Objective To investigate the change of serum Nogo-A protein in patients with acute closed brain injury, and explore its relationship with the severity of neuronal damage and prognosis. Methods Thirty-one patients with acute closed brain injury were enrolled. Venous blood samples (2 mL) were obtained 1, 3 and 5 d after injury. Serum concentrations of Nogo-A protein were determined by ELISA. Patients were divided into mild (n =7), moderate (n = 10) and severe (n = 14) injury groups according to Glasgow coma score (GCS), and were divided into favorable prognosis (n = 23) and poor prognosis (n = 8) groups according to Glasgow outcome score (GOS). Another 20 healthy adults were served as controls. Results The mass concentrations of serum Nogo-A protein in mild, moderate and severe injury groups 1, 3, 5 d after injury were significantly higher than those in control group (P < 0.01), and the mass concentrations of serum Nogo-A protein in moderate and severe injury groups 1, 3, 5 d after injury were significantly higher than those in mild injury group (P <0.05, P <0.01). The mass concentrations of serum Nogo-A protein 1, 3, 5 d after injury were significantly higher in poor prognosis group than those in favourable prognosis group (P < 0.01). Conclusion Serum Nogo-A protein level significantly increases after brain injury, and is related to the degree of injury and prognosis.

Objective: To investigate the effect of histone deacetylase inhibitor apicidin on the glioblastoma U87 cells and its regulation of OCT-4 gene expression. Methods: Glioblastoma U87 cells were treated with different concentrations of apicidin, and dimethyl sulfoxide instead of apicidin was negative control. Methyl thiazolyl tetrazolium (MTT) assay was used to detect the proliferative ability of U87 cells treated by apicidin. The cell apoptosis was observed under the fluorescence microscope, and the cell cycle was detected by using flow cytometry. Reverse transcription-polymerase chain reaction and Western blot was used to detect the expression of mRNA and protein of U87 cells, respectively relative to the expression of GAPDH. Results: MTT assay results showed that apicidin inhibited U87 cells proliferation in a dose-dependent and time-dependent manner, and half of the inhibitory concentration of cell proliferation at 48 h was (1.74±0.13) μmol/L. The cell proportion of U87 cells in S-phase of the negative control, 0.2, 0.5, and 1.0 μmol/L apicidin was (32.68±0.49)%, (33.73±0.76)%, (42.92±0.56)%, and (56.95±0.53)%, respectively after 48 h apicidin administration (P < 0.05), while the proportion of G₁ and G₂ phase cells was decreased. The karyopyknosis and other apoptotic changes were detected in U87 cells after 48 h treatment of 1.0 μmol/L apicidin under the confocal fluorescence microscope. Western blot and RT-PCR showed that the mRNA and protein relative levels of U87 cells OCT-4 were reduced after 1.0 μmol/L apicidin treatment for 48 h compared with the negative control group (mRNA: 72.44±0.00 vs. 56.66±0.23; protein: 86.59±0.19 vs. 56.04±0.15, both P < 0.01). Conclusions Apicidin can inhibit the growth of glioblastoma U87 cells, induce cell cycle arrest and apoptosis. Its mechanism may be related to the expression of OCT-4 inhibited by apicidin.

Objective: In this study, we tested for the presence of four human coronaviruses (HCoVs) in children with respiratory tract disease in Fuzhou, Fujian, China. Methods: Nasopharyngeal aspirates were collected from children with respiratory tract disease from Nov, 2007 to Jan, 2015. A total of 266 clinical samples were tested for HCoVs using reverse-transcription polymerase chain reaction (RT-PCR). The positive products were sequenced and compared with those in GenBank by BLAST. The positive samples were then tested for HCoV-HKU1 and HCoV-NL63 using RT-PCR method . We compared the 440 bp pol gene sequence of the 8 HCoV isolates in Fuzhou, China to other HCoV isolates documented in the GenBank database by using MEGA software version 6.06 and the neighbor-joining method . Results: HCoVs were detected in 8 patients (3.0%) out of the 266 children. Two of 266 (0.38%) were positive for HCoV-HKU1; 1 of 266(0.38%)were positive for HCoV-NL63; 1 of 266 (0.38%) were positive for HCoV-229E; 4 of 266 (1.5%)were positive for HCoV-OC43. All of children who were positive for HCoV had respiratory illness. Two HCoV-HKU1 were found to co-infect with human parainfluenza virus type 3 (HPIV-3). The 8 HCoV strains in our study fell into four clusters. Two strains of HCoV-HKU1 were genotype A. Conclusions HCoV infections were probably associated with upper and lower respiratory illness in children. Additional studies are needed to investigate the potential roles of these HCoVs in diseases.