Emerging data indicate that chromatin licencing and DNA replication factor 1 (CDT1) plays an important role in several cancers. However, it remains unclear whether CDT1 is functionally indispensable in lung cancer. Here, constructing tissue microarrays and performing in vitro and vivo experiments, we showed that CDT1 was significantly overexpressed in lung adenocarcinoma tissues, and its expression level significantly correlated with pathological stage, tumour invasiveness, and overall patient survival. Mechanistic investigations revealed that CDT1 possibly interacted with the transcription factor adenovirus early region 2 binding factor 1 (E2F1), thereby cooperatively enhancing the transcriptional activity of the targeting protein for Xenopus kinesin-like protein 2 (TPX2) gene. This phenomenon subsequently increased the expression of glycolysis-related molecules aldolase C and pyruvate kinase M2 via the PI3K/AKT signalling pathway, which promoted the proliferation and migration of non-small cell lung cancer (NSCLC) cells. Critically, knockdown of TPX2 or treatment with either the AKT pathway inhibitor MK-2206 2HCl or the glycolysis inhibitor AZ33 effectively reversed the promoting effects of CDT1 on AKT pathway activity, glycolytic metabolism, and tumour progression in CDT1-overexpressing NSCLC cells. Collectively, this study elucidates that CDT1 and E2F1 mutually promote the glycolysis and progression of NSCLC cells by activating the TPX2/AKT pathway. These findings provide novel therapeutic targets for refractory NSCLC treatment.

Paraptosis plays a critical role in mediating anti-tumor effects by inducing cell death in cancer cells. However, its specific involvement in lung adenocarcinoma (LUAD) remains inadequately understood. This study aims to systematically investigate the prognostic significance and underlying mechanisms of paraptosis-related genes (PRGs) in LUAD. Differentially expressed genes were identified between LUAD and control samples from the training set and cross-referenced with PRGs to generate candidate genes (CGs). Prognostic genes were selected from CGs using regression analysis, leading to the development of a LUAD risk model, which was validated in an independent validation set. Clinical characteristics were analyzed to identify independent prognostic factors for constructing a nomogram. Functional and immune infiltration analyses were performed on high-/low-risk cohorts from the training set. Drug predictions related to prognostic genes were made and subsequently validated through molecular docking. Polymerase chain reaction was performed to validate the expression of prognostic genes. Four prognostic genes (CDKN3, PEBP1, TNFRSF19, and PHB) were identified from 27 CGs through regression analysis. The prognostic risk model demonstrated robust predictive capacity for LUAD prognosis and exhibited generalizability. Significant associations were observed between risk scores and clinical features, including age, TNM.stage, T-stage, and N-stage (P < .05). These risk scores served as independent prognostic factors for the nomogram model, offering strong predictive power for LUAD. Vorinostat and raloxifene exhibited notable binding affinity for PEBP1. Elevated CDKN3 expression was observed in LUAD, while PEBP1 and TNFRSF19 expressions were reduced. This study highlights the prognostic value of PRGs, specifically CDKN3, PEBP1, TNFRSF19, and PHB. CDKN3 and PHB emerged as risk factors for LUAD prognosis, whereas PEBP1 and TNFRSF19 did not. In-depth analysis of the tumor microenvironment revealed the distribution and correlations of immune cell types influenced by PRGs and risk score. Furthermore, an independent prognostic model for LUAD was developed, enhancing our understanding of high-/low-risk cohorts' functional pathways. Drug prediction results provided valuable insights into potential therapeutic strategies for LUAD, warranting further investigation.

