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Histopathology of hereditary progressive muscular dystrophy in inbred strain 129 mice.

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Histopathology of Hereditary, Progressive Muscular
Dystrophy in Inbred Strain 129 Mice’
Roscoe B. Jackson Memorial LaboratoTy, Bar Harbor, Maine
A stock of mice segregating for animals
suffering from a form of hereditary, progressive muscular dystrophy has been established from a mutation which occurred
in the breeding stocks of inbred strain 129
mice at the Jackson Memorial Laboratory
(Michelson, Russell and Harman, ’55).
The disease is characterized by progressive
muscular weakness and gross atrophy of
muscles. It is recognizable by three
weeks of age and, in some cases, as early
as two weeks. On a standard regimen for
laboratory mice, the affected animals have
an average life span of about 10 weeks,
with a few survivors reaching the age of
6 months. Inheritance has been shown to
follow the pattern of an autosomal recessive gene (Stevens, Russell, and Southard,
This disease in mice is being extensively
studied in many laboratories, particularly
from the points of view of biochemistry
and physiology. There has been a need for
a systematic study of the pathological
changes in the muscles of these mice and
a comparison of the changes with those
of the human dystrophies. No lesions
have been observed in the central or peripheral nervous system (Michelson, Russell and Harman, ’55). The studies reported here are concerned with the histologic features of the dystrophic process
in skeletal muscle.
The mice studied were dystrophics (dydy ) and heterozygous “carriers” (Dydy )
from strain 129/Redy,2 and homozygous normals (DyDy) from strain 129/J.’
Animals of these two sublines of strain
129, separated since 1948, freely accept
each other’s ovarian transplants and survive a full lifespan in inter-subline parabiosis. All animals were fed a pelleted commercial diet (Purina Laboratory Chow)
and given water ad libitum. Males and females were sacrificed at the ages of two,
three, 4, 8, 12 and 26 weeks. Muscles of
the thigh, calf, brachium, lumbar and cervical regions, and the masseter, were compared in 46 dystrophic and 30 normal
animals. The cases for detailed comparison were selected on the basis of histologic quality, particularly of longitudinal
sections, from a larger series of autopsies.
Animals were killed with chloroform,
skinned and eviscerated, and the carcasses
fixed, with limbs extended, in Zenker’s
acetic fluid for 24 hours. The carcass was
decalcified in Evans-Krajian formic acid
fluid for an average period of 48 hours.
These studies were supported by a grant-inaid from the Muscular Dystrophy Associations of
America, Inc.
The following revised classification of strain
129 mice applies to all such mice used in the
present report as well as in all previous communciations by other authors concerning an
hereditary progressive muscular dystrophy in mice
derived from the Jackson Memorial Laboratory
dystrophy colony. This classification is in accordance with the rules and standard symbols
given in “Standardized Nomenclature for Inbred
Strains of Mice, second listing” prepared by the
Committee on Standardized Genetic Nomenclature for Mice, to be published in Cancer Research,
20: February, 1960.
I. 129/Re- dy designates the subline of the
129 inbred strain in which the dy (dystrophic)
mutation arose. The following classes of mice
stem from non-sibling matings in the 129/Redy subline:
A. all dydy dystrophic individuals.
B. all known D y d y heterozygous carrier individu als.
C. some mice of normal phenotype, which
may be ,either Dydy carriers or DyDy homozygous normals, derived from matings
between known heterozygous carriers.
11. 129/J designates a subline of the 129 inbred strain maintained i n the Jackson Memorial
Laboratory Foundation Stocks. Dystrophy has
never been observed in this sublne. All guaranteed DyDy homozygous normals are offspring of
full-sibling matings between animals descended
from this 129/J Foundation Stock colony.
Standardized cross and/or longitudinally
oriented samples of the skeletal musculature were embedded in paraffin, sectioned
at 6-8 p, and stained with hematoxylin
and eosin. Selected material was stained
with gallocyanin and eosin, Masson's trichrome, Mallory's phosphotungstic acid
hematoxylin, or tested for ribonucleic
acids by a method previously described
(West and Mason, '58).
The animals were obtained from a large
production colony having the primary function of providing animals for research in
many laboratories. It is likely that the
quotas of 4 and 8 week old animals for
this study were biassed toward those in
poorer general health, since animals of
these ages were in greatest demand, and
the healthier ones were selected for shipment.
