Vertical limits of bat echolocation

Contrary to popular belief, bats are not actually blind—this misconception stems from the fact that more than half of the 900 species do rely upon echolocation to navigate during their nocturnal activities. Echolocation, the use of sonar (sound navigation and ranging) with special morphological and physiological adaptations, enables bats to “see” with sound! Bats emit high-frequency calls and listen for the returning echoes, which provide them with the information they need to negotiate complex terrain and track moving prey in the dark. This echolocation is so precise they can discriminate differences of less than one millimeter in surface textures [1]!

I was surprised to learn that this impressive capability has a big flaw. In a recently published paper [2], scientists found that bat echolocation has a tough time with some environmental features. Specifically, smooth, vertical surfaces (think metal or glass plates on a building) provide a false environmental cue to the bat, tricking the animal into sensing that it is actually flying into open air! As you can imagine, this does not end well for the bats. Sadly, bats are often found dead or injured near buildings and other smooth structures, and the false cues the bats pick up from the buildings may be a major culprit. 

The sensory trap that a smooth building may create is not the only one that bats can fall prey to. In fact, Dr. Stefan Grief demonstrated in a previous study [3] that smooth metal or plastic plates also act as a sensory trap when laid on the ground; bats mistook these surfaces for water. In his recent study [3] at the Max Planck Institute for Ornithology, Dr. Grief and his colleagues flew greater mouse-eared bats around a dark, rectangular flight tunnel. Near one of the tunnel’s corners, the researches placed a metal plate either on the ground or against the wall. The result? All but two of the bats out of 21 hit the vertical plate at least once, but none of the bats ever hit the horizontal plate of any other part of the tunnel.

However, as noted previously, bats are not blind and they do integrate echolocation and vision to navigate. Why then do smooth, vertical structures pose such a navigational hazard to bats? That is still a question pondered by bat biologists, and one that Dr. Greif aims to explore in the future.


  1. Simmons, J. A., Ferragamo, M. J., & Moss, C. F. (1998). Echo-delay resolution in sonar images of the big brown bat, Eptesicus fuscusProceedings of the National Academy of Sciences of the United States of America95(21), 12647–12652.
  2. Greif, S., Zsebok, S., Schmieder, D., & Siemers, BM. (2017). Acoustic mirrors as sensory traps for bats. Science, 357(6355), 1045-1047.
  3. Greif, S., & Siemers, B. M. (2010). Innate recognition of water bodies in echolocating bats. Nature Communications1, 107–. http://doi.org/10.1038/ncomms1110.





Making insulin at Eli LillyWho am I to disagree? – Well I like sweet things but being a type I diabetic for 20 years, I remember times when technology wasn’t quite where it is today. March 5, 1997, southern Germany, a little kid drinks roughly 20 bottles of soda and feels dizzy at night. That was the day I was diagnosed with type I diabetes. I went to the hospital and was put on the top notch therapy available at the time. To test my blood sugar, I had to squeeze a huge drop of blood onto a little strip. After a minute, I wiped it down, checked the color indicating a rough estimate how my blood sugar was doing, and then inserted the strip into a little machine that would count down from 120, one count per second, to zero, when I would then learn that my sugar was out of range, or roughly 7-8 times the amount a healthy person has in their blood. I got insulin – the fancy kind that the founders of Genentech (a big pharma company!) developed in E.coli and made some of their riches with- not the old fashioned insulin that was isolated from pigs’ pancreases at the slaughterhouse. You know, it was way better than just staying alive, I would have a normal life, so I was told. That being said, my mum got up every night to check my blood sugar at midnight, 3 am, 6 am and then throughout the day of course. I had to inject two different insulins with syringes – one every time I ate, the other one every 4-6 hours. Yet it seemed so much better than the stories I heard from other people about not knowing their sugar levels most of the time, except the one time a week you got to see the doctor who had a meter. It also seemed better than the life of the child I was in a room with, who had 3 hours of dialysis every day because he had no working kidneys. And it was of course all free, because Germany has a working healthcare system.

I traveled the world and the seven seas… Fast forward 20 years to 2017. I live in the US and diabetes care has undergone quite a revolution. I test my blood sugar now with a barely visible drop of blood and get a result within five seconds – no wiping, no color codes. The meter directly sends the results to my insulin pump, which I carry 24/7. I only use one type of insulin, which basically works instantaneously, and I don’t need to worry about injecting it regularly because the pump is programmed to do that. My pump does basically everything for me, it actually learns how my blood sugar reacts to things I eat and does all the insulin dosing for me. I just tell it what I’m eating and hope I make good estimates. I’m in a priority access program for this “artificial pancreas” and can’t quite believe how we far we have come to get to this point. It comes with a price tag (since we’re in the US, where we haven’t figured out health insurance yet) but it is closer to a “normal” life than I’ve ever had. It is an amazing feeling to look back at how treatment has progressed for a condition that killed people mercilessly until the middle of the last century and still does in many parts of the world.

