
Prions, Nearly Indestructible and Universally Lethal, Seed the Eyes of Victims - tshannon
https://blogs.scientificamerican.com/artful-amoeba/prions-nearly-indestructible-and-universally-lethal-seed-the-eyes-of-victims/
======
arkades
Prion disease is exceedingly rare. CJD is the most common, with an incidence
of 1 per 1,000,000 person-years worldwide, inclusive of all transmission
vectors (including medical procedures).

Iatrogenic transmission is a rarer subset still: the riskiest transplants
(with respect to CJD) are in the central nervous system. The UK tracked their
transmission rates from 1970 to 2003 (a long period is needed because surgical
transmission usually occurs in folks with long incubation periods - up to ten
years or so) for dura transplants (something that goes into the CNS) and found
a total of eight.

This article is one good step above scare-mongering, but only one.

~~~
travisoneill1
Infectious disease is one area where fear of the unknown is rational. We don't
just need to defend against existing diseases, but also diseases yet to
emerge. Just because CJD is rare doesn't mean that the next prion disease will
be, so it would make sense to take measures to prevent transmission of prions
now.

~~~
arkades
We take measures now, for tissues where prions are a possible transmission
risk. The article mis-represented that. But:

(1) there are only so many resources to go around. Should we be devoting them
to vanishingly rare things rather than things that might actually affect you?

(2) prions will never be a wildfire plague. They have little or no tranmissive
ability, by nature of being absolutely naked protein. One step up from that -
encoding the protein for space constraints and encapsulating it - is called a
virus.

~~~
nwallin
> (2) prions will never be a wildfire plague. They have little or no
> tranmissive ability, by nature of being absolutely naked protein.

Chronic wasting disease (CWD) (affects deer) can be transmitted by infected
saliva. One of the symptoms of symptoms of CWD is excessive saliva production.
It is very transmissible, and is devastating captive populations of deer,
although it is relatively rare in the wild.

I think if a similar TSE affected humans, spreadable by infected saliva, it
would absolutely be a wildfire plague.

[https://en.wikipedia.org/wiki/Chronic_wasting_disease](https://en.wikipedia.org/wiki/Chronic_wasting_disease)

~~~
subroutine
Is there any mammalian prion disease not linked to the PRNP gene (which is
fairly conserved across mammals)?

At first I assumed that 'prions' came in many flavors, like virus. However
from my brief lit search, it seems like people are talking about (p)rion
proteins as if they were't all (P)rion proteins (PRNP). If all mammalian
'prion' disease can be traced to a single conserved gene, I think the risk of
another 'prion-like' disease cropping up is pretty low.

But then again, who knows? Prion disease still seems shrouded mystery, which I
find odd given (1) how inherently interesting this topic seems, and (2) we've
gotten really, really good at molecular biology.

I feel like we are missing a key piece of the puzzle when it comes to
understanding prion disease. The literature seems to want people to
conceptualize the disease etiology as such: an alternately folded (disease
causing) variant of PRNP protein (PrPs) bumps into a normal version of PRNP
(PrPc), causing a normal copy of PrPc to also misfold into PrPs. Rinse,
repeat. So you can basically think of it like an enzyme that catalyzes a
conformational change on versions of itself, in a feed-forward cascade. I feel
like an alternative hypothesis however, could be one of an autoimmune
response. The mammalian immune system, particularly the antibody system, is
mind blowing. This system can recognize virtually any foreign protein -- it
can even recognize specific sub-moieties and conformations of proteins
(antigens). It must, do this while never mistaking an endogenous protein to be
foreign; if it does, you get an autoimmune disease. My idea is basically that
PrPs is just slightly different enough from PrPc to get tagged as foreign by
the antibody system (which it absolutely can do, given that we can perform
western blots to detect the PrPs variant), but also just similar enough for
the antibody system to mistake some endogenous PRNP for the foreign version.

