lec 12 - pt.2 - rsystem
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r systemTRANSCRIPT
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Henley Beach, South Australia
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Slides includes material (direct or modified) from © 2013 Pearson Education, Inc. Human Anatomy & Physiology, Ninth Edition and materialsupplied by Dr J Carnegie and other sources as referenced
The Respiratory System
Lecs 3 & 4
ANP 1105A&EAnthony Krantis, [email protected]
These slides contain material to be presented in lecture*.The information from the lecture should be used in combination with the
relevant chapters of the recommended Text book(s).Throughout this presentation, there are references to and use of figures
from the text book. In addition, specific animations/videosare also referenced and can be used by the student forstudy purposes, if they wish.*Slides marked with a STAR will not be covered in the lecture but are
provided as additional learning material
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Respiratory SystemRespiration
Respiration = the series of exchanges that leads to theuptake of oxygen by the cells, and the release of carbondioxide to the lungs
Step 1 = ventilation –
Inspiration & expiration
Step 2 = exchange between alveoli (lungs) and pulmonarycapillaries (blood)
–
Referred to as External Respiration
Step 3 = transport of gases in blood
Step 4 = exchange between blood and cells – Referred to as Internal Respiration
– Cellular respiration = use of oxygen in ATP synthesis
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Gas Exchanges Between Blood, Lungs, and Tissues
• External respiration –diffusion of gases in lungs
–
Thickness and surface area of respiratory membrane – Partial pressure gradients and gas solubilities
– Ventilation-perfusion coupling
•
Internal respiration –diffusion of gases at body
tissues
• Both involve
– Physical properties of gases
– Composition of alveolar gas
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External Respiration
Internal Respiration
Ventilation
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Basic Properties of Gases:
Dalton's Law of Partial Pressures
•
Total P exerted by mixture of gases
= sum of pressures exerted by each gas
•
Partial pressure (PP)
– Pressure exerted by each gas inmixture
– Directly proportional to its % inmixture
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Table 22.4 Comparison of Gas Partial Pressuresand Approximate Percentages in theAtmosphere and in the Alveoli
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Basic Properties of Gases:
Henry's Law
• Gas mixtures in contact with liquid
– Each gas dissolves in proportion to its PP
– At equilibrium, PP’s in two phases will be
equal – Amount of each gas that will dissolve
depends on
• Solubility: CO2 20x more soluble in
water than O2; little N2 dissolves inwater
• Temperature: as T0 rises, solubility
decreases
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Partial Pressure Gradients and Gas Solubilities
• Steep PP gradient for O2 in lungs
–
Venous blood Po2 = 40 mm Hg
– Alveolar Po2 = 104 mm Hg
•
Drives O2 flow to blood• Equilibrium reached across respiratory
membrane in ~0.25 seconds, about 1/3time a red blood cell is in pulmonary
capillary!
– Adequate oxygenation even if blood
flow increases 3X
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Figure 22.18 Oxygenation of blood in the pulmonary capillaries at rest.
100
5040
0 0 0.25 0.50 0.75
PO2 104 mm Hg
Time in thepulmonary capillary (sec)
End ofcapillary
Start ofcapillary
P O 2 ( m
m H g )
150
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Partial Pressure Gradients and Gas Solubilities
•
PP gradient for CO2 in lungs less steep – Venous blood Pco2 = 45 mm Hg
– Alveolar Pco2 = 40 mm Hg
• However CO2 diffuses in equal amounts with
oxygen
– CO2 is 20X more soluble in plasma than O2
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Ventilation-Perfusion Coupling
• Perfusion- blood flow reaching alveoli
• Ventilation- amount of gas reaching alveoli
• Ventilation and Perfusion matched
(coupled) for efficient gas exchange
– Never balanced for all alveoli due to
• Regional variations due to effect ofgravity on blood and air flow
• Some alveolar ducts plugged with
mucus
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Ventilation-Perfusion Coupling
Perfusion
–
Changes in gasses in alveoli cause changes in
diameters of arterioles
• Where alveolar O2 is high, arterioles - dilate
• Where alveolar O2 is low, arterioles - constrict
•
Directs most blood where alveolar oxygen high
• Where alveolar CO2 is high, bronchioles - dilate
•
Where alveolar CO2 is low, bronchioles - constrict• Allows elimination of CO2 more rapidly
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Figure 22.19 Ventilation-perfusion coupling
Ventilation less than perfusion Ventilation greater than perfusion
Mismatch of ventilation and perfusion ventilation and/or perfusion of alveoli
causes local P and PCO2 O2
Mismatch of ventilation and perfusion ventilation and/or perfusion of alveoli
causes local P and PCO2 O2
O2 autoregulatesarteriolar diameter
O2 autoregulatesarteriolar diameter
Pulmonary arteriolesserving these alveoli
constricts
Pulmonary arteriolesserving these alveoli
dilate
Match of ventilation
and perfusionventilation, perfusion
Match of ventilation
and perfusionventilation, perfusion
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Internal Respiration
Capillary gas exchange in body tissues
•
Partial pressures and diffusion gradients reversed
compared to external respiration
– Tissue Po2 always lower than in systemicarterial blood O2 from blood to tissues
–
CO2 from tissues to blood
– Venous blood Po2 40 mm Hg and Pco2 45 mm Hg
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Figure 22.17 Partialpressure gradients
promoting gas
movements in thebody.
