目的 观察妊娠中晚期缺铁性贫血现状并研究血清铁蛋白水平对缺铁性贫血、妊娠结局的影响效应.方法 选取2018年1月至2021年1月宁德师范学院附属宁德市医院门诊建档立卡的妊娠中晚期妇女190例作为研究对象.比较190例妊娠中晚期妇女贫血现状,分别按照不同妊娠时期及不同血清铁蛋白水平进行分组,分析血清铁蛋白水平与妇女妊娠中晚期缺铁性贫血发生及妊娠结局的关系,以及血清铁蛋白、血红蛋白水平及二者联合检测对妊娠结局的评估价值.结果 妊娠晚期缺铁性贫血发生率高于妊娠中期,差异有统计学意义(χ2=7.161,P<0.05).妊娠晚期轻度贫血发生率低于妊娠中期,中度及重度贫血发生率均高于妊娠中期,差异有统计学意义(Z=2.216,P<0.05).随着血清铁蛋白水平升高,妊娠中晚期缺铁性贫血发生率逐渐下降,差异有统计学意义不同血清铁蛋白水平者妊娠晚期缺铁性贫血发生率比较,差异有统计学意义(χ2=107.820,P<0.05).妊娠期贫血妇女不良妊娠结局发生率明显高于正常妇女,血清铁蛋白水平10～19.9 ng/mL的妊娠期贫血妇女不良妊娠结局发生率明显高于正常者,差异有统计学意义(χ2=7.797 P<0.05).ROC曲线结果显示,血清铁蛋白、血红蛋白及其联合应用对妊娠结局的早期评估的AUC(0.95%CI)分别为0.728(0.512～0.950)、0.684(0.431～0.935)、0.805(0.635～0.976).结论 妊娠晚期妇女缺铁性贫血患病率高于妊娠中期,加强血清铁蛋白水平检测能够为临床适时补充铁剂并监测妊娠期妇女体内铁含量、减少缺铁性贫血对不良妊娠结局的影响提供参考依据.

PurposeTo investigate the application value of 3D arterial spin labeling (3D-ASL) for evaluating distal limb ischemic preconditioning to improve acute ischemic stroke (AIS) perfusion.Materials and MethodsA total of 40 patients with AISs treated in our hospital from January 2020 to December 2020 were recruited, and 15 healthy individuals who were examined in our hospital during the same period were included as the control group; all of these participants were scored on the National Institutes of Health Stroke Scale (NIHSS) and examined by MRI. Sequences included conventional sequences, diffusion-weighted imaging (DWI), magnetic resonance angiography (MRA), and 3D-ASL, and cerebral infarct volume and cerebral blood flow (CBF) in the area of the infarct lesion were measured. After 3 months of treatment, patients with AIS were scored on the modified Rankin Scale (mRS) and divided into good prognosis and poor prognosis groups. In total, 55 adult male Sprague–Dawley rats were divided randomly into three groups: 20 in the middle cerebral artery occlusion (MCAO) group, 20 in the MCAO + limb remote ischemic preconditioning (LRP) group, and 15 in the sham group. In total, 48 h after the procedures, conventional MRI, DWI, and 3D-ASL sequence data were collected, and 2,3,5-trphenyltetrazolium chloride monohydrate (TTC) staining and behavioral scoring were performed. CBF was recorded in the infarct lesion area and the corresponding contralateral area, and the affected/contralateral relative values (rCBF) were calculated to compare the differences in rCBF between different groups. The pathological changes in brain tissues were observed by HE staining, and the expression of vascular endothelial growth factor (VEGF) and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) in brain tissues was detected by immunofluorescence and real-time quantitative polymerase chain reaction (RT-qPCR). The protein expression of VEGF was detected by western blotting.ResultsHypertension and internal carotid atherosclerosis are high-risk factors for ischemic stroke, and CBF values in the infarct area are significantly lower than those in the corresponding areas on the contralateral side. NIHSS and mRS scores and CBF values have higher specificity and sensitivity for the prognosis of patients with AIS. LRP significantly reduces the infarct area, improves behavioral deficits in rats with cerebral ischemia, reduces neurological injury and histological damage, protects vascular structures, and promotes neovascularization. In addition, 3D-ASL showed a significant increase in brain tissue perfusion in the ischemic area after LRP, and the expression of VEGF and CD31 showed a significant positive correlation with CBF values.ConclusionThree dimensional (3D) ASL can be used to evaluate LRP to improve stroke perfusion, and its protective effect may be closely related to LRP-induced vascular regeneration.

