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System Injury (system + injury)
Kinds of System Injury Selected AbstractsBinding characteristics of chondroitin sulfate proteoglycans and laminin-1, and correlative neurite outgrowth behaviors in a standard tissue culture choice assayDEVELOPMENTAL NEUROBIOLOGY, Issue 4 2002Diane M. Snow Abstract Neuronal growth cones are capable of sophisticated discrimination of environmental cues, on cell surfaces and in the extracellular matrix, to accomplish navigation during development (generation) and following nervous system injury (regeneration). Choices made by growth cones are commonly examined using tissue culture paradigms in which molecules of interest are purified and substratum-bound. From observations of growth cone behaviors using these paradigms, assertions are made about choices neuronal growth cones may make in vivo. However, in many cases, the binding, interactions, and conformations of these molecules have not been determined. In the present study, we investigated the binding characteristics of two commonly studied outgrowth regulatory molecules: chondroitin sulfate proteoglycans (CSPGs), which are typically inhibitory to neurite outgrowth during development and following nervous system injury, and laminin, which is typically outgrowth promoting for many neuronal types. Using a novel combination of radiolabeling and quantitative fluorescence, we determined the precise concentrations of CSPGs and laminin-1 that were bound separately and together in a variety of choice assays. For identically prepared cultures, we correlated neurite outgrowth behaviors with binding characteristics. The data support our working hypothesis that neuronal growth cones are guided by the ratio of outgrowth-promoting to outgrowth-inhibiting influences in their environment, i.e., they summate local molecular cues. The response of growth cones to these molecular combinations is most likely mediated by integrins and subsequent activation of signal transduction cascades in growth cones. © 2002 Wiley Periodicals, Inc. J Neurobiol 51: 285,301, 2002 [source] Cooperative effects of bcl-2 and AAV-mediated expression of CNTF on retinal ganglion cell survival and axonal regeneration in adult transgenic miceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2006Simone G. Leaver Abstract We used a gene therapy approach in transgenic mice to assess the cooperative effects of combining anti-apoptotic and growth-promoting stimuli on adult retinal ganglion cell (RGC) survival and axonal regeneration following intraorbital optic nerve injury. Bi- cistronic adeno-associated viral vectors encoding a secretable form of ciliary neurotrophic factor and green fluorescent protein (AAV-CNTF-GFP) were injected into eyes of mice that had been engineered to over-express the anti-apoptotic protein bcl-2. For comparison this vector was also injected into wildtype (wt) mice, and both mouse strains were injected with control AAV encoding GFP. Five weeks after optic nerve injury we confirmed that bcl-2 over-expression by itself promoted the survival of axotomized RGCs, but in contrast to previous reports we also saw regeneration of some mature RGC axons beyond the optic nerve crush. AAV-mediated expression of CNTF in adult retinas significantly increased the survival and axonal regeneration of RGCs following axotomy in wt and bcl-2 transgenic mice; however, the effects were greatest in the transgenic strain. Compared with AAV-GFP-injected bcl-2 mice, RGC viability was increased by about 50% (mean, 36 738 RGCs per retina), and over 1000 axons per optic nerve regenerated 1,1.5 mm beyond the crush. These findings exemplify the importance of using a multifactorial therapeutic approach that enhances both neuroprotection and regeneration after central nervous system injury. [source] Correlations between clinical and historical variables, and cerebral structural variables in people with mild intellectual disability and schizophreniaJOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 2 2001T. L. Sanderson Abstract The increased prevalence of schizophrenia in the population with mildly intellectual disability (ID) remains unexplained. The present study explores several possibilities by examining historical/clinical findings in relation to structural neuroimaging findings in three groups: (1) comorbid mild ID and schizophrenia; (2) schizophrenia alone; and (3) mild ID alone. Information about clinical and historical variables was obtained from 101 subjects (39 with comorbidity, 34 with schizophrenia and 28 with mild ID), out of whom 68 (23, 25 and 20, respectively) had had a cerebral magnetic resonance imaging (MRI) scan. Although a number of significant correlations exist between clinical variables and structural MRI abnormalities in all three groups, no clearly predictive inter- or between-group differences emerged. More striking was the finding that showed small amygdalo-hippocampal size to be associated with a history of central nervous system injury, especially meningitis. These findings provide support for the view that cognitive impairment and comorbid psychosis can result from a common cause, such as meningitis or obstetric complications, possibly interacting with other factors, such as family history. [source] Therapeutic potential of melatonin in traumatic central nervous system injuryJOURNAL OF PINEAL RESEARCH, Issue 2 2009Supriti Samantaray Abstract:, A vast literature extolling the benefits of melatonin has accumulated during the past four decades. Melatonin was previously considered of importance to seasonal reproduction and circadian rhythmicity. Currently, it appears to be a versatile anti-oxidative and anti-nitrosative agent, a molecule with immunomodulatory actions and profound oncostatic activity, and also to play a role as a potent neuroprotectant. Nowadays, melatonin is sold