Wednesday, October 29, 2014

Almost This Or Almost That? Must Be The Other


Biology concepts – Protista, taxonomy, phylum, kingdom, monophyletic, paraphyletic, cladistics, algae, diatom, dinoflagellate


Euglena gracilis is an organism in the Kingdom Protista. It has
one long flagellar undulipodium, but it can also move by
amoeboid movement. It has chloroplasts and can do
photosynthesis, but it also can eat other organisms. Is it any
wonder that classifying protists is so hard?
Classifying living organisms is self-perpetuating job. Imagine if the dentist sold candy in his/her office, “Here’s your root canal and your Laffy Taffy.” Scientists try their best, but whenever you start sorting things out, you always have that pile left over that doesn’t seem to fit anywhere. So you have to rethink your categories and try again.

The best example of the inanity of classification is Kingdom Protista. The word means, “the very first,” probably because it is supposed that these were the first eukaryotes. How do we define the organisms of this Kingdom? The best we can manage is to say that they are the eukaryotes that aren't animals, plants, or fungi. Really, is that the best we can do?

In a perfect system, all the organisms of one kingdom would be descended from a single common ancestor (be monophyletic, mono = one, and phulon = tribe). But it don’t work like that. And this is where Kingdom Protista serves as a good example.

There are protists that look a lot like animals, those that resemble plants, and those that share features of fungi. No way did they all come from a single ancestor. Protista is a paraphyletic (para = near) kingdom, the group may exclude a member with a common ancestor. As such, the protists are a catch-all, those that don’t fit in some other kingdom. Protists are like pornography – hard to define, but you know it when you see it.


Classification isn’t perfect, some groups come from
different ancestors. A shows a group (in yellow) that
is monophyletic, they all come from one ancestor.
The paraphyletic group (B) shows that some groups
can’t include all descendents of a common ancestor.
And if a group is made from descendents of different
ancestors, it is called polyphyletic (C).
We already said that some behave like animals, plants, or fungi. Some are unicellular, some are multicellular, and some can be either. Some do photosynthesis, while some eat other organisms. How can you break these up into phyla, classes, orders, families, genera, and species when they are all so different?

You might do it by common ancestor; let their genes do the talking. We are learning more and more about who begot who – this is the study of cladistics. But if you break down protists into their clades – they don’t seem to make sense. Organisms that look or act similar might be in different clades, with wildly different organisms linked close together.

Alternatively, you might divide them up based on the characteristics, as Linneaus did - the animal-like protists in one phylum, the plant-like protozoans in another. But this may separate genetically related organisms into very different phyla. Same problem. How about by the way they get around? Some use flagella-like undulipodia, some use undulipodia called cilia, some use cytoplasmic crawling called pseudopodia, and others are immotile. Again, disparate organisms may be lumped together just based on their preferred mode of travel.

The idea of the "phylum" is to place the organisms in categories so that they are “more related to each other than they are to any other group.” Wow, that sounds scientific. Related based on what? We just discussed motility, genetics, and physical characteristics or behaviors.


The Kingdom Protista sits between the modern plants,
animals, and fungi, and the ancient prokaryotes. As such,
they end up being a catch all group. The right image
shows how some people group the protists based on
undulipodia characteristics, not ancestry.
And this assumes that we even know how related they are to each other and to organisms outside each phylum. Genome studies haven’t even begun to get close to establishing the ancestral relationships between all the organisms.

So we guess. And then we change things as new information becomes available. The work never ends, and the students never get to just memorize the categories.

As of today, some scientists classify protists based on a combination of the characteristics above. In the system I like best, there are 15 phyla, and we can roughly divide them as we show below. But there are six different phyla just for the protists that perform photosynthesis! The reason I like this system best -it roughly mimics the way they use undulipodia. And this is what we’re interested in today.

