I wish they'd do this for cats. Here's a few other things they do: http://www.bing.com/visualsearch
Sunday 28 February 2010
Dog Breeds - A cool Bing feature
Check this out (click the image). Basically it lists the dog breeds alphabetically by image:
I wish they'd do this for cats. Here's a few other things they do: http://www.bing.com/visualsearch
I wish they'd do this for cats. Here's a few other things they do: http://www.bing.com/visualsearch
Monday 22 February 2010
Dolly & Royana, we hardly knew ye!
RIP sheep.
PHP now supports anonymous functions
Did you know PHP 5.3 now supports anonymous functions? Let's look at some code.
This is the old way how you used to do it:
<?php
//the array we're working with
$arr = array(1,2,3,4,5);
//declare a function for use as callback
function callback($i){
echo $i;
}
//use the callback
array_walk($arr, 'callback'); //outputs 12345
?>
Now, this is the new way:
<?php
$arr = array(1,2,3,4,5);
//use anonymous callback method
array_walk($arr, function($i){echo $i;}); //outputs 12345
?>
And here's another interesting thing you can now do with PHP:
<?php
$arr = array(5,4,3,2,1);
//create a variable which will be a reference to a new function later
$fn = null;
//$fn's function is declared within the arguments of another function
array_walk($arr, $fn = function($i){echo $i;}); //outputs 54321
//calls the new function in $fn
$fn(68); //outputs 68
?>
Did you know you could use external variables inside of closures? You need the use keyword and pass the variables into it separated by commas like so:
$basePath = "/usr/home/";
$getPathFor = function($name) use ($basePath) {return "$basePath$name";}
echo $getPathFor("bob"); // /usr/home/bob
Nice.
This is the old way how you used to do it:
<?php
//the array we're working with
$arr = array(1,2,3,4,5);
//declare a function for use as callback
function callback($i){
echo $i;
}
//use the callback
array_walk($arr, 'callback'); //outputs 12345
?>
Now, this is the new way:
<?php
$arr = array(1,2,3,4,5);
//use anonymous callback method
array_walk($arr, function($i){echo $i;}); //outputs 12345
?>
And here's another interesting thing you can now do with PHP:
<?php
$arr = array(5,4,3,2,1);
//create a variable which will be a reference to a new function later
$fn = null;
//$fn's function is declared within the arguments of another function
array_walk($arr, $fn = function($i){echo $i;}); //outputs 54321
//calls the new function in $fn
$fn(68); //outputs 68
?>
Did you know you could use external variables inside of closures? You need the use keyword and pass the variables into it separated by commas like so:
$basePath = "/usr/home/";
$getPathFor = function($name) use ($basePath) {return "$basePath$name";}
echo $getPathFor("bob"); // /usr/home/bob
Nice.
Pachnoda sinuata - That's one wierd looking beetle
That's not it's face... no, it's its' bum! The first time I saw this I thought it was painted on for a joke but no, it's real! Here's what he looks like from above:
Morbidly obese 'may have missing genes'
A small number of extremely overweight people may be missing the same chunk of genetic material, claim UK researchers. The findings, published in the journal Nature, could offer clues to whether obesity can be "inherited" in some cases. Imperial College London scientists found dozens of people - all severely obese - who lacked approximately the same 30 genes. The gene "deletion" could not be found in people of normal weight. While much of the "obesity epidemic" currently affecting most Western countries has been attributed to a move towards high-calorie foods and more sedentary lifestyles, scientists have found evidence that genes may play a significant role in influencing weight gain in some people.