Inspired air:
PO2
PCO2
160 mm Hg
0.3 mm Hg
Alveoli of lungs:
PO2
PCO2
104 mm Hg
40 mm Hg
Externalrespiration
Pulmonaryarteries
AlveoliPulmonary
veins (PO2
100 mm Hg)
Blood leaving
tissues andentering lungs:PO2
PCO2 40 mm Hg
45 mm Hg PO2
PCO2
Blood leaving
lungs andentering tissue
capillaries:
100 mm Hg
40 mm Hg
Systemicveins Systemicarteries
Internalrespiration
Tissues:PO2
less than 40 mm Hg
PCO2
greater than 45 mm Hg
Heart
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O2 Transport in Blood
Molecular O2 carried in blood
–
1.5% dissolved in plasma
– 98.5% loosely bound to each Fe of hemoglobin (Hb)in RBCs
• Maximum 4 O2 per Hb = Oxyhemoglobin (HbO
2)
Reduced Hb(has released it’s O2 )
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O2 and Hemoglobin
Rate of loading and unloading of O2 regulated to
ensure adequate oxygen delivery to cells
– Po2
– Temperature
– Blood pH
– Pco2
– Concentration of BPG–1,3-
bisphosphoglycerate, metabolite of glycolysis
in RBCs; levels rise when oxygen levels
chronically low promotes the release of the remainingoxygen molecules bound to the
hemoglobin, thus enhancing the ability ofRBCs to release oxygen near tissues that
need it most.
Figure 22 20 The amount of oxygen carried by hemoglobin depends on the P (the amount of oxygen) available
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Figure 22.20 The amount of oxygen carried by hemoglobin depends on the PO2 (the amount of oxygen) available
locally.
This axis tells you how much
O2 is bound to Hb. At 100%,
each Hb molecule has 4 bound
oxygen molecules.
In the lungs, where PO2 is
high (100 mm Hg), Hb isalmost fully saturated
(98%) with O2.
If more O2 is present,more O2 is bound.
However, because of
Hb’s properties (O2 binding strength
changes with
saturation), this is an
S-shaped curve, not astraight line.
Hemoglobin
Oxygen
100
80
60
40
20
0
0 20 40 60 80 100
P e r c e n t O 2 s a t u r a t i o n o f h e m o g l o b i n
P (mm Hg)
This axis tells you the relative
Amount (partial pressure) of
O2 disslolved in the fluid
Surrounding the Hb.
In the tissues of other organs,where PO2
is low (40 mm Hg), Hb
is less saturated (75%) with O2.
