主动脉夹层术后患者心理状况及躯体症状对生活质量的影响

目的 探讨主动脉夹层术后患者心理状况、躯体症状对其生活质量的影响及作用机制，为制订干预计划提供参考。方法 采用广泛性焦虑障碍量表、患者健康问卷抑郁量表、躯体症状量表、12项简明健康状况调查表对327例主动脉夹层术后患者进行调查，根据相关性分析结果提出假设，应用AMOS软件进行结构方程模型分析。结果 主动脉夹层术后患者生活质量得分（81.56±7.36）分，焦虑得分2.00(0, 3.00)分，抑郁得分2.00(0, 3.00)分，躯体症状得分5.00(2.00, 8.00)分；焦虑、抑郁、躯体症状对生活质量有直接影响，焦虑、抑郁通过躯体症状对生活质量有间接影响（均P<0.05）。结论 主动脉夹层术后患者生活质量处于中等偏上水平，应早期对主动脉夹层术后患者的心理状况与躯体症状进行动态评估与监测，及时进行心理干预和症状管理，以改善其生活质量。     

Comparison of in vitro and in vivo biological effects of trabectedin,lurbinectedin (PM01183) and Zalypsis® (PM00104)

This study: (i) investigated the in vitro cytotoxicity and mode of action of lurbinectedin (PM01183) and Zalypsis® (PM00104) compared with trabectedin in cell lines deficient in specific mechanisms of repair, (ii) evaluated their in vivo antitumor activity against a series of murine tumors and human xenografts. The antiproliferative activity, the DNA damage and the cell cycle perturbations induced by the three compounds on tumor lines were very similar. Nucleotide Excision Repair (NER) deficient cells were approximately fourfold more resistant to trabectedin, lurbinectedin and Zalypsis®. Cells deficient in non‐homologous end joining (NHEJ), MRN complex and translesion synthesis (TLS) were slightly more sensitive to the three compounds (approximately fivefold) while cells deficient in homologous recombination (HR) were markedly more sensitive (150–200‐fold). All three compounds showed a good antitumor activity in several in vivo models. Lurbinectedin and trabectedin had a similar pattern of antitumor activity in murine tumors and in xenografts, whereas Zalypsis® appeared to have a distinct spectrum of activity. The fact that no relationship whatsoever was found between the in vitro cytotoxic potency and the in vivo antitumor activity, suggests that in addition to direct cytotoxic mechanisms other host‐mediated effects are involved in the in vivo pharmacological effects.     

Thoracic Computed Tomographic Manifestations of Tuberous Sclerosis in Adults

The purpose of this article is to illustrate the various manifestations that can be encountered on thoracic computed tomography of tuberous sclerosis in adults. The pulmonary findings include lymphangioleiomyomatosis and multifocal micronodular pneumocyte hyperplasia. The extrapulmonary manifestations are divided into cardiac, vascular, mediastinal, osseous, and upper abdominal findings.     

Nucleostemin deletion reveals an essential mechanism that maintains the genomic stability of stem and progenitor cells

Stem and progenitor cells maintain a robust DNA replication program during the tissue expansion phase of embryogenesis. The unique mechanism that protects them from the increased risk of replication-induced DNA damage, and hence permits self-renewal, remains unclear. To determine whether the genome integrity of stem/progenitor cells is safeguarded by mechanisms involving molecules beyond the core DNA repair machinery, we created a nucleostemin (a stem and cancer cell-enriched protein) conditional-null allele and showed that neural-specific knockout of nucleostemin predisposes embryos to spontaneous DNA damage that leads to severe brain defects in vivo. In cultured neural stem cells, depletion of nucleostemin triggers replication-dependent DNA damage and perturbs self-renewal, whereas overexpression of nucleostemin shows a protective effect against hydroxyurea-induced DNA damage. Mechanistic studies performed in mouse embryonic fibroblast cells showed that loss of nucleostemin triggers DNA damage and growth arrest independently of the p53 status or rRNA synthesis. Instead, nucleostemin is directly recruited to DNA damage sites and regulates the recruitment of the core repair protein, RAD51, to hydroxyurea-induced foci. This work establishes the primary function of nucleostemin in maintaining the genomic stability of actively dividing stem/progenitor cells by promoting the recruitment of RAD51 to stalled replication-induced DNA damage foci.