大白鼠皮肤Ⅱ度、Ⅲ度碱烧伤模型复制

目的 根据大白鼠皮肤碱烧伤创面早期病理组织学观察复制Ⅱ、Ⅲ度碱烧伤模型,研究碱烧伤的临床治疗.方法 Wistar纯种健康大白鼠20只,以不同浓度2mol/l、2.5mol/l、5mol/lNaOH,作用时间分别为30秒、45秒、60秒、75秒,涂抹于脱毛后的表皮.结果 2mol/L(60s)、2.5mol/L(45s),5mol/L(30s)即可直接造成Ⅱ度～深Ⅱ度烧伤;2mol/L(75s)、2.5mol/L(60s)、5 mol/L(45s)即可造成Ⅲ度烧伤,其烧伤深度与NaOH溶液浓度和作用时间呈正比.结论 Ⅱ度、Ⅲ度碱烧伤均为渐进性烧伤,与文献中介绍的潜拙样损伤似乎不同.另外,不同浓度NaOH溶液在相同时间对皮肤组织的损伤及同一浓度NaOH溶液在不同时间对大白鼠皮肤的损伤病理学变化均有差异.     

当前中职学生管理工作面临的问题及对策

随着教育形势的发展,中等职业学校学生管理工作也显现了一些新的问题:生源匮乏,素质下降;独生子女、单亲离异家庭学生增多,工作难度加大;社会不良因素对学生的影响;就业形势严峻,使学生学习积极性受到一定的影响;学生自我驾驭能力和心理抗挫能力较弱。要解决这些问题,教师要转变教育观念,给学生以成功的自信;真诚对待学生,塑造学生健全的人格;开展“心育”,培养学生良好的心理品质;突出专业特色教育,激发学生学习兴趣;严格学生管理,规范学生行为;完善就业机制,激发学生学习积极性。     

我们对发生在急诊科的死亡病例了解多少？

目的：通过尸体解剖检查结果来观测临床死亡诊断与实际死凶之间的差异，本研究中的死亡病例均发生在急诊科并向苏格兰地方检查院上报，随后进行尸检。方法：这是在格拉斯哥某医院急诊科进行的一个为期1年的前瞻性研究，所有入选病例系来院前死亡和在急诊科死亡的患者。由有经验的急诊科医师在场判断死亡原因，然后与尸枪结果确定的真正死因进行对照，比较两者之间的差异。     

Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats.

Cerebral ischemic preconditioning protects against stroke, but is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role in cerebral injury after stroke; we tested the hypothesis that interrupting reperfusion lessens ischemic injury. We found for the first time that such postconditioning with a series of mechanical interruptions of reperfusion significantly reduces ischemic damage. Focal ischemia was generated by permanent distal middle cerebral artery (MCA) occlusion plus transient bilateral common carotid artery (CCA) occlusion. After 30 secs of CCA reperfusion, ischemic postconditioning was performed by occluding CCAs for 10 secs, and then allowing for another two cycles of 30 secs of reperfusion and 10 secs of CCA occlusion. Infarct size was measured 2 days later. Cerebral blood flow (CBF) was measured in animals subjected to permanent MCA occlusion plus 15 mins of bilateral CCA occlusion, which demonstrates that postconditioning disturbed the early hyperemia immediately after reperfusion. Postconditioning dose dependently reduced infarct size in animals subjected to permanent MCA occlusion combined with 15, 30, and 60 mins of bilateral CCA occlusion, by reducing infarct size approximately 80%, 51%, and 17%, respectively. In addition, postconditioning blocked terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling-positive staining, a marker of apoptosis, in the penumbra 2 days after stroke. Furthermore, in situ superoxide detection using hydroethidine suggested that postconditioning attenuated superoxide products during early reperfusion after stroke. In conclusion, postconditioning reduced infarct size, most plausibly by blocking apoptosis and free radical generation. With further study it may eventually be clinically applicable for stroke treatment.     

