Neural - Spinal Cord Development

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Stage10 sem6.jpg


Neural groove closing to neural tube
Embryo early week 4 (Stage 10)
Spinal cord transverse section week 8
Spinal cord transverse section
Embryo week 8 (Carnegie Stage 22)

The spinal cord is the central nervous system part that extends into the axial skeleton and provides the two-way traffic required to interact with our environment. During pregnancy, early development of the spinal cord is influenced by the maternal dietary requirement for folate for closure of the neural tube. Later development requires the contribution of neural crest associating with the cord to form the dorsal root ganglia and ventral sympathetic ganglia. The animal models of spinal cord development has also been a key models of patterning, establishing ventral and dorsal compartments based upon surrounding signals.

The early central nervous system begins as a simple neural plate that folds to form a groove then tube, open initially at each end. Failure of these opening to close contributes a major class of neural abnormalities (neural tube defects).

Neural development is one of the earliest systems to begin and the last to be completed after birth. This development generates the most complex structure within the embryo and the long time period of development means in utero insult during pregnancy may have consequences to development of the nervous system.

Within the neural tube stem cells generate the 2 major classes of cells that make the majority of the nervous system: neurons and glia. Both these classes of cells differentiate into many different types generated with highly specialized functions and shapes. This section covers the establishment of neural populations, the inductive influences of surrounding tissues and the sequential generation of neurons establishing the layered structure seen in the brain and spinal cord.

  • Neural development beginnings quite early, therefore also look at notes covering Week 3- neural tube and Week 4-early nervous system.

Neural Links: ectoderm | neural | neural crest | ventricular | sensory | Stage 22 | gliogenesis | neural fetal | Medicine Lecture - Neural | Lecture - Ectoderm | Lecture - Neural Crest | Lab - Early Neural | neural abnormalities | folic acid | iodine deficiency | Fetal Alcohol Syndrome | neural postnatal | neural examination | Histology | Historic Neural | Category:Neural
Human embryo (Carnegie stage 13) spinal cord (shown in cross-section at the bottom of image).

Some Recent Findings

  • Differentiation and localization of interneurons in the developing spinal cord depends on DOT1L expression[1] "Genetic and epigenetic factors contribute to the development of the spinal cord. Failure in correct exertion of the developmental programs, including neurulation, neural tube closure and neurogenesis of the diverse spinal cord neuronal subtypes results in defects of variable severity. We here report on the histone methyltransferase Disruptor of Telomeric 1 Like (DOT1L), which mediates histone H3 lysine 79 (H3K79) methylation. Conditional inactivation of DOT1L using Wnt1-cre as driver (Dot1l-cKO) showed that DOT1L expression is essential for spinal cord neurogenesis and localization of diverse neuronal subtypes, similar to its function in the development of the cerebral cortex and cerebellum. Transcriptome analysis revealed that DOT1L deficiency favored differentiation over progenitor proliferation. Dot1l-cKO mainly decreased the numbers of dI1 interneurons expressing Lhx2. In contrast, Lhx9 expressing dI1 interneurons did not change in numbers but localized differently upon Dot1l-cKO. Similarly, loss of DOT1L affected localization but not generation of dI2, dI3, dI5, V0 and V1 interneurons. The resulting derailed interneuron patterns might be responsible for increased cell death, occurrence of which was restricted to the late developmental stage E18.5. Together our data indicate that DOT1L is essential for subtype-specific neurogenesis, migration and localization of dorsal and ventral interneurons in the developing spinal cord, in part by regulating transcriptional activation of Lhx2."
  • The Hedgehog receptor Patched1 regulates proliferation, neurogenesis, and axon guidance in the embryonic spinal cord[2] "The formation of the vertebrate nervous system depends on the complex interplay of morphogen signaling pathways and cell cycle progression to establish distinct cell fates. The sonic hedgehog (Shh) signaling pathway is well understood to promote ventral cell fates in the developing spinal cord. A key regulator of Shh signaling is its receptor Patched1 (Ptch1). However, because the Ptch1 null mutation is lethal early in mouse embryogenesis, its role in controlling cell cycle progression, neurogenesis, and axon guidance in the developing spinal cord is not fully understood. An allele of Ptch1 called Wiggable (Ptch1Wig), which was previously shown to enhance Shh signaling, was used to test its ability to regulate neurogenesis and proliferation in the developing spinal cord. Ptch1Wig/Wig mutants displayed enhanced ventral proneural gene activation, and aberrant proliferation of the neural tube and floor plate cells, the latter normally being a quiescent population. The expression of the cell cycle regulators p27Kip1 and p57Kip2 were expanded in Ptch1Wig/Wig mutant spinal cords, as was the number of mitotic and S-phase nuclei, suggesting enhanced cell cycle progression. However, Ptch1Wig/Wig mutants also showed enhanced apoptosis in the ventral embryonic spinal cord, which resulted in thinner spinal cords at later embryonic stages. Commissural axons largely failed to cross the floor plate of Ptch1Wig/Wig mutant embryos, suggesting enhanced Shh signaling in these mutants led to a dorsal expansion of the chemoattraction front. These findings are consistent with a role of Ptch1 in regulating neurogenesis and proliferation of neural progenitors, and in restricting the influence of Shh signaling in commissural axon guidance to the floor plate."
  • Species-specific Posture of Human Foetus in Late First Trimester[3] The ontogeny associated with the arm-hanging posture, which is considered ape-specific, remains unknown. To examine its ontogeny, we measured foetal movements of 62 human foetuses aged 10-20 gestation weeks using four-dimensional sonography. We observed that the first-trimester foetuses show this particular species-specific posture. After 11 weeks of gestation, all foetuses showed the arm-hanging posture, and the posture was most frequently observed at 14-16 weeks of gestation. Moreover, this posture often involved extension of both arms and both legs, indicating that it is not myogenic but neurogenic. Furthermore, early ontogeny suggests that it originates because of subcortical activity. Such posture extension bias and persistence indicates that vestibulospinal tract maturation involves the ontogeny of arm-hanging posture during 14-16 weeks of gestation." limb
More recent papers  
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Search term: Spinal Cord Development | Spinal Cord Embryology |