BACKGROUND:Checkpoint inhibitor-related pneumonitis (CIP) represents a highly lethal immune-related adverse event. Early diagnosis of CIP is crucial for timely intervention and improved prognosis; however, the absence of precise and effective diagnostic techniques often leads to underdiagnosis and misdiagnosis. This study aims to identify microRNA (miRNA) features from serum and extracellular vesicles (EVs) for the early CIP detection and prognosis. METHODS:Small RNA sequencing identified candidate miRNAs in 27 serum-derived EV samples from persons with lung cancer and CIP (CIP group) and those without, including immunotherapy-treated persons with lung cancer without CIP (immune checkpoint inhibitor, ICI group) and patients with infectious pneumonia (PNE group). These miRNAs were validated in EV samples in a discovery cohort (n=48) using a quantitative reverse transcription-PCR (qRT-PCR). Diagnostic models for the biomarkers were developed using a training cohort (ICI:47, PNE:28, CIP:31) and validated in a separate validation cohort (ICI:32, PNE:19, CIP:21) using qRT-PCR in both EV and serum samples, and logistic regression. Using a Cox regression model, we built a prognostic risk stratification for patients with CIP based on three miRNAs. RESULTS:Sequencing analysis initially screened and identified 13 overexpressed miRNAs in patients with CIP. Subsequently, qRT-PCR demonstrated that three miRNAs (EVs miR-193a-5p, serum miR-193a-5p, and serum miR-378a-3p) effectively distinguished CIP from non-CIP individuals (training cohort: area under the curve (AUC)=0.870; validation cohort: AUC=0.837). Notably, this miRNA signature was equally robust in differentiating CIP from ICI (training cohort: AUC=0.823; validation cohort: AUC=0.845) and PNE groups (training cohort: AUC=0.892; validation cohort: AUC=0.907). Furthermore, when combined with lymphocyte levels, the miRNA signature significantly enhanced the overall diagnostic accuracy in distinguishing CIP from the non-CIP group (training cohort: AUC=0.900; validation cohort: AUC=0.932), and maintained its robustness in distinguishing CIP from the ICI group (training cohort: AUC=0.898; validation cohort: AUC=0.946) and the PNE group (training cohort: AUC=0.938; validation cohort: AUC=0.959). Additionally, the three-miRNA panel was independently and significantly associated with overall survival in patients with CIP (HR: 2.827; p=0.040). CONCLUSIONS:Our circulating miRNA-based signature represents a non-invasive and robust diagnostic tool for patients with CIP and could accurately predict their prognosis. This signature may facilitate early detection and personalized management of these patients.

BACKGROUND Hepatoid adenocarcinoma of the lung (HAL) is a rare type of non-small cell lung cancer (NSCLC), histologically similar to hepatocellular carcinoma. HAL has high malignancy and poor prognosis, and a better treatment plan needs further study. CASE SUMMARY In order to deeply understand the occurrence and development of HAL, here we report a case of HAL with extensive metastasis of alpha fetoprotein negative KRAS A146T mutation. The patient refused chemotherapy and received one course of treatment (immune checkpoint inhibitors), and died three months later due to progressive disease. CONCLUSION HAL is a special type of NSCLC. The surgical treatment of HAL in the limited stage can achieve long-term survival, but most of them were in the advanced stage when they were found, and the prognosis was poor, which requires multidisciplinary comprehensive treatment.

BackgroundLung adenocarcinoma (LUAD), the most common histotype of lung cancer, may have variable prognosis due to molecular variations. The research strived to establish a prognostic model based on malignancy-related risk score (MRRS) in LUAD.MethodsWe applied the single-cell RNA sequencing (scRNA-seq) data from Tumor Immune Single Cell Hub database to recognize malignancy-related geneset. Meanwhile, we extracted RNA-seq data from The Cancer Genome Atlas database. The GSE68465 and GSE72094 datasets from the Gene Expression Omnibus database were downloaded to validate the prognostic signature. Random survival forest analysis screened MRRS with prognostic significance. Multivariate Cox analysis was leveraged to establish the MRRS. Furthermore, the biological functions, gene mutations, and immune landscape were investigated to uncover the underlying mechanisms of the malignancy-related signature. In addition, we used qRT-PCR to explore the expression profile of MRRS-constructed genes in LUAD cells.ResultsThe scRNA-seq analysis revealed the markers genes of malignant celltype. The MRRS composed of 7 malignancy-related genes was constructed for each patient, which was shown to be an independent prognostic factor. The results of the GSE68465 and GSE72094 datasets validated MRRS’s prognostic value. Further analysis demonstrated that MRRS was involved in oncogenic pathways, genetic mutations, and immune functions. Moreover, the results of qRT-PCR were consistent with bioinformatics analysis.ConclusionOur research recognized a novel malignancy-related signature for predicting the prognosis of LUAD patients and highlighted a promising prognostic and treatment marker for LUAD patients.

