Your blood is better than my blood

Siamese tomatoes. Taken from here.

Parabiosis is a surgical procedure that lets two animals to share the same blood; it’s a case of reverse conjoined twins restricted to the circulatory system.

The procedure is over 150 years old and is a useful technique in physiology, though rarely used, probably due to the perceived cruelty towards the animals, although today is performed under anesthesia and aseptic condition. It delivered good data; for example, it was a parabiosis experiment with rodents that showed is not the sugar in the blood that causes cavities but the sugar in the mouth. Similarly, parabiosis has been proven useful in cancer, diabetes, and ageing research.

Scudellari (2015) wrote a News piece for Nature describing some advancements in the ageing field using the parabiosis technique. Namely, by joining the circulatory systems of a young and an old mouse, researchers have observed that the old mouse is faster, smarter, with rejuvenated muscles and glossier fur. Now the race is to find out what in the blood does it. Researchers caution that the young blood is not effectively reversing ageing, but may have factors circulating in it that promote tissue repair. Already a muscle-rejuvenating protein has been identified.

I am not going through the original papers themselves as I usually do (they are provided as links in the Reference paper). Instead, I am featuring the news piece by Scudellari because in addition of looking at parabiosis and ageing result, it also provides a nice historical account of the use of parabiosis. Enjoy!

Reference: Scudellari, M. (22 Jan 2015). Ageing research: Blood to blood. Nature, 517: 426-429. Article | FREE Fulltext PDF

By Neuronicus, 4 January 2015

Beer spoiling bacteria, oh no! But we know now how you’re made, suckers!

64 - Copy

Over 250 years ago today, on 31 December 1759, Arthur Guinness started brewing one of the most loved adult drinks today, the Guinness beer.

As with all food and drink products, beer can be also suffer spoiling due to various bacteria. The genomes of two of these culprits – Megasphaera cerevisiae PAT 1T and Lactobacillus brevis BSO 464 – have been sequenced in 2015 by two different groups.

Funny thing though: the papers that announce the completion of the genome sequencing (see bellow References) do not talk abut the significance of their discovery. The usual template for a biology paper (or as a matter of fact any science paper) is:

Introduction: x is important because y,
Methods and Results: here is what we did to understand x,
Conclusion: now we can better tackle y.

Not these papers, which basically say, in less than a page: “This bacterium spoils beer; here is its genome. You’re welcome!”

Well played, geneticists, well played… And we are, indeed, grateful. Oh, yes, we are…


1. Kutumbaka KK, Pasmowitz J, Mategko J, Reyes D, Friedrich A, Han S, Martens-Habbena W, Neal-McKinney J, Janagama HK, & Nadala C, Samadpour M (10 Sep 2015). Draft Genome Sequence of the Beer Spoilage Bacterium Megasphaera cerevisiae Strain PAT 1T. Genome Announcements, 3(5). pii: e01045-15. doi: 10.1128/genomeA.01045-15. Article | FREE Fulltext PDF | FREE GENOME

2. Bergsveinson J, Pittet V, Ewen E, Baecker N, & Ziola B (3 Dec 2015). Genome Sequence of Rapid Beer-Spoiling Isolate Lactobacillus brevis BSO 464. Genome Announcements, 3(6). pii: e01411-15. doi: 10.1128/genomeA.01411-15. Article | FREE Fulltext PDF | FREE GENOME

By Neuronicus, 31 December 2015

I am blind, but my other personality can see


This is a truly bizarre report.

A woman named BT suffered an accident when she was 20 years old and she became blind. Thirteen year later she was referred to Bruno Waldvogel (one of the two authors of the paper) for psychotherapy by a psychiatry clinic who diagnosed her with dissociative identity disorder, formerly known as multiple personality disorder.

The cortical blindness diagnosis has been established after extensive ophtalmologic tests in which she appeared blind but not because of damage to the eyes. So, by inference, it had to be damage to the brain. Remarkably (we shall see later why), she had no oculomotor reflexes in response to glare. Moreover, visual evoked potentials (VEP is an EEG in the occipital region) showed no activity in the primary visual area of the brain (V1).

During the four years of psychotherapy, BT showed more than 10 distinct personalities. One of them, a teenage male, started to see words on a magazine and pretty soon could see everything. With the help of hypnotherapeutic techniques, more and more personalities started to see.

“Sighted and blind states could alternate within seconds” (Strasburger & Waldvogel, 2015).

The VEP showed no or very little activity when the blind personality was “on” and showed normal activity when the sighted personality was “on”. Which is extremely curious, because similar studies in people with psychogenic blindness or anesthetized showed intact VEPs.

There are a couple of conclusions from this: 1) BT was misdiagnosed, as is unlikely to be any brain damage because some personalities could see, and 2) Multiple personalities – or dissociate identities, as they are now called – are real in the sense that they can be separated at the biological level.

The visual pathway that mediates conscious visual perception. a) A side view of the human brain with the retinogeniculocortical pathway shown inside (blue). b) A horizontal section through the brain exposing the same pathway.

Fascinating! The next question is, obviously, what’s the mechanism behind this? The authors say that it’s very likely the LGN (the lateral geniculate nucleus of the thalamus) which is the only relay between retina and V1 (see pic). It can be. Surely is possible. Unfortunately, so are other putative mechanisms, as 10% of the neurons in the retina also go to the superior colliculus, and some others go directly to the hypothalamus, completely bypassing the thalamus. Also, because it is impossible to have a precise timing on the switching between personalities, even if you MRI the woman it would be difficult to establish if the switching to blindness mode is the result of a bottom-up or a top-down modulation (i.e. the visual information never reaches V1, it reaches V1 and is suppressed there, or some signal form other brain areas inhibits V1 completely, so is unresponsive when the visual information arrives).

