第三組翻譯黃疸

影片連結：https://en.wikipedia.org/wiki/File:Jaundice-video-osmosis.webm

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Jaundice, which doesn’t have the most intuitive
「黃疸症」沒有甚麼太直觀式的名稱，
name, comes from the french jaunice, meaning
其名癌自於法語jaunice，意指「黃色」
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yellowing. It’s also sometimes referred
to as icterus though, the origin of which
它有時也涉指「黃疸」，而他的由來
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is even less intuitive, coming from the thought
that jaundice could once be cured by looking
更加地不直觀，覺得可以靠看黃鳥
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at a yellow bird, the more you know! Anyways,
as you’ve probably gathered, jaundice involves
來治癒。不論如何，正如你所知的，
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someone taking on yellow pigments, specifically
in the skin and eyes. The yellowing pigment
「黃疸症」和一個人的皮膚和眼睛有黃色素有關。
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is caused by a compound called bilirubin,
a component of bile and the main cause of
而「黃疸症」是由化合物「膽紅素」所造成，
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bruises being yellow, and after its metabolism,
the yellow-ness of urine and brown-ness of
其主要成份有膽汁和挫傷，在代謝後，
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feces. So since bilirubin’s our main culprit
of yellow-ness, it’s super important to
就成了尿液的黃色與糞便的棕色。
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know where it comes from. As red blood cells
near the end of their lifespan—which is
所以它就是造成「黃色」的罪魁禍首，它的由來很重要，
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about 120 days—they’re eaten up or phagocytosed
by macrophages in the reticuloendothelial
當紅血球約120天的生命週期接近尾聲時，他們就會被網狀內皮系統，
又名巨噬細胞系統中的巨噬細胞給吞噬，
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system, aka the macrophage system, where the
spleen plays the largest part, but it’s
脾臟在此發揮極大的作用，但其同時是部分的淋巴系統所組成
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also made of parts of the lymph nodes. K so
first the macrophage eats up the blood cell,
所以血紅素被網狀內皮系統後，
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and hemoglobin is broken up into heme and
globin, the globin is further broken into
血紅素被分解成原血紅素與血紅蛋白。
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amino acids. The heme on the other hand is
split into iron and protoporphyrin, protoporphyrin
血紅蛋白再被分解成胺基酸。原血紅素則被分為鐵質和原紫質
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is then converted into unconjugated bilirubin,
or UCB. Unconjugated bilirubin is the form
原紫質再轉換成非結合膽紅素或是UCB。非結合膽紅素
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of bilirubin that’s lipid-soluble, meaning
it’s not water-soluble, sometimes it’s
是一種汁融性膽紅素的形式，並非水溶性，有時
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also known as indirect bilirubin. Albumin
in the blood then binds to UCB and gives it
被稱作間接膽紅素。血液中的蛋白素
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a lift over to the liver where it’s taken
up by hepatocytes, where it’s conjugated
與UCB結合後轉移到肝臟，在到肝臟被肝細胞吸收，
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by an enzyme called uridine glucuronyl transferase
(UGT), making it now water soluble. At this
並與稱為尿苷葡萄糖醛酸的酶結合，使之可溶於水。
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point the conjugated bilrubin is secreted
out the bile canaliculi where it drains into
因此，結合膽紅素從膽小管分泌出來，被排入膽管和
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the bile ducts and sent to the gallbladder
for storage as bile. Now when you eat a donut
送到膽囊作為膽汁儲存。現在，當你吃了一個甜甜圈什麼的，
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or something, your gallbladder secretes the
bile and CB, it moves through the common bile
你的膽囊就會分泌膽汁和CB，它透過膽總管分泌至小腸中的
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duct to the duodenum of the small intestine
and is converted to urobilinogen, or UBG,
十二指腸，並轉換為尿膽原或UBG，
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by intestinal microbes in the gut. Now it
undergoes spontaneous oxidation, turning it
透由腸道中的微生物，它正自然地氧化，轉變
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into urobilin, which is excreted and responsible
for the brown color of feces. About 20% of
成尿後膽色素。尿後膽色素是種排泄物，也是造成排泄物是咖啡色的原因。大概有百分之二十的
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that UBG is actually recycled, though, in
other words it doesn’t get oxidized and
UBG是回收再利用的，所以換句話說，它並有氧化而且
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instead gets reabsorbed into the blood and
gets sent to the liver and kidneys, about
還被重新吸收至血液中，然後輸送至肝臟和腎臟，大約
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90% going to the liver and 10% going to the
kidneys. The 10% that goes to the kidneys
有百分之九十輸送至肝臟，百分之十則輸送至腎臟。而至腎臟的百分之十
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and is excreted causes the yellow-ness of
urine! And there you have it, bilirubin metabolism
是排泄物病造成尿液變黃！簡單來說就是這樣，膽紅素代謝。
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in a nutshell.
