Thứ Tư, 26 tháng 7, 2017

Youtube daily Or Jul 26 2017

What is Good Youtube Its Your Boy Chris On the Mic and Today I'll Be Showing You

guys the comparison between NBA 2k17 and 2k18 to show you guys the differences

between the two games graphically just yesterday NBA 2k Studios released some

screenshots of their latest game NBA 2k from there we can see in game action

Paul George DeMar DeRozan and Isiah Thomas the 2k 17

gameplay I'll be showing you will be on the corner and it's from our ps4 there

if you guys really enjoyed this video please like it first off I want to thank

you for making it to the end of this video and second of all if you guys want

For more infomation >> NBA 2K18 vs NBA 2K17 Gameplay Comparison🔥 - First Screenshots Released!!(BETTER OR WORSE) - Duration: 2:01.

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#TechTuesday Chat: Anchor OR LiveLeap -- YOU DECIDE! #31DaysLIVE Day 21 - Duration: 41:07.

For more infomation >> #TechTuesday Chat: Anchor OR LiveLeap -- YOU DECIDE! #31DaysLIVE Day 21 - Duration: 41:07.

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EASIEST SLIME EVER (NO BORAX OR CONTACT SOLUTION) !!! - Duration: 1:55.

And today I am going to make the easiest slime ever

First I am going to put glue (any white glue)

And next we are going to put Persil gel

put a little bit

now we mix it with hands

now we put coloring (optional - food coloring or any water based colors)

Now I am going to make bubbles

The last thing is baby oil ( a little bit to avoid sticking)

For more infomation >> EASIEST SLIME EVER (NO BORAX OR CONTACT SOLUTION) !!! - Duration: 1:55.

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Is Insulin Really a Response to Carbohydrate or Just a Gauge of Energy Status? | MWM 2.23 - Duration: 35:18.

Insulin. Is the control of insulin

secretion finally something we've

arrived at that is all about

carbohydrate or is even insulin

secretion mostly just about

cellular energy status?

Find out in today's lesson.

A ketogenic diet has neurological benefits.

Why do we have to eat such

an enormous amount of food?

Complex science.

Clear explanations.

Class is starting now.

Hi. I'm Dr. Chris Masterjohn of

chrismasterjohnphd.com. And you're

watching Masterclass with Masterjohn.

We are now in our 23rd in a series of

lessons on the system of energy metabolism.

And today we are layering in for the first

first time the effects of hormones.

And to begin our discussion of insulin

we're going to talk about what controls

insulin secretion. We still at this point have

been talking about fat versus

carbohydrate, we're not ready yet to

layer in protein because of its

complexity. So although protein effects

insulin secretion, we're going to talk

about it only to a limited extent today and

we're primarily going to focus

on fat versus carbohydrate.

Nevertheless we're going to tackle

what seems like an incredible conflict

between what we know about the

effects of nutrition and what

happens at the cellular level. Because

we know nutritionally that you get more

insulin when you have more carbohydrate

and less when you have less. And yet when

we look at the mechanisms governing energy

secretion in the pancreatic beta-cell,

it seems to be all about energy status.

So let's carve out this problem and show it

exists and then let's try to explain it.

Shown on the screen is the design of a

study looking at the effects of

different meal patterns on insulin and

glucagon. Glucagon is a hormone that

opposes the action of insulin.

Although it's associated with the fasted state,

you also get a lot of glucagon when you

eat things that aren't carbohydrates,

especially protein.

One of the reasons for this is that insulin,

in the case of protein, is taking amino acids

into cells, and if you just had protein

stimulating insulin for that purpose it would

lower your blood sugar. So you need to have the

opposing effect of glucagon to allow

certain functions of insulin and prevent

other functions of insulin that are

undesirable in that context. We'll

talk about that in much more detail when

we get to protein, but for now let's just

take a look at these meals. We have an

oral glucose tolerance test which is a

100% glucose. We have a high-fat

meal that's deriving from fat 72% of

its calories and only 23% from

carbohydrate. We have a high protein

meal that's deriving 64% of its energy

from protein and 26% from

carbohydrate. And we have a mixed meal which

is really the high carbohydrate meal, it's the

meal that is 60% carbs. So all of these

are mixed, but there's more emphasis on fat

versus protein versus carbohydrate.

In this diagram plasma insulin following

the meal is shown on the left and plasma

glucagon is shown on the right. You can

see that the glucose is shown with the

filled in circles and the glucose

produces the most insulin and it

produces the least glucagon. In fact what

you see here is that glucose on its own

not only raises insulin, but it

suppresses glucagon; high insulin and low

glucagon gives you the most activity of

most of the processes downstream from

insulin. In other words a high insulin-to-

glucagon ratio gets you the most insulin

signaling. The mixed meal, which is really

a high carbohydrate meal, is next in line

for high insulin and next in line for

lowest glucagon. You see that protein and

fat both stimulated similar amounts of

insulin, again this is in the context of

a mixed meal where there is carbohydrate

in the meal, but having the predominant

source of calories be protein or fat led

to considerable insulin and considerable

glucagon. For insulin the rise was fairly

similar between the high-fat meal and

the high-protein meal, but the insulin

peaked earlier for the protein meal and

peaked later for the fat meal. And for

glucagon the glucagon was highest in a

high-protein meal and was next highest

in the high-fat meal. So carbohydrate

gives you the highest insulin to

glucagon ratio and the highest absolute

insulin amount, that translates into the

greatest insulin signaling. Contrast this

with what we know about what governs the

secretion of insulin by the pancreatic

beta-cell. Inside the pancreatic beta-cell,

the single most important governor

of insulin secretion is a high ratio of

ATP to ADP. That means that it's the

cellular energy status that is the

central governor of insulin secretion in

the pancreatic beta-cell. This diagram

shows what happens in more detail.