Background and objective: Activating transcription factor 3 (ATF3) plays a crucial role in regulating tumor development depending on the cellular context or cancer cell type. However, the effect of ATF3 on stem cells-like features in colorectal cancer (CRC) has yet to be elaborated. Methods: In this study, we overexpressed ATF3 in SW620 CRC cells to investigate its effects on stem cells-like features. Results: Our results indicated that overexpressing ATF3 inhibited the proliferation, invasion, migration, and sphere formation capacity of SW620 CRC cells. ATF3 overexpression also decreased the size of tumorspheres and reduced expression of the cancer stem cell markers CD44 and CD133 in SW620 cells. Conclusion: In summary, our study revealed that ATF3 suppresses CRC growth and stem cells-like features. ATF3 is considered a potential target in CRC therapy.

BACKGROUND:Gastric cancer (GC) is one of the most common cancers and the third leading cause of cancer related mortality worldwide. The 5-year survival rate is rather low owing to advanced unresectable and distant metastasis. The EMT has been widely implicated in the stemness, metastatic dormancy, and chemoresistance of different solid tumors. Given the fact that activating transcription factor-3 (ATF3) is a member of the ATF/CREB family of transcription factors and its role in regulation of GC recurrence and metastasis remain poorly understood, the aim of the present study was to investigate its potential impact in epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties and GC aggression. METHODS:To elucidate the potential role of ATF3 in gastric cancer, we utilized SGC-7901 and MGC-803 gastric cancer cell lines as research models and constructed stable cell lines overexpressing ATF3. We conducted a series of assays including cell proliferation, colony formation, cell migration, tumorsphere formation, and invasion to investigate the functional roles of ATF3 in stemness of gastric cancer. The possible effect of ATF3 on epithelial-mesenchymal transition (EMT) was assessed through flow cytometry and qRT-PCR. In vivo functional effect of upregulation of ATF3 on tumor growth was examined in a mouse xenograft model. RESULTS:We found that overexpression of ATF3 inhibited cell proliferation, colony formation, cell migration and invasion. In addition, up-regulation of ATF3 attenuated tumorsphere formation, cell stemness, and potentially decreased expression of EMT markers. Moreover, ATF3 overexpression inhibited tumorigenesis in mouse xenograft model. CONCLUSION:Our data suggest a suppressive role of ATF3 in gastric cancer development. Our findings will provide a potential therapeutic strategy and novel drug target for gastric cancer.

OBJECTIVE:Elder abuse (EA) is a critical social, health, and economic issue worldwide. To date, there is limited information on EA in certain similar culture-specific subpopulations, especially in East Asia. This study aims to summarize EA incidence in East Asia through a systematic review and meta-analysis and identify its variations and heterogeneity in the incidence estimates. METHODS/DESIGN:The study followed the Preferred Reporting Items for Systematic reviews and Meta-Analyses protocol. Systematic review registration number PROSPERO CRD42020197131. A systematic literature search was performed to identify relevant articles published before July 5th, 2020, from six electronic databases. Two reviewers screened for relevance of the studies against eligible criteria and assessed the bias of the included studies independently. A random-effect model was adopted to estimate the incidence of EA, followed by subgroup analyses and multi meta-regression. Sensitivity and publication bias tests were performed to verify the robustness of the meta-analysis by Stata version 15.1. RESULTS:Twelve eligible studies were included in the meta-analysis, which involved 79,395 subjects from 3 East Asian countries (China, Japan, and South Korea) ranging from 2004 to 2020. The overall incidence of EA was 78.33 per 1000 person-year (95% CI: 39.12-156.87) with high between-study variability (χ2  = 15,568, d.f. = 11, p<0.001; I2  = 99.9%). The sampling method, sample size, scope, instrument, data collection method, income classification, types of participants, and urbanity are all the sources of heterogeneity, which can explain nearly 100% of the variance between studies. CONCLUSIONS:The incidence of EA in this study is not as high as the global level. It may be furtherly underestimated in East Asia due to cultural norms. It is imperative to develop a culture-tailored EA assessment instrument to evaluate potential victims. Future studies should also identify more effective educational programs to raise the public's awareness and promote recognition ability.

