Electromyographic activity and thickness of masticatory muscles in children with unilateral posterior crossbite.

The aim of this study was to assess the electromyographic (EMG) activity and thickness of the masseter and anterior temporalis muscles in children with unilateral posterior crossbite (PCB). Thirty-six children (22 boys, 14 girls, and mean age of 8.8 +/- 1.1 years) were divided into the following groups: The case group with 20 PCB patients (10 on the left side, 10 on the right side); the control group with 16 normal occlusion (NOccl) subjects. EMG activity was recorded with bipolar surface electrodes at rest and during maximal clenching. The muscle thickness was measured with real-time ultrasound. Data were compared between groups and between sides. The correlation between EMG activity and muscle thickness was also evaluated. The data were analyzed using the Shapiro-Wilks test, Pearson's correlation and Spearman as appropriate, paired and unpaired t- test, and Mann-Whitney test. The results revealed that the masseter of the crossbite side was more active than that of the non-crossbite side in PCB group during maximal clenching. The comparisons of EMG activity between PCB and NOccl groups revealed some variability in the results, depending on the crossbite side. The ultrasonographic evaluation did not show statistically significant differences between groups, nor between sides in the PCB and NOccl groups. Significant correlation between EMG activity and thickness was observed only in the left masseter in the NOccl group. In conclusion, these findings showed that asymmetric muscle activity of the masticatory muscles was not related to the thickness of these muscles in children with PCB.

The full length HLA-G1 and no other alternative form of HLA-G is expressed at the cell surface of transfected cells.

In contrast to HLA class Ia, the HLA-G class Ib transcripts can be alternativeley spliced to yield several isoforms including four potentially membrane-bound variants, namely HLA-G1, -G2, -G3 and G4. It is so far unclear whether each of these splice variants lacking one or two external domains is properly translated and expressed at the cell surface. We used targeted Enhanced Green Fluorescence Protein (EGFP)-HLA-G fusion cDNA to track HLA-G isoform expression in living murine (L-human beta2m) and human (JAR) transiently transfected cells. It was demonstrated that the four HLA-G1, -G2, -G3, and -G4 isoforms were translated in these transfectants by the means of (i) Western blotting analysis, using an anti-EGFP mAb; (ii) intracellular double labeling flow cytometry analysis, using the EGFP natural fluorescence and phycoerythrin-labeled HCA2 anti-HLA-G mAb; and (iii) immunocytochemistry on isolated acetone fixed transfectants with the use of different anti-HLA-G mAbs. Cell surface flow cytometry analysis using the HCA2 mAb revealed that only the HLA-G1 isoform was expressed as a membrane-bound protein. Two color confocal microscopy performed on fixed, permeabilized cells further showed that the EGFP green fluorescence co-localized with anti-calnexin rhodamine fluorescence in the four HLA-G isoform transfectants but only in HLA-G1 transfectant was the green EGFP fluorescence also detectable at the outer part of the cells, suggesting that the HLA-G2, -G3, and G4 were retained in the endoplasmic reticulum. Such intracellular retention of the three shorter forms of HLA-G suggest that they may play a role in regulating cell surface expression either of the full length HLA-G1 form or of HLA-E.