DWI评估N-乙酰-5-羟色胺对脑缺血再灌注大鼠脑水肿的影响

目的 采用DWI观察N-乙酰-5-羟色胺（NAS）对急性局灶性脑缺血再灌注（IR）大鼠脑水肿的神经保护作用。方法 将66只大鼠随机分为假手术组（n=10）、大脑中动脉阻塞（MCAO）组（n=28）和NAS组（n=28）。对MCAO组和NAS组大鼠IR后6 h、24 h、72 h、7天,对假手术组于72 h,分别行DWI和病理学检查,比较3组不同时间点脑梗死区相对ADC值（rADC）、相对指数ADC值（reADC）、水通道蛋白4（AQP4）阳性细胞数的变化。IR后72 h,测量各组脑组织含水量的变化。结果 假手术组大鼠MRI检测未见异常信号。NAS组与MCAO组大鼠DWI图均可见损伤侧大脑皮层及纹状体异常高信号,ADC图为低信号,eADC图为高信号。IR后6、24、72 h,NAS组rADC值均高于MCAO组（P均<0.05）,reADC值和AQP4阳性细胞数低于MCAO组（P均<0.05）;IR后7天,各组rADC值、reADC值及AQP4阳性细胞数差异无统计学意义（P均>0.05）。IR后72 h,NAS组大鼠脑组织水含量低于MCAO组（P<0.05）。结论 NAS可减轻急性IR脑损伤大鼠脑水肿,其机制可能与下调AQP4蛋白的表达有关;DWI对评价NAS的神经保护作用具有重要价值。     

逐层匀场技术弥散加权成像评价膀胱癌

目的 对比基于逐层匀场技术弥散加权成像（iShim-DWI）与常规弥散加权成像（DWI）图像质量,评估iShim-DWI对膀胱癌的应用价值。方法 回顾性分析70例经手术病理证实的膀胱癌患者,依据TNM分期将其分为肌层浸润性膀胱癌（MIBC）组（n=34）和非肌层浸润性膀胱癌（NMIBC）组（n=36）,根据术后病理分级分为低级别尿路上皮癌组（n=38）和高级别尿路上皮癌组（n=32）。观察常规DWI和iShim-DWI图像质量的差异。测量iShim-DWI病灶表观弥散系数（ADC）,比较NMIBC组与MIBC组、高、低级别尿路上皮癌组ADC差异。以受试者工作特征（ROC）曲线评估ADC鉴别膀胱癌肌层浸润及高、低级别膀胱癌和T2WI、传统DWI及iShim-DWI诊断膀胱癌肌层浸润的效能。结果 2名医师对iShim-DWI图像的主观评分均高于传统DWI（P均<0.01）。NMIBC组ADC[1.12（1.06,1.18）×10^－3 mm²/s]大于MIBC组[0.81（0.75,0.83）×10^－3 mm²/s,Z=－6.79,P<0.01],ADC鉴别MIBC与NMIBC的AUC为0.97;低级别尿路上皮癌组ADC[1.13（1.06,1.17）×10^－3 mm²/s]大于高级别尿路上皮癌组[0.80（0.74,0.82）×10^－3 mm²/s,Z=－6.79,P<0.01],AUC为0.99。基于T2WI+常规DWI诊断膀胱癌肌层浸润的AUC均低于T2WI+iShim-DWI（P均<0.05）。结论 iShim-DWI有助于评估膀胱癌病理分级及肌层浸润,且图像质量优于常规DWI。     

分化型甲状腺癌术后患者131I治疗后全身显像中肝脏弥漫性摄取的临床意义

目的 探讨分化型甲状腺癌（DTC）术后患者¹³¹I治疗后全身显像（Rx-WBS）中肝脏弥漫性摄取（DHU）的临床意义。方法 回顾性分析178例DTC,根据Rx-WBS所示DHU程度将其分为G0组（n=41）、G1组（n=69）、G2组（n=56）和G3组（n=12）;将P<0.2的因素纳入有序Logistic回归分析,筛选DHU影响因素。结果 178例DTC中,137例（137/178,76.97%）可见DHU。单因素分析显示4组患者促甲状腺激素（TSH）、¹³¹I剂量及远处转移（M）差异均有统计学意义（P均<0.05）,而年龄、甲状腺球蛋白（Tg）等11个因素差异均无统计学意义（P均>0.05）。多因素有序Logistic回归分析显示¹³¹I剂量（β=0.013,P=0.036）是DHU程度的独立影响因素;4组间TSH、M、治疗次数及Tg差异均无统计学意义（P均>0.05）。结论 ¹³¹I剂量是DHU程度的独立影响因素,且具有显著正向影响。     

