On the face of it it sounds like the nice narrative we are fed every time something like this happens. I haven’t been following the international scene, and frankly it wouldn’t even surprise me if Europe headed for nativism and blood-related nationality. It is what is at the basis of their nation states (even if it’s often a lie. For instance I’d hazard that a lot of people in Portugal — yes, d*mn it, I’ll do the DNA testing. Let the house sell and let me have some money first — are as mixed as Americans. My kids call Portugal the reservoir tip at the end of Europe, which is unkind but somewhat accurate since that portion of land was part of the Celtic commonwealth, before being invaded by Carthaginians, Greeks, Romans, Germanic tribes, Moors (though their contribution in the North is minimal as the North was usually administered by overseers with little or no actual colonization) French crusaders, Viking raiders. Then there were British and Irish merchants due to ties going back before the Carthaginians who would set up trading posts, send their younger sons over, sometimes engage in a bit of raiding, etc. There are unkind proverbs about blue eyed Portuguese, but there are also a lot of them. (Two of my grandparents. A third was green eyed.) And in the end sometimes I think all of us are the result of some girl who tripped (on purpose or not) while evading a foreigner. All this to say that when my dad talks of the “The Portuguese Race” (and boy, does he) he’s mostly talking of a mythical entity. But it’s one they all believe in as hard as they can.)
Sarah A. Hoyt, “Multiculturalism IS Racism”, According to Hoyt, 2015-04-04.
May 15, 2015
March 20, 2015
Epigenetic researchers – “We can double the size of these bugs!” Everyone else – “No, thanks. We’re good.”
Science can be a great source of fascinating experiments. Doubling the size of insects is perhaps not the best way to advertise your particular speciality, however:
Researchers have changed the size of a handful of Florida ants by chemically modifying their DNA, rather than by changing its encoded information. The work is the latest advance from a field known as epigenetics and may help explain how the insects — despite their high degree of genetic similarity — grow into the different varieties of workers needed in a colony.
This discovery “takes the field leaps and bounds forward,” says entomologist Andrew Suarez of the University of Illinois, Urbana-Champaign, who wasn’t connected to the study. “It’s providing a better understanding of how genes interact with the environment to generate diversity.”
Ant nests have division of labor down pat. The queen spends her time pumping out eggs, and the workers, which are genetically similar sisters, perform all the other jobs necessary to keep the colony thriving, such as tending the young, gathering food, and excavating tunnels. Workers in many ant species specialize even further, forming so-called subcastes that look different and have different roles. In Florida carpenter ants (Camponotus floridanus), for example, workers tend to fall into two groups. Minor workers, which can be less than 6 mm long, rear the young and forage for food. Major workers, which can be almost twice as long, use their large jaws to protect the colony from predators.
A team from McGill University in Montreal, Canada, suspected that the mechanism involves DNA methylation: the addition of a chemical to DNA. Genome sequencing and other methods suggest that these physical differences don’t usually stem from genetic differences between individual ants. Instead, environmental factors help push workers to become majors or minors — specifically, the amount of food and coddling that young ants receive. But just how do these factors change the size of ants?
February 20, 2015
In Nature, Claire Ainsworth explains why it’s becoming more difficult to discuss sex as a binary:
Sex can be much more complicated than it at first seems. According to the simple scenario, the presence or absence of a Y chromosome is what counts: with it, you are male, and without it, you are female. But doctors have long known that some people straddle the boundary — their sex chromosomes say one thing, but their gonads (ovaries or testes) or sexual anatomy say another. Parents of children with these kinds of conditions — known as intersex conditions, or differences or disorders of sex development (DSDs) — often face difficult decisions about whether to bring up their child as a boy or a girl. Some researchers now say that as many as 1 person in 100 has some form of DSD.
