准分子激光角膜原位磨镶术治疗近视合并中度以上散光疗效观察

目的 :评价小光斑飞点扫描准分子激光系统应用于准分子激光原位角膜磨镶术 (LASIK)治疗近视合并中度以上散光的疗效。　方法 :对 96例患者 14 4只眼按术前屈光度分成三组 ,Ⅰ组 75只眼 ,近视 0～ - 6D ,散光 - 2～ - 4DC ;Ⅱ组 5 7只眼 ,近视 - 6 .2 5～ 10 .0 0D ,散光 - 2～ - 4DC。Ⅲ组 12只眼 ,近视 - 10 .2 5D以上 ,散光 - 2～- 4DC ;术后随访半年以上 ,并将结果进行比较分析。　结果 :术后 1个月裸眼视力达到 0 .6以上者 ,Ⅰ组为5 .3% ,Ⅱ组为 15 .8% ,Ⅲ组为 6 6 .7% ;术后 1个月裸眼视力达到 1.0以上者 ,Ⅰ组为 94 .7% ,Ⅱ组为 84 .2 % ,Ⅲ组为 33.3%。术后半年裸眼视力达到 0 .6以上者 ,Ⅰ组为 4 % ,Ⅱ组为 14 % ,Ⅲ组为 75 % ;术后半年裸眼视力达到 1.0以上者 ,Ⅰ组为 96 % ,Ⅱ组为 86 % ,Ⅲ组为 2 5 %。术后屈光度在± 1.0D以内者 ,Ⅰ组中为 8% ,Ⅱ组为 14 % ,Ⅲ组为 5 8.3%。术后屈光度在± 0 .5 0D以内者 ,Ⅰ组为 92 % ,Ⅱ组为 86 % ,Ⅲ组为 4 1.7%。术后散光度在± 1.0DC以内者 ,Ⅰ组为 8% ,Ⅱ组为 10 .5 % ,Ⅲ组为 5 0 %。术后散光度在± 0 .5 0DC以内者 ,Ⅰ组为 92 % ,Ⅱ组为 89.5 % ,Ⅲ组为 5 0 %。平均实际切削区直径为 (8.0 2± 0 .0 6 9)mm。　结论 :使用小光斑飞点显像LASIK治疗低     

巨噬细胞炎性蛋白4的突变和原核表达

目的 探索如何抑制嗜酸细胞的趋化作用，选择β-趋化因子巨噬细胞炎性蛋白4（MIP4）的突变性（Met-MIP4)作为趋化因子受体3的拮抗剂，将Met-MIP4基因在原核细胞中进行表达。方法 设计MIP4基因的PCR引物并进行氨基酸突变，将MIP4N末端的丙氨酸突变为蛋氨酸，以正常人肺酸突变，将MIP4N末端的丙氨酸突变为蛋氨酸。以正常人肺cDNA文库为模板，PCR方法获取Met-MIP4基因，克隆入载体pUC19，测序验证序列已得到突变，将正确的基因插入到GST融合表达载体pGEX-4T中，以IPTG诱导表达。结果 PCR产物为220bp左右的片段，连接入pUC19质粒后测序验证获得正确突变，构建的pGEX-4T融合表达载体在大肠杆菌中表达，经SDS-PAGE凝胶电泳显示有大小约34kU的新生融合蛋白表达。结论 成功突变并克隆了β-趋化因子MIP4基因，SDS-PAGE表明，与GST融合的Met-MIP4突变体已得到表达，为进一步研究其生物学活性奠定了基础。     

胸腺切除后血清乙酰胆碱受体抗体改变及与疗效关系

随访２３例因重症肌无力行胸腺切除术的病人。运用灵敏度高、特异性强的ＢＡＳ—ＥＬＩＳＡ法检测手术前、后血清乙酰胆碱受体抗体（ＡｃｈＲ抗体）水平，所得结果均进行统计学分析。２３例病人胸腺切除后，１８例临床症状改善，有效率７８％。术后１４例（６１％）病人血清ＡｃｈＲ抗体水平下降，统计结果表明，手术前后血清ＡｃｈＲ抗体水平差异有显著性（Ｐ＜０．０５），但与症状改善无关（Ｐ＞０．０５）。手术前后血清ＡｃｈＲ抗体水平不影响疗效（Ｐ＞０．０５）。     

