i. Here are my thoughts on the upcoming Danish election:
(And here are my thoughts on voting in general.)
“Office in the morning. This morning my dining-room was finished with green serge hanging and gilt leather, which is very handsome.
This night I sat up late to make up my accounts ready against to-morrow for my Lord. I found him to be above 80l. in my debt, which is a good sight, and I bless God for it.”
Here’s a background article. I learned about the existence of this diary through Bryson. I should point out that navigation is easier at the site where the diary is located; you can get brief explanations of key terms simply by hovering over the linked words, and so you often don’t really need to click any links.
I don’t actually think the lecture is all that great, but I watched it anyway and I figured I might as well blog it.
iv. I got a draw against a ~2050 Elo opponent last Monday – you can watch the game here, I was white. This was actually I game I was reasonably satisfied with – my opponent was the one who offered the draw, which was in itself a small victory (I graciously accepted). The draw was not a result of a blunder in a time scramble or something like that; I played semi-accurate moves and so did my opponent, and so we ended up in a dead drawn position. I didn’t exactly play ambitiously in this game but with opponents like this most people will probably consider a draw a satisfactory outcome (my opponent was in the top 25 in the last Danish Championship), and keeping it simple seemed the best strategy, especially as I got completely crushed in the first game I played against him. Today I won a bullet game against a much stronger opponent, but I often do that and those games don’t really count nearly as much as these; games like this one are serious games, and in these kinds of time controls it seems I can still play along with some of the best players in the club. This is nice. After 8 games of the tournament my performance rating is now slightly above 1950.
Okay – on to you guys: What have you been up to? Have you read anything during the last couple of weeks that I ought to read as well? Have you seen an amazing TV series I’ve never heard about? A good online lecture? Found an amazing website?
This is probably also a good place for a new reader to step forward and tell me a little about yourself. I like to know at least a little bit about who’s reading along here.
“The metric expansion of space is the increase of the distance between two distant parts of the universe with time. It is an intrinsic expansion whereby the scale of space itself is changed. That is, a metric expansion is defined by an increase in distance between parts of the universe even without those parts “moving” anywhere. […]
This kind of expansion is different from all kinds of expansions and explosions commonly seen in nature. What we see normally as “space” and “distance” are not absolutes, but are determined by a metric that can change. In the metric expansion of space, rather than objects in a fixed “space” moving apart into “emptiness”, it is space itself which is changing. It is as if without objects themselves moving, space is somehow growing or shrinking between them: if it were possible to place a tape measure between even stationary objects, one would observe the scale of the tape measure changing to show more distance between them.
Because this expansion is caused by changes in the distance-defining metric, and not by objects themselves moving in space, this expansion (and the resultant movement apart of objects) is not restricted by the speed of light upper bound of special relativity. So objects can be moving at sub-light speed yet appear to be moving apart faster than light. […]
“The expansion of space is sometimes described as a force which acts to push objects apart. Though this is an accurate description of the effect of the cosmological constant, it is not an accurate picture of the phenomenon of expansion in general. For much of the universe’s history the expansion has been due mainly to inertia. The matter in the very early universe was flying apart for unknown reasons (most likely as a result of cosmic inflation) and has simply continued to do so, though at an ever-decreasing rate due to the attractive effect of gravity.
In addition to slowing the overall expansion, gravity causes local clumping of matter into stars and galaxies. Once objects are formed and bound by gravity, they “drop out” of the expansion and do not subsequently expand under the influence of the cosmological metric, there being no force compelling them to do so.”
This is complicated (if also fascinating) stuff, as there’s a lot of math doing work ‘behind the scenes’ and reasonably few people around who actually understands all that math. As they put it in the introduction:
“Due to the non-intuitive nature of the subject and what has been described by some as “careless” choices of wording, certain descriptions of the metric expansion of space and the misconceptions to which such descriptions can lead are an ongoing subject of discussion in the realm of pedagogy and communication of scientific concepts.”
Despite the fact that the article deals with very complex stuff this is not a ‘mathy’ article; I’d say the article is not too technical for most people with an interest in these matters to read it and obtain a greater understanding of the universe in which he or she lives. Note that progress in the field of observational cosmology is continually being made, so it’s not like the final version of this article has been written at this point. For example the article states that the most distant quasar currently known is 28 billion light years away (comoving distance), however the most distant object we have observed (discovered earlier this month) is now 30 lightyears away – even if that’s technically a galaxy and not a quasar, it’s highly likely that another, more distant quasar, will be found in the future (if you don’t feel like clicking the link to the wiki article about that galaxy, here’s one sentence from the article that may change your mind: “The galaxy in its observable timeframe was producing stars at a phenomenal rate, equivalent in mass to about 300 suns per year.“).
ii. Cell membrane. These things are very important, yet most people probably don’t know a great deal about them. This article will teach you more. Khan Academy has stuff on this topic as well (you can start here – I’ve been thinking about blogging these videos, and maybe I will later on).
iii. Axe Murder incident. Short version: Two US Army officers got killed by North Korean soldiers while trying to cut down a tree in the Joint Security Area between North and South Korea. Some people higher up got angry about that and decided that that tree had to go, and so Operation Paul Bunyan was launched. With the aid of 23 American and South Korean vehicles, some detonation charges, two 30-man security platoons, a 64-man South Korean special forces company (..and a total task force of 813 men), a U.S. infantry company in 20 utility helicopters and 7 Cobra attack helicopters, some B-52 Stratofortresses escorted by F-4 Phantom II fighter-bombers and South Korean F-5 Freedom Fighters, as well as a nearby aircraft carrier and a dozen C-130s ready to provide support plus 12,000 additional troops which were ordered to Korea, two eight-man teams of military engineers managed to cut down the tree. Here’s what all the fuss was about:
(Do note that the reason why the tree was not cut down completely was not interference from NK soldiers: “The stump of the tree, almost 6 m (20 ft) tall, was deliberately left standing.”)
iv. Maggot therapy.
“Maggot therapy is also known as maggot debridement therapy (MDT), larval therapy, larva therapy, larvae therapy, biodebridement or biosurgery. It is a type of biotherapy involving the introduction of live, disinfected maggots (fly larvae) into the non-healing skin and soft tissue wound(s) of a human or animal for the purpose of cleaning out the necrotic (dead) tissue within a wound (debridement) and disinfection. […]
While at Johns Hopkins University in 1929, Dr. Baer introduced maggots into 21 patients with intractable chronic osteomyelitis. He observed rapid debridement, reductions in the number of pathogenic organisms, reduced odor levels, alkalinization of wound beds, and ideal rates of healing. All 21 patients’ open lesions were completely healed and they were released from the hospital after two months of maggot therapy.
After the publication of Dr. Baer’s results in 1931, maggot therapy for wound care became very common, particularly in the United States. The Lederle pharmaceutical company commercially produced “Surgical Maggots”, larvae of the green bottle fly, which primarily feed on the necrotic (dead) tissue of the living host without attacking living tissue. Between 1930 and 1940, more than 100 medical papers were published on maggot therapy. Medical literature of this time contains many references to the successful use of maggots in chronic or infected wounds including osteomyelitis, abscesses, burns, sub-acute mastoiditis, and chronic empyema.
More than 300 American hospitals employed maggot therapy during the 1940s. The extensive use of maggot therapy prior to World War II was curtailed when the discovery and growing use of penicillin caused it to be deemed outdated. […] While in the past it was believed that maggots do not damage healthy tissue, this is in doubt now. […]
The wound must be of a type which can actually benefit from the application of maggot therapy. A moist, exudating wound with sufficient oxygen supply is a prerequisite. Not all wound-types are suitable: wounds which are dry, or open wounds of body cavities do not provide a good environment for maggots to feed. […] In about 1/3 of all patients pain is increased.”
v. Oil shale (featured article).
“Oil shale, also known as kerogen shale, is an organic-rich fine-grained sedimentary rock containing kerogen (a solid mixture of organic chemical compounds) from which liquid hydrocarbons called shale oil (not to be confused with tight oil—crude oil occurring naturally in shales) can be produced. Shale oil is a substitute for conventional crude oil; however, extracting shale oil from oil shale is more costly than the production of conventional crude oil both financially and in terms of its environmental impact. […]
Heating oil shale to a sufficiently high temperature causes the chemical process of pyrolysis to yield a vapor. Upon cooling the vapor, the liquid shale oil—an unconventional oil—is separated from combustible oil-shale gas (the term shale gas can also refer to gas occurring naturally in shales). Oil shale can also be burned directly in furnaces as a low-grade fuel for power generation and district heating or used as a raw material in chemical and construction-materials processing.
Oil shale gains attention as a potential abundant source of oil whenever the price of crude oil rises. At the same time, oil-shale mining and processing raise a number of environmental concerns, such as land use, waste disposal, water use, waste-water management, greenhouse-gas emissions and air pollution. Estonia and China have well-established oil shale industries, and Brazil, Germany, and Russia also utilize oil shale. […]
Oil shale, an organic-rich sedimentary rock, belongs to the group of sapropel fuels. It does not have a definite geological definition nor a specific chemical formula, and its seams do not always have discrete boundaries. Oil shales vary considerably in their mineral content, chemical composition, age, type of kerogen, and depositional history and not all oil shales would necessarily be classified as shales in the strict sense. According to the petrologist Adrian C. Hutton of the University of Wollongong, oil shales are not “geological nor geochemically distinctive rock but rather ‘economic’ term.” Their common feature is low solubility in low-boiling organic solvents and generation of liquid organic products on thermal decomposition. […]
The largest deposits in the world occur in the United States in the Green River Formation, which covers portions of Colorado, Utah, and Wyoming; about 70% of this resource lies on land owned or managed by the United States federal government. Deposits in the United States constitute 62% of world resources; together, the United States, Russia and Brazil account for 86% of the world’s resources in terms of shale-oil content. These figures remain tentative, with exploration or analysis of several deposits still outstanding. […] As of 2009, 80% of oil shale used globally is extracted in Estonia […]
The shale oil derived from oil shale does not directly substitute for crude oil in all applications. It may contain higher concentrations of olefins, oxygen, and nitrogen than conventional crude oil. Some shale oils may have higher sulfur or arsenic content. […] The higher concentrations of these materials means that the oil must undergo considerable upgrading (hydrotreating) before serving as oil-refinery feedstock. […] Shale oil serves best for producing middle-distillates such as kerosene, jet fuel, and diesel fuel.”
i. “To be perfectly intelligible one must be inaccurate, and to be perfectly accurate, one must be unintelligible.” (attributed Bertrand Russell – the quote is from Clinical Epidemiology, however I have not been able to find independent verification that Russell ever actually said this.)
ii. “Quotation confesses inferiority.” (Emerson)
iii. “Money often costs too much.” (-ll-)
iv. “People seem not to see that their opinion of the world is also a confession of character.” (-ll-)
v. “Let me never fall into the vulgar mistake of dreaming that I am persecuted whenever I am contradicted.” (-ll-)
vi. “Discontent is the want of self-reliance: it is infirmity of will.” (-ll-)
vii. “For every thing you have missed, you have gained something else; and for every thing you gain, you lose something.” (-ll-)
viii. “That man is richest whose pleasures are the cheapest.” (Henry David Thoreau)
ix. “It takes two to speak the truth, — one to speak, and another to hear.” (-ll-)
x. “The greatest compliment that was ever paid me was when one asked me what I thought, and attended to my answer.” (-ll-)
xi. “Knowledge both enlarges and multiplies our Desires, and the fewer things a Man wishes for, the more easily his Necessities may be supply’d.” (Bernard Mandeville)
xii. “Every one that flatters thee
Is no friends in misery.
Words are easy, like the wind;
Faithful friends are hard to find.
Every man will be thy friend
Whilst thou hast wherewith to spend;
But if store of crowns be scant,
No man will supply thy want.” (Richard Barnfield)
xiii. “Ah, well! We live and learn, or, anyway, we live.” (Will Cuppy)
xiv. “The Mexicans gave the Spaniards malaria, and the Spaniards gave the Mexicans smallpox, whooping cough, diphtheria, and syphilis. The Spaniards believed it was better to give than to receive.” (-ll-)
xv. “A book which, above all others in the world, should be forbidden, is a catalogue of forbidden books.” (Georg Christoph Lichtenberg)
xvi. “A good means to discovery is to take away certain parts of a system to find out how the rest behaves.” (-ll-)
xvii. “The most heated defenders of a science, who cannot endure the slightest sneer at it, are commonly those who have not made very much progress in it and are secretly aware of this defect.” (-ll-)
xviii. “Man is always partial and is quite right to be. Even impartiality is partial.” (-ll-)
xix. “There is no more important rule of conduct in the world than this: attach yourself as much as you can to people who are abler than you and yet not so very different that you cannot understand them.” (-ll-)
xx. “There are very many people who read simply to prevent themselves from thinking.” (-ll-)
xxi. “We accumulate our opinions at an age when our understanding is at its weakest.” (-ll-)
“The aim of this article is to integrate empirical research on divorce risks in Europe and to explain the variation of empirical findings between European countries by the different levels of modernization and differences in the strength of marriage norms. We focus on the effects of premarital cohabitation, the presence of children, and the experience with parental divorce on marital stability. More than 260 studies on divorce risks could be identified, and 120 were used for further meta-analytical examinations. We show that there is considerable heterogeneity of divorce risks within as well as between countries. Explaining the variation of effect sizes between European countries, it could be shown that in countries where more rigid marriage norms prevail cohabitation has a stronger effect on marital stability than in countries where marriage norms are weaker. Furthermore, the lower the divorce barriers are, the weaker is the association between the parental divorce and the divorce risk of the offspring.”
