Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterized by a poor prognosis. Mitochondrial dysfunction, including alterations in metabolism, dynamics, and DNA, is increasingly recognized as a critical factor in the initiation and progression of pancreatic cancer. This study aimed to systematically investigate the role of mitochondrial dysfunction in PDAC to identify mitochondria-related genes (MitoRGs) of prognostic significance, explore associated molecular subtypes, and examine their effects on the tumor immune microenvironment. Methods: We integrated transcriptomic data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to identify a set of MitoRGs with significant prognostic value for PDAC. Their expression was further validated in PDAC cells and using single-cell RNA-sequencing data. Unsupervised clustering was employed to classify PDAC patients into distinct subtypes based on MitoRG expression patterns. A robust prognostic model was subsequently constructed using least absolute shrinkage and selection operator-Cox regression analysis. The predictive accuracy of the model for 1-, 3-, and 5-year overall survival (OS) was assessed. The immune cell infiltration and genomic features of the risk groups defined by the model were also analyzed. Finally, a clinically applicable nomogram was developed to facilitate prognostic prediction. Results: Based on MitoRG expression, PDAC patients were classified into two distinct subtypes (clusters A and B). Patients in cluster A exhibited significantly better OS than those in cluster B. A prognostic model based on a seven-MitoRG signature was established, which demonstrated high predictive accuracy. The high-risk group, as defined by the model, was characterized by an immunosuppressive tumor microenvironment, featuring reduced cytotoxic T-cell activity and increased stromal components. This group also showed significant enrichment of driver mutations such as KRAS and TP53. Conclusions: This study established a significant link between mitochondrial dysfunction and PDAC molecular subtypes, immune microenvironment remodeling, and clinical prognosis. The developed seven-MitoRG signature and nomogram could serve as reliable prognostic tools. These findings provide insights into the role of mitochondria in the pathogenesis of PDAC and offer potential targets for developing personalized therapeutic strategies.

Recent advancements in genetically engineered pigs have spurred research into pig-to-human xenotransplantation, particularly involving heart, kidney and liver. Here we characterize immune cell populations cells in both peripheral blood and transplanted liver in a human decedent who received a pig liver xenograft and who was monitored over the course of 10 days. Using single-cell RNA sequencing and spatial RNA sequencing, we found that T cells were progressively activated in the peripheral blood, whereas γδT cells and exhausted T cells infiltrated the pig liver extensively, indicating impaired adaptive immunity. Additionally, we identified two distinct monocyte clusters that may influence the coagulation and immune response after xenotransplantation. First, at an early phase after transplantation, THBS1+ monocytes had the potential to regulate coagulation through interaction with platelets via the THBS1-CD36 signaling pathway. Second, at a later phase, C1QC+ monocytes infiltrated the pig liver, potentially promoting T cell exhaustion through induction of CD274 (PD-L1) expression. In summary, our study highlights how innate immune cells may affect thrombotic and immune pathways after liver xenotransplantation and should spur further research to clarify the roles of THBS1+ and C1QC+ monocytes.

The shortage of donors is a major challenge for transplantation; however, organs from genetically modified pigs can serve as ideal supplements1,2. Until now, porcine hearts and kidneys have been successively transplanted into humans3–7. In this study, heterotopic auxiliary transplantation was used to donate a six-gene-edited pig liver to a brain-dead recipient. The graft function, haemodynamics, and immune and inflammatory responses of the recipient were monitored over the subsequent 10 days. Two hours after portal vein reperfusion of the xenograft, goldish bile was produced, increasing to 66.5 ml by postoperative day 10. Porcine liver-derived albumin also increased after surgery. Alanine aminotransferase levels remained in the normal range, while aspartate aminotransferase levels increased on postoperative day 1 and then rapidly declined. Blood flow velocity in the porcine hepatic artery and portal and hepatic veins remained at an acceptable level. Although platelet numbers decreased early after surgery, they ultimately returned to normal levels. Histological analyses showed that the porcine liver regenerated capably with no signs of rejection. T cell activity was inhibited by anti-thymocyte globulin administration, and B cell activation increased 3 days after surgery and was then inhibited by rituximab. There were no significant peri-operative changes in immunoglobulin G or immunoglobulin M levels. C-reactive protein and procalcitonin levels were initially elevated and then quickly declined. The xenograft remained functional until study completion. A gene-edited pig liver transplanted into a human recipient remains functional after 10 days and indicates that porcine organs could help meet the growing demand for liver transplants.

