促渗剂对水合胼胝类脂热转变影响的差示扫描热分析研究

从人胼胝组织提取出类脂经水合后代替人皮肤角质层用作差示扫描热分析研究促渗剂作用的简单模型。研究了１，８－桉油精，月桂氮酮和丙二醇等促渗剂对水合胼胝类脂热转变特征的影响。三种促渗剂均不同程度地降低水合胼胝类脂的热变温度，作用强弱依次为１，８－桉油精＞月桂氮酮＞丙二醇。丙二醇与１，８－桉油精或月桂氮酮混合应用时对热转变的影响具有协同作用。结果提示促渗剂可能改变脂质分子的排列和增加其流动性。同时，水的存在对脂质分子物理结构的形成具有重要作用。     

Œdème cérébral aigu mortel chez un enfant diabétique

A case is reported of fatal acute cerebral oedema occurring in a 15-year-old child suffering diabetic ketoacidosis. He had severe gastro-enteritis, with a weight lose of 8 kg over a period of 8 days (initial weight = 50 kg). He was admitted in a stupor with pH 7.15, 129 mmol.l-1 natraemia, and 31 mmol.l-1 blood glucose concentration. Blood osmolaity was calculated to be 310 mosmol.l-1. He was rehydrated with 416 ml.h-1 normal saline and 416 ml.h-1 of 1.4% sodium bicarbonate. At the same time a total dose of 75 i.u. of ordinary insulin was given. After 2 h, the patient's condition suddenly worsened with unreactive coma, bilateral fixed mydriasis, respiratory pauses, and impairment of haemodynamic state (heart rate 150 b.min-1, blood pressure 80/50 mmHg). The diagnosis of cerebral oedema with severe intracranial hypertension was confirmed by different investigations. Despite ventilatory support and continued intensive care, the patient died a few hours later. It is concluded that some degree of subclinical brain swelling could be common occurrence during diabetic ketoacidosis, present maybe even before the start of treatment. Such cases of cerebral oedema are often reported, but the pathophysiological mechanisms remain unclear. However, unlike this case, rehydration must be moderate (less than 41.m-2.day-1), especially in case of hyponatraemia. Insulin and sodium bicarbonate must be used with care. Early rigorous clinical and biological monitoring is essential. Treatment should aim at a progressive correction of the metabolic disturbances.     

1,3-Dipropyl-8-cyclopentylxanthine attenuates the NMDA response to hypoxia in the rat hippocampus

Excitatory amino acids may cause neuronal damage and death in cerebral hypoxia and ischemia, through the activation of different subtypes of glutamate receptors, in particular of the (NMDA) receptor. In the present work, the effect of hypoxia on the component of the field excitatory postsynaptic potential (fepsp) mediated by the NMDA receptor was studied in the hippocampal CA1 area of the rat. A period of 15 min of hypoxia induced virtual abolition of the NMDA receptor-mediated fepsp and a 94.8 ± 0.7% maximal decrease in the fepsp. A period of 3 min of hypoxia induced a 89.3 ± 12.3% maximal decrease in the NMDA receptor-mediated component of the fepsp and only a 50.8 ± 11.5% maximal decrease in the fepsp. Both periods of hypoxia thus induced a more pronounced depression of the NMDA receptor-mediated component of the fepsp than of the fepsp. We found that 48.5 ± 9.1% decrease (about half of the total decrease) in the NMDA receptor-mediated fepsp, and 51.6 ± 19.6% decrease (approximately all decrease) in the fepsp induced by hypoxia (3 min) were reversed in the presence of the selective adenosine A₁ receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (50 nM), and thus likely to be mediated by endogenous adenosine, through the activation of adenosine A₁ receptors. On the other hand, under the conditions we assumed to be normoxic in our slices, DPCPX (50 nM) induced a much larger increase in the amplitude of the NMDA receptor-mediated fepsp compared to the increase in the fepsp, which suggest that endogenous adenosine is inhibiting predominantly the NMDA receptor-mediated fepsp under these conditions. Hypoxia markedly decreases the NMDA receptor-mediated fepsp in the hippocampal CA₁ area. The contribution of endogenous adenosine to the inhibition of the NMDA receptor-mediated fepsp may be fundamental for its neuroprotective effects.     

Allergen activates peripheral blood eosinophil nuclear factor-κB to generate granulocyte macrophage-colony stimulating factor, tumour necrosis factor-α and interleukin-8

