zs株弓形虫P22基因片段在巨噬细胞中的表达

目的　克隆表达ZS株弓形虫表膜抗原P2 2编码基因的巨噬细胞株。方法　扩增P2 2编码基因ORF的全长 5 6 1bp片段 ,经PstI、XbaI双酶切后 ,定向克隆于质粒 pBudCE 4 .1,构建真核重组表达质粒 pBudCE 4 .1/P2 2 ,通过脂质体介导转染入小鼠巨噬细胞RAW2 6 4 .7,以RT PCR方法鉴定目的基因在巨噬细胞中的表达。结果　成功获取pBudCE 4 .1/P2 2转染的巨噬细胞阳性克隆 ,并证实P2 2 mRNA在阳性克隆细胞中的表达 ,为P2 2蛋白对巨噬细胞的免疫调节功能作用的研究奠定基础。     

Lithospermum erythrorhizon Alleviates Atopic Dermatitis-like Skin Lesions by Restoring Immune Balance and Skin Barrier Function in 2.4-Dinitrochlorobenzene-Induced NC/Nga Mice

The incidence of atopic dermatitis (AD), a disease characterized by an abnormal immune balance and skin barrier function, has increased rapidly in developed countries. This study investigated the anti-atopic effect of Lithospermum erythrorhizon (LE) using NC/Nga mice induced by 2,4-dinitrochlorobenzene. LE reduced AD clinical symptoms, including inflammatory cell infiltration, epidermal thickness, ear thickness, and scratching behavior, in the mice. Additionally, LE reduced serum IgE and histamine levels, and restored the T helper (Th) 1/Th2 immune balance through regulation of the IgG1/IgG2a ratio. LE also reduced the levels of AD-related cytokines and chemokines, including interleukin (IL)-1β, IL-4, IL-6, tumor necrosis factor-α (TNF-α), thymic stromal lymphopoietin, thymus and activation-regulated chemokine, macrophage-derived chemokine, regulated on activation, normal T cell expressed and secreted, and monocyte chemoattractant protein-1 in the serum. Moreover, LE modulated AD-related cytokines and chemokines expressed and secreted by Th1, Th2, Th17, and Th22 cells in the dorsal skin and splenocytes. Furthermore, LE restored skin barrier function by increasing pro-filaggrin gene expression and levels of skin barrier-related proteins filaggrin, involucrin, loricrin, occludin, and zonula occludens-1. These results suggest that LE is a potential therapeutic agent that can alleviate AD by modulating Th1/Th2 immune balance and restoring skin barrier function.     

人精子蛋白SP22在睾丸、精子中的分布与定位

目的：以原核表达的人精子蛋白SP22制备其兔多克隆抗体,研究人精子蛋白SP22在人睾丸和精子中的分布与定位。方法：在E.Coli中诱导表达SP22基因,以纯化出的重组人精子蛋白htSP22为抗原制备兔抗人SP22多克隆抗体,运用免疫组织化学分析SP22在人睾丸和精子中的分布与定位。结果：表达出了分子量约22000的重组htSP22蛋白,制备获得了能特异性识别睾丸、精子中天然SP22蛋白的兔抗人SP22多克隆抗体。免疫组织及细胞化学证明SP22存在于曲细精管中各类生精细胞及精子头部表面。结论：制备的抗体具有特异性,SP22存在于睾丸曲细精管中各类生精细胞及精子头部表面。     

中药复方止痛胶囊的药效学实验研究

目的　研究中药复方止痛胶囊的药效。方法　观察中药复方止痛胶囊镇痛抗炎作用 ,研究其相关抗炎镇痛机制。结果　中药复方止痛胶囊对多种炎症及疼痛模型有较好的抑制作用 ,同时能明显降低AA大鼠疼痛模型血清炎症介质及氧自由基水平 ,提高下丘脑β- 内啡肽含量。 结论　中药复方止痛胶囊具有抗炎镇痛作用 ,其作用机制可能与其降低外周血清炎症介质、氧自由基水平以及提高中枢β-内啡肽含量有关。     

Effect of Thermo-Mechanical Treatment on the Microstructure and Tensile Properties of the Fe-22Cr-5Al-0.1Y Alloy