Exposure to lead (Pb) or copper (Cu) is common and has been associated with increased risk of neurodegenerative disease. However, combined neurotoxic effects of co-exposure to these elements remain unclear. This study aimed to determine the toxic effects of Pb and Cu co-exposure on HT22 cells. In this study, Pb and Cu co-exposure exhibited enhanced toxicity, including increased reactive oxygen species (ROS) and Malondialdehyde (MDA) levels, Superoxide Dismutase 1 (SOD1) activity, lower cell viability and higher apoptotic rates, compared to single-element exposure. Pb and Cu co-exposure also resulted in significantly increased cellular labile Cu level by altering the protein levels of Cu transporters, including Copper Transporter-1 (CTR1), ATPase Copper Transporting-alpha(ATP7A) and ATPase Copper Transporting-beta (ATP7B). Treating with antioxidants or Cu chelator to the co-exposed cells blocked the reduction cell viability and elevation of apoptotic rates. This study suggests that Pb and Cu co-exposure can result in a synergistic toxicity in neuronal cells by inducing oxidative stress and apoptosis. The cellular Cu accumulation may play an important role in inducing these synergistic effects, and both antioxidation and Cu chelation may be promising control measures to alleviate the neurotoxicity of Pb and Cu co-exposure.

Mitochondria dysfunction has been closely linked to a wide spectrum of human cancers, whereas the molecular basis has yet to be fully understood. SLC25A35 belongs to the SLC25 family of mitochondrial carrier proteins. However, the role of SLC25A35 in mitochondrial metabolism reprogramming, development and progression in human cancers remains unclear. Here, we found that SLC25A35 markedly reprogramed mitochondrial metabolism, characterized by increased oxygen consumption rate and ATP production and decreased ROS level, via enhancing fatty acid oxidation (FAO). Meanwhile, SLC25A35 also enhanced mitochondrial biogenesis characterized by increased mitochondrial mass and DNA content. Mechanistic studies revealed that SLC25A35 facilitated FAO and mitochondrial biogenesis through upregulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) via increasing acetyl-CoA-mediated acetylation of PGC-1α. Clinically, SLC25A35 was highly expressed in HCC and correlated with adverse patients’ survival. Functionally, SLC25A35 promoted the proliferation and metastasis of HCC cells both in vitro and in vivo, as well as the carcinogenesis in a DEN-induced HCC mice model. Moreover, we found that SLC25A35 upregulation is caused, at least in part, by decreased miR-663a in HCC cells. Together, our results suggest a crucial oncogenic role of SLC25A35 in HCC by reprogramming mitochondrial metabolism and suggest SLC25A35 as a potential therapeutic target for the treatment of HCC.

