You can do exactly that with the ‘invention kit for everyone’, MaKey MaKey, a simple little circuit board that allows you to make computer keys from pretty much anything.
The kit does not require software, all you need is the circuit board, your computer, a USB cable, a couple of crocodile clips, an imagination and something even slightly electrically conductive, from coins and pencil graphite to fruit and your favourite tinned food.
So how does it work? Attach the MaKey MaKey circuit board to your computer, and from it attach a crocodile clip to yourself and to an object, eg. apple. When you touch the apple you make a connection and complete the circuit; your computer recognises the your ‘key’ as a normal computer key.
MaKey MaKey is a project for anyone, children can design simple keys to play games, while grad students have designed pressure sensitive swtiches with springs and play doh and expert designers can create more complex product prototypes.
The project is currently campaigning for funding on creative platform Kickstarter; still with 18 days to go the project has been pledged a massive $224,817 despite its target of only $25k. With this money MaKey MaKey intend to fund the first large production run of kits, reducing manufacturing and retail costs; making MaKey MaKey largely accessible to anyone.
Waaaah, I really want one to play around with, I hope they come to the UK! For more information visit makeymakey.com or to pledge and find the real techy info visit MaKey MaKey’s Kickstarter campaign page. I wish creators Jay Silver and Eric Rosenbaum all the best for their inventive project.
I have an Anatomy and Physiology exam on Monday, I’m stressing out a little at the strain on my poor memory this weekend, but I can’t help but love the nervous system, I wish I was a neuron sometimes.
So here’s a diagram summarising the events taking place at a neuromuscular junction (between a neuron and a muscle cell).
Synaptic transmission begins when an action potential (impulse) reaches an axon terminal; this results in depolarisation due to the opening of voltage gated sodium channels. This initiates the sequence of events leading to the release of a neurotransmitter.
Depolarization of the axon terminal membrane causes voltage gated calcium channels to open, and calcium ions rush into the axon terminal.
The calcium ions trigger the release of a neurotransmitter (in this case acetylcholine or ACh) by causing synaptic vesicles to fuse with the presynaptic membrane.
When the vesicles fuse with the membrane they release their content of neurotransmitter into the synaptic cleft (the space between the pre- and postsynaptic membranes. The neurotransmitter moves aross this space and binds to receptors on the postsynaptic membrane.
In this case, acetylcholine is the neurotransmitter, it bind to an ion channel, opening the channel and sodium ions enter the postsynaptic cell. The signal is then propagated in the postsynaptic cell.
This is my favourite part, the acetylcholine is broken down to be used again, I love recycling. An enzyme in the synaptic cleft, acetylcholinerae, breaks down the ACh into acetyl CoA and choline. The choline is taken back into the presynaptic terminal for resynthesis into ACh.
Endocytosis of the presynaptic membrane ensures the synaptic vesicles are also recycled. The ‘new’ vesicles are filled with the newly reformed neurotransmitter and ready for the next synaptic transmission.
And to think nerve impulses travel at 100 metres per second, I wonder how many nerve impulses it has taken to write this post, isn’t science wonderful?
If you have never taken Biology to an A2 level you’re unlikely to understand what I have been babbling on about; but the nervous system is pretty so watch this video:
Also, this one of the best books of my life: http://www.amazon.co.uk/Life-Science-Biology-International-Edition/dp/1429254319/ref=sr_1_1?ie=UTF8&qid=1336768303&sr=8-1
I’ve been working on this for a while, though its not yet finished.
