Ok everyone. Lets Talk About; Blood (DNA Next Thursday)
Some facts about blood: 1. A newborn baby has about one cup of blood in his body. 2. One pint of blood can save up to three lives. 3. Four main red blood cell types: A, B, AB and O. Each can be positive or negative for the Rh factor. AB is the universal recipient; O negative is the universal donor of red blood cells.
Here are some things that you do NOT want living in your blood: http://www.sciencephoto.com/image/262525/530wm/M2600205-Colour_SEM_of_Trypansoma_brucei_protozoa_in_blood-SPL.jpg (Electron micrograph) http://www.eoearth.org/images/182851/500x0/scale/TrypanosomaCDCDrMyron_GSchultz1315619092.jpg (Light microscope image of individuals of the same species) http://upload.wikimedia.org/wikipedia/commons/thumb/3/3c/Plasmodium.jpg/300px-Plasmodium.jpg (Light microscope image) Who knows what illnesses those two species cause?
I'm pretty sure 1. is African sleeping sickness .....
2. Chagas disease 3. Malaria
Trypanosoma brucei is indeed the parasite that causes sleeping sickness. It's a flagellate, but the flagellum doesn't wave freely like in most flagellates and instead forms an undulating membrane. Both of the first two photos show this species, with the light micrograph showing the flagellum a bit more clearly and the electron micrograph showing the general "body" shape. A different Trypanosoma parasite causes Chagas disease, but it looks more like this: http://upload.wikimedia.org/wikipedia/commons/0/0b/Trypanosoma_cruzi_crithidia.jpeg And you're right about the other one too. It shows Plasmodium parasites inside a blood cell, which is one of the locations where they asexually reproduce.
Interesting. Another thing for me to learn. Thanks for sharing it. :)
Hm, actually, I'm looking at other photos of Trypanosoma cruzi (the species that causes Chagas disease) and it does look VERY similar to Trypanosoma brucei (sleeping sickness) in a lot of micrographs. The photo that I linked to is allegedly Trypanosoma brucei (according to accompanying text), but I honestly don't know how to reliably tell them apart. I see on some websites a reference to the "long, thin" form of T. cruzi (this, I guess: http://upload.wikimedia.org/wikipedia/commons/0/0b/Trypanosoma_cruzi_crithidia.jpeg), but in other micrographs that also claim to show T. cruzi, it looks very much like what I see in standard images of T. brucei.
Now I'm reading that T. brucei ALSO has a "long, thin" form. But I guess they are closely-related, so it shouldn't be surprising that they look so similar.
Here's an article: The genus Trypanosoma contains a large number of parasitic species which infect wild and domesticated animals and humans in Africa. Commonly known as African sleeping sickness, human trypanosomiasis is caused by the species Trypanosoma brucei and is transmitted to humans through either a vector or the blood of ingested animals. The most common vector of Trypanosoma brucei is the tsetse fly, which may spread the parasite to humans and animals through bites. Through a process known as antigenic variation, some trypanosomes are able to evade the host's immune system by modifying their surface membrane, esentially multiplying with every surface change. As the disease progresses, Trypanosoma brucei gradually infiltrates the host's central nervous system. Symptoms include headache, weakness, and joint pain in the initial stages; anaemia, cardiovascular problems, and kidney disorders as the disease progresses; in its final stages, the disease may lead to extreme exhaustion and fatigue during the day, insomnia at night, coma, and ultimately death. Human trypanosomiasis affects as many as 66 million people in sub-Saharan Africa. Trypanosomes are also found in the Americas in the form of Trypanosoma cruzi, which causes American human trypanosomiasis, or Chagas' disease. This disease is found in humans in two forms: as an amastigote in the cells, and as a trymastigote in the blood. The vectors for Trypanosoma cruzi include members of the order Hemiptera, such as assassin flies, which ingest the amastigote or trymastigote and carry them to animals or humans. The parasites enter the human host through mucus membranes in the nose, eye, or mouth upon release from the insect vectors. Left untreated, Chagas' disease may cause dementia, megacolon, and megaesophagus, and damage to the heart muscle, and may result in death. Genome Structure Also: Do you know what illnesses this species causes?
