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Staphylococcus aureus infections 总被引:2,自引:0,他引:2
FD Lowy 《Canadian Metallurgical Quarterly》1998,339(8):520-532
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G Guillemin J Croitoru FD Boussin R Le Grand M Franck-Duchenne D Dormont 《Canadian Metallurgical Quarterly》1998,192(1):179-186
OBJECTIVE: The aim was to examine the effects of lysophosphatidylcholine (LPC), an amphiphilic lipid metabolite in ischemic myocardium, on intracellular pH (pH(i)) regulatory systems in guinea pig papillary muscles. METHODS: In CO2/HCO(3-)-buffered Tyrode solution, pH(i), intracellular Na+ activity (aNai) and membrane potential of isolated guinea pig papillary muscles were measured using ion-selective microelectrode and conventional microelectrode. Standard ammonium prepulsing with 20 mM NH4Cl was used to produce an intracellular acid load, and effects of LPC on the pH(i) recovery from acidosis were evaluated in the absence and presence of a transport inhibitor. RESULTS: LPC acidified the resting pH(i) by 0.03 +/- 0.01 pH units (n = 15, p < 0.01) concomitantly with a slight decrease in resting membrane potential and an increase in aNai in quiescent preparations. The pH(i) recovery rate from an intracellular acid load was decreased to 83 +/- 4% of the control value by 30 microM LPC (n = 8, P < 0.05) but not by 30 microM phosphatidylcholine (PC). In the presence of 10 microM 5-(N,N-hexamethylene) amiloride (HMA), a Na(+)-H+ exchange inhibitor, LPC still slowed pH(i) recovery from an intracellular acid load to 77 +/- 4% of the control (n = 5, P < 0.05). However, LPC failed to alter the pH(i) recovery rate in the presence of 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 0.5 mM), a Na(+)-HCO3- symport inhibitor. CONCLUSION: LPC impairs Na(+)-HCO3- symport but not Na(+)-H+ exchange, and LPC may potentiate its arrhythmogenic action by intensifying the intracellular acidosis in ischemic myocardium. 相似文献
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FD Brenneman BR Boulanger BA McLellan JP Culhane DA Redelmeier 《Canadian Metallurgical Quarterly》1995,39(2):320-324
Long-term outcomes after blunt trauma remain poorly defined. The purpose of this study was to document such outcomes in extremely injured adults (Injury Severity Score > or = 50). From April 1990 to June 1993, 76 patients (5% of all trauma victims) had an ISS > or = 50 at a single trauma center. Thirty-five (46%) survived to hospital discharge. The mean duration of hospital stay was longer for survivors than for nonsurvivors (92 days versus 16 days, p < 0.001). Of the 35 survivors, 26% were discharged directly home, 60% to a rehabilitation hospital, 8% to a chronic care facility, and 6% to an acute care hospital. After a mean follow-up of 27 months, 6% had died, 9% refused participation, and the remaining 30 patients (91% of long-term survivors) demonstrated significant residual disabilities in physical, emotional, and mental health status. We suggest that extremely injured patients comprise a small proportion of blunt trauma victims, consume substantial acute care hospital resources, often survive, and yet frequently have residual disability. A reduction in this long-term disability may represent the greatest challenge in modern trauma care. 相似文献
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DA Grillot R Merino JC Pena WC Fanslow FD Finkelman CB Thompson G Nunez 《Canadian Metallurgical Quarterly》1996,183(2):381-391
We have assessed during B cell development, the regulation and function of bcl-x, a member of the bcl-2 family of apoptosis regulatory genes. Here we show that Bcl-xL, a product of bcl-x, is expressed in pre-B cells but downregulated at the immature and mature stages of B cell development. Bcl-xL but not Bcl-2 is rapidly induced in peripheral B cells upon surface immunoglobulin M (IgM) cross-linking, CD40 signaling, or LPS stimulation. Transgenic mice that overexpressed Bcl-xL within the B cell lineage exhibited marked accumulation of peripheral B cells in lymphoid organs and enhanced survival of developing and mature B cells. B cell survival was further increased by simultaneous expression of bcl-xL and bcl-2 transgenes. These studies demonstrate that Bcl-2 and Bcl-xL are regulated differentially during B cell development and activation of mature B cells. Induction of Bcl-xL after signaling through surface IgM and CD40 appears to provide mature B cells with an additional protective mechanism against apoptotic signals associated with antigen-induced activation and proliferation. 相似文献
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A 5-HT2-receptor antagonist (LY53857) was evaluated in the livers of male Sprague-Dawley rats receiving a dose of serotonin (5-HT) producing systemic (arterial) hypotension and low flow. The specific aim of this investigation was to determine the cross-blocking potential of a 5-HT2 blocker having low affinity for alpha-adrenergic and histamine H 1-receptors. This was a follow-up study to one which characterized the effects of normo- and hypotensive doses of 5-HT on intralobular perfusion and volumetric rates of blood flow at the inlet of periportal and outlet of centrivenous sinusoids. Twenty rats were injected intraperitoneally (i.p.) with 0.05 mg per g b.w. pentobarbital five min following an i.p. injection of 0.1 mg per 100 g b.w. LY53857. The left lobes of the livers from these rats were exteriorized and examined with intravital videomicroscopic and electro-optical methods following surgical implantation of a catheter into the ileocecal vein. This venous catheter served as the route for endoportal infusion of hypotensive dose of 5-HT (10 micrograms per 100 g b.w.) in 10 rats, while the remaining 10 rats were given an equivalent volume of its carrier as a control (0.1 ml per 100 g b.w. Ringer's solution). Injection of LY53857 completely antagonized 5-HT-elicited low flow at the inlet of periportal and outlet of centrivenous sinusoids. In addition, no change in sinusoidal internal diameter was observed following blockade of 5-HT2 receptors. These results, in the concert with those from previous studies characterizing 5-HT vasoresponsiveness in the liver, suggest that: a) constrictor 5-HT2 receptors are localized on hepatic sinusoids, and b) 5-HT-provoked hypoperfusion is mediated by activation of the 5-HT2-receptor subtype. 相似文献
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FD Bartholomew NB Isada MI Evans 《Canadian Metallurgical Quarterly》1993,269(6):746; author reply 746-746; author reply 747
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