No abstract

Abnormality in the number and function of CD4 + CD25 + FOXP3 + regulatory T cells (Tregs) in peripheral blood has been linked to the initiation and progression of rheumatoid arthritis (RA). Effect of chemokine CCL22 on the number of Tregs in CD4 + T cells and the underlying mechanism were investigated. Downregulation of peripheral Tregs were observed while upregulation of serum chemokine CCL22 in RA patients. Tregs count and the expression of FOXP3 (Tregs function-related maker) and phosphorylated-signal transducer and activator of transcription 5 (p-STAT5) in CD4 + T cells from RA patients were increased while CC chemokine receptor 4 (CCR4) was decreased by anti-CCL22 antibody, however, recombinant CCL22 resulted in the opposite effects in CD4 + T cells from the healthy control. STAT5 inhibitor significantly reversed the effects of anti-CCL22 antibody. Similarly, sinomenine, an anti-arthritis drug, which decreased CCL22 and CCR4, showed the same trends as the above events, and was reversed by recombinant CCL22 or STAT5 inhibitor. Collectively, anti-CCL22 induced the number of Tregs via STAT5 pathway, leading to expansion of Tregs and subsequently to control of the autoimmune reaction in RA patients. Our study provides s novel strategy for RA treatment.

Gastric cancer is the most common digestive malignant tumor worldwild. EDD1 was reported to be frequently amplified in several tumors and played an important role in the tumorigenesis process. However, the biological role and potential mechanism of EDD1 in gastric cancer remains poorly understood. In this study, we are aim to investigate the effect of EDD1 on gastric cancer progression and to explore the underlying mechanism. The results showed the significant up-regulation of EDD1 in -gastric cancer cell tissues and lines. The expression level of EDD1 was also positively associated with advanced clinical stages and predicted poor overall patient survival and poor disease-free patient survival. Besides, EDD1 knockdown markedly inhibited cell viability, colony formation, and suppressed tumor growth. Opposite results were obtained in gastric cancer cells with EDD1 overexpression. EDD1 knockdown was also found to induce gastric cancer cells apoptosis. Further investigation indicated that the oncogenic role of EDD1 in regulating gastric cancer cells growth and apoptosis was related to its PABC domain and directly through targeting miR-22, which was significantly down-regulated in gastric cancer tissues. Totally, our study suggests that EDD1 plays an oncogenic role in gastric cancer and may be a potential therapeutic target for gastric cancer.

No abstract

Intracranial aneurysm may appear even after the removal of the cardiac myxoma. However, the pathogenesis and treatment of such aneurysm lesions are not clear. The study aimed to explore the clinical and imaging manifestation, hypothetical pathogenesis, and therapy in one case of left atrial myxoma causing multiple intracranial aneurysms. A 14-year-old male displayed a 3-hour history of episodic loss of consciousness and right hemiplegia after a leapfrog-like movement. The myxoma was diagnosed by a combination of clinical examination, leading to the diagnosis of mitral dynamic obstruction with a Grade III mitral diastolic murmur and tumor plop; magnetic resonance imaging, revealing multiple ischemic sites in both semi-oval centers; and transthoracic echocardiography, demonstrating a mitral valve obstruction.The myxoma was removed surgically; however, computed tomography angiography showed multiple intracranial aneurysms in both middle cerebral arteries 18 months after resection of the atrial myxoma. After conservative treatment, the patient had no neurological dysfunction symptoms for 5 years after myxoma resection. His condition is relatively stable. In conclusion, resection of the atrial myxoma may eliminate the early neurological symptoms, but it cannot ensure the nonoccurrence of delayed intracranial aneurysms. The neoplastic process theory was favored for explaining the aneurysm development in this case. According to the specific conditions of the patient, a combination of open surgery, chemotherapy, radiotherapy, and coil embolization is recommended.