Despite the limitations, I would certainly try to get the woman into an fMRI. C’mon, people, this is an extraordinary subject and if she gave permission for the case study report, surely she would not object to the scanning.

Reference: Strasburger H & Waldvogel B (Epub 15 Oct 2015). Sight and blindness in the same person: Gating in the visual system. PsyCh Journal. doi: 10.1002/pchj.109.  Article | FULLTEXT PDF | Washington Post cover

By Neuronicus, 29 November 2015

Pesticides reduce pollination

Close-up of a bee with pollen flying by a flower. Credit: Jon Sullivan. License: PD

Bees have difficult times these days, what with that mysterious colony collapse disorder on top of various viral, bacterial and parasitical diseases. Of course, the widespread use of pesticides did not help the thriving of the hive, as many pesticides have various deleterious effects on the bees, from poor foraging or less reproduction to even death.

The relatively new (’90s) class of insecticide – the neonicotinoids – has been met with great hope because has low toxic effects on birds and mammals, as opposed to the organophosphates, for example. Why that should be the case, is a mystery for me, because the neonicotinoids bind to the nicotinic receptors present in both peripheral and central nervous system in an irreversible manner, which does not put the neonicotinoids in a favorable light.

Now Stanley et al. (2015) have found that exposure to the neonicotinoid thiamethoxam reduces the pollination provided by the bumblebees to apples. They checked it using 24 bumblebee colonies and the exposure was at low levels over 13 days, trying to mimic realistic in-field exposure. The apples visited by the bumblebees exposed to insecticide had 36% reduction in apple seeds.

Almost 90% of the flowering plants need pollination to reproduce, so any threat to pollination can cause serious problems. Over the paste few years, virtually all USA corn had been treated with neonicotinoids; EU banned the thiamethoxam use in 2013. And, to make matters worse, neonicotinoids are but only one class of the many toxins affecting the bees.

Related post: Golf & Grapes OR Grandkids (but not both!)

Reference: Stanley DA, Garratt MP, Wickens JB, Wickens VJ, Potts SG, & Raine NE. (Epub 18 Nov 2015). Neonicotinoid pesticide exposure impairs crop pollination services provided by bumblebees. Nature, doi: 10.1038/nature16167. Article

By Neuronicus, 21 November 2015

Will you trust a pigeon pathologist? That’s right, he’s a bird. Stop being such an avesophobe!


From Levenson et al. (2015), doi: 10.1371/journal.pone.0141357. License: CC BY 4.0

Pigeons have amazing visual skills. They can remember facial expressions, recall almost 2000 images, recognizes all the letters of the alphabet (well, even I can do that), and even tell apart a Monet form a Picasso! (ok, birdie, you got me on that one).

Given their visual prowess, Levenson et al. (2015) figured that pigeons might be able to distinguish medically-relevant images (a bit of a big step in reasoning there, but let’s go with it). They got a few dozen pigeons, starved them a bit so the birds show motivation to work for food, and started training them on recognizing malignant versus non-malignant breast tumors histology pictures. These are the same exact pictures your radiologist looks at after a mammogram and your pathologist after a breast biopsy; they were not retouched in any way for the pigeon’s benefit (except to make it more difficult, see below). Every time the pigeon pecked on the correct image, it got a morsel of food (see picture). Training continued for a few weeks on over 100 images.

For biopsies, the birds had an overwhelming performance, reaching 99% accuracy, regardless of the magnification of the picture, and for mammograms, up to 80% accuracy, just like their human counterparts. Modifying the pictures’ attributes, like rotation, compression or color lowered somewhat their accuracy, but they were still able to score only marginally less than humans and considerably better than any computer software. More importantly, the pigeons were able to generalize, after training, to correctly classify previously unseen pictures.

Let’s be clear: I’m not talking about some fancy breed here, but your common beady-eyed, suspicious-sidling, feral-looking rock pigeon. Yes, the one and only pest that receives stones and bread in equal measures, the former usually accompanied by vicious swearings uttered by those that encountered their slushy “gifts” under the shoes, on the windshield or in the coffee and the latter offered by more kindly disposed and yet utterly naive individuals in the misguided hopes of befriending nature. Columba livia by its scientific name, at the same time an exasperating pest and an excellent pathologist! Who knew?!

The authors even suggest using pigeons instead of training and paying clinicians. Hmmm… But who do I sue if my mother’s breast cancer gets missed by the bird, in one of those 1% chances? Because somehow making a pigeon face the guillotine does not seem like justice to me. Or is this yet another plot to get the clinicians off the hook for misdiagnoses? Leave the medical profession alone, birdies – is morally sensitive as it is -, and search employment in the police or Google; they always need better performance in the ever-challenging task of face-recognition in surveillance videos.

P.S. The reason why you didn’t recognized the word “avesophobe” in the title is because I just invented it, to distinguish the hate for birds from a more serious affliction, ornithophobia, the fear of birds.

Reference: Levenson RM, Krupinski EA, Navarro VM, & Wasserman EA (18 Nov 2015). Pigeons (Columba livia) as Trainable Observers of Pathology and Radiology Breast Cancer Images. PLoS One, 10(11):e0141357. doi: 10.1371/journal.pone.0141357.  Article | FREE FULLTEXT PDF

By Neuronicus, 19 November 2015

Terrorist attacks increase the male fetal loss

effelThe odds of having a baby boy decreases after terrorist attacks, natural or man-made disasters, or economical depression. There are several studies worldwide that support this finding. This is somewhat counter-intuitive, because there are anecdotal accounts that report an increase in male births after a war, presumably to make up for the lost men.

Bruckner et al. (2010) wanted to see if this decrease in the odds of a male births, also called the secondary sex ratio, is due to a failure to conceive male babies or the male fetuses die in the womb before birth. They looked at the public databases from 1996-2002 fetal deaths and births from the U.S. National Center for Health Statistics.

