The FIRSTS: Increase in CO2 levels in the atmosphere results in global warming (1896)

Few people seem to know that although global warming and climate change are hotly debated topics right now (at least on the left side of the Atlantic) the effect of CO2 levels on the planet’s surface temperature was investigated and calculated more than a century ago. CO2 is one of the greenhouse gases responsible for the greenhouse effect, which was discovered by Joseph Fourier in 1824 (the effect, that is).

Let’s start with a terminology clarification. Whereas the term ‘global warming’ was coined by Wallace S. Broecker in 1975, the term ‘climate change’ underwent a more fluidic transformation in the ’70s from ‘inadvertent climate modification’ to ‘climatic change’ to a more consistent use of ‘climate change’ by Jule Charney in 1979, according to NASA. The same source tells us:

“Global warming refers to surface temperature increases, while climate change includes global warming and everything else that increasing greenhouse gas amounts will affect”.

But before NASA there was one Svante August Arrhenius (1859–1927). Dr. Arrhenius was a Swedish physical chemist who received the Nobel Prize in 1903 for uncovering the role of ions in how electrical current is conducted in chemical solutions.

S.A. Arrhenius was the first to quantify the variations of our planet’s surface temperature as a direct result of the amount of CO2 (which he calls carbonic acid, long story) present in the atmosphere. For those – admittedly few – nitpickers that say his views on the greenhouse effect were somewhat simplistic and his calculations were incorrect I’d say cut him a break: he didn’t have the incredible amount of data provided by the satellites or computers, nor the work of thousands of scientists over a century to back him up. Which they do. Kind of. Well, the idea, anyway, not the math. Well, some of the math. Let me explain.

First, let me tell you that I haven’t managed to pass past page 3 of the 39 pages of creative mathematics, densely packed tables, parameter assignments, and convoluted assumptions of Arrhenius (1896). Luckily, I convinced a spectroscopist to take a crack at the original paper since there is a lot of spectroscopy in it and then enlighten me.

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The photo was taken in 1887 and shows (standing, from the left): Walther Nernst (Nobel in Chemistry), Heinrich Streintz, Svante Arrhenius, Richard Hiecke; (sitting, from the left): Eduard Aulinger, Albert von Ettingshausen, Ludwig Boltzmann, Ignaz Klemenčič, Victor Hausmanninger. Source: Universität Graz. License: PD via Wikimedia Commons.

Second, despite his many accomplishments, including being credited with laying the foundations of a new field (physical chemistry), Arrhenius was first and foremost a mathematician. So he employed a lot of tedious mathematics (by hand!) together with some hefty guessing along with what was known at the time about Earth’s infrared radiation, solar radiation, water vapor and CO2 absorption, temperature of the Moon,  greenhouse effect, and some uncalibrated spectra taken by his predecessors to figure out if “the mean temperature of the ground [was] in any way influenced by the presence of the heat-absorbing gases in the atmosphere” (p. 237). Why was he interested in this? We find out only at page 267 after a lot of aforesaid dreary mathematics where he finally shares this with us:

“I certainly not have undertaken these tedious calculations if an extraordinary interest had not been connected with them. In the Physical Society of Stockholm there have been occasionally very lively discussions on the probable causes of the Ice Age”.

So Arrhenius was interested to find out if the fluctuations of CO2 levels could have caused the Ice Ages. And yes, he thinks that could have happened. I don’t know enough about climate science to tell you if this particular conclusion of his is correct today. But what he managed to accomplish though was to provide for the first time a way to mathematically calculate the amount of rise in temperature due the rise of CO2 levels. In other words, he found a direct relationship between the variations of CO2 and temperature. Today, it turns out that his math was incorrect because he left out some other variables that influence the global temperature that were discovered and/or understood later (like the thickness of the atmosphere, the rate of ocean absorption  of CO2 and others which I won’t pretend I understand). Nevertheless, Arrhenius was the first to point out to the following relationship, which, by and large, is still relevant today:

“Thus if the quantity of carbonic acid increased in geometric progression, the augmentation of the temperature will increase nearly in arithmetic progression” (p. 267).

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P.S. Technically, Joseph Fourier should be credited with the discovery of global warming by increasing the levels of greenhouse gases in the atmosphere in 1824, but Arrhenius quantified it so I credited him. Feel fee to debate :).

