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Suzuki SX4 S-Cross - Duration: 1:04.
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Geometric Distributions & The Birthday Paradox: Crash Course Statistics #17 - Duration: 10:19.
Hi, I'm Adriene Hill, and Welcome back to Crash Course, Statistics.
We have to wait for a lot of things in life.
We wait until we're old enough to live on our own, or go to college, or drive a car.
Waiting can suck, and it's even worse when you don't know how long you'll have to wait.
Luckily, in certain situations, probabilities can help you guess how long it might take
for something to happen, like getting a full house in poker, having your first daughter,
or winning the lottery.
INTRO
For example, you're eating from a box of Bertie Bott's Every Flavour Beans during
a fun, if risky, hang out with your friends.
These Jelly Beans have some flavors that are awesome like Cherry and Peppermint, and some
not so awesome like Grass, or Boogers, or Vomit. Ewww.
The problem: you don't know if you're gonna get a good or gross flavor until you eat it.
And you know that your affinity for this game will go away if you're ever unlucky enough
to come across one of those Vomit flavored beans.
Cinnamon!
It's delicious.
But how likely is it that you'll be able to eat 4 of these odd Jelly Beans before you
get that dreaded Vomit flavor and decide to get new friends?
Turns out, there's a formula to do this.
The Geometric Probability Formula.
This formula comes from The Geometric Probability Distribution, which looks similar to the Binomial
Probability Distribution that we talked about in the last episode.
But they do something a little bit different.
Geometric probabilities tell you the probability that your first success will be on your nth try.
And success here just means the event we're interested in happens, it's not always a good thing.
For example, the probability that your first Vomit flavored jelly bean will be your 5th
Jelly Bean this means that the first 4 beans were all not vomit flavored.
Let's pretend the probability of getting a Vomit flavored bean is 5%, then there's
a 95% chance that you'll get any other flavor.
As you remember from the multiplication rule.
Our chance of getting four non-vomit beans in a row is 0.95 x .95 x .95 x .95 or .95^4.
The probability of then getting the Vomit bean is 0.05, so all together, the probability
of getting 4 non-vomit beans and then 1 Vomit flavored bean is this or about 4.07%
In a more general form, The Geometric Probability Formula says that the probability of the kth
try being your first success, is the probability of failure to the k-1 power, times the probability
of success to the first power.
Which is what we just did in the vomit jellybean example..
The probability of the 5th try being your first success was the probability of 5-1 or
4 failures and then one success.
If we graph the geometric probability for all possible values of k, we get a Geometric
distribution that shows us the probability of each trial being the first time we get a success.
For example let's look at a section of the geometric distribution for finding the probability
that each trial is the first time we'd eat a vomit flavored jelly bean.
You'll notice that I said "a section of" because the geometric distribution could go
on forever technically we could eat thousands of Bertie's Beans and still not find any
Vomit Flavored ones...in fact that's pretty much what I hope when I eat them.
It's just very unlikely, which we can see on our graph.
As k increases, the probability of that being your first success gets incredibly low, mostly
because you'll probably have found the flavor that shall not be named already.
Let's look at another example: You're finishing up basketball practice and your
coach announces that you'll have to make one free throw before you can leave.
You're really bad at free throws, and you have a 20% probability of making any given shot.
So we can calculate the probability that the first shot you make is your 10th shot.
Plugging everything into our formula, we discover that the probability of this particular scenario
is this: or about 2.7%.
The Geometric distribution for this example looks like this which gives us all the probabilities
that a certain trial is the first time you make a shot: But you'd also get to leave
if you made it before your 10th shot.
To calculate the probability that you'll have to shoot 10 or fewer free throws before
you make one, we can add up all the geometric probabilities from 1 up to 10.
This essentially tells us the probability that it takes k or fewer tries before your
first success which you might remember from when we talked about cumulative distributions.
A cumulative geometric distribution is incredibly useful because often when we ask questions
about how long we have to wait for a certain outcome, we want to consider whether it happens
before the nth trial.
Like we said, whether it's the first or 10th shot, you still get to leave practice,
and it turns out that there's a 89.3% chance that before your 10th shot, You will have
made a basket.
That make for a total of about 92% chance that you'd make it on or before your 10th shot.
If you want to find the average number of shots you need to take before you score, you
can use the geometric distribution to calculate its mean, which is 1 divided by the probability
of success or this.
