Why are Dead Bugs Always on Their Backs?

Why are Dead Bugs Always on Their Backs?


[ intro ] You might notice something odd about those
flies you just swatted, or the cockroaches you nuked with insecticide. It seems like they almost always wind up on
their backs. And that’s not your imagination. Dead bugs really do end up belly up quite
often thanks to a combination of physics and biology. If you think about the shape of your typical
insect, like a cockroach or fly, it’s rounded with fairly thin legs relative to its body. That means most of its body weight is concentrated
near the top of its body, so it has a high center of mass. That’s the point of an object where external
forces like gravity appear to act. And the higher it is, the less tilt is required
before it’s no longer over the object’s base—at which point the object, or insect
in this case, topples. In fact, many bugs would just tip over if
it weren’t for the constant work of their teeny leg muscles—they’re pretty much
always doing a push up to stay upright. Sure, a bug will occasionally stumble onto
its back or purposely roll over as a defense mechanism. But whenever it finds itself in a supine position,
it can right itself with a little coordinated leg or wing action. There’s even one family of insects called
click beetles that launch themselves into a somersault to land right way up. But that all kind of falls apart when an insect
is injured or sick because it loses the ability to perform complex muscular movements. I mean, just picture trying to do a cartwheel
when you’ve got the flu or a broken arm. And any weakness in those leg muscles and
they’ll naturally curl inwards, a bit like how your fingers curl when you rest your hand. Curled legs can’t support that top-heavy
body. The chemicals used to kill bugs also usually
mess with their nervous system directly. Insecticides generally contain neurotoxins,
like organophosphates or pyrethroids, which cause convulsions or paralysis in insects
by over-stimulating or inhibiting their neuronal signals. Either way, the loss of muscular coordination
combined with a high center of mass means the animal probably ends up on its back before
it dies. In fact, if you see a bug on its back, it’s
likely not long for this world. In a 2002 study on Mediterranean fruit flies,
researchers found that as flies aged, they were more likely to go belly up temporarily—and
when that happened, their chances of dying jumped by close to 40 percent. Bugs pretty much never choose to be supine
unless they’re playing dead, so their inability to get up quickly is probably an indicator
that something is wrong. Thanks to our patron Carol for asking, and
to all our other patrons that voted for this question in our Patreon poll. If you want to suggest questions like this
one, vote on which questions we should answer, or just get some really cool rewards like
exclusive blooper reels, you can head over to Patreon.com/SciShow to learn more about
becoming one of our patrons. [ outro ]

Mathematics of Epidemics | Trish Campbell | TEDxYouth@Frankston

Mathematics of Epidemics | Trish Campbell | [email protected]