REFERENCE: Arrhenius, S. (April 1896). XXXI. On the Influence of Carbonic Acid in the Air upon the Temperature of the Ground, The London, Edinburgh, and Dublin Philosophical Magazine and Journal of Science (Fifth Series), 49 (251): 237-276. General Reference P.P.1433. doi: http://dx.doi.org/10.1080/14786449608620846. FREE FULLTEXT PDF

By Neuronicus, 24 June 2017

Arnica and a scientist’s frustrations

angry-1372523 - CopyWhen you’re the only scientist in the family you get asked the weirdest things. Actually, I’m not the only one, but the other one is a chemist and he’s mostly asked about astrophysics stuff, so he doesn’t really count, because I am the one who gets asked about rare diseases and medication side-effects and food advice. Never mind that I am a neuroscientist and I have professed repeatedly and quite loudly my minimum knowledge of everything from the neck down, all eyes turn to me when the new arthritis medication or the unexpected side-effects of that heart drug are being brought up. But, curiously, if I dare speak about brain stuff I get the looks that a thing the cat just dragged in gets. I guess everybody is an expert on how the brain works on account of having and using one, apparently. Everybody, but the actual neuroscience expert whose input on brain and behavior is to be tolerated and taken with a grain of salt at best, but whose opinion on stomach distress is of the utmost importance and must be listened to reverentially in utter silence [eyes roll].

So this is the background on which the following question was sprung on me: “Is arnica good for eczema?”. As always, being caught unawares by the sheer diversity of interests and afflictions my family and friends can have, I mumbled something about I don’t know what arnica is and said I will look it up.

This is an account of how I looked it up and what conclusions I arrived to or how a scientists tries to figure something out completely out of his or her field. First thing I did was to go on Wikipedia. Hold your horses, it was not about scientific information but for a first clarification step: is it a chemical, a drug, an insect, a plant maybe? I used to encourage my students to also use Wikipedia when they don’t have a clue what a word/concept/thing is. Kind of like a dictionary or a paper encyclopedia, if you will. To have a starting point. As a matter of fact Wikipedia is an online encyclopedia, right? Anyway, I found out that Arnica is a plant genus out of which one species, Arnica Montana seems to be popular.

Then I went to the library. Luckily for me, the library can be accessed online from the comfort of my home and my favorite pajamas in the incarnation of PubMed or Medline as it used to be affectionately called. It is the US National Library of Medicine maintained by the National Institutes of Health, a wonderful repository of scholarly papers (yeah, Google Scholar to PubMed is like the babbling of a two-year old to the Shakespearian sonnets; Google also has an agenda, which you won’t find on PubMed). Useful tip: when you look for a paper that is behind a paywall in Nature or Elsevier Journals or elsewhere, check the PubMed too because very few people seem to know that there is an obscure and incredibly helpful law saying that research paid by the US taxpayers should be available to the US taxpayer. A very sensible law passed only a few years ago that has the delightful effect of having FREE full text access to papers after a certain amount of months from publishing (look for the PMC icon in the upper right corner).

I searched for “arnica” and got almost 400 results. I sorted by “most recent”. The third hit was a review. I skimmed it and seemed to talk a lot about healing in homeopathy, at which point, naturally, I got a gloomy foreboding. But I persevered because one data point does not a trend make. Meaning that you need more than a paper – or a handful – to form an informed opinion. This line of thinking has been rewarded by the hit No. 14 in the search which had an interesting title in the sense that it was the first to hint to a mechanism through which this plant was having some effects. Mechanisms are important, they allow you to differentiate speculation from findings, so I always prefer papers that try to answer a “How?” question as opposed to the other kinds; whys are almost always speculative as they have a whiff of post factum rationalizations, whats are curious observations but, more often than not, a myriad factors can account for them, whens are an interesting hybrid between the whats and the hows – all interesting reads but for different purposes. You want to publish in Nature or Science? Design an experiment that answers all the questions. Gone are the days when answering one question was enough to publish…

Digressions aside, the paper I am covering today sounds like a mechanism paper. Marzotto et al. (2016) cultured a particular line of human cells in a Petri dish destined to test the healing powers of Arnica montana. The experimental design seems simple enough: the control culture gets nothing and the experimental culture gets Arnica montana. Then, the authors check to see if there are differences in gene expressions between the two groups.

The authors applied different doses of Arnica montana to the cultures to see if the effects are dose-dependant. The doses used were… wait, bear with me, I’m not familiar with the system, it’s not metric. In the Methods, the authors say

Arnica m. was produced by Boiron Laboratoires (Lyon, France) according to the French Homeopathic pharmacopoeia and provided as a first centesimal dilution (Arnica m. 1c) of the hydroalcoholic extract (Mother Tincture, MT) in 30% ethanol/distilled water”.

Wait, what?! Centesimal… centesimal… wasn’t that the nothing-in-it scale from the pseudoscientific bull called homeopathy? Maybe I’m wrong, maybe there are some other uses for it and becomes clear later:

Arnica m. 1c was used to prepare the second centesimal dilution (Arnica m. 2c) by adding 50μl of 1c solution to 4.95ml of distilled ultra-pure water. Therefore, 2c corresponds to 10−4 of the MT”.