前列腺癌ADC值与Gleason评分及Ki-67、P53蛋白表达的相关性

目的 探讨DWI ADC值与前列腺癌Gleason评分及Ki-67、P53蛋白表达的相关性。方法 收集59例接受DWI检查并经病理证实的前列腺癌患者,病理组织均经Ki-67和P53免疫组织化学染色。根据镜下癌细胞及间质的分化程度进行Gleason评分,将其分别纳入高分化组（<7分,n=17）、中分化组（7~8分,n=23）或低分化组（>8分,n=19）。比较各组间ADC值的差异,分析病灶ADC值与Gleason评分及Ki-67、P53蛋白表达的相关性。结果 59例前列腺癌病灶的ADC值为（0.98±0.19）×10^-3 mm²/s,高分化、中分化和低分化组ADC值分别为（1.14±0.17）×10^-3 mm²/s、（1.05±0.17）×10^-3 mm²/s和（0.88±0.24）×10^-3 mm²/s,总体和两两比较差异均有统计学意义（P均<0.05）。前列腺癌ADC值与Gleason评分、Ki-67和P53蛋白表达均呈负相关（r_s=-0.611、-0.491、-0.511,P=0.019、0.016、0.021）。结论 前列腺癌ADC值分别与Gleason评分及Ki-67、P53蛋白表达呈负相关。通过ADC值可初步评价前列腺癌的恶性程度及细胞分化、增殖程度。     

剪切波弹性成像评估重型β-地中海贫血患儿肝脏超铁负荷:与肝脏MR T2*值及血清铁蛋白的相关性

目的 观察剪切波弹性成像（SWE）评估重型β-地中海贫血（β-TM）患儿超铁负荷的价值,及其参数与肝脏MR T2^*值及血清铁蛋白的相关性。方法 回顾性分析96例β-TM患儿及100名健康儿童（对照组）,根据是否接受造血干细胞移植（HSCT）将患儿分为HSCT组（n=41）或无HSCT组（n=55）,比较3组SWE参数;采用Spearman相关分析观察肝脏剪切波速度（LSWV）与肝脏MR T2^*值及血清铁蛋白、杨氏模量与肝脏MR T2^*值及血清铁蛋白的相关性。结果 HSCT组、无HSCT组LSWV及杨氏模量均高于对照组（P均<0.001）;HSCT组与无HSCT组LSWV及杨氏模量差异均无统计学意义（P均>0.05）。β-TM患儿SWE参数与MR T2^*值均呈中度负相关（r=－0.501,P<0.05;r=－0.514,P<0.05）、与血清铁蛋白均呈低度正相关（r=0.488,P<0.05;r=0.470,P<0.05）。结论 SWE可用于评估β-TM患儿肝脏超铁负荷;SWE参数与MR T2^*值呈负相关、与血清铁蛋白呈正相关。     

体素内不相干运动成像在体检测人类结肠癌SW480裸鼠耐药性

目的 探讨体素内不相干运动（IVIM）成像活体评价人类结肠癌SW480裸鼠耐药性及其可行性。方法 对耐药组（n=5）和不耐药组（n=5）人类结肠癌SW480荷瘤裸鼠于肿瘤最长径大于1.50 cm后分别行IVIM DWI检查,测量肿瘤真扩散系数（D）、假扩散系数（D^*）及灌注分数（f）。处死荷瘤鼠,检测肿瘤坏死（HE染色）、凋亡（TUNEL法）及P-糖蛋白（P-gp）、多药耐药相关蛋白1（MRP1）、蛋白激酶C（PKC）蛋白表达（Western Blot）,对IVIM参数和肿瘤蛋白表达情况进行相关分析。结果 不耐药组D较耐药组增高（P<0.05）,2组D^*和f差异无统计学意义（P均>0.05）。2组肿瘤组织坏死区域范围相似;耐药组细胞核较不耐药组增大,且细胞间排列更紧密,细胞密度较大。2组肿瘤细胞凋亡指数差异无统计学意义（P>0.05）。耐药组PKC、P-gp、MRP1蛋白表达均较不耐药组增加（P均<0.05）。肿瘤D值与P-gp、MRP1、PKC表达均呈负相关（P均<0.05）。结论 IVIM成像参数D值可能成为评估小鼠人类结肠癌SW480耐药性的指标。     