There is considerable individual variation in the severity of the lesions among
animals of the same age group, as well
as among animals of different age groups,
to the extent that serial age sampling of
the mice does not guarantee material representative of chronological progression
of the disease. In any one animal, the various muscle groups studied show considerable consistency among themselves in the
severity of the lesions.
The major histological changes that
were observed are: variability in fiber size,
relative and absolute increase in the endomysial connective tissue, coagulation necrosis of segments of muscles fibers, subsarcolemmic nuclear accumulations and
internal nuclear rowing, and regenerative
activity. In terms of general morphological
description, the latter three phenomena
are quite similar to those observed in muscles of vitamin E-deficient hamsters (West
and Mason, '58). In all animals both
flexors and extensors, preaxial and postaxial musculature are affected. A survey
of 13 skeletal muscle groups and individual
muscles showed that all were affected.
No attempt was made in this study to
grade the severity of involvement of identified individual muscles. Specific lesions
of cardiac and smooth muscle were not observed, nor were any sex differences detected.
Variability in fiber size and changes in
Connective tissues. The most conspicous
change, observed in animals of all ages,
is the extreme variation in the diameter
of the muscle fibers, best seen in cross
section (fig. 1). Very small and very large
fibers, haphazardly distributed throughout
the muscle, contrast with the more uniform size of fibers in normal muscle (fig.
2). Most of the small and many of the
large fibers tend to be rounded (figs. 1, 3 ) .
It should be noted, however, that in normal animals two weeks of age most fibers
still show rounding (fig. 4), but by 4
weeks the fibers of normal muscle are
polygonal in outline. This tendency toward
rounding in dystrophic muscle fibers becomes more apparent in severely affected
animals, to the point that almost all fibers may be rounded (figs. 1 and 5 ) .
Similarly, the variability in fiber diameter
becomes more extreme in the more severe
cases of the disease.
In comparing photomicrographs, at the
same magnification, of sections of specific
muscles in normal and dystrophic animals
of the same age, it was consistently noted
that many of the large caliber fibers of
the dystrophic were distinctly larger than
the largest fibers in the normal (figs. 1,
2, 3 , 4). No evidence of true swelling of
fibers could be detected, in that the myofibrils in the larger fibers of dystrophic
muscle were as closely packed as in the
large fibers of normal muscle. Therefore,
such fibers are considered to be hypertrophic.
Associated with the size variation of fibers is a relative and absolute increase in
the connective tissue. The increase appears, for the most part, as a thickening
of the endomysium, especially around the
small caliber fibers (fig. 5). Some evidence of this change may be seen in animals two weeks of age. In some of the
older animals, 12 to 26 weeks of age,
fatty replacement may be observed (figs.
6, 7), but is never as great as has been
described in human dystrophy. It is quite
probable that the animals do not live long
enough for conspicuous fatty replacement
to develop.
Nuclear changes. There appears to be
an increase in the number of nuclei in fi-
28 1
In general, nuclear rows extend through
bers of dystrophic muscle as compared to
the fibers of normal muscle, in all age longer segments of fibers than does coagugroups studied. No mitotic figures were ob- lation necrosis (described below). Rowed
served that could account for this appar- fibers are more numerous than are fibers
ent increase. Nuclei of dystrophic muscle showing coagulation in all stages of dystend to be larger and more vesicular than trophy.
There is little evidence of the focal
those of normal muscle, thus resembling
down of myofibrils and associated
fetal muscle nuclei.
Internal nuclear rowing is a conspicuous nuclear degeneration observed in Vitamin
feature of the dystrophic lesions at all E-deficient hamsters (West and Mason,
stages of the disease studied. The nuclei ’58) and of vacuolation or granular deare aligned in rows of variable length generation of fibers observed in human
at a level deeper than the usual subsarco- muscular dystrophy (Adams, Dennylemmic position (figs. 5, 7, 8, 9 and 10). Brown and Pearson, ’53). The dystrophic
A single fiber may contain one or more process appears to involve mainly progressuch nuclear rows (fig. 10). Rowed fibers sive atrophy with gradual wasting of the
may also possess nuclei in the usual sub- contractile material, until the muscle fisarcolemmic position, and these also may bers completely disappear, leaving scatbe increased in number. A number of fi- tered chains of muscle nuclei lying in
bers, except for internal rowing and the connective tissue.
