Science Tidbits for July 17, 2012

Right. I’ll get to the science stuff in a minute. There’s a meteorite that hit the ground near here. I want to check it out. It won’t take long.

If you are teaching an astronomy class, I have a challenge for you. Introduce your students to minority astronomers. Neil deGrasse Tyson isn’t the only black astronomer! When I teach introductory biology I make sure to teach about women that are scientists and at the end of the semester, I often give a bonus point on the final if students can name a single female scientist that isn’t Marie Curie. Some can, some can’t.

Via Boing Boing, a heartwarming discussion of how your bellybutton is a special place for bacteria. OK, so it isn’t heartwarming, but what class from high school biology on up doesn’t involve sampling skin bacteria and growing them on petri dishes. It becomes slightly more intensive when you get into actually identifying all the bacteria present, but this is probably something that upper level courses might consider, if they have the required technology and resources.

Speaking of bacteria, and why not, since we are just walking, talking bacteria hosts and vectors, is this neat little bit on how certain bacteria have distinct smells. A well stocked lab with good safety controls could easily show off some of these lovely little bugs and remind students to use all their senses when making observations.

This piece actually reminds me of something I came across years ago about the naming of several short chain fatty acids (which happened to tie into my dissertation, another story for another day) and guess what, thank the interwebs, it still exists! If you are teaching a primary, secondary or introductory chemistry course, this would be a neat little thing to toss into a lab. It would only take a few minutes, perhaps while something else is going on, but having some samplers of things like butyric acid and a bit of rancid butter to compare it with would be a neat sensory lab. I’m not sure how you get a goat to compare caproic (hexanoic) acid with, but maybe some goat hair would do?

Worrying response to fatal shark attacks off the coast of Australia. While five fatal attacks in ten months sounds like it should be a definite concern, is it a trend marking a change in behavior? I’m not so sure.

If you look at the number of fatal attacks for all of Australia for the last decade, there is no clear trend that can be discerned. It is highly disturbing that there are now calls for a hunt for the shark responsible for the most recent attack. Attempting to hunt down the one large great white shark in an ocean that attacked a person is simply not a feasible idea. Great white sharks can roam dozens of miles in a day and can migrate thousands of miles seasonally. Without clear identification of the shark, checking stomach contents of a killed shark would be the only way to determine if you had caught and killed the right shark.

Revenge hunts won’t convince other sharks not to attack. People watching for sharks in the vicinity of beaches is a good preventative, but is not any more functional with a long coastline.

Tara C. Smith describes using zombies to teach about diseases, pandemics and other public health issues. How cool is that? What an excellent opportunity for discussion and fostering an active learning environment!

More joy from the Philipines, sea turtles saved from poacher’s nets. This probably should be viewed in the context of a larger dispute over territorial waters claimed by both China (where the poachers were from) and the Philipines, as noted in the link.

Lemurs are facing some serious threats and may be at risk of extinction.

Apparently moon dust is bad for you. Well, I could have told you that! Sharp pieces of regolith could get in your eyes and scratch your cornea or irritate your airways, not unlike inhaling ground glass. Here is the paper for specifics.

E. coli strain 0157 is a very nasty bug, and since there is no good reason to assume that the Germantown, Ohio outbreak came from meat (a recent outbreak was linked to feral hogs foraging in fields being used to produce vegetables), it will be interesting to see if a source is found. I’ll be keeping my eyes on the MMWR. In fact, students in any microbiology, disease ecology or public health course dealing with epidemiology should be asked to read and present reports from the MMWR as part of their course in order to see how the things they are studying are reflected in the real world.

There is a belief that lies can be detected via body language hint of looking up to the left. Apparently (surprise), it isn’t true, or at least is unreliable. Just like so many other lie detection tools.

The placebo effect is a very important concept to understand when examining any claim that a drug, intervention, device, whatever, has a positive effect. Well designed clinical trials can help researchers separate false effects from real ones (which is why alternative medicine seems powerful in small trials with poor statistical power, but when examined in large randomized double blind trials, the effect is no different from placebo. Hope plus effective treatment is very powerful. Hope plus nothing may make a person feel good in the short term, but in the long run can lead to dangerous delays in treatment.

