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Saturday, 26 April 2008

S282: Chapter 5-7 Formation, Main Sequence, and decay

The next three chapters are all about the main sequence for stars. This is the thick band of stars that is evident on the old Hertzsprung-Russell diagram. Most stars appear on this main sequence somewhere, hence if being the main sequence...

Chapter 5 - The formation of stars - covers how stars assemble themselves from clouds of dust, and how they first appear. It looks at some of the maths of dust clouds, first work out by James Jeans. He worked on a number of areas, but in this one he looked at the dynamics of gas clouds. He found if they were above a certain density depending on temperature, a cloud of gas would contract and depending on how much was present, form a star - sooner or later. Such stars then start life initially off the main sequence, such as the T Tauri stars, but rapidly hop on following Hayashi tracks and then spend most of their time there.

Chapter 6 - The main sequence life of stars - covers the general structure of stars as they spend their life on the main sequence. It looks at the main nuclear reactions, such as the 3 main ppi types, and the CNO cycle which kick in at different temperatures and pressures. It also considers a minimum and maximum size that stars can reach and how long such stars live for. Broadly speaking, the bigger the star, the shorter its life.

Chapter 7 - The life of stars beyond the main sequence - covers what happens towards the end of a stars life. Stars reach the end of their lives when they run out of fuel. This is basically hydrogen that is in the core of the star. Thats the hottest and densest part, and the only place fusion can take place. As it uses it up, things get increasingly desperate. If the star is big enough, it runs out, contracts, warms up a bit more, and can burn a small shell of hydrogen around the core. It can also start to burn helium if things get warm enough, using the triple alpha process, which burns 3 helium -> 1 carbon. At this stage it swell up into a much larger Red Giant star, which is the fate of our Sun. After this, things get increasingly desperate. Carbon burning is possible and will keep a large star going for 10,000 years maybe, followed by neon burning (1 year), oxygen burning (6 months) and finally silicon burning lasting a day. At this point there is nothing left to burn! What could possibly happen next.

Thursday, 24 April 2008

S320: Book 3 - Immunology

OK - now this book is a bit of a struggle. There are an awful lot of molecules and proteins introduced here, and any number of interactions between them. There is also the two disk interactive CD to take in, and all in all there is a lot going on here.

Let me see what I can remember. Well first there are the leukocytes, which come in all sorts of flavours. There are
  • Macrophages - which attempt to gobble up bacteria and similar agents and kill them with bursts of free radicals.
  • B cells - which were first discovered in the Bursa of chickens, hence B, but happily are manufactured in the bone in humans - so can still be called B cells without anyone getting confused. B cells produce antibodies, when requested to. They start as naive cells, and then go through a selection process where their antibodies are refined and the best survive to become plasma B cells which produce antibodies. Some also go on to become memory B-cells.
  • NK cells - these are natural killer cells, licensed to kill. They inspect cells of the body, and any that are not presenting the right documentation are terminated. This often happens under viral infection when MHC presenting is turned off by the virus in an attempt to avoid Tc cells. They usual kill by triggering the self destruct sequence built into all cells, but they also carry a gun, a protein called perforin which can punch holes in the cells surface and so start it leaking its contents.
  • Basophils - help in the control of inflammation.
  • Neutrophils - mainly used for anti-bacterial defence.
  • Eosinphils - used for defence against parasitic worms.
  • Mast cells - produce histamines and cause inflammation responses.
  • Dendritic cells - look a bit like nerve cells. They consume stuff and present it for inspection using MHC2. They tend to hang around in lymph glands.
  • T cells, of which there are many, and are produced in the Thymus - hence the T.
    • T helper cells, which come in at least two varieties. TH1, TH2. They use MHC1 and CD4 receptors for detection.
    • TH1 cells work in conjunction with macrophages, recognising antigens presented by macrophages, and releasing TNF and IFN╬│ cytokines that activate macrophages (but damp down TH2 activity).
    • TH2 work with B cells, recognising antigens presented on them, and activating them with various interluekin cytokines, and so help to make antibodies. They also prompt B-cells into class switching behaviour.
    • T-memory cells, which help in the memory of infection and so help ward off subsequent attacks.
    • Tc cells, also know as cytotoxic T cells, which are killers. They sample the MHC presented fragments of proteins presented on the cells surface. If they recognise one of these fragments as foreign, they press the cells self destruct button. They also carry the perforin guns as backup. They use the CD8 and MHC1 together for detection.
So TH1 work with macrophages (cell mediated response), and TH2 with B cells (antigen response). The body will usually use one pathway or the other, and if it chooses TH1, then the interaction between TH1 and macrophages acts to shut down the TH2 and B cell pathway, and vice versa.

