Macroscopic technique for the evaluation of oral tongue tumour thickness: a reliable intraoperative method.

There is no reliable method to assess tumour thickness preoperatively or intraoperatively in cases of oral tongue squamous cell carcinoma (SCC). The purpose of this study was to evaluate the efficacy of a macroscopic technique to measure tumour thickness. This was a prospective study of 51 consecutive patients with T1/T2 primary SCC of the oral tongue. All patients underwent primary resection with ipsilateral neck dissection. Thickness measurements were obtained using Vernier calipers on the fresh specimen. The technique was correlated with the microscopic evaluation statistically using (1) Pearson's correlation coefficient, (2) intra-class correlation, and (3) Bland-Altman plot with 95% confidence intervals. On comparing the macroscopic technique to the microscopic evaluation, Pearson's correlation (r) was 0.915 (P<0.001). The inter-rater reliability using the intra-class correlation coefficient was 0.955. The Bland-Altman plot to test the agreement between the techniques showed the average difference between macroscopic thickness and microscopic thickness (bias) to be -0.421, with 95% limits of agreement of -3.166 and 2.82. There was a significant correlation and agreement between the macroscopic and microscopic measures of tumour thickness. The macroscopic technique could be used as a reliable tool to measure tumour thickness intraoperatively, prior to neck dissection.

Extraction of ternary complexes of thorium(IV) with 3-phenyl-4-benzoyl-5-isoxazolone and neutral donors from nitric acid medium.

The extraction behaviour of thorium(IV) from aqueous nitric acid employing 3-phenyl-4-benzoyl-5-isoxazolone (HPBI) in the presence of tri-n-octyl phosphine oxide (TOPO) as well as tri-n-butyl phosphate (TBP) in xylene medium was investigated. The extraction constant (log k(ex)) for the binary organic phase species Th(PBI)(4) was determined to be 8.26 which is by far the largest amongst the corresponding values known for other beta-diketones. The overall extraction constant (log K) for the ternary species Th(PBI)(4) TBP and Th(PBI)(4).2TOPO were estimated to be 14.96 and 20.96 respectively. An inverse correlation of the adduct formation constant (log K(s)) with the pK(a) of the beta-diketones, 2-thenoyltrifluoroacetone, 1-phenyl-3-methyl-4-benzoyl-5-pyrazolone and HPBI, was observed. The steric as well as the electronic effects of adduct formation have been discussed. Analytical application of HPBI for the separation of (234)Th radiotracer from natural uranium (99.3% (238)U) has been suggested.

Potassium channel activators differentially modulate the effect of sodium channel blockade on cardiac conduction.

AIMS: Diminished repolarization reserve contributes to the arrhythmogenic substrate in many disease states. Pharmacological activation of K(+) channels has been suggested as a potential antiarrhythmic therapy in such conditions. Having previously demonstrated that I(K1) and I(Kr) can modulate cardiac conduction, we tested here the effects of pharmacological I(KATP) and I(Ks) activation on cardiac conduction and its dependence on the sodium current (I(Na)). METHODS AND RESULTS: Bath electrocardiograms (ECGs) recorded from Langendorff-perfused guinea pig ventricles revealed QRS prolongation during I(KATP) activation by pinacidil but not during I(Ks) activation by R-L3 relative to control. In contrast, when I(Na) was partially blocked by flecainide, R-L3 but not pinacidil prolonged the QRS relative to flecainide alone. Conduction velocity (θ) was quantified by optical mapping during epicardial pacing. Both longitudinal (θ(L)) and transverse (θ(T)) θ were reduced by pinacidil (by 10 ± 1 and 9 ± 3%, respectively) and R-L3 (by 11 ± 2% and 15 ± 4%, respectively). Flecainide decreased θ(L) by 33 ± 4% and θ(T) by 36 ± 5%. Whereas pinacidil did not further slow θ relative to flecainide alone, R-L3 decreased both θ(L) and θ(T). CONCLUSION: Pharmacological activation of I(KATP) and I(Ks) slows cardiac conduction; however, they demonstrate diverse effects on θ dependence on I(Na) blockade. These findings may have significant implications for the use of K(+) channel activators as antiarrhythmic drugs and for patients with Na(+) channel abnormalities or being treated with Na(+) channel blockers.