•
•
O2
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Influence of Po2 on Hemoglobin Saturation
•
Venous blood
–
Po2 = 40 mm Hg
–
Contains 15 vol % oxygen
–
Hb is 75% saturated
–
Venous reserve
•
Oxygen remaining in venous blood
•
Arterial blood
–
Po2 = 100 mm Hg
–
Contains 20 ml oxygen per 100 ml blood
(20 vol %)
–
Hb is 98% saturated
•
Further increases in Po2 (e.g., breathing deeply) produce minimalincreases in O2 binding
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In the lungs100
80
60
40
20
00 20 40 60 80
P e r c e n t O 2 s a
t u r a t i o n o f h e m o g l o b i n
100
PO2 (mm Hg)
At high PO2, large changes in PO2 cause only
small changes in Hb saturation. Notice that the
curve is relatively flat here. Hb’s properties
produce a safety margin that ensures that Hb is
almost fully saturated even with a substantial PO2
decrease. As a result, Hb remains saturated even
at high altitude or with lung disease.
At high altitude, there is less O2.
At a PO2 in the lungs of only 80
mm Hg, Hb is still 95% saturated.
At sea level, there is lots of O2.
At a PO2 in the lungs of 100 mm Hg,
Hb is 98% saturated.
98%
95%
Figure 22.20 The amount of oxygen carried by hemoglobin depends on the PO2 (amount of oxygen) available locally
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Figure 22.21 Effect oftemperature, PCO2
, and blood pHon the oxygen-hemoglobin
dissociation curve.
P e r c e n t O 2 s a t u r a
t i o n o f h e m o g l o b i n
P e r c e n t O 2 s a t u r a
t i o n o f h e m o g l o b i n
10ºC
20ºC38ºC
43ºC
0
20
40
60
80
100
0
20
40
60
80
100
Normal bodytemperature
Decreased carbon dioxide(PCO2
20 mm Hg) or H+ (pH 7.6)
Normal arterial
carbon dioxide
(PCO2 40 mm Hg)or H+ (pH 7.4)
Increased carbon dioxide
(PCO2 80 mm Hg)
or H+ (pH 7.2)
20 40 60 80 100
P
mm Hg)
O
2
a)
b)
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Factors that Increase Release of O2 by Hemoglobin
As cells metabolize glucose and use O2 – As Pco2 and H+ increase in capillary blood!
Bohr effect - Hb-O2 bond weakens! oxygenunloading where needed most
– As Heat production increases! directly andindirectly decreases Hb affinity for O2 !
increased oxygen unloading to active tissues
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Homeostatic Imbalance
Hypoxia
–
Inadequate O2 delivery to tissues! cyanosis
– Anemic hypoxia –too few RBCs; abnormal or toolittle Hb
– Ischemic hypoxia –impaired/blocked circulation
– Histotoxic hypoxia –cells unable to use O2, as inmetabolic poisons
– Hypoxemic hypoxia –abnormal ventilation;
pulmonary disease
– Carbon monoxide poisoning –especially from fire;
200X greater affinity for Hb than oxygen
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CO2 Transport in blood
CO2 transported in three forms
–
7 to 10% dissolved in plasma
– 20% bound to globin of hemoglobin(carbaminohemoglobin)
– 70% transported as bicarbonate ions (HCO3
– ) in
plasma
Occurs primarily in RBCs and is very fastIn plasma this reaction is slow
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Haldane Effect: Property of Hemoglobin(Hb)
De-oxygenation of blood increases its ability to carry CO2
• Reduced Hb (less O2 saturation) forms
carbaminohemoglobin and buffers H+ more easily!
– Lower Po2 and Hb saturation with O2; more CO2 carried in blood
• Encourages CO2 exchange in tissues and lungs
•
As more CO2 enters blood, more O2 dissociates fromhemoglobin (Bohr effect)
• As HbO2 releases O2, it more readily forms bonds withCO2 to form carbaminohemoglobin
Bohr Effect: hemoglobin's oxygen binding affinity is inversely related bothto acidity and to the concentration of carbon dioxide.
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Figure 22.22a Transport and exchange of CO2 and O2.
