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991.
TH Grayson JM Ellis S Chen RM Graham RD Brown CE Hill 《Canadian Metallurgical Quarterly》1998,293(3):435-444
This article reports results from a meta-analysis on adult age differences in the negative priming effect (21 studies on identity negative priming and 8 on location negative priming). Both younger and older adults were found to be susceptible to the negative priming effect in identity and location tasks. Effect sizes were homogeneous for both tasks, indicating that the data are adequately described without reference to moderator variables. State trace analysis on identity tasks, in which mean latencies in negative priming conditions were regressed onto mean latencies in baseline conditions, showed (a) that in both age groups the negative priming effect is proportional rather than additive and (b) that the negative priming effect is smaller in older adults as compared with younger adults. 相似文献
992.
JM Chabot 《Canadian Metallurgical Quarterly》1998,48(6):651-652
993.
S Roul-Bouriat C Léauté-Labrèze P Bobin JM Tamisier P Vernhes M Geniaux 《Canadian Metallurgical Quarterly》1998,125(12):888-890
BACKGROUND: We report a case of leprosy observed in a French woman who had lived in Africa 30 years earlier. The clinical presentation was misleading, suggesting connective tissue disease. CASE REPORT: A 69-year-old woman was hospitalized in April 1996 for inflammatory joint disease. The first manifestations had developed three years earlier and the patient had been on systemic corticosteroid therapy associated with anti-malarials since 1993. The clinical presentation progressively included neurological and skin manifestations. Histology examination gave the diagnosis of lepromatous leprosy. Three-drug anti-leprosy treatment in one oral dose was initiated. DISCUSSION: Chronic Mycobacterium leprae infection usually leads to overt leprosy with neurological and cutaneous involvement. Rheumatological forms are less common and found almost exclusively during leprous reactions. The association of inflammatory join pain with neurological and skin manifestations wrongly suggested vasculitis. In addition, the general corticosteroid therapy certainly was implicated in disease activation and progression to a purely lepromatous form. 相似文献
994.
TE Goldberg EF Torrey JM Gold LB Bigelow RD Ragland E Taylor DR Weinberger 《Canadian Metallurgical Quarterly》1995,17(1):77-84
We investigated the effect of the adenosine receptor agonist 5'-(N-ethylcarboxamido)adenosine (NECA) in catecholamine secretion from adrenal chromaffin cells that exhibit only the A2b subtype adenosine receptor. NECA reduced catecholamine release evoked by the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) in a time-dependent manner. Inhibition reached 25% after 30-40-min exposure to NECA. This effect on DMPP-evoked catecholamine secretion was mirrored by a similar (27.7 +/- 3.3%), slowly developing inhibition of [Ca2+]i transients induced by DMPP that peaked at 30-min preincubation with NECA. The capacity of the chromaffin cells to buffer Ca2+ load was not affected by the treatment with NECA. Short-term treatment with NECA failed both to modify [Ca2+]i levels and to increase endogenous diacylglycerol production, showing that NECA does not activate the intracellular Ca2+/protein kinase C signaling pathway. The inhibitory effects of NECA were accompanied by a 30% increase of protein phosphatase activity in chromaffin cell cytosol. We suggest that dephosphorylation of a protein involved in DMPP-evoked Ca2+ influx pathway (e.g., L-type Ca2+ channels) could be the mechanism of the inhibitory action of adenosine receptor stimulation on catecholamine secretion from adrenal chromaffin cells. 相似文献
995.
We have used the technique of cell electrorotation within a microfabricated planar gold electrode array as a means of detecting changes in the physical properties of a single human neutrophil, when activated by the chemotactic factor, phorbol myristate acetate (PMA). The results, which have been analyzed using a double-shell model to represent the cell and its nucleus, provide an indication of the changes in biophysical parameters that occur during cell activation. The methods used in this study have potential applications in the development of single-cell assays for pharmaceutical screening, as a means of determining rapidly the action of drugs. 相似文献
996.
JC Freeburn JM Wallace JJ Strain DG Sinnamon BM Craig D Johnson WS Gilmore 《Canadian Metallurgical Quarterly》1998,102(2):605-608
It is widely recognized that thrombosis is the major event in the evolution of stable vascular disease to unstable ischaemic syndromes including myocardial infarction and stroke. The purpose of this case-control study was to establish clinical and laboratory data on the possible relationship between specific components of the haemostatic system and coronary heart disease. The procoagulant activity (PCA) of peripheral monocytes and polymorphonuclear neutrophils was assessed in 21 males who had suffered a myocardial infarction (MI) and in age-matched controls. In addition, total factor VII activity, fibrinogen, tissue factor pathway inhibitor (TFPI). D-dimers, tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1), tumour necrosis factor-alpha (TNF-alpha) and full blood counts were measured. Post MI patients had significantly higher monocyte PCA, higher plasma concentrations of TFPI, fibrinogen, t-PA, T/P100 and also higher total white blood cell and neutrophil counts compared to age-matched controls. This elevated procoagulant state in post MI patients could further exacerbate the disease process and increase the risk of subsequent acute ischaemic events. 相似文献
997.