The results showed that in the months following the September 11, 2001 terrorist attacks the deaths of male fetuses older that 20 weeks increased significantly. The authors make reference to the communal bereavement hypothesis, which stipulates that stress increases in persons not directly affected by a tragedy. Although the effects of stress on pregnant females is well documented, why the male fetuses seem to be more susceptible to mother’s stress is unknown.

I chose to feature this paper because of the recent Paris atrocities.

Reference: Bruckner TA, Catalano R, & Ahern J. (25 May 2010). Male fetal loss in the U.S. following the terrorist attacks of September 11, 2001. BMC Public Health.;10:273. doi: 10.1186/1471-2458-10-273. Article | FREE FULLTEXT PDF

By Neuronicus, 15 November 2015

Kinesin in axon regeneration

Fig. 8 from Lu, Lakonishok, & Gelfand (2015). License: Creative Commons 2.
Fig. 8 from Lu, Lakonishok, & Gelfand (2015). License: Creative Commons 2.

The longest neuron that a human has is from the spinal cord to the tip of the toes. As a cell, it needs various proteins in various places. How is this transport done? Surely not by diffusion, the proteins would degrade or would arrive at inopportune membrane-moments (I just coined that). Molecular motors, on the other hand, are toiling proteins which haul huge cargoes for the benefit of the cell in an incredibly ingenious manner (they have feet and sticky soles and gears and so on). Notable motors are kinesin and dynein, the former brings stuff to the terminal buttons of the axon, the latter goes in the opposite direction, to the soma. They walk on a railway-like scaffold in a very funny manner, if you are to believe the simulations. Go on, I dare you, search kinesin or dynein animation on Google or YouTube and tell me then that biology is not funny.

And because no self-respectable scientist can work with the molecular motors without adding his/her contribution to the above-mentioned wealth of animations, the paper below comes with no less than 9 movies (as online supplemental material)! Lu et al. (2015) focused their attention on the role of kinesin in injured neurons. The authors dyed several types of proteins in fly neurons and then cultured the cells in a Petri dish. And then cut their axons with a glass needle. After that, they used a really fancy microscope (and a good microscopist, you should look at their pictures) to look at what happens. Which is this: the cut activates a c-Jun N-terminal kinase cascade (the cell’s response to stress), which leads to sliding of microtubules (part of cell’s cytoskeleton), which is com­pletely dependent on kinesin-1 heavy chain. This sliding initiates axonal regeneration (see picture).

I believe the kinesins and dyneins are the most charming, funny, and endearing proteins out there. Yes, I’m anthropomorphizing clumps of amino acids. I know, I’m a geek.

Reference: Lu W, Lakonishok M, & Gelfand VI (1 Apr 2015, Epub 5 Feb 2015). Kinesin-1–powered microtubule sliding initiates axonal regeneration in Drosophila cultured neurons. Molecular Biology of the Cell, 26(7):1296-307. doi: 10.1091/mbc.E14-10-1423. Article | FREE FULLTEXT PDF | Supplemental movies

Some youtube videos I mentioned before, quite accurate, too: best in show

by Neuronicus, 12 November 2015

Putative mechanism for decreased spermatogenesis following SSRI

fishThe SSRIs (selective serotonin reuptake inhibitors) are the most commonly prescribed antidepressants around the world. Whether is Prozac, Zoloft or Celexa, chances are that 1 in 4 Americans (or 1 in 10, depending on the study) will be making a decision during their lifetime to start an antidepressant course or not. And yet adherence to treatment is significantly low, as many people get off the SSRI due to their side effects, one of the main complains being sexual dysfunction in the form of low libido and pleasure.

Now a new study finds a mechanism for an even more worrisome effect of citalopram, (Celexa), an SSRI: the reduction of spermatogenesis. Prasad et al. (2015) used male zebrafish as a model and exposed them to citalopram in 3 different doses for 2- or 4-weeks period. They found out that the expression in the brain of the serotonin-related genes (trp2 and sert) and gonadotropin genes (lhb, sdhb, gnrh2, and gnrh3) were differently affected depending on the dose and durations of treatment. In the testes, the “long-term medium- and high-dose citalopram treatments displayed a drastic decrease in the developmental stages of spermatogenesis as well as in the matured sperm cell count” (p. 5). The authors also looked at how the neurons are organized and they found out that the serotonin fibers are associated with the fibers of the neurons that release gonadotropin-releasing hormone 3 (GnRH3) in preoptic area, a brain region in the hypothalamus heavily involved in sexual and parental behavior in both humans and fish.

Shortly put, in the brain, the citalopram affects gene expression profiles and fiber density of the serotonin neurons, which in turn decreases the production of GnRH3, which may account for the sexual dysfunctions that follow citalopram. In the testes, citalopram may act directly by binding to the local serotonin receptors and decrease spermatogenesis.

Reference: Prasad P, Ogawa S, & Parhar IS. (Oct 2015, Epub 8 Jul 2015). Serotonin Reuptake Inhibitor Citalopram Inhibits GnRH Synthesis and Spermatogenesis in the Male Zebrafish. Biololy of Reproduction. 93(4):102, 1-10. doi: 10.1095/biolreprod.115.129965. Article | FREE FULLTEXT PDF

By Neuronicus, 11 November 2015

The culprit in methamphetamine-induced psychosis is very likely BDNF

Psychoses. Credit: NIH (Publication Number 15-4209) & Neuronicus.
Psychoses. Credit: NIH (Publication Number 15-4209) & Neuronicus. License: PD.

Methamphetamine prolonged use may lead to psychotic episodes in the absence of the drug. These episodes are persistent and closely resemble schizophrenia. One of the (many) molecules involved in both schizophrenia and meth abuse is BDNF (brain derived neurotrophic factor), a protein mainly known for its role in neurogenesis and long-term memory.