Holy Mother of God, this is worse than gibberish; this is voluntary misdirection, crap wrapped up in glitter, medieval tinkering sold as state-of-the-art 21st century science. Speaking of state-of-the-art, the authors submit their “doses” to a liquid chromatograph, a thin layer chromatograph, a double-beam spectrophotometer, a nanoparticle tracking analysis (?!) for what purposes I cannot fathom. On, no, I can: to sound science-y. To give credibility for the incredulous. To make money.

At which point I stopped reading the ridiculous nonsense and took a closer look at the authors and got hit with this:

“Competing Interests: The authors have declared that no competing interests exist. This study was funded by Boiron Laboratoires Lyon with a research agreement in partnership with University of Verona. There are no patents, products in development or marketed products to declare. This does not alter our adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.”

No competing interests?? The biggest manufacturer of homeopathic crap in the world pays you to see if their product works and you have no competing interest? Maybe no other competing interests. There were some comments and replies to this paper after that, but it is all inconsequential because once you have faulty methods your results are irrelevant. Besides, the comments are from the same University, could be some internal feuding.

PLoS One, what have you done? You’re a peer-reviewed open access journal! What “peers” reviewed this paper and gave their ok for publication? Since when is homeopathy science?! What am I going to find that you publish next? Astrology? For shame… Give me that editor’s job because I am certain I can do better.

To wrap it up and tell you why I am so mad. The homeopathic scale system, that centesimal gibberish, is just that: gibberish. It is impossible to replicate this experiment without the product marketed by Boiron because nobody knows how much of the plant is in the dose, which parts of the plant, what kind of extract, or what concentration. So it’s like me handing you my special potion and telling you it makes warts disappear because it has parsley in it. But I don’t tell you my recipe, how much, if there anything else besides parsley in it, if I used the roots or only the leaves or anything. Now that, my friends, it’s not science, because science is REPLICABLE. Make no mistake: homeopathy is not science. Just like the rest of alternative medicine, homeopathy is a ruthless and dangerous business that is in sore need of lawmakers’ attention, like FDA or USDA. And for those who think this is a small paper, totally harmless, no impact, let me tell you that this paper had over 20,000 views.

I would have oh so much more to rant on. But enough. Rant over.

Oh, not yet. Lastly, I checked a few other papers about arnica and my answer to the eczema question is: “It’s possible but no, I don’t think so. I don’t know really, I couldn’t find any serious study about it and I gave up looking after I found a lot of homeopathic red flags”. The answer I will give my family member? “Not the product you have, no. Go to the doctors, the ones with MDs after their name and do what they tell you. In addition, I, the one with a PhD after my name, will tell you this for free because you’re family: rub the contents of this bottle only once a day – no more! – on the affected area and you will start seeing improvements in three days. Do not use elsewhere, it’s quite potent!” Because placebo works and at least my water vial is poison free.

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Reference: Marzotto M, Bonafini C, Olioso D, Baruzzi A, Bettinetti L, Di Leva F, Galbiati E, & Bellavite P (10 Nov 2016). Arnica montana Stimulates Extracellular Matrix Gene Expression in a Macrophage Cell Line Differentiated to Wound-Healing Phenotype. PLoS One, 11(11):e0166340. PMID: 27832158, PMCID: PMC5104438, DOI: 10.1371/journal.pone.0166340. ABSTRACT | FREE FULLTEXT PDF 

By Neuronicus, 10 June 2017

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Vanity and passion fruit

Ultraviolet irradiation exposure from our sun accelerates the skin aging, process called photoaging. It can even cause skin cancers. There has been some considerable research on how our beloved sun does that.

For example, one way the UV radiation leads to skin damage is by promoting the production of free radicals as reactive oxygen species (ROS), which do many bad things, like direct DNA damage. Another bad thing done by ROS is the upregulation of the mitogen-activated protein kinase (MAPK) signaling pathway which activates all sorts of transcription factors which, in turn, produce proteins that lead to collagen degradation and voilà, aged skin. I know I lost some of you at the MAPK point; you can think of MAPK as a massive proteinaceous hub, a multi-button console with many inputs and outputs. A very sensitive and incredibly complex hub that controls nearly all important aspects of cell function, with many feedback loops, so if you mess with it, cell Armageddon may be happening. Or nothing at all. It’s that complex.

But I digress. What MAPK is doing is less relevant for the paper I am introducing to you today than the fact that we have physiological markers for skin aging due to UV. Bravo et al. (2017) cultured human skin cells in a Petri dish, treated them with various concentrations of an extract of passion fruit (Passiflora tarminiana) and then bombarded them with UV (the B type, 280–315 nm). The authors made the extract themselves, is not something you just buy (yet).