Multiple myeloma (MM) is a malignant cancer with an increasing in incidence that can be alleviated through bortezomib (BTZ) treatment. Activating transcription factor 3 (ATF3) plays a major role in cancer development. Moreover, microRNAs (miRNAs) regulate carcinogenic pathways, apoptosis, and programmed necrotic cell death. However, the detailed mechanism by which ATF3 modulates BTZ drug sensitivity/resistance remains elusive. In the current study, expression of ATF3 was significantly increased under BTZ treatment in a dose-dependent manner in MM cell lines. In addition, ATF3 could regulate cell apoptosis under BTZ treatment. The effect of ATF3 was negatively regulated by its binding miRNA, miR-135a-5p. When either ATF3 was silenced or miR-135a-5p mimics were added to MM cells, they partially lost sensitivity to BTZ treatment. This was accompanied by low levels of Noxa, CHOP, and DR5, and a decrease in mitochondrial membrane potential. These results revealed the combinatorial regulatory patterns of ATF3 and miR-135a-5p in the regulatory protein interactome, which indicated a clinical significance of the miR-135a-5p-ATF3 protein interaction network in BTZ therapy. This study provides potential evidence for further investigation into BTZ resistance.

Introduction: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with poor prognosis. The tumor microenvironment (TME) plays a vital role in HCC progression. Thus, this research was designed to analyze the correlation between the TME and the prognosis of HCC patients and to construct a TME-related long noncoding RNA (lncRNA) signature to determine HCC patients’ prognosis and response to immunotherapy. Methods: We assessed the stromal–immune–estimate scores within the HCC microenvironment using the ESTIMATE (Estimation of Stromal and Immune Cells in Malignant Tumor Tissues Using Expression Data) algorithm based on The Cancer Genome Atlas database, and their associations with survival and clinicopathological parameters were also analyzed. Thereafter, differentially expressed lncRNAs were filtered out according to the immune and stromal scores. Cox regression analysis was performed to build a TME-related lncRNA risk signature. Kaplan–Meier analysis was used to explore the prognostic value of the risk signature. Furthermore, we explored the biological functions and immune microenvironment features in the high- and low-risk groups. Lastly, we probed the association of the risk model with treatment responses to immune checkpoint inhibitors (ICIs) in HCC. Results: The stromal, immune, and estimate scores were obtained utilizing the ESTIMATE algorithm for patients with HCC. Kaplan–Meier analysis showed that high scores were significantly correlated with better prognosis in HCC patients. Six TME-related lncRNAs were screened to construct the prognostic model. The Kaplan–Meier curves suggested that HCC patients with low risk had better prognosis than those with high risk. Receiver operating characteristic (ROC) curve and Cox regression analyses indicated that the risk model could predict HCC survival exactly and independently. Functional enrichment analysis revealed that some tumor- and immune-related pathways were activated in the high-risk group. We also revealed that some immune cells, which were important in enhancing immune responses toward cancer, were significantly increased in the low-risk group. In addition, there was a close correlation between ICIs and the risk signature, which can be used to predict the treatment responses of HCC patients. Conclusion: We analyzed the influence of the stromal, immune, and estimate scores on the prognosis of HCC patients. A novel TME-related lncRNA risk model was established, which could be effectively applied as an independent prognostic biomarker and predictor of ICIs for HCC patients.

