伴随着对医疗领域人才水平要求的逐步提高,医院人力资源管理尤其是医院人才引进工作正在由规模化发展向精细化发展转变。当前医院人才引进过程中存在缺乏人力资源发展规划、高层次人才引进方法有待完善、人才管理能力亟须提高、科室用人需求脱离实际、忽视对于岗位胜任力的分析等问题。人力资源成熟度模型（People Capability Maturity Model,P-CMM）作为一种系统的管理理论,其具备很强的实践性,文章对人力资源成熟度模型在医院人才引进工作中的本土化应用进行相关讨论与研究,将P-CMM不同成熟度等级、过程域目标与医院人才引进工作相结合,并提出可操作性指导,具有一定的理论与实践价值。

With the gradual improvement of the requirements for talents in the medical field,hospital human resource management,especially the introduction of talents in hospitals,is changing from large-scale development to refined development．At present,there are some problems in the process of hospital talent introduction,such as lack of human resource development plan,improvement of high-level talent introduction method,improvement of talent management ability,separation of department employment demand from reality,neglect of post competency analysis,etc．People Capability Maturity Model（P-CMM）,as a systematic management idea,has strong practicality．This study discusses and studies the localization application of human resource maturity model in hospital talent introduction,combines different maturity levels and process area objectives of P-CMM with hospital talent introduction,and puts forward operational guidance It has certain theoretical and practical value．

目的 探讨老年吸入性肺炎的危险因素,建立风险预测模型,以期降低老年吸入性肺炎的发病率。方法 选取2017年8月28日—2020年 10月30日广州市第一人民医院老年病科住院治疗的老年肺炎患者205例,按照是否发生吸入性肺炎分为吸入性肺炎组和非吸入性肺炎组,对比2组患者的各项指标,分析老年吸入性肺炎的危险因素,建立风险预测模型,采用ROC曲线对模型进行预测效果检验。结果 多因素Logistic回归分析结果显示,脑梗塞、帕金森、留置胃管、长期卧床为老年吸入性肺炎的危险因素(P<0.05)。模型公式为Logit(P)=-2.952+1.221X₂+2.417X₃+2.388X₈+1.683X₁₀。该模型ROC曲线下面积为0.894。结论 本研究中的模型预测效果良好,可为医护人员预测老年患者发生吸入性肺炎的概率,及时采取相应的预见性护理及干预性治疗。

Objective To explore the risk factors of aspiration pneumonia in the elderly and establish the risk prediction model, in order to reduce the incidence of aspiration pneumonia in the elderly. Methods A total of 205 elderly patients with pneumonia who were hospitalized in the department of geriatrics, Guangzhou First People's Hospital from August 28, 2017 to October 30, 2020, were divided into aspiration pneumonia group and non-aspiration pneumonia group according to whether aspiration pneumonia occurred. The indicators of the two groups of patients were compared, the risk factors of aspiration pneumonia in the elderly were analyzed, the risk prediction model was established, and the prediction effect of the model was tested by receiver operating characteristic curve. Results Multivariate Logistic regression analysis showed that cerebral infarction, Parkinson's disease, indwelling nasogastric tube, and being bedridden were risk factors for aspiration pneumonia in elderly patients (P<0.05). The model formula was Logit (P)=-2.952+1.221X₂+2.417X₃+2.388X₈+1.683X₁₀. The area under receiver operating characteristic curve of this model was 0.894. Conclusion The prediction effect of the model in this study was good, which could predict the probability of aspiration pneumonia in elderly patients for medical staff, and to timely take the corresponding predictive care and interventional treatment.

