Things are going to be alright

Saturday, January 21st, 2017

Recent studies showed that a single dose of psilocybin reduces anxiety and depression in cancer patients:

About 80 percent of cancer patients showed clinically significant reductions in both psychological disorders, a response sustained some seven months after the single dose. Side effects were minimal.

In both trials, the intensity of the mystical experience described by patients correlated with the degree to which their depression and anxiety decreased.

The studies, by researchers at New York University, with 29 patients, and at Johns Hopkins University, with 51, were released concurrently in The Journal of Psychopharmacology. They proceeded after arduous review by regulators and are the largest and most meticulous among a handful of trials to explore the possible therapeutic benefit of psilocybin.


One theory is that psilocybin interrupts the circuitry of self-absorbed thinking that is so pronounced in depressed people, making way for a mystical experience of selfless unity.

More from another article:

In the Johns Hopkins study, half of the 51 participants were given a low dose of psilocybin as control, followed by a high dose five weeks later. (For the other half, the order of the doses was reversed.) The results were remarkable: Six months later, 78 percent of the participants were less depressed than they started, as rated by a clinician, and 83 percent were less anxious. Furthermore, 65 percent had almost fully recovered from depression, and 57 percent from their anxiety, after six months. By comparison, in past studies antidepressants have only helped about 40 percent of cancer patients, performing about as well as a placebo. At the six-month follow-up, two-thirds of the participants rated the experience as one of the top five most meaningful of their lives. They attributed their improvements to positive changes in their attitudes about their lives and their social relationships. Their quality of life improved, as did their feelings of “life meaning” and optimism—even though several of them would later die. “People will say, ‘I know I’m dying, I’m sad that I’m dying, but it’s okay,” Griffiths said. “Things are going to be alright.”

The New York University study was very similar, but it had only 29 participants and used niacin, a vitamin, as a placebo. (Halfway through the experiment, the participants switched groups.) It also included a more formal psychotherapy component, in which the participants would discuss their trips. That study similarly found that the psilocybin had both immediate and enduring effects. Six months after the treatment, 60 to 80 percent of the participants saw improvements in various measures of depression and anxiety, and 70 percent considered it one of the top five most personally meaningful experiences of their lives.

“The most surprising thing to me is that this actually worked. I was highly skeptical,” said Ross, the lead NYU study author. Before the treatment, some of the participants would cry and shake when they talked about their cancer. But “the moment they get psilocybin, their distress comes down. That’s very new in psychiatry, to have a medication that works immediately for depression and anxiety and can last for that long.”

The researchers aren’t sure exactly how psilocybin works—a rather common problem in drugs aimed at brain chemistry. Psilocybin seems to quiet the prefrontal cortex, a part of the brain where increased activity has been associated with depression. It also might be acting on the brain’s use of glutamate, a neurotransmitter that affects learning and memory. Ross said what might be happening is a sort of “inverse PTSD”—a profoundly positive memory that affects participants for months, much like a severe trauma might in post-traumatic stress disorder.

It’s also possible that the sheer mysticism of the experience was enough to prompt a change in mood. “There’s a sacredness or a reverence to that experience … it’s also accompanied by positive mood, in the sense of an open-heartedness, love or benevolence,” Griffiths said. Participants might have a sense that “the experience is more real and more true than everyday waking consciousness. Although the effects of the drugs are gone by the end of the day, the memories of these experiences and the attributions made to them endure.” It’s not uncommon, he said, for study participants to say they think about their psilocybin experience every day.


Smaller studies have hinted at the drug’s effectiveness in treating alcoholism, obsessive-compulsive disorder, treatment-resistant depression, and smoking. It’s also been found to help change peoples’ personalities, making them more “open,” meaning imaginative or broad-minded.

There has never been a more powerful biological tool

Friday, January 20th, 2017

White-footed mice are the principal reservoir of Lyme disease, which they pass, through ticks, to humans — which presents an ecological solution:

There is currently no approved Lyme vaccine for humans, but there is one for dogs, which also works on mice. Esvelt and his team would begin by vaccinating their mice and sequencing the DNA of the most protective antibodies. They would then implant the genes required to make those antibodies into the cells of mouse eggs. Those mice would be born immune to Lyme. Ultimately, if enough of them are released to mate with wild mice, the entire population would become resistant. Just as critically, the antibodies in the mice would kill the Lyme bacterium in any ticks that bite them. Without infected ticks, there would be no infected people. “Take out the mice,” Esvelt told me, “and the entire transmission cycle collapses.”