[目的]探究微小RNA(microRNA,miR)-216a靶向调控酪氨酸蛋白激酶2/信号转导和转录激活因子3(Janus protein tyrosine protein kinase 2/signal transducer and activator of transcription 3,JAK2/STAT3)信号通路对鼻咽癌细胞增殖、侵袭、自噬及血管生成的影响.[方法] Target Scan Human预测miR-216a与JAK2的结合位点,双荧光素酶实验验证miR-216a与JAK2是否结合;免疫组化染色检测正常鼻咽黏膜组织、鼻咽癌组织标本p-JAK2、p-STAT3的表达水平,并分析p-JAK2、p-STAT3表达水平与患者临床病理参数的关系.采用LipofectamineTM3000将miR-216a模拟物双链小RNA、阴性对照双链小RNA转染至CNE-2细胞构建过表达miR-216a细胞系,细胞分为对照组、miR-NC组、miR-216a组.将抑制剂双链小RNA,抑制剂对照双链小RNA转染至CNE-2细胞构建低表达miR-216a细胞系,细胞分为对照组、抑制miR-NC组、抑制miR-216a组.采用qRT-PCR检测细胞JAK2、STAT3 mRNA表达水平;MTT法、Transwell小室、皮下种植瘤模型、小管形成实验、吖啶橙染色分别检测细胞增殖、侵袭、移植瘤生长、血管形成和自噬泡形成的能力;Western blot检测JAK2、p-JAK2、STAT3、p-STAT3、微管相关蛋白轻链3-Ⅱ(microtubule-associated protein light chain 3-Ⅱ,CL3-Ⅱ)、酵母自噬相关基因6的哺乳动物同源体(autophagy related protein ATG6,Beclin1)、血管内皮生长因子(vascular endothelial growth factor,VEGF)的表达水平.[结果]双荧光素酶实验验证了miR-216a对JAK2的靶向调控作用.鼻咽癌组织p-JAK2、p-STAT3阳性表达率(75.0％,68.3％)明显高于正常鼻咽黏膜组织(10％,13.3％)(P＜0.05).p-JAK2、p-STAT3表达越高,浸润深度越严重,越容易发生淋巴结和远处转移(P均＜0.05).细胞实验显示:与miR-NC组相比,miR-216a组细胞24、48、72、96 h吸光度值(0.32±0.03 vs 0.15±0.04、0.58±0.07 vs 0.24±0.06、0.86±0.10 vs 0.41±0.06、1.48±0.11 vs 0.75±0.07)、细胞侵袭数目(101.00±11.00 vs 22.67±5.77)、血管形成数目(127.53±10.61 vs 74.36±8.48)明显降低,移植瘤体积[(1545.21±70.71)mm3 vs (485.24±91.92)mm3)]减小,JAK2、p-JAK2、p-STAT3、VEGF蛋白表达量(1.85±0.07 vs 0.93±0.11、1.03±0.07 vs 0.32±0.05、0.92±0.09 vs 0.44±0.08、1.17±0.05 vs 0.55±0.07)明显减少(P均＜0.05);细胞自噬能力、Beclin1、CL3-Ⅱ蛋白表达量(0.30±0.08 vs 1.03±0.11、0.38±0.04 vs 1.00±0.08)均显著性升高(P＜0.05).与抑制miR-NC组相比,抑制miR-216a组JAK2、p-JAK2、p-STAT3蛋白表达量(1.35±0.07 vs 1.93±0.11、0.55±0.07 vs 1.28±0.11、0.45±0.07 vs 1.23±0.11)明显升高(P均＜0.05).[结论]JAK2、STAT3在鼻咽癌组织及细胞中表达量升高且发挥促癌作用,其作用机制可能是miR-216a通过靶向调控JAK2/STAT3信号通路,提高了细胞自噬水平,抑制了增殖、迁移和血管形成能力,对鼻咽癌患者的治疗和预后具有指导意义.