链置换式扩增检测羊水中巨细胞病毒DNA

目的：介绍一种简便快速准确检测羊水中ＣＭＶ－ＤＮＡ的改良ＰＣＲ－链置换式扩增用于诊断胎儿先天感染ＣＭＶ。方法，将组成套式ＰＣＲ的外内两对引物按照一定比例（外：内＝１：５０－１００）加在同一试管中一次扩增羊水和胎儿组织中ＣＭＶ－ＤＮＡ。结果：９０例异常孕产史的孕妇羊水检测ＣＭＶ－ＤＮＡ，阳性率为３８．９％（３５／９０），其中合并染色数目异常２例（４７，ＸＹＹ和４７，ＸＸ，＋２１）（已引产）核型及染色     

A method of cephalometric analysis]

In this paper, 220 children ranging from age 11 to 15 were selected. Each of them received a cephalometric roentgenographic examination. 153 cephalometric items from 13 types of methods which had been widely in use were studied through statistic analysis. By means of "t" test, several items which expressed little difference between the normal occlusion and the malocclusion were eliminated. By using of the cluster analysis we selected one item to represent the items which were with similar effect. Finally, 17 cephalometric items were pick out to provide references for clinical work.     

TREATMENT OF HYALINEMEMBRANE DISEASE BYHUMAN AMNIOTIC FLUIDSURFACTANT

A case of hyaline membrane disease was treated successfully with pulmonary surfactant (PS) isolated from human amniotic fluid. Dosage was 150 mg phospholipid/kg. The exogenous surfactant was instilled into the airway via a tracheal cannula. Clinical symptoms, PO2 and FiO2 improved evidently 24 hours after administration. L/S ratio and phosphatidylglycerol recovered gradually in aspirates. Lung X-ray film manifested "white lung" before instillation of surfactant and showed a striking improvement 3 days after treatment. The duration of mechanical ventilation was 6 days. During the period of recovery complications of patent ductus arteriosus and bacterial pneumonia developed. However, the patient recovered completely and was discharged 32 days after admission.     

Stress analysis between implant prostheses with different moduli and surrounding bones北大核心

背景:应力遮挡效应会导致植入假体修复骨缺损手术失败,其主要原因是由于植入假体的弹性模量大于骨组织弹性模量。目的:分析植入假体弹性模量对应力分布的影响,寻求消除应力遮挡现象的方法。方法:通过CT扫描的方式获取实验犬与人体骨组织的模型,分别对其优化后进行梯度赋值,建立较为可靠的骨骼力学模型,并与植入假体组合后进行有限元仿真。首先,通过对比格犬骨骼模型和人体骨骼模型及其对应的植入假体进行有限元仿真,模拟了不同弹性模量对植入假体修复术后的应力和位移分布情况;其次,分析了较小弹性模量差仍会形成应力遮挡现象的原因,建立了骨骼模型及植入假体模型,确立了材料属性赋予方法;最后,验证了该模型及材料属性赋予方法的可行性,并通过随机选取受力点的方式,定量分析植入假体弹性模量与骨骼弹性模量之间的关系对应力遮挡形成的影响。结果与结论:通过梯度赋值法建立与骨骼力学性质更加接近的实验犬骨骼模型和人体骨骼模型,该方法重建的力学模型与真实骨骼的力学性质更为接近;通过有限元仿真力学测试证明,不同弹性模量植入假体对假体本身与周围骨骼间相对位移的影响较小;另外量化弹性模量对假体植入骨骼后对应力分布的影响,可为后续的相关研究提供帮助。     

Modulation of B-cell abnormalities in lupus-prone (NZB x NZW)F1 mice by normal bone marrow-derived B-lineage cells.

