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3–1 Nuclei of large, active cells.
Liver cells have large, central nuclei. One or more highly ‐basophilic nucleoli are visible
within each nucleus, ‐indicating intense protein synthesis by these cells. Most of the
chromatin is light staining or euchromatic, with small areas of more darkly stained
heterochromatin ‐scattered throughout the nucleus and just inside the ‐nuclear envelope.
This superficial heterochromatin allows the boundary of the organelle to be seen more
easily by light microscopy. One cell here has two nuclei, which is fairly common in the liver.
X500. Pararosaniline–toluidine blue.
1
Figure 3–2 Relationship of nuclear envelope to the rough ER (RER).
Three‐dimensional representation of a cell nucleus shows a single large nucleolus and the
distribution of the nuclear pores in the nuclear envelope. The outer membrane of the
nuclear envelope is continuous with the RER TEM X20,000.
2
Figure 3–3 Ultrastructure of a nucleus.
Regions of euchromatin and heterochromatin display variable electron densities with the
transmission electron microscope (TEM). An active nucleus typically has much diffuse,
light‐staining euchromatin and smaller subdomains of electron‐dense heterochromatin (H),
with many of these associated at the periphery associated with the nuclear lamina. The
more heterogeneous electron‐dense subdomain is the ‐nucleolus (N), the site of rRNA
synthesis and ribosomal ‐subunit assembly. X25,000.
3
Figure 3–4 The nuclear envelope, nuclear lamina, and nuclear pore complexes.
(a) Bound to the inner membrane of the nuclear envelope is the nuclear lamina, a
meshwork assembled from lamins (class V intermediate filament proteins). Nuclear pore
complexes contain more than 30 core proteins (nucleoporins), span both membranes of
the nuclear envelope, and regulate the bidirectional transfer of macromolecular complexes
between the nucleus and cytoplasm.
(b) Scanning EM of the inner nuclear membrane (nucleoplasmic face) showing portions of
the nuclear lamina (NL) meshwork with many embedded nuclear pore complexes (NPC).
The preparation is from an actively growing amphibian oocyte. Nuclei of these very large
cells can be isolated manually, facilitating ultrastructural studies of the nuclear envelope.
X100,000.
(Used, with permission, of Dr M.W. Goldberg, Department of Biological and Biomedical
Sciences, Durham University, UK.)
4
Figure 3–5 Nuclear pores.
(a) A TEM section through the nuclear envelope between nucleus (N) and cytoplasm (C)
shows its two‐membrane structure. The electron‐dense nuclear pore complexes bridging
the nuclear envelope can also be seen (arrows). Electron‐dense heterochromatin is
adjacent to the envelope, except at the nuclear pores. (b) A tangential section through a
nuclear envelope shows the nuclear pore complexes (arrows) and the electron‐lucent
patches in the peripheral heterochromatin, which represent the areas just inside pores.
X80,000.
5
Figure 3–5 Nuclear pores.
(a) A TEM section through the nuclear envelope between nucleus (N) and cytoplasm (C)
shows its two‐membrane structure. The electron‐dense nuclear pore complexes bridging
the nuclear envelope can also be seen (arrows). Electron‐dense heterochromatin is
adjacent to the envelope, except at the nuclear pores. (b) A tangential section through a
nuclear envelope shows the nuclear pore complexes (arrows) and the electron‐lucent
patches in the peripheral heterochromatin, which represent the areas just inside pores.
X80,000.
6
Figure 3–6 Cryofracture of nuclear envelope showing nuclear pores.
An electron micrograph obtained by freeze‐fractured cell shows the two layers of the
nuclear envelope and nuclear pores. The fracture plane occurs partly between the two
nuclear envelope membranes (left) but mostly just inside the envelope with the chromatin
removed. The size and distribution of the nuclear pore complexes are clearly seen.
X60,000.
7
Figure 3–7 Chromosome territories of a human fibroblast nucleus.
Fluorescence in situ hybridization (FISH) can be used with a combination of labeled probes,
each specific for sequences on different chromosomes. A nucleus of a cultured human
fibroblast was processed by 24‐color FISH, photographed by confocal microscopy in
appropriate channels, and the results superimposed to form an RGB (red‐green‐blue )
image (a) of the 24 differently labeled chromosome types (1‐22, X, and Y). Individual
chromosome territories in the image were identified and false‐colored after classification
by software developed for such analyses (b).
(Used, with permission, of Dr Thomas Cremer, Department of Biology II, Anthropology and
Human Genetics, Ludwig ‐Maximilian University, Munich, Germany.)
8
Figure 3–8 Components of a nucleosome.
Nucleosome is a structure that produces the initial organization of free double‐stranded
DNA into chromatin. Each nucleosome has an octomeric core complex made up of four
types of histones, two copies each of H2A, H2B, H3, and H4. Around this core is wound
DNA approximately 150 base pairs in length. One H1 histone is located outside the DNA on
the surface of each nucleosome. DNA associated with nucleosomes in vivo thus resembles
a long string of beads. Nucleosomes are very dynamic structures, with H1 loosening and
DNA unwrapping at least once every second to allow other proteins, including transcription
factors and enzymes, access to the DNA.
9
Figure 3–9 From DNA to chromatin.
Several orders of DNA packing occur in chromatin and during chromatin condensation of
mitotic prophase. The top drawing shows the 2‐nm DNA double helix, followed by the
association of DNA with histones to form 11‐nm filaments of nucleosomes connected by
the DNA (“beads on a string”). Nucleosomes on the DNA then interact in a manner not well
understood to form a more compact 30‐nm fiber. For transcription, DNA forms loops that
remain tethered to and stabilized by interactions with protein scaffolds that eventually
make up a central framework at the long axis of each chromosome. Heterochromatin is
not transcribed and remains more highly condensed. The bottom drawing shows a
metaphase chromosome, with maximum packing of DNA. The chromosome consists of
two chromatids held together at a constriction called the centromere.
10
Figure 3–10 Human karyotype.
Karyotypes provide light microscopic information regarding the number and morphology of
chromosomes in an organism. Such preparations are made by staining and photographing
the chromosomes of a cultured cell arrested with colchicine during mitosis, when
chromosomes are maximally condensed. From the image individual chromosomes are
typically placed together in pairs. With certain stains each chromosome has a particular
pattern of banding that facilitates its identification and shows the relationship of the
banding pattern to genetic anomalies. Hybridization with fluorescent probes specific for
each chromosome (FISH) followed by karyotyping yields an image like that shown here.
