The functional and structural abnormalities of the ACC in FGIDs have been widely investigated. Similar to the insula, the activation of the ACC was commonly seen in neuroimaging studies on FGIDs. Our previous PET-CT study indicated that cerebral glycometabolism of the ACC in FD patients was significantly higher than that in the HS, and that the abnormal hyperactivity of the ACC was associated with symptoms and QOL of patients. Furthermore, some neuroimaging studies on IBS patients found a cortical thinning and a GMD increase in the ACC. In this study, we found that regional GMD in the bilateral ACC of the meal-related FD patient significantly decreased compared to the HS, and that the GMD decrease in the ACC was negatively correlated with the scores of symptoms and disease duration respectively. However, after correcting for depression and anxiety, the peak of GMC decrease within the ACC did not survive. Our result are consistent with Seminowicz DA’ s findings. His study on IBS patients also showed that inclusion of anxiety and depression together as covariates removed the group differences in the left pregenual ACC. A recent metaanalysis indicated that gray matter reduction in the ACC was the most consistent finding in VBM studies of major depressive disorder. The present results indicated that although the ACC is involved in multiple functions, such as the gastrointestinal signal process and emotional and cognitive controls, the anatomic alterations in the ACC in the meal-related FD patients were more likely to be associated with emotional changes and could be attributed neither to the durations nor to the symptoms. In summary, this study demonstrated the cerebral morphometric alterations in the meal-related FD patient and the influence of psychological factors on the regional brain structure. Although the majority of the structure-changed regions were related to emotional and cognitive processes, psychosocial dysfunction could not fully explain the microstructural alterations. The cerebral microstructural changes in the meal-related FD patients might be induced by multiple factors, including abnormal sensory input and psychosocial dysfunction, etc.Is HE4 secreted by ovarian cancer patients in the highly glycosylated form? Is there a heteroplasmon of HE4 like AFP-L3? Can Lewis y antigen be effectively utilized as a specific marker for monitoring the disease? These issues remain to be resolved.Our preliminary data indicated that Lewis y antigen is a component of HE4, and both are expressed at high levels in ovarian cancer, which was further confirmed using correlation analysis. Lewis y antigen of HE4 may thus contribute to changes in specific biological behaviors, including adhesion and migration of ovarian carcinoma cells, via the corresponding signal transduction pathways. However, the specific mechanisms underlying the activities of HE4 and Lewis y antigen in ovarian cancer development are currently unclear. To explain the occurrence and development of ovarian cancer, and aid in clinical diagnosis and assessment.