Kingdom Protista contains the organisms that seem to have made the most obvious uses of undulipodia. Eukaryotic flagella and cilia abound, some protists have both, and some have them only part of the time. There are six phylums of plant-like protists. Many have flagella, none that I could find have cilia. Here are some examples:


Pyrrophyta organisms will bloom and then bioluminesce
in order to scare predators away. Movement in the water
causes vesicles in the dinoflagellate to rupture via action
potential and release the reagents to make light. It’s exactly
the same system that fireflies use.
Phylum Pyrrhophyta The dinoflagellates are in this phylum; they have two flagella, one from that side that beats and one on the posterior that whips more traditionally. Some species of this protist are responsible for the red tides that poison fish and can (and have) killed humans who eat the fish. Other dinoflagellates are bioluminescent and make the water appear to be on fire (hence the phylum pyrro = fire).
             
Phylum Euglenophyta This phylum includes the Euglena gracilis organism shown in the animation at the beginning of the post. These protists also have two flagella, but one of them is reduced and doesn’t stick out. They have an eyespot, perhaps the genesis of our own eye. The eyespot helps them to move away from strong light sources, sources that would overheat them.

Euglena are common model organisms, on this world and in (near) space. They traveled on the parabolic flights to have their flagellar motions studied in zero gravity. The 2010 publication that resulted from the experiments showed that the process of beating is regulated and physiologic, as the change from hypergravity to microgravity stopped the flagellum from moving. The opposite change in gravity reoriented the cells and they started swimming to the bottom of their tank again.

The remaining phyla of plant-like protists can be included in a supergroup called the Chromista (colored organisms).  In terms of their undulipodia, the chromists tend to have two flagella, one on each end. The forward flagellum is usually longer and has lateral growths called mastigonemes. The best description for this type of flagellum is that it looks like Christmas tinsel.  The back flagellum is shorter and smooth.


These are the phyla of the Chromista; the colored protists.
Problem is, not all of them are colored and some colored
protists aren’t included in this group. Top right and bottom
left are the chlorophyta, the green algae. These are the most
recognizable algae. The bottom right is the diatoms, they have
the most interesting shapes. Look them up.
The Chrysophyta are the golden algae and diatoms. The diatoms are only flagellated when undergoing sexual reproduction, and is just the male gametes that have the flagella, sounds like male gametes in mammals doesn’t it?
  
Green algae are the ones we recognize; they belong to the Chlorophyta phylum. These are the ancestors of the land plants, and some have flagella in all stages, while others only have flagellated gametes.  We will see soon how some land plants still have flagellated gametes.

Brown algae belong to the Phaeophyta phylum. They are exceptional amongst the protists because every organism in this phylum is multicellular. No brown algae live as individual cells. Kelp is an example of brown algae. Kelp forests are multicellular example of brown algae thalli, growing to 40-60 m (130-200 ft) in height! Kelp forests are some of the most productive ecosystems on earth.      
The gametes of the brown algae are flagellated like in most of the other chromists. A 2014 study has started to look at the flagella of the chromists, using brown algae as the model organism. The study found that the flagella have functions in motility, signal transduction, and even metabolic activities.  The two different types of flagella had common proteins and proteins specific to each form, for a total of 495 different proteins associated with flagellar function and structure. For instance, only the posterior flagellum has a protein that senses blue light, and may be used for steering the organism. 


The Rhodophyta are where we get food stuffs. On the left
represents agar that can be used to make things that are like
Jello, it fills the role of the gelatin. In the middle, agar is also
used as a polysaccharide source of nutrition for growing
bacteria in the lab. On the right, nori is a rhodophyta
seaweed used in sushi.
Finally, Phylum Rhodophyta is the last of the Chromists. They are known as red algae, but you may know this protist better as seaweed. We saved them for last because they are the biggest exception in the plant-like protists.

If you’ve eaten Japanese sushi rolls, then you’ve eaten red algae in the nori that the rice and fish are wrapped in. Nori is made from several species of red algae of the genus Porphyra. Not a sushi fan? How about ice cream? Carageenans that make ice cream smooth also come from red algae.

Ice cream is reason enough to love the red algae, but there’s more. A 2014 study indicates that one compound found in the Porphyra is a strong antibiotic. Studies of 1,8-dihydroxy-anthraquinone from this red algae genus can disrupt the cell wall of Staphylococcus aureus. This is hugely important, since many strains of S. aureus (like MRSA and VRSA) are now resistant to most existing antibiotics.