Note that the 22 pairs of autosomes, as well as the X and Y chromosomes, differ in size,
morphology, and location of the centromere.
11
Figure 3–11 Regions within a nucleolus.
TEM reveals morphologically distinct regions within a nucleolus. Small, light‐staining areas
are fibrillar centers (FC), containing the DNA sequences for the rRNA genes (the nucleolar
organizers). The darker fibrillar material (F) surrounding the fibrillar centers consists of
accumulating rRNA transcripts. More granular material (G) of the nucleolus contains mainly
the large and small ribosomal subunits being assembled from rRNA and ribosomal proteins
synthesized in the cytoplasm. Various amounts of heterochromatin (H) are also typically
found near the nucleolus, scattered in the euchromatin (E), and adjacent to the nuclear
envelope (NE) that separates chromatin from cytoplasm (C). X35,000.
12
Figure 3–12 The cell cycle.
The ability to recognize microscopically cells during both mitosis and DNA replication (by
autoradiography after administering radiolabeled thymidine) led to the concept of the cell
“cycle” with the phases occurring as shown here. In rapidly dividing cells, G1 is a period in
which cells accumulate the enzymes and nucleotides required for DNA replication, S is the
period devoted primarily to DNA replication, G2 is a usually short period of preparation for
mitosis, and M includes all phases of mitosis itself. In rapidly growing human tissues the
cell cycle varies from 24 to 36 hours. The length of G1 depends on many factors and is
usually the longest and most variable period; the length of S is largely a function of the
genome size. G2 and mitosis together normally last only 2‐3 hours. Differentiating cells in
growing tissues may have very long G1 periods and such cells are often said to be in the G0
phase of the cell cycle.
13
Figure 3–13 Controls at cell cycle checkpoints.
Each phase of the cell cycle has one or more checkpoints where the quality of specific cell
activities is checked. Progression to the next phase of the cycle does not occur until all
activities of the preceding phase are completed satisfactorily. Three important checkpoints
are shown here, including
• The start or restriction checkpoint just before the start of S
• The G2 /M checkpoint that ensures that DNA replication is complete
• The metaphase spindle checkpoint that ensures that all chromosomes will be segregated
Overall progression in the cycle is regulated by proteins called cyclins and cyclin‐dependent
kinases (CDKs) that phosphorylate/activate enzymes and other proteins needed for phase‐
specific functions. Major cyclins, their CDKs, and important protein targets are summarized
in Table 3–1.
14
Figure 3–14 Stages of mitosis in cultured cells. (Opposite)
The phases of mitosis are shown well in these images of cultured cells obtained with a
confocal laser scanning microscope, with chromosomes stained orange and microtubules,
green. (a) Prophase: The chromosomes have undergone DNA replication and each consists
of two very close sister chromatids. Two microtubule‐organizing centers, the centrosomes,
have moved apart and each is associated with microtubules forming the mitotic spindle. (b)
Prometaphase: Chromosomes attach to spindle microtubules at their kinetochores and ‐
begin to be moved. (c) Metaphase: Chromosomes have become aligned at the middle of
the spindle, near the cell equator. Kinetochore microtubules attach to each sister
chromatid and to opposite poles of the spindle. (d) Anaphase: Sister chromatids separate
from each other to become individual chromosomes that are pulled toward the spindle
poles. The poles move apart and the kinetochore microtubules get shorter. (e) Telophase:
The two sets of daughter chromosomes arrive at the spindle poles. (f) Late telophase and
cytokinesis: A contractile ring of myosin‐associated actin filaments forms a cleavage furrow
that pinches the cell into two daughter cells, each with one nucleus and a complete set of
chromosomes ready to undergo another round of DNA replication. a, d, e, and f: X1500; b
and c: X3000.
(With permission, from Drs Julie C. Canman and Ted Salmon, Department of Biology,
University of North Carolina, Chapel Hill.)
15
Figure 3–15 Mitotic spindle and metaphase chromosomes.
TEM of a sectioned metaphase cell shows several features of the mitotic apparatus,
including the very electron‐dense chromosomes bound at kinetochores (arrows) to the
microtubules of the spindle. The microtubules converge on the centrosomes (C), each
containing a pair of centrioles. The flattened membrane vesicles near the mitotic spindle
may represent fragments of the nuclear envelope, which begin to reassemble during late
telophase. X19,000.
(With permission, from Richard McIntosh, Department of Molecular, Cellular and
Developmental Biology, University of Colorado, Boulder.)
16
Figure 3–16 Mitotic cells in adult tissues.
Dividing cells in recognizable stages of mitosis are rarely observed in adult tissues because
they are rare and the cells are small, with variable shapes and orientations. However,
mitotic figures, nuclei with clumped, darkly stained chromatin, can sometimes be
identified, as shown here in various rapidly renewing tissues.
(a) In the lining of the small intestine, many mitotic transit amplifying cells can be found in
the area above the most basal region of the intestinal crypts. Condensed chromosomes
of cells in late anaphase and prophase phase can be distinguished here. (b) Metaphase cell
in a gland of proliferating uterine endometrium. (c) Telophase cell in the esophagus lining.
(d) Metaphase in the basal layer of epidermis. X400. H&E.
17
Figure 3–17 Stem cells.
In rapidly growing adult tissues and perhaps in other tissues there are slowly dividing
populations of stem cells. Stem cells divide asymmetrically, producing one cell that remains
as a stem cell and another that becomes committed to a differentiative pathway but
divides a few more times at a more rapid rate. Such cells have been termed progenitor
cells, or “transit amplifying cells,” each of which eventually stops dividing and becomes
fully differentiated.
18
Figure 3–18 Mitosis and meiosis.
Mitosis and meiosis share many aspects of chromatin condensation and separation but
differ in key ways. Mitosis produces two diploid cells that are the same genetically. In
meiosis, the two homologous maternal and paternal chromosomes physically align in
synapsis and regions are exchanged during crossing over or genetic recombination. This is
followed by two meiotic divisions with no intervening S phase, producing four haploid
cells.