Esvelt and his colleagues were the first to describe, in 2014, how the revolutionary gene-editing tool CRISPR could combine with a natural phenomenon known as a gene drive to alter the genetic destiny of a species. Gene drives work by overriding the traditional rules of Mendelian inheritance. Normally, the progeny of any sexually reproductive organism receives half its genome from each parent. But since the nineteen-forties biologists have been aware that some genetic elements are “selfish”: evolution has bestowed on them a better than fifty-per-cent chance of being inherited. That peculiarity makes it possible for certain characteristics to spread with unusual speed.

Until CRISPR came along, biologists lacked the tools to force specific genetic changes across an entire population. But the system, which is essentially a molecular scalpel, makes it possible to alter or delete any sequence in a genome of billions of nucleotides. By placing it in an organism’s DNA, scientists can insure that the new gene will copy itself in every successive generation. A mutation that blocked the parasite responsible for malaria, for instance, could be engineered into a mosquito and passed down every time the mosquito reproduced. Each future generation would have more offspring with the trait until, at some point, the entire species would have it.

There has never been a more powerful biological tool, or one with more potential to both improve the world and endanger it.

Really, what’s the worst that could happen?

Oxytocin levels surge in troops of chimpanzees preparing for conflict with rival groups

Thursday, January 19th, 2017

Oxytocin levels surge in troops of chimpanzees preparing for conflict with rival groups:

The finding is at odds with the prevailing image of oxytocin as something that helps strengthen bonds between parent and infant, or foster friendships. But given its capacity to strengthen loyalty, oxytocin could also be a warmonger hormone that helps chimps galvanise and cooperate against a common enemy.

Catherine Crockford of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and her colleagues monitored two rival groups of chimpanzees in the Taï National Park in Ivory Coast, each containing five males and five females, for prolonged periods between October 2013 and May 2015.

Thanks to trust built up between the team and the chimps, the team could safely track and video the groups – even during conflict, observing at close quarters what was happening. Crucially, the team was also able to pipette up fresh samples from soil when chimps urinated.

The samples revealed that oxytocin levels surge in the mammals whenever the chimps on either side prepared for confrontation, or when either group took the risk of venturing near or into rival-held territories. These surges dwarfed the oxytocin levels seen during activities such as grooming, collaborative hunting for monkey prey or food sharing.

Building a 21st Century FDA

Monday, January 16th, 2017

Building a 21st Century FDA shouldn’t be hard:

A 2010 study in the Journal of Clinical Oncology by researchers from the M.D. Anderson Cancer Center in Houston, Texas found that the time from drug discovery to marketing increased from eight years in 1960 to 12 to 15 years in 2010. Five years of this increase results from new regulations boosting the lengths and costs of clinical trials. The regulators aim to prevent cancer patients from dying from toxic new drugs. However, the cancer researchers calculate that the delays caused by requirements for lengthier trials have instead resulted in the loss of 300,000 patient life-years while saving only 16 life-years. If true, this is a scandal.

How much higher are the costs of getting a new drug through the FDA gantlet? A new study, “Stifling New Cures: The True Cost of Lengthy Clinical Drug Trials,” by Manhattan Institute senior fellow Avik Roy points out that in 1975 the pharmaceutical industry spent about $100 million on research and development (R&D) before getting a new drug approved by the FDA. By 1987, that had tripled to $300 million and that has since quadrupled to $1.3 billion. But even these figures may be too low. Roy cites calculations done by Matthew Herper of Forbes, who divides up the R&D spending of $802 billion by 12 big pharma companies since 1997 by the 139 drugs that have since gotten FDA approval to yield costs of $5.8 billion per drug.

Currently, new pharmaceuticals typically go through Phase I trials using fewer than 100 patients to get preliminary information on the drug’s safety. Phase II trials involve a few hundred subjects and further evaluate a new drug’s safety and efficacy. Phase III trials enroll thousands of patients to see how well it works compared to either placebo and/or other therapies and to look for bad side effects.

“The biggest driver of this phenomenal increase has been the regulatory process governing Phase III clinical trials of new pharmaceuticals on on human volunteers,” notes Roy. Between 1999 and 2005, clinical trials saw average increases in trial procedures by 65 percent, staff work by 67 percent, and length by 70 percent.

