9 Muscle Teaching Slides PDF

Elaine N.

Marieb PowerPoint® Lecture Slides

prepared by Vince Austin,
Katja Hoehn
Bluegrass Technical
and Community College
CHAPTER
Human
Anatomy
9
Muscles and
Muscle Tissue
PART A

& Physiology
SEVENTH EDITION
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Muscle Overview
 The three types of muscle tissue are skeletal,
cardiac, and smooth
 These types differ in structure, location, function,
and means of activation
PLAY InterActive Physiology ®:

Anatomy Review: Skeletal Muscle Tissue, page 3

Muscle Similarities
 Skeletal and smooth muscle cells are elongated and
are called muscle fibers
 Muscle contraction depends on two kinds of
myofilaments – actin and myosin
 Muscle terminology is similar
 Sarcolemma – muscle plasma membrane
 Sarcoplasm – cytoplasm of a muscle cell
 Prefixes – myo, mys, and sarco all refer to muscle

Skeletal Muscle Tissue
 Packaged in skeletal muscles that attach to and cover the
bony skeleton
 Has obvious stripes called striations
 Is controlled voluntarily (i.e., by conscious control)
 Contracts rapidly but tires easily
 Is responsible for overall body motility
 Is extremely adaptable and can exert forces ranging from a
fraction of an ounce to over 70 pounds

Cardiac Muscle Tissue
 Occurs only in the heart
 Is striated like skeletal muscle but is not voluntary
 Contracts at a fairly steady rate set by the heart’s
pacemaker
 Neural controls allow the heart to respond to
changes in bodily needs

Smooth Muscle Tissue
 Found in the walls of hollow visceral organs, such
as the stomach, urinary bladder, and respiratory
passages
 Forces food and other substances through internal
body channels
 It is not striated and is involuntary

Functional Characteristics of Muscle Tissue
 Excitability, or irritability – the ability to receive
and respond to stimuli
 Contractility – the ability to shorten forcibly
 Extensibility – the ability to be stretched or
extended
 Elasticity – the ability to recoil and resume the
original resting length

Muscle Function
 Skeletal muscles are responsible for all locomotion
 Cardiac muscle is responsible for coursing the
blood through the body
 Smooth muscle helps maintain blood pressure, and
squeezes or propels substances (i.e., food, feces)
through organs
 Muscles also maintain posture, stabilize joints, and
generate heat

Structure and Organization of Skeletal Muscle
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 9.1a
Structure and Organization of Skeletal Muscle
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 9.1b
Skeletal Muscle
 Each muscle is a discrete organ composed of
muscle tissue, blood vessels, nerve fibers, and
connective tissue

Skeletal Muscle
 The three connective tissue sheaths are:
 Endomysium – fine sheath of connective tissue
composed of reticular fibers surrounding each
muscle fiber
 Perimysium – fibrous connective tissue that
surrounds groups of muscle fibers called fascicles
 Epimysium – an overcoat of dense regular
connective tissue that surrounds the entire muscle

Skeletal Muscle

Anatomy Review: Skeletal Muscle Tissue, pages 4-6
Figure 9.2a
Skeletal Muscle: Nerve and Blood Supply
 Each muscle is served by one nerve, an artery, and
one or more veins
 Each skeletal muscle fiber is supplied with a nerve
ending that controls contraction
 Contracting fibers require continuous delivery of
oxygen and nutrients via arteries
 Wastes must be removed via veins

Skeletal Muscle: Attachments
 Most skeletal muscles span joints and are attached
to bone in at least two places
 When muscles contract the movable bone, the
muscle’s insertion moves toward the immovable
bone, the muscle’s origin

Microscopic Anatomy of a Skeletal Muscle
Fiber
 Each fiber is a long, cylindrical cell with multiple
nuclei just beneath the sarcolemma
 Fibers are 10 to 100 m in diameter, and up to
hundreds of centimeters long

Microscopic Anatomy of a Skeletal Muscle
Fiber
 Sarcoplasm has numerous glycosomes and a
unique oxygen-binding protein called myoglobin
 Fibers contain the usual organelles, myofibrils,
sarcoplasmic reticulum, and T tubules

