磁共振成象诊断出血性胆囊炎——离体及活体研究

在离体研究的基础上,对三个出血性胆囊炎的病人术前做出诊断,出血性胆囊炎可分为混合性及非混合性.在离体实验中,如果血液未与胆汁混合,T₁加权象可发现加于10mL胆汁中的0.2mL的血液表现为高信号区;质子密度加权象可发现加于10mL,胆汁中的0.4mL血液表现为稍高信号区;T₂加权象对此不敏感.如果血液与胆汁完全混合,在所有采用的磁共振成象上均使胆汁信号增高.非混合性出血性胆囊炎的磁共振成象具有特征性:在T₁加权象及质子密度加权象胆囊内有高信号区,T₂加权象此区为等信号、低信号或其中心为低信号周围与胆汁相接的为高信号。混合性出血性胆囊炎在所采用的磁共振成象图象中,相对于肝脏,胆囊内容物表现为均匀高信号,临床资料及胆囊壁、胆囊周围渗出有助于这种出血性胆囊炎的诊断.     

慢性电刺激海马结构诱发大鼠脑磁共振成像异常信号分析

为探讨海马结构(hippocampal formation)功能失衡与癫痫源性脑损伤的关系,本工作采用 慢性强直电刺激大鼠海马(hippocampus, HPC) CA1顶树突区（apical dendrite region, A DR）或齿状回（dentate gyrus, DG）诱发大鼠癫痫模型,一天一次,连续刺激6～8天后, 观察人工致痫灶以外的横向弛豫时间加权的核磁共振(T₂ weighted magnetic reson ance im age, T₂-WI) 绝对信号值变化（片厚1mm）,以及深部电图和原发性湿狗颤抖（pri mary wet dog shakes, WEDS）,并对被检测动物T₂-WI信号异常的相应脑区进行组织学鉴定. 结果表明：（1）电 刺激大 鼠ADR或DG的作用基本相似,引起深部电图的癫痫样电活动和侧脑室区域T₂值增强.（2）含有电极尖端痕迹的核磁共振（magnetic resonance image,MRI）脑切片出现对称性腹部侧脑室区域T₂值增强,连续向后1mm取MRI脑切片进行观察发现,对侧腹部侧脑室区域信号异常. （3）组织学切片观察到：MRI检测的侧脑室区域T₂-WI信号增强与组织切片的侧脑室扩大相吻合,可见扩大的侧脑室中脉络丛上皮细胞病理性增生现象. 提示：在大鼠癫痫点燃现象出现之前,过度激活DG或ADR均可引起相似的早期癫痫源性脑损伤.     

基于磁共振弛豫时间实现加权像和压脂技术

磁共振成像是根据生物磁性核在磁场中表现的共振特性进行成像的新技术,其中弛豫时间是实现和控制成像的重要物理量.本文使用磁共振成像实验仪,对相关样品的纵向弛豫时间T₁、横向弛豫时间T₂进行测量,并且基于不同弛豫时间采用自旋回波序列实现T₁、T₂加权像,用反转恢复成像序列实现磁共振成像对脂肪的抑制.     

超极化Xenon 对慢阻肺的可视化加权成像

超极化气体3He 或者¹²⁹Xe 扩散加权成像已经被证明了能够有效检测慢性阻塞性肺部疾病(COPD)中肺部微结构的改变．相比于³He,¹²⁹Xe 更便宜而且更容易获得,但是¹²⁹Xe 成像中较低的信噪比致使¹²⁹Xe 的肺部表面扩散系数(ADC)的测量面临着许多困难．在该研究中,为了得到更高的图像信噪比,作者对气球模型,健康大鼠和COPD大鼠进行了单个b 值(14 cm2/s)的扩散加权超极化¹²⁹Xe 磁共振成像(MRI)．所有的COPD模型大鼠是通过烟熏和注射内毒素(LPS)进行诱导得到的．在7 T 磁共振成像仪上面获得了大鼠肺实质的超极化¹²⁹Xe ADC 值分布图．COPD 大鼠肺实质的¹²⁹Xe ADC 值是0.044 22±0.002 9 和0.042 34±0.002 3 cm2/s (Δ = 0.8/1.2 ms),远大于健康大鼠肺实质的¹²⁹Xe ADC 值0.037 7±0.002 3 和0.036 7±0.001 3 cm2/s．而且COPD 大鼠肺实质相关的¹²⁹Xe ADC 直方图也表现出了一定的展宽．这些结果说明了COPD 大鼠肺泡空腔的增大能够通过129Xe 在肺里面的ADC 增长和相关直方图的拓宽反应出来,从而证明了单个b 值的扩散加权MRI 方法可以有效地对COPD 大鼠进行检测．     