The UV produced the expected damage, translated as increased matrix mettoproteinase-1 (MMP-1), collagenase, and ROS production and decreased procollagen. Pretreatment with passion fruit extract significantly mitigated these UV effects in a dose-dependant manner. The concentration of their concoction that worked best was 10 μg/mL. Then the authors did some more chemistry to figure out what in their concoction is responsible, or at least probably responsible, for the observed wonderful effects. The authors believe the procyianidins and flavonoids are the culprits because 1) they have been proven to be strong antioxidants before and 2) this plant has them in very high amounts.

Good news then for the antiaging cosmetics industry. Perhaps even for dermatologists and their patients.

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Reference: Bravo K, Duque L, Ferreres F, Moreno DA, & Osorio E. (EPUB ahead of print: 3 Feb 2017). Passiflora tarminiana fruits reduce UVB-induced photoaging in human skin fibroblasts. Journal of Photochemistry and Photobiology, 168: 78-88. PMID: 28189068, DOI: 10.1016/j.jphotobiol.2017.01.023. ARTICLE

By Neuronicus, 13 February 2017

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Aging and its 11 hippocampal genes

Aging is being quite extensively studied these days and here is another advance in the field. Pardo et al. (2017) looked at what happens in the hippocampus of 2-months old (young) and 28-months old (old) female rats. Hippocampus is a seahorse shaped structure no more than 7 cm in length and 4 g in weight situated at the level of your temples, deep in the brain, and absolutely necessary for memory.

First the researchers tested the rats in a classical maze test (Barnes maze) designed to assess their spatial memory performance. Not surprisingly, the old performed worse than the young.

Then, they dissected the hippocampi and looked at neurogenesis and they saw that the young rats had more newborn neurons than the old. Also, the old rats had more reactive microglia, a sign of inflammation. Microglia are small cells in the brain that are not neurons but serve very important functions.

After that, the researchers looked at the hippocampal transcriptome, meaning they looked at what proteins are being expressed there (I know, transcription is not translation, but the general assumption of transcriptome studies is that the amount of protein X corresponds to the amount of the RNA X). They found 210 genes that were differentially expressed in the old, 81 were upregulated and 129 were downregulated. Most of these genes are to be found in human too, 170 to be exact.

But after looking at male versus female data, at human and mouse aging data, the authors came up with 11 genes that are de-regulated (7 up- and 4 down-) in the aging hippocampus, regardless of species or gender. These genes are involved in the immune response to inflammation. More detailed, immune system activates microglia, which stays activated and this “prolonged microglial activation leads to the release of pro-inflammatory cytokines that exacerbate neuroinflammation, contributing to neuronal loss and impairment of cognitive function” (p. 17). Moreover, these 11 genes have been associated with neurodegenerative diseases and brain cancers.

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These are the 11 genes: C3 (up), Cd74  (up), Cd4 (up), Gpr183 (up), Clec7a (up), Gpr34 (down), Gapt (down), Itgam (down), Itgb2 (up), Tyrobp (up), Pld4 (down).”Up” and “down” indicate the direction of deregulation: upregulation or downregulation.

I wish the above sentence was as explicitly stated in the paper as I wrote it so I don’t have to comb through their supplemental Excel files to figure it out. Other than that, good paper, good work. Gets us closer to unraveling and maybe undoing some of the burdens of aging, because, as the actress Bette Davis said, “growing old isn’t for the sissies”.

Reference: Pardo J, Abba MC, Lacunza E, Francelle L, Morel GR, Outeiro TF, Goya RG. (13 Jan 2017, Epub ahead of print). Identification of a conserved gene signature associated with an exacerbated inflammatory environment in the hippocampus of aging rats. Hippocampus, doi: 10.1002/hipo.22703. ARTICLE

By Neuronicus, 25 January 2017

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100% Effective Vaccine

A few days ago I was reading random stuff on the internet, as is one’s procrastination proclivity, catching up after the holiday, and I exclaimed out loud: “They discovered an 100% effective Ebola Vaccine!”. I expected some ‘yeay’-s or at least some grunts along the lines of ‘that’s nice’ or ‘cool’. Naturally, I turned around from my computer to check the source of unaccustomed silence to the announcement of such good news or, at least, to make sure that everybody is still breathing and present in the room. What met my worried glare was a gloom face and a shaking head. That’s because news like that are misleading, because, duh, it finally dawned on me, there is no such thing as ‘100% effective vaccine’.

And yet…, and yet this is exactly what Henao-Restrepo et al. (2016) say they found! The study is huge, employing more that 10 000 people. Such a tremendous endeavor has been financed by WHO (World Health Organization) and various departments from several countries (UK, USA, Switzerland, South Africa, Belgium, Germany, France, Guinea, and Norway) and, I’m assuming, a lot of paid and unpaid volunteers. I cannot even imagine the amount of work and the number of people that made this happen. And the coordination required for such speedy results!

