Uptake of calcium by brush-border membrane vesicles from rat small intestine is composed of saturable and nonsaturable components. We studied regulation of calcium uptake using the divalent cations strontium, a foreign ion that mimics calcium biologically and magnesium, a physiologically important ion that resembles calcium physically, although not biologically. Strontium present outside the vesicle inhibited saturable calcium uptake competitively, consistent with binding to the transporter at the same site as calcium. Strontium inside the vesicle accelerated saturable calcium uptake from the outside (countertransport), also consistent with binding to the same transporter site as calcium. Thus the calcium transporter shows functional characteristics of a mobile carrier. In the uptake medium (extracellular), magnesium was a noncompetitive inhibitor of saturable calcium transport, consistent with a regulatory role in calcium uptake by binding to the transporter at a locus other than that for calcium. Magnesium at 1 mM concentration inside the vesicle had no effect on saturable calcium uptake and a high concentrations functioned as a week uncompetitive inhibitor. Thus intracellular magnesium appears to have no major role in regulating saturable calcium uptake at the brush border of the enterocyte.
The effect of insulin or glutathione treatment on glutathione content of liver and jejunal mucosa and on superoxide dismutase (SOD) activity of liver, kidney, and erythrocytes was investigated in pair-fed animals with streptozocin (STZ)-induced diabetes. Diabetes lowered hepatic glutathione concentration, but glutathione concentration of the jejunal mucosa was not affected. Insulin, but not oral glutathione, restored hepatic glutathione concentration to normal levels. Diabetes depressed activity of the cytosolic form of SOD in liver, kidney, and erythrocyte. Treatment of diabetic rats with oral glutathione or intramuscular insulin increased cytosolic SOD activity of renal cortex and liver (but not erythrocytes) to control levels. These results suggest a link between glutathione metabolism and cytosolic SOD activity in diabetes.
Two cases of nafcillin-induced neutropenia in children are discussed. A seven-year-old girl was referred to the hospital after the pain and swelling in her foot persisted despite five days of oral penicillin VK therapy. Administration of intravenous nafcillin 150 mg/kg/day was started upon admission. The patient's leukocyte count was normal upon admission; further, her leukocyte and neutrophil counts were normal on the 10th and 17th days of hospitalization. After 22 days of nafcillin therapy, her leukocyte and neutrophil counts fell to 2300 and 162/cu mm, respectively. Three days after the nafcillin was discontinued, the leukocyte count was 5800/cu mm. The patient was given dicloxacillin 50 mg/kg/day, and had no recurrence of neutropenia. The second case involved a 28-month-old girl admitted to the hospital with fever, irritability, and skin rash. Her leukocyte count was normal upon admission. She received 10 days of penicillin G 100,000 units/kg/day, followed by 10 days of nafcillin 150 mg/kg/day, before neutropenia was discovered. On the ninth day of nafcillin therapy, here leukocyte and neutrophil counts were 4200 and 822/cu mm, respectively. Nafcillin was discontinued and cefazolin therapy was initiated at 100 mg/kg/day. Blood counts returned to normal, and there was no recurrence of neutropenia. Differential blood cell counts should be performed on patients receiving nafcillin, and, if neutropenia develops, nafcillin should be discontinued and treatment with a nonpenicillin antimicrobial considered.
We determined whether a β-lactam and an aminoglycoside have efficacy greater than a β-lactam alone in the management of a pulmonary exacerbation in patients with cystic fibrosis. Study design: Azlocillin and placebo or azlocillin and tobramycin were administered to 76 patients with a pulmonary exacerbation caused by Pseudomonas aeruginosa in a randomized double-blind, third-party monitored protocol. Improvement was assessed by standardized clinical evaluation, pulmonary function testing, sputum bacterial density, sputum DNA content, and time to the next pulmonary exacerbation requiring hospitalization. Results: No significant difference was seen between the 2 treatment groups in clinical evaluation, sputum DNA concentration, forced vital capacity, forced expiratory volume in second 1, or peak expiratory flow rate at the end of treatment (33 receiving azlocillin alone and 43 both antibiotics); adverse reactions were equivalent in each group. Sputum P. aeruginosa density decreased more with combination therapy (P = .034). On follow-up evaluation, an average of 26 days after the end of treatment, all outcome indicators had worsened in both groups. Time to readmission for a new pulmonary exacerbation was significantly longer in the group receiving azlocillin plus tobramycin (P < .001). Treatment-emergent tobramycin resistance occurred in both groups and was more frequent with combination therapy. Conclusion: We conclude that the combination of a β-lactam and an aminoglycoside produces a longer clinical remission than a β-lactam alone and slightly better initial improvement. (J Pediatr 1999;134:413-21)
Abstract The antibiotic concentration of the fluid from either lateral ventricle was determined 104 times in 37 patients through direct ventricular puncture, external ventricular drainage (EVD). or cerebrospinal fluid shunt sampling. The patients were 1 month to 12 years old. When the patients were receiving maximal intravenous antibiotic therapy alone, the concentrations for the most part were below 5 μg/ml. whereas patients receiving an antibiotic through direct ventricular puncture, EVD. or a shunt reservoir usually had concentrations over 5 μ/ml. However, wide variations from patient to patient were found with all forms of treatment despite similar dosages. Clustering of the concentration tended to occur in each individual patient. The authors conclude that, to obtain a high concentration of an antibiotic in the ventricular fluid, one should administer it directly into the ventricle.
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