Based on the description of the wiring to the motor (24V, GND, POT1, POT2, NC), it doesn't sound like the original setup would have been drawing much power through the pot either -- there's probably something else on the other end of that wire that is doing modulation based on the sense resistance, and the motor is itself drawing power from the 24V line. So while it's true that there should be a check for the allowable limits on the digipot, I don't think it's actually being used to sink much power.
Hey, author here. That's correct. The potentiometer has 5V going through it, with a current range of 30-164μA, which fell within limits of the digipot. I opted to use the digipot instead of my own PWM because something else must be doing PWM closer to the motor, where I didn't want to go modifying.
>Everything joined up via a 2-pin and 5-pin connector on the PCB. From there, it was a straightforward matter of measuring voltages and continuity to work out what connected to what: the 2-pin connector was offering 24V DC. The 5-pin connector was what went off to the motor itself. Two of its pins were passing through the 24V DC and ground directly. Two more pins were connected to the potentiometer. The fifth pin was not connected.
> there's probably something else on the other end of that wire that is doing modulation based on the sense resistance
And it would have been great if that arbitrary assumption had been tested by the OP and the results were documented in the article so that they wouldn't come off as somewhat clueless as to the limitations of their design.. oh well.
These passive aggressive posts are a far worse violation of the HN Guidelines than what they're in reply to almost all of the time - and this is no exception.
No, no they're not. I would much rather people are warned about the guidelines and adhere to them going forward than the opposite and we then just let violations run rampant.
There are a lot of people who read or watch stuff from the Internet and then play with mains voltages without giving a though to how dangerous that is.
See: any craze which uses the high voltage transformers from microwaves
If this (or, more accurately, a drug developed downstream of this technology) worked, they absolutely would.
A great example of this in relatively recent history is the treatment of hepatitis C. The treatments pre-circa-2011 were pretty crappy: interferon/ribavirin had poor cure rates and bad side effects. But it was still better than hepatitis destroying your liver, so people dealt with it.
Then, in 2011, as the culmination of years of trials, telaprevir (from Vertex/J&J) [1] and boceprevir (Schering-Plough/Merck) [2] were approved and were DRAMATICALLY BETTER than interferon/ribavirin.
...and then just two years later both of these drugs got nuked by the approval of sofosbuvir (aka Sovaldi, from Pharmasset/Gilead) [3], which has _cure_ rates in excess of 90%. Telaprevir and boceprevir were pulled from the market because there was simply no more market for them once sofosbuvir hit. Scientific competition at its finest.
There is absolutely a dark side to pharmaceutical pricing and licensing, but please don't let the existence of that dark side cloud your vision of the transformative impact that those of us in biotech R&D want to have (and in many cases, have had). I was at Vertex when the early trial data on telaprevir started coming out and it became clear that we might be able to offer patients real hope who did not have it before.
Those wondering about the mouthful of a name that is "orforglipron" may be interested in the INN (international nonproprietary name) standard for generic drugs. That name is a "generic" or "nonproprietary" name.
Those typically have a "stem" which indicate the mechanism by which the drug works. In this case, it's "-glipron", which you can parse as "glipr" -- GLP-1 receptor -- and "on" -- it's an "agonist", or something that turns "on" the receptor. So "-glipron"s are drugs which agonize, or activate, the GLP-1 receptor. There are other gliprons in trials, including danuglipron (https://en.wikipedia.org/wiki/Danuglipron) from Pfizer, and many others that don't have assigned INNs.
Semaglutide and liraglutide also agonize GLP-1, so why aren't they gliprons? Because chemically they are analogs of the naturally occurring GLP-1 peptide, so they get the -glutide (GLUcagon-like pepTIDE) stem.
No, it's not a reformulation of tirzepatide. Orforglipron is a small molecule with a molecular mass of 883 g/mol and tirzepatide is a large molecule peptide six tims larger, with a molecular mass of 4813 g/mol.
The Wikipedia pages are decent -- the picture makes it fairly obvious how much smaller orforglipron is than tirzepatide even if you don't know how to read chemical structures; just count atoms!
I should point out that we are hiring! Software engineering, data science/ML, and IT positions are available in Salt Lake City, Toronto, New York, and London:
Not that I know of! Note that the positions we list are typically in different teams so it's worth reading the descriptions to make sure you're picking whichever one is most appropriate to your experience+interests (and, as a corollary, if you weren't a fit for a previous position, you may be one for one that comes up in the future).
Yes, we (and plenty of others) have prior data showing that perturbations (things that you can do to cells, like knocking out genes or putting drug-candidates on them) have different effects at different times, so we are excited to see the potential for time course imaging.
Note that "video" is a little different here than the way we all usually think of it - think "minutes or hours between frames" not "frames per second".
These are tests of circulating cell-free DNA (cfDNA), not circulating cells. The fraction of circulating _cancer cells_ is too low (outside of blood cancers or metastatic cancers) to be technically feasible to detect; ditto in pregnancy. By contrast, while there isn't much cfDNA (DNA fragments floating around in blood plasma outside of cells) -- on the order of 1-10 ng/mL -- there's enough to extract reliably, and critically, the fraction of that that is tumor-derived (or fetally-derived, for prenatal testing) can be high. It's already high single to low double digit percent at 10-12 weeks of gestation, and can go much higher in some cancers.
But the biggest challenge for these tests is that this "tumor fraction" can be very very low in early stage cancers, which is why stage I sensitivity tends to be quite poor.
Biological microscopes illuminate the sample from below, as the samples are typically transparent. Metallurgical microscopes illuminate reflective samples from above.
*"Below" meaning "on the opposite side from the objective" - you illuminate _through_ the sample.
