KAI1和P53在滋养细胞疾病中的表达及意义

目的：探讨KAI1和P53蛋白在滋养细胞疾病中的表达及与滋养细胞肿瘤侵袭的关系。方法：应用免疫组织化学SP法检测正常早孕绒毛组织及滋养细胞肿瘤组织中KAI1和P53蛋白的表达情况。结果：①KAI1在恶性葡萄胎及绒癌中的表达与正常早孕绒毛及葡萄胎比较明显下降（P〈0．05），KAI1的表达与滋养细胞肿瘤患者的年龄和浸润情况相关（P〈0．05）；②P53在恶性葡萄胎及绒癌中的表达与正常早孕绒毛及葡萄胎比较明显升高（P〈0．05）；③P53和KAI1表达之间无明显相关（P〉0．05，rs=-0．8）。结论：P53、KAI1对预测滋养细胞的恶变，判断预后有一定的参考价值。     

Cathepsin D在滤泡型淋巴瘤及淋巴滤泡过度增生中的表达及意义

目的 检测溶酶体蛋白酶cathepsin D在滤泡型淋巴瘤(FL)和淋巴滤泡过度增生(FH)生发中心的表达。方法 收集10例FL和9例FH的淋巴结石蜡标本，用免疫组化LSAB法检测cathepsin D在各例标本中的表达。结果 在10例FL标本中，cathepsin D阳性信号较弱，位于瘤性滤泡生发中心树突状细胞浆内。滤泡中心部分的阳性细胞数目少，而靠近边缘部位较多。所有病例的滤泡生发中心瘤细胞cathepsin D表达阴性。在9例FH标本中，胞浆染色阳性的树突状细胞均匀弥散地分布于生发中心，阳性信号比FL组强。滤泡内少许组织细胞胞浆内也呈阳性，而滤泡内其他细胞均为阴性。滤泡生发中心周围有由T淋巴细胞组成的外套层。有4例FL的瘤性滤泡被反应性T淋巴细胞包绕，这些被包绕的滤泡中阳性细胞数目较其他6例无反应性T淋巴细胞包绕的滤泡多。在部分无T淋巴细胞包绕的滤泡中，cathepsin D阳性染色细胞甚至缺如。结论 cathepsin D可以作为滤泡树突状细胞和组织细胞良好的标志物。Cathepsin D在FL瘤性滤泡和FH滤泡树突状细胞中的差异表达可作为鉴别两种疾病的一项指标。FL瘤性滤泡中cathepsin D阳性树突状细胞的减少，可能与机体免疫系统对肿瘤细胞的免疫识别能力低下有关。     

恶性组织细胞增生症铁蛋白免疫组化定位及其临床意义

36例恶性组织细胞增生症铁蛋白免疫组化定位表明,恶组瘤细胞铁蛋白阳性率为100％,经图象分析证实,分化较好的瘤细胞铁蛋白含量较高,分化较差的异型组织细胞铁蛋白含量较低(P<0.01)。10例临床确诊为恶组的患者血清铁蛋白含量远高于正常,提示铁蛋白是恶组瘤细胞肿瘤相关抗原。瘤细胞合成并释放铁蛋白是恶组患者血清铁蛋白升高的原因之一,对铁蛋白的定位及血清学检测有助于恶组的诊断,并可能成为恶组复发及缓解的一个指标。     

兔肺动脉栓塞再灌注肺泡细胞凋亡及调控基因的实验研究

目的 探讨兔肺动脉栓塞／再灌注损伤中的细胞凋亡及其基因调控机制。方法 健康新西兰白兔36只，雌雄不拘，运用5F Berman球囊堵塞左下肺动脉，然后球囊放气，复制肺动脉栓塞缺血再灌注模型，随机分为6组：对照组，假手术组，肺栓塞1h组、肺栓塞2h组，肺栓塞2h再灌注1h组、肺栓塞2h再灌注2h组。实验结束取肺组织，测定肺组织湿干比，采用流式细胞分析法检测肺组织细胞凋亡率和免疫组织化学法检测肺上皮细胞Bax、Bcl-2、Fas／FasL蛋白表达的变化。结果兔肺动脉栓塞时肺组织细胞凋亡明显增加，再灌注后1h、2h凋亡细胞继续增加，并随着再灌注时间延长而增加（P〈0．05），Bax、Fas及FasL蛋白表达在肺动脉栓塞缺血及再灌注后明显增加（P〈O．01）。肺泡上皮细胞凋亡指数与肺组织湿干比、Bax、Fas、FasL蛋白表达之间存在非常显著的正相关关系（r=0．721，0．806，0．820，0．820；P〈0．01），与Bcl-2、Bcl-2／Bax比值呈显著负相关关系（r=-0．602，-0．829；P〈0．01）。结论肺动脉栓塞／再灌注中诱导肺组织细胞凋亡增加，肺组织细胞凋亡和Bax、Bcl-2，Fas、FasL系统活化可能参与了肺栓塞缺血再灌注肺损伤的发生。     

