Pic of the day: The most prevalent infection

00cat toxo - Copy (2)

Reference: Flegr J, Prandota J, Sovickova M, Israili ZH (2014). Toxoplasmosis – A Global Threat. Correlation of Latent Toxoplasmosis with Specific Disease Burden in a Set of 88 Countries. PLoS ONE, 9(3): e90203. doi:10.1371/journal.pone.0090203. Article | FREE fulltext PDF

By Neuronicus, 22 March 2016

Advertisements

Now, isn’t that sweet?

80sugar - Copy

When I opened one of my social media pages today, I saw a message from a friend of mine which was urging people to not believe everything they read, particularly when it comes to issues like safety and health. Instead, one should go directly at the original research articles on a particular issue. In case the reader is not familiar with the scientific jargon, the message was accompanied by one of the many very useful links to blogs that teach a non-scientist how to cleverly read a scientific paper without any specific science training.

Needless to say, I had to spread the message, as I believe in it wholeheartedly. All good and well, but what happens when you encounter two research papers with drastically opposite views on the same topic? What do you do then? Who do you believe?

So I thought pertinent to tell you my short experience with one of these issues and see if we can find a way out of this conundrum. A few days ago, the British Chancellor of the Exchequer (the rough equivalent of a Secretary of the Treasury or Minister of Finance in other countries) announced the introduction of a new tax on sugary drinks: the more sugar a company puts in its drinks, the more taxes it would pay. In his speech announcing the law, Mr. George Osborne was saying that the reason for this law is that there is a positive association between sugar consumption and obesity, meaning the more sugar you eat, the fatter you get. Naturally, he did not cite any studies (he would be a really odd politician if he did so).

Therefore, I started looking for these studies. As a scientist, but not a specialist in nutrition, the first thing I did was searching for reviews on the association between sugar consumption and obesity on peer-reviewed databases (like the Nature journals, the US NIH Library of Medicine, and the Stanford Search Engine). My next step would have been skimming a handful of reviews and then look at their references and select some dozens or so of research papers and read those. But I didn’t get that far and here is why.

At first glance (that is, skimming about a hundred abstracts or so), it seems there are overwhelmingly more papers out there that say there is a positive correlation between sugar intake and obesity in both children and adults. But, when looking at reviews, there are plenty of reviews on both sides of the issue! Usually, the reviews tend to reflect the compounded data, that’s what they are for and that’s why is a good idea to start with a review on a subject, if one knows nothing about it. So this dissociation between research data and reviews seemed suspicious. Among the reviews in question, the ones that seemed more systematic than others are this one and this one, with obvious opposite conclusions.

And then, instead of going for the original research and leave the reviews alone, I did something I am trying like hell not to do: I looked the authors and their affiliations up. Those who follow my blog might have noticed that very rarely do I mention where the research has taken place and, except in the Reference section, I almost never mention the name of the journal where the research was published in the main body of the text. And I do this quite intentionally as I am trying – and urge the readers to do the same thing – to not judge the book by the cover. That is, not forming a priori expectations based on the fame/prestige (or lack thereof) of the institution or journal in which the research was conducted and published, respectively. Judge the work by its value, not by its authors; and this paid off many times during my career, as I have seen crappy-crappity-crap papers published in Nature or Science, bloopers of cosmic proportions coming from NASA (see arsenic-DNA incorporation), or really big names screwing up big time. On the other hand, I have seen some quite interesting work, admittedly rare, done in Thailand, Morocco or other countries not known for their expensive research facilities.

But even in research the old dictum “follow the money” is, unfortunately, valid. Because a quick search showed that most of the nay-sayers (i.e. sugar does not cause weight gain) were 1) from USA and 2) had been funded by the food and beverage industry. Luckily for everybody, enter the scene: Canada. Leave it for the Canadians to set things straight. In other words, a true rara avis poked its head amidst this controversy: a meta-review. Lo and behold – a review of reviews! Massougbodji et al. (2014) found all sorts of things, from the lack of consensus on the strength of the evidence on causality to the quality of these reviews. But the one finding that was interesting to me was:

“reviews funded by the industry were less likely to conclude that there was a strong association between sugar-sweetened beverages consumption and obesity/weight gain” (p. 1103).

