Pathways into childlessness: evidence of gendered life course dynamics

Using data from the first wave of the Netherlands Kinship Panel Study (NKPS) for 2867 women and 2195 men aged 40 to 79, this study examines to what extent educational, employment and marital pathways shape the likelihood of remaining childless, and whether these pathways are gendered. The findings indicate that women and men have distinctive pathways into childlessness. Educational attainment increases the likelihood of remaining childless among women only. A stable career increases the likelihood of remaining childless among women, but it increases the likelihood of entering fatherhood. Years without a partner is positively associated with childlessness among both women and men. Not having had a partnership and having had multiple partnerships are strong determinants of childlessness, especially among men.     

Minimal model for membrane oscillations in the pancreatic beta-cell.

Following the experimental findings of Atwater et al. (In Biochemistry Biophysics of the Pancreatic-beta-Cell, George Thieme Verlag, New York, 100-107), we have formulated a mathematical model for ionic and electrical events that take place in pancreatic-beta-cells. Our formulation incorporates a Hodgkin-Huxley type gating mechanism for Ca2+ and K+ channels, in addition to Ca2+ gated K+-channels. Consistent with the experimental observations, our model generates spikes and bursts in beta-cell membrane potentials and gives the correct responses to additions of glucose, quinine, and tetraethylammonium ions. The response of the oscillations to ouabain and changing concentrations of external K+ can be incorporated into the present model, although a more complete treatment would require inclusion of the Na+/K+ pump.     

ATP-sensitive potassium channel and bursting in the pancreatic beta cell. A theoretical study.

Based on the existence of ATP-sensitive potassium channels in the plasma membrane of pancreatic beta cells, we develop a quantitative explanation of the electrical activity observed in pancreatic islets. The proposed mechanism involves the voltage-dependent inward calcium and outward potassium currents described by Rorsman and Trube (1986), which are voltage-activated when an increase in the cytoplasmic ATP/ADP ratio decreases the conductance of the ATP-sensitive potassium channels. It is proposed that modulation of the ATP/ADP ratio occurs through calcium inhibition of oxidative phosphorylation. In this picture the mitochondria serve as a transducer of metabolic activity whose sensitivity is modulated by cytosolic calcium. Solution of the differential equations that describe this mechanism gives rise to both bursting and continuous spiking electrical activity similar to that observed experimentally. While the mechanism for bursting in this model involves the ATP/ADP ratio, the feedback is still provided by calcium, as originally proposed by Chay and Keizer (1983) using a Ca2+-activated potassium conductance. A mixed-model, which includes both ATP-sensitive and Ca2+-activated potassium conductances, also reproduces the experimentally observed electrical activity and may correspond more closely to the actual situation in vivo.