目的 探讨固摄补肾针刺法配合经颅直流电刺激治疗脑卒中尿失禁的效果.方法 选择2020 年12 月—2021 年12 月空军军医大学第一附属医院收治的脑卒中尿失禁患者84 例,随机分成对照组和观察组各42 例.2 组患者均予内科常规治疗和排尿反射训练,对照组联合经颅直流电刺激治疗,观察组联合经颅直流电刺激及固摄补肾针刺法治疗,2 组均连续治疗8 周.观察比较2 组患者治疗前及治疗8 周后国际尿失禁咨询委员会尿失禁问卷简表(ICIQ-UI SF)评分、尿失禁生活质量问卷量表(I-QOL)评分、72 h排尿日记、膀胱最大容量、残余尿量变化,评估 2 组临床疗效及治疗安全性.结果 与治疗前比较,治疗8 周后2 组患者ICIQ-UI SF评分明显降低,夜尿次数、白天排尿次数、总排尿次数、尿失禁次数、残余尿量均明显减少,I-QOL评分明显升高,平均每次尿量、膀胱最大容量均明显增加,且观察组上述指标较对照组改善更明显,差异均有统计学意义(P均<0.05);观察组总有效率为92.9％(39/42),明显高于对照组的69.0％(32/42),差异有统计学意义(P<0.05);2 组治疗期间均未发生与经颅直流电刺激和针刺治疗相关的不良事件.结论 固摄补肾针刺法配合经颅直流电刺激治疗脑卒中尿失禁疗效十分显著,能够减少尿失禁次数,减轻尿失禁程度,增大膀胱容量,改善患者生活质量,有助于促进患者机体功能康复.

Globally, hepatocellular carcinoma (HCC) is one of the most common causes of cancer-associated mortalities. The clinical outcome of HCC patients remains poor due to distant metastasis and recurrence. In recent years, growing evidences have confirmed that the coiled-coil domain-containing (CCDC) family proteins are involved in the progression of several diseases. However, the expression and clinical significance of the coiled-coil domain-containing 137 (CCDC137) in hepatocellular carcinoma (HCC) have not been investigated. Level 3 mRNA expression profiles and clinicopathological data were obtained in TCGA-LIHC. Differentially expressed genes (DEGs) were screened between 371 HCC and 50 nontumor specimens. The prognostic value of CCDC137 was analyzed in HCC patients. The correlations between CCDC137 and cancer immune infiltrates were investigated. In this study, a total of 2897 DEGs were obtained: 2451 genes were significantly upregulated and 446 genes were significantly downregulated. KEGG assays revealed that these DEGs were involved in tumor progression. Among 2897 DEGs, we found that CCDC137 expression was distinctly increased in HCC specimens compared with nontumor specimens. A high level of CCDC137 expression was related to an advanced tumor stage and grade. Moreover, patients with higher levels of CCDC137 expression had a shorter overall survival and disease-free survival than patients with lower CCDC137 levels. CCDC137 expression was positively correlated with infiltrating levels of several immune cells, such as CD8 T cells and Th2 cells. Finally, in vitro experiments confirmed that CCDC137 expression was highly expressed in HCC cells, and its knockdown suppressed the proliferation of HCC cells. Taken together, our findings revealed that CCDC137 might be used as a biomarker for immune infiltration and poor prognosis in HCC, which offered fresh insight on potential therapies for HCC.

Solute carrier family 25 member 20 (SLC25A51) is a newly identified mammalian mitochondrial NAD+ transporter. However, the clinicopathological and biological significance of SLC25A51 in human cancers, including hepatocellular carcinoma (HCC), remains unclear. The aim of this study was to define the role of SLC25A51 in HCC progression. Here we demonstrate that SLC25A51 is significantly overexpressed in human HCC specimens and cell lines, caused by, at least in partial, the decrease of miR-212-3p. SLC25A51 overexpression is positively correlated with the clinicopathological characteristics of vascular invasion and tumor diameter, as well as poor survival in patients with HCC. Knockdown of SLC25A51 attenuated, while overexpression of SLC25A51 enhanced the growth and metastasis of HCC cells both in vitro and in vivo. Mechanistically, glucose metabolism reprogramming from oxidative phosphorylation to glycolysis by activation of mitochondrial sirtuin 5 (SIRT5) was found to contribute to the promotion of growth and metastasis by SLC25A51 in HCC cells. Together, these findings reveal important roles of SLC25A51 in HCC tumorigenesis and suggest SLC25A51 as a promising prognostic marker and therapeutic target for treating HCC.