Not only do FDA demands for bigger Phase III clinical trials delay the introduction of effective new medicines, they dramatically boost costs for bringing them to market. Roy acknowledges that pre-clinical research that aims to identify promising therapeutic compounds absorbs 28 percent of the R&D budgets of pharmaceutical companies. Setting those discovery costs aside, Roy calculates that the Phase III trials “typically represent 90 percent or more of the cost of developing an individual drug all the way from laboratory to market.”

Does Fungal Infection Cause Male Pattern Baldness and Heart Disease?

Sunday, January 15th, 2017

Mangan has gone down another rabbit hole in his health research, prompted by a reader’s unusual experience:

This started when a reader told me that he had started donating blood after reading this site and my book on iron.

He said that he had had seborrheic dermatitis of many years standing. (Click here if you want to see what that looks like.) It’s basically something like really terrible dandruff, but can be on any part of the body. He had tried both anti-fungal medication and topical steroids, and nothing worked. Since it didn’t bother him much, he quit worrying about it.

After his first blood donation, it started clearing up, and after his third donation, it completely disappeared.

What in the world? It turns out that both dandruff and seborrheic dermatitis are linked to a fungal infection by the fungus Malassezia. So is tinea versicolor, a skin infection; when I lived in Sierra Leone, virtually everyone had it to some degree.

Dandruff is caused by a fungal infection.

All microorganisms that invade man and cause disease require iron. (Every living thing requires iron.) Withholding iron from microbes is at the center of an evolutionary arms race. It stands to reason that donating blood can treat fungal infections of the skin by lowering skin iron levels. (Donating blood will also make you look younger.)

Shampoo that contains salicylate and ciclopirox effectively treats dandruff. Ciclopirox is an iron chelator (attaches and removes iron). So is salicylate. By attaching and removing iron, they deprive fungus of required growth material, it dies, and dandruff is treated.

Ketoconazole, an anti-fungal chemical that works by inhibiting fungal steroid synthesis, also treats dandruff.

Male pattern baldness has been linked to fungal infection as well, and the antifungal drug ketoconazole treats male pattern baldness just as well as minoxidil (Rogaine).

If this holds true for many or all cases of male pattern baldness (androgenic alopecia), then our notions of why some men go bald (that it’s due to testosterone metabolites) may be all wrong. Curiously, folklore has it that hats cause baldness — perhaps by giving fungus a warm, moist environment in which to grow?

Male pattern baldness is also associated with heart disease. Severe baldness was associated with a 2.5 fold greater risk of death from heart disease. Huge increase.

If fungal infection in the skin causes both male pattern baldness and dandruff, then iron is implicated, because all invasive microorganisms must take iron from their hosts.

High iron (ferritin) is also associated with heart disease. The mechanism usually postulated is increased oxidative stress of the walls of arteries; iron is a very reactive metal capable of damaging biological structures.

But another mechanism might be the stimulation of fungal growth. “Occult fungal infection is the underlying pathogenic cause of atherogenesis” (from the journal Medical Hypotheses).

Africa and the cold beauty of Maths

Saturday, January 14th, 2017

PISA has the capacity to spread embarrassment far and wide, in rich as well as poor countries, and Dr. James Thompson is “all in favour of that” — but that means that many countries opt out of it (and TIMMS), especially poorer countries in Africa, but a new working paper from the Center for Global Development gets around this:

Internationally comparable test scores play a central role in both research and policy debates on education. However, the main international testing regimes, such as PISA, TIMSS, or PIRLS, include very few low-income countries. For instance, most countries in Southern and Eastern Africa have opted instead for a regional assessment known as SACMEQ. This paper exploits an overlap between the SACMEQ and TIMSS tests—in both country coverage, and questions asked— to assesses the feasibility of constructing global learning metrics by equating regional and international scales. I compare three different equating methods and find that learning levels in this sample of African countries are consistently (a) low in absolute terms, with average pupils scoring below the fifth percentile for most developed economies; (b) significantly lower than predicted by African per capita GDP levels; and (c) converging slowly, if at all, to the rest of the world during the 2000s. While these broad patterns are robust, average performance in individual countries is quite sensitive to the method chosen to link scores. Creating test scores which are truly internationally comparable would be a global public good, requiring more concerted effort at the design stage.