When genetics is taken into consideration, the boundary between the sexes becomes even blurrier. Scientists have identified many of the genes involved in the main forms of DSD, and have uncovered variations in these genes that have subtle effects on a person’s anatomical or physiological sex. What’s more, new technologies in DNA sequencing and cell biology are revealing that almost everyone is, to varying degrees, a patchwork of genetically distinct cells, some with a sex that might not match that of the rest of their body. Some studies even suggest that the sex of each cell drives its behaviour, through a complicated network of molecular interactions. “I think there’s much greater diversity within male or female, and there is certainly an area of overlap where some people can’t easily define themselves within the binary structure,” says John Achermann, who studies sex development and endocrinology at University College London’s Institute of Child Health.
These discoveries do not sit well in a world in which sex is still defined in binary terms. Few legal systems allow for any ambiguity in biological sex, and a person’s legal rights and social status can be heavily influenced by whether their birth certificate says male or female.
“The main problem with a strong dichotomy is that there are intermediate cases that push the limits and ask us to figure out exactly where the dividing line is between males and females,” says Arthur Arnold at the University of California, Los Angeles, who studies biological sex differences. “And that’s often a very difficult problem, because sex can be defined a number of ways.”
February 19, 2015
Published on 18 Feb 2015
Almost every cell in your body has the same DNA sequence. So how come a heart cell is different from a brain cell? Cells use their DNA code in different ways, depending on their jobs. Just like orchestras can perform one piece of music in many different ways. A cell’s combined set of changes in gene expression is called its epigenome. This week Nature publishes a slew of new data on the epigenomic landscape in lots of different cells. Learn how epigenomics works in this video.
February 9, 2015
Last month, in his Times column, Matt Ridley explained why — until we discover a treatment for aging itself — rising cancer rates are a weird form of good news:
If we could prevent or cure all cancer, what would we die of? The new year has begun with a war of words over whether cancer is mostly bad luck, as suggested by a new study from Johns Hopkins School of Medicine, and over whether it’s a good way to die, compared with the alternatives, as suggested by Dr Richard Smith, a former editor of the BMJ.
It is certainly bad luck to be British and get cancer, relatively speaking. As The Sunday Times reported yesterday, survival rates after cancer diagnosis are lower here than in most developed and some developing countries, reflecting the National Health Service’s chronic problems with rationing treatment by delay. In Japan, survival rates for lung and liver cancer are three times higher than here.
Cancer is now the leading cause of death in Britain even though it is ever more survivable, with roughly half of people who contract it living long enough to die of something else. But what else? Often another cancer.
In the western world we’ve conquered most of the causes of premature death that used to kill our ancestors. War, smallpox, homicide, measles, scurvy, pneumonia, gangrene, tuberculosis, stroke, typhoid, heart disease and cholera are all much rarer, strike much later in life or are more survivable than they were fifty or a hundred years ago.
The mortality rate in men from coronary heart disease, for instance, has fallen by an amazing 80 per cent since 1968 — for all age groups. Mortality rates from stroke in both sexes have halved in 20 years. Cancer’s growing dominance of the mortality tables is not because it’s getting worse but because we are avoiding other causes of death and living longer.
It is worth remembering that some scientists and anti-pesticide campaigners in the 1960s were convinced that by now lifespans would be much shorter because of cancer caused by pesticides and other chemicals in the environment.
In the 1950s Wilhelm Hueper — a director of the US National Cancer Institute and mentor to Rachel Carson, the environmentalist author of Silent Spring — was so concerned that pesticides were causing cancer that he thought the theory that lung cancer was caused by smoking was a plot by the chemical industry to divert attention from its own culpability: “Cigarette smoking is not a major factor in the causation of lung cancer,” he insisted.
In fact it turns out that pollution causes very little cancer and cigarettes cause a lot. But aside from smoking, most cancers are indeed bad luck. The Johns Hopkins researchers found that tissues that replicate their stem cells most run the highest risk of cancer: basal skin cells do ten trillion cell divisions in a lifetime and have a million times more cancer risk than pelvic bone cells which do about a million cell divisions. Random DNA copying mistakes during cell division are “the major contributors to cancer overall, often more important than either hereditary or external environmental factors”, say the US researchers.