There are an estimated 700,000 of these people in the UK. 'Learning difficulties' The first clue came by looking at a group of teenagers and adults with learning difficulties, who are known to be at higher risk of obesity, although the reasons for this are not entirely clear. They researchers found 31 people who had nearly identical "deletions" in their genetic code, all of whom had a BMI of over 30, meaning they were obese. Then a wider scan of the genetic makeup of a mixture of more than 16,000 obese and normal weight people revealed 19 more examples of the missing genes. All of the people involved were classed as "morbidly obese", with a BMI of over 40, and at the highest risk of health problems related to their weight. Most of them had been normal weight as toddlers, but then became overweight during later childhood. None of the people studied with normal weight had the missing code. The precise function of the missing genes is unclear, as is the precise nature of the relationship between learning difficulties and obesity - none of the people with the deletions in the wider study had learning problems. Weight-loss surgery Professor Philippe Froguel, from Imperial College, said: "It is becoming increasingly clear that for some morbidly obese people, their weight gain has an underlying genetic cause. "If we can identify these individuals through genetic testing, we can then offer them appropriate support and medical interventions, such as the option of weight loss surgery, to improve their long-term health." Dr Robin Walters, also from Imperial, said that while this particular set of deletions was rare - affecting some seven in 1,000 morbidly obese people - there were likely to be other variations yet to be found. "The combined effect of several variations of this type could explain much of the genetic risk for severe obesity, which is known to run in families." Dr Sadaf Farooqi, from Cambridge University, who collaborated with this research, and was involved in similar research published in December which pointed to another gene flaw which could be linked to obesity. She said it was likely that a "patchwork" of different genetic variations would eventually emerge to explain more cases of obesity - perhaps by affecting appetite, or the rate at which the body burns fat. She said: "There is still an important public health message about diet and exercise, but simply blaming people for their obesity is no longer appropriate." http://news.bbc.co.uk/1/hi/health/8496938.stm | |||
Xenophyophores - That's one wierd looking single-celled organism
Despite such impressive dimensions, mention of them is likely to garner blank looks from most of the general public, and even from many biologists who probably should know better. This is because xenophyophores are restricted to the deep sea, not usually regarded as a prime holiday destination. Those that are occasionally pulled up from below are probably not recognised. Like benthic Steptoes, xenophyophores surround themselves with all sorts of junk they find lying around, which they use to make their shells, stuck together with a cement of polysaccharides. Id. Foraminiferan and radiolarian shells, sponge spicules, mineral grains – all are potential building materials (though individual species are often quite picky with regard to exactly what they use, and some species eschew foreign particles altogether). The particles used are referred to as xenophyae. When the fragile test is brought up, these particles tend to all fall apart, and are hence not recognised as having once been part of a larger whole.
Image: Syringammina from the web page of J. Alan Hughes.
http://www.newscientist.com/article/dn18468-zoologger-living-beach-ball-is-giant-single-cell.html?DCMP=NLC-nletter&nsref=dn18468
http://www.palaeos.com/Eukarya/Units/Rhizaria/Xenophyophorea.html
Close encounters with Japan's 'living fossil', the Giant Salamander
Dr Takeyoshi Tochimoto gives a guided tour of the world's biggest amphibian
"This is a dinosaur, this is amazing," he enthuses.
"We're talking about salamanders that usually fit in the palm of your hand. This one will chop your hand off."
As a leader of Conservation International's (CI) scientific programmes, and co-chair of the Amphibian Specialist Group with the International Union for the Conservation of Nature (IUCN), Dr Gascon has seen a fair few frogs and salamanders in his life; but little, he says, to compare with this.
 |  The skeleton of this species is almost identical to that of the fossil from 30 million years ago; therefore it's called the 'living fossil'  Dr Takeyoshi Tochimoto |
But impressive it certainly is: about 1.7m (5ft 6in) long, covered in a leathery skin that speaks of many decades passed, with a massive gnarled head covered in tubercles whose presumed sensitivity to motion probably helped it catch fish by the thousand over its lifetime.
If local legend is to be believed, though, this specimen is a mere tadpole compared with the biggest ever seen around Maniwa.
A 17th Century tale, related to us by cultural heritage officer Takashi Sakata, tells of a salamander (or hanzaki, in local parlance) 10m long that marauded its way across the countryside chomping cows and horses in its tracks.
 The hanzaki shrine is an attempt to make up for a mythical killing |
It proved not to be such a good move, however.
Crops failed, people started dying in mysterious ways - including Mr Hikoshiro himself.
Pretty soon the villagers drew the obvious conclusion that the salamander's spirit was wreaking revenge from beyond the grave, and must be placated. That is why Maniwa City boasts a shrine to the hanzaki.