People are less familiar with the nocebo effect, wherein something has a negative effect, even if there is nothing there.

In one study, 44 percent of lactose-intolerant people reported gastrointestinal problems after taking a fake lactose tablet. (Impressively, a quarter of people without lactose intolerance also reported digestive troubles after taking the tablet.) And in a somewhat cruel prostate drug study, one group of subjects was told that sexual dysfunction was a possible side effect, while the other group wasn’t. The better-informed group reported sexual side effects at a rate of 44 percent, compared to only 15 percent in the blissfully ignorant group.

People can actually make themselves more likely to experience side effects by simply knowing about them. Medical and nursing students would be well served by reading and discussing how this affects their interactions with patients and communicating risks of treatments. There is a fine line between communicating and providing informed consent and negatively influencing a patient’s treatment.

Undergraduate students in psychology or communication courses would also benefit from class discussions about interactions and how they affect both patient expectations and patient compliance (the linchpin of slowing the development and spread of antibiotic resistance).

It can be difficult to express the sheer diversity of ferns, but this SA blog post does that in spades. Don’t just show your students a fern from the florist. Show them the wild variety of these ancient plants and toss in some examples of ferns from the fossil record. If you can afford it, add some to your personal or department fossil collection.

Mixing live virus vaccines that can mix genes is causing problems in chicken farms. Could this happen in humans? Except for the oral polio vaccine, no, because our live virus vaccines that are given simultaneously can’t mix genes. The oral polio vaccine can recombine, but this is uncommon, and the oral vaccine is only used where polio is still a common disease. Is this virus a risk to people? No, people can’t catch this particular virus. If this sounds like the flu strains swapping genes, it should.

I love cats and cats go so well with science. Cats aren’t just something that students are familiar with, but they have some great features that make them good teaching tools. For example, calico and tortoiseshell cats are almost always female because the mix of alleles that cause a tricolor cat can only occur in a cat with two X chromosomes. A male cat that is calico is going to be the feline equivalent of Klinefelter’s syndrome. If it is as common in cats as it is in people, an assumption for which I have absolutely no evidence, then only 1 in 500 to 1 in 1000 male cats would be feline Klinefelter’s, even before the color pattern is determined.

So why are calico cats important? Find me an introductory biology text that doesn’t have a picture of a tricolor cat in the section about X chromosome interaction. They give us a visible examples of the mosaics formed during development as one X chromosome or another is inactivated, and only the color gene on the active chromosome is expressed. The presence of two active X chromosomes in a cell is probably toxic on some level to the animal. This likely has to do with the effect that the dosage of genes on a single chromosome being just right, while two is too much. More on cats in the classroom and the effects of aneuploidy on cells in the future, just not simultaneously.

Gorgeous video of a variety of insects getting a tasty, nutrient rich snack of pollen. Don’t worry, the flower will probably benefit by having a little bit (just enough) pollen finding its way to a stigma and then on to an ovary. (via @BugGirl on the twitter machines)

And here is another video of a critically endangered Lord Howe Island stick insect emerging from its egg. Wow. How nice it must be to not have a hard exoskeleton immediately upon hatching! More info here.

Lord Howe Island Stick Insect hatching from Zoos Victoria on Vimeo.

Keep an eye out for baby spiders doing their best impersonation of beloved literary characters!

Auroras are pretty neat. Maybe I’ll get a chance to see one some time. I just hope it doesn’t come with a solar flare powerful enough to be visible in Central Kentucky. Phil Plait not only has coverage of the most recent flare, but like he suggests, check out his related links for far more information than I could possibly impart. Just don’t forget to enjoy this video of the aurora from the BBC.

Enjoy this 360 panorama view of the inside of the Large Hadron Collider.


There are now suspects in the vandalism of a fossil bed in Alberta. I hope they get put away for geologic time.

Edinburgh’s Legionaires’ outbreak is continuing, with the total reported cases topping 100.

Ever wonder how creationists respond to major news items regarding evolution, say, regarding fossil dinosaurs with type 1 feathers? Check it out at Playing Chess with Pigeons.

And if you are on Twitter, Follow me!

