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Annotation 1417711324428

Subject 3. Market Equilibrium
#cfa #cfa-level-1 #economics #has-images #microeconomics #reading-13-demand-and-supply-analysis-introduction #subject-3-market-equilibrium
Aggregate Demand and Aggregate Supply

An aggregate demand curve is simply a schedule that shows amounts of a product that buyers collectively desire to purchase at each possible price level.

An aggregate supply curve is simply a curve showing the amounts of a product that all firms will produce at each price level.

Example 1

Refer to the graph below. What is the market quantity that would be supplied at a price of $2.00?

Market quantity is the sum of individual quantities supplied at each price. At a price of $2.00, Ann supplies 4, Barry supplies 3, and Charlie supplies 0. The market supply is 7.

Market Equilibrium

Equilibrium is a state in which conflicting forces are in balance. In equilibrium, it will be possible for both buyers and sellers to realize their goals simultaneously.

The following graph depicts the market supply and demand for concert tickets at Madison Square Garden in New York City.

Equilibrium price and quantity are where the supply and demand curves intersect. Draw a horizontal line from the intersection to the price axis. This is equilibrium price: $60. Draw a vertical line from the intersection to the quantity axis. This is equilibrium quantity: 300. It is equilibrium because quantity demanded equals quantity supplied at $60 per ticket. At this price, there is neither surplus (excess supply) nor shortage (excess demand), so there is no downward or upward pressure for the price to change.

Surplus will push prices downward towards equilibrium.

  • Suppose the price is initially above the equilibrium price (P2) and sits at P1.
  • Quantity supplied (Q1s) will exceed quantity demanded (Q1D), creating a surplus.
  • The surplus will put downward pressure on prices since producers will begin to lower their prices to sell the surplus.
  • As a result, the price will fall, the quantity supplied will decrease, and the quantity demanded will increase until the equilibrium price (P2) is restored.
  • This process involves movements along supply-and-demand curves since the changes are caused by price fluctuations.

Similarly, shortages push prices upward towards equilibrium.

Because the price rises if it is below equilibrium, falls if it is above equilibrium, and remains constant if it is at equilibrium, the price is pulled toward equilibrium and remains there until some event changes the equilibrium. We refer to such an equilibrium as being stable because whenever price is disturbed away from the equilibrium, it tends to converge back to that equilibrium.

An unstable equilibrium is an equilibrium that is not restored if disrupted by an external force. While most equilibria studied in economics are of the stable variety, a few cases of unstable equilibria do emerge from time to time, in limited circumstances.
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Annotation 1419556556044

Aggregate Demand and Aggregate Supply
#cfa #cfa-level-1 #economics #has-images #microeconomics #reading-13-demand-and-supply-analysis-introduction #subject-3-market-equilibrium

An aggregate demand curve is simply a schedule that shows amounts of a product that buyers collectively desire to purchase at each possible price level.

An aggregate supply curve is simply a curve showing the amounts of a product that all firms will produce at each price level.

Example 1

Refer to the graph below. What is the market quantity that would be supplied at a price of $2.00?

Market quantity is the sum of individual quantities supplied at each price. At a price of $2.00, Ann supplies 4, Barry supplies 3, and Charlie supplies 0. The market supply is 7.

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Subject 3. Market Equilibrium
Aggregate Demand and Aggregate Supply An aggregate demand curve is simply a schedule that shows amounts of a product that buyers collectively desire to purchase at each possible price level. An aggregate supply curve is simply a curve showing the amounts of a product that all firms will produce at each price level. Example 1 Refer to the graph below. What is the market quantity that would be supplied at a price of $2.00? Market quantity is the sum of individual quantities supplied at each price. At a price of $2.00, Ann supplies 4, Barry supplies 3, and Charlie supplies 0. The market supply is 7. Market Equilibrium Equilibrium is a state in which conflicting forces are in balance. In equilibrium, it will be possible for both buyers and sel



Annotation 1419565468940

#cfa #cfa-level-1 #economics #has-images #microeconomics #reading-13-demand-and-supply-analysis-introduction #subject-3-market-equilibrium
Market Equilibrium

Equilibrium is a state in which conflicting forces are in balance. In equilibrium, it will be possible for both buyers and sellers to realize their goals simultaneously.