1. Go on safari in Africa
2. Ride a camel in the desert
3. See the Giant’s Causeway, Ireland (my sister always wanted to go there)
4. Go to Svalbard and see the Aurora Borealis (a childhood dream)
5. See the Taj Mahal
6. Grow vegetables in the backgarden (carrots carrots carrots)
7. Buy spices from a market in Morocco
8. Visit the temples and teach English to children in Nepal
9. Read all the novels I own (this may never happen in my lifetime; too many)
10. Give a whole month’s wages to parents (though I own them more than money)
11. Give a whole month’s wages to British Heart Foundation
12. Give blood
12. Dress up and go to the Jack-in-the-Green festival, Hastings
13. Stay at the Mermaid Inn, Rye (really old and said to be haunted)
14. Take part in a Holi Colour Fight
15. Ride an elephant
16. See a Ballet
17. See an opera (secretly would love to be an opera singer)
18. Learn another language (maybe Finnish?)
19. Go surfing
20. Stand at the North Pole
22. Go stargazing
23. Stay in an igloo
24. Build a sandcastle masterpiece
25. Catch a fish and cook it (looking for a simple life)
26. Own chickens
27. Take a vow of silence for a whole week
28. Grow my hair to my hips
29. Go skinnydipping at midnight at the beach
30. Have an article published in a science magazine
31. Run the London Marathon
32. Start tap dancing again
33. Ride in a hot air balloon
34. Ride in a helicopter
35. Climb Mount Everest, Nepal or Mount Kilimanjaro, Tanzania
36. Ride on the Orient Express
37. Own axolotls
38. Visit the Galapagos Islands
39. Visit Ayers Rock, Australia
40. Travel along Route 61 (blues route)
41. Visit St Basil’s Cathedral, Russia
42. Visit the Louvre
43. See ‘The Scream’ by Edvard Munch
44. Paint friends and family in the style of Art Nouveau
45. Get a tattoo (maybe)
46. Visit Portmeirion, again, but stay overnight
47. Learn to say “Llanfairpwllgwyngyllgogerychwyrndrobwllllantysiliogogogoch”
48. Help deliver a baby animal
49. Take operatic singing lessons
50. Visit Durham’s Lumiere Festival of Light
51. Solve a Rubik’s cube
52. Take a photo of something everyday
53. Make toys to donate to the Parents Consortium
54. Be an extra in a film, again
55. Get married
56. Start a family
57. Renovate a property
58. See a bush baby
59. Hold a baby chimp
60. Milk a cow
61. Try oysters, lobster and caviar
62. Take part in scientific research
63. Learn to crochet
64. Put locks on the Eiffel Tower and Empire State Building
65. See a lightening bolt (is it weird that I have never seen one?)
66. Visit every continent
67. Hold a baby sloth (and freak out like Kristen Bell)
Get a tattoo Stop repeating life goals
69. Name a star
70. Go to a German christmas market
71. Cook a roast from scratch
72. Host a dinner party
73. Go camping for a whole month
74. See an outdoor theatre performance
75. Visit Stratford-Upon-Avon (Shakespeare’s birthplace)
76. Go to Glastonbury Festival
77. Go on holiday with friends (to be completed soon)
78. Buy a dutch bike
79. Visit CERN, Geneva
80. Live a medieval life for a week
81. Make a lemon cream pie
82. Swim with bioluminescent phytoplankton, Maldives
83. Spend 4 hours in Canterbury Cathedral
84. Take a tour of Liverpool, visit the Cavern Club and Strawberry Fields
85. Visit the Eden Project, Cornwall
I made this dinosaur cuddly toy (called Percy Pippin) about a year ago from a pattern I found in my Ma’s 1972 copy of Reader’s Digest Complete Guide to Sewing. I was so excited to get him finished that I wasn’t very careful when cutting the pieces, he turned out looking suspsciously like an anteater but we love him despite his imperfections.
The scales were made by cutting a gazillion pentagon shapes in felt, sewing 2 together, inserting pipe cleaners and topstitching to hold in place.
Last Christmas I made a couple more as gifts for my cousins of 1 and 3 years. I took a little more care with my 2nd attempts and I was pleased with the results. I love using buttons for eyes but they are not suitable for little mouths! I have a few orders placed by friends and family, I had better get cracking! I hope to document their creation in greater depth.
I created Toad (a Nintendo character) for my Toad-obsessed 10 year old cousin for her birthday gift. I search endlessly for patterns, but could find no such thing, so this creation was played completely by ear (eye?) and the help of Google images. I started with the head, I cut about 15 thin white isosceles triangles and attached them by their long sides to create a circle. From here I ruched the outer edges to form his mushroom hat. The arms and body were improvised with a little help from an old pattern I had for a teddy bear. He is a little rough around the edges and a bit wonky but I was pretty pleased with him, and my cousin LOVED him.
