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Secondary Damage (secondary + damage)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Cytoplasmic Extracts from Adipose Tissue Stromal Cells Alleviates Secondary Damage by Modulating Apoptosis and Promotes Functional Recovery Following Spinal Cord Injury

BRAIN PATHOLOGY, Issue 3 2007
Soo Kyung Kang
Spinal cord injury (SCI) typically results from sustained trauma to the spinal cord, resulting in loss of neurologic function at the level of the injury. However, activation of various physiological mechanisms secondary to the initial trauma including edema, inflammation, excito-toxicity, excessive cytokine release and apoptosis may exacerbate the injury and/or retard natural repair mechanisms. Herein, we demonstrate that cytoplasmic extracts prepared from adipose tissue stromal cells (ATSCs) inhibits H2O2 -mediated apoptosis of cultured spinal cord-derived neural progenitor cells (NPCs) resulting in increased cell survival. The ATSC extracts mediated this effect by decreasing caspase-3 and c-Jun,NH2-terminal kinase (SAPK/JNK) activity, inhibiting cytochrome c release from mitochondria and reducing Bax expression levels in cells. Direct injection of ATSC extracts mixed with Matrigel into the spinal cord immediately after SCI also resulted in reduced apoptotic cell death, astrogliosis and hypo-myelination but did not reduce the extent of microglia infiltration. Moreover, animals injected with the ATSC extract showed significant functional improvement of hind limbs as measured by the BBB (Basso, Beattie and Bresnahan) scale. Collectively, these studies show a prominent therapeutic effect of ATSC cytoplasmic extracts on SCI principally caused by an inhibition of apoptosis-mediated cell death, which spares white matter, oligodendrocytes and neurons at the site of injury. The ability of ATSC extracts to prevent secondary pathological events and improve neurologic function after SCI suggests that extracts prepared from autologous cells harvested from SCI patients may have clinical utility. [source]

Astrocytic factors protect neuronal integrity and reduce microglial activation in an in vitro model of N -methyl- d -aspartate-induced excitotoxic injury in organotypic hippocampal slice cultures

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2001
Nils P. Hailer
Abstract Acute CNS lesions lead to neuronal injury and a parallel glial activation that is accompanied by the release of neurotoxic substances. The extent of the original neuronal damage can therefore be potentiated in a process called secondary damage. As astrocytes are known to secrete immunomodulatory and neuroprotective substances, we investigated whether astrocytic factors can attenuate the amount of neuronal injury as well as the degree of microglial activation in a model of excitotoxic neurodegeneration. Treatment of organotypic hippocampal slice cultures with N-methyl- d -aspartate (NMDA) resulted in a reproducible loss of viable granule cells, partial destruction of the regular hippocampal cytoarchitecture and a concomitant accumulation of amoeboid microglial cells at sites of neuronal damage. Astrocyte-conditioned media reduced the amount of NMDA-induced neuronal injury by 45.3%, diminished the degree of microglial activation and resulted in an improved preservation of the hippocampal cytoarchitecture. Transforming growth factor (TGF)-, failed to act as a neuroprotectant and even enhanced the amount of neuronal injury by 52.5%. Direct effects of astrocytic factors on isolated microglial cells consisted of increased microglial ramification and down-regulated expression of intercellular adhesion molecule-1, whereas incubation with TGF-, had no such effects. In summary, our findings show that hitherto unidentified astrocyte-derived factors that are probably not identical with TGF-, can substantially enhance neuronal survival, either by eliciting direct neuroprotective effects or by modulating the microglial response to neuronal injury. [source]

Age-associated changes in viscoelastic properties of the bovine temporomandibular joint disc

EUROPEAN JOURNAL OF ORAL SCIENCES, Issue 1 2006
Eiji Tanaka
To test the hypothesis that compressive properties of the temporomandibular joint (TMJ) disc change with age, we investigated its viscoelastic properties and stress-relaxation behavior under compression. Compressive stress-relaxation tests were performed in different regions of bovine discs of various ages. For each disc, specimens were derived from three different regions (anterior, central, and posterior). For four strain levels (5, 10, 15, and 20%), a stress-relaxation test was conducted over a 5-min period. Values of the instantaneous modulus, E0, appeared to be larger in the anterior than in the posterior region of the disc, irrespective of age. The E0 value increased with age, especially in the central region. Values of the relaxed modulus, ER, also increased significantly with age. There were no regional differences in values of the relaxed modulus. Under stress-relaxation, the relaxation time became longer with age, especially in the posterior region. The results suggest that the compressive properties, instantaneous and relaxed moduli, increase with age, while the relaxation time becomes longer. This implies that the TMJ disc becomes harder with age. Furthermore, the compressive properties of the TMJ disc are region-specific. As a result of the harder disc, it is likely that the TMJ becomes more vulnerable to secondary damage, such as fracture and tissue degradation. [source]

Thrombin attenuation is neuroprotective in the injured rat optic nerve

JOURNAL OF NEUROCHEMISTRY, Issue 3 2001
Igor Friedmann
The functional loss that often follows injury of the mammalian CNS has been attributed not only to the immediate neural loss, but also to secondary neuronal degeneration caused by toxic biochemical mediators in the environment of the injured nerve. We report here that a high thrombin content, produced as a result of injury-induced activation of prothrombin, appears to be an important mediator of secondary damage. Measurement of post-traumatic neuronal survival in vivo revealed that post-traumatic local application of the thrombin inhibitor N -,-(2-naphthylsulphonylglycyl)-4-(d,l)-amidinophenylalanine piperidide acetate in the rat optic nerve subjected to mild partial crush injury left twice as many retinal ganglion cells with functioning axons as in controls. Thus, by readjusting thrombin activity, thereby possibly obtaining a moderate post-traumatic increase and thus gaining the benefit of thrombin without its toxic effects, it may be possible to create an environment that is more favourable towards post-traumatic survival. [source]