Peritoneal dialysis treatment in children and parental stress

The burden placed on the parents of a child in dialysis treatment can induce negative effects on the medical treatment and on the psychological development of the child. To identify which families are at risk, both parents of 14 out of 16 eligible patients in continuous ambulatory peritoneal dialysis (CAPD) answered an extensive questionnaire three times during one year. Large differences were found between the families with regard to the amount of stress experienced. Parents of older children (< 5 years) (and particularly parents of children with a failed transplantation) experienced significantly more stress. The nature of the stress was determined more by the psychological aspects than by the medical aspects of the treatment. Concern about the future contributed most to the stress experienced. Therefore, emotional support as well as practical help for families at risk is recommended.     

The geometry of triple-balloon dilation

Triple-balloon dilation (TBD) of a variety of luminal structures has been successfully, though infrequently, used. A mathematical model is presented for the selection of balloon sizes, and equations and tables are derived that allow the user to estimate more accurately the size of balloons needed for TBD of structures with large lumina. With TBD, an approximately circular lumen can be formed. Also, TBD allows smaller, higher-pressure balloons to be used instead of single, low-pressure, large balloons. However, multiple puncture sites may be required for TBD.     

Effects of monensin on conversion of proinsulin to insulin and secretion of newly synthesized insulin in isolated rat islets

When isolated rat islets were incubated with 10(-10) - 10(-6) M monensin, a sodium and proton ionophore, glucose-stimulated insulin release was inhibited in a concentration- and time-dependent manner. After removal of monensin, inhibition of insulin secretion persisted during stimulation with a variety of secretagogues, including 5 mM glucose plus 15 mM arginine, 20 mM glucose, and 20 mM glucose plus 1 mM 3-isobutyl-1-methylxanthine. Within the same low range of monensin concentrations, proteolytic conversion of newly synthesized proinsulin to insulin was also blocked. At each concentration, prohormone-to-hormone conversion was inhibited to almost the same extent as inhibition of insulin secretion. Therefore, both processes may have equal or common dependency on a subcellular ionic gradient. Although monensin decreased total insulin secretion, the glucose-regulated marking process was unaffected. Regardless of the monensin concentration or the overall rate of insulin secretion, the percentage of secreted newly synthesized versus older insulin remained the same, and the threefold differences in the fractional secretory rates of newly synthesized versus total insulin also remained the same. Thus, rather than specifically blocking protein traffic through the Golgi apparatus of the beta cell, monensin probably first inhibited insulin secretion by disrupting proton gradients in secretory vesicles and, thereby, also inhibited other processes occurring within this organelle.     

Interrelationships between alpha and beta-anomers of glucose affecting both insulin and glucagon secretion in the perfused rat pancreas. II.

Temporal and quantitative relationships between the alpha and beta anomers of glucose on insulin and glucagon secretion were studied in two surgical preparations of the in vitro perfused rat pancreas. Alpha-Glucose was a more effective stimulator of insulin release. Beta-Glucose, however, though less effective, was a positive modulator when admixed with alpha-glucose. Dose-response studies showed that alpha-glucose probably had a smaller apparent Km for insulin secretion, while the Vmax for the two anomers was the same-the effects of the two anomers being indistinguishable at high glucose concentrations (300 mg/dl). Alpha-Anomeric stereospecificity was demonstrable equally on both phases of insulin release and was maintained throughout 60-min perfusions. Spontaneous or arginine-stimulated glucagon release was also preferentially inhibited by alpha-glucose. Since others have shown that glucose uptake and phosphorylation in islets are not alpha-stereospecific, the data suggest that the initial signal for the first and second phases of insuulin release and glucose suppression of glucagon secretion is at the level of a glucoreceptor prior to, or indedendent of, major pathways of glucose metabolism.