Wait, what about people whose brain hemispheres that have been split reporting one "side" not being able to observe what the other side does? Or are those reports misreported/misinterpreted somehow?

Thanks for the correction. I am unaware of anything more specific but that sounds plausible.

I would also add that it is by no means essential to consume milk for its nutrient value.

I was just pointing out that primarily lactose intolerant people cannot breakdown lactose and therefore cannot absorb it in any meaningful way as far as i am concerned. Since the question was about nutrients in general.

You seem to know more than me about this. I imagine the reduction in nutrient absorption is not that large?

Despite what everyone is going to say, this has nothing to do with antigenic drift in flu (i.e. accumulated mutations in circulating viruses) and certainly nothing to do with antigenic shift (genome segment rearrangement).

While antigenic drift is a concern and shift is a much rarer concern, the fact is that influenza vaccine immunity wanes extremely fast regardless of shift or drift. This is very well known and there are literally hundreds of publications about it; you can start with Waning of Measured Influenza Vaccine Effectiveness Over Time or Waning Vaccine Effectiveness Against Influenza-Associated Hospitalizations Among Adults, 2015-2016 to 2018-2019, United States Hospitalized Adult Influenza Vaccine Effectiveness Network or many others.

This waning with the influenza vaccine is generally much worse than most vaccines and in particular it’s much worse than tetanus vaccine. The sad truth, though, is we don’t know why immunity wanes so fast. Part of it is that the conventional inactivated influenza vaccine, which has no adjuvant, is poorly immunogenic - but that’s kind of going in circles because “poorly immunogenic” means its immunity wanes rapidly.

Even many more modern influenza vaccines, made through different approaches, are weakly immunogenic and have rapid waning of immunity. So maybe there’s something specific about influenza, that means it has adapted to be poorly immunogenic in people. If so, we don’t have a clear idea what it is.

Including adjuvants with the vaccine does help, and that’s used in the elderly.

But in a sense, it’s not a critical problem now because even if immunity didn’t wane, we’d still need to give nearly annual vaccines because of the antigenic drift problem. It’s annoying, it does mean that people vaccinated in fall are already less well protected by spring, but by summer flu has mostly gone away and mostly you need a new vaccination by fall again anyway.

If and when new vaccines against flu are introduced, with broader reactivity, that don’t need to be modified every year - then this will need to be solved too. But they’re not out yet.

Reading up on how quadriplegics cope with a lack of body movement while still eating whole foods is quite interesting.

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I've heard the retina described as an extension of the brain.

It is amazing to think the foundations of those processing pathways can develop from genes.

Some bacterial infections don't necessarily require an adaptive immunity response. Our innate immunity cells have receptors that recognize common pathogens. We even have a system that is just an elegant sequence of proteins being modified to create a pore in bacteria. This is just kicked off by sugars on the outside of the bacteria cell wall (although one such pathway is initiated by antibodies). In fact, certain organs are "immune privileged" and (mostly) do not allow T cells and B cells to infiltrate. But in all cases the invaders are destroyed by the immune system and the debris will find its way (whether or not it goes to the spleen first) to the liver or kidneys and get excreted like any other waste.

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Thank you for a much better answer than mine!!

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I don't know about Dying Light but most instances of zombie fiction where the zombie disease is caused by a variant of rabies, it's usually taken to be a novel strain of rabies that DOES cause excessively aggressive behaviour in it's hosts. It would seem kinda silly to just say "it's rabies" because we have rabies in the real world and we don't (yet) have a zombie apocalypse.

Thank you for sharing this.

Where did inflammation come from?

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However, if someone is lactose intolerant they might not be able to absorb as much of those nutrients due to inflammation.

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Additionally, tetanus vaccine is inactivated toxin which targets a very specific binding site. It's easier to block that toxin from binding than an entire virus, which can target an array of cell types and binding sites.

Hm... There's not a detailed answer here yet, so I guess I'll jump in.

First thing to realize: in reach retina, there's over 100 million photoreceptors, but only 1 million axons in the optic nerve. How's that work? The answer, is that it's completely accurate to say that the earliest part of visual processing is in the eye. There's 5 layers to the retina. The million ganglion cells sending the optic nerve to central command, a middle 'processing' layer with three main types of interneurons, and the actual photoreceptor cell layer (the other two layers are 'in between' layers made up of the cabling connecting these three cell body layers).

