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Studies have shown cell鄄 free microRNA (miRNA) circulating in the serum and plasma with specific expression in cancer, indicating the potential of using miRNAs as biomarkers for cancer diagnosis and therapy. This study was to investigate whether plasma miRNA鄄 21 (miR鄄 21) can be used as a biomarker for the early detection of non-small cell lung cancer (NSCLC) and to explore its association with clinicopathologic features and sensitivity to platinum鄄 based chemotherapy. We used real鄄 time RT鄄 PCR to investigate the expression of miR鄄 21 in the plasma of 63 NSCLC patients and 30 healthy controls and correlated the findings with early diagnosis, pathologic parameters, and treatment. Thirty鄄 five patients (stages IIIB and IV) were evaluable for chemotherapeutic responses: 11 had partial response (PR); 24 had stable and progressive disease (SD+ PD). Plasma miR鄄 21 was significantly higher in NSCLC patients than in age鄄 and sex鄄 matched controls (P < 0.001). miR鄄 21 was related to TNM stage (P < 0.001), but not related to age, sex, smoking status, histological classification, lymph node status, and metastasis (all P > 0.05). This marker yielded a receiver operating characteristic (ROC) curve area of 0.775 (95% CI: 0.681 -0.868) with 76.2% sensitivity and 70.0% specificity. Importantly, miR鄄 21 plasma levels in PR samples were several folds lower than that in SD plus PD samples (P = 0.049), and were close to that in healthy controls (P = 0.130). Plasma miR鄄 21 can serve as a circulating tumor biomarker for the early diagnosis of NSCLC and is related to the sensitivity to platinum鄄 base chemotherapy.

Pulse field gradient diffusion measurements of pentane in a random copolymer of tetrafluoroethylene (TFE) and 2,2-bis(trifluoromethyl)-4,5-difluoro-1,3-dioxole (PDD) were made as a function of the time allowed for diffusion to occur. The initial change in echo amplitude at low values of q = γδg was used to determine the apparent diffusion constant. The apparent diffusion constant determined in this way decreases to a constant value as time increases. At a time of 12.4 ms the apparent diffusion constant was 2.2 × 10-7 cm2 s-1, and it decreases to 5.87 × 10-8 cm2 s-1 at 1 s. This change in the apparent diffusion constant was interpreted in terms of morphological structure on the micron length scale in this completely amorphous glassy polymer. This polymer has been considered to have high free volume regions which lead to the observed rapid permeation of gases and vapors. These regions are interspersed in lower free volume regions, and the low free volume regions constitute the majority component. In the pulse field gradient NMR experiment, regions allowing for rapid diffusion interspersed with regions allowing only slow diffusion can lead to changes in the apparent diffusion constant as a function of diffusion time. The data observed in this system were compared with two simple models for the topology of the regions allowing for rapid diffusion:  restricted diffusion and tortuous diffusion. The observed behavior is qualitatively similar to tortuous diffusion and can be fit with an equation describing this type of diffusion.

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Abstract. Tanshinone IIA is known to induce apoptosis in several types of cancer cells. However, little is known about its activity in chemoresistant cells. The aim of this study was to investigate the anticancer properties of tanshinone IIA in cisplatin-resistant human ovarian cancer COC1/DDP cells in vitro. We used a variety of methods to measure cell viability, the resistance index (RI) of cisplatin, cellular apoptosis, p38 mitogen-activated protein kinase (MAPK) expression and phosphorylation, and the mRNA expression of several genes implicated in drug resistance including survivin, Caspase-3, excision repair cross-complementing gene 1 (ERCC1), multidrug resistance (MDR), lung resistance protein (LRP) and glutathione-S-transferase-π (GST-π). We found that tanshinone IIA time-and dose-dependently inhibited the proliferation of COC1/DDP cells and caused significant apoptosis. Western blotting revealed that tanshinone IIA also increased phospho-p38 MAPK in a time-and dose-dependent manner. After treatment by tanshinone IIA for 48 h, the RI of cisplatin and the mRNA expression of survivin, ERCC1 and LRP were all significantly decreased. Furthermore, blockade of p38 signal transduction decreased apoptotic cell rates and dramatically elevated the mRNA expression of the survivin, ERCC1 and LRP genes. We therefore conclude that tanshinone IIA induces apoptosis and reduces cisplatin resistance in COC1/DDP cells and thus causes significant growth inhibitory effects. This mechanism appears to involve p38-mediated downregulation of survivin, ERCC1 and LRP mRNA expression.