Why making money in the stock market is as stressful than a missile attack (for me)

I made a ton of money in stock market in the past 7 weeks. I hated every minute of it. I found the stress very hard to take, particularly the anxiety and the inability to think of little else. As wives often do, my wife told me I’m nuts. “Don’t you remember how hard you worked for those neurosurgeons? This is the easiest money you’ve ever made”. I made probably more than half a year’s salary from them in absolute amount, and I was well paid.

But that was 25 years ago. For details see https://luysii.wordpress.com/2015/04/19/hilarys-stroke/. Yes, I was on every other night and probably was out between midnight and 8 AM every third night on call with a full day’s work to follow before sleep. It was physically demanding, but not particularly stressful mentally. “All you could lose was money, but in practice you could lose a life”. True, but I knew that I’d never make a mistake of omission, or commission or due to lack of knowledge (fairly arrogant but true, I really kept up with the literature in practice). Decisions didn’t always work out, initial diagnoses weren’t always correct, untoward reactions ensued (particularly to drugs), but I always knew that I given it my best shot. The stress came from doing everything right but still being unable to help, watching helplessly as patients deteriorated.

Thinking this over, after what my wife said, I realized that I was very much like a patient who really educated me.

Neurologists see headaches, lots of headaches. This young man came to see me about them, complete with his own (correct) diagnosis of their cause — a divorce in progress. Taking the history always starts things off, and a standard question is “When did the headaches start?” Oh, just after I got back from Riyadh. (This was during the Gulf War). Riyadh? Wasn’t there a missile attack that killed people while you were over there? Yes. Didn’t you have headaches then? No, but this divorce is killing me, doc. He was right.

So just like the shrinks say, it isn’t the situation itself, but how you perceive it.

Don’t get your hopes up — but

Amyotrophic lateral sclerosis (ALS) is a God-awful disease, where patients progressively weaken and die because they aren’t strong enough to breathe, remaining mentally intact the entire time. A recent paper [ Science vol. 348 pp. 239 – 242 ‘ 15 ] showed that a drug already released by the FDA for treating hypertension — Wytensin (Guanabenz) was of benefit in a mouse model of the disease. So the drug is out there. If I were still in practice, I’d certainly give it a shot in my patients — off-label use be damned. Even better, enterprising organic chemists synthesized an analogue of Wytensin (Sephin1) which doesn’t lower blood pressure, but which still works in the mouse model.

Here’s why you shouldn’t get your hopes up too high. [ Nature vol. 4564 pp. 682 – 685 ’08 ] The work using SOD1 mutant mice (the mouse model of ALS mentioned above) is quite sloppy and nearly 12 drugs with benefit in mouse models have had no benefit in clinical trials. Minocycline which was effective in 4 studies in mice actually made things worse in a clinical trial of over 400 patients .

Now for a bit of background. Most cases of ALS aren’t familial, but a few are. One protein Superoxide Dismutase 1 (SOD1) was found to mutated in about 20% of familial ALS. It’s been studied out the gazoo, and some 140 different mutations have been found in its 153 amino acids in familial cases.

It’s hard to conceive of them all acting the same way, and literally thousands of papers have been written on the subject. It does seem clear that aggregated proteins occur in the dying neurons of ALS patients, but whether they are made mostly of SOD1 remains controversial (although it is present in the inclusions to some extent). Mature SOD1 is a 32 kiloDalton homodimeric metalloenzyme, in which each monomer contains Cu and Zn and one intrasubunit disulfide bond. It is one of the most abundant cellular proteins. It has a tendency to aggregate when overexposed.

The mouse results are impressive, as it improved established disease. In vivo, Sephin1 prevented the motor morphological and molecular defects of two unrelated protein misfolding diseases in mice (Charcot Marie Tooth 1B and ALS ! ! !). The mice had a mutant SOD1 (G93A). SOD1 mutants bind to Derlin1 on the the cytosolic side of the endoplasmic reticulum (ER) membrane blocking degradation of ER proteins causing ER stress. Very impressive ! ! ! !

Read Einstein

Devoted readers of this blog (assuming there are any) know that I’ve been studying relativity for some time — for why see https://luysii.wordpress.com/2011/12/31/some-new-years-resolutions/.

Probably some of you have looked at writings about relativity, and have seen equations containing terms like ( 1 – v^2/c^2)^1/2. You need a lot of math for general relativity (which is about gravity), but to my surprise not so much for special relativity.

