Category Archives: Year 13

Nitrogen Cycle

disclaimer: this lesson has not yet been tested on school children

the quality of your lesson can go down as well as up

So there are some topics which just bring a cold chill to the heart when you contemplate planning the relevant lesson. A classic example of this is the Nitrogen Cycle. I’ve never taught it well, and I’ve seen several other people teach it to no useful effect. I’m bored, the students are bored – and we’re both slightly cross that any exam board would decide to include it in a specification. Covering important ideas is one thing, but we’re trying to get young people excited by science!

So is it just something you write off as a bad lot, hold your nose, teach the lesson as quickly as possible, and race on to something with more obvious appeal?

In a spirit of confession and openness, here is my Nitrogen Cycle lesson of recent years.

Nitrogen Cycle Exercise plus The Nitrogen Cycle

The idea is that they try to figure it out using the pictures as clues. Please note that I am at least trying to provoke active learning. I don’t expect them to get all of the blanks, but they should surely be able to figure out the middle bit with wee and poo and death and food. Shouldn’t they?

But no – they look blank, they look helpless, they look pathetic. No two ways about it, the lesson doesn’t work.

Back to the drawing board. To come up with something more successful, we need to determine the problem. I think a large part of it is that The Nitrogen Cycle comes from nowhere. It’s just this random topic that we insert into some convenient gap in the time table. There’s no reference point, no indication as to why it matters, and it’s just not interesting when all you’re expected to do is learn the various pathways and the unpronounceable and virtually unspellable micro-organisms.

But how to make it interesting? I wonder if we need to start with the atom itself….

So here are some ideas I’ll be trying next time the Nitrogen Cycle has to be taught. I’m thinking of A-level students. And I think I’ll cover it at the end of Photosynthesis in Year 13….

Opening question:

Name 5 biological molecules that contain a nitrogen atom…

With a bit of discussion between them I’d expect at least amino acids/proteins, nucleic acids, ATP, chlorophyll, NAD…

What does nitrogen bring to the party?

At this point I want them to think about why the properties of nitrogen make it so important to the biological molecules they’ve named. They already know about carbon and oxygen, so why does life also require nitrogen?

I’d expect this to take quite a lot of thought, discussion and prompting. I would want to remind them of carbon’s 4 bonds and the ability to form long chains. We would revise oxygen’s electro-negativity and the central importance of hydrogen bonds. Eventually, I’d hope to arrive at a point where they see that nitrogen is a bit like carbon and a bit like oxygen. It can form multiple bonds, but it doesn’t share its electrons nicely.

Where exactly are these properties important? Give specific examples.

This is great thinking fodder. Remember, the top universities are looking for students who both understand ideas and can apply them. Remember, the GCSE and A-level assessment is changing – factual recall is down (represents a max. 15% at iGCSE), using your brain is up. Will a question come up on the properties of nitrogen? Who knows! But it’s not a relevant query. This is training them in thinking, in not being afraid of the unfamiliar but tackling it head on.

Come on, describe some specific examples that you’ve met as part of the A-level course.

That generally puts the cat among the pigeons. An accusation that they’ve done this and should know it.

Tell me about proteins. What’s the role of nitrogen in building a protein?

Or maybe I’ll put the questions into an exercise and get them to work together in groups. Perhaps with some helpful diagrams that they can work with.

For DNA, proteins and chlorophyll, explain the importance of nitrogen in their structure and function.

So I would expect them to track down the nitrogen in the organic bases – maybe look at their own DNA model


and realise that the electronegativity of nitrogen is vital for the hydrogen bonds that connect the two stands.

And for protein, again referring to their models….

….they can trace it back to the peptide bond and the hydrogen bonds that stabilise the secondary structure.

As for chlorophyll, it needs that porphyrin ring to hold the magnesium ion. That ring is made possible by a combination of carbon and nitrogen…

So it’s key! We need to know more about it. The scene is set….

Question: where is most of the nitrogen on earth?

Right, now it’s time to consider diatomic nitrogen and why it’s so difficult to insert nitrogen atoms into large molecules. Let’s check out some enthalpy data.

N to N = 945.4 kJ/mol-1

Compare water (464 x 2) or carbon dioxide (805 x 2) kJ/mol-1

Basically, this is a molecule that’s less reactive than water! Demo trying to burn water for comedy value.

At this point I’d get them to research, in outline, the Haber process. What do we have to do when we want to rip nitrogen out of the atmosphere and combine it with other atoms?

450’C at 200atm with an iron catalyst. Yikes!