The story illustrates the cultural importance that this remarkable creature has in some parts of Japan.
Its scientific importance, meanwhile, lies in two main areas: its "living fossil" identity, and its apparently peaceful co-existence with the chytrid fungus that has devastated so many other amphibian species from Australia to the Andes.
Close family
"The skeleton of this species is almost identical to that of the fossil from 30 million years ago," recounts Takeyoshi Tochimoto, director of the Hanzaki Institute near Hyogo.
"Therefore it's called the 'living fossil'."
The hanzaki (Andrias japonicus) only has two close living relatives: the Chinese giant salamander (A. davidianus), which is close enough in size and shape and habits that the two can easily cross-breed, and the much smaller hellbender (Cryptobranchus alleganiensis) of the south-eastern US.
Creatures rather like these were certainly around when dinosaurs dominated life on land, and fossils of the family have been found much further afield than their current tight distribution - in northern Europe, certainly, where scientists presumed the the lineages had gone extinct until tales of the strange Oriental forms made their way back to the scientific burghers of Vienna and Leiden a couple of centuries ago.
"They are thought to be extremely primitive species, partly due to the fact that they are the only salamanders that have external fertilisation," says Don Church, a salamander specialist with CI.
Scientists at the Hanzaki Insitute filmed a fight between two of the giant beasts
Into a riverbank den that is usually occupied by the dominant male (the "den-master") swim several females, and also a few other males.
The den-master and the females release everything they have got, turning incessantly to stir the eggs and spermatozoa round in a roiling mass.
Maybe the lesser males sneak in a package or two as well; their function in the ménage-a-many is not completely clear.
| They have bacteria living on their skin that produce peptides that are lethal to the amphibian chytrid fungus Don Church, Conservation International |
It is not an ideal method of reproduction.
Research shows that genetic diversity among the hanzaki is smaller than it might be, partly as a result of the repeated polygamy, which in turn leaves them more prone to damage through environmental change.
But for the moment, it seems to work.
Outside the breeding season, the salamander's life appears to consist of remaining as inconspicuous as possible in the river (whether hiding in leaves, as the small ones do, or under the riverbanks like their larger fellows) and snapping whatever comes within reach, their usual meandering torpor transformed in an instant as the smell of a fish brushes by.
The adults' jaws are not to be treated lightly.
Among Dr Tochimoto's extensive collection of photos is one of bloodied human hands; and as he warns: "you may be attacked and injured; please be careful".
The giant Maniwa hanzaki brought gasps from experienced amphibian-watchers
When the chytrid fungus was identified just over a decade ago, indications were that Japan would be an unlikely place to look for its origins.
With the discovery of chytrid on museum specimens of the African clawed frog (Xenopus laevis), an out-of-Africa migration spurred by human transportation of amphibians once seemed the simple likelihood.
But just last year, a team of researchers led by Koichi Goka from Japan's National Institute for Environmental Studies published research showing that certain strains of chytrid were present on Japanese giant salamanders, and only on Japanese giant salamanders, including museum specimens from a century or so back; and that the relationship seemed benign.
| AMPHIBIANS: A QUICK GUIDE  First true amphibians evolved about 250m years ago There are three orders: frogs (including toads), salamanders (including newts) and caecilians, which are limbless Adapted to many different aquatic and terrestrial habitats Present today on every continent except Antarctica Many undergo metamorphosis, from larvae to adults |
Unravelling all that, says Don Church, might tell us something about the origins and spread of chytrid - and there is so much diversity among Japanese chytrid strains that the country is now being touted as a possible origin, as diversity often implies a long evolutionary timeframe.
More importantly, the discovery might also provide options for treating the infection.
"In the case of the North American salamanders, what was found was that they have bacteria living on their skin that produce peptides that are lethal to the amphibian chytrid fungus," says Dr Church.
"And those bacteria might be able to be transplanted to other species that can't fight off the fungus."
This is a line of research that is very much in play in laboratories around the world.
It appears likely now that studies of the Japanese giant salamander can expand the number of chytrid-fighting bacteria known to science, and so extend the options for developing treatments for an infection that currently cannot be controlled in the wild.