With the increasing use of neoadjuvant therapy (NAT) in patients with pancreatic cancer to reduce tumor burden on prognosis, preoperative biliary drainage (PBD) is becoming increasingly necessary. The aim of this study was to summarize the latest evidence and compare the clinical efficacy of metal stents (MS) and plastic stents (PS) in patients undergoing neoadjuvant therapy for operable pancreatic cancer. Eligible studies were searched in PubMed, Embase and Cochrane Library from their inception to September 2021. In this study, RevMan 5.4 was used to perform the analyses. Two randomized controlled trials (RCTs) and six retrospective studies with 316 patients were included. All patients had pancreatic cancer and received NAT before surgical resection. Meta-analysis showed that the rate of endoscopic reintervention in MS (26/143, 18%) group was lower than that of PS (122/153, 80%) group (P < 0.05). The rate of stent-related complications in MS group was lower (18/118, 15%) than that of PS (52/117, 44%) group (P = 0.02). But there were no significant differences in operative time, operative blood loss, overall postoperative complications, postoperative hospitalization days and total medical costs between the two groups. For operable pancreatic cancer patients undergoing NAT surgery, MS was preferred over PS in terms of the incidence of endoscopic reintervention and stent-related complications. More clinical trials are needed in the future to confirm these data with higher levels of evidence.

Background A better understanding of the molecular mechanisms that manifest in the immunosuppressive tumor microenvironment (TME) is crucial for developing more efficacious immunotherapies for hepatocellular carcinoma (HCC), which has a poor response to current immunotherapies. Regulatory T (Treg) cells are key mediators of HCC-associated immunosuppression. We investigated the selective mechanism exploited by HCC that lead to Treg cells expansion and to find more efficacious immunotherapies. Methods We used matched tumor tissues and blood samples from 150 patients with HCC to identify key factors of Treg cells expansion. We used mass cytometry (CyTOF) and orthotopic cancer mouse models to analyze overall immunological changes after growth differentiation factor 15 (GDF15) gene ablation in HCC. We used flow cytometry, coimmunoprecipitation, RNA sequencing, mass spectrum, chromatin immunoprecipitation and Gdf15–/–, OT-I and GFP transgenic mice to demonstrate the effects of GDF15 on Treg cells and related molecular mechanism. We used hybridoma technology to generate monoclonal antibody to block GDF15 and evaluate its effects on HCC-associated immunosuppression. Results GDF15 is positively associated with the elevation of Treg cell frequencies in patients wih HCC. Gene ablation of GDF15 in HCC can convert an immunosuppressive TME to an inflammatory state. GDF15 promotes the generation of peripherally derived inducible Treg (iTreg) cells and enhances the suppressive function of natural Treg (nTreg) cells by interacting with a previously unrecognized receptor CD48 on T cells and thus downregulates STUB1, an E3 ligase that mediates forkhead box P3 (FOXP3) protein degradation. GDF15 neutralizing antibody effectively eradicates HCC and augments the antitumor immunity in mouse. Conclusions Our results reveal the generation and function enhancement of Treg cells induced by GDF15 is a new mechanism for HCC-related immunosuppression. CD48 is the first discovered receptor of GDF15 in the immune system which provide the possibility to solve the molecular mechanism of the immunomodulatory function of GDF15. The therapeutic GDF15 blockade achieves HCC clearance without obvious adverse events.

