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Persons with Type 1 diabetes can participate safely in prolonged fasts provided they reduce their usual insulin dose significantly and adhere to guidelines regarding glucose monitoring and indications for terminating fasting.

Since the first implantation of a cardiac pacemaker in the second half of the 20th century, there have been evolutionary and revolutionary advances in the technology developed for patients with heart rhythm disturbances. These advances, however, have instead failed to demonstrate that mimicry of physiology by a pacing system would deliver a longer and better life to its recipient. Indeed, we are just now in the process of developing a new paradigm in pacing that may finally deliver physiology to the hyperbolically named "physiologic pacing." This article will discuss the reasons for the discrepancy between the earlier studies and the more recent ones, as well as a review of implantable cardioverter-defibrillator trials, keeping in focus the special needs of aged heart rhythm device recipients.

Shamouti phosphofructokinase (PFP) activation depends on the presence of fructose 2,6-bisphosphate (Fru-2,6-P2) in the glycolytic reaction. The effect of activation by Fru-2,6-P2 differs considerably, however, according to the buffer (pH 8.0) in which the reaction is performed: Ka = 2.77 +/- 0.3 nM in Hepes-NaOH and 7.75 +/- 1.49 nM in Tris-HCl. The presence of chloride ions (39 mM) in the Tris-HCl buffer inhibits PFP. Indeed, when using a Hepes-NaOH buffer and then adding 39 mM NaCl, Ka = 8.12 +/- 0.52 nM. The Ki for chloride ions is approximately 21.7 mM. In the gluconeogenic reaction, Shamouti PFP generally showed a high endogenous activity. Addition of Fru-2,6-P2 did not modify the velocity and the Vmax of the enzyme; however, its presence increased the affinity of the enzyme for Fru-1,6-P2 from 200 +/- 15.6 microM in absence of Fru-2,6-P2 to 89 +/- 10.3 microM in its presence (10 microM). In the presence of chloride (39 mM), the affinity for the substrate decreased with K(m) = 150 +/- 14 microM. The calculated Ki for chloride ions equals 56.9 mM. In both the glycolytic and the gluconeogenic reactions, Vmax is not affected; therefore, the inhibition mode of chloride is competitive.