------
OldFatCactus
I had project in college on Prions. Some interesting things I remember:

* Kuru (laughing disease) was transmitted from cannibalism. Women and children of the tribe were more likely to contract it because they were more often given the less palatable parts of the bodies, which included brains

* Some countries do not trust American cattle because our standards for Prion screening are too low

* Kentucky has issues with Prions because Squirrel brains are a popular dish

Try not to eat animal or human brains and you can dramatically reduce your
chances of getting Prions

~~~
ergothus
A few questions:

* Do we have a good grasp on the number of prions in the world? My recollection from when MadCow became a big thing in the late 90s was that prions weren't even looked for and were hard to find as a general rule, but that was 20+ years ago. Might there be many common-but-harmless prions that we haven't even noticed?

* WHY is brain consumption (both in humans and in animals) such a source of prions? What makes that situation more likely to create prions?

~~~
subroutine
Get this... there is only one (1) prion protein! All mammalian prion diseases
are directly related to the PRNP gene.

People talk about Mad Cow, Kuru, Creutzfeldt-Jacobs, Chronic Wasting Disease,
Scrapie, and a dozen other diseases like they are not all manifestations of
the same underlying problem with PRNP gene variants.

------
than
If you're interested in prions and some heavy science, I would highly
recommend reading the research blogs of Eric and Sonia.

[http://www.cureffi.org/](http://www.cureffi.org/) and
[http://www.prionalliance.org/blog/](http://www.prionalliance.org/blog/)

> Wife-husband team Sonia Vallabh and Eric Minikel are on a very personal
> mission to find a cure to prion diseases. When Sonia was diagnosed as a
> genetic carrier of a rare disease called Fatal Familial Insomnia (FFI), she
> and Eric quit their regular jobs and began studying molecular biology to
> learn as much as they could.

Theirs is an incredible story so far. [https://www.newyorker.com/books/page-
turner/a-prion-love-sto...](https://www.newyorker.com/books/page-
turner/a-prion-love-story)

~~~
theprotocol
This is pretty inspiring. Thanks for posting it.

------
chc4
A few months ago I was talking at a family gathering and learned that one of
my distant relatives has CJD. They're a high-ranking company executive, but
their cognition is rapidly wasting away and will be dead within a few years.
Another family member that was a nurse in Kentucky(?) said they have a high
rate of prion disease due to farmers inhaling contaminated dirt for years.

There are a few comments here about how talking about prion diseases are
basically fearmongering. It shook me a bit, though. I always thought of CJD as
one of those freak diseases that you hear about in the news, but is such low
likely hood that it's basically non-existent. Not so much anymore.

~~~
stef25
> A few months ago I was talking at a family gathering and learned that one of
> my distant relatives has CJD. They're a high-ranking company executive, but
> their cognition is rapidly wasting away and will be dead within a few years

Are you sure it's CJD? Article says 95% of CJD patients won't live 12 months
after diagnosis.

> Another family member that was a nurse in Kentucky(?) said they have a high
> rate of prion disease due to farmers inhaling contaminated dirt for years.

What kind of prion disease and what kind of dirt?

~~~
chc4
I was told mad cow disease and CJD interchangably, which looking it up seems
to be slightly different. I don't know the difference between CJD and vCJD and
Wikipedia isn't helping much. Honestly, I don't know how fast it's
progressing, so it may in fact be months. They may already be dead for all I
know, but it sounded like they were diagnosed several months before - they
don't know how long ago she _got_ it though, due to the long incubation. The
family member mentioned mood swings, improper outbursts in conversation, and
memory degeneration and how they're nearly bedbound now due to loss of
balance.

The nurse family member said cow farmers, so I assume cow feces contaminated
dirt, and that their brains looked "like Swiss cheese". This was also in the
context of mad cow disease. I checked my notes from the day and it was North
Carolina, not Kentucky.

------
marsrover
As someone with anxiety and eye problems, I'm not feeling great.

~~~
katuskoti
Same here. I've had strange eye problems that my doctor hasn't been able to
explain, and I feel like my cognition is declining. It's easy to buy into
unknowns like this which seem to explain everything wrong with you, but it's
exceedingly unlikely.