Abstract Background Lung squamous cell carcinoma (LUSC) is a main subgroup of non-small cell lung cancer that accounts for ~ approximately 80% of all lung cancer. Studies have demonstrated that tumor microenvironment is essential for the occurrence and development of LUSC. The present study identified the immune- and metabolic-related genes to construct a prognostic model for LUSC patients. Methods We downloaded RNA-sequence data and clinical information of LUSC patients from The Cancer Genome Atlas database. The differentially expressed metabolic-related genes (DMRGs) and the differentially expressed immune-related genes (DIRGs) between the control samples and LUSC patient samples were identified. Gene ontology analysis and Kyoto Encyclopedia of Genes and Genomes analysis were performed to explore the potential biological processes of harvested DMRGs and DIRGs. To develop a prognostic model for LUSC patients, we selected prognostic genes from DMRGs and DIRGs through the univariate and multivariate Cox regression. The prognostic value of the risk model was detected via the Kaplan-Meier curve and the area under the receiver operating characteristic curve analysis. Gene set enrichment analysis (GSEA) was operated to investigate the underlying latent pathways associated with the high-risk group. The infiltration of immune cells in the high- and low-risk groups were analyzed using the single-sample gene-set enrichment analysis. Results A total of 178 DMRGs were identified, which were mainly enriched in nucleoside phosphate biosynthetic process, carboxylic acid biosynthetic process, and cofactor metabolic process. Around 264 DIRGs were primarily associated with chemotaxis regulation, leukocyte migration, and positive regulation of cytokine production. After the univariate and multivariate Cox regression analyses, a prognostic risk model containing four prognostic genes was constructed, which performed better in prognosing LUSC patients via the ROC analysis. Moreover, the risk score was found to be an independent prognostic factor through the multivariate Cox regressions analysis. The GSEA suggested that the chemokine signaling pathway, cytokine-cytokine receptor interaction, and IL-17 signaling pathway were mainly enriched in the high-risk group. Finally, the risk score was mostly correlated with immune-related score and immune infiltration cells. Conclusion We constructed an immune- and metabolic-related gene signature that was quite reliable in predicting prognosis of LUSC patients.

Lung cancer has become the primary cause of cancer-related deaths because of its high recurrence rate, ability to metastasise easily, and propensity to develop drug resistance. The wide-ranging heterogeneity of lung cancer subtypes increases the complexity of developing effective therapeutic interventions. Therefore, personalised diagnostic and treatment strategies are required to guide clinical practice. The advent of innovative three-dimensional (3D) culture systems such as organoid and organ-on-a-chip models provides opportunities to address these challenges and revolutionise lung cancer research and drug evaluation. In this review, we introduce the advancements in lung-related 3D culture systems, with a particular focus on lung organoids and lung-on-a-chip, and their latest contributions to lung cancer research and drug evaluation. These developments include various aspects, from authentic simulations and mechanistic enquiries into lung cancer to assessing chemotherapeutic agents and targeted therapeutic interventions. The new 3D culture system can mimic the pathological and physiological microenvironment of the lung, enabling it to supplement or replace existing two-dimensional culture models and animal experimental models and realize the potential for personalised lung cancer treatment.

