联合雾化吸入对老年支气管哮喘急性发作的疗效观察及护理

支气管哮喘是一种由多种细胞及细胞因子参与的慢性炎症性疾病。气道慢性炎症导致气道高反应,从而产生反复发作的喘息、胸闷、呼吸困难、咳嗽等相关症状,尤其多发于夜间及凌晨。我科自2005年6月开始采用特布他林、异丙托溴胺、布地奈德联合雾化吸入治疗老年哮喘急性发作取得满意疗效。现报告如下。1一般资料1.1对象我科2005年6月—2007年5月共收治老年支气管哮喘急性发作病人78例,年龄65岁~95岁(73.0岁±6.0岁),均符合诊断标准[1]。随机分为两组,对照组38例:男30例,女8例;治疗组40例:男35例,女5例。两组年龄、性别比较,差异无统计学意义(P>0…     

胸腺瘤与重症肌无力的外科处理

10例胸腺瘤中3例合并重症肌无力症,经手术治疗配合抗胆碱酯酶药物治疗,9例治愈。     

Serum modulates cyclic AMP-dependent morphological changes in cultured neurohypophysial astrocytes

The effects of serum on the morphological plasticity exhibited by pituicytes in explant cultures of the neurohypophysis of adult rats have been examined. Cultured pituicytes are normally nonstellate, protoplasmic, amorphous cells (< 25% are stellate with a distinct cell body and phase bright processes). After incubation (90 min) of pituicyte cultures in a HEPES buffered salt solution (HBSS) supplemented with isoproterenol or forskolin, the fraction of stellate pituicytes significantly increased. The increase in the fraction of stellate cells induced by isoproterenol was not reversed by subsequent incubation in isoproterenol-free HBSS for 90 min. In contrast, after stellation was induced in cultures by exposure to forskolin (90 min), the fraction of stellate cells was significantly reduced if these cultures were incubated in forskolin-free, serum (0.5%) supplemented HBSS for the same duration. Serum also blocked the increase in the fraction of stellate pituicytes induced by forskolin. These experiments suggest that serum components may have a significant role in controlling the plasticity of neuroglial relations in the neurohypophysis priviously demonstrated in vivo.     

不同状态人体牙槽骨的弹性性质

人体下颌牙槽骨皮质骨是各向异性复合生物材料,组织结构上类似于胶原羟磷灰石纤维增强的单向纤维增强复合材料。本文应用电测法测试了不同状态人体下颌牙槽骨皮质骨在平面应力状态下的各向异性弹性常数。     

新生鼠和成年鼠脑7种微量元素含量的比较

利用高频电感耦合等离子体原子发射光谱法（ICP－AES）测定Sprunge－Dawley大鼠新生期大脑皮层、海马、小脑、间脑和脑桥等部位的锌、铁、铜、锰、铬、锶、钼等7种微量元素的含量，并与成年动物做了比较。结果表明：（1）新生期大鼠全脑7种微量元素含量的多寡依次为：锌、铁、铬、锶、锰、铜、钼；成年期时钢跃居第四位，总含量低于新生期。（2）脑内不同部位微量元素的含量不同。新生大鼠海马和小脑内多数元素含量高于其他脑区，钼在间脑和海马中含量较高。成年鼠皮层、海马微量元素含量较高，皮层内铜、锶、钼含量最低。     

自制“茎突分离保护器”及茎突过长症的治疗应用

本文介绍了自制“茎突分离保护器”的质地、规格、性能。茎突截短术应用代用器械手术18例,每侧截除长度平均为1.75cm;应用自制器械30例,每侧平均截除长度为2.52cm,且比代用器械每侧可缩短手术时间30～40分钟。文章还评价了包括颈外切开的6例,共54例手术的疗效。     

Gaucher disease: in vivo evidence for allele dose leading to neuronopathic and nonneuronopathic phenotypes

Gaucher disease, a common lysosomal storage disorder, is associated with mutations at the acid beta-glucosidase (GCase) locus. Two affected individuals are described to share a common mutant allele, but manifest different clinical categorical phenotypes. A 57-year-old female, with Gaucher disease type 1 and Cherokee ancestry, was homozygous for a rare mutant allele encoding Lys79Asn (K79N). A 2-year-old Caucasian male, with Gaucher disease type 3 and Cherokee ancestry, was a heteroallelic homozygote for this same allele (K79N) and a novel complex mutation (null allele). The shared alleles were identical as determined by complete gene sequencing, suggesting a founder effect. The discrepant phenotypes (types 1 and 3) in these two patients provide support for a threshold of residual activity necessary to "protect" the central nervous system (CNS) from the pathogenic effects of Gaucher disease, indicating an allele dose-effect. Designation of genotype associations with specific phenotypes must be assessed with this perspective.     