Coagulation necrosis and regenerative
larger, vesicular nuclei, appear otherwise
morphologically normal (figs. 8 and 10). activity. Coagulation of fiber segments
There are always many fibers which are (fig. 16) is the major form of necrosis
indistinguishable from those in non-dystro- observed. It is essentially similar to that
described in nutritional muscular dystrophic animals.
Nuclear rows are found predominantly phy of the hamster (West and Mason,
in the small caliber fibers (fig. 11) at all ’58). In some fiber segments, the necrosis
stages of dystrophy. However, they are is incomplete, leaving remnants of myoalso present in some large fibers in mild fibrils embedded in the coagulated matecases and the number of large fibers so rial (fig. 17).
Invasion of the coagulum by macroaffected increases with the severity of the
disease. Fibers are seen in which linear phages and polymorphonuclear leukocytes
accumulations of subsarcolemmic nuclei occurs, together with proliferation of musoccur (fig. 12); these fibers may or may cle nuclei with investing sarcoplasm that
not also contain more centrally located have survived the degenerative change,
converting the affected segment into a
rows of nuclei.
Many rowed fibers show a general sar- mass of cells and debris similar to
coplasrnic basophilia (fig. 13), but more the “Muskelzellenschlauche” of Waldeyer,
frequently there may be observed an in- (1865) (fig. 18).
Regeneration occurs essentially as deternuclear basophilic zone connecting
many or all of the rowed nuclei (figs. 8 scribed by West and Mason (’58) both
and 14). This basophilic reaction is pre- from the isolated muscle nuclei described
vented by digestion with ribonuclease above and by plasmodia1 budding (figs. 19
prior to staining (fig. 15), demonstrating and 20) from viable portions of the affected fiber. Before phagocytosis is comthe presence of ribonucleic acids.
These findings are similar to those ob- plete, myoblast-like basophilic cells appear
served in the vitamin E-deficient hamster (fig. 19); these represent the first evidence
(West and Mason, ’58), and have much of regenerative activity. The regenerating
the same implications: namely, that nu- cells, some round in form and others spinclear rowing may represent a response to dle-shaped, often become separated by conan underlying reparative effort as well as nective tissue which thus destroys the origa response to sublethal injury, since large inal architecture of the endomysial tube.
amounts of cytoplasmic ribonucleic acids This connective tissue appears to be newly
are generally indicative of anabolic ac- proliferated rather than a result of condensation of existing endomysium. At a
slightly later stage, small caliber, basophil
bands with central nuclei appear (fig. 21).
The fate of this regenerative activity
could not be clearly determined. Peripheral cross-striated myofibrils could be
found in many of these early regeneration
forms stained with phosphotungstic acid
hematoxylin (fig. 22). It is possible that
regeneration may give rise to some of the
rowed fibers. However, when proliferation
of connective tissue is associated with regenerative activity, it is doubtful that full
maturation of new fibers is possible.
Of interest is the point that the greatest degree of coagulation necrosis occurs
primarily in dystrophic animals 4 and 8
weeks of age; in the other age groups
studied this necrosis is much less conspicuous. Regenerative activity is found only
in muscles giving evidence of coagulation
necrosis and seems to vary in incidence in
direct proportion to the extent of coagulation.
The muscle lesions of hereditary progressive muscular dystrophy in the mouse,
involving alterations in fiber size, muscle
nuclei, connective tissues, and contractile
components, are similar in many respects
to those described for other spontaneous
and experimental myopathies. The lesions
are particularly analogous to those of the
hereditary human muscular dystrophies.
The variations in size of individual muscle fibers and the random spatial arrangement of such fibers are strikingly similar
to the findings in the human dystrophies
(Adams, Denny-Brown and Pearson, '53),
and are present at all stages of the disease
that we have studied. These changes are
not common in myopathly produced by
vitamin E deficiency, and in the species
in which they have been described they appear at relatively late stages of the disease.
The histologic appearance of the large caliber fibers in dystrophic muscle, as described in the text, is not indicative of
swelling but rather of hypertrophy. This
hypertrophy occurs even though progressive gross atrophy of muscle may be observed. Within the age range of this
material we found no evidence of an initial swelling of muscle fibers preceding
atrophy as inferred in cases of human dystrophy (Adams, Denny-Brown and Pear-
son, '53). It may be postulated that the
enlargement of certain muscle fibers represents work hypertrophy of the more
normal fibers. The origin of the small
caliber fibers poses a more complex problem. The possibilities include atrophy, failure of growth and regeneration, and
combinations of these processes. Fiber
branching has been observed in both the
dystrophics and normals, and may be more
readily observed in the less crowded sections of dystrophic muscle. We have not
found convincing evidence of fiber splitting
in this material.