In conclusion, I would add a morsel of advice to my friend’s message: in addition to looking up the original research on a topic, also look where the money funding that research is coming from. Money with no strings attached usually comes only from governments. Usually is the word, there may be exceptions, I am sure I am not well-versed in the behind-the-scenes money politics. But if you see Marlboro paying for “research” that says smoking is not causing lung cancer or the American Beverage Association funding studies to establish daily intake limits for high-fructose corn syrup, for sure you should cock an eyebrow before reading further.

Reference: Massougbodji J, Le Bodo Y, Fratu R, & De Wals P (2014). Reviews examining sugar-sweetened beverages and body weight: correlates of their quality and conclusions. The American Journal of Clinical Nutrition, 99:1096–1104. doi: 10.3945/ajcn.113.063776. Article | FREE PDF

By Neuronicus, 20 March 2016

All mammals bigger than 3 Kg pee in 21 seconds

pee in 21 - Copy (2)The Ig Nobel is a prize awarded for “research that makes people LAUGH, then THINK — real research, about anything and everything, from everywhere”. Although it started as a parody of the real Nobel prize, over the past two decades it gained much respect and is coveted by many researchers, almost – but not quite – like the real Nobels.

The 2015 Ig Nobel Prize in Physics went to a group of researchers who established, once and for all, how long it takes for a mammal to pee. That’s right, pee.

Sometimes, the time spent procrastinating on YouTube, where you start by looking for something specific and end up 3 hours later watching funny cat video compilations, may not be a complete waste. For example, Yang et al. (2015) gathered 28 YouTube videos of various animals peeing. They also went to the local zoo and videotaped 16 more animals at the Atlanta Zoo emptying their bladders and collected their urine.

Their analysis showed that any mammal larger than 3 Kg pees in an amazing constant amount of time: 21 ± 13 s. That’s right: the cat and the elephant, the dog and the zebra, all pee in about 21 seconds. Too bad they didn’t include the humans in this experiment. I guess there would have been serious questions regarding the videotaping of a man or a woman’s privates…(but they could have sent their students to the toilet with a stopwatch…) Nevertheless, the knowledge about human urethra diameter, bladder size and flow rate (mL/s) can give an estimate of human urination duration, which is about the same as other mammals.

So…. why is that? After all, you would expect that emptying the 160 L of urine (that’s the capacity of an elephant bladder ) will to take longer than 1.4 L (the dog’s bladder capacity). The answer lies in the specifications of the urethra. The longer and wider the urethra is, the faster the urine flow. As the researchers put it, “the urethra is analogous to Pascal’s Barrel: by providing a water-tight pipe to direct urine downward, the urethra increases the gravitational force acting on urine and therefore, the rate at which urine is expelled from the body” (p. 11936). Therefore, the urethra is not just a tube between bladder and genitals, as the medical textbooks define it, but is and amazingly adaptive, robust and efficient system. Contrary to previous thinking, the peeing time is not dictated by muscular contraction resulting in bladder pressure, but by the length and width of the emptying tube.

Of important note, animals smaller than 1 Kg do not follow the what is probably called by now the Hu Constant Urination Law (Hu is the Principal Investigator of the lab and last author of the paper). Why? Because their urethrae are so small that gravity may not help them much. In other words, capillary and viscous forces force them to expel urine in drops in less than 2 seconds. (So astronauts in space pee in drops?)

The researchers also produced a mathematical model of their data (of course). Such model can be used for studying urological disorders in humans. Until now, these studies have been conducted in rodents, which turns out that may not be as good models after all. Another application is in engineering, when designing draining that does not depend on the size of the system.

Overall, a funny, very graphic (has videos attached), highly mathematical and interesting paper to read. The prize is well-deserved.