Back in the early 50’s we were told not to study Calculus before reaching 18, as it was simply to hard for the young brain, and would harm it, the way lifting something too heavy could bring on a hernia. That all changed after Sputnik in ’58 (but too late for me).

I had similar temerity in approaching anything written by Einstein himself. But somehow I began looking at his book “Relativity” to clear up a few questions I had. The Routledge paperback edition (which I got in England) cost me all of 13 pounds. Routledge is a branch of a much larger publisher Taylor and Francis.

The book is extremely accessible. You need almost no math to read it. No linear algebra, no calculus, no topology, no manifolds, no differential geometry, just high school algebra.

You will see a great mind at work in terms you can understand.

Some background. Galileo had a theory of relativity, which basically said that there was no absolute position, and that motion was only meaningful relative to another object. Not much algebra was available to him, and later Galilean relativity came be taken to mean that the equations of physics should look the same to people in unaccelerated motion relative to each other.

Newton’s laws worked out quite well this way, but in the late 1800’s Maxwell’s equations for electromagnetism did not. This was recognized as a problem by physicists, so much so that some of them even wondered if the Maxwell equations were correct. In 1895 Lorentz figured out a way (purely by trying different equations out) to transform the Maxwell equations so they looked the same to two observers in relative motion to each other. It was a classic kludge (before there even were kludges).

The equation to transform the x coordinate of observer 1 to the x’ of observer 2 looks like this

x’ = ( x – v*t) / ( 1 – v^2/c^2)^1/2)

t = time, v = the constant velocity of the two observers relative to each other, c = velocity of light

Gruesome no ?

All Lorentz knew was that it made Maxwell’s equations transform properly from x to x’.

What you will see on pp. 117 – 123 of the book, is Einstein derive the Lorentz equation from
l. the constancy of the velocity of light to both observers regardless of whether they are moving relative to each other
2. the fact that as judged from observer1 the length of a rod at rest relative to observer2, is the same as the length of the same rod at rest relative to observer1 as judged from observer2. Tricky to state, but this just means that the rod is out there and has a length independent of who is measuring it.

To follow his derivation you need only high school algebra. That’s right — no linear algebra, no calculus, no topology, no manifolds, no differential geometry. Honest to God.

It’s a good idea to have figure 2 from p. 34 in front of you

The derivation isn’t particularly easy to follow, but the steps are quite clear, and you will have the experience of Einstein explaining relativity to you in terms you can understand. Like reading the Origin of Species, it’s fascinating to see a great mind at work.


A Touching Mother’s Day Story

Yes, a touching mother’s day story for you all. It was 48 years ago, and I was an intern at a big city hospital on rotation in the emergency room. The ER entrance was half a block from an intersection with a bar on each corner. On a Saturday night, we knew better than to try to get some sleep before 2AM or until we’d put in 2 chest tubes (to drain blood from the lungs, which had been shot or stabbed). The bartenders were an intelligent lot — they had to be quick thinking to defuse situations, and we came to know them by name. So it was 3AM 48 years ago and Tyrone was trudging past on his way home, and I was just outside the ER getting some cool night air, things having quieted down.

“Happy Mother’s day, Tyrone” sayeth I

“Thanks Doc, but every day is Mother’s day with me”

“Why, Tyrone?”

“Because every day I get called a mother— “

The neuron as motherboard

Back in the day when transistors were fairly large and the techniques for putting them together on silicon were primitive by today’s standards, each functionality was put on a separate component which was then placed on a substrate called the motherboard. Memory was one component, the central processing unit (CPU) another, each about the size of a small cellphone today. Later on as more and more transistors could be packed on a chip, functionality such as memory could be embedded in the CPU chip. We still have motherboards today as functionality undreamed of back then (graphic processors, disc drives) can be placed on them.

It’s time to look at individual neurons as motherboards rather than as CPUs which sum outputs and then fire. The old model was to have a neuron look like an oak tree, with each leaf functioning as an input device (dendritic spine). If enough of them were stimulated at once, a nerve impulse would occur at the trunk (the axon). To pursue the analogy a bit further, the axon has zillions of side branches (e.g,. the underground roots) which than contact other neurons. Probably the best example of this are the mangrove trees I saw in China, where the roots are above ground.

How would a contraption like this learn anything? If an impulse arrives at an axonal branch touching a leaf (dendritic spine) — e.g. a synapse, the spine doesn’t always respond. The more times impulses hit the leaf when it is responding to something else, the more likely the spine is to respond (this is called long term potentiation aka LTP).

