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Trimethylated histone H3 lysine 27 (H3K27me3) is a repressive histone marker that regulates a variety of developmental processes, including those that determine flowering time. However, relatively little is known about the mechanism of how H3K27me3 is recognized to regulate transcription. Here, we identified BAH domain-containing transcriptional regulator 1 (BDT1) as an H3K27me3 reader. BDT1 is responsible for preventing flowering by suppressing the expression of flowering genes. Mutation of the H3K27me3 recognition sites in the BAH domain disrupted the binding of BDT1 to H3K27me3, leading to de-repression of H3K27me3-enriched flowering genes and an early-flowering phenotype. We also found that BDT1 interacts with a family of PHD finger-containing proteins, which we named PHD1-6, and with CPL2, a Pol II carboxyl terminal domain (CTD) phosphatase responsible for transcriptional repression. Pull-down assays showed that the PHD finger-containing proteins can enhance the binding of BDT1 to the H3K27me3 peptide. Mutations in all of the PHD genes caused increased expression of flowering genes and an early-flowering phenotype. This study suggests that the binding of BDT1 to the H3K27me3 peptide, which is enhanced by PHD proteins, is critical for preventing early flowering.

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This study was designed to investigate triterpenoids from the roots of Rosa laevigata Michx. The silica gel column chromatography was used to separate the chemical constituents from the roots of Rosa laevigata Michx. HPLC was used to analyze its purity and chemical constitution. Spectroscopy methods were used to determine their structures. Five constituents were isolated and identified as19α-OH-3ß-E-feruloyl corosolic acid (1), 23-hydroxy-tormentic acid (2), 2α, 3ß, 19α, 23- tetrahydroxy-12-en-28-oleanolic acid (3), 2α, 3α, 20ß- trihydroxyurs-13 (18)-en-28-oic-acid (4), 2α, 3ß, 20ß-trihydroxyurs-13 (18)-en-28-oic-acid (5). Compound 1 was assigned as a new compound, compounds 4, 5 were obtained from the genus Rosa for the first time.

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Objective To observe the tropism ofboue marrow stromal stem cells for malignantglioma in rats. Methods The immunophenotype of in vitro cultureA Fisher344 rat BMSCs wereidentified using flow cytometry. The BMSCs or NIH3T3 cells were cocultured with 9L glioma cells in aTranswell system, and 24 h later, the cell migration rate was calculated. For in vivo experiment, aFisber344 rat model bearing malignant glioma was established by stereotactic injection of 9L glioma cellsinto the brain. After validation of the model 2 weeks after the injection by neurobehavioral test, magneticresonance imaging and HE staining, the BMSCs or NIH3T3 cells were transplanted via the internalcarotid artery in the rats. Two weeks after the transplantation, the rats were sacrificed by routine cardiacperfusion, and BMSCs migration in the brain was detected immunohistochemically. Results Thethird to six passages of the BMSCs were negative for CD34 and CD45 but positive for CD29 and CD44.Transwell assay demonstrated BMSCs tropism for 9L cells in vitro. In Fisher344 rats bearing 9L glioma,neurobehavioral changes characteristic of glioma were observed, and the BMSCs transplanted via theinternal carotid artery were found to migrate to the glioma tissue, residing mostly on the boundarybetween the normal tissue and the tumor tissue. Conclusion Rat BMSCs show a tropism formalignant glioma both in vitro and in vivo, and administration via the internal carotid artery can be aneasy and effective means for BMSCs transplant.

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OBJECTIVE: To observe the ways of diagnosis and treatment of bilateral facial nerve palsy. METHODS: Seven cases of bilateral facial nerve paralysis in 1996 - 2003 were retrospectively reviewed, and then the ways of diagnosis and therapies of these cases were analyzed. There were 6 patients with doubtless diagnosis. They were diagnosed as acute leukaemia, Vogt-Koyanagi-Harada disease (VKH), Machado-Jesoph disease, bilateral mandible fractures, Guillain-Barré syndrome, and Bell's palsy. The last one was diagnosed as Herpes zoster virus infection or Lyme disease. In all these cases, there were 4 of 5 positive cerebrospinal fluids test, 1 of 6 positive lyme antibody test, 2 of 5 positive images test, 7 of 7 EMG and Br test showed that the paralysis was peripheral palsy. All the 7 cases were treated with steroid and vitamin. RESULTS: House-Brackmann I was defined as complete recovery, after up to 2 months follow up, there were four cases got completely recovery while 2 cases incomplete recovery, and 1 case was not reacted to the therapy. CONCLUSIONS: Bilateral facial nerve paralysis was rare, and it was difficult to diagnosis and differentiation, while diagnostic mistakes would be serious. More attention should be paid to it in clinic.

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OBJECTIVE: To study the clinical value of muscle autograft denatured by microwave for repair of gaps in removal of facial neuromas. METHODS: Two cases of patients with facial nerve Schwann cell neuromas were reported. The operations for removal of facial neuromas were completed, and the gaps of the nerves were repaired with muscle autograft denatured by microwave of 250 W for 120 sec. RESULTS: The patients were followed up for two years, and the recovery of facial function on the affected sides were satisfactory. CONCLUSION: Muscle autograft denatured by microwave technique is convenient, highly efficient for repairing facial nerve gap after removal of facial neuroma.

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