(NZB x NZW)F1(NZB/WF1) mice spontaneously develop an autoimmune disease characterized by abnormality of haemopoietic stem cells. The present study examined a possible regulatory cell interaction between NZB/WF1 and normal bone marrow cells using radiation-induced chimeras. We demonstrated that the ability of NZB/WF1 bone marrow cells to transfer the typical disease with hypergammaglobulinemia including autoantibodies into lethally irradiated normal recipients was prevented by cotransfer of bone marrow from normal CBA/J mice but not from xid CBA/N mice carrying a selective defect in B-cell function. Flow cytometric analysis revealed that the generation of NZB/WF1 cells was reduced in the mixed chimeras given CBA/J but not CBA/N bone marrow cells. Interestingly, radiation chimeras reconstituted with a mixture of NZB/WF1 bone marrow and CBA/J splenic B cells did not show elevation of serum immunoglobulin levels, although most of the spleen cells were dominated by NZB/WF1 cells. On the other hand, NZB/WF1 B cells maturated in vivo in the presence of CBA/J bone marrow or splenic B cells lost the hyper-responsiveness to lipopolysaccharide (LPS) in the autoantibody production in vitro. These results suggest that radiosensitive normal B-lineage cells have the regulatory activity to ameliorate the hypergammaglobulinemia of NZB/WF1 mice by reducing the generation of NZB/WF1 B cells and/or by correcting their hyper-responsiveness, and that NZB/WF1 mice may have a defect(s) in the regulatory cell function. In addition, CBA/J splenic B cells were shown to modulate the B-cell abnormality even when injected into non-irradiated NZB/WF1 mice manifesting autoimmunity.     

Leukotriene B4 Receptor (BLT-1) Modulates Neutrophil Influx into the Peritoneum but Not the Lung and Liver during Surgically Induced Bacterial Peritonitis in Mice

Leukotriene B₄ (LTB₄) is a rapidly synthesized, early neutrophil chemoattractant that signals via its cell surface receptor, BLT-1, to attract and activate neutrophils during peritonitis. BLT-1-deficient (BLT-1^−/−) mice were used to determine the effects of LTB₄ on neutrophil migration and activation, bacterial levels, and survival after cecal ligation and puncture (CLP). Male BLT-1^−/− or wild-type (WT) BALB/c mice underwent CLP. Tissues were harvested for determination of levels of bacteria, myeloperoxidase (MPO), LTB₄, macrophage inflammatory protein 2 (MIP-2), and neutrophil (polymorphonuclear leukocyte [PMN]) numbers at 4 and 18 h after CLP. PMN activation was determined by an assessment of phagocytosis ability and CD11b expression. Survival was also determined. BLT-1^−/− mice had decreased numbers of PMNs in the peritoneum at both 4 and 18 h after CLP but increased numbers of PMNs in the blood at 18 h compared with WT mice. Liver and lung MPO levels were significantly higher in BLT-1^−/− mice at both 4 and 18 h after CLP, with increased bacterial levels in the blood, the liver, and peritoneal fluid at 4 h. Bacterial levels remained higher in peritoneal fluid at 18 h, but blood and liver bacterial levels at 18 h were not different from levels at 4 h. PMN phagocytosis and CD11b levels were decreased in BLT-1^−/− mice. LTB₄ levels were similar between the groups before and after CLP, but MIP-2 levels were decreased both locally and systemically in BLT-1^−/− mice. Survival was significantly improved in BLT-1^−/− mice (71%) compared with WT mice (14%) at 48 h post-CLP. Thus, LTB₄ modulates neutrophil migration into the mouse peritoneum, but not the lung or liver, after CLP. Despite higher bacterial and PMN levels at remote sites, there was increased survival in BLT-1^−/− mice compared to WT mice. Decreased PMN activation may result in less remote organ dysfunction and improved survival.