Translator: Yifat Adler
Reviewer: Hussain Laghabi It starts with just one person, and after 8 hours
100 have been infected. 16 hours later, 10,000 people. And a million after the first day. How many people by tomorrow? This is the story of #TheDress. And was it blue and black?
Or was it white and gold? [Laughter] This question was first posed
by a Facebook user who was a family member
of the person who owned the dress. There had been a disagreement
about the color of the dress, and later another user
posted the photo on Tumblr and the rest is history. With over ten million tweets
in the first week, this is an extreme case of going viral. So, let’s take a look at how
#TheDress spreads through a population. The population is divided
into three groups of people. People who haven’t seen the dress, people who have seen
and have started sharing the dress, and people who are
no longer sharing the dress because they’re sick of the dress and never want to hear about it again. And people change groups over time. So, how do the numbers
in each of these groups change? Well, the people who
haven’t seen the dress reduce by the number of people
who start sharing the dress. So, they see it and they start sharing. And the more people that we have sharing, the more new sharers that we get. The people who are sharing the dress increase by the number
of new sharers that we get. But they also decrease by the number
of people who give up sharing. And the people who are
no longer sharing the dress just keep increasing
by the sharers who give up. And we can track what happens to the numbers of people
sharing the dress over time. So, here in a population of ten million. The number of people sharing the dress
starts growing very slowly at first. But then it starts to take off. And once it does so,
it does so very rapidly, and reaches about 4 million people
sharing at any one time up to just a day and a half. Then the numbers fall away to nothing. At the same time, the number of people
who haven’t seen the dress reduces slowly at first and then plummets,
as they start to become new sharers. And the number of people
who are no longer sharing the dress rises really slowly at first
and then it quite reaches its maximum. So, why does the dress stop spreading? Has everybody in the population
seen the dress? Well, no. By the time that
the dress stops spreading, not everybody has seen it. The number of people
who are no longer sharing the dress never quite reaches back up
to a population of ten million. It stops because the people
that are sharing the dress can’t find any new people
to share it with. So they lose interest before they get
to pass it on to anybody else. And, so, the sharing numbers
drop to zero. This is a very simple picture
of how #TheDress spreads in population. And they’ve ignored some realities, like, not everyone has computers
or internet access and not everyone is interested
in sharing memes. So, even if they see it,
they won’t share it. And people have different numbers
of virtual friends. So, it’s not an exact representation, it’s a model, one that is based on
a set of assumptions. So, why should we even care about how a meme spreads through the internet? Well, it turns out that going viral
has its origin in the term virus. So, the way that a meme spreads
through the internet shares many characteristics with the way that an infectious disease
spreads through a real population. So, diseases like Ebola or influenza,
whooping cough, or measles… And fortunately none of these diseases,
or indeed any others known to man, spread any way near as quickly
as #TheDress does through a population. So, while it’s very difficult to stop
a meme such as #TheDress from spreading once it starts going, we’ve got an arsenal of weapons
with which to fight infectious diseases. Vaccines, antibiotics, quarantine,
just to name a few. And a very powerful weapon
behind the scenes: mathematics. Using mathematics to study
infectious diseases isn’t new. A scientist called Daniel Bernoulli
first used probability and statistics nearly 250 years ago to calculate the benefits
of vaccination against smallpox. And the model that I used
to describe the spread of #TheDress has actually been used by epidemiologists
for nearly a hundred years. It’s used to investigate the causes
and spread of infectious diseases and to help develop strategies
to prevent and control them. So, just like we did with #TheDress, we now have a population
that’s made up of people who are susceptible to catch a disease. People who are infectious
and spreading the disease, and people who have recovered
and can no longer pass on the disease. And people will move from these groups. This is called an SIR model, and it’s the basic infectious
disease model. Just like we did with #TheDress, we can keep track of the number of people that are in each
of these groups over time. But just like #TheDress,
we’re also ignoring a lot realities which influence the spread
of infectious diseases. And importantly what we are doing as well
is assuming that everybody in these groups has identical characteristics
and behaviors. And not many diseases or populations
behave quite so simply. So, we often have to allow for
new members to join the population, or for old members to leave. Or we have to account for the fact that for some diseases
just because you’ve had them, it doesn’t mean
that you can’t have them again. And we need to add in vaccination
and treatment for some diseases as well, if we really want to know
how they spread through a population. So, we can run virtual experiments
to answer questions like: how many cases could we prevent
if we had an effective vaccine against Ebola, for example? We can answer questions that
we can’t answer using real people. Sometimes because
the type of experiments that we would need to run
in a population are unethical. And at other times, just because collecting information
is really just too difficult. So, bear in mind that when these models were
first developed a hundred years ago, all the calculations
would have been done by hand. So, increasing computational power,
though, has meant that the process of mathematically modeling
infectious diseases has got much much faster, and we can now add
a lot more data into models to try and build a match
what’s really happening in a population. So, in this era of big data with rapid advances
in science and technology, we are seeing a rapid evolution in
the field of infectious disease modelling. So, here is just a few of the things
that are happening. We now have individual base models which follow the history
of individuals in a population and track the information that changes
their chance of catching a disease. So, things like their infection history,
their vaccination history, the number and ages of people
that they live with. People are even now using
radio frequency identification tags to start collecting information
on how people contact other people, how they move through a population. Because how you mix with
other members of a population is very important
to the spread of infectious disease. So, we’ve gone from modeling
groups of people in a population to modeling individual characteristics
and behaviors of individuals, to modeling the genomes,
the genetic material of the organisms that actually cause disease,
viruses and bacteria. And we are doing that so we can
find out who patient zero was, and to look at how the infection
has spread through a population. And we’re also using mathematics
to investigate how infectious diseases,
viruses and bacteria actually spread within a human body, and how our immune system
is fighting back. And all of this work is hoping
to give us a better understanding of how infectious diseases spread
and how we can stop them. In my lifetime, we’ve seen
the eradication of smallpox. And we’re on track to see
the eradication of polio in yours. Through careful planning aided by
the use of mathematical models, we wipe diseases that have caused millions of deaths
off the face of the Earth. But infectious diseases isn’t
the only application of mathematics to health problems. There are many biological processes
that are still a mystery and lend themselves
to mathematical exploration. So, what questions will you
answer using mathematics? Thank you.
[Applause]