Reference: Yang PJ, Pham J, Choo J, & Hu, DL (19 Aug 2014, Epub 26 Jun 2014). Duration of urination does not change with body size. Proceedings of the National Academy of Sciences of the United States of America, vol. 111 no. 33, pp. 11932–11937, doi: 10.1073/pnas.1402289111 Article | FREE PDF

By Neuronicus, 9 March 2016

You were not my first choice either!

lego
Sexually receptive mice females prefer a Lego brick over a male if their oxytocin neurons are silenced.

Over the past five years or so, dopamine stepped down from the role of the “love molecule” in favor of oxytocin, a hormone previously known mostly for its crucial role in pregnancy, labor, delivery, lactation, and breastfeeding. Since some interesting discoveries in monogamous vs. polygamous voles (a type of rodent) pointing to oxytocin as essential for bonding, many studies implicated the chemical in all sorts of behaviors, from autistic to trusting, from generosity to wound healing.

Nakajima, Görlich, & Heintz (2015) add to that body of knowledge by finding that only a small group of cells in the medial prefrontal cortex express oxytocin receptors: a subpopulation of somatostatin cortical interneurons. Moreover, these neurons are gender dimorphic, meaning they differ from male to female: the female ones have twice as many action potentials upon application of oxytocin as compared to male’s.

And here is the more interesting part:
– Females in the sexually receptive phase of their estrus whose oxytocin neurons were silenced preferred to interact with a Lego brick over a male mouse (which, as you might have guessed, in not what they typically choose).
– Females that were not in their sexually receptive phase when their oxytocin neurons were silenced still preferred to interact with a mouse (male or female) over the Lego brick.
– Silencing of other neurons had no effect on their choice.
– Silencing had no effect on the males.

Hm… there are such things out there as oxytocin inter-nasal sprays… How soon do you think until the homeopaths, naturopaths, and other charlatans market oxytocin as a potent aphrodisiac? And it will take some deaths until the slow machine of beaurocracy turns its wheels and tightens the regulations on the accessibility to the hormone. Until then… as the cartoons say, don’t try this at home! Go buy some flowers or something for your intended one… it would work better, trust me on this.

Reference: Nakajima M, Görlich A, & Heintz N (9 October 2014). Oxytocin modulates female sociosexual behavior through a specific class of prefrontal cortical interneurons. Cell. 159(2): 295–305. doi:10.1016/j.cell.2014.09.020. Article | FREE FULLTEXT PDF

By Neuronicus, 23 October 2015

Making new neurons from glia. Fully functional, too!

NeuroD1 transforms glial cells into neurons. Summary of the first portion of the Guo et al. (2014) paper.
Fig. 1. NeuroD1 transforms glial cells into neurons. Summary of the first portion of the Guo et al. (2014) paper.

Far more numerous than the neurons, the glial cells have many roles in the brain, one of which is protecting an injury site from being infected. In doing so, they fill up the injury space, but they also prohibit other neurons to grow there.

Guo et al. (2015) managed to turn these glial cells into neurons. Functioning neurons, that is, fully integrated within the rest of the brain network! They did it in a mouse model of stab injury and a mouse model of Alzeihmer’s in vivo. Because a mouse is not a man, they also metamorphosized human astrocytes into functioning glutamatergic neurons in a Petri dish, that is in vitro.

It is an elegant paper that crossed all the Ts and dotted all the Is. They went to a lot of double checking in different ways (see Fig. 1) to make sure their fantastic claim is for real (this kind of double, triple, quadruple checking is what gets a paper into the Big Name journals, like Cell). Needles to say, the findings show a tremendous therapeutic potential for people with central nervous system injuries, like paralyses, strokes, Alzheimer’s, Parkinson’s, Huntington, tumor resections, and many many more. Certainly worth a read!

Reference: Guo Z, Zhang L, Wu Z, Chen Y, Wang F, & Chen G (6 Feb 2014, Epub 19 Dec 2013). In vivo direct reprogramming of reactive glial cells into functional neurons after brain injury and in an Alzheimer’s disease model. Cell Stem Cell, 14(2):188-202. doi: 10.1016/j.stem.2013.12.001. Article | FREE FULLTEXT PDF | Cell cover

By Neuronicus, 18 October 2015