新型Gd基T2造影剂的制备和应用

设计并合成了结构为TPP-Lys（Acp-DOTA-Gd）-COOH（简称Gd-DOTA-TPP）的小分子磁共振探针,通过电转染的方式用探针标记人源脐带间充质干细胞（hMSCs）.11.7 T磁共振成像（MRI）扫描结果表明,Gd-DOTA-TPP标记的hMSCs在细胞内Gd含量为9×10⁹ Gd/cell时,T₂加权信号强度即可低至背景信号强度,呈现较强暗信号.将Gd-DOTA-TPP标记的hMSCs移植入小鼠脑室,可明显提高移植干细胞在MRI设备上的检测灵敏度,检测限可低至10³个细胞.     

猕猴桃的磁共振成象及核磁共振定域波谱研究

以猕猴桃鲜果为样品,在4.7T核磁共振成象仪上测量了质子密度象、扩散系数D的分布象、纵向弛豫时间T₁分布象和横向弛豫时间TT₂分布象,得到了鲜果不同部位的TT₁、TT₂和D的值,此外还进行了抑制水峰的定域波谱测量.所测得的定域波谱与猕猴桃果汁的¹H高分辨核磁共振(NMR)谱进行了比较和归属.无损地获得了有关猕猴桃的形态结构和物质组成的一些信息.     

用核磁共振成象研究大白鼠的光化学反应脑缺血模型

用不同权重的核磁共振T₂加权成象数据在采样过程中完成叠加,所得到的核磁共振T₂加权图象清晰地显示出大白鼠大脑中缺血损伤区域的位置和大小.用该方法研究大白鼠的光化学反应局部脑缺血模型,在大白鼠脑缺血发生后大约一小时即可以用T₂加权的MRI图象发现缺血区,证明该种方法有很大的应用潜力.     

超顺磁性氧化铁-胶束体系的制备和T2弛豫增强作用 

制备了在负离子型胶束十二烷基硫酸钠（SDS）、羧甲基纤维素钠（CMC），正离子型胶束十六烷基三甲基溴化铵（CTAB）和非离子型胶束Triton X-100、PEG-400中的氧 化铁粒子(SPIO)溶胶分散体系. 测定了这些SPIO胶束体系水质子的横向弛豫时间T₂, 并讨论了不同胶束性质对T₂的影响. 对PEG-400分散SPIO溶胶体系进行了动物急性毒性测试和活体T₂加权成像实验. 结果表明：该溶胶体系无明显急性毒性，且对大鼠肝区有显著的负增强.     

小白鼠肌肉组织的NMR质子自旋交换分析

本文在Zimmerman-Brittin两相质子交换核磁共振弛豫模型基础上,分析了NMR弛豫实验中检测信号与各相表现和本征弛豫多数的关系,编写了自动化处理实验数据的计算机程序,这一技术可用于复相系统中不同成分的NMR表现和本征弛豫特性研究中,本文中的样品是选用健康新鲜的小白鼠肌肉,没加任何处理,用h-h,s-h,s-s脉冲序列,反转恢复法(π-τ-π/2)在强场下(0.92T)做T₁、T₂测定实验,分析结果表明本征弛豫参数T₁=1050ms,T₂=4500μs的成分是由肌肉中的"自由水"引起的,其质子相对含量为69%;本征弛豫参数T₁=530ms,T₂=26μs的成分是由肌肉中的"束附水"引起的,其质子相对含量为9%,本征弛豫多数T₁=530ms,T₂=1250μs的成分是由肌肉中的各种大分子和有机物引起的,其质子相对含量为9%,本征弛豫参数T₁=470ms,T₂=1250μs的成分由样品中的脂肪引起的,其质子相对含量为13%,在肌肉组织中的质子与水中质子之间有强烈的交换作用,其交换率k=1000s^-1.在脂肪中的质子与其它成分之间没有交换作用。     