Rhodophyta algae are red because although they use some chlorophylls for photosynthesis, they also use phycoerythrins and phycocyanins. Interestingly, these are the same pigments that are present in the cyanobacteria. This suggests that there is an ancestral link. The link is supported by one other factoid. Both cyanobacteria and red algae lack undulipodia!


The seaweed Rhodophyta organisms often live in the tidal
pools. The spongy material in the stalks and “leaves” is the
agar and is related to the mucin product that attaches to the
male gametes as they are released. I couldn’t find a picture of
the gametes with their mucin tails, so this will have to do.
The male gametes of red algae are at a deficit; they don’t have flagella to swim toward the female eggs. They must relay on water movement to disperse them. An older study showed that when the male spermatia are released by the discharge from vesicles, the vesicle contents can hang on to the gametes and form mucin appendages. These are then more likely to be moved around by the water.

Whatever it is, the system seems to work. A 2014 study found that fertilization success was dependent on male organism biomass, but neared 100% when there were relatively few male gametes present. This was hypothesized to be possible because low tides in the tidal pools where the organisms live greatly increase the chances of male/female interaction and fertilization. Seaweed takes advantage of the moon’s effect on the tides to ensure reproductive success – who needs flagella!?

So far we have met protists that use flagella at some point in their life cycle (except for the red algae). Notice that none of them have used cilia. Next week, how about the animal-like protists? I bet there are some exceptions there as well.




Fu G, Nagasato C, Oka S, Cock JM, & Motomura T (2014). Proteomics Analysis of Heterogeneous Flagella in Brown Algae (Stramenopiles). Protist, 165 (5), 662-675 PMID: 25150613

Wei Y, Liu Q, Yu J, Feng Q, Zhao L, Song H, & Wang W (2014). Antibacterial mode of action of 1,8-dihydroxy-anthraquinone from Porphyra haitanensis against Staphylococcus aureus. Natural product research, 1-4 PMID: 25259418

Maggs CA, Fletcher HL, Fewer D, Loade L, Mineur F, & Johnson MP (2011). Speciation in red algae: members of the Ceramiales as model organisms. Integrative and comparative biology, 51 (3), 492-504 PMID: 21742776

Strauch SM, Richter P, Schuster M, & Häder DP (2010). The beating pattern of the flagellum of Euglena gracilis under altered gravity during parabolic flights. Journal of plant physiology, 167 (1), 41-6 PMID: 19679374




For more information or classroom activities, see:

Kingdom Protista –


Euglena –

Red tide –

Pyrrophyta –

Kelp –



Wednesday, October 22, 2014

Death By Haunted House


Halloween is a time when fear is invited. The rush of
adrenaline in a controlled environment is life-
affirming. Not much else to comment on here,
except that he seems to have excellent oral hygiene
for a chainsaw-wielding maniac.
A big man with the chainsaw and the gaping wound on his face jumps out from around the corner and growls. You leap backward and scream, your heart pounding in your ears. You’re ready to either take that power tool and teach him a lesson or to run like the kid from Home Alone. Sure you're scared, but could it kill you?

Haunted houses are great examples of stimuli that induce the fight or flight response. The name suggests that two mechanisms are fighting it out, but there is really only one biologic pathway. Whether an animal tries to escape or tries to defend itself, its muscles and mind need to be ready.

In response to a threat, the brain triggers the release of epinephrine and cortisol from your adrenal glands into the blood. As a result, your heart beats faster and stronger, your blood vessels dilate to move more blood, and your lung vessels dilate to exchange more oxygen for carbon dioxide. Equally as important, your liver breaks down glycogen (a sugar storage molecule) to glucose and dumps it into your bloodstream.

All these processes work together to increase your alertness and increase the power of your muscles for a short time - like when mothers who lift cars off their small children. You are now ready to respond to the threat; however, there is an exception – you may do nothing at all.

One of the major control mechanisms of the fight or flight response is the autonomic nervous system. This is part of the peripheral nervous system (PNS, outside the brain and spinal cord) and transmits information from the central nervous system to the rest of the body. The autonomic system controls involuntary movements and some of the functions of organs and organ systems.

