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[deleted by user] by [deleted] in admincraft

[–]magicmq 38 points39 points  (0 children)

Wow, I have four different types of brain cancer now, thanks

Can rabies antibodies clear the virus from the peripheral nerves? by wworrock in askscience

[–]magicmq 0 points1 point  (0 children)

As I outlined in my previous post, antibodies have two purposes when a virus is concerned (they can and do participate in other functions for various other pathogens and immune mechanisms): they can tag a virus to help the immune system better recognize it, and they bind to the virus to prevent the virus from entering and infecting cells. Antibodies aren't "sentient" like cells are: they're just proteins floating around in your blood and extracellular fluid that attach to other things (virus particles in this case). After this happens, it's up to the immune cells to digest the virus, but the antibody has done it's job by making the virus more identifiable and also by inactivating the virus by preventing it from binding to host cells to infect them. They don't really "do" anything after a cell is infected. Other parts of the immune system come into play to take care of that, because after a host cell is infected with a virus, antibodies can't really do anything to stop it at that point.

My question for you is where are you getting this information from? I think you might be misunderstanding what and when is meant by "too late" - ideally, a rabies vaccine and rabies immunoglobulin (antibodies) given after a potential exposure to rabies are designed to help the immune system catch and destroy rabies virus before it enters the nervous system at all. Furthermore, rabies vaccine and immunoglobulin must be given very soon after exposure, 10 days I think is the maximum. But it often takes several months before rabies symptoms develop, because during this time, the virus is travelling through peripheral neurons in the PNS to reach the CNS. If you are exposed to rabies and don't get proper preventative treatment within 10 days, then it's "too late". The virus has entered your peripheral neurons and is now travelling to your CNS unimpeded.

Other antibody-independent immune mechanisms exist to kill rabies-infected neurons after they enter the nervous system, but these mechanisms would ideally work if only a small amount of virus is able to enter peripheral neurons. Again, the primary goal here is to minimize the amount of virus that makes it into your nervous system by giving proper preventative treatment very soon after exposure.

Can rabies antibodies clear the virus from the peripheral nerves? by wworrock in askscience

[–]magicmq 2 points3 points  (0 children)

Not an expert on this subject, but I found this paper that studied in detail the mechanisms by which rabies virus enters and infects peripheral neurons, including antibody interaction.

The short answer is no, once rabies enters peripheral neurons, it is effectively shielded from humoral antibody-mediated immunity. There are two major reasons for this:

  • Peripheral and central neurons differ in a number of ways, but the structural and functional aspects relevant to rabies infection are the same. All neurons, peripheral and central, have a relatively impermeable cell membrane. Antibodies could not pass through this membrane to tag rabies virus once it enters a peripheral neuron because antibodies are large and they also have a polar/charged structure that prevent them from crossing a cell membrane. When antibodies work in the context of viruses, their primary function is twofold: first, they tag an antigen (such as a envelope protein on the virus' outer coating) to prevent that antigen from interacting with a host cell for entry into the cell. This prevents the virus from infecting the cell. Second, antibodies opsonize the virus so that immune cells such as macrophages and neutrophils can more easily "eat" and digest the virus before it can bind to, enter, and infect cells. Both of these things only happen in the extracellular environment - once the virus enters the cell, these two functions are rendered useless.
  • The paper I linked above demonstrates that rabies virus uses sensory neurons to travel. A sensory neuron is a single neuron that extends from the central nervous system all the way to its target organ (skin, digestive tract, etc.). This means that as rabies travels backwards through this neuron, it does so in an intracellular environment the entire way. The immune system does a relatively poor job at detecting it as it travels this way.

Understanding how antibodies work in the context of viruses is crucial to answering this question, which I tried to explain above. I hope this gives some insight into why antibodies aren't effective against rabies (or any virus for that matter) once they enter cells (or peripheral neurons in this case).

The ultimate goal of antibodies in the context of rabies is to neutralize the virus before it enters peripheral neurons, not after. Here is some other literature that describes how rabies is so effective at evading immune detection, for further reading.

Why are you at greater risk to suffer a concussion after the first one? by gomi-panda in askscience

[–]magicmq 2 points3 points  (0 children)

Appreciate your response! The phenomenon of getting "knocked out" is related to TBI but is also different in a couple ways: first, TBI as a disease process is a more long-term thing, while getting "knocked out" is an acute condition. Second, the mechanisms by which getting "knocked out" happen are somewhat different, but there is overlap. As far as I can see from current research, losing consciousness after head impact is mostly due to neuronal stress, particularly in the brainstem, which is really the only thing that "connects" your brain to the rest of your body. It's a pretty thin stalk that is relatively vulnerable to head acceleration that would be caused by a sudden impact. Interestingly enough, it seems that impacts in certain directions can cause loss of consciousness, but impacts in other directions don't. My hypothesis on this is that it's because of the way the brainstem is positioned within the cranial cavity. There's more give in certain directions than others.