More likely is that my eye problems are from wearing contacts in for too long
and staring too long at a computer in a low-humidity environment and never
blinking. My cognitive issues are probably from not eating healthily, not
getting enough sleep, not exercising, and from being depressed.

~~~
ThrowMeDown01
> _I 've had strange eye problems that my doctor hasn't been able to explain,
> and I feel like my cognition is declining_

You could also explain this with low-level heavy metal exposure, e.g. mercury,
as well as a large amount of other possibilities :-)

I thought hard if I should write this, as a joke and only the above line at
first, but here it goes. Having read your second paragraph too, that is pretty
much exactly what I said to myself a decade ago and before. Then some things
escalated a little bit and I was forced to either accept all my increasing
issues, or do some research myself.

Turned out I had chronic heavy metal poisoning from mercury. Fortunately
diagnosis was made easy because I actually had high levels of it in hair and
blood (and urine - same as blood since that's where that comes from). Anyway,
the scale of the problem was only made clear during chelation therapy, when
both I as well as my (university clinic researcher) doctor were amazed at all
the things that improved, including "miracles" such as thyroid normalization
(had been enlarged and with a nodule for decades, completely gone within half
a year of DMPS chelation, left the endocrinologist speechless, literally, he
checked me _twice_ with ultrasound to make sure he had not make a mistake).
This issue is next to impossible to diagnose with today's methods, unlike
acute poisoning, because how much you see in blood, urine or even hair does
not say anything about the size of the problem, it only shows up when it
actually moves around the body which it only does after exposure.

I had had dry eyes too, and of course the ophthalmologist as well as I myself
attributed it to too much screen work. Today, after years of chelation, I sit
in front of a monitor much more than ever before - but now I have _zero_
issues. Same with RSI. Sooo many little things are completely gone from my
body, depression too.

The crazy thing is, up to that point ~10 years ago when I had to confront that
something was not quite right, I called myself "healthy". And why not? I could
run a half marathon just for fun and still come back feeling relaxed. All the
many little issues I had, such as a few warts on the feet (more and more over
the decades but I ignored the trend), winter depression (many people have
that, it's normal!), eye problems (not really severe, so not worth thinking
about it) and many many other, my brain refused to think about it. The reality
my brain created of my world was highly distorted, but I did not know it. Only
the huge and unexpected changes happening after I began chelation (DMPS, later
DMSA) showed me the extend of the thus far ignored problem.

