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Destructive Processes (destructive + process)
Selected AbstractsForests, marketization, livelihoods and the poor in the Lao PDRLAND DEGRADATION AND DEVELOPMENT, Issue 2 2006J. D. Rigg Abstract The Lao PDR is making the transition from subsistence to cash, and command to market. Rural communities are being drawn ever more tightly into the embrace of the market economy and of the central state. The construction of roads, schools and health centres, the provision of credit and new crops and technologies, and the arrival of traders and the panoply of the consumer economy are all, in their different ways, remoulding rural economy and society. This paper looks at one aspect of this multi-stranded process of agrarian transformation: the role and place of forests and, in particular, non-timber forest products, in rural people's lives and livelihoods. The paper highlights the contradictory and uneven livelihood-eroding/enhancing effects of these transformations. In many upland areas of Laos livelihoods are being squeezed from ,below' by environmental degradation and from ,above' by the operation of government policies and, more generally, by evolving market relations. While market pessimists see market integration as a largely destructive process, the paper highlights the opportunities that market integration can provide through diversification and livelihood reorientation. The challenge is that these opportunities are unequally available and are likely to promote social differentiation. Some households find themselves in a position to embrace new opportunities while others are forced to continue to rely on a declining and degrading forest resource. Copyright © 2006 John Wiley & Sons, Ltd. [source] Comparative analysis of neonicotinoid binding to insect membranes: II.PEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 10 2004An unusual high affinity site for [3H]thiamethoxam in Myzus persicae, Aphis craccivora Abstract Neonicotinoids represent a class of insect-selective ligands of nicotinic acetylcholine receptors. Imidacloprid, the first commercially used neonicotinoid insecticide, has been studied on neuronal preparations from many insects to date. Here we report first intrinsic binding data of thiamethoxam, using membranes from Myzus persicae Sulzer and Aphis craccivora Koch. In both aphids, specific binding of [3H]thiamethoxam was sensitive to temperature, while the absolute level of non-specific binding was not affected. In M persicae, binding capacity (Bmax) for [3H]thiamethoxam was ca 450 fmol mg,1 of protein at 22 °C and ca 700 fmol mg,1 of protein at 2 °C. The negative effect of increased temperature was reversible and hence not due to some destructive process. The affinity for [3H]thiamethoxam was less affected by temperature: Kd was ca 11 nM at 2 °C and ca 15 nM at 22 °C. The membranes also lost binding sites for [3H]thiamethoxam during prolonged storage at room temperature, and upon freezing and thawing. In A craccivora, [3H]thiamethoxam was bound with a capacity of ca 1000 fmol mg,1 protein and an affinity of ca 90 nM, as measured at 2 °C. Overall, the in vitro temperature sensitivity of [3H]thiamethoxam binding was in obvious contrast to the behaviour of [3H]imidacloprid studied in parallel. Moreover, the binding of [3H]thiamethoxam was inhibited by imidacloprid in a non-competitive mode, as shown with M persicae. In our view, these differences demonstrate that thiamethoxam and imidacloprid, which represent different structural sub-classes of neonicotinoids, do not share the same binding site or mode. This holds also for other neonicotinoids, as we report in a companion article. Copyright © 2004 Society of Chemical Industry [source] Trophic factors attenuate nitric oxide mediated neuronal and axonal injury in vitro: roles and interactions of mitogen-activated protein kinase signalling pathwaysJOURNAL OF NEUROCHEMISTRY, Issue 6 2005Alastair Wilkins Abstract Inflammation in the central nervous system occurs in diseases such as multiple sclerosis and leads to axon dysfunction and destruction. Both in vitro and in vivo observations have suggested an important role for nitric oxide (NO) in mediating inflammatory axonopathy. The purposes of this study were to model inflammatory axonopathy in vitro and identify modulators of the process. Rat cortical neurones were cultured and exposed to an NO-donor plus potential protective factors. Cultures were then assessed for neuronal survival, axon survival and markers of intracellular signalling pathways. The NO-donor produced dose-dependent neuronal loss and a large degree of axon destruction. Oligodendrocyte conditioned medium (OCM) and insulin-like growth factor type-1 (IGF-1), but not glial cell line-derived neurotrophic factor (GDNF), improved survival of neurones exposed to NO donors. In addition p38 MAP kinase was activated by NO exposure and inhibition of p38 signalling led to neuronal and axonal survival effects. OCM and IGF-1 (but not GDNF) reduced p38 activation in NO-exposed cortical neurones. OCM, IGF-1 and GDNF improved axon survival in cultures exposed to NO, a process dependent on mitogen-activated protein kinase/extracellular signal-related kinase signalling. This study emphasizes that different mechanisms may underlie neuronal/axonal destructive processes, and suggests that trophic factors may modulate NO-mediated neurone/axon destruction via specific pathways. [source] Citicoline: neuroprotective mechanisms in cerebral ischemiaJOURNAL OF NEUROCHEMISTRY, Issue 1 2002Rao Muralikrishna Adibhatla Abstract Cytidine-5,-diphosphocholine (citicoline or CDP-choline), an intermediate in the biosynthesis of phosphatidylcholine (PtdCho), has shown beneficial effects in a number of CNS injury models and pathological conditions of the brain. Citicoline improved the outcome in several phase-III clinical trials of stroke, but provided inconclusive results in recent clinical trials. The therapeutic action of citicoline is thought to be caused by stimulation of PtdCho synthesis in the injured brain, although the experimental evidence for this is limited. This review attempts to shed some light on the properties of,citicoline that are responsible