The successful vaccine in rodents and non-human primates, called the recombinant, replication-competent, vesicular stomatitis virus-based vaccine expressing the glycoprotein of a Zaire Ebolavirus (rVSV-ZEBOV) has been taken to the Republic of Guinea and rapidly administered to volunteers who were in contact with somebody that had Ebola symptoms. And their contacts. I mean the contacts and the contacts of contacts of the Ebola patient. Who were contacted by the researchers within 2 days of a new Ebola case based on the patient’s list of contacts. And of contacts of contacts. Is not that complicated, honest.

After vaccinations, the “vaccinees were observed for 30 min post-vaccination and at home visits on days 3, 14, 21, 42, 63, and 84” (p.4). Some volunteers received the vaccine immediately, others after 3 weeks. No one who received the vaccine immediately developed Ebola, which lead the researchers to claim that the vaccine is 100% effective. Only 9 from the delayed vaccination group developed Ebola within 10 days of vaccination, but the researchers figured that these people probably contacted Ebola prior to the vaccination, since the disease requires typically about 10 days to show its ugly  horns.

So this is great news. Absolutely great. Even if, as always, I could nitpick thorough the paper, squabble over the “typically” 10-day incubation period, and cock an eyebrow at the new-fangled ring vaccination design as opposed to the old-fashioned placebo approach. Even after these minor criticisms this is – I repeat – GREAT NEWS!

P.S. Don’t ever say that the UN didn’t do anything for you.

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Reference: Henao-Restrepo AM, Camacho A, Longini IM, Watson CH, Edmunds WJ, Egger M, Carroll MW, Dean NE, Diatta I, Doumbia M, Draguez B, Duraffour S, Enwere G, Grais R, Gunther S, Gsell PS, Hossmann S, Watle SV, Kondé MK, Kéïta S, Kone S, Kuisma E, Levine MM, Mandal S, Mauget T, Norheim G, Riveros X, Soumah A, Trelle S, Vicari AS, Røttingen JA, Kieny MP. (22 Dec 2016). Efficacy and effectiveness of an rVSV-vectored vaccine in preventing Ebola virus disease: final results from the Guinea ring vaccination, open-label, cluster-randomised trial (Ebola Ça Suffit!). Lancet. pii: S0140-6736(16)32621-6. doi: 10.1016/S0140-6736(16)32621-6. PMID: 28017403 [Epub ahead of print] ARTICLE | FREE FULLTEXT PDF | Good Nitpicking in The Conversation

By Neuronicus, 18 January 2017

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Don’t eat snow

Whoever didn’t roll out a tongue to catch a few snowflakes? Probably only those who never encountered snow.

The bad news is that snow, particularly urban snow is bad, really bad for you. The good news is that this was not always the case. So there is hope that in the far future it will be pristine again.

Nazarenko et al. (2016) constructed a very clever contraption that reminds me of NASA space exploration instruments. The authors refer to this by the humble name of ‘environmental chamber’, but is in fact a complex construction with different modules designed to measure out how car exhaust and snow interact (see Fig. 1).

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Fig. 1 from Nazarenko et al. (2016, DOI: 10.1039/c5em00616c). Released under CC BY-NC 3.0.

After many experiments, researchers concluded that snow absorbs pollutants very effectively. Among the many kinds of organic compounds soaked by snow in just one hour after exposure to fume exhaust, there were the infamous BTEX (benzene, toluene, ethylbenzene, and xylenes). The amounts of these chemicals in the snow were not at all negligible; to give you an example, the BTEX concentration increased from virtually 0 to 50 and up to 380 ug kg-1. The authors provide detailed measurements for all the 40+ compounds they have identified.

Needles to say, many these compounds are known carcinogenics. Snow absorbs them, alters their size distributions, and then it melts… Some of them may be released back in the air as they are volatile, some will go in the ground and rivers as polluted water. After this gloomy reality check, I’ll leave you with the words of the researchers:

“The accumulation and transfer of pollutants from exhaust – to snow – to meltwater need to be considered by regulators and policy makers as an important area of focus for mitigation with the aim to protect public health and the environment” (p. 197).

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Reference: Nazarenko Y, Kurien U, Nepotchatykh O, Rangel-Alvarado RB, & Ariya PA. (Feb 2016). Role of snow and cold environment in the fate and effects of nanoparticles and select organic pollutants from gasoline engine exhaust. Environmental Science: Processes & Impacts, 18(2):190-199. doi: 10.1039/c5em00616c. ARTICLE | FREE FULTEXT PDF 

By Neuronicus, 26 December 2016

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Soccer and brain jiggling

There is no news or surprise that strong hits to the head produce transient or permanent brain damage. But how about mild hits produced by light objects like, say, a volley ball or soccer ball?

