Wednesday, April 27, 2016

Your Body Has A Photographic Memory

Biology Concepts – innate immunity, acquired immunity, memory response, influenza

Your body is exposed to tens of thousands of foreign molecules every day. Some can do you harm, some can’t. Your immune system sorts them by matching receptors on immune cells to molecules on the foreign objects.

Legos and biology are a good fit. They can be used to analogize the 
rearrangement T cell receptor genes or hypervariable regions 
of antibody genes, or they can be used to model the entire 
body. One scientist uses them to model building 
complex systems from repetitive units. And they’re fun.
Think of the receptors as Legos; your DNA provides for several different types of Lego blocks to be made, and your immune cells can rearrange the different types and put them together as a receptor, so there can be millions of different receptors. Each immune cell has just one type of Lego receptor, although it may have many copies of that one form. Each different Lego receptor will fit, key in lock style, with a specific foreign molecule.

The receptors exist on many types of cells, and antibodies sometimes function as receptors when attached to the surface of specialized immune cells. Even circulating antibodies (Ab) in the blood take the form of key and lock systems, whether as single Ab, dimers (2) or pentamer (5) complexes.

The immune system of higher animals can be described as several sets of pairs. Each member of a pair attacks a problem in a certain way, and has independent pathways, but each pair also has overlap and must work together in an overall response. We could spend weeks just on this system, but lets look at the major parts by describing each pair, from largest to smallest.

Innate immunity vs. adaptive immunity – the innate immune responses are fast but short. They don’t depend on your immune system recognizing the specific foreign molecule (antigen) with a specific receptor, but respond with the same types of reactions no matter what it is. Almost all plants and animals have some form of innate immune system.

Vertebrates take the immune system further. They have developed an adaptive immune system that does depend on your immune system recognizing the specific foreign invader. It then generates a tailored response to that one foreign organism or molecule. The faster, but more general, innate response helps the slower, but longer lasting and more specific, adaptive response to kick in.

These are cartoons of an antibody. The model on the left is a much 
more realistic image. The Fc portion is the same through most 
antibodies (c= constant), while the gene rearrangement takes place 
in the light chain and heavy chain variable regions. The 
different variable regions are the Lego blocks that can be put 
together differently to make the millions of different antigen 
binding sites.
Humoral immunity vs. cellular immunity – when an antigen is recognized by an adaptive immune cell (often through antigen presentation by the innate system), an early response is for the cell to divide and make more of itself. You don’t get sick from one bacterium infecting you; many infect you at once and then divide to become many more. You need many copies of that specific immune cell in order to battle the invading horde of bacteria.

The immune cells can generate an antibody response (humoral immunity) and/or trigger specific killing and directing cells to be produced (cellular immunity). The antibody (produced by B lymphocytes) is a protein that recognizes the specific antigen. The cellular immune response is mediated primarily by T lymphocytes.

However, B cell-produced antibodies are important for T cells to do their work, and antibodies also help the innate immune response to keep working after specific recognition has been made. In addition, the cellular immune response can control and ramp-up the humoral response. You see what I mean about each pair being separate but connected.

Effector T cells vs. regulatory T cells – There are pairs of T cells as well. I use the term “effector T” cells to lump CD8+ and CD4+ lymphocytes together (CD = cluster of differentiation markers on the cell surfaces). Effector T lymphocytes are either directly cytotoxic (CD8+, cyto = cell and toxic = damaging) or command (CD4+) the many adaptive responses. Effector cells are contrasted with regulatory cells, which include regulatory and suppressor T lymphocytes. The purpose of these cells is to stem the effector response so it doesn’t get out of hand; parts of the immune response are inflammation and non-specific cell killing – too much of that and you die too.

Memory Immune System – This last part of the immune response is not a member of a pair. When your innate immune system is activated, it ramps up, does its job, and hopefully is turned back off. The adaptive immune system responds to the antigen by producing more cells, antibodies and chemical signals (cytokines), and after the invader is vanquished you want this response to diminish as well. The innate system always starts over from zero, but the adaptive system remembers the infection you had.

The dendritc cell on the left is an innate immune cell that works 
to present the antigen to the adaptive immune cells (Th1, 
Th2, and B cells). The adaptive cells reproduce and make 
cytokines to stimulate other immune cells. They also generate 
some memory cells that recognize the same antigen, but stay 
around for a long time and can react strongly and quickly.
During the adaptive response, some of the produced immune cells become “memory cells,” they still recognize the antigen from the initial infection, but hang around in larger numbers; in many cases they circulate in your body for the rest of your life. If your body sees that specific antigen again, the memory response can be re-initaited very quickly and very aggressively. You might be infected again, but your memory response is so fast and effective that you never know it.

