The Correlation Between 18F-Fluorodeoxyglucose-Positron Emission Tomography/Computed Tomography Semiquantitative Parameters and the Clinical Features and Pathological Biological Indexes of Gastric Cancer.

Objective: This study explored the application value of the maximum standard uptake value (SUVmax) of 18F-fluorodeoxyglucose-positron emission tomography/computed tomography (18F-FDG PET/CT) in gastric cancer. Materials and Methods: Data of 164 patients with gastric cancer who had undergone18F-FDG PET/CT before a biopsy were collected, and the correlation of SUVmax with clinical stage, pathological differentiation degree, human epidermal growth factor receptor-2 (HER-2) status, and Ki-67 index of gastric cancer was analyzed. Results: The SUVmax of poorly differentiated adenocarcinoma was significantly higher than that of moderately differentiated adenocarcinoma and signet-ring cell carcinoma (p < 0.01), and SUVmax in the well-differentiated adenocarcinoma group was higher than that in the signet-ring cell carcinoma group (p < 0.01). The SUVmax in the HER-2 negative group was higher than that in the HER-2 positive group (p < 0.01). The SUVmax was higher in the Ki-67 high expression group than in the low expression group (p < 0.01), and there was a significant positive correlation between the two (p < 0.01). Conclusion: 18F-FDG PET/CT SUVmax can, to some extent, predict the degree of differentiation, HER-2 status, and Ki-67 index of gastric cancer patients.

[Effect of Bone Marrow Mesenchymal Stem Cells in Patients with Multiple Myelima on Migration of Myeloma Cells In Vitro].

OBJECTIVE: To explore the effect of bone marrow mesenchymal stem cells (MSC) in patients with multiple myeloma(MM) on chemotactic migration of myeloma cells in vitro. METHODS: By in vitro co-culture with diffferent MSC, the myeloma cell U266 was divided into 2 groups: group A in which the U266 cells were co-cultured with normal person MSC (N-MSC) and group B in which the U266 cells were co-cultured with MM-MSC. The expression level of CCR1 in U266 cells, migration rate of U266 cells in Transwell, and the effect of supernantant from co-culture of U266 cells with N-MSC and MM-MSC on the migration in Transwell were compared in condition with or without bortezomib. RESULTS: After co-culture of U266 cells with N-MSC or MM-MSC, the migration rate of U266 cells in Transwell in B group was higher than that in A group(P<0.05). The difference between 2 groups could not be eliminated after treatment of U266 cells with bortezomib. The CCR1 expression level of U266 cells in B group was higher than that in A group (P<0.05). The culture supernatant of bone marrow MSC showed that in condition without bortezomib the culture supernatant of MSC in MM patients and normal persons both possessed more strong chemotactic ability and enhanced the migration rate of cells in Transwell, compared with SDF-1, meanswhile the culture supernatant in 3 groups reduced the migration rate of cells in condition with bortezomib (P<0.05), but there were no statistical difference in migration rate of U266 cells in Transwell between supernatant of N-MSC and MM-MSC culture (P>0.05), no matter the bortezonib was used or not. CONCLUSION: The bone marrow MSC in MM patients have same intrinsic defects that affect the chemotaxis of cells in vitro by directly interacting with myeloma cells.

Treatment of thoracic hemorrhage due to rupture of traumatic mediastinal hematoma.

Patients in traffic accidents are usually presented with pain and bleeding due to fractures or soft tissue injury. On some occasions, more severe complications may be triggered by the trauma. A review of the published English language literature reveals no survival case once the traumatic mediastinal hematoma is ruptured. In our case, a 54-year-old man suffering motorcycle accident was admitted to emergency department. Computed tomography scan revealed subdural hematoma combined with posterior mediastinal hematoma. The patient was saved and discharged with a satisfactory outcome. Here we hope to share our treatment experience in dealing with the patient with severe multiple trauma.

Mimic of manganese superoxide dismutase induces apoptosis in human acute myeloid leukemia cells.

Abstract Increasing manganese superoxide dismutase (MnSOD) expression can suppress the malignant phenotype in various cancer cell lines and suppress tumor formation in xenograft and transgenic mouse models. A mimic of manganese superoxide dismutase (MnSODm), synthesized by a chemical method, has been shown to possess antitumor properties. However, the anticancer activity of MnSODm in acute myeloid leukemia (AML) is still obscure. In this study, we investigated the effects of MnSODm on the apoptosis of human leukemia HL-60 cells. Results showed that MnSODm significantly reduced the proliferation of HL-60 cells in a concentration- and time-dependent manner. By flow cytometric analysis, we found that MnSODm treatment resulted in increased apoptosis in HL-60 cells. Further analysis demonstrated involvement of activation of the caspase cascade, cleavage of poly(ADP-ribose) polymerase (PARP) and release of cytochrome c in MnSODm-induced apoptosis. The results also showed that the expression of anti-apoptotic Bcl-2 and Bid were dose-dependently decreased, whereas the expression of pro-apoptotic Bax protein was increased. Thus, MnSODm induced apoptosis in HL-60 cells via mitochondria-mediated, caspase-dependent pathways. MnSODm inhibition of Akt phosphorylation may contribute to MnSODm-mediated acute myeloid leukemia cell growth inhibition and apoptosis induction.

Mimic of manganese superoxide dismutase to induce apoptosis of human non-Hodgkin lymphoma Raji cells through mitochondrial pathways.

Increased reactive oxygen species (ROS) such as superoxide have been implicated as causal elements of oncogenesis. A variety of cancers have displayed changes in steady-state levels of key antioxidant enzymes, with the mitochondrial form of superoxide dismutase (MnSOD) being commonly implicated. Increasing MnSOD expression suppresses the malignant phenotype in various cancer cell lines and suppresses tumor formation in xenograft and transgenic mouse models. In this study, we examined the anti-proliferation effect of mimic of manganese superoxide dismutase (MnSODm) on human non-Hodgkin lymphoma Raji cells. The results showed that MnSODm significantly reduced the proliferation of Raji cells in a concentration and a time-dependent manner. By flow cytometric analysis, we found that MnSODm treatment resulted in an increased apoptosis in Raji cells. MnSODm also increased the production of ROS and the expression levels of cleaved caspase-9, caspase-3, poly (ADP-ribose) polymerase (PARP) and Bax in Raji cells. Moreover, the expression of Bcl-2 protein showed down-regulation in the MnSODm treatment group. In addition, MnSODm significantly elevated the level of cytochrome c in cytosol. These findings suggest that the activation of the mitochondrial pathway is involved in MnSODm-induced apoptosis in Raji cells.