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Eventual Death (eventual + death)
Selected AbstractsQuantitation of non-motor symptoms in Parkinson's diseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 2008K. Ray Chaudhuri Background:, Disabling non-motor symptoms (NMS) associated with Parkinson's disease (PD), such as dementia and loss of balance, do not respond well to levodopa therapy and can lead to eventual death in patients with the disease. In 2006, a multidisciplinary group of experts and patient representatives developed an NMS screening questionnaire (NMSQuest) and a unified Non-Motor Symptoms Scale (NMSS) to address the need for simple identification and comprehensive assessment of NMS in patients with PD. Methods and Results:, An international pilot study of 96 healthy controls and 123 patients with various stages of treated and untreated PD was conducted to demonstrate that the NMSQuest is a feasible, valid, and accepted tool. Conclusion:, The majority of patients and caregivers felt that the questionnaire was clear and relevant to their daily lives. Data from 242 PD patients with no dementia were analysed in a pilot study on the clinimetric validation of NMSS. Similar to the NMSQuest study, the NMSS study revealed a significant correlation between progression of PD and increasing NMS burden. These studies suggest that the NMSQuest accurately detects the NMS, and that the NMSS closely correlates with quality of life for PD patients. [source] Complement and its implications in cardiac ischemia/reperfusion: strategies to inhibit complementFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 5 2001Tiphaine Monsinjon Although reperfusion of the ischemic myocardium is an absolute necessity to salvage tissue from eventual death, it is also associated with pathologic changes that represent either an acceleration of processes initiated during ischemia or new pathophysiological changes that were initiated after reperfusion. This so-called ,reperfusion injury' is accompanied by a marked inflammatory reaction, which contributes to tissue injury. In addition to the well known role of oxygen free radicals and white blood cells, activation of the complement system probably represents one of the major contributors of the inflammatory reaction upon reperfusion. The complement may be activated through three different pathways: the classical, the alternative, and the lectin pathway. During reperfusion, complement may be activated by exposure to intracellular components such as mitochondrial membranes or intermediate filaments. Two elements of the activated complement contribute directly or indirectly to damages: anaphylatoxins (C3a and C5a) and the membrane attack complex (MAC). C5a, the most potent chemotactic anaphylatoxin, may attract neutrophils to the site of inflammation, leading to superoxide production, while MAC is deposited over endothelial cells and smooth vessel cells, leading to cell injury. Experimental evidence suggests that tissue salvage may be achieved by inhibition of the complement pathway. As the complement is composed of a cascade of proteins, it provides numerous sites for pharmacological interventions during acute myocardial infarction. Although various strategies aimed at modulating the complement system have been tested, the ideal approach probably consists of maintaining the activity of C3 (a central protein of the complement cascade) and inhibiting the later events implicated in ischemia/reperfusion and also in targeting inhibition in a tissue-specific manner. [source] Transgenic Drosophila reveals a functional in vivo receptor for the Bacillus thuringiensis toxin Cry1Ac1INSECT MOLECULAR BIOLOGY, Issue 6 2002Michael Gill Abstract The bacterium Bacillus thuringiensis synthesizes toxins (,-endotoxins) that are highly specific for insects. Once ingested, the activated form of the toxin binds to a specific receptor(s) located on the midgut epithelial cells, inserts into the membrane causing the formation of leakage pores and eventual death of the susceptible insect larvae. Manduca sexta larvae are highly susceptible to Cry1Ac1, a toxin that is believed to bind M. sexta Aminopeptidase N, a glycoprotein located on the apical membrane. However, the binding data obtained to date only support the interaction of Cry1Ac1 with APN in vitro. To explore the in vivo role of APN, we have utilized the GAL4 enhancer trap technique to drive the expression of M. sexta APN in both midgut and mesodermal tissues of Cry1Ac1 insensitive Drosophila larvae. Transgenic Drosophila fed the toxin were now killed, demonstrating that APN can function as a receptor for Cry1Ac1 in vivo. [source] Gamma,delta T cell subsets are differentially associated with granuloma development and organization in a bovine model of mycobacterial diseaseINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 6 2009Brandon L. Plattner Summary The characteristic lesion in bovine tuberculosis is well-organized respiratory granulomas. This is typically associated with a strong T-helper 1 biased cell-mediated immune response and eventual containment of the infection. In bovine paratuberculosis, the classic lesion is unorganized granulomatous intestinal inflammation. Clinical paratuberculosis is associated with a T-helper 2 biased humoral immune response and eventual death