Lower BDNF levels have been observed in schizophrenia, therefore Manning et al. (2015) wondered if it’s also involved in meth-induced psychosis. So they got normal mice and mice that were genetically engineered to express lower levels of BDNF. They gave them meth for 3 weeks, with escalating doses form one week to the next. Interestingly, no meth on weekends, which made me rapidly scroll to the beginning of the paper and confirm my suspicion that the experiments were not done in USA; if they were, the grad students would not have had the weekends off and mice would have received meth every day, including weekends. Look how social customs can influence research! Anyway, social commentary aside, after the meth injections, the researchers let the mice untroubled for 2 more weeks. And then they tested them on a psychosis test.

How do you measure psychosis in rodents? By inference, since the mouse will not grab your coat and tell you about the newly appeared hypnotizing wall pattern and the like. Basically, it was observed that psychotic people have a tendency to walk in a disorganized manner when given the opportunity to explore, a behavior that was also observed in rodents on amphetamines. This disorganized walk can be quantifies into an entropic index, which is thought to reflect occurrence of psychosis (I know, a lot of inferring. But you come up with a better model of psychosis in rodent!).

Manning et al. (2015) gave their mice amphetamine to mimic psychosis and then observed their behavior. And the results were that the genetically engineered mice to express less BDNF showed reduced psychosis (i.e. had a lower entropic index). In conclusion, the alteration of the BDNF pathway may be responsible for the development of psychosis in methamphetamine users.

Reference: Manning EE, Halberstadt AL, & van den Buuse M. (Epub 9 Oct 2015). BDNF-Deficient Mice Show Reduced Psychosis-Related Behaviors Following Chronic Methamphetamine. International Journal of Neuropsychopharmacology, 1–5. doi: 10.1093/ijnp/pyv116. Article | FREE FULLTEXT PDF

By Neuronicus, 9 November 2015

Hope for a new migraine medication

Headache clipart. Courtesy of ClipArtHut.
Headache. Courtesy of ClipArtHut.

The best current anti-migraine medication are triptans (5-HT1B/1D receptor agonists). Because these medications are contra-indicated in patients with a variety of other diseases (cardiovascular, renal, hepatic, etc.), the search for alternative drugs continues.

The heat- and pain-sensitive TRPV1 receptors (Transient Receptor Potential Vanilloid 1) localized on the trigeminal terminals (the fifth cranial nerve) have been implicated in the production of headaches. That is, if you activate them by, say, capsaicin, the same substance that gives the chili peppers their hotness, you get headaches (you’d have to eat an awful lot of peppers to get the migraine, though). On the other hand, if you block these receptors by triptans, you alleviate the migraines. All good and well, so let’s hunt for some TRPV1 antagonists, i.e. blockers. But, as theory often doesn’t meet practice, the first two antagonists that were tried were dropped in the clinical trials for lack of efficiency.

Meents et al. (2015) are giving another try to two different TRPV1 antagonists, by their fetching names of JNJ-38893777 and JNJ-17203212, respectively. Because you cannot ask a rat if it has a headache, it is very difficult to have a rodent model for migraine. Instead, researchers focused on giving rats some inflammatory soup directly into the subarachnoid space or capsaicin directly into the carotid artery, actions which they have reasons to believe produce severe headaches and some biological changes, like increase in a certain gene expression (c-fos, if you must know) in the trigeminal brain stem complex and release of the neurotransmitter calcitonin gene-related peptide (CGRP).

JNJ-17203212 got rid of all those physiological changes in a dose-dependent manner, presumably of the migraine, too. The other drug, JNJ-38893777, was effective only on the highest dose. Give these drugs a few more tests to pass, and off to the clinical trials with them. I’m joking, it takes a lot more research than just a paper between discovery and human drug trials.

Reference: Meents JE, Hoffmann J, Chaplan SR, Neeb L, Schuh-Hofer S, Wickenden A, & Reuter U (December 2015, Epub 24 June 2015). Two TRPV1 receptor antagonists are effective in two different experimental models of migraine. The Journal of Headache and Pain. 16:57. doi: 10.1186/s10194-015-0539-z. Article | FREE FULLTEXT PDF

By Neuronicus, 8 November 2015

Is religion turning perfectly normal children into selfish, punitive misanthropes? Seems like it.

Screenshot from
Screenshot from “Children of the Corn” (Director: Fritz Kiersch, 1984)

The main argument that religious people have against atheism or agnosticism is that without a guiding deity and a set of behaving rules, how can one trust a non-religious person to behave morally? In other words, there is no incentive for the non-religious to behave in a societally accepted manner. Or so it seemed. Past tense. There has been some evidence showing that, contrary to expectations, non-religious people are less prone to violence and deliver more lenient punishments as compared to religious people. Also, the non-religious show equal charitable behaviors as the religious folks, despite self-reporting of the latter to participate in more charitable acts. But these studies were done with adults, usually with non-ecological tests. Now, a truly first-of-its-kind study finds something even more interesting, that calls into question the fundamental basis of Christianity’s and Islam’s moral justifications.

Decety et al. (2015) administered a test of altruism and a test of moral sensitivity to 1170 children, aged 5-12, from the USA, Canada, Jordan, Turkey, and South Africa. Based on parents’ reports about their household practices, the children had been divided into 280 Christian, 510 Muslim, and 323 Not Religious (the remaining 57 children belonged to other religions, but were not included in the analyses due to lack of statistical power). The altruism test consisted in letting children choose their favorite 10 out of 30 stickers to be theirs to keep, but because there aren’t enough stickers for everybody, the child could give some of her/his stickers to another child, not so fortunate as to play the sticker game (the researcher would give the child privacy while choosing). Altruism was calculated as the number of stickers given to the fictive child. In the moral sensitivity task, children watched 10 videos of a child pushing, shoving etc. another child, either intentionally or accidentally and then the children were asked to rate the meanness of the action and to judge the amount of punishment deserved for each action.

