1.The clinical study of perioperative depression in brain tumor patients
Hongbo ZHANG ; Yanhui SUN ; Linsen MU ; Jiefei LI ; Mengkai LI ; Boyuan HUANG ; Hui SHEN ; Shichao GUO
Chinese Journal of Nervous and Mental Diseases 2014;(3):129-132
Objective To investigate the clinical features and incidence of depression in patients with different lo-cations and pathological types of brain tumors. Methods Hamilton Depression Scale (HRSD) was used to assess the de-pression in 140 patients with brain tumor before and after operation. Results The preoperative mean depression rating score was 15.36 ± 6.52 and the prevalence rate of depression was 50 cases (35.7%) in 140 patients with brain tumor. The postoperative mean score of depression was 9.71 ± 5.55 and the prevalence rate of depression was 9 cases (6.4%) in 140 patients with brain tumor. The postoperative depression score and the prevalence rate was significantly decreased after op-eration (P<0.05)(χ2=36.10,P<0.05). The postoperative depression score in either benign or malignant brain tumors was significantly lower after than before operation(all P<0.05)The postoperative depression score in either the left or right or bilateral brain lesions were significantly decreased after than before operation(all P<0.05).Conclusion Pa-tients with brain tumors have different degrees of depression in perioperative. Depression may be associated with brain tu-mour pathological types and lesion sites in patients with brain tumors.
2.Macrophage LMO7 deficiency facilitates inflammatory injury via metabolic-epigenetic reprogramming.
Shixin DUAN ; Xinyi LOU ; Shiyi CHEN ; Hongchao JIANG ; Dongxin CHEN ; Rui YIN ; Mengkai LI ; Yuseng GOU ; Wenjuan ZHAO ; Lei SUN ; Feng QIAN
Acta Pharmaceutica Sinica B 2023;13(12):4785-4800
Inflammatory bowel disease (IBD) is a formidable disease due to its complex pathogenesis. Macrophages, as a major immune cell population in IBD, are crucial for gut homeostasis. However, it is still unveiled how macrophages modulate IBD. Here, we found that LIM domain only 7 (LMO7) was downregulated in pro-inflammatory macrophages, and that LMO7 directly degraded 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) through K48-mediated ubiquitination in macrophages. As an enzyme that regulates glycolysis, PFKFB3 degradation led to the glycolytic process inhibition in macrophages, which in turn inhibited macrophage activation and ultimately attenuated murine colitis. Moreover, we demonstrated that PFKFB3 was required for histone demethylase Jumonji domain-containing protein 3 (JMJD3) expression, thereby inhibiting the protein level of trimethylation of histone H3 on lysine 27 (H3K27me3). Overall, our results indicated the LMO7/PFKFB3/JMJD3 axis is essential for modulating macrophage function and IBD pathogenesis. Targeting LMO7 or macrophage metabolism could potentially be an effective strategy for treating inflammatory diseases.