There is also a number of antibodies, which can appear in several different forms, such as
  • IgA - produced by B-cells and makes its way across mucosal surfaces to help block infection.
  • IgD, helps activate B cells, but not used much elsewhere.
  • IgE - produced by B cells, they attach to mast cells and basophils. When these then pick up antigen using these antibodies, they release inflammatory cytokines which attract macrophages.
  • IgG - produced by B cells, and found in plasma, and attaches to bacteria to labelled them to be attacked.
  • IgM - expressed by naive B-cells as receptors.
(no - I'm not sure what happened to B,C,F,H etc.)

The main signalling is done via the Major Histocompatible Complex, in two versions, called MHC1, and MHC2. All cells express MHC1, and the MHC1 contains within a groove bits of proteins found in the cell during cleanup. So all cells display what they are currently using, which allows Tc cells to check they are valid. MHC2 is expressed by macrophages, B-cells and dendritic cells, and is used to show bits of proteins that they have ingested recently. So in the case of macrophages, this might be bits of bacteria or viral particles. Its important they don't use MHC1 for this, or else the Tc cells would come round and have (fatal) words with them.

Then there is a profusion of chemicals that are produced by these cells and work with one another. Signalling molecules which include
  • interleukins (ILs) - produced by TH2 cells to kick B cells into action. This also slows down macrophages, so they don't fight too much.
  • interferons (IFNs) - produced as a result of viral infection to signal to other cells they are under attack. Also produced by TH1 cells to kick macrophages into action. This also slows down B cells.
  • colony stimulating factors - that bits a blur
  • chemokines - lots of these
  • tumour necrosis factors - another signalling molecule
Then there is the complement system. This is yet another arm of the immune system, which encourages macrophages to come towards the site of infection, and can also promote its own attack using a membrane attack complex that punches holes in the cell walls.

All in all there is a lot to keep straight, and to keep track of what influences what.

Wednesday, 23 April 2008

S282: Chapter 4 - Comparing Stars

This chapter is a major overdose on the Hertzsprung-Russell diagram. Its a popular diagram in astrophysics, and by the end of this chapter, and a few subsequent ones, you'll feel right at home with it. It looks at the location of the main sequence stars, like our Sun, which is towards the more insignificant end of the chart. Also at things like Red Giants, SuperGiants and white dwarfs which fall off the main bad somewhat.

You also pick up a few other lesser known types, such as Cephids, and T-Tauri stars, which turn out to be a bit more important later on.

After the H-R diagram has been done almost to death, the remainder of the chapter focuses on the interstellar medium and its affects on observations.

Tuesday, 8 April 2008

S282: Chapter 3 - Measuring the stars

Chapter 3 is all about how the stars are analysed from the Earth. So here we meet all sorts of remote analysis techniques.
It starts with a look at how we can measure the distance to the stars, starting with measuring parallax. This allows distances to the nearer stars to be measured. It also discusses the proper motion of the stars, and also the radial and space velocity from these details.

Following that there is a look at how other things can be worked out. If you know the distance, you can work out the luminosity of the star. From this you can also work out things like radius, temperature and some other things. Spectroscopy features quite highly here, as there are a number of things that can be worked out from this. Radial velocity is one thing based on the Doppler shift. However there are a number of other things you can work out from this, including some clues to the mass and temperature.

This leads to the categorisation of stars into the stellar classes such as O,B,A,F,G,K,M etc.

Tuesday, 1 April 2008

S320: TMA-1

Its time to face up to TMA-1 for this course. What is a level 3 TMA like?

Well firstly its a bit relentless. There are 7 questions in all, and most of them broken into sub parts.

Question 1 gives a table of data relating to bacterial infection rates. It gets you to do some simple statistics derived from these, such as working out case fatalities, and so on. It then gets you to write a few sentences on why the data may not be fully accurate. 18 marks for this part.

Question 2 is more simple, in that it is 12 marks to discuss three reasons why bacteria are likely to cause hospital acquired infections. This isn't too bad, except I struggle to find 12 worthwhile points in just a few sentences.

Question 3 looks at the disease syphilis, and the pathogen that causes it. The question ranges across the cause, change in incidence, and treatments for the disease. There are 22 marks available here, and again I struggle to find enough points to account for all the marks.

Question 4 covers Koch's postulates, and how it might be applied to the evidence that influenza might cause atherosclerosic plaques. 12 marks available here, but there seems precious little related information in the course book about this so I trawled through a number of papers..

Question 5 is a bit of a change. You are given a set of cases where the first sentence is true, and the second sentence may be true. You have to decide if the 2nd is, and if it is whether this is explained by the first statement. Another 12 marks here.

Question 6 is more descriptive asking why a knowledge of a pathogens biology might be useful in treating it. Another 12 marker.

Finally question 7 looks at viruses and what morphological changes there infection can cause.
Once again 12 marks.

I've spent quite some time on this TMA in fits and starts, but I'm struggling to pin down the connection between marks and salient points to make.

Oh well, its done now.