883 resultados para systemic sclerosis
Resumo:
The aims of the present study were to compare the perceptual assessments of deviant speech signs (dysarthria) exhibited by Australian and Swedish speakers with multiple sclerosis (MS) and to explore whether judgements of dysarthria differed depending on whether the speakers and the judges spoke the same or different languages. Ten Australian and 10 Swedish individuals with MS (matched as closely as possible for age, gender, progression type and severity of dysarthria) were assessed by 2 Australian and 2 Swedish clinically experienced judges using a protocol including 33 speech parameters. Results show that the following perceptual dimensions were identified by both pairs of judges in both groups of speakers to a just noticeable or moderate degree: imprecise consonants, inappropriate pitch level, reduced general rate, and glottal fry. The reliability (Spearman rank-order correlation) of the consensus ratings from the Australian and the Swedish judges was high, with a mean rho of 85.7 for the Australian speakers and mean rho of 84.3 for the Swedish speakers. The most difficult perceptual parameters to assess (i.e. to agree on) included harshness, level of pitch and loudness, precision of consonants and general stress pattern. The study indicated that perceptual assessments of speech characteristics in individuals with MS are informative and can be achieved with high inter-judge reliability irrespective of the judge's knowledge of the speaker's language. Copyright (C) 2003 S. Karger AG, Basel.
Resumo:
Pathogen challenge can trigger an integrated set of signal transduction pathways, which ultimately leads to a state of high alert, otherwise known as systemic or induced resistance in tissue remote to the initial infection. Although large-scale gene expression during systemic acquired resistance, which is induced by salicylic acid or necrotizing pathogens has been previously reported using a bacterial pathogen, the nature of systemic defense responses triggered by an incompatible necrotrophic fungal pathogen is not known. We examined transcriptional changes that occur during systemic defense responses in Arabidopsis plants inoculated with the incompatible fungal pathogen Alternaria brassicicola. Substantial changes (2.00-fold and statistically significant) were demonstrated in distal tissue of inoculated plants for 35 genes (25 up-regulated and 10 down-regulated), and expression of a selected subset of systemically expressed genes was confirmed using real-time quantitative polymerase chain reaction. Genes with altered expression in distal tissue included those with putative functions in cellular housekeeping, indicating that plants modify these vital processes to facilitate a coordinated response to pathogen attack. Transcriptional up-regulation of genes encoding enzymes functioning in the beta-oxidation pathway of fatty acids was particularly interesting. Transcriptional up-regulation was also observed for genes involved in cell wall synthesis and modification and genes putatively involved in signal transduction. The results of this study, therefore, confirm the notion that distal tissue of a pathogen-challenged plant has a heightened preparedness for subsequent pathogen attacks.
Resumo:
For most complex emergent technologies, product-market success depends on efficient linkages between changing lead innovators within the R&D process. In this paper, our unit of analysis is a complex high technology product and the system of alliance linkages formed to progress a product through R&D milestones. We present a model and evidence for advancing our understanding of how achieving early-to-market returns depends on systemic absorptive capacity. This systemic absorptive capacity is the cumulative efficiency in the use of absorptive capacity to link changing lead innovators across successive milestones in R&D product development. We advance propositions of how systemic absorptive capacity can explain performance differences between rival product development systems competing for early-to-market returns with similar products through accelerating speed to market, cost and quality advantages. These explanations are contrasted with the conclusions of previous studies that have focused on absorptive capacity of single firms or single alliances in RD.
Resumo:
Background: Periodontitis has been associated with a number of systemic diseases such as atherosclerosis, coronary heart diseases, and respiratory diseases. This study aimed to determine whether there is a significant difference in the prevalence of systemic diseases (a) in patients referred for periodontal care compared to the general practice population, (b) in patients attending a public hospital and private practices, (c) in patients attending public and private periodontal practices, and (d) among patients with periodontitis of varying severity. Methods: Charts of 1000 adult patients were selected from four clinics (University of Queensland (UQ) School of Dentistry Admissions Clinic, UQ School of Dentistry Periodontics Clinic, Private Periodontal Practice, and Private General Dental Practice). The prevalence of medical conditions was evaluated using validated self-reported health questionnaires. The periodontal condition was assessed from the most recent relevant radiographs in the files. Results: Periodontal patients had a higher prevalence of systemic diseases compared to the general practice population. Public patients had a greater prevalence of systemic diseases compared to patients in private practice for both general practice and periodontal patients. In patients with advanced periodontitis, bronchitis, hepatitis and rheumatoid arthritis were most prevalent. Patients with periodontitis also took more medications and were more likely to suffer from multiple conditions compared to the general dental population. Conclusions: Patients attending public dental facilities have an increased prevalence of systemic disease compared to those attending private practices. Furthermore periodontal patients have a greater prevalence of disease compared to general practice patients. Patients with moderate or advanced periodontitis show an increase in the prevalence of some systemic diseases previously reported to be risk factors for periodontal disease.
