The last week of the immersion program has come to an end,
and it was definitely one of the most productive weeks here in NYC. All the preparations----IACUC
protocol, surgical and rodent cadaver trainings-----payed off as we finally
went in to the OR in the animal facility to practice ACLT on live rats. I am
very glad that we were able to do this, as I realized that cadaver practices
cannot capture the scope of complications on live animal surgeries. I learned
how to manage and monitor the depth of anesthesia, when and where to administer
pain killers and antibiotics, and all the little details that you can only pick
up in a real OR (such as how to effectively maintain sterile barrier, how to minimize
pain and discomfort of the subjects, and etc.). One thing I overlooked when I
was preparing myself for the live animal training is the importance of monitoring
the depth of anesthesia. The depth of anesthesia affects the heart rate and respiratory
rate of the animal (the respiratory rate is actually one of the ways to monitor
depth of anesthesia), and thus affects the bleeding when incisions are made. Unlike
cadavers where there are no bleeding, the live animals can bleed excessively if
it is heart rate has not slow down properly from anesthesia, resulting obstructed
views by the blood and thus longer and more complicated procedures.
The other good news it that our closed PTOA apparatus is now
functional. After numerous iterations and trails and errors, we have finally achieved
control speed, displacement and alignment, and ease of operation. As it turns out,
the ease of operation was actually more changeling than we originally thought. Because
we were modeling our system based on the previously existing PTOA apparatus in rats,
we often forget how small mice are. For example, mounting the tibia to the feet
clamp is a easy task on rats, but it has proven to be much harder on mice which
are around ten times smaller. The size limited the space we can operate, and
many mechanisms of stabilizing ended up being too bulky to be practical. Luckily,
we gotten it almost figure out by Friday and proceeded to testing on some
cadaver mice. Our measurements agrees with the mechanical testing of ACL and
the data from the manual methods. However, with manual methods when the force
is greater than 10N the PCL are often also ruptured. With our device, we can exert
>20N of force and rupture the ACL only, as a result of the controlled displacement.
This is great because we know the strength of ACL varies greatly from animal to
animal, and with the apparatus, we don’t have to sacrifice the ones with
stronger tendons just because we cannot rupture it properly. The ongoing theory
of why the manual method always rupture the PCL with the ones of greater force is
that once the ACL is ruptured the human hand will accelerate due to the sudden decrease
of resistance and hit the PCL. The great the force requires to rupture the ACL
(tougher ACL), the greater this acceleration will be and the more likely the
PCL will be ruptured. This is precisely why we went to the more controlled methods
with a loader in the first place----with a control displacement, no matter the
force needed to rupture the ACL, the PCL will remain intact as the loader will
never reach it.
I am very happy that all my goals have been accomplished. I
am glad that I was able to challenge myself and try new things, both in lab and
in life. I had a fantastic summer here in NYC and I will certainly miss the
city. In truth, I am already missing it as I am typing my last immersion blog
in Newark Airport, but who knows, since my flight has already been delayed for
four hours I may never get to leave here after all.
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