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Jul 23 2014

AtheistTV, next week

I hope AtheistTV is good — they’ve announced they’ll be putting 50 years worth of their video archives on there, so I’m hoping for some interesting content. On the other hand, if it’s recycling crap from youtube as a fast way to get lots of noise online, well…it could get embarrassing. There has to be some quality control, somewhere.

I’ll check it out next Tuesday and let you know what’s on.

Jul 22 2014

Big News: God was not a Klingon

Poor Ken Ham: the media has been distorting his words. They claim that he said all the space aliens are damned to hell. He did not! He plainly said:

And I do believe there can’t be other intelligent beings in outer space because of the meaning of the gospel.

See? They aren’t going to hell, because they don’t exist. He continues with a beautiful example of fundagelical creologic:

You see, the Bible makes it clear that Adam’s sin affected the whole universe. This means that any aliens would also be affected by Adam’s sin, but because they are not Adam’s descendants, they can’t have salvation. One day, the whole universe will be judged by fire, and there will be a new heavens and earth. God’s Son stepped into history to be Jesus Christ, the “Godman,” to be our relative, and to be the perfect sacrifice for sin—the Savior of mankind.

Jesus did not become the “GodKlingon” or the “GodMartian”!  Only descendants of Adam can be saved.  God’s Son remains the “Godman” as our Savior.  In fact, the Bible makes it clear that we see the Father through the Son (and we see the Son through His Word).  To suggest that aliens could respond to the gospel is just totally wrong.

An understanding of the gospel makes it clear that salvation through Christ is only for the Adamic race—human beings who are all descendants of Adam.

Now that’s impressive arrogance and delusions of grandeur. So there are 1011 galaxies and almost 1023 stars in the universe, and they’re all entirely empty of intelligent life, and they’re all going to be burned away and discarded when a Magic Jew comes reappears on Planet Earth. We know this because of an ancient book written by people who thought the earth was flat and the sky was held up on pillars.

Ooooookay.

Jul 22 2014

Can someone dig up the corpse of Norman Vincent Peale and drive a stake through its heart?

He’s still stalking about, giving the complacent a lie to shut the dissatisfied up. No, positive thinking doesn’t work; affirmations have no power; The Secret is a scam. The @SciCareer guy put his foot in it again by touting some paper titled “Happy Thoughts May Help Postdocs Handle Stress.” As you might guess, the reactions of young academics aren’t exactly enthusiastic.

Are you for actual serious with this?? The article describes a new study–and I use this word lightly because it’s based on a one-time survey of 200 postdocs–that found less anxiety and depression in folks who self-reported more frequent positive emotions. So, not only do we have a clear correlation vs. causation issue here – who can say that it was the positive emotions that prevented the development of clinical symptoms and not vice versa – but it belittles the many real stressful problems that postdocs face that cannot simply be "thought" away.

The real money quote is this:  "When we suggest that people need more positive emotions in their lives, I know it sounds kind of frou-frou, but it’s actually a very simple practice.” OK. a) I don’t think you know what frou-frou means (frilly or ornamented, not fluffy or insubstantial, which is what you probably mean and you’d be right). b) No, it is not simple. Postdocs have personal, financial, and professional stresses on a daily basis. They are busy as fuck. To suggest that watching a sit-com or going for a run can change that reality not only presumes they have time for something like that, but has very strong undertones of "stop complaining and just change your attitude."

Anger is fuel for change, “positive thinking” is a worthless analgesic for the masses. Get angry, and do something about it.

Jul 22 2014

Commitment

Jonathan Eisen is walking the walk, turning down an endowed lecture opportunity because of their gender imbalance.

Thank you so much for the invitation and the respect it shows to me that I would be considered for this.  However, when I looked into past lectures in this series I saw something that was disappointing.  From the site XXXX where past lectures are listed I see that the ratio of male to female speakers is 14:3.  I note – the XXXX lecture series – also from XXXX – also has a skewed ratio (11:2).  As someone who is working actively on multiple issues relating to gender bias in science, I find this very disappointing.  I realize there are many issues that contribute to who comes to give a talk in a meeting or seminar series or such. But I simply cannot personally contribute to a series which has such an imbalance and I would suggest that you consider whether anything in your process is biased in some way. 