But that can only come to pass if the giant salamanders endure; something that is not guaranteed, with the challenges they face in modern Japan including, perhaps, new strains of chytrid itself.
There is as yet no modern hero able to still the pace of habitat loss or prevent invasion from rival species.
Tuesday 2 February 2010
Pelecinus - that's one weird looking wasp
Ever seen a wasp like this?
Pelecinus is a large, 7cm long, black wasp, who's ancestors are extinct, so there are no similar wasp family around today. It is native to the US and Mexico so we don't have to worry here ;). Oddly enough I can't find a single picture of Pelecinus thoracicus or Pelecinus dichrous; What you see above is Pelecinus polyturator which is the most common species. The females are parthogenic and don't need to sexually reproduce, but can if they choose to. They lay their eggs in scarab larvae.
Monday 1 February 2010
I, virus: Why you're only half human
WHEN, in 2001, the human genome was sequenced for the first time, we were confronted by several surprises. One was the sheer lack of genes: where we had anticipated perhaps 100,000 there were actually as few as 20,000. A bigger surprise came from analysis of the genetic sequences, which revealed that these genes made up a mere 1.5 per cent of the genome. This is dwarfed by DNA deriving from viruses, which amounts to roughly 9 per cent.
On top of that, huge chunks of the genome are made up of mysterious virus-like entities called retrotransposons, pieces of selfish DNA that appear to serve no function other than to make copies of themselves. These account for no less than 34 per cent of our genome.
All in all, the virus-like components of the human genome amount to almost half of our DNA. This would once have been dismissed as mere "junk DNA", but we now know that some of it plays a critical role in our biology. As to the origins and function of the rest, we simply do not know.
The human genome therefore presents us with a paradox. How does this viral DNA come to be there? What role has it played in our evolution, and what is it doing to our physiology? To answer these questions we need to deconstruct the origins of the human genome - a story more fantastic than anything we previously imagined, with viruses playing a bigger part than you might care to believe.
Around 15 years ago, when I was researching my book Virus X, I came to the conclusion there was more to viruses than meets the eye. Viruses are often associated with plagues - epidemics accompanied by great mortality, such as smallpox, flu and AIDS. I proposed that plague viruses also interact with their hosts in a more subtle way, through symbiosis, with important implications for the evolution of their hosts. Today we have growing evidence that this is true (New Scientist, 30 August 2008, p 38), and overwhelming evidence that viruses have significantly changed human evolution.
Symbiosis was defined by botanist Anton de Bary in 1878 as the living together of dissimilar organisms. The partners are known as symbionts and the sum of the partnership as the holobiont. Types of symbiotic relationships include parasitism, where one partner benefits at the expense of the other, commensalism, where one partner profits without harming the other, and mutualism, in which both partners benefit.
Symbiotic relationships have evolutionary implications for the holobiont. Although selection still operates on the symbionts at an individual level since they reproduce independently, it also operates at partnership level. This is most clearly seen in the pollination mutualisms involving hummingbirds and flowers, where the structure of flower and bill have co-evolved to accommodate each other and make a perfect fit. When symbiosis results in such evolutionary change it is known as symbiogenesis.
Viruses as partners
Symbiosis works at many different levels of biological organisation. At one end of the spectrum is the simple exchange of metabolites. Mycorrhizal partnerships between plant roots and fungi, which supply the plant with minerals and the fungus with sugars, are a good example. At the other end are behavioural symbioses typified by cleaning stations where marine predators line up to have their mouths cleared of parasites and debris by fish and shrimps.
Symbiosis can also operate at the genetic level, with partners sharing genes. A good example is the solar-powered sea slug Elysia chlorotica
, which extracts chloroplasts from the alga it eats and transfers them to cells in its gut where they supply the slug with nutrients. The slug's genome also contains genes transferred from the alga, without which the chloroplasts could not function. The slug genome can therefore be seen as a holobiont of slug genes and algal genes.
This concept of genetic symbiosis is crucial to answering our question about the origin of the human genome, because it also applies to viruses and their hosts. Viruses are obligate parasites. They can only reproduce within the cells of their host, so their life cycle involves forming an intimate partnership. Thus, according to de Bary's definition, virus-host interactions are symbiotic.