During a game of soccer, a player is allowed to touch the ball with any part of his/her body minus the hands. Therefore, hitting the ball with the head, a.k.a. soccer heading, is a legal move and goals marked through such a move are thought to be most spectacular by the refined connoisseur.

A year back, in 2015, the United States Soccer Federation forbade the heading of the ball by children 10 years old and younger after a class-action lawsuit against them. There has been some data that soccer players display loss of brain matter that is associated with cognitive impairment, but such studies were correlational in nature.

Now, Di Virgilio et al. (2016) conducted a study designed to explore the consequences of soccer heading in more detail. They recruited 19 young amateur soccer players, mostly male, who were instructed to perform 20 rotational headings as if responding to corner kicks in a game. The ball was delivered by a machine at a speed of approximately 38 kph. The mean force of impact for the group was 13.1 ± 1.9 g. Immediately after the heading session and at 24 h, 48 h and 2 weeks post-heading, the authors performed a series of tests, among which are a transcranial magnetic stimulation (TMS) recording, a cognitive function assessment (by using the Cambridge Neuropsychological Test Automated Battery), and a postural control test.

Not being a TMS expert myself, I was wondering how do you record with a stimulator? TMS stimulates, it doesn’t measure anything. Or so I thought. The authors delivered brief  (1 ms) stimulating impulses to the brain area that controls the leg (primary motor cortex). Then they placed an electrode over the said muscle (rectus femoris or quadriceps femoris) and recorded how the muscle responded. Pretty neat. Moreover, the authors believe that they can make inferences about levels of inhibitory chemicals in the brain from the way the muscle responds. Namely, if the muscle is sluggish in responding to stimulation, then the brain released an inhibitory chemical, like GABA (gamma-amino butyric acid), hence calling this process corticomotor inhibition. Personally, I find this GABA inference a bit of a leap of faith, but, like I said, I am not fully versed in TMS studies so it may be well documented. Whether or not GABA is responsible for the muscle sluggishness, one thing is well documented though: this sluggishness is the most consistent finding in concussions.

The subjects had impaired short term and long term memory functions immediately after the ball heading, but not 24 h or more later. Also transient was the corticomotor inhibition. In other words, soccer ball heading results in measurable changes in brain function. Changes for the worst.

Even if these changes are transient, there is no knowing (as of yet) what prolonged ball heading might do. There is ample evidence that successive concussions have devastating effects on the brain. Granted, soccer heading does not produce concussions, at least in this paper’s setting, but I cannot think that even sub-concussion intensity brain disruption can be good for you.

On a lighter note, although the title of the paper features the word “soccer”, the rest o the paper refers to the game as “football”. I’ll let you guess the authors’ nationality or at least the continent of provenance ;).

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Reference: Di Virgilio TG, Hunter A, Wilson L, Stewart W, Goodall S, Howatson G, Donaldson DI, & Ietswaart M. (Nov 2016, Epub 23 Oct 2016). Evidence for Acute Electrophysiological and Cognitive Changes Following Routine Soccer Heading. EBioMedicine, 13:66-71. PMID: 27789273, DOI: 10.1016/j.ebiom.2016.10.029. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 20 December 2016

Scientists don’t know the risks & benefits of science

If you want to find out how bleach works or what keeps the airplanes in the air or why is the rainbow the same sequence of colors or if it’s dangerous to let your kid play with snails would you ask a scientist or your local priest?

The answer is very straightforward for most of the people. Just that for a portion of the people the straightforwardness is viewed by the other portion as corkscrewedness. Or rather just plain dumb.

Cacciatore et al. (2016) asked about 5 years ago 2806 American adults how much they trust the information provided by religious organizations, university scientists, industry scientists, and science/technology museums. They also asked them about their age, gender, race, socioeconomic status, income as well as about Facebook use, religiosity, ideology, and attention to science-y content.

Almost 40% of the sample described themselves as Evangelical Christians, one of the largest religious group in USA. These people said they trust more their religious organizations then scientists (regardless of who employs these scientists) to tell the truth about the risks and benefits of technologies and their applications.

The data yielded more information, like the fact that younger, richer, liberal, and white people tended to trust scientists more then their counterparts. Finally, Republicans were more likely to report a religious affiliation than Democrats.

I would have thought that everybody would prefer to take advice about science from a scientist. Wow, what am I saying, I just realized what I typed… Of course people are taking health advice from homeopaths all the time, from politicians rather than environment scientists, from alternative medicine quacks than from doctors, from no-college educated than geneticists. From this perspective then, the results of this study are not surprising, just very very sad… I just didn’t think that the gullible people can also be grouped by political affiliations. I though the affliction is attacking both sides of an ideological isle in a democratic manner.