基于患者体质量指数的68Ga-DOTA-NOC PET/CT最佳采集条件

目的 探讨基于患者体质量指数（BMI）的⁶⁸Ga-1,4,7,10-四氮杂环十二烷-1,4,7,10-四乙酸-1-柰丙氨酸-奥曲肽（DOTA-NOC）PET/CT最佳采集条件。方法 收集89例接受⁶⁸Ga-DOTA-NOC PET/CT全身扫描的神经内分泌肿瘤患者,根据体质量指数分为偏瘦组（n=13）、正常组（n=40）、超重组（n=31）和肥胖组（n=5）。以真符合计数率、随机符合计数率、等效噪声比（NECR）、随机分数和变异系数（CV）评估PET图像质量,分析其与BMI的关系,并比较4组间差异。结果 89例患者平均BMI为（22.99±3.77）kg/m²,⁶⁸Ga-DOTA-NOC注射剂量为（1.04±0.27）MBq/kg体质量。真符合计数率、随机符合计数率和NECR均与显像剂注射剂量呈线性正相关（r=0.71、0.71、0.72,P均<0.01）。NECR在显像剂注射剂量约为1.65 MBq/kg体质量时获得最大值。4组真符合计数率差异有统计学意义（F=6.26,P<0.01）,且BMI正常组患者真符合计数率与偏瘦组、超重组和肥胖组的比值分别为0.82、1.12和1.28。CV值随显像剂注射剂量的增加而下降（r=0.78,P<0.01）,4组间差异有统计学意义（F=16.48,P<0.01）。4组间随机分数差异无统计学意义（F=1.33,P=0.27）。结论 基于患者BMI,⁶⁸Ga-DOTA-NOC PET/CT推荐方案如下：偏瘦患者显像剂注射剂量参考范围为1.05~1.15 MBq/kg体质量,最大不超过1.30 MBq/kg体质量;超重患者和肥胖患者的每床位采集时间分别延长1.2~1.3倍和1.3~1.5倍。     

1H-MRS定量分析糖尿病大鼠腓肠肌代谢物早期评估糖尿病周围神经病变

目的 观察氢质子磁共振频谱（¹H-MRS）检测腓肠肌代谢物对早期评估大鼠糖尿病（DM）模型周围神经病变的价值。方法 将40只SD雄性大鼠随机分为实验组（n=20）与正常组（n=20）。实验组以高糖高脂饲养+注射链脲菌素法建立DM模型。于造模前和造模后7、14、21天采集2组大鼠右下肢腓肠肌¹H-MRS，获得胆碱复合物（Cho）、肌酸复合物（Cr）、细胞内脂质（IMCL）、Cho/Cr及IMCl/Cr值。正常组大鼠予普通饲料喂养。造模后21天行右下肢坐骨神经电生理及病理检查，测量2组坐骨神经运动神经传导速度（MNCV）及感觉神经传导速度（SNCV）。比较实验组内各时间点代谢物浓度值差异及2组间MNCV和SNCV差异，观察病理结果。结果 实验组内不同时间点Cho、Cr、IMCL、Cho/Cr及IMCL/Cr值差异均有统计学意义（F=6.69、5.41、3.65、3.51、3.10，P均<0.05）；造模后14、21天Cr和Cho值均高于造模前（P均<0.05），造模后7天IMCL值高于造模前（P<0.05）。造模后21天实验组右下肢坐骨神经MNCV和SNCV均低于正常组（t=2.74、4.62，P均<0.01）。相比正常组，实验组神经纤维稀疏松散，排列紊乱，部分髓鞘着色浅且不均匀，轴索变细萎缩。结论 ¹H-MRS可无创定量分析骨骼肌代谢，进而早期评估大鼠DM模型DPN。     