Resumo:
Background. The development of therapeutic interventions to prevent progressive valve damage is more likely to limit the progression of structural damage to the aortic valve with normal function (aortic sclerosis [ASC]) than clinically apparent aortic stenosis. Currently, the ability to appreciate the progression of ASC is compromised by the subjective and qualitative evaluation of sclerosis severity. Methods: We sought to reveal whether the intensity of ultrasonic backscatter could be used to quantify sclerosis severity in 26 patients with ASC and 23 healthy young adults. images of the aortic valve were obtained in the parasternal long-axis view and saved in raw data format. Six square-shaped 11 X 11 pixel regions of interest were placed on the anterior and posterior leaflets, and calibrated backscatter values were obtained by subtracting the regions of interest in the blood pool from the averaged backscatter values obtained from the leaflets. Results. Mean ultrasonic backscatter values for sclerotic valves exceeded the results in normal valve tissue (16.3 +/- 4.4 dB vs 9.8 +/- 3.3 dB, P < .0001). Backscatter values were greater (22.0 +/- 3.5 dB) in a group of 6 patients with aortic stenosis. Within the sclerosis group, the magnitude of backscatter was directly correlated (P < .05) with a subjective sclerosis score, and with transvalvular pressure gradient. mean reproducibility was 2.4 +/- 1.8 dB (SD) between observers, and 2.3 +/- 1.7 dB (SD) between examinations. Conclusion: Measurement of backscatter from the valve leaflets of patients with ASC may be a feasible means of following the progression and treatment response of aortic sclerosis.
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Using Fos immunolabelling as a marker of neuronal activation, we investigated the role of the parabrachial nucleus in generating central neuronal responses to the systemic administration of the proinflarnmatory cytokine interleukin-1beta (1 mug/kg, i.a.). Relative to intact animals, parabrachial nucleus lesions significantly reduced the number of Fos-positive cells observed in the central amygdala (CeA), the bed nucleus of the stria terminalis (BNST), and the ventrolateral medulla (VLM) after systemic interleukin-1beta. In a subsequent experiment in which animals received parabrachial-directed deposits of a retrograde tracer, it was found that many neurons located in the nucleus tractus solitarius (NTS) and the VLM neurons were both retrogradely labelled and Fos-positive after interleukin-1beta administration. These results suggest that the parabrachial nucleus plays a critical role in interleukin-1beta-induced Fos expression in CeA, BNST and VLM neurons and that neurons of the NTS and VLM may serve to trigger or at least influence changes in parabrachial nucleus activity that follows systemic interleukin-1beta administration. (C) 2004 Elsevier B.V. All rights reserved.
Resumo:
The intestinal absorption of the essential trace element iron and its mobilization from storage sites in the body are controlled by systemic signals that reflect tissue iron requirements. Recent advances have indicated that the liver-derived peptide hepcidin plays a central role in this process by repressing iron release from intestinal enterocytes, macrophages and other body cells. When iron requirements are increased, hepcidin levels decline and more iron enters the plasma. It has been proposed that the level of circulating diferric transferrin, which reflects tissue iron levels, acts as a signal to alter hepcidin expression. In the liver, the proteins HFE, transferrin receptor 2 and hemojuvelin may be involved in mediating this signal as disruption of each of these molecules decreases hepcidin expression. Patients carrying mutations in these molecules or in hepcidin itself develop systemic iron loading (or hemochromatosis) due to their inability to down regulate iron absorption. Hepcidin is also responsible for the decreased plasma iron or hypoferremia that accompanies inflammation and various chronic diseases as its expression is stimulated by pro-inflammatory cytokines such as interleukin 6. The mechanisms underlying the regulation of hepcidin expression and how it acts on cells to control iron release are key areas of ongoing research.
Resumo:
In opiate addicts or patients receiving morphine treatment, it has been reported that the immune system is often compromised. The mechanisms responsible for the adverse effects of opioids on responses to infection are not clear but it is possible that central and/or peripheral opioid receptors may be important. We have utilised an experimental immune challenge model in rats, the systemic administration of the human pro-inflammatory cytokine interleukin-1 beta (IL-1 beta) to study the effects of selectively blocking peripheral opioid receptors only (using naloxone methiodide) or after blocking both central and peripheral opioid receptors (using naloxone). Pre-treatment with naloxone methiodide decreased (15%) IL-1 beta-induced Fos-immunoreactivity (Fos-IR) in medial parvocellular paraventricular nucleus (mPVN) corticotropin-releasing hormone (CRH) neurons but increased responses in the ventrolateral medulla (VLM) C1 (65%) and nucleus tractus solitarius (NTS) A2 (110%) catecholamine cell groups and area postrema (136%). However no effect of blocking peripheral opioid receptors was detected in the central nucleus of the amygdala (CeA) or dorsal bed nucleus of the stria terminalis (BNST). We next determined the effect of blocking both central and peripheral opioid receptors with naloxone and, when compared to the naloxone methiodide pre-treated group, a further 60% decrease in Fos-IR mPVN CRH neurons induced by IL-1 beta was detected, which was attributed to block of central opioid receptors. Similar comparisons also detected decreases in Fos-IR neurons induced by IL-1 beta in the VLM A1, VLM C1 and NTS A2 catecholamine cell groups, area postrema, and parabrachial nucleus. In contrast, pre-treatment with naloxone increased Fos-IR neurons in CeA (98%) and dorsal BNST (72%). These results provide novel evidence that endogenous opioids can influence central neural responses to systemic IL-1 beta and also suggest that the differential patterns of activation may arise because of actions at central and/or peripheral opioid receptors that might be important in regulating behavioural, hypothalamic-pituitary-adrenal axis and sympathetic nervous system responses during an immune challenge. (c) 2005 Elsevier Ltd. All rights reserved.