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Now if some point in this process is disrupted,
for example if your liver cells are damaged
如果在這個過程中的一些點差錯，例如，如果你的肝臟細胞被破壞
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and can’t conjugate bilirubin anymore, or
if they die and release their bilirubin, you
而且不能使用膽紅素了，或者
如果細胞死去然後釋放膽紅素，你
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can end up with increased bilirubin in the
blood, which can be conjugated or unconjugated,
血液中的膽紅素可能會升高，它可能是共軛的、非共軛的
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or both! This is what accounts for the yellow
color in the skin and eyes. Usually it takes
或是兩者皆是！這是造成皮膚和眼睛變黃的原因。通常需要
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about 2.5 mg/dL or greater of serum bilirubin
to give the skin that Simpsons-esque yellow
大約2.5 mg/dL或更多的血清膽紅素，皮膚才會變成"辛普森式"的黃
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skin tone. The earliest sign of jaundice and
increased bilirubin in the blood is by looking
膚色。初期可以從眼裡的鞏膜來判斷的是否有黃疸和血液中的膽紅素是否升高。
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at the sclera of the eyes. Scleral tissue
is high in elastin, which has a particular
鞏膜組織的彈性蛋白含量很高，而彈性蛋白對
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fondness for bilirubin and binds it with a
high affinity, giving the scleral tissue a
膽紅素有很強的吸引力並特別喜歡與之結合，並在讓皮膚變黃之前
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yellow color often before the skin. Now as
you might imagine after looking at this process,
先影響鞏膜組織的顏色。現在，你可能在看過這個過程後想像，
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there’re quite a few potential pitfalls
along the way that can lead to jaundice, and
有很多潛在的隱疾有可能導致罹患黃疸，而且
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they’re lumped together depending on whether
they have more UCB in the blood, more CB in
它們取決於是否有很多UCB(非結合膽紅素)、CB(結合膽紅素)、
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the blood, or more of both in the blood.
或是兩者皆集中在血液中。
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Two types of disorders that have increased
UCB and similar presentation of jaundice are
有兩種疾病混增加血液中的非結合膽紅素並且跟黃疸有類似的病徵，
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extravascular hemolytic anemias, where red
blood cells are broken down earlier than they
其中一種是溶血性貧血，在這種情況下紅血球會不正常分解，
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normally would, and ineffective hematopoesis,
where your blood cells don’t form quite
並無法正常造血，造成骨隨中血液的組成不正常，
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right in your bone marrow, causing macrophages
to break them down. In both cases, the red
引起巨噬細胞分解它們。在這兩種情況下，紅血球
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blood cells are broken down, causing high
levels of UCB. Since your hepatocytes can
被分解，從而導致非結合膽紅素過高。由於你的肝細胞只能
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only work so hard converting UCB to CB, they
can get overwhelmed. As an imaginary example,
將一定數量的非結合膽紅素轉換成結合膽紅素，它們可能會受不了。作一個假想的例子，
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say that this liver cell can conjugate 10
molecules of UCB a minute, max, but normally
假設一個肝細胞一分鐘內最多能結合10分子的非結合膽紅素，但通常
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they only see 5, so that’s easy. If all
the sudden your body starts breaking down
它們只看到5，所以5對肝細胞來說是很容易的。如果突然你的身體開始
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more blood cells and the UCB molecules on
this cell’s docket jumps to 15/min, this
以每分鐘15分子的速度分解更多的血液細胞和非結合膽紅素分子，
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liver cell can’t keep up, and that excess
of 5 molecules of UCB stays in the blood,
肝細胞會跟不上，那多餘的非結合膽紅素5分子就會停留在血液中，
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that’s the first issue. In addition, as
the liver cells max out, now there’s all
這就是首要問題。另外，肝細胞輸出過大，造成現在所有
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this CB that goes to the bile, which increases
the risk for pigmented bilirubin gallstones.
結合膽紅素融入膽汁，這增加了色素膽紅素膽結石的風險。
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Not only that, once all that CB is sent to
the duodenum, it’s converted to urobilinogen.