Some data and results from the paper (click tables and figures to see them in a higher resolution):
The table shows the estimated effect sizes of premarital cohabitation on the divorce risk in various European countries; a positive effect size indicates a higher likelihood of divorce among couples who lived together before they got married, whereas a negative effect size indicates a smaller divorce risk for couples who did not cohabitate before they got married. They note in the paper that, “The European overall effect indicates a positive relationship between cohabitation and the risk of divorce, that is, cohabiting couples have a 33 per cent higher risk to divorce than couples who do not share a common household before marriage.” However the effecs are highly heterogenous across countries, and more specifically they find that: “In countries in which traditional marriage norms are strongly institutionalized, cohabitation has a stronger effect than in countries in which marriage norms are weaker.” The institutional framework is important. The Q-statistic is a heterogeneity-measure – read the paper if you want the details..
What about children? Here’s a brief summary:
Effect sizes are almost universally negative (children = smaller risk of divorce) and a lot of them are highly significant (more than half of them are significant at the 1% confidence level). As they note, “The presence of children strongly decreases the risk of divorce”. Note that the effect sizes vary but tend to be large; in the Netherlands, the country with the largest effect size, married couples with children are 70% less likely to divorce than are couples without children. The average estimated effect size is 50% so this is a huge effect. However I would be cautious about making a lot of inferences based on this finding without at the very least having a closer look at the studies on which these results are based; for example it’s unclear if they have taken into account that there may be unobserved heterogeneity problems playing a role when comparing married couples with- and without children here; lots of marriages break up early on (using Danish data I have previously estimated that once the marriage has lasted 9 years, half of the total divorce risk the Danish couple confronted ex ante will basically have been accounted for; i.e. the total risk that you’ll divorce your partner during the first 9 years is as big as is the risk that you’ll do it at any point after the 9th year of marriage – see the last figure in this post), and it does not seem unlikely e.g. that sampled marriages involving children may, ceteris paribus, have lasted a longer time on average than have sampled marriages without children (most European couples get married before they have children so the likelihood that a couple will have children is positively correlated with the marriage duration), meaning that these marriages were less likely to get broken up, regardless of the children. If they conditioned on marriage duration when calculating these effects this particular problem is dealt with, but I don’t know if they did that (and I’m not going to go through all those studies in order to find out..) and there may be a lot of other ways in which marriages with and without children differ; differences that may also relate to divorce probability (education, income, labour market status, …). Note that the fact that the studies included in the meta-study are longitudinal studies does not on its own solve the potential ‘duration problem’ (/selection problem); you can easily follow two couples for the same amount of time and still have radically different (ex ante) divorce likelihoods – and comparing unadjusted (group?) hazard rates and making conclusions based on those seems problematic if you have selection issues like these. Researchers aren’t stupid, so the studies here may all have taken care of this particular potential problem. But I’m sure there are problems they haven’t handled. Caution is warranted – part of the estimated ‘children effect’ is likely not to go through the children at all.
How about the parents? How does the fact that your parents got divorced impact your own likelihood of divorce?
“Nearly all the reported effect sizes indicate positive associations between the stability of the parental marriage and the stability of children’s marriage”. There are huge cross-country differences – in Italy an individual whose parents got divorced is almost three times as likely to get divorced him/herself as is an individual whose parents did not divorce, whereas the risk increase in Poland amounts to only (a statistically insignificant) 14%.
Lastly, I’ll note that:
“No empirical support was found for any of our hypotheses which link the level of modernization to the risk of divorce. A least with respect to the divorce risk, we considered the level of socioeconomic development not to be an important macro-variable. Also, we could not find any significant relationships between the strength of divorce barriers and the effect of children on marital stability.”
I would not have expected these results if you’d asked me beforehand. Then again e.g. the differences in socioeconomic development among the countries included here are not that big, so it may just be a power issue.
Various people have recommended this book to me, including people who’ve commented here on the blog. Now I’ve read it.
I must admit I didn’t think much of it. I gave it two stars on goodreads. If it hadn’t been recommended to me by multiple people, I’m pretty sure I’d have thrown the book away around pages 50-60 at the latest.
To avoid spoilers I’ve written the rest of this post in rot-13 below the fold. You can decrypt the ciphertext here.
I decided to do a tally.
There’s a small overlap with last year’s reading because I started #3 and #5 last year but only finished them this year. On the other hand I’ve only included books I’ve finished, which means that more than a few books are left out of the equation; including some books where I’ve actually read a substantial number of pages. I was wondering whether to include novellas and plays – I decided to include them here, but you can mentally remove Dickens, Abbott and Stoppard from the list if you prefer to. I like to think it sort of evens out in the end in terms of ‘proper book equivalents’; there are only a few of them on the list, and on the other hand all the Martin books I read and added to the list were single volume publications, even though some of these books have been “divided into two, three, or even four volumes“. There are also quite a few textbooks on this list which should help ‘even things out’. Either way I think the goal of 50 books has been reached at this point. It seems that I’ve read a few more non-fiction books than fiction books overall, but it’s almost 50/50 – naturally I spend a lot more time reading non-fiction than fiction. In terms of the language breakdown, there are 57 books in English and one book in Danish – I wasn’t really aware that it was that bad, but it seems I’ve pretty much stopped reading Danish books at this point.
The list below includes one link/book to a post I’ve written here on the blog about the specific book in question. In cases where I’ve written multiple posts about the book I’ve only linked to one of the posts (most often the last one) – linking takes time, making a list like this one takes time, and the blog does have a search button for a reason.
Books I’ve read:
IV. Close Relationships.
XIII. A Christmas Carol.
XVII. Ten days in a mad-house.
XIX. A Game of Thrones.
XXI. Carpe Jugulum.
XXII. Daily Negations.
XXIII. A Clash of Kings.
XXV. A Storm of Swords.
XXVII. A Feast for Crows.
XXIX. Men at arms.
XXXI. The Devotion of Suspect X.
XXXIII. The Mysterious Affair at Styles.
XXXIV. The Murder on the Links.
XXXV. Lord Edgware Dies.
XXXVII. Three Act Tragedy.
XXXVIII. Gender, Physical Activity, and Aging.
XXXIX. The ABC murders.
XLIII. A Dance With Dragons.
XLIV. Handbook of critical care.
XLV. Evil Under the Sun.
XLVI. One, Two, Buckle My Shoe.
XLVIII. The (Honest) Truth about Dishonesty.
L. The Double Helix.
LI. Dumb Witness.
LIII. Five Little Pigs.
LV. Why sex matters.
LVII. Murder on the Orient Express.
I started the book on Friday and I just finished it. I should point out that it doesn’t actually take that long to read; I had social obligations this weekend as I was visiting family, and so I didn’t read very much Saturday and Sunday.
Like A short History…, the book covers a lot of ground. It’s really hard to summarize, but here are some introductory remarks from the first pages of the book:
“I don’t know how many hours of my school years were spent studying the Missouri Compromise or the War of the Roses, but it was vastly more than I was ever encouraged or allowed to give to the history of eating, sleeping, having sex or endeavouring to be amused. So I thought it might be interesting, for the length of a book, to consider the ordinary things in life, to notice them for once and treat them as if they were important, too. Looking around my house, I was startled and a little appalled to realize how little I knew about the domestic world around me. Sitting at the kitchen table one afternoon, playing idly with the salt and pepper shakers, it occurred to me that I had absolutely no idea why, out of all the spices in the world, we have such an abiding attachment to those two. Why not pepper and cardamom, say, or salt and cinnamon? And why do forks have four tines and not three or five? There must be reasons for these things. […] Suddenly the house seemed a place of mystery to me. So I formed the idea to make a journey around it, to wander from room to room and consider how each has featured in the evolution of private life. The bathroom would be a history of hygiene, the kitchen of cooking, the bedroom of sex and death and sleeping, and so on.”
How was life like for servants living in Victorian England? Which materials did American settlers have problems procuring, and how did this change over time? Which kinds of building materials have people been using over time? Which kinds of clothes were popular in 1650 (…and which clothes were you even allowed to wear..?)? What about furniture like chairs and beds? What did people eat and drink during the Middle Ages? Child labour during the Industrial Revolution. The construction of the Eiffel Tower. The history of incandescent lighting. Crop rotation. English country houses. The Sepoy Rebellion. Flushing toilets. Ötzi the Iceman. The power loom. The Columbian Exchange. There’s a lot of stuff covered in this book. Did you know that Britain used to have a tax on bricks? And another tax on glass? And a wallpaper tax? I didn’t.
A few times while reading the book I had a, ‘Hey, based on what I know that doesn’t sound quite right’-experience. Or a, ‘Whereas this may not be completely wrong, it also does not seem entirely accurate.’ This was especially the case in the beginning of the book, where Bryson writes about stuff which I’ve read about before; e.g. he briefly discusses the Völkervanderung and how this period affected Britain, but he doesn’t seem to have deep knowledge about the period or what was actually going on. At the very least he makes some questionable conclusions along the way without providing a lot of supporting evidence in the text. His knowledge of prehistory and stuff like the origins of farming, which he briefly touches upon in the beginning, also doesn’t seem extensive; I don’t think he’s read Scarre or an equivalent work (just as he most certainly hasn’t read Heather). He’ll occasionally make inferences about specific aspects of home life such as the timing of the introduction of specific types of furniture based on (sparse) linguistic evidence. He includes an extended form of Bayes’ Theorem in the book early on (one of only two equations in the book, if I remember correctly) but doesn’t actually convince me that he understand how the theorem works; he doesn’t explain what the parameters in the equation he’s written down actually are, and it seems as if even though he knows what the equation looks like, it’s still just a black box to him.
But the comments above refer to minor specific points of small relevance to the overall reading experience. In general I’d have to say that the book is well written, and it’s occasionally hilariously funny. To me the far most problematic thing about the book is that there is no way to link a specific piece of information to a specific source (wikipedians would say that there are no inline citations). There’s an extensive bibliography with 508 books, according to one review (I haven’t counted them), which is almost, though not quite, a book per page. So don’t for a second think Bryson hasn’t read a lot of stuff in order to write this book, including a lot of interesting original sources. But I still can’t figure out where a given piece of information comes from, and when I can’t do that I tend to get annoyed. Especially as there were quite a few errors in A Short History… I subtract roughly a star from my final goodreads rating because of this problem. Which means that I’ve given it four stars. The average rating on goodreads is 3.93.
I’ve added some random observations from the book below:
“By 1851, one-third of all the young women in London – those aged from about fifteen to twenty-five – were servants. Another one in three was a prostitute. For many, that was about all the choice there was.” (I’d love to see a source for these estimates, but I’m not going to go through the bibliography in order to figure out where those numbers are derived from. However even if the estimates are inaccurate, it’s beyond doubt that this was a very different world.)
“Visiting his daughter in the 1920s, in a house too small to keep his servants with him, the tenth Duke of Marlborough emerged from the bathroom in a state of helpless bewilderment because his toothbrush wasn’t foaming properly. It turned out that his valet had always put the toothpaste on the brush for him and the duke was unaware that toothbrushes didn’t recharge automatically.”
“We forget just how painfully dim the world was before electricity. A candle – a good candle – provides barely a hundredth of the illumination of a single 100-watt light bulb. Open your refrigerator door and you summon forth more light than the total amount enjoyed by most households in the eighteenth century. The world at night for much of history was a very dark place indeed. […] The widespread belief that people in the pre-electrical world went to bed at nightfall seems to be based entirely on the presumption that anyone deprived of robust illumination would be driven by frustration to retire. In fact, it appears that most people didn’t retire terribly early – nine or ten o’clock seems to have been standard for most people in the days before electricity, and for some, particularly in cities, it was even later. […] Visitors to eighteenth-century London often noted that the shops were open till 10 at night, and clearly there would be no shops without shoppers. When guests were present it was usual to serve supper at 10 and for company to stay till midnight or so.”
