固真方对~(60)Coγ射线照射大鼠神经内分泌及免疫系统的调节作用

作者以６．８Ｇｙ（６０）Ｃｏγ射线一次全身照射的大鼠为研究对象，以四君子汤作为对照，同步观察了（６０）Ｃｏγ射线照射后的大鼠下丘脑单胺类神经递质及其代谢产物的含量，血清促黄体生成激素，雌二醇、睾酮、血浆β－内啡肽和脾淋巴细胞免疫功能等方面的变化以及由首乌，肉苁蓉等补肾中药组成的固真方对这些变化的影响．结果发现：（６０）Ｃｏγ射线照射以后大鼠下丘脑单胺类神经递质及其代谢产物发生紊乱；血浆β－内啡肽浓度持续性增高；下丘脑－垂体－性腺轴功能亢进，脾淋巴细胞免疫功能低下，而固真方能不同程度地改善上述老年性改变．     

急性心肌梗塞早期MRI与病理对照研究

将１６支结扎冠状动脉左前降支的犬分为两组。第一组９只，第二组７只，分别进行手术前和术后３０ｍｉｎ到３ｈ的ＭＲ平扫和Ｇｄ－ＤＴＰＡ增强扫描。观察其ＭＲＩ征象，并与病理改变相对照。平扫组部分犬出现心前壁高信号和腔内流动信号，而增强组７只犬在注射Ｇｄ－ＤＴＰＡ后３～３０ｍｉｎ均有增强效应，其信号增强区与相对应层面的心肌大切片ＴＴＣ染色所示梗塞区大小形态相同。结果表明Ｇｄ－ＤＴＰＡ增强ＭＲＩ能够敏感可靠地显示早期心肌梗塞。     

脾动脉栓塞的临床应用

本文采用经皮导管脾动脉部分栓塞的方法，对门脉高压并脾亢、原发性血小板减少性紫癜、溶血性贫血及外伤性脾破裂进行了栓塞治疗（３１例３３次栓塞），取得了良好效果。并发症为１６．１％，死亡率为３．３％，均较国内（３０％与２０％）国外（２１％与１５．８％）同类水平为低。该方法扩大了栓塞治疗的应用范围，达到了内科久治不愈，病情难以控制，需要外科切脾的目的，既保证了人体解剖的完整性，又保留了脾的免疫功能，具有肯定的临床应用价值。     

小鼠组织神经生长因子的免疫组织化学定位观察

在获得神经生长因子（ＮＧＦ）ＩｇＧ后，以其为第一抗体建立了ＮＧＦ免疫组织化学方法，并观察了成年小鼠组织中ＮＧＦ的定位和分布。在颌下腺内，ＮＧＦ主要定位于粒曲小管细胞及纹状导管细胞，而且雌、雄动物之间ＮＧＦ样免疫反应存在明显差异。第一抗体吸收试验观察到颌下腺显示免疫反应阴性，提示该反应是ＮＧＦ特异性的。舌下腺内仅可见到反应阳性的散在的小导管细胞。输精管平滑肌和心房肌也显示免疫反应阳性。肾组织的观察表     

椎小关节病的CT诊断：附402例分析

笔者对１０１７例肩背和／或腰腿痛患者的临床、Ｘ线及ＣＴ资料进行了回顾性分析。ＣＴ显示椎小关节异常４０２例，Ｘ线显示１８３例。ＣＴ对本病的显示率比Ｘ线高１２倍。ＣＴ能有效地显示关节突增生肥大、骨赘形成、关节间隙变窄、骨性关节面改变、关节脱位及半脱位、侧隐窝或椎间孔狭窄、关节囊钙化及关节“真空”征等。后二者Ｘ线检查难以显示。ＣＴ易于显示椎小关节病及其并存症，对肩背腰腿痛患者的合理施治有重要意义。     

3种光敏剂对5株人鼻咽癌细胞PDT量效关系的研究

用ＭＴＴ法比较了不同能量的脉冲铜蒸气激光、不同浓度的３种光敏剂（ＰＳＤ－００７、ＢＨｐＤ和ＹＨ－ｐＤ）对５株人鼻咽癌细胞（ＣＮＥ２、ＨＮＥ１、ＨＮＥ２、ＨＮＥ３，和ＨｏＮＥ１的体外杀伤效应。结果表明：（１）激光合并光敏剂即令能量较低、剂量较小，也能显示明显的杀伤效应，而单用激光或单用光敏药物则只在较高能量和较大剂量时才显示轻微杀伤效应。（２）５株鼻咽癌细胞对３种光敏剂的ＰＤＴ敏感性彼此存在着差异。（３）在一定激光能量和光敏剂浓度时，ＰＳＰ－００７的杀伤效应优于ＢＨｐＤ和ＹＨｐＤ，而ＹＨｐＤ又稍优于ＢＨｐＤ。     

