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About Immunologist

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  • Location
    Montréal, Qc, Canada
  • College Major/Degree
    McGill University, M.Sc
  • Favorite Area of Science
    Micro & Immuno
  • Occupation
    Grad Student
  1. This one is free: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=stryer.TOC&depth=2 The classic University textbook in biochemistry is: Biochemistry by Donald Voet, Judith Voet J.Wiley&Sons It will be hard to find "good" in the meaning of "entertaining" one though! Good intro to the field!
  2. No in fact I even prefer your way of saying it. What is important is the gene pool and the "new gene-bearer". The concept of its eventual offspring and the foundation of the gene pool will come after the initial survival of this new individual (and its replication). So natural selection is not acting on the gene pool itself, but on each gene-bearer in function of the concerned gene. So the distinction being: Species: Arbitrary decision of 2 different groups each containing heterogeneity in their respective gene pool. Saying that natural selection occurs on new species is therefore impossible because it acts simply at the level of the individual (gene-bearer). I am having a complicated issue here essentialy over a semantic question: a mutated individual and its first descendants do not form a different specie from their originating specie until they diverged enough. One gene difference is not enough to have a different specie. Is it better?
  3. You should not address this relation in this regard. Theoricaly, the 2 beings -mother and foetus- are one and only until the birth, so they cannot "interact" together as two individuals do. It is biologicaly the same than a yeast budding from another yeast. The best I could find to describe it would be "nourishing" for mother to foetus and "being nourished" for foetus towards mother. But it is not quite proper in scientific language, although appealing in common language. I feel there should be more appropriate word, but I don't think it will be one of the one you suggested as they refer to 2 different individuals.
  4. In fact, your first observation that it is useless against viruses is quite sufficient in itself not to prescribe it. Second, as noted, it favors the apparition of resistance. Usually, in a normal organism (human), a bacteria that mutated and is now resistant to antibiotics (yes, this occurs sporadicaly and naturally without presence of antibiotics) have it more as a burden than an advantage when there is no antibiotics. The use f antibiotics will provide it with an advantage and favors an improvement of this new strain by selecting the better ones. Thus, pretty bad for the rest of us. Third, antibiotics kill many bacterias, not just pathogenic ones. Importantly, it will kill bacterias of the normal flora of the body and particularly the gut. This population is important and each antibiotic treatment affects them and rarely for the better. Among other things the normal flora prevents us from getting recurrent diarhea from opportunistic pathogens passing in the gut. If you trouble the normal flora, this could occur. Althought Frostbite is correct in saying that antibiotics are not perfectly specific (I don't know about his precise example), they usually do not harm ourselves too badly and this argument, although probably true, would not be a major reason not to prescribe the antibiotic. Why? Because we also have to concede that physicians have reasons to act this way: a viral infection could hide or allow a bacterial infection to occur as the immune system is occupied with the virus. So sometimes they prescribe the antibiotic in this idea, a risk that outweight the risk of non-specific killing of human cells (because often eucaryotic cells are sensitive to antibiotics, but to a concentration 2 or 3 logs higher than what is needed for bacterias) Hope it helps!
  5. I think that as the first thinker of the idea, you should be sent there to supervise the operation, no? And eat the same thing??? I think that you don't need to invent poisoned food, just don't provide them any if you think this way. I a not a supporter of ethics, but seeing that people have ideas like that could convert me.