And.. the highlighted results are:

  1. “Family religious identification decreases children’s altruistic behaviors.
  2. Religiousness predicts parent-reported child sensitivity to injustices and empathy.
  3. Children from religious households are harsher in their punitive tendencies.”
Current Biology DOI: (10.1016/j.cub.2015.09.056). Copyright © 2015 Elsevier Ltd
From Current Biology (DOI: 10.1016/j.cub.2015.09.056). Copyright © 2015 Elsevier Ltd. NOTE: ns. means non-significant difference.

Parents’ educational level did not predict children’s behavior, but the level of religiosity did: the more religious the household, the less altruistic, more judgmental, and delivering harsher punishments the children were. Also, in stark contrast with the actual results, the religious parents viewed their children as more emphatic and sensitive to injustices as compared to the non-religious parents. This was a linear relationship: the more religious the parents, the higher the self-reports of socially desirable behavior, but the lower the child’s empathy and altruism objective scores.

Childhood is an extraordinarily sensitive period for learning desirable social behavior. So… is religion really turning perfectly normal children into selfish, vengeful misanthropes? What anybody does at home is their business, but maybe we could make a secular schooling paradigm mandatory to level the field (i.e. forbid religion teachings in school)? I’d love to read your comments on this.

Reference: Decety J, Cowell JM, Lee K, Mahasneh R, Malcolm-Smith S, Selcuk B, & Zhou X. (16 Nov 2015, Epub 5 Nov 2015). The Negative Association between Religiousness and Children’s Altruism across the World. Current Biology. DOI: 10.1016/j.cub.2015.09.056. Article | FREE PDF | Science Cover

By Neuronicus, 5 November 2015

Only the climate change scientists are interested in evidence. The rest is politics

Satellite image of clouds created by the exhaust of ship smokestacks (2005). Credit: NASA. License: PD.
Satellite image of clouds created by the exhaust of ship smokestacks (2005). Credit: NASA. License: PD.

Medimorec & Pennycook (2015) analyzed the language used in two prominent reports regarding climate change. Climate change is not a subject of scientific debate anymore, but of political discourse. Nevertheless, it appears that there are a few scientists that are skeptical about the climate change. As part of a conservative think tank, they formed the “Nongovernmental International Panel on Climate Change (NIPCC) as an alternative to the Intergovernmental Panel on Climate Change (IPCC). In 2013, the NIPCC authored Climate Change Reconsidered II: Physical Science (hereafter referred to as ‘NIPCC’; Idso et al. 2013), a scientific report that is a direct response to IPCC’s Working Group 1: The Physical Science Basis (hereafter referred to as ‘IPCC’; Stocker et al. 2013), also published in 2013″ (Medimorec & Pennycook, 2015) .

The authors are not climate scientists, but psychologists armed with nothing but 3 text analysis tools: Coh-Metrix text analyzer, Linguistic Inquiry and Word Count, and AntConc 3.3.5 concordancer analysis toolkit). They do not even fully understand the two very lengthy and highly technical papers; as they put it,

it is very unlikely that non-experts (present authors included) would have the requisite knowledge to be able to distinguish the NIPCC and IPCC reports based on the validity of their scientific arguments“.

So, they proceed on counting nouns, verbs, adverbs, and the like. The results: IPCC used more formal language, more nouns, more abstract words, more infrequent words, more complex syntax, and a lot more tentative language (‘possible’, ‘probable’, ‘might’) than the NIPCC. Which is ironic, since the climate scientists proponents are the ones accused of alarmism and trumpeting catastrophes. On the contrary, their language was much more refrained, perhaps out of fear of controversy, or just as likely, because they are scientists and very afraid to put their reputations at stake by risking type 1 errors.

In the authors’ words (I know, I am citing them 3 times in 4 paragraphs, but I really enjoyed their eloquence),

“the IPCC authors used more conservative (i.e., more cautious, less explicit) language to present their claims compared to the authors of the NIPCC report […]. The language style used by climate change skeptics suggests that the arguments put forth by these groups warrant skepticism in that they are relatively less focused upon the propagation of evidence and more intent on discrediting the opposing perspective”.

And this comes just from text analysis…

Reference: Medimorec, S. & Pennycook, G. (Epub 30 August 2015). The language of denial: text analysis reveals differences in language use between climate change proponents and skeptics. Climatic Change, doi:10.1007/s10584-015-1475-2. Article | Research Gate full text PDF

By Neuronicus, 4 November 2015

TMS decreases religiosity and ethnocentrism

Medieval knight dressed in an outfit with the Cross of St James of Compostela. From Galicianflag.
Medieval knight dressed in an outfit with the Cross of St. James of Compostela. Image from Galicianflag.

Rituals are anxiolytic; we developed them because they decrease anxiety. So it makes sense that when we feel the most stressed we turn to soothing ritualistic behaviors. Likewise, in times of threat, be it anywhere from war to financial depression, people show a sharp increase in adherence to political or religious ideologies.

Holbrook et al. (2015) used TMS (transcranial magnetic stimulation) to locally downregulate the activity of the posterior medial frontal cortex (which includes the dorsal anterior cingulate cortex and the dorsomedial prefrontal cortex), a portion of the brain the authors have reasons to believe is involved in augmenting the adherence to ideological convictions in times of threat.

They selected 38 U.S. undergraduates who scored similarly on political views (moderate or extremely conservative, the extremely liberals were excluded). Curiously, they did not measure religiosity prior to testing. Then, they submitted the subjects to a group prejudice test designed to increase ethnocentrism (read critique of USA written by an immigrant) and a high-level conflict designated to increase religiosity (reminder of death) while half of them received TMS and the other half received shams.

