Jetlag, HIV and a Moon with an Oxygen Atmosphere
In this NewsFlash we explore the link between jetlag and forgetfulness, discover a moon with an oxygen atmosphere, and a new technique to tell someones age from their blood. Plus, in time for World AIDS Day, we find out how HIV infection lays waste to non-infected, or "bystander" cells, leading to the destruction of the immune system.
In this episode
00:25 - Jet-lag linked to forgetfulness
Jet-lag linked to forgetfulness
Psychologists working at the University of Berkeley have found that jet lag affects the brain's ability to retain facts long after returning to a more regular schedule.
The researchers came to this conclusion after they had subjected a group of female Syrian hamsters to six-hour shifts in their circadian rhythms - which is the same as flying London to New York. They applied quite a tough regime to these hamsters, exposing them to this artificial jet lag twice a week for four weeks.
They also kept a control group of hamsters whose schedules remained unchanged. Lance Kriegsfield and his colleagues then put both sets of hamsters through tests which measured their ability to learn and remember simple tasks, such as locating hidden food.
As expected, the jet-lagged hamsters didn't perform as well as the control group. But what was surprising is that the jet-lagged ones continued to perform poorly even a month after their rhythms returned to normal.
They also found that the jet-lagged hamsters only had half the usual number of new neurons in the hippocampus area of the brain, which is crucial for memory and learning.It's already known that human frequent flyers and rotating night shift workers can suffer problems with their memory but what this study implies is that those problems could persist, even after they've settled into a more regular working pattern - at least we know that's true for hamsters, anyway.
02:23 - Aged by blood
Aged by blood
In a move that could make a critical contribution to forensic investigations, scientists have developed a powerful new technique to predict a person's age from a sample of their blood.
Writing in the journal Current Biology, Erasmus MC Medical Centre, Rotterdam, researcher Manfred Kayser and his colleagues demonstrate that it's possible to age a blood donor with a precision of plus or minus nine years by studying the DNA present in the donor's T lymphocytes, which are a type of white blood cell.
The technique makes use of an observation that T cells contain additional small, circular pieces of DNA known as signal joint TCR excision circles - sj TRECS for short. These are produced when the cells rearrange their DNA in order to mount a targeted immune response and there are usually a large number of them, although, critically, this number declines with age in a predictable fashion.
What the Dutch team do is to quantify the number of sj TRECS and then work out how much DNA is present overall in order to standardise the count. This enables them to make their prediction of the age of the person who produced the blood, which might be the only sample found at a crime scene.
According to Kayser, this is currently the most accurate ageing method currently available. But where it will really come into its own is that it can be combined with other DNA techniques that can now make predictions as to a person's appearance based on their genetic make-up. However, knowing roughly how old a victim or perpetrator is can be used to dramatically improve the power of such techniques because more accurate descriptions can be produced.
Commenting on the work, Kayser points out that "conventional DNA profiling applied in forensics can oly identify persons already known to the investigating bodies, because the approach is completely comparative. Hence, every forensic lab is confronted with cases where the DNA profile obtained from the evidence material does not match that of any known suspect tested, nor anybody in the criminal DNA database, and such cases therefore cannot be solved so far. In such cases, it is expected that appearance information estimated from evidence material will help in finding unknown persons..."
05:32 - Bose-Einstein condensate of photons
Bose-Einstein condensate of photons
Normally if you cool a gas the atoms exist in a variety of different energies, but Einstein and Bose predicted that if you cool certain types of atoms enough they start to condense into a single state all with exactly identical energy momentum etc., essentially a new state of matter.
Although it was predicted in 1938 it wasn't achieved until 1995 when Eric Cornell and Carl Wieman cooled a very low pressure rubidium gas to about 170 billionths of a degree above absolute zero and they formed a bose-einstein condensate. This got physicists very interested as it is a fascinating example of a quantum mechanical effect, but at that temperature they could almost never be used for anything practical.
If you used light for this purpose the same thing could happen at much higher temperatures, however the problem is that you can't confine and cool down light, it tends to get absorbed by the walls far too quickly.