We’ve always thought that different parts of the dendritic tree (leaves and branches) receive different sorts of information, and can remember (by LTP). Only recently have we been able to study different leaves and branches of the same neuron and record from them in a living intact animal. Well we can, and what the following rather technical description says, its that different areas of a single neuron are ‘trained’ for different tasks. So a single neuron is far more than a transistor or even a collection of switches. It’s an entire motherboard (full fledged computer to you).

Presently Intel can put billions of transistors on a chip. But we have billions of neurons, each of which has tends of thousands of leaves (synapses) impinging on it, along with memory of what happened at each leaf.

That’s a metaphorical way of describing the results of the following paper (given in full jargon mode).

[ Nature vol. 520 pp. 180 – 185 ’15 ] Different motor learning tasks induce dendritic calcium spikes on different apical tuft branches of individual layer V pyramidal neurons in mouse motor cortex. These branch specific calcium spikes cause long lasting potentiation of postsynaptic dendritic spines active at the time of spike generation.

Disentangling Heredity and Environmental effects on IQ

No sensible person thinks intelligence is completely determined by heredity or by environment. Recent Swedish work [ Proc. Natl. Acad. Sci. vol. 112 pp.4612 – 4617 ’15 ] tries to control for heredity while measuring environmental effects on IQ, assuming that IQ measures intelligence, a position some find contentious. Every Swedish 18 year old man is conscripted into the military apparently. IQ tests are given to all. Amazingly the authors found 436 sibships where the brothers had been raised apart.

The intelligence of the biological and adoptive parents wasn’t measured. Rather the surrogate of educational level was used instead. It was divided into 5 classes.

What did they find? Adopted sibs had an IQ 4.41 points higher than the nonAdopted sib (recall that average IQ is stated to be 100 points although it’s been rising, and that IQ levels of the population fall on the Bell (Gaussian) curve, with a standard deviation of 15 points). These results are not surprising, as few willingly give children up for adoption, so the adopted environment was quite likely better. The educational level of the adoptive parents was an average of 2.6 points higher.

Next, the authors measured the effect of the surrogate marker for intelligence (educational level) on IQ. For each point in the 5 point scale that the adoptive parent was at a higher educational level than the biologic ones there was an increase in IQ of the adopted sib relative to the unadopted one. This is as unequivocal evidence as we have for the effect of environment and educational level on IQ.

We’ll never have perfect data, and many caveats about this work are possible, but it is an impressive effort. 436 sibs is a huge number compared to the twins who’ve been reared apart and studied this way.

Just how large an effect do you think it was? I’ve already told you everything you need to know.

Each additional unit of rearing parental education was associated with 2 IQ units. Are you surprised? I was, because I thought the effect would be much larger. So environment is important in determining intelligence, just not so much.

Hillary’s stroke

Hillary Clinton had a stroke toward the end of 2012. It was not due to the faint she had presumably because of the flu in mid December. The information given out at the time was extremely sketchy and confusing (see the copy of the post of 31 Dec ’12 at the end).

She fainted while giving a speech in Buffalo according to one account and at her home in Washington according to another and was not hospitalized. She is said to have suffered a concussion when she fell. Then on the 30th of December she was hospitalized because a blood clot was found (more later) and placed on blood thinners. She suffered double vision and had to wear corrective glasses (Fresnel lenses) for congressional testimony 23 January 2013.

So she had a blood clot in her head and a neurologic deficit persisting for a few weeks. That’s what a stroke is.

Could it have been due to the head trauma? This is extremely doubtful based on an intense 42 month experience managing acute head injuries.

To get my kids through college, I took a job working for two busy neurosurgeons. When I got there, I was informed that I’d be on call every other night and weekend, taking first call with one of the neurosurgeons backing me up. Neurologists rarely deal with acute head trauma although when the smoke clears we see plenty of its long term side effects (post-traumatic epilepsy, cognitive and coordination problems etc. etc.). I saw plenty of it in soldiers when I was in the service ’68 – ’70, but this was after they’d been stabilized and shipped stateside. Fortunately, my neurosurgical backup was excellent, and I learned and now know far more about acute head trauma than any neurologist should.

We admitted some of the head trauma cases to our service, but most cases had trauma to other parts of the body, so a general surgeon would run the show with our group as consultants. The initial consultant in half the cases was me. If I saw them initially, I followed the patients until discharge. On weekends I covered all our patients and all our consults, usually well over 20 people.

