For those interested in more, I found this People Make Games video to be super interesting. https://youtu.be/lYaDXZ2MI-k?si=pxrioKZq_S7ka9il

For me and mine, it’s carrots. Do you know how difficult it is to find carrot-free items? Impossible.

Agreed, seems like a no-brainer. Typically this stuff is handled at an institutional level, with bad professors losing/ failing to achieve tenure. But some results have much bigger implications than just “Uh oh, I cited that paper and it was a bad one.” Often, entire clinical pipelines are developed off of bad research, which wastes millions of dollars.

See also, the recent scandals in Alzheimer’s research. https://www.science.org/content/article/potential-fabrication-research-images-threatens-key-theory-alzheimers-disease

In grad school I worked with MRI data (hence the username). I had to upload ~500GB to our supercomputing cluster. Somewhere around 100,000 MRI images, and wrote 20 or so different machine learning algorithms to process them. All said and done, I ended up with about 2.5TB on the supercomputer. About 500MB ended up being useful and made it into my thesis.

Don’t stay in school, kids.

Nah. Fenced epee for a bit in a college club. Height advantage was pretty great. I guess it just depends on the weapon.

Can’t say I’ve heard anything since launch, so take my advice with a grain of salt.

Grim Dawn Item Assistant is your best friend. While you’re at it, Rainbow Item Names (or whatever it’s called).

Well if you liked PoE I doubt you’ll like D4. It’s a much simpler game. Sadly my only advice is to try GD and Last Epoch again. I’ve got hundreds of hours in the former and I just got 10 hours into the latter.

Last Epoch feels like a more approachable PoE. I thoroughly enjoy how the skills interplay with one another, but I still prefer the itemization in Grim Dawn.

The only reason I’m not playing GD currently is because I have too many QoL mods installed so my cloud saving doesn’t work, but I can cloud save for Last Epoch for my steam deck lmao.

I’m not sure I agree here - I think the resin printer might not be a good entry point, but I’m curious to hear what others think. I’ve heard resin printers require special ventilation and the photo-resin is carcinogenic. Once dialed in, an FDM can do pretty great for detailed parts. Especially with a smaller nozzle. So I’m not convinced jumping straight into a resin printer is wise.

I used my Ender 3 for a few years making miniatures, and they came out pretty great. Of course, then I tried switching to a larger nozzle and I still haven’t managed to get it running… but that’s my fault.

My job is 8:30 - 5 with a 30 minute lunch break. So almost.

But, we also get 2 days/week at home, and can flex time as required. Tons of international work, so the flexible hours are a godsend when time zones are against us.

It’s a salaried position and depending on your supervisor and stage of your career, you’re expected to work 40-45 hours a week. Deadlines and ugly projects tend to increase hours work. I’m very lucky, as my industry can be pretty brutal with sudden ends to projects and unexpected layoffs.

https://youtu.be/ainyK6fXku0?si=hTSP3-5T3oH8JOjt

We’ve got some really good theories, though. Neurons make new connections and prune them over time. We know about two types of ion channels within the synapse - AMPA and NMDA. AMPA channels open within the post-synapse neuron when glutamate is released by the pre-synapse neuron. And the AMPA receptor allows sodium ions into the dell, causing it to activate.

If the post-synapse cell fires for a long enough time, i.e. recieves strong enough input from another cells/enough AMPA receptors open, the NMDA receptor opens and calcium enters the cell. Typically an ion of magnesium keeps it closed. Once opened, it triggers a series of cellular mechanisms that cause the connection between the neurons to get stronger.

This is how Donald Hebb’s theory of learning works. https://en.wikipedia.org/wiki/Hebbian_theory?wprov=sfla1

Cells that fire together, wire together.

Actually, neuron-based machine learning models can handle this. The connections between the fake neurons can be modeled as a “strength”, or the probability that activating neuron A leads to activation of neuron B. Advanced learning models just change the strength of these connections. If the probability is zero, that’s a “lost” connection.

Those models don’t have physical connections between neurons, but mathematical/programmed connections. Those are easy to change.

I’ve been quoting Jordan Peterson for years?! Ahhh fuck.

Actually, we’ve got some pretty sophisticated models of neurons. https://en.wikipedia.org/wiki/Blue_Brain_Project?wprov=sfla1

See my other comment for an example of how little we truly understand about neurons.

Even assuming we can model the same number of (simple machine learning model) neurons, it’s the connections that matter. The number of possible connections in the human brain is literally greater than the number of atoms in the universe.

It’s not a terrible idea by any means. It’s pretty hard to do, though. Check out the Blue Brain Project. https://en.wikipedia.org/wiki/Blue_Brain_Project?wprov=sfla1

ETA: not to mention the brain is a heck of a lot more than a collection of neurons. Other commenters pointed out how we just discovered a new kind of brain cell - the brain is filled with so many different types of neurons (e.g. pyramidal, Purkinje, dopamine-based, myelinated, unmyelinated, internet Ron’s, etc.). Then there’s an entire class of “neuron support” cells called neuralgia. This includes oligodendrocytes (and Schwann cells), microglia, satellite cells, and most importantly, astrocytes. These star-shaped cells can have a huge impact on how neurons communicate by uptaking neurotransmitters and other mechanisms.

Here’s more info: https://en.wikipedia.org/wiki/Tripartite_synapse?wprov=sfla1

Heck, we barely know how neurons work. Sure, we’ve got the important stuff down like action potentials and ion channels, but there’s all sorts of stuff we don’t fully understand yet. For example, we know the huntingtin protein is critical to neuron growth (maybe for axons?), and we know if the gene has too many mutations it causes Huntington’s disease. But we don’t know why huntingtin is essential, or how it actually effects neuron growth. We just know that cells die without it, or when it is misformed.

Now, take that uncertainty and multiply it by the sheer number of genes and proteins we haven’t fully figured out and baby, you’ve got a stew going.

Time to reboot and replay!!!

My understanding was you needed to have a second copy to 100% - I was always missing a specific mission item. So I never completed the game.