Jan Klaers and collegues have however got around this problem, they have trapped photons with two curved mirrors very close together only about 3.5 wavelengths, this means that the photons can only exist at certain wavelengths, and if those can't be absorbed by the walls or medium in between they stay in the cavity, and the photons of light can be cooled by interacting with dye molecules in between the mirrors causing the differences in state between them to slowly tend towards the temperature of the dye molecules. This has produced a Bose Einstein Condensate of photons for the first time, which is pretty impressive but what is more impressive is that they made it at room temperature, so it could be practical to use.
They haven't got to that point yet, but photon Bose Einstein Condensates may be able to produce high quality laser like light at wavelengths that are difficult to make lasers at, such as the ultraviolet, plus other more exotic applications that a new state of matter may open up.
08:34 - How HIV Kills Bystander Cells
How HIV Kills Bystander Cells
Professor Warner Greene, University of California at San Francisco
Chris - Wednesday, December the 1st is going to be World Aids Day and 2011 actually marks the 30th anniversary of the discovery of HIV - the agent that causes AIDS. So it's very timely that this week scientists have announced that they have solved one of the big outstanding questions that surrounds HIV infection, which is why the virus is so damaging to the immune system. Professor Warner Greene is the Director of the Gladstone Institute of Virology and Immunology at the University of California in San Francisco. He's with us now. Warner, hello. Welcome to the Naked Scientists. First, can you give us a brief potted history of what actually happens during HIV infection? In other words, how does the virus get into cells and what's its life cycle?
Warner - Good evening, Chris. I'm happy to do that and it's too bad as we're celebrating the 30th World AIDS day that we haven't ended this epidemic but the number of new infections are in fact declining markedly throughout world which is very good news. In terms of the life cycle of HIV, HIV binds to the cell surface, micro-injects its RNA genome into the cytoplasm of the cell, and then converts that RNA into DNA, a double-stranded version of the DNA, hence, the name retrovirus - reverse flow of genetic information. The DNA is then integrated into our own chromosomes, the DNA is then expressed into new proteins and RNA which is packaged into new virions which bud from the cell, and starts the entire infection process over again.
Chris - And the cells that are targeted are white blood cells, CD4, they carry that marker on their surface, T-cells, without which the immune system can't function properly. So one logical conclusion is the virus infects the very cells that orchestrate the immune response. So if you damage them then the immune system is harmed.
Warner - Correct. But the real question is, how are these CD4 T-cells dying? It was quite clear that the number of cells productively infected with HIV could not explain. In other words, direct killing could not explain the massive CD4 T-cell loss that occurs during HIV infection. Then a theory was advanced that it's not the directly infected cells but cells surrounding the infected cell, bystander cells, that are dying. Our study now shows for the first time that in fact, it is these bystander cells which are the principal cause of CD4 T-cell loss, but they themselves are becoming infect but in an abortive manner, an incomplete infection that arrests early after the virus begins the reverse transcription process.
Chris - How did you do this work? How did you prove that?
Warner - Well the first key was to use a primary lymphoid tissue. We used tonsil and in this tissue, we were then able to use each of the different types of new HIV drugs that interfere with precise steps in the viral life cycle. We were able to interrupt the life cycle with these drugs and ask whether or not, CD4 T-cell killing was blocked or not.
Chris - Ingenious. So, by adding a different drug that works on a different aspect of the life cycle, you interrupt at that stage, see if the cell dies. If it doesn't die, that tells you that the effect that you see, the bystander death, in an infected patient must lie downstream of that blockade. If the cell does die, it's upstream of where the drug works and that confines a bit of the viral life cycle that must be doing the damage.
Warner - Right. We were able to narrow-in the death window - as we called it - to a step during the reverse transcription process, whereby, the DNA is elongated into a chain longer than 150 base pairs. One of the real surprises in our study was, it's not the virus that's causing the CD4 T-cells to die, but rather, it's the host cell's response to the occurrence or to the accumulation of cytoplasmic DNA in the cell cytoplasm. That's what triggers a defensive response in the cell. In an attempt to protect the host, the CD4 T-cell commits suicide.