目的 体外构建胶原—壳聚糖复合支架材料,分析其物理化学性质及生物相容性,探讨其应用于组织工程支架材料的可行性。方法 利用冷冻干燥的方法构建三维多孔的胶原支架材料,通过甲醛交联以及添加壳聚糖的方法改善其物理化学性能。通过体外降解实验以及电镜扫描的方法检测材料的各项物理化学指标;通过细胞接种的方法研究材料的生物相容性。结果 胶原—壳聚糖复合材料通过冷冻干燥的方法,能够获得稳定的三维多孔结构,电镜显示孔隙贯通,体外降解速度降低,并且能够支持细胞生长。理化性质分析显示该结构适合细胞生长,具有良好的生物相容性。结论 本课题体外构建胶原—壳聚糖复合支架材料,满足组织工程生物材料的理化以及生物相容性要求,为其应用于组织工程支架材料提供重要的依据。

Objective We build up the Collagen-Chitosan compound scaffold in vitro,and study the physical,chemical and biological properties,to analyze the feasibility in tissue engineering. Methods The three-dimensional porous scaffold was obtained by freezing-drying method,and optimized by using formaldehyde and Chitosan.We used hydrolysis in vitro and SEM scanning to investigate its physical and chemical properties.The biocompatibility of scaffold was analyzed in MEF cells. Results Collagen-Chitosan compound scaffold we obtained by freezing-drying method was a kind of stable 3D vesicular structure.The scaffold degenerated in decreased velocity in vitro.The physical and chemical properties showed that it was suitable for the cells grow in it,which suggested that it has a good biocompatibility. Conclusion This kind of Collagen-Chitosan compound scaffold is constructed.It's qualified by the physical and chemical properties,and biocompatibility which the biomaterials require.The evidence are important for its application in tissue engineering.

目的 构建抑癌基因SEMA3B真核表达载体pcDNA3.1-SEMA3B,并检测其对肺癌A549细胞恶性生物学行为的影响。方法 应用PCR扩增SEMA3B全长cDNA片段,构建真核表达载体pcDNA3.1-SEMA3B。克隆PCR、双酶切法、基因测序验证过表达载体构建成功。将pcDNA3.1-SEMA3B真核表达载体和空载体pcDNA3.1分别转染入A549细胞中,应用qRT-PCR、Western blot检测SEMA3B mRNA、蛋白表达水平的变化;MTS法检测细胞增殖;流式细胞仪检测细胞凋亡、细胞周期;克隆形成实验检测细胞集落形成能力。结果 SEMA3B基因扩增片段与预测片段一致,克隆成功,且测序鉴定证实真核表达载体构建成功。转染pcDNA3.1-SEMA3B真核表达载体可上调SEMA3B mRNA、蛋白表达水平,且可抑制A549细胞的增殖,诱导凋细胞亡,细胞被阻滞在G1期,抑制细胞集落形成能力。结论 成功构建了SEMA3B基因真核表达载体,抑癌基因SEMA3B在肺癌恶性生物学进程中可能发挥重要作用。

Objective To construct the eukaryotic expression vector of the cancer suppressor gene, SEMA3B, and research the effects on malignant biological behavior of lung cancer A549 cells. Methods By reverse transcriptase-polymerase chain reaction (RT-PCR), the full length SEMA3B gene was amplified and then was inserted into pcDNA3.1. The recombinant plasmid pcDNA3.1-SEMA3B was confirmed correctly through double enzyme digestion and PCR identification, which was transfected into lung cancer A549 cells by lipid media transfection. The untransfected A549 and A549 transfected with pcDNA3.1 were used as controls. SMEA3B gene was detected by qRT-PCR and western blot. MTS assay, flow cytometry, and colony formation test were performed to evaluate the effect of overexpression of SEMA3B gene on A549 cell proliferation, apoptosis, cell cycle, and colony forming ability. Results The amplied fragment of SEMA3B gene by PCR was consistent with the anticipated result, the SEMA3B gene was cloned successfully. And the recombinant plasmid pcDNA3.1-SMEA3B was constructed successfully through gene sequence identification. After transfection of pcDNA3.1-SEMA3B, SEMA3B mRNA and protein expression levels were raised, and overexpression of SEMA3B gene in A549 cells significantly inhibited the proliferation of A549 cells, induced apoptotic cell death, blocked cell cycle in the G1 phase, and suppressed cell colony-forming ability. Conclusion The recombinant pcDNA3.1-SEMA3B is constructed successfully. SEMA3B gene can significantly inhibit the malignant biological behavior of lung cancer A549 cells.