“electric lighting was ultimately irresistible. It was clean, steady, easy to maintain, and available instantaneously and in infinite amounts at the flick of a switch. Gas lighting had taken half a century to establish itself, but electric lighting happened much more quickly. By 1900, in cities anyway, electric lighting was increasingly the norm – and electric appliances ineluctably followed: the electric fan in 1891, the vacuum cleaner in 1901, the washing machine and iron in 1909, the toaster in 1910, the refrigerator and dishwasher in 1918.”
“A typical stove in 1899, according to a study in Boston, burned some three hundred pounds of coal in a week, produced twenty-seven pounds of ash, and required three hours and eleven minutes of attention. […] By 1842, Britain was using two-thirds of all the coal produced in the western world.”
“Between 1699 and 1721 tea imports [to Britain] increased almost a hundredfold, from 13,000 pounds to 1.2 million pounds, then quadroupled again in the thirty years to 1750. […] By 1800 tea was embedded in the British psyche as the national beverage, and imports were running at 23 million pounds a year. Virtually all that tea came from China. This caused a large and chronic trade imbalance. The British resolved this problem in part by selling opium produced in India to the Chinese. […] tea cultivation was introduced to India in […] 1851 […] In half a century, from a base of nothing in 1850, tea production in India rose to 140 million pounds a year.”
“Throughout history Britons have used and needed a lot of wood. A typical farmhouse of the fifteenth century contained the wood of 330 oak trees. […] Hauling a cartload of stone ten or twelve miles could easily double its costs, so medieval stone didn’t travel far, which is why there are such appealing and specific regional differences of stone use and architectural style throughout Britain.”
“By the early twentieth century, 10 per cent of all British aristocratic marriages were to Americans”
“By the early 1880s America had sixty thousand telephones in operation. In the next twenty years that figure would increase to over six million.”
“One of the conventions of the age was to feed and put up any respectable-looking person who presented himself at the door. [George] Washington was plagued with guests – he had 677 of them in one year – and many of those stayed for more than one night.”
“By the late nineteenth century, 80 per cent of English wallpapers contained arsenic, often in very significant quantities. […] It has […] been suggested that poisonous wallpaper could well account for why a change of air was so often beneficial for the chronically ill. In many cases they were doubtless simply escaping a slow poisoning.”
“For much of history a bed was, for most homeowners, the most valuable thing they owned. In William Shakespeare’s day, for instance, a decent canopied bed cost £5, half the annual salary of a typical schoolmaster. […] Privacy was a much different concept in former times. In inns, sharing beds remained common into the nineteenth century, and diaries frequently contain entries lamenting how the author was disappointed to find a late-arriving stranger clambering into bed with him.”
“In 1954 just one French residence in ten had a shower or bath.”
“Halley was a tireless investigator into scientific phenomena of all kinds, and produced papers on everything from magnetism to the soporific effects of opium. In 1693, he came across figures for annual births and deaths in Breslau, Silesia (now Poland), which fascinated him because they were so unusually complete. […] In Breslau, slightly over a quarter of babies died in their first year, and 44 per cent were dead by their seventh birthday.”
“Between 1872 and 1902, American wheat production increased by 700 per cent. In the same period, British wheat production fell by more than 40 per cent.”
“And now a passenger lies dead in his berth – stabbed.”
I read the book yesterday.
This is one of the few Christie stories that I remember having watched a film version of in my youth. Because of that I was considering beforehand whether to read it now or to leave it for another decade. I decided to read it, as I became aware while trying to recall the plot that I couldn’t really remember any of it. I’m glad I made that decision – my goodreads review sums it up quite nicely: ‘This book is awesome.’ I gave it 5 stars. Average goodreads rating is 4.08 (based on tens of thousands of ratings) – the average rating of (one specific edition of) The Murder of Roger Ackroyd is 4.10, so the two books seem to the goodreads community to be of comparable quality. I like the latter a little better, but this book is to me up there in broadly the same category. This is very clever stuff. Recommended.
I was curious to know how my blog looks like when I’m not logged into my wordpress account and my adblocker is disabled. I know that wordpress occasionally displays adds in the sidebar and below my posts, and so I wanted to see which kinds of advertisements they were displaying – I don’t see those adds normally.
Before I ever got to watching adds, I noticed while I was logged out that recent comments do not display in the sidebar (“There are no public comments available to display.”). I should point out that this is not what the blog looks like when I’m logged in – when I’m logged in I have no problems viewing recent comments in the sidebar, and so I had no idea this problem existed. Is it a new problem, or has it been that way for a while?
If things look bad/wrong for some reason, you should never hesitate to tell me in the comments – odds are I don’t know about it. Even if I can’t do anything about it, I prefer knowing to not knowing. I actually spend a non-negligible amount of time on formatting and related stuff in order to make things look reasonably okay when I post (e.g. in order to make sure quotes don’t come out all wrong because of formatting issues etc.). That work is completely in vain if things look like crap or doesn’t work because of issues I’m unaware of.
I’m told that it’s a problem on wordpress’ end, so it’s not something I’ve done. I hope it’ll be solved quickly. To be updated.
I started reading this book last year – here’s a post from back then. It’s a great book – it’s well written, I’m learning a lot. But on the flip-side the book is, and was, hard work to read – so when I was last reading it I simply decided at one point to put it away (temporarily?) because I couldn’t be arsed to do the work it took to actually finish this book (not even close – there’s a lot of stuff in there). I recently decided I should have another go at it, partially on account of having learned some relevant stuff in the meantime which might result in some of the chapters being perhaps a little easier for me to read; I never really read any chapters ‘cold’ – i.e. without knowing anything about the topic – but a few of the topics covered I didn’t know much about, and these were really hard to read. Knowing stuff like what’s in here, here, here, here, here, here, and here will help make the book easier for you to read and I don’t think this should be the first medical textbook you read.
When I ‘stopped reading’ I had gotten to chapter 7, which is about nervous system disorders. It’s a very long chapter, which was probably part of the reason why that was where I stopped. I’ve now finished this chapter, as well as chapter 8 on diseases of the skin, chapter 9 on pulmonary disease, and chapter 10 on heart disease. I’ve started reading chapter 11 on vascular disease – I’m almost half way through the book at this point. A chapter takes a significant amount of time to read and I can’t possibly cover all the stuff they talk about in these chapters here, but I’ve added some general remarks related to chapters 7-9 below. I may cover chapter 10 later.
The nervous system chapter is as mentioned quite long and it covers a lot of stuff; the way I see it, there’s more interesting stuff about how these things actually work in a quarter of this chapter alone than there is in Oliver Sacks entire book The Man Who Mistook His Wife for a Hat. You do not find sentences like the first one below in Sacks:
“The prefrontal cortex (Figure 7-9) generally refers to the areas 9, 10, 11, 12, 45, 46, and 47 of Broadmann on the superior and lateral surfaces of the frontal lobes and the anterior cingulate, parolfactory, and orbitofrontal cortex inferiorly and mesially. These regions are essential for orderly planning and sequencing of complex behaviors, attending to several stimuli or ideas simultaneously, concentrating and flexibly altering the focus of concentration, grasping the context and meaning of information, and controlling impulses, emotions, and thought sequences. Damage to the frontal lobes or connections to the caudate and dorsal medial nuclei of the thalamus cause the frontal lobe syndrome. Patients may suffer dramatic alterations in personality and conduct, while most sensorimotor functions remain intact.” (You may find this link to anatomical terms of location to be helpful)
The chapter as always covers first how things are supposed to work, what is going on in that system, and then it has some stuff about what happens when things go wrong. That said, the line drawn between the parts dealing with physiology and the parts dealing with pathophysiology felt more fluid to me in this chapter than it did in most chapters in this book. There’s an obvious reason for that: The neurological system handles a huge amount of specific types of activities, and subcomponents of this system are often highly specialized; so I thought it made a lot of sense for them to include a few remarks about ‘what might go wrong if this specific mechanism is impacted for some reason’ while talking about ‘how things generally work’, and I found remarks such as the one above quite helpful. Aside from frontal lobe syndrome they also talk along the way about e.g. various forms of hearing loss, vision problems and how they might be caused by neurological problems (and how different neurological problems may manifest in different ways – i.e., which type of vision loss you can expect will depend on which specific neurological pathway is damaged), anatomy of sensory loss while dealing with the somatosensory system, as well as how language might be impacted by damage to specific regions of the brain. To take a few examples. They naturally couldn’t possibly cover all neurological pathologies in detail in a chapter like this, so they don’t try to do this either; what they do instead is that in the latter half they select out a few neurological disorders which are then covered in some detail in order to illustrate some central themes. The disorders covered are motor neuron diseases (primarily ALS), Parkinson’s disease, Myasthenia Gravis, epilepsy, dementia and Alzheimer’s disease, and stroke.
Chapter 8 deals with diseases of the skin. It’s a short chapter, much shorter than the neurology chapter, and I won’t talk too much about it. It spends a few pages talking about how skin works and how it normally looks like, then there’s an overview of skin diseases and how to classify them, and then there’s a section about the pathophysiology of selected skin diseases (psoriasis, lichen planus, erythema multiforme, bullous pemphigoid, and leukocytoplastic vasculitis). Here’s an observation from this chapter which I’d never thought about:
“Physicians interested in the skin learned decades ago that the accurate diagnosis and classification of the many patterns of dermatitis were dependent upon a standardized nomenclature for the description and documentation of rashes. […] To illustrate the importance of terminology, imagine trying to describe a patient’s condition over the phone to another physician. Talking about a “red raised rash” may truthfully describe the eruption in some sense, but the mental image evoked could be any one of dozens of skin diseases. As the describer, the only way to accurately portray an eruption is through the use of precisely defined terms.”
So how does one go about describing these things? Well, here’s the system they’ve come up with and apply:
“The most important types of primary lesions include macules and patches, papules and plaques, vesicles and bullae, postules and nodules. The terms macule and patch denote flat areas of discoloration, without any discernible change in texture. Macules are 1 cm or less in diameter, while patches exceed 1 cm in size. Papules and plaques are elevated, palpable skin lesions, in which the breadth of the lesion exceeds its thickness. A papule is small, 1 cm or less in diameter, while a plaque exceeds 1 cm in size. Vesicles and bullae are fluid-filled spaces within the skin. Vesicles are less than 1 cm in diameter, while bullae exceed 1 cm in size. A vesicle or bulla containing purulent fluid is known as a postule. A nodule is a solid, rounded skin lesion in which diameter and thickness are roughly equal.”
Chapter 9 is about pulmonary disease. I assume these Khan Academy videos cover stuff similar to what’s covered in the beginning of the chapter (I’ve seen all the videos about gas exchange aside from the last one, but I’ve only seen the last one in the introduction section so I don’t really know in detail what’s covered in the first ones) – at least I’ll say having watched some of these beforehand was helpful. The first part of the chapter talks about the normal structure of the lungs, basic anatomical features, static properties like compliance and elastic recoil as well as dynamic properties related to flow and resistance (I watched the fluid dynamics videos on Khan Academy a while back so some of this stuff was review), how matching of ventilation and perfusion is achieved (and what happens when there’s a mismatch between the two), and how breathing is controlled. The second part deals with the pathophysiology of some specific lung diases; asthma, COPD (treatment split up into two parts, dealing with chronic bronchitis and emphysema separately), idiopathic pulmonary fibrosis, pulmonary edema, and pulmonary embolism. Some observations from the chapter:
“At rest, the lungs take 4 L/min of air and 5 L/min of blood, direct them within 0.2 µm of each other, and then return both to their respective pools. With maximal exercise, flow may increase to 100 L/min of ventilation and 25 L/min of cardiac output. The lungs thereby perform their primary physiologic function of making oxygen available to the tissues for metabolism and removing the major by-product of that metabolism, carbon dioxide. The lungs perform this task largely free of conscious control, all the while maintaining PaCO2 within 5% tolerance. It is a magnificent feat of evolutionary plumbing and neural control. […] The amount of energy needed to maintain the respiratory muscles during quiet breathing is small, approximately 2% of basal oxygen consumption. Increasing ventilation in normal humans consumes relatively little oxygen until ventilation approaches 70 L/min. In patients with lung disease, the energy requirements are greater at rest and increase dramatically with exercise. Patients with emphysema may not be able to increase their ventilation by more than a factor of 2 because the oxygen cost of breathing exceeds the additional oxygen made available for the body.”
“The functional role of the lungs is to place ambient air in close proximity to circulating blood to permit gas exchange by simple diffusion. To accomplish this, air and blood flow must be directed to the same place at the same time. In other words, ventilation and perfusion must be matched. A failure to match ventilation to perfusion […] lies behind most abnormalities in O2 and CO2 exchange.”
