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judgestarling · 4 months

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How to Ignore More than a Century Worth of Scientific Literature and Make Headline-Grabbing Claims on One of the Deadliest and Exhaustively Studied Pandemics in History Based on Flawed Data and Questionable Analysis

The 1918 influenza pandemic, also erroneously referred to as the “Spanish flu,” has affected up to one billion people—half the world’s population at the time—and has killed an estimated 20–30 million people in the Western World and God-only-knows-how-many people in other countries. Previous and subsequent influenza pandemics usually hit infants and the elderly the hardest. The 1918 influenza pandemic was a weird one because of the atypically high mortality among young adults. The peak mortality rate during the fall wave of the 1918 influenza pandemic in Canada and the USA was 28 years. The death of young adults lowered the average life expectancy in the United States by more than 10 years. Numerous studies have confirmed these findings.

A typical picture illustrating the haunting age peculiarity of this pandemic is shown below.

Even in poor, medically underserved communities, it was the young healthy adults that perished leaving many very young orphans behind.

In the early 2000s scientists started looking for samples of the 1918 virus. They reasoned that their best chance was to find it inside an influenza victim buried in permafrost. Brevig Mission in Alaska had 89 inhabitants in 1918 of which 87 died of influenza. It was a good bet that some sequenceable genetic material could be recovered from the graves of these flu victims. Indeed, genomic RNA of the 1918 virus was recovered from frozen lung tissues of an Alaskan influenza victim who was buried in permafrost in November of 1918.

In 2005, scientists used reverse genetics to generate an influenza virus bearing all eight genome segments of the 1918 virus to study its properties. The deadly 1918 virus has thus been resurrected!

The reconstructed virus turned out to be as deadly as the original one with a 100% mortality in mice. Another conclusion of this “resurrection” study was that the virus kills by overreaction of the body’s immune system, which explained the weird age distribution of deaths due to the "Spanish Flu." The strong adaptive immune systems of young adults ravaged their body, whereas the underdeveloped immune systems of young children and the weakened immune system of old people resulted fewer deaths. It was inflammation that killed people, not the viral infection directly or secondary infections. These studies seemed like the end of the 1918 influenza story.

Imagine my surprise, then, when at the end of 2023, I started noticing that the 1918 influenza pandemic is in the news again. “Killer 1918 flu didn't pick on the healthy, after all,” declared Science (the same Science that “killed” Junk DNA a decade earlier). “History Says the 1918 Flu Killed the Young and Healthy. These Bones Say Otherwise,” quipped WIRED. And US News and World Reports headlined the findings as “Contrary to Popular Belief, 1918 Flu Did Not Target the Healthy Young.”

The origin of these headlines was a 2023 paper in Proceedings of the National Academy of Science entitled “Frailty and Survival in the 1918 Influenza Pandemic” by Amanda Wissler, currently an Assistant Professor of Anthropology at McMaster University in Hamilton, Ontario and Sharon DeWitte, Professor of Anthropology at University of Colorado in Boulder. The paper was largely based largely on Wissler’s PhD dissertation at Arizona State University under the supervision of Professor Jane Buikstra.

One would have thought that a study that purports to discard more than a hundred years of observations, refute dozens of analyses, refute the conclusions in about 18,000 peer-reviewed articles, and generate headlines in serious news media would require a great amount of unimpeachable data and an analysis that is—if not infallible—close to infallible. If you thought that, you will be sorely disappointed.

Let us start with the Materials and Methods section. The study is based on a bone sample from the Hamann-Todd Osteological Collection which contains skeletons of people who died in Cleveland, Ohio between 1910 and 1939. The skeletons belong to people whose bodies were not claimed within 36 hours of death (i.e., the poor, the homeless, the socially isolated, the incarcerated, the institutionalized as “mentally defectives,” and those whose relatives couldn’t possibly collect their loved ones’ bodies within a day and a half. Black and indigenous people most probably made the bulk of this collection. Wissler and DeWitte euphemistically called their sample as consisting of “individuals of low socioeconomic status,” who mostly “died in almshouses or public hospitals.” Is this sample representative of the population in Cleveland between 1910 and 1939? I very much doubt it. And don’t even start me on the ethical crimes committed to assemble this collection. Of course, the bodies in this collection were legally obtained following an Ohio legislation that permitted people whose bodies were not claimed within 36 hours of death to be “donated” for scientific study, but was the collection ethically assembled? I think not! The ethics of this collection reminds me of a joke my dad used to tell. “A religious Jewish woman goes to the Rabbi in a panic. ‘Rabbi, the chicken I cooked for Shabbat dinner fell into a soiled baby's diaper. Is it still kosher?’ she asks. The Rabbi replies, ‘It's kosher, of course, but I would I eat it?’” But, I digress.

Wissler and DeWitte’s sample consisted of 369 individuals: 310 males (84%) and 59 females (16%). This fact immediately tells the reader that something is off; the sample is not representative of the general population.

Curiously, the Materials and Methods section also contains the following statement, “to maximize the sample size, both the 1918 flu and the control groups include individuals who died from influenza and pneumonia as well as other diseases such as tuberculosis and myocarditis.” (No data is provided as to how many individuals were included for the purpose of padding the sample size.) Finally, medical history for the individuals in the study is mostly not known. Thus, it is impossible to know whether “an individual suffered another disease during life unless it was listed as the cause of death or left diagnostic evidence on their skeleton.”

Finally, we have the problem of missing data. In the previous paragraph, we have seen one method of padding the data. Here comes another one. The last sentence of the Analytical Methods section states that missing skeletal data “were imputed using the ‘pmm’ function of the mice R package following previous recommendations.” Now, I need to tell the reader that I get hives and homicidal thoughts whenever I read the terms “imputed” or “imputation,” which nowadays essentially mean conjuring data out of thin air. Interestingly, “imputed” was originally a theological term meaning to falsely ascribe guilt to a person. The way data analysts use the word “imputed” started with economists in 1893 when a step in a multistep process was assigned a value by inference from the value of the process to which it contributes. More recently, the term “impute” was used by the Internal Revenue Service to assign interest to an investment when the interest rate is not known. The fact that imputation is used in scientific research to artificially increase the sample size is an inexcusable obscenity.

In the abstract of the article, it is stated that “frail or unhealthy individuals were more likely to die during the pandemic than those who were not frail.” Now, “frailty” is a nebulous and inexact term often defined as “an aging-related syndrome of physiological decline, characterized by marked vulnerability to adverse health outcomes.” https://www.uptodate.com/contents/frailty Thus, the authors used a skeletal proxy to identify frailty. The proxy was lesions on the shinbones (periostosis). Whether this proxy has anything to do with anything is unknown.

The choice of lesions on the shinbones reminds me on of the Streetlight effect or the Drunkard's search principle—both examples of an observational bias whereby one limits the variables used in a study to those that are easy to obtain regardless of whether the choice is actually relevant to the study question.

Let us now discuss the article’s statistical analyses, results, and conclusions. A good piece of advice that I once got from one of my mentors was “Before you subject your data to complicated analyses and reach extravagant conclusions, do yourself a favor and look at the data carefully and perform some simple analyses.” In this case, subjecting the data to complicated (and frankly confusing) Kaplan–Meier survival analysis, Cox proportional hazards analysis, and Schoenfeld test, one should look at the data and do some long division or at most some simple 2×2 contingency analyses.

The following data was extracted from Table 1 of Wissler and DeWitte (2023).

The first thing I noticed was that 67% of the skeletons in the sample belonged to "frail" people. Does this look like a representative sample of the population of Cleveland, Ohio in 1918? The second thing I noticed is that 69% of the control group have had lesions on their shinbones (either active or healed) versus 59% in the group that succumbed to flu. Thus, by the definition used by Wissler and DeWitte, the group of people that succumbed to influenza were 14–17% less “frail” than the group that survived. Of course, in my simple analysis I can use the skeletons exhibiting active or mixed lesions versus the rest of the skeletons (healed and no lesions). In this case, 25% of the control group turn out to be frail, versus 20% in those that succumbed to flu. This result seemed to support the thesis of Wissler and DeWitte, until you realize that the difference is not statistically significant (Fisher's exact test, P = 0.3074).

After reading this paper very carefully, I am left with one open question. It remains unclear to me how this paper managed to get published in PNAS and become a news sensation. Is this another example of the power of the press release?

#influenza #data padding

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judgestarling · 6 months

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A Paternity "Test" Based on the "Science of Eugenics": The Case of Abraham Lincoln

Dr. James Caswell Coggins (1865-1958) was the first President of Atlantic Christian College (now Barton College) in Wilson, North Carolina. His academic degrees consisted of a Bachelor of Arts from Milligan College and three law degrees. In 1940, he published a book entitled “The Eugenics of Abraham Lincoln,” in which he “irrefutably" established that the 16th President of the United States was of pure German-Scottish ancestry. In other words, that Abraham Lincoln’s father wasn’t his biological father.

According to Dr. Coggins, Abraham Lincoln’s mother, Nancy Hanks Lincoln, was an intelligent woman, who in her youth was described as "a bold, reckless, daredevil kind of woman,” and later in life was said to have been "mild, tender, and intellectually inclined." Abraham Lincoln’s father, Thomas Lincoln, on the other hand, was a ne’er-do-well farmer and carpenter, who could neither read nor write.