表面活性剂CTAB水溶液中的T2弛豫分散研究

用CPMG脉冲序列测定了表面活性剂十六烷基三甲基溴化铵（CTAB）分子中的氮甲基(N-CH₃)质子的横向弛豫时间（T₂表观）,并发现测得的T₂表观\}与序列中的重聚脉冲间隔时间的一半τ _cp有关,说明存在横向弛豫分散现象. 当在τ_cp≤1 ms时,T₂表观与τ²_cp}呈线性关系;而当τ_cp≥4.6 ms时,T₂表观变得与τ_cp无关. 利用Luz-Meiboom两体化学交换模型计算了不同浓度的CTAB溶液中的N-CH₃质子的本征横向弛豫时间（T₂本征）和化学交换速率k_ex,发现k_ex与T₂本征和自扩散系数D一样,在临界胶束浓度（CMC）附近发生突变. 这个突变反映了CTAB分子在从单体到胶束的转变过程中其动力学特性发生了改变.      

In Vivo Temporal EPR Measurements in the Lung of Mice by a Selected-Region Intensity Determination Method

Selected-region intensity determination (SRID) is a method for obtaining the temporal changes in electron paramagnetic resonance (EPR) signal intensity from a selected region without complicated procedures used in the previous imaging method. We used an in vivo 700 MHz radiofrequency EPR spectrometer equipped with a bridged loop-gap resonator and the SRID method to perform temporal EPR measurements of the lung area of mice which had received a nitroxide radical (3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl) administration via the intravenous route. The half-life and initial level of nitroxide radical in the lung or the mediastinum were calculated from temporal changes in the signal intensity. A mathematical model was devised to determine the nitroxide radical concentration in the lung, which is connected to other organs via the circulatory system. Using this model and the results of the EPR measurements, the degrees of influence of the nitroxide reduction in the lung and other organs were simulated. It was found that the reaction rate (=log2/half-life) obtained from the lung mainly reflected the reduction of nitroxide radical there. Authors' address: Hidekatsu Yokoyama, National Institute of Advanced Industrial Science and Technology, 2266-98 Anagahora, Shimoshidami, Moriyama-ku, 463-8560 Nagoya, Japan     

癫痫大鼠海马神经元生化分子的同步辐射显微红外光谱成像研究

癫痫是影响所有年龄段的慢性脑功能障碍,主要特征为整个或局部脑区神经元异常同步化高频群集动作电位发放。利用神经毒素海人藻酸（KA）立体定位注射入大鼠海马,诱导大鼠产生癫痫持续状态,建立颞叶癫痫大鼠模型。应用同步辐射显微光谱和同步辐射显微光谱成像分析癫痫持续状态发作后24小时的颞叶癫痫大鼠海马角（CA）1区神经元生物化学分子的胞内浓度和分布是否改变。结果显示反映蛋白质二级结构的酰胺Ⅰ在1 655 cm-1的振动频率和属于脂类功能集团的2 800～3 000 cm-1振动频率,在正常对照大鼠海马CA1神经元胞体内呈高浓度分布,但在癫痫大鼠海马CA1神经元胞体,反映蛋白质二级内呈低浓度分布,并且以细胞核分布浓度最低,但在神经元胞体外围分布浓度相对较高。属于核酸集团的1 055～1 054 cm-1 PO₂反对称拉伸振动在正常和癫痫大鼠海马CA1神经元胞体内分布趋势没有差异,都在胞体内呈高浓度分布,尤其在细胞核分布浓度最高。对属于酰胺Ⅰ的吸收频率进行二级导数分析显示癫痫海马神经元的酰胺Ⅰ相对于正常对照多出1个1 653 cm-1附近的负峰。以上结果提示在发生癫痫持续发作后海马神经元生物化学分子的细胞分布会出现变化。     

Estimation of the in vivo decay rate of EPR signals for a nitroxide radical in rat brains by a region-selected intensity determination method