不僅如此，一旦所有的結合膽紅素輸送至十二指腸，它會轉換成尿膽素。
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Remember 20% of that urobilinogen is recycled
back into the blood and some of it is excreted
記得尿膽素中有20％被回收到血液中而其他的一些
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in the urine, giving it a much darker color.
The UCB is not excreted because it’s not
在尿中被排泄出體外，使尿液有較暗的顏色。非結合膽紅素則沒有排出體外
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water soluble!
，因為它不溶於水。
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In the previous two cases, too much UCB was
created, but you can also have hepatocytes
在前面的兩種情況下，生產了過多的非結合膽紅素，但你也可以有肝細胞，
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that just can’t work hard enough and keep
up. Physiologic jaundice of newborn is one
只是不夠努力運作並趕上進度。生理上新生兒黃疸是其中
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of these cases; newborn livers having a lower
amount of UGT in the liver to convert UCB,
一個案例;新生兒的幹臟不具有足夠的UGT來轉換非結合膽紅素，
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and after birth, UCB levels can be high due
to the natural process of macrophages destroying
出生後，UCB可能由於巨噬細胞破壞胎兒的紅血球的自然過程而增加。
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fetal red blood cells. Typically this is normal,
but can cause complications if UCB rises a
胎兒的紅血球的自然過程而增加。通常這是正常的，但可能引起並發症，如果非結合膽紅素上升
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LOT; since it’s fat soluble, it can collect
in the basal ganglia of the brain, which is
太多;因為它是脂溶性，它可能集中在大腦，這就是
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called kernicterus, and cause damage to the
brain or death. Treatment of this condition
所謂的核黃疸基底節，並造成大腦損害甚至死亡。通常這種情況的治療方法
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is usually phototherapy, which uses light
to induce structural and configurational changes
是光線療法，使用光誘導膽紅素分子中的結構和構型變化
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in the bilirubin molecule, basically it absorbs
the energy from the light and changes shape.
，基本上它是從光吸收能量並改變形狀。
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These new shapes are more soluble, and can
be excreted in the urine. This can be a super
這些新的形體是比較具可溶性的，並且可以藉由尿液排出。這可能是一個超級
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effective and non-invasive way to get excess
UCB out of the blood.
有效且非侵入性的治療方式，來從血液中取出過量的非結合膽紅素。
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Another potential case where not enough UCB
can be conjugated is through hereditary defects.
另一種可能的案例是由於遺傳缺陷造成沒有結合足夠的非結合膽紅素。
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One case is called Gilbert’s syndrome, where
their UGT enzyme activity is low and has a
一種情況是所謂的吉式症候群，它們的UGT活性較低，
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hard time cranking up when needed, so maybe
this liver cell can only pump through a max
也很難在必要的時候增強，所以或許這種肝細胞只能
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of 6 molecules/minute. Unfortunately, if something
comes along that increases hemolysis, like
以每分鐘6分子的極限運作。不幸的是，如果有任何會增加溶血的附加物，例如
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infection, stress, or starvation, the unconjugated
bilirubin load will increase which can easily
感染，壓力，或飢餓時，非結合膽紅素負荷會增加，這樣這些肝細胞很容易
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overwhelm these hepatocytes, cause buildup
of unconjugated bilirubin in the blood and
無法負荷，造成血液中非結合膽紅素的堆積，
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lead to jaundice.
導致黃疸。
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Another genetic example is called Crigler
Najjar syndrome, where gilbert’s syndrome
另一個基因上的例子被稱為克果納傑氏症候群。吉式症候群是
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was a low amount of UGT, Crigler Najjar is
where there’s pretty much no UGT and therefore
UGT不足，克果納傑氏症候群是幾乎沒有UGT，因此
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no ability to conjugate UCB, this will lead
to SUPER high levels of UCB, and likely UCB
沒有結合非結合膽紅素的能力。這將導致非結合膽紅素的量變得"超級"多，且
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deposits in the brain and kernicterus; Crigler
Najjar syndrome is usually fatal.
非結合膽紅素可能堆積至腦部和腦核性黃疸;克果納傑氏症候群通常是致命的。
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The previous couple examples focused on high
levels of unconjugated bilirubin in the blood,
前面的幾個例子專注於血液中含有高水平的非結合膽紅素，
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but there are also examples of jaundice with
high levels of conjugated bilirubin in the
但也有血液中含有高水平的結合膽紅素的黃疸
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blood.