Background: Efficient and specific induction of cell death in liver cancer is urgently needed. In this study, we aimed to design an exosome-based platform to deliver ferroptosis inducer (Erastin, Er) and photosensitizer (Rose Bengal, RB) into tumor tissues with high specificity. Methods: Exosome donor cells (HEK293T) were transfected with control or CD47-overexpressing plasmid. Exosomes were isolated and loaded with Er and RB via sonication method. Hepa1-6 cell xenograft C57BL/6 model was injected with control and engineered exosomes via tail vein. In vivo distribution of the injected exosomes was analyzed via tracking the fluorescence labeled exosomes. Photodynamic therapy was conducted by 532 nm laser irradiation. The therapeutic effects on hepatocellular carcinoma and toxic side-effects were systemically analyzed. Results: CD47 was efficiently loaded on the exosomes from the donor cells when CD47 was forced expressed by transfection. CD47 surface functionalization (ExosCD47) made the exosomes effectively escape the phagocytosis of mononuclear phagocyte system (MPS), and thus increased the distribution in tumor tissues. Erastin and RB could be effectively encapsulated into exosomes after sonication, and the drug-loaded exosomes (Er/RB@ExosCD47) strongly induced ferroptosis both in vitro and in vivo in tumor cells after irradiation of 532 nm laser. Moreover, compared with the control exosomes (Er/RB@ExosCtrl), Er/RB@ExosCD47 displayed much lower toxicity in liver. Conclusion: The engineered exosomes composed of CD47, Erastin, and Rose Bengal, induce obvious ferroptosis in hepatocellular carcinoma (HCC) with minimized toxicity in liver and kidney. The proposed exosomes would provide a promising strategy to treat types of malignant tumors.

空军军医大学西京医院针对临床教学中存在的"照本宣科、天马行空和千篇一律"等问题,坚持突破模式束缚,破而后立,在遵循临床医学教学内在规律的基础上重构教学设计,提出了以"破立有道"为基本理念,以"循规'导'矩"为实践策略的课堂设计新思路,总结出针对教学对象、内容取舍、整体设计、方法选择和效果评估等五方面的"ABCDE"模式,并应用于临床医学教学实践,在促进教学实施效果和教师队伍水平方面取得了良好成效.

目的 通过生物信息学分析探讨胰岛素样生长因子结合蛋白(IGFBP)家族成员在肝细胞癌(肝癌)中表达情况和预后价值.方法 利用GEPIA在线分析IGFBP家族在肝癌中的基因表达,Kaplan-Meier生存曲线分析IGFBP与预后关系,采用cBioPortal for Cancer Genomics分析肝癌患者中IGFBP基因改变情况.采用GeneMANIA构建IGFBP相关基因作用网络,Metascape数据库基因网络进行基因本体(GO)富集分析.结果 GEPIA在线分析显示肝癌IGFBP3 mRNA相对表达量明显低于正常肝组织(P<0.05).IGFBP3表达与肿瘤病理分期有关(F=5.52,P<0.05).Kaplan-Meier生存分析显示,IGFBP3和IGFBP4 mRNA表达水平与不良预后密切相关(HR=1.50,0.43;P<0.05).cBioPortal分析显示肝癌中IGFBP发生基因改变,包括突变、融合、扩增、深缺失和多重改变,其中突变、扩增和深缺失是最常见改变.IGFBPs遗传改变0～1％.GeneMANIA分析确定了20个与IGFBPs密切相关的基因,GO富集分析发现IGFBP主要富集在与生长及细胞运动相关的信号通路中.结论 基于生物信息学研究发现IGFBP3在肝癌患者组织中表达异常,且与患者预后相关,IGFBP3可能作为肝癌预后生物标志物和治疗潜在靶点.

Exosomes are emerging as a promising drug delivery vehicle, while the low yield from the cell culture medium restricts their potential application. Exploring strategies boosting the yields would be of significant importance. In this study, we aimed to explore whether low intensity ultrasound (LIUS) irradiation could booster the exosome yield, while having no significant effects on the characteristics. Treatment of LIUS at 0.5 w/cm2 60 min significantly promotes exosomes secretion in A2780 cells, an ovary cancer cell model used to produce exosomes. Moreover, the resultant exosomes had no significant change in morphology, size, and in vivo distribution. Mechanistical study further suggest that LIUS boosts exosome secretion possibly via promoting the expression of exosome biosynthesis/secretion-related genes. Taken together, our data indicate that LIUS could promote exosome biosynthesis, which could be an effective method to increase exosome yield for drug delivery.

