分类: 物理学 >> 基本粒子与场物理学 提交时间: 2017-08-05
摘要: The tensor network/geometry correspondence is a proposed discrete version of the holographic duality. We show how important features in the AdS/CFT dictionary, such as the bulk operator reconstruction via the HKLL relation and the map between bulk isometry and boundary global symmetry, can emerge naturally from the tensor network construction. Furthermore, we propose that the tensor network living on the Bruhat-Tits tree gives a concrete realization of the recently proposed p-adic AdS/CFT (a holographic duality based on the p-adic number field Qp); in particular, the wavefunction of the tensor network defines the ground state of the boundary p-adic CFT.
分类: 核科学技术 >> 核材料与工艺技术 提交时间: 2023-06-18 合作期刊: 《Nuclear Science and Techniques》
摘要: This study was to determine the Semaphorin3B (SEMA3B) role in glioma cells responding to irradiation. Two glioma cell lines, which were used here was wild-type p53 (U-87MG), and the other was harboring mutated p53 (U-251). The SEMA3B mRNA could be detected in the two cell lines. The expression level of SEMA3B mRNA was higher in U-87MG cells than in U-251 cells, and increased with time in U-87MG cells after irradiation. Knockdown of SEMA3B expression by shRNA decreased the radiosensitivity of U-87MG cells, this may be associated with the increased G2 accumulation after irradiation. In addition, G2 accumulation after irradiation was enhanced in SEMA3B low-expressing U-87MG cells. These results showed that the SEMA3B was implicated in glioma cells responding to irradiation.
分类: 生物学 >> 生物物理学 >> 肿瘤学 提交时间: 2016-05-11
摘要: Hereditary multiple exostosis (HME) is an autosomal inherited skeletal disease whose etiology is not fully understood. To further understand the genetic spectrum of the disease, we analyzed a five-generation Chinese family with HME that have observable inheritance. Exome sequencing was performed on three HME individuals and three unaffected individuals from the family. A downstream study confirmed a new C deletion at codon 442 on exon 5 of the exostosin-1 (EXT1) gene as the only pathogenic site which generated a stop codon and caused the truncation of the protein. We rediscovered the deletion in other affected individuals but not in the unaffected individuals from the family. Upon immunohistochemistry assay, we found that the EXT1 protein level of the patients with the novel mutation in our study was less than the level in the patients without the EXT1 mutation from another unrelated family. For a deeper understanding, we analyzed the mutation spectrum of the EXT1 gene. The present study should facilitate a further understanding of HME.