F Herranz Amo F Camú?ez JM Díez Cordero F Verdú Tartajo E Lledo García G Bueno Chamon 《Canadian Metallurgical Quarterly》1998,51(8):818-820
OBJECTIVE: To describe a case of uretero-iliac fistula, an extremely rare condition that is not easily diagnosed. METHODS/RESULTS: Herein we describe a 76-year-old female who had undergone repeated pelvic surgery for adenocarcinoma of the sigmoid. She had a right ureteral fistula that had been managed conservatively by insertion of a ureteral catheter. Diagnosis was made by selective arteriography of the iliac arteries. The patient was submitted to surgery; primary closure of the arterial fistula and nephroureterectomy were performed. CONCLUSIONS: Uretero-iliac fistula should be suspected in patients with a history of repeated pelvic surgery and ureteral catheter placement that present with massive hematuria. 相似文献
998.
M Clodi P Vollenweider J Klarlund N Nakashima S Martin MP Czech JM Olefsky 《Canadian Metallurgical Quarterly》1998,139(12):4984-4990
We investigated the effects of general receptor for phosphoinositides-1 (GRP1), a recently cloned protein that binds 3,4,5-phosphatidylinositol [PtdIns(3,4,5)P3] with high affinity, but not PtdIns(3,4)P2 nor PtdIns(3)P, on insulin and insulin-like growth factor I (IGF-I)-induced cytoskeletal rearrangement, glucose transporter-4 (GLUT4) translocation, and DNA synthesis. GRP1 consists of an NH2-terminally located coiled coil domain followed by a Sec7 domain and a COOH-terminal pleckstrin homology (PH) domain that is required for PtdIns binding. We used microinjection of glutathione-S-transferase fusion proteins containing residues 239-399 (PH domain), residues 52-260 (Sec7 domain), residues 5-71 (N-terminal domain), full-length GRP1, and an antibody (AB) raised against full-length GRP1 coupled with immunofluorescent detection of actin filament rearrangement, GLUT4 translocation, and 3'-bromo-5'-deoxyuridine incorporation. Microinjection of these constructs and the AB had no effect on insulin-induced GLUT4 translocation or DNA synthesis. However, microinjection of the GRP1-PH and the GRP1-Sec7 domain as well as the alpha-GRP1-AB significantly inhibited insulin- and IGF-I-stimulated actin rearrangement in an insulin receptor-overexpressing cell line (HIRcB) compared with that in control experiments. Coinjection of GRP1-Sec7 along with constitutively active Rac (Q67L) did not inhibit Rac-induced actin rearrangement. Furthermore, GRP1 is not able to bind and act as a nucleotide exchange factor for the small GTP-binding proteins of the Rho family. As GRP1 acts as a guanine nucleotide exchange factor for ARF6 proteins, we propose a signaling pathway distinct from the small GTP-binding protein Rac, connecting PtdIns(3,4,5)P3 via GRP1 to ARF6, leading to insulin- and IGF-I-induced actin rearrangement. 相似文献
999.
We describe a genetic model for neurodegeneration in the nematode Caenorhabditis elegans. Constitutive activation of the GTP-binding protein Galphas induces neurodegeneration. Neuron loss occurs in two phases whereby affected cells undergo a swelling response in young larvae and subsequently die sometime during larval development. Different neural cell types vary greatly in their susceptibility to Galphas-induced cytotoxicity, ranging from 0 to 88% of cells affected. Mutations that prevent programmed cell death do not prevent Galphas-induced killing, suggesting that these deaths do not occur by apoptosis. Mutations in three genes protect against Galphas-induced cell deaths. The acy-1 gene is absolutely required for neurodegeneration, and the predicted ACY-1 protein is highly similar (40% identical) to mammalian adenylyl cyclases. Thus, Gs-induced neurodegeneration is mediated by the second messenger cAMP. Mutations in the unc-36 and eat-4 genes are partially neuroprotective, which indicates that endogenous signaling modulates the severity of the neurotoxic effects of Galphas. These experiments define an intracellular signaling cascade that triggers a necrotic form of neurodegeneration. 相似文献
1000.
S Rae JM Raboud B Conway P Reiss S Vella D Cooper J Lange M Harris MA Wainberg P Robinson M Myers D Hall JS Montaner 《Canadian Metallurgical Quarterly》1998,12(16):2185-2192
OBJECTIVE: To assess the potential discrepancies in reported changes in plasma viral load (PVL) depending on how values below the detection limit of the assay are handled in the data analysis phase of a randomized controlled clinical trial. DESIGN: Data from a recently completed clinical trial comparing combinations of zidovudine, didanosine and nevirapine were analysed. In this trial, PVL was measured using an assay with a lower quantification limit of 400 HIV-1 RNA copies/ml initially. All PVL values less than 500 copies/ml were retested with a more sensitive assay with a lower quantification limit of 20 copies/ml. METHODS: Several summary measures for assessing change in PVL were calculated using three different methods to adjust for PVL values less than the quantification limit of the assay. The differences between these measures were evaluated. RESULTS: We found that the magnitude of the discrepancy between summary measures used to report changes in PVL depended on the proportion of subjects with PVL less than the quantification limit of the assay, how those observations were handled in the data analysis, and the relative difference between the quantification limits of the conventional and more sensitive assay. CONCLUSION: The lack of consensus in reporting of PVL data in the literature makes the interpretation of published trial results difficult. In the absence of agreement on the most appropriate summary measure of PVL data, we recommend that all summaries include information on the quantification limit of the assay used, the proportion of observations at or below the quantification limit and how these observations were handled in the data analysis. 相似文献