The following graph depicts the market supply and demand for concert tickets at Madison Square Garden in New York City.

Equilibrium price and quantity are where the supply and demand curves intersect. Draw a horizontal line from the intersection to the price axis. This is equilibrium price: $60. Draw a vertical line from the intersection to the quantity axis. This is equilibrium quantity: 300. It is equilibrium because quantity demanded equals quantity supplied at $60 per ticket. At this price, there is neither surplus (excess supply) nor shortage (excess demand), so there is no downward or upward pressure for the price to change.

Surplus will push prices downward towards equilibrium.

  • Suppose the price is initially above the equilibrium price (P2) and sits at P1.
  • Quantity supplied (Q1s) will exceed quantity demanded (Q1D), creating a surplus.
  • The surplus will put downward pressure on prices since producers will begin to lower their prices to sell the surplus.
  • As a result, the price will fall, the quantity supplied will decrease, and the quantity demanded will increase until the equilibrium price (P2) is restored.
  • This process involves movements along supply-and-demand curves since the changes are caused by price fluctuations.

Similarly, shortages push prices upward towards equilibrium.

Because the price rises if it is below equilibrium, falls if it is above equilibrium, and remains constant if it is at equilibrium, the price is pulled toward equilibrium and remains there until some event changes the equilibrium. We refer to such an equilibrium as being stable because whenever price is disturbed away from the equilibrium, it tends to converge back to that equilibrium.

An unstable equilibrium is an equilibrium that is not restored if disrupted by an external force. While most equilibria studied in economics are of the stable variety, a few cases of unstable equilibria do emerge from time to time, in limited circumstances.
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Subject 3. Market Equilibrium
; Market quantity is the sum of individual quantities supplied at each price. At a price of $2.00, Ann supplies 4, Barry supplies 3, and Charlie supplies 0. The market supply is 7. <span>Market Equilibrium Equilibrium is a state in which conflicting forces are in balance. In equilibrium, it will be possible for both buyers and sellers to realize their goals simultaneously. The following graph depicts the market supply and demand for concert tickets at Madison Square Garden in New York City. Equilibrium price and quantity are where the supply and demand curves intersect. Draw a horizontal line from the intersection to the price axis. This is equilibrium price: $60. Draw a vertical line from the intersection to the quantity axis. This is equilibrium quantity: 300. It is equilibrium because quantity demanded equals quantity supplied at $60 per ticket. At this price, there is neither surplus (excess supply) nor shortage (excess demand), so there is no downward or upward pressure for the price to change. Surplus will push prices downward towards equilibrium. Suppose the price is initially above the equilibrium price (P 2 ) and sits at P 1 . Quantity supplied (Q 1s ) will exceed quantity demanded (Q 1D ), creating a surplus. The surplus will put downward pressure on prices since producers will begin to lower their prices to sell the surplus. As a result, the price will fall, the quantity supplied will decrease, and the quantity demanded will increase until the equilibrium price (P 2 ) is restored. This process involves movements along supply-and-demand curves since the changes are caused by price fluctuations. Similarly, shortages push prices upward towards equilibrium. Because the price rises if it is below equilibrium, falls if it is above equilibrium, and remains constant if it is at equilibrium, the price is pulled toward equilibrium and remains there until some event changes the equilibrium. We refer to such an equilibrium as being stable because whenever price is disturbed away from the equilibrium, it tends to converge back to that equilibrium. An unstable equilibrium is an equilibrium that is not restored if disrupted by an external force. While most equilibria studied in economics are of the stable variety, a few cases of unstable equilibria do emerge from time to time, in limited circumstances.<span><body><html>



Annotation 1420204576012

M2-receptorer decreases heartrate by the G beta gamma subunit of the G protein coupled to M2.
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M2-receptors modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate.