And this is, in the context of a field over

insulin secretion in which there are

many controversies and disagreements,

this right here on the screen is the one

least controversial thing that you will

find as the consensus in any scientific

paper about what triggers insulin

secretion. When you have a low energy

state you have more ADP and less ATP.

This doesn't literally mean that you

have more ADP than ATP,

it just means relative to higher energy

conditions ADP is predominating. And when

you have a low-energy state mediated

through the ADP-to-ATP ratio, this

activates potassium channels in the cell

membrane. Those channels allow potassium

to leave the cell. Potassium is

positively charged, so having those

channels open means a net loss of

positive charge from the inside of the

cell and a net gain of positive charge

outside the cell. This leads to a

polarization of charge across the

membrane. Outside the cell is more

positive in general because of the

potassium, inside the cell is more

negative. When you have a polarization of

charge across the membrane you have a

voltage. You have voltage-sensitive

calcium channels that are blocked when

the membrane is polarized; they're

blocked in response to the voltage

across the membrane. When the calcium

cannot enter the cell, the calcium

concentration inside the cell is low.

Calcium is very frequently used as an

intracellular messenger. A low

concentration of intracellular calcium

ions keeps insulin from being secreted.

Some of that insulin is stored in the

middle of the cell where it's ready to

be moved at a later time; some of that

insulin is right associated with the

inside of the membrane ready to go when

first called. If the energy state of the

beta-cell increases, you get an abundance

of ATP relative to ADP. This change in

the ratio inhibits the potassium

channels.The potassium now cannot get

outside and that depolarizes the

membrane, meaning the polarity across the

membrane of charge, the voltage across

the membrane, now dissipates.

Positive charges can't get out.

So now you have an equilibration

where you have closer to electric

neutrality on each side of the membrane.

Since the calcium channels are sensitive

to the voltage this loss of voltage or

depolarization opens up those calcium

channels. Calcium comes into the cell, the

rise in intracellular calcium stimulates

a cascade of events that lead to insulin

being delivered to the cell membrane

with the vesicles opening up and

allowing insulin to travel outside of

the cell. This idea of changes

in membrane polarization triggering

some other event or cascade

of events, is extremely common in

cellular biology. This is just one

example of a common phenomenon.

So this being the part of insulin secretion that

is not controversial means that what we

know best about insulin secretion is

that it's governed by the amount of ATP

in the pancreatic beta-cell. How can it

be that nutritionally there's a specific

effect of glucose and yet at the level

of molecular biology and biochemistry

it's all about cellular energy status,

it's all about ATP? I believe the answer

is that we cannot explain the specific role

of glucose in insulin signaling by invoking

biochemistry or molecular biology.

I believe instead we need to

invoke anatomy and physiology.

Anatomy is the relationship between the organs

and the other structural features of our

body; physiology is how metabolism is

coordinated between those different

organs to orchestrate some overall net

result in the body that's more than the

sum of its parts. So let's take a look at

the anatomy and physiology of how

carbohydrates and fats would reach

a pancreatic beta-cell.

The pancreas is closely associated with the

organs of the digestive system.

Inside your torso underneath the cavity where

your lungs are, you have the liver,

you have the gallbladder located tucked

into the liver, you have ducts that lead

together into the small intestine,

you have the stomach, and you have that

lead into the small intestine, the first

section of which is the duodenum.

The pancreas is tucked underneath the

stomach relatively close to the liver

and gallbladder, but tucked into the

curve of the duodenum, giving it very close

access to the small intestine.

It's important to realize that glucose or fat

when we first eat it is going to go from

the stomach into the small intestine.

That does not mean at all that they have

direct access to the pancreas. The reason

The pancreas is tucked in with the

duodenum is because it plays a role in

digestion. Its role in responding to

nutrients to secrete insulin is not

related to the direct proximity to the

duodenum. The key role of the pancreas

in the digestive system is to make

digestive enzymes. So we have bile acids that are

made in the liver and come through the

hepatic duct, can be stored in the

gallbladder and come to the cystic duct

into the common bile duct and then the

pancreatic duct takes digestive

secretions from the pancreas, mixes them

with the bile acids and they

get carried into the duodenum so that

they can begin the digestive processes.

If we look inside a pancreas what we

will find is one to two million islets.

An islet is a collection of many cells

involved in hormone secretion, which

constitute the endocrine function of the

pancreas. The islets are surrounded by

circular arrangements of acinar cells in

acini that are responsible for

digestive secretions. These arrange

circularly around the islet and each of

the acini is itself a circle of cells

that can input the digestive secretions

into the middle of those cells to be

carried through the pancreatic duct into

the duodenum.

Inside the islet we have many, many cells.

We have alpha-cells, beta-cells, delta-cells

and F-cells. The alpha-cells make

glucagon, the beta-cells make insulin, the

delta-cells make somatostatin and the F-

cells make pancreatic polypeptide.

Somatostatin and pancreatic polypeptide

play special regulatory roles that are

not of concern to us in this discussion.

We're briefly touching on glucagon here

but we're primarily going to focus on it

once we get to protein. For our purposes

what we care most about is that 70% of

the cells in the islet are beta-cells.

How would carbohydrate and fat reach the

pancreatic beta-cell? Well in fact their

transport is completely different. If you

have carbohydrate coming into the small

intestine, it's going to travel through

the portal vein directly to the liver.