局部应用壳聚糖膜防止术后关节粘连的临床研究

目的评价局部应用壳聚糖膜防止术后关节粘连的效果。方法对涉及膝、肘关节及屈指肌腱断裂手术的患者随机分为两组，对照组行常规手术，壳聚糖膜组术中置入医用壳聚糖膜。随访包括测量关节活动范围（ROM），按HSS标准评价膝关节整体功能，按Morrey评分系统评价肘关节整体功能，按Stricldand总主动运动度评价近侧指间关节功能。结：纛壳聚糖膜组关节ROM明显大于对照组：壳聚糖膜组关节整体功能明显优于对照组。结论在骨科手术中可能引起关节粘连的部位置入壳聚糖膜，有效地防止了术后关节粘连的形成。     

霍奇金淋巴瘤组织中H／RS细胞与其背景细胞的微切割及其IgH基因重排检测

目的 从基因水平探讨霍奇金淋巴瘤(HL)组织中H／RS细胞(Hodgkin and Reed-Sternberg cells)是否起源于B细胞、H／RS细胞的克隆性以及与背景淋巴细胞的相互关系。方法 对33例经典霍奇金淋巴瘤(cHL)石蜡刮片组织进行IgH基因重排分析，并对其中6例重排阳性的病例经B细胞特异性激活蛋白(BSAP)免疫标记，将标记阳性的H／RS细胞和背景淋巴细胞进行微切割后进一步行IgH基因重排分析。结果 16例石蜡刮片组织IgH基因重排阳性。对6例经BSAP标记的cHL成功进行了微切割，其中19管H／RS细胞中，有14管出现重排阳性，细胞数目不同的各管阳性率无显著性差异(P=0．290)；12管背景淋巴细胞有2管出现重排阳性，H／RS细胞与背景淋巴细胞的阳性率有显著性差异(P=0．002)。结论 支持H／RS细胞来源于B细胞的理论，认为部分背景淋巴细胞可能具有瘤性增生活性，参与H／RS细胞的前体细胞组成。     

微波凝固对变应性鼻炎患者T淋巴细胞亚群的影响及意义

目的　探讨常年性变应性鼻炎 (PAR)患者细胞免疫功能状态及微波凝固治疗的作用机制。方法　观察组 2 5例PAR患者分别于微波治疗前以及治疗 1个月后应用免疫组化法检测鼻粘膜上皮和外周血CD3、CD4、CD8、CD4/CD8水平。健康对照组 1 5例亦作相应检测。结果　PAR患者治疗前鼻粘膜及外周血CD3、CD4明显高于正常人 ,CD8低于正常人 ,CD4/CD8比值升高 ,与正常人比较差异有显著性 (P <0 .0 5)。微波治疗后CD4明显减少 ,CD8升高 ,CD4/CD8接近于健康对照组。结论　PAR患者存在明显的细胞免疫功能障碍 ;微波局部凝固治疗可改善PAR患者的细胞免疫状况。     

Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.     

脑创伤致迟发性脑梗死临床分析

目的探讨脑创伤后迟发脑梗死的发生机制,临床诊断及救治措施。方法对32例经影像学证实为颅脑创伤后迟发脑梗死患者的临床资料进行回顾分析。结果出院时按GOS标准评价:恢复良好12例、中残5例、重残4例、植物生存3例,死亡8例,其中非手术治疗20例,存活14例,死亡6例,死亡率30%;手术治疗12例,存活10例,死亡2例,死亡率17%。结论及时诊断与合理有效的治疗是提高脑创伤后迟发性脑梗死的治愈率及提高患者生存质量的关键。     

重睑术后继发上睑下垂的成因及防治

重睑术为最常见的、操作简单的门诊手术,但若想术后取得满意的效果却并非易事[1],术后并发症相对较多,其中继发上睑下垂是较严重的并发症之一,我们复习相关文献发现,关于如何在重睑术中、术后早期发现、早治疗,避免医疗纠纷及并发症发生的报道不多见。本文就重睑术后继发上睑下