So … Sometimes Fireflies Eat Other Fireflies | Deep Look

So … Sometimes Fireflies Eat Other Fireflies | Deep Look


If you think there’s something romantic
about fireflies glowing on a warm summer night… You’d be right. But what you don’t see, is the dark side
of this luminous display. Firefly flashes are a secret code, a language
of light. The light comes from a masterful bit of chemistry. A bioluminescent reaction that generates light
but no heat. So what are they saying? Well, males on the wing are advertising themselves
to females with a bit of sexy skywriting. Take the common Eastern firefly. His signature move? A fishhook-shaped maneuver. Which is why his species is sometimes called
the “Big Dipper.” Her reply is more subtle: a single, slow pulse
from her heart-shaped lantern. Our “Big Dipper” comes bearing a “nuptial
gift,” a present of more than 200 assorted nutrients… kind of like a box of chocolates. Here’s the handoff. Some are lucibufagins — defensive chemicals
fireflies secrete to ward off predators like spiders and birds. These defensive chemicals may help protect
her. Firefly codes are so reliable that anyone
can speak the language. But we’re not the only codebreakers listening
in. Meet Photuris. She’s also a firefly — a larger, stronger
one than the Big Dippers. But she has a weakness. Her species can’t make its own lucibufagins. They have fewer defenses against predators. So she sets a trap to get some. She mimics the glow of other firefly females
— luring in the males of that species. When Mr. Big Dipper shows up with his chemical
gift, she moves in… sucks up those defensive chemicals that she
desperately needs… …then makes a meal of the rest of him. Most fireflies don’t even eat during the
few weeks they spend as adults. But he’s not totally defenseless. If she’s not quick enough, he can secrete
a gooey compound that sticks in her jaw and lets him escape. Another gift from the master chemist. Hey there, it’s Lauren. I know you see that ‘Subscribe’ button there. Here’s what it’ll get you. New Deep Look episodes every two weeks. Keep up with all the weird, gross, and wonderful
things we’re working on. Thanks, and see you soon.

How Mosquitoes Use Six Needles to Suck Your Blood  |  Deep Look

How Mosquitoes Use Six Needles to Suck Your Blood | Deep Look


This is the deadliest animal in the world. Mosquitoes kill hundreds of thousands of people
each year… the most vulnerable people: children, pregnant women… No other bite kills more humans… or makes
more of us sick. So what makes a mosquito’s bite so effective? For starters, they’re motivated. Only females bite us. They need blood to make
eggs… And a pool of water for their babies to hatch in. Even a piece of trash can hold enough. At first glance, it looks simple — this mosquito
digging her proboscis into us. But the tools she’s using here are sophisticated. First, a protective sheath retracts – see
it bending back? If you look at a mosquito’s head under a
microscope, you can see what that sheath protects. And inside *there* are six needles! Two of them have tiny teeth. She uses those to saw through the skin. They’re so sharp you can barely feel her pushing. These other two needles hold the tissues apart while she works. From under the skin, you can see her probing, looking for a blood vessel. Receptors on the tip of one of her other needles pick up on chemicals that our blood vessels exude naturally and guide her to it. Then she uses this same needle like a straw. As her gut fills up, she separates water from the blood and squeezes it out. See that drop? That frees up space to stuff herself with
more nutritious red blood cells. With another needle, she spits chemicals into us. They get our blood flowing more easily, and give us itchy welts afterwards. And sometimes, before she pries herself away, she leaves a parting gift in her saliva: a virus or a parasite that can sicken or kill
us. There’s nothing in it for her. The viruses
and parasites are just hitching a ride. But this is what makes mortal enemies out of us
and mosquitoes. They take our blood. Sometimes we take theirs.
But often, not soon enough. Good. You’re still there. . These are the
larvae of Culex pipiens, a.k.a. the common house mosquito here in California. Gross, right?
Well, you can avoid them by emptying your rain gutters. Pet water dishes too. While
you’re at it, subscribe! We have so many more science videos coming your way. See you next
time!