It's going to go to the liver with all the

other water-soluble nutrients in the

diet. That means the liver gets first

access to the carbohydrate. Well that's

important because the first thing you

want to do with carbohydrate is replete

your hepatic glycogen supply because

hepatic glycogen is what keeps your

blood sugar stable between meals. So you

can imagine already that if you're

running low on carbohydrate that in

itself is going to make less

carbohydrate ever reach the pancreas

because it's going to go to the liver

first to replete the glycogen stored

there. The hepatic veins then take

remaining carbohydrate into the inferior

vena cava, which is the vein that's going

to take those nutrients into the heart.

From the heart those nutrients reach the

aorta and they can go through multiple

arteries to either circulate to many

other organs or to go specifically to

the pancreas. By contrast if fats are in

the small intestine they're going to get

packaged into lipoproteins, which are

spherical particles that help them

transport through our system and are

called chylomicrons.

The chylomicrons are going to leave the small

intestine through the thoracic duct,

which is part of the lymphatic system.

These chylomicrons are going to

have long-chain fats and any other

fat-soluble nutrients. These fats are going

to go through the thoracic duct as part

of the chylomicrons and then empty into

the inferior vena cava, which is where

they first reach the circulatory system

and which is the part where they share

in common with the travel of

carbohydrate that had come from the

liver. Like the carbohydrates that came

from the liver, the fat that came from

the lymphatic system that never yet went

into the liver, is going to reach the

heart first; it's going to go through the

aorta; from the aorta it goes through

multiple arteries that can take it to

the pancreas or to the many other

organs. So the two key differences

between carbohydrate and fat so far is

that carbohydrate goes through the

portal vein and the liver has first

access before it ever gets to the heart

or pancreas. Fat goes from the small

intestine through the lymphatic system and

never goes to the liver until after it

goes through the heart, which has first

access, and then to the general

circulation where it can reach the liver

or the pancreas. If we look at how the

fat or carbohydrate would get inside

cells, it gets even more different.

We digest carbohydrate to free sugars.

In the case of starch, for example, we digest

it into glucose, or if we eat glucose we

get free glucose. If we have free glucose,

it transports

right into the cell through the glucose

transporters in the cell membrane.This

is a very simple transport system. The

transport of chylomicrons, of fats

contained in chylomicrons, is quite

different. In certain cells that make the

enzyme lipoprotein lipase, they can send

the enzyme out into the capillary beds

that nourish them. So let's say this is

the heart, the heart cell makes LPL, puts

it out into the capillaries nourishing the

heart. Same thing with the muscle, the

muscle cell makes the LPL sends it out

into the capillary bed. The capillary bed

is made of capillaries and the lumen of

the capillary is the area in which blood

flows. That lumen is enclosed by the

capillary endothelial cells, which make

the lining of the capillary.

The lipoprotein lipase, or LPL, will come out

of a cell that made it and become

embedded in the capillary endothelial

cell. That LPL will then take

chylomicrons and digest their fats into

glycerol and fatty acids. The chylomicron

gets digested into a chylomicron remnant

and that chylomicron remnant

gets taken up by the liver.

Meanwhile the glycerol and fatty acids

are available to the tissue that

made the LPL because the job of this

capillary is to feed that tissue.

So those nutrients get digested in the

capillary and infused into the cell.

The expression of glucose transporters and

LPL is very different. If you look at

glucose transporters, all tissues in the

entire body express GLUT1 and GLUT3.

These glucose transporters are high

affinity for glucose and not dependent

on insulin. That gives all tissues access

to the glucose that they need under any

condition. The liver and pancreatic

beta-cells also make GLUT2. GLUT2 has

low affinity, meaning it's only activated

at high concentrations of glucose and

it's not dependent on insulin. That

allows the liver and the pancreas to

ramp up glucose uptake when blood

glucose concentrations rise beyond their

normal level. In addition, muscle, heart

and adipose tissue make GLUT4.

GLUT4 has moderate affinity and it's

increased by insulin and AMPK.

AMPK increases GLUT4 because the cell

needs more energy.

Insulin increases GLUT4 because

the body needs the cell to take up

energy or to take up specifically glucose.

So we have all tissues expressing

GLUTs, some more than others,

some extra GLUTs that play specific

functions such as a response to insulin,

response to energy status or response to

circulating glucose. If you look at the

expression of LPL, it's expressed much

more limitedly. Almost all of the LPL is

expressed in muscle, heart and adipose

tissue. We know most about the LPL that's

expressed in those tissues. What we know

is that high energy status shifts

expression away from muscle and heart

and toward adipose. By contrast

low energy status does the opposite.

So think of the fat traveling through the meal,

remember it goes to the heart first.

If it goes to the heart first then if energy

status is low and the heart really needs

fat, the heart gets first access to that

fat and takes it up. But if energy status

is high the heart just looks at the fat and

it's like, "No I don't want this," that leaves

more available to muscle and adipose

tissue, but muscle also looks at that fat

and says "No, I don't want this." By contrast adipose LPL

is high under conditions of high energy

status. That makes fat go to adipose

tissue under conditions of high energy

status. Meanwhile there is also LPL

expression in macrophages, lung, kidney,

brain and lactating mammary glands.

The expression is much smaller than in

muscle, heart and adipose tissue; the

the regulatory mechanisms are

diverse and poorly understood. A typical

review of LPL expression across tissues

won't even mention its expression in the

pancreas, but if the pancreas doesn't

make LPL, how is it supposed to take up

postprandial fat from chylomicrons?

If you know studies that look at human

beta-cell LPL, please send them to me.

I couldn't find any, but I found studies in

mice. And what these studies show is that

in mice pancreatic beta-cells do make LPL.

However, under almost any condition the LPL is

inside the beta-cell. If the LPL is

inside the beta-cell that means there's

no LPL in the capillary lumen. That means

there's no LPL to digest chylomicrons.

