Overexpression of CDCA8 Predicts Poor Prognosis and Promotes Tumor Cell Growth in Prostate Cancer.

Human cell division cycle-related protein 8 (CDCA8) is an essential component of the vertebrate chromosomal passenger complex (CPC). CDCA8 was confirmed to play a role in promoting malignant tumor progression. However, the exact function of CDCA8 in the development and progression of prostate cancer (PCa) remains unclear. In this study, the database GSE69223 was downloaded by the gene expression omnibus (GEO) database, as well as CDCA8 expression differences in multiple tumor tissues and normal tissues were detected by The Cancer Genome Atlas (TCGA), TIMER, Oncomine, and Ualcan databases. Kaplan-Meier and Cox regression methods were used to analyze the correlation between CDCA8 expression and prognosis in PCa. We confirmed the expression of CDCA8 in PCa tissues by HPA. We also analyzed the association of CDCA8 expression with PCa clinical characteristics in the TCGA database. To further understand the role of CDCA8 in PCa, we assessed the effects of CDCA8 on PCa cell growth, proliferation, and migration in vitro studies. As a result, CDCA8 was significantly overexpressed in PCa cells compared with normal prostate cells. High CDCA8 expression predicts poor prognosis in PCa patients, and CDCA8 expression was higher in high-grade PCa. In addition, silencing of CDCA8 significantly inhibited PCa cell proliferation and migration. In summary, CDCA8 promoted the proliferation and migration of PCa cells.

[Comparative analysis of trace elements in five marine-derived shell TCM using multivariate statistical analysis].

A comparable study were carried out by determination of trace elements on five marine-derived shell traditional Chinese medicine (TCM) (Ostreae Concha, Haliotidis Concha, Margaritifera Concha, Meretricis Concha, and Arcae Concha), which were recorded in the Chinese Pharmacopoeia (2010 version). Seven trace elements in 51 batches of this type of shell TCM were analyzed by Inductively Coupled Plasma Mass Spectrometry (ICP-MS), combined with principal component analysis (PCA) methods. The content of element Se, which exhibited significant differences among different drugs, could be used as a key element to distinguish this type of drugs. Meanwhile, the contents of elements Co, Cu, Mo, and Ba in Haliotidis Concha, Co and As in Margaritifera Concha, Mo and As in Meretricis Concha, Mo, As, and Ba in Arcae Concha, and Zn in Meretricis Concha were relatively stable. In the PCA plot, Arcae Concha and Meretricis Concha could be efficiently distinguished from Ostreae Concha together with Haliotidis Concha, and Margaritifera Concha. The results also showed a correlation with their medicinal function. In conclusion, trace elements in marine-derived shell TCM could not be neglected for their quality control.

Effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, ROS production and lipid peroxidation in broiler chickens.

In order to investigate the effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, production of reactive oxygen species (ROS) and lipid peroxidation in broiler chickens, 128 six-week-old broiler chickens were kept in a controlled-environment chamber. The broiler chickens were initially kept at 25 degrees C (relative humidity, RH, 70+/-5%) for 6d and subsequently exposed to 35 degrees C (RH, 70+/-5%) for 3h, then the heat stress was removed and the temperature returned to 25 degrees C (RH, 70+/-5%). Blood and liver samples were obtained before heat exposure and at 0 (at the end of the three-hour heating episode, this group is also abbreviated as the HT group), 1, 2, 4, 8, 12h after the stress was removed. The results showed that acute heat stress induced a significant production of ROS, function of the mitochondrial respiratory chain, antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activity, and formation of malondialdehybe (MDA). Within the first 12h after removal of the heat stress, the acute modification of the above parameters induced by heat stress gradually approached to pre-heat levels. The results of the present study suggest that acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This leads to over-production of ROS, which ultimately results in lipid peroxidation and oxidative stress. When the high temperature was removed, the production of ROS, mitochondrial respiratory function and oxidative injury that were induced by acute heat exposure gradually approached the levels observed before heating, in a time-dependent manner.