19
Figure 3–19 Apoptotic cells.
Apoptotic cells in adult tissues are rare because the process is completed very rapidly.
Moreover, with their highly condensed chromatin in pyknotic nuclei and rounded shape,
cells early in apoptosis may superficially resemble some mitotic cells. Shown here are
apoptotic cells (A) in the epithelium covering an intestinal villus (a), in a corpus luteum
beginning to undergo involution (b), in the epithelium of a uterine endometrial gland at the
onset of menstruation (c), and in the liver (d). X400. H&E.
20
Figure 3–19 Apoptotic cells.
Apoptotic cells in adult tissues are rare because the process is completed very rapidly.
Moreover, with their highly condensed chromatin in pyknotic nuclei and rounded shape,
cells early in apoptosis may superficially resemble some mitotic cells. Shown here are
apoptotic cells (A) in the epithelium covering an ‐intestinal villus (a), in a corpus luteum
beginning to undergo involution (b), in the epithelium of a uterine endometrial gland at the
onset of menstruation (c), and in the liver (d). X400. H&E.
21
Figure 3–20 Late apoptosis—apoptotic bodies.
TEM of a cell in late apoptosis shows radical changes in cell shape, with membrane
blebbing and the formation of many membrane‐bound cytoplasmic regions. These
apoptotic bodies may separate from one another but remain enclosed by plasma
membrane so that no contents are released into the extracellular space. The membrane
changes are recognized by neighboring cells, and macrophages and apoptotic bodies are
very rapidly phagocytosed. X10,000.
22
Figure Credits
Figure numbers in boldface indicate those appearing for the first time in this text; figure numbers in lightface indicate those taken from other sources.
Berman I. Color Atlas of Basic Histology. 3rd ed. New York, NY: McGraw‐Hill; 2003.
Eckel CM. Human Anatomy Lab Manual. New York, NY: McGraw‐Hill; 2008.
Fitzpatrick TB, et al. Dermatology in General Medicine. New York, NY: McGraw‐Hill; 1971.
Hartwell L, Hood L, Goldberg M., et al. Genetics: From Genes to Genomes. 4th ed. New York, NY: McGraw‐Hill; 2010.
Kaushansky K, Lichtman M, Beutler E, et al. Williams Hematology. 8th ed. New York, NY: McGraw‐Hill; 2010.
Lewis R, Gaffin D, Hoefnagels M, et al. Life. 5th ed. New York, NY: McGraw‐Hill; 2004.
Lichtman MA, Shafer MS, Felgar RE, Wang N: Lichtman’s Atlas of Hematology. New York, NY: 2007. http://www.accessmedicine.com.
McKinley M, O’Loughlin VD. Human Anatomy. 2nd ed. New York, NY: McGraw‐Hill; 2008.
McKinley M, O’Loughlin VD. Human Anatomy. 3rd ed. New York, NY: McGraw‐Hill; 2012.
McKinley MP, O’Loughlin VD, Bidle TS. Anatomy & Physiology: An Integrative Approach. New York, NY: McGraw‐Hill; 2013.
Murray RK, Bender DA, Botham KM, et al. Harper’s Illustrated Biochemistry. 28th ed. New York, NY: McGraw‐Hill; 2009.
Raven P, Johnson GB, Losos JB, et al. Biology. 7th ed. New York, NY: McGraw‐Hill; 2005.
Weiss L, Greep RO. Histology. 4th ed. New York, NY: McGraw‐Hill; 1977.
Widmaier EP, Raff H, Strang KT. Vander’s Human Physiology. 11th ed. New York, NY: McGraw‐Hill; 2008.
Chapter 1
1‐14: McKinley et al 1‐5.
Chapter 2
2‐3: McKinley et al 4‐5a; 2‐6: McKinley, O’Loughlin (2nd ed) 2‐7; 2‐8: McKinley et al 4‐19; 2‐10a: McKinley, O’Loughlin 2‐8; 2‐10b: McKinley, O’Loughlin 2‐8; 2‐13a (left side): McKinley, O’Loughlin 2‐9; 2‐16b: McKinley, O’Loughlin 2‐10; 2‐16c: McKinley, O’Loughlin 2‐10; 2‐20 (top part): McKinley, O’Loughlin (2nd ed) 2‐12; 2‐21b: McKinley, O’Loughlin 2‐11; 2‐24:
McKinley, O’Loughlin (2nd ed) 2‐35.
Chapter 3
3‐2: McKinley, O’Loughlin 2‐17; 3‐10: Hartwell et al 17‐22b; 3‐12 (right): McKinley, O’Loughlin 2‐19; 3‐18: Lewis et al 9‐10.
Chapter 4
4‐4: Raven 7‐13; 4‐5: Weiss 3‐12; 4‐20: McKinley, O’Loughlin (2nd ed) 4‐4; 4‐15d: Berman 1‐16; 4‐21a: McKinley, O’Loughlin 4‐6; 4‐21b: McKinley, O’Loughlin 4‐6; 4‐21c: McKinley, O’Loughlin 4‐6c; 4‐27: McKinley et al 4‐14.
Chapter 5
5‐2: McKinley et al 16‐3; 5‐3a: Berman 2‐6; 5‐8a: Berman 2‐7; 5‐12b: Berman 2‐24; 5‐17b: Murray et al 48‐6.
Chapter 6
6‐1c: Berman 2‐20; 6‐1d: Berman 2‐19.
Chapter 7
7‐1: McKinley, O’Loughlin (2nd ed) 6‐1; 7‐5a: Berman 3‐4.
Chapter 8
8‐1: McKinley et al 7‐7; 8‐9: Berman 4‐4; 8‐13a: Berman 5‐7; 8‐14: McKinley, O’Loughlin (2nd ed) 6‐11; 8‐16: McKinley, O’Loughlin (2nd ed) 6‐12a,b; 8‐17a: Berman 5‐3; 8‐17b: Berman 5‐4; 8‐18: McKinley, O’Loughlin (2nd ed) 6‐16; 8‐19a: McKinley, O’Loughlin (2nd ed) 9‐4.