Original toplevel document

Muscarinic acetylcholine receptor M2 - Wikipedia
is claim instead found no significant association between the CHRM2 gene and intelligence. [8] Olfactory behavior[edit] Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating) [9] Mechanism of action[edit] <span>M 2 muscarinic receptors act via a G i type receptor, which causes a decrease in cAMP in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors. [10] In addition, they modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate. Ligands[edit] Few highly selective M 2 agonists are available at present, although there are several non-selective muscarinic agonists that stimulate M 2 , and a number of selectiv



Annotation 1420413242636

#instalacje #ogrzewanie
COP Jest to stosunek:
ilości uzyskanej energii użytecznej (np. ciepła do ogrzewania),
do energii włożonej – napędowej (np. energia elektryczna do zasilania sprężarki).
COP (ang. coefficent of performance):
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Flashcard 1420469079308

Question
Pompy ciepła wykorzystują zjawisko przepływu [...].
Answer
ciepła

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Pompy ciepła wykorzystują zjawisko przepływu ciepła.

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Flashcard 1420470652172

Question
Pompy ciepła wykorzystują zjawisko [...] ciepła.
Answer
przepływu

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Pompy ciepła wykorzystują zjawisko przepływu ciepła.

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Annotation 1420472225036

Pompy ciepła wykorzystują zjawisko zmiany stanu fizycznego substancji.
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Pompy ciepła wykorzystują zjawisko przepływu ciepła. Pompy ciepła wykorzystują zjawisko zmiany stanu fizycznego substancji. Przykład. Jeżeli do gotującej się w naczyniu wody będziemy dalej dostarczać energię (ciepło), to cała woda wyparuje, a jej temperatura nie wzrośnie. Ilość energii związana ze

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Annotation 1420704484620

#dieta #tcm
PIERWSZA Słuchać sygnałów płynący ch z w łasnego o rganizm u.
Nie jeść, jeżeli nie odczuwa się głodu. M ożna wypić sok, zjeść jakiś owoc lub m ałą porcję surówki albo poprzestać na szklance wody. To za lecenie dotyczy również tych, którzy aktualnie stosują dietę oczysz czającą wątrobę i zastanaw iają się, czy powinni jeść, jeżeli nade szła pora posiłku. Nie należy jednak głodzić się i doprowadzać do bólów głodo wych, które m ogą pow odow ać wrzody i wyw oływ ać hipoglike- mię. Zbyt w iele osób trzym a się sztyw no ustalonego planu posił ków i jada na przykład regularnie o 8.00, 13.00 i 19.00 bez w zglę du na to, czy odczuwa głód czy nie. Znacznie zdrowiej będzie, je żeli porę posiłku w skaże głód, a nie zegar, podobnie jak to robią dzieci, które jedzą wtedy, gdy są głodne i nie zw racają uwagi na zegar. Jeżeli ktoś ma naw yk spożyw ania regularnych posiłków bez uczucia głodu, zm usza sw oją wątrobę do nadm iernego w ysił ku, wskutek czego cierpi ona z przepracow ania i przeciążenia, podobnie jak zartretyzow ane stawy zmuszane do ruchu
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Annotation 1420706843916

#b21 #instalacje #ogrzewanie #seo
Parowanie i skraplanie odbywa się przy stałym ciśnieniu
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Annotation 1420708416780

#instalacje #ogrzewanie
entalpia to zawartość energii
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/head>Entalpia – określa zawartość energii w układzie termodynamicznym, oznaczana jako: H, I [kJ; Wh]; entalpia właściwa: h, i [kJ/kg, Wh/kg]. Entalpia, ze starogreckiego: „en” – „w” i „thalpein” – „rozgrzewać”. entalpia to zawartość energii <html>

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Annotation 1420710251788

#b21 #instalacje #ogrzewanie #seo
Im mniejsza jest różnica temperatur pomiędzy temperaturą zasilania obiegu grzewczego i temperaturą wejściową źródła ciepła (∆T), tym wyższy jest współczynnik wydajności COP (efektywności). temperatura zasilania ogrzewania niższa o 1 K – COP wyższy o 2,5% temperatura źródła, np. solanki, wyższa o 1 K – COP wyższy o 2,7%
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Annotation 1420711824652