The mean number of shots we'd need to take before we made our first would be
1/0.2, which is 1/(1/5) or 5.
And this makes some sense.
The smaller the probability of success is, the more tries we'll need--on average--before
we get a success.
For example, if there's only a 10% chance that we'd make the shot, we're really
bad basketball players we'd now need to try an average of 1/(1/10) or 10 throws
before we sink that perfect shot.
The mean and cumulative frequency of the geometric distribution can help you weigh your options.
Say you're at Target, and you see the display of Pokemon cards.
You really want that Pikachu card, but let's say that the probability of getting one is
1/200.
You have enough money to either buy 4 packs of cards, or Star Wars Episode VI on Blu-Ray.
Star Wars guarantees ewoks.
Pokemon means maybe Pikachu.
You're really into small cute animals...small cute animals with Static ability...even better.
You want that Pikachu.
Is is worth it?
If each pack of Pokemon cards has 10 cards, you'll have 40 cards, each with a 1/200
chance of being a coveted Pikachu.
The probability that you wouldn't get a Pikachu until your 40th card is only about
.04 %, but the cumulative probability that you'd get a Pikachu on your 40th card or
earlier is about 18%, which isn't bad.
So now you're left to decide whether it's worth it to forgo an evening with ewoks for
an 18% shot at getting your beloved Pikachu.
That part is something statistics can't decide for you.
Before we wrap up probability...let's look a really fun statistical paradox...the birthday paradox.
There are 365 birthdays that anyone can have, we're not going to count leap days-- to
keep things simple.
So let's say there are 20 people in your classroom.
What's the likelihood that there would be any shared birthdays?
To me...it seemed like it'd be pretty low.
Let's assume that there's an equal probability of having a birthday on each day of the year.
That's not quite true, but it's close enough.
The first person we look at has a 100% chance of having a unique birthday, simply because
we haven't looked at anyone else yet.
The second person also has a pretty high chance of having a unique birthday, they could be
born on any of the 364 days on which person #1 wasn't born, so there's a 364/365 chance
of having a unique birthday.
Similarly person #3 can be born on any of the 363 days on which neither person #1 or
person #2 are born, so there's a 363/365 chance that they'll have a unique birthday as well.
And this pattern continues for all the people in the room.
By the 20th person, there is a 346/365 chance that they have a unique birthday.
Using the multiplication rule, we know that the probability of ALL of these events happening--in
other words each person having a unique birthday-- is the product of all these probabilities.
So the probability that everyone has a unique birthday is about 59%.
That means that the other 41% of the time at least two people will share a birthday.
Once you get up to a group of 70 there's a 99.9% chance of someone will be sharing a birthday with someone else.
This is one of those instances where statistics trumps my own intuition.
And a good reason to be prepared for the possibility of double cupcakes if you have a big class.
Probabilities are important.
They're things we use all the time.
When you're at your local diner and see those super cool Crane machines, you might
estimate the probability that you can snag that sweet stuffed otter by the time your
food arrives and whether it's worth your time and money to even try.
Or you can use them to figure out that on average, you'll probably have to wait a
looooong time before you win the California State Lottery , like a really long time, on
average it should take you about 15 million tries.
That's a lot o' lotto tickets.
Brandon made me say that.
Geometric probabilities, and probabilities in general, allow you to guess how long you'll
have to wait for something, so you can decide whether it's worth it.
As the famous mathematician Pierre-Simon Laplace once said, probability "is basically just
common sense reduced to calculus; it makes one appreciate with exactness that which accurate
minds feel with a sort of instinct, often without being able to account for it."
In other words, it allows us to quantify things we already feel.
Probability assigns numbers to common sense.
And we all need a little more of that.
Thanks for watching, I'll see you next time.
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Constable Kile Blanchard Named Police Officer of the Year | @TorontoPolice @TorontoRBOT - Duration: 2:58.
So presenters, please stand by, we have one last honour to bestow, and that of
course is to announce the 2017 Police Officer of the Year....