Sincerely, 

Jonathan Eisen

Jul 22 2014

Caricature, corrected

MRA’s have been sending me this video they’re very excited about — it’s done by a pretty young woman who comically repeats every stupid stereotype of feminists by anti-feminists everywhere. Did you know feminists don’t want you to be young and slender and pretty, and you shouldn’t wear makeup or pretty clothes, and most of them hate men, and it’s all about competing to see who is most oppressed? We don’t need feminism any more, because men and women are already equal in all things, and besides, she has never experienced any discrimination, so nobody else can have. It is funny. Funnily bad.

I thought about writing a rebuttal, but shortly I have to go to work, and it would take hours to dismantle it nonsensical misconception by outright flaming stupidity, sentence by sentence. There’s so much of it.

Fortunately, I don’t have to. One of the sensible people who sends me things (They exist! Really, my in-box isn’t just a shitstorm of derp. Usually.) sent me this most excellent common sense general defense of feminism by the Bloggess, so I’ll just tell you all to go read that instead.

Feminism is inherently good.  It’s not even close to perfect and still needs lots of work and sometimes it gets all fucked up and backward and awful but that doesn’t mean it’s not still worth fighting for.  Now go back and replace “Feminism” with “The human race”.  It works, right?.  That’s because feminists are made of human.  Men and women.  In fact, one of my favorite feminists is Sir Patrick Stewart.

Patrick Stewart, feminist. His mother made 3 pounds 10 shillings for working a forty hour week in a weaving shed. She was also an abuse victim and he’s an anti-domestic violence advocate.

Patrick Stewart, feminist. His mother made 3 pounds 10 shillings for working a forty hour week in a weaving shed. She was also an abuse victim and he’s an anti-domestic violence advocate.

I’m not saying you can’t choose to not be a feminist but know what you’re choosing.  Don’t make a decision about a group based on the most radical beliefs of a group.  Don’t get defensive if you get deeper and are exposed to difficult ideas about intersectionality and race and gender and colonialism and patriarchy and male liberation.  Just listen.  Some of it will make sense.  Some of it won’t.  Some of it will later when you’re a different person.  Some of it you’ll change your mind about throughout your life and the world will change too.  Some of it is bullshit.  Some of it is truth.  All of it is worth listening to.

And now you get to decide.  Are you a feminist?  Yes?  No?  Well, don’t worry because tomorrow you get to choose again.  And that keeps happening every day for the rest of your life.

As for me, I am a feminist (among so, so many other things).  I believe in equality and I think we still have work to do.  I’m thankful to the men and women who worked to give me the freedom and rights I have today and I am proud to be a part of a movement that I hope will make the world better and safer for my daughter (and for the men and women she’ll share that world with).  I’m happy we’ve come so far and I’m glad that we’re becoming more aware of feminist issues that don’t just focus on straight, white women, even though confronting those issues is sometimes painful. And I’m happy that the womenagainstfeminism tumblr exists.  Because even though I disagree with most of them I’m glad that those women have a platform on which to speak, and also because if we know what the arguments or misperceptions are against feminism then we can better address them.  Or agree with them.  Or ignore them.  Or discuss them with our sons and daughters so they can make informed decisions for themselves.  It’s up to you.

That pretty young woman’s video? The most important part of the description is that she’s young. I hope she grows up to be just like the Bloggess.

Jul 22 2014

Those sneaky forms of academic bias…

It’s Tuesday…that must mean it’s “Let’s point out flaws in the academic system!” day.

Here’s another example: some investigators did a study of the value of screening cancer patients for distress — they asked whether such screening actually contributed to patient’s feelings of well-being and willingness to follow medical recommendations, and whether it was cost-effective. Their answer was no on all counts. Kudos to the Journal of Clinical Oncology for publishing a negative result.

Raspberries to the Journal of Clinical Oncology for what they did next, though. They brought in a proponent of screening to write a dismissal of the study.

Hollingsworth and colleagues were surely disappointed to discover that their article was accompanied by a negative editorial commentary. They had not been alerted or given an opportunity to offer a rebuttal. Their manuscript had made it through peer review, only to get whomped by a major proponent of screening, Linda Carlson.

After some faint praise, Carlson tried to neutralize the negative finding

despite several strengths, major study design limitations may explain this result, temper interpretations, and inform further clinical implementation of screening for distress programs.

And if anyone tries to access Hollingworth’s  article through Google Scholar or the Journal of Clinical Oncology website, they run smack into a paywall. Yet they can get through to Carlson’s commentary without obstruction and download a PDF for free.  So, easier to access the trashing of the article than the article itself. Doubly unfair!

Why we need open access, reason #21035.

