Cortical plasticity: effect of high and low intensity conditioning electrical stimulations (100 Hz) on SEPs to painful finger stimulation.

OBJECTIVE: To study the effect of high-frequency (100 Hz) repetitive conditioning electrical stimulation (CES, 10 min) on human somatosensory evoked potentials (SEPs) to evaluate if short-term cortical plasticity could be induced. METHODS: Painful electrical stimulations were applied to thumb (D1) and little finger (D5) fingertips, respectively. The 124-channel EEG was recorded from 10 healthy male volunteers. Peak stages around 34, 45, 212, 331 ms were analyzed with focal maximum amplitude (FA) and area magnitude (AM) of scalp field potential, topography, and equivalent current dipole source localisation, comparing before and after two-level CES (high- vs. low-level) applied to the He-Gu acupoint. RESULTS: After a high-level CES, the positive FA and AM of the current efflux showed a significant increase at the early phase 34 ms, and significantly decreased at 45 ms in D1 SEPs. The negative FA and AM of the current influx were significantly increased at late phase 350 ms of the D5 SEPs. Only 36 ms, the z-axis position of dipole was significantly changed from (x: -15.9 mm, y: 29.6 mm, z: 43.9 mm) to (x: -12.9 mm, y: 29.4mm, z: 51.5mm) for the D5 SEPs. CONCLUSIONS: The high-level CES significantly attenuated the subsequent cortical activation (45 ms peak for D1 stimulation). Both low- and high-level CES significantly enhanced the late activities (226, 350 ms) in D5 stimulation. This may be explained by pain sensation change at the level of subcortical cingulate cortex induced by the site-dependent post-effect of CES. SIGNIFICANCE: This study showed cortical plasticity induced by conditioning somatosensory stimulation.     

Inter- and intraobserver variability in sonographic measurement of the lower uterine segment after a previous Cesarean section.

OBJECTIVE: To evaluate the reproducibility of sonographic measurement of the lower uterine segment in pregnant women at term. METHODS: Two independent observers performed transabdominal sonography on 129 women between 36 and 38 weeks of gestation who had had a previous Cesarean section. Sonography was performed when the patients had a full and a half-full bladder; in 100 patients, the measurements were also performed transvaginally, with the patients having an empty bladder. Agreement was quantified by the intraclass correlation coefficient and, using a cut-off of 3.5 mm, by the kappa coefficient. RESULTS: The intraobserver agreement was generally high (intraclass correlation coefficient > 0.90). The interobserver agreement was higher on transvaginal (intraclass correlation coefficient, 0.94) compared with transabdominal (0.70 and 0.84, with full and half-full bladder, respectively) ultrasound. The kappa coefficient was 0.75 transvaginally, compared with 0.34 and 0.54 using the transabdominal approach, with full and half-full bladder, respectively. CONCLUSION: The agreement between two observers for sonographic transvaginal measurement of the lower uterine segment can be considered good, compared with poor to moderate agreement using the transabdominal approach.     

Delayed and persistent suppression of bronchoconstriction by trypsin in the airway lumen.

Mucosal trypsin, a protease-activated receptor (PAR) stimulant, may have an endogenous bronchoprotective role on airway smooth muscle. To test this possibility the effects of lumenal trypsin on airway tone in segments of pig bronchus were tested. Bronchial segments from pigs were mounted in an organ chamber containing Kreb's solution. Contractions were assessed from isovolumetric lumen pressure induced by acetylcholine (ACh) or carbachol added to the adventitia. Trypsin, added to the airway lumen (300 microg x mL(-1)), had no immediate effect on smooth muscle tone but suppressed ACh-induced contractions after 60 min, for at least 3 h. Synthetic activating peptides (AP) for PAR1, PAR2 or PAR3 were without effect, but PAR4 AP caused rapid, weak suppression of contractions. Lumenal thrombin was without effect and did not prevent the effects of trypsin. Effects of trypsin were reduced by N(omega)-nitro-L-arginine methyl ester but not indomethacin. Trypsin, thrombin and PAR4 AP released prostaglandin E2. Adventitially, trypsin, thrombin and PAR4 AP (but not PAR2 AP) relaxed carbachol-toned airways after <3 min. The findings of this study show that trypsin causes delayed and persistent bronchoprotection by interacting with airway cells accessible from the lumen. The signalling mechanism may involve nitric oxide synthase but not prostanoids or protease-activated receptors.