Introduction: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with poor prognosis. Tumor microenvironment (TME) plays a vital role in the tumor progression of HCC. Thus, we aimed to analyze the association of TME with HCC prognosis, and construct an TME-related lncRNAs signature for predicting the prognosis of HCC patients. Methods: We firstly assessed the stromal/immune /Estimate scores within the HCC microenvironment using the ESTIMATE algorithm based on TCGA database, and its associations with survival and clinicopathological parameters were also analyzed. Then, different expression lncRNAs were filtered out according to immune/stromal scores. Cox regression was performed to built an TME-related lncRNAs risk signature. Kaplan–Meier analysis was carried out to explored the prognostic values of the risk signature. Furthermore, we explored the biological functions and immune microenvironment feathers in high- and low risk groups. Lastly, we probed the association of the risk signature with the treatment responses to immune checkpoint inhibitors (ICIs) in HCC by comparing the immunophenoscore (IPS). Results: Stromal/immune /Estimate scores of HCC patients were obtained based on the ESTIMATE algorithm. The Kaplan-Meier curve analysis showed the high stromal/immune/ Estimate scores were significantly associated with better prognosis of the HCC patients. Then, six TME-related lncRNAs were screened for constructing the prognosis model. Kaplan-Meier survival curves suggested that HCC patients in high-risk group had worse prognosis than those with low-risk. ROC curve and Cox regression analyses demonstrated the signature could predict HCC survival exactly and independently. Function enrichment analysis revealed that some tumor- and immune-related pathways associated with HCC tumorigenesis and progression might be activated in high-risk group. We also discovered that some immune cells, which were beneficial to enhance immune responses towards cancer, were remarkably upregulated in low-risk group. Besides, there was closely correlation of immune checkmate inhibitors (ICIs) with the risk signature and the signature can be used to predict treatment response of ICIs. Conclusions: We analyzed the impact of the tumor microenvironment scores on the prognosis of patients with HCC. A novel TME-related prognostic risk signature was established, which may improve prognostic predictive accuracy and guide individualized immunotherapy for HCC patients.

目的:观察对妊娠期合并缺铁性贫血应用蛋白琥珀酸铁治疗的临床效果.方法:择选我院2018年7月-2019年6月收诊的92例妊娠合并缺铁性贫血患者为观察对象,按随机数表法分成对照组和研究组,每组46例.给予对照组三维亚铁咀嚼片治疗,给予研究组蛋白琥珀酸铁治疗.治疗6周后评价疗效,于治疗前后对两组RBC、Hb、HCT、SF水平进行检测,并统计治疗过程中出现的不良反应.结果:治疗后对照组总有效38例,总有效率为82.61％(38/46),研究组总有效44例,总有效率为95.65％(44/46),差异显著(P＜0.05);治疗前,两组RBC、Hb、HCT、SF差异不显著(P＞0.05);治疗后,两组RBC、Hb、HCT、SF水平均明显升高,与同组治疗前差异显著(P＜0.05),两组之间差异显著(P＜0.05);两组治疗过程中均未发生明确的严重不良反应.结论:应用蛋白琥珀酸铁治疗妊娠期合并缺铁性贫血,不仅能够改善临床症状,提高疗效,而且能够显著提高因子水平,安全可靠,值得临床上推广.

目的 探讨长链非编码RNA(LncRNA)人母系表达基因3(MEG3)在表阿霉素抑制T细胞淋巴瘤增殖和诱导细胞凋亡中的作用及可能机制.方法 实时定量PCR(RT-qPCR)检测T细胞淋巴瘤组织、临近正常组织、T细胞淋巴瘤细胞(Jurkat、CCRF-CEM、SUP-T1)、人类T细胞细胞株H9以及不同浓度表阿霉素处理的Jurkat细胞中MEG3的表达水平.将Jurkat细胞分为对照组、表阿霉素(Epirubicin)处理组、表阿霉素+pcDNA组、表阿霉素+MEG3组、表阿霉素+MEG3+miR-con组和表阿霉素+MEG3+miR-191组.采用CCK-8法、流式细胞术分别检测检测细胞活力和凋亡.蛋白质印记(Westernblot)检测B细胞淋巴瘤2(Bcl-2)和Bcl相关X蛋白(Bax)表达.双荧光素酶报告基因实验和RT-qPCR确定MEG3与miR-191靶向调控关系.结果 与临近正常组织比较,T细胞淋巴瘤组织中MEG3表达明显降低(P＜0.05).与H9细胞比较,T细胞淋巴瘤细胞中MEG3表达明显降低(P＜0.05).不同浓度表阿霉素处理后Jurkat细胞中MEG3表达明显升高(P＜0.05).表阿霉素处理后Jurkat细胞存活率、Bcl-2蛋白表达明显降低,凋亡率、Bax蛋白表达明显升高(P＜0.05).过表达MEG3可提高表阿霉素对Jurkat细胞的增殖抑制和凋亡促进作用(P＜0.05).MEG3靶向miR-191并负调控其表达.过表达miR-191可逆转MEG3过表达对表阿霉素处理的Jurkat细胞增殖、凋亡以及Bcl-2和Bax蛋白表达的影响,差异有统计学意义(P＜0.05).结论 LncRNA MEG3通过下调miR-191能够增强表阿霉素对T细胞淋巴瘤细胞的增殖抑制和凋亡促进作用.