What is the challenge for any living organism wanting to go it alone and DIY its own nitrogen containing molecules?

Time for them to do some more research. What organisms can do this, what conditions do they need in order to do it, and where are these conditions found?

So, finally, after all this preamble, we’re dipping our toes tentatively into the nitrogen cycle. But this is seriously amazing and worth lingering over a bit. I like the contrast with our clumsy, clunky human chemistry, using sheer brute force to break the triple bond, and the beautiful elegance of biology, able to achieve the same ends at atmospheric pressure and the temperature of the soil. Primo Levi says this about photosynthesis:

“if the elaboration of carbon were not a common daily occurrence, on the scale of billions of tons a week, wherever the green of a leaf appears, it would by full right deserve to be called a miracle.”

I think the same sense of wonder is appropriate here.

There are some great images of the Rhizobium inside the legume nodules. What a cool relationship!

Rhizobium and nodules

This feels like the end of the lesson to me, so homework would be writing the diary of a nitrogen atom, detailing its adventures as it passes through every point of the nitrogen cycle…

As I say, I’ve not taught this, so caveat emptor. What do you think?



Your modelling career…

Last week I burbled briefly on Genetic Drift and said I would return to Hardy Weinberg in a future post. Well, here it is… (in a curious case of deja vu, part of me is convinced I’ve already written about this, but can find no evidence! if you’ve read this before, just put it down to advancing senility…).

I think most students find Hardy Weinberg difficult. It’s abstract, it’s got an equation that just seems circular and self-referencing, and it’s hard for teachers to avoid a chalk and talk approach followed by lots of practice of number crunching.

There are some super resources to help with this and I reckon you could usefully get your class to teach themselves the entire topic from this Pearson LabBench Activity.

But, as you know, I like my lessons to involve students doing things, and especially I like making them think. So I came up with this lesson plan.

First, the Powerpoint. What’s wrong with this woman?

Allele frequency intro

Of course, they can’t tell there’s anything wrong just by looking, though they come up with some very creative guesses.

The only clue is in her ethnic origin. Usually, at this point, someone gets sickle cell anaemia. Time out to talk about sickle cell anaemia, why it is a bad thing, and how it is inherited. A picture of a normal vs sickled cell, and then a heterozygote genotype.

The next slide shows a population – stress population – of individuals of varying genotypes. But we’re not going to count individuals, we’re going to count alleles.

The slide helpfully separates them to aid this. I get them to count the HbN alleles, and right at the start it’s worth pointing out the basic principle that they don’t then have to count the HbS alleles – if they know one, they know the other!

We then work out frequency. Easy, isn’t it? Again, look, if you know one, you don’t have to work out the other – they have to add up to 1.

Back to the population. What about the next generation? Are all of those individuals going to pass on their alleles? Why not? We quietly vanish the HbSHbS genotype. What’s the effect on the respective allele frequency?

So, there’s the setting. We’re looking at allele frequency in populations.

Now it’s time to start the modelling. The sheet…

Modelling Allele Frequency in Populations

introduces them to HardyWeinberg without any attempt to explain or use the equation. That can come later. For now, we’re interested in this assumption that allele frequency doesn’t change (you can demonstrate this quite nicely with a pack of cards dealt into pairs, picked up and shuffled, and re-dealt). The exercise mentions the assumptions required, and describes 3 of them. The idea of the exercise is for them to identify 4 more.

The rest is fairly self-explanatory. They divide into pairs, count out some coloured beads, and play around with them as per the instructions. You could talk a little bit about why this kind of thing can only be done as model, rather than an experiment. But they get practice in counting model alleles and working out frequency so they become very comfortable with the process.

The bit they will find difficult is imagining what events these might represent in real life. But with a bit of discussion, a bit of prompting, they figure it out. So for the first event, what could cause half your population (with their alleles!) to disappear overnight? For the second event, what can you say about the blue allele? Why aren’t those alleles being passed on? The third and fourth are more straightforward, though it helps to stress the correct terminology.

And you can then have a discussion about how realistic HW is and when/why you might find allele frequencies changing at a higher rate. This exercise …

Changes in Allele Frequency in real life

gives a few ideas.

I also wasn’t aware until recently that HardyWeinberg assumptions can be used to assess the accuracy of DNA sampling in a population. The slides here show the results of two genotypic assaying samples. You want to check whether they are valid samples. So you compare the numbers given to the Hardy Weinberg equilibrium. What does this tell you about the two samples?