Enhanced tumor detection in the presence of fatty liver disease: Cell-specific contrast agents

It is assumed that hepatobiliary, cell-specific contrast agents will be adversely affected by the presence of diffuse liver disease. The diagnostic efficacy for tumor detection in the presence of fatty liver disease was experimentally studied at contrast-enhanced magnetic resonance (MR) imaging with manganese-DPDP (N,N′-dipyridoxylethylenediamine-N,N′-diacetate 5,5′-bis[phosphate]) and gadobenate dimeglumine (Gd-BOPTA/dimeg) and compared with conventional and chemical shift imaging. Carcinosarcoma was implanted into the liver of rats, and fatty liver was induced with L-ethionine. Without contrast agents, the tumor-fatty liver contrast-to-noise ratio (C/N) was increased on T1-weighted and decreased on T2-weighted MR images relative to tumor-bearing control rats without fatty liver. Chemical shift imaging (phase-contrast method) increased the tumor—fatty liver C/N from 2.3 ± 1.0 to 6.1 ± 1.7 (P <.001). Mn-DPDP and Gd-BOPTA/dimeg increased the tumor—fatty liver C/N from -5.4 ± 1.6 to -11.0 ± 1.9 and ?9.8 ± 3.4, respectively (P <.001). The hepatobiliary, cell-specific contrast agents were equally effective in both fatty and nonfatty liver and outperformed both chemical shift and conventional MR imaging in detecting liver tumors.     

Time after excision and temperature alter ex vivo tissue relaxation time measurements

Previously unreported effects of tissue storage were recently observed in the authors' experimental magnetic resonance (MR) studies. To evaluate the effect of elapsed time after excision and storage temperature on tissue relaxation time measurements, tissue samples from the liver, pancreas, kidney, testis, spleen, and brain were obtained in rats. T1 and T2 were first measured within 5 minutes of excision, and between subsequent measurements, tubes were kept in a water bath at 40°C, at room temperature (28°C), or in an ice bath (4°C). Cellular and organellar integrity was assessed with electron microscopy and correlated with the MR findings. At 40°C (20-MHz spectrometer), the T1 of liver decreased from 280 msec ± 8 to 212 msec ± 10 during the first 60 minutes; the T1 of pancreas decreased from 276 msec ± 3 to 208 msec ± 2. Other tissues showed less than a 5% decrease in T1. T2 changes were smaller than T1 changes in all tissues. Electron microscopy of pancreatic acinar cells showed postmortem changes in mitochondria evolving over the first 60 minutes after death. Manganese loading experiments implicated mitochondrial manganese stores in the observed enhanced postmortem decrease in T1. This study calls into question reported relaxation time data for liver and pancreas. MR studies of excised tissues must account for time and temperature to prevent systematic experimental errors.     

Atorvastatin enhances kainate‐induced gamma oscillations in rat hippocampal slices

Atorvastatin has been shown to affect cognitive functions in rodents and humans. However, the underlying mechanism is not fully understood. Because hippocampal gamma oscillations (γ, 20–80 Hz) are associated with cognitive functions, we studied the effect of atorvastatin on persistent kainate‐induced γ oscillation in the CA3 area of rat hippocampal slices. The involvement of NMDA receptors and multiple kinases was tested before and after administration of atorvastatin. Whole‐cell current‐clamp and voltage‐clamp recordings were made from CA3 pyramidal neurons and interneurons before and after atorvastatin application. Atorvastatin increased γ power by ~ 50% in a concentration‐dependent manner, without affecting dominant frequency. Whereas atorvastatin did not affect intrinsic properties of both pyramidal neurons and interneurons, it increased the firing frequency of interneurons but not that of pyramidal neurons. Furthermore, whereas atorvastatin did not affect synaptic current amplitude, it increased the frequency of spontaneous inhibitory post‐synaptic currents, but did not affect the frequency of spontaneous excitatory post‐synaptic currents. The atorvastatin‐induced enhancement of γ oscillations was prevented by pretreatment with the PKA inhibitor H89, the ERK inhibitor U0126, or the PI3K inhibitor wortmanin, but not by the NMDA receptor antagonist D‐AP5. Taken together, these results demonstrate that atorvastatin enhanced the kainate‐induced γ oscillation by increasing interneuron excitability, with an involvement of multiple intracellular kinase pathways. Our study suggests that the classical cholesterol‐lowering agent atorvastatin may improve cognitive functions compromised in disease, via the enhancement of hippocampal γ oscillations.