I also found it interesting that the critical opinion piece had references…but most were to the author, or lab groups that had published with the author. Signs of a circle-jerk in the citations are always a warning sign.

The opinion piece also talks at length about problems with the Hollingworth paper’s protocols. I think it’s important to point out such failings, but shouldn’t they be done by editors and reviewers before publication? And why nitpick at studies that disagree with you, while ignoring major methodological flaws in your own approach?

Try this experiment: Ignore what is said in abstracts of screening studies and instead check the results section carefully. You will see that there are actually lots of negative studies out there, but they have been spun into positive studies. This can easily be accomplished by authors ignoring results obtained for primary outcomes at pre-specified follow-up periods. They can hedge their bets and assess outcome with a full battery of measures at multiple timepoints and then choose the findings that make screening looked best. Or they can just ignore their actual results when writing abstracts and discussion sections.

Especially in their abstracts, articles report only the strongest results at the particular time point that make the study looked best. They emphasize unplanned subgroup analyses. Thus, they report that breast cancer patients did particularly well at 6 months, and ignore that was not true for 3 or 12 month follow up. Clever authors interested in getting published ignore other groups of cancer patients who did not benefit, even when their actual hypothesis had been that all patients would show an improvement and breast cancer patients had not been singled out ahead of time. With lots of opportunities to lump, split, and selectively report the data, such results can be obtained by chance, not fraud, but won’t replicate.

Oh, boy, another of my peeves: fishing with statistics, gaming with your data.

Jul 22 2014

Behold the wrath of god

Remember, everything has a purpose.

Jul 22 2014

Biology is a hard problem

New genetic disorders pop up all the time — each one represents a child who may face incredible challenges, or even be doomed to death. A child named Bertrand exhibited some serious symptoms — profound developmental disabilities — shortly after he was born, and no one could figure out what was wrong with him. So they took advantage of 21st century biotechnology and sequenced his genome, and the genome of both of his parents, and asked what novel mutations the child carried.

For years, sequencing was too expensive for common use—in 2001, the cost of sequencing a single human genome was around a hundred million dollars. But by 2010, with the advent of new technologies, that figure had dropped by more than ninety-nine per cent, to roughly fifty thousand dollars. To reduce costs further, the Duke researchers, including Shashi and a geneticist named David Goldstein, planned to sequence only the exome—the less than two per cent of the genome that codes for proteins and gives rise to the vast majority of known genetic disorders. In a handful of isolated cases, exome sequencing had been successfully used by doctors desperate to identify the causes of mysterious, life-threatening conditions. If the technique could be shown to be more broadly effective, the Duke team might help usher in a new approach to disease discovery.

For their study, Shashi, Goldstein, and their colleagues assembled a dozen test subjects, all suffering from various undiagnosed disorders. There were nine children, two teen-agers, and one adult; their symptoms included everything from spine abnormalities to severe intellectual disabilities. The researchers began by sequencing each patient and both biological parents—what’s known as a parent-child trio. There are between thirty and fifty million base pairs in the human exome; the average child’s exome differs from each of his parents’ in roughly fifteen thousand spots. The researchers could dismiss most of those variations—either they corresponded to already known conditions, or they occurred frequently enough in the general population to rule out their being the cause of a rare disease, or they were involved in biological processes that were unrelated to the patient’s symptoms. That left a short list of about a dozen genes for each patient.

In Bertrand’s case, they narrowed it down to one likely gene responsible for his condition — one gene that they also found that each of his parents carried variants for, although paired in both cases with normal functional alleles. Bertrand was unlucky: he inherited one bad copy from his mother, and another bad (but different) copy from his father.

Then there was Bertrand. The Duke team thought it was likely that mutations on one of his candidate genes, known as NGLY1, were responsible for his problems. Normally, NGLY1 produces an enzyme that plays a crucial role in recycling cellular waste, by removing sugar molecules from damaged proteins, effectively decommissioning them. Diseases that affect the way proteins and sugar molecules interact, known as congenital disorders of glycosylation, or CDGs, are extremely rare—there are fewer than five hundred cases in the United States. Since the NGLY1 gene operates in cells throughout the body, its malfunction could conceivably cause problems in a wide range of biological systems.

The article points out that one of the things that has made tracking down the genetic cause of this disorder is academic competition. Lots of people are born with novel genetic disorders, and they go to their high-powered geneticist/MD, and they get parts or their entire genome sequenced, and then the sequence is kept private. This is now the doctor’s discovery: making it open knowledge would also make it likely that someone else would use it and publish it, and that they wouldn’t get credit for it. That doesn’t help patients, but it does help careers.