“All blood vessels leak. In the adult human, leakage from the pulmonary circulation represents less than 0.01% of pulmonary blood flow, or a baseline filtration of approximately 10-20 mL/h. […] Pulmonary edema occurs when the transmural pressure is excessive for a given capillary permeability. […] in the presence of damaged capillary endothelium, small increases in otherwise normal transmural pressure may cause large increases in edema formation. Similarly, if the alveolar epithelial barrier is damaged, even the baseline filtration across an intact endothelium may cause alveolar flooding.”
“The English word “embolus” derives from a Greek root meaning “plug” or “stopper.” A pulmonary embolus consists of material that gains access to the venous system and then to the pulmonary circulation. Eventually, it reaches a vessel whose caliber is too small to permit free passage, and there it forms a plug, occluding the lumen and obstructing perfusion. […] It is a normal function of the pulmonary microcirculation to remove venous emboli. The lungs possess both excess functional capacity and a redundant vascular supply, making them a superb filter for preventing small thrombi and platelet aggregates from gaining access to the systemic circulation. However, large thromboemboli – or an accumulation of smaller ones – can cause substantial impairment of cardiac and respiratory function, including death. […] Pulmonary thromboemboli are quite common and cause significant morbidity. They are found at autopsy in 25-50% of hospitalized patients [my emphasis, US] and are considered a major contributing cause of death in a third of those. However, the diagnosis is made antemortem in only 10-20% of cases. […] More than 95% of pulmonary thromboemboli arise from thrombi in the deep veins of the lower extremity: the popliteal, femoral, and iliac veins. […] The most prevalent risk factor in hospitalized patients is stasis from immobilization, especially in those undergoing surgical procedures. The incidence of calf vein thrombosis in patients who do not receive heparin prophylaxis following total knee replacement is reported to be as high as 84%; it is more than 50% following hip surgery or prostatectomy. The risk of fatal pulmonary thromboembolism in these patients may be as high as 5%. […] The most devastating and feared complication of acute thromboembolism is sudden occlusion of the pulmonary outflow tract, reducing cardiac output to zero and causing immediate cardiovascular collapse and death. Large emboli that do not completely occlude vessels, particularly in patients with compromised cardiac function, may cause an acute increase in pulmonary vascular resistance. This leads to acute right ventricular strain and a fatal fall in cardiac output. Such dramatic presentations represent less than 5% of cases and are essentially untreatable. They serve to highlight the importance of primary prevention of venous thrombosis.”
On gnxp Razib Khan posts regular ‘Open Threads’ where people can share links, talk about stuff they’ve read or thought about, etc. I have been thinking about introducing similar posts here for a while, and I’ve now decided to give it a go. If it turns out the readership isn’t willing to ‘give anything back’ and ‘participate’, I’ll not make this a regular feature – consider this post a test-case.
Here are my contributions to the discussion:
I’ll quote a friend: “His speaking is horrible. […] He sounds like a drunk homeless guy who likes howling speeches in the middle of the night and disturbing everyone who wants to sleep. […] If I didn’t know he was Winston Churchill I would have stopped the video after 5 seconds.”
Here are a few other important speeches from this period:
(This one made me laugh out loud after 15 seconds. He sounds like Daffy Duck. But if you can look past this, it’s an important speech.)
The word is yours…
“Thirty-five percent of U.S. adults say that at one time or another they have gone online specifically to try to figure out what medical condition they or someone else might have.
These findings come from a national survey by the Pew Research Center’s Internet & American Life Project. Throughout this report, we call those who searched for answers on the internet “online diagnosers”.
When asked if the information found online led them to think they needed the attention of a medical professional, 46% of online diagnosers say that was the case. Thirty-eight percent of online diagnosers say it was something they could take care of at home and 11% say it was both or in-between.
When we asked respondents about the accuracy of their initial diagnosis, they reported:
41% of online diagnosers say a medical professional confirmed their diagnosis. An additional 2% say a medical professional partially confirmed it.
35% say they did not visit a clinician to get a professional opinion.
18% say they consulted a medical professional and the clinician either did not agree or offered a different opinion about the condition.
1% say their conversation with a clinician was inconclusive.
Women are more likely than men to go online to figure out a possible diagnosis. Other groups that have a high likelihood of doing so include younger people, white adults, those who live in households earning $75,000 or more, and those with a college degree or advanced degrees.”
The quotes above are from a Pew report, Health Online 2013, published earlier this year. Below I’ve added some more data from the report, as well as a few comments. You can click the tables to view them in a higher resolution.
“Looking more broadly at the online landscape, 72% of internet users say they looked online for health information of one kind or another within the past year. […] 77% of online health seekers say they began at a search engine such as Google, Bing, or Yahoo. Another 13% say they began at a site that specializes in health information, like WebMD. Just 2% say they started their research at a more general site like Wikipedia […] 39% of online health seekers say they looked for information related to their own situation. Another 39% say they looked for information related to someone else’s health or medical situation. […] As of September 2012, 81% of U.S. adults use the internet and, of those, 72% say they have looked online for health information in the past year. [Incidentally, according to this Pew report, the number of online Americans is actually 85%, but it’s in that neighbourhood… Note that 72% of 81% is just 58% (they say 59% in the report later, probably due to rounding) – so almost half of all Americans don’t look for health information online. That’s a lot of people.] […]
Females are more likely to be online diagnosers, as are young people, whites, rich people, and college-educated individuals (when we compare the females with males, the young people with the old, the white people with the non-white, etc. See also the remarks in the update..). Note that education is basically a step-function here; the more education you get, all else equal the more likely you are to try to diagnose yourself online. Note also that some of these differences are really huge; roughly 10 percent of people without a HS diploma answered that they’d looked online to diagnose a condition during the last year, whereas half of all college-educated individuals answered in the affirmative.
A potentially important thing to have in mind when comparing the numbers for insured and uninsured individuals is that internet usage and health insurance status probably covary; I believe it’s likely that uninsured people are also less likely to use the internet. Low-income individuals with short educations are much less likely to be online, independent of age (see the link above).
“Twenty-six percent of internet users who look online for health information say they have been asked to pay for access to something they wanted to see online. […] Of those who have been asked to pay, just 2% say they did so. [I was very surprised that that number was strictly larger than zero…] Fully 83% of those who hit a pay wall say they tried to find the same information somewhere else. Thirteen percent of those who hit a pay wall say they just gave up. […] Respondents living in lower-income households were significantly more likely than their wealthier counterparts to say they gave up at that point. Wealthier respondents were the likeliest group to say they tried to find the same information elsewhere.”
Do remember when looking at the numbers above that health status and education are related variables; lower educated people are more likely to be in poorer health than are higher educated people on average, in part because of lifestyle choices (I’ve written about these differences before – see e.g. this post (and note that there’s a lot of stuff in those links – and that I have a lot more links for you if you don’t find them satisfactory, as I’ve done academic work in this field and am quite familiar with the literature on the links between education and health.)). Yet even when conditioning on online status (low-educated individuals are less likely to be online), individuals with low educations are still, all other things being equal, much less likely than are the college educated to look online for many types of health information.
Update: To illustrate how much trouble you might get into if you don’t have in mind the differences in internet adoption rates across social strata, I decided to add a few more numbers. The numbers are from the Offline Adults report, to which I also link above:
People without a high school diploma are roughly 10 times as likely not to use the internet as are people with a college degree; 41% of people without a HS diploma don’t use the internet – 4% of college-educated don’t. For individuals with an income below $30k, one in four don’t use the internet, whereas roughly 5% of those with an income north of $50k don’t. It’s very safe to say that not all subgroups included in some of the specific types of response data above are equally representative of the groups from which they are derived. Note also that potential drivers of the relevant intragroup differences here may be very important if one were to try to find ways to ‘bridge the information gap’; for example if some of the low-educated individuals who don’t use the internet can’t read, finding ways to provide them with internet access may not make much difference.
I should point out here that based just on the observations above it’s impossible to say anything about the details of what drives these results. It’s not clear e.g. how big a role the age variable plays when it comes to the contribution from income and education; old people on a pension have much lower incomes (but higher net savings) than most people who’re still active in the labour market (link), and older people are also significantly less likely to have college degrees and more likely to not have a high school diploma. The significance tests they report which are meant to indicate whether or not e.g. the results for people with an income of $30-50k are different from the results for people with incomes below $30k don’t take stuff like that into account, they’re just of a ‘let’s ignore everything else and compare the numbers’-kind and so can’t really be trusted. Maybe income doesn’t matter once you’ve taken age and education into account. I’m not saying this is the case, but given the data you can’t say if that’s true or not. Disentangling the ‘pure partial effects’ would be nice, but that’s likely to be a lot harder than it looks; multicollinearity is likely a problem, and some of the correlated regressors display non-linear relationships (e.g. income-age – see the link above). Be careful about which conclusions you draw.
I’ve posted a few of Carolin Crawford’s astronomy lectures before – in this post I’ve added a few more:
If you want a more detailed account, Rory Barnes’ Formation and Evolution of Exoplanets is probably a good try, even though it’s a couple of years old and things are – as Crawford points out – changing rather fast in this field of exploration. I read the first couple of chapters of that book a while back and browsed a few of the other chapters a bit later on, but I decided against finishing it because it was too much work – the mathematics gets a bit ugly along the way, and if you don’t happen to have a rather strong foundation in physics and(/or?) maths it’s probably not worth your time as you’ll not understand much of what’s going on.
It’s sometimes a bit annoying that you can’t tell what she’s pointing at when she’s explaining what going on in a given picture or illustration (I find that this is a very common problem when it comes to online lectures, and it’s also sometimes an issue during the other lectures in this series), but it’s still a great lecture.
This one is actually the most recent one I’ve watched, even though it turns out it’s her first Gresham lecture. The sound quality of this lecture is a bit worse than that of the ones above, especially during the first minutes (perhaps I just got used to it? I don’t know…) but it’s pretty awesome anyway:
I think Crawford’s doing a splendid job and that’s she’s given some very interesting and educational videos. Please don’t skip/ignore these videos just because they’re somewhat longer than ‘the standard youtube video‘ – there’s some really awesome stuff here (the same thing applies, I think, to the various medical lectures I’ve posted recently as well – you can go back to those posts now and have a look if you skipped them the first time around; they’re all still there…). Wikipedia incidentally has great coverage of many astronomy-related topics and I’m sure (because I’ve read some of them before, e.g. the article about Enceladus) that there are some featured articles about stuff covered in these lectures waiting for you if you want to learn more. You don’t need to start at the Enceladus article if you want to learn more about Saturn’s moons – a better place to start would probably be this article.
As Razib Khan put it recently, this is truly a golden age of the mind, if you want it. As some of the readers who read my most recent post (I pulled it later, and there wasn’t much to read, really – so the rest of you didn’t miss out on anything..) might have inferred, I often have doubts about if this will keep being ‘enough’ for me, for some rather narrow definitions of ‘enough’ – but I should point out that I do derive (…/and so it is possible to derive…) a great deal of pleasure from living in an age where you at least in theory (but to a greater and greater extent also in practise) have the option of exploring and learning (/trying to learn..) stuff about almost any topic you’d care to have a go at. Even though I from time to time find myself depressed on account of wanting/desiring much more from life than what such a life of the mind on its own can possibly give me, I do think that most people do not take enough advantage of the opportunities they have today in this area of life.
i. Golden Eagle.
I checked out the wiki article after I’d come across this article with some amazing pictures (“While the three photos were taken over the course of just two seconds, they made scientific history.”).