HW assay

That’s enough for now. We’re being inspected and I think that’s someone at the door of the lab….


One spin off from the BTOY award was being invited to chair a series of talks on Biology in the Real World at this year’s ASE conference in Birmingham. It was my first time at this event and it was brilliant. Indeed, I’ll be back next year, if I can wangle the time off, as I was only there for the day and didn’t have nearly enough time to explore everything that was going on. But the overall effect was energising, exciting, inspiring – I came back to Oxford buzzing with new ideas and a bag bursting at the seams with bumpf. Many thanks to the Royal Society of Biology for the invite…

The talks were brilliant – here’s the briefest of summaries….

  1. Professor Joanna Verran (Manchester Uni) on Biofilms. Amazing images of e.g. 1000s of bacterial cells on a single grain of sand
    3. I, SuperOrganism – popular book on human body’s biofilms
    4. Fascinating stuff on quorum sensing and possible role in bacterial control
    5. 99% of planet’s bacteria live in biofilm communities.


  1. Dr Charles Lane (FERA and SAPS) on Killer Plant Diseases.
    1. Great practical on SAPS website on how to demonstrate Koch’s postulates with rotten apples
    2. Ash dieback first plant disease to be discussed in COBRA meeting


    3. Professor Saffron Whitehead (Society of Endocrinology) on Hormones and Homeostasis

    1. Steroids highly conserved – found across Animal Kingdom
    2. Ketoacidosis only occurs in Type 1 Diabetes (because ketone body production inhibited by insulin)
    3. Glycosylated haemoglobin main problem from diabetes leading to similar complications of CVD

4. Professor Greg Hurst (University of Liverpool) on Microbial Partners

  1. e.g. 10-20% of human calorific intake from bacterial digestion in gut (short chain fatty acids – acetate, propionate, butyrate)antibiotics bad for cows/horses because e.g. horses get 80% plus of calories from bacterial digestion. aphids have specialised organ for cultivating symbiotic bacteria that make essential amino acids lacking in phloem – 200 million year old symbiosis. desert rats eat leaves of creosote bush – only because their bacteria detoxify the creosote – a desert rat on antibiotics becomes sensitive to creosote
  2. breast mile contains complex polysaccharides specifically to encourage growth of particular bacteria
  3. aphids not found in tropics because bacteria temperature sensitive
  4. insects dependent on blood/phloem become sterile if fed antibiotics – because they rely on bacteria to produce vital nutrients otherwise lacking in diet
  5. apologising for breaking wind is taking responsibility for the microbial part of you, as methane/hydrogen sulphide are only produced by bacterial enzymes
  6. Review of idea of Holiobionts and how organisms can borrow skills from other Kingdoms by forming a symbiosis/symbiosis opens up new ways of life/niches

5. Dr Ginny Acha (Association of the British Pharmaceutical Industry & British Pharmacological Society) on Personalised Medicines

  1. Interesting data on efficacy of drugs – numbers show percentage of patients who do not respond to drugs for that condition
  • Anti-depressants 38%
  • Diabetes 40%
  • Arthritis 50%
  • Alzheimers 70%
  • Cancer 75%
  • Nice review of history of understanding of blood cancer and how increasing understanding has led to more effective treatment
  • 100 years ago – “disease of blood” – 100% mortality
  • 80 years ago – leukaemia vs lymphoma
  • 60 years ago – 3 types of leukaemia and 2 types of lymphoma
  • Today – too many classifications to note down! 70% survival

Back at school and a lovely lesson with my Year 13s, exploring Genetic Drift through retinitis pigmentosa on Tristan da Cunha (use Google Earth to dramatically show the geographic isolation of this volcanic island)and a rather splendid colour worm game, followed by allele frequency and selection with sickle cell anaemia Sickle Cell Anaemia change in allele freq.

I came up with the idea of applying rates of mutation through Sean B Carroll’s excellent The Making of the Fittest where he does the same with colour vision in birds (brilliant chapter!). It works quite well but, boy, do they struggle with calculating the probabilities! How do you get on?

One way to help is to rephrase the problem. If the rate of mutation was 1 base in 3,000,000,000, what would be the probability of any one person having that mutation? So if the rate is 175 in 3,000,000,000….? And so on. Of course, a point mutation will only have an effect if it’s the right point mutation…. so what do you have to do to the probability?

I send them off to do some homework on Eugenics and applying Hardy Weinberg to the elimination of cystic fibrosis by selective breeding eugenics worksheet with Hardy Weinberg. Yields dramatic results!

