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Biomedical subjects

C Little

Publications and source records attributed to C Little.

135 records · Page 8Linked to original sources

The effectiveness of a lipid peroxide in oxidizing protein and non-protein thiols.

1. Thiol oxidation by a lipid peroxide or hydrogen peroxide was as efficient in denatured non-haem proteins as in small thiols. Both peroxides were relatively ineffective in oxidizing haemoprotein thiols, especially at low pH. Increased amounts of haematin decreased greatly the efficiency of GSH oxidation by peroxides especially at low pH. 2. Other than the haematin ring, the thiol group was found to be probably the group in proteins most sensitive to modification by peroxides. 3. At low concentrations, the fatty acid moiety of a lipid peroxide appeared to impede thiol oxidation in proteins, probably by hydrophobic bonding to the protein, rather than to stimulate thiol oxidation by denaturing the protein and thereby increasing the exposure and reactivity of the thiol group. 4. The relative rates of thiol oxidation by peroxides in the different thiols were: haemoprotein thiols>small thiols>other protein thiols. In all cases, thiol oxidation was much more rapid by the lipid peroxide than by hydrogen peroxide.

Adult↗

Phospholipase C-evoked glycerol release in energy depleted rat myocardial cells.

Preincubation of rat myocardial cells in hypoxic substrate-free Krebs-Ringer bicarbonate buffer (pH 7.4, 37 degrees C) resulted in a substantial decline in high energy phosphates (ATP and CP). Thus, 20 and 60 min preincubation produced a 18 and 72% decline in ATP content, whereas the parallel decline in CP content was 51 and 73%. This energy depletion was accompanied by a change in cell morphology from the initial rod-shaped form to rounded up (hyper-contracted) myocytes. In cells preincubated in substrate-free normoxic buffer, both normal morphology and energy homeostasis were maintained. When energy depleted myocytes later were incubated in the presence of phospholipase C (PLC), this resulted in a substantial release of glycerol, amounting to 92 and 137 nmol/10(6) cells.2 h in 20 and 60 min energy depleted myocytes, respectively. In addition, PLC caused an increased leakage of lactate dehydrogenase in energy depleted myocytes. Normal cells, on the other hand, were apparently not affected by PLC. These data suggest that PLC selectively attacks energy depleted and/or structurally damaged myocytes. This could well enhance the breakdown of the natural barrier between the extra- and intracellular compartments and thus augment the cellular damage during ischemia. Moreover, energy depleted myocytes appeared exceptionally sensitive to this enzyme, since the levels required to cause glycerol or lactate dehydrogenase release were several orders of magnitude lower than that required to cause membrane permeation in other cell types.

Adenosine Triphosphate↗

Ollier disease: an interdisciplinary approach.

Ollier disease is a bone disorder characterized by the development of cartilaginous lesions which lead to a variety of bony deformities. Orthopaedic treatment is specific to the resulting deformity, and nursing care will vary according to the individual treatment plan. Successful intervention requires an interdisciplinary approach to care that addresses both physiologic and psychologic concerns. Nursing plays a vital role in both direct interaction with the patient and family and coordination with other disciplines. Long-range care must also include monitoring patients for possible malignant changes.

Aftercare↗

Comparison of intramuscular betamethasone and oral prednisone in the prevention of relapse of acute asthma.

OBJECTIVE: To compare the relapse rate after a single intramuscular injection of a long acting corticosteroid, betamethasone, with oral prednisone in patients discharged from the emergency department (ED) for acute exacerbations of asthma. PATIENTS AND METHODS: Patients with acute exacerbations of asthma who were suitable for discharge from the ED were enrolled in a double-blind, randomized, placebo controlled pilot study. At discharge, patients were randomly assigned to receive either intramuscular betamethasone 12 mg and placebo capsules, or a placebo intramuscular injection and prednisone 50 mg daily for seven days. At days 7 and 21, patients were contacted by telephone to determine relapse. Relapse was defined as an unscheduled visit to a physician for treatment of continuing or worsening symptoms of asthma. RESULTS: One hundred and seventy-one patients were enrolled, of whom 87 were randomly assigned to the betamethasone group and 84 to the prednisone group. Baseline characteristics were matched evenly between the groups, with the exception of asthma duration (15.5 versus 21.2 years, respectively) and use of inhaled corticosteroids (46% versus 64.3% respectively) (P<0.05). Using intention-to-treat analysis, the relapse rates for betamethasone and prednisone at day 7 were 14.9% (13 of 87 patients) and 25% (21 of 84 patients), respectively (P=0.1), and at day 21, the rates were 36.8% (32 of 87 patients) and 31% (26 of 84 patients), respectively (P=0.4). There were no differences in symptom score, peak flows and adverse effects between the two groups at days 7 and 21. CONCLUSIONS: A single dose of intramuscular betamethasone 12 mg was safe and as efficacious as prednisone in preventing the relapse of acute asthma. There was a trend toward a reduced relapse rate at seven days. In select ED patients discharged for acute asthma, intramuscular betamethasone may be an effective alternative to prednisone.

Acute Disease↗