“The Golden Eagle (Aquila chrysaetos) is one of the best-known birds of prey in the Northern Hemisphere. It is the most widely distributed species of eagle. Like all eagles, it belongs to the family Accipitridae. These birds are dark brown, with lighter golden-brown plumage on their napes. Immature eagles of this species typically have white on the tail and often have white markings on the wings. Golden Eagles use their agility and speed combined with extremely powerful feet and massive, sharp talons to snatch up a variety of prey (mainly hares, rabbits, marmots and other ground squirrels). […]
Golden Eagles are sometimes considered the most superlative fliers among eagles and perhaps among all raptorial birds. They are equipped with broad, long wings with somewhat finger-like indentations on the tips of the wing. Golden Eagles are unique among their genus in that they often fly in a slight dihedral, which means the wings are often held in a slight, upturned V. When they must engage in flapping flight, Golden Eagles appear at their most labored but this flight method is generally less common than soaring or gliding flights. Flapping flight usually consists of 6–8 deep wing-beats, interspersed with 2 to 3 second glides. While soaring the wings and tail are held in one plane with the primary tips often spread. A typical, unhurried soaring speed in Golden Eagles is around 45–52 kilometers per hour (28–32 mph). When hunting or displaying, the Golden Eagle is capable of very fast gliding, attaining speeds of up to 190 km/h (120 mph). When diving (or stooping) in the direction of prey or during territorial displays, the eagle holds its wings tight and partially closed against their body and the legs up against tail. In a full stoop, a Golden Eagle can reach spectacular speeds of up to 240 to 320 kilometers per hour (150 to 200 mph) when diving after prey. Although less agile and maneuverable, the Golden Eagle is apparently quite the equal and possibly even the superior of the Peregrine Falcon’s stooping and gliding speeds. This places the Golden Eagle as the one of the two fastest moving living animals on earth. [Note though that: “The Peregrine is renowned for its speed, reaching over 322 km/h (200 mph) during its characteristic hunting stoop (high speed dive), making it the fastest member of the animal kingdom. According to a National Geographic TV programme, the highest measured speed of a Peregrine Falcon is 389 km/h (242 mph).” – from the (featured) wikipedia article about the Peregrine Falcon]. […]
One of the most fascinating, though relatively little studied, aspects of the Golden Eagle’s biology is how it interacts with other predators in a natural environment, especially other large predatory birds. The Golden Eagle is a powerful hunter with few avian rivals in size or strength, although what it gains in these areas it loses somewhat in its agility and speed. Golden Eagles are avian apex predators, meaning a healthy adult is not generally preyed upon. There are several other large birds of prey that inhabit the Northern Hemisphere that may be attracted to the same prey, habitats and nesting sites as the Golden Eagles. Two examples are the Common Raven and Peregrine Falcon (Falco peregrinus) as these are two fairly large-bodied, mostly predatory birds that co-exist with Golden Eagles in almost every part of their range, although the former occurs in much larger numbers and the latter has a much larger natural distribution in more varied habitats. Both the Raven and the Peregrine are often attracted to much the same precipitous habitat as the Golden Eagle. However, both are generally dominated by the much larger eagle and will actively avoid nesting in the same area as a Golden Eagle pair.”
It’s a very long article, so there’s a lot of stuff there if you’re curious to learn more.
ii. Triton (moon) (featured).
“Triton is the largest moon of the planet Neptune, discovered on October 10, 1846, by English astronomer William Lassell. It is the only large moon in the Solar System with a retrograde orbit, which is an orbit in the opposite direction to its planet’s rotation. At 2,700 kilometres (1,700 mi) in diameter, it is the seventh-largest moon in the Solar System. Because of its retrograde orbit and composition similar to Pluto‘s, Triton is thought to have been captured from the Kuiper belt. Triton has a surface of mostly frozen nitrogen, a mostly water ice crust, an icy mantle and a substantial core of rock and metal. The core makes up two-thirds of its total mass. Triton has a mean density of 2.061 grams per cubic centimetre (0.0745 lb/cu in) and is composed of approximately 15–35% water ice.
Triton is one of the few moons in the Solar System known to be geologically active. As a consequence, its surface is relatively young, with a complex geological history revealed in intricate and mysterious cryovolcanic and tectonic terrains. Part of its crust is dotted with geysers thought to erupt nitrogen. […]
Triton’s revolution around Neptune has become a nearly perfect circle with an eccentricity of almost zero. Viscoelastic damping from tides alone is not thought to be capable of circularizing Triton’s orbit in the time since the origin of the system, and gas drag from a prograde debris disc is likely to have played a substantial role. Tidal interactions also cause Triton’s orbit, already closer to Neptune than the Moon’s to Earth, to slowly decay further; predictions are that some 3.6 billion years from now, Triton will pass within Neptune’s Roche limit. This will result in either a collision with Neptune’s atmosphere or the breakup of Triton, forming a ring system similar to that found around Saturn. […]
iii. Myth of the Flat Earth.
“The myth of the Flat Earth is the modern misconception that the prevailing cosmological view during the Middle Ages saw the Earth as flat, instead of spherical. The idea seems to have been widespread during the first half of the 20th century, so that the Members of the Historical Association in 1945 stated that:
During the early Middle Ages, virtually all scholars maintained the spherical viewpoint first expressed by the Ancient Greeks. From at least the 14th century, belief in a flat Earth among the educated was almost nonexistent, despite fanciful depictions in art, such as the exterior of Hieronymus Bosch‘s famous triptych The Garden of Earthly Delights, in which a disc-shaped Earth is shown floating inside a transparent sphere. […]
Since the early 20th century, a number of books and articles have documented the flat earth error as one of a number of widespread misconceptions in popular views of the Middle Ages. Both E.M.W. Tillyard’s book The Elizabethan World Picture and C.S. Lewis’ The Discarded Image are devoted to a broad survey of how the universe was viewed in Renaissance and medieval times, and both extensively discuss how the educated classes knew the world was round. […] Although the misconception was frequently refuted in historical scholarship since at least 1920, it persisted in popular culture and in some school textbooks into the 1960s.”
This is what a tank looked like in 1918 (…’A’):
And here’s how a tank looked like 21 years later (…’B’):
v. Golden Horde.
The Golden Horde (Tatar: Алтын Урда Altın Urda; Mongolian: Зүчийн улс, Züchii-in Uls; Russian: Золотая Орда, tr. Zolotaya Orda) was a Mongol and later Turkicized khanate, established in the 13th century, which comprised the northwestern sector of the Mongol Empire. The khanate is also known as the Kipchak Khanate or as the Ulus of Jochi.
After the death of Batu Khan in 1255, the prosperity of his dynasty lasted for a full century, until 1359, though the intrigues of Nogai did instigate a partial civil war in the late 1290s. The Horde’s military power peaked during the reign of Uzbeg (1312–41), who adopted Islam. The territory of the Golden Horde at its peak included most of Eastern Europe from the Urals to the right bank of the Danube River, extending east deep into Siberia. In the south, the Golden Horde’s lands bordered on the Black Sea, the Caucasus Mountains, and the territories of the Mongol dynasty known as the Ilkhanate.
The khanate experienced violent internal political disorder beginning in 1359, before it was briefly reunited under Tokhtamysh in 1381. However, soon after the 1396 invasion of Tamerlane, it broke into smaller Tatar khanates that declined steadily in power. At the start of the 15th century the Horde began to fall apart. By 1433 it was being referred to simply as the Great Horde. Within its territories there emerged numerous, predominantly Turkic-speaking, khanates. These internal struggles allowed the northern vassal state of Muscovy to rid itself of the “Tatar Yoke” at the Great stand on the Ugra river in 1480. The Crimean Khanate and the Kazakh Khanate, the last remnants of the Golden Horde, persisted until 1783 and 1847, respectively. […]
After Uzbeg (Öz-Beg) mounted the throne in 1313, he adopted Islam as the state religion. He proscribed Buddhism and Shamanism among the Mongols in Russia, thus reversing the spread of the Yuan culture. By 1315, Uzbeg had successfully Islamicized the Horde, killing Jochid princes and Buddhist lamas who opposed his religious policy and succession of the throne.
Mohammed Uzbeg Khan continued the alliance with the Mamluks which Berke and his predecessors had begun. He kept a friendly relationship with the Mamluk Sultan and his shadow Caliph in Cairo. After a long delay and much discussion, he married a princess of the blood to Al-Nasir Muhammad, Sultan of Egypt.
The Mongol rulers’ Rus’ policy was one of constantly switching alliances in an attempt to keep Russia and Eastern Europe weak and divided. […]
Uzbeg, whose total army exceeded 300,000, repeatedly raided Thrace, partly in service of Bulgaria’s war against both Byzantium and Serbia from 1319 on. The Byzantine Empire, beginning in the reign of Andronikos II Palaiologos and continuing in that of Andronikos III Palaiologos, was raided by the Golden Horde between 1320 and 1341, until the Byzantine port of Vicina Macaria was occupied. Some sources report that Uzbeg also married Andronikos III’s illegitimate daughter, who had taken the name Bayalun, and who later, after relations between the Horde and the Byzantines deteriorated, fled back to the Byzantine Empire, apparently fearing her forced conversion to Islam. His armies pillaged Thrace for forty days in 1324 and for fifteen days in 1337,taking 300,000 captives. However, his attempt to reassert Mongol control over Serbia was unsuccessful in 1330.”
(The article has much more.)
vi. Caesium (featured).
The book is an introductory textbook about clinical epidemiology. I don’t think I’ve ever actually read an epidemiology textbook (..a big part of why I wanted to read this), but I’ve read a lot of other stuff on related matters and I think it would be fair to say that this is not a new field to me. Most of the stuff in the book was well known to me and there actually wasn’t a lot of new stuff in there. I happen to know a lot more about many of the topics covered than what’s written in the book; data analysis is data analysis, and whether you’re performing survival analysis using Cox proportional hazard models on medical data or on unemployment data doesn’t really change all that much, except perhaps how to interpret the results.. But I didn’t know that I knew beforehand, and the book did contain enough interesting observations along the way to keep me going; even though many of the things covered were things I’d read about before, I did read the book from cover to cover. Though I should also point out that I emphatically did not spend an equal amount of time on all of it, and that I went over some of it quite fast (I didn’t really need to be reminded what a p-value is…).
The book defines a lot of concepts and shows how they are connected. I think I’d categorize it as ‘methodological, but informal’, in the sense that there’s very little explicit math here aside from the math required to introduce/explain variables of interest. Given the informal structure and the fact that it’s an introductionary text it’s natural that a few imprecise statements creep in here and there; there was in particular one paragraph in the middle of the book where I felt unsure what they were actually trying to say (they were basically saying that you shouldn’t ever use a specific research method, described in a very vague manner, but I knew that if they were criticizing what I believed them to be criticizing then they were obviously overlooking/disregarding benefits of the method which should be traded off against the costs they emphasized). A couple of places they make semi-questionable assumptions about e.g. attrition rate dynamics and selection mechanisms related to stuff like compliance patterns – but given the nature of the book this is perfectly understandable and, I think, forgivable, as a person who’s completely new to the field probably shouldn’t worry too much about those kinds of details yet (you can easily end up confusing people more than you help them by adding too much complexity to an intro textbook). Most of the time the language is precise and to the point.
If you don’t know a lot about this stuff, I think this book is a good starting point. It provides you with a good basis. It’s well written. But it’s not detailed enough (/too informal) and it didn’t teach me enough new stuff for me to really start getting excited about the book – I ended up giving it 3 stars on goodreads. To give you a sense of what the book is like, below I’ve added a few quotes from the book, with my own comments italized and bracketed:
“Although clinical distributions often resemble a normal distribution the resemblance is superficial. As one statistician (4) put it, “The experimental fact is that for most physiological variables the distribution is smooth, unimodal, and skewed, and that mean +/- 2 standard deviations does not cut off the desired 95%. We have no mathematical, statistical, or other theorems that enable us to predict the shape of the distributions of physiologic measurements.”
The shapes of clinical distributions differ from one another because many differences among people, other than random variation, contribute to distributions of clinical measurements. Therefore, if distributions of clinical measurements resemble normal curves, it is largely by accident. Even so, it is often assumed, as a matter of convenience […] that clinical measurements are “normally distributed”.”
“most distributions of clinical variables are not easily divided into “normal” and “abnormal.” They are not inherently dichotomous and do not display sharp breaks or two peaks that characterize normal and abnormal results. This is because disease is usually acquired by degrees, so there is a smooth transition from low to high values with increasing degrees of dysfunction. Laboratory tests reflecting organ failure, such as serum creatinine for kidney failure or ejection fraction for heart failure, behave in this way. Another reason why normals and abnormals are not seen as separate distributions is that even when people with and without a disease have substantially different frequency distributions, the distributions almost always overlap.”
“patients in clinical trials are usually a highly selected, biased sample of all patients with the condition of interest. As heterogeneity is restricted, the internal validity of the study is improved; in other words, there is less opportunity for differences in outcome that are not related to treatment itself. But exclusions come at the price of diminished generalizability.” [As RCT’s (potentially) limited external validity is closely related to questions about compliance/adherence, this aspect was naturally extensively covered in Davies and Kermani – so it’s not exactly news to me. Nevertheless it’s an important aspect often overlooked when evaluating studies of this type, so I figured I should include a remark/quote on the topic here].
“Lead time is the period of time between the detection of a medical condition by screening and when it ordinarily would be diagnosed because a patient experiences symptoms and seeks medical care […] The amount of lead time for a given disease depends on the biological rate of progression of the disease and how early the screening test can detect the disease. When lead time is very short […] treatment of medical conditions picked up on screening is likely to be no more effective than treatment after symptoms appear. On the other hand, when lead time is long […] treatment of the medical condition found on screening can be very effective. […] How can lead time cause biased results in a study of the efficacy of early treatment? […] because of screening, a disease is found earlier than it would have been after the patient developed symptoms. As a result, people who are diagnosed by screening for a deadly disease will, on average, survive longer from the time of diagnosis than people who are diagnosed after they get symptoms, even if early treatment is no more effective than treatment at the time of clinical presentation. In such a situation, screening would appear to help people live longer, spuriously improving survival rates when, in reality, they have been given not more “survival time” but more “disease time.”” [I knew about this phenomenon, but I didn’t know that it had a name. I do now.]