I’ll say a bit more about Hardy Weinberg next week, as it’s a nice example of how to make what appears to be dry and theoretical into a hands on, student led learning activity.

But there’s also an Inspection next week, so if it seems a bit rushed, you’ll know why!

Retrieving the Krebs’ Disaster

Last year (October 16th: Chemiosmosis and DNP) I came clean about an idea that simply hadn’t worked. In my endless search for ways of making students do figure things out for themselves – I had designed an activity whereby they would work out Krebs’ Cycle for themselves.

I wasn’t expecting them to do this completely from scratch! They had already covered ATP, Chemiosmosis, and proton pumping by electrons fed into the ETC by reduced NAD. They knew that the NAD was reduced with hydrogens originally stripped from glucose by dehydrogenase enzymes. They had carried out an investigation with yeast and TTC and interpreted the results (INSERT). And they had met Glycolysis and the Link Reaction, so had met metabolic pathways and the slow tweaking and adjusting of the molecules as each enzyme makes its own small contribution. So the foundation was there. Could they complete the jigsaw?

It looked good on paper. First, a bit of human interest, the story of Krebs fleeing Nazi Germany and finally settling in Sheffield for his entire career because the people were so friendly. Then a list of the various molecules that you find in actively respiring cells (liquidised liver, I believe) – the citrate and the oxaloacetate and so on, along with their basic chemical formula. Next, a brief account of Krebs’ approach – enzyme inhibition followed by measuring the relative concentrations of these molecules. Finally, an outline of what some of the results of the enzyme inhibition.

From that, I reckoned they could figure it out. But when I trialled it on a class of intimidatingly bright students, it failed. They got frustrated and annoyed and ultimately confused. Not great.

At this point, I had two choices. Throw the whole thing in the bin and abandon it as a basically bad idea – and revert to just chalking and talking through the process. Or I could try and figure out why it didn’t work, adjust the exercise accordingly, and try again. Given the inestimable value of giving students ownership of their learning, of the understanding and recall that result from them finding things out for themselves, I opted for the latter.

The trial class had struggled, I realised, because they were trying to account for all of the atoms in the molecules, and couldn’t make any sense of the oxygens. But oxygen is not an important atom to follow in the Krebs’ Cycle – they need to keep track of the carbons and the process of decarboxylation producing CO2 – and they need to appreciate the over-arching importance of dehydrogenation and the production of NADH to power the Electron Transport Chain and thus maintain the proton gradient for chemiosmosis. But oxygen can be safely ignored.

So I went back to the drawing board and re-worked the exercise, summarising the oxygen content of each molecule with (n). Unravelling metabolic pathways a la Hans Krebs

And last week I ran it again. It worked beautifully. They quickly figured out the sequence of the metabolic pathway from the enzyme inhibition results. From there, they deduced that carbon dioxide was being produced as the number of carbon atoms went down AND they identified when dehydrogenation was taking place. To put the icing on the cake, they then figured out that by attaching Acetyl(2C) to Oxaloacetate (4C) it would take them back to Citrate (6C) and the whole thing could start again. It was bloody wonderful.

So I would urge you to try new things. That’s the only way you can find out if they work! Your students will appreciate the effort, even if it’s not 100% successful, and even an apparent disaster will teach you something about your students, your approach, your idea.

Finally, a couple of pictures taken with our Celestron Digital Imager, a bit of kit that is proving so popular with the department that I’ve had to order two more.

cheek cells by Mariablood

These are student slides of blood cells and cheek cells respectively (cheek cells extracted from the micro-centrifuge approach – look how plump, juicy and numerous they are!). With the imager, you can project live microscope work on to your white board, capture images (as here) and even take video footage.

Have a good week!

A good week

nb: this will the last burble of the academic year 2014-15 – the summer holidays are nigh and I want to think about anything other than teaching for at least 6 weeks. But it’s nice to end the summer term on a high note and I’m going to tell you about my 15 minutes of fame.

It’s been a good week.

I started with the glorious weather last weekend that finally enabled us to dig out the water slide and set our sons loose on it. As you can see, George is very happy.


I bought a £2 scratch card that had a £5 prize.

We took our first honey harvest of the year.

And then there was this.

I won’t bore you with details of the process, other than to say that it was very thorough. But, for the final burble of the academic year 2014-2015, I thought I’d tell you about the lesson the judges from the Society of Biology observed.

Year 13. Gene Therapy.

