In this study, we applied cognitive behavioural intervention to subjects who had painful limited mouth opening, with or without posture correction in daily life. The efficacy of non-intervention control was then compared with it in order to study the effectiveness of posture correction as part of a biobehavioural therapy. The visual analogue scale (VAS) value of pain intensity at maximum mouth opening and disturbance in daily life sharply declined in the group which received only cognitive behavioural intervention and those who received it together with posture correction in daily life compared to the non-intervention control group although there was little difference between the intervention groups. Moreover, pain-free unassisted mouth opening was restored earlier in the group which had added posture correction. This suggests that posture correction in daily life has a positive effect in alleviating myofascial pain with limited mouth opening.
The aim of this study was to clarify the relationship between changes in the occlusal contact area and cervical muscle activity. A decreases in the occlusal contact area using bite planes (stage 1: full contact bite plane, stage 2: bilateral molar removed from contact, and stage 3: bilateral molar and premolar removed from contact) was experimentally simulated in seven subjects (aged 23-25 years) with normal dentition, and muscle activity of the sternocleidomastoid muscle (SCM) and trapezius muscle (TRM) during 50 and 10% of maximum voluntary contraction (MVC) was measured by surface electromyography. The SCM activity during 50% MVC was stage 1: 31.2 +/- 9.4 microV and stage 3: 35.3 +/- 12.3 microV. The TRM activity during 50% MVC was stage 1: 15.2 +/- 0.7 microV and stage 3: 18.3 +/- 2.9 microV. At the 50% MVC, stage 3 showed significant differences in comparison with stage 1 (P < 0.05, anova). These findings suggested that the sternocleidomastoid and TRM play roles in the exertion of occlusal force, and decreases in the occlusal contact area influence the amount of SCM and TRM activity.
The expression of epidermal growth factor receptor (EGFR), epidermal growth factor (EGF), transforming growth factor α (TGFα) and the labeling index of proliferating cell nuclear antigen (PCNA LI) were examined immuno-histochemically in 288 gastric cancer patients, and the relationships between these results and the lymph node metastasis were studied. To investigate the relation between the expression of EGFR and PCNA LI, we divided the patients into the following three groups according to the immunohistochemi-cal findings: group A, EGFR(+); group B, EGFR(-), and EGF(+) or TGFa(+); group C, EGFR(-), EGF(-) and TGFα(-). In the cancers invading submucosal or proper muscle layer, high-PCNA tumors (PCNA LI ≥ 70) in both groups A and B had more frequent lymph node metastasis than in the intermediate-(40-69) and low- ( ≤ 39) PCNA tumors. In the cancers invading subserosal layer or further, the frequency of metastasis in group A was over 78% and was not related to the PCNA range. In group B, metastasis was more frequent in high- and intermediate-PCNA tumors (about 80%) than in low-PCNA tumors (44%). These results suggest that growth regulation by EGFR is related to lymph node metastasis in gastric cancer, and the higher the PCNA LI of cancer cells becomes, the more frequent the occurrence of lymph node metastasis.
The luminal membrane and subapical area of dark cells in the semicircular canal were immunolabeled. The stainable substance in the endolymphatic space was strongly stained. The cytoplasm of epithelial cells was also stained in various patterns.
With regard to the severity of the damage, higher drug concentrations were associated with more severe effects. The severity of damage was the same when the same total dose was used; however, it was found that when the dose was administered over a longer period, the damage region was wider. The functional changes also corresponded with the morphological changes.
We previously purified lysophospholipase D (lysoPLD), which hydrolyzes lysophosphatidylcholine (lysoPC) to lysophosphatidic acid (LPA), from rat brain and identified the heterotrimeric G protein subunits Gαq and Gβ1 in the lysoPLD active fractions. Tag-affinity purified Gαq exhibits lysoPLD activity but a mutant that affected cellular localization or interaction with the Gβ subunit reduced lysoPLD activity. Size exclusion chromatography revealed that active lysoPLD is a much higher molecular mass complex than is heterotrimeric G protein, suggesting the presence of other components. Liquid chromatography–tandem mass spectrometry of lysoPLD purified from rat brain identified glycerophosphodiesterase 4 (GDE4), recently reported as lysoPLD, in the same fraction as G proteins. The overexpressed and tag-purified Gαq fractions, which exhibit lysoPLD activity, contained GDE4. Exogenously expressed GDE4 was co-immunoprecipitated with endogenous Gαq and Gβ and exhibited high lysoPLD activity. The results of confocal microscopy and cell fractionation experiments indicated that exogenously expressed GDE4 in cells mainly localized at the endoplasmic reticulum and partially co-localized with Gαq protein at the plasma membrane. Proteinase K protection assay results suggested that the catalytic domain of GDE4 faces the lumen/extracellular space. Mutations at the conserved amino acids in the C-terminus cytoplasmic regions amongst GDE1, 4 and 7, dramatically suppressed GDE4 enzyme activities. When both the Gαq and Gα11 genes in Neuro2A cells were disrupted using the CRISPR–Cas9 system, endogenous lysoPLD activity was partially reduced but rescued by overexpression of Gαq. These results suggest that GDE4 is a new effector of G protein signaling that produces bioactive phospholipid LPA and/or modulates membrane homeostasis.
Atrial fibrillation (AF) is a progressive disease that starts with structural or functional changes in the left atrium and left ventricle, and evolves from paroxysmal toward sustained forms. Early detection of structural or functional changes in the left atrium and left ventricle in the paroxysmal stage could be useful for identifying higher risk of progression to persistent AF and future cardio-cerebrovascular events. The aim of this study was to test the hypothesis that feature tracking (FT) left atrial (LA) strain and left ventricular (LV) extracellular volume fraction (ECV) derived from cardiovascular magnetic resonance (CMR) could detect the early changes of remodeling in the left atrium and ventricle in the stage of paroxysmal AF (PAF).Participants comprised 106 PAF patients (age, 66.1 ± 10.7 years; 66% male) who underwent clinical CMR before pulmonary vein isolation and 20 control subjects (age, 68.3 ± 8.6 years; 55% male). CMR-FT LA strain/phasic function and LV-ECV were compared between the PAF and control groups. Total and passive LA empty fraction (LAEF) and LA strain (corresponding to LA reservoir and conduit function) were decreased in the PAF group compared to the control group. However, active LAEF (corresponding to LA booster pump function) did not differ significantly between the PAF group (33.9 ± 10.9%) and control group (37.9 ± 13.3%, p = 0.15), while active LA strain (corresponding to LA booster pump function) was significantly decreased in the PAF group (11.4 ± 4.3 vs. 15.2 ± 5.6%, p = 0.002). LV-ECV was significantly greater in the PAF group (28.7 ± 2.8%) than in the control group (26.6 ± 2.0%, p = 0.002). In the PAF group, LV-ECV correlated significantly with E/e’ and LA volume index. Regarding LA strain, correlations were seen between LV-ECV and both reservoir function and conduit function.CMR-FT LA strain in combination with LV-ECV offers a potential imaging marker that identifies LA/LV remodeling including subtle LA booster pump dysfunction undetectable by conventional booster pump LAEF in the stage of PAF. These findings provide new insights into LA-LV interactions and further investigation regarding association between perpetuation of AF and LA functional remodeling in PAF patients.
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