There's actually about 20 different kinds of ganglion cells, so you can look at it as there being 20 different image filters sent in to central. Some with blue/yellow contrast, others for pure luminance contrast, etc. Some of these 'views' have very tiny 'receptive fields' (the part of the retina their signal contains information for). So-called 'P' ganglions for example can have one single cone that causes them to depolarize and fire, though they all have surrounding parts/colors that inhibits firing. Each ganglion cell actually has a fairly complex 'optimal' pattern that makes them fire... Usually either 'light in the center, dark on the edges', the reverse of that, or a color version (blue light but no yellow light, for example). So even by the time the signal's leaving the eye, you're already getting various size views containing different kinds of contrast information. It should be said too, the closer to the fovea (center of the view) the smaller the receptive field gets, so the more detail you can perceive... So the 'resolution' of your view is actually not consistent even just across the eye.

Anyway. So: the optic nerve. These million axons aren't sending pixel information, they're sending 20 pictures, each with larger or smaller receptive fields depending on type and distance from the fovea, and different activation patterns they're 'looking for' to fire. This tract splits off on the way to the central switchboard (the LGN in the thalamus). For the left hemisphere of the LGN (say), you get the right eye's ear half of the view, and the left eye's nose half of the view. Opposite that for the right hemisphere.

So, the left hemisphere switchboard gets input from the right half of the visual field. But these two views don't perfectly line up... Maybe 80% of that view does, but the most peripheral part of the view only gets a signal from the outside edge, not the nose-side edge, so your peripheral vision doesn't have a binocular signal to put together in the first place.

Input from different eyes is totally separate still in this central switchboard. Each hemisphere's LGN has 6 main layers, 3 from each eye, with thin middle layers in between carrying the comparatively small amount of color information (koniocellular layers), also still separated by eye.

Among other places (pupil and eye muscle autonomic circuits in particular) this tract then gets sent to the primary visual cortex in V1, at the very back of your head. Here, it's still separated by eye. You've got these stripes running from the back to the front, with alternating left eye, right eye input. Perpendicular to that, you've got simple edge detectors going through different orientations, and mixed into all that, you've got these barrel shaped blobs of cells that respond to color information. You can see a picture of what I mean here. One 'cycle' of left eye/right eye, and 180 degrees of orientation preference for edges marks out a roughly 1mm x 1mm 'hypercolumn', that takes in input from a chunk of the retina. These hypercolumn are the basic processing unit here in V1, and they tile over the visual field. The receptive field here is larger than a single cone or rod certainly, but it's still fairly small. You can see that the same parts of the visual field are at least nearby now though, that's what those stripes are... Lined up regions from the same part of the visual field from different eyes.

Once it gets to V2, the next layer of processing, this is where you start to have 'binocular integration', neurons that selectively fire based on visual input from both eyes.

As you climb up in levels, you'll see larger and larger receptive fields. By the time you get deep into the ventral visual stream (very loosely speaking, ventral stream is identifying things you're seeing, dorsal stream is for helping to guide hands and stuff for grabbing things and so on) you're seeing cells that selectively fire given complex input from anywhere in the visual field. A 'Jennifer Aniston' neuron for example that might fire anytime you're seeing her face... Or her name written, or a drawing of her, or so on, from anywhere in the visual field.

But anyway. You get the gist. The full complex view of even the early visual system is hilariously intricate, and there's no really simple description that captures all the detail. But maybe a partway answer that's close enough... Peripheral vision has no binocular component, since only one eye captures that outside edge. For the bulk of your visual field though, yes... Things get tied together eventually, but it's not until V2... After many layers of processing in the retina, LGN, and V1. By then, you're talking about receptive fields with hundreds of input photoreceptors, and you're already talking about integrating signals for fairly high level information... Direction of movement, edge orientations, color information and so on, all in separate parallel feeds, to be integrated into even more high level, abstract tracts of information with even larger receptive fields as you continue climbing up towards the dorsal (hand eye coordination) and ventral (object recognition) tracts.

Note too: every step here is more tightly interconnected than I'm describing. In particular, there's 10x connections coming BACKWARDS from downstream than there are coming in from upstream towards the retina, so you probably do have some binocular signal affecting neuron firing even before you get to the binocular integration part in V2. Those incredibly numerous backpropagating connections aren't well understood, but it does definitely complicate the question of where you can start pointing to neurons influenced by input from both eyes in the same part of the visual field.

So anyway... There you go, haha. This is largely cobbled together from Kandel's 'principles of Neuroscience, 6th edition', there's a half dozen chapters in the low 20's going through how the brain processes visual information in pretty heavy detail.

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