Myofibrils
 Myofibrils are densely packed, rodlike contractile
elements
 They make up most of the muscle volume
 The arrangement of myofibrils within a fiber is
such that a perfectly aligned repeating series of
dark A bands and light I bands is evident

Myofibrils

Anatomy Review: Skeletal Muscle Tissue, pages 7-8
Figure 9.3b
Sarcomeres
 The smallest contractile unit of a muscle
 The region of a myofibril between two successive
Z discs
 Composed of myofilaments made up of contractile
proteins
 Myofilaments are of two types – thick and thin

Sarcomeres

Figure 9.3c
Myofilaments: Banding Pattern
 Thick filaments – extend the entire length of an A
band
 Thin filaments – extend across the I band and
partway into the A band
 Z-disc – coin-shaped sheet of proteins (connectins)
that anchors the thin filaments and connects
myofibrils to one another

 Thin filaments do not overlap thick filaments in
the lighter H zone
 M lines appear darker due to the presence of the
protein desmin

Figure 9.3c,d
Ultrastructure of Myofilaments: Thick
Filaments
 Thick filaments are composed of the protein
myosin
 Each myosin molecule has a rod-like tail and two
globular heads
 Tails – two interwoven, heavy polypeptide chains
 Heads – two smaller, light polypeptide chains called
cross bridges

Ultrastructure of Myofilaments: Thick
Filaments
Figure 9.4a,b
Ultrastructure of Myofilaments: Thin
Filaments
 Thin filaments are chiefly composed of the protein
actin
 Each actin molecule is a helical polymer of globular
subunits called G actin
 The subunits contain the active sites to which myosin
heads attach during contraction
 Tropomyosin and troponin are regulatory subunits
bound to actin

Ultrastructure of Myofilaments: Thin
Filaments
Figure 9.4c
Arrangement of the Filaments in a Sarcomere
 Longitudinal section within one sarcomere
Figure 9.4d
Sarcoplasmic Reticulum (SR)
 SR is an elaborate, smooth endoplasmic reticulum
that mostly runs longitudinally and surrounds each
myofibril
 Paired terminal cisternae form perpendicular cross
channels
 Functions in the regulation of intracellular calcium
levels

 Elongated tubes called T tubules penetrate into the
cell’s interior at each A band–I band junction
 T tubules associate with the paired terminal
cisternae to form triads

Figure 9.5
T Tubules
 T tubules are continuous with the sarcolemma
 They conduct impulses to the deepest regions of
the muscle
 These impulses signal for the release of Ca2+ from
adjacent terminal cisternae

Triad Relationships
 T tubules and SR provide tightly linked signals for
muscle contraction
 A double zipper of integral membrane proteins
protrudes into the intermembrane space
 T tubule proteins act as voltage sensors
 SR foot proteins are receptors that regulate Ca2+
release from the SR cisternae


Sliding Filament Model of Contraction
 Thin filaments slide past the thick ones so that the
actin and myosin filaments overlap to a greater
degree
 In the relaxed state, thin and thick filaments
overlap only slightly
 Upon stimulation, myosin heads bind to actin and
sliding begins

Sliding Filament Model of Contraction
 Each myosin head binds and detaches several
times during contraction, acting like a ratchet to
generate tension and propel the thin filaments to
the center of the sarcomere
 As this event occurs throughout the sarcomeres,
the muscle shortens

Skeletal Muscle Contraction
 In order to contract, a skeletal muscle must:
 Be stimulated by a nerve ending
 Propagate an electrical current, or action potential,
along its sarcolemma
 Have a rise in intracellular Ca2+ levels, the final
trigger for contraction
 Linking the electrical signal to the contraction is
excitation-contraction coupling

Nerve Stimulus of Skeletal Muscle
 Skeletal muscles are stimulated by motor neurons
of the somatic nervous system
 Axons of these neurons travel in nerves to muscle
cells
 Axons of motor neurons branch profusely as they
enter muscles
 Each axonal branch forms a neuromuscular
junction with a single muscle fiber

Neuromuscular Junction
 The neuromuscular junction is formed from:
 Axonal endings, which have small membranous
sacs (synaptic vesicles) that contain the
neurotransmitter acetylcholine (ACh)
 The motor end plate of a muscle, which is a
specific part of the sarcolemma that contains ACh
receptors and helps form the neuromuscular
junction

