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Urs Rutishauser - One of the best experts on this subject based on the ideXlab platform.
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Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
Neuroscience, 1998Co-Authors: S.h Hrynkow, Craig Brumwell, D. Kent Morest, Urs RutishauserAbstract:Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.
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Multiple roles of neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1 Adhesion Molecules during sensory innervation of the otic epithelium in vitro
Neuroscience, 1998Co-Authors: S.h Hrynkow, Masako M. Bilak, D. Kent Morest, Urs RutishauserAbstract:Abstract To explore the role of cell Adhesion Molecules in the innervation of the inner ear, antibody perturbation was used on histotypic co-cultures of the ganglionic and epithelial anlagen derived from the otocyst. When unperturbed, these tissues survived and differentiated in this culture system with outgrowth of fasciculated neuronal fibers which expressed neural cell Adhesion Molecule and L1. The fibers exhibited target choice and penetration, then branching and spreading within the otic epithelium as individual axons. Treatment of the co-cultures, or of the ganglionic anlagen alone, with anti-neural cell Adhesion Molecule or anti-L1 Fab fragments produced a defasciculation of fibers but did not affect neurite outgrowth. In the co-cultures this defasciculation was accompanied by a small increase in the number of fibers found in inappropriate tissues. However, the antibodies did not prevent fiber entry to the otic epithelium. In contrast, removal of polysialic acid from neural cell Adhesion Molecule with endoneuraminadase-N, while producing a similar fiber defasciculation, also increased the incidence of fibers entering the epithelium. Nevertheless, once within the target tissue, the individual fibers responded to either Fab or to desialylation by spreading out more rapidly, branching, and growing farther into the epithelium. The findings suggest that fasciculation is not essential for specific sensory fibers to seek out and penetrate the appropriate target, although it may improve their tracking efficiency. Polysialic acid on neural cell Adhesion Molecule appears to limit initial penetration of the target epithelium. Polysialic acid as well as neural cell Adhesion Molecule and L1 function are involved in fiber–target interactions that influence the arborization of sensory axons within the otic epithelium.
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Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
Neuroscience, 1998Co-Authors: S.h Hrynkow, Craig Brumwell, D. Kent Morest, Urs RutishauserAbstract:Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.
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Neural cell Adhesion Molecule in aged mouse muscle
Neuroscience, 1992Co-Authors: H Kobayashi, N. Robbins, Urs RutishauserAbstract:Abstract Expression of the neural cell Adhesion Molecule was compared in endplate and non-endplate regions of skeletal muscles of mature and old CBF-1 mice, in order to determine whether age-related changes in neuromuscular morphology were correlated with age changes in neural cell Adhesion Molecule expression. Three muscles were examined: two (soleus and sternomastoid) showed age-related regionalization of nerve terminals as one manifestation of increased synaptic remodelling, while the third (diaphragm) did not. Relative neural cell Adhesion Molecule content in these muscles was measured by densitometry of immunoblots after concentration by affinity chromatography. Expression of the major 140,000 mol. wt form of neural cell Adhesion Molecule, which was most abundant in the endplate region, was increased in sternomastoid and soleus of old compared to adult mouse, but was unchanged with age in diaphragm. A 70,000–80,000 mol. wt presumably proteolytic polypeptide fragment of neural cell Adhesion Molecule was increased in immunoblots of all old muscles. Immunocytochemical studies of skeletal muscles showed no difference in neural cell Adhesion Molecule cellular distribution in mature vs old mice, but in motor nerve of sternomastoid, the number of neural cell Adhesion Molecule-positive nerve fibers was increased in old mice. Several lines of evidence indicated that partial denervation was rare in old CBF-1 mice, and therefore could not account for the findings above. Selective increase of 140,000 mol. wt neural cell Adhesion Molecule expression in the junctional regions of those muscles of old mice which show neuromuscular remodelling indicates that this Adhesion Molecule may play a role in the age-related instability of motor nerve terminals.
S.h Hrynkow - One of the best experts on this subject based on the ideXlab platform.
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Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
Neuroscience, 1998Co-Authors: S.h Hrynkow, Craig Brumwell, D. Kent Morest, Urs RutishauserAbstract:Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.