Parts of the autonomic system acts like a teeter-totter, it's their relative balance that controls the outcomes. In the fight or flight response, the sympathetic system predominates and your heart rate increases and your blood vessels dilate.

The autonomic nervous system is divided into sympathetic
and parasympathetic. Much of the sympathetic innervation
comes from the thoracic and lumbar regions, while most
parasympathetic innervation is carried by the vagus nerve.
You can see that the two systems have largely opposite effects.
But what if the parasympathetic system gained an upper hand for a short time? The parasympathetic system controls what is sometimes called the rest and digest response – the opposite, get it? The heart slows, the blood vessels constrict in the muscles, blood moves from muscles to the gut, and glycogen is produced from glucose. Remember the old adage - don’t swim after your dine; eating puts you in a parasympathetic state of mind! (O.K., I just made it up)

Many people have had the experience of parasympathetic domination coincident to a threat, for some folks it proceeds long enough to have an observable result – they faint. The vagus nerve (a primarily parasympathetic cranial nerve) controls much of this response, so it may be called the vasovagal response. The parasympathetic-mediated reduction in blood oxygen and glucose do not spare the brain - and when your brain is starved of oxygen and glucose, you pass out. Fighting or fleeing is difficult when you are unconscious.

Lower animals will faint as well, but they have additional defenses along these lines. Mammals, amphibians, insects and even fish can be scared enough to fake death – ever hears of playin’ opossum?

There are overlapping mechanisms for feigned death, from tonic immobility (not moving) to thanatosis (thanat = death, and osis = condition of, playing dead). When opossums employ thanatosis, they fall down, stick their tongue out, and even emit a foul smelling odor from glands around their anus. One study in crickets showed that those who feigned death the longest were more likely to avoid being attacked, so this is definitely a survival adaptation – except for the opossums scared by cars and decide to play dead in the street.

Feigned death deters predation, so being scared ain’t all bad. Many predators won’t eat something that is already dead, so not moving could protect them from attack. Another theory is the clot formation hypothesis; it contends that slowing the heart and blood flow forces blood clots to form faster. This will reduce the amount of blood lost during an attack, improving chances for survival.

New evidence is suggesting that even humans undergo tonic immobility. Post-traumatic stress patients asked to relive their trauma show definite signs of tonic immobility, although first they show signs of "attentive immobility," which is more voluntary then the tonic form.

I highly recommend this new book for popular
biology and medicine readers. Zoobiquity explores
a powerful reality. No disease--whether physical or
psychiatric--is uniquely  human. We have much to
learn from animal patients and from the doctors who
care for them.  The impact on human medicine
will be significant.
We have discovered one exception to the rule; instead of fight or flight, it is really fight, flight or faint – but can we take it further? Should it be fight, flight, faint, or fatality? The answer is yes, but it's very rare. Sometimes animals (including us) don’t just feign death when afraid – they actually die.

In their book, Zoobiquity, What animals can teach us about health and the science of healing, Barabara Natterson-Horowitz and Kathyrn Bowers talk about capture myopathy in animals. Small traps that limit movement, cause pain, or are associated with loud noises can cause spontaneous death in live-trapped animals. Several decades ago it was not unusual for 10% of trapped animals to die. In birds, the death rate often rose to 50%! More humane methods of live trapping have reduced the death rate, but point is made – these animals were scared to death.

A human analogy of capture myopathy may have been identified. People that have had a sudden emotional shock, perhaps the death of a loved one, some other tragic occurrence, or crippling fear can undergo something that looks a lot like a heart attack, even if they have no history of heart disease.

This sudden loss of heart rhythm has been called broken-heart syndrome, but is more accurately termed stress cardiomyopathy (SCM). In these cases, the heart actually changes shape! The part of the heart that pumps blood out to the body (left ventricle) balloons out and loses the ability to pump efficiently. Dramatically less efficient pumping leads to symptoms just like a heart attack.