The region-selected intensity determination (RSID) method was proposed to obtain the temporal changes in electron paramagnetic resonance (EPR) signal intensity from a selected region by a stationary magnetic field gradient. To select the region, the subtraction field that was derived from the distance between the center and the projection of the selected region to the direction of the field gradient was applied to the main field. The directions of the stationary magnetic field gradient at a constant strength were systematically changed in a three-dimensional space after each acquisition of the spectrum. All spectra under the field gradient were accumulated and the resultant spectrum was deconvoluted by a spectrum without the field gradient. The center height of the deconvoluted spectrum indicates the signal intensity of the selected region. To verify this method, a phantom or in vivo study was conducted on a 700 MHz radio-frequency EPR spectrometer equipped with a bridged loop-gap resonator. In the temporal EPR measurements of phantoms including a nitroxide radical aqueous solution with and without ascorbic acid, the selected regions were alternatively changed at the position of the two phantoms. The signal intensity derived from the one phantom showed an exponential decay, and for the other phantom, no temporal changes. The spatial resolution of this method was estimated to be 2.7 mm by using a pinpoint phantom that included diphenylpicrylhydrazyl powder. In the in vivo temporal EPR measurements, the selected regions were alternatively changed at the cerebral cortex and the striatum of rats that had received a blood-brain barrier-permeative nitroxide radical. The decay rate of the signal intensity at each region obtained by this method was consistent with those previously reported.     

Magnetic resonance imaging and pulsed Doppler sonography of poststenotic jets: Correlation between signal void and flow velocity distribution

To correlate the appearance of poststenotic jets on gradient echo images with features of localized Doppler spectra of the jets, we studied an in vitro model of steady flow-through stenoses of 86, 96, and 99% area reduction. As fluids, water and a 40% glycerol solution in water were used. MRI was performed with a 1.5 T whole body imager and gradient echo images were obtained in planes parallel to the direction of flow. Doppler spectra were acquired separately from the MR measurements at 1 cm intervals for a distance of 10 cm downstream from the stenosis. Poststenotic signal void was observed for water and for the 40% glycerol solution only if the mean velocity within the stenosis exceeded a limit of 50–60 cm/sec. On the MR images, the jets could be divided into two segments: A proximal jet segment of uniform width equal to the diameter of the stenosis, followed by a distal jet segment which was characterized by broadening and then dissipating signal void. Except for the 99% stenosis, a high signal intensity core was present within the proximal jet segment. In the proximal jet segment, the Doppler measurements showed a low temporal fluctuation of the maximal flow velocity and only little flow opposite to the main flow direction. In the distal jet segment, the velocity fluctuation and the intensity of reverse flow increased sharply. The high signal intensity core of the jet was associated with a poststenotic zone of constant maximal flow velocity. The results demonstrate a close relationship between characteristic features of poststenotic jets in MRI and pulsed Doppler sonography.     

小脑齿状核MRI功能成象研究

通过测量齿状核T₁弛豫时间,设计出齿状核功能成象破坏稳态梯度回波序列的成象参数,并用此序列在一正常志愿者,在静止和刺激时交替扫描3次,进行齿状核功能成象,刺激时齿状核信号平均强度是静止时的1.2倍.静止和刺激时齿状核信号强度没有重叠     

Proton magnetic resonance imaging and phosphorus-31 magnetic resonance spectroscopy studies of bromobenzene-induced liver damage in the rat.

Respiratory-gated proton magnetic resonance imaging was used to study the response of the rat liver in situ to bromobenzene, a classic hepatotoxicant. A localized region of high proton signal intensity in the perihilar region of the liver was seen 24-48 hr after an intraperitoneal injection of bromobenzene. Localized proton magnetic resonance spectra from within this region indicated that the increased proton signal intensity was not due to accumulation of fat in the liver, but primarily due to a longer T2 for the proton resonance of water. This is consistent with acute edema in this localized region. In vivo 31P magnetic resonance spectroscopy studies of the same rat livers in situ were performed. Spectroscopic conditions were determined whereby localized, quantitative 31P spectra could be obtained. Using these methods, 10 mmol/kg bromobenzene was found after 24 hr to cause a number of statistically significant (p less than 0.05) effects: a decrease in adenosine 5'-triphosphate levels from 4.1 +/- 0.5 to 3.0 +/- 0.5 mM, a decrease in phosphodiester levels from 11.3 +/- 0.9 to 9.3 +/- 0.7 mM and an increase in the phosphomonoesters from 3.0 +/- 0.4 to 5.5 +/- 1.2 mM (mean +/- standard deviation). High resolution in vitro 31P spectra of perchloric acid extracts of these rat livers showed that the increased phosphomonoester resonance was due to a selective 4.3-fold increase in phosphocholine. Thus, our in vivo and in vitro 31P magnetic resonance spectra are consistent with the hypothesis that a phosphatidylcholine-specific phospholipase C (generating phosphocholine and diacylglycerol) is activated during tissue damage. Both the imaging and spectroscopy results obtained with bromobenzene closely resemble CCl4-induced liver changes previously reported, and may reflect a generalized response of the liver to any acutely acting toxic chemical.     

