化疗对淋巴瘤伴乙肝病毒感染患者肝功能影响的回顾性分析

目的研究化疗对淋巴瘤伴乙肝病毒感染患者肝功能的影响。方法回顾性病例分析，比较50例HBsAg（-）、20例HBsAg（＋）和18例小三阳的恶性淋巴瘤患者化疗后肝功能变化情况。结果HBsAg（-）组、HBsAg（＋）组和小三阳组化疗后Ⅲ级以上肝功能损害分别是0％、15％、55％。结论伴乙肝病毒感染的淋巴瘤患者化疗后肝功能损害明显，尤其小三阳患者损害更为严重，甚至死亡。     

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     

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     

An Autopsy Case of Dermatomyositis with Rapidly Progressive Diffuse Alveolar Damage

A 47-year-old woman visited a clinic with dyspnea which had continued for two months and was followed by general fatigue and fever. Antibiotics were not effective. Edematous erythema occurred on her face, elbows, knees and feet, and she entered our hospital. A skin biopsy revealed interface dermatitis with severe edema and mucinosis in dermis. Diffuse bilateral infiltration was observed in the chest X-ray, and laboratory findings showed increased LDH, GPT, GOT and CPK. No antinuclear factor was detected. Her respiratory condition rapidly worsened, and she died eight days after hospitalization in spite of corticosteroid pulse therapy. The autopsy revealed that the main cause of death was diffuse alveolar damage (DAD). Interstitial pneumonia related to dermatomyositis is not histologically uniform; the response to the therapy depends on its histological type. The patients with dermatomyositis who have poor prognosis are clinically characterized by acute onset with general symptoms and less pronounced muscle weakness; they generally show DAD in their lungs. We need to establish a simple method for distinguishing histological types of interstitial pneumonia and adequate therapy for each one.     

Role of neutrophils in gastric damage induced by platelet activating factor

Summary Platelet-activating factor (PAF) has recently been shown to be a potent ulcerogenic agent in the stomach and intestinal mucosa. Its exact mechanism of action is not yet known although histological studies suggest that vasocongestion is an important feature of PAF-induced damage. We have therefore studied the activity of various agents with different modes of action toward PAF-induced gastrointestinal lesions in the rat (PAF 2 g/kg i.v. ; macroscopic lesions of tissues scored 20 min later; arbitrary scale from 0 to 4). Drugs were administered either i. m., s. c. (5 min) or orally (30 min) before PAF injection. PAF-induced gastric lesions were strongly inhibited by the natural PAF-antagonist BN 52021 as well as by atropine sulphate and cimetidine which implicates cholinergic stimulation in the ulcerogenic activity of PAF. The somatostatin analog BIM 23014 was also very potent against PAF, perhaps by reducing the parasympathetic stimulation in the gastric wall as described for somatostatin. Allopurinol, which is a free radical scavenger also almost totally inhibited PAF-induced gastric damage, suggesting that neutrophils are involved in the mucosal lesions. The considerable inhibition of the gastric effects of PAF found in neutrophil-depleted animal supports this hypothesis. Theophylline and disodium cromoglycate, mast cell stabilizing drugs which were also active in our model, could act by protecting mast cell degranulation induced by free radicals released from activated neutrophils. A multifunctional process seems to determine the mucosal gastric damage induced by PAF, but parasympathetic stimulation and neutrophil activation play a major role in this pathology.Send offprint requests to A. Etienne at the above address