BACKGROUND: Allergic inflammation is characterized by the influx and activation of eosinophils. Cytokines generated by both resident and infiltrating cells are responsible for the initiation and maintenance of this pathogenesis. This study focuses on allergen-induced activation of eosinophil NF-kappaB and generation of granulocyte macrophage-colony stimulating factor (GM-CSF), TNF-alpha, and IL-8. METHODS: Peripheral blood eosinophils were enriched to >99.9% by Percoll gradient sedimentation and negative magnetic affinity chromatography. NF-kappaB activation by 10 microg/mL house dust mite (HDM) extract was demonstrated immunocytochemically using a monoclonal antibody against the active form of NF-kappaB (NF-kappaBa). The authenticity of NF-kappaB was confirmed by Western blot. Cytokine production was assessed both by immuno-staining of eosinophils and by assay of cytokines in the cell supernatant. RESULTS: Activation of peripheral blood eosinophils from atopic, but not non-atopic, donors induced activation of NF-kappaB, which peaked at 4 h and was accompanied by a decline in IkappaB-alpha. The activation of authentic NF-kappaB was confirmed in gel shift assays. Supershift assays showed p65 to be the major subunit of eosinophil NF-kappaB. Immunofluorescent confocal microscopy demonstrated localization of NF-kappaBa to the nucleus. Following activation, cytokine immunoreactivity was seen in a fraction of the eosinophils and cytokines were released into the supernatant. The NF-kappaB inhibitors, calpain inhibitor 1 (10 microm), pentoxifylline (0.5 mm), pyrrolidine dithiocarbamate (PDTC, 10 microm) or gliotoxin (1 pg/mL) reduced the generation of GM-CSF, TNF-alpha and IL-8 in parallel with their inhibition of NF-kappaB. CONCLUSIONS: HDM allergen activates human eosinophil NF-kappaB leading to the production of the cytokines GM-CSF, TNF-alpha and IL-8. We speculate that a role for eosinophil NF-kappaB-dependent cytokines is to act as an autocrine loop augmenting the survival of eosinophils in vivo.     

Deep brain stimulation for Parkinson''s disease: electropermeabilization and activation

Deep brain stimulation, DBS, is an accepted technique for the treatment of Parkinson's disease. DBS affects the electrical functions of neurons, but exactly how it alters those functions is not clearly explained. An electrical model is determined to simulate treatment with DBS of the sub thalamic nucleus. This model shows the difference in electrical fields between the inside and the outside the neurons. The generated electrical field near the electrodes is high enough to perform an electropermeabilization of the cell membranes, which most likely blockade normal nerve pulses or reduce the nerve impulse speed. Further away from the electrodes activation of large axons is performed.     

Factors associated with quality of life in Menière's disease

The aim of this study was to identify the factors associated with better or worse quality of life in a sample of people with Menière's disease drawn from a UK self‐help group (the Menière's Society) and to assess the forms of support on which the respondents could draw. A postal survey was sent to 1000 randomly selected group members, containing validated questionnaires assessing: (1) quality of life (the Short Form 36 (SF‐36)); (2) factors that might predict quality of life; and (3) usage of resources provided to members by the Menière's Society. A total of 509 members completed the main survey, and 370 the second part of the survey. Factors associated with a less good quality of life included more severe vertigo, pressure in the ear, hearing loss and tinnitus, being younger, being female, living alone, having a lower occupational status and believing that the attitude of the consultant is unhelpful. Levels of vertigo severity in this sample were similar to those found in hospital samples, but it is possible that these respondents may differ in other respects from patients who do not join a self‐help group.     

小肠吸收胆固醇的分子生物学研究进展

胆固醇通过分布于十二指肠和近段空肠黏膜上皮细胞刷状缘膜的Niemann—Pick C1样蛋白1摄取，ATP结合盒G5、G8抑制小肠对胆固醇的摄取过程。进入上皮细胞的胆固醇大多数被乙酰辅酶A，胆固醇转乙酰基酶2酯化，随后通过组装形成乳糜微粒，经淋巴管进入血循环；另一部分胆固醇则以未酯化形式直接进入血循环形成高密度脂蛋白颗粒。这些过程受核受体——肝脏X受体的调控。年龄、性别、黏膜屏障和小肠传输速度也影响胆固醇的吸收。     

Microvascular decompression for hemifacial spasm: postoperative neurologic follow-up and evaluation of life quality

Microvascular decompression (MVD) is an effective and safe treatment in hemifacial spasm (HFS). Postoperative evaluations are usually made by neurosurgeons. Follow-up studies performed by neurologists and postoperative quality of life (QoL) investigations are lacking. All 25 HFS patients operated with MVD in our centre between 2000 and 2004 were evaluated with the recently validated HFS-7 scheme, extended with the item 'sleep disturbance due to HFS' (HFS-8). The patients underwent a careful neurological examination median 3 years after the operation. The evaluation focused on clinical aspects, changes in blood pressure and time until observable effect of MVD. The evaluation of HFS-7 questionnaire and the extended form (HFS-8) showed significant improvement in QoL after MVD. Neurological outcome was in almost all cases excellent or good. Eleven (44%) patients had no neurological deficits at all. Only one patient had serious complications with ipsilateral facial palsy, deafness, balance problems and vertigo. The other patients had minor neurological findings or symptoms. Eighteen (72%) patients experienced early effect within 3 months after MVD; seven (28%) patients had late effect between 6 and 14 months. Median age of the patients with late effect (62.6 years) was significantly higher than in those with early effect (52.7 years).     

红斑狼疮皮损中CD4^＋和CD8^＋T细胞的表达

目的检测红斑狼疮皮损区T淋巴细胞亚群CD4 和CD8 T细胞的表达情况。方法采用免疫组织化学法对红斑狼疮皮损区淋巴细胞进行检测,并与正常皮肤作对照。结果红斑狼疮患者皮损CD4 T细胞百分数明显高于正常对照组。CD8 T细胞百分数明显低于正常对照组。结论红斑狼疮患者可能存在CD4 T细胞活性增强,CD8 T细胞功能抑制,从而导致免疫紊乱而发病。