BACKGROUND:Lots of in vitro experiments have explored the toxicity of upconversion nanoparticles, but its toxicity in vivo is little reported. OBJECTIVE:To investigate the toxicity of upconversion nanoparticles in mouse organs. METHODS:After tracheotomy, 36 Balb/c mice were randomly divided into three groups, fol owed by instil ed with 28 mg/kg upconversion nanoparticle (experimental group), the same volume of normal saline (control group), and nothing (sham operation group), respectively. The functional changes of the lung, liver and kidney were detected at 1 day, 1 and 2 weeks postoperatively, and meanwhile, the morphological changes of the lung, liver, kidney, and heart were observed. RESULTS AND CONCLUSION:At 1 day postoperatively, the pH values in the experimental group were lower than those in the control and sham operation groups (P<0.05), while the glutamic-pyruvic transaminase level was higher than that in the control and sham operation groups (P<0.05). The oxygen partial pressure in the sham operation group was higher than that in the other two groups at 1 day postoperatively (P<0.05). The oxygen partial pressure and glutamic-pyruvic transaminase level did not significantly differ among groups at 1 and 2 weeks postoperatively. The carbon dioxide differential pressure and kidney function showed no significant differences among groups at different time points after surgery. At postoperative 1 day, in the experimental group, hyperplasia and inflammation were most obvious, distorted alveolar cavity and congestion of blood vessels were visible. In the control group, obvious hyperplasia and inflammation were found, the alveolar cavity was crimped and the gap between alveoli was broadened. The sham operation group had normal alveoli with no inflammations. Lung lesions in the experimental and control groups became mild with time at postoperative 1 and 2 weeks. One day postoperatively, hepatocyte swel ing and vacuolar degeneration were severer in the experimental group. Moderate hepatocyte swel ing and vacuolar degeneration occurred in the control group. The sham operation group showed mild hepatocyte swel ing and vacuolar degeneration. The morphology of the liver in each group returned to normal at 2 weeks postoperatively. Fortunately, the heart and kidney structure showed no overt changes in each group. These findings suggest that upconversion nanoparticles cause transient damage to the mouse lung and liver.

Objective To study the relationship between viral infection and chronic obstructive pulmonary disease (COPD),and the effect of viral infections on the changes of Th1/Th2 in COPD patients. Methods The se-ra from 81 patients with acute exacerbations of COPD,25 patients with stable COPD and 22 healthy subjects were tested for specific IgM of respiratary syncytial virus(RSV) ,herpes simplex virus type 1 (HSV-1), parainfluenza vi-rus (PIV), adenovirus (ADV) and cytomegalovirus (CMV) by indirect enzyme-linked immunosorbent assay (ELISA). Supernatant INF-γ and IL-4 cultured with PHA were determined. Results The positive rates of IgM in patients with acute exacerbations of COPD compared with those in patients with stable COPD and healthy subjects were significantly different(P <0.001 ). The level of INF-γ, and IL-4 in patients with acute exacerbations of COPD and stable COPD compared with normal control group;the level of INF-γ (242±43) and the of IL-4(42±9) in pa-tients with acute exacerbations of COPD was not significantly different as compared with the level of INF-γ( 198±32) and the level of IL-4(56±11 ) in patients with stable COPD (P<0.05), but the level of INF-γ was increased (90±18)and IL-4 was decreased (141±24) in control group (P<0.05). Compared with those in IgM negative group, the levels of INF-γ were significantly higher and the levels of IL-4 were significantly lowerIL-4 in lgM positive group( P<0.01 ). Conclusion Virus infection is a rather important factor in acute exacerbations of COPD, and COPD is characterized by a predominance of Th1-type response,and there is more significant Th1 response predomi-nance in COPD with virus infection.