Constable Kile Blanchard... (applause)
In January 2015 Constable Kile Blanchard was working at
43 Division and a Youth and Family Violence Unit he had received
information that a father had been sexually assaulting his daughter on a
regular basis during the investigation and lengthy court proceedings, Constable
Blanchard and the victim developed a very strong rapport... this is where the person
came through... Constable Blanchard worked with various
organizations to ensure the victim received the proper support and
counseling that she needed. He also cancelled a contacted T.R.O.O.P. and arranged
to send this girl on a camping trip. This experience allowed this girl to shine,
and show who she really was, and rise above, and as a result of all of this
hard work and dedication, the girl never had to testify in court, the accused pled
guilty to various charges, and due to her strong rapport with Constable Blanchard,
the girl returned to disclose further abuse at the hands of another family
member who was also charged with multiple sexual offences offences. That
is incredible..... [Constable Blanchard] it's an honour and privilege to work for the Toronto Police
Service and this is...shocking and exciting ... everyone here tonight....
their stories are fantastic just an honour to serve with them. I think everyone
here's a winner. I can tell you that it was a team effort, it wasn't just me
I just happened to be the case manager that case there was several other people
in my office that I worked with - in concert with - with not even just police
officers, but other agencies Victim Witness boost of the Children's Aid
Society it just goes to show what a team effort can do and I just hope that the
victim in this case and I know what the victim of this case is doing well and
much better and I wish that she continues to do so and we all work
together - like I said - with other agencies and our outcome and our goal is to
provide the best services for them and I think in this example so far this victim
hasn't had to testify and that's a huge thing and she's been put in the proper
support systems and hopefully that's gonna mean the difference for her in the
future. Being a Toronto Police Officer means everything to me. It's the only
service I've ever applied to and this is the only service that I want to serve
and like I said it's the people that you work with every day that makes the
difference and I hope to have several more successful cases like this and I
know we will as a team.
(music)
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BREAKING NEWS !!! Samsung Galaxy S7 And S7 Edge Android Oreo Update Has Been Paused Temporarily - Duration: 1:53.
Samsung recently released the Android Oreo update for the Samsung Galaxy s7
and the galaxy s7 edge now it looks like the update has been paused because some
people were having issues with their handsets after installing it some owners
of the handsets have reported that their device has been rebooting after
installing the update samsung has now decided to put the update on hold until
they get the issue resolved a spokesperson from Samsung's European
help forum has said that following a limited number of cases where galaxy s7
devices have rebooted unexpectedly with the Android 8.0 Oreo we have temporarily
stopped the rollout of the update we are investigating the issue internally to
ensure that the impact to the affected devices is minimized and the rollout of
the update can resume as quickly as possible
it is not clear as yet on how long it will take Samsung to fix this issue and
restart the update as soon as we get some more details we will let you guys
know if you have installed the update on your handset and have had this issue
please leave a comment below and let us know
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Oomiya Jinja - Oshima Tokyo Island - 大宮神社 - 4K Ultra HD - Duration: 3:33.
Oomiya Jinja is a nice little Shinto shrine located on the west side of Oshima Island.
While not a lot of information is available on this shrine, it is said that it used to be located on the northern part of the island
before a fire destroyed not only the temple but also the surrounding area.
What makes Oomiya Jinja unique to our eyes is its beautiful and long approach that step by step
will guide you through a dense and almost mystical forest surrounded by some small stone structures and alters.
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Introduction to the immune system - Duration: 16:20.
Despite being surrounded by harmful microorganisms, toxins, and the threat of our own cells turning
into tumor cells, humans manage to survive; largely thanks to our immune system.
The immune system is made up of organs, tissues, cells, and molecules that all work together
to generate an immune response that protects us from microorganisms, removes toxins, and
destroys tumor cells - hopefully not all at once!
The immune response can identify a threat, mount an attack, eliminate a pathogen, and
develop mechanisms to remember the offender in case you encounter it again - all within
10 days.
In some cases, like if the pathogen is particularly stubborn or if the immune system starts attacking
something it shouldn't like your own tissue, it can last much longer, for months to years,
and that leads to chronic inflammation.
Your immune system is like the military - with two main branches, the innate immune response
and the adaptive immune response.
The innate immune response includes cells that are non-specific, meaning that although
they distinguish an invader from a human cell, they don't distinguish one invader from
another invader.
The innate response is also feverishly fast - working within minutes to hours.
Get it?
"Feverishly" - that's cause it's responsible for causing fevers.
The trade off for that speed is that there's no memory associated with innate responses.