In 1940, common lore dictated that intelligence was inherited from the father, while mothers contribute little to mental development. Dr. Coggins could not reconcile Abraham Lincoln’s “splendid intellect” with Thomas Lincoln’s “subnormal mind.” Nor he could bring himself to accept an alternative hypothesis, i.e., that Nancy Lincoln was the parent who endowed Lincoln with the brains. Finally, Coggins refused to entertain the idea that intellect has nothing to do with genetics.

So, he built a 284-page argument according to which Abraham Lincoln was not the son of Thomas Lincoln but was actually the illegitimate son of a Smoky Mountain man, Abram Enloe. This story was first propagated in an 1893 article in the Charlotte Observer by a writer who called himself a “Student of History,” and subsequent authors embellished the story further. Coggins's account was merely a late such reincarnation, distinguished from previous stories by the claim that the Abram Enloe paternity was the most consistent with the “Science of Eugenics.”

Coggins builds his case as a lawyer who defends a guilty party. He embellishes and regresses, he uses metaphors and old-wives’ tales, he attacks and retreats as if in an attempt to confuse the jury. His prose is sometimes endearing, sometimes annoying, and always irrelevant. He calls the orthodoxy of Abraham Lincoln’s paternity akin to believing that "Santa Claus comes down the chimney," while “the Truth is hiding behind the door laughing up his sleeve.”

He presents a caricature of the theory of evolution and then proceeds to refute it:

“It has often been contended, that Abraham Lincoln furnished a good example of the doctrine of evolution, as something great coming from almost nothing, and this case is the favorite proof text for this popular theory. But one does not need a high brow to be able to see the sophistry lying at the foundation of all such foolishness.”

Later, he uses “common-sense” analogies sprinkled with more than a modicum of racism to prove his thesis.

“But one can see the utter impossibility of "pouring out" a bucket of water, if there is no water in the bucket to start with. And if the bucket is full of milk it is impossible to pour out water. Now this gets right at the foundation of that whole high-sounding question that any schoolboy or schoolgirl can—in a few words—furnish an unanswerable puzzle to such teachers. It has been proved over and over again that something cannot come from nothing; and that any kind of egg must "evolute" the same kind of life, bird or animal, that produced the egg. It does not switch off to something different. The seed of the African Race can only produce Negroes; the seed of the Chinese can only produce the Chinese, and it takes the seed of the White Race to produce White People. This is an unchangeable law. Not only is this a fixed law as applied to the different Races of people, but this is also true of families and of different individuals.”

At this point in the narrative, he resorts to a story that was repeatedly told by eugenicists but whose veracity has since been proven doubtful. He compares Lincoln father to the low-grade family described in an 1877 book called "The Jukes," who for almost a century has been America's most despised family—a case study of dysfunction, a bunch of hereditary paupers, criminals, harlots, epileptics, and mental defectives, whose care had placed a huge financial burden on taxpayers. As a contrast, he describes the family of slaver Robert E. Lee which is described in the book as the epitome of virtue.

James Coggins book is an example of a pseudoscientific book written by a person who has no knowledge of the subjects he writes about. Such crooks and quacks abound in the modern era to such an extent that the findings of real scientists are drowned in an ocean of self-serving nonsense and the musings of snake oil peddlers.

James Caswell Coggins. 1940. The Eugenics of Abraham Lincoln. Crown Rights Book Company, Dahlonega, Georgia

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judgestarling · 7 months

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Anti-vaxxers, alternative medicine and Martha Jefferson

Reading the musings of prominent anti-vaxxers and promoters of alternative medicine, I started thinking about Martha Wayles Skelton Jefferson, famous for being the wife of Thomas Jefferson, our third president, and a tragic figure in the Greek sense of the word.

Our story starts with Bathurst Skelton who was born in 1744, graduated from the College of William and Mary in Williamsburg, Virginia, and at 22, married Martha Wayles, then 18-years-old. He and 19-year-old Martha had one son, John, who died of an unspecified contagious disease before his fifth birthday. No vaccines or antibiotics, you see. John was preceded in death by his 24-year-old father, who expired before his son's first brthday. No antibiotics, sorry!

Thomas Jefferson was one of the richest people in the United States. For starters, he owned vast swathes of land and about 600 enslaved human beings. There was something, however, that he lacked: Modern medicine. Life in the eighteenth century was, in the words of Thomas Hobbes, “nasty, brutish, and short.” You had to do things early to accomplish anything in life.

On January 1, 1772, 29-year-old Jefferson married his third cousin Martha Wayles Skelton, the 23-year-old widow of Bathurst Skelton. During their ten years of marriage, Martha bore six children: Martha (1772–1836); Jane (1774–1775); an unnamed son who lived for only a few weeks in 1777; Mary (1778–1804); Lucy Elizabeth (1780–1781); and another Lucy Elizabeth who was born after the death of the first Lucy Elizabeth (1782–1784). Only Martha and Mary survived to adulthood, 64 and 26 years, respectively. All the four children who died young, died of what now are preventable diseases. Sadly, what they had in the eighteenth century was only alternative medicine.

So, when I hear anti-vaxxers and promoters of alternative medicine airing their views to the blockhead masses and the ignoramuses, I wonder, are these people aware that they themselves have reached a respectable age because of modern medicine? Why would they want to deny these benefits from the younger generation?

Martha Wayles Skelton Jefferson died in 1782, aged 33. It is now thought that she died of postpartum sepsis, a condition that can now be either prevented or treated with Intravenous antibiotics, blood transfusion, and medication to control blood pressure. None of these existed in the alternative-medicine world of the Commonwealth of Virginia in 1782.

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judgestarling · 1 year

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What is biological function?

In biology, there are two main concepts of function: the selected-effect and causal-role functions. The selected-effect function is a historical concept; it explains the origin, the cause (etiology), and the subsequent evolution of a trait. In other words, the selected-effect function of a trait is the effect for which the trait was selected and/or by which it is maintained. The selected-effect function answers the question, Why does the trait exist?

The causal-role function is an ahistorical and nonevolutionary concept. That is, for a trait to have a causal-role, it is necessary and sufficient that trait performs an activity. The causal-role function answers the question, What does the trait do?

To illustrate the difference between these two concepts of function, let us consider two examples.

The first is a molecular example based on Griffiths (2009). There are two identical sequences in the genome. The first, TATAAA, has been maintained at a certain genomic position by natural selection for the purpose of binding a transcription factor; hence, its selected-effect function is to bind this transcription factor. A second sequence has arisen by mutation and, purely by chance, has come to be identical to the first sequence. Therefore, it also binds the same transcription factor. However, the existence of the second transcription-factor-binding site indicates that it has neither adaptive nor maladaptive consequences. Thus, the second TATAAA sequence has no selected-effect function, but its causal role is to bind a transcription factor.

The second example is based on my own experience of living in Houston, Texas during very hot summers. The selected-effect function of the soles of my shoes is to protect the soles of my feet. Invariably, however, the soles of my shoes bind melted chewing while walking on hot sidewalks. The protection function is a selected-effect function, the chewing-gum binding is a causal role.

Causal roles are easy to detect; selected-effect functions require much work, which is also the reason why evolutionary ignoramuses and creationist dogmatics are so quick in claiming that junk DNA doesn’t exist.

Griffiths PE. 2009. In what sense does “Nothing make sense except in the light of evolution?” Acta Biotheoretica 57:11–32.

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judgestarling · 1 year

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Women who vote Republican are Suckers or Cretinous or Both

In 2022, 42% of women voted Republican; 57% voted for the Democrats.

Who got a better return on their vote? Let us do a simple cost-benefit analysis by using the percentage of women from both parties in Congress.

We start with the expectation. Given the above numbers, the percentage of Republican women in in Congress should be 74% of the percentage of Democratic women in Congress.

There are 202 Democratic representatives in the House, of which 91 are women (45%). Thus, the expected percentage among Republicans should be 33%. There are 222 Republican representatives in the House. Thus, the expectation is that there should be 73 Republican women in the House. In reality, there are only 33 (15%).

There are 51 Democratic senators, of which 16 are women (31%). There are 49 Republican senators, so the expectation is that 23% should be women. Alas, instead of 11 Republican women in the Senate, there are only 9.

Thus, women who vote for Republicans are suckers or cretinous or both. (I actually did not need all that math to prove my point, I should merely have pointed out that Marjorie Taylor-Greene is a Republican woman.

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judgestarling · 1 year

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Academic Five-Year Plans: The Art of Saying Nothing and Sounding Grand

One of the most ridiculous and inadvertently hilarious genres in nonfiction is the “five-year plan.” I became acquainted with this literary form in my first grade in Communist Romania. At the end of the year, I stood in front of an audience of teachers, parents, and party bosses and read aloud the following immortal sentence: “We, the proletariat, pledge to fulfill the five-year plan in four years.” The local communist bosses seemed pleased with my reading of their text. It is now more than 60 years after my first encounter with a five-year plan, and I still cringe painfully whenever I read about these obscenities.

Following the fall of the Berlin Wall, I thought I shall never encounter this style again. I was wrong. Silly five-year plans are everywhere, especially in the academia. (Recently, the President of my University put forward five-year plan defined as “a bold new initiative to advance the University beyond a comprehensive research institution to better position it for the future.”)

