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Molecular markers for the detection of lymph node micrometastases of malignant tumors have been extensively investigated. However, epigenetic signatures have rarely been reported for identification of metastatic lymph nodes and disease relapse. Septin 9 is the most frequently reported hypermethylated gene in colorectal cancer (CRC). This study aimed to assess the clinical relevance of Septin 9 methylation in regional lymph nodes in recurrence/metastases of CRC.We analyzed Septin 9 methylation of DNA from resected lymph nodes in 75 CRC patients with or without tumor recurrence using quantitative methylation-sensitive PCR (qMS-PCR).Of the 30 histologically negative lymph node CRC patients without recurrence (group 1), methylated Septin 9 was detected in 3 (10 %) cases. The positivity rate of methylated Septin 9 in group 2 containing 30 histologically node-negative CRC patients with recurrence was 30 % (9/30). For group 3, lymphatic invasion as well as tumor recurrence, 11 (73 %) out of 15 subjects had Septin 9 methylation-positive lymph nodes. Moreover, patients in group 3 had a higher level of methylated Septin 9 compared to subjects in group 1 and group 2 (p 0.05). In addition, CRC patients with Septin 9 methylation in lymph nodes had significantly reduced survival (Log-rank P 0.0001).Our data support the predictive role of Septin 9 methylation analysis of lymph node micrometastases for tumor relapse after surgery.

Phosphatidylserine (PS) is distributed asymmetrically in the plasma membrane of eukaryotic cells. Phosphatidylserine flippase (P4-ATPase) transports PS from the outer leaflet of the lipid bilayer to the inner leaflet of the membrane to maintain PS asymmetry. The β subunit TMEM30A is indispensable for transport and proper function of P4-ATPase. Previous studies have shown that the ATP11A and TMEM30A complex is the molecular switch for myotube formation. However, the role of Tmem30a in skeletal muscle regeneration remains elusive. In the current study, Tmem30a was highly expressed in the tibialis anterior (TA) muscles of dystrophin-null (mdx) mice and BaCl2-induced muscle injury model mice. We generated a satellite cell (SC)-specific Tmem30a conditional knockout (cKO) mouse model to investigate the role of Tmem30a in skeletal muscle regeneration. The regenerative ability of cKO mice was evaluated by analyzing the number and diameter of regenerated SCs after the TA muscles were injured by BaCl2-injection. Compared to the control mice, the cKO mice showed decreased Pax7+ and MYH3+ SCs, indicating diminished SC proliferation, and decreased expression of muscular regulatory factors (MYOD and MYOG), suggesting impaired myoblast proliferation in skeletal muscle regeneration. Taken together, these results demonstrate the essential role of Tmem30a in skeletal muscle regeneration.

Familial exudative vitreoretinopathy (FEVR) is a hereditary eye disease characterized by defects in the development of periphery retinal vessels. However, the clinical phenotypes of FEVR vary widely from asymptomatic to complete blindness. We analyzed patients from three Chinese families and one sporadic patient with FEVR to investigate the clinical features and disease-causing mutations. Ocular phenotypes included increased ramification of the peripheral retinal vessels, a peripheral avascular zone, inferotemporal dragging of the optic disc and macula, and retinal folds. Peripheral blood DNA samples were obtained from patients with FEVR and their family members. Primers were designed to amplify the coding exons and adjacent intronic regions of the FEVR-causing genes FZD4, LRP5, NDP and TSPAN12. By polymerase chain reactions, each amplicon was subjected to direct Sanger sequencing analysis. Potential pathogenic changes of the sequence variants were analyzed by the orthologous protein sequence alignment and computational prediction software. We identified five LRP5 mutations: three novel heterozygous mutations-p.M181R, p.R399S and p.G503R and two known mutations that were never reported in FEVR patients: p.R494Q and p.G876S. All five mutations involved highly conserved residues and were predicted to be damaging by SIFT and PolyPhen-2. None was present in 500 normal individuals. To assess the pathogenesis of these mutations, wild-type and all five mutant LRP5 proteins were assayed for the ability to activate the Norrin/β-catenin pathway by established luciferase reporter assays, and all mutants failed to activate the pathway. This study extends the genetic database of the FEVR disease in China and provides a basis for molecular diagnosis of the disease.

To construct a MYH9 gene knockout model in MGC803 cell line using transcription activator-like effector nuclease (TALEN) and observe its effect on cell cycle and apoptosis.According to FastTALE(TM) TALEN Kit, we designed TALEN pairs and constructed the plasmids targeting to MYH9 gene. After detecting their activity in MGC803 cells by plasmid transfection, DNA sequencing, RT-PCR and western blot, we selected the monoclonal cells and studied the changes in the cell cycle and apoptosis.MYH9 gene could not be knocked out but knocked down in selected MGC803 monoclonal cells, which caused cell cycle arrested at G2/M phase (P0.05) and a significant increase in the cell number with early apoptosis (P0.01).We successfully generated a MYH9 knockdown model in MGC803 cell lines by TALEN, which could be in favor of MYH9 function study in gastric cancer.

Two three-dimensional (3D) coordination polymers {[NaFe(dipic)2(H2O)2]}∞ (1) and {[NaCr(dipic)2(H2O)2]}∞ (2) containing Fe5Na5 and Cr5Na5 mixed d-/s-block subunits were synthesized by the reactions of tridentate ligand H2dipic (pyridine-2,6-dicarboxylic acid) with Fe(ClO4)3 · 6H2O or Cr(ClO4)3 · 6H2O through the self-assembly process with sodium ions. The X-ray diffraction analyses reveal that both complexes have 3D (10,3) topology. Magnetic susceptibility measurements of both complexes in the temperature range of 2–300 K reveal the occurrence of weak antiferromagnetic interactions together with zero-field splitting effects.

Samples of LiNi0.85Co0.15−2x(TiMg)xO2 (x = 0.0125, 0.025 and 0.05), prepared by solid state reaction at 725 °C for 24 h from LiOH·H2O, Ni2O3, Co2O3, TiO2 and Mg(OH)2 under oxygen flow, were characterized by TG–DTA, XRD and electrochemical tests. LiNiO2 simultaneously doped by Co-Ti-Mg has been tried to improve the cathode performance. The results show that co-doping (x = 0.025) definitely has a large beneficial effect in increasing the capacity (182.7 mA h g−1 of the first discharge capacity for LiNi0.85Co0.10(TiMg)0.025O2) and cycling behavior (170.6 mA h g−1 after 15 cycles). Differential capacity versus voltage curves indicate the co-doped LiNiO2 show suppression of the phase transitions as compared with LiNiO2.

A tin–cobalt oxide film with a 3-dimensional (3D) reticular structure has been prepared by electrostatic spray deposition (ESD). X-Ray diffraction (XRD) and transmission electron microscopy (TEM) make it clear that the film is amorphous. X-Ray photoemission spectroscopy (XPS) indicates that the 3D grid is composed of SnO2 and CoO. As an anode for the lithium ion battery, the film has 1240.2 mAh/g of initial discharge capacity, shows a gradually increasing capacity after the first cycle, and has 845 mAh/g of discharge capacity up to the 50th cycle. The high porosity of the 3D reticular structure can provide more reaction sites on the electrode surface and accommodate volume variation of Sn particles during Li alloying–dealloying. The CoO in the complex composite film plays an important role, allowing the formation of a polymeric gel-like film to improve its electrochemical performance, preventing Sn aggregation during charging and discharging. Such a composite film can be used as an anode for lithium ion batteries with higher energy densities.