Chapter 9
9‐1: McKinley, O’Loughlin (2nd ed) 14‐1; 9‐2: McKinley, O’Loughlin (2nd ed) 14‐16; 9‐3: McKinley et al 12‐2; 9‐4: McKinley et al 12‐1 (table); 9‐5: Berman 6‐8; 9‐6a: McKinley, O’Loughlin (2nd ed) 14‐14b; 9‐7: McKinley, O’Loughlin (2nd ed) 14‐13c; 9‐8b: Eckel 4‐28b; 9‐9: McKinley, O’Loughlin (2nd ed) 14‐7; 9‐10a: Berman 9‐11a; 9‐17: Eckel 16‐1c; 9‐18a:
McKinley, O’Loughlin (2nd ed) 16‐2b; 9‐19: McKinley, O’Loughlin 15‐4; 9‐20c: McKinley, O’Loughlin (2nd ed) 15‐7a; 9‐21a: McKinley, O’Loughlin (2nd ed) 14‐8(1); 9‐21b: McKinley, O’Loughlin (2nd ed) 14‐8(2); 9‐21c: McKinley, O’Loughlin (2nd ed) 14‐8(3); 9‐21d: McKinley, O’Loughlin (2nd ed) 14‐8(4); 9‐22: Berman 6‐21; 9‐25: McKinley, O’Loughlin (2nd ed) 14‐
10a; 9‐26a: McKinley, O’Loughlin (2nd ed) 14‐12a; 9‐26b: Berman 6‐15; 9‐26d: McKinley, O’Loughlin (2nd ed) 14‐12b; 9‐28b: Berman 6‐19; 9‐28d: Berman 6‐18; 9‐29a: Berman 6‐10; 9‐29c: Berman 6‐12.
Chapter 10
10‐1: Widmaier 9‐1; 10‐2: McKinley, O’Loughlin (2nd ed) 10‐4; 10‐3: McKinley et al 10‐1; 10‐7a: Berman 7‐2; 10‐7c: Berman 7‐4; 10‐8: McKinley, O’Loughlin (2nd ed) 10‐6; 10‐9: McKinley et al 10‐4; McKinley, O’Loughlin 10‐9; 10‐12: McKinley et al 10‐12; 10‐13: Widmaier 9‐14; 10‐14a: Widmaier 10‐4; Berman 7‐6; 10‐14b: Berman 7‐7; 10‐15: McKinley, O’Loughlin
(2nd ed) 10‐12; 10‐16: McKinley, O’Loughlin (2nd ed) 22‐10a; 10‐17a: Berman 7‐10; 10‐17b: Berman 7‐11; 10‐19a: Berman 7‐12; 10‐21a: McKinley, O’Loughlin (2nd ed) 10‐16.
Chapter 11
11‐1: McKinley, O’Loughlin 22‐1; 11‐2: McKinley, O’Loughlin (2nd ed) 22‐11; 11‐5: Berman 11‐2; 11‐6: McKinley, O’Loughlin (2nd ed) 23‐1; 11‐8a: Berman 11‐11; 11‐8b: Berman 11‐12; 11‐13: McKinley et al 20‐5; 11‐14a: Berman 11‐20; 11‐14b: Berman 11‐22; 11‐15: McKinley et al 20‐8; 11‐16: Berman 11‐25; 11‐21b: Berman 11‐21; 11‐22b: Berman 11‐18; 11‐22c:
Berman 11‐13; 11‐22d: Berman 11‐19;11‐24b: McKinley, O’Loughlin (2nd ed) 24‐2b.
Chapter 12
12‐1: McKinley, O’Loughlin (2nd ed) 21‐2; 12‐3: McKinley et al 18‐2; 12‐4a: Widmaier 12‐67; 12‐4b,c: McKinley, O’Loughlin (2nd ed) 21‐4; 12‐8: Lichtman II.A.4; 12‐10d: Lichtman II.E.7; 12‐11b: Berman 8‐5; 12‐12c: Berman 8‐6; 12‐12d: Berman 8‐1; 12‐13a: Berman 8‐9; 12‐14: McKinley, O’Loughlin (2nd ed) 21‐10.
Chapter 13
13‐1: Kaushansky et al 4‐1; 13‐5: McKinley et al 18‐4b; 13‐7a: Berman 9‐6 through 9‐9; 13‐7b: Berman 8‐8; 13‐10 top, bottom, insets: Berman 9‐2, 9‐1; 9‐4, 9‐5; 13‐13a: Berman 9‐11; 13‐13b: Berman 9‐13; 13‐14: Berman 9‐14.
Chapter 14
14‐1: McKinley et al 21‐1; 14‐2: McKinley et al 22‐17; 14‐3: McKinley et al 22‐18a; 14‐5: McKinley et al 22‐9; 14‐6: McKinley et al 22‐18; 14‐8a: McKinley et al 21‐5; 14‐8c: McKinley et al 21‐5; 14‐11: McKinley et al 22‐14; 14‐13a: Berman 10‐5; 14‐16: McKinley et al 21‐6.
Chapter 15
15‐1: McKinley, O’Loughlin (2nd ed) 26‐1; 15‐2: McKinley, O’Loughlin (2nd ed) 26‐9; 15‐4: McKinley et al 16‐7; 15‐5a: Berman 12‐10; 15‐5b: Berman 12‐12; 15‐6a: McKinley, O’Loughlin 26‐6c; 15‐6b: McKinley/O’Loughlin (2nd ed) 26‐5; 15‐10a: Berman 12‐1; 15‐10b: Berman 12‐4; 15‐12: McKinley, O’Loughlin 26‐10; 15‐13a: Berman 12‐16; 15‐14a: McKinley et al
26‐9a; 15‐14b: McKinley et al 26‐10; 15‐15: Berman 12‐22; 15‐17d: McKinley et al 26‐10c; 15‐22: McKinley, O’Loughlin (2nd ed) 26‐15; 15‐31: McKinley, O’Loughlin (2nd ed) 26‐26; 15‐32a: McKinley et al 26‐23a; 15‐32b: McKinley et al 26‐23b; 15‐33a: Berman 12‐41; 15‐33b: Berman 12‐43.
Chapter 16
16‐1: McKinley, O’Loughlin (2nd ed) 26‐4a; 16‐3b: Berman 13‐26; 16‐5a: Berman 13‐29; 16‐5b: Berman 13‐32; 16‐7: McKinley, O’Loughlin 26‐20; 16‐8: Berman 13‐17; 16‐9a: Berman 13‐21; 16‐11a,b: McKinley, O’Loughlin 26‐19; 16‐12a: Berman 13‐3; 16‐12b: Berman 13‐4; 16‐13b: Berman 13‐7; 16‐19: McKinley et al 26‐17; 16‐20a: Berman 13‐15.
