In the spinal cord, neurons and glial cells actively interact and contribute to neurofunction. Surprisingly, both cell types have similar receptors, transporters and ion channels and also produce similar neurotransmitters and cytokines. The neuroanatomical and neurochemical similarities work synergistically to maintain physiological homeostasis in the normal spinal cord. However, in trauma or disease states, spinal glia become activated, dorsal horn neurons become hyperexcitable contributing to sensitized neuronal-glial circuits. The maladaptive spinal circuits directly affect synaptic excitability, including activation of intracellular downstream cascades that result in enhanced evoked and spontaneous activity in dorsal horn neurons with the result that abnormal pain syndromes develop. Recent literature reported that spinal cord injury produces glial activation in the dorsal horn; however, the majority of glial activation studies after SCI have focused on transient and/or acute time points, from a few hours to one month, and peri-lesion sites, a few millimeters rostral and caudal to the lesion site. In addition, thoracic spinal cord injury produces activation of astrocytes and microglia that contributes to dorsal horn neuronal hyperexcitability and central neuropathic pain in above-level, at-level and below-level segments remote from the lesion in the spinal cord. The cellular and molecular events of glial activation are not a simple event, rather it is the consequence of a combination of several neurochemical and neurophysiological changes following SCI. The ionic imbalances, neuroinflammation and alterations of cell cycle proteins after SCI are predominant components for neuroanatomical and neurochemical changes that result in glial activation. More importantly, SCI induced release of glutamate, proinfloammatory cytokines, ATP, reactive oxygen species (ROS) and neurotrophic factors trigger activation of postsynaptic neurons and glial cells via their own receptors and channels that, in turn, contribute to neuronal-neuronal and neuronal-glial interaction as well as microglia-astrocytic interactions. However, a systematic review of temporal and spatial glial activation following SCI has not been done. In this review, we describe time and regional dependence of glial activation and describe activation mechanisms in various SCI models in rats. These data are placed in the broader context of glial activation mechanisms and chronic pain states. Our work in the context of work by others in SCI models demonstrate that dysfunctional glia, a condition called “gliopathy”, are key contributors in the underlying cellular mechanisms contributing to neuropathic pain.
The effects of guava leaves extracted using solvents of water, ethanol, methanol, and different concentrations of hydroethanolic solvents on phenolic compounds and flavonoids, and antioxidant properties have been investigated. The antioxidant capability was assessed based on 2,2-diphenyl-1-picrylhydrazyl radical and 2,2′-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) radical-scavenging abilities, reducing power, and nitric oxide-and nitrate-scavenging activities. The results demonstrated that the antioxidant ability of guava leaf extracts has a strong relationship with phenolic compound content rather than flavonoid content. Phenolic compound content of water extracted guava leaves was higher compared to pure ethanol and methanol extracts. However, phenolic compound content extracted using hydroethanolic solvent was higher than water, whereas 50% hydroethanolic was observed to be the most effective solvent showing high antioxidant ability.
Ventricular CSF shunting surgery has changed the overall outcome figures for hydrocephalic patients over the past three decades. The factors that have improved the outcome are evolution of the shunt systems, improvement of the surgical environment and use of potent antibiotics, technological advances in brain imaging, and refinements in the assessment of cognitive and functional outcomes and of actuarial statistical techniques. But the recent large studies revealed that nearly half of all shunt placements were for revision, and there is a low but real percentage of cases in which death and neurological impairment are related to shunt surgery. The most frequent complication was shunt obstruction, followed by infection, disconnection, hematoma and slit ventricle syndrome. This clearly means that the shunt systems and the techniques in current use involve many problems that have yet to be solved. To solve these problems, new shunt systems should be developed and continuous efforts at reducing shunt infection should be made. The overall complication rate in the authors' series was 31.7%, but we have been able to reduce the complication rate from 37% to 25% by exercising special care focused on the surgical environment and techniques. Careful, long-term follow-up using various parameters and proper statistical analysis is another important factor in improving surgical outcome. Multicenter and international studies will be easier with the development of a network, and it will give us a strong background to treat hydrocephalus.
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