  6. Hello Dims, First, part of Scicop says is true, these are notions you would easily get in a basic immunology book, but there is no need to be as agressive as he is. Second, Dr. Dalek provided come clues, but he is not absolutly right... So third, here goes my answer: Phagocytes are usually wandering around in different tissues and engulf by phagocytosis many things, self and non-self. Once it is said, we must conclude that they also "eat" things that are not dangerous! So your idea that they are eating in a preventive manner is not absolutly wrong, but inexact. For example, they are eating dead cells from the body to remove them from the tissue. But in this case, as it is not a danger signal, there is antigen presentation, but no activation of the immune response against it! How does it happens? Well antigen presenting cells (APCs) have different cell receptors, commonly reffered as "Pattern Recognition Receptors" PRRs. These receptors include the Toll-Like Receptors (TLRs) that the others discussed before. These receptors do recognize non-self and therefore "activate" the phagocyte. In the case of a self molecule, it is phagocytosed, but not recognized by these receptors, so the APC does not get activated. What is activation? Activation ensures that the APC will be presenting the antigen (Ag) to the Tcells concurently with a second signal (co-signal). This co-signal is NECESSARY for activation of the immune response, without it, Tcells will not respond. Think this should be clear. So yes the engulfed pathogen (or other) is killed, but it is important that Ag presentation occurs so that the immune system is made aware of the presence of this pathogen, because all chances are that others are present! Is it ok
  7. Hello Kirlian, Cancers form due to an abnormal growth of cells (from any type of cells). These cells are directed to proliferate all the time when they should not. Most of the time, a mutation of a gene that regulate the growth of cells is the origin of the disregulation. These mutations can be induced by many factors, like viruses that insert in the genome, exposition to radiations, chemicals (ethidium bromide)... anything that will induce affect DNA and cause an improper repair of the DNA strand. In the lung, the most common cause of cancers is, sadly, cigarette smoke. Among all the stuff in cigarette smoke, there is (if I remember correctly) over hundred cancerigens and 20 (I'm sure of that one) cancerigens that are aiming specially at the lungs. Genetic predispositions are also involved in cancer. By example, if you have a specific allele of a regulatory gene (for cell growth), it can change the odds that this gene's protein work badly. Hope it helps understand! A good reference for cancer: http://www.cancer.org/docroot/home/index.asp For lung: http://www.lungusa.org
  8. http://kentsimmons.uwinnipeg.ca/16cm05/16lab05/lb1pg7.htm fig. 16
  9. I think you should find this answer by yourself, but take the hints of people: I am rephrasing your question as follow: You have 3 non-sense mutations in a LacZ gene in 3 strains of E.coli. You will use UV on these strains to try and revert these non-sense mutations to coding codons. For each of the 3 stated codons (TAA,TAG and TGA), what is the expected codon after UV irradiation when referring to the "A rule" (hint: what UV do to nucleotides??? How these modified nucleotides will be interpreted by polymerases?). The post-UV irradiation codons will result in what? 1. which amino acid (or stop) 2. functional or not functional gene. Everything revolves around the effect of UVs on nucleotides and the mutation induced by UVs... Good luck!
  10. I think Dak got a more simple approach (and probably more verifiable). If a recombination occured in the parents, finding it in the child would allow to trace the parent. If that was a teacher's question, recombination would surely be the answer.
  11. Here is a call for discussion. In March (Science, March 2, Evidence for a functional second thymus in mice) a German team reported having isolated a second thymus (YES A BRAND NEW PREVIOUSLY UNIDENTIFIED ORGAN) in the mouse http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16513945&query_hl=3&itool=pubmed_docsum. This has clear consequences for teams who were previously doing thymectomy to prevent lymphocyte development. Does anyone performed thymectomy in mice? If yes, what is the remaining population found in periphery? How did you address that it was peripheral expansion?
  12. I think I would personnaly repeat the serum Ig testing, just in case your subject was exposed to something irrelevant the week before the sampling... As IgG2 are a more rare form, an acute elevation in their amount is more likely to be noted than an increase in IgG1 for example. So it could be only some irrelevant (to your idiopathic fatigue context) observation. Can you correlate this observation with leucocyte counts in the blood? If an increased amount of neutrophils is found, search no more: infection with something. In a case where there is nothing like that, could it be that increased [igG2] is only a consequence of something deeper, like overexpression of hormones leading to increased IL-6 or else? Having measured anything else in this serum? Philippe
  13. Autoantibodies and auto-reactive T cells are always generated in our body. But they are kept silent by 2 mechanisms. The first one involve not letting them out of their maturing organ (thymus): t cells that recognize self antigens (presented in the thymus) are sent in apoptosis (programmed cell death). In the periphery, if they were not killed in thymus, they are anergized by antigen presenting cells (APCs) if they recognize self-antigens (APCs do not express co-stimulation molecules necessary for activation). So how can you have auto-reactive antibodies? 1. a self-antigen is expressed out of its context. Some proteins are expressed only in the eye, so are never presented as "self" in the thymus. But if someone get an injury to an eye and inflammatory cells can now get in the eye, they can be activated by these never-seen proteins. 2. Some proteins (antigens actually) are very similar to some pathogens, so after an infection, you get autoimmunity against your own self because it is similar to the previous infectious agent (see rheumatic fever with gr A b-hemolytic Streptcocci: http://www.life.umd.edu/classroom/bsci424/BSCI223WebSiteFiles/Chapter23.htm) 3. Also, in periphery, some cells are there to keep immune reactions low, the T regulatory cells (Treg). If for a reason or another, they do not perform their task, you can have autoimmunity. 4. Plenty of other known or still debated reasons. Hope it helped.
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