Neural cell adhesion molecules are present in the fetal human primary olfactory pathway.
ABSTRACT Olfactory tissues from human fetuses (17.5-28 weeks of gestation) were stained by immunofluorescence for neural cell adhesion molecules (N-CAMs). Staining for N-CAMs was most prominent in the olfactory nerve bundles in the lamina propria, while in the olfactory epithelium, it was present on the olfactory receptor neurons and globose basal cells. The basal cells proper and supporting cells lacked N-CAMs. In the olfactory bulb, only the olfactory nerve and glomerular layers showed moderate labeling for N-CAMs. Western blot analysis showed that the N-CAMs of the fetal human primary olfactory pathway consisted of three molecular isoforms, N-CAM180, N-CAM140 and N-CAM120.
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ABSTRACT: Case report. Report rapid neurological changes in a complete tetraplegic following a cell injection procedure. Beijing, China. ASIA/IMSOP neurological scale. Immunostaining of cell cultures. Cellular transplantation to effect functional restoration following spinal cord injury (SCI) has been hypothesized to cause improvements through axonal regeneration, increased plasticity, or axonal remyelination. Several human trials are in preliminary phases. We report a rapid improvement in motor and sensory functions in the segment adjacent to the level of complete SCI within days following cellular transplantation of cultured fetal olfactory bulb-derived cells. The patient was an 18-year-old C3 ASIA A complete tetraplegic 18 months post-injury who had been neurologically stable for more than 6 months. Within 48 h of cell transplantation, the patient improved one ASIA motor grade in the left elbow flexors and began to show right wrist extensor function. Descent of the sensory level occurred within 4 days and then the rate of change slowed. He is now a C5 motor and C4 sensory complete tetraplegic. Cellular cultures prepared in the same facility showed viable human cells that labeled for nestin and GFAP. We hypothesize that improved transmission in intact fibers subserving the zone of partial preservation accounts for these early improvements. We emphasize the need for further independent analysis of the outcomes of this and other preliminary cell transplant studies.Spinal Cord 04/2006; 44(3):135-42. · 1.90 Impact Factor
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ABSTRACT: The peptide urotensin II (U-II) is the cognate ligand of the G-protein coupled receptor UT (formerly GPR14). A role in the regulation of cardiovascular functions has been proposed for this novel peptide/receptor system. In the present study, we evaluated the ability of U-II to induce plasma extravasation in mice and attempted to characterize the receptor involved using the novel UT receptor ligand, [Orn(8)]U-II. The Evans blue technique was used to quantify plasma extravasation. U-II (0.01, 0.1, 1 and 10 nmol/kg) dose-dependently stimulated plasma extravasation in airways, gastrointestinal and urogenital tract tissues from mice, but not in the skin. In most tissues, the dose/response curves to U-II were bell shaped with the maximal effect induced by 1 nmol/kg. [Orn(8)]U-II at 30 nmol/kg was per se either inactive or produced a non-significant increase in plasma extravasation; in the presence of 30 nmol/kg [Orn(8)]U-II, the effects of 1 nmol/kg U-II were always reduced and, in some tissues, abolished. The present findings demonstrate that U-II promotes plasma extravasation in various mouse vascular regions via activation of UT receptors. The mouse plasma extravasation assay will be a useful tool in future studies aimed at characterizing the pharmacological features of novel UT receptor ligands in vivo.Archiv für Experimentelle Pathologie und Pharmakologie 12/2004; 370(5):347-52. · 2.15 Impact Factor
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ABSTRACT: 1. SB-706375 potently inhibited [(125)I]hU-II binding to both mammalian recombinant and 'native' UT receptors (K(i) 4.7+/-1.5 to 20.7+/-3.6 nM at rodent, feline and primate recombinant UT receptors and K(i) 5.4+/-0.4 nM at the endogenous UT receptor in SJRH30 cells). 2. Prior exposure to SB-706375 (1 microM, 30 min) did not alter [(125)I]hU-II binding affinity or density in recombinant cells (K(D) 3.1+/-0.4 vs 5.8+/-0.9 nM and B(max) 3.1+/-1.0 vs 2.8+/-0.8 pmol mg(-1)) consistent with a reversible mode of action. 3. The novel, nonpeptidic radioligand [(3)H]SB-657510, a close analogue of SB-706375, bound to the monkey UT receptor (K(D) 2.6+/-0.4 nM, B(max) 0.86+/-0.12 pmol mg(-1)) in a manner that was inhibited by both U-II isopeptides and SB-706375 (K(i) 4.6+/-1.4 to 17.6+/-5.4 nM) consistent with the sulphonamides and native U-II ligands sharing a common UT receptor binding domain. 4. SB-706375 was a potent, competitive hU-II antagonist across species with pK(b) 7.29-8.00 in HEK293-UT receptor cells (inhibition of [Ca(2+)](i)-mobilization) and pK(b) 7.47 in rat isolated aorta (inhibition of contraction). SB-706375 also reversed tone established in the rat aorta by prior exposure to hU-II (K(app) approximately 20 nM). 5. SB-706375 was a selective U-II antagonist with >/=100-fold selectivity for the human UT receptor compared to 86 distinct receptors, ion channels, enzymes, transporters and nuclear hormones (K(i)/IC(50)>1 microM). Accordingly, the contractile responses induced in isolated aortae by KCl, phenylephrine, angiotensin II and endothelin-1 were unaltered by SB-706375 (1 microM). 6. In summary, SB-706375 is a high-affinity, surmountable, reversible and selective nonpeptide UT receptor antagonist with cross-species activity that will assist in delineating the pathophysiological actions of U-II in mammals.British Journal of Pharmacology 08/2005; 145(5):620-35. · 5.07 Impact Factor