Which brings me to last Saturday and my cleaning of some folders on my laptop. Among the piles of disjointed junk and articles I shall never read, I discovered a 2012 paper in Cancer Epidemiology, Biomarkers & Prevention in which the National Cancer Institute and the Centers for Disease Control resurrected the silly Soviet five-year plan with gusto.

The five-year plan by the NCI and CDC brilliantly mixed bureaucratese with meaningless gibberish while pretending to deliver a scientific vision of the future. Economist Priya A. Roy called such prose “sanitized rhetoric and stale platitudes.” The intention, as always, was to sound grand while saying absolutely nothing.

What can be more inspiring that the slogan “Develop, evaluate, and use novel technologies appropriately”? Well, this is how NCI and CDC envisioned the aims of science in the 21st century. The most important development in epidemiology in the 21st century, COVID, was nowhere in their 2012 futuristic divinations.

The paper is a blueprint to “Transforming Epidemiology for 21st Century Medicine and Public Health.” Since the writers were also the ones who decided where the CDC and NCI money went, this ridiculous blueprint most certainly dictated the types of grants that were funded by these two agencies. Anyone wishing to get money from these exalted benefactors, most probably mentioned their aims in their proposals.

The aims were grand and praiseworthy:

1. Extend the reach of epidemiology. (Translation: Train more postdocs and paste their names at position 234 out of 547 coauthors, also known as the “mass grave.”)

2. Balance the epidemiology research portfolio beyond traditional emphasis on discovery and etiologic research to encompass development and evaluation of clinical and population interventions, implementation, dissemination, and outcomes research. (Translation: The only meaningful word in this interminable sentence is “portfolio.” At last, the bureaucrats that run the scientific show admit that they manage portfolios.)

3. Maximize the output and productivity from existing cohorts and assess the need for new cohorts of etiology and outcomes including multiple health-related outcomes and intermediate biomarkers. (Translation: Perform the same studies as your predecessors with a bigger sample sizes. Do not forget to state at the end of each article that much bigger samples are needed for any meaningful insight.)

4. Develop, evaluate, and use novel technologies appropriately. (Translation: This is my absolute favorite of all the recommendations: We must always use technologies appropriately. Inappropriate use of technologies will not be tolerated!)

5. Expand knowledge integration to drive research, policy, and practice. Support knowledge integration and meta research (systematic reviews, modeling, decision analysis, etc.) to identify gaps, inform funding, and to integrate epidemiologic knowledge into decision making. (Translation: Despite my best efforts and the waste of 8.36 minutes of my life, I have no idea what this paragraph means.) I ran out of steam.

The complete list of aims can be found here. If you like pain and whips, this article is for you.

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judgestarling · 2 years

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GWASturbation, ENCODE, AI and Pentecostalism (2nd Edition)

Pentecostalism is a renewal movement within Christianity, and like many such movements, it adheres to the inerrancy of scripture and the necessity of accepting Christ as personal Lord and Savior, while placing special emphasis on direct personal experiences. A main tenet of Pentecostalism is the belief in empowerment, which leads to spiritual gifts, such as speaking in tongues (glossolalia), divine healing, and the ability to handle snakes without being harmed.

The interesting thing about speaking in tongues is that no Pentecostal has never been caught speaking a real minority language like Albanian, Romansh, or Irish Gaelic. Neither were they caught speaking a dead language. The “tongues” Pentecostals speak are always a sort of guttural gibberish that only a high Pentecostal priest can understand and interpret.

Divine healing involves the irrational belief that by performing a series of rituals in a certain order, diseases will disappear, cancer will regress, and demons will be exorcised. The snake bit is of particular interest since it involves the belief that the practitioner is immune from even the worst of the worst, let alone criticism by outsiders and twitter trolls. This immunity from everything is of particular importance to the story I am about to tell.

My story concerns people who are convinced that genome-wide association studies (GWAS), which I call GWASturbation and machine learning, will bring joy and salvation to the human race. These people seem to have quite a lot in common with Pentecostals. First, they adhere to the irrational belief that by performing a series of rituals in a certain order, diseases will disappear and cancers will regress. The belief is irrational since nothing ever came out of these endeavors except huge headlines in the news media and a bit of scandal. Second, these people have a tendency to speak in tongues. Take for example the following paragraph from a PLoS Genetics article entitled: “Integrative Modeling of eQTLs and Cis-Regulatory Elements Suggests Mechanisms Underlying Cell Type Specificity of eQTLs” by Christopher D. Brown, Lara M. Mangravite, and Barbara E. Engelhardt:

“We identified, for each gene expression trait, the most highly associated SNP within each local linkage disequilibrium (LD) block. We tested the independence of each SNP by multivariate regression and took the union of the independently associated SNPs for each gene. We refer to, for example, the first and second most significant, independently associated SNPs as primary and secondary SNPs, respectively, and we refer to the set of primary SNPs as first tier, or tier 1, extending in the straightforward way through tier 4. We do not consider tiers beyond the fourth tier because of lack of statistical power. For each study, and within each tier, we independently estimated false discovery rates (FDRs) by permutation. Although we computed a BF for every SNP-gene pair, we limit our subsequent analysis to cis-linked SNPs, or SNPs within 1 Mb of the transcription start site (TSS) or transcription end site (TES) of a gene. While we have standardized analysis and reporting across studies, we have not considered the scope of differences in eQTL discovery based on alternative data analysis pipelines.”

I challenge any person who is not intimately involved with Pentecostalism or does not GWASturbate regularly to translate the above paragraph into English.

Or take this paragraph:

“We chose to control for the confounding effects of both known covariates and unknown factors by removing the effects of principal components (PCs; Figure S1, Table S1) [36], [37]. Given that a diverse set of demographic (e.g., age, sex), environmental (e.g., BMI, drug use), and technical (e.g., post-mortem interval, array batch, ozone levels, identity of the technician who handled the arrays) variables are known to be associated with gene expression measurements and to confound eQTL ascertainment [26], [36], [37] we felt it was critical to control for these effects in the most consistent way possible prior to eQTL mapping. Across the diverse set of studies examined here, the covariate annotation ranges from non-existent to detailed. To address this non-uniformity, we analyzed each data set with the same approach, irrespective of covariate annotation. Multiple independent studies demonstrate the effectiveness of controlling for latent variables with respect to eQTL ascertainment; indeed, controlling for PCs substantially increases power to detect cis-eQTLs within these studies [26]. Importantly, it has also been demonstrated that each of these eQTL discoveries is also more likely to replicate across studies [26].”

Or this one:

“We next sought to investigate the biological characteristics associated with the reproducibility and cell specificity of eQTLs. To do this, we quantified the overlap between cis-eQTL SNPs and genomic features associated with functional cis-regulatory elements (CREs), including DHS sites, chromatin marks, and binding sites for transcription factors and other DNA associated regulatory proteins (see Table S3 for full list of data sets). We categorized regions of open or activating chromatin, and regions of transcription factor or DNA protein binding as activating CREs, and regions of repetitive, repressive, or heterochromatic chromatin domains as repressive CREs, to draw a contrast between genomic regions where transcription factor binding is frequent and regions where it is discouraged or unlikely. We focused analyses of LCL eQTL SNPs on CRE data sets produced in LCLs (primarily GM12878) and analyses of liver eQTLs on CRE data sets produced in HepG2 cells, a well-characterized, if imperfect, proxy for hepatocyte biology. We note that the quantification of eQTL SNP-CRE overlap enrichments is inherently conservative, given that the boundaries of most genomically defined CRE types are imprecise and that eQTL SNPs are typically tag SNPs, rather than the exact causal variants.”

At this point, there are three possibilities: The first is that the authors indeed possess the secret of “empowerment,” which enables them to speak in tongues and perform divine healing, while at the same time rendering them immune to "snakes” like me. If this is so, we should all genuflect and accept their superior authority. The second possibility is that the GWAS-ENCODE-AI crowd does not speak in tongues, but that the rest of the scientists in all branches of genomics, molecular evolution, molecular biology, genetics, and biochemistry are low-grade imbeciles (see below) deficient in their ability to comprehend the superior knowledge of the empowered. If this is so, then again, we should all genuflect and accept their intellectual supremacy.

The third possibility is that the GWAS-ENCODE-AI people are pulling a Sokal-like hoax on all of us. I, for one, would be very surprised if any of the so-called reviewers who were supposed to read the Brown, Mangravite, and Engelhardt paper in PLoS Genetics would have noticed anything bizarre in the paragraph below (which I have written in the Alan Sokal style). Will the paragraph below be out of place in the midst of the Pentecostal gibberish spewed by Brown, Mangravite, and Engelhardt in their so-called scientific paper.

“The different intuitive pictures which we use to describe CRE systems, although fully adequate for given experiments, are nevertheless mutually exclusive. Thus, for instance, the overlap between cis-eQTL SNPs and genomic features, including DHS sites, can be described as a small-scale hepatic system, having a central nucleus about which the external cytoplasm revolves. For other experiments, however, it might be more convenient to imagine that the activating chromatin and regions of transcription-factor binding are surrounded by a system of stationary SNPs whose frequency is characteristic of species. Finally, we can consider the cell from a chemical point of view. Each covariate annotation is legitimate when used in the right place, but the different covariate may be contradictory and therefore we call them mutually controlling for latent variables with respect to eQTL ascertainment.”

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judgestarling · 2 years

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How Do You Portray the Moral Inferiority of Christians at a Baptist University?