For the birth of a second cousin last August I made a sweet little teddy bear from a lovely floral pillowcase I acquired from a charity shop, unfortunately I don’t have any pictures of him, but I intend to make more soon, I shall post the patterns I used! When uni work is out the way in June I can’t wait to make some more cuddly toys using this pattern given to me by my Nanna, gaaaah I love making these things!
Maternal malnutrition can have a great detrimental effect on the fitness of her offspring and more surprisingly; her grandchildren. Findings have shown that a poor maternal diet can increase the susceptibility to disease during the adult lives of her children; such traits can be inherited by future generations. The phenomena of the ‘inheritance of acquired traits’ is investigated in the study of ‘epigenetics’.
It has been seen that “adverse pregnancy conditions” can influence ”physiological function and disease patterns” in progeny’s adult lives; suboptimal intrauterine conditions, namely a maternal diet deficient in calories, protein and fats, appears bear association to a “constellation of adult diseases” (Johnson and Everitt, 2007). Such pathological consequences were observed in the children of the ‘Dutch Hunger Winter’ of World War II. In autumn 1944, German-controlled Holland was faced with a mass starvation; Nazis had disallowed food supplies to enter the country to punish them for their reluctance to aid the Nazi war effort (Murphy Paul, 2010). The famine that ensued killed 10,000 people, but also affected the 40,000 foetuses in utero. Maternal malnourishment had many immediate observable effects, such as still births, lower birth weights and increased infant mortality (Hart, 1993). But other, unanticipated effects would not be seen for many years; in adult life, the children of the Dutch malnourished mothers were seen to have more obesity, diabetes, heart disease, cancers and other disorders (Murphy-Paul, 2010). The most surprising outcome of the Dutch Hunger Winter was its effects on the grandchildren of those affected; in addition to immediate descendants, grandchildren and great-grandchildren were seen to have smaller birth weights and adult complications (Pray, 2004). This phenomenon poses the question; could a grandmother’s diet have affected the health of her children and her grandchildren?
Until recently such an argument may have been deemed a ‘scientific heresy’; it suggests an acceptance of Lamarck’s disproved theory of the inheritance of acquired characteristics (Pray, 2004). Eighteenth century Lamarck’s crude theory, though false, may be applied at a molecular level in the study of epigenetics; simply, alterations in gene expression caused by other mechanisms (such as nutrition) will occur rather than changes in DNA sequence; such alterations may be inherited (Pray, 2004). The genome can be likened to the hardware of a computer, whilst the epigenome may be compared with the software that directs the operation of the computer (Dolinoy et al., 2007). Whilst the ‘genomic hardware’ comes in the form of DNA sequence, the ‘epigenomic software’ acts via various mechanisms such as DNA methylation and histone modification (see Figure 1) (Dolinoy et al., 2007).
One epigenetic mechanism, DNA methylation, involves the cytosine methylation of CpG dinucleotides. Dietary protein methionine is combined with ATP to produce S-Adenosyl methionine (SAM), which plays a role in DNA methylation (Dolinoy et al., 2007). A methyl group is transferred from SAM to the carbon-5 position of the cytosine ring, forming 5-methylcytosine (5Mc); this reaction is catalysed by DNA methyl tranferase enzymes (Sadava et al., 2010). The 5Mc produced “acts like a fifth base” and its presence can have great effects on the expression of the DNA in which it resides; since it extends into the DNA it inhibits transcription “by interfering with transcription binding proteins”, methylated genes are effectively “silenced” (Dolinoy et al., 2007). A maternal diet containing healthy amounts of “methyl donating substances” such as choline, Vitamin B12, folic acid and betaine can markedly alter foetal gene expression; “epigenetic tags” mask disease causing genes, therefore offspring tend to be healthy and the risk of disease is reduced (Dolinoy et al., 2007). Maternal diets deficient in methionine will lead to decreased levels of methylation, allowing disease causing genes to be expressed (Heijmans et al., 2008). Malnutrition can also lead to methyl groups binding themselves to the wrong genes or not at all, often producing abnormal cells and resulting in disease (Portela and Esteller, 2010). Such methylation modifications can take place in the mitotically dividing foetal cells in utero and can be passed transgenerationally for many generations (Portela and Esteller, 2010). The foetuses of the Dutch Hunger Winter were undernourished and so decreased DNA methylation and detrimental gene expression resulted from a lack of methionine; the ‘Hunger Winter children’ experienced many complications in adult life (Heijmans et al., 2008).
