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DrZoidberg

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Posts posted by DrZoidberg

  1. The complement system is a complex cleavage cascade involving many C proteins (C1-9), if you need un-necessary detail a good immunology text will cover this. Generally you should only know the importance of the activation of C3 convertase to cleave C3 to create C3b! (via classical or alternate pathways). C3b is a major product that then permits further cascades, resulting in enhanced phagocytosis of antigen (e.g organism) known as opsonisation, or lysis of target via membrane attack complex formation, and initiation of acute immflamatory reactions. The latter is important for enhanced immune responses and C-reactive protein is vital for responses to bacterial infection (activation of complement).

  2. Inbreeding as you stated, increases recessive gene expression in a confined gene pool, hence increased genetic disease; however more potently, inbreeding depression results due to lack of gene pool variation. It is becoming clear that inbreeding decreases DNA fidelity such that mutations in cell replication or development (ie embryonic development) can occur more frequently when a fetus results from two closely related individuals. This is why inbreed children are more frequently stillborn, or if the mutation allows life, born with extra appendages or poor limb development etc

  3. I remember doing an essay on germline gene therapy a few years back, so not sure if the situation is the same today but for what i knew....

     

    Yes, the body does attack the virus and this is one of the problems with using a viral DNA vector, the virus is attacked before it can inject its package. Secondly it is important to make sure the virus injects the DNA into the correct target cell (e.g. correct insulin gene into right pancreatic cells), so synthesising a virus which can evade the immune system to deliver DNA to the right target AND have a limited lifespan (so not to persist) is the current obstacle in gene therapy (although there are other vectors being explored).

  4. Well' date=' the problem is simply that your definition does not match the actual termini used to describe evolution. And they were in fact misleading.

    There are for instance bacteria that have adapted to parasitic life-styles and in that process eliminated a lot of its own core genome (a more dramatic examples are probabl plastids and mitochondria). In your definition this would be accounted as "backward" or at least as de-evolution. However the process is clearly evolution and not the reversal of it.

    As such your definitions are simply not suited or accurate enough to describe this. Sorry.[/quote']

     

    Top post! Along the same lines as to what i mentioned waaaay back on this thread. Genetic evolution in any sense is the presence of DNA over time, whether new genes arise or old dissapear.

  5. Sounds promising, however the details are sketchy i.e. growing a 3D organ from a monolayer of bladder cells - interested to find more on this. Can foresee potential problems already with an organ bank i.e. staff transplanting organs into wrong hosts!

     

    Ahhh, go to lancet and download the paper, fascinating methods used, painstaking work to reform a dual layer of tissue (smooth muscle and urethrial cells) about an organ shaped scaffold.

  6. references? there are many. look in pubmed/google scholar with the keywords

    >male female autoimmunity (review)

    or

    >c57 balb strain th1 th2

     

    if this begins to get interesting' date=' i'll discuss the ideas and data more; a bit of a daunting task but i'll try.

     

    the act of child bearing is well known to boost the immune system of mothers to be, and pregnancy itself diminishes autoimmunity despite the fact that the mother is carrying a child with a different immunogenecity to herself. in other words, immunologically there is an argument that the mother should be mounting an immune response against the fetus.

     

    but this is a long way from the initial question![/quote']

     

     

    I am interested yes, although i come from a more molecular biological background, immunology was a subject i really enjoyed and am now re-revising since my current research is immunologically based (am concerned with gene expression in mature dendritic cells).

    From what i read in a good paper, and by your logic, it appears T helper cells play a big role in protecting fetal growth by creating a tolerant micro-environment, and to do this T helper cell count is greater than normal male numbers to accomplish this protection (which works to the advantage of the fetal host by enhancing immune responses)>>?

  7. simple to complex? No' date=' not necessarily.

    forward? No, that's an arbitrary distinction, and the root of your misunderstanding. Evolution has no overall "direction." That is dictated solely by the environment at the time.[/quote']

     

    Well stated! evolution IS de-evolution and vice versa. In otherwords de-evolution does not exist, evolution takes unstated pathways and if that means refining complexity to simplicity so be it.

  8. Great medical advancements for me would be the use of ether in surgery and the discovery and advancement of anaethesia. This overwhemingly increased patient survival.

    Others would be Pastuer's work on isolating microbes as source of infection, Metchnikoff's work on starfish (immune cells) or Garrod's pioneeringwork on enzymopathies linking genetic defects and deformed proteins to congenital disease.

  9. it may be of interest to this thread that there is evidence for certain animals, eg[/i'] strains of mice, that stronger immune responses can contribute to stronger autoimmune responses too. perhaps the most interesting research on this issue, but the most difficult to draw conclusions from, relates to the observation that human females are more prone to autoimmune diseases and that human males comparatively to females have weaker immune responses.

     

     

    Interesting comment, any references? Perhaps a stronger and more sensitive immune system serves a greater importance in child-bearing mammals?

  10. In any sense ALL wild animals have competant immune systems otherwise they would not be there. Of course the strength of immune response differs between individuals due to genetic roots and environmental upbringing. Immune strengths can differ between species but all are susceptible to disease that is generic or specialist. For example the HIV virion is exclusive to invade human T cells and not monkey T cells. We now know why due to certain recognition markers lacking in monkey cells (so we are exploring other animal immune systems and learning). However, monkeys are liable to SIV infection whilst we usually aren't.

  11. Interesting topic. Firstly i should highlight that 'creating a monkey' from a human transcript or vice versa is impossible at this point in time. It is simply not a case of transferring missing genes. The importance of gene interaction and expression is becoming more evident in the way DNA 'works'. Alot of important differences may for example exist within introns of other genes or genes shared by us and our primate cousins. Furthermore novel signal codons (or novel genes) within 'junk' DNA stretches (obselete term i know, should be DNA of no known or lacking function) may of yet to be uncovered and play vital gene regulatory roles.

    The point really is genomes work collectively and 'cut and paste' of sequences have a high chance of missense or complete confusion.

     

    However with the advance of microarrays, greater understanding of gene interaction may one day lead to a monkey with the ability of speech via vocal chord/neural/brain enhancements!

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