Craft an Insect! | Project for Kids

Craft an Insect! | Project for Kids


Hi everyone! Squeaks and I were just outside,
and while we were enjoying the sun, we spotted a few different insects. They were so colorful and wonderful to look
at, that we thought we would make some insect-inspired art to brighten up our lab! We’ve talked about insects before on SciShow
Kids, so you may remember what makes an insect an insect. One thing that all insects have in common,
is that they have three main body parts! There’s the head … …the part in the middle is called the thorax… …and the abdomen at the end! The second thing that makes an insect an insect
is that they have an exoskeleton. Insects don’t have bones the way we do, instead
they have hard skeletons on the outside of their body that they use to stand up, move
around, and protect their insides. The final thing that makes an insect different
from other animals is the number of legs they have! Do you remember how many? That’s right: six! So keeping these things in mind, let’s make
some insect art! I’m going to make my insect out of construction
paper, but you can paint your insect, make it out of clay, or use stuff you find around
your house! If you want to follow along with me and use
construction paper, you’ll need scissors, glue, a pencil, pen or crayon, and a few different
markers. Remember, if you’re gonna use scissors, tell a grown up! First, I’m gonna to choose a few different
colored pieces of paper to make my head, thorax, and abdomen. Now that I have my colors, I’ll start off by marking where I want to
cut with my pencil. Now that I have my insect parts outlined,
I’ll cut the different shapes out. Once I’ve cut out the shapes, I’ll glue
them together. Remember which goes where? The head goes wherever you want the front
to be… …the thorax goes right in the middle… …and the abdomen brings up the rear! Since our insects are flat, we won’t need
to worry about making an exoskeleton. But we should add some legs! I’ll cut another piece of construction paper into six strips, for our six insect legs. Now let’s glue them to our insect’s body.
An insect has three legs on each side, and they attach to the thorax, the middle part
of the body! That looks great! What do you think Squeaks? [Squeaks asks a question] You’re right, we should add a little personality!
How about a face? On the head of an insect you’ll find their antennae, mouth, and eyes.
So let’s add those to our insect’s head. Insects are special because they have compound
eyes. This means that each of their eyes are made up of smaller eyes that all work together to make one picture. And their mouths are different from ours because they have a mouth as well
as biting parts that help them eat! Alright! What do you think? Is she ready to
hang up in the lab? Well there you go! We made some insect inspired
art and the lab has some bright new decorations! Would you like to share your insect art with
Squeaks and me? Just grab a grown up and send us an e-mail at [email protected]! And if
you have any questions about anything at all, leave a comment down below! Thanks for joining us
on SciShow Kids! And we’ll see you next time here at the fort!