Under these conditions, the TMS decreased the belief in God and also the negative evaluations of the critical immigrant, compared to the people that received sham TMS.

The paper is, without doubt, interesting, despite the many possible methodological confounds. The authors themselves acknowledged some of the drawbacks in the discussion section, so regard the article as a pilot investigation. It doesn’t even have a picture with the TMS coordinates. Nevertheless, reducing someone’s religiosity and extremism by inactivating a portion of the brain… Sometimes I get afraid of my discipline.

Reference: Holbrook C, Izuma K, Deblieck C, Fessler DM, & Iacoboni M (Epub 4 Sep 2015). Neuromodulation of group prejudice and religious belief. Social Cognitive and Affective Neuroscience. DOI: 10.1093/scan/nsv107. Article | Research Gate full text PDF

By Neuronicus, 3 November 2015

How long does it take for environmental enrichment to show effects?

From funnyvet.
From funnyvet.

Environmental enrichment is a powerful way to give a boost to neurogenesis and alleviate some anxiety and depression symptoms. For the laboratory rodents, who spend their lives in cages with water and food access, environmental enrichment can refer to as little as a toy or two or as much as large room colonies with different size tubes, different levels to explore, nesting materials, plenty of toys with various shapes, textures, and colors, exercise wheels, and even the occasional fruit or peanut butter snack. But for how long does a mouse need to be exposed to enrichment to show cognitive and emotional improvement?

Leger et al. (2015) ran several anxiety, depression, and long-term memory tests in mice who have been exposed to environmental enrichment for 24 h, 1, 3, or 5 weeks. Although 24 h exposure was enough to improve memory, only after 3-week exposure some anxiety behaviors were attenuated. No effect on depressive behaviors or coticosterone levels, which may be due to that particular strain of mouse (several other studies found that environmental enrichment ameliorates depressive symptoms in other mice strains and rats). The 3-week exposure also increased the levels of serotonin in the frontal cortex. Only after 5-eweek exposure there was a significant survival rate of the hippocampal new cells. Of note, these were normal mice, i.e. they were not suffering from any disorder prior to exposure.

Mice raised in an impoverished environment (a) show less dendrite growth (c) than do mice raised in an enriched environment (b, d). Copyright: BSCS.
Mice raised in an impoverished environment (a) show less dendrite growth (c) than do mice raised in an enriched environment (b, d). Copyright: BSCS.

The findings give us a nice timeline for environmental enrichment to show its desired effects. But… if there are differences in the timeline and effects of environmental enrichment exposure from mouse strain to mouse strain, then what can we say for humans? Probably not much, unfortunately. As the ad nauseam overused phrase goes at the end of so many papers, ‘more research is needed to elucidate this problem’.

Reference: Leger M, Paizanis E, Dzahini K, Quiedeville A, Bouet V, Cassel JC, Freret T, Schumann-Bard P, & Boulouard M. (Nov 2015, Epub 5 Jun 2014). Environmental Enrichment Duration Differentially Affects Behavior and Neuroplasticity in Adult Mice. Cerebral Cortex, 25(11):4048-61. doi: 10.1093/cercor/bhu119. Article | FREE PDF

By Neuronicus, 1 November 2015

The Atlantic cod is driven to extinction by overfishing and global warming

Say bye-bye to this tasty beauty. Atlantic cod (Gadus morhua) picture by Hans Hillewaert (CC BY-SA 4.0)
Say bye-bye to this tasty beauty: the Atlantic cod (Gadus morhua). Picture by Hans Hillewaert released under CC BY-SA 4.0 license.

Pershing et al. (2015) analyzed a lot data from 1982-2013 about the Gulf of Maine temperatures, cod population metrics, and global warming indices. Global warming has hit the Gulf of Maine harder than anywhere else on the planet, with temperatures rising much faster than the rest of the global ocean during the last decade (about 0.23 Cº per YEAR). As a direct consequence, the cod population has declined very rapidly in the last two decades: “The most recent assessment found that the spawning biomass in this stock is now less than 3,000 mt, only 4% of the spawning stock biomass that gives the maximum sustainable yield” (p. 2)., which means, to my non-marine biologist understanding, that 96% of the little fishes required to make a sustainable pool for fishing are dead.

The authors go further and analyze predator behavior, zooplankton availability (which has declined due to… you are correct, that pesky global warming again) coupled with the recent heat waves and they say that, despite the horribly rapid decline in the population, the cod would have bounced back if it wasn’t for overfishing. That’s right, folks! Is not enough that global warming (which is also man-made, the nay-sayers are deluded, period) has jeopardized this species, but we made sure is on the brink of extinction by overfishing it. The quotas set for the fishing industry failed to take into the account the global warming effect of the population, setting fishing quotas for a steady-state system, which obviously the Gulf of Maine is not.

You may say, “All righty, then. Let’s fish some less cod until it bounces back. Some major fisheries will go bankrupt, but, hey, we’re saving the fishes so we can eat them later. Easy-peasy”. Not so fast. The gravity of the situation is further accentuated by the very doom and gloom predictions of a basic population dynamics model that the authors publish in the form of Fig. 3 of the paper. The cod population may bounce back, if we stop the fishing now COMPLETELY. Not a little bit, not a few here and there, not the slow and the weak, but ALL fishing needs to stop now if we want to rebuild the cod stock population. And you don’t get to say “damn the cod, I don’t eat it anyway’, because you don’t know what else might be driven to extinction by the disappearance of the cod.

I am not exaggerating here with metaphors. Read the paper and take a look at the scientists’ simulations and predictions yourselves.