Background: Inhibitor of DNA binding 1 (Id1) is upregulated in multiple cancers, and Id1 overexpression correlates with cancer aggressiveness and poor clinical outcomes in cancer patients. However, its roles in cancer stem-like cells (CSCs) and epithelial-mesenchymal transition (EMT) are still elusive. Purpose: This study aimed to examine the role of Id1 on the mediation of CRC sternness and explore the underlying mechanisms. Methods: Id1 and CD133 expression was detected by qPCR assay and immunohistochemistry (IHC) in normal mucosal and primary colorectal cancer (CRC) specimens. Id1 was stably knocked down (KD) in human CRC cell lines. Spheres forming assay and tumorigenic assay were performed to evaluate self-renewal capacity and tumor initiation. Expression of CSC- and EMT-related markers and TCF/LEF activity were assessed in HCT116 cells after Id1 KD. Results: qPCR assay showed higher Id1 and CD133 expression in CRC specimens than in normal mucosal specimens (P<0.05). IHC detected high cytoplasmic Id1 expression in 35 CRC specimens (46.7%), and high CD133 expression in 22 CRC specimens (29.3%) and negative expression in 18 normal mucosal specimens. High Id1 expression positively correlated with poor differentiation (P=0.034), and CD133 expression correlated with T category in CRC patients (P=0.002). Spearman correlation analysis revealed a positive correlation between Id1 and CD133 expression in CRC patients (P<0.05). Id1 KD resulted in suppression of proliferation, cell-colony formation, self-renewal capability and CSC-like features in HCT116 cells, and impaired the tumor-initiating capability in CRC cells. In addition, Id1 maintained the sternness of CRC cells via the Id1-c-Myc-PLAC8 axis through activating the Wnt/beta-catenin and Shh signaling pathways. Conclusions: Id1 expression significantly correlates with CD133 expression in CRC patients, and Id1 KD impairs CSC-like capacity and reverses EMT traits, partially via the Wnt/beta-catenin signaling. Id1 may be a promising therapeutic target against colon CSCs.

目的 在本研究中主要针对宁德地区产前诊断中心共计1500例α地中海贫血以及650例β地中海贫血产前基因诊断进行文献分析.方法 针对2018年1月—2019年1月α地中海贫血产前基因诊断采用裂隙聚合酶链反应以及点杂交方法,而对于β地中海贫血产前诊断采用PCR以及RDB方法.如果其中一位夫妇携带少见突变则需要采用DNA测序方法.结果 对于1500例α型地中海贫血产前诊断患者,检测出有800例患有水肿胎.对于650例β型地中海贫血产前基因诊断中检测出共计174例患有重型β地中海贫血.结论 针对地中海贫血进行产前基因诊断能够从一定程度上减少水肿胎以及重型β地中海贫血患者的出生,进一步对于指导优生优育,减少患者围术期并发症产生具有十分重要的作用.