In other words, the innate response will respond to the same pathogen in the exact same way
no matter how many times it sees the pathogen.
The innate immune response includes things that you may not even think of as being part
of the immune system.
Things like chemical barriers, like lysozymes in the tears and a low pH in the stomach,
as well as physical barriers like the epithelium in the skin and gut, and the cilia the line
the airways to keep invaders out.
In contrast, the adaptive immune response is highly specific for each invader.
The cells of the adaptive immune response have receptors that differentiate one pathogen
from another by their unique parts - called antigens.
These receptors can distinguish between friendly bacteria and potentially deadly ones.
The trade off is that the adaptive response relies on cells being primed or activated,
so they can fully differentiate into the right kind of fighter to kill that pathogen, and
that can take a few weeks.
But the great advantage of the adaptive immune response is immunologic memory.
The cells that are activated in the adaptive immune response undergo clonal expansion which
means that they massively proliferate.
And each time the adaptive cells see that same pathogen, they massively proliferate
again, resulting in a stronger and faster response each time that pathogen comes around.
Once the pathogen is destroyed, most of the clonally expanded cells die off, that's
called clonal deletion.
But some of the clonally expanded cells live on as memory cells and they're ready to
expand once more if that pathogen ever resurfaces.
Now, it's time to meet the soldiers - which are the white blood cells or leukocytes.
Hematopoiesis is the process of forming white blood cells, as well as red blood cells, and
platelets and it takes place in the bone marrow.
Hematopoiesis starts with a multipotent hematopoietic stem cell which can develop into various cell
types - it's future is undecided.
Some become myeloid progenitor cells whereas others become lymphoid progenitor cells.
The myeloid progenitor cells develop into myeloid cells which include neutrophils, eosinophils,
basophils, mast cells, dendritic cells, macrophages, and monocytes, all of which are part of the
innate immune response and can be found in the blood as well as in the tissues.
The neutrophils, eosinophils, basophils, and mast cells are considered granulocytes, because
they contain granules in their cytoplasm, and the trio of neutrophils, eosinophils,
and basophils are also referred to as polymorphonuclear cells, or PMNs, because they're nuclei contain
multiple lobes instead of being round.
The mast cells, aren't considered PMNs because their nucleus is round.
During an immune response, the bone marrow produces lots of PMNs, most of which are neutrophils.
Neutrophils use a process called phagocytosis - that's where they get near a pathogen
and reach around it with their cytoplasm to "swallow" it whole, so that it ends up
in a phagosome.
From there, the neutrophils can destroy the pathogen using two methods - they can use
their cytoplasmic granules or oxidative burst.
First, the cytoplasmic granules fuse with the phagosome to form the phagolysosome.
The granules contain molecules that lower the pH of the phagolysosome, making it very
acidic, and that kills about 2% of the pathogens.
Now, the neutrophil doesn't stop there.
It keeps swallowing up more and more pathogens until it's full of pathogens, and at that
point, it unleashes the oxidative burst.
During an oxidative burst, the neutrophil produces lots of highly reactive oxygen molecules
like hydrogen peroxide.
These molecules start to destroy nearby proteins and nucleic acids - a bit like the neutrophil
dumping bleach on itself and then lighting itself on fire.
This process kills the neutrophil - a bit of a suicide mission - but each neutrophil
takes out a lot of pathogens with it.
Now, in comparison to neutrophils, eosinophils and basophils are far less common.
They both contain granules that contain histamine and other proinflammatory molecules.
Eosinophils stain pink with the dye eosin - which is where they get their name.
Eosinophils are also phagocytic, and they're best known for fighting large and unwieldy
parasites because eosinophils are much larger than neutrophils and have receptors that are
specific for parasites.
Unlike neutrophils and eosinophils, basophils are non-phagocytic.
They stain blue with the dye hematoxylin, and like eosinophils they can be helpful at
combatting large parasites but also cause inflammation in asthma and allergy responses.
Finally, there are the mast cells which are also non-phagocytic and they're involved
in asthma and allergic responses.
Next up are the monocytes, macrophages, and dendritic cells which are also phagocytic
cells - they gobble up pathogens and release cytokines - tiny molecules that help attract
other immune cells to the area.
Monocytes only circulate in the blood.
Some monocytes migrate into tissues and differentiate into macrophages, which remain in tissues
and aren't found in the blood.