幻灯是医学教学中重要的辅助工具,良好的幻灯能直观、形象地展示医学教学的主要内容和重要知识点,幻灯的设计是教学目标的充分体现,而幻灯的美感则是决定幻灯质量和教学效果的关键点之一.笔者从所在医院教学实践中存在的教学幻灯美感问题出发,针对性地总结出医学教学幻灯美学设计的基本原则和方法:整体上应构图优美、页面简洁、用色恰当;细节上宜精准配图、美化文字、图文并茂、巧用动画等动态媒体元素.需要注意的是:教学幻灯美化不能"为了美而美",而应以提高教学效果为目标;掌握通用的幻灯美学设计原则和技巧固然重要,但美感的创作更多地需要教师在生活实践中不断培养和提升自身内在的美学修养.

Hepatocellular carcinoma (HCC) is one of the most lethal malignant diseases worldwide. Despite advances in the diagnosis and treatment of HCC, its overall prognosis remains poor. Recent studies have shown that long noncoding RNAs (lncRNAs) play crucial roles in various pathophysiological processes, including liver cancer. In the current study, we report that lncRNA SLC2A1‐AS1 is frequently downregulated in HCC samples, as shown by quantitative real‐time polymerase chain reaction analysis. SLC2A1‐AS1 deletion is significantly associated with recurrence‐free survival in HCC. By performing glucose uptake, lactate production and ATP detection assays, we found that SLC2A1‐AS1‐mediated glucose transporter 1 (GLUT1) downregulation significantly suppressed glycolysis of HCC. In vitro Cell Counting Kit‐8, colony formation, transwell assays as well as in vivo tumorigenesis and metastasis assays showed that SLC2A1‐AS1 overexpression significantly suppressed proliferation and metastasis in HCC through the transcriptional inhibition of GLUT1. Results from fluorescence in situ hybridization, ChIP and luciferase reporter assays demonstrated that SLC2A1‐AS1 exerts its regulatory role on GLUT1 by competitively binding to transketolase and signal transducer and activator of transcription 3 (STAT3) and inhibits the transactivation of Forkhead box M1 (FOXM1) via STAT3, thus resulting in inactivation of the FOXM1/GLUT1 axis in HCC cells. Our findings will be helpful for understanding the function and mechanism of lncRNA in HCC. These data also highlight the crucial role of SLC2A1‐AS1 in HCC aerobic glycolysis and progression and pave the way for further research regarding the potential of SLC2A1‐AS1 as a valuable predictive biomarker for HCC recurrence.

Objectives: To propose a novel clinical classification system of gallbladder cancer, and to investigate the differences of clinicopathological characteristics and prognosis based on patients who underwent radical resection with different types of gallbladder cancer. Methods: The clinical data of 1 059 patients with gallbladder cancer underwent radical resection in 12 institutions in China from January 2013 to December 2017 were retrospectively collected and analyzed.There were 389 males and 670 females, aged (62.0±10.5)years(range:22-88 years).According to the location of tumor and the mode of invasion,the tumors were divided into peritoneal type, hepatic type, hepatic hilum type and mixed type, the surgical procedures were divided into regional radical resection and extended radical resection.The correlation between different types and T stage, N stage, vascular invasion, neural invasion, median survival time and surgical procedures were analyzed.Rates were compared by χ(2) test, survival analysis was carried by Kaplan-Meier and Log-rank test. Results: Regional radical resection was performed in 940 cases,including 81 cases in T1 stage,859 cases in T2-T4 stage,119 cases underwent extended radical resection;R0 resection was achieved in 990 cases(93.5%).The overall median survival time was 28 months.There were 81 patients in Tis-T1 stage and 978 patients in T2-T4 stage.The classification of gallbladder cancer in patients with T2-T4 stage: 345 cases(35.3%)of peritoneal type, 331 cases(33.8%) of hepatic type, 122 cases(12.5%) of hepatic hilum type and 180 cases(18.4%) of mixed type.T stage(χ(2)=288.60,P<0.01),N stage(χ(2)=68.10, P<0.01), vascular invasion(χ(2)=128.70, P<0.01)and neural invasion(χ(2)=54.30, P<0.01)were significantly correlated with the classification.The median survival time of peritoneal type,hepatic type,hepatic hilum type and mixed type was 48 months,21 months,16 months and 11 months,respectively(χ(2)=80.60,P<0.01).There was no significant difference in median survival time between regional radical resection and extended radical resection in the peritoneal type,hepatic type,hepatic hilum type and mixed type(all P>0.05). Conclusion: With application of new clinical classification, different types of gallbladder cancer are proved to be correlated with TNM stage, malignant biological behavior and prognosis, which will facilitate us in preoperative evaluation,surgical planning and prognosis evaluation.