In a world without vaccines, you are infected, get the disease, recover (hopefully), and then have a memory immune system for that antigen. Vaccines take the initial infection and disease out of the equation; you get to develop a memory without having had the experience!

As we discussed last week with smallpox, vaccines present your immune system with the antigen in the form of a dead or weakened pathogen, or just the antigen molecule itself. Your body doesn’t know the difference, it develops an adaptive and memory response just as if it were the real infection.

In the majority of cases, you develop memory B and T lymphocytes when infected or vaccinated. However, there are exceptions. Most antigens cannot fully activate B cells to make antibody, they have to be helped along by antigen-activated T cells. But there are T cell-independent antigens that can fully activate B cells on their own. In these infections, you can develop a B cell memory without a T cell memory.

On the other hand, there are other infections that develop a full memory response, but it is not useful. Influenza is an example of this. Influenza has been around for thousands of years; some years we have severe epidemics or even world-wide pandemics. The 1918-1919 Spanish flu pandemic killed over 50 million people, many more than the contemporaneous WWI (16 million deaths).

Flu is difficult to vaccinate against because it keeps changing. Influenza virus has two antigens, called H (hemagglutinin) and N (neuraminidase). These are the molecules on the virus particle that your body mounts an immune response against.

The H molecule on the viral coat binds to sialic acid receptors on respiratory cells and allows the virus to enter. When the newly produced viruses bud off of the cell, they place H on the cell surface, but there are still host sialic acid receptors there as well. These receptors would bind up the H and prevent the new viral particles from attaching to and infecting other cells, so the N molecule cleaves the sialic acid receptors from the new viral particles.

Influenza virus can mutate by antigenic drift or antigenic
shift. The top line shows that by passing from person to
person, the antigens (and virulence) shift slightly. The lower
line shows that by passing through other animals and
recombining, the antigens can have small or big changes. When
shifted virus moves into humans, it’s a recipe for a pandemic.
The problem arises when the H and N antigens mutate.... and they do. Scientists have identified 16 different classes of H’s and 9 different N’s, and they can be paired up in many combinations. Small changes (antigenic drift) usually mean that memory might have a slight protective effect, and major epidemics do not occur. But major changes in H and N (antigenic shift) mean that previously infected people have no memory protection.

Different strains of influenza virus can infect the same animal (often pigs and ducks – thus avian flus and swine flus) and can mix their H’s and N’s. What emerges and might be transmitted to humans can be a virus with H’s and N’s similar to years past, or with new H’s or N’s. That is why a new vaccine must be produced each year, after scientists see which H’s and N’s the new virus has and how much they have drifted. Avian flu is H5N1, while swine flu is H1N1. However, antigenic drift means that each H1N1 will not be exactly like the previous H1N1 to emerge. The 1918 pandemic was caused by an antigenically shifted H1N1 sub-strain.

Like flu, other infections may not provide life-long memory. If the memory response is weak or the initial response was not strong, then memory may fade over time. This is why some vaccinations require boosters in later years. A fading of the memory response to influenza is also implicated in the need for yearly vaccinations.

Here's a great book that discusses both the biology
and sociology of influenza. There are great personal
stories as well as medical detective work. This
pandemic was a jolt that brought infectious
disease research into a new century. I highly
recommend it.
Now for the exception to the exception. Influenza changes each year, so memory does not help much, but a 2010 report from scientists in Hong Kong suggests that prior exposure to any seasonal influenza (either by infection or vaccination) might have been a contributing factor as to why the 2009 pandemic of antigenically shifted swine flu (H1N1) was much milder than expected.

The 2009 seasonal flu vaccine did not have any cross-reactivity with pandemic H1N1, so the scientists suggest that previous years seasonal influenzas did generate some memory response that was partially effective against 2009’s H1N1 swine flu. Cross-reactivity means that the H and N antigens were not identical to previous version; the Legos don’t fit together exactly, but they were similar enough to fit together and initiate a partial response. Once again, we see that getting sick may save your life down the line.

Next week will look at examples wherein having one disease can protect you from catching another.