Chapter 17
17‐1: McKinley, O’Loughlin (2nd ed) 25‐1; 17‐3: McKinley et al 16‐6; 17‐4: Berman 14‐1; 17‐6: McKinley, O’Loughlin (2nd ed) 25‐8; 17‐7: Berman 14‐10; 17‐8a: Berman 14‐11; 17‐8b: Berman 14‐12; 17‐9a: Berman 14‐13; 17‐9c: Berman 14‐14; 17‐11a: McKinley et al 26‐11; 17‐11b,c: McKinley, O’Loughlin (2nd ed) 25‐9; 17‐12: Berman 14‐18; 17‐13a: McKinley et al
23‐12; 17‐13b: McKinley, O’Loughlin (2nd ed) 25‐10; 17‐14: Berman 14‐20; 17‐18a: McKinley, O’Loughlin (2nd ed) 25‐11.
Chapter 18
18‐1: McKinley et al 6‐6; 18‐2: McKinley, O’Loughlin (2nd ed) 5‐2; 18‐3: Berman 15‐4; 18‐5: Berman 15‐3; 18‐6a: Berman 15‐2; 18‐6b: McKinley, O’Loughlin (2nd ed) 5‐4a; 18‐7b: Fitzpatrick 70‐9; 18‐9: Fitzpatrick 7‐6; 18‐10: McKinley, O’Loughlin (2nd ed) 19‐5; 18‐11: McKinley et al 16‐3; 18‐12: Eckel 17‐2; 18‐13a: McKinley et al 6‐9; 18‐13c: McKinley, O’Loughlin
(2nd ed) 5‐9; 18‐14a: Berman 15‐15; 18‐14b: Berman 15‐14; 18‐14c: Berman 15‐13; 18‐15a,b: McKinley, O’Loughlin (2nd ed) 5‐8; 18‐16: McKinley et al 6‐10a; 18‐17a: Berman 15‐10; 18‐19: Fitzpatrick 81‐2; 18‐20: McKinley et al 6‐12.
Chapter 19
19‐1: McKinley et al 24‐3 (right side); 19‐2: McKinley et al 24‐4; 19‐3: McKinley et al 24‐8; 19‐4: Berman 16‐4; 19‐5a: McKinley, O’Loughlin (2nd ed) 27‐6; 19‐5c: McKinley et al 24‐11a; 19‐5d: McKinley, O’Loughlin (2nd ed) 27‐6; 19‐6b: Berman 16‐11; 19‐6c: McKinley et al 24‐11b; 19‐8a: Berman 16‐8; 19‐9a,b,c: McKinley, O’Loughlin (2nd ed) 27‐7; 19‐13:
McKinley et al 24‐9; 19‐16: McKinley, O’Loughlin (2nd ed) 27‐8; 19‐17a: Berman 16‐18.
Chapter 20
20‐1: McKinley et al 17‐3; 20‐2: McKinley, O’Loughlin (2nd ed) 20‐4; 20‐3: McKinley, O’Loughlin (2nd ed) 20‐15; 20‐4: Berman 17‐1; 20‐5a: McKinley, O’Loughlin 20‐8; 20‐5b: McKinley, O’Loughlin 20‐6; 20‐6: Berman 17‐3; 20‐8: McKinley et al 17‐4; 20‐9: Berman 17‐4, McKinley, O’Loughlin (2nd ed) 20‐10; 20‐12: McKinley, O’Loughlin (2nd ed) 20‐13a; 20‐14:
McKinley, O’Loughlin (2nd ed) 20‐13c,d; 20‐17c: Berman 17‐13; 20‐17e: McKinley, O’Loughlin (2nd ed) rt qt; 20‐18: McKinley, O’Loughlin (2nd ed) 20‐9; 20‐19: Berman 17‐15; 20‐21 (upper right): McKinley et al 17‐18; 20‐22: McKinley, O’Loughlin (2nd ed) 20‐11a; 20‐23: Berman 17‐17.
Chapter 21
21‐1: McKinley, O’Loughlin (2nd ed) 28‐11; 21‐2: McKinley, O’Loughlin (2nd ed) 28‐13; 21‐3: Berman 18‐2; 21‐4a: Berman 18‐5; 21‐5: McKinley et al 28‐18; 21‐6a: Berman 18‐7; 21‐6b: Berman 18‐8; 21‐9a: Berman 18‐10; 21‐9b: Berman 18‐11; 21‐10b: Berman 18‐13; 21‐11a: Berman 18‐14; 21‐12a: Berman 18‐16; 21‐13a: McKinley et al 28‐19; 21‐14a: Berman 18‐
18; 21‐16a: Berman 18‐20; 21‐16b: Berman 18‐21; 21‐17: McKinley, O’Loughlin (2nd ed) 18‐17b; 21‐18: Berman 18‐23.
Chapter 22
22‐1a,b: McKinley, O’Loughlin (2nd ed) 28‐11; 22‐2: McKinley, O’Loughlin (2nd ed) 28‐4; 22‐9: McKinley, O’Loughlin (2nd ed) 3‐7; 22‐10: McKinley et al 28‐6; 22‐11: McKinley et al 28‐8; 22‐13: Berman 19‐8; 22‐14: McKinley, O’Loughlin (2nd ed) 28‐7; 22‐15a: Berman 19‐16; 22‐17: McKinley, O’Loughlin (2nd ed) 28‐6; 22‐19a: Berman 19‐19; 22‐19b: Berman 19‐
20; 22‐19c: Berman 19‐21; 22‐20: McKinley, O’Loughlin (2nd ed) 2‐6; 22‐21c: McKinley et al 29‐7 22‐23a: Berman 19‐22; 22‐24a: Berman 19‐23; 22‐26a: Berman 19‐24; 22‐26b: Berman 19‐25; 22‐26c: Berman 19‐26; 22‐27a: Berman 19‐27.
