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Kolmer-Agduhr (KA) cells are a subgroup of interneurons positioned adjacent to the neurocoele with cilia on the apical surface protruding into the central canal of the spinal cord. Although KA cells were identified almost a century ago, their development and functions are only beginning to be unfolded. Recent studies have revealed the characteristics of KA cells in greater detail, including their spatial distribution, the timing of their differentiation, and their specification via extrinsic signaling and a unique combination of transcription factors in zebrafish and mouse. Cell lineage-tracing experiments have demonstrated that two subsets of KA cells, named KA' and KA" cells, differentiate from motoneuronal progenitors and floor-plate precursors, respectively, in both zebrafish and mouse. Although KA' and KA" cells originate from different progenitors/precursors, they each share a common set of transcription factors. Intriguingly, the combination of transcription factors that promote the acquisition of KA' cell characteristics differs from those that promote a KA" cell identity. In addition, KA' and KA" cells exhibit separable neuronal targets and differential responses to bending of the spinal cord. In this review, we summarize what is currently known about the genetic programs defining the identities of KA' and KA" cell identities. We then discuss how these two subgroups of KA cells are genetically specified.
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http://dx.doi.org/10.3389/fnins.2020.577879 | DOI Listing |
Neural Regen Res
September 2015
Institute of Clinical Anatomy, Southern Medical University, Guangzhou, Guangdong Province, China.
Chemically extracted acellular nerve allografts loaded with brain-derived neurotrophic factor-transfected or ciliary neurotrophic factor-transfected bone marrow mesenchymal stem cells have been shown to repair sciatic nerve injury better than chemically extracted acellular nerve allografts alone, or chemically extracted acellular nerve allografts loaded with bone marrow mesenchymal stem cells. We hypothesized that these allografts compounded with both brain-derived neurotrophic factor- and ciliary neurotrophic factor-transfected bone marrow mesenchymal stem cells may demonstrate even better effects in the repair of peripheral nerve injury. We cultured bone marrow mesenchymal stem cells expressing brain-derived neurotrophic factor and/or ciliary neurotrophic factor and used them to treat sciatic nerve injury in rats.
View Article and Find Full Text PDFNeural Regen Res
October 2014
Institute of Clinical Anatomy, Southern Medical University, Guangzhou, Guangdong Province, China.
In this study, we chemically extracted acellular nerve allografts from bilateral sciatic nerves, and repaired 10-mm sciatic nerve defects in rats using these grafts and brain-derived neurotrophic factor transfected bone marrow mesenchymal stem cells. Experiments were performed in three groups: the acellular nerve allograft bridging group, acellular nerve allograft + bone marrow mesenchymal stem cells group, and the acellular nerve allograft + brain-derived neurotrophic factor transfected bone marrow mesenchymal stem cells group. Results showed that at 8 weeks after bridging, sciatic functional index, triceps wet weight recovery rate, myelin thickness, and number of myelinated nerve fibers were significantly changed in the three groups.
View Article and Find Full Text PDFPlane-to-point transformations are used to develop a version of the Hydrolight computer program with which to compute the spatial dependence of the irradiance and the scalar irradiance of the light field away from an isotropic point source deep within a spatially uniform ocean. The transformations are also used to derive analytic approximations for determining the diffuse attenuation coefficient and the mean cosine of the radiance far from an isotropic point source. Approximations for determining the asymptotic diffuse attenuation coefficient from measurements at only two distances far from the source are derived and numerically tested with the modified version of the Hydrolight computer program.
View Article and Find Full Text PDFInt J Palliat Nurs
November 2003
Interactive Education Unit, The Institute of Cancer Research, 15 Cotswold Road, Sutton, SM2 5NG, UK.
Chem Res Toxicol
April 2002
University of Minnesota Cancer Center, Minneapolis, Minnesota 55455, USA.
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a tobacco-specific lung carcinogen which may play an important role as a cause of lung cancer in smokers. NNK is extensively metabolized to 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), which like NNK is a potent pulmonary carcinogen. NNAL in turn is glucuronidated, and both NNAL and its glucuronides are excreted in human urine.
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