脐疗配合耳穴贴压治疗便秘26例

目的 探讨济疗配合耳穴疗法对便秘的疗效。方法 将50例便秘患随机分成两组，治疗组用济部药物贴敷配合耳穴贴压治疗；对照组单纯用于穴贴压治疗，所获数据采用t检验。结果 治疗组有效率96．15％，对照组有效率83．33％，经统计学处理，P＜0．01，有显性差异。结论 济疗联合耳穴贴压治疗便秘疗效较单纯耳穴贴压效果好，且简单方便，无副作用。     

"同病异治"原则与中医缺血脑保护药物干预策略

溶栓治疗和神经保护治疗是缺血性脑卒中的两大药物干预策略,其中广义的神经保护治疗包括神经保护和神经修复两种方法,而目前存在的中西医结合缺血性脑卒中的药物干预策略可能也存在多层次、分阶段干预的特点,体现了祖国医学"同病异治"的原则,我们认为现有的缺血脑保护方法主要针对缺血性脑卒中的不同发展阶段,而神经修复的研究,尤其是中医药促进神经干细胞再生的研究,可能蕴涵着巨大的发展潜力和无限商机.     

Cardioprotective effects of stimulation of peripheral μ-opiate receptors and the role of opiatergic mechanisms in the pathogenesis of stress-induced heart damage

Immobilization induces stress damage to the heart. DAGO, an agonist of μ-opiate receptors potentiates, while an agonist of peripheral μ-opiate receptors prevents this damage. Naltrexone reduces, while methylnaltrexone, an inhibitor of peripheral μ-opiate receptors, potentiates the stress-induced damage to the heart. Other opiate ligands have no effect on heart damage. It is suggested that the stress-induced damage to the heart is promoted by activation of central μ-opiate receptors and prevented by stimulation of peripheral μ-opiate receptors. Translated fromByulleten'Eksperimental'noi Biologii i Meditsiny, Vol. 123, No. 3, pp. 276–278, March, 1997     

Temporal Lobe Epileptogenesis and Epilepsy in the Developing Brain: Bridging the Gap Between the Laboratory and the Clinic. Progression, But in What Direction?

Summary:  The origins of human mesial temporal lobe epilepsy and hippocampal sclerosis are still not well understood. Hippocampal sclerosis and temporal lobe epileptogenesis involve a series of pathologies including hippocampal neuronal loss and gliosis, axonal reorganization, and maybe hippocampal neoneurogenesis. However, the causality of these events is unclear as well as their relation to the factors that may precipitate epileptogenesis. Significant differences between temporal lobe epileptogenesis in the adult and immature brain may require differential approaches. Hereditary factors also may participate in some cases of hippocampal sclerosis. The key point is to identify the significance of these age-dependent changes and to design preventive treatments. Novel strategies for the prevention and treatment of mesial temporal lobe epilepsy and hippocampal sclerosis may include rational use of neuroprotective agents, hormonotherapy, immunizations, and immunotherapy.     

肝钳与肝门阻断的肝损害及其防治的实验研究

本实验观察不同阻断时刻肝钳与肝门阻断的肝损害以及预防性应用抗氧化剂的缓解作用。结果表明：（１）ＳＧＰＴ、ＴＢ在肝钳组的变化比肝门阻断组表现得更为一过性。而肝门阻断给药组的改变要比非给药组的轻微且恢复得快。（２）肝门阻断时，ＭＤＡ含量显著升高，机体的Ｔ－ＡＯＣ和ＳＯＤ下降。而给药组可明显减轻上述改变。（３）随着肝门阻断时间的延长，肝组织损害也相应加重，抗氧化剂的给予缓解了肝缺血和再灌注造成的组织损害。肝钳组由于健肝血供未受干扰，因此，不同阻断时刻肝组织学形态与对照组相似无甚改变。结论：（１）肝钳较肝门阻断的肝损害轻，且实用安全。（２）肝门阻断预防性使用抗氧化剂，可明显减轻肝缺血再灌注损害。（３）肝门阻断时经门静脉较外周静脉输注抗氧化剂，其保护作用更直接、明显     