Other monocytes differentiate into dendritic cells which roam around in the lymph, blood,
and tissue.
When dendritic cells are young and immature they're excellent at phagocytosis, constantly
eating large amounts protein found in the interstitial fluid.
But when a dendritic cell phagocytoses a pathogen for the first time - it's a life-changing,
coming of age moment.
Mature dendritic cells will destroy the pathogen and break up it's proteins into short amino
acid chains.
Dendritic cells will then move through the lymph to the nearest lymph node and they'll
perform antigen presentation which is where they present those amino acid chains - which
are antigens - to T cells.
Antigen presentation is something that can be done by dendritic cells, macrophages residing
in the lymph node, and monocytes which can travel to a lymph node after phagocytosing
a bloodborne pathogen - which is why all of these cells are referred to as antigen presenting
cells.
Now, only T cells with a receptor that can bind to the specific shape of the antigen
will get activated - that's called priming.
It's similar to how a lock will only snap open when a key with a very specific shape
goes in.
However, T cells can only see their antigen if it is presented to them on a silver platter
- and on a molecular level that platter is the Major Histocompatibility complex or MHC
for short.
So the antigen presenting cell will load the antigen onto an MHC molecule and display it
to T cells - and when the right T cell comes along - it binds!
Now the other group - the lymphoid progenitor cells - become lymphoid cells which are the
B cells, natural killer cells -quite a name huh?, and the T cells, which we've already
talked a little about.
B cells and NK cells complete their development where they started - in the bone marrow, whereas
some lymphoid progenitor cells migrate to the thymus where they develop into T cells.
All of the lymphocytes are able to travel in and out of tissue and the bloodstream.
NK cells are large lymphocytes with granules and they target cells infected with intracellular
organisms, like viruses, as well as cells that pose a threat like cancer cells.
NK cells kill their target cells by releasing cytotoxic granules in their cytoplasm directly
into the target cell.
These granules contain some molecules that cause target cells to undergo apoptosis which
is a programmed cell death and some that punch holes in the target cell's membrane by binding
directly to the phospholipids and creating pores.
B cells, like T cells, also have a receptor on their surface that allows them to only
bind to an antigen that has a very specific shape.
The main difference is that B cells don't need antigen to be presented to them on an
MHC molecule, they can simply bind an antigen directly.
When a B cell binds to an antigen that's on the surface of a pathogen, it is capable
of phagocytosis and antigen presentation - so technically, they're also antigen presenting
cells as well.
Like other antigen presenting cells, the B cell will load the antigen onto an MHC molecule
called MHC II, and display it to T cells.
When a T cell gets activated it helps the B cell mature into a plasma cell, and a plasma
cell can secrete lots and lots of antibodies.
Typically, it takes a few weeks for antibody levels to peak.
The antibodies, or immunoglobulins, have the exact same antigen specificity as the B cell
they come from.
Antibodies, are just the B cell receptor in a secreted form, so they can circulate in
serum, which is the non-cellular part of blood - attaching to pathogens and tagging them
for destruction.
Because antibodies aren't bound to cells and float freely in the blood, this is considered
humoral immunity - a throwback to the term "humors" which refers to body fluids.
Now the final type of lymphoid cell is the T cell and its in charge of cell mediated
immunity.
T cells are antigen specific, but they can't secrete their antigen receptor.
A naive T cell can be activated or primed to allow it to turn into a mature T cell by
any of the antigen presenting cells, but most often it's done by a dendritic cell.
Now, there are two main types of T cells, CD4 T cells and CD8 T cells - where "CD"
stands for cluster of differentiation.
There are hundreds of CD markers in the immune system, and these CD markers are useful in
telling them apart.
For example, all T cells are CD3+, because CD3 is part of the T cell receptor.
So, CD4+ T cells, are actually CD3+CD4+, and these cells are called helper cells because
they're like generals on the battlefield, they secrete cytokines that help coordinate
the efforts of macrophages, B cells, and NK cells.
Helper T cells can only see their antigen if it is presented on an MHC II molecule.
CD8+ T cells are CD3+CD8+, and they're called cytotoxic T cells because they kill target
cells, really similarly to how NK cells do it with one major difference.