We report a female patient, who presented as a carcinoma of unknown primary site with multiple tumors in breast, lung, stomach, and ovary, was confirmed to be lung adenocarcinoma as primary cancer through detecting EML4-ALK rearrangement by the next generation sequencing (NGS). The patient was treated with crizotinib and resulted in significant regression of the primary and metastatic tumors, but resistance to crizotinib was developed 5 months after the treatment. Targeted therapy was, therefore, switched to alectinib, one of the second-generation of anaplastic lymphoma kinase (ALK) inhibitors, with excellent therapeutic response till November 16th, 2021. This study suggested that NGS be recommended to detect ALK rearrangement in the patients with carcinoma of unknown primary site, and that resistance to targeted therapy with ALK inhibitors should be considered for personalized precision medicine.

Background Vascular air embolism (VAE) is a rare but important complication that has not been paid enough attention to in the medical process such as surgery and anesthesia. Case presentation We report for the first time that a 54-year-old male patient with central lung cancer developed severe complications of CAE after right pneumonectomy. After targeted first-aid measures such as assisted breathing, mannitol dehydration and antibiotic treatment, the patient gradually improved. The patient became conscious at discharge after 25 days of treatment but left limb was left with nerve injury symptoms. Conclusion We analyzed the possible causes of CAE in this case, and the findings from this report would be highly useful as a reference to clinicians.

Sterol O-acyltransferase 1 (SOAT1) is a key enzyme in lipid metabolism, which mediates cholesterol esterification metabolism and is closely associated with many cancers. However, the role of SOAT1 in lung cancer invasion remains unclear. We found that SOAT1 expression was positively correlated with lung cancer invasion. Downregulation of SOAT1 inhibited invasion, mitochondrial fragmentation, AKT phosphorylation, and phospho-Drp (Ser616) in lung cancer cells and promoted intracellular free cholesterol accumulation. Mechanistically, the AKT phosphorylation inhibitor MK-2206 alleviated both SOAT1 overexpression and high expression-induced mitochondrial fragmentation and lung cancer cell invasion. Furthermore, intracellular free cholesterol accumulation reduced AKT phosphorylation, SREBP1 mRNA expression, cell invasion, and mitochondrial fragmentation in lung cancer cells with high SOAT1 expression. In summary, our findings suggest that SOAT1 promotes lung cancer invasion by activating the PI3K/AKT signaling pathway by downregulating intracellular free cholesterol levels, thereby affecting the regulation of mitochondrial fragmentation.

Sterol O-acyltransferase 1 (SOAT1) is a key enzyme in lipid metabolism, which mediates cholesterol esterification metabolism and is closely associated with many cancers. However, the role of SOAT1 in lung cancer invasion remains unclear. We found that SOAT1 expression was positively correlated with lung cancer invasion. Downregulation of SOAT1 inhibited invasion, mitochondrial fragmentation, AKT phosphorylation, and phospho-Drp (Ser616) in lung cancer cells and promoted intracellular free cholesterol accumulation. Mechanistically, AKT phosphorylation inhibitor MK-2206 alleviated both SOAT1 overexpression or high expression-induced mitochondrial fragmentation and lung cancer cell invasion. Furthermore, intracellular free cholesterol accumulation reduced AKT phosphorylation, SREBP1 mRNA expression, cell invasion, and mitochondrial fragmentation in lung cancer cells with high SOAT1 expression. In summary, our findings suggest that SOAT1 promotes lung cancer invasion activates the PI3K/AKT signaling pathway by downregulating intracellular free cholesterol levels, thereby affecting the regulation of mitochondrial fragmentation.