Chapter 23
23‐1: McKinley 19‐12b; 23‐2: McKinley, O’Loughlin (2nd ed) 19‐19; 23‐8: McKinley et al 16‐16; 23‐10a: Berman 20‐4; 23‐14: McKinley, O’Loughlin (2nd ed) 19‐14a,b; 23‐15: Berman 20‐9; 23‐21: McKinley, O’Loughlin (2nd ed) 19‐20; 23‐23: McKinley et al 16‐25; 23‐24: McKinley et al 26‐26; 23‐25: McKinley et al 16‐32; 23‐28: McKinley, O’Loughlin (2nd ed) 19‐25;
23‐29a,b: McKinley et al 16‐27a,b; 23‐29c: McKinley 19‐27; 23‐29d: McKinley et al 16‐27d; 23‐32: McKinley et al 16‐28; 23‐33: McKinley et al 16‐29.
23
Figure Credits
Figure numbers in boldface indicate those appearing for the first time in this text; figure numbers in lightface indicate those taken from other sources.
Berman I. Color Atlas of Basic Histology. 3rd ed. New York, NY: McGraw‐Hill; 2003.
Eckel CM. Human Anatomy Lab Manual. New York, NY: McGraw‐Hill; 2008.
Fitzpatrick TB, et al. Dermatology in General Medicine. New York, NY: McGraw‐Hill; 1971.
Hartwell L, Hood L, Goldberg M., et al. Genetics: From Genes to Genomes. 4th ed. New York, NY: McGraw‐Hill; 2010.
Kaushansky K, Lichtman M, Beutler E, et al. Williams Hematology. 8th ed. New York, NY: McGraw‐Hill; 2010.
Lewis R, Gaffin D, Hoefnagels M, et al. Life. 5th ed. New York, NY: McGraw‐Hill; 2004.
Lichtman MA, Shafer MS, Felgar RE, Wang N: Lichtman’s Atlas of Hematology. New York, NY: 2007. http://www.accessmedicine.com.
McKinley M, O’Loughlin VD. Human Anatomy. 2nd ed. New York, NY: McGraw‐Hill; 2008.
McKinley M, O’Loughlin VD. Human Anatomy. 3rd ed. New York, NY: McGraw‐Hill; 2012.
McKinley MP, O’Loughlin VD, Bidle TS. Anatomy & Physiology: An Integrative Approach. New York, NY: McGraw‐Hill; 2013.
Murray RK, Bender DA, Botham KM, et al. Harper’s Illustrated Biochemistry. 28th ed. New York, NY: McGraw‐Hill; 2009.
Raven P, Johnson GB, Losos JB, et al. Biology. 7th ed. New York, NY: McGraw‐Hill; 2005.
Weiss L, Greep RO. Histology. 4th ed. New York, NY: McGraw‐Hill; 1977.
Widmaier EP, Raff H, Strang KT. Vander’s Human Physiology. 11th ed. New York, NY: McGraw‐Hill; 2008.
Chapter 1
1‐14: McKinley et al 1‐5.
Chapter 2
2‐3: McKinley et al 4‐5a; 2‐6: McKinley, O’Loughlin (2nd ed) 2‐7; 2‐8: McKinley et al 4‐19; 2‐10a: McKinley, O’Loughlin 2‐8; 2‐10b: McKinley, O’Loughlin 2‐8; 2‐13a (left side): McKinley, O’Loughlin 2‐9; 2‐16b: McKinley, O’Loughlin 2‐10; 2‐16c: McKinley, O’Loughlin 2‐10; 2‐20 (top part): McKinley, O’Loughlin (2nd ed) 2‐12; 2‐21b: McKinley, O’Loughlin 2‐11; 2‐24:
McKinley, O’Loughlin (2nd ed) 2‐35.
Chapter 3
3‐2: McKinley, O’Loughlin 2‐17; 3‐10: Hartwell et al 17‐22b; 3‐12 (right): McKinley, O’Loughlin 2‐19; 3‐18: Lewis et al 9‐10.
Chapter 4
4‐4: Raven 7‐13; 4‐5: Weiss 3‐12; 4‐20: McKinley, O’Loughlin (2nd ed) 4‐4; 4‐15d: Berman 1‐16; 4‐21a: McKinley, O’Loughlin 4‐6; 4‐21b: McKinley, O’Loughlin 4‐6; 4‐21c: McKinley, O’Loughlin 4‐6c; 4‐27: McKinley et al 4‐14.
Chapter 5
5‐2: McKinley et al 16‐3; 5‐3a: Berman 2‐6; 5‐8a: Berman 2‐7; 5‐12b: Berman 2‐24; 5‐17b: Murray et al 48‐6.
Chapter 6
6‐1c: Berman 2‐20; 6‐1d: Berman 2‐19.
Chapter 7
7‐1: McKinley, O’Loughlin (2nd ed) 6‐1; 7‐5a: Berman 3‐4.
Chapter 8
8‐1: McKinley et al 7‐7; 8‐9: Berman 4‐4; 8‐13a: Berman 5‐7; 8‐14: McKinley, O’Loughlin (2nd ed) 6‐11; 8‐16: McKinley, O’Loughlin (2nd ed) 6‐12a,b; 8‐17a: Berman 5‐3; 8‐17b: Berman 5‐4; 8‐18: McKinley, O’Loughlin (2nd ed) 6‐16; 8‐19a: McKinley, O’Loughlin (2nd ed) 9‐4.
Chapter 9
9‐1: McKinley, O’Loughlin (2nd ed) 14‐1; 9‐2: McKinley, O’Loughlin (2nd ed) 14‐16; 9‐3: McKinley et al 12‐2; 9‐4: McKinley et al 12‐1 (table); 9‐5: Berman 6‐8; 9‐6a: McKinley, O’Loughlin (2nd ed) 14‐14b; 9‐7: McKinley, O’Loughlin (2nd ed) 14‐13c; 9‐8b: Eckel 4‐28b; 9‐9: McKinley, O’Loughlin (2nd ed) 14‐7; 9‐10a: Berman 9‐11a; 9‐17: Eckel 16‐1c; 9‐18a:
McKinley, O’Loughlin (2nd ed) 16‐2b; 9‐19: McKinley, O’Loughlin 15‐4; 9‐20c: McKinley, O’Loughlin (2nd ed) 15‐7a; 9‐21a: McKinley, O’Loughlin (2nd ed) 14‐8(1); 9‐21b: McKinley, O’Loughlin (2nd ed) 14‐8(2); 9‐21c: McKinley, O’Loughlin (2nd ed) 14‐8(3); 9‐21d: McKinley, O’Loughlin (2nd ed) 14‐8(4); 9‐22: Berman 6‐21; 9‐25: McKinley, O’Loughlin (2nd ed) 14‐
10a; 9‐26a: McKinley, O’Loughlin (2nd ed) 14‐12a; 9‐26b: Berman 6‐15; 9‐26d: McKinley, O’Loughlin (2nd ed) 14‐12b; 9‐28b: Berman 6‐19; 9‐28d: Berman 6‐18; 9‐29a: Berman 6‐10; 9‐29c: Berman 6‐12.