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Multiple roles of neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1 Adhesion Molecules during sensory innervation of the otic epithelium in vitro
Neuroscience, 1998Co-Authors: S.h Hrynkow, Masako M. Bilak, D. Kent Morest, Urs RutishauserAbstract:Abstract To explore the role of cell Adhesion Molecules in the innervation of the inner ear, antibody perturbation was used on histotypic co-cultures of the ganglionic and epithelial anlagen derived from the otocyst. When unperturbed, these tissues survived and differentiated in this culture system with outgrowth of fasciculated neuronal fibers which expressed neural cell Adhesion Molecule and L1. The fibers exhibited target choice and penetration, then branching and spreading within the otic epithelium as individual axons. Treatment of the co-cultures, or of the ganglionic anlagen alone, with anti-neural cell Adhesion Molecule or anti-L1 Fab fragments produced a defasciculation of fibers but did not affect neurite outgrowth. In the co-cultures this defasciculation was accompanied by a small increase in the number of fibers found in inappropriate tissues. However, the antibodies did not prevent fiber entry to the otic epithelium. In contrast, removal of polysialic acid from neural cell Adhesion Molecule with endoneuraminadase-N, while producing a similar fiber defasciculation, also increased the incidence of fibers entering the epithelium. Nevertheless, once within the target tissue, the individual fibers responded to either Fab or to desialylation by spreading out more rapidly, branching, and growing farther into the epithelium. The findings suggest that fasciculation is not essential for specific sensory fibers to seek out and penetrate the appropriate target, although it may improve their tracking efficiency. Polysialic acid on neural cell Adhesion Molecule appears to limit initial penetration of the target epithelium. Polysialic acid as well as neural cell Adhesion Molecule and L1 function are involved in fiber–target interactions that influence the arborization of sensory axons within the otic epithelium.
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Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
Neuroscience, 1998Co-Authors: S.h Hrynkow, Craig Brumwell, D. Kent Morest, Urs RutishauserAbstract:Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.
J. Joseph Walshe - One of the best experts on this subject based on the ideXlab platform.
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Circulating vascular cell Adhesion Molecule–1 in pre-eclampsia, gestational hypertension, and normal pregnancy: Evidence of selective dysregulation of vascular cell Adhesion Molecule–1 homeostasis in pre-eclampsia
American Journal of Obstetrics and Gynecology, 1998Co-Authors: John R. Higgins, Aikaterina Papayianni, Hugh R. Brady, Michael R. N. Darling, J. Joseph WalsheAbstract:Abstract OBJECTIVE: Our purpose was to investigate circulating levels of vascular cell Adhesion Molecule–1 in the peripheral and uteroplacental circulations during normotensive and hypertensive pregnancies. STUDY DESIGN: This prospective observational study involved 2 patient groups. Group 1 consisted of 22 women with pre-eclampsia and 30 normotensive women followed up longitudinally through pregnancy and post partum. There were an additional 13 women with established gestational hypertension. Group 2 consisted of 20 women with established pre-eclampsia and 19 normotensive control subjects undergoing cesarean delivery. Plasma levels of vascular cell Adhesion Molecule–1 were measured in blood drawn from the antecubital vein (group 1) and from both the antecubital and uterine veins (group 2). Data were analyzed by analysis of variance. RESULTS: In group 1 vascular cell Adhesion Molecule–1 levels did not change significantly throughout normal pregnancy and post partum. Women with established pre-eclampsia had increased vascular cell Adhesion Molecule–1 levels compared with the normotensive pregnancy group ( P = .01). Vascular cell Adhesion Molecule–1 levels were not elevated in women with established gestational hypertension. In group 2 significantly higher levels of vascular cell Adhesion Molecule–1 were detected in the uteroplacental ( P P P = .06). In contrast to vascular cell Adhesion Molecule–1, circulating levels of E-selectin and intercellular Adhesion Molecule–1, other major leukocyte Adhesion Molecules expressed by the endothelium, were not different in pre-eclamptic and normotensive pregnancies. CONCLUSION: Established pre-eclampsia is characterized by selective dysregulation of vascular cell Adhesion Molecule–1 homeostasis. This event is not an early preclinical feature of pre-eclampsia, does not persist post partum, is not a feature of nonproteinuric gestational hypertension, and is not observed with other major leukocyte Adhesion Molecules. Induction of vascular cell Adhesion Molecule–1 expression in pre-eclampsia may contribute to leukocyte-mediated tissue injury in this condition or may reflect perturbation of other, previously unrecognized, functions of this Molecule in pregnancy. (Am J Obstet Gynecol 1998;179:464-9.)
