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1.
Clinical experience with short-time hemodialysis. 总被引:4,自引:0,他引:4
After at least 6 months on conventional hemodialysis (cellulosic dialyzers, acetate dialysate, and a 3- to 4-hour treatment time), 56 patients were changed to short-time hemodialysis (less than 180 minutes) using polysulfone dialyzers and bicarbonate-containing dialysate. Treatment time decreased (191 +/- 5 v 147 +/- 5 min; P = 0.001), while Kt/V (1.22 +/- 0.04 v 1.29 +/- 0.06; P = NS) and normalized protein catabolic rate (pcr) (1.10 +/- 0.05 v 1.10 +/- 0.07 g/kg/d; P = NS) remained constant. When compared with the conventional period, 30 months of short-time hemodialysis resulted in no changes in predialysis blood pressure (BP) (151 +/- 2/84 +/- 1 v 151 +/- 2/86 +/- 1 mm Hg), postdialysis BP (144 +/- 2/81 +/- 1 v 143 +/- 3/84 +/- 1 mm Hg), interdialytic weight gain (2.4 +/- 0.1 v 2.7 +/- 0.2 kg), or blood urea nitrogen (BUN) (26.1 +/- 0.71 v 25.3 +/- 1.07 mmol/L [73 +/- 2 v 71 +/- 3 mg/dL]). Shorter treatment times were not associated with an increase in intradialytic complications. Actually, the frequency (%) of dialysis treatments associated with nausea (5.94 +/- 1.33 v 2.21 +/- 0.52), vomiting (3.12 +/- 0.87 v 0.54 +/- 0.14; P less than 0.05), headaches (5.60 +/- 1.13 v 2.03 +/- 0.52; P less than 0.05), and back pain (0.91 +/- 0.25 v 0.05 +/- 0.05; P less than 0.05) was decreased.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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U K Ganu D D Khandalekar S V Gokhale 《Indian journal of physiology and pharmacology》1984,28(1):21-26
The ability of Amphotericin B ('Fungizone') to alter the natural resistance of leukemia L1210 to vincristine was studied in BDF1 mice Neither Fungizone nor the "solubilizing agent" sodium deoxycholate, when used in combination with vincristine potentiated the activity of the drug against L1210. There was no change in the activity pattern of 5-fluorouracil against L1210 or vincristine against P388 lymphocytic leukemia respectively, which are sensitive to these drugs. Thus, both Fungizone and sodium deoxycholate failed to improve the activity of the drugs in either a naturally resistant or sensitive murine leukemia in vivo. 相似文献
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Kyung-Heup Ahn Andrew Sewell Jacqueline Elander Brian Pittman Mohini Ranganathan Handan Gunduz-Bruce John Krystal Deepak Cyril D'Souza 《Neuropsychopharmacology》2015,40(12):2822-2831
Some schizophrenia patients are more sensitive to amphetamine (AMPH)-induced exacerbations in psychosis–an effect that correlates with higher striatal dopamine release. This enhanced vulnerability may be related to gamma-aminobutyric acid (GABA) deficits observed in schizophrenia. We hypothesized that a pharmacologically induced GABA deficit would create vulnerability to the psychotomimetic effects to the ‘subthreshold'' dose of AMPH in healthy subjects, which by itself would not induce clinically significant increase in positive symptoms. To test this hypothesis, a GABA deficit was induced by intravenous infusion of iomazenil (IOM; 3.7 μg/kg), an antagonist and partial inverse agonist of benzodiazepine receptor. A subthreshold dose of AMPH (0.1 mg/kg) was administered by intravenous infusion. Healthy subjects received placebo IOM followed by placebo AMPH, active IOM followed by placebo AMPH, placebo IOM followed by active AMPH, and active IOM followed by active AMPH in a randomized, double-blind crossover design over 4 test days. Twelve healthy subjects who had a subclinical response to active AMPH alone were included in the analysis. Psychotomimetic effects (Positive and Negative Syndrome Scale (PANSS)), perceptual alterations (Clinician Administered Dissociative Symptoms Scale (CADSS)), and subjective effects (visual analog scale) were captured before and after the administration of drugs. IOM significantly augmented AMPH-induced peak changes in PANSS positive symptom subscale and both subjective and objective CADSS scores. There were no pharmacokinetic interactions. In conclusion, GABA deficits increased vulnerability to amphetamine-induced psychosis-relevant effects in healthy subjects, suggesting that pre-existing GABA deficits may explain why a subgroup of schizophrenia patients are vulnerable to AMPH. 相似文献
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Giri Prerna Mukhopadhyay Amrita Gupta Mohini Mohapatra Bhagyalaxmi 《Heart failure reviews》2022,27(2):431-454
Heart Failure Reviews - Heart failure is a global health burden responsible for high morbidity and mortality with a prevalence of greater than 60 million individuals worldwide. One of the major... 相似文献
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Barnett Alana Edwards Katie Harper Rebecca Evans Elizabeth Alexander Derina Choudhary Mohini Richards Gareth 《Journal of autism and developmental disorders》2021,51(6):1866-1879
Journal of Autism and Developmental Disorders - Previous studies have reported positive correlations between autistic traits and disordered eating, though it is unclear whether the association is... 相似文献
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HMG-CoA reductase inhibitors promote cholesterol-dependent Akt/PKB translocation to membrane domains in endothelial cells 总被引:5,自引:0,他引:5
Skaletz-Rorowski A Lutchman M Kureishi Y Lefer DJ Faust JR Walsh K 《Cardiovascular research》2003,57(1):253-264
OBJECTIVE: Recent results have shown that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors referred to as statins rapidly activate the protein kinase Akt/PKB in endothelial cells (ECs) and endothelial precursor cells (EPCs). This pathway is critical for cellular responses that contribute to angiogenesis and EC function including nitric oxide production, cellular survival and migration. METHODS: Here we tested whether statins control the translocation of recombinant and endogenous Akt to the plasma membrane of endothelial cells in a cholesterol-dependent manner. RESULTS: Low doses of statins rapidly induce the translocation of Akt to discrete sites in endothelial cell plasma membrane that colocalize with F-actin-positive, focal adhesion kinase (FAK)-negative lamellipodia and filopodia. This translocation event requires the lipid-binding, pleckstrin homology domain of Akt. Treatment with phosphoinositide 3-kinase (PI 3-kinase) inhibitors or the HMG-CoA reductase reaction product L-mevalonate blocks the translocation of Akt in response to statin stimulation. Furthermore, the ability of statins to promote Akt activation and translocation to the membrane is inhibited by cholesterol delivery to cells, but cholesterol loading had no effect on VEGF-induced Akt activation. CONCLUSIONS: These results suggest that statin activation of Akt signaling is mediated by the translocation of Akt to cholesterol-sensitive membrane structures within activated ECs. 相似文献
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Mohini Ranganathan R. Andrew Sewell Michelle Carbuto Jacqueline Elander Ashley Schnakenberg Rajiv Radhakrishnan Brian Pittman Deepak Cyril D’Souza 《Psychopharmacology》2014,231(12):2385-2393