Chapter 10
10‐1: Widmaier 9‐1; 10‐2: McKinley, O’Loughlin (2nd ed) 10‐4; 10‐3: McKinley et al 10‐1; 10‐7a: Berman 7‐2; 10‐7c: Berman 7‐4; 10‐8: McKinley, O’Loughlin (2nd ed) 10‐6; 10‐9: McKinley et al 10‐4; McKinley, O’Loughlin 10‐9; 10‐12: McKinley et al 10‐12; 10‐13: Widmaier 9‐14; 10‐14a: Widmaier 10‐4; Berman 7‐6; 10‐14b: Berman 7‐7; 10‐15: McKinley, O’Loughlin
(2nd ed) 10‐12; 10‐16: McKinley, O’Loughlin (2nd ed) 22‐10a; 10‐17a: Berman 7‐10; 10‐17b: Berman 7‐11; 10‐19a: Berman 7‐12; 10‐21a: McKinley, O’Loughlin (2nd ed) 10‐16.
Chapter 11
11‐1: McKinley, O’Loughlin 22‐1; 11‐2: McKinley, O’Loughlin (2nd ed) 22‐11; 11‐5: Berman 11‐2; 11‐6: McKinley, O’Loughlin (2nd ed) 23‐1; 11‐8a: Berman 11‐11; 11‐8b: Berman 11‐12; 11‐13: McKinley et al 20‐5; 11‐14a: Berman 11‐20; 11‐14b: Berman 11‐22; 11‐15: McKinley et al 20‐8; 11‐16: Berman 11‐25; 11‐21b: Berman 11‐21; 11‐22b: Berman 11‐18; 11‐22c:
Berman 11‐13; 11‐22d: Berman 11‐19;11‐24b: McKinley, O’Loughlin (2nd ed) 24‐2b.
Chapter 12
12‐1: McKinley, O’Loughlin (2nd ed) 21‐2; 12‐3: McKinley et al 18‐2; 12‐4a: Widmaier 12‐67; 12‐4b,c: McKinley, O’Loughlin (2nd ed) 21‐4; 12‐8: Lichtman II.A.4; 12‐10d: Lichtman II.E.7; 12‐11b: Berman 8‐5; 12‐12c: Berman 8‐6; 12‐12d: Berman 8‐1; 12‐13a: Berman 8‐9; 12‐14: McKinley, O’Loughlin (2nd ed) 21‐10.
Chapter 13
13‐1: Kaushansky et al 4‐1; 13‐5: McKinley et al 18‐4b; 13‐7a: Berman 9‐6 through 9‐9; 13‐7b: Berman 8‐8; 13‐10 top, bottom, insets: Berman 9‐2, 9‐1; 9‐4, 9‐5; 13‐13a: Berman 9‐11; 13‐13b: Berman 9‐13; 13‐14: Berman 9‐14.
Chapter 14
14‐1: McKinley et al 21‐1; 14‐2: McKinley et al 22‐17; 14‐3: McKinley et al 22‐18a; 14‐5: McKinley et al 22‐9; 14‐6: McKinley et al 22‐18; 14‐8a: McKinley et al 21‐5; 14‐8c: McKinley et al 21‐5; 14‐11: McKinley et al 22‐14; 14‐13a: Berman 10‐5; 14‐16: McKinley et al 21‐6.
Chapter 15
15‐1: McKinley, O’Loughlin (2nd ed) 26‐1; 15‐2: McKinley, O’Loughlin (2nd ed) 26‐9; 15‐4: McKinley et al 16‐7; 15‐5a: Berman 12‐10; 15‐5b: Berman 12‐12; 15‐6a: McKinley, O’Loughlin 26‐6c; 15‐6b: McKinley/O’Loughlin (2nd ed) 26‐5; 15‐10a: Berman 12‐1; 15‐10b: Berman 12‐4; 15‐12: McKinley, O’Loughlin 26‐10; 15‐13a: Berman 12‐16; 15‐14a: McKinley et al
26‐9a; 15‐14b: McKinley et al 26‐10; 15‐15: Berman 12‐22; 15‐17d: McKinley et al 26‐10c; 15‐22: McKinley, O’Loughlin (2nd ed) 26‐15; 15‐31: McKinley, O’Loughlin (2nd ed) 26‐26; 15‐32a: McKinley et al 26‐23a; 15‐32b: McKinley et al 26‐23b; 15‐33a: Berman 12‐41; 15‐33b: Berman 12‐43.
Chapter 16
16‐1: McKinley, O’Loughlin (2nd ed) 26‐4a; 16‐3b: Berman 13‐26; 16‐5a: Berman 13‐29; 16‐5b: Berman 13‐32; 16‐7: McKinley, O’Loughlin 26‐20; 16‐8: Berman 13‐17; 16‐9a: Berman 13‐21; 16‐11a,b: McKinley, O’Loughlin 26‐19; 16‐12a: Berman 13‐3; 16‐12b: Berman 13‐4; 16‐13b: Berman 13‐7; 16‐19: McKinley et al 26‐17; 16‐20a: Berman 13‐15.
Chapter 17
17‐1: McKinley, O’Loughlin (2nd ed) 25‐1; 17‐3: McKinley et al 16‐6; 17‐4: Berman 14‐1; 17‐6: McKinley, O’Loughlin (2nd ed) 25‐8; 17‐7: Berman 14‐10; 17‐8a: Berman 14‐11; 17‐8b: Berman 14‐12; 17‐9a: Berman 14‐13; 17‐9c: Berman 14‐14; 17‐11a: McKinley et al 26‐11; 17‐11b,c: McKinley, O’Loughlin (2nd ed) 25‐9; 17‐12: Berman 14‐18; 17‐13a: McKinley et al
23‐12; 17‐13b: McKinley, O’Loughlin (2nd ed) 25‐10; 17‐14: Berman 14‐20; 17‐18a: McKinley, O’Loughlin (2nd ed) 25‐11.