In the normal left ventricle of the heart (left image), the muscle is
thick around the space (in red) and contracts strongly. In SCM, the
space is ballooned at the based (middle image) and the muscular wall
is thin, giving a weak contraction. The change in shape can be seen in
the superimposed images on the right, as is the octopus trap (tako-tsubo)
that the original Japanese describers thought the lesion looked like,
hence the early name takotsubo cardiomyopathy.
In most cases, SCM and the change in heart shape resolve after a time and there is little left to show they were present, but if they go too far for too long, they can cause death – called sudden cardiac death. There are many causes for sudden cardiac death, but emotion and fear are definitely among them.

I was wondering if there was a link between SCM in humans and capture myopathy in animals, so I asked Dr. Natterson-Horowitz. She told me that those studies have not been done yet; we don’t know if there is a heart shape change in captured animals. I think it would be hard to get approval for studies that would intentionally scare animals to death.

One interesting connection amongst fight or flight, capture myopathy, and SCM is the catecholamine dump involved. Epinephrine and norepinephrine control all three responses, and in humans they control even more. Recent evidence shows that catecholamines mediate the production of fear memories.

You remember fearful events more readily and more vividly as a survival adaptation. Strong memories help you to avoid dangerous situations in the future. In this way, your mind can affect how your body responds to a threat. We will see this again in just a bit.

All babies have an exaggerated startle reflex until
they are several months old, but in some cases it may
contribute to SIDS. An exaggerated startle can lead to
apnea (temporary breathing cessation) and this can be
compounded by a depressed heart rate if the baby is
sleeping on its stomach. Some clinicians also theorize
that swaddling may contribute by exaggerating the startle
due to confinement stress, but by far the greatest
association with SIDS is stomach sleeping.
However, dying or nearly dying from fright isn’t all in your head either; some conditions can predispose you to dying from a sudden shock. One unfortunate condition is called hyperekplexia, or startle disease of the newborn. Newborns with one or more of several mutations in the glycine receptor (an inhibitory receptor in the brain used in neuron signal transmission) can lead to these babies dying from loud noises or a sudden touch.

The startle reflex involves squinting to protect the eyes, raising the arms, hunching the body to protect the back of the neck, as well as inducing the fight or flight response. With the loss of inhibitory signaling, the signals that ramp up a startle response are unchecked and can lead to uncontrolled beating of the heart (ventricular fibrillation, VF) and sudden cardiac death.

Just as some cases of the fight or flight response going too far, the startle can sometimes lead to VF. A recent study has shown that the bigger the perceived threat, the bigger the startle reflex will be. Also, if there is a fearful environment prior to the threat, then the startle will be bigger. Once in a long while, it goes too far.

Similar to hyperekplexia, there is another condition that could lead to VF and death in the environment of fear. Long QT syndrome can either be inherited or acquired later in life, and affects the time between beats of the heart. In long QT, the interval is variable and longer, and can lead to inefficient beating and VF.

On echocardiogram tracings a heartbeat has a certain shape, and 
each point has a corresponding name which is represented 
by a letter. If the time between the Q point and the T point 
is too long, the heart rhythm is subject to disintegrating 
into chaos. In the 1990’s, the antihistamine Seldane was 
taken off the market due to QT interaction when it was 
given with the antibiotic erythromycin.
Highlighting our circle of fear and the body, evidence presented here and here suggest that SCM can cause acquired long QT syndrome. Dr. Natterson-Horowitz said today many patients with long QT may have implantable defibrillators. In earlier days, however, these patients were warned not to use alarm clocks or to jump into cold water – they could startle themselves to death.

Long ago we talked about premature burial. It would be easy to envision a person waking up inside a coffin, and then dying from the fright of being buried alive! Does this mean that you are putting yourself in peril every time you visit a haunted house at Halloween? Probably not, remember that deaths from fright are exceedingly rare. Maybe you could just feign death, and the horrible monster will leave you alone.

For the next couple weeks - back to the science of flagella. Undulipodia are present in many phylums, except for where they aren’t. On the other hand, some types of organisms don’t have undulipodia - except for those that do.