Reference: Pershing AJ, Alexander MA, Hernandez CM, Kerr LA, Le Bris A, Mills KE, Nye JA, Record NR, Scannell HA, Scott JD, Sherwood GD, & Thomas AC (Epub 29 October 2015). Slow adaptation in the face of rapid warming leads to collapse of the Gulf of Maine cod fishery. Science, DOI: 10.1126/science.aac9819. Article | FREE FULLTEXT PDF

By Neuronicus, 30 October 2015

Grooming only half side of the body

Grooming only half side of the body. Credit:
Grooming only half side of the body. Credit:

Contrary to popular belief, rats and mice are very fastidious animals; they keep themselves scrupulously clean by engaging in a very meticulous routine of self-grooming. The routine is so rigorous that allows the researchers to divide the grooming sequence into four different phases, starting with the nose and whiskers and ending with the genitalia and tail. It is also a symmetrical behavior (no whisker left ungroomed, no paw unlicked).

Grooming is sensitive to dopaminergic manipulations, so Pelosi, Girault, & Hervé (2015) sought to see what happens if they destroy the dopamine fibers in the mouse brain. So they lesioned the medial forebrain bundle, which is a bunch axon fibers that contains over 80% of the midbrain dopaminergic axons. But they were tricky, they lesioned only one side.

And the results were that the lesioned mice not only exhibited less self-grooming on the opposite side to the lesion, but the behavior was rescued by L-DOPA, which is medication for Parkinson’s. That is, they gave the mice some L-DOPA and they began to merrily self-groom again on both sides of the body. The authors discuss in depths other findings, like the changes (or absence thereof) in grooming bouts, grooming time, grooming bouts, completeness of grooming etc.

The findings have significance in the Parkinson’s research, where the mild to moderate phases of the disease often present with asymmetrical motor behavior.

Reference: Pelosi A, Girault J-A, & Hervé D (23 Sept 2015). Unilateral Lesion of Dopamine Neurons Induces Grooming Asymmetry in the Mouse. PLoS One. 2015; 10(9): e0137185. doi: 10.1371/journal.pone.0137185. PMCID: PMC4580614. Article | FREE FULLTEXT PDF

By Neuronicus, 29 October 2015

Fat & afraid or slim & brave (Leptin and anxiety in ventral tegmental area)

A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right). Courtesy of Wikipedia. License: PD
A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right). Courtesy of Wikipedia. License: PD

Leptin is a small molecule produced mostly by the adipose tissue, whose absence is the cause of morbid obesity in the genetically engineered ob/ob mice. Here is a paper that gives us another reason to love this hormone.

Liu, Guo, & Lu (2015) build upon their previous work of investigating the leptin action(s) in the ventral tegmental area of the brain (VTA), a region that houses dopamine neurons and widely implicated in pleasure and drug addiction (among other things). They did a series of very straightforward experiments in which the either infused leptin directly into the mouse VTA or deleted the leptin receptors in this region (by using a virus in genetically engineered mice). Then they tested the mice on three different anxiety tests.

The results: leptin decreases anxiety; absence of leptin receptors increases anxiety. Simple and to the point. And also makes sense, given that leptin receptors are mostly located on the VTA neurons that project to the central amygdala, a region involved in fear and anxiety (curiously, the authors cite the amygdala papers, but do not comment on the leptin-VTA-dopamine-amygdala connection). For the specialists, I would say that they are a little liberal with their VTA hit assessment (they are mostly targeting the posterior VTA) and their GFP (green fluorescent protein) is sparsely expressed.

Reference: Liu J, Guo M, & Lu XY (Epub ahead of print 5 Oct 2015). Leptin/LepRb in the Ventral Tegmental Area Mediates Anxiety-Related Behaviors. International Journal of Neuropsychopharmacology, 1–11. doi:10.1093/ijnp/pyv115. Article | FREE PDF

By Neuronicus, 28 October 2015

How grateful would you feel after watching a Holocaust documentary? (Before you comment, READ the post first)

form Fox et al. (2015)
form Fox et al. (2015)

How would you feel if one of your favourite scientists published a paper that is, to put it in mild terms, not to their very best? Disappointed? Or perhaps secretly gleeful that even “the big ones” are not always producing pearl after pearl?

This is what happened to me after reading the latest paper of the Damasio group. Fox et al. (2015) decided to look for the neural correlates of gratitude. That is, stick people in fMRI, make them feel grateful, and see what lights up. All well and good, except they decided to go with a second-hand approach, meaning that instead of making people feel grateful (I don’t know how, maybe giving them something?), they made the participants watch stories in which gratitude may have been felt by other people (still not too too bad, maybe watching somebody helping the elderly). But, the researchers made an in-house documentary about the Holocaust and then had several actual Holocaust survivors tell their story (taken from the SC Shoah Foundation Institutes Visual History Archive), focusing on the part where their lives were saved or they were helped by others by giving them survival necessities. Then, the subjects were asked to immerse themselves in the story and tell how grateful they felt if they were the gift recipients.

I don’t know about you, but I don’t think that after watching a documentary about the Holocaust (done with powerfully evocative images and professional actor voice-overs, mind you!) and seeing people tell the horrors they’ve been through and then receiving some food or shelter from a Good Samaritan, gratitude would not have been my first feeling. Anger perhaps? That such an abominable thing as the Holocaust was perpetrated by my fellow humans? Sorrow? Sadness? Sick to my stomach? Compassion for the survivors? Maybe I am blatantly off-Gauss here, but I don’t think Damasio et co. measured what they thought they were measuring.

Anyway, for what is worth, the task produced significant activity in the medial prefrontal cortex (which is involved in so many behaviors that is not even worth listing them), along with the usual suspects in a task as ambiguous as this, like various portions of the anterior cingulate and orbitofrontal cortices.