Chapter 18
18‐1: McKinley et al 6‐6; 18‐2: McKinley, O’Loughlin (2nd ed) 5‐2; 18‐3: Berman 15‐4; 18‐5: Berman 15‐3; 18‐6a: Berman 15‐2; 18‐6b: McKinley, O’Loughlin (2nd ed) 5‐4a; 18‐7b: Fitzpatrick 70‐9; 18‐9: Fitzpatrick 7‐6; 18‐10: McKinley, O’Loughlin (2nd ed) 19‐5; 18‐11: McKinley et al 16‐3; 18‐12: Eckel 17‐2; 18‐13a: McKinley et al 6‐9; 18‐13c: McKinley, O’Loughlin
(2nd ed) 5‐9; 18‐14a: Berman 15‐15; 18‐14b: Berman 15‐14; 18‐14c: Berman 15‐13; 18‐15a,b: McKinley, O’Loughlin (2nd ed) 5‐8; 18‐16: McKinley et al 6‐10a; 18‐17a: Berman 15‐10; 18‐19: Fitzpatrick 81‐2; 18‐20: McKinley et al 6‐12.
Chapter 19
19‐1: McKinley et al 24‐3 (right side); 19‐2: McKinley et al 24‐4; 19‐3: McKinley et al 24‐8; 19‐4: Berman 16‐4; 19‐5a: McKinley, O’Loughlin (2nd ed) 27‐6; 19‐5c: McKinley et al 24‐11a; 19‐5d: McKinley, O’Loughlin (2nd ed) 27‐6; 19‐6b: Berman 16‐11; 19‐6c: McKinley et al 24‐11b; 19‐8a: Berman 16‐8; 19‐9a,b,c: McKinley, O’Loughlin (2nd ed) 27‐7; 19‐13:
McKinley et al 24‐9; 19‐16: McKinley, O’Loughlin (2nd ed) 27‐8; 19‐17a: Berman 16‐18.
Chapter 20
20‐1: McKinley et al 17‐3; 20‐2: McKinley, O’Loughlin (2nd ed) 20‐4; 20‐3: McKinley, O’Loughlin (2nd ed) 20‐15; 20‐4: Berman 17‐1; 20‐5a: McKinley, O’Loughlin 20‐8; 20‐5b: McKinley, O’Loughlin 20‐6; 20‐6: Berman 17‐3; 20‐8: McKinley et al 17‐4; 20‐9: Berman 17‐4, McKinley, O’Loughlin (2nd ed) 20‐10; 20‐12: McKinley, O’Loughlin (2nd ed) 20‐13a; 20‐14:
McKinley, O’Loughlin (2nd ed) 20‐13c,d; 20‐17c: Berman 17‐13; 20‐17e: McKinley, O’Loughlin (2nd ed) rt qt; 20‐18: McKinley, O’Loughlin (2nd ed) 20‐9; 20‐19: Berman 17‐15; 20‐21 (upper right): McKinley et al 17‐18; 20‐22: McKinley, O’Loughlin (2nd ed) 20‐11a; 20‐23: Berman 17‐17.
Chapter 21
21‐1: McKinley, O’Loughlin (2nd ed) 28‐11; 21‐2: McKinley, O’Loughlin (2nd ed) 28‐13; 21‐3: Berman 18‐2; 21‐4a: Berman 18‐5; 21‐5: McKinley et al 28‐18; 21‐6a: Berman 18‐7; 21‐6b: Berman 18‐8; 21‐9a: Berman 18‐10; 21‐9b: Berman 18‐11; 21‐10b: Berman 18‐13; 21‐11a: Berman 18‐14; 21‐12a: Berman 18‐16; 21‐13a: McKinley et al 28‐19; 21‐14a: Berman 18‐
18; 21‐16a: Berman 18‐20; 21‐16b: Berman 18‐21; 21‐17: McKinley, O’Loughlin (2nd ed) 18‐17b; 21‐18: Berman 18‐23.
Chapter 22
22‐1a,b: McKinley, O’Loughlin (2nd ed) 28‐11; 22‐2: McKinley, O’Loughlin (2nd ed) 28‐4; 22‐9: McKinley, O’Loughlin (2nd ed) 3‐7; 22‐10: McKinley et al 28‐6; 22‐11: McKinley et al 28‐8; 22‐13: Berman 19‐8; 22‐14: McKinley, O’Loughlin (2nd ed) 28‐7; 22‐15a: Berman 19‐16; 22‐17: McKinley, O’Loughlin (2nd ed) 28‐6; 22‐19a: Berman 19‐19; 22‐19b: Berman 19‐
20; 22‐19c: Berman 19‐21; 22‐20: McKinley, O’Loughlin (2nd ed) 2‐6; 22‐21c: McKinley et al 29‐7 22‐23a: Berman 19‐22; 22‐24a: Berman 19‐23; 22‐26a: Berman 19‐24; 22‐26b: Berman 19‐25; 22‐26c: Berman 19‐26; 22‐27a: Berman 19‐27.
Chapter 23
23‐1: McKinley 19‐12b; 23‐2: McKinley, O’Loughlin (2nd ed) 19‐19; 23‐8: McKinley et al 16‐16; 23‐10a: Berman 20‐4; 23‐14: McKinley, O’Loughlin (2nd ed) 19‐14a,b; 23‐15: Berman 20‐9; 23‐21: McKinley, O’Loughlin (2nd ed) 19‐20; 23‐23: McKinley et al 16‐25; 23‐24: McKinley et al 26‐26; 23‐25: McKinley et al 16‐32; 23‐28: McKinley, O’Loughlin (2nd ed) 19‐25;
23‐29a,b: McKinley et al 16‐27a,b; 23‐29c: McKinley 19‐27; 23‐29d: McKinley et al 16‐27d; 23‐32: McKinley et al 16‐28; 23‐33: McKinley et al 16‐29.
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