Baylor University is a Baptist university. Thus, at Baylor, they celebrate a research creed whereby “research, scholarship and faith guide the mind in understanding the complex diversity of God’s creation.” At Baylor University evolution is taught, but the Biology Department finds it necessary to provide an explanation as to why they do that. Most universities do not provide an explanation.

What do researchers do when their findings contradict elements of the Christian faith or the Christian practice? Do they manipulate the data? Do they burry the results in a drawer. No! They burry the data inside the publication and emphasize the parts that fit the Christian dogma. The most important results are buried deep in almost impenetrable tables and socio-psycho-babble. (They follow G.K. Chesterton’s advice: “Where does a wise man hide a leaf? In the forest.”

Take for example, Sung Joon Jang and Aaron Franzen from and their study Is being “spiritual” enough without being religious? A study of violent and property crimes among emerging adults that was published in 2013 in the journal Criminology.

From the abstract:

“This study first examines differences in crime between “spiritual-but-not-religious” individuals and their “religious-and-spiritual,” “religious-but-not-spiritual,” and “neither-religious-nor-spiritual” peers in emerging adulthood. Specifically, we hypothesize that the “spiritual-but-not-religious” young adults are more prone to crime than their “religious” counterparts, while expecting them to be different from the “neither” group… The overall results tend to provide a partial support for the hypotheses. Implications for criminology and future research are discussed.”

C'est tout! There is nothing more of any substance in the abstract.

The expectation of the “scientists” at Baylor was that “religious-and-spiritual” commit the least number of crimes, followed by the “religious but not spiritual,” “spiritual but not religious,” and “neither religious nor spiritual.”

The “partial support” in the abstract seems to indicate that the actual data confirmed their expectation. Indeed, a press release by the Media Relations Department at Baylor was entitled “Spiritual” Young People Are More Likely to Commit Crimes than “Religious” Ones, Baylor Study Finds.“

This conclusion was picked up by the authors of the Findings column of the the August 2013 issue of Harper’s Magazine (unfortunately behind a paywall). (I wish Harper’s would hire me once in a while to do the heavy lifting and rummage through obscurantist tables.)

In reality, the group that was least prone to criminal behavior was the “neither religious nor spiritual.” Given these results, the title of the article by the gentlemen from Baylor should have been “Is being religious and/or spiritual enough? The dearth of property crimes among neither-religious-nor-spiritual emerging adults.”

Such a title would, of course, be unthinkable at a university where “faith guides the complex understanding of God’s subjects.” So what do the authors do. Prevaricate!

Prevaricators in the Name of Christ: Sung Joon Jang, associate professor in the Department of Sociology and the Institute for Studies of Religion at Baylor University, and Aaron B. Franzen, then Ph.D. candidate at Baylor and currently Associate Professor at Hope College, a four-year liberal arts college emphasizing “vibrant Christian faith”

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judgestarling · 2 years

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Robert G. Ingersoll on Theologians and Theology

“As a rule, theologians know nothing of this world, and far less of the next; but they have the power of stating the most absurd propositions with faces solemn as stupidity touched by fear.”

“It is a part of their business to malign and vilify the Voltaires, Humes, Paines, Humboldts, Tyndalls, Haeckels, Darwins, Spencers, and Drapers, and to bow with uncovered heads before the murderers, adulterers, and persecutors of the world. They are, for the most part, engaged in poisoning the minds of the young, prejudicing children against science, teaching the astronomy and geology of the bible, and inducing all to desert the sublime standard of reason.”

― Robert G. Ingersoll, 1880. Mistakes of Moses

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judgestarling · 3 years

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The Origin of the Term “Junk DNA”: A Scientific Whodunnit (3rd edition)

As most textbooks would have it, the term “junk DNA” was coined in 1972 by Susumu Ohno as part of his work on the role of gene and genome duplication. The first time I met Susumu Ohno was at a meeting in Crete many years ago, and the way I remember it, he told me that he “deliberately” chose a “provocative term” for “junk DNA” to emphasize the “uselessness” of this DNA fraction. (Indeed, the term “junk” comes with a “semantic baggage” since it used as a synonym for heroin and male genitalia—two terms that are verboten in polite company.) At the conference dinner, Ohno also told me (and other newbies) that rosé wine is produced by mixing red and white wines. I no longer believe either of these “narratives.”

It all started with my obsession to read very thoroughly every article that I quote, instead of relying on indirect references. In this day and age, in which articles are signed by hundreds of authors, the vast majority of whom don’t even bother to read their “own” publications, I stand out like a nigella seed in mayonnaise. This disorder is probably due to my association with Mina Graur, who is a historian that only trusts “primary sources.” Indeed, so strong is her belief in primary sources, that I am quite certain she wouldn’t even trust a textbook description of the double helix—she would want to read Watson and Crick’s (1953) article, as well as their notebooks, correspondences, and preliminary drafts, and if possible interview each and every one associated with the lab in Cambridge including the janitors. What can I say? She does NOT trust “secondary” sources!

For a few years, I engaged in a bitter fight with the quacks of the ENCODE Project over “junk DNA,” and to my dismay, I realized that I cannot find a copy of Susumu Ohno’s (1972) article “So much ‘junk’ DNA in our genome.” So, I started searching the net for the article. My searches led me to discover three publications from 1972 that mention “junk DNA.” The above-mentioned paper by Susumu Ohno, an article in Advances in Human Genetics by David Comings, and a New Scientist commentary by Tim Hunt.

Solving the origin of Comings’ “junk DNA” was easy. He got it from Susumu Ohno, who was his colleague at City of Hope National Medical Center in Duarte, California. Indeed, Comings quotes two “in press” papers by Ohno. The most interesting thing about Comings’ article, however, is that his treatment of junk DNA is much more thorough and much more informative and much more considerate than Ohno’s cryptic 1972 article, in which the term “junk” is only mentioned in the title.

The origin of Tim Hunt’s “junk DNA” proved to be much more interesting. In 1972, the future Nobel Prize winner was a 29-year-old researcher at Cambridge trying to understand messenger RNA and the great amounts of DNA that never produce mRNA. In time, his research led him into a completely different area of study, and in 2001, Tim Hunt shared the Nobel Prize in Physiology and Medicine with Paul Nurse and Leland Hartwell. The work for which he was conferred the highest accolade in the sciences had nothing to do with either mRNA or junk DNA—the Nobel was in recognition of his discovery of proteins that control cell division.

In his 1972 commentary, Tim Hunt uses the term “junk DNA” to refer to “the large amount of nucleic acid that never finds its way out of the nucleus, which does not fit in with the old categories of genes and messages.” Note that Hunt’s 1972 “junk DNA” employs a mechanistic definition of junk DNA that is different from but not at odds with our current functional—or actually nonfunctional—understanding of junk DNA as “useless and harmless” per the definition of Sydney Brenner in 1998.

Where did Tim Hunt get the term? On September 18, 2013, I sent him the following email.

“I have recently realized that although the late Susumu Ohno is credited solely with the coinage ‘junk DNA,’ he was not the only person to have used the term in 1972. In your ‘How mammals get the message’ in New Scientist, you have an entire section entitled ‘Why all that junk?’ In this section you mention “junk DNA.” I am curious whether (1) you got the term from Susumu Ohno, (2) he got it from you, (3) you coined it independently, or (4) you got it from a third person. I would greatly appreciate your help with this historical puzzle.”

The next day, Dr. Hunt replied and his reply pointed me in a new direction.

“Gosh, yes! I did write that piece, and I never met Ohno. I got it from Sydney Brenner and/or Francis Crick—it was certainly current in Cambridge at the time. Maybe they got it from Ohno? You should ask Sydney.”

So, I wrote Dr. Brenner who stated that he was not the originator of the term “junk DNA.” One of the sentences in his reply made the puzzle even more profound.

“I can confirm that we were using the idea of “junk” in the genome in the sixties at Cambridge.”

Really? The sixties? If the term was indeed current in the sixties, it is entirely possible that the term may have found its way into the literature and hasn’t been detected thus far. If it was there, I was determined to find it.

Enter Google Ngram, with which one can find short phrases in over 6 million books (published since 1500) that have been digitized by Google.

With Google Ngram, I struck gold, a 1963 paper by Charles Ehret and Gérard de Haller entitled “Origin, development, and maturation of organelles and organelle systems of the cell surface in Paramecium.” The paper which was published in Journal of Ultrastructure Research is huge—42 pages and 86 figures. On page 39 it is written:

“While current evidence makes plausible the idea that all genetic material is DNA (with the possible exception of RNA viruses), it does not follow that all DNA is competent genetic material (viz. ‘junk’ DNA), nor that all Feulgen-positive material is active DNA.”

This was completely unexpected. Nine years before Susumu Ohno, two authors referred to “junk DNA” in a casual manner without even bothering to explain what junk DNA is. If we assume that “non-competent” genetic material is the same as nonfunctional DNA, then their use of “junk DNA” was entirely modern. The problem was that I have never heard of the authors before. Who was Charles F. Ehret? Who was Gérard de Haller?

A little more digging revealed that Charles F. Ehret was a very important person, as evidenced by the fact that The Washington Post published an obituary on his death in 2007.

