> These are not hard and fast rules, more of a system
This is key. You’re trying to build a base of good behaviors but it’s flexible because the world is full of complexity and having overly strict rules is impossible.
There’s also the hold/tap key thing where you don’t have to move the key physically. Between that and layers the keyboard is an infinite canvas for customizations.
I played around with different tap&hold durations (how long you have to hold before it registers as a hold rather than a tap), but I just couldn't find a duration that matched my rhythm. I kept getting holds when I wanted taps (for short durations) or vice versa for longer durations. My current config uses tap&hold on two keys (home and end, which I don't use often anyway). Holding leads to "hyper" and "meh" which are two extra modifier keys (like control or alt/option/meta). I'm an emacs user so extra modifiers means I can basically store as many macros as I want!
The default Kinesis firmware is fairly limited. It has what they call tap&hold, but it is too limited to be useful in practice. So, it’s mostly limited to simple remaps and macros. That does have the advantage that you don’t fall in the customization rabbit hole.
That said, I made a KinT controller for my advantage, so that I can run QMK.
I love these kinds of projects. Each time I move to another keyboard I inevitably “lose” keys - numpad, then function keys. So I’m maybe a couple of iterations away before I’m ready for this ultimate challenge.
Thanks for your very honest comment. At my office we’re hybrid and people oscillate between the home and in-office for the same reasons as you - sometimes it’s just nice to hang out with people, even if you’re working.
I would hope you wouldn’t have to abandon your career and maybe a little job hopping is in order. I don’t think the world will go full remote, even if that’s personally the way I enjoy it.
I wish I did. The hints in the literature are spread far and wide among older papers, often misinterpreted as something else. A lot of it is unpublished data from my graduate work.
First, penicillin does bind to enzymes that cross link cell wall. It's getting from there to dead cells that's the problem. First, if you knock out a set of proteins called autolysins, cultures exposed to penicillin plateau in population, but the population does not decrease. That is, there is a suicide response. Second, changing the external turgor pressure, such as by adding PEG to the medium, doesn't change the rate of death. Third, if you watch a culture under a microscope when you add penicillin, all the cells in the culture stop growing long before they die. So the unbalanced growth model can't work. I have a vague memory that the kinetics don't work out either, but it's been too many years.
More interestingly, other antibiotics, such as rifampicin and chloramphenicol, which don't target anything related to cell wall, cause bacteria to stop growing when they are added to the medium. That implies that there are active mechanisms involved, not some random fact about cell wall synthesis that happens to stop when something is inhibited. Rifampicin is supposed to inhibit protein production (and does mess up ribosome activity), but there was an interesting paper that showed that a few mRNAs were translated as normal in the presence of rifampicin, even though most were messed up. And how would inhibiting protein synthesis lead to cells exploding (which they do) by a direct, physical mechanism?
I've thought about going back and writing a review article on all this stuff, but biology is a long ways in my past at this point.
This is key. You’re trying to build a base of good behaviors but it’s flexible because the world is full of complexity and having overly strict rules is impossible.