because of inability of the host to contain the infection. Recent reports have suggested that gamma,delta (,,) T cells play a significant role in granuloma development and/or maintenance during initial stages of infection and may influence the subsequent adaptive immune response. The objective of this study was to use an in vivo bovine model to evaluate ,, T cells during the early host immune response to mycobacterial infection. We used immunofluorescent staining, hyperspectral microscopy, and computerized assisted morphometry to evaluate staining and distribution of ,, T cells during development of organized and unorganized granulomas. Our data suggest that bovine ,, T cell subsets are differentially recruited to early infection sites, and may be instrumental during the initial antimycobacterial host immune response as well as for granuloma organization. [source] Expression of mutant SOD1G93A in astrocytes induces functional deficits in motoneuron mitochondriaJOURNAL OF NEUROCHEMISTRY, Issue 5 2008Lynsey G. Bilsland Abstract Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by motoneuron degeneration resulting in paralysis and eventual death. ALS is regarded as a motoneuron-specific disorder but increasing evidence indicates non-neuronal cells play a significant role in disease pathogenesis. Although the precise aetiology of ALS remains unclear, mutations in the superoxide dismutase (SOD1) gene are known to account for approximately 20% of familial ALS. We examined the influence of SOD1G93A expression in astrocytes on mitochondrial homeostasis in motoneurons in a primary astrocyte : motoneuron co-culture model. SOD1G93A expression in astrocytes induced changes in mitochondrial function of both SOD1G93A and wild-type motoneurons. In the presence of SOD1G93A astrocytes, mitochondrial redox state of both wild-type and SOD1G93A motoneurons was more reduced and mitochondrial membrane potential decreased. While intra-mitochondrial calcium levels [Ca2+]m were elevated in SOD1G93A motoneurons, changes in mitochondrial function did not correlate with [Ca2+]m. Thus, expression of SOD1G93A in astrocytes directly alters mitochondrial function even in embryonic motoneurons, irrespective of genotype. These early deficits in mitochondrial function induced by surrounding astrocytes may increase the vulnerability of motoneurons to other neurotoxic mechanisms involved in ALS pathogenesis. [source] Knockdown resistance to DDT and pyrethroids: from target-site mutations to molecular modellingPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 11 2008TG Emyr Davies Abstract Naturally derived insecticides such as pyrethrum and man-made insecticides such as DDT and the synthetic pyrethroids act on the voltage-gated sodium channel proteins found in insect nerve-cell membranes. The correct functioning of these channels is essential for the normal transmission of nerve impulses, and this process is disrupted by binding of the insecticides, leading to paralysis and eventual death. Some insect pest populations have evolved modifications of the sodium channel protein that inhibit the binding of the insecticide and result in the insect developing resistance. This perspective outlines the current understanding of the molecular processes underlying target-site resistance to these insecticides (termed kdr and super-kdr), and how this knowledge may in future contribute to the design of novel insecticidal compounds. Copyright © 2008 Society of Chemical Industry [source] A green fluorescent protein-based screening method for identification of resistance in anthurium to systemic infection by Xanthomonas axonopodis pv. dieffenbachiaePLANT PATHOLOGY, Issue 5 2007W. Elibox Resistance of cultivars of Anthurium andraeanum to systemic infection by Xanthomonas axonopodis pv. dieffenbachiae, the causal organism of bacterial blight disease of anthurium, was investigated using a bioengineered bacterial strain containing p519ngfp plasmid. Successful infection establishment in anthurium was found to be cultivar and inoculum density dependent, but independent of plant age. Injection of cut petioles (stage-2 leaf) with 100 µL inoculum (109 CFU mL,1) resulted in 100% infection establishment in susceptible cultivars on a repeatable basis, and differentiated between various levels of observed field resistance. Time to death (weeks) and proportion of dead plants best differentiated between levels of resistance and cultivars were placed in four groups based on these criteria. The susceptible group (32 cultivars) rapidly declined within 6,12 weeks of inoculation (WAI) and resulted in 100% plant death; the moderately resistant group (10 cultivars) declined within 12 WAI, but resulted in less than 100% plant death; the resistant category had less than 100% plant death with a slow decline taking over 20 weeks; and the highly resistant category (15 cultivars) showed 0% infection. The correlation coefficient between green fluorescent protein (GFP)-fluorescence and eventual death of plants was 0·90, indicating that the final death of individual plants can be reasonably well predicted based on GFP-fluorescence data at 5 WAI. Hence GFP data at 5 WAI can be used for early detection of latently infected plants and may assist screening for resistance in segregating populations of anthurium. [source] | |||||||||||||