CD8+ T cells only kill cells that present a specific antigen on an MHC I molecule - which
is structurally similar to the MHC II molecule, whereas NK cells aren't nearly as specific
in who they kill.
So now let's go through a complete immune response with a bacterial pathogen in the
lungs.
To start, the bacteria will have to get breathed in, slip by your nose hairs, past the cilia
in the airways, and will then have to penetrate past the epithelium layer of the lungs.
Once it's in the lung tissue, the bacteria will start to divide and might encounter a
resident macrophage in the lung tissue which will ingest the bacteria and start releasing
cytokines.
Those cytokines start the inflammatory process by making blood vessels leaky and attracting
nearby eosinophils, basophils, and mast cells, which release their own cytokines and granules
amplifying the inflammation.
Neutrophils from the blood as well as fresh new ones from the bone marrow dive into the
tissue and join the battle.
If the pathogen was a virus, NK cells would help destroy the the infected cells at this
point.
Around this point in the infection, immature dendritic cells digest the pathogens and move
from the lung tissue over to a nearby lymph node where they present the processed antigen
on an MHC II protein to a naive T cell.
Sometimes, if the infection is spreading, bacteria might find its own way to a lymph
node without the help of the dendritic cell.
In this case, B cells might directly phagocytose the bacteria and present it to a naive T CD4+
cell.
Either way, if the antigen is the right "fit" for the T cell it will begin to differentiate
and undergo clonal expansion.
Differentiated CD4+ T cells will release cytokines that will induce B cells to differentiate
into plasma cells which secrete antibodies that will go into the lymph and then the bloodstream.
The antibodies will tag pathogens making it easier for phagocytes to eat them.
Once again, at this point, if the pathogen was a virus, the CD8+ T cells would kill any
infected cells that express the viral antigen on an MHC I.
Over time, as the invading pathogen dies off, most of the B and T cells die of neglect,
but a few turn into memory B cells and memory T cells, which linger for years in case their
needed in the future.
So, to recap - the immune system has innate and adaptive response.
The innate immune response is immediate, but non-specific, and lacks memory, whereas the
adaptive immune response is highly specific and remembers everything, but it takes several
days to get started and almost two weeks to peak.
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Les Marseillais Australia: Camille explique pourquoi Jessica l'a prise sous son aile ! - Duration: 3:18. For more infomation >> Les Marseillais Australia: Camille explique pourquoi Jessica l'a prise sous son aile ! - Duration: 3:18. -------------------------------------------
Anticipazioni Uomini e donne, la scelta di Sara: la promessa damore di Lorenzo - Duration: 4:13.
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Al Bano si confessa da Costanzo e va in onda la dichiarazione d'amore a Romina Power - Duration: 11:58.
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Baratunde Cola: From Football to Nanotechnology - Duration: 4:16.
I was a curious kid. I think that I started having an interest in books and
things and widgets and fixing things when I was young. But I think centrally I
always just wanted to be someone that made a difference. I convinced myself as
a kid that I could do that playing sports and doing engineering. And fortunately
I got to do a little bit of both. Vanderbilt's a good place to do that.
So I walked on; I was a walk-on. You know, if you're a scholarship player and you have a lab
and you got to miss practice, that's one thing. But if you're a walk-on and you're
trying to get respect and you have to miss practice for a lab, that's a
challenge. And I was put in those situations and had to deal with that, and
it was not easy. I had several semesters where I had 18 or 19 hours and you know,
that's, you know, those semesters you really don't have a life outside of
school and football. But I had a happy ending with it all. I, you know, came back,
I got a scholarship my last year, and I was the starting fullback, and scored a
couple touchdowns, so that was awesome. But it was hard. It's a
challenge, but it does shape you to be disciplined, and to learn how to manage
your time, all these basic life skills that you eventually have to get to be a
successful adult, you get those earlier when you balance sports and engineering.
I applied to one graduate institution, which is Purdue. I enjoyed it! It was one
of the best decisions I've made in my life.
The environment was perfect to do a PhD, great resources, great people. I was the
first graduate student. first student to move into the Birck Nanotechnology
Center. This great nano center is gonna be the best in the country.
