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S M Douglas

Publications and source records attributed to S M Douglas.

5 recordsLinked to original sources
PubMed1992

Maternal depression, assessment methods, and physical symptoms affect estimates of depressive symptomatology among children with cancer.

Investigated the incidence of depressive symptoms and their covariates in a sample of 99 children undergoing treatment for cancer and their mothers. Although the prevalence of depressive symptoms falling within the clinical range was low (7 to 8%), classification of these children was highly dependent upon the informant and instrument used. Interrater reliabilities did not differ from chance levels. Separate multiple regression analyses of the mother's and nurse's ratings of the child's level of depression, the child's self-report on the Child Depression Inventory, and the mother's responses to the Child Behavior Checklist depression scales revealed different statistical models for each method of assessment. However, increased severity of the mother's self-report of depressive symptoms on the Beck Depression Inventory, which was predicted by low perceived social support and hospitalization of her child, was associated with higher levels of child depression on all child- and parent-report measures. Parental adjustment, sociodemographic, and medical factors as well as methods of assessment must be addressed by models explaining the etiology of depressive symptoms among pediatric oncology patients.

Adult↗
PubMed1986

Amiloride-sensitive sodium-hydrogen exchange in osmotically shrunken rabbit red blood cells.

As part of a detailed study of cell volume regulation in high-potassium mammalian erythrocytes, we have characterized ouabain-insensitive sodium transport in normal and osmotically shrunken rabbit red cells. In cells of normal volume and physiological pH, there is no amiloride-inhibited component of the sodium efflux (into either sodium-containing or sodium-free media). Osmotic shrinkage activates an amiloride-sensitive (50% inhibitory concentration = 10(-5) M) sodium transport system that can catalyze net sodium movement in either direction. This system appears to be distinct from the sodium-sodium (sodium-lithium) counter-transporter that operates in cells of normal volume. Replacement of chloride with acetate does not inhibit the sodium flux, but replacement with either nitrate or thiocyanate is inhibitory. An inward sodium gradient in shrunken cells induces a net uphill efflux of acid equivalents, indicating that the sodium transport is a sodium-hydrogen exchange. However, a sevenfold inward gradient of hydrogen ions (pHo = 6.4; pHi = 7.2) does not stimulate net sodium efflux in shrunken cells. This suggests that the extracellular affinity of the transport site for hydrogen ions is high, and that there is an extracellular noncompetitive inhibitory site for proton binding. Bilateral pH reduction stimulates an amiloride-inhibitable sodium flux in cells of normal volume; this indicates that, as has been found in kidney, brain, and lymphocytes, there is an intracellular protonation site that can activate the transport. Shrinkage of the cells shifts the pH dependence of the transport, suggesting that part of the signal for the osmotic activation of the transport is a shift in the pKa of this modifier site.

Amiloride↗
PubMed1985

Functions of extracellular lysine residues in the human erythrocyte anion transport protein.

The extracellular lysine residues in the human erythrocyte anion transport protein (band 3) have been investigated using chemical modification with the impermeant homobifunctional active ester bis(sulfosuccinimidyl)-suberate (BSSS). This agent forms covalent intra- and intermolecular cross-links in human band 3 in intact cells (Staros and Kakkad. 1983. J. Membr. Biol. 74:247). We have found that the intermolecular cross-link has no detectable effect on the anion transport function of band 3. The intramolecular cross-link, however, causes major changes in the characteristics of the anion transport. These functional alterations are caused by the modification of lysine residues at the stilbene disulfonate binding site. BSSS pretreatment at pH 7.4 irreversibly inhibits Cl-Br exchange by at least 90% when the transport is assayed at extracellular pH above 8. In the same BSSS-pretreated cells, however, the Cl-Br exchange rate is activated by lowering the pH of the flux medium (intracellular pH fixed at 7). The flux is maximal at pH 5-6; a further lowering of the extracellular pH inhibits the anion exchange. This acid-activated Cl-Br exchange in the BSSS-treated cells is mediated by band 3, as indicated by phenylglyoxal and phloretin inhibition of the flux. Thus, the BSSS pretreatment has little effect on the maximal Cl-Br exchange flux catalyzed by band 3, but it shifts the alkaline branch of its extracellular pH dependence by approximately 5 pH units. BSSS also eliminates the self-inhibition of Cl-halide exchange by high extracellular Br or I concentrations. These results indicate that the BSSS-modified lysines do not participate directly in anion translocation, but that one of the lysines normally provides a positive charge that is necessary for substrate anion binding. This positive charge is removed by the BSSS treatment but can be replaced by lowering the extracellular pH. The results also provide insight regarding the halide selectivity of the maximal rate of chloride-halide exchange: the native selectivity (Br much greater than I) is nearly abolished by BSSS treatment, which suggests that the selectivity results from the very strong binding of iodide to an outward-facing modifier site.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1979

Evaluation of the Gambro Lundia Major 1.36 m2 disposable parallel plate dialyzer.

The Gambro Lundia Major 1.36 m2 dialyzer was assessed in vivo in ten hemodialysis patients. Urea and creatinine clearances (measured as whole blood values at 60 minutes with a blood flow rate of 200 ml/minute) were 166 +/- 8 m/minute (mean +/- standard error of the mean, n = 9) and 115 +/- 4 ml/minute (n = 11). The creatinine clearance is 15% lower than in vitro data. There was a marked decrease in urea and creatinine clearance with third use of the dialyzer. The ultrafiltration rate was 490 ml/hour/100 mmHg. The priming volume was 125 ml (at a transmembrane pressure of 100 mmHg) and residual blood volume in the dialyzer was 0.57 +/- 0.11 ml (n = 5). The handling, storage and ease of disposal of the dialyzer is better than previous models and its performance characteristics are clinically acceptable.

Adult↗