~~~
joadha
Can I ask how you were exposed to mercury?

~~~
ThrowMeDown01
Beginning the story indirectly, when I began the treatment I was not even
close to being sure about it all. The only reason I had even tested for
mercury was because I was desperate, there just was no other option left,
after consulting many doctors finding nothing. After having been given PPIs
for the problems that had forced me to start looking in the first place my
issues exploded in severity: I had never felt so bad in my life. With barely
any stomach acid from the PPIs - I could hardly digest anything, it would lie
in my stomach for way too long - I had reflux near constantly. Each time I lay
down to sleep, really every single time. With much reduced stomach acid, which
seemed to have a very strong opposite effect of what it was intended to do. I
also had incredible bloating and my mouth felt funny. The professor
gastroenterologist treating me thought it was just nerves.

The first thing I found was, after having first dismissed it as esoterics when
I found it on the net, that I had a candida problem. Proven by the significant
immediate effect of taking Nystatine (anti-fungal) and a doctor confirmed it.
Later I even got Fluconazole, an internal antifungal, again with huge effects.
Just an aside, funnily enough, the warts on the sole of my feet that every
doctor would say were caused by a virus disappeared by 95% after Fluconazole.

Anyway, I learned Candida never is a cause but itself just a symptom, and
since I had none of the conditions that are listed in the text books that
might cause it I had to continue looking. Heavy metal poisoning was one of the
only options that would explain the Candida, but also everything else. And I
had only one possible source: amalgam fillings.

When the tests confirmed high levels of mercury in my hair as well as in my
urine I still was not completely sure: It was high but not high enough to
explain the severity of my issues. The doctor I went to said it was high
enough to justify starting chelation, but I must have something else. I had
the remaining three fillings removed with special equipment and protection. I
had had three or four removed decades earlier without protection, just normal
drilling, at the beginning of my CS study, and now something made sense: At
the time I had suddenly, out of nowhere and pretty much overnight, developed
almost-asthma level pollen allergy, and for half a year I had severe problems
with the right leg joint. I never went to a doctor for the joint because the
symptoms clearly showed me it was not "physical", I can't explain it with a
few words. I also developed severe insomnia and - as I understand now but not
at the time - "dumb". I had always been good at math, for example, but
suddenly it was a problem. Stuff that today, after all my chelation, again
looks very easy to me. I still passed and I was still very good at everything
more practical so getting through the study was no problem. At the time I
completely ignored all those sudden issues and took it as "that's just live".

Everything started to improve greatly during the first year of chelation, and
after the fifth or so DMPS treatment in the following weeks the tissue around
my right-side thyroid became very active. That was very curious, because I had
had a double-sized right thyroid with a nodule for at least two decades, re-
diagnosed just a year prior. Recommendation back then was surgery to get rid
of the nodule. The tissues in that area became active after two or three DMPS
treatments. I went to the endocrinologist again when I felt nothing else
there. He did an ultrasound, and when he was done he started casually looking
through his notes and became more and more agitated. He asked me to lie down
again and he repeated the ultrasound, right side only this time. At the end
the result still was this: Thyroid size nearly completely normal, and the
nodule had disappeared completely. That was the point when I actually believed
that yes, I had found the source of the problem.

Regarding an even more clear proof for amalgam fillings as the cause:

After about a year the doctor wanted to make an injection in to my buccal
mucosa. It's just mucosa, so you don't need any force, but his needle ended up
_deep inside jaw bone_. He found several places where the needle easily
penetrated into bone. All those places where where amalgam fillings had been
for two or three decades. He injected DMPS and just like in the thyroid area
the are began to "work". Very actively. A year later the needle could not
penetrate anywhere any more. The jaw remained a very very active area though
for years, and it still reacted to chelation. An aside: The are had been OPG
x-rayed a few times in the years before because I had finally gotten my
crooked teeth fixed and jaw extension surgery too (now I have perfect bite and
teeth, wonderful!!!). No doctor ever saw anything in my jaw. One wasn't sure
about seeing a tiny shadow near one root - the one where I had the most issues
and that was the most active later during chelation - but didn't take it
serious enough and didn't follow up (when patients don't complain why would
you if it's so subtle). But bone that can be penetrated by a needle easily is
_very_ broken. This shows how much (more) broken something has to be to show
up even in an OPG x-ray.

My doctor never found anything else and now he too thinks that the only
problem there ever was were the amalgam fillings. A lot - _a lot!_ \- of very
interesting stuff happened to me, the chelators only paved the way out and
started it, 99% of the actual work was done by my body (most chelators only
work in extracellular space anyway). For example, there were three months of
nightly 3-4 am kidney pain, but after the nephrologist found that despite
elevated protein levels in urine there was no sign of kidney disease I didn't
worry about it. It fit into the pattern of stuff happening at various times
all over my body and my brain, a new phase starting every few months in
another area of the body. For those three kidney pain months I simply got up
when it started at 3 am or so, went to bed when it stopped at 5 am and slept
until 10 and still got my sleep. No problem.

Even tough I'm a CS person, I actually have a background not in medicine, but
(for fun and out of interest) I've also have many courses in biology,
chemistry, org.chemistry, biochemistry, anatomy, physiology, neuroscience,
several courses in each. I don't care about pathologies, I only wanted to
understand the basics of biology and life and of human physiology.

------
nkurz
In related prion news, does anyone have insight into the recent studies
suggesting that Chronic Wasting Disease (CWD, increasingly prevalent in North
American deer and elk) may be transmissible from infected animals to humans
via cooked muscle meat?

In 2017, there was a Canadian study that seemed to show that feeding macaque
monkeys raw muscle meat from infected deer was capable of transmitting the
disease. I don't think the study has been published yet, but it's described in
detail in this Norwegian report
([https://vkm.no/download/18.25950e0715e84a118a6ec492/15069251...](https://vkm.no/download/18.25950e0715e84a118a6ec492/1506925175221/Statement%20CWD.pdf))
and forms the basis of an advisory by the Canadian government
([https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-
Op...](https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-
CWD-2017.pdf)) suggesting that consumption of all potentially infected meat be
avoided.

Then in 2018, a separate seemingly very similar American study was published
([http://sci-hub.tw/10.1128/JVI.00550-18](http://sci-
hub.tw/10.1128/JVI.00550-18)) , saying that no evidence was found for
transmission to macaques, even after direct cerebral exposure. The NIH issued
a press release ([https://www.nih.gov/news-events/news-releases/nih-study-
find...](https://www.nih.gov/news-events/news-releases/nih-study-finds-no-
chronic-wasting-disease-transmissibility-macaques)) with the headline "NIH
study finds no chronic wasting disease transmissibility in macaques".

Suffice it to say, there seem to be contradictory messages here. Is there some
overview that would help to clear things up?