“Charles F. Ehret, 83, a scientist whose study of circadian rhythms led to a widely popular anti-jet lag regimen that improved the trips of untold numbers of world travelers, died February 24 of multiple illnesses at his home in Grayslake, Ill.”

“In more than 35 years of experimentation, Dr. Ehret found that the headaches, nausea, disorientation, fatigue, and malaise suffered by globe-trotters had almost nothing to do with thin air and the dizzying effects of supersonic speed, as was commonly assumed. Rather, jet lag is a matter of crossing too many time zones too quickly for the body to adjust. It can be ameliorated by adjusting eating, activity and sleep schedules according to a strict system that Dr. Ehret developed.”

A search of the literature revealed that the paper in Journal of Ultrastructure Research represented quite a detour in the scientific life of Dr. Ehret. With the exception of a 1948 paper in The Anatomical Record, entitled “The mating reaction of multimicronuclear monstrosities in Paramecium bursaria,” his entire research program dealt with circadian rhythms, jet lag, and light exposure.

Interestingly, Dr. Ehret worked on many different organisms which, according to The Washington Post, included “single-celled organisms, rats, his eight children, and volunteers.” Rats and eight children? That sounds like a winning combination!

The amount of information I could find on Gérard de Haller was quite minimal. He became Professor of Protistology at the University of Geneva in 1969. He mostly published in French, and the last known address for him was the Molecular Systematics Group at the University of Geneva. As far as I could ascertain, he published his last paper in 1993. In October, 2013, I wrote to the head of the Molecular Systematics Group, Jan Wojciech Pawlowski. He replied promptly.

“Prof. Gérard de Haller is a Honorary Professor of the University of Geneva. He was one of the jurors of my PhD thesis and the head of Protistology Laboratory since 1969. His specialty was the biology of ciliates. As far as I know he is still alive, although he is not scientifically very active since his retirement. I saw him last time about 2 years ago when he came to the University to participate in a ceremony for one of his younger assistants. He is still on the list of University Professors.”

I was looking for more information about him but could not find anything more. However, I can easily find someone from his family who live in Geneva if this is necessary.”

In the end, the person who managed to find Gérard de Haller was Robert Hirt, Professor of Evolutionary Parasitology at Newcastle University. Through him, in May 2014, I got an email from Prof. de Haller himself.

“As far as I can remember, the first time we spoke of junk DNA was at a seminar with Werner Arber around 1958 or so, and I know that Eduard Kellenberger’s department, where Werner was working, was in close contact with the big bosses of the raising DNA science [at Cambridge]. Unfortunately, that’s all I can remember, except that these were great times!”

“I asked Werner Arber, but he couldn’t add anything. He mentioned Francis Crick as a possible “inventor” of the term.”

At this point, I was quite certain that Ehret and de Haller did not invent the term “junk DNA.” They used it properly and in the right context, but it wasn’t theirs.

I wrote about my findings in my blog, and ended the article with an appeal.

“In the manner of the appeals by Oxford English Dictionary, I would like to ask the readers: Do you have an earlier record of the term “junk DNA”? Please submit your evidence by email.”

Soon afterwards, an anonymous reader found an example of “junk DNA” from 1960.

“Following your example, I’ve been trying to find earlier “junk DNA” quotes using Google. I found this quote in the Year Book of the Carnegie Institution, Washington July 1, 1959- June 30, 1960 (Volume 59, page 278).”

The quote from the Year Book was quite straightforward.

“It is much more difficult to imagine how the different DNA’s could act as templates for the similar RNA’s. This is the problem that can be avoided most easily by considering a large part of the DNA to be junk.’”

The authors, however, did not like the concept of “junk DNA’, although they admitted that there were precedents.

“The idea that a large part of the nucleic acid is nonfunctional is repugnant. It seems unlikely that such an inefficient mechanism would have survived through evolution, although it must be remembered that enzyme molecules are very large in comparison with their active centers.”

The Carnegie Institution report was written by eight members of the Biophysics Group within the Department of Terrestrial Magnetism. Yes, “Terrestrial Magnetism”!

Several names stood out. Sadly, Richard Roberts died in 1980, Ellis Bolton in 2006, and Roy Britten in 2012. The person with which I was most familiar with was Roy Britten, who was the discoverer of repeated DNA sequences in the genomes of eukaryotic organisms, and later studied their effects on the evolution of genomes. I have met Britten several times at scientific meetings, and if there was one thing clear, it was the fact that he was not a fan of “junk DNA.” When Roy Britten died in 2012 at the age of 92, his obituary in the journal Science was written by his close collaborator Eric Davidson.

So, I wrote to Eric Davidson, and got the following email on November 11, 2013.

“First off, I wouldn’t exactly consider that citation as related to the later nonsense about junk DNA of the Leslie Orgel/Francis Crick variety. At Carnegie they were strictly concerned that year with the protein coding sequence load of the DNA, as seen through the lens of ribosome structure/function, without considering the function of mRNA and tRNA.”

“As for Roy, you are right, he couldn’t stand the idea of junk DNA, but that was in reference to the Crick usage (which we heard about verbally all the time from him and others of his circle; in those days, late 60s and early 70s Roy and I were hotly involved in arguments about the organization of animal genomic DNA). Anyway, Roy could not possibly have been responsible for the Year Book citation you sent because that particular report concerned the year Roy wasn’t even at Carnegie; he was in Denmark working on yeast. The Biophysics report then and in the succeeding few years at the Department of Terrestrial Magnetism was written by the senior people, Bolton and Roberts, I think mainly Bolton (with whom Roy did not get along particularly well in intellectual terms). Roy was then very junior in the hierarchy and he wrote his own report on that year’s activity; it is very doubtful he could have inserted anything like that even ex post facto. So, I don’t think it is a likely hypothesis that Roy originated that term in any way shape form or manner, then or later.”

Is it possible that Davidson was wrong and one of the authors of the Carnegie report did coin the term “junk DNA” as a pejorative? One such precedent comes to mind. In 1955, British cosmologist Fred Hoyle derided a theory by American physicist George Gamow and called it by a ridiculous name, “Big Bang.” The name stuck. As far as “junk DNA” is concerned, however, there is little evidence for the pejorative-nickname hypothesis.

Why did the Biophysics group at the Department of Terrestrial Magnetism at Carnegie found the concept of “junk DNA” to be repugnant in 1959? The historical context was explained to me by Alexander Palazzo from the University of Toronto.

“To understand this report, you need to remember that it was written two years before the discovery of mRNA. Back then it was believed that each gene made a separate RNA that got incorporated into a ribosome (i.e., ribosomal RNA). Thus, according to this model, each ribosome contained information within it to make a single protein. Of course, today we understand that ribosomes are only enzymes, and that the protein-information is contained in mRNA. But considering that >90% of cellular RNA is rRNA, their old faulty model is understandable.”

“The Roberts’ group was analyzing the length of E. coli rRNA. In the discussion they write about the size of proteins and note that some of these are very small. In contrast, there was too much rRNA in each ribosome. This discrepancy indicated that in these cases the additional RNA was likely non-functional. Interestingly, Roberts missed a critical fact that was pointed out by others—that rRNA was not large enough to code for certain large proteins (beta-galactosidase, for example).”

“Roberts’ group also noted that all rRNAs looked the same, whereas the nucleotide composition of DNA varied considerably. Thus, some DNA must not code for ribosomal RNA and this is where they invoke the idea of junk DNA.”

“Note that a new form of RNA (messenger RNA) was recognized in a landmark paper by Brenner, François Jacob and Matthew Meselson in 1961 making this whole discussion moot. (And yes, I’m aware that James Watson’s group also demonstrated the existence of mRNA…).”

How should I summarize my current understanding on the origin of “junk DNA”—the term and the concept?

First, there is evidence that the term “junk DNA” was already in use in the early 1960s (e.g., Aronson et al. 1960; Ehret and de Haller 1963). I am, however, almost certain that none of these authors coined the term. All clues point to Cambridge in the late 1950s. My guess is that the term originated with Francis Crick, but at present I have no evidence for this claim.

And what about Susumu Ohno? I was reminded by a reader that “a conceptual discovery is usually ascribed to one who first stuck his/her neck out to push the viewpoint.” It doesn’t really matter who said what first.

We remember Charles Darwin, not because he discovered natural selection (and sexual selection) or because he was the first to propose that adaptive evolution is due to selection. Others, e.g., William Charles Wells, Patrick Matthew, James Cowles Prichard, William Lawrence, and John Sebright, may (or may not) have recognized evolution by natural selection long before him. It was Darwin, however, who staked his reputation on what was considered at the time a grave heresy. It is, of course, interesting that Hunt, Brenner, De Haller, Roberts and perhaps others toyed explicitly with the idea of “junk DNA” before 1972, not to mention others who may have entertained the same idea without calling it “junk.” However, it was Susumu Ohno who stuck his neck out and put his reputation on the line by advocating a very unpopular and contentious idea.

In my book, Molecular and Genome Evolution, I decided on the following phrasing:

“We have written evidence that the term “junk DNA” was already in use in the early 1960s (e.g., Aronson et al. 1960; Ehret and de Haller 1963); however, it was Susumu Ohno (1972, 1973) who formalized its meaning and provided an evolutionary rationale for its existence.”

Will we ever know who coined "junk DNA”? I am hopeful that one day a scholar rummaging the archives of Francis Crick will find the answer.