目的 分析医院血液科感染患者的病原菌分布和耐药性,并探讨发生感染的危险因素. 方法 选取2013年2月至2018年12月在本院血液科感染患者1182例,采集分泌物、痰(唾)液、尿液、血液等标本,进行病原学和耐药性检测;收集患者临床资料,采用x2检验分析感染发生的相关因素. 结果 1182例感染患者共分离出病原菌1 305株,其中分离自分泌物标本占25.0％、分离自痰(唾液)、尿液、血液及脓肿标本分别占24.1％、21.5％、12.0％和9.6％.在1305株病原菌中,G-菌826株,占63.3％;G+菌334株,占25.6％;真菌145株,占11.1％.G-菌中检出率较高的是大肠埃希菌、肺炎克雷伯菌、铜绿假单胞菌,3种菌对氨苄西林舒巴坦、氨曲南、复方新诺明、头孢唑林、头孢呋辛钠的耐药率较高(16.58％～100％),对阿米卡星、厄它培南、美洛培南、哌拉西林/他唑巴坦、妥布霉素的耐药率较低(0～9.41％).G+菌中检出率较高的是金黄色葡萄球菌和肺炎链球菌,2种菌对阿奇霉素、克林霉素、四环素的耐药率较高(22.22％～100％),对利福平、利奈唑烷、莫西沙星、万古霉素的耐药率较低(0～8.89％).经单因素分析,年龄、病程、侵入性操作是血液科患者发生感染的相关因素(P＜0.05). 结论 血液科患者感染的致病病原菌种类广泛且对部分抗菌药物的耐药性较高;感染的发生与患者年龄、病程、侵人性操作等因素有关,可供临床医师参考.

目的 探讨系统性红斑狼疮(S L E)患者尿酸水平与肾损害的关系.方法 选取2015年3月至2017年3月在福建医科大学附属宁德市医院血液风湿科治疗的S L E患者,共210例,其中男14例,女196例.采用系统性红斑狼疮国际合作诊所/美国风湿病学会(SLICC/ACR)损伤指数SDI对疾病损害程度、疾病持续时间、代谢综合征并发症和狼疮性肾炎进行评估,根据患者有无肾损伤,将其分为有肾损伤组(Y组,182例),无肾损伤组(W组,28例).运用单变量和多变量C o x回归分析肾损伤风险.结果 两组尿酸、血肌酐水平比较,差异有统计学意义(P<0.05).诊断肾损伤的最佳临界值为5.5 mg/dL,曲线下面积(AUC)为0.776,灵敏度为68.8％,特异度为87.1％.基线尿酸水平与肾损害具有一定相关性,将尿酸作为连续变量时,单变量分析的风险比为2.24,95％C I为1.50～3.34,P<0.001;多变量分析的风险比为2.82,95％C I为1.05～7.57,P=0.040.将尿酸作为二分类变量时,较高的尿酸水平(>5.5 mg/dL)与肾损伤具有相关性(P<0.05).结论 SLE患者存在尿酸水平的异常变化,较高的尿酸水平会增加SLE患者发生肾脏损害的风险.

目的 分析系统性红斑狼疮伴中重度血小板减少患者白细胞计数、血红蛋白浓度及补体C3水平.方法 对我院2015年1月-2017年1月收治的40例系统性红斑狼疮伴中重度血小板减少患者的临床资料进行回顾性分析,将这些患者作为中重度组,另将我院同期收治的40例系统性红斑狼疮血小板正常患者为正常组,对两组患者的临床症状和体征、血小板计数、淋巴细胞计数、IgG、SLE-DAI评分、白细胞计数、血红蛋白浓度及补体C3、C4水平进行统计分析.结果 中重度组患者的血小板计数低于正常组(P＜0 05),白细胞计数、血红蛋白浓度、补体C3水平均低于正常组(P＜0 05),APL阳性率25.0％高于正常组的APL阳性率0(P＜0.05).结论 系统性红斑狼疮伴中重度血小板减少患者白细胞计数、血红蛋白浓度及补体C3水平均较血小板正常患者低.

