When the universe was very young – less than a millionth of a second after the big bang – it was also very hot (around 1013K to be more precise). At that time, there were no “ordinary” particles as we know them today, only quarks and photons. These were in approximate equilibrium, with quarks and antiquarks annihilating each other to make photons, and the photons spontaneously changing back to quark-antiquark pairs (“pair production“).
As the universe cooled, photons no longer had enough energy for pair production to occur, and the existing quarks and antiquarks mostly then annihilated each other – but not entirely, since (obviously) some quarks (but hardly any antiquarks) remained, eventually to form the protons and neutrons of ordinary matter. Two consequences of this process are observable today. There are far more photons than quarks in the universe, by a very large ratio of more than a billion to 1. And there are far more quarks than antiquarks (bound up in protons and neutrons), by a similarly large ratio.
The only conceivable way this could have happened is for some asymmetry in the laws of particle physics to favor quarks over antiquarks. This imbalance need not have been large at all to account for the results – an excess of quarks over antiquarks of only 3 in a billion would have been enough. However, the existing Standard Model of particle physics has no explanation for this asymmetry, and therefore it can’t predict the imbalance between matter and antimatter. Experiments, however, can actually measure imbalances in some cases. Such imbalances will be quantities that any successful theory refining the Standard Model must predict.
Experiments at Fermilab that measure the results of decay of B mesons into muons have found an excess of muons over antimuons of about 1%. As more data is collected, the probability that this excess is not a statistical fluke has risen, and the latest results, just reported, place the odds of a meaningless fluke at about 1 part in 20,000.
- New Tevatron collider result may help explain the matter-antimatter asymmetry in the universe (6/30/11)
- Antimatter Tevatron mystery gains ground (7/1/11)
- A step closer to explaining our existence (7/1/11)
Quantum graininess of space
Einstein’s General Theory of Relativity says nothing about the properties of spacetime on a small scale, and that’s why it is both generally compatible with, yet completely independent of, quantum mechanics. The latter theory, however, suggests that spacetime could have a discrete “grainy” structure at very small dimensions.
Often the Planck length of 1.616×10-35 m is suggested as the proper scale for the graininess to appear. But this length is physically rather arbitrary, and recent astrophysical observations impose much more stringent limits on the scale at which graininess appears – if it even occurs at all.
The most recently published astrophysical results are from ESA’s Integral gamma-ray observatory. The gamma-ray burst GRB 041219A was detected on December 19, 2004. It was extremely bright, in the top 1% of all gamma-ray bursts. In part this is because its source was “only” about 300 million light years away. This brightness made it possible to deduce sufficiently precise values for the amount of polarization of its gamma-ray emissions at different wavelengths. Together with a recent good determination of the distance of GRB 041219A, this has made it possible to deduce that any quantum graininess must be at a length of less than 10-48 m – more than 10 trillion times smaller than the Planck length.
This is not the first use of astrophysical observations to constrain spacetime graininess. A result reported in November 2009, and discussed in detail here, placed limits on the length scale below the Planck length – but not nearly so small as the latest results.
- Integral challenges physics beyond Einstein (6/30/11)
- Study challenges physics beyond Einstein (7/1/11)
- New Space Technologies Search for Quantum Fabric of the Universe (7/1/11)
Physical Review D DOI: Constraints on Lorentz Invariance Violation using integral/IBIS observations of GRB041219A
Masturbation as mating call?
Perhaps because the study was done by Europeans or (more likely?) because the findings might be too upsetting to delicate American sensibilities, some rather interesting entomological research hasn’t received the notice it deserves on the U. S. side of the Atlantic. To put it bluntly, a somewhat obscure aquatic bug, the lesser water boatman, serenades its hoped-for romatic conquests by… masturbating. And not only that, but in so doing the bug makes the loudest noise, in proportion to its size, of any animal on the planet. (Including human rock vocalists.) At least, if electronic amplification isn’t a factor.
It doesn’t seem to be known whether the insect finds the activity pleasurable in itself, let alone whether it can lead to orgasm. However, the research did determine that the sound is produced by rubbing of the bug’s genital equipment against its abdomen. And at a sound level peaking at 99.2 decibels (as measured by sound pressure level), the output in proportion to body size exceeds that of any other animal. Evidently it has the desired effect on female water boatmen – the researchers describe it as the outcome of
runaway sexual selection. That makes some sense – the ability to make a lot of noise with one’s genitalia is evidence of good reproductive health, or horniness (or both).
Telomeres and cancer
The link between cancer and teleomeres gets quite a lot of attention among researchers, as evidenced by the award of a Nobel Prize in 2009 for foundational work on telomeres. Since telomeres are segments of DNA that protect the ends of chromosomes from damage during the DNA replication that occurs during cell division, and cancer is a result of uncontrolled cell division, the connection is apparent.
In non-cancerous cells, the telomeres gradually erode with each cell division. The enzyme telomerase, which is generally present in normal cells only during embryonic development, is able to rebuild telomeres, and so it is, not surprisingly, often present in cancerous cells. However, not all cancerous cells contain telomerase, yet their telomeres are still maintained to allow uncontrolled cell division. The mechanism that enables this is not understood, but it has been given a name: “Alternative Lengthening of Telomeres” (ALT). One possibility is that ALT enables homologous recombination of telomere segments, which is normally prevented.
There is new research that gives some clues about the ALT mechanism. Detailed examination of the proteins expressed in pancreatic neuroendocrine tumors and various other tumor types has identified two genes, ATRX and DAXX, as being of special interest. In particular, in tumor cells with ALT (i. e., no evidence of telomerase), one or both of the genes are either mutated or not expressed at all. This doesn’t directly elucidate the ALT mechanism, but it does help because it implies that the protein products of these genes inhibit ALT somehow – and therefore raises hopes for therapeutics in cancers where ALT is a factor.
Neuronal plaques and Alzheimer’s disease
There is a long-noticed connection between Alzheimer’s disease and accumulation of amyloid-β peptide in plaques around neurons in the brains of disease victims. The connection isn’t perfect – such plaques are also found (on autopsy) in the brains of people without Alzheimer’s disease symptoms. But the hypothesis that such plaques contribute to neuronal death (through an unknown mechanism), and hence Alzheimer’s disease, is still taken pretty seriously.
It’s also well-known that there’s a correlation between having a particular version (ε4) of the APOE gene and risk for developing Alzheimer’s disease. In fact, having one copy of the APOE4 allele increases the risk by a factor of 3, and two copies multiplies the risk another 5-fold. So the question is: what’s APOE4 doing (or not doing) to raise the risk so dramatically?
New research suggests that amyloid-β plaques are strongly implicated as a disease factor. There are (at least) two ways that APOE4 might play an important role. It might cause increased production of amyloid-β plaques, or it could hinder normal clearance of such plaques from the brain. The research now shows that (at least in mice) APOE4 does not do the latter – but it does do the latter.
What is still not known is how APOE4 hinders plaque clearance. Having that knowledge ought to suggest how to overcome the hindrance, or at least how to speed up the clearance in other ways.
- Alzheimer’s plaques due to purging flaw (6/29/11)
Science Translational Medicine abstract: Human apoE Isoforms Differentially Regulate Brain Amyloid-β Peptide Clearance