Serum periostin is useful for detecting chronic rhinosinusitis with nasal polyps and predicting radiological chronic rhinosinusitis severity in patients with asthma. Clinical trial registered with the UMIN Clinical Trials Registry (UMIN000017533).

BackgroundAlthough several computer-aided computed tomography (CT) analysis methods have been reported to objectively assess the disease severity and progression of idiopathic pulmonary fibrosis (IPF), it is unclear which method is most practical. A universal severity classification system has not yet been adopted for IPF.ObjectiveThe purpose of this study was to test the correlation between quantitative-CT indices and lung physiology variables and to determine the ability of such indices to predict disease severity in IPF.MethodsA total of 27 IPF patients showing radiological UIP pattern on high-resolution (HR) CT were retrospectively enrolled. Staging of IPF was performed according to two classification systems: the Japanese and GAP (gender, age, and physiology) staging systems. CT images were assessed using a commercially available CT imaging analysis workstation, and the whole-lung mean CT value (MCT), the normally attenuated lung volume as defined from −950 HU to −701 Hounsfield unit (NL), the volume of the whole lung (WL), and the percentage of NL to WL (NL%), were calculated.ResultsCT indices (MCT, WL, and NL) closely correlated with lung physiology variables. Among them, NL strongly correlated with forced vital capacity (FVC) (r = 0.92, P <0.0001). NL% showed a large area under the receiver operating characteristic curve for detecting patients in the moderate or advanced stages of IPF. Multivariable logistic regression analyses showed that NL% is significantly more useful than the percentages of predicted FVC and predicted diffusing capacity of the lungs for carbon monoxide (Japanese stage II/III/IV [odds ratio, 0.73; 95% confidence intervals (CI), 0.48 to 0.92; P < 0.01]; III/IV [odds ratio. 0.80; 95% CI 0.59 to 0.96; P < 0.01]; GAP stage II/III [odds ratio, 0.79; 95% CI, 0.56 to 0.97; P < 0.05]).ConclusionThe measurement of NL% by threshold-based volumetric CT analysis may help improve IPF staging.

In this paper we demonstrate that the residual stress introduced by several different surface finishes affects the critical current density for passivation and the passive current density in the anodic polarization curve of austenitic stainless steel and that those critical current densities can be reduced by controlling the residual stress by applying a cavitating jet to the backs of specimens. The results show that the current density either increased or decreased depending on the surface finish, and that was decreased by introducing compressive residual stress for all surface finishes.

The c-MET receptor tyrosine kinase is the receptor for hepatocyte growth factor. Recently, activation of the c-MET/hepatocyte growth factor signaling pathway was associated with poor prognosis in various solid tumors and was one of the mechanisms of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor, gefitinib. But the link between c-MET activation and the cytotoxic anticancer drug has not been fully examined. Here, we found that the enhanced expression and activation of c-MET in cytotoxic anticancer agent-resistant small-cell lung cancer cells. Downregulation of c-MET expression by siRNA against the c-MET gene or inhibition of c-MET activation by SU11274, a c-MET inhibitor, in the resistant cells altered resistance to the cytotoxic anticancer agent. These results indicated that c-MET overexpression might play an important role in acquired resistance to cytotoxic anticancer drugs. Furthermore, the number of c-MET gene loci was increased in the resistant cells compared to the parental cells. In conclusion, increased c-Met expression through an increase in the number of c-MET gene loci is one of the mechanisms of acquired resistance to cytotoxic anticancer drugs. Our results add a new strategy, the targeting of c-MET, for overcoming resistance to cytotoxic agents in small-cell lung cancer.

A new model for hydrogen-assisted fatigue crack growth (HAFCG) in BCC iron under a gaseous hydrogen environment has been established based on various methods of observation, i.e., electron backscatter diffraction (EBSD), electron channeling contrast imaging (ECCI) and transmission electron microscopy (TEM), to elucidate the precise mechanism of HAFCG. The FCG in gaseous hydrogen showed two distinguishing regimes corresponding to the 2 unaccelerated regime at a relatively low stress intensity factor range, ΔK, and the accelerated regime at a relatively high ΔK. The fracture surface in the unaccelerated regime was covered by ductile transgranular and intergranular features, while mainly quasi-cleavage features were observed in the accelerated regime. The EBSD and ECCI results demonstrated considerably lower amounts of plastic deformation, i.e., less plasticity, around the crack path in the accelerated regime. The TEM results confirmed that the dislocation structure immediately beneath the crack in the accelerated regime showed significantly lower development and that the fracture surface in the quasi-cleavage regions was parallel to the {100} plane. These observations suggest that the HAFCG in pure iron may be attributed to "less plasticity" rather than "localized plasticity" around the crack tip.

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We have previously shown that overexpression of thymidylate synthetase (TS) resulted in pemetrexed (MTA) resistance. To investigate another mechanism of MTA resistance, we investigated the expression of ATP-binding cassette (ABC)-transporters in MTAresistant lung cancer cell lines and found that the gene and protein expression of ABCC11 ⁄ MRP8 (ABCC11) was higher in MTA-resistant cells than in the parental cells. The MTA resistant cells showed cross-resistance to methotrexate (MTX), which is a substrate for ABCC11, and intracellular MTX accumulation in MTA-resistant cells was lower than in the parental cells. We then tested the effect of decreasing the expression of ABCC11 by siRNA and found that decreased expression of ABCC11 enhanced MTA cytotoxicity and increased intracellular MTX accumulation in MTA-resistant cells. These findings suggested that ABCC11 directly confers resistance to MTA by enhancing efflux of the intracellular anti-cancer drug. Next, we analyzed the relationship between ABCC11 gene expression and MTA sensitivity of 13 adenocarcinoma cells, but there was no correlation. The ABCC11 gene has been shown to have a functional single-nucleotide polymorphism (SNP), 538G>A. We then classified 13 lung adenocarcinoma cell lines into three groups based on the genotype of this ABCC11 SNP: G ⁄ G, G ⁄ A and A ⁄ A. The A ⁄ A group showed a significant reduction in the IC 50 of MTA compared with the combined G ⁄ G and G ⁄ A groups, indicating that the SNP (538G>A) in the ABCC11 gene is an important determinant of MTA sensitivity. These results showed that ABCC11 may be one of the biomarkers for MTA treatment in adenocarcinomas. (Cancer Sci 2010; 101: 2404-2410 C urrently, several folate-based antimetabolites are used for cancer treatment and have been studied intensively in clinical trials. Nearly 60 years ago, methotrexate (MTX) was the first antifolate used in oncology clinics that was shown to be active for the chemotherapeutic treatment of childhood acute lymphoblastic leukemia.(1) Methotrexate and its polyglutamate forms are potent inhibitors of the dihydrofolate reductase (DHFR) enzyme that plays a key role in intracellular metabolism and is essential for DNA synthesis and cell growth.(2) Recently, a new generation antifolate, pemetrexed (MTA) was approved for the treatment of malignant pleural mesothelioma and non-small-cell lung cancer (NSCLC). (3,4) Pemetrexed is transported into the cell, predominantly via the reduced folate carrier (RFC), and is metabolized to polyglutamated forms. Pemetrexed was found to be one of the best substrates for mammalian folylpoly-c-glutamate synthetase (FPGS), and it is believed that MTA polyglutamation and its polyglutamated metabolites play important roles in determining both the selectivity and antitumor activity of this agent. The polyglutamated metabolites of MTA are most active against thymidylate synthase (TS), followed by DHFR, glycinamide ribonucleotide formyltransferase (GARFT) and aminoimidazole carboxamide formyl transferase (AICARFT), and natural folate c...

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