We are told that Hillary had a clot in one of the large draining veins in the back of her head (venous sinuses actually). In all the head trauma I saw (well over 300 I’d guess), I never saw a clot develop there. I’ve spoken to two neuroradiologists still in practice, and they can’t recall seeing such a clot without a skull fracture near the vein. Nothing like this was mentioned at any time about Hillary.

Hillary’s neurologic deficit involved a nerve going to the muscles of her left eye. These start in the brainstem, a part of the brain quite near the site where she is said to have the clot in her vein. The brainstem is crucial in maintaining consciousness, and it is far more likely that the faint in early December was a warning sign of the stroke she had subsequently.

I can’t believe that she would not have been hospitalized had she complained of double vision when she fainted in early December, so it must have come on later.

So the issue is why did she have the stroke, and how likely is it to recur. I seriously doubt that it had anything to do with the head injury she sustained when she fainted. We’ve have two presidents neurologically impaired by stroke in the past century (Woodrow Wilson after World War I and Franklin Delano Roosevelt at Yalta). The results were not happy for the USA or the World.

Certainly all this would be cleared up if her medical records were released. Only Hillary can do this, but at least she cannot destroy them, as although she ‘owns’ them, they are not in her sole possession.

The following is a post written 31 December ’12 when the news of Hillary’s illness first broke showing how fragmentary the information about it was back then (it isn’t a good deal better now).

Medical tribulations of politicians — degrees of transparency

Remarkably on the last day of the year, 3 political figures and their medical problems are in the news. Here they are in order of medical transparency (highest first).

l. George Bush Sr. — the most transparent. We are told what he has (pneumonia), when he was admitted to hospital when he was in the ICU, when he came out. Docs call pneumonia ‘the old man’s friend’ not out of cynicism, but because its a mode of death with (relatively) little suffering. The patient lapses into unconsciousness and usually dies quickly and quietly. It took my cellist’s father only a day or two to pass away this month. Clearly it isn’t invariably fatal, and Bush Sr. was now out of the ICU at last count (he’s 88).

2. Hillary Clinton — admitted to the hospital yesterday with a ‘blood clot’ somewhere, said to be a complication of the concussion she suffered a few weeks ago. Also said to be under treatment with anticoagulants. Most clots due to head trauma are inside the head and treating them with anticoagulants is a disaster. The most likely type of clot given the time from the concussion is a subdural hematoma. It is possible that she’s been so inactive since the concussion that she developed thrombophlebitis in her legs, in which case anticoagulation would be indicated.

More disturbingly, is that her passing out a few weeks ago is a sign of something more serious going on. Hopefully not.

The powers that be should have told us where the clot actually is.

Update 5:50 PM EST — Well the powers that be did open up and it is a most unusual complication of head injury (and one I’d never seen in nearly 4 decades of practice) — a venous thrombosis in the head. I’m not even sure it’s due to her head injury. It might have even caused her syncope, but presumably she had some sort of radiologic study of her head when she fainted, which should have picked it up. The venous sinuses draining the brain in the back of the head are notoriously asymmetric, so a narrowing attributable to a clot could just be a variant anatomy. One very bad complication of cerebral venous thrombosis back there (which I saw as a complication of chronic mastoid bone infection — not head trauma) is pseudotumor cerebri. I really wonder if these guys have the right diagnosis.

3. Hugo Chavez — Yesterday it was announced that he’s had a third complication since his surgery for cancer 3 weeks ago. Naturally, we’re not told just what this complication actually is. This is consistent with the information that has been released about his case. We know almost nothing about his actual tumor (except that he has one). He most assuredly is not free of cancer as he stated last fall. He is said to have have a bleeding problem and a lung infection as the first two complications.

My guess for this third complication is that it is a dehiscence of his abdominal incision, which must have been fairly large for a 6 hour operation. Dehiscence just means that the wound has spontaneously opened up exposing abdominal contents (which means that peritonitis is not far behind). Why should this happen? Two reasons — he’s had radiation to the area which inhibits wound healing, and he’s been on high dose steroids in the past (and perhaps presently) which also inhibits wound healing.

I don’t think he’s going to be able to take office 10 days hence, and doubt that he’ll come back to Venezuela alive. Transparency has been zilch. Hopefully the people of Venezuela are beginning to realize just how misleading the information they’ve been fed about his health has been.