“Length-time bias […] occurs because the proportion of slow-growing lesions diagnosed during screening is greater than the proportion of those diagnosed during usual medical care. [This is because the speed of tumor growth is related to the likelihood that a screening test will ‘be necessary’ to find the cancer – a fast-moving cancer will produce symptoms before the screening test/in between screening tests, whereas a slow-moving cancer will not]. As a result, length-time bias makes it seem that screening and early treatment are more effective than usual care.” [For those who don’t know, I should note that some similar problems may pop up in models applied in labour economics, e.g. when dealing with unemployment data. So the math/intuition behind problems such as these are not unknown to me – as mentioned in the beginning data analysis is to some extent just data analysis, no matter which field of inquiry it’s being applied to.]
“To many people in the Western world, the suggestion that sticking needles into the body and twirling them can decrease pain and control vomiting seems biologically implausible. However, randomized controlled trials of acupuncture have found acupuncture effective.” [I include this quote here only because it cost the book one star in my evaluation. I was probably at around ~3.5 or so before reading this. After reading this, I was at ~2.5. I considered it a serious hit to the credibility of the authors, because it to me displayed a lack of critical thinking and a signal of poor judgment. Here’s a cochrane review on the matter (“We concluded that there was insufficient evidence to judge whether acupuncture is effective in relieving cancer-related pain in adults.”).]
Here’s what I wrote in my goodreads review:
“This book isn’t written by someone who read a few books and then decided to publish her own work on the subject – the book has 56 pages of references.
It’s a very solid piece of work with a lot of interesting stuff. A lot of work went into writing this book, and you can tell. Recommended.”
Razib Khan gave it 5 stars. So did I. Not all chapters are equally great and in general I’d say that I liked the first half of the book better than the second half. But I really couldn’t justify giving it any other rating.
I read the first couple of chapters while I was finishing the Adipose Tissue and cancer book – although this is a university press publication (published by Princeton University Press) it’s still a much easier read than the Springer publication, so I read it while taking breaks from the textbook. I should note that I read most of the book today and so it doesn’t actually take that long to read. Though I didn’t actually do a lot of other stuff today…
I was considering the problem of how to blog this book early on, and I decided to limit my coverage of it somewhat as I’d otherwise have to spend a lot of time on it; there’s a lot of good stuff in there and book-blogging takes time which I can’t spend reading (or, you know, doing other stuff). Some of this stuff was review and there are topics covered here which I’ve read about in a lot more detail elsewhere (e.g. stuff covered in Miller, or Dawkins), but the book also had a lot of new stuff. A nice thing about the book is that Low actually provides the data and the evidence for a lot of things which you’ve perhaps sort of assumed to be true but didn’t actually have great reasons for believing were true. Another nice thing is that she asks some questions you’d probably never thought about asking, and she also provides some interesting answers along the way. There are a lot of interesting observations in there.
I should note that in (/quite?) a few chapters she covers work done by Robert Boyd and Peter Richerson. I’ve known for a while that I ought to have a go at some of their stuff, and I actually recently purchased The Origin and Evolution of Cultures – but at this point I’ve skimmed parts of it, and that book just looks like a lot of hard work, so I’ve sort of shied away from it so far.. I think Low convinced me that I really ought to have a look at that stuff ‘at some point’ when I feel up to it.
I have added some hopefully illustrative quotes from the book below:
She gives a breakdown of what the book is about in the introduction:
“I will begin with the basic arguments and assumptions of behavioral and evolutionary ecology: selfish genes, conflicts of interest, and why two (and not more or fewer) sexes have specialized to reproduce through different behaviors (chapters 1–3). Then I ask: How do these basic sex differences, whose theory we understand, actually play out in other primates, as well as humans (chapters 4–6)? Next, I take an empirical glance at the diverse ways in which both traditional and transitional societies make a living, how men’s and women’s roles and lives diverge, and how even marriage is affected by ecology and resources (chapters 7, 8). The complexity of these patterns leads us back to basic theory to explore how conflicts of interest are mediated, literally from the level of genes in genomes to whole societies (chapters 9, 10). Sex differences and conflicts of interest help us predict why there are so few women warriors or high-roller politicians in most societies—and the kinds of societies in which they are likely to occur (chapters 11–14). And finally I ask: How does our evolutionary past interact with current global population and resource consumption problems (chapter 15)?”
Some other quotes:
“many people may be appalled at the approach I will use here, that is, to assume that we humans are as predictable as other animals in our behavior, and are governed by the same rules. And I want to begin with simple rules, no less. Many of us assume that humans operate under rules that are different from those of other species, that our rules are culturally based rather than biological. I will ask: What can we learn if we begin without assuming that this were true? […] My explorations here assume that humans are indeed animals, even if elegantly complex ones, and that they are therefore subject without special exemption to the general rules of natural selection, the rules that govern behavior and life history among living things. […] In their “deep” objectives—in what they evolved to do—humans are not qualitatively different from other living organisms. Like other living things, they evolved to get and use resources to survive and enhance the spread of their genes.”
“When societies lack rules of inheritance, suggesting that there is little to inherit, men typically do not exchange goods for women, but exchange women;37 when there are no societal rules about wealth or hereditary class stratification, men are similarly more likely to exchange women than goods. But even in such societies, resources are not irrelevant to the pattern of exchange. […] when men purchase wives (bridewealth societies), younger (higher reproductive value) women are worth a higher bride price.38 The currency of choice varies: sometimes women are purchased with cattle, as among the Kanuri people; sometimes with sheep, as among the Yomut Turkmen; sometimes with pigs, as among the Tsembaga-Maring; or a combination.” [Some more details are given later in the book and I couldn’t help myself from quoting this part:] “the Turkmen are a bridewealth society, and bridewealth is high. A man of median wealth will pay two to four years’ income for a virgin bride. In concrete terms, this is ten camels for the bride’s father and one camel for her mother, or the bridewealth can be paid in cash or other livestock. One camel equals two horses, one really good race horse, two cows, ten sheep, or ten goats.”
“We can break preferences down into signals that reflect health (shiny hair, clear skin) or youth (no wrinkles or sags) and current reproductive stage (waist-hip ratio, color of nipples); signals that suggest other reproductively important attributes like wealth; signals that reflect social awareness (stylishness, which may be purely culturally defined); signals of belonging to a certain group. Cross-culturally among traditional societies, the things people describe as attractive in the other sex turns up all of these categories. […] selectively relevant traits consistently rank high. […] Certainly cultural and historical factors strongly influence these preferences, but some preferences—healthy, young, not pregnant— are virtually universal. […] Put simply, in our evolutionary history, it seems likely that a woman’s value was usually her reproductive value, and a man’s value was his resource value.”
“in most societies, the reproductive interests of more than the two who mate can matter. In traditional societies, the potential bride had greater say than the would-be groom in marriage negotiations in only 3.7 percent (3/81) of societies.27 Grooms had greater— or sole—say in 39.5 percent (32/81). In most of these societies, the older generation had considerable power in these decisions.” [the source given is ‘Whyte, 1978, 1979’ – I feel reasonably certain the data used is from the Standard cross-cultural sample, an oft-used resource in this book.]
“Typically, perhaps sentimentally, we view pregnancy as a time of maternal support and care for the growing embryo. But genetic conflicts over resources start here. An infant in utero is only half like its mother […] Thus the stage is set for conflict, both with mother and any siblings who share the womb […] Fetal genes from Dad that increase Mom’s transfer of nutrients to the fetus will be favored. Will such a transfer harm Mom? No matter, so long as she is healthy enough to continue investing, from the fetus’s point of view. In fact, if her ability to produce other (competing) siblings is reduced, so much the better. […] As early as the implantation of the zygote on the uterine wall, trophoblast cells (fetally derived) invade the lining of the mother’s womb and remodel certain arteries so that they cannot constrict to shut down blood flow to the fetus. This means several things. A mother cannot control the blood or nutrient flow to the fetus without affecting herself as well, and the placenta can now release hormones directly into the mother’s blood stream. Some of these manipulations are countered by maternal strategies. Fetus and mother are truly combatants in an arms race. As biologist David Haig has cogently pointed out, a number of unpleasant accompaniments of pregnancy (as well as serious medical conditions like preclampsia) are better explained as maternal-fetal conflict than by any competing theories.”
“The importance of resource value for men versus reproductive value for women means that in many societies it may be harder for a man to get a wife than for a woman to get a husband […] If the reproduction of sons is more variable than that of daughters, and especially if wealth or status matters more to men’s success than women’s, investment is likely to be biased toward sons. […] when parental investment can influence the reproductive success of one sex more than the other (as in baboons), there should be a correlation between parental condition and investment in that sex.”
“in Locknevi parish [Sweden] during the period of this study [1824-1896], resources shifted from being relatively uneven with some very large holdings, to being more even but limited. […] Locknevi folk married early but delayed having children. A man’s best occupation influenced his chances of marrying: 74 percent of agricultural workers and servants living their entire life in the parish failed to marry, compared to 20 percent of lower-middle-class men. […] Sixty-one percent of women failed to marry while in the parish […]
The quote above, and a few others in that chapter, basically made me aware that I have had some questionable ideas about how this part of human history was like for most people. I have sort of implicitly assumed that most people in this historical period had relatively few problems getting married, even those in the ‘poor peasants’ segment [and do remember that there were a lot of poor peasants in the past] – but the data presented in this chapter, including also data from three other areas of Sweden during this period, tells a quite different story. And this is good data, as good as it gets. In Nedertorneå, another Swedish parish, almost two-thirds of all women who didn’t leave the parish didn’t get married: “Sixty-four percent of women failed to marry while in the parish”. Incidentally, in some places resources mattered a great deal; here’s what things were like in the Tuna parish:
“Landowners [men] were almost certain to marry (95 percent), in stark contrast to other men (35 percent); they married women about 2.5 years younger than other men, and had about one to 1.5 more children.”
Such effects were not always present, but as Low remarks in the chapter, “whenever wealth or resource differentials existed, resources and reproductive success were positively correlated.” And differences across social groups, even in an ethnically homogenous country like Sweden, were huge and persistent back then – here’s another observation:
“Of men who stayed in their birth parish, poor [occupational status of cottar – tenant farmers – or proletariat and no land ownership record, US] sons of poor fathers were most likely to remain unmarried (57 percent); 97 percent of such poor, unmarried men had fewer children than other men. Rich [owned land and/or had an occupational status of upper middle class, lower middle class, or bönder [farmer], US] sons of rich fathers had an approximately equal chance of marrying or not (48 percent versus 52 percent), and once married had a 59 percent chance of having relatively large families. Rich sons of rich fathers who did not marry were, like poor sons of poor fathers, likely to have fewer than the median number of children. Although 97 percent of poor sons had this fate, only 55 percent of rich sons did.”
As I mentioned, there’s a lot of interesting stuff in this book.
I’ve finished the book.
It’s a Springer book, so those of you who’ve encountered these books before will know that this is not an easy-to-read popular-science book. The general level is high and occasionally I felt almost completely lost; chapter 8 for example was very technical. As I’ve pointed out before, I don’t like to fault authors for not taking into account the possibility that their books may also be picked up by ignorant fools who don’t know anything, but if you have a hard time understanding what the author is getting at it will affect your reading experience in a negative manner. It should be noted, though, that although it’s not an easy book to read you’ll learn a lot of stuff if you put in some effort (…and/but if you don’t put in some effort you’ll never finish it, and you’ll get nothing out of it at all).
Some of the chapters deal with similar stuff, and I got the impression a couple of times that the authors of a specific chapter had not read the other chapters. On the other hand it’s very clear in other chapters/contexts that they most certainly did, but even so there are a few things which are repeated a few times along the way which perhaps did not need to be repeated. On the third hand the book is structured in such a way that each chapter is pretty much self-contained (which is presumably part of the explanation for the occasional repetitions), and the fact that you probably don’t necessarily need to read it cover to cover from chapter one to chapter 9 the way I did to get a lot out of the book would presumably be appealing to some people.
I gave it four stars on goodreads, because of the high quality of the material included.