Literature

Aronson AI, Bolton ET, Britten RJ, Cowie DB, Duerksen JD, McCarthy BJ, McQuillen K, Roberts RB. 1960. Biophysics. pp. 229–289. In: Year Book: Carnegie Institution of Washington. Volume 59. Lord Baltimore Press, Baltimore, MD.

Brenner S. 1998. Refuge of spandrels. Curr. Biol. 8:PR669.

Comings DE. 1972. The structure and function of chromatin. Adv. Hum. Genet. 3:237–431.

Davidson EH. 2012. Roy J. Britten (1919–2012). Science 335:1183.

Ehret CF, G. Haller G. 1963. Origin, development and maturation of organelles and organelle systems of the cell surface in Paramecium. J. Ultrastruct. Res. 23:S1–S42.

Graur D. 2016. Molecular and Genome Evolution. Sinauer Associates

Hunt T. 1972. How mammals get the message. New Scientist 18 May:373–375.

Ohno S. 1972. So much “junk” DNA in our genome. In: Smith HH (ed.) Evolution of Genetic Systems: Brookhaven Symposia in Biology. Gordon and Breach, New York. 23:366–370.

Ohno, S. 1973. Evolutional reason for having so much junk DNA. In: Pfeiffer RA (ed.) Modern Aspects of Cytogenetics: Constitutive Heterochromatin in Man. Schattauer Verlag, Stuttgart, Germany. pp. 169–180.

Watson JD, Crick F.HC. 1953. Molecular structure of nucleic acids: A structure for deoxyribose nucleic acid. Nature 171:737–738.

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judgestarling · 3 years

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The #Evolution of the Term “Evolution”

(a) 1616: A movement or change of position, e.g., “The nature of this Euolution is clearely to leaue the File-leaders in front, and Bringers in reare.”

(b) 1624: The process of unrolling, opening out, or revealing.

(c) 1671: The process by which living organisms or their parts develop from a rudimentary to a mature or complete state. These days, this process is referred to as “development.” The first use of “evolution” in this sense appears in an anonymous book review published in Philosophical Transactions of the Royal Society. The book being reviewed was the first part of Historiæ Generalis Insectorum (General History of Insects) by Johannis Swammerdani. The book is described in the review as “a curious and philosophical book, written in the Belgick tongue.” The review is shown below.

(d) 1764: Introduction of (b) into biology. Emergence or release from an enclosed structure, e.g., “Our author asserts, that every fungus is contained in an entire and perfect state… in the egg, or as it is called, the seed, and wants nothing but evolution, in order to imbibe the necessary juices.

(e) 1783: The process of emission or release of such entities as gas, heat, and light, e.g., “The method put in practice by Mr. Hutchins to settle the freezing point of quicksilver depends entirely upon the evolution of heat.”

(f) 1832: The use of “evolution” à la Darwin started with Charles Lyell’s second edition of Principles of Geology, where on page 11 it is written “The testacea of the ocean existed first, until some of them by gradual evolution, were improved into those inhabiting the land.”

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judgestarling · 3 years

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Protections against #COVID19 as They Apply to Poor and Rich Students: A #Texas Comparison @UHouston @RiceUniversity #Texas @GregAbbott_TX @UHpres

A letter from the President of University of Houston, Renu Khator, landed in my inbox on August 10 at 1:00 PM. I was waiting for such a letter to see how a responsible university president will deal with the inane rules of Texas governor, Greg Abbott, who decreed that public schools are require marks, proof of vaccination, testing, or social distancing. I was also looking—most probably naively—at some signs of civic responsibility, of putting the interests of her “subjects” above the fear of being fired by the Republican Governor of Texas, who is now a full-fledged Trump boot-licking lackey. I was thoroughly disappointed.

The first two paragraphs of the letter started with a typical “caring-while-presidential” tone and promised to outline measures to protect faculty, students, and staff.

Dear Faculty and Staff,

I hope you and your families are safe and healthy. The current resurgence of COVID-19 caused by the Delta variant has given rise to a new round of anxiety and concern, which is entirely understandable. To be honest, I feel the same way.

While I trust that we all will take personal responsibility to mitigate the risk of the COVID-19 spread as we open for Fall Semester on August 23, I also feel that some institutional decisions regarding vaccinations, masks, meetings, exemptions, and course delivery are necessary to keep our community safe.

Sadly, the tone of the letter changed very quickly from concerned, understanding, and reassuring, to a hodgepodge litany of bureaucratese and empty words.

“Rapidly changing and increasingly complex environment” was quickly followed by “ready to pivot,” “finding the right balance,” and “local flexibility.” A reinstated committee was announced, the “Instructional Format Committee,” and the faculty is told to “address this challenge,” “innovate,” “be prepared,” “work together,” and take “personal responsibility.”

We were also told that University of Houston has a “COVID-19 Response Team,” new “safe air filtration systems,” “sanitization stations,” and “strict cleaning protocols.”

The higher-ups, we are further told, “will continue to monitor,” “promote alternatives,” weigh “vaccination options,” while maintaining “data transparency.” Further, details will be provided by the Provost.

The University of Houston President is “cautious yet optimistic,” and she ends the letter with “I look forward to seeing you around the campus.” Whether “dead or alive” is not spelled out.

In short, blah-blah, gobbledygook, and mumbo jumbo. The word “mandate” is verboten, umentionable, and everything that is common sense, logical, and necessary is a mere optional recommendation.

Let us now compare the policies of University of Houston with those of Rice University. Because the median family income of a student from University of Houston is $58,000 and only 26% come from the top 20%, while the median family income of a student from Rice is $160,800 and 64% come from the top 20%, the comparison will serve as an illustration how Texas protections against COVID-19 apply to poor and rich students.

The campus COVID policies at Rice University are listed here.

The rules are quite simple:

1. Face masks are required indoors at all times for faculty, staff, students, and visitors. 2. Vaccination is not mandatory, however, every fully vaccinated person at Rice must register his identity with the university. By default the identity of unvaccinated people is revealed. 3. Fully vaccinated people at Rice must schedule a test at least once every two weeks. 4. Unvaccinated people must test twice per week, regardless of whether they come into contact with other people or not. 5. Large gathering are forbidden.

To summarize, rich kids must be protected at all costs. Poor kids? Who cares?

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judgestarling · 3 years

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The darwin, the simpson, the haldane, the pauling, the kimura, and the Darwin: Five Mostly Forgotten Units of Evolutionary Rates and One Measure of Scientific Fame

See article here

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judgestarling · 3 years

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A Perfect Question for a #Genetics Course Final (Make It a Bonus Question)

A painting hangs in the Nijmegen Town Hall showing a young woman with an old man lying in her lap, and six sons standing next to her: two in red, two in green, and two in white.

It is accompanied by the following text:

The wife of the old man says:

“Remark and see that I declare The two in red are my father’s brothers. The two in green are my mother’s brothers. The two in white are my children and I, the mother, am married to the father of these six There is no forbidden degree of kinship among us.”

Two two sons in red say:

“We would have regretted if not our niece had been given to our father Because she is not our father’s niece Which nobody would easily guess.”

The two sons in green say:

“It is remarkable to show in these figures that he is our natural father And has married our niece Which we don’t regret.”

The two in white say:

“Our father is the old man. Our mother is the young lady. But tell us how it is possible That our brothers are our mother’s uncles?”

Assignment: Draw the family tree for all these individuals.

Solution: Huybert, the old man (yellow square) married his first wife, Anna (red circle), a widow who had a prior son called Gijsbert (blue square marked with G). Huybert and Anna had two sons (small red squares): Adam and Arent. After Anna died, Huybert married a second wife, a widow named Beel (green circle), who had a prior daughter named Jacomijn (blue circle marked with J). Huybert and Beel had two sons (small green squares): Bertel and Barent. In the meanwhile, the prior son of the first wife, Gijsbert, married the prior daughter of the second wife, Jacomijn. Gijsbert and Jacomijn had a daughter named Charlotte (white circle). After Beel’s death, Charlotte became the third and current wife of Huybert. Charlotte and Huybert have two sons, Casper and Coenraat (small white squares). Deceased individuals are marked with the dagger sign.

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judgestarling · 3 years

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4 Jokes about Engineers

Engineering student #1: "Where did you get this great bike?"

Engineering student #2: "Well, I was walking yesterday, minding my own business, when a beautiful woman rode up on this bike, threw it to the ground, took off all her clothes and said, 'Take what you want'.”

Engineering student #1: "Good choice: The clothes probably wouldn't have fitted you anyway."

A priest, a physician, and an engineer are waiting for a particularly slow group of golfers to finish their game.

All: "What's up with those guys? We've been waiting for a very long time!"

Golf Official: “That's a group of blind firemen. They lost their sight saving our clubhouse from a fire last year, so we always let them play for free anytime!"

The group fell silent for a moment.

Priest: "That's so sad. I'll say a special prayer for them tonight."

Physician: "I'll contact my ophthalmologist and see if there's anything she can do for them."

Engineer: "Why don’t they play at night?"

An engineer was crossing a road one day, when a frog called out to him and said, "If you kiss me, I'll turn into a beautiful princess."

He bent over, picked up the frog, and put it in his pocket.

The frog spoke up again and said, "If you kiss me, I'll turn back into a beautiful princess and stay with you for one week."

The engineer took the frog out of his pocket, smiled at it and returned it to the pocket.