That means that LPL does nothing to get

fat into that beta-cell. They've taken

the mice and they've subjected them to

fasting, to refeeding, to a normal chow diet,

to a high-fat diet, and the LPL just

sits in the pancreatic beta-cell.

The only conditions that make it leave the

beta-cell and go into the capillary

lumen, in these mouse and mouse cell

experiments, is high glucose

concentrations. We're talking 20 millimolar,

conditions of untreated diabetic

concentrations of high glucose.

That means that only under conditions of

very high glucose would you ever get fat

going into the pancreatic beta-cell

through locally expressed LPL.

But there's another way that fat in the

postprandial state could reach the

pancreatic beta-cell and that's from

fatty acid spillover. Let's say you have

an LPL-producing tissue that puts LPL

into the local capillary bed; it digests

chylomicron triglycerides into free

fatty acids and glycerol. In general

these are completely or mostly taken up

by the LPL-expressing tissue. But what if

you have so much fat that you overwhelm

that tissue and there's no room to take

up all the fat that's been digested?

Or what if you're fat, what if that tissue

is fat, and all the room within that cell

is taken up by fat; or what if the energy

status of that cell is so high that it's

blocking the uptake of everything?

In those cases you may get digestion of the

chylomicrons into free fatty acids and

glycerol that get left in the blood.

And since they don't get taken up by the

tissue, they leave the capillaries through

the veins and then they eventually make

their way into the circulation to get to

other tissues such as the pancreas.

That's called fatty acid spillover, and it's

thought to be increased by

high-fat diets, obesity and insulin resistance.

So, so far we have glucose

going to the liver first and we're

repleting the hepatic glycogen. Whatever

glucose is left over, it goes to the heart

and eventually can make its way

to the pancreas.

By contrast fat goes through the

lymphatic system, it goes first to the heart

and if the energy status in the heart is

low the heart gets first dibs on the fat,

if it's high that fat preferentially

goes to adipose tissue, not necessarily

ever making it to the pancreas. Glucose

transporters are expressed in the

pancreas. In fact the pancreas also

expresses GLUT2, a special glucose

transporter that makes glucose uptake

kick in even higher than normal whenever

circulating concentrations of glucose are high.

The liver does the same thing.

That means that high blood glucose goes

preferentially first to the liver to

replete hepatic glycogen, and second to

the pancreas for insulin stimulation.

In addition, the pancreas also has a special

form of hexokinase that doesn't get

inhibited by glucose-6-phosphate.

We talked before about how if you don't go

through glycolysis, glucose 6-phosphate

builds up and that rejects the glucose.

In the pancreatic beta-cell we have

glucokinase, a special form of hexokinase

that is not inhibited by

glucose-6-phosphate. That means that the

pancreatic expression of glucose

transporters and hexokinase isoforms is

designed to facilitate glucose uptake

into the pancreas, not because the

pancreas needs more glucose, but

specifically because the circulating

glucose concentrations are high. This is

not true for fat because

the pancreatic beta-cell appears not to

move LPL into its local capillary bed

unless possibly exposed to very high

concentrations of glucose mimicking

untreated diabetes. But the pancreatic

beta-cell still gets some fatty acids in

the postprandial state from fatty acid

spillover if the meal is very high in

fat or if the person is obese or insulin

resistant. So it seems then that it is

the anatomy and the physiology that

coordinate the inter-organ distribution

of these nutrients that drives the

effect on insulin secretion instead of

the biochemistry and the molecular and

cellular biology that occurs within the

pancreatic beta-cell. Nevertheless the

mechanism that I showed you at the very

beginning is what's called "triggering."

There's also an amplification step to

insulin secretion, and the amplification step

is much more complex and much more

controversial. So let's say that it's

glucose that is primarily the nutrient

that can raise ATP levels in the

pancreas, inhibiting the potassium

channels, depolarizing the membrane,

activating the calcium channels, getting

a rise of intracellular calcium,

initiating a cascade of events that

leads insulin to be secreted.

Well there's that and that's the

uncontroversial consensus part of this.

But the amplification step can make the

cell more sensitive to the influx of

calcium or can increase the capacity to

respond to that calcium by making more

insulin ready to be mobilized. And these

amplification signals are, number 1,

very complex, and, number 2, not at all

agreed upon. We may be moving toward a

consensus eventually, but if you look at

even recent reviews of this topic you'll

see lots of controversy about which

mechanisms are more important,

and even some controversy over which

mechanisms actually play out in the live

human at all. If we look at these

amplification signals what we will see

is that anaplerosis, which is the

filling up of citric acid cycle

intermediates, can occur in a way that

overfills the citric acid cycle and leads

to cataplerosis, which is the leaving of

citric acid cycle metabolites including

their transport into the cytosol. Since

anaplerosis is primarily the domain of

carbohydrate and as a secondary source

protein rather than fat, then that means

that cataplerosis is primarily enabled

by carbohydrate and secondarily protein.

That cataplerosis then leads to

amplification signals. Lipogenesis leads

to various downstream processes from the

accumulation of fat in the cell. Lipogenesis

is driven by malonyl CoA.

Malonyl CoA can be derived from

anything that makes acetyl CoA and

citrate because citrate activates the

conversion of acetyl CoA to malonyl CoA,

as we talked about in the

lesson on fat burning. Since carbs,

protein, and fat can all generate acetyl CoA,

and can all generate citrate, and carbs, protein,

and fat can all lead to malonyl Coa and

lipogenesis and can all, to some extent,

lead to that amplification symbol.

That amplification signal.

Some of this is driven by the

pentose phosphate pathway's production

of NADPH, a topic that we haven't covered yet.

It's carbs specifically that support

the pentose phosphate pathway and

provide that NADPH that go into that

amplification signal. So what we see

then is that all of the macronutrients

can make some contribution to

amplification. But carbohydrates are the

most versatile out of all of them and

fats are the least versatile.