节细胞神经瘤的影像学表现

目的：分析节细胞神经瘤的影像学征象，以提高其诊断的正确性。资料与方法：回顾性分析经手术与病理证实的节细胞神经瘤11例，男4例，7列，除1例发生于后纵隔者为9岁儿童外，其余10例发病年龄22－63岁，中位年龄44．6岁。10例患者经CT扫描（包括平扫和增强扫描5例，平扫3例，直接增强2例）；3例患者经MR检查（平扫2例，平扫＋增强扫描1例）。结果：（1）节细胞神经瘤以青年和成年人多见（10例，90．9％）；（2）腹膜后6例（54．5％），后纵隔3例（27．3％），颈部2例（18．2％）；（3）肿物边界清晰，位于腹膜后者多沿周围器官间隙呈嵌入性生长，邻近大血管被包绕穿行于肿物之中或受压移位为其特征性表现之一。CT平扫为均匀低密度（8／8例），可伴有钙化，增强扫描后强化不明显（4／7）或仅见少量条线形强化（3／7例）；MR T2WI为明显不均匀高信号（3例），注射对比剂后呈延迟强化（1例）。结论：CT的MRI有助于提高节细胞神经瘤诊断的准确性，并可进一步观察病变与周围血管及器官的关系，为临床及手术提供更多的参考信息。     

MTAP在人BEP2D细胞辐射致癌模型和肺癌中表达研究

目的探索甲硫腺苷磷酸化酶(Methyhhioadenosine Phosphorylase，MTAP)在人支气管上皮BEP2D永生化细胞的恶性转化过程和临床非小细胞肺癌中的表达变化。方法培养BEP2D和BERP35T-2细胞，制备细胞总蛋白，进行双相电泳和质谱分析；选择有表达差异的蛋白质点MTAP，在细胞模型中进行NorthernBlot分析；对获得的15例肺癌标本用RT—PGR方法分析验证MTAP的表达水平。结果双相电泳发现MTAP在恶性转化细胞BERP35T-2中表达降低；Northern Blot分析表明MTAP mRNA在BEP2D永生化细胞中表达水平很高，而在BERP35T-2恶转细胞中表达极低；对15例非小细胞肺癌进行RT-PCR分析，发现MTAP在73．3％(11／15)的肿瘤组织中低表达；在中／低分化组肺癌的低表达频率(90．9％)显著高于高分化组(25％)，在腺癌与鳞癌组则没有显著性差异。结论MTAP低表达现象与肺癌恶性转化密切相关，可能发挥抑癌基因的生物学功能。     

恶性组织细胞增生症的X线表现（附25例分析）

恶性组织细胞增生症的Ｘ线表现（附２５例分析）孟繁禄，徐德永，田军，尹洪臣，曲凤声，李家忠恶性组织细胞增生症（简称恶组）是一种系统性组织细胞恶性增生的全身性疾病。由于本病的临床及Ｘ线表现缺乏特异性征象而易于误诊。笔者分析了；临床资料完整并经病理证实的２...     

X射线诱导survivin在EL-4细胞中的表达及与P53表达的相互关系

目的观察电离辐射对EL-4细胞survivin蛋白表达的影响及与P53表达的关系。方法采用流式细胞术（FCM）观察EL-4细胞接受4GyX射线照射后，survivin蛋白的表达、P53表达及细胞凋亡的变化。结果4Gy X射线照射EL-4细胞，Survivin蛋白表达受抑制，在4h明显降低，与对照组相比，差异有统计学意义（P〈0．001）；照射组P53蛋白表达水平均高于对照组，在此时间点上与对照组相比，差异有统计学意义（P〈0．01）。照射后4h细胞凋亡率显著升高，与对照组相比差异有统计学意义（P〈0．001）。结论survivin与P53在细胞凋亡调控中发挥重要作用，survivin表达与P53表达水平相关。     