And that’s the next step. It’s clear that Bertrand has an anomalous form of NGLY1, but that doesn’t demonstrate that that is the cause (remember, he’s got 15,000 other variations from his parents’ genome). The clincher would be to find other kids with similar phenotypes who also had NGLY1 variants, and then you’d be relatively certain you’d found the cause. If you had lots of sequence data, you might also find people who had the NGLY1 variants but none of the disease symptoms, which would rule out NGLY1 as the cause. It’s a real problem that information gets locked up in little academic kingdoms, and is difficult to pry out without promising authorship on a paper…and who wants to be the 63rd author on a paper that has 200 contributors, anyway?

So the article ends up pointing out a flaw in poor Bertrand’s genome, and another flaw in the institution of science.

I have to point out another problem, though, and this one has been known about in genetics for a long, long time: the high visibility of mutations of large effect, and how they skew our perception of how the genome works. These mutations exist, and Bertrand’s case is an excellent example: a single point mutation wreaks global havoc on the system, causes profoundly disruptive symptoms, and draws a bulls-eye around itself to attract the attention of geneticists. But the overwhelming majority of allelic variants do nothing detectable at all — again, witness Bertrand’s 15,000 differences that were ruled out as causal — yet we can’t rule out the possibility in other genetic disorders that multiple genes are required to be messed up to trigger the problem, and that focusing on them just one at a time means you miss the causes.

We know this is the case in cancer, for instance. There are central players that frequently end up mutated to cause oncogenesis — myc, ras, and p53, for instance — but no cancer is caused by just one genetic change, and it requires multiple steps to initiate. Further, there are multiple components, each with their own likely cause: proliferation is different from suppression of apoptosis is different from metastasis, and every patient has a different genetic profile. That’s why you’re not going to find any responsible doctor claiming that they found THE gene that causes cancer and have THE cure.

But here’s another example: a large genetic study that used similar techniques to those applied to Bertrand, looking for the heritable cause for a more complex and subtle disorder, schizophrenia. They didn’t find one. They found a hundred.

One clue to this complexity, and how schizophrenia as a disease is "built", has come this week in new research published in Nature which looks at the genetic basis for the illness. In one of the largest genetic studies of its kind, a team of scientists from around the world compared the genomes of 36,989 people with schizophrenia with 113,075 control participants. They identified 128 independent genes in the people with schizophrenia, 83 of which were not known about until now.

Although this is an important study, it would be false to say that genomics work will lead to an imminent breakthrough in terms of a cure for mental illnesses. What we can do with this information is to ask better questions about what to research next in this field, for example some of the new genes identified are involved with immune processes, which provides the first real evidence for a long-held hypothesis that connects schizophrenia with immune system problems.

The medical team studying Bertrand got lucky and found a single gene as the likely source of his problems (Bertrand is not lucky at all, though: that we know what’s wrong with him is a world away from being able to fix him). What makes people tick is a constellation of genes interacting cooperatively with one another, and you generally can’t map single genes to single phenotypic traits.

It’s going to be hard to figure that out. That’s why we need more biologists!

Jul 21 2014

Mary’s Monday Metazoan: Cruel flower

This flower, over many generations, has warped the poor buff-tail sicklebilled hummingbird’s beak into that bizarre curve.

Jul 21 2014

The dose makes the poison

Princeton physicist William Happer is still getting invited on television to say stupid things.

I keep hearing about the "pollutant CO2," or about "poisoning the atmosphere" with CO2, or about minimizing our "carbon footprint." This brings to mind another Orwellian pronouncement that is worth pondering: "But if thought corrupts language, language can also corrupt thought." CO2 is not a pollutant and it is not a poison and we should not corrupt the English language by depriving "pollutant" and "poison" of their original meaning….CO2 is absolutely essential for life on earth.

Did you know oxygen, while not a poison at standard concentrations, is highly reactive and will kill you at high concentration? Or that CO2 is vital for plants and is measured to regulate your breathing, but too much and you’ll suffocate?

What makes a substance poisonous is how much of it there is. Paracelsus figured this out in the 16th century. So Princeton physicists are unaware of developments and explanations that predate even Newton? That’s kind of amazing.

Maybe CNBC and other networks ought to take a lesson from the BBC on ginned up controversies and false dichotomies, and cut this bozo Happer from their invitation list.

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