The results are grim:

Substantively, the results here are daunting for African education systems. Most of the national test-score averages I estimate for the thirteen African countries in my sample fall more than two standard deviations below the TIMSS average, which places them below the 5th percentile in most European, North American, and East Asian countries. In contrast, scores from the SACMEQ test administered to math teachers are much higher, but fall only modestly above the TIMSS sample average for seventh- and eighth-grade pupils, in line with earlier analysis by Spaull and van der Berg (2013). African test scores appear low relative to national GDP levels; in a regression of average scores on per capita GDP in PPP terms, average scores in the SACMEQ sample are significantly below the predicted value using all three linking methodologies. Furthermore, there is little sign that African scores were improving rapidly or converging to OECD levels during the 2000s.

Really grim:

In some African countries teachers seem to have lower abilities than students in Europe or East-Asia!

Raising scholastic attainment is unlikely to be a simple question of investing money, Dr. Thompson notes:

A summary of investment in education suggests that the pay-off is front-end loaded: the first $5000 has a big effect, and then it tends to plateau thereafter. Another way of looking at it is to note that once countries get to $16,000 GDP per capita then schooling in those countries accounts for only 10% of the variance of student attainment. So, poor countries (most of Africa is well below this level) should have plenty of scope for educational gains.

Scientists Say the Clock of Aging May Be Reversible

Friday, January 13th, 2017

Researchers at the Salk Institute are resetting the clock of the aging process — in genetically engineered mice:

Ten years ago, the Japanese biologist Shinya Yamanaka amazed researchers by identifying four critical genes that reset the clock of the fertilized egg. The four genes are so powerful that they will reprogram even the genome of skin or intestinal cells back to the embryonic state. Dr. Yamanaka’s method is now routinely used to change adult tissue cells into cells very similar to the embryonic stem cells produced in the first few divisions of a fertilized egg.

Scientists next began to wonder if the four Yamanaka genes could be applied not just to cells in glassware but to a whole animal. The results were disastrous. As two groups of researchers reported in 2013 and 2014, the animals all died, some because their adult tissue cells had lost their identity and others from cancer. Embryonic cells are primed for rapid growth, which easily becomes uncontrolled.

But at the Salk Institute, Juan Carlos Izpisua Belmonte had been contemplating a different approach. He has long been interested in regeneration, the phenomenon in which certain animals, like lizards and fish, can regenerate lost tails or limbs. The cells near the lost appendage revert to a stage midway between an embryonic cell, which is open to all fates, and an adult cell, which is committed to being a particular type of cell, before rebuilding the missing limb.

This partial reprogramming suggested to him that reprogramming is a stepwise process, and that a small dose of the Yamanaka factors might rejuvenate cells without the total reprogramming that converts cells to the embryonic state.

With Alejandro Ocampo and other Salk researchers, Dr. Izpisua Belmonte has spent five years devising ways to deliver a nonlethal dose of Yamanaka factors to mice. The solution his team developed was to genetically engineer mice with extra copies of the four Yamanaka genes, and to have the genes activated only when the mice received a certain drug in their drinking water, applied just two days a week.

The Salk team worked first with mice that age prematurely, so as to get quick results. “What we saw is that the animal has fewer signs of aging, healthier organs, and at the end of the experiment we could see they had lived 30 percent longer than control mice,” Dr. Izpisua Belmonte said.

Newton made three bets

Thursday, January 12th, 2017

Paul Graham knows a thing or two about risk and discovery:

Because biographies of famous scientists tend to edit out their mistakes, we underestimate the degree of risk they were willing to take. And because anything a famous scientist did that wasn’t a mistake has probably now become the conventional wisdom, those choices don’t seem risky either.

Biographies of Newton, for example, understandably focus more on physics than alchemy or theology. The impression we get is that his unerring judgment led him straight to truths no one else had noticed. How to explain all the time he spent on alchemy and theology? Well, smart people are often kind of crazy.

But maybe there is a simpler explanation. Maybe the smartness and the craziness were not as separate as we think. Physics seems to us a promising thing to work on, and alchemy and theology obvious wastes of time. But that’s because we know how things turned out. In Newton’s day the three problems seemed roughly equally promising. No one knew yet what the payoff would be for inventing what we now call physics; if they had, more people would have been working on it. And alchemy and theology were still then in the category Marc Andreessen would describe as “huge, if true.”

How a Guy From a Montana Trailer Park Overturned 150 Years of Biology

Saturday, January 7th, 2017

Toby Spribille grew up in a Montana trailer park, where he was educated by a fundamentalist cult, before somehow getting into a German university and then overturning 150 years of biology:

He joined the lab of symbiosis specialist John McCutcheon, who convinced him to supplement his formidable natural history skills with some know-how in modern genetics.