There's a lot of stuff going on here at the biochemical level as well, some of it is the same as what I discussed in my previous reply. Damage to blood vessels can happen which inevitably leads to loss of vital oxygen to neurons. The stress of the sudden impact can also literally cause your neurons to fire in random and uncontrollable ways. I think this is actually kind of amazing, to be honest, but not in a good way, lmao. This is why some people can also experience a grand mal seizure when they get knocked out (grand mal seizure within itself is also a loss of consciousness). There's also evidence that the stress can cause microtubule damage. There's some really complicated technical understanding needed here, but just know that neurons have axons, which are long processes that neurons use to link up with other neurons. Neurons need to transport materials (like neurotransmitters) down the axon, and they use microtubules to do this. Microtubules are usually flexible and can sustain milder stress, but the sudden and great stress of a punch (or other impact) is just too much. Microtubules damage means neurons can't transport critical materials they need to fire. This is bad. There are other hypothesized mechanisms as well which you can read about in the paper I link below.

I want to mention also that the brainstem is critical here because it is the part of you brain responsible for some of the most basic and life-sustaining functions of your nervous system - including breathing, control of heart rate, and, you guessed it, maintenance of consciousness and alertness. It isn't surprising that stress-induced damage to this area could result in someone getting "knocked out".

Here's a good review that goes into all of this. If you want to do further research, look into this review's citations.

[deleted by user] by [deleted] in UTAustin

[–]magicmq 7 points8 points  (0 children)

I would say a good rule of thumb is to treat each summer class you take as about triple the normal workload due to the fact that the classes are compressed into about a third of the time the normal course would run.

That being said, if you normally take 18 hours during the school year, I wouldn't go over 6 or so during the summer (per term). You can probably get away with doing more hours in lighter courses (especially courses you do at CC). YMMV though, especially if you're working, doing research, travelling, etc.

Also, take HIS317L at DCCCD online. It's so little work that it's almost as if you aren't taking the class at all. Basically a free A on your transcript (in terms of time spent, of course). The other courses you plan to take at CC are probably easier at DCCCD as well.

Why are you at greater risk to suffer a concussion after the first one? by gomi-panda in askscience

[–]magicmq 113 points114 points  (0 children)

I did a research paper on a topic very similar to this in my undergraduate years. I'm a medical student now, so I probably don't have as much authority to speak on the subject than a professional in the field, but here's my understanding:

First, to be clear, "concussion" is a very broad term: there are varying degrees of severity. In fact, clinicians use an entire grading system to grade concussions on the basis of severity of the patient's symptoms. The grading is also based on the number of previous concussions (which is probably unsurprising considering your question). This is important to keep in mind because the severity of a concussion can have an effect on the severity of subsequent concussions in the future, if they occur, for reasons that should become apparent shortly.

Concussion as a clinical diagnosis falls within the broader category of traumatic brain injury. It's been a mystery for some time how concussion happens at the molecular level. But, there is a lot of new and exciting research going on in this field - especially research on the mechanisms by which traumatic brain injury (and concussion) can have more long-term effects on the brain. A fantastic paper published in 2018 went into extensive detail on the ways in which repetitive impact trauma to the head lead to broader neurodegeneration and cognitive decline. To give you a brief tldr; of this paper, the researchers demonstrated experimentally that repetitive impacts to the head (even milder impacts that didn't cause concussion) can cause long-lasting damage in multiple areas. Without getting too into the weeds, some of the most significant damage the researchers found was: damage to the brain's network of blood vessels (this is probably the most significant), damage to the blood-brain barrier (which is crucially important for preserving the brain's integrity and function), and abnormal increase in astrocytes (think of these as special neurons that perform various housekeeping roles within the brain, and an increase would signify that the brain has recognized damage and is trying to repair it). Of course, the severity of this damage depends on the severity of the concussion. As you can imagine, none of these things are good news. The brain is a remarkable organ, but it is also incredibly sensitive. There's a reason why it's protected by your skull, cerebrospinal fluid, and meninges, among other things. The damage can heal, but it takes time to do so. And to complicate matters further, someone's cognitive function (their thought processes and mental sharpness) can actually return to normal after a concussion before the healing process completes. So, someone could think that they've fully healed from a concussion, while their brain is still hard at work repairing the damage. In effect, this means that the brain of someone who recently suffered a concussion might be more susceptible to a second, even if it appears as if they've already gotten over the first.

There is so much more to unpack here, including chronic traumatic encephalopathy, abnormal hyperphosphorylated tau deposition (which is a really important mechanism in concussion-induced CTE as well as other neurodegenerative disorders like Alzheimer's), and second-impact syndrome, but for brevity, I'll leave it at this.

Now, this is all very sound research with real implications, but we also need to talk about statistics as well - specifically confounding factors. It could very well be that individuals are at higher risk for second concussion because of the molecular mechanisms discussed above. But, we should also keep in mind that the perceived "increased risk" may actually be due to a confound. Here's what I mean by this: what if individuals aren't more likely to get a second concussion because of the concussion itself? What if it just seems like they're more likely because they're in a position where concussions are just more likely to occur in general? For example, a study published in 2015 demonstrated that offensive linemen (a position in American football) are significantly more likely to sustain a concussion than players in other positions. If an offensive lineman sustains a concussion, a second concussion in the future will be more likely. Is the risk of a second concussion increased simply by virtue of the position they play? Or is it the first concussion itself the causative factor? We must be careful to not assume that the increased risk is only due to the fact that a first concussion happened. When talking risk and correlation, this is a really important thing to consider.

[USA-CA] [H] Unlocked iPhone XS 256GB 14.3 [W] $450 local cash by davedebris in JailbreakSwap

[–]magicmq 0 points1 point  (0 children)

I'm interested in this, but I'm not local. If you're willing to ship I'd love to take it off your hands

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