Further, if you are on twitter, follow Joanne Manaster @sciencegoddess for some great science information and teaching goodies like this!


Science Tidbits for June 29, 2012

How cool are worms? Really cool. Worms are freaking neat. Annelids (the phylum including earthworms, leeches and polychaetes) are just flat out odd sometimes, and odd makes for teachable concepts.

Zombie worms are polycheates that live in the deep ocean, and have a very odd way of eating.

They don’t, not exactly.

They don’t have mouths. They don’t have stomachs, intestines or anuses either, and yet, they eat the bones of dead whales, and are called bone eating worms or osedax, which means bone eating in Latin.

They use a branching anchor with rootlike structures, covered in microvilli, to secrete acid, which breaks down the calcium structure, liberating fats, which are absorbed and then digested by bacteria living in the tissues of the worm. And zombie worms aren’t even the most grossly named of these critters. Behold the bone eating snot flower worm!

So they don’t eat, but do break down bone and absorb food from their surroundings.

It sounds a bit like a fungus, actually. And this can be a great chance for you to talk about how what a normal defining characteristic of a kingdom (ingesting food for Animalia, photosynthesis for Plantae) are sometimes abandoned, but the organism never hops to another kingdom. A ghost orchid that doesn’t photosynthesize is still a plant, existing as a parasite on fungi underground, only poking up to flower on rare occasion. Students often want to think of non-photosynthesizing plants as fungi, and might want to do the same with bone eating worms, but they still have all the other features of their kingdoms. The osedax still doesn’t have cell walls or mycorrhizae like a fungus. It still has closer genetic ties to other polychaetes and annelids than to anything else. The ghost orchid still has cellulose cell walls instead of chitin. It may not have chloroplasts, but it still is a plant. Great chance to have a lesson on phylogenetic trees.

Another topic you can bring up is the use it or lose it concept. Osedax don’t use a digestive tract and don’t need one. The genes for a digestive tract are turned off and over the millions of years since they evolved, the genes probably have become mutated into a non-functional state. It was once assumed that once you go down this tract, you can’t go back, but scientists have found that geckos have gained and lost their adhesive toe pads several times, and some lineages of scorpions have gone from surface to cave dwelling and back, and lost their eyesight and regained it. The longer you don’t use something and it remains unexpressed, the harder it is to reactivate, but it isn’t impossible.

I would really love to see a study of the early development of these worms, especially to see if their larval forms have digestive tracts.

One other cool detail… Osedax have both male and female sexes, but the males live in a larva like state inside the female.

Worms = cool

A new gene in the influenza virus has been discovered. Let me pick up my teeth. Influenza just went from a genome of 10-11 genes to 11-12.

The gene is hidden in the code of another gene, and it appears to limit the severity of the immune response. If the mouse model is correct, when this gene works, the flu symptoms are less severe. If it is mutated, the flu is more severe and is more likely to kill otherwise healthy people.

The gene wasn’t discovered until now because it is found after the main gene on segment three starts. It basically is a second open reading frame (this is the link to the original paper in the journal Science), and is activated by a ribosomal frame shift. (Does this sound like it may be for an undergraduate genetics course? Oh yeah. But don’t be afraid of handing it to a gifted high school student.)

Basically, the gene is transcribed as normal, making the viral mRNA. The mRNA is then translated, and when the ribosome reaches the start of the internal gene, it slips, missing a nucleotide and the rest of the protein is produced according to the internal gene. This is similar to eukaryotic alternative splicing, and is a very cool way to get two genes coded into the space of one.

This produces a protein that represses the genes of the cell, and probably inhibits the cell from putting up the little red flags that tell the immune system that it has been infected. Less immune response, less chance for a cytokine storm, the nightmare scenario for flu.

Misc science goodness:
Neutron star racing across space 
Graphene may make for an efficient way to make salt water into fresh
Nice way to explain the different parts of the electromagnetic spectrum (xrays to visible light to radio waves) and their significance to astronomy
Why does coal become rare in the fossil record around 300 million years ago? Fungus that could break down lignin evolved about that time.
A rare freshwater mussel is facing extinction.
Animals from the Ediacaran period preserved by volcanic ash.

Teach on.