NF1 mutations in neurofibromatosis 1 patients with plexiform neurofibromas

Neurofibromatosis 1 (NF1) is an autosomal dominant disorder caused by genetic alterations of the NF1 gene on 17q11.2. About 30% of NF1 patients develop plexiform neurofibromas (PNFs), which often cause severe clinical deficits. To determine whether there is a certain genotype underlying PNFs or subtypes of PNFs, we screened 42 NF1 patients from 41 families with PNFs for mutations in the NF1 gene. In 33 out of the 41 (80%) unrelated patients NF1 mutations were found, 24 are novel while the other 9 have been described in previous studies. The 33 mutations included 23 nonsense and frameshift, six splice and four missense mutations. The tumors in these patients had various sizes and features/growth characteristics. No correlation was found between the type or location of the NF1 mutations and size, location or feature of the PNFs, suggesting that many types of NF1 mutations can lead to development of PNFs.     

Short-term enzyme replacement in the murine model of Sanfilippo syndrome type B

The Sanfilippo syndrome type B (MPS III B) is an autosomal recessive disease caused by deficiency of alpha-N-acetylglucosaminidase (EC 3. 2.1.50), one of the lysosomal enzymes required for the degradation of heparan sulfate. The disease is characterized by profound neurodegeneration but relatively mild somatic manifestations, and is usually fatal in the second decade. A mouse model had been generated by disruption of the Naglu gene in order to facilitate the study of pathogenesis and the development of therapy for this currently untreatable disease. Recombinant human alpha-N-acetylglucosaminidase (rhNAGLU) was prepared from secretions of Lec1 mutant Chinese hamster ovary cells. The enzyme, which has only unphosphorylated high-mannose carbohydrate chains, was endocytosed by mouse peritoneal macrophages via mannose receptors, with half-maximal uptake at ca. 10(-7) M. When administered intravenously to 3 month-old mice, rhNAGLU was taken up avidly by liver and spleen but marginally if at all by thymus, lung, kidney, heart, and brain (in order of diminishing uptake). The half-life of the enzyme was 2.5 days in liver and spleen. Immunohistochemistry and electron microscopy showed that only macrophages were involved in enzyme uptake and correction in these two organs, yet the storage of glycosaminoglycan was reduced to almost normal levels. The results show that the macrophage-targeted rhNAGLU can substantially reduce the body burden of glycosaminoglycan storage in the mouse model of Sanfilippo syndrome III B.     

Effects of x-ray and CT image enhancements on the robustness and accuracy of a rigid 3D/2D image registration

A rigid body three-dimensional/two-dimensional (3D/2D) registration method has been implemented using mutual information, gradient ascent, and 3D texturemap-based digitally reconstructed radiographs. Nine combinations of commonly used x-ray and computed tomography (CT) image enhancement methods, including window leveling, histogram equalization, and adaptive histogram equalization, were examined to assess their effects on accuracy and robustness of the registration method. From a set of experiments using an anthropomorphic chest phantom, we were able to draw several conclusions. First, the CT and x-ray preprocessing combination with the widest attraction range was the one that linearly stretched the histograms onto the entire display range on both CT and x-ray images. The average attraction ranges of this combination were 71.3 mm and 61.3 deg in the translation and rotation dimensions, respectively, and the average errors were 0.12 deg and 0.47 mm. Second, the combination of the CT image with tissue and bone information and the x-ray images with adaptive histogram equalization also showed subvoxel accuracy, especially the best in the translation dimensions. However, its attraction ranges were the smallest among the examined combinations (on average 36 mm and 19 deg). Last the bone-only information on the CT image did not show convergency property to the correct registration.