The changes in the connective tissue in
the muscle of the dystrophic mouse follow
the general pattern found in human dystrophies as well as in other myopathies.
There appears to be both a condensation
of existing endomysium and perimysium
and an actual proliferation of connective
tissue; however, our material does not
permit evaluation of the extent of these
two processes. Fatty replacement or infiltration occurs but does not become extensive in the age range of these animals.
Preliminary study of hybrid dystrophics
which live 9 months or more shows a
much larger amount of fatty tissue in the
affected muscles. It is quite probable that
the strain 129 dystrophic mice maintained
on a standard laboratory regimen do not
live long enough for conspicuous fatty replacement to develop.
An increased number of muscle nuclei,
their arrangement in rows within the fiber,
and subsarcolemmic accumulation of muscle nuclei are common phenomena in muscle injury and disease (Kirschbaum, '52;
Adams, Denny-Brown and Pearson, '53;
West and Mason, '58). In dystrophy, these
changes may represent fibers which fail
to mature, fibers which undergo atrophy
or dedifferentiation, and fibers arising
from regenerative activity, as well as a
reparative reaction to sublethal injury
(West and Mason, '58).
Coagulation necrosis, of common occurrence in these dystrophic mice at the ages
of 4 and 8 weeks, is not usually a conspicuous feature of human dystrophy. As
has been pointed out, our dystrophics of
these age groups were biassed toward
those in poorer general health. Factors
such as inanition, specific nutritional de-
ficiencies and intercurrent infections may
play a role in these animals, in addition
to possible selection of more rapidly progressing cases of dystrophy. Examination
of muscles obtained from dystrophic mice
of corresponding age, reared on a diet containing high quality protein and fat (Coleman, unpublished data), showed that
coagulation necrosis was significantly decreased, although other lesions were unchanged. It is likely that the commerical
pelleted diets that are commonly used for
the maintenance of laboratory mice are
inadequate for optimal maintenance of
dystrophic mice.
Regenerative activity parallels coagulation necrosis, being increased or decreased
in direct proportion to necrosis. Adams,
Denny-Brown and Pearson ( ' 5 3 ) consider
the absence of regenerative activity to be
a fundamental characteristic of the human
dystrophies. However, Walton and Adams
('56) described regenerative processes in
childhood dystrophy of rapid progression,
in which segments of muscle fibers show
an acute degeneration similar to coagulation necrosis. It can be postulated that
the presence or absence of acute degeneration and regeneration in progressive muscular dystrophy is dependent upon
whether the particular case is severe and
rapid or mild and slow in progression.
The opportunity to study the regenerative
capacity of human dystrophic muscle has
been necessarily limited. Preliminary studies in the dystrophic mouse have indicated
that heat injury is followed by early regenerative activity comparable to that of
non-dystrophic mice (West, unpublished
data). The end result of this regenerative
activity in the dystrophic mouse has not
been determined. It is possible that regeneration may give rise to some of the
small caliber fibers. However, when the
endomysial sheaths are thickened and distorted, it is doubtful that full maturation
of new fibers can occur.
Our autopsy material, which was limited
to clinically diagnosed cases, does not permit observations on the pre-clinical stages
of the disease necessary for the development of an adequate concept of the histogenesis of this disease in young mice. All
the basic changes were present in the
youngest animals studied (two weeks of
age). Preliminary studies of entire new
born litters, obtained from normal females
bearing transplanted dystrophic ovaries
and mated with male heterozygotes, in
which the theoretical incidence of dystrophy should be 5 0 % , have shown a variation in the amount of endomysial connective tissue in some of the animals. No
coagulation necrosis was observed. The
fibers were of course much smaller than
in mature muscle, and the nuclei tended
to be centrally located at this stage of development in the mouse which is only 19
or 20 days after fertilization. The problem is one of the cellular pathology of developing muscle for which there is little
background information. Attempts at producing 100% dystrophic litters by artificial insemination have been successful
in a few instances. If this technique can
be utilized on a predictable experimental
basis, a rapid advance in this field may
be possible.