Science Tidbits for June 26, 2012

Two quick news items for today and one video.

First up, more information on the effect that the 2009 H1N1 pandemic virus had. The H1N1 “swine” flu inflicted a particularly severe toll based on an interesting application of a couple concepts from the world of epidemiology and public health.

There are multiple ways to describe the death rates of a disease, one of which is simply the number of people that die from the disease. This simple measurement of mortality doesn’t tell us everything. Influenza typically kills a mix of the very young and very old. The 2009 H1N1 pandemic flu killed far more young people than the seasonal flu normally does, which changes the effect on society.

The concept to stress here is that of patient or person years. Functionally, every person that lives one year lives a person year. If you have fifty people that live one year, you can express this as fifty person years. If they are patients, you would say that there were fifty patient years.

A good way to bring this to the classroom is to compare one young person and one older person. Let’s say that the young person can expect to live sixty more years, while the older person can expect to live twenty more years. If both people die from the same disease, at the same time, the young person lost more years than the older person. Sure, if either one of them had survived the disease, either could have been hit by a bus the very next day, but statistically, the death of the younger person was a greater loss of potential years of life. If we have a very large population, with perhaps tens of thousands of young people and old people falling into our patient group. For every young person that dies, three older people have to die to add up to the same number of patient years.

It sounds like a very cold and callous way to look at the lives and deaths of real people, but this system is used to determine what level of risk is acceptable for a medication. How many patient years are saved from the treatment and how many are lost from side effects? How severe was an outbreak? How useful was a new safety technology installed in automobiles? Many concepts in public health take an impersonal look at an issue because of the sheer number of people involved.

This can lead to a great discussion of the differences between patient and population centered medicine, if that is in the scope of the class you are teaching.

The second tidbit is a quick explanation of a piece that was in the news a couple of weeks ago. A woman eating parboiled squid bit into what appeared to be a tasty piece of meat, but was in reality a reproductive organ of the male meal. This can either be passed along to students asking if it was real, or be used in a zoology course when discussing the reproductive strategies of a variety of invertebrates.

Finally, a video that I have used in teaching about the process of mitosis.

I have shown the video as is to a course, muted it and described the steps in the video, pausing to point out specific features, and have included it as a link on a course website (both Moodle and Blackboard). However you approach the multimodal classroom, videos like this can be very useful in helping students understand how something like mitosis works, and can be used at multiple levels of difficulty, from simply learning the phases of mitosis in order to beginning to understand the function of spindle fibers.

Teach on.

Science Tidbits for June 21 and 22, 2012

Good Morning, Tokyo. I promised tidbits by morning, and it is still morning on the other side of the planet.

Whenever I teach about the cell cycle, I discuss cancer, and when I discuss cancer and the cell cycle, I talk about how some anticancer drugs work in relation to the cell cycle. While my own dissertation work focuses on using cell cycle dependent drugs and making them more effective by tricking the cell into dividing with a second drug, all before it has repaired damage caused by first, I’m always looking for recent work that hits on this topic. This press release talks about using just such a “one two punch” to attack cancer cells. The full paper can be found here, but access is subscription limited. I suppose I’ll be hitting up the University library.

I love talking about flu as an example of… well, lots of things. Mutation rates, genes, viruses, zoonotic pathogens, genetic recombination, etc. One of the things I talk about is how close we are to an H5N1 pandemic. Right now, the H5N1 strains that are being monitored don’t pass from human to human very efficiently, which is one thing that keeps it from running rampant through the population. All it takes is a few small mutations and the virus can pick up the ability to pass from human to human, and it is only a matter of time before just such a mutant strain evolves. Hopefully, by that point in time, we will have universal influenza vaccines ready, or at least have methods approved for rapid vaccine production via cell culture. The chicken egg method is just too slow.

Do you know that the color you call blue is seen in precisely the same way as another person? A wavelength of 460 nm is a specific shade of blue. Do you see the same exact shade as another person? Does your brain interpret in precisely the same way?

We have no good way of knowing if my color blue is the same as yours, since every person has different eyes and different brains. Your brain, when you look around you, is receiving information from the surrounding world from your eyes, transferred along the occular nerves, and is decoding it. As it does this, it produces a simulation from that information. You can’t see some things that are there. You can’t see pigments that reflect in the ultraviolet range, but they are present, and many insects can see them. Illusions and mirages are excellent examples of errors in your interpretation of the world and how it is in reality.