背景 严重气管狭窄是一种危重症,患者在清醒状态时无法耐受纤维支气管镜检查,还存在全身麻醉诱导后无法建立有效气管的风险.既往实施复杂气管病变手术患者术中常规使用双套气管插管,但会影响手术视野,延长手术时间,而术中应用体外膜肺氧合(ECMO)可解决上述问题.目的 探讨ECMO在严重气管狭窄及复杂气管病变手术中的应用效果.方法 选取2013年9月—2017年5月南方医科大学深圳医院和兰州大学第二医院收治的严重气管狭窄和复杂气管病变患者8例,均在ECMO支持下行严重气管狭窄及复杂气管病变外科手术,分析患者预后.结果 8例患者中,6例恢复良好,1例死亡,1例行探查术.随访2年7个月～6年3个月,4例创伤后气管狭窄患者及2例气管腺样囊性癌患者术后未见气管狭窄或肿瘤复发迹象;1例气管食管瘘患者因高位截瘫无自主呼吸致肺部严重感染,呼吸衰竭死亡;1例因气管狭窄位置较高,胸外科未能行气管端端吻合术,后就诊于外院耳鼻喉科,行气管甲状软骨吻合术,术后未出现狭窄复发.结论 ECMO在严重气管狭窄及复杂气管病变患者手术中安全可行.

This study aimed to explore the molecular mechanism by which mesenchymal stem cells (MSCs) mediate lung cancer progression. Extracellular vesicles (EVs) were isolated from transfected or untransfected MSCs, and were co-cultured with lung cancer cells with/without microRNA-130b-3p (miR-130b-3p) inhibitor, mimic, overexpression plasmids of FOXO3/NFE2L2, or shRNAs. CCK-8 assay, colony formation, transwell assay, and flow cytometry were carried out to determine the biological functioning of lung cancer cells. Furthermore, FOXO3, Keap1, NFE2L2, and TXNRD1 expression was determined by qRT-PCR and western blot analysis. A tumor xenograft mouse model was used to determine role of EVs-miR-130b-3p and its target FOXO3 in lung cancer progression in vivo. miR-130b-3p was highly expressed in lung cancer tissues and MSC-derived EVs. Moreover, the MSC-derived EVs transferred miR-130b-3p to lung cancer cells to promote cell proliferation, migration, and invasion while repress cell apoptosis. miR-130b-3p directly targeted FOXO3, and FOXO3 elevated Keap1 expression to downregulate NFE2L2, thus inhibiting TXNRD1. FOXO3 overexpression or silencing of NFE2L2 or TXNRD1 diminished lung cancer cell proliferation, invasion, and migration but enhanced apoptosis. EV-delivered miR-130b-3p or FOXO3 silencing promoted lung cancer progression in vivo. In summary, MSC-derived EVs with upregulated miR-130b-3p suppressed FOXO3 to block the NFE2L2/TXNRD1 pathway, thus playing an oncogenic role in lung cancer progression.

BACKGROUND:Pneumonectomy and sleeve resection are routine operations for the treatment of central non-small cell lung cancer (NSCLC), but some patients suffered of central NSCLC, whose pulmonary function is too poor to tolerate pneumonectomy, or the tumor involves the bronchus and pulmonary artery extensively,it is hard to perform bronchovascular sleeve lobectomy. The aim of this study is to assess the feasibility of lung autotransplantation in the treatment of central NSCLC.METHODS:The clinical data of 3 cases with central NSCLC treated by lung autotransplantation was reviewed from December 2016 to December 2018. One patient underwent double sleeve resection of left upper lobe with end-to-end anastomosis of the bronchus. Because the resection of the pulmonary artery was too long to perfrom a tension-free anastomosis, the inferior pulmonary vein was cut off, then the left lower lobe was moved up for an anastomosis of the inferior pulmonary vein and the stump of the superior pulmonary vein. In the other 2 cases, left pneumonectomy was performed directly, and the upper left lobe was excised in vitro. The lower left lobe was reset to the chest after trimming and flushing and then the bronchus, pulmonary artery and pulmonary vein were anastomosed in turn.RESULTS:The average operation time was 333 min, the average time of vascular occlusion was 86 min, the average blood loss was 450 mL, and the average hospital stay was 18.7 d; Perioperative complications included a case of bronchial obstruction, which improved after sputum aspiration through bronchofibroscope. The average follow-up period was 20 mon; One case died of cancer, one case had recurrence of anastomotic stoma and brain metastasis, one case had 4R lymph node metastasis (stable condition after chemotherapy), and one case survived without recurrence.CONCLUSIONS:For patients with central NSCLC with extensive tumor invasion, thus inability to tolerate sleeve resection or pneumonectomy, autologous lung transplantation can preserve lung function to the greatest extent with a complete tumor resection and improve postoperative quality of life.