The frog then cried out, "If you kiss me and turn me back into a princess I'll stay with you for one week and do anything you want."

Again, the engineer took the frog out, smiled at it and put it back into his pocket.

Finally, the frog asked, "What's the matter? I've told you I'm a beautiful princess and that I'll stay with you for one week and do anything you want. Why won't you kiss me?"

The engineer responded, "Look, I'm an engineer. I don't have time for a girlfriend. But a talking frog - now that's cool."

Two engineers were standing at the base of a flagpole, looking at its top. A woman walked by and asked what they were doing

"We're supposed to find the height of this flagpole," said Sven, "but we don't have a ladder."

The woman took a spanner from her purse, loosened a couple of bolts, and laid the pole down on the ground. Then she took a tape measure from her purse, took a measurement, announced, "6.5 meters," and walked away.

One engineer shook his head and laughed, "A lot of good that does. We asked for the height and she gives us the length!"

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judgestarling · 4 years

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Theophilus Painter, the Geneticist on the Wrong Side of History... Not Once, But Three Times

Theophilus Painter (1889–1969) joined the faculty at the University of Texas in 1916 and except for a military stint during World War I stayed there his whole career. He was, in succession, instructor, associate professor, professor, distinguished professor, acting president (1944–1946), and president (1946–1952) of the University of Texas.

These days, he is remembered for three things (1) erroneously claiming that humans possess 48 chromosomes—an error that plagued human cytogenetics for 33 years, (2) his willingness to curry favor with corrupt politicians in Texas at the expense of academic freedom, and (3) his support of racist practices.

The number of human chromosomes

Probably the first effort to determine the chromosome number of humans was that of Hansemann (1891), who counted 18, 24 and more than 40 chromosomes in three cells. In between 1891 and 1932, many investigators published papers reporting various chromosome number in humans. With two exceptions, the counts were low, ranging from 8 to 24 as the diploid number. However, for a long time the most influential paper in human cytogenetics was that of van Winiwarter* (1912), who reported a chromosome number of 47 in males and 48 in females. He concluded that humans, like locusts, had an XX/X0 male sex-determining mechanism. Nine years later, de Winiwarter* (1921) confirmed his observations, and added a racial component to the findings by claiming that the diploid number of chromosomes in Africans was 24.

In the early 1920, Theophilus Painter decided to settle the question of chromosome number in humans. To do that, he enlisted the help of a physician at Texas State Insane Asylum to provide him with freshly harvested “testes.” Here are some excerpts from the Material and Methods section in his 1923 article:

“The material upon which this study is based was obtained from three inmates of the Texas State Insane Asylum through the interest and cooperation of Dr. T. E. Cook, a physician at that institution. Two of these individuals were negroes and one was a young white man. In all three cases, the cause for the removal of the testes was excessive self abuse… The operation for the removal of the testes was made, in all three cases, under local anesthesia. An hour or two prior to the operation, the patients were given hypodermic injections of morphine in order to quiet them. This was followed by local injections of Novocain in the operating room. None of the patients exhibited any interest or excitement during the operation, nor did they show any signs of pain except when the vas deferens and the accompanying nerves were cut. One of the negroes went to sleep during the operation.”

[There are two noteworthy sentences in this paragraph. The first refers to the main manifestation of the mental illness, which presumably caused these unfortunate souls to be forcefully interred in the insane asylum in the first place and subsequently subjected to the inhumane experiments of Theophilus Painter and his accessories. It was self abuse, i.e., masturbation, which was regarded originally as a Biblical sin (onanism) and then as a mental disease or as a cause of mental disease (e.g., Hagenbach 1879).

The second noteworthy sentence is the last one. It encapsulates a common racist canard used by slave owners since the 17th century, according to which black people are impervious to pain and can therefore be mistreated, beaten, and mutilated (Villarosa 2019). Many scientists, including Harvard’s rabid anti-Darwinian zoologist, Louis Agassiz, provided scientific support for this claim. Painter’s statement concerning “one of the negroes” falling asleep during the operation can be understood in this context.]

In 1923, Painter published his article. His conclusions were simple and straightforward: The spermatogonia of both the white man and the negroes has 48 chromosomes. Two of these chromosomes, X and Y, are unpaired.

And that was it.

For 33 years, from 1923 to 1956, every microscope-peering Tom, Dick and Harry saw the wrong number of chromosomes. For example, in 1947, P. C. Koller from the Royal Cancer Hospital in London noted that while some tumor cells exhibited great variation in chromosome number, many of them, such as cervical carcinoma cells retained “the normal 48 chromosomes.”

In 1934 Painter was awarded the Daniel Giraud Elliot Medal from the National Academy of Sciences for “meritorious work in zoology or paleontology.” Named after founder of the American Ornithologist Union, the medal was first awarded in 1917, and has since been awarded at irregular intervals.**

In 1955, Joe Hin Tjio, a Chinese-Indonesian working in the lab of Albert Levan at the University of Lund, perfect some advanced techniques to visualize chromosomes in human somatic cells. By using these techniques he discovered that humans have 46 chromosomes. With Tjio and Levan (1956), the human chromosome number was finally corrected. According to Trask (2002), the field of human cytogenetics was launched in 1956 with the following hesitant statement.

“Before a renewed, careful control has been made of the chromosome number in spermatogonial mitoses of man, we do not wish to generalize our present findings into a statement that the chromosome number of man is 2n = 46, but it is hard to avoid the conclusion that this would be the most natural explanation of our observations.”

Some postscripts to Painter (1923)

In 1925, Theophilus Painter published a comparative study of chromosome numbers in mammals. There is one feature in Painter (1925) that is quite troubling. Despite the fact that he could not find differences between whites and blacks, he continued to report the identical results separately. It was as if he couldn’t believe that such different creatures have the same number of chromosomes.

Painter continued to publish scientific articles on chromosomes for the rest of his career. In fact, his last contribution was published two years after his death. Interestingly, he never mentioned Tjio and Levan (1956).

In the 1980s, T. C. (Tao-Chiuh) Hsu at the M.D. Anderson Cancer Center in Huston, Texas, reexamined some of the original preparation, on the basis of which Painter based his erroneous chromosome count. According to Painter's biographer Bentley Glass, Hsu found chromosomes that stuck together or clumped, chromosomes cut into segments by the microtome knife, and other artifacts which made it hard to tell how anyone can get any chromosome count out of these misshapen slides, let alone a clear chromosome count.

The continuing reporting of the incorrect chromosome count in the 1923–1956 period was attributed to “preconception” (Kottler 1974). The number was supposed to be 48, so subsequent investigators did everything possible to make their counts 48. Preconception aside, I am puzzled by the lack of criticisms of the drawings published by Painter. As everyone can see, it is impossible to tell how many chromosomes are in the drawing. I would agree that preconception was an important impediment to the delayed discovery of the correct human chromosome number, but I think that the reluctance to criticize so-called scientific authorities might have been equally important in thwarting scientific progress.

Academic freedom

In 1939, the board of regents of the University of Texas named Homer P. Rainey, a former President of Franklin College and Bucknell University as the 12th President of University of Texas, at the time not only the largest university in Texas, but the entire southern half of the United States. The makeup of the board of regents, however, soon changed due to appointments over the next several years by two extremely reactionary governors (even by Texas standards at the time), W. Lee O'Daniel and Coke R. Stevenson. The Board started to clash with Rainey in 1941, when several members of the Board pressured Rainey to fire four full professors of economics who espoused New Deal views. In 1942 the regents fired three untenured economics instructors and a fourth who had only a one-year appointment for having attempted to defend federal labor laws at an antiunion meeting in Dallas. Rainey protested their dismissals, and also protested the fact that tenure was weakened and funding for social science was cut completely. His communications to the Board of Regents were answered most rudely. For instance, Regent D. F. Strickland wrote Rainey that the president of the University of Texas had “no business suggesting anything to the regents” and that “if the abolition of tenure would make it more difficult to recruit out-of-state professors, Texas would be better off.” The most spectacular single issue dividing Rainey from the regents was the board's repression of John Dos Passos's USA and its efforts to fire the professor who placed the third volume of the trilogy on the English department's sophomore reading list. The regents deemed the work subversive and perverted. Since the selection had been a committee decision, however, no one was fired, but Rainey was outraged at what he believed to be a witch-hunt. All this, along with the fact that he tried to move the Medical Branch from Galveston to Austin a couple years earlier, cause the board to fire him on November 1, 1944, without citing any reason.

After the firing, 8,000 students went on strike and protested in the campus and at the state capitol. Less than three months after Rainey's firing, the governor appointed new board members. While the new members increased funding for social science and rehired the aforementioned fired professors, they did not re-hire Rainey. Several organizations, including the American Association of University Professors, the Southern Association of Colleges and Secondary Schools, and Phi Beta Kappa, reprimanded the university for firing Rainey. The censorship by the American Association of University Professors lasted nine years, until the organization was convinced that the regents changed their policies.

Enter Theophilus Painter. Following the dismissal of the university president who had defended academic freedom, the Regents of the University looked for a caretaker who could be expected to refrain from political action (or any other action) and at the same time would be of high academic reputation. A committee of three members of the faculty met with the Regents in order to make suggestions for a resolution of the difficulties, and Painter was one of the three.