Perhaps that versatility in providing

the amplification signal is simply a way

to gauge the versatility of

carbohydrate. Because carbohydrate is

also the most versatile in supporting

the biochemical pathways that you

actually need. So if the body is trying

to judge whether it has enough energy, it

makes sense that part of that signal

would be specifically driven by

carbohydrate because carbohydrate is the

thing that supports the pentose

phosphate pathway, whereas fat doesn't.

Carbohydrate is the thing that supports

anaplerosis of the citric acid cycle,

which fat doesn't to anywhere

near the same extent. And so it

may actually be that the pancreatic

beta-cell is, as the mechanism of

triggering would suggest, simply gauging

energy status. And it may be that the

pancreas correctly looks at carbohydrate

as especially valuable source of energy

because the energetic uses of

carbohydrate are more versatile than

those of other macronutrients,

especially fat. And if carbs provide

energy plus the specific uses of energy

that fat can't, then carbs are a uniquely

valuable source of energy. So when I look

at this what I see is the pancreatic

beta-cell wants to make sure that we

have enough energy; but it wants to

specifically make sure that we have

enough glucose because of the specific

things we can do with that energy that

are much harder to do with the energy we

derive from fat. So is insulin responding

to carbohydrate specifically or is it

responding to energy status in general?

The answer is both.

The anatomy and physiology bias

carbohydrate to the pancreas when

it reaches high concentration providing

the liver has the first opportunity

to replete the hepatic glycogen pool.

That same anatomy and physiology biases

fat toward the heart and muscle under

low-energy conditions and toward adipose

tissue under high-energy conditions, and

biases it away from the pancreas under

any conditions except possibly severe

hyperglycemia.

Then the biochemical pathways

within the pancreatic beta-cell

are mostly responding to cellular energy

status. But because the pancreatic

beta-cell's energy status is best

nourished by carbohydrate, then

carbohydrate plays a specific role in

triggering insulin. Carbohydrate also

plays the dominant role, with protein second

and fat a distant third in amplifying

that insulin signal. Because, perhaps, the

pancreas cares that we don't just have

enough total energy, but that we have the

versatility that we get from having

carbohydrate as a part of that energy.

The audio of this lesson was generously

enhanced and post-processed by

Bob Davodian of Taurean Mixing, giving

you strong sound and dependable quality.

You can find more of his work at

taureanonlinemixing.com.

To continue watching these lessons, you

can find them on my YouTube channel at

youtube.com/chrismasterjohn.

Or on my Facebook page at

facebook.com/chrismasterjohn.

Or you can sign up for MWM Pro, to get

early access to content, enhanced keyword

searching, self-pacing tools,

downloadable audio and transcripts,

a rich array of hyperlinked further

reading suggestions, and a community

forum for each lesson. If you really

want to own these lessons, study them

and get the most out of them, you can

sign up for MWM Pro at

chrismasterjohnphd.com/pro.

Signing off, this is Chris Masterjohn of

chrismasterjohnphd.com.

You've been watching

Masterclass with Masterjohn.

And I will see you in the next lesson.

For more infomation >> Is Insulin Really a Response to Carbohydrate or Just a Gauge of Energy Status? | MWM 2.23 - Duration: 35:18.

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ANNE BANCROFT IN TO BE OR NOT TO BE - Duration: 0:14.

For more infomation >> ANNE BANCROFT IN TO BE OR NOT TO BE - Duration: 0:14.

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Superman or Batman - Which Kind of Leader Are You? | TIAnimate - Duration: 2:38.

Before defining your leadership style,

you need to find out which type of leader are you:

Superman or Batman?

If you are a Superman-typed leader,

you might realize that

you are a naturally-born leader.

You might have leadership traits such as confidence, charisma,

intelligence, and some other traits.

But it does not mean that Superman

would just become a great leader from that.

Nonetheless, Superman needs to know himself first

so that he could find certain values that he believes in.

Just like when he believed he could fly,

then he actually did.

Unlike Superman, Batman does not have those advantages

since he was born.

Batman, a.k.a Bruce Wayne

was just a normal human being without possessing superpower.

So, if you're a Batman leader,

you need to understand your competitors

and their strengths over you

to excel Superman Leaders.

Although Superman has extraordinary talents,

he never settles down with his achievements.

If you're a Superman leader,

you need to follow his example.

Because you'll never know how far you can go

if you don't keep exploring your talents.

On the other hand, Batman has limitations.

So if you're a Batman leader

remember that your limitations

are not your barriers for success.

In contrast, these limitations can motivate you

to think creatively and continue to innovate

and to solve various problems.

Just like Batman who utilizes his belt,

you can also use technology to help you.

But keep in mind: use it only when it's needed.

Despite their differences, both Superman and Batman leaders

have the same opportunities to be great leaders.

As long as you're resilient and you don't see failure as a defeat,

your chance to becoming a great leader is widely opened.

For more infomation >> Superman or Batman - Which Kind of Leader Are You? | TIAnimate - Duration: 2:38.

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5 Home Remedies To Get Rid Of Slipped Or Herniated Disc - Duration: 3:07.

In this video you will learn about 5 Home Remedies To Get Rid Of Slipped Or Herniated

Disc.

The vertebrae are the backbone of the body.

Any problems in our spine can lead to problems in your daily movement and activities.

Our spinal cord is made up of small bones known as vertebrae that are attached to each

other.

These bones are lined by discs which protect them from shock.

These discs have gel-like inner portion and a strong outer portion.

Any kind of injury or damage to the discs can cause the inner portion to come out and

cause a bulge like appearance on the outer part.

This disorder is known as herniated disc or a slipped disc.

