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W e have made a retrospective review of 185 cemented Charnley total hip arthroplasties performed between 1970 and 1974 to determine the relationships between radiological variables and failure of the femoral and acetabular components. We measured the acetabular wear, the orientation of the cup, the thickness and consistency of acetabular and femoral cement mantles, radiolucency and femoral alignment. The mean follow-up was for 11.7 years. Femoral loosening was demonstrable radiologically in 15 hips (8.1%), ten (5.4%) of which were revised during the period of follow-up. Only when the first postoperative radiograph showed a thin cement mantle in Gruen zone 5 was there a significant association with failure of the femoral component. There were 12 loose acetabular components (6.5%), nine (4.8%) of which were revised. When the initial radiograph after operation showed radiolucency in DeLee and Charnley zone 1, the incidence of acetabular loosening was 28.21%. If such radiolucency was not present, the incidence of acetabular loosening was only 0.69%. Our findings emphasise the importance of careful cementing.

This study investigated removal of five haloacetic acids (HAA5) (monochloroacetic acid, dichloroacetic acid, trichloroacetic acid, monobromoacetic acid, and dibromoacetic acid) in biologically active carbon (BAC) columns. An acclimated granular activated carbon (GAC), or BAC, column effectively removed four of the HAA5 that had been spiked in the influent at 50 µg/L each. Only trichloroacetic acid, detected at 10 µg/L in the effluents, was not completely removed. After the biological activity on acclimated GAC was eliminated by autoclaving, the HAA removal efficiency was significantly reduced. In another experiment, the removal of HAAs in a new GAC column was continuously monitored for 76 days. The new GAC effectively removed HAAs. HAA removal at the beginning of this experiment was from carbon adsorption, whereas biodegradation was the HAA removal mechanism later in the experiment. The results of this study are significant to the water industry-removal of HAAs using BAC may provide a new technology for control of disinfection by-products.

Abstract. The purpose of the present study was to investigate the effects of bafilomycin A1 (BafA1) on proliferation, apoptosis and autophagy in MG63 osteosarcoma cells. The growth rate of MG63 cells was determined using a Cell Counting Kit-8 assay. The mitochondrial membrane potential (Δψ) was measured using a fluorescent probe, JC-1, and the inhibition of autophagy and apoptosis was monitored by transmission electron microscopy. In addition, the inhibition of autophagy was monitored by western blot analysis of microtubule-associated protein 1 light chain 3 (LC3), and the ratio of LC3-II/LC3-I protein levels was calculated as an indicator of the extent of autophagy. Furthermore, the expression levels of specific proteins associated with autophagy, including p53, Beclin1 and p62, were detected in cultured MG63 cells by western blotting. It was shown that the viability of MG63 cells was inhibited following the use of BafA1, and an induction in the expression levels of the apoptosis-related protein p53 and the autophagic protein Beclin1 was detected. Furthermore, a collapse in Δψ was observed, together with an induction of apoptotic cell death, following treatment with BafA1. Therefore, following BafA1-mediated inhibition of autophagy, the inhibition of MG63 cell proliferation and induction of apoptosis were observed.

Although androgen-deprivation treatment (ADT) is the main treatment for advanced prostate cancer (PCa), it eventually fails. This failure invariably leads to castration-resistant prostate cancer (CRPC) and the development of the neuroendocrine (NE) phenotype. The molecular basis for PCa progression remains unclear. Previously, we and others have demonstrated that the sex-determining region Y-box 4 ( SOX4 ) gene, a critical developmental transcription factor, is overexpressed and associated with poor prognosis in PCa patients. In this study, we show that SOX4 expression is associated with PCa progression and the development of the NE phenotype in androgen deprivation conditions. High-throughput microRNA profiling and bioinformatics analyses suggest that SOX4 may target the miR-17-92 cluster. SOX4 transcriptionally upregulates miR-17-92 cluster expression in PCa cells. SOX4-induced PCa cell proliferation, migration, and invasion are also mediated by miR-17-92 cluster members. Furthermore, RB1 is a target gene of miR-17-92 cluster. We found that SOX4 downregulates RB1 protein expression by upregulating the miR-17-92 expression. In addition, SOX4-knockdown restrains NE phenotype and PCa cell proliferation. Clinically, the overexpression of miR-17-92 members is shown to be positively correlated with SOX4 expression in PCa patients, whereas RB1 expression is negatively correlated with SOX4 expression in patients with the aggressive PCa phenotype. Collectively, we propose a novel model of a SOX4/miR-17-92/RB1 axis that may exist to promote PCa progression.

Osteoarthritis (OA) is a chronic degenerative disease featured by cartilage erosion and inflammation. Luteolin, a member of the flavonoid family, has been shown to exert anti-inflammatory and antioxidative activities. However, the potential biological effects and underlying mechanism of luteolin on chondrocytes and OA progression remain largely elusive. In this study, the potential effect and mechanism of luteolin on OA were investigated in vitro and in vivo. Our data revealed that luteolin inhibited H2O2-induced cell death, apoptosis, oxidative stress, programmed necrosis, and inflammatory mediator production in primary murine chondrocytes. In addition, luteolin could activate the AMPK and Nrf2 pathways, and AMPK serves as a positive upstream regulator of Nrf2. In vivo results demonstrated the therapeutic effects of luteolin on OA in the DMM mouse model. Collectively, our findings showed that luteolin might serve as a novel and effective treatment for OA and provided a new research direction for clinical OA therapies.