@Miss_Deva Bone marrow disease. :)
Blood is sterile in a healthy person, but is a medium of choice for quite a few nasty pathogens. As nasty as the big ones mentioned above are the small ones, particularly Staphylococcus aureus. When the body can't mount a proper immune response or when the bacteria is not treated, these bacteria cause disease by being carried everywhere the blood goes and by changing the chemistry and constitution (both cellular and chemical) of the blood itself. One of the nastier effects of blood borne bacterial infection is on the heart and on the endocardium, or layer of cells lining the heart. It sprouts growths, often on the heart valves, in a condition called "infective vegetative endocarditis." The type of growth depends on what bacteria causes it (and often pathologists get an idea for what might have infected a person by seeing what sort of growths are in their heart) and are harmful to the person both because they decrease the heart's efficiency and because they are carried off and lodge in the lungs or systematic circulation, cutting off blood flow. That's the pathology stuff inspired by what others posted. ---- Often not appreciated either is how important the actual fluid pressure the blood exerts on the vessel walls is to the health (or lack of health) in a person. A lot of ink in textbooks is devoted to the types of cells and proteins in the blood so people tend not to consider fluid forces, but they are incredibly important. The endothelial cells which line blood vessels have cell surface proteins called integrins. These integrins are very small proteins - they consist of one short alpha helix and a small disordered region - but they are incredibly important. They anchor cells to its extracellular matrix. In the case of blood, where that matrix is a moving fluid, they are incredibly sensitive to the sheer forces of the fluid molecules sliding past them. Depending on the types of forces being exerted on them, they trigger signalling pathways inside the endothelial cells which mediate cellualr decisions (like division, migration, etc.) implicated in many clinically relevant processes. Some important examples are hypertensive vascular disease, aneurysm formation and metastatic cancer cells wiggling their way through the endothelium into the blood stream. That's what I intended to post before I thought about pathology.
here are some videos hope u guys enjoy it :) blood platelets story :) 1) http://www.youtube.com/watch?v=vEmsaXA-go0&feature=related 2) http://www.youtube.com/watch?v=JvOH5skxqoA&feature=endscreen&NR=1 3) http://www.youtube.com/watch?v=M_YpLaWdBpk&feature=fvwp&NR=1
Erythrocytes can only utilize Anaerobic respiration Erythrocytes lacks the Major histocompability complex recognized by certain immunecells. Hemoglobin has 4 different states depending on how many O2 are currently bound to it. Can't think of anything other that hasn't been mentioned at the moment.
Thanks for everyone and there great facts, Bravo :)
special thanks to u ;)
:D Thanks :D
A late (but interesting) addition, if you don't mind. There is a minute probability that the offspring of two type AB parents can end up being type O! This odd phenomena, known as the Bombay phenotype, is actually a simple case of recessive epistasis. The locus here codes for the relatively unknown H antigen. "The H antigen is produced by a specific fucosyltransferase. Depending upon a person's ABO blood type, the H antigen is converted into either the A antigen, B antigen, or both. If a person has blood group O, the H antigen remains unmodified. Therefore, the H antigen is present in the highest amounts in blood type O and in the least amounts in blood type AB." Only one copy of the H antigen is needed for the "regular" (A, B, O) blood phenotype to be displayed. If you have Hh, that's fine - however, if you have hh, then you'll lack all of your ABO antigens. What this means is parents who have Hh genotypes can have a child that appears to have a type O phenotype (even though he/she may have inherited A or B genes), if the child inherits double recessive h alleles. No production of H antigens = no modification of them = no presence of ABO antigens. Technically speaking, what the child actually has is the "Oh" phenotype - slightly different from just an O phenotype. He/she also can't receive blood even from type O donors. Type O does not indicate a complete lack of antigens - as mentioned before, type O donors do have significant amounts of the H antigen. The h/h genotype recipient however produces anti-H antibodies, making a transfusion dangerous. For a more in-depth and better explanation, see this: http://www.ncbi.nlm.nih.gov/books/NBK2268/
Thanks to all the posters, closing the question and next one is going up
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