Mathews, J., McBryde, E., McVernon, J., Pallaghy, P., & McCaw, J. (2010). Prior immunity helps to explain wave-like behaviour of pandemic influenza in 1918-9 BMC Infectious Diseases, 10 (1) DOI: 10.1186/1471-2334-10-128

Kash, J., Qi, L., Dugan, V., Jagger, B., Hrabal, R., Memoli, M., Morens, D., & Taubenberger, J. (2010). Prior infection with classical swine H1N1 influenza viruses is associated with protective immunity to the 2009 pandemic H1N1 virus Influenza and Other Respiratory Viruses, 4 (3), 121-127 DOI: 10.1111/j.1750-2659.2010.00132.x

Cowling, B., Ng, S., Ma, E., Cheng, C., Wai, W., Fang, V., Chan, K., Ip, D., Chiu, S., Peiris, J., & Leung, G. (2010). Protective Efficacy of Seasonal Influenza Vaccination against Seasonal and Pandemic Influenza Virus Infection during 2009 in Hong Kong Clinical Infectious Diseases, 51 (12), 1370-1379 DOI: 10.1086/657311

For more information or classroom activities, see:

innate immunity:

adaptive immunity:

memory immune response:

influenza virus:

Wednesday, April 20, 2016

Lucky For Me, I’m Diseased

Biology Concepts – disease, vaccination, single nucleotide polymorphisms

Jill Bolte Taylor is an Indiana University neuroscience
professor who suffered a massive stroke. She recognized
what was happening and has translated her thoughts
and feelings into a narrative to help us understand. She
is eloquent in describing how her stroke has affected her
in a positive way. --- Soon to be a major motion picture!

You rarely hear someone say how glad they are to be sick – unless a business meeting, unit test, or visit to the in-laws is involved. Robust health is a sign of good genes, and animals (including humans) instinctually seek out good genes when selecting mates. We don’t like to be sick, and we don’t want others (potential mates) to see us being sick.

True, there is that one person in a thousand who argues quite eloquently that an illness showed them another side of life, expanding their world-view and making them a better person. I applaud this attitude, but did you ever notice that it’s only the survivors that can gain this insight?

Our entire health care system is based on the idea that it is preferable to not be sick. The best way to bring this about is to reduce the chances that we will encounter anything that might provoke a response from our body, including pathogens (disease causing organisms, from pathos = disease and genique = to produce) and allergens (living or non-living molecules that can induce an allergic response).

But what does it mean to be “sick?” If you are infected by a pathogen, are you necessarily sick? There are infections that are subclinical or asymptomatic (without signs of disease), and there are carrier states, when a person is infected and can transmit the disease, but does not have symptoms. Are these people still sick?

You can be in a social situation where you feel empathy or regret, “I feel just sick about how I treated her.” Is this true sickness? Your mental state of mind is important in your health; if you talk yourself into being sick, are you really sick?

Single nucleotide polymorphisms (SNPs) are one base
changes in a gene sequence. “Polymorphism” means
that the population will show different sequences at this
point. SNPs may produce no change in the protein, but in
some cases they may change the shape or function of the
protein just slightly. This may not cause disease, but may
affect the course of a disease, or how drugs will work in
that individual. SNPs may one day lead to personalized
medicines in a new science called pharmacogenomics.
Drugs will be designed to work best for your particular
DNA sequence.

What about genetic mutations? Can everyone with a genetic mutation be considered sick? If yes, then we are all sick, because everyone one of us has thousands, perhaps millions of single nucleotide polymorphisms (differences in a single base of DNA that might lead to change in function of a protein). I would suspect that most of us have larger mutations as well; the older we are, the more mutations we have. Some mutations render a person predisposed (more likely) to develop a disease – is this person sick even before he/she acquires the illness?

Osteoarthritis is a disease that can wear away joint surfaces and necessitate hip or knee replacement. My father has two artificial hips due to osteoarthritis, but does that make him sick or ill?

You see someone coughing, sneezing and blowing his/her nose. It could be due to respiratory allergies or a bacterial or viral infection. Are they sick in one instance, but not the other? I have seen TV ads that try to convince allergy sufferers that they are a menace to society, and should be embarrassed about their condition (unless they use their wonderful product). The entirety of the message in our society is that any illness or condition is a deficit.

To summarize our man-made rule: diseases are bad, and being exposed to diseases is bad, so keep your environment clean and antiseptic. Don’t get me wrong – I am not mocking the rule. I would rather not be sick - so much so that I am careful where I go and what I touch – in some places I simply choose not to breathe, just to be on the safe side. Disease prevention is an important part of life expectancy.

