Some things to note: - This is NOT a professional video! It's my Grade 12 Biology assignment. Heck the only reason it's up on YouTube is because I couldn't get the computer there to play the video file. - The music used is actually "Comptine d'un autre été" by Yann Tiersen, from the movie 'Amelie'. - I do NOT own rights to any of the clips, images or music in this video. - There is no actual part 2 to this. It was just made to look like one of those typical information videos teachers show their students. The spinal cord (aka part 2) was covered by another student in powerpoint. - I've been getting a lot of comments about this (funny when I wasn't expecting any): once and for all, I'm sorry about my voice. I'm not exactly my favourite speaker, and combined with my fatigue at the time and the hurriedness to get this thing out of the way, the sound of my voice obviously isn't exactly on par with Morgan Freeman...and, unfortunately, he was busy at the time. I prefer editing and behind-the-scenes work over speaking. So, please, forgive me for that.
http://www.nucleusinc.com/medical-animation This 3D medical animation shows how antibodies stop harmful pathogens from attaching themselves to healthy cells in the blood stream. The animation begins by showing normal red and white blood cells flowing through the blood stream. Next, a single pathogen appears onscreen slowly moving toward its destination on the surface of a cell. The tubular extensions on the pathogen are surface proteins which attach to corresponding surface proteins on a white blood cell, or leukocyte. As the animation continues, more pathogens continue to attach to the white blood cell, rendering it ineffective.
During the immune system response, Y-shaped antibodies begin attacking the pathogen, binding to its surface proteins as the pathogen attempts to anchor to the blood cell. The antibodies completely block the pathogen from attaching to the blood cell, "tagging" the pathogen so that one of the immune system's leaner cells, a macrophage, appears onscreen to engulf and digest the pathogen.
Nucleus Medical Art is a leading creator and licensor of medical illustrations, 3D medical animations and interactive multimedia for medical devices, pharmaceutical companies, education, biotechnology, advertising agencies, lawyers, and more. online at http://www.nucleusinc.com/youtube.
Permission to use ADEAR materials is not required. When you use our materials in print, on the Web, or in a video or audio format, we simply request that you credit the "Alzheimer's Disease Education and Referral Center, a service of the National Institute on Aging."
The human brain is a remarkable organ. Complex chemical and electrical processes take place within our brains that let us speak, move, see, remember, feel emotions and make decisions. Inside a normal healthy brain, billions of cells called neurons constantly communicate with one another.They receive messages from each other as electrical charges travel down the axon to the end of the neuron. The electrical charges release chemical messengers called neurotransmitters. The transmitters move across microscopic gaps, or synapses, between neurons. They bind to receptor sites on the dendrites of the next neuron.This cellular circuitry enables communication within the brain. Healthy neurotransmission is important for the brain to function well. Alzheimer's disease disrupts this intricate interplay. By compromising the ability of neurons to communicate with one another, the disease over time destroys memory and thinking skills. Scientific research has revealed some of the brain changes that take place in Alzheimer's disease. Abnormal structures called beta amyloid plaques and neurofibrillary tangles are classic biological hallmarks of the disease. Plaques form when specific proteins in the neuron's cell membrane are processed differently. Normally, an enzyme called Alpha-secretase snips amyloid precursor protein, or APP, releasing a fragment. A second enzyme, Gamma-secretase, also snips APP in another place. These released fragments are thought to benefit neurons. In Alzheimer's disease, the first cut is made most often by another enzyme, Beta-secretase. That, combined with the cut made by Gamma-secretase, results in the release of short fragments of APP called Beta-Amyloid. When these fragments clump together, they become toxic and interfere with the function of neurons. As more fragments are added, these oligomers increase in size and become insoluable, eventually forming Beta-Amyloid plaques. Neurofibrillary tangles are made when a protein called tau is modified. In normal brain cells, tau stabilizes structures critical to the cell's internal transport system. Nutrients and other cellular cargo are carried up and down the structures called microtubules to all parts of the neuron. In Alzheimer's disease, abnormal tau separates from the microtubules, causing them to fall apart. Strands of this tau combine to form tangles inside the neuron, disabling the transport system and destroying the cell. Neurons in certain brain regions disconnect from each other and eventually die, causing memory loss. As these processes continue, the brain shrinks and loses function. We now know a great deal about changes that take place in the brain with Alzheimer's disease, but there is still much to learn. What other changes are taking place in the aging brain and its cells and what influence do other diseases, genetics, and lifestyle factors have on the risk of developing Alzheimer's disease as the brain and body age? Scientific research is helping to unravel the mystery of Alzheimer's and related brain disorders As we learn more, researchers move ever closer to discovering ways to treat and ulimately prevent this devestating, fatal disease