What if all Insects Disappeared? | #aumsum

What if all Insects Disappeared? | #aumsum


It’s AumSum Time. What if all insects disappeared? No worries. I have their photographs. You might think insects are inconsequential,
but the reality is. Without them, there probably would be no life
on earth. The first life to get affected, would be plant
life. Most plants in the world are angiosperms,
that is, flowering plants. Without insects pollinating them, plant life
would gradually disappear. Gradually, birds and mammals feeding on plants
would also disappear. Further, insects are food for many birds,
frogs, reptiles, etc. Without insects, they would also start dying. Then, animals eating those animals would also
start dying. This would ultimately lead to a domino effect. Finally wiping out the top of the food chain,
that is, human beings. Also, don’t be surprised, if you suddenly
see a lot of dead things everywhere. This is because insects are decomposers. Without insects, decomposition process would
take much longer. What if earth lost oxygen for 5 seconds? We would need to organize a search party. No. If it was just 5 seconds. We wouldn’t notice changes in our breathing. But do you know what would happen around us? Earth’s crust contains 45% oxygen. Without oxygen, crust would crumble. Causing the ground to crumble and we would
be in freefall. Buildings, bridges and concrete structures
would crumble into dust. As oxygen is the binding agent for concrete. Cars would stop. And planes would fall from sky as their combustion
engines wouldn’t work without oxygen. Also, losing oxygen means losing almost 21%
air pressure. This would cause our inner ear to explode,
causing hearing loss. It would also become darker suddenly. Why? For sunlight to reach us, it needs to bounce
off air particles like oxygen, dust etc. No oxygen means much fewer particles to bounce
off, thus much darker. What if the sun disappeared? We would need a lot of flashlights. No. The sun’s enormous mass and gravitational
power locks the planets in their orbits. If the sun disappeared, the earth would fly
off in a straight line into space. Earth would collapse into darkness only after
8 minutes. As sunlight takes about 8 minutes to reach
earth. Moon would disappear as it doesn’t produce
light of its own. Plants would die, as no sunlight means no
photosynthesis. Within a week, earth’s temperature would drop
below 0 degrees Fahrenheit. Dropping to negative 100 degrees Fahrenheit
within a year. Making it impossible for us to survive. Ocean surfaces would freeze. However, water in the interior would stay
liquid, due to heat from the Earth’s core. Only microorganisms who don’t require photosynthesis. Would survive by converting core’s heat into
the energy they need. Thus, without the sun, humans wouldn’t exist. What if everyone went vegetarian? Then I will turn Pizzaterian. No. Meat industry requires a lot of land to feed
and maintain livestock. This leads to deforestation and an increase
in greenhouse gases. Turning vegetarian would free up that land. Restoring at least 70% of it to natural forests. Thus cooling the planet. Also, today there are around 1 billion cows. Who excrete large amounts of methane. Methane is a deadly poisonous gas, 20 times
more harmful than other greenhouse gases. Cutting out meat would decrease methane in
the atmosphere. Human deaths would also go down. Chronic illnesses, cancers, strokes, etc. Would drastically reduce, leading to reduced
medical costs as well. However, the meat industry generates a lot
of employment. We would need to think of alternative employment
measures if everybody goes vegetarian. But the overall positive impact on the climate,
our health and the planet cannot be ignored.

Scientists Put the Brain of a Worm Into a Robot… and It MOVED

Scientists Put the Brain of a Worm Into a Robot… and It MOVED


Worms. They’re weird, primitive creatures that
seem to just squirm around senselessly. BUT this simplistic behavior is exactly what
we are looking for in our endeavours to digitize a living brain. Now look at this. This..this looks like a robot being controlled
by an ewok. But actually, this robot isn’t being controlled
AT ALL. What you are looking at is a copy of the brain
of a Caenorhabditis elegans, or C. elegans. This is the digital brain of a worm ON a computer
chip IN a lego robot. This little guy is a simulated brain navigating
on its own. Well, navigating the best way a wormbot can. The scientists put sensors on their robots
“noses” and “tails”so if they meet a wall, they know to turn around. Just like the C.elegans. But, as simple as this robot seems to be,
getting to this point took a long time. Researchers spent decades looking at each
and every cell in the C.Elegans,and at how each cell works with the cells around it. Then other researchers built a program that
could mimic that interaction.Each one of these boxes represents a neuron interacting with
the environment. They could do this, because scientists have
a complete map of every single cell in the C.Elegans and their functions. It’s the worm’s CONNECTOME, and it holds
around 1000 cells and all 302 neurons of this little worm. So, once you’ve digitized how every cell
and neuron interact, you have the digital version of the C. Elegans brain! Sort of. By simulating a brain at a cellular level,
the researchers can watch the larger aspects, like movement, emerge…naturally. Or, put another way, they turned it on and
let the wormbot be a worm… bot. To do this they took the connectome, some
algorithms, and a precise anatomical map and combined them. Then they threw it in a simulator — which
is super complicated, and I don’t really understand how it all works — but the important
thing is what happened once they flipped it on. The robot behaved like a living C.Elegans! Well, almost. The researchers are starting small. They want to get the neuron’s interacting
with the “muscles” of the robot. It still doesn’t have independent instinct,
it’s not going to start looking for food or anything yet. Those behaviours are definitely on the agenda
for our researchers, but they just want to get the digital organism moving first. Now, I know what you’re thinking, is this
a huge step towards some crazy scientists digitizing and uploading human brains into
robuts! AHH!! But, no. Not really. No. These scientists are mapping this worm’s
brain and creating an accurate digital simulation because WE still don’t know a lot about
how OUR brain works. This project’s success could completely
change the way we map and understand our own brain. Plus, with this application we could possibly
get rid of squishy living organisms in labs and could rely on computer simulations instead. There’s nothing to fear… C.elegans are only 1mm long.It will take a
while before we start digitizing your brains guys. For more science in your day, subscribe to
Seeker and are you wondering how our brains power our thoughts in the first place? We explain it right here. Did you know that the C.elegans is the first
animal and currently, ONLY animal with an entirely mapped connectome? Pretty cool. Thanks for watching.