Of course, this is a survey study, therefore a lot more work is needed to properly generalize these results, from expanding the survey sections (beyond the meager 1 or 2 questions per section) to validation and replication. Possibly, even addressing different aspects of science because, for instance, climate change is a much more touchy subject than, say, apoptosis. And replace or get rid of the “Scientists know best what is good for the public” item; seriously, I don’t know any scientist, including me, who would answer yes to that question. Nevertheless, the trend is, like I said, sad.

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Reference:  Cacciatore MA, Browning N, Scheufele DA, Brossard D, Xenos MA, & Corley EA. (Epub ahead of print 25 Jul 2016). Opposing ends of the spectrum: Exploring trust in scientific and religious authorities. Public Understanding of Science. PMID: 27458117, DOI: 10.1177/0963662516661090. ARTICLE | NPR cover

By Neuronicus, 7 December 2016

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The oldest known anatomically modern humans in Europe

A couple of days ago, on December 1st, was the National Day of Romania, a small country in the South-East of Europe. In its honor, I dug out a paper that shows that some of the earliest known modern humans in Europe were also… dug out there.

Trinkaus et al. (2003) investigated the mandible of an individual found in 2002 by a Romanian speological expedition in Peștera cu Oase (the Cave with Bones), one of the caves in the SouthWest of the country, not far from where Danube meets the Carpathians.

First the authors did a lot of very fine measurement of various aspects of the jaw, including the five teeth, and then compared them with those found in other early humans and Neanderthals. The morphological features place the Oase 1 individual as an early modern human with some Neanderthal features. The accelerator mass spectrometry radiocarbon (14C) direct dating makes him the oldest early modern human discovered to that date in Europe; he’s 34,000–36,000 year old. I’m assuming is a he for no particular reason; the paper doesn’t specify anywhere whether they know the jaw owner’s gender and age. A later paper (Fu et al., 2015) says Oase 1 is even older: 37,000–42,000-year-old.

After this paper it seemed to be a race to see what country can boast to have the oldest human remains on its territory. Italy and UK successfully reassessed their own previous findings thusly: UK has a human maxilla that was incorrectly dated in 1989 but new dating makes it 44,200–39,000 year old, carefully titling their paper “The earliest evidence for anatomically modern humans in northwestern Europe” (Higham et al., 2011) while Italy’s remains that they thought for decades to be Neanderthal turned out to be 45,000-43,000 years old humans, making “the Cavallo human remains […] the oldest known European anatomically modern humans” (Benmazzi et al., 2011).

I wonder what prompted the sudden rush in reassessing the old untouched-for-decades fossils… Probably good old fashioned national pride. Fair enough. Surely it cannot have anything to do with the disdain publicly expressed by some Western Europe towards Eastern Europe, can it? Surely scientists are more open minded than some petty xenophobes, right?

Well, the above thought wouldn’t have even crossed my mind, nor would I have noticed that the Romanians’ discovery has been published in PNAS and the others in Nature, had it not been for the Fu et al. (2015) paper, also published in Nature. This paper does a genetic analysis of the Oase 1 individual and through some statistical inferences that I will not pretend to fully understand they arrive to two conclusions. First, Oase 1 had a “Neanderthal ancestor as recently as four to six generations back”. OK. Proof of interbreeding, nothing new here. But the second conclusion I will quote in full: “However, the Oase individual does not share more alleles with later Europeans than with East Asians, suggesting that the Oase population did not contribute substantially to later humans in Europe.”

Now you don’t need to know much about statistics or about basic logic either to know that from 1 (one) instance alone you cannot generalize to a whole population. That particular individual from the Oase population hasn’t contributed to later humans in Europe, NOT the entire population. Of course it is possible that that is the case, but you cannot scientifically draw that conclusion from one instance alone! This is in the abstract, so everybody can see this, but I got access to the whole paper, which I have read in the hopes against hope that maybe I’m missing something. Nope. The authors did not investigate any additional DNA and they reiterate that the Oase population did not contribute to modern-day Europeans. So it’s not a type-O. From the many questions that are crowding to get out like ‘How did it get past reviewers?’, ‘Why was it published in Nature (interesting paper, but not that interesting, we knew about interbreeding so what makes it so new and exciting)?’, the one that begs to be asked the most is: ‘Why would they say this, when stating the same thing about the Oase 1 individual instead about the Oase population wouldn’t have diminished their paper in any way?’ .

I must admit that I am getting a little paranoid in my older age. But with all the hate that seems to come out and about these days EVERYWHERE towards everything that is “not like me” and “I don’t want it to be like me”, one cannot but wonder… Who knows, maybe it is really just as simple as an overlooked mistake or some harmless national pride so all is good and life goes on, especially since the authors of all four papers discussed above are from various countries and institutions all across the Globe. Should that be the case, I offer my general apologies for suspecting darker motives behind these papers, but I’m not holding my breath.