Tissue cell Interstitial fluid
(dissolved in plasma)
Binds to
plasma
proteins
Chlorideshift
(in) via
transport
protein
Blood plasma
(dissolved in plasma)
Slow
Carbonic
anhydrase
(Carbamino-
hemoglobin)
Red blood cell
Fast
Oxygen release and carbon dioxide pickup at the tissues
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Influence of CO2 on Blood pH
Carbonic acid–bicarbonate system – buffers blood pH
– If H+ concentration in blood rises, excess H+ isremoved by combining with HCO3
– ! H2CO3
– If H+ concentration begins to drop, H2CO3 dissociates, releasing H+
– HCO3 – is the alkaline reserve of carbonic acid-
bicarbonate buffer system
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Influence of CO2 on Blood pH
Respiratory rate & depth affect blood pH
–
Slow, shallow breathing increased CO2 in
blood drop in pH
– Rapid, deep breathing decreased CO2 inblood rise in pH
• Changes in ventilation can adjust pH whendisturbed by metabolic factors
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Influence of CO2 on Blood pH
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Control of Respiration
Involves brain centers, chemoreceptors, and other reflexes
•
Brain control
–
Reticular formation of Medulla and Pons
– Pons neurons Influence and modify activity of VRG neurons
–
Smooth out transition between inspiration and expiration
–
Modify and fine-tune breathing rhythms during vocalization,sleep, exercise
–
Clustered neurons in medulla important
•
Ventral respiratory group
•
Dorsal respiratory group
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Medullary Respiratory Centers
• Ventral respiratory group (VRG) –
Rhythm-generating & integrative center
– Sets eupnea –normal breathing (12–15 breaths/min)
– Its inspiratory neurons excite inspiratory muscles via phrenic (diaphragm) and intercostal nerves (external intercostals)
–
Expiratory neurons inhibit inspiratory neurons
• Dorsal respiratory group (DRG) – Near root of cranial nerve IX
–
Integrates input from peripheral stretchand chemoreceptors; sends information! VRG
Figure 22 23 Locations of
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Pons
Medulla
Pontine respiratory centers
interact with medullaryrespiratory centers to smooththe respiratory pattern.
Ventral respiratory group (VRG) contains rhythm generatorswhose output drives respiration.
Pons
Dorsal respiratory group (DRG) integrates peripheral sensoryinput and modifies the rhythmsgenerated by the VRG.
To inspiratorymuscles
Externalintercostalmuscles
Diaphragm
Medulla
Figure 22.23 Locations ofrespiratory centers and theirpostulated connections.
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Factors influencing Breathing Rate and Depth
• Depth = how actively the respiratory center stimulates
respiratory muscles• Rate = duration of inspiratory center activity
• Both modified in response to changing body demands
– Most important are changing levels of CO2, O2, and H+
– Sensed by central and peripheral chemoreceptors
• Hyperventilation- depth & rate of breathing thatexceeds body's need to remove CO2
! decreases blood CO2 levels (hypocapnia)
! cerebral vasoconstriction and cerebralischemia ! dizziness, fainting
• Apnea – breathing cessation from abnormally lowPco2
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Chemical Factors
Rising CO2 levels most powerful respiratory stimulant
–
If blood Pco2 rises (hypercapnia), CO2
accumulates in brain!
– CO2 in brain hydrated to carbonic acid! dissociates, releasing H+ ! pH drops
–
H+ stimulates chemoreceptors of brain stem
– Chemoreceptors synapse with respiratoryregulatory centers! increased depth and rate
of breathing! lower blood Pco2 ! pH risesNormally blood Po2 affects breathing only indirectly by influencingperipheral chemoreceptor sensitivity to changes in Pco2
But when arterial Po2 <60 mm Hg, it becomes major stimulus forrespiration (via peripheral chemoreceptors)
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Chemical Factors
Influence of Po2
–
Peripheral chemoreceptors inaortic & carotid bodies – sense
arterial O2 level
– When stimulated, causerespiratory centers to increase
ventilation
–
Declining Po2 normally slighteffect on ventilation
• Huge O2 reservoir bound toHb
• Requires substantial drop in
arterial Po2 (to 60 mm Hg)to stimulate increased
ventilation
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Chemical Factors
Influence of arterial pH
–
Can modify respiratory rate & rhythm even if CO2 &
O2 levels normal
– Involves peripheral chemoreceptors
– Decreased pH may reflect
•
CO2 retention; accumulation of lactic acid; excessketone bodies
– Respiratory system controls attempt to raise pH by
increasing respiratory rate and depth
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Inflation Reflex
Hering-Breuer Reflex (inflation reflex)
•
Stretch receptors in pleurae and airways
stimulated by lung inflation
- Inhibitory signals to medullary respiratorycenters end inhalation and allow expiration
- Acts as protective response more than
normal regulatory mechanism
Figure 22.24 Neural and chemical influences on brain stem respiratory centers.