Oxide dispersion strengthened ferritic steel is considered an important structural material in fusion reactors due to its excellent resistance to radiation and oxidation. Fine and dispersed oxides can be introduced into the matrix via the powder metallurgy process. In the present study, large grain sizes and prior particle boundaries (PPBs) formed in the FeCrAlY alloy prepared via powder metallurgy. Thermo-mechanical treatment was conducted on the FeCrAlY alloy. Results showed that microstructure was optimized: the average grain diameter decreased, the PPBs disappeared, and the distribution of oxides dispersed. Both ultimate tensile strength and elongation improved, especially the average elongation increased from 0.5% to 23%.     

miRNA-146a在溃疡性结肠炎大鼠结肠组织与血浆中浓度表达意义

目的探讨miRNA-146a在溃疡性结肠炎(ulcerative colitis, UC)大鼠结肠组织及血浆中浓度表达意义。方法建立溃疡性结肠炎模型,采取病变结肠组织与血浆提取miRNA,并采用核酸测定仪测定浓度,琼脂糖凝胶电泳检测完整性,采用荧光定量PCR技术检测溃疡性结肠炎miRNA-146a在组织及血浆中表达差异。结果模型组中溃疡性结肠炎大鼠结肠组织与血浆miRNA-146a表达量低于空白组(P<0.05)。模型组中组织核酸测定及琼脂糖凝胶电泳示浓度、纯度及完整性较血浆好。结论 miRNA-146a在溃疡性结肠炎大鼠组织与血浆中呈低表达,并且溃疡性结肠炎大鼠结肠组织较血浆更具稳定性可作为UC诊断的指标之一。     

A novel homozygous variant extending the peripheral myelin protein 22 by 9 amino acids causes early‐onset Charcot‐Marie‐Tooth disease with predominant severe sensory ataxia

Peripheral myelin protein 22 (PMP22) related neuropathies account for over 50% of inherited peripheral neuropathies. A gene copy variation results in CMT1A (duplication) and hereditary neuropathy with liability to pressure palsies (HNPP; single deletion). Point mutations comprise both phenotypes. The underlying pathological mechanisms are incompletely understood and biallelic mutations of PMP22 are very rare. We describe a 9‐year‐old girl who presented before the age of 1 year with severe locomotor delay. She now requires support for standing and walking in view of her severe sensory ataxia. Strikingly, her muscle power and bulk are close to normal in all segments. Nerve conduction studies showed sensory‐motor velocities below 5 m/s. Genetic analysis revealed a homozygous sequence change in the PMP22 gene causing the loss of termination codon (c.483A > G; p.[*161Trpext*10]), extending the protein by 9 amino acids. Both heterozygous parents have neurophysiological abnormalities consistent with HNPP, consistent with this being a loss‐of‐function mutation. PMP22‐deficient human models are rare but important to decipher the physiological function of the PMP22 protein in vivo. The predominance of large fiber sensory involvement in this and other rare similar cases suggests a pivotal role played by PMP22 in the embryogenesis of dorsal root ganglia in humans.     

Diagnosis of metachromatic leukodystrophy in a patient with regression and Phelan-McDermid syndrome

Phelan-McDermid syndrome (PMS) is a 22q13.3 deletion syndrome. Most PMS patients show global developmental delay and some of them suffer from developmental regression. The deleted region contains ARSA, which is responsible for metachromatic leukodystrophy (MLD). Here we report an extremely rare case of PMS characterized by unusual, rapidly progressive developmental regression due to additional pathogenic mutation in ARSA. Considering the 1 in 100 chance of an MLD carrier, co-occurrence of PMS and MLD in a patient is possible if either parent carries a heterozygous ARSA mutation. Therefore, MLD should be ruled out in PMS patients with severe neurological phenotype.     

Microdeletion 22q11.2 syndrome: Does thymus incidental surgical resection affect its immunological profile?

Background

The del22q11 syndrome patients present immunological abnormalities associated to thymus alterations. Up to 75% of them present cardiopathies and thymus is frequently removed during surgery. The thymectomy per se has a deleterious effect concerning lymphocyte subpopulations, and T cell function. When compared to healthy controls, these patients have higher infections propensity of variable severity. The factors behind these variations are unknown. We compared immunological profiles of del22q11.2 Syndrome patients with and without thymectomy to establish its effect in the immune profile.