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References:

1) Trinkaus E, Moldovan O, Milota S, Bîlgăr A, Sarcina L, Athreya S, Bailey SE, Rodrigo R, Mircea G, Higham T, Ramsey CB, & van der Plicht J. (30 Sep 2003, Epub 22 Sep 2003). An early modern human from the Peştera cu Oase, Romania. Proceedings of the National Academy of Sciences U S A,  100(20):11231-11236. PMID: 14504393, PMCID: PMC208740, DOI: 10.1073/pnas.2035108100. ARTICLE  | FREE FULLTEXT PDF

 2) Higham T, Compton T, Stringer C, Jacobi R, Shapiro B, Trinkaus E, Chandler B, Gröning F, Collins C, Hillson S, O’Higgins P, FitzGerald C, & Fagan M. (2 Nov 2011). The earliest evidence for anatomically modern humans in northwestern Europe. Nature. 479(7374):521-4. PMID: 22048314, DOI: 10.1038/nature10484. ARTICLE | FULLTEXT PDF via ResearchGate

3) Benazzi S, Douka K, Fornai C, Bauer CC, Kullmer O, Svoboda J, Pap I, Mallegni F, Bayle P, Coquerelle M, Condemi S, Ronchitelli A, Harvati K, & Weber GW. (2 Nov 2011). Early dispersal of modern humans in Europe and implications for Neanderthal behaviour. Nature, 479(7374):525-8. PMID: 22048311, DOI: 10.1038/nature10617. ARTICLE | FULLTEXT PDF via ResearchGate

4) Fu Q, Hajdinjak M, Moldovan OT, Constantin S, Mallick S, Skoglund P, Patterson N, Rohland N, Lazaridis I, Nickel B, Viola B, Prüfer K, Meyer M, Kelso J, Reich D, & Pääbo S. (13 Aug 2015, Epub 22 Jun 2015). An early modern human from Romania with a recent Neanderthal ancestor. Nature. 524(7564):216-9. PMID: 26098372, PMCID: PMC4537386, DOI:10.1038/nature14558. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 3 December 2016

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Earliest memories

I found a rather old-ish paper which attempts to settle a curiosity regarding human memory: how far back can we remember?

MacDonald et al. (2000) got 96 participants to fill a 15-minute questionnaire about their demographics and their earliest memories. The New Zealand subjects were in their early twenties, a third of Maori descent, a third of European descent and the last third of Asian descent.

The Maori had the earliest memories, some of them as early as before they turned 1 year old, though the mean was 2 years and 8 months. Next came the Europeans with the mean of 3 years and a half, followed by the Asians with the mean of 4 and 9 months. Overall, most memories seem to occur between 3 and 4 years. There was no difference in gender except for the Asian group where the females reported much later memories, around 6 years.

The subjects were also required to indicate the source of the memory as being personal recollection, family story or photographs. About 86% reported it as personal recollection. The authors argue that even without the remaining 14% the results looks the same. I personally would have left those 14% out if they really don’t make a difference, it would have made the results much neater.

There are a few caveats that one must keep in mind with this kind of studies, the questionnaire studies. One of them is the inherent veracity problem: you rely on human honesty because there is no way to check the data for truth. The fact that the memory may be true or false would not matter for this study, but whether is a personal recollection or a family story would matter. So take the results at face value. Besides, human memory is extremely easy to manipulate, therefore some participants may actually believe that they ‘remember’ an event when in fact it was learned much later from relatives. I also have very early memories and while one of them I believe was told ad nauseam by family members at every family gathering so many times that I incorporated it as actual recollection, there are a couple that I couldn’t tell you for the life of me whether I remember them truly or they too have been subjected to family re-reminiscing.

Another issue might be the very small sample sizes with sub-groups. The authors divided their participants in many subgroups (whether they spoke English first, whether they were raised mainly by the mother etc.) that some subgroups ended up having 2 or 3 members, which is not enough to make a statistical judgement. Which also leads me to multiple comparisons adjustments, which should be more visible.

So not exactly the best paper ever written. Nevertheless, it’s an interesting paper in that even if it doesn’t really establish (in my opinion) when do most people have their earliest true memories, it does point to cultural differences in individuals’ earliest recollections. The authors speculate that that may be due to the emphasis put on detailed stories about personal experiences told by the mother in the early years in some cultures (here Maori) versus a lack of these stories in other cultures (here Asian).

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Reference: MacDonald S, Uesiliana K, & Hayne H. (Nov 2000). Cross-cultural and gender differences in childhood amnesia. Memory. 2000 Nov;8(6):365-76. PMID: 11145068, DOI: 10.1080/09658210050156822. ARTICLE | FULLTEXT PDF

By Neuronicus, 28 November 2016

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