内皮抑素基因联合放射治疗对大鼠Walker-256细胞种植性肿瘤的抑制作用

目的探讨鼠源性内皮抑素（endostatin）基因联合放射治疗对大鼠种植性肿瘤的抑制效应。方法制作大鼠乳腺癌Walker-256细胞种植性肿瘤的动物模型，通过检测肿瘤重量和肿瘤生长速率观察内皮抑素基因治疗联合放疗的抑瘤效应。体外采用Western blot检测构建pCMV-endostatin质粒转染的Walke-256细胞endostatin蛋白表达，体内采用BT-PCR观察各组endostatin mRNA表达。结果基因治疗组和基因治疗联合放射治疗组均可见到endostatin mRNA及其蛋白明显表达，但两组间表达无统计学意义；基因与放射联合组肿瘤的生长速率和重量均明显小于单纯基因治疗和放疗组（P〈0．01），后两组其肿瘤的生长速率和重量明显低于对照组（P〈0．01），但二者之间差异无统计学意义。结论pCMV-endostatin在Walker-256细胞内有明显表达endostatin mRNA及其蛋白；endostatin基因治疗有明显的抑瘤作用，但endostatin基因联合放疗的抑瘤效应更明显，促进放疗的抑瘤效果。     

99Tcm-HL91乏氧显像评价小鼠移植瘤放疗疗效

目的为^99Tc^m-4，9-二氮-3，3，10，10-四甲基十二烷-2，11-二酮肟（HL91）乏氧显像评价肿瘤放疗疗效提供依据。方法15只H22肝癌细胞小鼠移植瘤模型分成3组，每组各5只。A组不进行放疗；B组单次放疗25Gy后即刻进行^99Tc^m-HL91显像；C组单次放疗25Gy48h后进行^99Tc^m-HL91显像，计算B、C组放疗前后同一感兴趣区（ROI）内肿瘤组织与正常脑组织放射性计数比值（T／N）；测定A、B、C组凋亡细胞、G1期和S期细胞比例及观察肿瘤组织放疗前后病理变化。结果（1）B组放疗后T／N值较放疗前显著增高（P〈0．05）；C组放疗后T／N值较放疗前显著降低（P〈0．05）。（2）A、B、C组凋亡细胞之间比例差异具有统计学意义（P〈0．05，A〈B〈C）。（3）C组S期细胞所占比例明显低于A、B组，G1期细胞比例明显高于A、B组（P〈0．05）；C组肿瘤组织光学显微镜下可见凋亡细胞和大量细胞碎片。结论^99Tc^m-HL91显像是一种有价值的评价放疗疗效的手段。     

缺氧诱导的UCHL5增强宫颈癌Hela细胞辐射抗性

目的 研究缺氧诱导的泛素羧基末端水解酶L5（UCHL5）在调节宫颈癌Hela细胞辐射敏感性中的作用。 方法 以宫颈癌Hela细胞为研究对象,1% O₂条件下培养观察UCHL5表达水平的变化。采用Western blot和实时定量聚合酶链反应（PCR）检测慢病毒载体感染Hela细胞后稳定调变UCHL5的效率,转录本分为空白对照组、过表达对照组、过表达UCHL5组转录本1~4和沉默对照组、沉默UCHL5组转录本1~2。将实验所用的细胞分为过表达对照组、过表达UCHL5组、沉默对照组和沉默UCHL5组。采用流式细胞术检测8 Gy γ射线照射48 h后细胞的凋亡率;采用细胞克隆形成实验检测0、2、4、6 Gy γ射线单次照射培养2周后4组细胞的克隆形成率;采用3-（4,5-二甲基噻唑-2）-2,5-二苯基四氮唑溴盐（MTT）实验检测4组细胞培养1周后的增殖率以及联合0、2、4、6、8、10 Gy γ射线照射后的增殖率。使用基因表达谱数据动态分析癌症基因组图谱数据库宫颈癌组织和正常组织中抗缺氧诱导因子1α（HIF-1α）与UCHL5表达的相关性。采用双荧光素酶报告基因实验观察HIF-1α对UCHL5的激活作用。组间比较采用单样本t检验,采用Pearson检验进行相关性分析。 结果 缺氧可诱导宫颈癌Hela细胞UCHL5的表达。Western blot和实时定量PCR结果显示,感染后的Hela细胞可显著上调或下调UCHL5的表达,其中,过表达UCHL5组转录本2和沉默UCHL5组转录本2的表达均较高,所以选择此2种转录本进行后续实验。克隆形成实验结果显示,与接受相同剂量照射的过表达对照组相比,上调UCHL5增加了Hela细胞的克隆形成率,在0 、2、4、6 Gy剂量照射后克隆形成率的差异均有统计学意义（t=14.16、19.22、8.76、6.79,均 P<0.05）。 流式细胞术结果显示,与沉默对照组相比,沉默 UCHL5 促进了 Hela 细胞的凋亡（t=10.29,P<0.05）,增加了 γ 射线诱导的细胞凋亡率 (t=52.01, P<0.05)。MTT 实验结果显示,与过表达对照组相比,上调 UCHL5 可升高宫颈癌 Hela 细胞的增殖率,增殖率在第3天时差异有统计学意义 (t=3.905,P<0.05);与过表达对照组相比,等剂量照射 UCHL5 上调组升高了受照细胞的增殖率,在剂量为6、8、10 Gy时,细胞的增殖率差异均有统计学意义（t=3.40、4.06、3.68,均P<0.05）。宫颈癌组织中 HIF-1α 表达水平和UCHL5 表达水平呈正相关（R=0.31,P<0.01）,双荧光素酶报告基因结果显示 HIF-1α 结合并激活 UCHL5 启动子的活性,其活性增加了2.5倍（t=30.47,P<0.05）。 结论 缺氧条件下,宫颈癌Hela细胞中UHCL5的诱导表达降低了细胞的辐射敏感性,其潜在的机制可能与HIF-1α转录激活UCHL5的表达有关。     