But are there exceptions? Is it sometimes good to get sick, either in general or with some specific disease? I think you know there must be exceptions, otherwise we would just be left with an interesting discussion of what it means to be sick. I bet you can even come up with at least example on your own. There are in fact boatloads of general and specific exceptions to this rule. Let’s take a few weeks and cover a few examples that are exceptions to "disease is bad" rule.

Our first exception is one that you may have already thought of – vaccines. With many vaccines, getting the disease is the key to not getting the disease – counterintuitive, isn’t it? I will use smallpox as an example of the idea that sickness prevents sickness, but there are many others.

Smallpox survivors had a very distinct look. It was
unfortunate that the lesions showed up most heavily on
the face and arms. Thankfully, the disease has been
eradicated, and the virus only exists now in two
laboratories, at the Centers for Disease Control in Atlanta
and the “vector” lab in Siberia. Whether these stocks
should be destroyed is a matter of some debate.
Smallpox, until recently, had been a scourge on mankind for thousands of years. The infection is caused by a virus (Variola major or minor) and may present in several different forms. It was a very dangerous disease, the hemorrhagic form was almost universally lethal. Those that survived smallpox were marked for life (see picture).

In the 1790’s, Edward Jenner of Gloucestershire, England noticed that milk hands and milkmaids seemed to be immune (from Latin, immunis = exempt) to smallpox and he wondered why that might be. The milking workers told him they felt protected because they worked with diseased cows, those that had a mild disease called cowpox. For some reason, having had cowpox kept the milkmaids from catching smallpox.

It turns out that cowpox and smallpox are enough alike that having one will prevent you from having the other. It was on this basis that Jenner developed the first vaccine (Latin from vaccinus = from cows, coined by Louis Pasteur as a tribute to Jenner). By pricking the skin of a young boy with a needle contaminated with the pus from a young milkmaid with cowpox, Jenner showed that this could prevent infection with smallpox (Jenner wasn’t the first to vaccinate with cowpox, just the first to prove it prevented smallpox).

Contracting cowpox, a mild disease that did not kill or scar, could prevent one from catching smallpox, a terrible disease that often killed and left survivors with permanent reminders of their ordeal. Maybe getting sick ain’t always so bad. We will talk more next week about just how vaccination works to produce a protective immune response.

Cowpox vaccination is an example of using one disease to prevent another, but even 100 years before Jenner it was recognized that you could prevent smallpox by giving people smallpox. Strange, isn’t it? Variolation was performed by blowing ground smallpox scabs up the nose of another person, or by pricking them to place the material under the skin.

The virus in the olds scabs was definitely variola, it was just weakened (attenuated) by its age and its time outside of healthy cells. The virus was recognized by the body and an immune response is mounted, but the virus was too weak to produce a fulminant infection was eliminated by the body. But not before it helped the vicitim become immune to subsequent smallpox infection.

Poliomyelitis infection led to a paralysis of the muscles.
This could include the respiratory muscles, so iron lungs
were used to force air in and out of the patients’ lungs.
Before a vaccine was developed, a treatment was
developed by an unaccredited nurse from Australia.
Sister Elizabeth Kenny overcame much professional and
gender prejudice to show that heat and passive exercise
to retrain muscles was better than the then used
immobilization therapy. Try to see the biopic “Sister
Kenny” on TCM some time.

Attenuated vaccines do carry some risk. Paralytic poliomyelitis has almost been eradicated thanks to Jonas Salk’s inactivated (dead) vaccine injections and Sabin’s orallly taken, attenuated vaccine. The attenuated vaccine is better at preventing a natural infection, but in rare cases the vaccine virus can revert back to a wild form and result in iatrogenic (iatro = doctor and genique = to cause) polio, also called vaccine associated paralytic poliomyelitis (VAPP). Thankfully, widespread use of the Salk and Sabin vaccines in the 1950’s has made vaccination in the US (as of 2000) and UK (2004) unnecessary.

Many of the vaccines used today are engineered in a laboratory from just a portion of the organism. By using only the antigenic portion (that part that elicits an immune response) of the virus, there is no risk of iatrogenic disease. If the viral portion is produced in a laboratory using DNA technologies, it is called a recombinant vaccine. In some cases, the antigenic part of the virus is weak on its own, so these subunit vaccines may be conjugated (joined to) some other molecule that will elicit a stronger immune response.