Everybody’s looking for something. I’ve also been looking at news articles about how we’ll be able to cure diabetes entirely for about as long as I have had the condition. Of course, it’s always only preclinical work and some mouse was successfully injected with an insulin producing cell or something along those lines, and to me the whole topic goes right along the lines of the many talks on science ethics I’ve been to, where misrepresentation or over-representation of results to the general public is always a topic. I’ve been called by many excited aunts who read in the newspaper that I was going to be cured but, I still think I’ll see a cure in my lifetime.

Some of them want to use you. I’m also sure that Big Pharma won’t be too excited when a cure is found. Diabetes is essentially a dream of any pharma company. Your life depends on their product, and it keeps you alive and paying for a long time. I sometimes wonder if that is part of why we’re still excited about a pump that manages your diabetes for you. It is time to push forward… we have come a very long way for sure from where we were 20 years ago, but I’m also a lot more cynical about it now.

- MGS -

image source: http://americanhistory.si.edu/blog/2013/11/two-tons-of-pig-parts-making-insulin-in-the-1920s.html


Sophia Spencer and #BugsR4Girls

In a story that has traveled across the globe, Sophia Spencer, an eight year old girl, who loves insects but was teased for it by her peers, has since been connected to myriad entomologists in large part due to her co-author, Morgan Jackson’s use of social media. Sophia – whose love for insects was inspired by a visit to a butterfly conservatory at the age of two - is now published in Annals of the Entomological Society of America. The publication, entitled, “Engaging for a Good Cause: Sophia's Story and Why #BugsR4Girls” [1] discusses Sophia’s experience of being mocked and teased in school for her love of bugs and her subsequent loss of engagement , which prompted her mother to reach out to the Entomological Society of Canada. Jackson, a social media volunteer at the Society, used twitter to rally support.  The piece evaluates the social media and wider media response following Jackson’s tweet, which garnered an outpouring of encouragement for this young scientist, and highlights the potential for social media to make positive impact across multiple platforms. The paper also delves into important topics such as stereotypes often imposed upon women in the workplace, as well as the underrepresentation of women in science.

More to the point, the wide-scale response brought back Sophia’s confidence and “old funny self”.  Sophia’s story is as heartwarming as it is important, and is especially poignant amidst our currently divisive political climate.  Public encouragement and support transformed the haunting spectre of bullying into a message of hope – and it is my hope that this story continues on and inspires children who might feel that they are judged or shunned because they might be different, because the truth is, we are all different! How much better to celebrate our differences! This story has many refreshing messages including that of the love of knowledge at the heart of scientific inquiry, how people can work together to overcome serious obstacles, and how science and social media can actually bring out the best in people.



[1] Jackson, MD, Spencer S. Engaging for a good cause: Sophia’s story and Why #BugsR4Girls. Annals of the Entomological Society of America.2017 110(5), 2017, 439–448 doi: 10.1093/aesa/sax055




Commonly used asthma medications appear to regulate epigenetic mechanisms and may be associated with decreased risk for Parkinson’s disease

Arrows indicate Lew bodies, arrowheads, Lewy neuritesIn an interesting new study, β2-adrenoreceptor ligands were found to regulate the α-synuclein gene (SNCA) via epigenetic mechanisms [1].  Further, prolonged use of the asmtha medication salbutamol, which is a β2-adrenoreceptor agonist, was linked to reduced risk associated with Parkinson’s disease [1]. Results from the study demonstrated that the β2-adrenoreceptor regulates histone H3 acetylation and DNA replication in the cell, controlling the amount of α-synuclein [1,2]. Lewy bodies, one of the neural hallmarks of Parkinson’s, are protein aggregates mainly formed from α-synuclein. Lewy bodies are connected to the death of neuronal cells as they are mainly found in brain areas where the most severe neuronal loss is seen [3]. Thus decreasing the amount of α-synuclein in neuronal cells is thought be one way to potentially prevent Parkinson's disease.

After a compound screen, the researchers identified four that reduced SNCA gene activity in human cells and further tests showed that β2-adrenoreceptor agonists led to reduced H3 acetylation, SNCA expression, and the amount of α-synuclein in both cell culture and in animal studies [1]. These results prompted researchers ask whether β2-adrenoreceptor agonist or antagonist medications might influence the prevalence of Parkinson’s disease. By studying the medical records of nearly 5 million Norwegians, they found that those with long term use of salbutamol for their asthma, had lower risk of Parkinson’s, whereas people using propranolol for heart conditions appeared to have increased risk [1]. These findings suggest that the β2-adrenoreceptor may play a role in Parkinson’s disease and opens new doors for Parkinson’s disease research. Perhaps in the future Parkinson’s could be treated, or even pre-treated using epigenetic drugs.