Forensic nanopore sequencing of microhaplotype markers using QitanTech’s QNome

In recent years, extraordinary progress has been made in genome sequencing technologies, which has led to a decrease in cost and an increase in the diversity of sequenced genomes. Nanopore sequencing is one of the latest genome sequencing technologies. It aims to sequence longer contiguous pieces of DNA, which are essential for resolving structurally complex regions, and provides a new approach for forensic genetics to detect longer markers in real time. To date, multiple studies have been conducted to sequence forensic markers using MinION from Oxford Nanopore Technologies (ONT), and the results indicate that nanopore sequencing holds promise for forensic applications. Qitan Technology (QitanTech) recently launched its first commercial nanopore genome sequencer, QNome. It could achieve a read length of more than 150 kbp, and could generate approximately 500 Mb of data in 8 h. In this pilot study, we explored and validated this alternative nanopore sequencing device for microhaplotype (MH) profiling using a custom set of 15 MH loci. Seventy single-contributor samples were divided into 7 batches, each of which included 10 samples and control DNA 9947A and was sequenced by QNome. MH genotypes generated from QNome were compared to those from Ion Torrent sequencing (Ion S5XL system) to evaluate the accuracy and stability. Twelve samples randomly selected from the last three batches and Control DNA 9947A were also subjected to ONT MinION sequencing (with R9.4 flow cell) for parallel comparison. Based on MHtyper, a bioinformatics workflow developed for automated MH designation, all MH loci can be genotyped and reliably phased using the QNome data, with an overall accuracy of 99.83% (4 errors among 2310 genotypes). Three occurred near or in the region of homopolymer sequences, and one existed within 50 bp of the start of the sequencing reaction. In the last 15 samples (12 individual samples and 3 replicates of control DNA 9947A), two SNPs located at 4-mer homopolymers failed to obtain reliable genotypes on the MinION data. This study shows the potential of state-of-the-art nanopore sequencing methods to analyze forensic MH markers. Given the rapid pace of change, sporadic and nonrepetitive errors presented in this study are expected to be resolved by further developments of nanopore technologies and analysis tools.     

Mononuclear cells in subcutaneous haemorrhage with special consideration of myeloid percursor cells

Various hematogenous markers were used to differentiate and quantify the types of mononuclear cells present in subcutaneous haemorrhages. Fifty samples of subcutaneous bleeding with a survival time of a few minutes to more than 48 hours were studied. The various cell types were detected using the following stains: Naphthol AS-D chloracetate esterase for myeloid cells, including mast cells; (alpha1-antichymotrypsin for monocytes/macrophages; UCHL1 for T-lymphocytes; and L26 for B lymphocytes. The percentage of monocytes/macrophages was found to increase in dependence on survival time, whereas T-lymphocytes declined. Within minutes of injury neutrophilic granulocytes had emigrated into the surrounding tissue and mast cell degranulation had occurred within the haemorrhagic zone. Esterase-positive mononuclear cells, namely metamyelocytes, were detected within minutes after injury and were still present after survival times exceeding 48 hours; however, no dependence on survival time or cause of death was found. Although the increasing number of monocytes/ macrophages and T-lymphocytes was expected, the sometimes high percentage of myeloid precursor cells within the wound were surprising. Possible explanations for this phenomenon are discussed.     

