The auditory midbrain implant: a new auditory prosthesis for neural deafness-concept and device description.

The auditory midbrain implant (AMI) is a new central auditory prosthesis designed for penetrating stimulation of the human inferior colliculus. The major group of candidates for the AMI consists of neurofibromatosis type 2 (NF2) patients who develop neural deafness because of growth and/or surgical removal of bilateral acoustic neuromas. Because of the absence of a viable auditory nerve, these patients cannot benefit from cochlear implants. An alternative solution has been the auditory brainstem implant (ABI), which stimulates the cochlear nucleus. However, speech perception performance in NF2 ABI patients has been limited. The fact that the ABI is able to produce high levels of speech perception in nontumor patients (with inaccessible cochleae or posttraumatic damage to the cochlear nerve) suggests that limitations in ABI performance in NF2 patients may be associated with cochlear nucleus damage caused by the tumors or the tumor removal process. Thus, stimulation of the auditory midbrain proximal to the damaged cochlear nucleus may be a better alternative for hearing restoration in NF2 patients. We propose the central nucleus of the inferior colliculus (ICC) as the potential site. A penetrating electrode array aligned along the well-defined tonotopic gradient of the ICC should selectively activate different frequency regions, which is an important elementfor supporting good speech understanding. The goal of this article is to present the ICC as an alternative site for an auditory implant for NF2 patients and to describe the design of the first human prototype AMI. Practical considerations for implementation of the AMI will also be discussed.     

黄芩苷、丹参酮ⅡA、三七皂苷R1对过氧化氢所致大鼠海马神经元损伤的保护作用

目的:探讨黄芩苷、丹参酮ⅡA、三七皂苷R1对过氧化氢所致的大鼠海马神经元损伤的保护作用.方法:采用新生1d SD大鼠海马神经元原代培养,以H2O2(50μM)造成细胞损伤模型,将黄芩苷、丹参酮ⅡA、三七皂苷R1的高(20μg/ml)和低(0.2μg/ml)两个剂量加入到培养细胞液中.在4h时,检测细胞形态及释放出的LDH活性变化,观察到上述药物对海马神经元损伤的直接保护作用.结果:低剂量黄芩苷和三七皂苷R1与模型组比较,未见明显差异,三种组分高剂量和丹参酮ⅡA低剂量组与模型组比较,均有明显差异.结论:黄芩苷、丹参酮ⅡA、三七皂苷R1对过氧化氢所致的大鼠海马神经元损伤具有一定的保护作用.     

Functional and Immunological Studies Revealed a Second Superantigen Toxin in Staphylococcal Enterotoxin C Producing Staphylococcus aureus Strains

Staphylococcus aureus is a human and animal pathogen as well as a commensal bacterium. It can be a causative agent of severe, life-threatening infections with high mortality, e.g., toxic shock syndrome, septic shock, and multi-organ failure. S. aureus strains secrete a number of toxins. Exotoxins/enterotoxins are considered important in the pathogenesis of the above-mentioned conditions. Exotoxins, e.g., superantigen toxins, cause uncontrolled and polyclonal T cell activation and unregulated activation of inflammatory cytokines. Here we show the importance of genomic analysis of infectious strains in order to identify disease-causing exotoxins. Further, we show through functional analysis of superantigenic properties of staphylococcal exotoxins that even very small amounts of a putative superantigenic contaminant can have a significant mitogenic effect. The results show expression and production of two distinct staphylococcal exotoxins, SEC and SEL, in several strains from clinical isolates. Antibodies against both toxins are required to neutralise the superantigenic activity of staphylococcal supernatants and purified staphylococcal toxins.     

