentials that form the substratum of drug abuse.

It is also the case that in some areas of the developing world education alone will not stem the epidemic. Education is necessary, but it must be accompanied by other measures. In central Africa--the part of the world most beleaguered by AIDs--there are few facilities for blood testing and few technicians trained to perform tests. Furthermore, the blood tests used in the U.S. and Western Europe are too expensive to be helpful. As a result the virus is still being spread by contaminated blood, long after that form of transmission has been practically eliminated in the industrial countries.

To help change this situation the World AIDS Foundation has made improving the situation in central Africa its highest priority. The foundation (along with its parent, the Franco-American AIDS Foundation) was formed as part of the agreement that resolved a lawsuit between France and the U.S. over the AIDS blood test. The parent foundation receives 80 percent of the royalties from the French and American blood tests; the World AIDS Foundation in turn receives 25 percent of that. Much thought has been given to how to allocate the funds, and the first project (carried out in conjunction with the World Health Organization) will be realized in several African countries. It will include training technicians to perform blood tests, establishing one HIV-free blood center and increasing public education about HIV transmission.

Efforts such as this one, coupling public and private funds and energies, will be essential to stopping AIDS. As we stated above, both of us are certain that science will ultimately find a cure and a vaccine for AIDS. But not tomorrow. The AIDS virus (and other human retroviruses) will be with us for a long time. During that time no intelligent person can expect the necessary solutions to come solely from authorities such as scientists, governments or corporations. All of us must accept responsibilities: to learn how HIV is spread, to reduce risky behavior, to raise our voices against acceptance of the drug culture and to avoid stigmatizing victims of the disease. If we can accept such responsibilities, the worst element of nightmare will have been removed from the AIDS epidemic.

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