This is especially true if you have certain genes for colorblindness. The “normal” person has three different types of cone cells in their eyes. They have trichromatic vision. These cones detect different ranges of color, and for each type of colorblindness, you lose one of those ranges. Your simulation is reduced pretty significantly for each malfunctioning cone cell type.

It turns out that there aren’t only people that have one fewer cone cell type, but some people have one extra type of cone cell, and are called tetrochromatic.

This is one of those little details that you can toss in to a lecture about vision or sex linked genes (some types of colorblindness are sex linked, and tetrochromatic vision definitely appears to be). I find that these kind of teaching tidbits can be a useful way of keeping students that are at the top of the curve right there, involved. They may already know a decent portion of the material, but if you toss in a few bits of trivia that they haven’t seen before, they pay attention for the new things that they didn’t already know about.

More fun Pollinator Week stuff from Bug Girl. Ignore the Burt’s Bees commercial part of the video, and enjoy the information about how bees are the true masters of interpretive dance, and how they are involved in pollination. Oh, did I mention that it is one of Isabella Rossellini’s wonderful videos about nature? Because it is.

Are you teaching a class about reproduction? Are you teaching a minimally mature class? Then fill them in on the oddities of animal penises (via Discovery News). The duck one is actually kind of useful if you are talking about prezygotic barriers to reproduction as a means of speciation. Ducks have penises and vaginas that can be species specific, which can prevent one species from being able to mate with another.

Ever have a student ask why you get brain freeze when you eat or drink something cold? Here is a nice video explanation.
Oh, and if you haven’t heard that Europe is working on increasing the involvement of girls in STEM (Science Technology Engineering Math) education, then you have missed out on one of the worst PR bungles ever. Why is it bad (other than being painful to watch)?

Sexist imagery decreases the performance of female students on tests in STEM subjects. Nicole (NoisyAstronomer) points out the problems in the campaign and also gives some good examples of what women doing science look like. (If you are on Google+, follow her for great astronomy news and information) Kylie Sturgess at Token Skeptic also has some great examples of women in science and a good takedown of the ad as well (Kylie’s podcast is pretty great, too).

Their examples are what get people interested in science. Normal people doing interesting things. And the great thing about this is that when you show minority groups involved in science, it increases their involvement, and doesn’t discourage people in majority groups. Their functional privilege makes such differences invisible to them. Well, except for the ones that need their privilege reinforced, and require that all discussions be about them.

Have a nice weekend. I’ll be calling people to push poll on evolution.

Teaching about swine flu

These are some notes I put up on the JREF forum last April. I have updated a bit of it, fixing some minor errors. I figured this would be a good place to start things off.

I moved a bit away from my planned lectures on environmental science for my two freshmen biology sections to focus on this current and very teachable event, and thought that other educators may find these lecture notes and resources useful.

First off, the google swine flu map provides an excellent resource for teaching how modern transportation can make preventing the spread of flu practically impossible. Unlike the original google map, this map has a very easily understood legend. For details on national and regional outbreaks, zoom in. For instance, Kentucky, my home state, currently has an orange circle with 167 in it. This means that there have been 167 confirmed cases, but no deaths. Florida on the other hand, has a tri colored circle with 2895. Click the circle, and you get these details.

Suspected Cases: 1
Confirmed Cases: 2865
Fatal Cases: 29

For more detail, zoom in further. Miami-Dade has these details, plus information on some cases.

Reported Location: Miami Dade County, FL
Confirmed Cases: 917
Fatal Cases: 10
This is an aggregated report based on 24 reports near the same location.

Next up is the structure of the virus. All viruses have genetic material that is either DNA or RNA, proteins that surround and protect the genetic material, and spike proteins that allow it to interact with the environment and bind to target receptors on the cells it can affect.