The herniated disc can affect any region of your spine but the lower part is more at risk

due to continuous bending and turnings.

The symptoms of herniated disc or slipped disc are: 1.

Pain and numbness which usually occurs on any one side of your body; 2.

Pain that moves up to arms or moves down to the legs; 3.

Tingling or a burning sensation in the region of the slipped disc.

The 5 Home Remedies to Get Rid of Slipped or Herniated Disc are:

1.

Heat or Cold Therapy You can use both hot and cold water bags on

the area where you feel the maximum pain.

Do the alterations between cold and hot water.

However, remember to keep at least half an hour gap between both of them.

2.

Physiotherapy and Yoga Physiotherapy is all about proper exercises

and stretches which will improve the disc shape to a great extent.

Physiotherapy helps in promoting faster healing of this disorder.

Doing some yoga poses also helps in healing herniated disc or slipped disc.

3.

Use Turmeric Turmeric contains curcumin which is a very

good anti-oxidant and anti-inflammatory agent.

Turmeric helps in reducing the pain because of slowed blood circulation to the area of

pain.

4.

Acupressure and Acupuncture It is an excellent pain management method.

The pressure is used for relieving the pain from the swelled area.

In acupressure fingers are used and in acupuncture needles are used.

5.

Take bath with Epsom Salt Epsom salt is widely used as a natural painkiller

and anti-inflammatory agent.

Add 3 to 4 cups of salt in a hot water bath.

Stay inside the bath for at least 15 minutes.

Doing this will help you to achieve maximum relaxation.

Note: Do not use this remedy if you are diabetic or pregnant.

So what are you waiting for, start taking these home remedies and consult a doctor whenever

you feel any kind of severe pain.

Thanks for watching this video, if you enjoyed this video, please do not forget to like and

subscribe to our channel.

In this channel you will get information about various health related topics.

Wishing you good health in your life, bye.

For more infomation >> 5 Home Remedies To Get Rid Of Slipped Or Herniated Disc - Duration: 3:07.

-------------------------------------------

how to install minecraft on you pc or mac tutorial - Duration: 5:51.

i hope you luv this video subscribe and leave a like and even tell your friends about it!!!! "if they want to know how but don't definitely tell them :)"

For more infomation >> how to install minecraft on you pc or mac tutorial - Duration: 5:51.

-------------------------------------------

Humanity does not need sex, color or religion - Duration: 11:36.

For more infomation >> Humanity does not need sex, color or religion - Duration: 11:36.

-------------------------------------------

UV Air Purifier - Home Or Business UV Air Purifier - Duration: 1:16.

Are you looking for Air Oasis UV Air Purifier?

Are you concerned about the air quality in your home or business or need allergy or asthma

relief?

Then you need our Air Oasis UV air purifier sanitizer.

Air Oasis UV isn't a filtration air cleaner but an air and surface sanitizer.

Unlike inefficient noisy HEPA cleaners that capture pollutants, the Air Oasis UV Air Purifier

uses ultraviolet light in conjunction with photocatalytic oxidation which sends out powerful

oxidizing cleaning agents eliminating odors, VOCs, mold, viruses and bacteria in the air

and on surfaces.

Air Oasis UV sanitizers have unmatched test data.

Air Oasis has the Mobile personal travel sanitizer, the 1000 and 3000 models for home or office,

and commercial models.

AirOasisUV.com has sold commercial models to food stores, kennels, vet clinics, doctors'

offices, hospitals, salons, churches, schools, NFL and MBL lockers rooms and many more.

For discounts on Air Oasis UV air purifier sanitizers, visit AirOasisUV.com or give us

a call toll free 855-488-8806.

For more infomation >> UV Air Purifier - Home Or Business UV Air Purifier - Duration: 1:16.

-------------------------------------------

A Street or a Zoo : Learn Hindi with subtitles - Story for Children "BookBox.Com" - Duration: 2:55.

For more infomation >> A Street or a Zoo : Learn Hindi with subtitles - Story for Children "BookBox.Com" - Duration: 2:55.

-------------------------------------------

[ [ MMD SHORT ] ] Why Bad Boy or Blue Can't Get Girls [Motion by Monica x Isabel] +Captions - Duration: 0:59.

But I told her!

That she's cute! That I love her!

Exactly, she probably thought it was a prank.

I mean, you do seem superficial (and gay).

Bad Boy: WHAT DID YOU JUST CALL ME IN DAT THERE PARENTHESIS >:d

I'll have you know I graduated top of my class in the Navy Seals, and I've been involved in numerous secret raids on Al-Quaeda, and I have over 300 confirmed kills. I am trained in gorilla warfare--

The FitnessGram™ Pacer Test is a multistage aerobic capacity test that progressively gets more difficult as it continues. The 20 meter pacer test will begin in 30 seconds. Line up at the start. The running speed starts slowly, but gets faster each minute after you hear this signal-

It's better than you who never says anything.

w0t u say m8

You couldn't even say hey to Neru or tell her that she's kawaii desuuuuuu.

I told you, it's not like that (it's because I'm gay.)

If you keep acting like this, you're going to miss your chance.

*triggered fist*

I TOLD YOU, I'M GAY--- I MEAN IT'S NOT LIKE THAT, YOU SUPERFICIAL BAKA D:<!!!!

W0T M8?!!!!!! I CAN'T HEAR YOUUUUUUUUUUUUU!!

YOU ARE A NASTY BOY ( ͡° ͜ʖ ͡°)

YOU ARE CLOSET PERVERT (and gay).

*constipation noises*

( ͡° ͜ʖ ͡°)( ͡° ͜ʖ ͡°)( ͡° ͜ʖ ͡°)

Bad Boy: STOP TOUCHING MY BUTT

Blue: Kay. ( ͡° ͜ʖ ͡°)

SHASH YA'LL MOUTHS

...