乌龙丹联合柳氮磺吡啶治疗强直性脊柱炎36例

目的：观察乌龙丹联合柳氮磺吡啶治疗强直性脊柱炎的疗效与安全性。方法：66例门诊患者随机分为治疗组36例和对照组30例,治疗组给予乌龙丹联合柳氮磺吡啶治疗,对照组给予柳氮磺吡啶治疗,两组均在必要时给予NSAIDs治疗并记录剂量及用药天数。观察治疗前后两组患者临床疗效及实验室指标改变情况。结果：治疗12周后,两组患者在晨僵时间、ESR、CRP、BASFI、BASDAI均比治疗前有显著改善（P＜0．05）,且治疗组优于对照组（P＜0．05）。治疗组有效率高于对照组（P＜0．05）,且不良反应较对照组少（ P＜0．05）。结论：乌龙丹联合柳氮磺吡啶治疗强直性脊柱炎有良好疗效。     

硫酸镁对普鲁帕酮致心律失常的干预作用

目的探讨静脉滴注硫酸镁对普鲁帕酮致心律失常作用的干预效果。方法将92例心律失常患者随机分为对照组和干预组,每组46例。两组均口服普鲁帕酮,干预组同时静脉滴注硫酸镁,于治疗1周后常规心电图观察心律失常变化及致心律失常作用。结果心律失常消失率对照组为43.4%(20/46)、干预组为82.6%(39/46),致心律失常率对照组为19.6%、干预组为4.4%,两组比较有统计学意义(P<0.01)。结论普鲁帕酮抗心律失常同时有致心律失常作用,使用硫酸镁干预可降低致心律失常发生率。     

细菌快速检测试纸片法与传统方法培养结果的比较

目的比较细菌快速检测试纸片法与传统的方法在细菌检测结果上的差异。方法用试纸片法对物体表面污染菌总数和大肠杆菌进行检测,同时与传统方法作平行比较。结果检测细菌总数,用常规方法培养48 h后,细菌生长正常;而纸片法培养48 h,营养琼脂平板上无菌生长,继续培养至72 h才出现菌落。大肠菌群检测中,传统9管发酵法培养24h即有菌生长,国产大肠菌群快速检测试纸法培养36 h和日本产试纸片培养48 h才出现肉眼可见菌落。结论细菌快速检测试纸片虽能简化操作,但存在技术缺陷,且成本高。     

Phenotyping of malignant hematopoietic cells

Summary 1255 cases of leukemia-lymphoma were tested between 1972 and 1984 by multiple marker analysis. Routine leukemia phenotyping was performed using standard morphological and cytochemical techniques in combination with clinical and histo-pathological information; the main emphasis was put on immunological surface marker analysis using erythrocyte rosette assays, TdT and a large panel of poly- and monoclonal antibody tests. The 1255 cases were divided into these major types and subtypes: 349 cases of ALL and related immature T- and Burkitt-lymphomas (cALL, pre B-ALL, B-ALL and Burkitt-lymphomas, T-ALL and immature, mostly leukemic T-lymphomas, Null-ALL), 454 cases of mature T- and B-cell malignancies (T-CLL, mycosis fungoides, Sezary-syndrome, T-lymphomas, B-CLL, hairy cell leukemia, multiple myeloma, B-lymphomas), 263 cases of acute myeloid leukemias (AML, AMMoL/AMoL), 182 cases of chronic myeloid leukemias (CML in chronic phase, CMoL, CML in blast crisis), 6 cases of erythroleukemia and 1 case of megakaryoblastic leukemia. A simplified classification scheme which has been used in our laboratories is presented. Phenotyping is of diagnostic, prognostic and therapeutic relevance, most evidently for patients with ALL. Routine leukemia phenotyping should be performed with highly standardized techniques and reagents and by combining information from several fields in the multiple marker analysis. New areas of leukemia research might become very useful for the routine procedure of phenotyping.Abbreviations ALL acute lymphoblastic leukemia - AML acute myeloblastic leukemia - AMMoL acute myelomonoblastic leukemia - AMoL acute monoblastic leukemia - cALL common ALL - CLL chronic lymphocytic leukemia - CML chronic myelocytic leukemia - CML-BC CML in blastic crisis - CMoL chronic monocytic leukemia