#b21 #instalacje #ogrzewanie #seo
Współczynnik efektywności chłodniczej – EER EER (Energy Efficiency Ratio) – współczynnik, który określa efektywność pompy ciepła, przy pracy w trybie chłodzenia. Jest to stosunek dostarczonej mocy chłodniczej, do pobranej mocy elektrycznej. Jeśli EER wynosi 3 to znaczy, że wykorzystując 1 kWh energii elektrycznej dostarczamy do pomieszczenia 3 kWh chłodu (lub usuwamy 3 kWh ciepła).
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Annotation 1420713397516

#b21 #instalacje #ogrzewanie #seo
COP określa stosunek ciepła użytecznego dostarczonego przez pompę ciepła, do pobranej przy tym energii elektrycznej - w konkretnym punkcie pracy (temperatur), w danej chwili. Może służyć do porównania pomp ciepła różnych producentów – dla tych samych warunków pracy.
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Annotation 1420714970380

#b21 #instalacje #ogrzewanie #seo
SPF, JAZ, SCOP - jest to stosunek dostarczonego ciepła użytecznego, do zużycia energii elektrycznej, ale wykorzystanej przez całą instalację ogrzewania (pompy, grzałki, siłowniki, itp.) - dla określonego przedziału czasu, np.: dla miesiąca, okresu grzewczego, całego roku, itp. Jest pomocny przy określaniu efektywności instalacji ogrzewania budynku z pompą ciepła, tym samym, do oszacowania kosztów ogrzewania, np. w ciągu całego roku.
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Annotation 1420716543244

#b21 #instalacje #ogrzewanie #seo
Kolektory wykorzystują ciepło, które dostarczone zostało do gruntu w wyniku promieniowania słonecznego, opadów deszczu lub z wodą pochodzącą z roztopów. Wykorzystują w miarę stabilną temperaturę gruntu w ciągu całego roku : rury z tworzyw sztucznych, zakopane ok. 20 cm poniżej strefy przemarzania gruntu: od 1,2 do 1,6 m (większe głębokości są nieuzasadnione ekonomicznie) pojedyncze pętle (kręgi): do100 m długości – dla uzyskania możliwie niewielkich spadków ciśnienia (>100 m – pompa o większej mocy) poszcz. pętle wymiennika łączą się w kolektorze zasilającym i powrotnym
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Flashcard 1420723621132

Question
[default - edit me]
Answer
This part of the G protein can open K+ channels, which causes an outward current of potassium, which slows down the heart rate.

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
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M2-receptorer decreases heartrate by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels, which causes an outward current of potassium, which slows down the heart rate.

Original toplevel document

Muscarinic acetylcholine receptor M2 - Wikipedia
is claim instead found no significant association between the CHRM2 gene and intelligence. [8] Olfactory behavior[edit] Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating) [9] Mechanism of action[edit] <span>M 2 muscarinic receptors act via a G i type receptor, which causes a decrease in cAMP in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors. [10] In addition, they modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate. Ligands[edit] Few highly selective M 2 agonists are available at present, although there are several non-selective muscarinic agonists that stimulate M 2 , and a number of selectiv






Annotation 1420724669708

G-Beta-gamma part of the G protein of M2 can open K+ channels, which slows down the heart rate
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M2-receptorer decreases heartrate by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels, which causes an outward current of potassium, which slows down the heart rate.

Original toplevel document

Muscarinic acetylcholine receptor M2 - Wikipedia
is claim instead found no significant association between the CHRM2 gene and intelligence. [8] Olfactory behavior[edit] Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating) [9] Mechanism of action[edit] <span>M 2 muscarinic receptors act via a G i type receptor, which causes a decrease in cAMP in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors. [10] In addition, they modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate. Ligands[edit] Few highly selective M 2 agonists are available at present, although there are several non-selective muscarinic agonists that stimulate M 2 , and a number of selectiv



Flashcard 1420728601868

Question
[...] decreases heartrate by the G beta gamma subunit of the G protein coupled to M2.
Answer
M2-receptorer

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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M2-receptorer decreases heartrate by the G beta gamma subunit of the G protein coupled to M 2 .