Resumo:
Purpose. This study examined benefit finding in MS carers including the dimensionality of benefit finding, relations between carer and care recipient benefit finding, and the effects of carer benefit finding on carer positive and negative adjustment domains. Method. A total of 267 carers and their care recipients completed questionnaires at Time 1 and 3 months later, Time 2 (n=155). Illness data were collected at Time 1, and number of problems, stress appraisal, benefit finding, negative (global distress, negative affect) and positive (life satisfaction, positive affect, dyadic adjustment) adjustment domains were measured at Time 2. Results. Qualitative data revealed seven benefit finding themes, two of which were adequately represented by the Benefit Finding Scale (BFS) [1] (Mohr et al. Health Psychology 1999; 18: 376). Factor analyses indicated two factors (Personal Growth, Family Relations Growth) which were psychometrically sound and showed differential relations with illness and adjustment domains. Although care recipients reported higher levels of benefit finding than carers, their benefit finding reports regarding personal growth were correlated. The carer BFS factors were positively related to carer and care recipient dyadic adjustment. Care recipient benefit finding was unrelated to carer adjustment domains. After controlling for the effects of demographics, care recipient characteristics, problems and appraisal, carer benefit finding was related to carer positive adjustment domains and unrelated to carer negative adjustment domains. Conclusion. Findings support the role of benefit finding in sustaining positive psychological states and the communal search for meaning within carer-care recipient dyads.
Resumo:
This study examined relations between stress and coping predictors and negative and positive outcomes in MS caregiving. A total of 222 carers and their care-recipients completed questionnaires at Time 1 and three months later, Time 2 ( n = 155). Predictors included care-recipient characteristics ( age, time since diagnosis, course and life satisfaction), and Times 1 and 2 carer problems, stress appraisal and coping. Dependent variables were Time 2 negative ( anxiety, depression) and positive outcomes ( life satisfaction, positive affect, benefits). Regressions indicated that, overall, the hypothesised direct effects of stress appraisal and coping strategies on positive and negative outcomes were supported. The hypothesised stress-buffering effects of positive reframing coping were also supported. All but one of the coping strategies were related to both positive and negative outcomes; specifically, practical assistance coping emerged as a unique predictor of distress. Of the model predictors, care-recipient life satisfaction emerged as the strongest and most consistent predictor of both positive and negative outcomes except benefit finding. Findings support the role of care-recipient characteristics and the carer's appraisal and coping processes in shaping both positive and negative outcomes. The guiding framework and findings have the potential to inform interventions designed to promote well-being in carers.
Resumo:
This study examined the direct and stress-buffering effects of benefit finding on positive and negative outcomes. A total of 502 people with multiple sclerosis completed a questionnaire at Time 1 and, 3 months later, at Time 2 (n = 404). Measures of illness were collected at Time 1, and number of problems, stress appraisal, benefit finding, subjective health, and negative (global distress, negative affect) and positive (life satisfaction, positive affect, dyadic adjustment) outcomes were measured at Time 2. Factor analyses showed the Benefit Finding scale to have 2 dimensions: Personal Growth and Family Relations Growth. Hierarchical regressions showed that after controlling for the effects of demographics, illness, problems, and appraisal, benefit finding showed strong direct effects on the positive outcomes. Benefit finding did not have a direct effect on distress, or subjective health but had a weak association with negative affect. Family Relations Growth had a stress-buffering effect on distress.
Resumo:
The mechanisms responsible for the immunosuppression associated with sepsis or some chronic blood infections remain poorly understood. Here we show that infection with a malaria parasite (Plasmodium berghei) or simple systemic exposure to bacterial or viral Toll-like receptor ligands inhibited cross-priming. Reduced cross-priming was a consequence of downregulation of cross-presentation by activated dendritic cells due to systemic activation that did not otherwise globally inhibit T cell proliferation. Although activated dendritic cells retained their capacity to present viral antigens via the endogenous major histocompatibility complex class I processing pathway, antiviral responses were greatly impaired in mice exposed to Toll-like receptor ligands. This is consistent with a key function for cross-presentation in antiviral immunity and helps explain the immunosuppressive effects of systemic infection. Moreover, inhibition of cross-presentation was overcome by injection of dendritic cells bearing antigen, which provides a new strategy for generating immunity during immunosuppressive blood infections.