两种缺氧刺激对大学生红细胞生成素及有氧能力的影响

目的:探讨缺氧刺激对血清红细胞生成素(EPO)和转铁蛋白受体(sTfR)的影响,观察在低氧刺激环境下血液EPO分泌和血清sTfR浓度的变化规律.方法:受试者为20名身体健康的男性大学生,随机分为3组:间歇吸低氧组(n=7)、模拟高住组(n=5)和对照组(n=8).间歇吸低氧组每天30分钟吸低氧,模拟高住组每天8小时低氧环境睡眠.所有受试者在实验期均从事相同的体育技术课和理论课学习及相同的生活作息,全部实验共包括4周试验期和2周恢复期.结果:(1)对照组血清EPO浓度在实验前、中和恢复期均无明显变化.间歇吸低氧组血清EPO浓度在实验第3天、第17天、第22天,模拟高住组血清EPO浓度在实验第15天、第17天、第22天、第24天及恢复期均显著高于实验前(P＜0.05),(2)间歇吸低氧组血清sTfR浓度在实验第3天、第10天、第17天及恢复期结束均显著高于实验前(P＜0.05),而模拟高住组和对照组血清sTfR浓度在实验期和恢复期均未发生明显变化.(3)实验后间歇吸低氧组受试者VO2max与实验前比较明显增加(P＜0.05).(4)除对照组外,实验后间歇吸低氧组、模拟高住组在定量负荷运动中的心率、血乳酸与实验前相比显著下降(P＜0.05).结论:血清EPO、sTfR浓度的变化受不同低氧浓度刺激时间和方式的影响,间歇吸低氧与运动刺激相结合可增加VO2max.     

Development and evaluation of a novel panel containing 188 microhaplotypes for 2nd-degree kinship testing in the Hebei Han population

Distant kinship identification is one of the critical problems in forensic genetics. As a new type of genetic marker defined and discussed in the last decade, the microhaplotype (MH) has drawn much attention in such identification owing to its specific advantages to traditional short tandem repeat (STR) or single nucleotide polymorphism (SNP) markers. In this study, MH markers were screened step by step from the 1000 Genomes Project database, and a novel multiplex panel containing 188 MHs (in which 181 are reported the first time, while 1 was reported in a previous study and the other 6 have partial overlaps with known markers) was constructed for application in 2nd- and 3rd-degree kinship identification. Along with the construction, a novel MH nomenclature was proposed, in which the SNP position information they contained was taken into account to eliminate the possibility that the same locus was named differently interlaboratory. After a series of evaluations, the panel was shown to have good sequencing accuracy, high sensitivity, species specificity, and resistance to anti-PCR inhibitors or degradation. Population data of the 188 MHs were calculated based on the genetic information of 221 unrelated Hebei Han individuals, and the effective number of alleles (Ae) ranged from 2.0925 to 8.2634 (with an average of 2.9267). For the whole system, the cumulative matching probability (CMP), the cumulative power of exclusion in paternity testing of duos (CPEduo) and that of trios (CPEtrio) reached 2.8422 × 10⁻¹³⁷, 1–1.3109 × 10⁻²¹, and 1–2.8975 × 10⁻³⁹, respectively, indicating that this panel was satisfactory for individual identification and paternity testing. Then, the efficiency of the 188 MHs in 2nd- and 3rd-degree kinship testing was studied based on 30 extended families consisting of 179 2nd-degree and 121 3rd-degree relatives, as well as simulations of 0.5 million pairs of those two kinships. The results showed that clear opinions would be given in 83.36% of 2nd-degree identifications with a false rate less than 10⁻⁵, when the confirming and excluding thresholds of cumulative likelihood ratio (CLR) were set as 10⁴ and 10⁻⁴, respectively. This panel is still not sufficient to solve the problem of 3rd-degree kinship identification alone, and approximately 300 or 870 MH loci would be needed in 2nd- or 3rd-degree kinship identification, respectively, to achieve a system efficiency not less than 0.99 with such a threshold set; such necessary numbers would be used only as a reference in further research.     