 Though exceedingly close, axonal ends and muscle fibers
are always separated by a space called the synaptic cleft

Figure 9.7 (a-c)

 When a nerve impulse reaches the end of an axon
at the neuromuscular junction:
 Voltage-regulated calcium channels open and
allow Ca2+ to enter the axon
 Ca2+ inside the axon terminal causes axonal
vesicles to fuse with the axonal membrane

The Neuromuscular Junction, pages 3-5

 This fusion releases ACh into the synaptic cleft via
exocytosis
 ACh diffuses across the synaptic cleft to ACh
receptors on the sarcolemma
 Binding of ACh to its receptors initiates an action
potential in the muscle

Destruction of Acetylcholine
 ACh bound to ACh receptors is quickly destroyed
by the enzyme acetylcholinesterase
 This destruction prevents continued muscle fiber
contraction in the absence of additional stimuli

The Neuromuscular Junction, pages 6-10

Action Potential
 A transient depolarization event that includes
polarity reversal of a sarcolemma (or nerve cell
membrane) and the propagation of an action
potential along the membrane

Role of Acetylcholine (Ach)
 ACh binds its receptors at the motor end plate
 Binding opens chemically (ligand) gated channels
 Na+ and K+ diffuse out and the interior of the
sarcolemma becomes less negative
 This event is called depolarization

Depolarization
 Initially, this is a local electrical event called end
plate potential
 Later, it ignites an action potential that spreads in
all directions across the sarcolemma

Excitation-Contraction Coupling
 Once generated, the action potential:
 Is propagated along the sarcolemma
 Travels down the T tubules
 Triggers Ca2+ release from terminal cisternae
 Ca2+ binds to troponin and causes:
 The blocking action of tropomyosin to cease
 Actin active binding sites to be exposed

Excitation-Contraction Coupling
 Myosin cross bridges alternately attach and detach
 Thin filaments move toward the center of the
sarcomere
 Hydrolysis of ATP powers this cycling process
 Ca2+ is removed into the SR, tropomyosin
blockage is restored, and the muscle fiber relaxes

Action Potential Scan
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 9.9
Excitation-Contraction (EC) Coupling
1. Action potential generated and
propagated along sarcomere to
T-tubules
2. Action potential triggers Ca2+
release
3. Ca++ bind to troponin;
blocking action of tropomyosin
released
4. contraction via crossbridge
formation; ATP hyrdolysis
5. Removal of Ca+2 by active
transport
6. tropomyosin blockage restored;
contraction ends
Neurotransmitter released diffuses
Axon terminal across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Synaptic
Synaptic cleft
vesicle Sarcolemma
T tubule
1 Net entry of Na+ Initiates

an action potential which
is propagated along the
sarcolemma and down
ACh ACh ACh the T tubules.
Ca2+ Ca2+
SR tubules (cut)
SR
Ca2+ Ca2+
2 Action potential in
T tubule activates
ADP voltage-sensitive receptors,
which in turn trigger Ca2+
Pi release from terminal
cisternae of SR
into cytosol.
Ca2+
Ca2+
6 Tropomyosin blockage restored, Ca2+ Ca2+
blocking myosin binding sites on
actin; contraction ends and
muscle fiber relaxes. 3 Calcium ions bind to troponin;
troponin changes shape, removing
Ca2+ the blocking action of tropomyosin;
actin active sites exposed.
5 Removal of Ca2+ by active transport