The duo started studying two local lichens that are common in local forests and hang from branches like unruly wigs. One is yellow because it makes a strong poison called vulpinic acid; the other lacks this toxin and is dark brown. They clearly look different, and had been classified as separate species for almost a century. But recent studies had suggested that they’re actually the same fungus, partnered with the same alga. So why are they different?

To find out, Spribille analyzed which genes the two lichens were activating. He found no differences. Then, he realized that he was searching too narrowly. Lichenologists all thought that the fungi in the partnership belonged to a group called the ascomycetes — so Spribille had only searched for ascomycete genes. Almost on a whim, he broadened his search to the entire fungal kingdom, and found something bizarre. A lot of the genes that were activated in the lichens belonged to a fungus from an entirely different group — the basidiomycetes. “That didn’t look right,” says McCutcheon. “It took a lot of time to figure out.”

At first, the duo figured that a basidiomycete fungus was growing on the lichens. Perhaps it was just a contaminant, a speck of microbial fluff that had landed on the specimens. Or it might have been a pathogen, a fungus that was infecting the lichens and causing disease. It might simply have been a false alarm. (Such things happen: genetic algorithms have misidentified plague bacteria on the New York subway, platypuses in Virginia tomato fields, and seals in Vietnamese forests.)

But when Spribille removed all the basidiomycete genes from his data, everything that related to the presence of vulpinic acid also disappeared. “That was the eureka moment,” he says. “That’s when I leaned back in my chair.” That’s when he began to suspect that the basidiomycete was actually part of the lichens — present in both types, but especially abundant in the yellow toxic one.

And not just in these two types, either. Throughout his career, Spribille had collected some 45,000 samples of lichens. He began screening these, from many different lineages and continents. And in almost all the macrolichens — the world’s most species-rich group — he found the genes of basidiomycete fungi. They were everywhere. Now, he needed to see them with his own eyes.

Down a microscope, a lichen looks like a loaf of ciabatta: it has a stiff, dense crust surrounding a spongy, loose interior. The alga is embedded in the thick crust. The familiar ascomycete fungus is there too, but it branches inwards, creating the spongy interior. And the basidiomycetes? They’re in the outermost part of the crust, surrounding the other two partners. “They’re everywhere in that outer layer,” says Spribille.

Despite their seemingly obvious location, it took around five years to find them. They’re embedded in a matrix of sugars, as if someone had plastered over them. To see them, Spribille bought laundry detergent from Wal-Mart and used it to very carefully strip that matrix away.

And even when the basidiomycetes were exposed, they weren’t easy to identify. They look exactly like a cross-section from one of the ascomycete branches. Unless you know what you’re looking for, there’s no reason why you’d think there are two fungi there, rather than one — which is why no one realised for 150 years. Spribille only worked out what was happening by labeling each of the three partners with different fluorescent molecules, which glowed red, green, and blue respectively. Only then did the trinity become clear.

Talk to a physicist

Thursday, January 5th, 2017

Sabine Hossenfelder is currently a research fellow at the Frankfurt Institute for Advanced Studies, but between gigs she has run a talk-to-a-physicist service:

‘Talk to a physicist. Call me on Skype. $50 per 20 minutes.’

A week passed with nothing but jokes from colleagues, most of whom thought my post was a satire. No, no, I assured them, I’m totally serious; send me your crackpots, they’re welcome. In the second week I got two enquiries and, a little nervous, I took on my first customer. Then came a second. A third. And they kept coming.

My callers fall into two very different categories. Some of them cherish the opportunity to talk to a physicist because one-to-one conversation is simply more efficient than Google. They can shoot up to 20 questions a minute, everything from: ‘How do we know quarks exist?’ to ‘Can atoms contain tiny universes?’ They’re normally young or middle-aged men who want to understand all the nerdy stuff but have no time to lose. That’s the minority.

The majority of my callers are the ones who seek advice for an idea they’ve tried to formalise, unsuccessfully, often for a long time. Many of them are retired or near retirement, typically with a background in engineering or a related industry. All of them are men. Many base their theories on images, downloaded or drawn by hand, embedded in long pamphlets. A few use basic equations. Some add videos or applets. Some work with 3D models of Styrofoam, cardboard or wires. The variety of their ideas is bewildering, but these callers have two things in common: they spend an extraordinary amount of time on their theories, and they are frustrated that nobody is interested.

