Coping in long-term survivors of childhood cancer: relations to psychological distress.

OBJECTIVE: The goal of this study was to describe coping strategies and their associations with psychological distress in young adult survivors of childhood cancer. METHODS: One hundred and sixty-four childhood cancer survivors, at least 7 years after diagnosis, completed questionnaires assessing demographics, health information, psychological distress, and different ways of coping (return rate: 61%). The Brief Symptom Inventory-18 (BSI-18) and the Post-traumatic Diagnostic Scale's (PDS) eight-item short form were used to measure psychological distress. Coping was assessed with the Cognitive Control Strategies Scale (CCSS), the Illness Perception Questionnaire-Revised (IPQ-R), and the White Bear Suppression Inventory (WBSI). RESULTS: Higher levels of distress were associated with the female sex, not being in a relationship, and with the presence of medical late effects. These predictors explained 12% of the variance in psychological distress. When coping variables were also entered into the equation, the amount of explained variance increased to 50%. The most important determinants of psychological distress in our sample were a tendency to suppress negative thoughts and a low level of optimism. CONCLUSION: These results contribute to a better understanding of the correlates of difficulties in long-term psychological adjustment after childhood cancer. Cognitive strategies, which are associated with or may increase the risk for concurrent psychological distress, in specific, avoidance of negative thoughts and a lack of positive future expectations, should be addressed in psychological counseling with survivors suffering from symptoms of distress.

Two different oxygen sensors regulate oxygen-sensitive K+ transport in crucian carp red blood cells.

The O2 dependence of ouabain-independent K+ transport mechanisms has been studied by unidirectional Rb+ flux analysis in crucian carp red blood cells (RBCs). The following observations suggest that O2 activates K+-Cl- cotransport (KCC) and deactivates Na+-K+-2Cl- cotransport (NKCC) in these cells via separate O2 sensors that differ in their O2 affinity. When O2 tension (PO2) at physiological pH 7.9 was increased from 0 to 1, 4, 21 or 100 kPa, K+ (Rb+) influx was increasingly inhibited, and at 100 kPa amounted to about 30% of the value at 0 kPa. This influx was almost completely Cl- dependent at high and low PO2, as shown by substituting Cl- with nitrate or methanesulphonate. K+ (Rb+) efflux showed a similar PO2 dependence as K+ (Rb+) influx, but was about 4-5 times higher over the whole PO2 range. The combined net free energy of transmembrane ion gradients favoured net efflux of ions for both KCC and NKCC mechanisms. The KCC inhibitor dihydroindenyloxyalkanoic acid (DIOA, 0.1 mM) abolished Cl- -dependent K+ (Rb+) influx at a PO2 of 100 kPa, but was only partially effective at low PO2 (0-1 kPa). At PO2 values between 0 and 4 kPa, K+ (Rb+) influx was further unaffected by variations in pH between 8.4 and 6.9, whereas the flux at 21 and 100 kPa was strongly reduced by pH values below 8.4. At pH 8.4, where K+ (Rb+) influx was maximal at high and low PO2, titration of K+ (Rb+) influx with the NKCC inhibitor bumetanide (1, 10 and 100 microM) revealed a highly bumetanide-sensitive K+ (Rb+) flux pathway at low PO2, and a relative bumetanide-insensitive pathway at high PO2. The bumetanide-sensitive K+ (Rb+) influx pathway was activated by decreasing PO2, with a PO2 for half-maximal activation (P50) not significantly different from the P50 for haemoglobin O2 binding. The bumetanide-insensitive K+ (Rb+) influx pathway was activated by increasing PO2 with a P50 significantly higher than for haemoglobin O2 binding. These results are relevant for the pathologically altered O2 sensitivity of RBC ion transport in certain human haemoglobinopathies.