The flu virus has RNA for genetic material, and typically has 8 short stretches of RNA, which exist in a fashion similar to mini chromosomes. It also has two spike proteins which also are the antigens that our immune system recognizes, and give the name and classifications for these viruses. Hemagglutinin targets the virus to infect a specific cell type, and is the H of the H1N1 of the current flu type. Neuraminidase helps the virus bud off of the cell, and is the remaining N. For each different group of flu virus, HxNy describes a related group with lots of strains with minor mutations between them.

Since most of us have had H1N1 flus or flu shots recently, we have some minor immunity to members of this group, which is great news. However, mutant strains may be different enough to sneak past our immune system and make us sick. Because the flu virus mutates quickly, this is why you need to get a flu shot every year. The strain is a little different every time. In the case of the H1N1 swine flu virus, it isn’t a minor mutant, but a new combination of genes, so we really don’t know if previous shots will offer any help at all.

Also of interest is that the flu virus is an envelope virus. As it buds off of the host cell, it surrounds itself with some of the host’s cell membrane. This means that the host cell doesn’t die when viruses are released. It may die later if the virus causes the cell to use too much of its own resources to make viruses, or if the immune system detects the infected cell and targets it for killing.

I mentioned that the genome is set up as mini chromosomes, each with one or two genes, and this is very important to this particular strain. You may have heard that his flu virus has a mix of avian (bird), swine and human flu genes. Well, this is unusual, but not unheard of, and is certainly not evidence of genetic engineering and conspiracy as some CTrs (conspiracy theorists)  are claiming.

Recombination of flu genes

First, many different groups of animals have their own flu viruses, but only these three groups do a particularly good job of infecting humans. Lets say we have a hog farm, maybe with some ducks and pigeons in the area, and of course, humans.

The birds pass one virus to a hog, which is also infected with its own flu virus. This means that the animal (Animal I in my blackboard notes) has two different viruses in it’s cells. The mini chromosomes would sort separately, just like chromosomes in meiosis, and each new virus would have a random mix of bird and swine flu genes.

Lets say this gets passed along for a bit from one pig to another, or perhaps back to some birds. At some time, another animal (Animal II) becomes infected with the hybrid virus and a third virus, this time from a human flu group. Again, we have a mixture of genes being produced, and the most fit ones (not necessarily the ones that cause the worst disease) spread through the population.

If the genes are just right, the virus ends up moving into the human population and can be spread from one person to another.

Also of great value is the HHMI’s biointeractive website. Under the lecture tab, holiday lectures, infectious disease, you can find the 1999 lecture, which is a little out of date, but there is one part of the 4th lecture that specifically deals with the flu, and you get most of the above information.

The Holiday lectures are targeted towards advanced high school students, but I think that the lecturer probably used words and terms that were a bit more advanced than are needed. I don’t mind showing it to my college students, but even so, I know that some probably still didn’t follow parts of it. Alas, you can’t reach them all.

One question I received on the JREF: What are the chances for a mutation to make it particularly deadly? That’s my biggest concern?

Well, it is possible. Since the flu is an RNA virus, the rate of mutation (1/10,000) is about the same as the length as the entire viral genome, you could expect every virus to have a mutation. Most of these do nothing (no appreciable change to the 3D shape of a protein), and some will be negative and inhibit the mutant and its offspring. Occasionally, a strain will get really a really nasty mutant coming from it, but that is completely unpredictable.

If a disease kills quickly, though, it won’t get a chance to spread very far, and the outbreak would burn itself out. That isn’t very likely for the flu though, because even really bad cases take several days to progress to pneumonia or cytokine storm (extreme immune response, very nasty), including time where you are feeling OK enough to be around people. The 1918 pandemic was around 2.5 – 5% mortality, and so far, this one isn’t nearly there (even though we don’t have good numbers yet).

It is hard to estimate the case fatality ratio, because we tend to undercount the number of real cases, especially if people don’t need to go to the hospital for mild cases. The we have to figure out how many people actually died from flu and not something else, so that number is hard to get. Divide deaths by cases, and you at least have an idea of how bad it is.

Of course, we now have some anti-flu drugs and better medical care, so at least the developed world shouldn’t be affected as badly. The reason we are so concerned about bird flu is that some strains of it don’t appear to respond to these drugs, so we may have one less tool to use (at least from the few cases that have been seen).

Best, and teach on.