S282: Chapter 8 and 9

The final two chapters of this tomb relate to the death of stars and what happens to them afterwards.

The death throws can result in stars doing all sorts of things. Some of them eject large rings of material called planetary nebulae. The bigger and brasher stars go out with a bang in a supernova explosion, which as a by product generates most of the common elements with atomic numbers greater than Iron. Supernovae can occur in a couple of ways, mostly its big brash stars blowing up, but occasionally its a white dwarf in a binary system given a second chance to shine.

The death of a star depends largely on how big it is. The smaller stars like our own after going through a red-giant phase tend to start to fizzle out into a white dwarf. In this stage, they are basically out of fuel, and all they can do is sit there and glow with the heat saved from their glory days. They eventually cool down to black dwarfs, but this takes so long to happen, that it probably hasn't had chance yet. However they are rather faint objects so they are difficult to see at the best of times. There is a fairly hard and fast limit (the Chandrasekhar limit) to the size of a white dwarf, and most stars sneak under this limit by blowing off much of their mass in their death throws.

Bigger stars end up as more exotic objects, including neutron stars, quark stars (possibly - the jury is still out on the existence of these) and the more famous black hole.

With that, book 1 is done, and book 2 beckons, but a TMA needs to be finished first!

Next S282 Prev S282

S320: Book 4 - Diagnosing infection

Well this is a much easier book after the alphabet soup of the Immunology.
It goes into some details of how infections can be diagnosed in practice. This is not the GP having you "Say ahhh" type of diagnosis, but the methods of isolation pathogens.

There are sections on how to culture bacteria, how to breed viruses and so on. What media you can grow them on and how you can tweak this to give you a pure culture. There is also an interesting video on life in the diagnostic lab.

After that, it moves onto the more high tech techniques. These generally involve antibodies, or gels and stuff. So it covers immunofluorescence, Enzyme-linked immunoabsorbent assay (thankfully abbreviated to ELISA) and then things like gel electrophoresis, SDS-PAGE, blotting, and PCR.

The final chapter takes you through the diagnosis of some common diseases, such as cholera, HIV, flu, malaria and flukes.

As I say, positively relaxing after book 3, but I bet the exam questions will be digging around in this material.

Next S320 Prev S320

SXR376: Molecular basis of Human Disease

Uh oh - this years residential material has arrived. I've opted for one of the 3rd level biology residentials which will take place at Nottingham. The pack arrived with:

• An introductory letter
• A course calender
• A course guide
• A ring binder and insert
• A stack of reading (well 180 pages worth)
  
• A CD-ROM with more stuff on and a virtual lab.

As the title says, its an investigation to the molecular basis of Human Disease. Now I'm not entirely sure what we're going to be doing in the weeks work, but I have a fair idea it will involve some PCR machines, and some immunoblotting, also known as western blotting.

The 3rd level residentials take a step up in pace, as you have to pass a computer marked assignment (CMA in the OU jargon), which is a 20 question multi-choice paper before you even get to the place. This, the lady assured me last year when I was scoping the place out, is to ensure you have fully read all the material beforehand. SXR103 I suspect you can wiggle your way through provided you have a bit of background and some luck without reading the materials, especially if you are doing S103/4. SXR270 it certainly helped to read the materials beforehand, but here they want to make sure!

The first few chapters of the material are great, as they are almost revision for the S320 course I'm doing at the moment. A whole batch of immunology, and the theory of PCR and blotting techniques. Then there is a whole load of stuff on the mechanisms of the HIV virus and how it attacks cells, and the mutations that can help or fight it. There is also a paper to read on the discovery of CCR5-delta32 mutation which renders some people almost immune to HIV.

The CD-ROM gets you to work through a simulated lab procedure for running PCR DNA amplification and the western blotting for proteins. This is quite useful, as most of my first experiments in this I messed up by using the wrong concentrations, picking the wrong temperature or the wrong primers. One click and you can try again. An inexpensive way to make mistakes!

There is also a mini-lecture on HIV infection and some PDFs on the disc, but most of the material, including the CMA has to be loaded from the course web site. There is the usual first class forum, and I've noticed a few people I've met on previous residential course. I think there are only a small number of people that can fit in the lab, so its typically only 20-30 people per week - which is somewhat smaller than either of the other two residentials. It's also the reason I signed up for this course at 7:30am on the day registration opened to ensure a place!

So - onwards trhough the reading, the CD and then the CMA (which you can submit online - yay!).

Next SXR376

S282: TMA-2

Its time to do the second TMA on this course and this one is relatively involved.

The first question is to write up an experiment you have performed, either on calculating the luminosity of the Sun, or on the sidereal day. I chose the former. For this we had to compare on a sunny day the output of a 150W lightbulb with the sun using a piece of paper with an oil spot on it. You move the paper in between the sun and the bulb until the oil spot is not visible anymore - then you have similar luminosity values. Unfortunately 150W lightbulbs are pretty much phased out especially the clear ones that are required and 100W clear are hard to find but I did managed to find a 100W clear eventually. I ended up with about 1/3 of the accepted value for the luminosity of the Sun, which considering there was some very hazy high level cloud around, and it was early in the year (and I was using 100W bulb) I didn't think was too bad. I've learnt not to expect too much from physics experiments without doing a fearsome amount of work.

This question is worth 40% of the marks. It means of course you have to do the experiment first, and then write it up using the appropriate section headings, titles, abstracts and stuff like that. It requires analysis of data, error calculations and how the experiment could be improved and so on.

Question 2 is another relentless one. Its split into 3 sub-questions on parallax measurement, doppler measurements and some planisphere work to work out rising and setting times. Each sub question is made up of 3 to 5 parts, so that's 11 questions you have to answer, for 24% of the marks.

Question 3 is similarly made up of 3 subsections on spectral classification, spectral measurement and magnitudes. Its again 11 questions in all and is again 24%.

Question 4 is about dust clouds and collapse to form suns. Three sub parts again looking at collapse conditions, Hertzsprung-Russell diagrams for forming clouds, and finally a wild card on detection of planets orbiting other suns. Only 7 questions in total to answer here for your 12%.

Next S282 Prev S282

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.

Next S282 Prev S282

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 IFNγ 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.

Next S320 Prev S320