Original toplevel document

Muscarinic acetylcholine receptor M2 - Wikipedia
is claim instead found no significant association between the CHRM2 gene and intelligence. [8] Olfactory behavior[edit] Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating) [9] Mechanism of action[edit] <span>M 2 muscarinic receptors act via a G i type receptor, which causes a decrease in cAMP in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors. [10] In addition, they modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate. Ligands[edit] Few highly selective M 2 agonists are available at present, although there are several non-selective muscarinic agonists that stimulate M 2 , and a number of selectiv






Flashcard 1420730174732

Question
M2-receptorer [...] heartrate by the G beta gamma subunit of the G protein coupled to M2.
Answer
decreases

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M2-receptorer decreases heartrate by the G beta gamma subunit of the G protein coupled to M 2 .

Original toplevel document

Muscarinic acetylcholine receptor M2 - Wikipedia
is claim instead found no significant association between the CHRM2 gene and intelligence. [8] Olfactory behavior[edit] Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating) [9] Mechanism of action[edit] <span>M 2 muscarinic receptors act via a G i type receptor, which causes a decrease in cAMP in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors. [10] In addition, they modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate. Ligands[edit] Few highly selective M 2 agonists are available at present, although there are several non-selective muscarinic agonists that stimulate M 2 , and a number of selectiv






Flashcard 1420731747596

Question
M2-receptorer decreases heartrate by the [...] of the G protein coupled to M2.
Answer
G beta gamma subunit

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M2-receptorer decreases heartrate by the G beta gamma subunit of the G protein coupled to M 2 .

Original toplevel document

Muscarinic acetylcholine receptor M2 - Wikipedia
is claim instead found no significant association between the CHRM2 gene and intelligence. [8] Olfactory behavior[edit] Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating) [9] Mechanism of action[edit] <span>M 2 muscarinic receptors act via a G i type receptor, which causes a decrease in cAMP in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors. [10] In addition, they modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate. Ligands[edit] Few highly selective M 2 agonists are available at present, although there are several non-selective muscarinic agonists that stimulate M 2 , and a number of selectiv






Flashcard 1420733320460

Question
[...] effect of vasopressin occurs via activation of V2R.
Answer

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Antidiuretic effect of vasopressin occurs via activation of V 2 R.

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Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri






Flashcard 1420734893324

Question
Antidiuretic effect of vasopressin occurs via activation of [...]
Answer
V2R.

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Antidiuretic effect of vasopressin occurs via activation of V 2 R.

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri






Flashcard 1420736466188

Question
Antidiuretic effect of [...] occurs via activation of V2R.
Answer
vasopressin

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Antidiuretic effect of vasopressin occurs via activation of V 2 R.

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri






Flashcard 1420738039052

Question
HUr sker antidiuretiska effekter av ADH? (receptor)
Answer
activation of V2R.

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Antidiuretic effect of vasopressin occurs via activation of V 2 R.

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri






Flashcard 1420740398348

Question
[Typ av vasopressinreceptor] are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.
Answer
V1 receptors (V1Rs)

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V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.

Original toplevel document

Vasopressin receptor - Wikipedia
f collecting duct, vascular endothelium and vascular smooth muscle cell insertion of AQP-2 water channels into apical membrane, induction of AQP-2 synthesis, releases von Willebrand factor and factor VIII, vasodilation V 1 receptor[edit] <span>V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade. [1] Cardiac myocytes also possess V 1 R. Additionally V 1 R are located in brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. [1] V 1 R is present on platelets, which upon stimulation induces an increase in intracellular calcium, facilitating thrombosis. Studies have indicated that due to polymorphism of platelet V 1 R there is significant heterogeneity in the aggregation response of normal human platelets to vasopressin. [1] V 1 Rs are found in kidney, where they occur in high density on medullary interstitial cells, vasa recta, and epithelial cells of the collecting duct. [1] Vasopressin acts on medullary vasculature through V 1 R to reduce blood flow to inner medulla without affecting blood flow to outer medulla. V 1 Rs on the luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus a






Flashcard 1420742757644

Question
V1 receptors (V1Rs) are found in high density on [...]