How a Sick Chimp Led to a Global Pandemic: The Rise of HIV

How a Sick Chimp Led to a Global Pandemic: The Rise of HIV


Here at SciShow, we talk a lot about the fascinating,
complicated, and often very weird stories of discovery and collaboration that led to
the science we know today. But one of the strangest is something we haven’t
covered in much detail before, and it’s a biggie: the decades it took to figure out
exactly what HIV and AIDS were, and how to prevent and treat them. Since the start of the AIDS crisis, some 70
million people have been infected with HIV, and 35 million of those people have died. Both those numbers are staggering in their
own way, and together, they tell the story of a disease that has led to an incredible
amount of loss, but also one that — if you’re lucky enough to have access to the right medicines
— is no longer a death sentence. So, in honor of World AIDS Day on December
1, we want to tell you that story. There’s a lot to cover, so we’ll do it
in two parts. This episode, we’ll go over how we figured
out what HIV is, when the infection morphs into AIDS, and where we think the virus came
from. Next time, we’ll look back to the earliest
treatments, the arrival of antiretroviral drugs, which were complete game-changers,
and go over the creative ways scientists are now thinking about prevention and possibly
even a cure. But first, the basics. HIV, or human immunodeficiency virus, is a
retrovirus that infects immune cells, most notably what are known as CD4 T cells. The “retrovirus” part just means that
the virus uses RNA — DNA’s more wily, less stable cousin — as its genetic material,
and that once HIV infects a cell, it makes a DNA version of its genome with a special
enzyme, then inserts that DNA into the host genome. If that sounds sneaky — well, it is. And it’s part of why HIV has been so difficult
to treat, which we’ll talk about more next time. Now, those CD4 T cells that HIV infects and
ultimately kills are a kind of white blood cell known as ‘helper’ T cells. When they recognize a threat, they pump out
proteins that help coordinate a bunch of different immune responses. You definitely want them around. HIV is spread by bodily fluids, including
blood, semen, vaginal fluid, and breast milk. That’s why HIV can be transmitted through
sex, dirty needles, breastfeeding, and any other swapping of fluids you might do — with
a major exception: saliva isn’t one of those fluids. Saliva is full of other stuff that prevents
HIV from being infectious, like antibodies and a bunch of antimicrobial proteins. So unless there’s a lot of blood in your
saliva for some reason, it can’t transmit HIV. When someone is first infected, they might
feel like they have a bout of the flu, with a fever, headache, rash, sore throat, and
muscle and joint pain. That’s because the virus is infecting lots
of cells and the immune system is trying to fight it off. But within a few weeks those symptoms pass
because by then the person has specific antibodies that can keep the virus from running totally
rampant. After that, they usually feel fine for a long
time — in many cases, a really long time, like several decades. Until, one day, they don’t, because the
virus has finally killed off too many T cells, leaving the body unable to properly defend
itself against pathogens — anything that might be dangerous or infectious. That’s when someone is said to have AIDS,
or acquired immune deficiency syndrome. Usually AIDS is diagnosed once the person’s
T cell count falls below 200 cells per microliter of blood, which is well below the normal 500-1500,
or if they develop what’s called an opportunistic infection. These are infections that anyone with a reasonably
strong immune system would be able to fight off, easy-peasy. But because HIV has obliterated most of their
T cells, AIDS patients get sick. And, they can die. Most of the time it’s an opportunistic infection
that killed them. So, some of that was probably familiar to
you, but pretend for a moment that you’ve never heard of HIV or anything else I just
mentioned. Because back in the ‘80s, we didn’t know
these basic facts. All doctors knew was that suddenly, healthy
young gay men were developing extremely rare infections and cancers — and, it was killing
them. One of the first people to notice the pattern
was an immunologist at UCLA. Between the fall of 1980 and the following
spring, he saw a string of five patients, all gay men in their 20s or 30s, with an unusual
kind of pneumonia. There was a fungus growing inside their lungs. Normally, the fungus was totally harmless
and would never infect the lungs, but in these men it had, and it was making it hard for
them to breathe. The patients also had oral thrush — basically
yeast infections in their mouths — and few CD4 T cells. By June, when the immunologist wrote up the
results for the CDC’s weekly Mortality and Morbidity report, two patients had died. A month later, a dermatologist in New York
chimed in with a similarly disturbing report, this time with Kaposi’s sarcoma, a rare
cancer where patients develop blotchy purple lesions on their skin. In two and a half years, 26 young gay men
in New York and LA had been diagnosed with Kaposi’s. Some also had the weird fungal pneumonia,
and 8 had died. It’s hard to imagine now, but at this point,
scientists had no idea what was making people sick. They didn’t know if it was some sort of
toxin or a pathogen. And if it was an infection of some kind, they
didn’t know how it was spreading. That meant they couldn’t warn people about
how to protect themselves. The association with gay men, though, was
certainly striking, and early on, many called the mystery disease GRID, for gay-related
immune deficiency. Lots of people would talk about it as the
“gay cancer” or “gay plague.” But the disease wasn’t limited to gay men. It was turning up in hemophiliacs — people
whose blood doesn’t clot properly and are treated with clotting factors taken from other
people’s blood. Doctors were also seeing cases in IV drug