To sum it up, until or unless medical research finds a way to stop the bodily effects of aging, cancer becomes the most likely way for all of us to die. Cancer is a generic rather than a specific term — it’s what we use to describe the inevitable breakdown of the cellular division process that happens millions or even trillions of times over our lifetime. As Ridley puts it, “even if everybody lived in the healthiest possible way, we would still get a lot of cancer.” I’m not a scientist and I don’t even play one on TV, but I suspect that the solution to cancers of all kinds are to boost our immune systems to more quickly identify aberrant cells in our bodies before they start reproducing beyond the capability of the immune system to handle. The short- to medium-term solution to cancer may be to make us all a little bit cyborg…
December 5, 2014
Michael White says we need to follow up our success in reading our own genetic code by decoding a different one:
There are thousands of mutations that occur in the breast cancer-linked genes BRCA1 and BRCA2. Some of these cause breast or ovarian cancer, while others are harmless. When we design a genetic test for predisposition to breast cancer, we have to know which ones to test for. The same is true of almost any gene that plays a role in disease — you’ll find many mutations in that gene in the general population, only some of which cause health problems. So how do we know which mutations to worry about?
We start by using the genetic code. The genetic code, cracked by scientists in the 1960s, makes it surprisingly easy to “read” our DNA and understand how a particular mutation affects a gene. As genetic testing takes on a bigger role in predicting, diagnosing, and treating disease, we rely on this code to help us make sense of the data. Unfortunately, the genetic code applies to less than two percent of our DNA. In an effort to read the rest, researchers are trying to crack a new genetic code — and this next one is turning out to be much more difficult to solve than the first. In fact, scientists may have to give up the idea that we can use a “code” to “read” the rest of our DNA.
When scientists were working out the original genetic code in the 1950s and ’60s, all sorts of complicated schemes were proposed to explain how information is stored in our genes. The problem they were trying to solve was how a gene, made of DNA, codes the information to make a particular protein — an enzyme, a pump, a piece of cellular scaffolding, or some other critical component of the cell’s working machinery. They were looking for a code that would translate the four-letter DNA alphabet of genes into the 20-letter amino acid alphabet of proteins.
Thanks to its simplicity, the genetic code is a powerful tool in our hunt for mutations that cause disease. Unfortunately, it has also led to the genetic equivalent of a drunk looking for his lost keys under the lamppost. Researchers have put much of their effort into looking for disease mutations in those parts of our genomes that we can read with the genetic code — that is, parts that consist of canonical genes that code for proteins. But these genes make up less than two percent of our DNA; much more of our genetic function is outside of genes in the relatively uncharted “non-coding” portions. We have no idea how many disease-causing mutations are in that non-coding portion — for some types of mutations, it could be as high as 90 percent.
May 7, 2014
In Forbes, Matthew Herper looks at how Novartis is transforming itself in an attempt to conquer cancer:
“I’ve been an oncologist for 20 years,” says Grupp, “and I have never, ever seen anything like this.” Emily has become the poster child for a radical new treatment that Novartis, the third-biggest drug company on the Forbes Global 2000, is making one of the top priorities in its $9.9 billion research and development budget.
“I’ve told the team that resources are not an issue. Speed is the issue,” says Novartis Chief Executive Joseph Jimenez, 54. “I want to hear what it takes to run this phase III trial and to get this to market. You’re talking about patients who are about to die. The pain of having to turn patients away is such that we are going as fast as we can and not letting resources get in the way.”
A successful trial would prove a milestone in the fight against the demon that has plagued living things since dinosaurs roamed the Earth. Coupled with the exploding capabilities of DNA-sequencing machines that can unlock the genetic code, recent drugs have delivered stunning results in lung cancer, melanoma and other deadly tumors, sometimes making them disappear entirely – albeit temporarily. Just last year the Food & Drug Administration approved nine targeted cancer drugs. It’s big business, too. According to data provider IMS Health, spending on oncology drugs was $91 billion last year, triple what it was in 2003.
