甲型H1N1流感的胸部影像学表现

目的 观察甲型H1N1流感患者的胸片及CT表现。 方法 回顾性分析51例甲型H1N1流感患者(实验室确诊47例,临床诊断4例)初始胸片及CT检查的病变表现形式、分布特点及病变程度。 结果 甲型H1N1流感患者的胸片及CT检查最主要表现是双侧或单侧多发磨玻璃密度影,伴或不伴单发或多发实变区。CT显示病变主要沿支气管血管周围中心肺区和(或)胸膜下区分布。 结论 影像学诊断甲型H1N1流感时,结合病史非常重要。     

甲型H1N1流感肺炎的胸部CT表现及动态变化特点

目的 探讨甲型H1N1流感肺炎的胸部CT表现及动态变化. 方法 对60例甲型H1N1流感确诊患者进行胸部CT扫描(含HRCT),回顾性分析、比较病变的影像学特点及动态变化并进行半定量CT评分. 结果 甲型H1N1流感胸部CT表现及动态变化特点:①主要表现为片状肺实质渗出病灶,早期和吸收期主要CT表现为磨玻璃密度影;②两肺小叶性或节段性散在分布,以胸膜下和支气管周围多见,下叶较重;③肺组织、胸膜及纵隔受累可同时存在;④病程早期CT评分4.41且逐渐下降,渗出性病灶短期内吸收较快,后期遗留纤维化病变CT评分1.64分. 结论甲型H1N1流感肺炎的动态胸部CT表现具有一定特征性.熟悉其胸部CT表现有助于该病的诊断、鉴别诊断与疗效观察,但确诊需依靠流行病学史及实验室检查.     

甲型H1N1流感胸部影像学表现

2009年3月,美国报道了发生在墨西哥的首例甲型H1N1流感病例,随后甲型H1N1流感波及到全世界。我院被确定为河北省重症甲型H1N1流感定点医院,自2009年9月至2010年1月共收治重症可疑甲型H1N1流感患者72例,经咽拭子核酸检测,其中确诊44例,28例排除。为提高对其影像学表现的认识,现将我院收治病例分析如下。     

重症甲型H1N1流感肺部的影像学表现

目的：探讨重症甲型H1N1流感患者的胸部X线和CT表现特征,以期提高对甲型H1N1流感的认识。方法：搜集我院2009年6月～2010年3月住院确诊重症甲型H1N1流感的患者11例,对其临床及影像学资料进行回顾性总结分析。结果：重症甲型H1N1流感临床的主要特征是持续高热、咳嗽,部分出现呼吸衰竭和神志改变。肺部影像学特点是：①早期最常见影像学表现为斑片状磨玻璃影;②发病后1～3天达到高峰,重症患者肺部病变变化较快且易反复;③治疗后患者肺部大部分病变可完全吸收,部分可见肺间质的改变。④肺部影像学表现与临床表现基本一致。结论：重症甲型H1N1流感患者的影像学表现可以反映病情变化,对指导临床治疗及判断预后具有重要的参考价值。     

天津市甲型H1N1流感重症患者的临床与影像学特点分析

随着甲型H1N1流感秋冬季的第2次爆发,重症患者日趋增多.本院共收治患者45例,32例治愈出院,2例死亡,11例住院治疗中.现回顾性分析23例重症患者的临床及影像学资料,探讨甲型H1N1流感重症患者临床及影像学特点、演变规律,以期对临床进行诊断和治疗有所指导,报告如下.     

甲型H1N1流感肺炎影像学表现

目的 总结甲型H1N1流感肺炎影像学表现,提高对本病的认识。方法 回顾性分析17例确诊甲型H1N1流感肺炎患者胸部X线片及64层螺旋CT检查系列影像学资料。结果 17例甲型H1N1流感肺炎患者均有1次以上胸部计算机X线摄影术(CR)检查,其中8例接受CT检查。17例胸部X线及CT表现均以斑片或大片实变影合并磨玻璃密度影为主要表现。病变累及单侧肺野者4例,占23.53%;双侧肺野均受累者13例,占76.47%;随访病例均有不同程度的纤维化改变。结论 甲型H1N1流感肺炎X线及CT表现具有一定特征性。肺部病变以多叶段分布渗出性改变为其共有表现,病程后期两肺以纤维化表现为主。     