Greek, R. (2012). Zoobiquity: What Animals Can Teach Us About Health and the Science of Healing. By Barbara Natterson-Horowitz and Kathryn Bowers. Knopf Doubleday Publishing: New York, NY, USA, 2012; Hardback, 320 pp; $16.23; ISBN-10: 0307593487 Animals, 2 (4), 559-563 DOI: 10.3390/ani2040559

Volchan, E., Souza, G., Franklin, C., Norte, C., Rocha-Rego, V., Oliveira, J., David, I., Mendlowicz, M., Coutinho, E., Fiszman, A., Berger, W., Marques-Portella, C., & Figueira, I. (2011). Is there tonic immobility in humans? Biological evidence from victims of traumatic stress Biological Psychology, 88 (1), 13-19 DOI: 10.1016/j.biopsycho.2011.06.002


For more information or classroom activities, see:

Fight or flight –

Autonomic nervous system –

Thantosis/tonic immobility –

Stress cardiomyopathy –

Hyperekplexia –

Long QT syndrome -


Wednesday, October 15, 2014

Frankenstein Meets Genetic Modification

Biology concepts – Frankenstein, asystole, ethics, genetically modified organisms, genetically modified foods, synthetic biology, decomposers, electroconvulsive therapy


Mary Shelly was wedded to Percy and friend to Lord
Byron, one of the great poets of the early 19th century.
But she was a fair writer on her own. Note the bolts on the
monster's neck. These were added by make-up artist Jack
P. Pierce. He said they were electrodes, not bolts, even
though Mary Shelly never actually wrote that
the good doctor used electrodes on the body.
Can you think of anything scarier for Halloween than an irresponsible scientist letting his creation loose on the world? Now imagine that his creation is something that violates our sense of decency and our reverence for the dead. Well, that’s the story behind Mary Shelly’s Frankenstein.

Who's the victim of the story? Is it Dr. Frankenstein, who’s family is murdered or is it perhaps his monster, who was brought into the world and abandoned? He lives his second life shunned by all, misunderstood, lonely, unable to live with dignity or even die at all.

This is a big story for a 17 year old to pen. Yep, that’s how old Mary Shelly was when she wrote Frankenstein (published when she was 21 in 1818). Despite her age and inexperience, she rolled out one of the greatest novels ever. It was both romantic and a criticism of romance. It sparked the science fiction genre and was the beginning of horror stories.

The movies and stories about Frankenstein’s monster usually highlight the way in which the monster was created and his ugliness and hatred, but that isn’t what the book is about. It’s a story of responsibility in science and toward others.

The Age of Enlightenment had just ended when Frankenstein was written, and the Romantic period was in full bloom. A switch from science to emotion meant that the facts and discoveries about the world now needed to be examined, not just accepted. Here was Mary found her message – a person must be responsible for the things he/she creates – be they physical things, knowledge, or opinion.


Electrical impulses make muscles move. Adding salt to
freshly skinned frog legs is a lot like hitting the with a
mild jolt of electricity. This is like Galvani demonstrated
with the corpse of the murderer and the image Mary
Shelly evoked in her novella.
The science of the monster’s reanimation was not the focus, but Mary had good knowledge of the latest science of the day, and this is what informed her making of the monster. Sir Humphrey Davy of the Royal Institution of Science had just stated that chemistry would, eventually, control the conversion of dead matter into living matter.

This was combined with the advances in electricity at the time. Just before 1800, Luigi Galvani had published on the ability of electricity to excite the muscles of dead animals – the innate electrical force of living tissue came to be known as “galvanism.” In 1803, Galvani applied an electrical charge to the corpse of executed murderer Thomas Forster, and the body jolted and moved – a good visual for Mary.

So could a body be reanimated as Shelly relates in the novel? Nope…. at least, not yet. Let’s examine why.

Dr. Frankenstein uses a corpse, with some implied modifications through surgery. Not good. Immediately after death, cells that are starved for oxygen stop making ATP. ATP is required to maintain lipid membrane compartments and in general for the integrity of the cell. Once there is no oxygen and no flow of energy, the enzymes designed to break down wastes, toxins, and old organelles for recycling are released to the cytoplasm and start to destroy the cell.

Consider the process of rigor mortis. Muscle contraction requires ATP not to contract, but to release the contraction (see this post). With no ATP, the muscles become rigid in their contraction about 3-4 hours after death. Rigor lasts for about 12-20 hours, and is only released by the process of cell destruction that we described above.