ABSTRACT This study aimed to explore the molecular mechanism by which mesenchymal stem cells (MSCs) mediate lung cancer progression. Extracellular vesicles (EVs) were isolated from transfected or untransfected MSCs, and were used to treat lung cancer with/without inhibitor, mimic, overexpression plasmid or shRNAs. CCK-8 assay, colony formation, transwell assay and flow cytometry were carried out to determine biological functioning of lung cancer cells. Furthermore, FOXO3, Keap1, NFE2L2 and TXNRD1 expression was determined by RT-qPCR and Western blot analysis. A tumor xenograft mouse model was used to determine role of EVs-microRNA-130b-3p (miR-130b-3p) and its target FOXO3 in lung cancer progression in vivo. miR-130b-3p was highly expressed in lung cancer tissues and MSC-derived EVs. Moreover, the MSC-derived EVs transferred miR-130b-3p to lung cancer cells to promote cell proliferation, migration and invasion while repressing cell apoptosis. miR-130b-3p directly targeted FOXO3, and FOXO3 elevated Keap1 expression to downregulate NFE2L2, thus inhibiting TXNRD1. FOXO3 overexpression or silencing of NFE2L2 or TXNRD1 diminished lung cancer cell proliferation, invasion, and migration but enhanced apoptosis. EV-delivered miR-130b or FOXO3 silencing promoted lung cancer progression in vivo. In summary, MSC-derived EVs with upregulated miR-130b-3p suppressed FOXO3 to block the NFE2L2/TXNRD1 pathway, thus playing an oncogenic role in lung cancer progression.

目的 探讨肺隔离症的诊断和治疗策略.方法 2017年7月至2019年6月收治的4例肺隔离症患者,3例患者行胸腔镜手术治疗,1例行介入下血管塞封堵迷走供血动脉,对其诊治过程和临床资料进行回顾性分析,总结诊治过程中的体会.结果 4例肺隔离症患者均接受治疗,1例患者接受介入下血管塞封堵迷走供血动脉后恢复顺利;1例患者胸腔镜下肺叶切除术后恢复顺利;2例患者接受胸腔镜下隔离肺叶切除术,其中1例恢复顺利,1例因胸腔进行性出血行胸腔镜下开胸止血术,后恢复顺利.术后3月复查胸部螺旋计算机体层摄影血管造影显示,3例行胸腔镜下隔离肺叶或肺叶切除手术患者的异常肺叶及供血动脉消失,行介入下血管塞封堵异常血管的1例患者的迷走供血动脉被栓塞,栓塞血管远端已无血流供应,隔离肺组织充血表现较前明显好转,4例患者随访7～31个月,未见复发.在手术时间、术中出血量、术后疼痛、术后胸腔闭式引流量、术后并发症、住院时间及住院费用等方面,介入栓塞治疗均优于胸腔镜手术治疗.结论 胸腔镜手术是目前处理肺隔离症的主要方式,介入栓塞治疗肺隔离症同样是一种安全、有效、微创的治疗方法,尤其对以咯血为主要症状,凝血功能异常且病情较重者效果佳.