Some stuff from the last chapters, with some hopefully helpful links added to make the passages easier to understand (perhaps needless to say no such links are included in the book, so if you find the links helpful you’ll probably need to look up some stuff along the way if you decide to read it yourself…) as well as some comments here and there:
“Emerging studies clearly indicate that a bidirectional crosstalk is established between all cellular components of AT [adipose tissue, US] and cancer cells and that the tumor-surrounding AT contributes to inflammation, extracellular matrix remodeling as well as energy supply within the tumors. In this chapter, we present evidences showing how AT locally affects tumor progression in given types of tumors and how these results might be attractive to explain the link between obesity and the poor prognosis of some cancers. This will be preceded by the overall description of AT composition and function with special emphasis on the specificity of adipose depots, key aspects that need to be taken in account when paracrine effects of AT on tumor progression is considered. […]
The past two decades have provided substantial evidence for the major role of the tissue local environment for tumor progression. Cancer is now considered as a tissue-based disease in which malignant cells interact dynamically with the surrounding supportive tissue, the tumor stroma, composed by multiple normal cell types such as fibroblasts, infiltrating immune cells, and endothelial cells within the context of extracellular matrix . This stroma/tumor cell interaction involves constant bidirectional crosstalk between normal and malignant cells. Cancer cells usually generate a supportive microenvironment by activating the wound-healing response of the host . Conversely, the stromal cells, such as for example, cancerassociated fibroblasts (CAFs) or tumor-associated macrophages (TAMs), promote tumor progression through different mechanisms including enhancement of tumor survival, growth, and spread, by secreting growth factors, chemokines, extracellular matrix (ECM) components, and ECM-modifying enzymes [3,4]. Constituents of the tumor microenvironment can arise from two major sources: recruitment from nearby local tissue or systemic recruitment from distant tissues via circulation. Among the different cell types frequently found at close proximity of evolving tumors, little attention has been given to cells that compose the adipose tissue (AT) although a growing interest can be noted in recent years. Throughout the body, AT is mainly described as subcutaneous (i.e., superficial and deep hypodermic location) and visceral depots. Visceral adipose tissue (VAT) surrounds the inner organs and can be divided into omental, mesenteric, retroperitoneal (surrounding the kidney), gonadal, perivascular, and pericardial depots . Of note, AT is also present in the breast (mammary adipose tissue or MAT) and in the bone marrow (BM). All these specific regional depots exhibit differences in structure, function, composition, and secretion profiles . […] The cellular heterogeneity of AT adds an additional degree of complexity when AT/cancer cells crosstalk is considered. […] All the cells from adipose tissue (including mature adipocytes) produces a large number of secretory bioactive substances, such as hormones, growth factors, chemokines, proangiogenic or proinflammatory molecules , which could directly affect adjacent tumors. AT is therefore an excellent candidate to influence tumor behavior through heterotypic paracrine signaling processes and might prove to be critical for tumor survival, growth, local, and distant invasion. […] Fat depots from different region of the body have different incidence in pathology because they display distinct functional and structural properties in terms of energy metabolism and bioactive molecule (adipokines) release as well. Regional heterogeneity plays a central role in mammalian AT homeostasis.” (I talked about these aspects in the last post, but I figured I should give at least part of the ‘medical textbook version’ here..) […]
“Ovarian cancer is a highly fatal disease, with only about 40 % of women with ovarian cancer still alive more than 5 years postdiagnosis. This poor survival is largely attributable to the fact that a majority of ovarian cancer in developed countries is diagnosed with metastatic spread. The omentum, a peritoneal organ rich in AT and immune cells, has been shown to be a preferred site of metastatic dissemination in ovarian cancer patients. Omental dissemination, which is often accompanied by ascites, facilitates the further spread of the tumors .” […]
“Prostate cancer is the most common malignancy in males in Western countries, representing the second leading cause of cancer death. Prostate is surrounded by AT and tumor admixed with periprostatic fat is the most easily recognized manifestation of extraprostatic extension, a well-established adverse prognostic factor for prostate cancer [79,80]. Periprostatic AT (PPAT) is considered as VAT, but the specificities of this depot in terms of metabolism and adipokines secretion remain largely unknown. At laboratory levels, the contribution of this tissue to cancer progression has been first suggested by the report of Finley et al. that analyzed the PPAT features in patients undergoing prostatectomy for cancer . In this study, the authors found that the level of IL-6 secreted by PPAT-conditioned medium (CM) was almost 375 times greater than the circulating levels of the cytokine in the same patient. Both IL-6 levels in PPAT and activation of IL-6 related signaling pathways were correlated to tumor aggressiveness . Therefore, this study strongly suggests that PPAT represents an important source of IL-6 that favors tumor progression. Interestingly, several studies already reported that increased serum IL-6 and soluble interleukin-6 receptor levels are associated with aggressiveness of the disease and with a poor prognosis in prostate cancer patients, underlying the importance of this pathway in PC progression (for review see ). […] Recent studies suggest that, like in breast cancer, a bidirectional crosstalk exists between PC cells and surrounding AT.” […]
“During the last decade, pancreatic cancer has become the fourth leading cause of cancer-related death in the USA and the sixth leading cause in Europe. Despite major advances in surgical techniques and adjuvant therapies, overall 5-year survival remains under 5 %. While very few, if any, laboratory studies have been performed to date on the crosstalk between pancreatic cancers and AT, several clinical data have suggested that an adipose-rich environment leads to a deleterious outcome on this disease. […] it has been demonstrated that peripancreatic fat invasion is correlated to a poorer survival for pancreatic cancers . Recent epidemiologic studies also suggest that obesity doubles the relative risk of pancreatic cancer . In addition, central adiposity has been shown to be an independent risk factor in development of pancreatic cancer as well as to contribute to a poorer survival . Interestingly, it has been demonstrated that increased pancreatic fat (pancreatic steatosis) promotes dissemination and lethality of pancreatic cancer .” […]
“The relationship between AT and cancer is complex and involves both paracrine and endocrine effects whose relative contribution to tumor progression remains to be determined. Regarding paracrine effects, we have underlined in this chapter the need to consider the appropriate neighboring AT for each cancer subtypes in experimental studies. […] there is clear variations between the different AT in terms of secretion and sensitivity to lipolysis […] Nevertheless, regarding AT/cancer crosstalk, there are common features found in several cancer subtypes. […] it is very important to underline that adipose cells are not inert to their surrounding and that their phenotype are profoundly modified by cancer cell secretions.” […]
“Present data suggest caution about the clinical use of lipotransfer-derived WAT cells for breast reconstruction in patients with breast cancer [15,16].”
I thought I should make a brief stop here to cover the observation above in a little more detail, because I think it’s a good illustration of why the finer details of how these things work actually matter. Now, one might well be tempted to say that if we know that fat people get cancer more often and have worse prognoses (this is, incidentally, a gross oversimplification – as should be clear from the posts), well – do we really need to know all that much more about how it all works out at the microscopical level and so on? Why not just tell people to lose weight and just leave it at that? Findings like the ones in [15,16] above indicate that it matters what goes on in these tissues. What did the studies tell us? Well, it has been observed that female breast cancer survivors who have undergone a specific type of reconstructive surgery (‘lipotransfer procedure for esthetical purposes’) had higher cancer recurrence risk than did females who had not undergone such a procedure; this is important information with clinical relevance. One basic idea behind what may be happening is that the adipose tissue that is transplanted into the reconstructed breast(/s) may work as a fuel source for any remaining cancerous cells still hiding in the tissues (/and it may spark new tumor development through the crosstalk and paracrine signalling mechanisms already mentioned). Note that this information may not yet be well known – see e.g. this webpage about reconstructive breast surgery from the website of Johns Hopkins University, which is hardly an institution to be found at the bottom of the barrel: “we try to give women the look and feel of an actual breast, using creative techniques such as fat grafting, also known as lipofilling or fat transfer. Fat can be taken from another part of your body, possibly the abdomen or somewhere on your buttocks, through liposuction. The fat will be purified and carefully layered within the new breast to create the desired shape. Our surgeons are experienced at these techniques.” They may want to reconsider at the very least the extent to which they are using these techniques. Anyway, back to the book:
“surgical options for treatment of the severely obese population have increased in popularity over the last few decades, with an estimated 344,000 cases performed globally in 2008 [40,41]. As previously noted, lifestyle therapy for weight loss intervention is generally insufficient for extremely obese patients and effective long-term weight loss using pharmacological therapy has been limited, leaving bariatric surgery as the only medical intervention providing substantial, long-term weight loss for most severely obese patients. […] Because post-bariatric surgical patients generally experience significant and sustained weight loss [2,47], they represent a unique population to study the relationship between voluntary weight loss and cancer risk. […] Generally, 80 % of patients who seek bariatric surgery are female.” […]
“Since 2009, there have been five reviews exploring the potential relationship between bariatric surgery and subsequent cancer risk [22,40,59–61], and two additional reviews of cancer risk associated with either weight loss from bariatric surgery or nonsurgical weight loss therapies [11,20]. […] [the following are some results from these studies:] Reported cancers subsequent to bariatric surgery were 117 cancers in the surgical group compared to 169 cancers among the control groups, representing an HR of 0.67 (95 % CI 0.53–0.85; p=0.0009). For female participants only, the surgical group had a reported 79 cancers compared to 130 cancers in the control females, giving an HR value of 0.58 (95 % CI 0.44–0.77; p = 0.0001). […] After a maximum of 5-year followup, the reported number of visits to the physician/hospital that led to a cancer-related diagnosis for the weight loss surgical group was 21 visits (2.0 %) compared with 487 visits (8.5 %) among the control group. This difference was reported to have a relative risk of 0.22 (95% CI 0.14–0.35; p=0.001) . […] the relative risk for breast cancer was 0.17 (95% CI 0.01–0.31; p=0.001). […] For cancer deaths, the bariatric surgical group was 60 % lower when compared the control group ( p = 0.001; 31 deaths among surgical group compared to 73 deaths in control groups). […] For all cancers combined, there was a 24 % reduction in cancer incidence among the surgical group compared to controls (HR 0.76, 95% CI, 0.65–0.89; p=0.0006). […] Based upon these analyses, it was estimated that about 71 gastric bypass surgeries would be necessary to prevent one incident cancer . […] [And so they conclude:] there are now studies that demonstrate a reduction in cancer mortality among postbariatric patients compared to severely obese, nonoperated controls. In addition, one prospective study (SOS study) and a few observational studies have also demonstrated a reduction in cancer incidence following metabolic surgery. To date, the reduced cancer risk benefits have been limited to females and there appears to be a stronger correlation of benefit associated with cancers that are “likely” to be obesity related. Given these limitations, the general consensus is that intentional weight loss does lead to a reduction in cancer incidence .” […]
“Multiple reviews have been published on the effect of metabolic surgery on diabetes, including a meta-analysis by Buchwald et al., which reported a 78.1 % remission of diabetes and an 86.6 % improvement or remission in diabetes following bariatric surgery . The intriguing element related to diabetes remission is that a significant number of bariatric surgical patients (i.e., gastric bypass patients) have discarded their antidiabetic medication and returned to a normal blood glucose by the time they are discharged from the hospital following their metabolic surgery (i.e., 2–3 days after surgery) and long before significant weight loss has occurred . Again, mechanisms accounting for this remarkable remittance or improvement of diabetes following surgery are multiple. In an analogous way, the reduced risk of cancer following metabolic surgery is also likely to be linked with several biological mechanisms, which may or may not be directly associated with weight loss.”
I’ve read roughly two-thirds of the book by now – I like it, pretty much every page contains new stuff which I didn’t know anything about and it’s quite interesting. Some more stuff from the book below, as well as some comments. As always you can click images to view them in a higher resolution.
“Obesity increases the incidence of many cancers, such as breast, prostate, and colon cancer. However, endometrial cancer is the mostly tightly linked with obesity. Estimates suggest that nearly 40 % of cases of endometrial cancer can be attributed to obesity. […] Obese women have a threefold higher risk of developing endometrial cancer than lean women . […] every increase in BMI of 5 kg/m^2 increases a woman’s risk of the developing of endometrial cancer by approximately 60 % (relative risk, 1.59; 95 % confidence interval [CI], 1.50–1.68) . Endometrial cancer in obese women is more likely to have lower risk features such as endometrioid histology and low/intermediate grade. […] An elevated waist-to-hip ratio, reflecting a preferential deposition of adipose in the abdomen, increases the risk of developing endometrial cancer by 220 % . […] Among the population as a whole, obesity increases the risk of death from endometrial cancer. In a study of 900,000 prospectively followed healthy patients, 57,145 individuals died of cancer over 16 years. The relative risk of death from endometrial cancer in this population was 6.25 for women with a BMI >40 and 2.77 with a BMI between 35 and 39 .”