目的:探讨心理治疗对风湿病患者精神状态、心理健康及预后的影响作用.方法:选取2016年1月-2017年1月本院收治的风湿病患者80例作为研究对象,按照随机数字表法将其分为观察组与对照组,各40例.对照组仅接受常规基础治疗,观察组则在基础治疗上实施心理治疗,比较两组风湿病治疗效果及精神状态、心理健康情况.结果:观察组治疗总有效率明显高于对照组,差异有统计学意义(χ2=8.538,P=0.003).干预后,观察组汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)评分、简易心理健康评分量表(SCL-90)总分均明显低于对照组,差异均有统计学意义(P<0.05).结论:在常规基础治疗上联合心理治疗可有效提升风湿病临床治疗效果,并对改善患者精神状态、心理健康具有重要作用.

Colorectal cancer is the third most common cancer and the fourth leading cause of cancer-related mortality worldwide. Activating transcription factor 3 ( ATF3) has been identified as both an oncogene and a tumor suppressor in colorectal cancer, which encourages further studies to validate the exact role of ATF3 in colorectal cancer development and progression. The aim of this study was to examine the effect of ATF3 overexpression on biological behaviors of human colorectal cancer HCT116 cells. A stable ATF3-overexpressed HCT116 cell line was established by transfecting HCT116 cells with lentivirus carrying a full-length of ATF3. Cell proliferation was measured with MTS and colony-formation assays, and cell migration and invasion was detected using Transwell migration/ invasion assays. In addition, a sphere-forming assay was performed to assess the cancer-initiation capacity, while the gene and protein expression was quantified with qRT-PCR, Western blotting and flow cytometry. ATF3 overexpression was found to suppress proliferation, migration and invasion of HCT116 cells as compared with the control cells, while down-regulation of Survivin and PCNA expression was detected in HCT116 cells at both translational and transcriptional levels, and a reduction was measured in the CyclinD1 protein expression in HCT116 cells overexpressing ATF3 than in the control cells. In addition, MMP2 and MMP9 expression was found to be down-regulated in HCT116 cells overexpressing ATF3 at both translational and transcriptional levels, and Western blotting detected up-regulation of TIMP-2 and TIMP-1 expression in HCT116 cells overexpressing ATF3 relative to the control cells. Overexpression of ATF3 resulted in reversal of epithelial-mesenchymal transition (EMT), as revealed by changes of cell morphology and altered expression of E-cadherin, Snail, Slug and Twist. Most importantly, ATF3-overexpressed HCT117 cells produced less and smaller spheres as compared with the control cells. The expression of multiple markers associated with colorectal cancer-initiation including CD24, CD133, CD166, EpCAM, EZH2 and ID1 were down-regulated in HCT116 cells overexpressing ATF3 at both translational and transcriptional levels, while lower beta-catenin protein expression was detected in ATF3-overexpressed HCT116 cells relative to the control cells. The results of this study demonstrate that ATF3 overexpression inhibits colorectal cancer progression and suggest that ATF3 exhibits antitumor activity through reversing EMT and impairing cancer-initiation ability.

Objective:To explore the correlation of procalcitonin (PCT) with liver metastasis of colorectal cancer (CRC).Methods:101 CRC patients admitted in our hospital form January 2013 to December 2015 were enrolled in this study,consisting of 55 CRC patients without distant metastasis (group A),27 CRC patients with only liver metastasis (group B),19 CRC patients with distant metastasis but not liver (group C).The serum PCT level was detected by ELISA,and the relationship between serum PCT levels with the metastasis of CRC was analyzed.Results:The serum PCT levels were 0.16 (0.07-0.28) ηg/mL,1.20 (0.32-2.89) ηg/mL and 0.67 (0.12-1.23) ηg/mL in group A,B and C.which was significantly increased in group B compared to groups A (p＜0.05),but no difference was observed in PCT levels between groups A and C or B and C.Multiple linear regression analysis shown that PCT was positively related to liver metastasis status of CRC ([3=0.577,p=0.002).On analysis of ROC,the cut-off for PCT was 0.56 ηg/mL,with 66.7％ scnsitivity and 92.7％ specificity for liver metastasis of CRC.Conclusions:PCT levels was related to the disease stage of CRC patients,which might be a specific marker of liver metastasis in CRC.