Unfortunately, there is a growing number of people ignoring history and putting are their children and the population at large at risk. Some parents’ reluctance to vaccinate is based on a single 1998 study in which vaccination was linked to autism, even though the author of the paper, Andrew Wakefield, has been convicted of scientific fraud and banned from the practice of medicine. Wakefield was an investor in a company that was going to offer medical testing for vaccine-associated autism and as well as assist in autism/vaccine lawsuits, so he falsified his data in an effort to make his company profitable.  

As a result of the vaccine scare, the UK has seen a rise in the number of measles, mumps, and rubella cases in the last decade. These are diseases associated with childhood, but can cause severe disease or death in many victims, especially adults.

Pertussis, also called whooping cough, is transmitted only
from person to person. If no around you has it, you can’t
get it. However, symptoms may not show for 6 weeks after
infection, so everyone should be vaccinated. The coughing
can be so violent that it breaks blood vessels around the
eyes and nose – and it can kill young children.

Many in the US are also selecting to apply for vaccination exemption due to medical, religious, or personal beliefs; therefore, disease incidence is rising in America as well. In July, 2012, the CDC reported that the US had 18,000 cases of pertussis (whooping cough) in the past year, including an epidemic of more than 2500 cases in Washington state from January to June. This points out the need for vigilance in monitoring, as some of these patients had been vaccinated. This suggests that that the protection may not be lifelong; a booster vaccination may be necessary, although it is also telling that Washington state has one of the highest vaccination exemption rates in the country.

This also brings up the idea of herd immunity. There are some people who have been vaccinated, but protection is not complete. The elderly may not be able to react completely even if vaccinated, as might the very young. Some vaccinations may not take - how many time have you had an antibody titer test to make sure your vaccine worked? It is very rare to get titers unless something is suspected and you are already sick. Therefore, many people must count on the vaccination of the herd - a critical percentage of population needs to be protected in order to keep the incidence of the disease below a crucial level. If the level rises - as with too many people choosing not to vaccinate - then the incidence will sky rocket because it will affect those people who don't happen to know they are not protected. Un vaccinated people affect everyone, not just themselves.

Next week we will look at vaccine driven immune responses in a bit more depth, in an effort to understand why we have to get a flu vaccination every year.

Centers for Disease Control and Prevention (CDC) (2012). Pertussis epidemic - washington, 2012. MMWR. Morbidity and mortality weekly report, 61, 517-22 PMID: 22810264

For more information on these subjects, or classroom activities, see:


Single nucleotide polymorphisms and pharmacogenomics:


Lack of vaccination:

Wednesday, April 13, 2016

Ivy League Climber

Wrigley Field was originally called Weeghman Park,
after a local lunchroom owner. The first team to call
the park home was the Chicago Whales - strange name
for a city on a freshwater lake. The ivy on the outfield
wall is actually Boston Ivy and Japanese Bittersweet,
since English Ivy would have a tough time with Chicago
winters- just like everyone else.
Wrigley Field is the venerable 1914 baseball stadium on Chicago’s north side. One of its most characteristic features is the ivy covered outfield wall that occasionally swallows a hit ball, never to be seen again – a ground rule double.

The question of the day:
Does ivy stick to a wall or grab it, and will ivy have enough strength to destroy the wall over time?

English ivy (Hedera helix) is of the Araliacae family, but doesn’t have spines like some other species in the family, like the aptly named devil’s walking stick (Aralia spinosa). I can’t imagine a Chicago Cub outfielder diving into a wall covered with devil’s walking stick to make a catch; although being a Cubs fan can feel like that.

English ivy is an evergreen climbing vine, but it will grow along the ground just fine if there is nothing available to climb. Not unlike Kudzu in the US south, ivy can become invasive and choke out other plants, creating “ivy deserts.”

As English ivy grows along the ground, it shows its juvenile form. It has light colored leaves with lobes and points, no flowers, and can form roots very easily. When the ivy finds something on which to grow vertically, it transitions to the adult stage, with leaves that are less lobed or pointy, less root growth and can produce flowers and berries.

The stem of ivy is not capable of supporting the weight of the vine – it can’t stand up on its own, but yet it easily grows 30 m (98 ft) against the force of gravity and can reach heights of more than 90 m (300 ft) in conifer trees with seemingly no problem whatsoever. The mechanism by which it accomplishes this was investigated by none other than Charles Darwin, but much more recent work is showing the ivy plant to be quite a surprise.

English ivy sends out thousands of adventitious roots
per foot. These roots are responsible for the ivy’s
adherence to the substrate. They are aerial roots, but
can also grow into the ground and act as regular roots
as well.

