AKA as the brain-eating amoeba.
These
guys are known to withstand higher temperatures and are typically found
in water. This includes ponds, rivers, moist soil, lakes, HOT springs,
and UNCHLORINATED POOLS.
This parasite enters the host via
nasal passage and feasts on the central nervous system (CNS) and brain
which causes Primary Amoebic Meningoencephalitis (PAM) taking down it’s
victim in less than 2 weeks 99% of the time. Initial
symptoms include fevers, change in taste and/or smell, headaches,
nausea and stiff neck. Eventually as the infection progresses due to
reproduction of the amoeba, the individual will experience photophobia
(low tolerance for light), mental status changes and seizures leading
them to a coma and die within 2 weeks upon contracting the disease. There
is no known cure for the disease as of today and the affected hosts
have a mortality rate of 98%, but there are survivors.
There is no exact way to prevent yourself from possibly being infected besides avoiding untreated warm bodies of water. N. fowleri has three stages: Cyst, trophozoite, and flagellate. Here is the bastard in its trophozoite stage: YES, I know. They look as terrifying as they sound. And here is what it would do to your brain: Whole brain necrosis
Artsy pictures borrowed from brainsenemy on wordpress.
I remember learning about these guys in the second year of my degree
and they definitely scared me off bathing in warmer waters. Luckily
they’re only found in fresh water and the number of actual cases is low,
but they still have ridiculously high mortality rate for a pathogen,
And the people who have survived are generally severely brain damaged.
I have always been fascinated with this. I am from the south and I
remember hearing about kids getting “the amoeba” after swimming in some
lake during the summer. Pretty much every summer you hear of at least a
couple of kids who get this and die soon after. Thanks for a great,
informative post!
The manual differential is one of my favorite tasks to
complete as a medical laboratory science student. Automation has largely
taken over the differential, but there will always be a need for
completing manual differentials. It’s something students tend to love or
absolutely hate. It takes a lot of skill and a ton of practice, but
when you’ve gotten good at it, it’s a skill that will set you apart from
other scientists and technicians. As a disclaimer, there are many
different ways to perform a manual differential, and every hospital’s
protocol is going to be a little different. If you do something
differently, or learned to do something a different way, I’m not saying
your way is wrong; I’m simply saying this is the way I was taught.
1.
First, examine your slide macroscopically. Make sure there are no
holes, your cells haven’t sloughed off and that your slide has stained
evenly. Remember, there will be an area of the slide where the film of
blood is thicker, so the staining will appear darker there, which is
normal. The stain should have a gradient effect. See image below
(source: http://www.medical-labs.net/feathered-edge-of-peripheral-blood-smear-2598/). Make
sure that you have a nice feathered edge. If there is no feathered
edge, you may not have a good area to count, known as the monolayer.
This is the area of the slide where red blood cells are barely touching
each other but are still abundant and have a nice central pallor.
2.
If you have a quality slide macroscopically, examine your slide
microscopically under the 10X objective. The main things you want to
look for are blast/immature cells in the feathered edge, platelet
clumping and parasites. Blast and immature cells tend to be larger, so
they are pushed into the feathered edge a lot of the time. Catching
these abnormal cells is one of the most important parts of performing a
manual differential. A lot of the time, this is why you will perform a
manual differential in a clinical lab, because a machine flagged it for
review due to abnormal cells (as in cells that shouldn’t be in
PERIPHERAL blood). If you see platelet clumping, you should not release a
platelet estimate. Check your tube for clots. If your tube is clotted,
you should request a new sample. Always follow your hospital’s protocol,
though. There are many different blood parasites. Microfilariae are
large, so they can be seen under the 10X objective, but you may have to
wait until you get under the 50X or 100X objectives to see things such
as Plasmodium spp. and Toxoplasma gondii.
3.