“As a component of adipose tissue in obese individuals, immune cells, and specifically macrophages, secrete a variety of growth, survival, and proangiogenic factors, as well as bioactive molecules that enable tumor growth and contribute to the remodeling of the tumor microenvironment to facilitate metastases. Furthermore, reactive oxygen and nitrogen species released by activated macrophages are mutagenic and accelerate oncogenic mutations that contribute to cancer risk and progression [30,33]. So, not only does inflamed visceral adipose tissue provide an ideal milieu for the growth of metastatic endometrial cancer but proinflammatory factors also secreted by infiltrating adipose immune cells mediate systemic effects on tumor progression at distant sites, including the endometrium.”
“Taken together, current evidence suggests that through a variety of mechanisms, weight loss and physical activity reduce proproliferative signaling and counteract environmental conditions that support the initiation and progression of endometrial cancer.” […as the figure above illustrates, endometrial cancer is far from the only cancer type where behavioral factors play a large role – US.]
“Multiple epidemiologic studies demonstrate that women who use combination estrogen and progesterone oral contraceptives (OCP) decrease their risk of endometrial cancer by 50 % [78–80]. While there is no data to support a decreased efficacy in endometrial cancer protection in obese women, there are studies that suggest that obese women have a slightly decreased contraceptive efficacy compared to thin women .”
“At the cellular level, overweight and obesity are characterized by the increase in number and size of adipocytes. A lean adult has 35 million adipocytes, each containing 0.4–0.6 μg of triglycerides, whereas an extremely obese person has 125 million adipocytes, each containing 0.8–1.2 μg of triglycerides . Traditionally, adipocytes have been viewed solely as energy depots, but after the discovery of leptin in 1994 and extensive research in the field in the last decades, it has been established that the adipose tissue is an active endocrine organ. The adipocyte is a major source of secreted proteins …”
A really important point which has been repeated, explicitly or implicitly, again and again in this book, and which I thought I should emphasize here using ‘non-textbook language’, is that fat cells aren’t just inactive cells that ‘hang around’ doing nothing. They do a lot of stuff while they’re ‘hanging around’. And when you have a lot of them hanging around in the wrong places, many of the things they’re doing are really quite bad for you. As you’ve probably already inferred, the book goes into a lot more detail about mechanisms and how these things work in detail (to the extent that we even know what’s going on in the first place), but if you don’t remember much from the posts about this book this is at least, I think, one of the key points you should try to remember; adipose tissues are active tissues and they – and the secretions derived from them – play a major role in a variety of contexts, including some contexts which are highly relevant to e.g. cancer pathogenesis. There’s still a lot we don’t know because this stuff is complicated; I link to leptin above, which has been intensively studied and is also relatively intensively covered e.g. in chapter 5 of the book, and the wiki link about adipokines mentions a few others – but I should note here that there are more than 50 different types of adipokines that we know of at this point. Different types of cancer start out in different types of tissues and a diverse set of mechanisms are involved in the disease processes, and so it seems likely that different types of adipokines play different roles in different types of cancers. There are still a lot of things which are not clear, but as they put it in the conclusion of chapter 5: “There are strong epidemiological, molecular, and clinical evidences showing associations between adipokines and the incidence and clinical outcome of cancer.” It should be noted that work on this stuff is not limited to work on just ‘human data’ – lab-work using rodents, which is covered in chapter 6 of the book, has added some details and some interesting observations regarding potential mechanisms of action, and such animal models seem to support ‘a causal link’ of some sort between body weight and the development of specific types of cancers in a number of important (…to humans…) cases, including breast cancer and colon cancer. However the precise mechanisms of action are still far from clear, as they note in their conclusion in chapter 6:
“As detailed here, overweight and/or obesity is associated with an elevated risk of several cancers; however, it is clear that a common disease mechanism was not identified. Although the current literature hypothesizes at least three major components such as sex hormones, insulin-related pathologies, and adipokines, these components cannot explain every aspect of clinical features/disease courses. But as models improve both for obesity and various cancers, hopefully it will become easier to identify mechanisms of action for the relationship of body weight and cancer.”
i. Troubadour, gainsay, sordid, repast, calumniate, skinflint, gentile, enjoin, prestidigitation, compunction, madrigal, bacchanalian, reify, effete, seamy, betoken, codicil, peripatetic, reactionary, mendicant, osculate, expiation, propitiation, viand, panegyric, fulsome, paean, rarefied, vitiate, bibulous, delineate, wistful, hirsute, staid, bandy, mettle, saturnine, prorogue, legerdemain, caesura, dilatory, prolix, din, hoary, obsequious, spoonerism, gratuitous, diverting, contrite, grouse, preen, poignant, roil, aver, importune, lampoon, flagitious, expedient, parlous, obdurate, piebald, dolorous, parsimony, mawkish, natty, blithely, fractious, pique, bathos, cant, recreant, plumb, diaphanous, argot, ursine, frisson, insouciant, meretricious, upbraid, pugnacious, curate, plaintively, spate, cabal, slake, odium, encomium, mulct, turgid, disport, ply, cavort, cloying, sable, svelte, idempotent, teleological, inchoate, comity, bucolic.
The above is a list of the first 100 words I’ve ‘mastered’ on the vocabulary.com site. Of course I knew some of them already, but I’ve also learned quite a few new words here along the way and it’d be incorrect to say that I haven’t also gotten a better grasp of some of the words with which I was already familiar. Here’s how it works. A few of the assessment questions so far have been in my opinion really poor (allowing for multiple correct answers, only one of which is accepted as correct), but in general this seems like an extremely useful site and the site does allow you to provide feedback if you think a question is poorly worded.
Do note that average vocabulary sizes are really rather small, all things considered: “Most adult native test-takers range from 20,000-35,000 words”. I think that you can probably progress rather rapidly with a tool like this, if you use it consistently. Note that the site doesn’t completely stop asking you questions about the words you’ve ‘mastered’; brush-up questions are added occasionally to aid retention. The starting point is as far as I can remember based on educational background, so if you’re a graduate student you shouldn’t worry that the site will start out by asking you if you know the word ‘house’ or ‘cat’. I’m pretty sure even walking dictionaries will find plenty of words along the way that they are unfamiliar with.
I’ll probably stop going on about the site now, but I really like it at this point and so I figured I should post at least a few posts about it before letting it go. It’s a very neat tool.
ii. For the last two years I have been involved in a medical trial aimed at figuring out if a specific drug might be used to delay the development of retinopathy in diabetics. My participation in the trial ended this week. The trial was more or less a direct result of a smaller trial in which I also participated, which showed some promising initial results – here’s the relevant paper. The researcher conducting the trial I just participated in will publish a paper about it later on, and I’ll naturally blog that when it’s published. There has been talk about continuing the project (/…that is, starting a new project) for the participants who got the active drug – half of the people in this trial got placebo – in order to increase the follow-up period. If I got the active drug (whether or not I did is not clear at this point, but I’ll be told relatively soon) I’ll probably participate in the new trial as well. No, the person who’s going to analyze the data will not be told whether or not I got the active drug – I asked about this part, but the study design is such that the double blind aspect is not compromised; the researcher who’ll figure out whether or not I got the active drug is not involved in the data analysis at all.
Medical trials often have trouble finding participants and selection into such trials is far from random. If you live in Denmark, you should check out this site. I assume similar resources exist in other countries…
A couple more 60 symbols videos below. I’ve now watched most of the videos they’ve posted, and I really like this stuff:
“He was a very strange man. And yet he’s absolutely wonderful!” – I could easily have said something similar about him. I’d much, much rather spend time with someone like that than with a ‘normal’ (boring) person. (Here’s a related link. Also, this.)
“The aim of the current study was to examine the relationship between individual differences in anxiety and the social judgements of trustworthiness and approachability. We assessed levels of state and trait anxiety in eighty-two participants who rated the trustworthiness and approachability of a series of unexpressive faces. Higher levels of trait anxiety (controlling for age, sex and state anxiety) were associated with the judgement of faces as less trustworthy. In contrast, there was no significant association between trait anxiety and judgements of approachability. These findings indicate that trait anxiety is a significant predictor of trustworthiness evaluations and illustrate the importance of considering the role of individual differences in the evaluation of trustworthiness. We propose that trait anxiety may be an important variable to control for in future studies assessing the cognitive and neural mechanisms underlying trustworthiness. This is likely to be particularly important for studies involving clinical populations who often experience atypical levels of anxiety.”
“The Cretaceous–Paleogene (K-Pg) boundary is marked by a major mass extinction, yet this event is thought to have had little effect on the diversity of lizards and snakes (Squamata). A revision of fossil squamates from the Maastrichtian and Paleocene of North America shows that lizards and snakes suffered a devastating mass extinction coinciding with the Chicxulub asteroid impact. Species-level extinction was 83%, and the K-Pg event resulted in the elimination of many lizard groups and a dramatic decrease in morphological disparity. Survival was associated with small body size and perhaps large geographic range. The recovery was prolonged; diversity did not approach Cretaceous levels until 10 My after the extinction, and resulted in a dramatic change in faunal composition. The squamate fossil record shows that the end-Cretaceous mass extinction was far more severe than previously believed, and underscores the role played by mass extinctions in driving diversification.”
A little more:
“Survival at the K-Pg boundary is highly nonrandom. Small size has been identified as a determinant of survival (36), yet size selectivity is evident even among the squamates. The most striking pattern is the extinction of all large lizards and snakes. […] The largest known early Paleocene lizard is Provaranosaurus acutus. Comparisons with varanids suggest an SVL [snout-vent length, US] of 305 mm and a mass of 415 g (Dataset S1), compared with an estimated SVL of 850 mm and mass of 6 kg for the largest Maastrichtian lizard, Palaeosaniwa. The largest early Paleocene snake is Helagras prisciformis, with an estimated SVL >950 mm and a mass >520 g, compared with >1,700 mm and 2.9 kg for the largest Maastrichtian snake, Cerberophis. […]
Size selectivity may help explain why nonavian dinosaurs became extinct, suggesting that it was nonavian dinosaurs’ failure to evolve a diverse fauna of small-bodied species, rather than a decrease in the diversity of large-bodied forms, that ultimately sealed their fate. A number of small, nonavian dinosaurs are now known from the Late Cretaceous, including alvarezsaurids (37) and microraptorine dromaeosaurids (38), and taphonomic biases almost certainly obscure the true diversity of small dinosaurs (38, 39). However, the fact remains that during the late Maastrichtian, small dinosaurs were vastly outnumbered by other small vertebrates, including a minimum of 30 squamates, 18 birds (15), and 50 mammal species (40). Strikingly, birds—the only dinosaurs to survive— were the only dinosaurs with a high diversity of smallbodied (<5 kg) forms (15). In this context, a discussion of a decline in large dinosaur diversity in the Maastrichtian (9) is perhaps beside the point. A high diversity of large herbivores and carnivores in the latest Maastrichtian would have been unlikely to change the fate of the nonavian dinosaurs, because no animals occupying these niches survived. Instead, the rarity of small dinosaurs—resulting perhaps from being outcompeted by squamates and mammals for these niches —led to their downfall. […]
Extinction at the K-Pg boundary was followed by recovery in the Paleocene and Eocene. A number of new lizard lineages occur in the basal Paleocene, notably the stem varanoid Provaranosaurus, xantusiids, and amphisbaenians (27). These may represent opportunistic invaders that colonized the area in the aftermath to exploit niches left vacant by the extinction, as seen among mammals (10, 44). Despite this, early Paleocene diversity is considerably lower than late Maastrichtian diversity (Fig. 3). Subsequently, ecological release provided by the extinction allowed the survivors to stage an adaptive radiation, paralleling the adaptive radiations staged by mammals (6, 45, 46), birds (46, 47), and fish (48). The community that emerges in the early Eocene is dominated by groups that are either minor components of the Cretaceous fauna or unknown from the Cretaceous […] diversity does not approach Cretaceous levels until the early Eocene, 10 My later […] Unlike mammals, […] squamates appear to have simply reoccupied the niches they occupied before the extinction. This reoccupation of niches was […] delayed; by the middle Paleocene, lizards had yet to recover the range of body sizes and morphotypes found in the Maastrichtian (Fig. 5).”
“‘What are you going to do?’
‘I am going to visit these five people – and from each one I am going to get his or her own story.’
Superintendent Hale sighed with a deep melancholy.
‘Man, you’re nuts! None of their stories are going to agree! Don’t you grasp that elementary fact? No two people remember a thing in the same order anyway. And after all this time! Why, you’ll hear five accounts of five separate murders!’
‘That,’ said Poirot, ‘is what I am counting upon. It will be very instructive.'”
I finished the book today. I felt very conflicted about how to rate it, so I decided not to – I should note that the average goodreads rating is 3.88, which is pretty high for a Christie novel. I really liked reading the book, but I felt cheated when I reached the end. Details below the fold, in rot-13 – decrypt that part only if you don’t mind spoilers (to spell out this point, you can translate the gibberish below into English by following the link and copy the text into the box and transform the data. But you should only do so if you don’t mind spoilers).