In order to investigate the feasibility of serum creatine kinase (CK) and blood urea nitrogen (BUN) in monitoring pre-competition training of badminton athletes, the pre-competition training load of 20 badminton athletes was studied, and serum CK and BUN were determined before, immediate and next morning after training. The results showed that after intensive training for one week, serum CK levels were significantly increased by 57.53 mmol/L (P<0.05). After regulation of the training intensity, average serum CK levels were increased by 21.79 mmol/L (P<0.05). BUN contents were increased by 0.83 mmol/L on average with the difference being not significant (P>0.05). After intermittent training, there was significant difference in the average increased levels of serum CK in athletes (P<0.05). There was significant difference before and after regulation of training (P<0.05). The increased levels of BUN were 0.78 mmol/L without significant difference (P>0.05). It was concluded that serum CK was one of the biochemical indicators monitoring the training load sensitivity of badminton athletes, but BUN was of little value in monitoring the training load. Both serum CK and BUN recovered slowly after one-week intensive training and intermittent training, suggesting the metabolic mechanism of human body in training needs further study.

In order to investigate the effect of curcumin on proliferation and apoptosis of human pterygium fibroblasts (HPF) in culture and search for a new method to prevent the recurrence after pterygium surgery, HPF was incubated with 0–160 μmol/L curcumin for 24–96 h. The MTT method was used to assay the biologic activities of curcumin at different time points and different doses. The expression of proliferating cell nuclear antigen (PCNA) in each group was detected by immunohistochemistry. The cell cycle distribution was detected by flow cytometry (FCM). Administration of 20–80 μmol/L curcumin for 24–72 h could significantly inhibit HPF proliferation in a dose-and time-dependent manner (P<0.05). After treatment with curcumin at different concentrations of 20, 40, 80 and 160 μmol/L for 24 h, FCM revealed there was a significant sub-G1 peak at each concentration. The number of HPF in G₀/G₁ phase was increased, while in S phase, it was decreased (P<0.05). At the concentration of 20–80 μmol/L, curcumin, in a dose-dependent manner (P<0.05), could inhibit the expression of PCNA in HPF. It was suggesterd that curcumin could significantly inhibit the proliferation of HPF, make HPF arrest in G₀/G₁ phase and induce the apoptosis of HPF in a dose-and time-dependent manner.

The validity of ^99mTc-YIGSR, a novel receptor radio-tracer, in imaging the Ehrlich ascites tumor was evaluated. YIGSR, a pentapeptide of laminin, was labeled with ^99mTc by using a bifunctional chelator S-Acetly-NH₃-MAG₃. The MIBI was labeled with ^99mTc by following the kit instruction. The mice of tumor group were intravenously injected 1–2 mCi of ^99mTc-YIGSR or ^99mTc-MIBI via caudal vein, immobilized and imaged under a Gamma camera. The same procedure was performed in mice of blockade group, in which the unlabeled YIGSR was previously injected to block the receptor-recognition sites, and inflammation group serving as control. The reverse-phase Sep-Pak C₁₈ chromatogram was found to have an essentially complete conjugation between YIGSR and S-Acetly-NH₃-MAG₃. The conjugated YIGSR could be radio-labeled successfully with ^99mTc at room temperature and neutral pH, with a radio-labeling yield of 62%. Without the chelator S-Acetly-NH₃-MAG₃, the YIGSR was labeled with ^99mTc at an efficiency of 4%. The imagological study revealed obvious tumor accumulation of ^99mTc-YIGSR 15 min after the injection, and the uptake peaked after 3 h with a tumor-to-muscle ratio (T/M) of 11.36. The radio-tracer was slowly cleared up and resulted in a T/M of 3.01 at the 8th h after the injection. As for blocked group, the tumor uptake of radiotracer was significantly lower, with the highest T/M being 4.61 after 3 h and 0.89 after 8 h. The T/M was 3.72 at the 3rd h and 1.29 at the 8th h after the ^99mTc-YIGSR injection in the inflammatory group. The T/M was significantly higher in tumor group than in inflammatory group or control group (P<0.001). In the 99mTc-MIBI group, the T/M was 1.40 at the 3rd h and 0.55 at the 8th h after the injection, which showed a significant difference as compared with ^99mTc-YIGSR (P<0.001). It is concluded that YIGSR can be successfully radiolabelled by using S-Acetly-NH₃-MAG₃. ^99mTc-YIGSR has many advantages in tumor imaging, such as quick and clear visualization, high sensitivity and specificity, and satisfactory target/non-target ratio (N/NT). It promises to be tumor radio-tracer.

In order to explore the role of TGF-β1 in scleral remodeling and the possible mechanism, the influence of high level TGF-β1 on scleral thickness and the expression of MMP-2 and TIMP-2 was investigated in a TGF-β1 transgenic mouse model. Alb/TGF-β1 (Cys^223,225Ser) TGF-β1 transgenic mice were used as experimental subjects and non-transgenic littermates as controls. Plasma levels of TGF-β1 were determined by ELISA. TGF-β1, MMP-2 and TIMP-2 levels in sclera were detected by using Western blot. The thickness of posterior sclera was measured by computerized image analysis of a midsagittal section. Mean difference was analyzed with independent t-test. The results showed plasma levels of TGF-β1 in transgenic mice were 1.68 times as much as that in the controls (P<0.01). TGF-β1 levels in the sclera of transgenic mice were 2.68 times of the controls (P<0.01). Posterior scleral thickness in transgenic mice were significantly thicker than in the controls. There was no significant difference in the MMP-2 levels between transgenic mice and controls, but the TIMP-2 levels were increased significantly in transsgenic mice as compared with those in the controls. It was suggested that high levels of TGF-β1 in transgenic mice could result in the increased scleral thickness by inducing the expression of TIMP-2 to suppress the activity of MMP-2, finally inhibiting the degradation of collagen.

In order to investigate the role of TNF-and ICAM-1 in the pathogenesis of lichen planus, immunohistochemistry was used to detect the expression of TNF-and ICAM-1 in skin lesions of the patients with lichen planus and skin tissues of normal subjects. The results showed that positive rates of TNF-α and ICAM-1 expressions in lichen planus were significantly higher than those in normal skins (both P<0.05). Meanwhile, there was a obvious correlation between the increase of TNF-α and that of ICAM-1 in lichen planus. The expression of TNF-α and ICAM-1 might play an important role in the development of lichen planus.