甲型H1N1流感首次胸部CT表现初步分析

目的:探讨甲型H1N1流感首次胸部CT影像学特点.方法:回顾性分析临床确诊22例甲型H1N1流感患者的首次胸部CT表现.结果:22例患者中,男10例,女12例,年龄4～63岁,平均46岁.22例患者CT表现共有268个肺段病变,包括磨玻璃密度影218段、斑片状实变影30段、结节影20段.肺部病变分布在中外带17例,弥漫分布3例,内带2例.胸膜增厚15例,其中右侧12例、左侧10例、双侧7例.纵隔淋巴结肿大3例,胸腔积液2例.结论:甲型H1N1流感患者首次胸部CT表现特点为以双侧、多段、外带肺部磨玻璃密度影改变为主.     

甲型H1N1流感合并呼吸衰竭孕产妇1年随访分析

已知妊娠是甲型H1N1流感感染的高危因素[1-3].国外研究资料表明,孕妇感染甲型H1N1流感后易进展为重症,病死率较高[4].本研究中通过分析甲型H1N1流感合并呼吸衰竭(呼衰)孕产妇住院及1年期随访的临床资料,总结妊娠合并甲型H1N1流感的临床特点及对患者健康状况的影响. 1对象与方法 1.1 研究对象:2009年8月20日至2010年1月10日北京地坛医院共收治甲型H1N1流感确诊孕妇32例,其中轻症20例,重症4例,危重症8例.8例危重症患者均合并呼衰,并作为研究对象,所有治疗获得患者或家属知情同意.     

甲型H1N1流感99例的诊断、治疗及预后

甲型H1N1流感是一种新型的呼吸道传染病,高居传染病死亡之首.我院发热门诊2009年5月～2010年1月确诊甲型H1N1流感99例,本文分析诊断、治疗及预后如下.     

烟台地区甲型H1N1流感住院患者临床特征分析

目的 了解甲型H1N1 流感的流行病学、临床表现、实验室检查等特点及重症甲型H1N1 流感病例的预测因子.方法 对2009 年6 月22 日至12 月31 日收治的226 例确诊病例的流行病学及临床资料进行回顾性分析.结果 患者中位年龄21 岁(4 ～72 岁),男128 例,女98 例.输入性病例3 例,本地病例223 例.常见症状为发热(100%)、咳嗽(84.5%)、咽痛(45.1 %)、头痛(34.1 %)、全身肌肉痛(21.2%)、有腹泻症状者少(2.2%).外周血白细胞大多正常或降低(94.25 %), 44.7%的病例有胸部影像学异常改变.多因素分析显示,高CRP 、低血钾及胸部影像学检查异常是重症甲型H1N1 流感病例的独立预测因子,相应的OR(95%CI )值分别为1.090(1.018 ～1.167 )、0.907(0.857 ～0.960 )和32.951(8.240 ～131.761 ).结论 烟台地区甲型H1N1 流感病例以本地人群为主,青少年为易感人群,大多数病情轻,预后良好,高CRP 、低血钾及胸部影像学检查异常是重症病例的独立预测因子.     

Identification of C-C Chemokine Receptor 1 (CCR1) as the Monocyte Hemofiltrate C-C Chemokine (HCC)-1 Receptor

Hemofiltrate C-C chemokine (HCC)-1 is a recently cloned C-C chemokine that is structurally similar to macrophage inflammatory protein (MIP)-1α. Unlike most chemokines, it is constitutively secreted by tissues and is present at high concentrations in normal human plasma. Also atypical for chemokines, HCC-1 is reported not to be chemotactic for leukocytes. In this paper, we have investigated the chemokine receptor usage and downstream signaling pathways of HCC-1. Cross-desensitization experiments using THP-1 cells suggested that HCC-1 and MIP-1α activated the same receptor. Experiments using a panel of cloned chemokine receptors revealed that HCC-1 specifically activated C-C chemokine receptor (CCR)1, but not closely related receptors, including CCR5. HCC-1 competed with MIP-1α for binding to CCR1-transfected cells, but with a markedly reduced affinity (IC₅₀ = 93 nM versus 1.3 nM for MIP-1α). Similarly, HCC-1 was less potent than MIP-1α in inducing inhibition of adenylyl cyclase in CCR1-transfected cells. HCC-1 induced chemotaxis of freshly isolated human monocytes, THP-1 cells, and CCR1-transfected cells, and the optimal concentration for cell migration (100 nM) was ∼100-fold lower than that of MIP-1α (1 nM). These data demonstrate that HCC-1 is a chemoattractant and identify CCR1 as a functional HCC-1 receptor on human monocytes.     