into the SR after the action
potential ends.
Ca2+
4 Contraction; myosin heads alternately attach to
actin and detach, pulling the actin filaments toward
the center of the sarcomere; release of energy by
ATP hydrolysis powers the cycling process.
Role of Ionic Calcium (Ca2+) in the Contraction
Mechanism
 At low intracellular Ca2+
concentration:
 Tropomyosin blocks
the binding sites on
actin
 Myosin cross bridges
cannot attach to
binding sites on actin
 The relaxed state of the
muscle is enforced
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 9.11a
Mechanism
 At higher intracellular
Ca2+ concentrations:
 Additional calcium
binds to troponin
(inactive troponin
binds two Ca2+)
 Calcium-activated
troponin binds an
additional two Ca2+ at
a separate regulatory
site
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 9.11b
Mechanism
 Calcium-activated
troponin undergoes a
conformational change
 This change moves
tropomyosin away from
actin’s binding sites
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 9.11c
Mechanism
 Myosin head can now
bind and cycle
 This permits contraction
(sliding of the thin
filaments by the myosin
cross bridges) to begin
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 9.11d
Sequential Events of Contraction
 Cross bridge formation – myosin cross bridge
attaches to actin filament
 Working (power) stroke – myosin head pivots and
pulls actin filament toward M line
 Cross bridge detachment – ATP attaches to myosin
head and the cross bridge detaches
 “Cocking” of the myosin head – energy from
hydrolysis of ATP cocks the myosin head into the
high-energy state
PLAY InterActive Physiology ®: Sliding Filament Theory, pages 3-29

Myosin head ADP
(high-energy
configuration) Pi
1 Myosin head attaches to the actin

myofilament, forming a cross bridge.
Thin filament
ADP
ATP ADP Thick filament
hydrolysis
Pi
4 As ATP is split into ADP and Pi, the myosin 2 Inorganic phosphate (Pi) generated in the
head is energized (cocked into the high-energy previous contraction cycle is released, initiating
conformation). the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released.
ATP
Myosin head
ATP
(low-energy
configuration)
3 As new ATP attaches to the myosin head, the link between

myosin and actin weakens, and the cross bridge detaches.
Contraction of Skeletal Muscle Fibers
 Contraction – refers to the activation of myosin’s
cross bridges (force-generating sites)
 Shortening occurs when the tension generated by
the cross bridge exceeds forces opposing
shortening
 Contraction ends when cross bridges become
inactive, the tension generated declines, and
relaxation is induced

Contraction of Skeletal Muscle (Organ Level)
 Contraction of muscle fibers (cells) and muscles
(organs) is similar
 The two types of muscle contractions are:
 Isometric contraction – increasing muscle tension
(muscle does not shorten during contraction)
 Isotonic contraction – decreasing muscle length
(muscle shortens during contraction)

Isotonic Contractions
 In isotonic contractions, the muscle changes in
length (decreasing the angle of the joint) and
moves the load
 The two types of isotonic contractions are
concentric and eccentric
 Concentric contractions – the muscle shortens and
does work
 Eccentric contractions – the muscle contracts as it
lengthens

Isometric Contractions
 Tension increases to the muscle’s capacity, but the
muscle neither shortens nor lengthens
 Occurs if the load is greater than the tension the
muscle is able to develop

Muscle Metabolism: Energy for Contraction
 ATP is the only source used directly for contractile
activity
 As soon as available stores of ATP are hydrolyzed
(4-6 seconds), they are regenerated by:
 The interaction of ADP with creatine phosphate
(CP)
 Anaerobic glycolysis
 Aerobic respiration
Muscle Metabolism, pages 3-15

Muscle Metabolism: Energy for Contraction
Muscle Metabolism: Anaerobic Glycolysis
 When muscle contractile activity reaches 70% of
maximum:
 Bulging muscles compress blood vessels
 Oxygen delivery is impaired
 Pyruvic acid is converted into lactic acid

Muscle Metabolism: Anaerobic Glycolysis
 The lactic acid:
 Diffuses into the bloodstream
 Is picked up and used as fuel by the liver, kidneys,
and heart
 Is converted back into pyruvic acid by the liver

Muscle Fatigue
 Muscle fatigue – the muscle is in a state of
physiological inability to contract
 Muscle fatigue occurs when:
 ATP production fails to keep pace with ATP use
 There is a relative deficit of ATP, causing
contractures
 Lactic acid accumulates in the muscle
 Ionic imbalances are present

Muscle Fatigue
 Intense exercise produces rapid muscle fatigue
(with rapid recovery)
 Na+-K+ pumps cannot restore ionic balances
quickly enough
 Low-intensity exercise produces slow-developing
fatigue
 SR is damaged and Ca2+ regulation is disrupted

Smooth Muscle
 Composed of spindle-shaped fibers with a
diameter of 2-10 m and lengths of several
hundred m
 Lack the coarse connective tissue sheaths of
skeletal muscle, but have fine endomysium
 Organized into two layers (longitudinal and
circular) of closely apposed fibers