对CT所见腰椎间盘突出的重新鉴别与治疗观察

目的：因临床发现有些经ＣＴ检查有腰椎间盘突出的患者，其症状体征与ＣＴ结果不符。对１１２ＣＴ阳性者根据症状体征进行重新鉴别。方法：将ＣＴ阳性者根据“三种试验”分为阳性、阴性两组，再选压痛点作注射治疗。结果：两组治疗结果阴性组优良率较高。结论：ＣＴ结果可供参考，但不能作临床考虑的主要依据。对腰椎间盘突出症的诊断与治疗要以症状体征为主     

耳穴压豆法治疗儿童哮喘50例

采用耳穴压豆法治疗儿童哮喘５０例，并随访１年。结果：痊愈１１例；好转３７例；无效２例，总有效率为９６％。认为此法不仅能预防哮喘的发作，还能避免药物引起的副作用。     

大鼠颌下腺切除对CCl4所致肝损伤修复的影响

实验大鼠分为颌下切除＋ＣＣｌ４组，假手术＋ＣＣｌ４对照组及正常对照组，结果假手术＋ＣＣｌ４第２ｄ时Ⅲ带细胞轻度受损，第４ｄ、８ｄ时受损面积略大，第１２ｄ时大部分细胞恢复，而颌下腺切除＋ＣＣｌ４组则损伤明显，第８ｄ时胞质极度稀疏，１２ｄ时大部分细胞尚未恢复，与假手术组比较，该组Ｆｅｕｌｇｅｎ反应略弱，ＰＡＳ反应减弱，第４～８ｄ时较明显，Ｇ－６－Ｐ，ＳＤＨ活性均减弱。结果表明颌下腺切除导致内源性表皮生     

A protease inhibitor attenuates gastric erosions and microcirculatory disturbance in the early period after thermal injury in rats

The effects of camostat mesilate, a synthetic serine protease inhibitor on gastric microcirculation and active oxygen species generated by leucocytes from the gastric and jugular veins in the early period after thermal injury were assessed. Male Wistar rats were anaesthetized and a 30% full skin-thickness dorsal burn was inflicted. Camostat mesilate (100 mg/kg) was dissolved in distilled water and administered orally to rats 40 min before thermal injury (the camostat group). The control animals (the vehicle group) were administered distilled water orally. Rolling leucocytes as well as Monastral blue B deposits in venules were observed using in vivo microscopy. Active oxygen species were measured by chemiluminescence. Camostat mesilate decreased the total length of gastric erosion, venular deposits of Monastral blue B, and rolling of leucocytes in venules, and relatively increased luminol-dependent chemiluminescence activity generated by zymosan-stimulated leucocytes 15 min after thermal injury. These results suggest that serine proteases are involved in the formation of gastric erosions and gastric microcirculatory disturbance in the early period after thermal injury.     

Neuropathology in non-human immunodeficiency virus-infected drug addicts: hypoxic brain damage after chronic intravenous drug abuse

Neuropathological studies were carried out on 180 human immunodeficiency virus-seronegative intravenous drug addicts. The findings in victims of acute heroin intoxication (n = 116) were congestion (99.1%), capillary engorgement (68.1%), and/or perivascular bleeding (68.1%) – hemodynamic processes attributable to toxic primary respiratory failure. In a high percentage of these cases (88%), cerebral edema was also present. In 18 cases of acute heroin intoxication who survived for periods of hours or days, the sole postmortem finding was ischemic nerve cell damage, resembling that typically seen in systemic hypoxia. Semiquantitative analysis revealed nerve cell loss in the hippocampal formation and/ or Purkinje cell layer in 26% of the 162 chronic drug abusers. By contrast, in nearly 80% of these cases, the hippocampus showed enhanced expression of glial fibrillary acid protein by astrocytes and/or a proliferation of microglia, demonstrated by CD68 expression. Since such reactive processes are produced by primary neuronal damage, it can be assumed that chronic intravenous drug abuse results in obviously ischemic nerve cell loss. This could be demonstrated in the hippocampus, but it must also occur throughout the whole brain. The demonstration of ischemic nerve cell damage and neuronal loss or secondary reactive alterations has not been described previously. Received: 31 March 1995 / Revised, accepted: 27 November 1995