长链非编码RNA DBH-AS1通过下调AKT1表达抑制胰腺癌进展

目的与背景 本研究旨在检测长链非编码RNA DBH-AS1在胰腺癌中的表达情况,探讨DBH-AS1在胰腺癌进展中的潜在分子作用。方法 采用实时定量PCR检测基因表达。细胞增殖、成克隆生长和迁移侵袭能力分别通过CCK-8、克隆形成和transwell检测。蛋白质水平用免疫印迹法测定。结果GEPIA数据库和定量PCR结果证实,DBH-AS1在胰腺癌组织中表达下调,与癌旁正常胰腺组织相比差异均有统计学意义(P 均＜0.05)。在胰腺癌肿瘤组织中DBH-AS1的低表达与肿瘤分化差、TNM分期晚期、淋巴结转移、以及预后不良(无瘤生存时间和总体生存时间)有关(P均＜0.05)。DBH-AS1基因敲除可促进胰腺癌细胞的增殖、克隆形成、迁移和侵袭能力,与对照组相比差异均有统计学意义(P均＜0.05)。机制研究表明,在胰腺癌中DBH-AS1通过下调AKT1表达抑制mTOR信号通路。结论DBH-AS1通过降低AKT1的表达抑制胰腺癌的进展。     

LncRNA SLC16A1‐AS1 contributes to the progression of hepatocellular carcinoma cells by modulating miR‐411/MITD1 axis

BackgroundHepatocellular carcinoma (HCC) is a common malignancy with high morbidity. The current study aimed to explore the molecular mechanism of lncRNA SLC16A1‐AS1 in the tumorigenesis of HCC.Material and methodsThe expression of SLC16A1‐AS1 and miR‐411 was examined in clinical HCC tissues. HCC cell lines Hep3B and Huh‐7 were employed and transfected with si‐SLC16A1‐AS1. The correlation between SLC16A1‐AS1 and miR‐411 was verified by luciferase reporter assay. Cell viability was detected by CCK‐8 assay. Cell migration and invasion capacity were examined by transwell assay. The protein level of MITD1 was analyzed by western blotting.ResultsThe expression of SLC16A1‐AS1 markedly increased in HCC tissues and cell lines. Subsequent studies identified SLC16A1‐AS1 as a downstream target of miR‐411. In addition, SLC16A1‐AS1 knockdown and miR‐411 overexpression significantly stagnated the progression of HCC cells. SLC16A1‐AS1 knockdown also downregulated MITD1 levels.ConclusionOur findings showed that SLC16A1‐AS1 was overexpressed in HCC cells and tissues. SLC16A1‐AS1 promoted the malignant characteristics of HCC cells and acted as an oncogene. Its regulatory effect may be associated with miR‐411/MITD1 axis. Therefore, SLC16A1‐AS1 has the potential to be used as a biomarker or therapeutic target for the treatment of HCC.     

AML1-ETO对p21 WAF1/CIP1启动子转录活性作用的研究

目的观察AML1-ETO融合基因对p21WAF1／CIP1基因启动子转录活性的影响，探讨AML1-ETO促进白血病发生的机制。方法构建p21WAF1／CIP1基因启动子的报告质粒，与AML1-ETO、AML1b和AML1a的表达质粒共转染非洲绿猴肾细胞系CV—1细胞，测定荧光素酶的活性，分析AML1-ETO、AML1b和AML1a对p21WAF1／CIP1基因启动子转录活性的影响。结果在CV—1细胞中，AML1-ETO对p21WAF1／CIP1基因启动子的转录具有明显的抑制作用，在pCMV5-AML1-ETO的剂量为1000ng时，p21WAF1／CIP1启动子的转录活性下降为对照组的（19±4）％，这种作用具有序列特异性和剂量依赖性；AML1b和AML1a对p21WAF1／CIP1基因启动子转录活性的抑制作用不明显，在剂量为1000ng时，p21WAF1／CIP1启动子的转录活性分别下降为对照组的（61±16）％和（594-16）％。结论AML1在与ETO形成融合基因后，其产物由于ETO蛋白能够更有效地募集转录共抑制复合物，其转录抑制活性要比AML1a和AML1b更强；外源的AML1-ETO对p21WAF1／CIP1的作用可能也与细胞系有关。     