( ͡° ͜ʖ ͡°) wow

[distant fujoshi screaming]

(me after watching boku no pico)

Bad Gir--

MOMMY RAC!!! BAD BOY BROTHER IS CHEATING aGAIN!!! SAVE US ALL!! I WANT LIGHTNINGBOY!!!

For more infomation >> [ [ MMD SHORT ] ] Why Bad Boy or Blue Can't Get Girls [Motion by Monica x Isabel] +Captions - Duration: 0:59.

-------------------------------------------

Which Rice Has Less Arsenic: Black, Brown, Red, White or Wild? - Duration: 5:15.

For more infomation >> Which Rice Has Less Arsenic: Black, Brown, Red, White or Wild? - Duration: 5:15.

-------------------------------------------

No Degree: Apply For Job Or Internship? - Duration: 8:09.

Hey, what's up?

John Sonmez here from simpleprogrammer.com.

Tired of pushy recruiters sending you LinkedIn requests for jobs you have no interest in?

Tired of blasting out resumes into the dark?

If so, you should check out Hired.com.

Hired.com flips job searching on its head by having top employers like Facebook come

to you after you fill out one simple application.

You also get your own job coach to help you on your next job search.

If you haven't checked it out, I highly recommend you at least fill out the application.

Just go to Hired.com/simpleprogrammer.

When you get hired with Hired, you'll get double the normal sign-on bonus for using

that link.

I got a question from—oh, and he gave me the pronunciation.

He's from Bulgaria.

He says Lyubomir.

At least I think that's Lyubomir.

Lyubomir says, "I can either go to the US to work for 14-16 hours a day for $10 an hour

(That's a lot of money in Bulgaria) or get an internship doing some programming for little

or no pay.

What should I do the 4 months in summer when I don't have college?"

He says he's from Bulgaria finishing up his second semester studying Computer Science

and Information Systems.

His college is extremely expensive, $5000 a year with a 60% scholarship.

For Bulgaria, that's expensive.

He's been doing freelance web development on the side for pretty lucrative amounts of

money, but it's not enough to pay for his education.

He'd either have to go to the US and work two jobs in the summer or have a large student

loan that I have to pay off after I graduate.

If I understand the question correctly, I think what he's saying is that he's either

going to go to the US and work 14-16 hours a day at about 10 bucks an hour or do an internship

doing some programming with no or little pay in Bulgaria.

What should you do in this case?

I would highly recommend—you know, I talked about this before in a video.

I think someone asked in a video about going to the US or staying in their country and

I had recommended going to the US.

If we can find that video, I don't remember the name of it, but I would highly recommend

going to the US and doing the 10-14-hour days for 10 bucks an hour just because of the connections

that you're going to make there, especially working at a company being paid in the US,

and the perspective change that you're going to have.

I mean I have my own world view and my own perspective, but I've seen on the flip side.

I went to China.

You can check out my videos in China and I've gone to a lot of third world kind of countries

or places where the cost of living is much less, where people make a lot less and they

live in a lot worse conditions.

I realized how plentiful the US is and how much opportunity there is here and how fortunate

I am to be here and to have that opportunity.

It's sort of made my perspective bigger to understand that opportunity that I maybe was

taking for granted.

I think, again, I haven't done this, but I think the other perspective is also valuable.

I think if you're from somewhere like Bulgaria and you come to the US and you see—I mean

I've actually had the other experience.

I'll talk about it in a second, but, essentially, I think if you come to US and you see how

much everyone's got—is making so much money and there's so many expensive stores, and

all of this stuff and how much things cost, it may motivate you and make you realize that

there is—because you're working in this global economy.

Maybe you're underpricing yourself.

Maybe you're undervaluing yourself because you're used to what is expensive or what is

the current value in Bulgaria, which is a lot less.

Seeing something more grand and more extravagant and of a higher level can make you want to—not

only want to reach that level, but it can make you realize that it's possible and that

there's—for a lot of people, it's the norm.

Now, again, there's opportunities and there's all of these things, but as we're moving to

more of a global economy especially for programmers, there is—a lot of it is perception.

A lot of it comes down to perception and I'll tell you like I've had this experience when

I've gone to places like Manhattan and gone to 5th Street in Manhattan.

You might think that you're doing pretty well, but you go to 5th Street in Manhattan and

you're like, "Man, I am poor."

Or you go to Vegas to some of these places in Vegas where—I went to this one restaurant

and they had this Japanese kobe beef.

Do you know how much that beef costs—like 4 ounces of beef?

I'm embarrassed to tell you how much it cost me, but it cost me like 200 bucks, something

like that.

It was like 150 or 200 bucks.

Somewhere around that range for like 4 ounces of beef.

Now, I wouldn't do that all the time.

Obviously, I'm not that rich but I wanted to try it once, and there are people that

do, that lived that way.

It expanded my mindset to say, "Wow.

This is interesting.

For some people, this is just a norm.

Why do I have such a limited mindset that I don't think this is the norm?"

I'm not saying that money is everything and that—you know, all this but I'm just saying

that sometimes seeing how the extravagant or seeing how the wealthy live can make you

realize that that could be your like—it could adjust you to that where it could set

your sights a little higher because a lot of times we set our sights too high or—I

mean too low.

We should set them a little bit higher.

I know this is kind of a weird way to go from your question, but, honestly, I would come

over to the US and take that opportunity and just—I feel like it will expand your perspective.

It will give you lot of opportunities in the future in the US versus doing an unpaid internship

in Bulgaria.

I think that it's going to carry more weight.