But the developments at Penn point, tantalizingly, to something more, something that would rank among the great milestones in the history of mankind: a true cure. Of 25 children and 5 adults with Emily’s disease, ALL, 27 had a complete remission, in which cancer becomes undetectable. “It’s a stunning breakthrough,” says Sally Church, of drug development advisor Icarus Consultants. Says Crystal Mackall, who is developing similar treatments at the National Cancer Institute: “It really is a revolution. This is going to open the door for all sorts of cell-based and gene therapy for all kinds of disease because it’s going to demonstrate that it’s economically viable.”
H/T to Megan McArdle for the link.
December 17, 2013
At Ace of Spades HQ, Ace explains why a court decision from the 1970s set a very bad precedent for today’s legal and technological world:
Fifty years ago the police had a very limited ability to utilize your fingerprints record to harm you. If you became a suspect in a case — and only in that case — they could painstakingly compare your fingerprints to those found at a crime scene using slow, precious human labor resources.
There were serious practical limits on what could be done with citizen data held in government files. Yes, the government could use that data to put people in jail, but analysis and comparison was a labor intensive process that at least served as a naturally-existing limiting principle on government intrusion: Sure, the government could search your personally-identifying data to connect you with a crime, but, as a practical matter, it was so time-consuming to do so that they generally would not do so, not unless they had a strong suspicion you were actually a culprit.
They wouldn’t just compare every fingerprint on file with every fingerprint found at unsolved crime scenes, after all.
Well, today, they can — and do — actually do that. So there is no longer any practical limitation on the government’s ability to use your DNA to connect you with unknown DNA found at a crime. They can run everyone’s DNA through the database with virtually no effort.
I exaggerate; there is some lab work needed to process the DNA and reduce it to a 13 allele “genetic fingerprint.” Nevertheless, this can all be done fairly inexpensively, and running it through the database once reduced to a short code is very nearly cost-free.
But within the next ten years all of this will become entirely cost-free.
This is why I disagreed with the Supreme Court’s reliance on an old precedent in claiming that the police can take a DNA sample from every single person arrested. Merely arrested, not convicted. They relied on a precedent established at the dawn of investigatory police science, that every arrestee’s fingerprints may be collected and catalogued.
But way ‘back then, there were natural limitations on the State’s power to make use of such data which simply no longer exist. What would have been considered a silly hypothetical sci-fi objection back then — “But what stops the state from merely searching these fingerprints against every fingerprint ever lifted at a crime scene?” — is actual reality now.
The same arguments apply to all police/FBI/NSA mass data collection: cell-phone usage, internet activity, license plate scanning, facial recognition software, and so on. It resets the baseline assumptions of civil society, where the authorities only look for suspects in actual criminal cases, rather than tracking everyone all the time and deducing “criminal” actions without needing to detect the crime. If your first reaction is to think “if you’ve done nothing wrong, you’ve got nothing to fear”, remember that you cannot possibly know all the laws of your country and that statistically speaking, you probably violate one or more laws every day without realizing it (one author suggests it’s actually three felonies per day).
Update: Ayn Rand explained this phenomenon fictionally in Atlas Shrugged.
“Did you really think that we want those laws to be observed?” said Dr. Ferris. “We want them broken. You’d better get it straight that it’s not a bunch of boy scouts you’re up against — then you’ll know that this is not the age of beautiful gestures. We’re after power and we mean it. You fellows were pikers, but we know the real trick, and you’d better get wise to it. There’s no way to rule innocent men. The only power any government has is the power to crack down on criminals. Well, when there aren’t enough criminals, one ‘makes’ them. One declares so many things to be a crime that it becomes impossible for men to live without breaking laws. Who wants a nation of law-abiding citizens? What’s there in that for anyone? But just pass the kind of laws that can neither be observed nor enforced nor objectively interpreted — and you create a nation of law-breakers and then you cash in on the guilt. Now that’s the system, Mr. Rearden, that’s the game, and once you understand it, you’ll be much easier to deal with.”