~~~
ff7f00
I don't have studies but I did email the National Prion Disease Pathology
Surveillance Center asking "is there a breakdown of cases of the individual
Animal Prion Diseases by location and possibly by year (i.e. cases of human
prion disease acquired by eating contaminated meat)?" and here was their
response:

> To date, in the US, there have been no known cases of variant CJD, or human
> prion disease acquired by eating contaminated beef. Here at the NPDPSC, we
> have diagnosed 4 cases, but they were all acquired out side the US; 1 case
> in 2044 acquired in UK, 2 cases in 2006 acquired in Saudi Arabia, and 1 case
> in 2014 acquired in the middle east.

> In several western US states, Canada, and now South Korea and Norway, there
> is concern that chronic wasting disease (CWD), the prion disease of elk and
> deer, may be transmissible to people who hunt, butcher, or eat the affected
> animals. Although transmission of CWD from animals to humans is unlikely,
> recent data indicate that the barriers between species may be weakened when
> CWD has been transmitted from animal to animal several times (as may happen
> in the wild). The NPDPSC, along with the CDC, Department of Health, and the
> Game and Wildlife Administration, is carefully monitoring any possible case
> of acquired CWD in humans.

Asked for extra clarification, "So although there is a concern with CWD
crossing that barrier, there still haven't been any recorded cases?"

> That is correct.

~~~
snowwrestler
This is such a great comment. Thank you for doing that legwork, and for
sharing it.

------
technological
Here is excellent documentary
[https://www.youtube.com/watch?v=vw_tClcS6To&list=PLdO1m6dMye...](https://www.youtube.com/watch?v=vw_tClcS6To&list=PLdO1m6dMyeyS58vB1wSpnNbc1bhv_N3jd)
anyone wants to see documentary related to Kuru (Prion Disease)

------
yourapostasy
Not all prions are bad [1]. We still need to study them and their protein
precursors to understand them more.

[1] [https://www.the-scientist.com/features/the-bright-side-of-
pr...](https://www.the-scientist.com/features/the-bright-side-of-prions-38210)

------
barking
About 20 or so years ago I was feeling bad about my chances of developing the
type of CJD associated with mad cow disease because of all the burgers I'd
eaten over the preceding years.

There were also human cases getting reported at a rate that some suggested
matched the pattern for the early days of an epidemic.

Luckily that never materialised. Still though having lived in the UK during a
certain time period precludes one from donating blood elsewhere, to this day.

~~~
dev_dull
Sorry friend. Not off the hook yet:

> _patients with very long incubation periods of at least 34 years, and
> probably more than 40 years._

[https://www.thelancet.com/journals/lancet/article/PIIS0140-6...](https://www.thelancet.com/journals/lancet/article/PIIS0140-6736\(06\)69362-8/fulltext)

~~~
barking
The uptick in cases should have started in about 2014 (if 34 years ) or 2020
(if 40 years) and start to tail off a decade later.

------
arbuge
The part about the possibility of contracting these from your doctor's
equipment when you go in for an eye exam is truly scary:

"Undiagnosed CJD patients may seek testing. And the diagnostic equipment used
to test them may then become contaminated, the authors write. They recommend
single-use instruments or the adoption of new decontamination procedures for
opthalmological equipment with better effectiveness on prions."

~~~
rladd
The fear of contracting something from equipment is one reason why I go to an
eye doctor who uses contactless air-puff glaucoma diagnostic machines rather
than the older style which touches the eye.

In my last several visits, nothing has touched my eye at all.

------
growlist
Slightly worrying given that I had a cataract operation in my mid-30s. OTOH, I
suspect I should be far more worried about the health impact of filthy diesel.

~~~
michaelcampbell
Isn't cataract surgery _removing_ something, only?

FWIW, both my parents had cataracts removed, and my father who'd worn
eyeglasses since the 1940's said he'd never seen better in his life. So, chin
up.