As always, when originally planning this lesson (it’s been in the files for about 4 years), I try to think how to make the students do all the work. Or, rather, how to engage them, make them think, and ensure effective learning. The idea is very simple. We start by covering the actual principle of gene therapy very quickly. Broken gene = broken protein = disease. Insert working gene = working protein = cure. But I want them to get a much fuller appreciation of what the process might involve.

So I divided them into teams of 4 and asked them to imagine that they were working on the development team at Glaxo-Smithkline – or possibly setting up a Young Enterprise Team, depending on the scale of their ambition. Gene therapy is on the research agenda and they’ve been asked to identify a potential genetic disease for gene therapy development. I give them a list of 6 different genetic diseases and ask them to carry out the research that will enable them to identify the most likely contender for successful gene therapy.

Gene Therapy revised 2015

At this point, it’s very important to clarify the rules. They must NOT go away and enter a search for “Cystic Fibrosis, gene therapy” into Google. They’re researching the disease itself, not gene therapy, and using that information to make their own decisions as to whether it’s worth investing zillions of dollars of development money into. They will need to consider lots of different criteria in order to justify their decision.

Now, if your lesson is being observed as part of deciding the Biology Teacher of the Year award, you obviously want to choose a goodie, and this particular example has always proved popular and successful in the past. It has everything I like in a lesson – challenge, interest, relevance, independent team learning and the chance for me to make a coffee and put my feet up catch up with vital administration. Nonetheless – and this is always a good reason to welcome lesson observation – I went away and updated/tightened up the instructions. In addition, I changed some of my original 6 diseases to include conditions currently being researched.

The girls were suitably and predictably brilliant. The judges were great too. There wasn’t any loitering in the back of the lab, doodling on note pads, they both immediately joined a group so that they could talk to the girls and see what was going on. After about 10 minutes of initial brain- storming they had all established a list of criteria to look for in their disease of choice. It needed to be:

  • common enough to make it commercially viable (and common in the developed world, where it could be afforded)
  • it needed to be a recessive condition so that the introduction of a functioning allele could make a difference
  • the affected gene and its associated protein needed to be known and the mechanism fully understood
  • and there needed to be a plausible way of getting at the affected cells.

At this point, they headed off to the IT rooms (pre-booked) and the judges dutifully trotted after them. I took the chance to make a coffee and put my feet up catch up with vital administration.

40 minutes later they were back.

It’s interesting how they divide the jobs up. One team decided to allocate a disease per person. The other team worked through the diseases in order, but with each person looking for a specific feature of each disease. Either way, it worked.

So, discussion time. Are there any diseases that they’ve managed to eliminate as possibilities?

Haemophilia is always one of the first to go. Why? Well, there’s a perfectly effective treatment so it’s hard to justify the cost. Plus, they add, completely straight faced, it only affects men, so why bother? Ah, the joys of teaching in a girls’ school!

Von Hippel-Lindau disease is also easy to eliminate (always good to include some diseases they haven’t heard of – this one sounds intriguing and adds a layer of interest to the research). It’s a truly horrendous condition, but it affects every single one of the 50,000,000,000,000 cells in the body – utterly impossible to deliver a working gene on that scale. Plus it’s thankfully very rare – so, brutal economic reality intruding, you’d never recover your research costs.

Parkinson’s disease raises interesting debate because it’s not a genetic disease. You don’t inherit it. There’s no obvious gene to correct. It’s caused by a specific set of brain cells dying (cells in an area of the brain called the substantia nigra) that deprive the brain of its ability to make the vital neurotransmitter dopamine. For all these reasons, they dismiss Parkinsons as a possible candidate for gene therapy. They do recognise, however, the vast and increasing market available for a successful treatment.

So, the thoughtful reader might enquire, why did I put Parkinson’s on the list at all? Aha, replies the faithful burbler, because there is a gene therapy for this disease currently being researched by a company called Oxford Biomedica (who are also working on Stargardt disease). They’re obviously chasing the potential billions in revenue, but how would this actually work? The students get there quicker than I thought they might – could you put Dopamine gene(s) into some other brain cells, so the ability to synthesize dopamine is restored?


OK, what about the other options? What did they decide for themselves?

Inevitably, cystic fibrosis is everyone’s favourite. It fulfils all the criteria for potential gene therapy. It’s common, particularly in the developed world. It’s recessive. The relevant protein and its mechanism are well understood. Best of all, the cells are readily accessible – lining the airways of the lungs, they are actually in contact with the outside world, so it’s very easy to deliver your treatment, whatever form it takes, to the very cells that need it.