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V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.

Original toplevel document

Vasopressin receptor - Wikipedia
f collecting duct, vascular endothelium and vascular smooth muscle cell insertion of AQP-2 water channels into apical membrane, induction of AQP-2 synthesis, releases von Willebrand factor and factor VIII, vasodilation V 1 receptor[edit] <span>V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade. [1] Cardiac myocytes also possess V 1 R. Additionally V 1 R are located in brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. [1] V 1 R is present on platelets, which upon stimulation induces an increase in intracellular calcium, facilitating thrombosis. Studies have indicated that due to polymorphism of platelet V 1 R there is significant heterogeneity in the aggregation response of normal human platelets to vasopressin. [1] V 1 Rs are found in kidney, where they occur in high density on medullary interstitial cells, vasa recta, and epithelial cells of the collecting duct. [1] Vasopressin acts on medullary vasculature through V 1 R to reduce blood flow to inner medulla without affecting blood flow to outer medulla. V 1 Rs on the luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus a






Flashcard 1420744330508

Question
V1 receptors causes [...]
Answer
vasoconstriction

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V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.

Original toplevel document

Vasopressin receptor - Wikipedia
f collecting duct, vascular endothelium and vascular smooth muscle cell insertion of AQP-2 water channels into apical membrane, induction of AQP-2 synthesis, releases von Willebrand factor and factor VIII, vasodilation V 1 receptor[edit] <span>V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade. [1] Cardiac myocytes also possess V 1 R. Additionally V 1 R are located in brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. [1] V 1 R is present on platelets, which upon stimulation induces an increase in intracellular calcium, facilitating thrombosis. Studies have indicated that due to polymorphism of platelet V 1 R there is significant heterogeneity in the aggregation response of normal human platelets to vasopressin. [1] V 1 Rs are found in kidney, where they occur in high density on medullary interstitial cells, vasa recta, and epithelial cells of the collecting duct. [1] Vasopressin acts on medullary vasculature through V 1 R to reduce blood flow to inner medulla without affecting blood flow to outer medulla. V 1 Rs on the luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus a






Flashcard 1420745903372

Question
Vilken typ av receptor är V1 receptor?
Answer
Gaq

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V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.</sp

Original toplevel document

Vasopressin receptor - Wikipedia
f collecting duct, vascular endothelium and vascular smooth muscle cell insertion of AQP-2 water channels into apical membrane, induction of AQP-2 synthesis, releases von Willebrand factor and factor VIII, vasodilation V 1 receptor[edit] <span>V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade. [1] Cardiac myocytes also possess V 1 R. Additionally V 1 R are located in brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. [1] V 1 R is present on platelets, which upon stimulation induces an increase in intracellular calcium, facilitating thrombosis. Studies have indicated that due to polymorphism of platelet V 1 R there is significant heterogeneity in the aggregation response of normal human platelets to vasopressin. [1] V 1 Rs are found in kidney, where they occur in high density on medullary interstitial cells, vasa recta, and epithelial cells of the collecting duct. [1] Vasopressin acts on medullary vasculature through V 1 R to reduce blood flow to inner medulla without affecting blood flow to outer medulla. V 1 Rs on the luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus a






Flashcard 1420748262668

Question
Var finns V1 receptorn?
Answer
vascular smooth muscle

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V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.