Darwin noted that ivy sends out adventitious roots from its stem. This is where the devil’s club or walking stick and the ivy are similar, but in the case of ivy, they are induced by a vertical substrate and don’t cause pain.

Adventitious roots are those that arise from someplace other there where you would expect them, like directly from the sides of stems, or off leaves, or off old woody roots. In the case of ivy, they are aerial, adventitious roots, since they do not get buried in dirt. They can still collect water, but are protected from dehydration by having a thicker, waxier surface.

Darwin also noted that ivy was not wrapping the adventitious roots around some protruberance on the vertical surface to allow the vine to cling. Those that do wrap around and grab are called tendril climbers, and include clematis, grapes, and sweet peas. In some cases, the clinging apparatus will have only that function, in other plants they will grasp, but can leaf or fruit as well.

Other vines use their stems to wrap around a vertical substrate, the stem twiners and tendril climbers are both examples of thigmotropism (thigmo = to touch, and trope = turn). Interestingly, honeysuckle always coils clockwise while wisteria always turns counterclockwise.

Pea plants grab hold of vertical surfaces using tendrils
that coil upon contact with a surface. The tendrils are
modified leaves, stems, or shoots. Supposedly they taste
good and are a vogue ingredient in cooking nowadays.

English ivy doesn’t twine, it doesn’t tendril wrap, and it doesn’t burrow into a flat surface to gain an anchor, although it will exploit a crack and grow through or along it. Neither does it just grow up until it touches something and then use its growth to ramble through and around the substrate. Climbing rose is an example of a rambler, it will use its hook shaped thorns to help it stand up as it grows through and around another plant.

No, English ivy uses a chemical adhesive secreted by it adventitious rootlet ends in order to stick to a vertical surface – it can even cling to something as smooth as glass. The secretion is yellowish and forms circular dots on the vertical surface. It is very sticky, and becomes stickier as it dehydrates.

The compound contains polysaccharides that act as a carrying agent for discrete nanoparticles (70 nm diameter) that are responsible for the adhesion to the wall. Amazingly, the way ivy clings to a wall is very similar to how a gecko walks up a wall or hang upside down.

This is an electron micrograph of the nanoparticles of
ivy adhesive. The particles have an average diameter
of about 65 nm and can get so close to the substrate
that the electrons and nuclei of each will interact and
attract one another.

The nanoparticles are like the nanohairs on a gecko’s (or fly’s) foot. They increase the surface area of the material greatly and are so small that they can make very intimate contact with the surface. They get so close to one other that they can use van der Waal’s forces on the atomic level to attract one surface to the other. Studies from 2010 showed that the interactions of the nanoparticles in the yellowish ivy secretion were enough to create the bond, and mimics using polystyrene nanoparticles have become excellent adhesives.

But the amazing abilities of the ivy nanoparticles don’t stop there. They seem to disperse and absorb light energy much better than the metal nanoparticles that we currently use in our sunscreens. Titanium oxide and zinc oxide are the current state of the art in terms of reflecting, dispersing and absorbing ultraviolet rays, but it seems that ivy nanoparticles are 70X better at these jobs than are the metal oxide particles. Our next generation of sunblock may come from ivy – talk about green technologies!

Ivy can help with sun damage in another way as well. By covering the walls of a building, ivy keeps the heat in during the winter by acting as insulation and reflects the sunlight away in the summer, keeping the building warmer or cooler as the case may be. Ivy also deflects much of the rain from getting to the surface that is covered, so it can protect against acid rain damage or other weathering.

But ivy can do damage as well. Any surface that has gaps, like shutters against a wall or wood siding will allow ivy to grow in the cracks and pull them from the wall over time.  It may not create holes in mortar or brick, but it will grow into them and then expand when the stem fills with water. This hydraulic action can break down stone over time and bring a building down if given enough time and opportunity.

The mass of an ivy vine can also cause damage. It can cover an entire plant and keep it from getting enough sunlight to live, but it can also make it top heavy and cause it to fall in a strong wind. I have wondered about this in terms of ivy growing on a building. How much weight does it add to the wall, and would it ever be enough to pull the wall down?

The quintessential ivy covered cottage. How much weight
must this add to the house? The roof could easily collapse,
and who knows what is living in there. But there is no
arguing that it looks great.

Look at an ivy-covered wall. How much must all that vine weigh? Forestry workers pulling ivy off of conifers say it is not unusual for there to be over 2000 lb.s (907 kg) of ivy on a single tree.