Chris - So this is something we've acquired through evolution to defend us against viral attack. Cells that sense this cytoplasmic DNA, genetic material in the cell where it shouldn't be, tells the cell, "I'm infected with a virus. I'll kill myself to protect the rest of the body." Unfortunately, when you've got the scale of infection going on like you have with HIV, this has deleterious effects then.
Warner - Right and the other twist of the story that was a real surprise was that these cells do not die silently, but rather they are dying a fiery death with the release of what's called pyroptosis which is the release of inflammatory cytokines. The entire cellular contents of the cell are dumped which increases the inflammatory response. We now know that there is a close relationship between HIV and inflammation, that these two go hand in hand, dictating disease progression.
Chris - What is the implication of this, just to finish this up? Does this mean that we're now closer to understanding how to intervene in the viral life cycle better, so people who are infected with HIV don't lose all their immune cells in this way?
Warner - Well, one of the great milestones in modern medicine is the creation of a panoply of anti-retroviral drugs, 26 FDA approved drugs for HIV therapy at last count. All of these drugs can interfere with this death pathway. However, the new link to inflammation, a death with inflammation, now allows us to explore the possibility of removing that inflammatory component which might allow the virus to grow in a non-pathogenic way. This might be important for certain clinical settings.
Chris - Let's hope so. Warner, thank you very much. That's Warner Greene who is Professor of medicine, microbiology and immunology at the University California, San Francisco.
14:30 - Is that face male or female? Look into my eyes, not around the eyes...
Is that face male or female? Look into my eyes, not around the eyes...
Researchers in Massachusetts this week have discovered that the ability of our brains to determine whether a human face is male or female is affected by where in the field of view they appear.
So for example, a typically male face in the centre of our vision might be interpreted as a female face when it appears left-of-centre.
In the real world this isn't usually a problem because we have so many other cues about the gender of the face's owner. Features like hair, clothing and body shape can all contribute to our conclusions as to whether a person is male or female.
The researchers removed all these extra cues and used computer-generated faces, which made a spectrum of very male to very female. These faces were shown in random order to study participants, of which there were 11.
Aresh Afraz and colleagues ensured that each face was displayed for 50 milliseconds and that the subjects kept their gaze fixed on the centre of the screen. The subjects were asked to assign a gender to each face. What they found was that, while gender judgements were consistent for those faces in the centre of the visual field, those faces lying off-centre received different judgements. And the tendency of each subject to judge an off-centre face as male or female seemed to be specific to the subject.
What Afraz think this means is that this comes down to how our visual cortex is organised. The visual cortex is the part of the brain that interprets images and inside it cells are grouped according to the part of the visual field that they interpret. So Afraz' conclusion is that the visual cortex has a limited number of neurons per visual field area that it uses to assign gender. If the image is small and is interpreted by one part of the visual cortex, it can come to a different conclusion than another part might make.
17:27 - NASA has found a moon with a mostly oxygen atmosphere
NASA has found a moon with a mostly oxygen atmosphere
One of the most unusual things about the Earth is the large amount of oxygen in its atmosphere, which isn't stable and is only there because plants keep producing it.
The Cassini probe orbiting Saturn has discovered that Saturn's moon Rhea has an atmosphere made of mostly oxygen, and 30% carbon-dioxide. Unfortunately this doesn't mean that captain Kirk could beam down there and be comfortable in his polyester jump suit, and it doesn't indicate that there is a colony of plants down on the surface photosynthesising.
' alt='Saturn's moon Rhea' >Rhea's surface is mostly made of water ice at -180C, and it is getting irradiated by particles of solar wind trapped by Saturn's magnetic field. This breaks up the water releasing oxygen, which is forming the atmosphere. There is also some carbon dioxide being released, possibly from deeper within the moon. Whilst the atmosphere is 100km thick there are still only a few tonnes of oxygen spread out over the whole moon, which if it was on the earth would just fill a large building, so compared to earth's atmosphere it is immensely tenuous.
So this certainly isn't the big story it first sounds like, but it does show that when looking for life you have to be careful when interpreting what atmospheres are made of as there are lots of strange forms of chemistry that can go on without life being involved at all.