See this video for an excellent explanation of superantigens and the sequence of events they induce. A prototypical example of a superantigen is toxic shock syndrome toxin (TSST) released by S. aureus.
In a nutshell:
1) Superantigen binds periphery of T-cell and MHC molecule receptors
2) Non-selective T-cell activation with release of IFN-gamma
3) Macrophage activation and release of IL-1, IL-6 and TNF-alpha
4) Non-specific inflammatory response
I’m definitely someone who struggles keeping stuff organized when things sound the same, so I was always getting these mixed up. Here is a helpful cartoon courtesy of Jorge Muniz on www.medcomic.com to help keep things straight. The website actually has a lot of great cartoons that can really help you learn in a fun way. Enjoy!
Can you answer the NEJM image challenge? Click here to vote and see the answer.
A great video that everyone should watch. People are made in all shapes and sizes! Obviously healthcare professionals should encourage a healthy lifestyle, I think many people fail to realize that a healthy lifestyle does not mean a runway model body.
Be fit. Be healthy. Be proud of who you are.
95,000 Child Study Proves That Measles Vaccine Doesn’t Cause Autism But The True Believers Won’t Be Satisfied
While I would have thought the overwhelming science on this issue would have put it to rest by now, it’s still controversial among some groups to say that the measles vaccine doesn’t cause autism but does protect children from measles. I know, it’s a shocking idea! Well, the Journal of the American Medical Association wants to put this to rest for good and they’ve conducted an enormous study using 95,000 children as subjects in order to check the “good science” box once and for all. Here’s the takeaway:
Conclusions and Relevance In this large sample of privately insured children with older siblings, receipt of the MMR vaccine was not associated with increased risk of ASD, regardless of whether older siblings had ASD. These findings indicate no harmful association between MMR vaccine receipt and ASD even among children already at higher…
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I’d like to apologize to all my followers for being absent lately. I’ve been finishing up semester courses, had a conference last weekend, present research next week and am trying to fit studying for Step 1 in there as well. Needless to say, it’s been pretty chaotic!
However, I will try to post more often and get some more podcast episodes up now that the semester is coming to a close, so stay tuned!
I remember when I used to get all the different parts of the sarcomere mixed up, but with a few simple tricks you can remember it easy and long-term.
First, understand the the I band is isotropic and the A band is anisotropic. Although these terms technically refer to the behavior of polarized light passing through, I like to think of isotropic = moving and anisotropic = non-moving (remember that “an-“ means “without”).
So how do you remember which is the thick filament and which is the thin filament? Just remember that the heavier something is, the less likely it’ll move! In other words, think of the thick filaments as too heavy to move which means they’re the A bands because “an-“ (or “a” if that’s easier for you) means “without”. By default, the thin filament will be the I band. Additionally, the letter “I” is thinner than the letter “A” so it’s gotta be the “thin” filament right?
Now Z lines are you endpoints which should be easy to remember, because the letter “Z” is at the end of the alphabet. This actually ties into the next point too.
The points that “move” during muscle contraction are the H band and I band which spell “HI”. In other words, the “HI” bands bring the ends of the sarcomere (Z lines) closer together so they can say “Hi”!
Obviously this doesn’t cover everything you should know about the sarcomere and muscle contraction, but hopefully it helps get you started if you were having trouble!
Background: Paroxysmal nocturnal hemoglobinuria is a rare, chronic condition in which patients experience breakdown of red blood cells (RBCs) which releases hemoglobin into the blood. This hemoglobin is then filtered into the kidneys and causes the patient to have dark-colored urine. Although patients can experience hemoglobinuria after a full nights sleep, this isn’t always the case, so the name is somewhat of a misnomer. The idea behind this process occurring mainly at night is that people have altered breathing patterns when sleeping which causes the blood to become more acidic. The acidic environment activates the complement system which goes on to cause hemolysis of RBCs. However, more recent studies have shown that hemolysis actually occurs anytime throughout the day and the urine just becomes more concentrated at night. Thus, it often appears darkest in the morning because of it being in a concentrated state.
Pathogenesis: I actually really like the image shown below for a visual explanation of the condition. Basically, patients with PNH lack the glycosyl-phosphotidylinositol (GPI) protein that functions as an anchor for CD55 (decay-accelerating factor or DAF) and CD59 (membrane inhibitor of reactive lysis or MIRL). This is due to an X-linked mutation on the PIGA gene. As a result, cells can’t “hold on” to the CD55 and CD59 proteins. Think of CD55 and CD59 as identification tags for the cells; without them, the cells can’t prove they belong! The complement system comes along and sees someone without proper identification, so it decides to do something about it. Thus, it attacks the “foreign” red blood cells which results in hemolysis and the release of hemoglobin. At first, a molecule called haptoglobin can go around and “sweep up” the hemoglobin. It’s like a specialized janitor for hemoglobin. Over time the janitors are all busy so the hemoglobin starts to accumulate in the blood and gets filtered into the urine for excretion.
Treatment: Also shown in the diagram, you can see that eculizumab blocks C5 which prevents formation of the membrane attack complex (MAC). As a result, there is decreased hemolysis of the RBCs. However, opsonization by C3b can still occur so that macrophages will eventually take care of business.
Additional Information: Hemolytic episodes can also be precipitated by drugs, trauma, infection etc. The most common cause of death in these patients is venous thrombosis. However, the thrombophilia present with PNH is not fully understood. Plasma hemoglobin can consume nitric oxide (NO) which is important for inhibiting platelet aggregation. Thus, one hypothesis is that the the reduction in NO causes increased clot formation. Patients are also at an increased risk of developing aplastic anemia.
Check out the latestMedical Minded Podcast episode, Gram Staining: Gram-Negative vs Gram-Positive Bacteria which covers what gram staining is, how it works and how it is used to differentiate gram-negative and gram-positive bacteria. This is a must know for anything who is a med student, premed or even just taking a biology course. I know this episode may be basic for some people, but it’s essential information and it’s always good to work on the fundamentals!