users, women, infants, and heterosexual men. In particular, 20 recent immigrants from Haiti
had gotten sick, and none said they were gay. Those clues were important, because they told
scientists the disease — which had finally been given the name AIDS — was probably
infectious, and probably transmitted by blood. There were other diseases that spread in similar
ways, like hepatitis B. So in March of 1983, the CDC issued a warning
that doctors needed to be careful about blood transfusions, and that the disease seemed
to spread through both gay and straight sex. Debates about the specifics, including whether
it could spread through saliva, would happen later. But what was the infectious agent? The race was on for scientists to figure out
what was causing the disease. French molecular biologist Luc Montagnier
suspected a virus because at the time, the blood products hemophiliacs used were filtered
for things like bacteria and fungi. But viruses were too small to catch. So along with his colleague Françoise Barré-Sinoussi,
he searched cells taken from AIDS patients and found a retrovirus. Around the same time, Robert Gallo at the
NIH in the US also identified a retrovirus in samples from AIDS patients. Both groups published their work in May 1983,
and shortly afterward another team found yet another retrovirus. All the viruses had been given different names,
and at first, it’s wasn’t totally obvious that they were the same thing. But they were, and in 1986, the cause of AIDS
had been given an official name: HIV. So, HIV was the problem, but where had it
come from, and why had the epidemic struck now, in the decade of big hair and Michael
Jackson? While some researchers were scrambling to
identify whatever it was that made AIDS infectious, others noticed that macaque monkeys also seemed
to suffer from an AIDS-like disease. One group decided to take some blood samples
from these sick monkeys, and in 1985 they found a virus that was similar to HIV. It was eventually called SIV, for simian immunodeficiency
virus. Researchers started to think that HIV might
have come from our primate relatives, jumping the species barrier. After a lot of work, they figured out that
the virus behind the epidemic was very similar to the chimpanzee version of SIV, and they
were the ones who had passed it to us. But how exactly? There’s no real way to put this delicately,
but most scientists agree that the reason why SIV made the leap into humans — what’s
called a spillover — is because we had a taste for bushmeat, or wild game. In this case, monkeys and chimps. This is known as the cut-hunter hypothesis. In the course of butchering a chimpanzee,
some SIV-infected chimp blood enters a small cut on the hunter’s hand. Or, a bit of blood splatters in their mouth. The virus is close enough to human biology
to infect the hunter, and over time, if the hunter passes the virus along to enough people,
it evolves into the HIV we know today. Spillovers like these happened many times
— we can tell because the virus mutates quickly, and by looking at genetic differences,
we can identify multiple lineages of the virus, each one corresponding to a spillover. We’ve traced the current epidemic to just
one of these, called ‘M’ for main. By analyzing chimpanzee pee and poop, researchers
think the chimps who passed that version of the virus to us lived in southwestern Cameroon,
in the forests near the Congo. And based on the oldest blood samples we can
find that we now know have HIV in them, which are from 1959 and 1960, scientists estimate
that HIV-1 first infected humans around 1908. If that seems like a long time ago, well,
it takes a while for a virus to take off. By the 1920s, it’s thought that the virus
traveled downriver — in a person, of course — to the burgeoning city of Kinshasa, then
known as the Belgian colonial city of Leopoldville. There weren’t many women around other than
prostitutes, so experts think HIV spread that way, and possibly through injectable drugs
the colonists used to treat some tropical and venereal diseases. This was before disposable syringes, and nurses
were trying to treat lots of people with just a few of them, so the syringes may have only
been rinsed with alcohol before being used on the next patient. So the very methods meant to stop the spread
of disease may have actually been
encouraging it. With time, infected people in Kinshasa left
to go to other places, and they did the unavoidable: they brought the virus with them. Because the virus mutates so quickly, we can
group the viruses into 9 different subtypes and get a sense of how HIV traveled around
the world from Central Africa. Several subtypes spread to other parts of
Africa. Subtype C went south and then landed in India. Subtype B went to Haiti — and then, through
several quirks of history, came to the US. First, in 1960, when the Belgians left the
Congo, French-speaking Haitians started to arrive in the Congo to work as doctors, lawyers,
and other professionals. But with the creation of Zaire in 1965, the
immigrants felt unwelcome, so they went back to Haiti, bringing HIV with them. There, HIV expanded especially quickly, possibly
because of a plasmapheresis center where people could get paid to donate their blood plasma. The center used a machine that mixed the blood
of different donors, allowing viruses to transfer. By 1982, nearly 8 percent of a group of young
mothers in a Port-au-Prince slum were HIV-positive — an astoundingly high number. HIV is thought to have entered the US around
1969, with just one infected person or unit of plasma from Haiti. It took about a decade for anyone to notice,
but by then it was too late. The epidemic had begun, and HIV was not only
in the Americas, but Europe and Asia, too. And now that it was here, we needed to figure
out how to fight it. But we’ll get to that in the next episode
of this mini-series. In the meantime, thanks for watching this
episode of SciShow, and if you want to learn more about HIV and all kinds of other science,
you can go to youtube.com/scishow and subscribe.

