日本血吸虫病的影像学诊断

日本血吸虫病的影像学诊断第一军医大学寄生虫学教研室（广州５１０５１５）马文峰综述刘国章审校在所有能感染人的血吸虫中，日本血吸虫被认为是能引起最严重疾病的虫种。虽然作为致病性和死亡之原因，其重要性正在减轻，但日本血吸虫病至今仍然是一个重要的公共卫生问题...     

用BALB／c基因型裸鼠的骨髓细胞重建昆明小白鼠的造血功能

用ＢＡＬＢ／ｃ基因型裸鼠的骨髓细胞重建昆明小白鼠的造血功能胡军，马文煜，杨涌峰，张海，姜绍谆（西安微生物学教研室７１００３３）关键词裸鼠；骨髓移植；Ｃ带染色中图号目前，国内骨髓移植治疗血液病及放射病的研究主要从组织配型、免疫抑制剂的使用和Ｔ淋巴细胞克...     

经皮肺动脉瓣狭窄球囊导管扩张术的方法和疗效评价(附7例报告)

应用经皮球囊导管扩张术治疗先天性肺动脉瓣狭窄7例(男3例,女4例,年龄5～32岁),均获成功。球囊直径较肺动脉瓣环大30～50％。扩张前后右室收缩压分别为65mmHg和46mmHg,下降19mmHg(P<0.05);扩张前后跨瓣压力阶差分别为45mmHg和21mmHg,降低24mmHg(P<0.05)。术后平均随访36个月,患者症状改善,活动耐受性增加,杂音减轻,提示近期疗效良好。     

纤维喉镜下治疗儿童声带小结、息肉190例体会

目的：探讨纤维喉镜下儿童声带小结及息肉的治疗方法与效果。方法：经纤维喉镜下治疗儿童声带小结136例，息肉54例。结果：近期(1周)疗效：治愈71例，显效91例，有效28例，总的有效率为100％，术中、术后均无并发症。结论：纤维喉镜下儿童声带小结及息肉摘除术是一种疗效好、操作方便、安全迅速、术后恢复快，值得推广的方法。     

Peripheral Nerve Injury Sensitizes the Response to Visceral Distension but Not Its Inhibition by the Antidepressant Milnacipran

Background: Manipulations that cause hypersensitivity to visceral stimuli have been shown to also result in hypersensitivity to somatic stimuli coming from convergent dermatomes, but the converse has not been examined. The authors tested whether lumbar spinal nerve ligation in rats, a common model of neuropathic pain that results in hypersensitivity to somatic stimuli, also leads to hypersensitivity to visceral stimuli coming from convergent dermatomes and whether pharmacology of inhibition differed between these two sensory modalities.

Methods: Female Sprague-Dawley rats were anesthetized, and the left L5 and L6 spinal nerves were ligated. Animals received either intrathecal saline or milnacipran (0.1-3 [mu]g), and withdrawal thresholds to mechanical testing in the left hind paw, using von Frey filaments, and visceral testing, using balloon colorectal distension, were determined.

Results: Nerve ligation resulted in decreases in threshold to withdrawal to somatic mechanical stimulation (from 13 +/- 1.8 g to 2.7 +/- 0.7 g) and also in decreases in threshold to reflex response to visceral stimulation (from 60 mmHg to 40 mmHg). Intrathecal milnacipran increased withdrawal threshold to somatic stimulation in a dose-dependent manner but failed to alter the response to noxious visceral stimulation.     

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

Background: Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) [kappa]B and its regulated inflammatory mediators expression were examined in the current study.

Methods: Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-[kappa]B activity was determined by electrophoretic mobility shift assay. The NF-[kappa]B inhibitor, I[kappa]B-[alpha], was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis.

Results: Nuclear factor [kappa]B-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic I[kappa]B-[alpha] was decreased. Supershift assay revealed the involvement of NF-[kappa]B p65 and p50 subunits. APC with sevoflurane attenuated NF-[kappa]B activation and reduced the expression of tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR.     

Morphine Enhances Pharmacological Preconditioning by Isoflurane: Role of Mitochondrial KATP Channels and Opioid Receptors

Background: Adenosine triphosphate-regulated potassium channels mediate protection against myocardial infarction produced by volatile anesthetics and opioids. We tested the hypothesis that morphine enhances the protective effect of isoflurane by activating mitochondrial adenosine triphosphate-regulated potassium channels and opioid receptors.

Methods: Barbiturate-anesthetized rats (n = 131) were instrumented for measurement of hemodynamics and subjected to a 30 min coronary artery occlusion followed by 2 h of reperfusion. Myocardial infarct size was determined using triphenyltetrazolium staining. Rats were randomly assigned to receive 0.9% saline, isoflurane (0.5 and 1.0 minimum alveolar concentration [MAC]), morphine (0.1 and 0.3 mg/kg), or morphine (0.3 mg/kg) plus isoflurane (1.0 MAC). Isoflurane was administered for 30 min and discontinued 15 min before coronary occlusion. In eight additional groups of experiments, rats received 5-hydroxydecanoic acid (5-HD; 10 mg/kg) or naloxone (6 mg/kg) in the presence or absence of isoflurane, morphine, and morphine plus isoflurane.

Results: Isoflurane (1.0 MAC) and morphine (0.3 mg/kg) reduced infarct size (41 +/- 3%; n = 13 and 38 +/- 2% of the area at risk; n = 10, respectively) as compared to control experiments (59 +/- 2%; n = 10). Morphine plus isoflurane further decreased infarct size to 26 +/- 3% (n = 11). 5-HD and naloxone alone did not affect infarct size, but abolished cardioprotection produced by isoflurane, morphine, and morphine plus isoflurane.