Signal characteristics of FLAIR related to water content: comparison with conventional spin echo imaging in infarcted rat brain

To examine the correlation between tissue water content and signal intensity on fluid-attenuated inversion recovery (FLAIR) images, we analyzed infarcted rat brain, verified the results by theoretical simulation, and compared them with conventional spin-echo images. We produced brain infarction with cavitation in five rats by middle cerebral artery occlusion. After in vivo MRI, histologic sections of the MRI plane were obtained. We measured the signal intensity of regions on FLAIR and spin-echo images, and measured the area of cavitation on histologic sections. We plotted curves of cavity percentage to signal intensity. Theoretical values were calculated using a two-compartment model. On the curve of cavity area to signal intensity, the signal on FLAIR images peaked in tissues with 20% to 30% area of cavitation. On the theoretical curve, the signal on FLAIR images peaked at 90% tissue water content. These results seem to be characteristic of FLAIR.     

An empirical investigation of motion effects in eMRI of interictal epileptiform spikes

We recently developed a functional neuroimaging technique called encephalographic magnetic resonance imaging (eMRI). Our method acquires rapid single-shot gradient-echo echo-planar MRI (repetition time=47 ms); it attempts to measure an MR signal more directly linked to neuronal electromagnetic activity than existing methods. To increase the likelihood of detecting such an MR signal, we recorded concurrent MRI and scalp electroencephalography (EEG) during fast (20-200 ms), localized, high-amplitude (>50 μV on EEG) cortical discharges in a cohort of focal epilepsy patients. Seen on EEG as interictal spikes, these discharges occur in between seizures and induced easily detectable MR magnitude and phase changes concurrent with the spikes with a lag of milliseconds to tens of milliseconds. Due to the time scale of the responses, localized changes in blood flow or hemoglobin oxygenation are unlikely to cause the MR signal changes that we observed. While the precise underlying mechanisms are unclear, in this study, we empirically investigate one potentially important confounding variable — motion. Head motion in the scanner affects both EEG and MR recording. It can produce brief “spike-like” artifacts on EEG and induce large MR signal changes similar to our interictal spike-related signal changes. In order to explore the possibility that interictal spikes were associated with head motions (although such an association had never been reported), we had previously tracked head position in epilepsy patients during interictal spikes and explicitly demonstrated a lack of associated head motion. However, that study was performed outside the MR scanner, and the root-mean-square error in the head position measurement was 0.7 mm. The large inaccuracy in this measurement therefore did not definitively rule out motion as a possible signal generator. In this study, we instructed healthy subjects to make deliberate brief (<500 ms) head motions inside the MR scanner and imaged these head motions with concurrent EEG and MRI. We compared these artifactual MR and EEG data to genuine interictal spikes. While per-voxel MR and per-electrode EEG time courses for the motion case can mimic the corresponding time courses associated with a genuine interictal spike, head motion can be unambiguously differentiated from interictal spikes via scalp EEG potential maps. Motion induces widespread changes in scalp potential, whereas interictal spikes are localized and have a regional fall-off in amplitude. These findings make bulk head motion an unlikely generator of the large spike-related MR signal changes that we had observed. Further work is required to precisely identify the underlying mechanisms.     

In vivo temporal EPR study using a region-selected intensity determination method to estimate cerebral reducing ability in rats treated with olanzapine

Region-selected intensity determination (RSID) is a method for obtaining the temporal changes in electron paramagnetic resonance (EPR) signal intensity from a target region, without the use of complicated procedures employed in the conventional imaging methods. An in vivo 700-MHz radio frequency EPR spectrometer equipped with a bridged loop-gap resonator was used with the RSID method to estimate intracerebral reducing ability in the rat following acute administration of olanzapine (OZP) or haloperidol (HPD). To this end, temporal changes in EPR signal intensity of target regions (the striatum and the prefrontal cortex) of rats which had received a blood-brain-barrier-permeable nitroxide radical (3-hydroxymethyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl) via an intravenous route were observed. The half-lives of EPR signal intensity in both regions of OZP- or HPD-treated rats were significantly longer than in control animals. This indicated that reducing abilities of the striatum and cerebral cortex decreased in the rats to which either OZP or HPD had been acutely administered.