It has been shown that hereditary muscular dystrophy in the mouse has much in
common morphologically with the muscular dystrophies in man. The differences
in lesions that do exist are ones of degree
rather than of kind. Further, the hereditary nature of the disease (Stevens, Russell and Southard, ' 5 7 ) , the progressive
muscular atrophy and weakness, and the
absence of lesions in the central and peripheral nervous system (Michelson, Russell and Harman, '55) are analogous in
the two diseases. Attempts by us to
classify this dystrophy in the mouse according to the existing classifications of
the human disease lead us to believe that
such comparison is neither practical nor
necessary. There is no reason to assume
that dystrophy in the mouse should conform to any specific type in man, or that
lack of such conformity rules out important similarities in mechanism and etiology. The important point is that in the
mouse there is available a primary, hereditary, progressive myopathy of skeletal
muscle which is analogous to human progressive muscular dystrophy and which
lends itself to experimental study not possible in man.
The hisopathology of skeletal muscle in
hereditary, progressive muscular dystro-
phy in strain 129 mice (two to 26 weeks
of age) is described. The major changes
observed were: variation in fiber size, a
relative and absolute increase in connective tissue, changes in muscle nuclei, coagulation necrosis and regeneration of
necrotic segments.
Wide variation in fiber size with haphazard distribution of very small and very
large fibers among those of more normal
diameter is the most striking change.
There is an associated relative and absolute increase of connective tissue, with
thickening of the endomysium especially
around the smaller caliber fibers. Fatty
replacement appears in some of the older
Changes in muscle nuclei are commonly
found in all stages of dystrophy, particularly alignment of the nuclei in chains
within the fiber (internal nuclear rowing),
subsarcolemmic nuclear accumulation,
and vesicular enlargement of the nuclei.
Coagulation necrosis of segments of
muscle fibers, although present to some
extent in most phases of the dystrophic
process, is more common in those mice 4
and 8 weeks of age. Necrosis is associated with invasion by macrophages and
polymorphonuclear leukocytes and with
evidence of regenerative activity in the
form of myoblast-like elements and plasmodial outgrowth from viable portions of
affected fibers.
The lesions are compared to those described for the herediatry human muscular dystrophies and the experimental myopathies produced by vitamin E deficiency.
The histopathology of muscle, especially
the haphazard distribution of large and
small caliber fibers and associated connective tissue changes, the hereditary nature of the disease, the progressive muscular atrophy and weakness, and the absence of lesions in the nervous system,
lead to the conclusion that dystrophy in
mice is most analogous to the human dystrophies. Existing morphologic differences are ones of degree rather than of
kind, and do not rule out the possibility of
important similarities in mechanism and
Adams, R. D., D. Denny-Brown and C. M. Pearson 1953 Diseases of Muscle. Paul B. Hoeher, Inc., New York, N. Y.
Coleman, D. L., unpublished data.
Kirschbaum, W. R. 1952 Histological studies
of muscle tissue in neuromuscular diseases.
J. Neuropathol. Exp. Neurol., 11: 373-391.
Michelson, A. M., E. S. Russell and P. J. Harman
1955 Dystrophia Muscularis: A heredietary
primary niyopathy in the house mouse. Proc.
Nat. Acad. Sci., 41: 1079-1084.
Stevens, L. C., E. S. Russell and J. L. Southard
1957 Evidence on inheritance of muscular dystrophy in a n inbred strain of mice using
ovarian transplantation. Proc. Soc. Exp. BioI.
Med., 95: 161-164.
Waldeyer, W. 1865 Ueber die Veranderungen
der quergestreiften Muskeln bei der Entziindung und dem Typhusprozess, sowie iiher die
Regeneration derselben nach Substanzdefecten.
Virchow’s Arch. path. Anat. u. Physiol., 34:
473-5 14.
Walton, J. N., and R. D. Adams 1956 The resuonse of the normal. the denervated and the
d;strophic muscle-cell’to injury. J. Path. Bact.,
72: 273-298.
West, W. T., and K. E. Mason 1958 Histopathology of muscular dystrophy in the vitamin
E-deficient hamster. Am. J. Anat., 102: 323-
Sacrospinalis from a normal 8 week male. The cross-sectional form of the fibers is
polygonal rather than rounded, the endomysial connective tissue is relatively inconspicuous, and the more uniform size of the fibers, as compared to those shown in
figure 1, can be easily seen. Gallocyanin and eosin. X 150.
Rectus femoris from a two week normal male. The fiber diameters tend to be more
rounded than in older normal animals. Contrast the more uniform fiber size with thc
size variability of fibers in figure 3. Gallocyanin and eosin. X 150.