体素内不相干运动DWI评估SD大鼠C6脑胶质瘤模型肿瘤微环境乏氧状态

目的 观察体素内不相干运动DWI（IVIM-DWI）评估SD大鼠C6脑胶质瘤模型肿瘤微环境乏氧状态的可行性。方法 建立SD大鼠C6脑胶质瘤模型（n=48）,于造模第14、21及28天分别取16只大鼠行IVIM-DWI,获得ADC、纯扩散系数（D）、伪灌注扩散系数（D^*）及灌注分数（f）。每次扫描后处死大鼠,取肿瘤组织行缺氧诱导因子1α（HIF-1α）免疫组织化学化染色并评分,比较造模后各时间点IVIM-DWI参数及HIF-1α评分差异,分析IVIM-DWI参数与HIF-1α评分的相关性。结果 造模第14、21及28天,IVIM-DWI各参数及HIF-1α评分比较差异均有统计学意义（P均<0.01）。造模第21天,D、D^*、f均与HIF-1α评分呈负相关（r=-0.73、-0.58、-0.67,P均<0.05）;造模第28天,D、f均与HIF-1α评分呈负相关（r=-0.60、-0.65,P均<0.05）。结论 IVIM-DWI能够评价SD大鼠C6脑胶质瘤模型肿瘤微环境乏氧状态。     

3D动脉自旋标记、弥散张量成像联合常规MRI鉴别诊断颅内血管外皮细胞瘤与血管瘤型脑膜瘤

目的 观察3D动脉自旋标记（3D ASL）、弥散张量成像（DTI）联合常规MRI鉴别诊断颅内血管外皮细胞瘤（HPC）与血管瘤型脑膜瘤（AM）的价值。方法 回顾性分析经手术病理证实的15例HPC（HPC组）与11例AM（AM组），分析2组临床表现、MRI（包括平扫、增强、DTI、3D ASL）征象及功能成像参数差异。结果 HPC组平均脑血流量（CBF）及各向异性分数（FA）均低于AM组（t=-8.99，P<0.01；t=-3.66，P<0.01），表观弥散系数（ADC）高于AM组（t=2.61，P=0.02）；HPC组高灌注区和低灌注区CBF均低于AM组（t=-15.13，P<0.01；t=-8.30，P<0.01）；HPC组平均发病年龄低于AM组（t=-2.39，P=0.02），性别差异无统计学意义（χ²=1.69，P=0.19）；相比AM组，HPC组更易出现分叶征（χ²=9.09，P<0.01）及囊变坏死（χ²=9.38，P<0.01），HPC病灶T1WI以等高信号为主（χ²=27.78，P<0.01）、T2WI以等低信号为主（χ²=16.33，P<0.01），瘤周水肿程度轻（χ²=19.25，P<0.01），血管流空影更常见且更粗大（χ²=9.02，P=0.01），多与硬脑膜多为窄基底相连（χ²=28.54，P<0.01）而脑膜尾征少见（χ²=25.00，P<0.01）。结论 HPC与AM的MRI征象及各功能成像参数值存在一定差异，可为鉴别诊断提供参考。     

The Hereditary Syndrome of Thrombocytopathia, Bleeding Tendency, Extreme Miosis, Muscular Fatigue, Asplenia, Headache, etc

SYNOPSIS
A new, autosomal dominantly inherited syndrome with a bleeding disorder was described in 1985 by Stormorken and his co-workers.1,2 In this multifaceted syndrome, there were the following integral components: thrombocytopathia, extreme miosis with Argyll Robertson-like traits, muscular fatigue, a tendency to spasms, asplenia, ichthyosis, dyslexia, etc.
Headache with migraine traits was also present in the family in all 4 generations in which this syndrome had been observed. Nasal and conjunctival bleeding were part of the headache picture in some of the individuals exhibiting the hemorrhagic syndrome. While the attack-related bleeding disturbances only involved family members who also suffered from the hemorrhagic syndrome, the headache per se may seem to behave differently: The affected son's headache seems to have developed into a headache with tension headache traits, whereas the other, unaffected, son's headache has common migraine traits. The familial headache which in earlier generations clearly had migraine traits, therefore, may be inherited independently from the hemorrhagic disorder. In other words, a migraine or migraine-like headache is most probably not an obligatory integral part of this syndrome. The thrombocytopathia in this disorder comprises abnormal serotonin storage, uptake, and release (Stormorken and co-workers, to be published).
The admittedly somewhat farfetched possibility also exists that the headache, although being similar to migraine, differs essentially from it and may be an expression of the serotonin aberration.     

