It can't be put off any longer - another TMA to submit.
Question 1 (25%) looks at stellar evolution and reactions - and its in three parts.
Part a) gives you 6 nuclear reactions and then asks a number of true/false type questions. However the joke in the pack is that if you think it is false, you have to give a reason why it is false. So this means getting your reasons in order.
Part b) is similar, in that you are given 8 statements, and told to pick out two that are false, and then explain why they are false. All the questions concern binary star systems in one way or another.
Part c) is another list of 8 statements about stellar evolution, and again pick out the true ones, and explain why the false ones are incorrect.
Question 2 (20%) is split into a-c with subparts for each.
Part a) looks at the stability of stars and you need to draw a diagram showing the forces in balance in a star, then to consider what forces are important in various sized stars.
Part b), with 4 subparts, looks at the collapse of a stellar remnant to a white dwarf and a neutron star and what conditions each are formed in.
Part c) takes the part b) further and introduces black holes into the mix and you have to do some calculations on back hole radii.
Question 3 (18%) looks at supernovae, and its just 4 subparts. Its based around a given table and you need to consider what type or supernova each represents, what they can be used for, and what would happen to the remnant left over.
Question 4 (22%) is a little different in that you are given a spreadsheet of cepheid data from M81 and you have to calculate various equations and end up with a value for its distance. There are a few formulas to rearrange and some averaging to be done, and then some general questions about the results.
Question 5 (20%) is again different in that you have to read one of three recent articles published on the website and then write a short account of its significance
Its not too bad as there is a bit of variety in amongst it, although I found the first question dragged on a bit as I trawled through various pages looking for clear refutation of this point or that.
Thursday, 10 July 2008
Tuesday, 8 July 2008
S282: Book2 - Chapter 3 & 4
Book 3 continues with some more chapters about galaxies. In chapter 3 we are considering active galaxies. This looks at all sorts of the more weird end of the galactic spectrum. It considers galaxies that have active cores - these include Seyfert galaxies, quasars and blazars - and whether they are the same thing viewed from different angles. Active galaxies appear to be associated with early galactic structure, at least in some cases. I found it all a bit dull to be honest after the first few pages. Maybe galaxies aren't my thing - or I'm missing the point!
Then chapter 4 looks at the distribution of galaxies. The fact that the milky way is just one of a local group of galaxies that includes a number of others. Then our local group is part of a supergroup of groups grouped together. Beyond that there doesn't seem to be any further discernible structure to the universe.
Then chapter 4 looks at the distribution of galaxies. The fact that the milky way is just one of a local group of galaxies that includes a number of others. Then our local group is part of a supergroup of groups grouped together. Beyond that there doesn't seem to be any further discernible structure to the universe.
Wednesday, 2 July 2008
S320: TMA-2
Another TMA comes around. There are only 3 in the course, but the 3rd counts double. Anyway, time to tackle this one.
Question 1 (14%) is about immunology. We have to draw a diagram with Interferon-γ in the middle of it, and around it all the things it affects and produce it. IFNγ is used a lot for signalling, and has over 20 interactions, but luckily the book doesn't list most of those, and I confine myself to those given in the book.
Question 2 (18%) we have to do a search of the literature to find a couple of papers that look at HLA haplotypes and their effect on tuberculosis.
Question 3 (8%) is about pathogen identification and asks you the steps you would take to identify a bacterial pathogen. Its rather a general question as the steps depend quite heavily on what you suspect it might be.
Question 4 (10%) is like in the last TMA where you are given two statements one true, and one that might be true, might be explained by the first, or might not. 5 sub-questions, related to worm infections, sterilisation, bacteriology, antibodies and PCR.
Question 5 (50%) you have to read a published article about dengue disease and:
(a) Comment on the general style of the article.
(b) Define a number of terms (with references) used in the article.
(c) Draw a diagram of the life cycle and intervention points of the disease.
(d) Write a 200 word summary of the article.
Its still hard to spot the marks in these TMAs and to ensure you have written enough points for the number of marks on offer, but I did ok on this one.
Question 1 (14%) is about immunology. We have to draw a diagram with Interferon-γ in the middle of it, and around it all the things it affects and produce it. IFNγ is used a lot for signalling, and has over 20 interactions, but luckily the book doesn't list most of those, and I confine myself to those given in the book.
Question 2 (18%) we have to do a search of the literature to find a couple of papers that look at HLA haplotypes and their effect on tuberculosis.
Question 3 (8%) is about pathogen identification and asks you the steps you would take to identify a bacterial pathogen. Its rather a general question as the steps depend quite heavily on what you suspect it might be.
Question 4 (10%) is like in the last TMA where you are given two statements one true, and one that might be true, might be explained by the first, or might not. 5 sub-questions, related to worm infections, sterilisation, bacteriology, antibodies and PCR.
Question 5 (50%) you have to read a published article about dengue disease and:
(a) Comment on the general style of the article.
(b) Define a number of terms (with references) used in the article.
(c) Draw a diagram of the life cycle and intervention points of the disease.
(d) Write a 200 word summary of the article.
Its still hard to spot the marks in these TMAs and to ensure you have written enough points for the number of marks on offer, but I did ok on this one.
S320: Book 6 - Modelling epidemics
This book looks at how epidemics happen, and what can be done to stop them.
It starts by looking at some very basic maths. It revolves around a number called R0, which is the average number of people who will be infected by a infective individual.