系统性红斑狼疮合并甲型H1N1流感重症型死亡1例

患者女,27岁.以"双手遇冷变白变紫7年,流涕5天,喘憋1天"为主诉于2009年10月20日入院治疗.查体:体温、血压均正常.双手皮肤发紫,皮温低,面部红斑,咽稍充血,双侧扁桃体不大,双肺呼吸音清,未闻及干湿啰音.三尖瓣听诊区、主动脉瓣听诊区可闻及舒张期3级隆隆样杂音.双踝关节肿胀无压痛.入院诊断:系统性红斑狼疮;肺动脉高压;阑尾切除术后.入院后给予对症、扩血管、激素、抗风湿等药物治疗,患者症状逐渐好转.于2009年11月18日患者出现咳嗽、咯少量白痰,2009年11月19日出现咳嗽、咯痰加重,胸部正位片示:双下肺纹理粗重,余未见异常(图1A).     

SIRT1与INS/IGF-1通路的关系及对NIT-1细胞胰岛素分泌的影响

目的探讨哺乳动物沉默信息调节因子沉默信息调节因子1（SIRT1）与胰岛素/胰岛素样生长因子（INS/IGF-1）通路的关系,观察SIRT1的表达是否可通过INS/IGF-1通路并影响胰岛素瘤细胞（NIT-1细胞）的胰岛素分泌,为2型糖尿病发病机制提供新的实验依据。方法利用SIRT1激活剂白藜芦醇（RE）和抑制剂尼克酰胺（NIC）分别对NIT-1细胞进行刺激,应用RT-PCR免疫细胞化学方法检测INS/IGF-1通路主要因子PI3K、AKT、FOXO1的mRNA及蛋白表达水平;放射免疫、免疫细胞化学、RT-PCR检测NIT-1细胞胰岛素分泌及表达量的变化,细胞计数法检测细胞倍增时间的变化。结果SIRT1激活剂和抑制剂分别使SIRT1在mRNA水平上出现高、低表达的同时影响了NIT-1细胞的胰岛素分泌量,并影响了INS/IGF-1通路主要因子PI3K、AKT的表达,但对FOXO1的影响,SIRT1的高表达并没有使其产生变化,提示SIRT1影响NIT-1胰岛素分泌通路的复杂性。结论SIRT1可以通过调控INS/IGF-1通路,进而影响NIT-1细胞胰岛素分泌。     

Knockdown of lncRNA MALAT1 ameliorates acute kidney injury by mediating the miR‐204/APOL1 pathway

BackgroundAcute kidney injury (AKI) was characterized by loss of renal function, associated with chronic kidney disease, end‐stage renal disease, and length of hospital stay. Long non‐coding RNAs (lncRNAs) participated in AKI development and progression. Here, we aimed to investigate the roles and mechanisms of lncRNA MALAT1 in AKI.MethodsAKI serum samples were obtained from 129 AKI patients. ROC analysis was conducted to confirm the diagnostic value of MALAT1 in differentiating AKI from healthy volunteers. After hypoxic treatment on HK‐2 cells, the expressions of inflammatory cytokines, MALAT1, miR‐204, APOL1, p65, and p‐p65, were measured by RT‐qPCR and Western blot assays. The targeted relationship between miR‐204 and MALAT1 or miR‐204 and APOL1 was determined by luciferase reporter assay and RNA pull‐down analysis. After transfection, CCK‐8, flow cytometry, and TUNEL staining assays were performed to evaluate the effects of MALAT1 and miR‐204 on AKI progression.ResultsFrom the results, lncRNA MALAT1 was strongly elevated in serum samples from AKI patients, with the high sensitivity and specificity concerning differentiating AKI patients from healthy controls. In vitro, we established the AKI cell model after hypoxic treatment. After experiencing hypoxia, we found significantly increased MALAT1, IL‐1β, IL‐6, and TNF‐α expressions along with decreased miR‐204 level. Moreover, the targeted relationship between MALAT1 and miR‐204 was confirmed. Silencing of MALAT1 could reverse hypoxia‐triggered promotion of HK‐2 cell apoptosis. Meanwhile, the increase of IL‐1β, IL‐6, and TNF‐α after hypoxia treatment could be repressed by MALAT1 knockdown as well. After co‐transfection with MALAT1 silencing and miR‐204 inhibition, we found that miR‐204 could counteract the effects of MALAT1 on HK‐2 cell progression and inflammation after under hypoxic conditions. Finally, NF‐κB signaling was inactivated while APOL1 expression was increased in HK‐2 cells after hypoxia treatment, and lncRNA MALAT1 inhibition reactivated NF‐κB signaling while suppressed APOL1 expression by sponging miR‐204.ConclusionsCollectively, these results illustrated that knockdown of lncRNA MALAT1 could ameliorate AKI progression and inflammation by targeting miR‐204 through APOL1/NF‐κB signaling.     