Roly Polies Came From the Sea to Conquer the Earth | Deep Look

Roly Polies Came From the Sea to Conquer the Earth | Deep Look


Pill bugs…… roly polies….. potato bugs… whatever you want to call them, somehow there’s something less creepy about these guys than other insects. More loveable, or something. Maybe it’s because they’re not insects
at all. Pill bugs are actually crustaceans. They’re more closely related to shrimp and
lobsters than crickets or beetles. Pill bugs even taste like shellfish, if you
cook them right. Some adventurous foragers call them wood shrimp. As early as 300 million years ago, some intrepid
ancestor crawled out of the ocean, sensing there might be more to eat, or less competition,
on dry land.” But unlike lobsters, pillbugs can roll up
into a perfect little ball for protection. If you look closely you can see the evidence
of where these guys came from. Like their ocean-dwelling cousins, pill bugs
still use gills to breathe. True insects — like this cricket — use a
totally different system. See those tiny holes on this cricket’s abdomen? They’re called spiracles. They lead to a series of tubes that bring
fresh air directly to the insect’s cells. But pill bugs don’t have any of that. To survive on land, they had to adapt. Their gills, called pleopods, are modified
to work in air. Folds in the pleopod gills developed into
hollow branched structures, almost like tiny lungs. In a way, the pillbug is only halfway to becoming
a true land animal. Because… they’re still gills. They need to be kept moist in order to work. Which is why you usually find pill bugs in
moist places, like under damp, rotting logs. They can’t venture too far away. Sure, pill bugs look like the most ordinary
of bugs. But they’re much more than that: evidence
that over evolutionary time, species make big, life-changing leaps. And those stories are written on their bodies. Hey, while we’re on the subject of oddball
crustaceans… check out this episode about mantis shrimp. Their eyes see colors we can’t even
comprehend. Their punch is faster than Muhammad Ali’s. And while we have you: Subscribe. OK? Thank you! And see you next time.