Blue light is important for night vision, so either of those options would lead to less of an ability to see well after sunset.

No, glia support neurons; they do things like redirecting blood flow to more-active-than-usual neurons, mylenate axons, etc. They wouldn’t form a mesh around neurons’ photoreceptors the same way they do neurons’ somas and axons. What the article describes is that glia actually are critical at allowing for color vision during the day and night vision at night, since on land we’d get too much blue light to see color with much fidelity were it not for glia, and a similar filtration process helps us see at night. It’s not that it’s not as bad as it could be, it’s actually that vision is better this way (barring one small blind spot outside of our fovea–which, being outside of the fovea, would have low acuity anyways).

This arrangement actually optimizes color vision in the daytime and night vision at night. Evolution selected for the correct arrangement for those of us living on land:

https://theconversation.com/look-your-eyes-are-wired-backwards-heres-why-38319

What if we 👉@👈 …? 🤭

My merit review this year specifically noted my high volume of peer review for why I exceeded expectations in the 20% service part of my contract. Again I say, faculty are remunerated for peer review. It’s better to do peer review for the service part of my contract than it is to sit on faculty senate. Doing peer review helps my research. It’s a win-win, unless I don’t want to get my full merit raise because i ignored service.

Faculty are paid for doing peer review just like we’re paid for publishing. We’re not paid directly for each of either, but both publishing (research) and peer review (service to the field) are stipulated within our contracts. Arxiv is also free to upload to and isn’t a journal with publication fees.

Methods sections are limited in word count, and if a lab is hoping to get a few more papers out of a paradigm, they may be intentionally terse. There’s a big difference between how we write protocols in-house and how we write limited-length methods sections.

While we’re on a thread about English grammar, “who’s” means “who is.” The possessive of “who” is “whose.”

Sorry.

ONLYOFFICE (sorry about the caps, poor name choice IMO) has even better docx compatibility, and its source code is open

I use Linux. I’m a researcher, not IT. Many of my colleagues use Linux.

When have we been talking about anyone’s diagnosis? We’ve been talking about the common misperception that depressive episodes caused by environmental triggers are not a result of treatable neurochemical dysfunction. MDD can certainly be a result of environmental triggers, and there are a wide variety of neurochemical bases of it. I distinctly said in my first comment that I was referencing a small part of your reply. I’m not trying to have a needless fight, I’m trying to correct a common public misperception that you reiterated. I do that whenever I see a misunderstanding of science; I care about public science education, especially on topics important enough as psychiatric conditions that are often fatal without treatment. If you feel like this is a pointless fight, sorry. I only commented because I understood your comment to mean something that, no matter my read of your wording, you clearly say you weren’t meaning.

MDD is a real disability. It can and often is precipitated by environmental triggers, and episodes can resolve once the environment is changed. Just because someone experiences remission in such a case doesn’t mean they don’t have a disorder that should be treated prior to another episode. Dichotomizing chemical and psychological/environmental is harmful.

My point is that such a lay interpretation isn’t helpful, and it may be harmful. Plenty of people with MDD have an environmental trigger prior to their first episode, and have their episode remit after that precipitating factor is managed. Convincing someone that their experience isn’t chemical suggests against treatment seeking during remission, such as seeking therapy, which could help prevent another episode (and one that may not have an environmental trigger). A depressive episode can be fatal. Telling someone that because their prior episode remitted spontaneously or after the environmental trigger changed might prevent them from getting the proactive and preventative treatment that they need to keep them from experiencing another episode and thus keep them alive. Don’t gatekeep depression.

And how do you think addressing stressors works? Some non-chemical means?

That first bit is totally untrue. Do you think our grief is not chemical? That we can’t have neural rewiring occur following the loss of a loved one? Don’t dichotomize experience and neurochemistry. They’re two sides of the same coin.

Trogdor was popular way before Reddit

It doesn’t have to be

https://www.mathworks.com/products/compiler.html

MATLAB can ruin all sorts of coding experiences, programming included

(⌐■ ͜ʖ■)

You’re normal in that respect:

https://onlinelibrary.wiley.com/doi/abs/10.1002/aur.1962

In fact, the idea that autistic individuals are immune to propaganda is, itself, media propaganda. The study that those articles report on was a single study that found that autistic individuals show less of a framing effect on their own preferences. It’s much more easily explained by autistic individuals having strong, internal preferences for their own likes/dislikes than it is by autistic individuals being immune to propaganda.

Speaking from experience here, too.

I go out of my way not to do so. Whenever I search for some specific items and see “Sponsored,” I’ll scroll down until I get the same listing without the ad link.