Relation between excessive CO2 expiration and performance in high-intensity exercise

This study examined the relation between excessive CO2 expiration and exercise performance in exercise exhausted for 1-2 min. First, the Wingate test was conducted to determine the exercise intensity of the performance test. The exercise intensity was set at 80% of the power exerted during the last 5 s of the Wingate test so that subjects could continue for 1-2 min. Total work, which was the value of the work rate times the performed duration was used as an index of the performance level. The excessive CO2 expiration rate (‡CO2excess) was defined as the difference between CO2 output and O2 uptake. Integration of ‡CO2excess from the start of exercise to the zero level of ‡CO2excess observed at around 10 min in recovery was defined as the amount of excessive CO2 expiration (CO2excess). The performance was associated with the peak value of blood lactate (peak La) obtained after exercise (r=0.744). The performance was also associated with CO2excess (r=0.848). It is likely that CO2excess is a better physiological index for assessing the performance in exercise exhausted for 1-2 min than peak La

Rectangular model of a ballistic spin interferometer in (001) InGaAs/InAlAs quantum wells

We report an unambiguous detection of the crytalline anisotropy of the spin-orbit interaction in (001) InAlAs/InGaAs/InAlAs quantum wells using nanofabricated rectangular loop arrays, where the sides of the constituent loops are aligned along either the [110] or [110￣] crystallographic axis. The fabrication and measurements were performed on the epi-wafer samples whose spin properties were characterized previously [Koga et al., Phys. Rev. Lett 89, 046801 (2002)]. We find that the experimentally observed spin interference patterns ― the amplitude modulation of the Al'tshuler-Aronov-Spivak oscillations as a function of the gate voltage ― are in good agreement with the results of the spin interferometer model extended for rectangular loops and including both the Rashba and Dresselhaus spin-orbit interactions

Heterozygous mutations in cyclic AMP phosphodiesterase-4D (PDE4D) and protein kinase A (PKA) provide new insights into the molecular pathology of acrodysostosis

Acrodysostosis without hormone resistance is a rare skeletal disorder characterized by brachydactyly, nasal hypoplasia, mental retardation and occasionally developmental delay. Recently, loss-of-function mutations in the gene encoding cAMP-hydrolyzing phosphodiesterase-4D (PDE4D) have been reported to cause this rare condition but the pathomechanism has not been fully elucidated. To understand the pathogenetic mechanism of PDE4D mutations, we conducted 3D modeling studies to predict changes in the binding efficacy of CAMP to the catalytic pocket in PDE4D mutants. Our results indicated diminished enzyme activity in the two mutants we analyzed (Gly673Asp and Ile678Thr; based on PDE4D4 residue numbering). Ectopic expression of PDE4D mutants in HEK293 cells demonstrated this reduction in activity, which was identified by increased CAMP levels. However, the cells from an acrodysostosis patient showed low cAMP accumulation, which resulted in a decrease in the phosphorylated CAMP Response Element-Binding Protein (pCREB)/CREB ratio. The reason for this discrepancy was due to a compensatory increase in expression levels of PDE4A and PDE4B isoforms, which accounted for the paradoxical decrease in cAMP levels in the patient cells expressing mutant isoforms with a lowered PDE4D activity. Skeletal radiographs of 10-week-old knockout (KO) rats showed that the distal part of the forelimb was shorter than in wild-type (WT) rats and that all the metacarpals and phalanges were also shorter in KO, as the name acrodysostosis implies. Like the G-protein a-stimulatory subunit and PRKAR1A, PDE4D critically regulates the cAMP signal transduction pathway and influences bone formation in a way that activity-compromising PDE4D mutations can result in skeletal dysplasia. We propose that specific inhibitory PDE4D mutations can lead to the molecular pathology of acrodysostosis without hormone resistance but that the pathological phenotype may well be dependent on an over-compensatory induction of other PDE4 isoforms that can be expected to be targeted to different signaling complexes and exert distinct effects on compartmentalized CAMP signaling. (C) 2014 Published by Elsevier Inc.X112521sciescopu