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Central
chemoreceptors
Other receptors (e.g., pain)and emotional stimuli actingthrough the hypothalamus
Peripheralchemoreceptors
Respiratory centers(medulla and pons)
Higher brain centers(cerebral cortex—voluntary
control over breathing)
-breath holding in anger
-gasping with pain-rise in body temperature
Stretch receptorsin lungs
Irritantreceptors
Receptors inmuscles and joints
+ –
+ –
+
–+
+
–
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Respiratory Adjustments: Exercise
Adjustments geared to intensity & duration of exercise
•
Hyperpnea – Increased ventilation (10 - 20 fold) in response to
metabolic needs
• Pco2, Po2, and pH remain surprisingly constant during
exercise•
Three neural factors increase ventilation as exercise begins
- Psychological stimuli — anticipation of exercise
- Simultaneous cortical motor activation of skeletal muscles
and respiratory centers
Excitatory impulses to respiratory centers from
proprioceptors in moving muscles, tendons, joints
R i t Adj t t E i
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Respiratory Adjustments: Exercise
•
Ventilation declines suddenly as exercise ends
because the three neural factors shut off
• Gradual decline to baseline because of declinein CO2 flow after exercise ends
• Exercise! anaerobic respiration! lactic acid
– Not from poor respiratory function; from
insufficient cardiac output or skeletal muscle
inability to increase oxygen uptake
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High Altitude
•
Quick move to > 2400m (8000 ft)! acute
mountain sickness (AMS) – Atmos P and Po2 levels lower
– Headaches, shortness of breath, nausea,dizziness
–
Possible, lethal cerebral & pulmonaryedema
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Acclimatization to High Altitude
• Respiratory & hematopoietic adjustments occur
•
Chemoreceptors more responsive to Pco2 when Po2 declines
• Lower Po2 directly stimulates peripheralchemoreceptors
• Ventilation increases to 2–3 L/min higher than sea
level• Always lower-than-normal Hb saturation levels
– Less O2 available
• Decline in blood O2 stimulates kidneys to accelerateproduction of EPO
•
RBC numbers increase slowly to provide long-termcompensation
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Chronic Obstructive Pulmonary Disease (COPD)
– Exemplified by chronic bronchitis & emphysema
–
Irreversible decrease in ability to force air out of lungs – Common features
• History of smoking in 80% of patients
• Dyspnea - labored breathing ("air hunger")
• Coughing & frequent pulmonary infections
•
Most develop respiratory failure (hypoventilation)accompanied by respiratory acidosis, hypoxemia
• Treated with bronchodilators, corticosteroids, oxygen,sometimes surgery
normal emphysema
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• Tobacco smoke• Air pollution
!-1 antitrypsindeficiency
Continual bronchialirritation and inflammation
Breakdown of elastin inconnective tissue of lungs
• Chronic productive cough• Loss of lung elasticity
• Frequent infections
• Respiratory acidosis
Chronic bronchitis
• Excess mucus production
Emphysema
• Destruction of alveolarwalls
• Airway obstructionor air trapping
• Dyspnea
• Hypoventilation• Hypoxemia
Figure 22.27 Thepathogenesis of COPD
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Asthma: Reversible COPD
– Characterized by coughing, dyspnea, wheezing, and
chest tightness
– Active inflammation of airways precedes bronchospasms
– Inflammation is immune response due to release ofinterleukins, production of IgE, and recruitment ofinflammatory cells
– Airways thickened with inflammatory exudate magnifyeffect of bronchospasms
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Tuberculosis (TB)
– Infectious disease caused by bacterium
Mycobacterium tuberculosis
– Symptoms-fever, night sweats, weight loss,racking cough, coughing up blood
– Treatment- 12-month course of antibiotics
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Cystic fibrosis
– Most common lethal genetic disease in North
America
– Abnormal, viscous mucus clogs passageways! bacterial infections
•
Affects lungs, pancreatic ducts, reproductive
ducts
– Cause–abnormal gene for Cl- membrane
channel
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