目的 探讨编织技术微创治疗鸡胸的可行性.方法 回顾性分析2011年1月至2018年12月收治的51例鸡胸患者的临床资料,其中男47例、女4例,年龄9～29(13.7±2.9)岁,均行胸腔镜直视下置入穿插走行于皮下、肋间、胸骨的矫形钢板微创治疗,置入钢板数量依胸壁畸形程度而定.术后2年取出钢板.结果 51例均顺利完成手术,钢板置入手术时间(63.9±15.8) min,出血量(19.8±8.8)mL,术后住院时间(4.6±1.6)d;并发症有2例肋间动脉损伤,4例气胸,3例胸腔积液,1例皮肤破裂,29例术后第1d中度疼痛(疼痛数字评价量表评分4～6分),无因不可耐受的不适而取出钢板者.37例于术后2年取出钢板,术后住院时间(1.4±0.5)d,常规随访33(1～48)个月,矫形效果评价22例优秀,9例良好,胸廓外形得到明显改善;5例一般,1例差;未发现置入钢板对患者生长发育存在不良影响.结论 编织技术微创治疗鸡胸安全、可行、有效,胸廓修复效果满意.

目的 探讨在护理科研教学过程中应用TBL教学模式对本科护生科研能力的效果.方法 采用自愿原则组成TBL学习小组,按照护理科研流程将TBL教学模式贯穿于我院大三本科护生护理科研教学全过程,通过问卷评价TBL教学模式对护生科研能力的作用.结果 学生课程期末考试成绩和总成绩呈正态分布,总成绩80分以上者占92.17％,优秀率达6.41％.课后教学效果反馈表明,96.80％的学生认可TBL教学模式.学生各项科研能力得分和总分均较开展教学前显著提高(P<0.01),科研水平较干预前明显提高(P<0.05),TBL教学模式可以显著提高学生的科研兴趣、胜任科研工作的自信度和科研活动的参与度(P<0.05).结论 TBL教学模式引导学生渐进式掌握和实践护理科研课程内容,有利于调动学生平时学习的积极性、主动性和协作性,激发学生科研兴趣,全面提高了学生的综合素质.

目的:了解本学院不同实习医院本科护生临床实习满意度的状况.方法:采用问卷调查法对7所三级甲等综合医院实习的120名本科护生进行临床实习满意度调查.结果:7家实习医院总体评分结果显示,总体带教满意度为(4.19±0.76)分,3个维度从高到低依次为临床带教为(20.74±3.21)分、教学环境(19.16±3.60)分,教学管理为(16.34±2.71)分;不同科室满意度评分分别为内科(17.73±2.26)分、外科(17.64±2.22)分、妇产科(17.31±2.35)分、儿科(16.96±2.55)分.结论:各实习医院均能满足学生的实习需求,但应重视护理实践教学环境,加强教学管理,以提高实习效果,稳定护生的职业稳定性.

目的 靶向程序性死亡分子1(programmed cell death ligand 1,PD-1)通路的肿瘤免疫治疗在多种类型肿瘤中取得了卓越的临床疗效,包括非小细胞肺癌(non-small cell lung carcinoma,NSCLC).本研究关注2种靶向结合PD-1受体的单克隆抗体Pembrolizumab和Nivolumab一线治疗在我国晚期NSCLC患者中的疗效.方法 2例未接受过任何治疗的确诊为晚期鳞状NSCLC患者,患者甲给予Pembrolizumab 100mg/3w、患者乙给予Nivolumab 2 mg/(kg·2 w),均静脉注射,定期评估疗效.结果 经2周期治疗后,2例患者肺部肿瘤均达部分缓解(partial response,PR),呼吸系统症状及炎症好转;患者甲最终因肺癌脑转移于免疫治疗第3周期后死亡.患者乙治疗期间肺部原发病灶逐渐缩小,疗效评价PR;拟行第4周期治疗时发现脑部多发转移瘤,拟行第5周期时脑部多发转移瘤较前略有增大,疗效评价稳定(stable disease,SD),迄今仍在维持治疗.治疗期间,2例患者肿瘤标志物CA125均显著下降.治疗期间未观察到不良反应.结论 初步研究显示PD-1抑制剂治疗晚期NSCLC原发病灶疗效显著,安全性好,血清CA125浓度可作为一个评价疗效的观察指标.但PD-1抑制剂对控制脑部转移灶的疗效需要进一步研究.由于本研究入组人数较少,此结论尚需得到进一步的论证.