Sociologists have long tried and failed to draw a line between science and pseudoscience. In physics, though, that ‘demarcation problem’ is a non-problem, solved by the pragmatic observation that we can reliably tell an outsider when we see one. During a decade of education, we physicists learn more than the tools of the trade; we also learn the walk and talk of the community, shared through countless seminars and conferences, meetings, lectures and papers. After exchanging a few sentences, we can tell if you’re one of us. You can’t fake our community slang any more than you can fake a local accent in a foreign country.

My clients know so little about current research in physics, they aren’t even aware they’re in a foreign country. They have no clue how far they are from making themselves understood. Their ideas aren’t bad; they are raw versions of ideas that underlie established research programmes. But those who seek my advice lack the mathematical background to build anything interesting on their intuitions. I try to help them by making connections to existing research. During our conversations, I point them towards relevant literature and name the important keywords. I give recommendations on what to do next, what they need to learn, or what problem lies in the way. And I make clear that if they want to be taken seriously by physicists, there’s no way around mathematics, lots of mathematics. Images and videos will not do.

One or two seemed miffed that I didn’t immediately exclaim: ‘Genius!’, but most of my callers realised that they can’t contribute to a field without meeting today’s quality standard. Then again, I hear only from those willing to invest in advancing their education to begin with. After our first conversation, they often book another appointment. One of them might even publish a paper soon. Not a proposal for a theory of everything, mind you, but a new way to look at a known effect. A first step on a long journey.

I haven’t learned any new physics in these conversations, but I have learned a great deal about science communication. My clients almost exclusively get their information from the popular science media. Often, they get something utterly wrong in the process. Once I hear their reading of an article about, say, space-time foam or black hole firewalls, I can see where their misunderstanding stems from. But they come up with interpretations that never would have crossed my mind when writing an article.

A typical problem is that, in the absence of equations, they project literal meanings onto words such as ‘grains’ of space-time or particles ‘popping’ in and out of existence. Science writers should be more careful to point out when we are using metaphors. My clients read way too much into pictures, measuring every angle, scrutinising every colour, counting every dash. Illustrators should be more careful to point out what is relevant information and what is artistic freedom. But the most important lesson I’ve learned is that journalists are so successful at making physics seem not so complicated that many readers come away with the impression that they can easily do it themselves. How can we blame them for not knowing what it takes if we never tell them?

The Atlantic is now trying to tar human genetics with the “racist” brush

Friday, December 30th, 2016

The Atlantic is now trying to tar human genetics with the “racist” brush:

Modern geneticists now take pains to distance their work from the racist assumptions of eugenics. Yet since the dawn of the genomic revolution, sociologists and historians have warned that even seemingly benign genetics research can reinforce a belief that different races are essentially different—an argument made most famously by Troy Duster in his book Backdoor to Eugenics. If a genetic test can identify you as 78 percent Norwegian, 12 percent Scottish, and 10 percent Italian, then it’s easy to assume there is such thing as white DNA. If scientists find that a new drug works works better in African Americans because of a certain mutation common among them, then it’s easy to believe that races are genetically meaningful categories.

If a drug works better on one race than another, then, yes, it is easy to believe that races are genetically meaningful categories — easy for a very good reason.

Can Hypothermia Save Gunshot Victims?

Friday, December 9th, 2016

E.P.R., or emergency preservation and resuscitation, has long been proved successful in animal experiments, but overcoming the institutional, logistical, and ethical obstacles to performing it on a human being has taken more than a decade:

When [the first patient to undergo E.P.R.] loses his pulse, the attending surgeon will, as usual, crack his chest open and clamp the descending aorta. But then, instead of trying to coax the heart back into activity, the surgeon will start pumping the body full of ice-cold saline at a rate of at least a gallon a minute. Within twenty minutes (depending on the size of the patient, the number of wounds, and the amount of blood lost), the patient’s brain temperature, measured using a probe in the ear or nose, will sink to somewhere in the low fifties Fahrenheit.

At this point, the patient, his circulatory system filled with icy salt water, will have no blood, no pulse, and no brain activity. He will remain in this state of suspended animation for up to an hour, while surgeons locate the bullet holes or stab wounds and sew them up. Then, after as much as sixty minutes without a heartbeat or a breath, the patient will be resuscitated. A cardiac surgeon will attach a heart-lung bypass machine and start pumping the patient full of blood again, cold, at first, but gradually warming, one degree at a time, over the course of a couple of hours. As soon as the heartbeat returns, perhaps jump-started with the help of a gentle electric shock, and as long as the lungs seem capable of functioning, at least with the help of a ventilator, the patient will be taken off bypass.