If all is well microscopically, find your monolayer. There are many
different ways to move your slide to begin counting. The two most
important things are to not leave the monolayer and not count the same
field over again by accident. A good way to move your slide can be see
in the image below (source: http://www.medical-labs.net/feathered-edge-of-peripheral-blood-smear-2598/). The
typical count is 100 WBCs but some hospitals will require counting 200
WBCs if the WBC count is high. I always count using the 100X objective
because I feel it’s far more accurate, but counting using the 50X
objective is very common for the experienced. While counting,
simultaneously look at RBC and WBC morphology and inclusions, as well as
platelet morphology and an estimate. Record all results according to
your hospital’s protocol, and you’re done! Another smear under your
belt.
Is there something you do differently during a manual differential? Let me know in my ask!
Breast Tumor Stiffness and Metastasis Risk Linked by Molecule’s Movement Stiffness drives cancer invasion through previously unknown mechanism
Researchers
at the University of California, San Diego School of Medicine and
Moores Cancer Center have discovered a molecular mechanism that connects
breast tissue stiffness to tumor metastasis and poor prognosis. The
study, published April 20 in Nature Cell Biology, may inspire new approaches to predicting patient outcomes and halting tumor metastasis.
“We’re
finding that cancer cell behavior isn’t driven by just biochemical
signals, but also biomechanical signals from the tumor’s physical
environment,” said senior author Jing Yang, PhD, associate professor of
pharmacology and pediatrics.
In breast cancer, dense clusters of
collagen fibers makes the tumor feel stiffer than surrounding tissue.
That’s why breast tumors are most often detected by touch — they feel
harder than normal breast tissue. But it’s also known that increased
tumor stiffness correlates with tumor progression and metastasis, as
well as poor survival.
To determine how tissue stiffness
influences tumor behavior, the team of cancer biologists and
bioengineers used a hydrogel system to vary the rigidity on 3D cultures
of breast cells from that typically experienced by normal mammary glands
to the high stiffness characteristic of breast tumors. They discovered
that high stiffness causes a protein called TWIST1 to lose its molecular
anchor and move into the cell’s nucleus. In the nucleus, TWIST1
activates genes that enable breast cancer cells to invade surrounding
tissue and metastasize to other places in the body.
The
researchers also compared mouse models of human breast cancer with and
without TWIST1’s anchor, a protein called G3BP2. Without G3BP2, tumors
were more invasive and developed more metastases in the lung, compared
to tumors with G3BP2.
The same mechanism plays out in human breast
cancers, too, the researchers found. Analysis of human breast cancer
patient samples showed that patients with stiffer tumors (meaning tumors
with more organized collagen structures) did not survive as long as
patients with more compliant tumors with disorganized collagen. Patients
with both low G3BP2 and stiffer tumors had even shorter survival times.
The correlations were so clear the team could use these factors — G3BP2
protein levels and collagen organization — to predict patient outcome.
“Next
we want to understand exactly how cells interpret mechanical cues into
biological responses,” said Laurent Fattet, PhD, a postdoctoral
researcher in Yang’s lab who led the study, along with former graduate
student Spencer Wei. “This cross-talk between a tumor’s biomechanical
microenvironment and the inter-workings of individual cancer cells may
someday provide new therapeutic strategies to slow cancer’s spread.”
I thought you might find this interesting. It’s a scanning electron
microscopic image of mouse beta-eyelet cells that I had differentiated
from mouse embryonic stem cells. It’s not the greatest image (I was
still learning the SEM) but it’s still pretty fascinating.
This is fantastic! Beautiful, thank you for sharing, darwin4life!
I'm a Biomedical science
graduate who is working in a hospital laboratory in Ireland. I try to
post things relating to what's going on in the laboratory and also some
other things of interest.
Feel free to submit any science-related posts or to ask questions. I'll try to get back to you as quickly as possible!
You can also follow my personal blog at http://amygdala-hijack.tumblr.com.
Disclaimer: I reblog and post images which are mostly from other
sources, so I try to cite them as best I can. I do not intend ot
infringe copyright, so if I give the wrong source, please tell me and
I'll try to fix it. curious scientists
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