If the R0 is less than 1, then the infection will die out, if its greater it will survive.
It also looks at the affect of Herd Immunity. This has a big effect on diseases. Its brought on either by lots of the population having caught the disease and so being immune, or else through vaccination. The key thing here is that it is related to R0, if enough of the population is immune, then the R0 will drop below 1. This is because obviously most people an infected individual meets will be immune so will not be infected themselves. So with something like smallpox, you only need to get more than 85% of the population immune, and the disease will die out. This doesn't work so well with zoonotic diseases, as there is a reservoir of infections.
On the other hand, partial herd immunity can sometimes be a bad thing. If only a fraction of the population are immune, then the disease still thrives, but not as well. However the age at which one becomes infected tends to move up. This can be a problem, as some diseases caught in childhood (mumps for instance) can have much more severe consequences in adulthood.
Its a balance, and not always obvious what is going to be good in the long run!
An interesting book - and at only 70 odd pages, not too difficult to digest.
It starts by looking at some very basic maths. It revolves around a number called R0, which is the average number of people who will be infected by a infective individual.
If the R0 is less than 1, then the infection will die out, if its greater it will survive.
It also looks at the affect of Herd Immunity. This has a big effect on diseases. Its brought on either by lots of the population having caught the disease and so being immune, or else through vaccination. The key thing here is that it is related to R0, if enough of the population is immune, then the R0 will drop below 1. This is because obviously most people an infected individual meets will be immune so will not be infected themselves. So with something like smallpox, you only need to get more than 85% of the population immune, and the disease will die out. This doesn't work so well with zoonotic diseases, as there is a reservoir of infections.
On the other hand, partial herd immunity can sometimes be a bad thing. If only a fraction of the population are immune, then the disease still thrives, but not as well. However the age at which one becomes infected tends to move up. This can be a problem, as some diseases caught in childhood (mumps for instance) can have much more severe consequences in adulthood.
Its a balance, and not always obvious what is going to be good in the long run!
An interesting book - and at only 70 odd pages, not too difficult to digest.
Wednesday, 18 June 2008
S282: Book2 - Chapter 1 & 2
Well - another weighty tomb awaits us in the shape of Book 2, An Introduction to Galaxies and
Cosmology (435p). The first book was all about the birth, life loves and death of stars. In this book we take a step back and look at the bigger picture of how galaxies are born, live and die.
If you thought finding out details of stars which are all tiny pin pricks of light was hard, well its much simpler than galaxies. Galaxies are orders of magnitude further away than stars so the amount of light you can capture is typically smaller.
Anyway - we start the book with Chapter 1 looking at the Milky Way - our own galaxy. This allows us to explore what it is made up of (and stars are are pretty minor component!), its shape such as the halo (including the dark matter one) and the bulge, some of the oddities within it such as open cluster and globular clusters.
Then Chapter 2 looks at regular galaxies. There are a lot of different galaxies out there and naturally the first thing the early people did was to lump them together into categories. So we have spirals (with and without bars), ellipticals, lenticular and irregulars. These are classified according to the Hubble scheme (or other variants).
Then there is quite a section on how we work out the distance to these galaxies - which is pretty hard work. Many techniques are not very accurate but give a good appreciation of the order of magnitude.
Cosmology (435p). The first book was all about the birth, life loves and death of stars. In this book we take a step back and look at the bigger picture of how galaxies are born, live and die.
If you thought finding out details of stars which are all tiny pin pricks of light was hard, well its much simpler than galaxies. Galaxies are orders of magnitude further away than stars so the amount of light you can capture is typically smaller.
Anyway - we start the book with Chapter 1 looking at the Milky Way - our own galaxy. This allows us to explore what it is made up of (and stars are are pretty minor component!), its shape such as the halo (including the dark matter one) and the bulge, some of the oddities within it such as open cluster and globular clusters.
Then Chapter 2 looks at regular galaxies. There are a lot of different galaxies out there and naturally the first thing the early people did was to lump them together into categories. So we have spirals (with and without bars), ellipticals, lenticular and irregulars. These are classified according to the Hubble scheme (or other variants).
Then there is quite a section on how we work out the distance to these galaxies - which is pretty hard work. Many techniques are not very accurate but give a good appreciation of the order of magnitude.
Friday, 13 June 2008
S320: Book 5 - Evolving infections
Book 5 now and at about 100 pages not too bad either.
It considers some of the theoretical basis of disease. The arms race between pathogen and the host and how they both evolve over time. It also looks at things like the manipulation of the host, particularly by some pathogens that can have a quite large effect on the behaviour of the host. This also considers the patterns of virulence and how the life of the pathogen is affected by the life of the host.
Transmission mechanisms also are looked at in detail, and how effective they are.
Finally in the last chapter it looks at a theoretical model for a host/pathogen infection in a population and how that can be modelled. This is apparently setting us up nicely for the next book on epidemiology.
It considers some of the theoretical basis of disease. The arms race between pathogen and the host and how they both evolve over time. It also looks at things like the manipulation of the host, particularly by some pathogens that can have a quite large effect on the behaviour of the host. This also considers the patterns of virulence and how the life of the pathogen is affected by the life of the host.
Transmission mechanisms also are looked at in detail, and how effective they are.
Finally in the last chapter it looks at a theoretical model for a host/pathogen infection in a population and how that can be modelled. This is apparently setting us up nicely for the next book on epidemiology.
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