December 2, 2013
Kyle Smith on the FDA’s sudden interest in shutting down private DNA testing company 23andMe:
… the FDA has the power to regulate medical devices, which is the pretext it is using to stop 23andMe. Ordering it to stop selling its personal genome service, the FDA declared that the tube “is a device within the meaning of section 201(h) of the FD&C Act, 21 U.S.C. 321(h), because it is intended for use in the diagnosis of disease or other conditions or in the cure, mitigation, treatment or prevention of disease, or is intended to affect the structure or function of the body.’
It would seem that 23andMe could simply put the words, “not intended for us in the diagnosis, cure, mitigation, treatment or prevention of disease” on its website and satisfy the FDA, but we all know that the motto of today’s federales is “We make it up as we go along.” The FDA seems determined to conduct a lengthy war with 23andMe.
Using the same reasoning, the FDA might as well shut down WebMd.com because people might type their symptoms into the site, and the response might affect whether or not they choose to go to a doctor. Any computer or iPhone thereby becomes a “medical device” that people can use for the “diagnosis, cure, mitigation, treatment or prevention of disease.”
Come to think of it, that thermometer you use to check your temperature is pretty dangerous too — it might give you either a false positive or a false negative — but why stop there? You exercise to mitigate or prevent disease, don’t you? Maybe the FDA should take your running shoes and your yoga pants away.
November 29, 2013
Nick Gillespie on the mindnumbingly awful exercise of FDA regulatory power in shutting down personal DNA testing company 23andMe:
Personal genetic tests are safe, innovative, and the future of medicine. So why is the most transparent administration ever shutting down a cheap and popular service? Because it can.
In its infinite wisdom, the Food and Drug Administration (FDA) has forbidden the personal genetic testing service 23andMe from soliciting new customers, claiming the company hasn’t proven the validity of its product.
The real reason? Because when it comes to learning about your own goddamn genes, the FDA doesn’t think you can handle the truth. That means the FDA is now officially worse than Oedipus’s parents, Dr. Zaius, and the god of Genesis combined, telling us that there are things that us mere mortals just shouldn’t be allowed to know.
23andMe allows you to get rudimentary information about your genetic makeup, including where your ancestors came from and DNA markers for over 240 different hereditary diseases and conditions (not all of them bad, by the way). Think of it as the H&M version of the haute couture genetic mark-up that Angelina Jolie had done prior to having the proactive mastectomy that she revealed this year.
Peter Huber of the Manhattan Institute, a conservative think tank, has an important new book out called The Cure in the Code: How 20th Century Law is Undermining 21st Century Medicine. Huber writes that whatever sense current drug-approval procedures once might have had, their day is done. Not only does the incredible amount of time and money — 12 years and $350 million at a minimum — slow down innovation, it’s based on the clearly wrong idea that all humans are the same and will respond the same way to the same drugs.
Given what we already know about small but hugely important variations in individual body chemistry, the FDA’s whole mental map needs to be redrawn. “The search for one-dimensional, very simple correlations — one drug, one clinical effect in all patients — is horrendously obsolete,” Huber told me in a recent interview. And the FDA’s latest action needs to be understood in that context — it’s just one more way in which a government which now not only says we must buy insurance but plans whose contours are dictated by bureaucrats who arbitrarily decide what is best for all of us.
March 18, 2013
Mark Lynas was one of the most prominent activists working against the adoption of genetically modified crops. Over time, he realized he was fighting the wrong battle and publicly recanted his decades-long struggle. He talks about it in an interview with Charlie Gillis in Maclean’s:
Q: You’ve disavowed a cause you were identified with for decades. How are you feeling about your decision?