D. Kent Morest - One of the best experts on this subject based on the ideXlab platform.
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Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
Neuroscience, 1998Co-Authors: S.h Hrynkow, Craig Brumwell, D. Kent Morest, Urs RutishauserAbstract:Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.
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Multiple roles of neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1 Adhesion Molecules during sensory innervation of the otic epithelium in vitro
Neuroscience, 1998Co-Authors: S.h Hrynkow, Masako M. Bilak, D. Kent Morest, Urs RutishauserAbstract:Abstract To explore the role of cell Adhesion Molecules in the innervation of the inner ear, antibody perturbation was used on histotypic co-cultures of the ganglionic and epithelial anlagen derived from the otocyst. When unperturbed, these tissues survived and differentiated in this culture system with outgrowth of fasciculated neuronal fibers which expressed neural cell Adhesion Molecule and L1. The fibers exhibited target choice and penetration, then branching and spreading within the otic epithelium as individual axons. Treatment of the co-cultures, or of the ganglionic anlagen alone, with anti-neural cell Adhesion Molecule or anti-L1 Fab fragments produced a defasciculation of fibers but did not affect neurite outgrowth. In the co-cultures this defasciculation was accompanied by a small increase in the number of fibers found in inappropriate tissues. However, the antibodies did not prevent fiber entry to the otic epithelium. In contrast, removal of polysialic acid from neural cell Adhesion Molecule with endoneuraminadase-N, while producing a similar fiber defasciculation, also increased the incidence of fibers entering the epithelium. Nevertheless, once within the target tissue, the individual fibers responded to either Fab or to desialylation by spreading out more rapidly, branching, and growing farther into the epithelium. The findings suggest that fasciculation is not essential for specific sensory fibers to seek out and penetrate the appropriate target, although it may improve their tracking efficiency. Polysialic acid on neural cell Adhesion Molecule appears to limit initial penetration of the target epithelium. Polysialic acid as well as neural cell Adhesion Molecule and L1 function are involved in fiber–target interactions that influence the arborization of sensory axons within the otic epithelium.
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Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
Neuroscience, 1998Co-Authors: S.h Hrynkow, Craig Brumwell, D. Kent Morest, Urs RutishauserAbstract:Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.
Masato Kusunoki - One of the best experts on this subject based on the ideXlab platform.
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Serum Level of Soluble Vascular Cell Adhesion Molecule 1 Is a Valuable Prognostic Marker in Colorectal Carcinoma
Diseases of The Colon & Rectum, 2009Co-Authors: Yoshinaga Okugawa, Chikao Miki, Yuji Toiyama, Yuhki Koike, Yasuhiro Inoue, Masato KusunokiAbstract:PURPOSE: Vascular cell Adhesion Molecule 1 plays an important role in solid tumor enlargement and/or metastasis. This study evaluated the clinical significance of measuring serum levels of soluble vascular cell Adhesion Molecule 1 in colorectal cancer and aimed to clarify the biologic significance of its local expression. METHODS: Serum was collected from 161 patients with colorectal cancer and 26 healthy volunteers. Cancer tissue was collected from 128 patients. The level of soluble vascular cell Adhesion Molecule 1 in serum and cancer tissue was measured by enzyme-linked immunosorbent assay. RESULTS: The mean soluble vascular cell Adhesion Molecule 1 level in patients was significantly higher than that in control subjects. Elevated serum soluble vascular cell Adhesion Molecule 1 was significantly associated with clinicopathologic parameters such as tumor size, lymph node metastasis, distant metastasis, and poor prognosis. In Cox multivariate analysis, distant metastasis and elevated serum soluble vascular cell Adhesion Molecule 1 level were independent risk factors predicting poor prognosis. The prognosis for Stage 2 patients positive for soluble vascular cell Adhesion Molecule 1 was comparable to that for Stage 3 patients. In addition, the serum level of soluble vascular cell Adhesion Molecule 1 level was correlated negatively with the cancer tissue level. CONCLUSION: The preoperative level of soluble vascular cell Adhesion Molecule 1 level reflected disease progression and was a sensitive biomarker for colorectal cancer, especially Stage 2 disease.