Background: There is no guideline recommendation for preventing hepatocellular carcinoma (HCC) recurrence after hepatic resection. Moreover, an unmet need exists on the effectiveness of sorafenib therapy in recurrent HCC. Purpose: We therefore assessed the efficacy and safety of sorafenib in Chinese HCC patients with high risk of recurrence. Patients and methods: Data were collected retrospectively from 15 Chinese research centers from January 1, 2012 to November 15, 2013, by chart reviews of patients with moderate-advanced HCC who received hepatic carcinectomy. The primary end point was recurrence-free survival rate at 1 year in patients with a high recurrence risk. Secondary end points included 1-year survival rate, time to recurrence and safety assessment. Results: A total of 209 high-risk patients (sorafenib, n=98; control, n=111) who underwent carcinectomy were analyzed. There was no significant difference in the proportion of patients with recurrence-free survival at 1 year between the sorafenib and control (70.43% vs 68.90%: χ2=0.007, P=0.934). One-year survival rate was significantly higher with sorafenib than observed with control (95.5% vs 83.35%; χ2=7.441, P=0.006). Time to recurrence between sorafenib and control groups was similar. Incidences of all the adverse events (AEs) were similar in both the groups and transaminase elevation was most common in both groups (20.37% vs 24.79%). Thrombocytopenia incidence was significantly lower with the sorafenib group than with control (1.85% vs 9.40%; P=0.015). Conclusion: Sorafenib may be considered as a feasible option in the treatment of HCC recurrence.

目的:探讨肝癌切除术后患者D-二聚体(D-Di)及纤维蛋白原降解产物(FDP)的变化与深静脉血栓形成(D V T)的关系,以指导D V T的防治.方法:回顾性分析381例手术切除的肝癌患者,对发生DV T的7例(A组)及符合入组条件、未发生DV T的68例(B组)的D-Di及FDP术前、术后变化进行研究分析.结果:两组患者术后D-Di及FDP值均较术前升高.两组的D-Di值在术后第1、3、5天均持续升高,但B组升高的幅度低于A组的半数.A组的FDP值术后第1、3、5天持续升高;B组的FD P在术后第1天达到高峰,之后开始波动式下降.两组FD P的组间、时点间的效应差异及组间时点间的交互效应差异均无统计学意义(P>0.05),而两组D-Di的组间、时点间的效应差异及组间时点间的交互效应差异均有统计学意义(P<0.01).结论:肝癌切除术后若D-Di及FDP呈持续上升态势,要高度警惕DVT发生.快速康复外科(ERAS)治疗有利于深静脉血栓的预防.

目的 探讨肝细胞腺瘤(HCA)的临床诊治.方法 回顾性分析西京医院2009年1月至2016年12月收治的12例HCA患者的临床资料,对患者的诊治过程进行分析总结.结果 12例患者均手术切除病变,术后行病理检查明确诊断.所有患者术后均恢复良好.5例(41.67％)患者诊断为腺瘤并局部癌变,最小癌变病灶3.7 cm.术后获随访12例,随访时间18～103个月,除1例亡故于心脏病外,其他无死亡病例.术后复发2例,经射频消融治疗后痊愈.结论 HCA临床少见,易误诊.>3.5 cm的病灶病变出血及恶变几率增加,应采取积极手术治疗;<3.5 cm的病灶射频消融效果良好,患者总体预后良好.