Serum thrombospondin-2 is a candidate diagnosis biomarker for early non-small-cell lung cancer.

Thrombospondin-2 (THBS2) is a secreted protein overexpressed in numerous cancers and may function as a diagnostic tumor marker. The objective of the present study was to investigate the diagnostic performance of serum THBS2 in early stage non-small-cell lung cancer (NSCLC). Serum THBS2 and Cyfra21-1 level were evaluated in blood samples of 112 patients from NSCLC groups and 51 healthy control (HC) groups. Receiver operator characteristic (ROC) curves were used to evaluate the diagnostic significance. Serum THBS2 level was significantly up-regulated in NSCLC patients compared with healthy control subjects (P<0.0001), and the postoperative THBS2 level decreased significantly (P<0.0001). ROC curves analysis demonstrated that THBS2 was a comparable biomarker as Cyfra21-1 to distinguish early stage NSCLC or lung squamous cell carcinoma (SC) from healthy control subjects. And Cyfra21-1 was observed with significantly improved performances by the combination of THBS2 to distinguish early stage NSCLC (P<0.05) as well as SC (P<0.05) from the control subjects. In addition, THBS2 was estimated to perform well in the diagnosis of patients with Cyfra21-1-negative NSCLC (area under the curve [AUC] = 0.73). In summary, the present study suggested that serum THBS2 might be an early diagnostic biomarker for NSCLC.

Changes in aortic endothelium ultrastructure in male rats following castration, replacement with testosterone and administration of 5alpha-reductase inhibitor.

AIM: To investigate the relationship between low androgen level and ultrastructure of vascular endothelium. METHODS: Forty-eight male Sprague-Dawley rats were randomly divided into four groups: group A, normal rats with sham castration; group B, castrated rats; group C, castrated rats given testosterone (T) undecanoate; and group D, intact rats treated with 5alpha-reductase inhibitor. After 10 weeks of treatment or castration, rats in different groups were killed and serum T, free T (FT) and dihydrotestosterone (DHT) were measured. The aortic endothelia were scanned under electron microcopy and the Vascular Endothelium Structure Score (VESS) was computed. RESULTS: Serum T and FT concentrations of rats in group B were significantly lower than those of the other three groups (P < 0.01); DHT concentrations of group D rats were significantly decreased (P < 0.01) when compared with those of groups A and C. Rats in groups B and D rats (with low androgen levels) had obvious damage to their endothelial surfaces, which appeared crimpled, rough, adhesive and ruptured, and had high destruction of VESS. CONCLUSION: These results suggest that low concentrations of T and DHT are associated with ultrastructural damage of the aortic endothelia in male rats.

[Protective effect of rosiglitazone on myocardium in diabetic cardiomyopathy of rats].

OBJECTIVE: To investigate the protective effect of PPARgamma ligands rosiglitazone on myocardium in diabetic cardiomyopathy of rats. METHODS: The rat model of diabetes was induced by administration of streptozotocin (STZ) for 6 or 10 weeks. In the treatment group the STZ-induced diabetic rats were treated with rosiglitazone. The left ventricular muscle specimens were taken from treatment and control group; then were examined under transmission electron microscope. RESULT: Cardiac myofibrils of diabetic rats in control group were obviously fewer and broken. There were fewer and smaller dissolved mitochondria with incomplete membrane and mixed cristae and karyopyknosis. Myocardium of diabetic rats treated with rosiglitazone was markedly improved although their blood glucose levels were still high. CONCLUSION: Hyperglycemia can cause destruction of myocardial cell structure. Rosiglitazone has protective effect on myocardial cells of diabetic rats, which seems to be independent of blood glucose levels.