Painter recalled that he was asleep, when he was asked to return to the meeting with the Board of Regents. He was asked to become the acting president of the university and like a damsel in distress he “reluctantly” agreed, despite the fact that “his research program was at a critical stage.” Later, Painter agreed to serve as president with the stipulation that the term would last only until a satisfactory president could be found. It took 8 years for the university to find a satisfactory president.

During these years, Theophilus Painter obediently and somewhat offhandedly carried the oppressive, racist, misogynist, and discriminatory policies of the Texas Governors and their appointees at University of Texas Board of Regents. The question of academic freedom seems not to have been raised again during his reign, but of course these were the heydays of McCarthyism and academic freedom was not a priority. Of particular interest is Painter’s undermining all attempts by black students to enter the University of Texas. As a consequence, he will forever be known as the small-minded racist bureaucrat in Sweatt v. Painter.

Sweat v. Painter

Painter was president of the University of Texas when Texas resident Heman Marion Sweatt applied for and was denied admission to the Law School due to his race. Subsequently, Painter was the named defendant in the civil rights case Sweatt v. Painter, 339 U.S.629 (1950), which proved an integral stepping stone in the landmark case Brown v. Board of Education of Topeka, Kansas 347 U.S. 483 (1954), that held that "separate is inherently unequal" and led to the integration of America's public schools.

The "separate but equal" doctrine of racial segregation was established in the 1896 case of Plessy v. Ferguson 163 U.S. 537 (1896), in which a majority of seven justices upheld the constitutionality of racial segregation laws for public facilities as long as the segregated facilities were equal in quality. A single justice dissented, while another decided not to take part in the case. The decision legitimized the many state laws reestablishing racial segregation that had been passed in the American South after the end of the Reconstruction Era (1865–1877).

The underlying case originated in 1892 when Homer Plessy, an "octoroon" (person of seven-eighths white and one-eighth black ancestry) resident of New Orleans, deliberately violated Louisiana's Separate Car Act of 1890, which required "equal, but separate" train car accommodations for white and non-white passengers.

In May 1896, the Supreme Court issued a 7–1 decision against Plessy ruling that the Louisiana law did not violate the Fourteenth Amendment to the U.S. Constitution, stating that although the Fourteenth Amendment established the legal equality of white and black Americans, it did not and could not require the elimination of all social or other "distinctions based upon color". The Court rejected Plessy's lawyers' arguments that the Louisiana law inherently implied that black people were inferior

“We consider the underlying fallacy of the plaintiff's argument to consist in the assumption that the enforced separation of the two races stamps the colored race with a badge of inferiority. If this be so, it is not by reason of anything found in the act, but solely because the colored race chooses to put that construction on it.”

So, there you have it. Enforced racial segregations has nothing to do with discrimination. If blacks are considered inferior it is because blacks decided that they are inferior. Plessy v. Ferguson is widely regarded as one of the worst decisions in U.S. Supreme Court history. Despite its infamy, the decision itself has never been explicitly overruled.

Sweatt v. Painter involved a black man, Heman Marion Sweatt, who was refused admission to the School of Law of the University of Texas, whose president was Theophilus Painter, on the grounds that the Texas State Constitution prohibited integrated education.

On February 26, 1946, Sweatt and Painter, along with representatives from the NAACP and other university officials, met at University of Texas Main Building. Sweatt presented his college transcript to Painter and asked for admission to the law school. Painter said that the school could not officially accept the transcript for consideration, but that he would seek counsel from the state's attorney general.

In a letter to Texas Attorney General Grover Sellers, Painter wrote: "This applicant is a citizen of Texas and duly qualified for admission to the Law School at the University of Texas, save and except for the fact that he is a negro." In a response that came several weeks later, Attorney Sellers upheld the constitutionality of segregation in education, but added that if separate but equal facilities could not be provided, Sweatt must be admitted to the law school of University of Texas. Painter, as was his life-long habit, decided to do nothing that will enrage the governor and the board of regents. In May 1946, Sweatt filed a case against Painter and the university in the county court. Among those representing him: a lawyer from the NAACP Legal Defense Fund named Thurgood Marshall.

According to law and given that no school for black people existed in Texas, the Travis County district judge should have granted the plaintiff a right of mandamus, i.e., ordered the University of Texas to properly fulfill their official duties and admit Sweatt to the Law School. Instead, Painter and the Travis County Judge conspired to drag the case for six more months, during which they tried to bribe Sweatt with the promise of covering his tuition at a school outside of Texas. When this ploy failed, the state hastily created a law school for black students only, which it established in Houston at the Texas State University for Negroes (now Texas Southern University). The judge, then, ruled that Sweatt has no reason to sue, since “a separate and equal school” exists in Texas. This ridiculous decision was affirmed by the Court of Civil Appeals, the Texas Supreme Court, and several federal courts.

The case ultimately reached the US Supreme Court. Robert Carter and Thurgood Marshall presented Sweatt's case. The case rested on the fact that the two schools were not even comparable, let alone equal. The University of Texas Law School had 16 full-time and 3 part-time professors, while the black law school had 5 full-time professors. The University of Texas Law School had 850 students and a law library of 65,000 volumes, while the black law school had 23 students and a library of 16,500 volumes.

Thurgood Marshall would go on to build a case around the idea of intangibles. Beyond differences in square footage of classrooms and numbers of faculty, course offerings, and books in the library, a separate facility for black students lacked opportunities to debate ideas with other students, a critical part of learning.

"The modern law school is operated so the student can understand ideas of all stratas of society, so he can go out and be of service to his community, his state and his nation," argued Marshall, a future Supreme Court justice.

On June 5, 1950, the court ruled unanimously that under the Equal Protection Clause, Sweatt must be admitted to the university. Chief Justice Fred Vinson referenced intangibles in the opinion:

"The law school, the proving ground for legal learning and practice, cannot be effective in isolation from the individuals and institutions with which the law interacts. Few students and no one who has practiced law would choose to study in an academic vacuum, removed from the interplay of ideas and the exchange of views with which the law is concerned."The Supreme Court reversed the lower court decision, saying that the separate school failed to qualify, both because of quantitative differences in facilities and experiential factors, such as its isolation from most of the future lawyers with whom its graduates would interact. The court held that, when considering graduate education, experience must be considered as part of "substantive equality."

Sweatt enrolled at the law school that fall, but dropped out before completing his second year. His legal struggles affected his health and his marriage. He later earned a masters degree in social work from Atlanta University and went on to have a career with the Urban League. He died in 1982.

On June 14, 2005, the Travis County Commissioners voted to rename the courthouse as the Heman Marion Sweatt Travis County Courthouse in honor of Sweatt's endeavor and victory.

And what about Theophilus Painter? Nothing of note happened to him afterwards. He returned to his lab, continued to publish insignificant papers, and died of old age on returning from a hunting trip.

The purpose of this note is to remind young people of an unsavory character in the history of genetics and to ask them to look around for small minded Painters, recognize their bigotry, and expose their vileness.

Notes

*In the literature, three versions of the name are found: Hans de Winiwarter (French), Hans van Winivarter (Flemish), and Hans Winivarter. This is most probably due to the fact that the guy was Belgian, so he used both the French honorific “de” and the Flemish honorific “van.”

**The last medal recipient was Günter P. Wagner (2018).

References

de Winiwarter, H. 1921. La formule chromosomale dans l’espèce humaine. C. R. Seances Soc. Biol. Fil. 85:266 –267. Ford CE, Hamerton JL. 1956. The chromosomes of man. Nature 178:1020–1023. Gartler S.M. 2006. The chromosome number in humans: A brief history. Nature Rev. Genet. 7:655–660. Glass B. 1990. Theophilus Painter (1889–1969): A Biographical Memoir. National Academy of Sciences, Washington DC ((http://www.nasonline.org/publications/biographical-memoirs/memoir-pdfs/painter-theophilus-shickel.pdf). Hagenbach AW. 1879. Masturbation as a cause of disease. Journal Nerv. Mental Dis. 6:603-612. Hansemann D. 1891. Über pathologische Mitosen. Arch. Pathol. Anat. Physiol. 123:356-370. Koller PC. 1947. Abnormal mitosis in tumours. Brit. J. Cancer 1:38–47. Kottler MJ. 1974. From 48 to 46: Cytological technique, preconception and the counting of the human chromosomes. Bull. Hist. Med. 48:465–502. Painter TS. 1923. Studies in mammalian spermatogenesis. II: The spermatogenesis of man. J. Exp. Zool. 37:291–336. Painter TS. 1925. A comparative study of the chromosomes of mammals. Am. Nat. 59:385-409. Painter TS. 1971. Chromosomes and genes viewed from a perspective of fifty years of research. Stadler Symp. 1-2: 33-42. Ruddle FH. 2004. Theophilus Painter: First steps toward an understanding of the human genome. J. Exp. Zool. 301A:375–377 Tjio JH, Levan A. 1956. The chromosome number of man. Hereditas 42:1–6 Trask BJ. 2002. Human cytogenetics: 46 chromosomes, 46 years and counting. Nature Rev. Genet. 3:769–778 van Winiwarter H. 1912. Études sur la spermatogenèse humaine. Arch. Biol. 27: 91-189. Villarosa L. 2019. Myths about physical racial differences were used to justify slavery—and are still believed by doctors today. https://www.nytimes.com/interactive/2019/08/14/magazine/racial-differences-doctors.html

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