Even if everything works perfectly, it will take between three and five days to determine whether the patient’s brain has been damaged, and, if so, to what extent. There will be more surgeries, followed by months of rehabilitation.

You can see why the homicide rate keeps going down.

Cancer drug sparks growth of new eggs

Tuesday, December 6th, 2016

Women who had been treated for Hodgkin’s Lymphoma with the chemotherapy drug ABVD had 10 times the eggs of healthy women:

Lead researcher Professor Evelyn Telfer, of the University of Edinburgh’s School of Biological Sciences, said: “We were astonished when we saw what had happened to the tissue. It looked like pre-pubescent tissue with a high density of follicles and clustering that you don’t normally see in an adult.

“We knew that ABVD does not have a sterilising effect like some cancer drugs can, but to find new eggs being made, in such huge numbers, that was very surprising to see.

“It looks like something is being activated probably in the germline or stem cells and we need to find out what that mechanism is. It could be that the harshness of the treatment triggers some kind of shock effect or perturbation which stimulates the stem cells into producing new eggs.

“I think it’s a pretty big deal. It is the first time that we have ever been able to see new follicles being formed within the ovary, and it may only be a small number of women, but it is significant that the same effect was seen in all of the women on ABVD. The outcome may be significant and far-reaching.”

Scientists analysed samples of ovarian tissue donated by 14 women who had undergone chemotherapy, alongside tissues from 12 healthy women.

They found that the tissue from eight of the cancer patients who had been treated with ABVD had between four and 10 times more eggs compared with tissue from women who had received a different chemotherapy, or healthy women of a similar age.

The ovarian tissue was seen to be in healthy condition, appearing similar to tissue from young women’s ovaries.

Although the eggs are still in an immature state, the scientists are now trying to discover how they were created in the first place, then work out a way to bring them to maturity. It is unclear if the eggs in their current form would be functional.

But if research can reveal the mechanism, it would help scientists understand how women could produce more eggs during their lifetime, which was until now thought to be impossible.

Future studies will examine the separate impact of each of the four drugs that combine to make ABVD — known as adriamycin, bleomycin, vinblastine and dacarbazine — to better understand the biological mechanisms involved.

(Hat tip to Mangan.)

Mammals Are Downright Drab

Sunday, December 4th, 2016

Compared to colorful fish, lizards, birds, and insects, we mammals are downright drab:

Unless you are a color scientist you are probably accustomed to dealing with chemical colors. For example, if you take a handful of blue pigment powder, mix it with water, paint it onto a chair, let it dry, then scrape it off the chair, and grind it back into powder, you expect it to remain blue at all stages in the process (except if you get a bit of chair mixed in with it.)

By contrast, if you scraped the scales off a blue morpho butterfly’s wings, you’d just end up with a pile of grey dust and a sad butterfly. By themselves, blue morpho scales are not “blue,” even under regular light. Rather, their scales are arranged so that light bounces between them, like light bouncing from molecule to molecule in the air.


This kind of structural color works great if your medium is scales, feathers, carapaces, berries, or even CDs, but just doesn’t work with hair, which we mammals have.

Compared to other animals, mammals also have bad color perception, which may be explained by the nocturnal bottleneck hypothesis:

The hypothesis states that mammals were mainly or even exclusively nocturnal through most of their evolutionary story, starting with their origin 225 million years ago, and only ending with the demise of the dinosaurs 65 millions years ago. While some mammal groups have later evolved to fill diurnal niches, the 160 million years spent as nocturnal animals has left a lasting legacy on basal anatomy and physiology, and most mammals are still nocturnal.

The Real War on Science

Wednesday, November 30th, 2016

John Tierney’s liberal friends sometimes ask him why he doesn’t devote more of his science journalism to the sins of the Right:

My friends don’t like my answer: because there isn’t much to write about. Conservatives just don’t have that much impact on science. I know that sounds strange to Democrats who decry Republican creationists and call themselves the “party of science.” But I’ve done my homework. I’ve read the Left’s indictments, including Chris Mooney’s bestseller, The Republican War on Science. I finished it with the same question about this war that I had at the outset: Where are the casualties?

Read the whole thing.