This is the sort of thing physicians taking care of really sick people deal with daily, which may explain why your doc friends aren’t as jolly as you are at the New Year’s Eve parties you’re about to attend.

Nonetheless, Happy New Year to all ! ! ! !

None dare call it junk

There has been a huge amount of controversy about whether all the DNA we carry about has some purpose to carry out — or not. Could some of it be ‘junk’?.

At most 2% of our DNA actually codes for the amino acids comprising our proteins. Some (particularly the ENCODE consortium) have used the criterion of transcription of the DNA into RNA (a process which takes energy) as a sign that well over 50% of our genome is NOT junk. Others regard this transcription as the unused turnings from a lathe.

All agree however, that bacteria use a good deal of their small genomes to code for protein. The following paper http://www.pnas.org/content/112/14/4251.full quotes a figure of 84 – 89%.

Consider the humble leprosy organism.It’s a mycobacterium (like the organism causing TB), but because it essentially is confined to man, and lives inside humans for most of its existence, it has jettisoned large parts of its genome, first by throwing about 1/3 of it out (the genome is 1/3 smaller than TB from which it is thought to have diverged 66 million years ago), and second by mutation of many of its genes so protein can no longer be made from them. Why throw out all that DNA? The short answer is that it is metabolically expensive to produce and maintain DNA that you’re not using

If you want a few numbers here they are:
Genome of M. TB 4,441,529 nucleotides
Genome of M. Leprae 3,268,203 nucleotides
1,604 genes coding for protein
1,116 pseudoGenes (e.g. genes that look like they could code for proteins, but no longer can because of premature termination codons.

This brings us to the organism described in the paper — Trichodesmium erythraeum — a photosynthetic bacterium living in the ocean. When conditions are right it multiplies rapidly causing a red algal bloom (even though it isn’t an algae which are cellular). It’s probably how the Red Sea got its name.

The organism only uses 64% of its genome to code for its protein. The most interesting point is that 86% of the nonCoding (for protein anyway) DNA is transcribed into RNA.

The authors wrestle with the question of what the nonCoding DNA is doing.

“Because it is thought that many bacteria are deletion-biased (47, 77), stable maintenance of these elements from laboratory isolates to the natural samples suggest that they may be required in some fashion for growth both in culture and in situ.”

Translation: The nonCoding DNA probably isn’t junk.

They give it another shot.

“Others have hypothesized that the conserved repeat structures observed in some bacteria could function as recombination-dependent “promoter banks” for adaptation to new conditions, thereby allowing relatively quick “rewiring” of metabolism in subpopulations”

Plausible, but why waste the energy transcribing the DNA into RNA if it isn’t doing anything for the organism doing the transcribing?

Never assume that what you can’t measure or don’t understand is unimportant.

Is natural selection disprovable?

One of the linchpins of evolutionary theory is that natural selection works by increased reproductive success of the ‘fittest’. Granted that this is Panglossian in its tautology — of course the fittest is what survives, so of course it has greater reproductive success.

So decreased reproductive success couldn’t be the result of natural selection could it? A recent paper http://www.sciencemag.org/content/348/6231/180.full.pdf says that is exactly what has happened, and in humans to boot, not in some obscure slime mold or the like.

The work comes from in vitro fertilization which the paper says is responsible for 2 -3 % of all children born in developed countries — seems high. Maternal genomes can be sequenced and the likelihood of successful conception correlated with a variety of variants. It was found that there is a strong association between change in just one nucleotide (e.g. a single nucleotide polymorphism or SNP) and reproductive success. The deleterious polymorphism (rs2305957) decreases reproductive success. This is based on 15,388 embryos from 2,998 mothers sampled at the day-5 blastocyst stage.

What is remarkable is that the polymorphism isn’t present in Neanderthals (from which modern humans diverged between 100,000 and 400,000 year ago). It is in an area of the genome which has the characteristics of a ‘selective sweep’. Here’s the skinny

A selective sweep is the reduction or elimination of variation among the nucleotides in neighbouring DNA of a mutation as the result of recent and strong positive natural selection.

A selective sweep can occur when a new mutation occurs that increases the fitness of the carrier relative to other members of the population. Natural selection will favour individuals that have a higher fitness and with time the newly mutated variant (allele) will increase in frequency relative to other alleles. As its prevalence increases, neutral and nearly neutral genetic variation linked to the new mutation will also become more prevalent. This phenomenon is called genetic hitchhiking. A strong selective sweep results in a region of the genome where the positively selected haplotype (the mutated allele and its neighbours) is essentially the only one that exists in the population, resulting in a large reduction of the total genetic variation in that chromosome region.