Fluorescent markers of hypoxic cells: a comparison of two compounds on three cell lines

Two compounds, nitroakridin 3582 (NA) and a 3-nitro-naphthalimide (DM113), have been tested as potential fluorescent markers for hypoxic cells. Cellular fluorescence in three cell lines (V79-379A, WHF1B, EMT6) was measured by flow cytometry and high-performance liquid chromatography (HPLC) after incubating the cells with the drugs for various times in air or hypoxia. In all three cell lines, both drugs showed greater fluorescence in hypoxic than in oxic cells. There were, however, differences between the cell lines in respect of the magnitudes of hypoxic and oxic cell fluorescence and in the ratio of hypoxic to oxic fluorescence. Differences in hypoxic cell fluorescence were due to differences in the rate and extent of nitroreduction. Drug uptake and DNA content per cell were relatively unimportant factors in determining the magnitude of fluorescence. There was not a good correlation between cytotoxicity of the drugs and hypoxic fluorescence. Nitroakridin was more toxic to hypoxic than to aerated cells but the reverse was true for DM113. The dependence of fluorescence and radiosensitivity on oxygen concentration were compared for the three cell lines and only small differences between the "K"-curves for the two end-points were found. Two problems with the present compounds which should be addressed in designing future fluorogenic compounds as hypoxic markers were oxic cell fluorescence and leakage of fluorescent products from hypoxic cells.     

Changes in glucose metabolism and gene expression after transfer of anti-angiogenic genes in rat hepatoma

Purpose Human troponin I (TROP), the soluble receptor for vascular endothelial growth factor (sFLT) and angiostatin (ASTAT) are potent inhibitors of endothelial cell proliferation, angiogenesis and tumour growth in vivo. Transfer of these genes into tumours may induce changes not only in perfusion, but also more general ones such as changes in metabolism. The aim of this study was to assess these reactions using FDG-PET and high-throughput methods such as gene profiling. Methods We established Morris hepatoma (MH3924A) cell lines expressing TROP, sFLT or ASTAT and quantified ¹⁸F-fluorodeoxyglucose (¹⁸FDG) uptake by dynamic positron emission tomography (PET) after tumour inoculation in ACI rats. Furthermore, expression of glucose transporter-1 and -3 (GLUT-1 and GLUT-3) as well as hexokinase-1 and -2 were investigated by RT-PCR and immunohistomorphometry. In addition, gene array analyses were performed. Results ¹⁸FDG uptake, vascular fraction and distribution volume were significantly higher in all genetically modified tumours. Immunohistomorphometry showed an increased percentage of hexokinase-1 and -2 as well as GLUT-1 and -3 immunoreactive (ir) cells. Using gene arrays and comparing all three groups of genetically modified tumours, we found upregulated expression of 36 genes related to apoptosis, signal transduction, stress or metabolism. Conclusion TROP-, sFLT- or ASTAT-expressing MH3924A tumours show enhanced influx of ¹⁸FDG, which seems to be caused by several factors: enhanced exchange of nutrients between blood and tumour, increased amounts of glucose transporters and hexokinases, and increased expression of genes related to apoptosis, matrix and stress, which induce an increased demand for glucose.     

脑胶质肉瘤的影像学表现与临床病理对照

目的探讨胶质肉瘤的影像学表现与临床病理特点。方法回顾性分析经手术病理证实的脑胶质肉瘤8例的CT、MR I表现和临床病理所见,并复习文献。结果7例位于幕上区,小脑1例,8例CT扫描5例为低等混杂密度,2例为低密度,1例为稍高密度,增强扫描为不规则强化,其内见囊变及坏死。3例行MR I检查,T1W I为低信号,T2W I为稍高混杂信号或高信号。增强扫描为不均匀强化,边界清楚,水肿明显。组织学检查,肿瘤由胶质母细胞和梭形细胞2种成分组成,免疫组化检查8例,脑胶质细胞成分GFAP为阳性,梭形细胞成分GFAP为阴性。结论脑胶质肉瘤少见,临床上无特异性,CT、MR I表现虽有一定特点,但确诊依靠病理检查。     

环氧酶抑制剂对创伤性代谢反应的影响

观察了环氧酶抑制剂对创伤性应激反应和蛋白质分解代谢的影响，将全胃切除术病人分为两组：消炎痛组，从术后２小时开始给予消炎痛肛栓剂５０ｍｇ，１／８小时；对照组按同样方法给予安慰剂。监测了手术前后体温，血清激素、血浆蛋白和尿中尿素氮、肌酐和３—甲基组氨酸的排出，结果显示消炎痛组体温、应激激素和尿中尿素氮，３—甲基组氨酸排出均明显低于对照组。表明环氧酶抑制剂可以减轻创伤时的应激反应和减少蛋白质分解代谢。