Original toplevel document

Vasopressin receptor - Wikipedia
f collecting duct, vascular endothelium and vascular smooth muscle cell insertion of AQP-2 water channels into apical membrane, induction of AQP-2 synthesis, releases von Willebrand factor and factor VIII, vasodilation V 1 receptor[edit] <span>V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade. [1] Cardiac myocytes also possess V 1 R. Additionally V 1 R are located in brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. [1] V 1 R is present on platelets, which upon stimulation induces an increase in intracellular calcium, facilitating thrombosis. Studies have indicated that due to polymorphism of platelet V 1 R there is significant heterogeneity in the aggregation response of normal human platelets to vasopressin. [1] V 1 Rs are found in kidney, where they occur in high density on medullary interstitial cells, vasa recta, and epithelial cells of the collecting duct. [1] Vasopressin acts on medullary vasculature through V 1 R to reduce blood flow to inner medulla without affecting blood flow to outer medulla. V 1 Rs on the luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus a






Flashcard 1420750621964

Question
Vad händer när ADH binder till V1-receptorn?

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V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.

Original toplevel document

Vasopressin receptor - Wikipedia
f collecting duct, vascular endothelium and vascular smooth muscle cell insertion of AQP-2 water channels into apical membrane, induction of AQP-2 synthesis, releases von Willebrand factor and factor VIII, vasodilation V 1 receptor[edit] <span>V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade. [1] Cardiac myocytes also possess V 1 R. Additionally V 1 R are located in brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. [1] V 1 R is present on platelets, which upon stimulation induces an increase in intracellular calcium, facilitating thrombosis. Studies have indicated that due to polymorphism of platelet V 1 R there is significant heterogeneity in the aggregation response of normal human platelets to vasopressin. [1] V 1 Rs are found in kidney, where they occur in high density on medullary interstitial cells, vasa recta, and epithelial cells of the collecting duct. [1] Vasopressin acts on medullary vasculature through V 1 R to reduce blood flow to inner medulla without affecting blood flow to outer medulla. V 1 Rs on the luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus a






Flashcard 1420752981260

Question
Vilken cell ökar i ICV när ADH binder till V1-receptor
Answer
calcium

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V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade.

Original toplevel document

Vasopressin receptor - Wikipedia
f collecting duct, vascular endothelium and vascular smooth muscle cell insertion of AQP-2 water channels into apical membrane, induction of AQP-2 synthesis, releases von Willebrand factor and factor VIII, vasodilation V 1 receptor[edit] <span>V 1 receptors (V 1 Rs) are found in high density on vascular smooth muscle and cause vasoconstriction by an increase in intracellular calcium via the phosphatidyl–inositol-bisphosphonate cascade. [1] Cardiac myocytes also possess V 1 R. Additionally V 1 R are located in brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. [1] V 1 R is present on platelets, which upon stimulation induces an increase in intracellular calcium, facilitating thrombosis. Studies have indicated that due to polymorphism of platelet V 1 R there is significant heterogeneity in the aggregation response of normal human platelets to vasopressin. [1] V 1 Rs are found in kidney, where they occur in high density on medullary interstitial cells, vasa recta, and epithelial cells of the collecting duct. [1] Vasopressin acts on medullary vasculature through V 1 R to reduce blood flow to inner medulla without affecting blood flow to outer medulla. V 1 Rs on the luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus a






Annotation 1420756126988

Vasopressin regulates water excretion by increasing the water permeability of the collecting duct
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he V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] <span>Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalize

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri



Flashcard 1420757699852

Question
Vilken typ av receptor är V2?
Answer
Gs

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the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate <span>G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes&quot

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri






Flashcard 1420760059148

Question
Vad uppreglerar ADH genom V2 receptor`?
Answer
aquaporin-2

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G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of <span>aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1]<span><body><html>

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri






Flashcard 1420762418444

Question
Vilka celler har V2-receptor?
Answer
principal cells

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plexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct <span>principal cells, increasing water reabsorption. [1]<span><body><html>

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri






Flashcard 1420764777740

Question
Var finns V2-receptorn?
Answer
collecting duct

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m "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the <span>collecting duct principal cells, increasing water reabsorption. [1]<span><body><html>

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri