No abstract

Patients with lung cancer often experience a state of depression, and these conditions may severely affect their quality of life (QoL) and prescription compliance. The current study was conducted to delineate the complex links between depression and the prognosis of patients with small cell lung cancer (SCLC) and the underlying mechanism was also explored.186 patients who received platinum-based chemotherapy for newly diagnosed stage III or stage IV SCLC were enrolled. The Self-Rating Depression Scale (SDS) questionnaire was completed the day before the start of chemotherapy to assess the depression status of the patients. Patients with stage IV SCLC or lower BMI have higher depression scores. In terms of the adverse effects of chemotherapy, depression severely decreases patient tolerance to chemotherapy and their QoL score (R2 = 0.2385) and is also associated with severe vomiting (P < 0.001), leukopenia (R2 = 0.2332), and prolonged hospital stay (R2 = 0.1961). More importantly, severe depression reduces the PFS (R2 = 0.1943) and OS (P < 0.01) of the patients. We found that patients with severe depression displayed a downregulated level of serum BDNF and that the level of serum BDNF was highly correlated with the OS of the patients (R2 = 0.2292). Using the MTT cell viability assay in vitro, we observed that cotreatment with BDNF clearly enhanced the chemosensitivity of NCI-H69 tumor cells to Cisplatin and induced the downregulation of ABCG2.Based on this evidence, it appears that a relationship does exist between depression and prognosis in SCLC and that the mechanism by which depression affects prognosis is achieved via the downregulation of BDNF expression.

This paper presents an experimental investigation on the wind-induced vibration of a transmission tower-line system. A discrete stiffness method is applied to design the aero-elastic model on the basis of similarity theory. The dynamic characteristics of the single tower and the tower-line system are identified and the displacement responses at different positions are obtained under a variety of wind speeds. The mean and the RMS of the displacements as well as their spectra are discussed. Moreover, the test results and the codal specifications are compared in terms of the wind-induced vibration coefficient. The first natural frequency of the single tower is slightly larger than that of the tower-line system. But the damping ratio of the former is smaller than that of the latter, especially in the direction normal to the conductors. At the wind attack angle of 90°, the conductors significantly increase the longitudinal and lateral displacement RMS as well as the longitudinal mean displacement. And more complicated forms of vibration are aroused by the conductors, especially in the lateral direction. The wind-induced vibration coefficient show a notable rise at the position of cross arm, which cannot be characterized by Chinese code. Besides, the wind-induced vibration coefficient specified by the code is much smaller than test results thus the codal value seems to be unsafe for the UHV transmission tower.

Cellular retinoic acid binding protein 2 (CRABP2) is essential for myoblast differentiation, however, little is known about its role in osteogenic differentiation. This study mainly aims to explore the biological functions and the underlying molecular mechanisms of CRABP2 in osteogenesis. Using quantitative polymerase chain reaction and western blot assays, we found that the expression of CRABP2 at both mRNA and protein levels were downregulated during osteogenesis. Furthermore, CRABP2 knockdown displayed significant changes in the cell phenotype and the actin filaments (F-actin) polymerization in C2C12 cells treated with BMP2. Moreover, the western blotting of osteogenic differentiation biomarkers, alkaline phosphatase (ALP) staining and Alizarin red staining showed that CRABP2 dramatically inhibited osteogenic differentiation. The following investigation of molecular mechanisms implicated that CARBP2 specifically interacted with LIMK1, a key factor in acin cytoskeletal rearrangements in osteogenesis, to interrupt its activity and stability in an ubiquitin-proteasome pathway to prevent C2C12 cells from osteogenic differentiation in response to BMP2. Above all, our data suggest a novel function of CRABP2 in regulating actin remodeling and osteogenic differentiation via LIMK1, thus presenting a possible molecular target for promoting the osteogenic differentiation in bone degenerative diseases.