[1] Mittal S, Bjørnevik K, Im DS, Flierl A, Dong X, Locascio JJ, Abo KM, Long E, Jin M, Xu B, Xiang YK, Rochet JC, Engeland A, Rizzu P, Heutink P, Bartels T, Selkoe DJ, Caldarone BJ, Glicksman MA, Khurana V, Schüle B, Park DS, Riise T, Scherzer CR: β2-Adrenoreceptor is a regulator of the α-synuclein gene driving risk of Parkinson's disease. Science. 2017;357(6354):891-98

[2] Bannister AJ, Kouzarides T: Regulation of chromatin by histone modifications. Cell Res. 2011;21(3):381-95

[3] Michael J. Fox Foundation for Parkinson’s Research: Alpha-synuclein and Parkinson's Disease. https://www.michaeljfox.org/understanding-parkinsons/living-with-pd/topic.php?alpha-synuclein

Image: Ingelsson M (2016) Alpha-Synuclein Oligomers—Neurotoxic Molecules in Parkinson's Disease and Other Lewy Body Disorders. Front. Neurosci. 10:408. doi: 10.3389/fnins.2016.00408


Not so fun facts about psychiatry...

Out of all the medical disciplines psychiatry may arguably have the worst reputation. Unfortunately, this view is not entirely undeserved; the first two Nobel Prizes awarded to psychiatrists were for the discovery that infecting patients with malaria - a form of pyrotherapy - could cure certain psychotic disorders (a consequence of syphilis, and the induced fevers either killed the pathogen - or the patient) and the invention of lobotomy, in which lesioning neural connections, or basically, scraping out pieces of the frontal lobes, made aggressive patients complacent. While much easier to manage afterwards, these patients also lacked any recognizable personality. In all fairness, while these approaches were both literal and metaphorical stabs into the dark, unknown realm of mental illness, terrible treatments such as pyrotherapy and lobotomy were the only alternatives to a lifetime shuttered away in an asylum.  Unfortunately, these institutions were often overcrowded, typically poorly maintained psychiatric hospitals with the main purpose of preventing patients from doing damage to themselves or society because no cures were available.

It is until the middle of the last century that Freud’s legacy firmly controlled the discipline of psychiatry in the United States. It was a widely held belief that all psychiatric illness stemmed from unresolved conflicts of the subconscious that simply needed to be uncovered and discussed to resolve the condition.  Though a neurologist by training, Freud’s approach was not based on biological data but rather on the interpretation of patient case studies fueled by theoretical considerations, many of which when judged by today’s standards appear to be based upon idiosyncratic convictions. For example, today we know that autism is not caused by “frigid mothers” and schizophrenia is not a consequence of obscure inner conflicts.

Initial attempts to classify neuropsychiatric illness in the United States grew out of the 1840 census.  The first Diagnostic and Statistical Manual (DSM) was a medical document which emerged from the assessment of soldiers during World War II. While some biological aspects of mental illness had been considered by this time, a major step forward was the development of the DSM-III, the first guidebook to facilitate the diagnosis of psychiatric illness in a systematic way, based on data rather than on purely Kraepelinian views or Freudian anecdotes. DSM-III was published in 1980(!) as a response to public frustration over inconsistent diagnoses and treatments in psychiatry. The practitioners realized that in order to maintain public trust in psychiatry, insurance coverage for psychiatric procedures, and to find actual cures for devastating illnesses such as depression, bipolar disorder and schizophrenia, a data-based approach was indispensable.

Now, almost 40 years and two DSM versions later, we have a variety of psychopharmacological treatment options. We have also realized that neither pharmacological treatment nor psychotherapy alone can solve the big problems in neuropsychiatric illness, and that combined, these approaches are only a small step towards actually understanding and curing the most devastating disorders. Even with our most advanced neuroimaging technology it is still painstakingly difficult to advance our knowledge. But, taking the history of treatment into perspective along with our evolving  understanding of mental illness, at least we no longer infect patients with malaria or blindly poke around in the frontal lobes of patients suffering from psychoses. We are still a long way from general, reliable solutions but psychiatric illness is no longer a life sentence to an asylum.



Sources/Further Reading:

Lieberman, J., Ogas, O., (2015). Shrinks: the Untold Story of Psychiatry. London: Weidenfeld and Nicolson.

Jamison, Kay Redfield, (1995). An Unquiet Mind. New York: Knopf.

Decker, Hannah, (2013). The making of DSM-III. Oxford: Oxford University Press.


Schematic of a transorbital lobotomy:

Source: https://www.theparisreview.org/blog/2017/04/18/the-art-of-the-lobotomy-and-other-news/