_ihaque
Joined 13 years ago
Joined 13 years ago
Let's say you want to run a single shower at 2.5gpm, the water comes into the home at 55F (12.8C, pretty temperate!) and you want your shower at 100F (37.8C), so a 25C rise. 2.5gpm = 9.463 L/min = 158mL/sec. Water's heat capacity is 4.184* J/mL/degC, so the sustained thermal power you need to deliver is:
4.184 x 158 x 25 = 16.5kJ/s = 16.5kW
At 240V, 16.5kW would be almost 70A.
What makes a heat pump heater more efficient is that it multiplies the electrical power input into a larger thermal power output, by "borrowing" thermal energy from the surroundings. So you could get (for example) 15kW thermal power from 5kW electrical power. In practice the heater will be tanked, rather than tankless, for two reasons:
1. The effective power will probably be less than that.
2. That was an estimate to run just one shower and you might want to run more than that!
So the tank lets you buffer the power draw over time; there will be some thermal loss over time, but insulation is cheap, and it's hard to fight a 3-5x amplification from the heat pump.
* Yes, yes, per gram/K but 1mL of water is close enough to 1g for this.
> the fact this is how hot it will be from now on
That sounds to me like an acknowledgement that, in fact, the climate has changed.
A fun but off-topic note: "behave the same chemically" is only approximately true. For heavy atoms like the ones discussed in the article, it's basically true. But for hydrogen, adding one neutron doubles its mass and you can get real effects on chemical reaction rates.
https://en.wikipedia.org/wiki/Kinetic_isotope_effect
And of course, an obligatory "In The Pipeline" link on how it's used in drug discovery: https://www.science.org/content/blog-post/isotopes-get-your-...
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.
[1] https://en.wikipedia.org/wiki/Telaprevir [2] https://en.wikipedia.org/wiki/Boceprevir [3] https://en.wikipedia.org/wiki/Sofosbuvir
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.
I don't know why tirzepatide got that name. It's a peptide, so "-tide" makes sense, but it's actually listed as a "various" exception in the master document of INNs: https://iris.who.int/bitstream/handle/10665/379226/978924009....
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