Which is why, of course, everyone has been chasing cystic fibrosis gene therapy for 20 years or more.

And, as a sobering return to reality, in all that time, and despite the billions spent and the careers of brilliant people dedicated to the research, there is still no gene therapy treatment for any genetic disease.

Thank you very much to everyone who has been following my blog. I hope you’ve found it interesting and, if a biology teacher, useful. I plan to be back in the autumn with more of the same. Have a fantastic summer. I’ll leave you with some photos of the Biological Cakes that the Year 12s have been making. Can you guess what they all are?

IMG_0642 IMG_0643 IMG_0645 IMG_0648 IMG_0649 IMG_0634

Co-operative pregnancy

The briefest of burbles this week as we’re setting up the Year 12 Practical Skills Assessments – 38 students – and it’s all a bit manic.

So, pregnancy testing kits. Even I would not ask for a student volunteer to donate urine to show how they work – finding out that you’re pregnant, whether it’s a moment of life-affirming joy, or an unmitigated disaster, is not something that should happen in a Biology lesson. Mind you, I would have no problem asking a volunteer to use a fertility testing kit – and several brave girls over the years have done so.

I did test the urine of the class female hamster (Hettie)


with a pregnancy testing kit, as she had recently mated with the male (Herbie)


and we had high hopes of baby hamsters. The test came up negative but, which turned out to be correct, but we still don’t know if HCG (Hamster Chorionic Gonadrotrophin) is sufficiently similar to HCG (Human Chorionic Gonadotrophin) for the test to work if she was pregnant. Maybe in the summer term when Hettie and Herbie will meet again…

Anyway, pregnancy testing is on the OCR A2 spec. How to teach it? Specifically, how to teach it so that they learn how it works, rather than telling them how it works so that they then have to go away and learn it?


I started by showing them the positive test for George, our youngest son. There he is, bless him, George’s first communication with the outside world, a little message saying, “I’m here! Look after me!” I still look on this as faintly miraculous. I give them a little bit of human detail – we had hoped for a girl, 3rd time round, but on the 20 week scan, along with the bones and kidneys and brain ventricles and beating heart, there was another structure visible that could only mean one thing, another bloody boy… A few tears in the carpark afterwards… but once George had actually manifested himself as George, we obviously wouldn’t change a thing.

But how does the actual test work?

I set it as a kind of Dragons Den/The Apprentice/Young Enterprise exercise. I asked them to imagine they were the development team at GSK and you’d come up with a brilliant idea to invent a pregnancy testing kit. Make millions from grateful women the world over! And then told them to invent it. From scratch. No research allowed.

It was joyous. They quickly decided that they needed to look at it from the consumer’s point of view as well as the biological point of view. What would the customer want? Has to be reliable and easy to use. So urine rather than blood. Something in the urine that is uniquely associated with being pregnant. That means it’s also got to be small enough to get through the basement membrane (i.e. molecular mass < 69,000 in the kidney.

At this point I provided a bit of scaffolding – the molecule you’re looking for is HCG. Released by the embryo very early on in pregnancy to prevent the yellow body breaking down and maintain the supply of progesterone. I love this – the idea that your baby is chemically manipulating you right from the start.

They quickly come up with the idea of some kind of receptors. They’ve picked up on my much repeated assertion that if you can do jigsaws, you can do Biology. But somehow they’ve got to colour code the receptor. And they’ve got to arrange things so that there’s a control line as well as the positive/negative line. Someone finally hits on antibodies, and I scaffold some more, telling them that specific antibodies can be manufactured in sheep, and that antibodies can be tagged at the end of the constant region with the colour of their choice. Much amusement when someone imagines centrifuging a sheep (rather than the sheep’s plasma).

They keep going. They hit on the principle of capillary action. Perhaps the antibodies could move along a fabric or something? But then they need to be stopped. But only if they’re bound to HCG. Er, this is getting complicated. But they sketch it out, and I provide a bit more help, and they’re there. Pretty much. So when we finally draw out the diagram and sketch a positive/negative test, and answer some interpretive questions, they already know and understand it. pregnancy tests

It was a fabulous example of co-operative learning – it wasn’t a particularly bright group, but they trusted my implicit assertion that, yes, you can do this, and they worked together, every student making suggestions and thinking aloud. None of them could have done it on their own. As a group, they did.

They were thrilled at their own cleverness, and fascinated by the cleverness of the testing kit. And to add to my own happiness at a lesson that had worked so well, SLT had popped in to observe it as part of one of their Learning Walks.

Back to the PSAs! Have a good week.