Frankenstein’s monster better have been a very fresh
corpse. Decomposers like bacteria and fungi are already
in and on your body; it’s your immune system that keeps
them at bay. Once dead, we’re all just food for worms,
prokaryotes, protists , fungi, and of course buzzards.
Mary doesn’t describe anything to overcome this problem. But there are other problems as well. No life, no immune system. This is what keeps our fungal, bacterial, and protist flora in check. Without a working immune system, the microorganisms that are normally growing in and on us will be unchecked and start to grow and feed on the corpse. This is where they get their name, “decomposers.” Mary doesn’t mention anyway to overcome that problem either.

What about the electrical problem? We use electricity in our neural system and in our heart. Your brain is an electrochemical machine, using ions to generate and electrical current down axons. Electroconvulsive therapy (ECT) is useful in treating some forms of depression and schizophrenia and mania, but we don’t really know how it works yet.

Several hypotheses exist; none or all of which may be correct. ECT may alter neurotransmitter concentrations, which would change the degree to which impulses are transferred or suppressed from one neuron to another. It may work to prune back some neural connections in the brain, or it may work to stimulate hormone release that could alter the brain chemistry. A 2014 review provides more information on the various theories of ECT mechanism.


From top to bottom we see a normal heart rhythm, and a
then a ventricular fibrillation that CAN be treated with
electric shock. Below that is a pulseless rhythm, which
looks normal but doesn’t move the heart, and then asystole,
with no pulse at all. The bottom two CANNOT be treated by
shocking the heart. That’s why they called it a defibrillator,
not a heart starter.
Electricity is used in the heart as well. We can modulate the rhythm of the heartbeat with a pacemaker, which is just a low voltage shocking device. When a person is dying from a poor heart rhythm (ventricular tachycardia or fibrillation), we can use a defibrillator to shock the heart back toward a normal rhythm.

Mary’s error: electrical shock won’t start a stopped heart (called asystole, a = not, and systole = contraction), despite what you’ve seen on the TV shows. For asystole, the treatment is CPR with a shockingly large dose of adrenaline every 5 minutes.

Dr. Frankenstein couldn’t have reanimated his self-digesting, microbiological dinner plate of a corpse with an electric shock, but if the muscles hadn’t gone into rigor yet, he might have been able to get a short slam dance out of him. But then, this isn’t really the point of the story.

Frankenstein’s monster was alive and wandering the world alone a mere 1/5 of the way through the story, so it’s really a story of how to deal with the products of science. Erasmus Darwin (Charles’ grandfather) had introduced the idea of mutations or “monstrosities” being passed on or inherited – so Mary now had the essence of the story. Who is the monstrosity - the monster or the scientist who creates and then abandons it?


Erasmus Darwin was Charles granddad. He was an
inventor, poet, natural philosopher and I hear a great
cook. One of his poems predicted the discovery of the
Big Bang, he also suggested the idea of natural
selection and mutation and sketched out a liquid
oxygen and hydrogen rocket.
One indication that a story is a classic is whether its themes are applicable in different eras. Frankenstein may be even more applicable to our times than it was to Mary’s. Current debates are boiling over concerning the uses and limitations of science.

The issue most often compared to Frankenstein’s monster is genetically modified organisms (GMOs). Have you heard the term, “Frankenfoods?” This is the name that opponents of GMOs and particularly GM foods use to taint the agricultural biotechnology industry.

The fear is that by tampering with nature and introducing genes into organisms, we are creating monsters that might have unexpected effects on us. It’s a good marketing campaign idea, and it has stuck in the minds of the public.

Europe and Russia have banned all GM foods out of fears that they may contain toxins or mutagens that would harm the consumers. One fear is that DNA from the genetically modified organisms would be transferred to the eater and combine with their own DNA. That is a scary sounding idea.

The problem is, you take up DNA from the food you eat every day, although not whole genes as the fear warrants. Digestion breaks down DNA, so we take up mostly nucleotides and short stretches of nucleic acid. No recorded evidence exists of uptake of an entire gene.