I have been wondering how to estimate the mass of ivy that is clinging to a wall. You might estimate the square footage covered, then cut out one square foot and find its mass, and then do the math to find the total. But if you cut from the bottom, then everything above it will die – not the best experimental design. If you cut from the top or edge, the vine will be immature and have less mass per sq/ft than the average along the entire wall.

Maybe you could advertise free ivy removal, find a client, measure the square footage and the find the mass of everything you take down. But remember, that is one great adhesive; you will probably leave a decent amount behind, leading to a low estimate. Or, you will bring parts of the wall with it, leading to an overestimation.  Any ideas?

Next week we will begin a series of posts on getting sick - the exceptional thing is that sometimes it is good for you to get sick.

Lijin Xia, Scott C Lenaghan, Mingjun Zhang, Zhili Zhang and Quanshui Li (2010). Naturally occurring nanoparticles from English ivy: an alternative to metal-based nanoparticles for UV protection Journal of Nanbiotechnology DOI: 10.1186/1477-3155-8-12

Wednesday, April 6, 2016

I’ll Fly Home—Or Not

The snowy owl is sedentary, meaning it does not
migrate. The males are almost perfectly white,
while the females and juveniles can have black
barring. They sit, look, and listen for their prey,
which includes small rodents and even other birds.
Their hearing is good enough to let them target a
mouse under the snow from hundreds of yards away.

The Arctic tern travels from north of the Arctic Circle to Antarctica and back again every year. On the other hand, the Snowy Owl lives in the arctic region year-round; it doesn't migrate at all.

The Question of the Day:
Why do some birds migrate while other birds stay in one place?

The possible explanations are many. Maybe the type of food they eat is present only part of the year, or maybe they can’t stand the cold temperature. They might need to have their babies in a place away from predators, or perhaps migration is an evolutionary holdover that had a reason in the past, but no longer is necessary.

How could you start to determine the reason for migration in only some bird species? I would start by looking at how closely related the migratory and non-migratory species are. Maybe all the birds that migrate are more closely related to one another than to the birds that don’t move around during the year. This would suggest that there is a genetic basis for why only some species migrate.

One research group did just this in 2007. The looked at 379 species of flycatchers, a closely related group of birds. They found that almost equal numbers of species were migratory or resident, so it doesn’t appear that genetic relatedness is the answer.

The painted bunting is among the most colorful
birds in North America. This male has several colors,
while the female is a brilliant green. They breed in
south central US or on the southern east coast, but
winter in Central America; therefore, they are
seasonally migratory.
Maybe the need to migrate has to do with the geographic region. About 90% of birds in the arctic migrate, some are present there only in the mid-summer months. The arctic tern is a good example. Arctic terns move with the summer, breeding in the arctic in May-July, moving down along continental coasts to arrive in Antarctica for the months of December to February. The entire distance traveled could be as much as 32,000 km (20,000 miles) in a single year.

Similar to the arctic region, the east coast of North America has species that migrate and species that are sedentary. About 80% of the birds species of the east coast move south during the colder months, but on the Pacific coast, almost all the bird species are non-migratory.

So migration is not due to the type of geography around the birds. However, the east coast of North America does have larger temperature swings than the west coast, so maybe it is just that some birds can’t deal with the cold. 

Some non-migratory birds can control the amount
of blood that travels to the legs in order to conserve
body heat. This works even better if they can reduce
the amount of contact with the cold surfaces, so some
of these birds perch on one leg at a time.
Many birds that do not migrate have special adaptations to deal with the cold. Trying to keep a constant body temperature (endothermy) takes a lot of energy, and birds live right on the edge of having enough energy anyway. Flying requires a huge amount of energy and they must eat almost constantly just to keep enough carbohydrates in their system to be able to move around to find more food.

Burning more energy to keep warm might tip them over the edge into starvation. To alleviate this problem, many birds can allow parts of their bodies cool down to freezing or near freezing, while keeping their internal organs at a temperature that will preserve their function. Blood flow is a major way to keep parts of the body warm, a duck standing on the ice can reduce the blood flow to its feet and reduce the amount of heat lost to the cold ice. The duck’s chest may be 40˚C, but its feet could be just one degree above freezing.

But let us look again at the arctic tern. It migrates from the north polar region to the Antarctic region in such a way that it sees two summers each year. But these are summers in name only. The arctic summer has an average temperature from -10˚C to 10˚C, so much of the time the tern is there, the temperatures are near zero.

