explain agglutination reaction?
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Aantibodies when they bind to the corresponding antigen(s) bring as many as 5 such antigens or antigen containing entities per antibody depending on the type of the antibodytogether. However such antigen containing cells/entities have many such antigens on their surface and therefore are attacked upon by many such antibodies which result in a meshwork like formation resulting in the phenomen of agglutination. The classic example for this is blood grouping.
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The Landsteiner system works like this, there are A and B antigens. Blood group AB means anyone who has this group (not many do, but I'm one!) has both anti A and anti B on the surface of the red blood cells, but neither in the serum.\nGroup A will have anti A on the red blood cells and anti B in the serum, whereas group B will have anti B on the red blood cells and anti A in the serum. \nBlood group O (usually the commonest) has no antigens on the red blood cells , but both anti A and anti B in the serum.\nYou may have heard of rhesus negative and positive? That refers to the D antigen and there are Cs and Es and loads of other ways to group blood, but the ABO Landsteiner system along with anti D are the most relevant and best known.\n(hopes she's remembered her stuff from the path labs donkey's years ago!)
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At higher temperatures, reactions proceed faster, so metablic activity increases.  Also, pressure and/or volume may increase.  At high enough temperatures, proteins will start to denature, but this usually doesn't happen with a fever.
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The Gram reaction is based on the structure of the bacterial cell wall.\nIn Gram-positive bacteria, the purple crystal violet stain is trapped by the layer of peptidoglycan which forms the outer layer of the cell.\nIn Gram-negative bacteria, the outer membrane prevents the stain from reaching the peptidoglycan layer in the periplasm. The outer membrane is then permeabilized by acetone treatment, and the pink safranin counterstain is trapped by the peptidoglycan layer.
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Hi Kitty,\nHere is what, I think, you need.\n\nExothermic, dH < 0, Entropy increases (dS > 0), Reaction is spontaneous and dG < 0\n\nExothermic, dH < 0, Entropy decreases (dS < 0), Reaction is spontaneous only at low temps, if |T dS| < |dH|\n\nEndothermic, dH > 0, Entropy increases (dS > 0), Reaction is spontaneous only  at high temps, if T dS > dH\n\nEndothermic, dH > 0, Entropy decreases (dS < 0), Reaction is not spontaneous, dG > 0
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basic chemistry\n\nthey neutralize each other by forming salt and H2O
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Hopefully this diagram can answer your questions:\nhttp://fachschaft.cup.uni-muenchen.de/~schleifi/reaktion/reaction/stobbe.html
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The chemical reaction from adding\nsalt lowers the temperature in which water freezes.\n\nThat is why they throw in onto the roads in areas of winter freezing.
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Humoral immune response has to do with the antibodies. The antibodies attach themselves to the virus and destroy them.  Look here: \nhttp://www.google.com.my/search?hl=en&hs=cwy&client=firefox-a&rls=org.mozilla:en-GB:official_s&sa=X&oi=spell&resnum=0&ct=result&cd=1&q=Humoral+Immune+response&spell=1\n\nGot a whole list!
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Cells of the immune system more specifically B cells produce antibodies with shapes similar to the receptors on the foreign cells. Therefore these antibodies fit into the receptor sites on the membrane of the foreign cell and causes its membrane to break down.
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The IgM will persist until the antigen is removed. The presence of IgM is usually taken to mean that the infection is still active. IgM usually appear 1-2 weeks after initial exposure, while IgG appear 3-4 weeks after initial exposure.\n\nThe exact numbers may vary a little, but this is what I remember.
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You are looking at a displacement reaction, in which the more reactive metal (Cu) is displacing the less reactive metal (Ag) from its salt solution (AgNO3).\nCu (s) + 2AgNO3 (aq) --> 2Ag (s) + Cu(NO3)2 (aq)\n\nHope this helps. :)
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For any molecule to perform its function it must recognize other molecules in the cell that it will react with them. the only way the reactants can meet is through binding to each other through their shapes. for example, if antibodies do not have their specific structures that can recognize specific antigens there will be no immune system and no disease will be treated. Another example is enzymes, the special 3-D structures create unique site called active sites that fit only the substrate of that enzyme, so any subtle change in the active site will make the enzyme nonfunctional and no reaction will be carried out.
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The venom of this species has been extensively studied. It contains specific phospholipases (enzymes capable of destroying cell membranes), and also a platelet inhibitor called applaggin (anticoagulant), as well as a specific lectin (these are glycoproteins that can agglutinate red blood cells).\nI'm sure there are other components, just use the links!\n\nSome publications (some are abstracts):\nhttp://www.pnas.org/cgi/reprint/86/20/8050\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3082870&dopt=Abstract\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10484740&dopt=Citation\n \nTry searching using Google Scholar :-)\nhttp://scholar.google.com
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antigen are the foerign organism to our body
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antibodies, white blood cells
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first you will need the blood sample, anti-A antibody and anti-B antibody. \nplace a drop of anti-A and anti-B antibody on separate slides.\nsmall amount of blood is taken from the patient's 4th finger. the blood sample is then mixed with the droplets of the antibodies.\nafter a few minutes, observe any signs of agglutination on the slides. if agglutination occurs on slide with anti-A antibody, the blood contains antigen A (blood type A). if agglutination occurs on slide with anti-B antibody, the blood contains antigen B (blood type B). if there's agglutination on both slides, the person has blood type AB. if there's no agglutination, the person has blood type O.