Genetic symbiosis is crucial to understanding the origin of the human genome, because it also applies to viruses
For many viruses, such as influenza, this relationship is parasitic and temporary. But some cause persistent infections, with the virus never leaving the host. Such a long-term association changes the nature of the symbiosis, making the evolution of mutualism likely. This process often follows a recognisable progression I have termed "aggressive symbiosis".
An example of aggressive symbiosis is the myxomatosis epidemic in rabbits in Australia in the 1950s. The European rabbit was introduced into Australia in 1859 as a source of food. Lacking natural predators, the population exploded, leading to widespread destruction of agricultural grassland. In 1950, rabbits infected with myxoma virus were deliberately released into the wild. Within three months, 99.8 per cent of the rabbits of south-east Australia were dead.
Although the myxomatosis epidemic was not planned as an evolutionary experiment, it had evolutionary consequences. The myxoma virus's natural host is the Brazilian rabbit, in which it is a persistant partner causing no more than minor skin blemishes. The same is now true of rabbits in Australia. Over the course of the epidemic the virus selected for rabbits with a minority genetic variant capable of surviving infection. Plague culling was followed by co-evolution, and today rabbit and virus coexist in a largely non-pathogenic mutualism.
Now imagine a plague virus attacking an early human population in Africa. The epidemic would have followed a similar trajectory, with plague culling followed by a period in which survivors and virus co-evolved. There is evidence that this happened repeatedly during our evolution, though when, and through what infectious agents, is unknown (Proceedings of the National Academy of Sciences, vol 99, p 11748).
Even today viral diseases are changing the course of human evolution. Although the plague culling effect is mitigated by medical intervention in the AIDS pandemic, we nevertheless observe selection pressure on humans and virus alike. For example, the human gene HLA-B plays an important role in the response to HIV-1 infection, and different variants are strongly associated with the rate of AIDS progression. It is therefore likely that different HLA-B alleles impose selection pressure on HIV-1, while HLA-B gene frequencies in the population are likely to be influenced by HIV (Nature, vol 432, p 769). This is symbiogenesis in action.
How does that move us closer to understanding the composition of the human genome? HIV-1 is a retrovirus, a class of RNA virus that converts its RNA genome into DNA before implanting it into host chromosomes. This process, known as endogenisation, converts an infectious virus into a non-infectious endogenous retrovirus (ERV). In humans, ERVs are called HERVs.
Germline invaders
Endogenisation allows retroviruses to take genetic symbiosis to a new level. Usually it is an extension of the normal infectious process, when a retrovirus infects a blood cell, such as a lymphocyte. But if the virus happens to get incorporated in a chromosome in the host's germ line (sperm or egg), it can become part of the genome of future generations.
Such germ-line endogenisation has happened repeatedly in our own lineage - it is the source of all that viral DNA in our genome. The human genome contains thousands of HERVs from between 30 and 50 different families, believed to be the legacy of epidemics throughout our evolutionary history. We might pause to consider that we are the descendents of the survivors of a harrowing, if brutally creative, series of viral epidemics.
Endogenisation is happening right now in a retroviral epidemic that is spreading among koalas in Australia. The retrovirus, KoRv, appeared about 100 years ago and has already spread through 75 per cent of the koala's range, culling animals on a large scale and simultaneously invading the germ line of the survivors.
Retroviruses don't have a monopoly on endogenisation. Earlier this month researchers reported finding genes from a bornavirus in the genomes of several mammals, including humans, the first time a virus not in the retrovirus class has been identified in an animal genome. The virus appears to have entered the germ line of a mammalian ancestor around 40 million years ago (Nature, vol 463, p 84). Many more such discoveries are anticipated, perhaps explaining the origin of some of that mysterious half of the genome.
The ability of viruses to unite, genome-to-genome, with their hosts has clear evolutionary significance. For the host, it means new material for evolution. If a virus happens to introduce a useful gene, natural selection will act on it and, like a beneficial new mutation, it may spread through the population.