Dr. Frankenstein used all natural body parts, no artificial
sweeteners, additives or preservatives, and good old-
fashioned electricity. If he was sold in the market, the
monster could be labeled as organic! No genetic
modification here.
Websites and books talk about the dangers of GM foods, but the evidence hasn’t shown up in the scientific literature. What few papers have announced negative ramifications of GM foods have been retracted or have such vague conclusions as to apply to any food at all. I’ll give a typical example.

In 2012, a researcher named Seralini from the U. of Caen announced that an herbicide used with GM foods (glyphosate in Roundup) causes tumors. He didn’t just publish it, he had a press conference and concurrent release of his book on the subject and videos in three different languages. It turns out that he also had a company that was preparing to market a product as a “protectant” against glyphosate. The study was subsequently retracted, but a modified version with a conclusion that “more study is needed” was re-published in a lesser journal (see note below).

Other studies on the dangers of GM foods have been correlative, meaning that when you see “A”, you often see “B.” But that doesn’t mean that A causes B, or that B causes A. Remember this: correlation does not imply causation.

The truth is, we need more studies. There are real issues to be dealt with, such as - does introduction of a particular gene cause plant toxins to be increased – this could be bad for us. The idea is the same as in Mary Shelly book – we must be responsible for those things we make. No GMO or GM food should go to market without extensive testing.

The testing to date shows that there are no health risks associated with GM foods. Longitudinal studies from 2014, 2013, and 2012 of live stock feeds showed that animals fed GM crops over five generations showed no ill health effects and their meat was exactly like that of animals fed conventional feed. By the middle of 2013, over 600 studies showing that GM foods carried no health risks had been peer-reviewed and published. The key is always the same - responsible and thorough testing.


Synthetic biology has arrived. Vanilla is a very expensive
crop to produce. But a gene has been constructed and
vanillin is now produced in yeast. They ferment sugar and
produce vanillin. This is more natural than artificial vanilla,
and contains many of the metabolites that make vanilla
taste like vanilla.
The problem of hidden agendas like Seralina's does go both ways; a 2014 editorial on the safety of GM foods was written by a Monsanto employee, the company that markets GM corn and soybeans. Society must be diligent and demand topnotch, transparent, and responsible science. This was one of Shelly’s themes, Frankenstein conducted his work in private, with no comment from society about how or whether it should be done at all.

The next generation of people will have more issues to deal with, like synthetic biology (not merely taking a gene from one organism and putting it another, but constructing a gene or genes from nucleotides and then inserting them). How to ensure good use of science? - transparent methods and results, no hidden agendas, no jumping to conclusions, and a very science literate population that can judge and reason for themselves. And that’s why we learn biology.

Next week - Halloween is a time to focus on what's scary and what's dead. Can you actually be scared to death?




The retraction of the 2012 study of Seralini in Food and Chemical Toxicology can be found here. It was republished in modified form in the journal, Environmental Sciences Europe in 2014, but with no peer-review.



Goldstein, D. (2014). Tempest in a Tea Pot: How did the Public Conversation on Genetically Modified Crops Drift so far from the Facts? Journal of Medical Toxicology, 10 (2), 194-201 DOI: 10.1007/s13181-014-0402-7

Tufarelli V, & Laudadio V (2013). Genetically Modified Feeds in Poultry Diet: Safety, Performance and Product Quality. Critical reviews in food science and nutrition PMID: 24915369

Van Eenennaam AL, & Young AE (2014). Prevalence and impacts of genetically engineered feedstuffs on livestock populations. Journal of animal science, 92 (10), 4255-78 PMID: 25184846

Snell C, Bernheim A, Bergé JB, Kuntz M, Pascal G, Paris A, & Ricroch AE (2012). Assessment of the health impact of GM plant diets in long-term and multigenerational animal feeding trials: a literature review. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 50 (3-4), 1134-48 PMID: 22155268

McCall WV, Andrade C, & Sienaert P (2014). Searching for the mechanism(s) of ECT's therapeutic effect. The journal of ECT, 30 (2), 87-9 PMID: 24755719

 
For more information or classroom activities, see:

Genetically modified organisms/foods –