3 Rectus femoris from a two week male dystrophic. Extreme variability in fiber size
can be observed as well as a tendency toward rounding of the fiher cross-section. The
endomysial connective tissue in this animal is only slightly thickened. Comparison
with figure 4 (rectus femoris from a two w.eek normal male) shows that many of
larger fibers of the dystrophic are distinctly larger than the largest in the normal.
Gallocyanin and eosin. X 150.
Cross-section of the lumbar sacrospinalis from an 8 week dystrophic male showing
extreme variation in the fiber diameters. Note the haphazard distribution of small and
large fibers among those of more normal size and the rounded rather than polygonal
shape of the fibers. The thickening of endomysial connective tissue is striking. Comparison with figure 2 (sacrospinalis from a normal 8 week male) shows that some
of the fibers of the dystrophic are of larger diameter than the largest in the normal.
Gallocyanin and eosin. X 150.
William T. West and Edwin D. Murphy
Cross-section of thigh muscle from 8 week dystrophic inale showing the rounded form
of most of the fibers and the thickened endomysiuni, especially around the small Caliber fibers ( A ) . Gallocyanin and eosin. X 450.
6 and 7 Longitudinal and cross-sections from a 12 week f.emale dystrophic. Fatty replacement of muscle fibers is evident. The internal location of muscle nuclei may be
observed in fibers pictured in figure 7. Gallocyanin and eosin. x 450.
William T. West and Edwin D. Murphy
8 and 9 Thigh musculature from a 4 week dystrophic female showing internal nuclear
rowing. A n internuclear basophilic zone connecting most of the nuclei can be seen i n
figure 8. Except for nuclear rowing and the enlarged vesicular nuclei the fib,ers i n
figure 8 are otherwise structurally normal. Gallocyanin and eosin. x 450.
Thigh muscle of 26 week dystrophic male. Two rows of nuclei lying in a single fiber
may be observed. Gallocyanin and eosin. X 450.
11 Thigh musculature of 4 week dystrophic female. Internal nuclear rowing in small
caliber fiben. Some internuclear basophilia may also be observed. Gallocyanin and
eosin. x 450.
William T. West and Edwin D. Murphy
Thigh muscle from 26 week dystrophic male, in which linear accumulations of sub
sarcoleinmic nuclei are clearly illustrated. Gallocyanin and eosin. x 450.
13, 14 and 15 Thigh muscle from 4 w.eek dystrophic female. A generalized sarcoplasmic
basophilia may b.e seen in rowed fibers (fig. 13). More frequently a n internuclear
basophilic zone connecting many or all of the rowed nuclei may be observed (fig. 14).
This basophilic reaction is prevented by ribonuclease digestion prior to staining as may
be seen i n figure 15 ( a section immediately adjacent to that shown in fig. 1 4 ) , indicating the presence of ribonucleic acids. Gallocyanin. x 720.
Thigh muscle from 4 week dystrophic female. Coagulation necrosis of a segment of
muscle fiber. The external form of the fiber is preserv.ed and early phagocytosis of
the necrotic material is in progress (A). Gallocyanin and eosin. X 450.
17 Thigh muscle from 4 week dystrophic female. Remnants of myofibrils remaining i n
a coagulated fiber; some cross striations may be seen (A). Phosphotungstic acid
hematoxylin. X 720.
William T. West and Edwin D. Murphy
Thigh muscle from 4 week dystrophic female. The coagulated material is being phagocytized by inacrophages. Nuclei structurally similar to muscle nuclei are visible. Gallocyanin and eosin. X 400.
19, 20, and 21 Thigh muscle from a v.ery severely affected two week dystrophic male.
Regeneration occurs from isolated, myoblast-like cells (fig. 19. A ) and by plasmodia1
budding from viable portions of the affected fiber (fig. 20, B ) . At a slightly later
stage, small caliber, basophil bands with central nuclei appear (fig. 21). Figure 19,
gallocyanin and eosin; figures 20 and 21, gallocyanin. X 720.
Thigh muscle from 4 week dystrophic female. Peripheral myofibrils i n regenerating
muscle fib.ers (A), which suggests that some complete regeneration of necrotic segments may occur. Phosphotungstic acid hematoxylin. x 720.
William T.West and Edwin D. Murphy
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histopathology, progressive, inbreds, 129, strait, mice, hereditary, muscular, dystrophy
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