Could a viral gene really be useful to a mammal? Don't bet against it. Retroviruses have undergone a long co-evolutionary relationship with their hosts, during which they have evolved the ability to manipulate host defences for their own ends. So we might expect the genes of viruses infecting humans to be compatible with human biology.
This is also true of their regulatory DNA. A virus integrating itself into the germ line brings not just its own genes, but also regulatory regions that control those genes. Viral genomes are bookended by regions known as long terminal repeats (LTRs), which contain an array of sequences capable of controlling not just viral genes but host ones as well. Many LTRs contain attachment sites for host hormones, for example, which probably evolved to allow the virus to manipulate host defences.
Retroviruses will often endogenise repeatedly throughout the host genome, leading to a gradual accumulation of anything up to 1000 ERVs. Each integration offers the potential of symbiogenetic evolution.
Once an ERV is established in the genome, natural selection will act on it, weeding out viral genes or regulatory sequences that impair survival of the host, ignoring those that have no effect, and positively selecting the rare ones that enhance survival.
Most ERV integrations will be negative or have no effect. The human genome is littered with the decayed remnants of such integrations, often reduced to fragments, or even solitary LTRs. This may explain the origin of retrotransposons. These come in two types: long and short interspersed repetitive elements (LINEs and SINEs), and it now appears likely that they are heavily degraded fragments of ancient viruses.
As for positive selection, this can be readily confirmed by looking for viral genes or regulatory sequences that have been conserved and become an integral part of the human genome. We now know of many such sequences.
The first to be discovered is the remnant of a retrovirus that invaded the primate genome a little less than 40 million years ago and gave rise to what is known as the W family of ERVs. The human genome has roughly 650 such integrations. One of these, on chromosome 7, contains a gene called syncytin-1, which codes for a protein originally used in the virus's envelope but now critical to the functioning of the human placenta. Expression of syncytin-1 is controlled by two LTRs, one derived from the original virus and another from a different retrovirus called MaLR. Thus we have a quintessential viral genetic unit fulfilling a vitally important role in human biology.
Virus genes
There are many more examples. Another gene producing a protein vital to the construction of the placenta, syncytin-2, is also derived from a virus, and at least six other viral genes contribute to normal placental function, although their precise roles are poorly understood.
There is also tentative evidence that HERVs play a significant role in embryonic development. The developing human embryo expresses genes and control sequences from two classes of HERV in large amounts, though their functions are not known (Virology, vol 297, p 220). What is more, disrupting the action of LINE retrotransposons by administration of the drug nevirapine causes an irreversible arrest in development in mouse embryos, suggesting that LINEs are somehow critical to early development in mammals (Systems Biology in Reproductive Medicine, vol 54, p 11).
It also appears that HERVs play important roles in normal cellular physiology. Analysis of gene expression in the brain suggests that many different families of HERV participate in normal brain function. Syncytin-1 and syncytin-2, for example, are extensively expressed in the adult brain, though their functions there have yet to be explored.
Other research groups have found that 25 per cent of human regulatory sequences contain viral elements, prompting suggestions that HERVs make a major contribution to gene regulation (Trends in Genetics, vol 19, p 68). In support of that, HERV LTRs have been shown to be involved in the transcription of important proteins. For example, the beta-globin gene, which codes for one of the protein components of haemoglobin, is partly under the control of an LTR derived from a retrovirus.
The answer to our paradox is now clear: the human genome has evolved as a holobiontic union of vertebrate and virus. It is hardly surprising that researchers who have made these discoveries are now calling for a full-scale project to assess the contribution of viruses to our biology (BMC Genomics, vol 9, p 354).
It is also probable that this "virolution" is continuing today. HIV belongs to a group of retroviruses called the lentiviruses. Until recently virologists thought that lentiviruses did not endogenise, but now we know that they have entered the germ lines of rabbits and the grey mouse lemur. That suggests that HIV-1 might have the potential to enter the human germ line (Proceedings of the National Academy of Sciences, vol 104, p 6261 and vol 105, p 20362), perhaps taking our evolution in new and unexpected directions. It's a plague to us - but it could be vital to the biology our descendants.
http://www.newscientist.com/article/mg20527451.200-i-virus-why-youre-only-half-human.html?full=true
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