Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phylogenetically "lower" species in some cases use different biological strategies for recovery after injury to the CNS than do "higher" species. One approach that we have taken in our laboratory has been to study the mechanisms of functional recovery of the CNS after injury in those vertebrate species where recovery does occur. The present report reviews recent studies on a model system, the spinal electromotor system of the gymnotiform teleost Sternarchus albifrons, which exhibits regeneration and neurogenesis after injury. Regeneration in this system leads to a recapitulation of relatively normal morphologic structure by the damaged or extirpated spinal cord. In Sternarchus, new spinal cord is generated from ependymal cells; some ependymal cells in the adult remain pluripotent and retain the capability to generate new neurons. The Sternarchus spinal cord thus represents an especially useful model for the study of neurogenesis after injury to the CNS. Recent studies in our laboratory indicate that neurogenesis in adult Sternarchus spinal cord tissue occurs both in vivo and in vitro. Neurogenesis has been demonstrated by incorporation of tritiated thymidine into explant cultures from the spinal cord of adult Sternarchus. Autoradiography reveals the presence of thymidine-labeled neurons. Neuronal identity of 3H-labeled cells has been confirmed by positive staining with neuron-specific monoclonal antibodies. Thymidine labeling occurs in cultured neurons derived from both normal (histologically and functionally mature) and regenerating spinal cord of adult Sternarchus albifrons. These results provide evidence that some cells in spinal cord of adult Sternarchus retain the ability to incorporate thymidine and undergo neuronal differentiation in vitro. This system provides a new model in which neurogenesis from adult tissue can be studied in vivo and in vitro.
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PMID:Neurogenesis in adult vertebrate spinal cord in situ and in vitro: a new model system. 391 65

Reactive oxygen species are generated during ischemia-reperfusion tissue injury. Oxidation of thymidine by hydroxyl radicals (HO*) causes formation of 5,6-dihydroxy-5,6-dihydrothymidine (thymidine glycol). Thymidine glycol excreted in urine can be used as a biomarker of oxidative DNA damage. The aim of this study was to investigate the oxidative DNA damage in patients showing immediate allograft function after kidney transplantation, and to find out whether this damage correlates with glomerular and tubular lesions. Time dependent changes in urinary excretion rates of thymidine glycol, but also of total protein, albumin, low molecular weight (alpha1-microglobulin, beta2-microglobulin) and high molecular weight proteins (transferrin, IgG, alpha2-macroglobulin) were analyzed quantitatively and by polyacrylamide-gel electrophoresis in six patients. Urinary thymidine glycol was determined by a fluorimetric assay in combination with affinity chromatography and HPLC. After kidney transplantation the urinary excretion rate of thymidine glycol increased gradually reaching a maximum within the first 48 hours (16.56+/-11.3 nmol/m mol creatinine, ref. 4.3+/-0.97). Severe proteinuria with an excretion rate of up to 7.2 g/mmol creatinine was observed and declined within the first 24 hours of allograft function (0.35+/-0.26 g/mmol creatinine). The gel-electrophoretic pattern showed a nonselective glomerular and tubular proteinuria. The initial nonselective glomerular proteinuria disappeared within 48 hours, changing to a mild selective glomerular proteinuria. In this period (12-48 hours) higher levels of thymidine glycol excretion were observed, when compared to the initial posttransplant phase (13.66+/-9.76 vs. 4.31+/-3.61 nmol/mmol creatinine; p<0.05). An increased excretion of thymidine glycol is seen after kidney transplantation and is explained by the ischemia-reperfusion induced oxidative DNA damage in the kidney. In the second phase higher levels of excretion were observed parallel to the change from a nonselective to a selective glomerular and tubular proteinuria. An explanation may be sought in the repair process of DNA in the glomerular and tubular epithelial cells, appearing simultaneously with functional recovery.
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PMID:Urinary thymidine glycol as a biomarker for oxidative stress after kidney transplantation. 1090 Nov 87

Functional recovery is poor after peripheral nerve injury and delayed surgical repair or when nerves must regenerate over long distances to reinnervate distant targets. A reduced capacity of Schwann cells (SCs) in chronically denervated distal nerve stumps to support and interact with regenerating axons may account for the poor outcome. In an in vitro system, we examined the capacity of adult, long-term denervated rat SCs to proliferate and to myelinate neurites in co-cultures with fetal dorsal root ganglion (DRG) neurons. Non-neuronal cells were counted immediately after their isolation from the distal sciatic nerve stumps that were subjected to acute denervation of 7 days or chronic denervation of either 7 weeks or 17 months. Thereafter, equal numbers of the non-neural cells were co-cultured with purified dissociated DRG neurons for 5 days. The co-cultures were then treated with 3H-Thymidine for 24 h to quantitate SC proliferation with S100 immunostaining and autoradiography. After a 24-day period of co-culture, Sudan Black staining was used to visualize and count myelin segments that were elaborated around DRG neurites by the SCs. Isolated non-neural cells from 7-week chronically denervated nerve stumps increased 2.5-fold in number compared to ~2 million in 7 day acutely denervated stumps. There were only <0.2 million cells in the 17-week chronically denervated stumps. Nonetheless, these chronically denervated SCs maintained their proliferative capacity although the capacity was reduced to 30% in the 17-month chronically denervated distal nerve stumps. Moreover, the chronically denervated SCs retained their capacity to myelinate DRG neurites: there was extensive myelination of the neurites by the acutely and chronically denervated SCs after 24 days co-culture. There were no significant differences in the extent of myelination. We conclude that the low numbers of surviving SCs in chronically denervated distal nerve stumps retain their ability to respond to axonal signals to divide and to elaborate myelin. However, their low numbers consequent to their poor survival and their reduced capacity to proliferate account, at least in part, for the poor functional recovery after delayed surgical repair of injured nerve and/or the repair of injured nerves far from their target organs.
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PMID:Long-Term Denervated Rat Schwann Cells Retain Their Capacity to Proliferate and to Myelinate Axons in vitro. 3066 88