The arctic tern has a ghastly commute each year.
The trip is even more amazing when you consider
that during its yearly molting, the tern flies very
little.  So, all that distance must be fit in to just a part
of the year, not the entire 365 days. I guess they
vacation by NOT traveling.
Then when they reach the Antarctic, the summer there has an average temperature of -2˚C to 2˚C. This is hardly a balmy vacation destination for the tern. The temperatures in both its breeding grounds and wintering grounds would require it to have elaborate temperature control and energy-saving adaptations. Therefore, inability to tolerate cold temperatures is not the reason for migration, at least not for many birds.

The group who carried out the 2007 study concluded that the main reason that only some flycatcher species migrate is not due to what they eat, or when they breed, or what is trying to et them, but to how available their food source is. Whether they are fruit eaters, or insect eaters, or seed eaters, how easy it is to find their food is the most common reason that migration has evolved for a specific species in a specific location.

The food availability hypothesis is supported by certain types of migration that are common in North America. Irruptive migration is characterized by a population moving to another place, but there is no yearly, seasonal, or geographic pattern. The birds may migrate one year, then not again for a dozen years, or they might go for several years in a row. North American seed-eating birds are famous for these migrations. The distance and number of individuals that migrate are also not very predictable, and this all makes it sound like the movement is linked to food availability. However, it could also be to escape some population explosion in a predator species or for some other reason.

It isn’t only birds that might undergo partial migration.
Some crab species will migrate for breeding purposes,
like these Christmas Island Red Crabs.  Individuals
that won't breed just don’t make the trip. They may be
too young, too old, too lazy. In other cases, when
populations migrate away from the breeding grounds,
some individuals may remain there the year round.
Another type of migration is partial migration, a pattern wherein not all birds of a species in a certain location will migrate, only some of them leave in non-breeding times, while others stick around year-round. Food may be available for some, but not all, or the environment may be unsuitable for some weaker individuals to have enough time to forage for a sufficient amount of food. These (and other reasons) might explain why partial migration exists, but one question remains, who stays and who goes? The choices could be based on age, altruism, suitability, dominance… laziness?

As an aside, it isn’t just birds that migrate. Mammals move from place to place, sometimes with a defined pattern during the year, but sometimes they just follow the food, a process called random migration. And some insects migrate as well.

For many years, the migration of the Monarch butterfly was believed to be the longest insect migration. But this is not the typical migration we think of, where an individual moves from one place to another and then back again. The migration of the monarch butterfly takes four generations to complete. Some generations are born and fly a long distance to lay their eggs, while others are born, live, and reproduce in a small area. But altogether, this butterfly moves from as far north as Canada to the high mountains of Mexico and back each year, about 7000 km (4400 miles).

Globe skimmer dragonflies breed in freshwater pools,
so they migrate from India’s monsoon season to the rainy
season in East Africa, all in search of a place to lay
eggs. They make stopovers on the Indian Ocean islands,
but only to rest, because there are very few
pools of freshwater on these coral cay islands.
A few years ago, a biologist in the Maldive Islands started to wonder about the movement of globe skimmer dragonflies where he lived. They seemed to be plentiful in some periods and absent in others. He started to track them, and found that they have an even larger migration pattern than the monarch butterfly. What is more, they fly long distances over the ocean with no place to stop and rest.

Over a series of generations, the dragonflies move from India to the Maldives, some 600-800 km across the open sea. Then they move to east Africa, from Uganda to Kenya and Mozambique. In January, they start back toward India, and complete their migration of more than 18,000 km (>11,000 miles).

So birds may get most of the publicity, but insects hold their own in the migration game. Of course, it does take four generations of dragonflies or butterflies to make their complete journey, where a single arctic tern may make its entire 20,000 mile trip thirty times in its lifetime. O.K., they are both pretty impressive when you consider most people need a car to go down the street to the grocery store and back.

Davenport LC, Goodenough KS, & Haugaasen T (2016). Birds of Two Oceans? Trans-Andean and Divergent Migration of Black Skimmers (Rynchops niger cinerascens) from the Peruvian Amazon. PloS one, 11 (1) PMID: 26760301

Ahola MP, Laaksonen T, Eeva T, & Lehikoinen E (2007). Climate change can alter competitive relationships between resident and migratory birds. The Journal of animal ecology, 76 (6), 1045-52 PMID: 17922701

Hobson KA, Anderson RC, Soto DX, & Wassenaar LI (2012). Isotopic evidence that dragonflies (Pantala flavescens) migrating through the Maldives come from the northern Indian subcontinent. PloS one, 7 (12) PMID: 23285106