Effect of 5-fluorouracil, mitoxantrone, methotrexate, and vincristine on the antibacterial activity of ceftriaxone, ceftazidime, cefotiam, piperacillin, and netilmicin

Using the checkerboard agar dilution technique, antibacterial activity and in vitro interactions of 4 antineoplastic agents and 5 antimicrobial drugs were examined against 56 strains of 7 bacterial species. 5-fluorouracil was found to inhibit all strains of Staphylococcus aureus and of Staphylococcus epidermidis at a concentration of 0.8 micrograms/ml or less. 84% of all gram-negative strains were inhibited synergistically when 5-fluorouracil was combined with beta-lactam antibiotics. Methotrexate and cefotiam were antagonistic in 42% of all combinations, especially when tested against Escherichia coli and Klebsiella pneumoniae.     

Susceptibilities of non-Pseudomonas aeruginosa gram-negative nonfermentative rods to ciprofloxacin, ofloxacin, levofloxacin, D-ofloxacin, sparfloxacin, ceftazidime, piperacillin, piperacillin-tazobactam, trimethoprim-sulfamethoxazole, and imipenem.

Agar dilution MICs of 10 agents against 410 non-Pseudomonas aeruginosa gram-negative nonfermentative rods were determined. MICs at which 50 and 90% of the isolates were inhibited, respectively, were as follows (in micrograms per milliliter): sparfloxacin, 0.5 and 8.0; levofloxacin, 1.0 and 8.0; ciprofloxacin, 2.0 and 32.0; ofloxacin, 2.0 and 32.0; D-ofloxacin, 32.0 and > 64.0; ceftazidime, 8.0 and 64.0; piperacillin with or without tazobactam, 16.0 and > 64.0; trimethoprim-sulfamethoxazole, 0.5 and > 64.0; imipenem, 2.0 and > 64.0. With the exception of those for Stenotrophomonas maltophilia, Burkholderia cepacia, and Alcaligenes faecalis-A. odorans, agar dilution MICs for all strains tested were within 1 dilution of inhibitory (bacteriostatic) levels as determined by time-kill methodology.     

品管圈在提高儿科住院患儿服药到口率中的应用

目的：探讨品管圈在儿科病房服药到口护理工作改进中的管理作用。方法：通过品管圈活动步骤,运用质量管理工具对儿科住院患儿服药不能到口的问题进行改进,并将改进前后状况进行比较讨论。结果：住院患儿服药到口率从42.5%提升到99.19%(P＜0.01)。结论：品管圈方法的应用提高了住院患儿服药到口率,提高了医护人员的团队精神,增强了护士的责任心,提升了护士的个人素质和自信心。     

Comparative ototoxicity of ribostamycin, dactimicin, dibekacin, kanamycin, amikacin, tobramycin, gentamicin, sisomicin and netilmicin in the inner ear of guinea pigs

Nine aminoglycoside antibiotics, ribostamycin (RSM), dactimicin (DAC), dibekacin (DKB), kanamycin (KM), amikacin (AMK), netilmicin (NTL), tobramycin (TOB), gentamicin (GM) and sisomicin (SISO) were administered intramuscularly to guinea pigs for 4 weeks, and ototoxicity and drug concentration in the inner ear fluid were determined. RSM and DAC showed the weakest ototoxicity against the cochlea and vestibular organs. AMK and KM were more toxic to cochlea than vestibular organs. DKB, TOM, GM and SISO were equally toxic to vestibular organs and cochlea. NTL was more toxic to vestibular organs than cochlea. As judged from the pinna reflex response and hair cell damage in the cochlea, the order of auditory toxicity was the following: SISO greater than GM greater than TOB greater than AMK greater than DKB greater than KM greater than NTL, DAC RSM, whereas the vestibular toxicity was in the following order: SISO greater than GM greater than DKB greater than TOB greater than NTL greater than AMK greater than KM greater than DAC, RSM. RSM, causing the weakest ototoxicity, showed a low drug concentration in the inner ear fluid, while GM, causing severe ototoxicity, showed the highest drug level under the same conditions.