Another epigenetic mechanism is that of histone modification of the chromatin structure. DNA is stored in nucleosomes, in which it is ‘wrapped’ around histone proteins, deeming DNA inaccessible to RNA polymerase, having effects on gene expression; when the chromatin is closed genes are inactivated and are expressed when the chromatin is open (Davis and Ross, 2008). Chromatins are opened by the influence of the enzymes histone acetyltransferases, which add acetyl groups to histone tails (Sadava et al., 2010). Such modification loosens the attachment of the nucleosome to the DNA, allowing transcription and gene expression to occur. It has been suggested that DNA methylation will induce histone modification, but whether the histones are susceptible to modifications as a direct result of the environment (similarly to DNA methylation patterns) is yet to be concluded (Dolinoy et al., 2007).
In regards to DNA methylation, an investigation was undertaken to determine nutritional effects. The test subjects were genetically identical agouti mice (Waterland and Jirtle, 2003). The mothers of group A received a restricted diet, mothers of group B received a diet supplemented with choline, folic acid, betaine and Vitamin B12 (Waterland and Jirtle, 2003).. The offspring of mothers of groups A and B were genetically identical, but through diet control received different epigenetic tags; offspring of group A (restricted) had yellow coats, were obese and were more prone to cancer and diabetes, those of group B (supplemented) were found to have brown coats, be of healthy size and less prone to disease (Waterland and Jirtle, 2003) (see Figure 2). This study highlights the considerable differences that arise through changes of diet on identical genomes.
The theory of epigenetics and its suggestions of Lamarckian inheritance are now widely accepted. It has become apparent that the genome is not the only controller of phenotype, and that environmental factors have significant effects on the genes expressed. Whether epigenetic mechanisms can have profound effects amounting to long term evolutionary change is yet to be seen (Futuyma, 2009); but it is clear that diet can have major though relatively short term effects on the epigenome. Epigenetic ‘tags’ can be passed onto your children and grandchildren; the dietary decisions one makes can affect not only one’s health but that of many generations of descendants.
DAVIS, C. and ROSS, S. (2008) Dietary Components Impact Histone Modifications and Cancer Risk, Nutrition Reviews, (65)2:88-94
DOLINOY, D., WEIDMAN, J. and JIRTLE, R. (2007) Epigenetic gene regulation: Linking early developmental environment to adult disease, Reproductive Toxicology, 23:297-307
FUTUYMA, D. (2009) Evolution, 2nd Edition, Massachusetts, USA, Sinauer Associates Inc.
MURPHY PAUL, A. (2010) Origins: How the Nine Months Before Birth Shape the Rest of Our Lives, 1st Edition, Free Press
HART, N. (1993) Famine, Maternal Nutrition and Infant Mortality: a re-examination of the Dutch Hunger Winter, Population Studies, 47:27-46
HEIJMANS, B., TOBI, E., STEIN, A., PUTTER, H., BLAUW, G., SUSSER,E., SLAGBOOM, P. and LUMEY, L. (2008) Persistent epigenetic differences associated with prenatal exposure to famine in humans, PNAS, (105)44:17046-17049
PRAY, L. (2004) Epigenetics: Genome, Meet Your Environment, The Scientist, (18):13
PORTELA, A. and ESTELLER, M. (2010) Epigenetic modifications and human disease, Nature Biotechnology, 28:1057-1068
WATERLAND, A. and JIRTLE, R. (2003) Transposable Elements: Targets for Early Nutritional Effects on Epigenetic Gene Regulation, American Society for Microbiology, 23(15):5293-5300