So here we have something that needs some serious explaining — something decreasing fecundity which is somehow ‘fitter’ (by the definition of fitness) because it spread in the human population. The authors gamely do their Panglossian best explaining “the mitotic-error phenotype (which causes decreased fecundity) may be maintained by conferring both a deleterious effect on maternal fecundity and a possible beneficial effect of obscured paternity via a reduction in the probability of successful pregnancy per intercourse. This hypothesis is based on the fact that humans possess a suite of traits (such as concealed ovulation and constant receptivity) that obscure paternity and may have evolved to increase paternal investment in offspring.

Nice try fellas, but this sort of thing is a body blow to the idea of natural selection as increased reproductive success.

There is a way out however, it is possible that what is being selected for is something controlled near to rs2305957 so useful, that it spread in our genome DESPITE decreased fecundity.

Don’t get me wrong, I’m not a creationist. The previous post https://luysii.wordpress.com/2015/04/07/one-reason-our-brain-is-3-times-that-of-a-chimpanzee/ described some of the best evidence we have in man for another pillar of evolutionary theory — descent with modification. Here duplication of a single gene since humans diverged from chimps causes a massive expansion of the gray matter of the brain (cerebral cortex).


Addendum 13 April

I thought the following comment was so interesting that it belongs in the main body of the text


Mutations dont need to confer fitness in order to spread through the population. These days natural selection is considered a fairly minor part of evolution. Most changes become fixed as the result of random drift, and fitness is usually irrelevant. “Nearly neutral theory” explains how deleterious mutations can spread through a population, even without piggybacking on a beneficial mutation; no need for panglossian adaptive hypotheses.

Here’s my reply

Well, the authors of the paper didn’t take this line, but came up with a rather contorted argument to show why decreased fecundity might be a selective advantage, rather than just saying it was random drift. They also note genomic evidence for a ‘selective sweep’ — decreased genomic heterogeneity around the SNP.

One reason our brain is 3 times that of a chimpanzee

Just based on the capacity of the skull, our brain is 3 – 4 times larger than that of our closest primate relative, the chimp. Most of the increase in size occurs in the cerebral cortex (the gray matter) just under the skull. Our cortex is thrown into folds because there is so much of it. Compare the picture of the mouse brain (smooth) and ours, wrinkled like a walnut http://www.nsf.gov/discoveries/disc_summ.jsp?cntn_id=130442.

We now may have part of the explanation. A fascinating paper http://www.sciencemag.org/content/347/6229/1465.full.pdf studied genetic differences between the progenitor cells from which the cortex arises (radial glia) in man and mouse. They found 56 protein coding genes expressed in our radial glia not present in the mouse (out of 20,000 or so).

One in particular called by the awful name ARHGAP11B is particularly fascinating. Why? Because it’s the product of a gene duplication of ARHGAP11A. When did this happen — after the human line split off from the chimp 6 million years ago. Chimps have no such duplication, just the original

Put ARHGAP11B into a developing mouse and its cortex expands so much it forms folds.

There has been all sorts of work on the genetic difference between man and chimp. There almost too many — [ Nature vol. 486 pp. 481 – 482 ’12 ] — some 20,000,000. Finding the relevant ones is the problem. ARHGAP11A is by far the best we’ve found to date.

Another fascinating story is the ‘language gene’ discovered in a family suffering from a speech and language disorder. It’s called FOXP2. Since the last common ancestor of humans and mice (70 megaYears ago) there have been only 3 changes in the 715 amino acids comprising the protein. 2 of them have occurred in the human lineage since it split with the chips 6 megaYears ago. So far no one has put the human FOXP2 gene into a chimp and got it to talk. For more details see http://en.wikipedia.org/wiki/FOXP2

There is all sorts of fascinating molecular biology about what these two genes actually do in the cell, but that would make this post too long,. This is, in part, a chemistry blog and just what FOXP2 and ARHGAP11A actually do involves some beautiful and elegant chemistry — look up RhoGAP and Winged Helix transcription factors. Ferrari’s are beautiful cars, and become even more beautiful when you understand what’s going on under the hood. Chemistry gives you that for molecular, cellular and organismal biology.


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