Reference: Fox GR, Kaplan J, Damasio H, & Damasio A (30 September 2015). Neural correlates of gratitude. Frontiers in Psycholology, 6:1491. doi: 10.3389/fpsyg.2015.01491. Article | FREE FULLTEXT PDF

By Neuronicus, 27 October 2015


The F in memory

"Figure 2. Ephs and ephrins mediate molecular events that may be involved in memory formation. Evidence shows that memory formation involves alterations of presynaptic neurotransmitter release, activation of glutamate receptors, and neuronal morphogenesis. Eph receptors regulate synaptic transmission by regulating synaptic release, glutamate reuptake from the synapse (via astrocytes), and glutamate receptor conductance and trafficking. Ephs and ephrins also regulate neuronal morphogenesis of axons and dendritic spines through controlling the actin cytoskeleton structure and dynamics" (Dines & Lamprecht, 2015, p. 3).
“Figure 2. Ephs and ephrins mediate molecular events that may be involved in memory formation. Evidence shows that memory formation involves alterations of presynaptic neurotransmitter release, activation of glutamate receptors, and neuronal morphogenesis. Eph receptors regulate synaptic transmission by regulating synaptic release, glutamate reuptake from the synapse (via astrocytes), and glutamate receptor conductance and trafficking. Ephs and ephrins also regulate neuronal morphogenesis of axons and dendritic spines through controlling the actin cytoskeleton structure and dynamics” (Dines & Lamprecht, 2015, p. 3).

When thinking about long-term memory formation, most people immediately picture glutamate synapses. Dines & Lamprecht (2015) review the role of a family of little known players, but with big roles in learning and long-term memory consolidation: the ephs and the ephrines.

Ephs (the name comes from erythropoietin-producing human hepatocellular, the cancer line from which the first member was isolated) are transmembranal tyrosine kinase receptors. Ephrines (Eph receptor interacting protein) bind to them. Ephrines are also membrane-bound proteins, which means that in order for the aforementioned binding to happen, cells must touch each other, or at least be in a very very cozy vicinity. They are expressed in many regions of the brain like hippocampus, amygdala, or cortex.

The authors show that “interruption of Ephs/ephrins mediated functions is sufficient for disruption of memory formation” (p. 7) by reviewing a great deal of genetic, pharmacologic, and electrophysiological studies employing a variety of behavioral tasks, from spatial memory to fear conditioning. The final sections of the review focus on the involvement of ephs/ephrins in Alzheimer’s and anxiety disorders, suggesting that drugs that reverse the impairment on eph/ephrin signaling in these brain diseases may lead to an eventual cure.

Reference: Dines M & Lamprecht R (8 Oct 2015, Epub 13 Sept 2015). The Role of Ephs and Ephrins in Memory Formation. International Journal of Neuropsychopharmacology, 1-14. doi:10.1093/ijnp/pyv106. Article | FREE FULLTEXT PDF

By Neuronicus, 26 October 2015

Are you in love with an animal?

Sugar Candy Hearts by Petr Kratochvil. License: PD
Sugar Candy Hearts by Petr Kratochvil taken from publicdomainpictures. License: PD

Ren et al. (2015) gave sweet drink (Fanta), sweet food (Oreos), salty–vinegar food (Lays chips) or water to 422 people and then asked them about their romantic relationship; or, if they didn’t have one, about a hypothetical relationship. For hitched people, the foods or drinks had no effect on the evaluation of their relationship. In contrast, the singles who received sweets were more eager to initiate a relationship with a potential partner and evaluated more favorably a hypothetical relationship (how do you do that? I mean, if it’s hypothetical… why wouldn’t you evaluate it favorably from your singleton perspective?) Anyway, the singles who got sweets tend see things a little more on the rosy side, as opposed to the taken ones.

The rationale for doing this experiment is that metaphors alter our perceptions (fair enough). Given that many terms of endearment include reference to the taste of sweet, like “Honey”, “Sugar” or “Sweetie”, maybe this is not accidental or just a metaphor and, if we manipulate the taste, we manipulate the perception. Wait, what? Now re-read the finding above.

The authors take their results as supporting the view that “metaphorical thinking is one fundamental way of perceiving the world; metaphors facilitate social cognition by applying concrete concepts (e.g., sweet taste) to understand abstract concepts (e.g., love)” (p. 916).

So… I am left with many questions, the first being: if the sweet appelatives in a romantic relationship stem from an extrapolation of the concrete taste of sweet to an abstract concept like love, then, I wonder, what kind of concrete concept is being underlined in the prevalence of “baby” as a term of endearment? Do I dare speculate what the metaphor stands for? Should people who are referred to as “baby” by their partners alert the authorities for a possible pedophile ideation? And what do we do about the non-English cultures (apparently non-Germanic or non-Mandarin too) in which the lovey-dovey terms tend to cluster around various small objects (e.g. tassels), vegetables (e.g. pumpkin), cute onomatopoeics (I am at a loss for transcription here), or baby animals (e.g. chick, kitten, puppy). Believe me, such cultures do exist and are numerous. “Excuse me, officer, I suspect my partner is in love with an animal. Oh, wait, that didn’t come out right…”

Ok, maybe I missed something with this paper, as half-way through I failed to maintain proper focus due to an intruding – and disturbing! – image of a man, a chicken, and a tassel. So take the authors’ words when they say that their study “not only contributes to the literature on metaphorical thinking but also sheds light on an understudied factor that influences relationship initiation, that of taste” (p. 918). Oh, metaphors, how sweetly misleading you are…

Please use the “Comments” section below to share the strangest metaphor used as term of endearment you have ever heard in a romantic relationship.

Reference: Ren D, Tan K, Arriaga XB, & Chan KQ (Nov 2015). Sweet love: The effects of sweet taste experience on romantic perceptions. Journal of Social and Personal Relationships, 32(7): 905 – 921. DOI: 10.1177/0265407514554512. Article | FREE FULLTEXT PDF

By Neuronicus, 21 October 2015