A: It’s been traumatic, but it’s also been something of a liberation. I’ve obviously been inconsistent in my life, but so are we all. In my view, it’s better to be inconsistent and half-right, than to be consistently wrong. Even the pope doesn’t claim these days to be infallible, yet that’s what most environmental groups do.
Q: Still, you’ve offended your former allies, a lot of whom are now trying to discredit you. Some say you exaggerated your part in founding the anti-GM movement to start with. What’s that been like on a personal level?
A: My whole social scene has been characterized by my environmentalism. I’m in a situation where I can go to a party and I don’t know who’s currently not speaking to me.
Q: On Twitter, Vandana Shiva, a prominent environmentalist in India, likened your calls for farmers to be able to plant GMOs to saying rapists should have the freedom to rape.
A: That was simply astonishing, and frankly, hurtful to people who have actually suffered the trauma of rape. Look, these attacks on me are obviously done in the interests of damage limitation. It’s sort of an emperor’s-new-clothes thing. I have helped expose the fact most people’s concerns about GM foods are based on mythology. Once you can get past the idea that there’s something inherently dangerous about GM foods, it’s a whole different conversation. We actually can tell whether GM foods are safe. They have been extensively tested hundreds and hundreds of times, using different techniques. Many of the tests were conducted independently. The jury is entirely in on this issue.
[. . .]
Q. You argue that opposing GMOs is actually anti-environmental.
A. That was the realization that changed my mind. That recombinant DNA is actually a potentially very powerful technology for designing crop plants that can help humanity tackle our food-supply shortages, and also reduce our environmental footprint. They can help us use less fertilizer, and dramatically reduce pesticide applications. We can reduce our exposure to climate change through drought and heat-tolerant crops. So the potential is enormous.
March 2, 2013
Matt Ridley on the soon-to-be-possible reversal of species extinction:
The founders of Revive and Restore aren’t mainstream scientists, but they’re not people to be taken lightly, either. Stewart Brand and Ryan Phelan are a husband-and-wife team with a track record of starting unusual but successful organizations — in his case, the Whole Earth Catalog and the Global Business Network; in hers, the consumer-focused startups Direct Medical Knowledge and DNA Direct. They’ve attracted the interest of the pioneering Harvard University DNA sequencing and synthesis expert George Church.
Their argument is that it’s time to start tentatively trying de-extinction and thinking through its ethical and ecological implications. There are already projects under way to revive extinct subspecies like the European aurochs (a type of wild cattle) and the Pyrenean ibex, or bucardo. In the latter case, when the last female (Celia) was killed by a falling tree in 2000, her tissue was cloned. At least one fetus survived to term in a surrogate mother goat, but it died soon after birth.
A full species that’s been extinct for decades like the thylacine (Tasmanian tiger) or the passenger pigeon — the last one of which, Martha, died in the Cincinnati Zoo 99 years ago — will be a taller order, since the DNA from long dead specimens is fragmented. Yet Ben Novak, a young researcher working with the ancient-DNA expert Beth Shapiro at the University of California, Santa Cruz, has extracted passenger pigeon DNA from the toe pad of a museum specimen and sequenced it. Dr. Church hopes to use one of the newly invented letter-by-letter gene-replacement techniques, such as Talens or Crispr, to transform the genome of a related species called the band-tailed pigeon into that of a passenger pigeon.
February 18, 2013
Tim Worstall on some of the issues with demands that all British beef for human consumption be tested for horsemeat:
Now let’s turn to that meat problem. We’re going to test something to make sure that it is indeed what it says. Most of the time, usually, we’d go looking for beef DNA and on finding it say, yup, that’s beef.
But now we’re talking about trace amounts of other species. Some of this horse contamination is someone deliberately substituting, yes. But a lot of it, those trace amounts, is someone not cleaning the pipes between species being processed. Or the knives even. Which leads us to something of a problem.