案例。
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Dubin-Johnson syndrome is an autosomal recessive
disorder where there’s a deficiency in the
杜賓- 強生症候群是一種常染色體隱性遺傳疾病，其中有一個缺陷
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protein that helps move CB from the liver
cell to the bile ducts, called MRP2, so CB
幫助移動結合膽紅素從肝細胞向膽管，這個缺陷叫做MRP2蛋白質，所以結合膽紅素
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builds up in the hepatocyte. It’s thought
that when the MRP2 transporter is defected,
在肝細胞積聚。人們認為，當MRP2的輸送出現缺陷，
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another transporter, MRP3 is upregulated,
though this transporter moves it into the
另一個輸送員MRP3接手，相對於膽汁小管，這種輸送可使其進入
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interstitial space and blood flow, as opposed
to the bile canaliculus, so in this case you’ll
間隙空間和血液，因此，在這種情況下，
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have increased CB in the blood, which also
gets excreted into the urine, giving it a
增加血液中的結合膽紅素，這也隨尿液排泄出體外，
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darker color, this leakage also causes the
liver itself to get super dark.
使尿液顏色變得較深，該洩漏也導致肝臟本身變得超級黑。
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Another high-CB category of jaundice is called
obstructive jaundice, and this is basically
另一高CB類的黃疸被稱為阻塞性黃疸，這基本上是
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where something blocks the flow of bile, these
blockages could be anything from gallstones,
指有物體阻擋膽汁的流動，這些障礙可能是膽結石、
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pancreatic carcinomas and cholangiocarcinomas,
to parasites like the liver fluke. Remember
胰腺癌和膽管癌、或是寄生蟲，例如肝吸蟲。請記住，膽汁是由結合膽紅素組成，這基本上對堵塞膽管造成壓力，導致膽汁洩漏通過肝細胞之間的緊密連接，但是這並不是唯一漏出來的東西;膽鹽、膽汁酸和膽固醇都可以可以進入血液。
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that bile’s made up of conjugated bilirubin
and this blockage basically causes pressure
膽汁是由結合膽紅素組成，這基本上增加了對堵塞膽管造成的壓力
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to rise in the bile duct, which literally
causes bile to leak through the tight junctions
，導致膽汁洩漏通過肝細胞
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between hepatocytes, but that’s not the
only thing that leaks out though; bile salts,
之間的緊密連接，但是這並不是唯一漏出來的東西;膽鹽、
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00:09:19,570 --> 00:09:24,510
bile acids, and cholesterol all can can get
into the blood. If they deposit in the skin,
膽汁酸和膽固醇都可以可以進入血液。如果他們在皮膚上沉積，
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it could lead to itchiness or pruritus, but
also lead to things like hypercholesterolemia
就可能導致發癢或搔癢症，還會導致高膽固醇血症和
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00:09:30,080 --> 00:09:39,460
and xanthomas. The excess CB is excreted in
the urine, leading again to dark urine. Also,
黃色瘤之類的病徵。多餘的結合膽紅素是從尿中排出，再次導致尿液色變深。此外，
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00:09:39,460 --> 00:09:44,100
since you’re losing bile, you won’t be
able to absorb fat as well, which (1) causes
因為你失去的膽汁，你將不能夠正常吸收脂肪，其中（1）使你
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00:09:44,100 --> 00:09:50,190
you to excrete a ton of fat, a condition called
steatorrhea, and (2) causes you to not be
排泄大量的脂肪，此症狀稱為脂肪瀉;（2）使你不能夠
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able to absorb as many fat-soluble vitamins
as you need.
吸收所需的脂溶性維生素。
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00:09:54,280 --> 00:10:01,060
Finally, viral hepatitis leads to both conjugated
and unconjugated bilirubin in the blood. When
最後，病毒性肝炎導致血液中的兩個共軛和非結合膽紅素。當
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hepatocytes get infected and start to die
off, they both lose the ability to conjugate
肝細胞受到感染，並開始死亡，它們都失去了共軛
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bilirubin, leading to excess UCB in the blood,
AND since they also line the bile ducts, when
膽紅素的能力，從而導致血液中有過剩非結合膽紅素，當
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they die they let bile leak out into the blood,
causing an increase in blood CB as well. Again,
它們死了，因為他們也行經膽管，他們讓膽汁洩漏出來進入血液，也讓血液中結合膽紅素增加。
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since CB is up, patients will have more CB
excreted and darker urine.
同樣，因為結合膽紅素增加了，病人將排泄出更多的膽紅素，使尿液顏色更深。