广东地区新甲型H1N1流感病毒对奥司他韦的耐药性分析

目的 调查广东省2009年新甲型H1N1流感病毒对奥司他韦的耐药情况,为临床用药提供指导,监测流感流行株的变异趋势.方法 2009年4-12月,对广东省流感监测哨点医院收集患者鼻咽拭子,用MDCK细胞或者鸡胚,分离得到流感毒株221株.利用神经氨酸酶化学荧光抑制实验检测毒株对奥司他韦的IC50,筛选出对神经氨酸酶抑制剂...     

Expression of caspase-3 and hypoxia inducible factor 1α in hepatocellular carcinoma complicated by hemorrhage and necrosis

BACKGROUNDHepatocellular carcinoma (HCC) is a malignant tumor that occurs in the liver. Its onset is latent, and it shows high heterogeneity and can readily experience intrahepatic metastasis or systemic metastasis, which seriously affects patients’ quality of life. Numerous studies have shown that hypoxia inducible factor1α (HIF-1α) plays a significant role in the occurrence and development of tumors, as it promotes the formation of intratumoral vessels and plays a key role in their metastasis and invasion. Some studies have reported that caspase-3, which is induced by various factors, is involved in the apoptosis of tumor cells.AIMTo investigate the expression of caspase-3 and HIF-1α and their relationship to the prognosis of patients with primary HCC complicated by pathological changes of hemorrhage and necrosis.METHODSA total of 88 patients with HCC complicated by pathological changes of hemorrhage and necrosis who were treated at our hospital from January 2017 to December 2019 were selected. The expression of caspase-3 and HIF-1α in HCC and paracancerous tissues from these patients was assessed.RESULTSThe positive expression rate of caspase-3 in HCC tissues was 27.27%, which was significantly lower than that in the paracancerous tissues (P < 0.05), while the positive expression rate of HIF-1α was 72.73%, which was significantly higher than that in the paracancerous tissues (P < 0.05). The positive expression rates for caspase-3 in tumor node metastasis (TNM) stage III and lymph node metastasis tissues were 2.78% and 2.50%, respectively, which were significantly lower than those in TNM stage I-II and non-lymph node metastasis tissues (P < 0.05). The positive expression rates of HIF-1α in TNM stage III, lymph node metastasis, and portal vein tumor thrombus tissues were 86.11%, 87.50%, and 88.00%, respectively, and these values were significantly higher than those in TNM stage I-II, non-lymph node metastasis, and portal vein tumor thrombus tissues (P < 0.05). The expression of caspase-3 and HIF-1α in HCC tissues were negatively correlated (r_s = − 0.426, P < 0.05). The median overall survival time of HCC patients was 18.90 mo (95% CI: 17.20–19.91). The results of the Cox proportional risk regression model analysis showed that TNM stage, portal vein tumor thrombus, lymph node metastasis, caspase-3 expression, and HIF-1α expression were the factors influencing patient prognosis (P < 0.05).CONCLUSIONThe expression of caspase-3 decreases and HIF-1α increases in HCC tissues complicated by pathological changes of hemorrhage and necrosis, and these are related to clinicopathological features and prognosis.