How many species do we test for? Some minced beef… or pink slime perhaps. Do we test for beef and horse? For beef, horse, mutton, pork, chicken, duck, goose? What about rat and mouse? For I’ll guarantee you that however much people try there will often be the odd molecule of either one of those in there. Sparrow? That’s more of a problem with grain processing but still.
For example, one lovely story about vegetarianism. Those (umm, OK, some) who have moved from the sub-continent to the UK. They carry on eating the (possibly Hindu caste based) vegetarian diet they are used to. And they start falling prey to all sorts of dietary deficiencies. Anaemia, there have even been reports of kwashikor (a protein deficiency). The grains and the pulses of the sub-continent have rather more insect and other residue in them than our more modern processing and storage systems provide.
People don’t test for hedgehog DNA in meat supplies, no. But how many species should they test for?
February 5, 2013
A facial reconstruction based on the skull of Richard III:
A facial reconstruction based on the skull of Richard III has revealed how the English king may have looked.
The king’s skeleton was found under a car park in Leicester during an archaeological dig.
The reconstructed face has a slightly arched nose and prominent chin, similar to features shown in portraits of Richard III painted after his death.
Historian and author John Ashdown-Hill said seeing it was “almost like being face to face with a real person”.
The development comes after archaeologists from the University of Leicester confirmed the skeleton found last year was the 15th Century king’s, with DNA from the bones having matched that of descendants of the monarch’s family.
I was unable to find an image of the reconstruction that is okay to use, but you can see various pictures on Google Image Search.
February 4, 2013
BBC News rounds up the details:
A skeleton found beneath a Leicester car park has been confirmed as that of English king Richard III.
Experts from the University of Leicester said DNA from the bones matched that of descendants of the monarch’s family.
Lead archaeologist Richard Buckley, from the University of Leicester, told a press conference to applause: “Beyond reasonable doubt it’s Richard.”
Richard, killed in battle in 1485, will be reinterred in Leicester Cathedral.
Mr Buckley said the bones had been subjected to “rigorous academic study” and had been carbon dated to a period from 1455-1540.
Dr Jo Appleby, an osteo-archaeologist from the university’s School of Archaeology and Ancient History, revealed the bones were of a man in his late 20s or early 30s. Richard was 32 when he died.
His skeleton had suffered 10 injuries, including eight to the skull, at around the time of death. Two of the skull wounds were potentially fatal.
One was a “slice” removing a flap of bone, the other caused by bladed weapon which went through and hit the opposite side of the skull, a depth of more than 10cms (4ins).
Dr Appleby said: “Both of these injuries would have caused an almost instant loss of consciousness and death would have followed quickly afterwards.
“In the case of the larger wound, if the blade had penetrated 7cm into the brain, which we cannot determine from the bones, death would have been instantaneous.”
Other wounds included slashes or stabs to the face and the side of the head.
Update: New Scientist still has concerns that the trail of evidence is not strong enough to constitute proof of identity:
Mitochondrial DNA is passed down the maternal line and has 16,000 base pairs in total. Typically, you might expect to get 50 to 150 fragments from a 500-year-old skeleton, says Ian Barnes at Royal Holloway, University of London, who was not involved in the research. “You’d want to get sequences from lots of those fragments,” he says. “There’s a possibility of mitochondrial mutations arising in the line from Richard III.”
“It’s intriguing to be sure,” says Mark Thomas at University College London. It is right that they used mitochondrial DNA based on the maternal line, he says, since genealogical evidence for the paternal lineage cannot be trusted.
But mitochondrial DNA is not especially good for pinpointing identity. “I could have the same mitochondrial DNA as Richard III and not be related to him,” says Thomas.
The researchers used the two living descendents to “triangulate” the DNA results. The evidence will rest on whether Ibsen and his cousin have sufficiently rare mtDNA to make it unlikely that they both match the dead king by chance.