I take a lot of pride saying that I was the first student there. I spent a
lot of late nights in that cleanroom. But I always considered it a privilege. And I
still talk about that today, that a select few people get the opportunity to go in
there and to chase their dreams, to have a chance to make something that never
existed before, a reality. To make it happen, right? That's my experience
at Purdue, and it is happening. The carbon nanotubes, which I worked on with Tim
Fisher, is a magical material, that
because it's made of carbon, when you combine them together, they do a lot of
amazing things. They're ten times stronger than steel, they are eight times
more conductive than copper. So they have all these fantastic properties. And what
I worked on was the thermal property. The fact that they can basically be the new
standard of thermal transfer in industry. It's the first new thermal material in
150 years, really. So Carbice Corporation commercializes
vertically aligned carbon nanotubes, the same material that I came to Purdue to
study, and I got my PhD on. We make the world's new standard of thermal adhesive.
We released two products last year: Space Tape and Infinity Tape. Space Tape has
become the leading product for assembling electronic components in
space builds, for satellites and vehicles. And Infinity has become a leading
product that's really changed how things are done in the chip making business.
Purdue is a special place, and a special community for one to develop oneself
into a better person. When you're here, you have an opportunity to be immersed
in this intentional experience of being in the Boilermaker community. To me,
there's no better training for life, and the challenges of the complex world that
we live in, and all the information being thrown at us today, to be able to filter
through. How do you filter through that information in a logical, thoughtful way?
These are the things that engineering teaches you, and this is why it's,
you know, there's no surprise why you have engineers that are the leaders of
our best Fortune 500 companies. Why there are engineers that are stalwarts in
their community. Peel back the layers of society, and that engineering training
shows up in places that you never could even imagine yourself being.
-------------------------------------------
Topolino Hackerino: La Conquista Del Mondo! | [HD] [1 Ep] [Sottotitoli] - Duration: 3:22.
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Striscia la Notizia difende Barbara D'Urso, una trappola nei suoi confronti? - Duration: 4:03.
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✅ Andrea Damante reagisce all'ospitata di Giulia De Lellis a UeD - Duration: 3:20.
Uomini e Donne: Andrea Damante commenta l'ospitata di Giulia De Lellis Andrea Damante e Giulia De Lellis sono la coppia che per ben due anni hanno fatto sognare i telespettatori di Uomini e Donne
Purtroppo, la loro storia d'amore è terminata qualche settimana fa e da allora i rapporti tra i due non sono dei migliori
Anche se da quel momento hanno deciso di non apparire più nei salotti televisivi più importanti
O almeno fino ad ora. L'esperta di tendenze più famosa del piccolo schermo è stata ospite della trasmissione ideata e condotta da Maria De Filippi su canale 5, proprio durante la scelta di Nilufar
Giulia De Lellis, durante la sua breve ospitata, si è lasciata andare alle lacrime, ripensando al momento in cui lei è stata la scelta del bel dj veronese a Uomini e Donne
Come prevedibile, la reazione di Andrea Damante sui social non è tardata ad arrivare
Ha scritto l'ex tronista di Maria De Filippi. Ovviamente, nemmeno la reazione dei fan della coppia è tardata ad arrivare, che in massa hanno ancora una volta accusato il dj di aver tradito la sua ormai ex fidanzata
Giulia De Lellis piange a Uomini e Donne pensando ad Andrea Damante Giulia De Lellis si è commossa a Uomini e Donne
Molto probabilmente, come già vi abbiamo accennato, essere ospite del programma di Maria De Filippi proprio durante il momento della scelta le avrà ricordato quei momenti in cui era lei a trovarsi sulla famosa sedia rossa, aspettando che Andrea Damante la scegliesse tra le tante ragazze presenti in studio
Purtroppo la favola dei due è durata meno del previsto e i fan sono sempre più curiosi di scoprire i motivi che hanno spinto i protagonisti di Uomini e Donne a dirsi addio
Sempre più insistenti sono le voci che vedrebbero Andrea Damante nei panni del traditore seriale
Giulia De Lellis, durante le poche volte che parlato della vicenda, sembrerebbe in un certo senso confermare le indiscrezioni trapelate in rete
I due, recentemente, si sono perfino incontrati a Verona. Ovviamente, l'incontro è stato del tutto casuale, visto che vivono nella stessa città e a pochi metri di distanza
In molti, tra l'altro, credono che la bella esperta di tendenze possa presto salire sul trono per avere la sua rivalsa
Sarà vero o sono soltanto sogni dei fan del programma?
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