Older papers  
  • Review - The Multiple Roles of FGF Signaling in the Developing Spinal Cord[4] "During vertebrate embryonic development, the spinal cord is formed by the neural derivatives of a neuromesodermal population that is specified at early stages of development and which develops in concert with the caudal regression of the primitive streak. Several processes related to spinal cord specification and maturation are coupled to this caudal extension including neurogenesis, ventral patterning and neural crest specification and all of them seem to be crucially regulated by Fibroblast Growth Factor (FGF) signaling, which is prominently active in the neuromesodermal region and transiently in its derivatives. Here we review the role of FGF signaling in those processes, trying to separate its different functions and highlighting the interactions with other signaling pathways." FGF
  • Coordination of progenitor specification and growth in mouse and chick spinal cord[5] "Our data show that domain proportions are first established by opposing morphogen gradients and subsequently controlled by domain-specific regulation of differentiation rate but not differences in proliferation rate. Regulation of differentiation rate is key to maintaining domain proportions while accommodating both intra- and interspecies variations in size. Thus, the sequential control of progenitor specification and differentiation elaborates pattern without requiring that signaling gradients grow as tissues expand."
  • Motor neuron position and topographic order imposed by β- and γ-catenin activities[6] "Neurons typically settle at positions that match the location of their synaptic targets, creating topographic maps. In the spinal cord, the organization of motor neurons into discrete clusters is linked to the location of their muscle targets, establishing a topographic map of punctate design. To define the significance of motor pool organization for neuromuscular map formation, we assessed the role of cadherin-catenin signaling in motor neuron positioning and limb muscle innervation. We find that joint inactivation of β- and γ-catenin scrambles motor neuron settling position in the spinal cord but fails to erode the predictive link between motor neuron transcriptional identity and muscle target. Inactivation of N-cadherin perturbs pool positioning in similar ways, albeit with reduced penetrance. These findings reveal that cadherin-catenin signaling directs motor pool patterning and imposes topographic order on an underlying identity-based neural map."
  • Dynamic imaging of mammalian neural tube closure[7]

Neural Development Overview

Neuralation begins at the trilaminar embryo with formation of the notochord and somites, both of which underly the ectoderm and do not contribute to the nervous system, but are involved with patterning its initial formation. The central portion of the ectoderm then forms the neural plate that folds to form the neural tube, that will eventually form the entire central nervous system.

Early developmental sequence: Epiblast - Ectoderm - Neural Plate - Neural groove and Neural Crest - Neural Tube and Neural Crest

Neural Tube Development
Neural Tube Primary Vesicles Secondary Vesicles Adult Structures
week 3 week 4 week 5 adult
neural plate
neural groove
neural tube

prosencephalon (forebrain) telencephalon Rhinencephalon, Amygdala, hippocampus, cerebrum (cortex), hypothalamus‎, pituitary | Basal Ganglia, lateral ventricles
diencephalon epithalamus, thalamus, Subthalamus, pineal, posterior commissure, pretectum, third ventricle
mesencephalon (midbrain) mesencephalon tectum, Cerebral peduncle, cerebral aqueduct, pons
rhombencephalon (hindbrain) metencephalon cerebellum
myelencephalon medulla oblongata, isthmus
spinal cord, pyramidal decussation, central canal

Early Brain Vesicles

In week 3, the neural plate forms and the caudal end of the neural plate remains narrow compared to the cranial end which rapidly expands.

In week 4, when the plate folds to form the neural tube, the cranial end of the tube then forms a series of enlarged cavities (vesicles) that will eventually form the brain. The caudal end of the tube forms a narrower tube of relatively the same size along its length that will eventually form the spinal cord.

Primary Vesicles Secondary Vesicles
CNS primary vesicles.jpg CNS secondary vesicles.jpg
early embryonic late embryonic

Human brain growth 01.jpg

Direct comparison of brain growth embryonic and fetal period. Note the relative size of the spinal cord seen at the lower end of each image.

Spinal Cord Regions

The neural tube forms similar regions around the wall along its length, including the spinal cord. The floor and roof plate are specialised developmental regions, important embryonic "patterning" regions.[8]

  • Floor plate - thin wall region that overlies the notochord. Ventral patterns the spinal cord, both floor plate and notochord produce Sonic hedgehog (Shh) (see also notochord)
  • Basal plate - thick wall region lying either side of the floor floor plate. The ventral horn motor neurons develop here and extend axons out of the spinal cord to innervate developing skeletal muscle. Tracts formed by axons surround these horns and project both up and down the spinal cord.
  • Alar plate - thick wall region lying either side of the roof floor plate. The sensory dorsal horn develops there and receives axons from the sensory structures outside the spinal cord. The adult horn is divided into 6 laminae (I to VI). Tracts formed by axons surround these horns and project both up and down the spinal cord.
  • Roof plate - thin wall region that underlies the dorsal ectoderm epithelium. Dorsal patterns the spinal cord, the roof plate produces Bone morphogenetic proteins (BMPs).[9][10]
  • Lumen - neuroepithelium lined fluid-filled space continuous with the brain ventricular system.
Week 4 Week 8
Stage13 spinal cord02.jpg Human Stage22 spinal cord02.jpg
Stage 13 Spinal cord cross-section (upper part of cord).
labeled image | unlabeled image
Stage 22 Spinal cord cross-section (ventral is at bottom of image)
labeled image | unlabeled image

Embryonic Development

Week 4

Spinal cord cross-section (upper part of cord) (Carnegie Stage 13)
Stage13 spinal cord01.jpg Stage13 spinal cord02.jpg

Week 8

Human Stage22 spinal cord02.jpg

Virtual Slide

Stage 22 - Spinal Cord (rotated)

Human Stage22 spinal cord03.jpg

 ‎‎Mobile | Desktop | Original

Stage 22 | Embryo Slides
These listed features link to zoomed views of the virtual slide with the named feature generally in the centre of the view.

Use the (-) at the top left of the screen to see where this feature is located.

Spinal Cord Features Other Features

Fetal Development

Links: fetal

Conus Medullaris

Human week 10 fetus
Conus Medullaris (week 10, GA week 12)

The conus medullaris (Latin, "medullary cone") is the tapered, lower end of the spinal cord. An ultrasound study of the position of the spinal cord conus medullaris at 18-22 weeks (20 to 24 weeks ((GA}}) showed that it ended adjacent to vertebrae L2, L2-3 vertebral space, and L3 (73/78, 93%).[11]

Plexus Development

The spinal nerves initially leave the spinal cord at each individual segmental levels. At various levels they then form an intersecting network of nerves, a plexus, from which mixed segmental nerves emerge.

Cervical Plexus

Adult Cervical Plexus

(plexus cervicalis)

  • formed by the anterior divisions of the upper four cervical nerves
  • each nerve, except the 1st, divides into an upper and a lower branch, and the branches unite to form three loops.
  • branches are divided into two groups, superficial and deep.

Search PubMed: cervical plexus embryology

Brachial Plexus

Adult Brachial Plexus

plexus brachial

  • plexus extends from the lower part of the side of the neck to the axilla.
  • nerves that form it are similar in size, mode of communication is subject to some variation.
  • formed by union of the anterior divisions of the lower 4 cervical nerves and the greater part of the anterior division of the first thoracic nerve.
  • 4th cervical usually gives a branch to the 5th cervical.
  • 1st thoracic frequently receives one from the 2nd thoracic.
Search PubMed: brachial plexus embryology

Lumbar Plexus

Adult Lumbar Plexus

plexus lumbalis

  • formed by anterior divisions of the first three and the greater part of the 4th lumbar nerves.
  • 1st lumbar often receives a branch from the last thoracic nerve.
Search PubMed: lumbar plexus embryology

Sacral Plexus


A dermatome represents the area of skin that is mainly supplied by a single spinal nerve. Therefore each spinal nerve can be "mapped" to a region of the external body surface and that this "map" is established before embryonic limb rotation.

Links: Sensory - Touch Development | Limb Development


Neural tube dorsoventral patterning SHH BMP.jpg|

Neural tube Dorsoventral Patterning by SHH BMP[12]

Dorsoventral domains are established by opposing concentration gradients of Sonic Hedgehog (Shh) and Bone Morphogenic Protein (BMP).

  • left - These regulate progenitor gene expression. The progenitor genes cross-repress each other to establish domain boundaries.
  • right - Each domain will give rise to a specific cell type that expresses various post-mitotic differentiation genes.

Links: SHH | BMP

Spinal Cord Histology

Identify gray and white matter, central canal (surrounded by ependymal cells), dorsal and ventral horns, meninges (pia, arachnoid and dura mater), subarachnoid space with dorsal and ventral rootlets, blood vessels, a motor neurone with a cell body (soma), nucleus, nucleolus, Nissl granules, an axon with axon hillock area, dendrites, glial cells (oligodendrocytes, astrocytes).

Spinal cord (Luxol Fast Blue)
Spinal cord histology 01.jpg Spinal cord histology 02.jpg
Spinal cord - Grey and white matter
Spinal cord histology 03.jpg Spinal cord histology 04.jpg
Spinal cord - Grey matter
Spinal cord histology 11.jpg

Grey matter (HE)

Spinal cord histology 12.jpg

Grey matter (silver)

Spinal Cord: Overview 1 | Overview 2 | Overview animation | Grey matter | Grey matter | Grey matter | White matter | Overview unlabeled | Grey matter unlabeled 1 | Grey matter unlabeled 2 | White matter unlabeled 1 | Ependymal cells unlabeled

Spinal cord histology 10.jpg
Mouse ependymal cilia 01-icon.jpg
 ‎‎Ependymal cilia
Page | Play
<mediaplayer width='600' height='230' image="">File:Mouse_ependymal_cilia_01.mp4</mediaplayer>


Spinal Muscular Atrophy

ICD-11 8B61 Spinal muscular atrophy (ICD-10-CM Diagnosis Code G12.9)

Spinal muscular atrophy (SMA) is a rare neural autosomal recessive genetic condition that leads to a loss of motor neurons and then progressive muscle wasting. A new drug treatment using nusinersen[13] (trade name Spinraza®), see reviews[14][15], has led to the recent inclusion of SMA in the newborn heel-prick test (Guthrie test). Clinical classification of SMA type depends upon the age of onset and highest level of motor function achieved.

This genetic disease exists in several different forms related to SMN1 gene on chromosome 5q13:
  • Type 1 - caused by mutation or deletion in the telomeric copy of the SMN1 gene.
  • Type 2 - caused by homozygous or compound heterozygous mutation in the SMN1 gene.
  • Type 3 - caused by homozygous or compound heterozygous mutation in the SMN1 gene.

SMN1 - (5q13) encodes a 38 kD protein expressed in neuronal cytoplasm and nucleus. Nuclear SMN is located in Cajal bodies ("GEMS", Gemini of the coiled bodies; nucleolar accessory bodies; coiled body) involved in mRNA metabolism. These are proposed sites where small nuclear ribonucleoproteins (snRNPs) and small nucleolar RNAs (snoRNPs) are modified. Cajal bodies were first reported in 1903 by the Spanish cytologist/histologist Cajal, who christened them "nucleolar accessory bodies".

Cajal bodies
Cajal bodies panel (D) EM purified CB, SMN (arrowheads).[16]

The Hammersmith Functional Motor Scale (HFMS), was first developed in 2003 and recently revised by international collaboration[17] as a tool for assessment of the physical abilities of SMA type 2 and type 3 patients with limited ambulation. (More? Hammersmith Functional Motor Scale - 2015 revision)

Links: skeletal muscle | Search PubMed Spinal muscular atrophy


  1. Gray de Cristoforis A, Ferrari F, Clotman F & Vogel T. (2020). Differentiation and localization of interneurons in the developing spinal cord depends on DOT1L expression. Mol Brain , 13, 85. PMID: 32471461 DOI.
  2. Iulianella A & Stanton-Turcotte D. (2019). The Hedgehog receptor Patched1 regulates proliferation, neurogenesis, and axon guidance in the embryonic spinal cord. Mech. Dev. , 160, 103577. PMID: 31634536 DOI.
  3. Ohmura Y, Morokuma S, Kato K & Kuniyoshi Y. (2018). Species-specific Posture of Human Foetus in Late First Trimester. Sci Rep , 8, 27. PMID: 29311655 DOI.
  4. Diez Del Corral R & Morales AV. (2017). The Multiple Roles of FGF Signaling in the Developing Spinal Cord. Front Cell Dev Biol , 5, 58. PMID: 28626748 DOI.
  5. Kicheva A, Bollenbach T, Ribeiro A, Valle HP, Lovell-Badge R, Episkopou V & Briscoe J. (2014). Coordination of progenitor specification and growth in mouse and chick spinal cord. Science , 345, 1254927. PMID: 25258086 DOI.
  6. Demireva EY, Shapiro LS, Jessell TM & Zampieri N. (2011). Motor neuron position and topographic order imposed by β- and γ-catenin activities. Cell , 147, 641-52. PMID: 22036570 DOI.
  7. Pyrgaki C, Trainor P, Hadjantonakis AK & Niswander L. (2010). Dynamic imaging of mammalian neural tube closure. Dev. Biol. , 344, 941-7. PMID: 20558153 DOI.
  8. Wilson L & Maden M. (2005). The mechanisms of dorsoventral patterning in the vertebrate neural tube. Dev. Biol. , 282, 1-13. PMID: 15936325 DOI.
  9. Chizhikov VV & Millen KJ. (2004). Mechanisms of roof plate formation in the vertebrate CNS. Nat. Rev. Neurosci. , 5, 808-12. PMID: 15378040 DOI.
  10. Chizhikov VV & Millen KJ. (2005). Roof plate-dependent patterning of the vertebrate dorsal central nervous system. Dev. Biol. , 277, 287-95. PMID: 15617675 DOI.
  11. Perlitz Y, Izhaki I & Ben-Ami M. (2010). Sonographic evaluation of the fetal conus medullaris at 20 to 24 weeks' gestation. Prenat. Diagn. , 30, 862-4. PMID: 20582935 DOI.
  12. Zannino DA & Sagerström CG. (2015). An emerging role for prdm family genes in dorsoventral patterning of the vertebrate nervous system. Neural Dev , 10, 24. PMID: 26499851 DOI.
  13. Finkel RS, Mercuri E, Darras BT, Connolly AM, Kuntz NL, Kirschner J, Chiriboga CA, Saito K, Servais L, Tizzano E, Topaloglu H, Tulinius M, Montes J, Glanzman AM, Bishop K, Zhong ZJ, Gheuens S, Bennett CF, Schneider E, Farwell W & De Vivo DC. (2017). Nusinersen versus Sham Control in Infantile-Onset Spinal Muscular Atrophy. N. Engl. J. Med. , 377, 1723-1732. PMID: 29091570 DOI.
  14. Gidaro T & Servais L. (2018). Nusinersen treatment of spinal muscular atrophy: current knowledge and existing gaps. Dev Med Child Neurol , , . PMID: 30221755 DOI.
  15. Vukovic S, McAdam L, Zlotnik-Shaul R & Amin R. (2018). Putting our best foot forward: Clinical, treatment-based and ethical considerations of nusinersen therapy in Canada for spinal muscular atrophy. J Paediatr Child Health , , . PMID: 30246272 DOI.
  16. Ogg SC & Lamond AI. (2002). Cajal bodies and coilin--moving towards function. J. Cell Biol. , 159, 17-21. PMID: 12379800 DOI.
  17. Ramsey D, Scoto M, Mayhew A, Main M, Mazzone ES, Montes J, de Sanctis R, Dunaway Young S, Salazar R, Glanzman AM, Pasternak A, Quigley J, Mirek E, Duong T, Gee R, Civitello M, Tennekoon G, Pane M, Pera MC, Bushby K, Day J, Darras BT, De Vivo D, Finkel R, Mercuri E & Muntoni F. (2017). Revised Hammersmith Scale for spinal muscular atrophy: A SMA specific clinical outcome assessment tool. PLoS ONE , 12, e0172346. PMID: 28222119 DOI.


Borodinsky LN. (2017). Xenopus laevis as a Model Organism for the Study of Spinal Cord Formation, Development, Function and Regeneration. Front Neural Circuits , 11, 90. PMID: 29218002 DOI.

Welniarz Q, Dusart I & Roze E. (2017). The corticospinal tract: Evolution, development, and human disorders. Dev Neurobiol , 77, 810-829. PMID: 27706924 DOI.

Greene ND & Copp AJ. (2009). Development of the vertebrate central nervous system: formation of the neural tube. Prenat. Diagn. , 29, 303-11. PMID: 19206138 DOI.

Ulloa F & Martí E. (2010). Wnt won the war: antagonistic role of Wnt over Shh controls dorso-ventral patterning of the vertebrate neural tube. Dev. Dyn. , 239, 69-76. PMID: 19681160 DOI.

Dasen JS & Jessell TM. (2009). Hox networks and the origins of motor neuron diversity. Curr. Top. Dev. Biol. , 88, 169-200. PMID: 19651305 DOI.

Dessaud E, McMahon AP & Briscoe J. (2008). Pattern formation in the vertebrate neural tube: a sonic hedgehog morphogen-regulated transcriptional network. Development , 135, 2489-503. PMID: 18621990 DOI.

Molyneaux BJ, Arlotta P & Macklis JD. (2007). Molecular development of corticospinal motor neuron circuitry. Novartis Found. Symp. , 288, 3-15; discussion 15-20, 96-8. PMID: 18494249

Glenn OA & Barkovich AJ. (2006). Magnetic resonance imaging of the fetal brain and spine: an increasingly important tool in prenatal diagnosis, part 1. AJNR Am J Neuroradiol , 27, 1604-11. PMID: 16971596

Glenn OA & Barkovich J. (2006). Magnetic resonance imaging of the fetal brain and spine: an increasingly important tool in prenatal diagnosis: part 2. AJNR Am J Neuroradiol , 27, 1807-14. PMID: 17032846

Sadler TW. (2005). Embryology of neural tube development. Am J Med Genet C Semin Med Genet , 135C, 2-8. PMID: 15806586 DOI.

Placzek M & Briscoe J. (2005). The floor plate: multiple cells, multiple signals. Nat. Rev. Neurosci. , 6, 230-40. PMID: 15738958 DOI.


Saitsu H & Shiota K. (2008). Involvement of the axially condensed tail bud mesenchyme in normal and abnormal human posterior neural tube development. Congenit Anom (Kyoto) , 48, 1-6. PMID: 18230116 DOI.


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Filum Terminale (1919)
Streeter GL. Factors involved in the formation of the filum terminale. (1919) Amer. J Anat. 22(1): 1-11.
Human Embryology And Morphology (1921)
Keith, A. Human Embryology And Morphology (1921) Longmans, Green & Co.:New York.

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Anatomy of the Human Body (1918)
Gray, H. Anatomy of the Human Body. Philadelphia: Lea & Febiger, 1918.

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