Plus, the other thing to think about too is that if you do try to get a job in the US

or you try to do freelancing, if you have US clients on your resume and on your portfolio,

that's going to make a bigger difference.

If it's all Bulgarian clients and you try to get a job somewhere else or you try to

court a US client, it's going to be harder because they're going to say, "Well, I don't

know like is this legit?

Does this measure up?"

They're going to have these perceptions and—if you're like, "Oh, I interned at IBM in the

US for four months," that's going to look much better for you.

Again, I don't know about this.

I don't have your perspective so I can't tell you 100%, but I would say that just for

my own experience and what I've seen and all the people that I know that—I know a ton

of developers that came over here from India.

There's one in particular that the dude started following my channel, I think like three or

four years ago and started reading my stuff and my blog, and he was making like nothing

in India like very little, and he came to US and he's making like almost $200,000 a

year in the US now.

I mean can you imagine that?

A lot of it was the mindset shift.

A lot of it was because—when I've talked to him, he said that a lot of watching my

videos and just realizing what was possible made him want that and set his bar that high,

and then all of a sudden he's—I mean it's unbelievable where he's been and there's couple

of stories like that.

I mean you've seen the one on my channel where i told about the story, the guy that emailed

me that—also from India—That end up being extremely successful.

I can't remember the—Skip MBA.

That's his name.

All right.

That's all I got for you.

Good luck.

If you have a question to email me, email me at john@simpleprogrammer.com.

Make sure that you click that Subscribe button if you haven't already and click the bell

to make sure you don't miss any videos when they come out.

I'll talk to next time.

Take care.

For more infomation >> No Degree: Apply For Job Or Internship? - Duration: 8:09.

-------------------------------------------

Overly Excited Tourist Loses It At San Diego Comic-Con - Duration: 2:29.

- Surf's up, honey.

I'm in sunny San Diego.

They're havin' some sort of a costume party or somethin'.

Let's go find us a cot-stume, and have a good time.

(seagulls cawing)

(fireworks exploding)

Yeah, buddy, that's the one.

Yeah, yeah, yeah, yeah, yeah, yeah, yeah, yeah.

Whoa baby boy,

I got my cat-stume, and I am ready to go.

I am Batman.

Hasta la vista, buddy.

Hey, Alexa, where are the restrooms at this costume party?

Alexa!

50 years of Penis in Japan.

Only in Santiago.

Scoogy boogy boo, how are you?

Are you joking my ass?

They got a life size Shrek.

Donkey.

One thing I'll say about Sandy Bagels

is they have a whole lot of danosaurs.

Look at these nasty bad skulls.

I'm spooked as heck.

♫ Transformers,

♫ Robots in-they are cars.

Shrek!

I'm an ogre.

Toly Crobus!

They got a life size Colin O'Brien.

Hi, honey.

- Psychosis.

- Are you jokin' my ass?

Get in my ass and think about what you've done.

Look at the size of this pineapple.

They say it's a 100 feet bit, and...

I am gay.

Wake up, silly ass, we're having a costume party.

Uh-oh, Batman and Brain,

we better not fight.

- I'm gonna break your back, Batman.

- Oh, Jesus Christ!

Toly Crobus!

They got a Lego...

Super...

man.

I'll smash his ass for a hundred bucks.

Holy snopes, they got a real live Henry Simpson

holding a...

a...

a ball.

Jumpin' Jefferson,

it's pro wrestler Sting!

Hi, boy!

Ew, icky bad, look at all these nasty poops.

Shrek!

Donkey,

I'm an ogre, Donkey.

I love Stan Liego!

Ass full o' nuts, what a day I've had

here at this impromptu Halloween party.

Everyone was pretty ugly,

but it was still a pretty good time.

I think it even was the best day of my whole life.

(upbeat techno music)

For more infomation >> Overly Excited Tourist Loses It At San Diego Comic-Con - Duration: 2:29.

-------------------------------------------

Will Trump be Impeached or become a Dictator? - Duration: 8:39.

For more infomation >> Will Trump be Impeached or become a Dictator? - Duration: 8:39.

-------------------------------------------

PROTECTIVE MOM! Kajol Will Be Angry If Yug Or Nysa Gets Papped Like Suhana Khan For Pictures - Duration: 1:45.

PROTECTIVE MOM! Kajol Will Be Angry If Yug Or Nysa Gets Papped Like Suhana Khan For Pictures

For more infomation >> PROTECTIVE MOM! Kajol Will Be Angry If Yug Or Nysa Gets Papped Like Suhana Khan For Pictures - Duration: 1:45.

-------------------------------------------

Is It a Common Cold or Allergies? - Duration: 1:43.

is it a common cold or allergies it's a question that worries lots of folks

windows common symptoms it is all that are coughing and sneezing from a cold or

hay fever it's sometimes the TAS call but how long your problems last is one

of the big clues what our colds and allergies they have different causes you

got a cold when a small living thing asked a virus gets into your body there

are numbers of different species that can get you sick once a cold virus gets

inside you your free system the body's protection against germs launches a

counter-attack it's this response that brings on the

typical symptoms like a cold or stuffed-up nose the viruses that cause

colds are contagious you can choose them up when someone who's infected sneezes

coughs or shakes hands by you after a couple of weeks at the maximum you

immune system fights off the attack and you should stop producing symptoms it's

a different story by allergies they move made by an overactive immune system for

some reason your build mistakes homeless things such as dirt or pollen for germs

also fixes an attack on them when that happens your heart releases chemicals

such as histamine just as it appears when fighting a cold

that can cause a swelling in the passageways of your nose and you'll

start sneezing and coughing unlike colds allergies aren't taking though some

people may inherit a tendency to get them differences between colds and

allergies take stock of your symptoms and how great they last to help you

decide what's causing your trouble your trouble

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