for its effectiveness. Our studies in transient cerebral ischemia suggest that citicoline might enhance reconstruction (synthesis) of PtdCho and sphingomyelin, but could act by inhibiting the destructive processes (activation of phospholipases). Citicoline neuroprotection may,include: (i) preserving cardiolipin (an exclusive inner mitochondrial membrane component) and sphingomyelin; (ii),preserving the arachidonic acid content of PtdCho and phosphatidylethanolamine; (iii) partially restoring PtdCho levels; (iv) stimulating glutathione synthesis and glutathione reductase activity; (v) attenuating lipid peroxidation; and (vi),restoring Na+/K+ -ATPase activity. These observed effects,of citicoline could be explained by the attenuation of,phospholipase A2 activation. Based on these findings, a singular unifying,mechanism has been hypothesized. Citicoline also provides choline for synthesis of neurotransmitter acetylcholine, stimulation of tyrosine hydroxylase activity and dopamine release. [source] Prostaglandin E2 secretion from gingival fibroblasts treated with interleukin-1,: effects of lipid extracts from Porphyromonas gingivalis or calculusJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2001Frank C. Nichols Complex lipids of Porphyromonas gingivalis have been identified in lipid extracts from calculus-contaminated root surfaces and in diseased gingival tissues. However, little is known about the biological effects of these complex lipids on host cells. The purpose of this study was to evaluate the effects of P. gingivalis or calculus lipids on prostaglandin secretion from gingival fibroblasts. Lipids were extracted from paired subgingival plaque and teeth samples, and calculus-contaminated root surfaces before and after scaling and root planing, in order to determine the relevant levels of lipid extracts for the treatment of gingival fibroblasts in culture. Primary cultures of gingival fibroblasts were exposed to lipid extracts from either P. gingivalis or calculus/teeth for a period of 7 days. Control and lipid-treated cultures were exposed to human recombinant interleukin-1, for 48 h and prostaglandin secretion from interleukin-1,-treated fibroblasts was compared with control and lipid-treated fibroblasts without interleukin-1, treatment. These experiments demonstrated that P. gingivalis lipids or calculus-tooth lipids potentiate interleukin-1,-mediated prostaglandin secretory responses from gingival fibroblasts. Additionally, P. gingivalis or calculus-tooth lipid extracts were readily taken up by gingival fibroblasts as measured by bacterial fatty acid recovery in lipid extracts of cultured fibroblasts. These results indicate that bacterial lipid penetration into gingival tissues in combination with a chronic inflammatory response may substantially potentiate prostaglandin secretion from gingival fibroblasts, thereby promoting tissue destructive processes associated with adult periodontitis. [source] Benign cysts in the central nervous system: Neuropathological observations of the cyst wallsNEUROPATHOLOGY, Issue 1 2004Asao Hirano A diverse variety of benign cysts exist in the CNS. Advances in diagnostic radiology have facilitated diagnoses and surgical intervention in many patients with CNS cysts. However, a fundamental understanding of the pathological features of these lesions is clinically vital. From an etiological point of view, the cysts can be divided into two groups. The first includes lesions that arise from within the CNS and may be static structures such as cavities arising from infarcts and other destructive processes while other lesions such as arachnoid cysts, ependymal cysts, cystic hemangioblastoma, cystic cerebellar astrocytoma and infectious processes, are progressive. The second group of cysts arise from the intrusion of non-nervous system tissue into the neuroaxis and are usually midline. They are frequently expanding congenital lesions although some become symptomatic only in adults. Examples include teratomas, dermoid cysts, epidermoid cysts, craniopharyngiomas, Rathke's cleft cysts, and other epithelial cysts presumably derived from the upper respiratory or intestinal tract. Chick embryos exposed to lead have been used as a model of cyst formation. [source] Heterogeneous requirement of I,B kinase 2 for inflammatory cytokine and matrix metalloproteinase production in rheumatoid arthritis: Implications for therapyARTHRITIS & RHEUMATISM, Issue 7 2003Evangelos Andreakos Objective To investigate the potential role of I,B kinase 1 (IKK-1) and IKK-2 in the regulation of nuclear factor ,B (NF-,B) activation and the expression of tumor necrosis factor , (TNF,), as well as interleukin-1, (IL-1,), IL-6, IL-8, vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs), in rheumatoid arthritis (RA). Methods Recombinant adenoviruses expressing ,-galactosidase, dominant-negative IKK-1 and IKK-2, or I,B, were used to infect ex vivo RA synovial membrane cultures and synovial fibroblasts obtained from patients with RA undergoing joint replacement surgery, or human dermal fibroblasts, human umbilical vein endothelial cells (HUVECs), and monocyte-derived macrophages from healthy volunteers. Then, their effect on the spontaneous or stimulus-induced release of inflammatory cytokines, VEGF, and MMPs from RA synovial membrane cells was examined. Results IKK-2 was not required for lipopolysaccharide (LPS),induced NF-,B activation or TNF,, IL-6, or IL-8 production in macrophages, but was essential for this process in response to CD40 ligand, TNF,, and IL-1. In synovial fibroblasts, dermal fibroblasts, and HUVECs, IKK-2 was also required for LPS-induced NF-,B activation and IL-6 or IL-8 production. In RA synovial membrane cells, IKK-2 inhibition had no effect on spontaneous TNF, production but significantly reduced IL-1,, IL-6, IL-8, VEGF, and MMPs 1, 2, 3, and 13. Conclusion Our study demonstrates that IKK-2 is not essential for TNF, production in RA. However, because IKK-2 regulates the expression of other inflammatory cytokines (IL-1,, IL-6, and IL-8), VEGF, and MMPs 1, 2, 3, and 13, which are involved in the inflammatory, angiogenic, and destructive processes in the RA joint, it may still be a good therapeutic target. [source] | ||||||||||