~~~
Invictus0
Yes, but the article says that the instruments used in opthalmology can be
vectors for the prions. OP is fine though assuming his operation was more than
a year ago and he's not currently dead.

~~~
erichurkman
[https://www.ncbi.nlm.nih.gov/pubmed/11721058?dopt=Abstract](https://www.ncbi.nlm.nih.gov/pubmed/11721058?dopt=Abstract)

> we estimate that the mean duration of the incubation period is 16.7 years

[https://www.thelancet.com/journals/lancet/article/PIIS0140-6...](https://www.thelancet.com/journals/lancet/article/PIIS0140-6736\(06\)69362-8/fulltext)

> A comprehensive statistical analysis had earlier reported that the mean
> incubation period was between 10.3 and 13.2 years, but the tail of the
> distribution was long. Using these estimates, we calculated that the upper
> 0.4% quantile was 40 years, and even larger for those infected young (>50
> years), very much in line with these new observations.

------
andrewingram
Well that's made me a bit more worried about my cornea transplant next year.

------
gumby
Given that prions are proteins, why can't we use immunotherapy and vaccinate?

~~~
Nasrudith
Well the immune system needs to be able to do something of use in response.
Just putting it in even with an immune sensitizing agent would add another
prion that it can't do anything useful about. But antibodies, if we had ones
that worked for a strain and weren't essentially prions themselves we could
vaccinate for it or use it to "chelate" assuming the prion grabbers wouldn't
cause other unacceptable problems.

~~~
folli
Passive immunization might indeed be a feasible option, but of course requires
timely detection.

~~~
gumby
Couldn't we immunize _before_ exposure as we do with, say polio, TB, influenza
et al? Then no detection would be needed.

Or are the abnormal prions in CJD and the like not uniform enough for general
prophylaxis?

I really have a naive understanding of immunotherapy, so sorry if my question
is dumb.

~~~
Nasrudith
Whatever it is isn't that simple given that CJD is just a standard of care.
I'm more an enthusiastic dabbler who occasionally checks if I could have been
capable technically than an expert admittedly.

I did some more cursory research. Interestingly I was half-wrong about the
immune system - while I was right about it not being equipped to stop it can
do something. Monoclonal antibody treatments delay it. However another problem
is that the body's own proteins which are deformed into prions aren't
recognized as foreign bodies. Given that notes mention that mice vaccines only
delay the onset along with monoclonal antibody treatments. Some sources seem
to indicate that it only blocks prions from deforming as opposed to
eliminating combined with the fact that native proteins will keep on
cascading.

I wonder how much processing power would be required just to get a candidate
'prion grabber' \- never mind going through ones which won't turn out to be
horrifyingly toxic in other ways.

Here are a few sources I skimmed I would be glad to know where I went wrong.

[https://www.researchgate.net/publication/233941323_Immunothe...](https://www.researchgate.net/publication/233941323_Immunotherapy_in_prion_disease)

[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2063508/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2063508/)

------
honestoHeminway
I guess, this is the weapon of choice for any patient spy unwilling to send a
message. One pinbrick, and the nuclear scientist/dissendent/oppossitional spy
has half a year to write his/her memoir.

Are there statistics on Creuzfeld-Jakobs in Langley?

------
paulpauper
It would seem the solution is to treat deceased CJD victims as bio hazard like
ebola

------
ryanmercer
Prions are one of the things that makes me go, hey wait maybe we do live in a
simulation. They're basically corrupted code (which we've yet to figure out
how they get that way in the first place) that corrupts other code... what is
that?!?! Reminds me a lot of the WoW 'corrupted blood incident'.

I understand how something like bacteria or a virus enters a host and
replicates, but an anomalous protein corrupting other protein is just so
strange. I'm sure science will adequately explain it someday but until then
it's a pretty WTF anomaly to me.

~~~
mrob
At the molecular scale, everything is effectively made of springs (molecular
and intermolecular bonds). Proteins are a big complicated tangle of springs,
and that means they have multiple possible configurations they can spring to
if you let them relax. If you bump another protein of the right shape against
them, you can nudge them into a different spring configuration.

Think of "slap bracelets", those curved metal strips that spring around your
wrist. If you push two straight ones together, nothing happens. But if you
push a curled one against a straight one it will make the straight one curl up
too. The curled slap bracelet is acting like a prion.

~~~
ryanmercer
>Think of "slap bracelets", those curved metal strips that spring around your
wrist

Wow, I've not heard someone mention those in probably 2 decades.