as a dietary supplement with differential availability as an over-the-counter aid in different countries. There is a widespread agreement that melatonin is nontoxic and safe considering its frequent, long-term usage by humans at both physiological and pharmacological doses with no reported side effects. Endeavors toward a designated drug status for melatonin may be enormously rewarding in clinics for treatment of several forms of neurotrauma where effective pharmacological intervention has not yet been attained. This mini review consolidates the data regarding the efficacy of melatonin as an unique neuroprotective agent in traumatic central nervous system (CNS) injuries. Well-documented actions of melatonin in combating traumatic CNS damage are compiled from various clinical and experimental studies. Research on traumatic brain injury and ischemia/reperfusion are briefly outlined here as they have been recently reviewed elsewhere, whereas the studies on different animal models of the experimental spinal cord injury have been extensively covered in this mini review for the first time. [source] Resolution of alcoholic neuropathy following liver transplantationLIVER TRANSPLANTATION, Issue 12 2004Edward Gane Between 10 and 20% of adult liver transplants are performed for end-stage alcoholic liver disease. Severe extrahepatic end-organ damage from alcoholism (cardiomyopathy, pancreatitis, central nervous system injury, and neuropathy) is widely regarded as an absolute contraindication to liver transplantation, despite a lack of data on the effect of transplantation on these complications. We describe such a patient who presented with decompensated alcoholic liver disease and moderately severe peripheral neuropathy. Both his liver failure and neuropathy progressed despite 9 months abstinence and intensive nutritional support. By 12 months post-transplant, however, this patient had regained almost normal muscle strength, with associated recovery in sensory and motor conduction velocities. Direct alcohol toxicity, nutritional and vitamin deficiencies, and liver failure were all likely etiologic factors in this patient's neuropathy. In conclusion, this case suggests that peripheral neuropathy in a patient with alcoholic cirrhosis may resolve following liver transplantation and should not constitute a contraindication to transplantation, even when it is disabling. (Liver Transpl 2004;10:1545,1548.) [source] The Meissner and Pacinian sensory corpuscles revisited new data from the last decade,MICROSCOPY RESEARCH AND TECHNIQUE, Issue 4 2009José A. Vega Abstract This article reviews the biochemical, physiological, and experimental data cumulated during the last decade on the Meissner and Pacinian corpuscles. It includes information about (i) the localization of molecules recently detected in sensory corpuscles; (ii) the unsolved problem of the accessory fibers in sensory corpuscles and the occurrence of myelin within them; (iii) the development of sensory corpuscles, especially their neuronal and growth factor dependency; (iv) the composition and functional significance of the extracellular matrix as an essential part of the mechanisms involved in the genesis of the stimuli generated in sensory corpuscles; (v) the molecular basis of mechanotransduction; (vi) a miscellaneous section containing sparse new data on the protein composition of sensory corpuscles, as well as in the proteins involved in live,death cell decisions; (vii) the changes in sensory corpuscles as a consequence of aging, the central, or peripheral nervous system injury; and finally, (viii) the special interest of Meissner corpuscles and Pacinian corpuscles for pathologists for the diagnosis of some peripheral neuropathies nd neurodegenerative diseases. Microsc. Res. Tech., 2009. © 2008 Wiley-Liss, Inc. [source] Nervous system,derived chondroitin sulfate proteoglycans regulate growth cone morphology and inhibit neurite outgrowth: A light, epifluorescence, and electron microscopy studyMICROSCOPY RESEARCH AND TECHNIQUE, Issue 5 2001Diane M. Snow Abstract Proteoglycans influence aging and plasticity in the nervous system. Particularly prominent are the chondroitin sulfate proteoglycans (CSPGs), which are generally inhibitory to neurite outgrowth. During development, CSPGs facilitate normal guidance, but following nervous system injury and in diseases of aging (e.g., Alzheimer's disease), they block successful regeneration, and are associated with axon devoid regions and degenerating nerve cells. Whereas previous studies used non-nervous system sources of CSPGs, this study analyzed the morphology and behavior of sensory (dorsal root ganglia) neurons, and a human nerve cell model (SH-SY5Y neuroblastoma cells) as they contacted nervous system,derived CSPGs, using a variety of microscopy techniques. The results of these qualitative analyses show that growth cones of both nerve cell types contact CSPGs via actin-based filopodia, sample the CSPGs repeatedly without collapse, and alter their trajectory to avoid nervous system,derived CSPGs. Turning and branching are correlated with increased filopodial sampling, and are common to both neurons and Schwann cells. We show that CSPG expression by rat CNS astrocytes in culture is correlated with sensory neuron avoidance. Further, we show for the first time the ultrastructure of sensory growth cones at a CSPG-laminin border and reveal details of growth cone and neurite organization at this choice point. This type of detailed analysis of the response of growth cones to nervous system,derived CSPGs may lead to an understanding of CSPG function following injury and in diseases of aging, where CSPGs are likely to contribute to aberrant neurite outgrowth, failed or reduced synaptic connectivity, and/or ineffective plasticity. Microsc. Res. Tech. 54:273,286, 2001. © 2001 Wiley-Liss, Inc. [source] | |||||||||||||