The effect of phenylephrine on the onset time of rocuronium

BACKGROUND: Several studies have demonstrated that ephedrine shortens the onset time of muscle relaxants, and it does so probably by increasing the cardiac output. However, elevation of the systemic blood pressure through α adrenergic stimulation via ephedrine may affect the onset of muscle relaxants during the induction of anesthesia. We investigated the effect of phenylephrine, which is a selective α-1 agonist, on the onset time of rocuronium and the intubating conditions in adults after the administration of propofol. METHODS: Sixty-four patients were randomly assigned to two groups. Phenylephrine (0.9 µg/kg) (P group) or the same volume of saline (S group) was injected before rocuronium (0.6 mg/kg) administration. Anesthesia was induced with fentanyl 2 µg/kg and propofol 2 mg/kg. The onset time was defined as the time from the end of rocuronium injection to the time when a single twitch height gets to 0% or the minimum level. A well-trained anesthesiologist who was 'blinded' to the treatment groups evaluated the intubating conditions. The mean arterial pressure and heart rate were recorded before induction, before intubation, immediately after intubation and 1 minute and 2 minutes after intubation. RESULTS: The onset time was 84 ± 18 sec in the P-group and 72 ± 14 sec in the S-group. There was no difference of the intubating conditions, the mean arterial pressure and the heart rate between the two groups. CONCLUSIONS: A small dose of phenylephrine, which has a limited effect on blood pressure, delayed the onset time of rocuronium after the administration of propofol, and the vasoconstriction effect of phenylephrine may affect the prolongation of the rocuronium onset time at the induction of anesthesia with using propofol.ope

Temperature dependence of Mott transition in VO_2 and programmable critical temperature sensor

The temperature dependence of the Mott metal-insulator transition (MIT) is studied with a VO_2-based two-terminal device. When a constant voltage is applied to the device, an abrupt current jump is observed with temperature. With increasing applied voltages, the transition temperature of the MIT current jump decreases. We find a monoclinic and electronically correlated metal (MCM) phase between the abrupt current jump and the structural phase transition (SPT). After the transition from insulator to metal, a linear increase in current (or conductivity) is shown with temperature until the current becomes a constant maximum value above T_{SPT}=68^oC. The SPT is confirmed by micro-Raman spectroscopy measurements. Optical microscopy analysis reveals the absence of the local current path in micro scale in the VO_2 device. The current uniformly flows throughout the surface of the VO_2 film when the MIT occurs. This device can be used as a programmable critical temperature sensor.Comment: 4 pages, 3 figure

Leukotactin-1/CCL15-induced chemotaxis signaling through CCR1 in HOS cells

AbstractLeukotactin-1 (Lkn-1)/CCL15 is a recently cloned CC-chemokine that binds to the CCR1 and CCR3. Although Lkn-1 has been known to function as a chemoattractant for neutrophils, monocytes and lymphocytes, its cellular mechanism remains unclear. To understand the mechanism of Lkn-1-induced chemotaxis signaling, we examined the chemotactic activities of human osteogenic sarcoma cells expressing CCR1 in response to Lkn-1 using inhibitors of signaling molecules. Inhibitors of Gi/Go protein, phospholipase C (PLC) and protein kinase Cδ (PKCδ) inhibited the chemotactic activity of Lkn-1 indicating that Lkn-1-induced chemotaxis signal is transduced through Gi/Go protein, PLC and PKCδ. The activities of PLC and PKCδ were also enhanced by Lkn-1 stimulation. Chemotactic activity of Lkn-1 was inhibited by the treatment of cycloheximide and actinomycin D suggesting that newly synthesized proteins are needed for chemotaxis. Nuclear factor-κB (NF-κB) inhibitor reduced chemotactic activity of Lkn-1. DNA binding activity of NF-κB was also enhanced by Lkn-1 stimulation. These results suggest that Lkn-1 transduces the signal through Gi/Go protein, PLC, PKCδ, NF-κB and newly synthesized proteins for chemotaxis

Price Rigidity and Means of Payment

The trade-off between cash and a debit card as a means of payment is incorporated into a search-theoretic model. A buyer incurs the proportional cost of carrying cash into the decentralized goods market, and a seller accepting a debit card bears a fixed recordkeeping cost. In an equilibrium, the price of a cash good turns out to be relatively sticky compared with that of a debit-card good. With money supply increasing at a constant rate, the carrying cost of cash proportional to its amount causes the cash balance net of cost to increase at a rate less than the money growth rate. Consumption smoothing also leads to a relatively small decrease in quantity traded in comparison with the increase in cash balance, implying rigid price. Further, the means-of-payment mechanism underlying price rigidity yields an additional distortionary effect of inflation on relative price between cash trade and debit-card trade, which implies higher welfare cost of inflation than that in the standard search-based model