Smooth Muscle
 Found in walls of hollow organs (except the heart)
 Have essentially the same contractile mechanisms
as skeletal muscle

Smooth Muscle
Microscopic Anatomy of Smooth Muscle
 SR is less developed than in skeletal muscle and
lacks a specific pattern
 T tubules are absent
 Plasma membranes have pouchlike infoldings called
caveoli

Microscopic Anatomy of Smooth Muscle
 Ca2+ is sequestered in the extracellular space near
the caveoli, allowing rapid influx when channels
are opened
 There are no visible striations and no sarcomeres
 Thin and thick filaments are present

Proportion and Organization of Myofilaments
in Smooth Muscle
 Ratio of thick to thin filaments is much lower than
in skeletal muscle
 Thick filaments have heads along their entire length
 There is no troponin complex

in Smooth Muscle
 Thick and thin filaments are arranged diagonally,
causing smooth muscle to contract in a corkscrew
manner
 Noncontractile intermediate filament bundles attach to
dense bodies (analogous to Z discs) at regular intervals

in Smooth Muscle
Contraction of Smooth Muscle
 Whole sheets of smooth muscle exhibit slow,
synchronized contraction
 They contract in union, reflecting their electrical
coupling with gap junctions
 Action potentials are transmitted from cell to cell

Contraction of Smooth Muscle
 Some smooth muscle cells:
 Act as pacemakers and set the contractile pace for
whole sheets of muscle
 Are self-excitatory and depolarize without external
stimuli

Contraction Mechanism
 Actin and myosin interact according to the sliding
filament mechanism
 The final trigger for contractions is a rise in
intracellular Ca2+
 Ca2+ is released from the SR and from the
extracellular space
 Ca2+ interacts with calmodulin and myosin light
chain kinase to activate myosin

Role of Calcium Ion
 Ca2+ binds to calmodulin and activates it
 Activated calmodulin activates the kinase enzyme
 Activated kinase transfers phosphate from ATP to
myosin cross bridges
 Phosphorylated cross bridges interact with actin to
produce shortening
 Smooth muscle relaxes when intracellular Ca2+
levels drop

Special Features of Smooth Muscle
Contraction
 Unique characteristics of smooth muscle include:
 Smooth muscle tone

 Slow, prolonged contractile activity
 Low energy requirements
 Response to stretch

Response to Stretch
 Smooth muscle exhibits a phenomenon called
stress-relaxation response in which:
 Smooth muscle responds to stretch only briefly,
and then adapts to its new length
 The new length, however, retains its ability to
contract
 This enables organs such as the stomach and
bladder to temporarily store contents

Types of Smooth Muscle: Single Unit
 The cells of single-unit smooth muscle, commonly
called visceral muscle:
 Contract rhythmically as a unit
 Are electrically coupled to one another via gap
junctions
 Often exhibit spontaneous action potentials
 Are arranged in opposing sheets and exhibit stress-
relaxation response

Types of Smooth Muscle: Multiunit
 Multiunit smooth muscles are found:
 In large airways to the lungs
 In large arteries
 In arrector pili muscles
 Attached to hair follicles
 In the internal eye muscles

Types of Smooth Muscle: Multiunit
 Their characteristics include:
 Rare gap junctions
 Infrequent spontaneous depolarizations
 Structurally independent muscle fibers
 A rich nerve supply, which, with a number of
muscle fibers, forms motor units
 Graded contractions in response to neural stimuli

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 9.3.1

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Elaine N.

Marieb PowerPoint® Lecture Slides

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

PLAY InterActive Physiology ®:

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

PLAY InterActive Physiology ®:

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

PLAY InterActive Physiology ®:

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

PLAY InterActive Physiology ®:

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

PLAY InterActive Physiology ®:

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 9.7 (a-c)

PLAY InterActive Physiology ®:

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

PLAY InterActive Physiology ®:

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

1 Net entry of Na+ Initiates

5 Removal of Ca2+ by active transport

PLAY InterActive Physiology ®: Sliding Filament Theory, pages 3-29

1 Myosin head attaches to the actin

3 As new ATP attaches to the myosin head, the link between

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings