STUDIES OF THE DEGENERATION AND REGENERATION OF AXIS CYLINDERS IN VITRO

1. The brains of chick embryos, of cats six weeks old, of rabbits two months old, and of dogs three weeks old, when cultivated in vitro, develop long filaments which, according to their growth and their anatomical and tinctorial characters, must be considered as true axis cylinders. 2. Similar structures develop from spinal ganglia of rabbits seven months old, and from the spinal cord of cats six weeks old, and of rabbits two months old. 3. When severed from their origin by section these threads undergo degenerative changes which do not appear after nine hours, but which are seen after twenty hours, and continue until in the course of the following two days the thread degenerates completely. 4. After twenty hours the development of new axis cylinders from the central part of the cut fibers is observed.

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Teratogenic activity of methadone hydrochloride in mouse and chick embryos

Development ◽

10.1242/dev.30.2.449 ◽

1973 ◽

Vol 30 (2) ◽

pp. 449-458

Author(s):

A. Jurand

Keyword(s):

Spinal Cord ◽

Central Nervous System ◽

Nervous System ◽

Neural Plate ◽

Mouse Embryos ◽

Chick Embryos ◽

In Ovo ◽

Cervical Area ◽

Extensive Necrosis

Teratogenic activity of methadone HCl (Physeptone, Burroughs Wellcome and Co.) was tested on inbred JBT/Jd and outbred Q strain mouse embryos and on chick embryos. 22–24 mg/kg injected subcutaneously on the 9th day of pregnancy caused by the 13th day exencephaly in 56 out of 479 JBT/Jd embryos but after 32 mg/kg only in 1 out of 220 of the Q strain. Some affected JBT/Jd embryos showed also rachischisis in the cervical area. The second abnormality shown by the embryos of both strains is Z-shaped kinkage of the spinal cord. In explanted chick embryos cultured in vitro as well as in embryos treated in ovo methadone causes non-closure of the neural tube with extensive necrosis of the neural plate cells in the cephalic region. The results of this study indicate that methadone, which is a neutropic drug, has an embryotoxic activity directed against the developing central nervous system.

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Chondrogenesis in chick embryo somites in vitro

Development ◽

10.1242/dev.21.2.331 ◽

1969 ◽

Vol 21 (2) ◽

pp. 331-340

Author(s):

M. L. Ellison ◽

E. J. Ambrose ◽

G. C. Easty

Keyword(s):

Spinal Cord ◽

Chick Embryo ◽

Embryonic Development ◽

Liquid Medium ◽

Culture Conditions ◽

Chick Embryos ◽

Cartilage Formation

During the embryonic development of vertebral cartilages, cells from the somite mesoderm differentiate into chondrocytes around the spinal cord and notochord. Grafting experiments in amphibian and chick embryos have indicated that the spinal cord and notochord have some influence on this differentiation of somite cells to cartilage (Holtzer & Detwiler, 1953; Watterson, Fowler & Fowler, 1954). Further analysis in vitro has established that, under specified culture conditions, cartilage formation from somites is, in fact, dependent on the presence of either spinal cord and/or notochord or their extracts (Grobstein & Parker, 1954; Grobstein & Holtzer, 1955; Strudel, 1962, 1963; Lash, 1963). For example, Lash (1963) showed that in his system on a liquid medium stage 16 (Hamburger & Hamilton, 1951, stages) somites alone formed no cartilage, but that cartilage did develop when notochord or spinal cord was cultured with the somites. This suggested that the spinal cord and notochord were ‘inducing’ somite mesoderm cells to form chondrocytes.

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Androgen target cells in spinal cord, spinal ganglia, and glycogen body of chick embryos

Experimental Brain Research ◽

10.1007/bf00236561 ◽

1981 ◽

Vol 44 (3) ◽

Cited By ~ 15

Author(s):

F.A. Reid ◽

J.-M. Gasc ◽

W.E. Stumpf ◽

M. Sar

Keyword(s):

Spinal Cord ◽

Spinal Ganglia ◽

Target Cells ◽

Chick Embryos ◽

Glycogen Body

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The in vitro neonatal rat spinal cord preparation: a new insight into mammalian locomotor mechanisms

Journal of Comparative Physiology A ◽

10.1007/s00359-004-0499-2 ◽

2004 ◽

Vol 190 (5) ◽

pp. 343-357 ◽

Cited By ~ 35

Author(s):

F. Clarac ◽

E. Pearlstein ◽

J. F. Pflieger ◽

L. Vinay

Keyword(s):

Spinal Cord ◽

Neonatal Rat ◽

Rat Spinal Cord ◽

Insight Into

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Knockdown of long non-coding RNA LEF1-AS1 attenuates apoptosis and inflammatory injury of microglia cells following spinal cord injury

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-020-02041-6 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Sheng-Yu Cui ◽

Wei Zhang ◽

Zhi-Ming Cui ◽

Hong Yi ◽

Da-Wei Xu ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Cell Viability ◽

Microglial Cells ◽

Protective Effects ◽

Loss Of Function ◽

Sprague Dawley ◽

Cord Injury ◽

Apoptosis And Inflammation

Abstract Background Spinal cord injury (SCI) is associated with health burden both at personal and societal levels. Recent assessments on the role of lncRNAs in SCI regulation have matured. Therefore, to comprehensively explore the function of lncRNA LEF1-AS1 in SCI, there is an urgent need to understand its occurrence and development. Methods Using in vitro experiments, we used lipopolysaccharide (LPS) to treat and establish the SCI model primarily on microglial cells. Gain- and loss of function assays of LEF1-AS1 and miR-222-5p were conducted. Cell viability and apoptosis of microglial cells were assessed via CCK8 assay and flow cytometry, respectively. Adult Sprague-Dawley (SD) rats were randomly divided into four groups: Control, SCI, sh-NC, and sh-LEF-AS1 groups. ELISA test was used to determine the expression of TNF-α and IL-6, whereas the protein level of apoptotic-related markers (Bcl-2, Bax, and cleaved caspase-3) was assessed using Western blot technique. Results We revealed that LncRNA LEF1-AS1 was distinctly upregulated, whereas miR-222-5p was significantly downregulated in LPS-treated SCI and microglial cells. However, LEF1-AS1 knockdown enhanced cell viability, inhibited apoptosis, as well as inflammation of LPS-mediated microglial cells. On the contrary, miR-222-5p upregulation decreased cell viability, promoted apoptosis, and inflammation of microglial cells. Mechanistically, LEF1-AS1 served as a competitive endogenous RNA (ceRNA) by sponging miR-222-5p, targeting RAMP3. RAMP3 overexpression attenuated LEF1-AS1-mediated protective effects on LPS-mediated microglial cells from apoptosis and inflammation. Conclusion In summary, these findings ascertain that knockdown of LEF1-AS1 impedes SCI progression via the miR-222-5p/RAMP3 axis.

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A Collagen-Based Scaffold for Promoting Neural Plasticity in a Rat Model of Spinal Cord Injury

Polymers ◽

10.3390/polym12102245 ◽

2020 ◽

Vol 12 (10) ◽

pp. 2245

Author(s):

Jue-Zong Yeh ◽

Ding-Han Wang ◽

Juin-Hong Cherng ◽

Yi-Wen Wang ◽

Gang-Yi Fan ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Rat Model ◽

Neural Plasticity ◽

Collagen Scaffold ◽

Glial Scar ◽

Beneficial Effects ◽

Cord Injury

In spinal cord injury (SCI) therapy, glial scarring formed by activated astrocytes is a primary problem that needs to be solved to enhance axonal regeneration. In this study, we developed and used a collagen scaffold for glial scar replacement to create an appropriate environment in an SCI rat model and determined whether neural plasticity can be manipulated using this approach. We used four experimental groups, as follows: SCI-collagen scaffold, SCI control, normal spinal cord-collagen scaffold, and normal control. The collagen scaffold showed excellent in vitro and in vivo biocompatibility. Immunofluorescence staining revealed increased expression of neurofilament and fibronectin and reduced expression of glial fibrillary acidic protein and anti-chondroitin sulfate in the collagen scaffold-treated SCI rats at 1 and 4 weeks post-implantation compared with that in untreated SCI control. This indicates that the collagen scaffold implantation promoted neuronal survival and axonal growth within the injured site and prevented glial scar formation by controlling astrocyte production for their normal functioning. Our study highlights the feasibility of using the collagen scaffold in SCI repair. The collagen scaffold was found to exert beneficial effects on neuronal activity and may help in manipulating synaptic plasticity, implying its great potential for clinical application in SCI.

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Transrectal electroejaculation combined with in-vitro fertilization: effective treatment of anejaculatory infertility due to spinal cord injury

Human Reproduction ◽

10.1093/humrep/12.12.2687 ◽

1997 ◽

Vol 12 (12) ◽

pp. 2687-2692 ◽

Cited By ~ 17

Author(s):

P. R. Brinsden ◽

S. M. Avery ◽

S. Marcus ◽

M. C. Macnamee

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

In Vitro Fertilization ◽

Effective Treatment ◽

Vitro Fertilization ◽

Cord Injury

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THE PATHOLOGIC EFFECTS OF STREPTOCOCCI FROM CASES OF POLIOMYELITIS AND OTHER SOURCES

Journal of Experimental Medicine ◽

10.1084/jem.25.4.557 ◽

1917 ◽

Vol 25 (4) ◽

pp. 557-580 ◽

Cited By ~ 25

Author(s):

Carroll G. Bull

Keyword(s):

Spinal Cord ◽

Guinea Pigs ◽

The Other ◽

Laboratory Animals ◽

Histological Changes ◽

Other Hand ◽

Brain And Spinal Cord ◽

The Brain

Streptococci cultivated from the tonsils of thirty-two cases of poliomyelitis were used to inoculate various laboratory animals. In no case was a condition induced resembling poliomyelitis clinically or pathologically in guinea pigs, dogs, cats, rabbits, or monkeys. On the other hand, a considerable percentage of the rabbits and a smaller percentage of some of the other animals developed lesions due to streptococci. These lesions consisted of meningitis, meningo-encephalitis, abscess of the brain, arthritis, tenosynovitis, myositis, abscess of the kidney, endocarditis, pericarditis, and neuritis. No distinction in the character or frequency of the lesions could be determined between the streptococci derived from poliomyelitic patients and from other sources. Streptococci isolated from the poliomyelitic brain and spinal cord of monkeys which succumbed to inoculation with the filtered virus failed to induce in monkeys any paralysis or the characteristic histological changes of poliomyelitis. These streptococci are regarded as secondary bacterial invaders of the nervous organs. Monkeys which have recovered from infection with streptococci derived from cases of poliomyelitis are not protected from infection with the filtered virus, and their blood does not neutralize the filtered virus in vitro. We have failed to detect any etiologic or pathologic relationship between streptococci and epidemic poliomyelitis in man or true experimental poliomyelitis in the monkey.

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Apoptosis in metanephric development.

The Journal of Cell Biology ◽

10.1083/jcb.119.5.1327 ◽

1992 ◽

Vol 119 (5) ◽

pp. 1327-1333 ◽

Cited By ~ 200

Author(s):

C Koseki ◽

D Herzlinger ◽

Q al-Awqati

Keyword(s):

Spinal Cord ◽

Protein Kinase ◽

Transcriptional Activation ◽

Phorbol Esters ◽

Dna Degradation ◽

Morphological Evidence ◽

Metanephric Mesenchyme ◽

Embryonic Spinal Cord

During metanephric development, non-polarized mesenchymal cells are induced to form the epithelial structures of the nephron following interaction with extracellular matrix proteins and factors produced by the inducing tissue, ureteric bud. This induction can occur in a transfilter organ culture system where it can also be produced by heterologous cells such as the embryonic spinal cord. We found that when embryonic mesenchyme was induced in vitro and in vivo, many of the cells surrounding the new epithelium showed morphological evidence of programmed cell death (apoptosis) such as condensed nuclei, fragmented cytoplasm, and cell shrinking. A biochemical correlate of apoptosis is the transcriptional activation of a calcium-sensitive endonuclease. Indeed, DNA isolated from uninduced mesenchyme showed progressive degradation, a process that was prevented by treatment with actinomycin-D or cycloheximide and by buffering intracellular calcium. These results demonstrate that the metanephric mesenchyme is programmed for apoptosis. Incubation of mesenchyme with a heterologous inducer, embryonic spinal cord prevented this DNA degradation. To investigate the mechanism by which inducers prevented apoptosis we tested the effects of protein kinase C modulators on this process. Phorbol esters mimicked the effects of the inducer and staurosporine, an inhibitor of this protein kinase, prevented the effect of the inducer. EGF also prevented DNA degradation but did not lead to differentiation. These results demonstrate that conversion of mesenchyme to epithelial requires at least two steps, rescue of the mesenchyme from apoptosis and induction of differentiation.

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