TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2

The I kappa B kinase (IKK), consisting of the IKK1 and IKK2 catalytic subunits and the NEMO (also known as IKK gamma) regulatory subunit, phosphorylates I kappa B proteins, targeting them for degradation and thus inducing activation of NF-kappa B (reviewed in refs 1, 2). IKK2 and NEMO are necessary for NF-kappa B activation through pro-inflammatory signals. IKK1 seems to be dispensable for this function but controls epidermal differentiation independently of NF-kappa B. Previous studies suggested that NF-kappa B has a function in the growth regulation of epidermal keratinocytes. Mice lacking RelB or I kappa B alpha, as well as both mice and humans with heterozygous NEMO mutations, develop skin lesions. However, the function of NF-kappa B in the epidermis remains unclear. Here we used Cre/loxP-mediated gene targeting to investigate the function of IKK2 specifically in epidermal keratinocytes. IKK2 deficiency inhibits NF-kappa B activation, but does not lead to cell-autonomous hyperproliferation or impaired differentiation of keratinocytes. Mice with epidermis-specific deletion of IKK2 develop a severe inflammatory skin disease, which is caused by a tumour necrosis factor-mediated, alpha beta T-cell-independent inflammatory response that develops in the skin shortly after birth. Our results suggest that the critical function of IKK2-mediated NF-kappa B activity in epidermal keratinocytes is to regulate mechanisms that maintain the immune homeostasis of the skin.     

Resistance to therapy caused by intragenic deletion in BRCA2

Cells with loss of BRCA2 function are defective in homologous recombination (HR) and are highly sensitive to inhibitors of poly(ADP-ribose) polymerase (PARP), which provides the basis for a new therapeutic approach. Here we show that resistance to PARP inhibition can be acquired by deletion of a mutation in BRCA2. We derived PARP-inhibitor-resistant (PIR) clones from the human CAPAN1 pancreatic cancer cell line, which carries the protein-truncating c.6174delT frameshift mutation. PIR clones could form DNA-damage-induced RAD51 nuclear foci and were able to limit genotoxin-induced genomic instability, both hallmarks of a competent HR pathway. New BRCA2 isoforms were expressed in the resistant lines as a result of intragenic deletion of the c.6174delT mutation and restoration of the open reading frame (ORF). Reconstitution of BRCA2-deficient cells with these revertant BRCA2 alleles rescued PARP inhibitor sensitivity and HR deficiency. Most of the deletions in BRCA2 were associated with small tracts of homology, and possibly arose from error-prone repair caused by BRCA2 deficiency. Similar ORF-restoring mutations were present in carboplatin-resistant ovarian tumours from c.6174delT mutation carriers. These observations have implications for understanding drug resistance in BRCA mutation carriers as well as in defining functionally important domains within BRCA2.     

钧窑名由及钧瓷源起刍议

窑以地名,钧窑名称之由来与＂古钧台＂关系密切。钧瓷之源起,除与＂唐花瓷＂等渊源至深外,更离不开＂柴窑＂匠师的精工绝技。正是在＂唐钧＂乳光蓝斑工艺的基础上,借鉴柴窑＂雨过天晴＂釉等精湛的制瓷工艺,才烧出了宋初的钧蓝釉（天青、天蓝）等分相乳光釉,钧瓷创烧才得以成功。     

Chilli anthracnose disease caused by Colletotrichum species

Anthracnose disease is one of the major economic constraints to chilli production worldwide, especially in tropical and subtropical regions. Accurate taxonomic information is necessary for effective disease control management. In the Colletotrichum patho-system, different Colletotrichum species can be associated with anthracnose of the same host. Little information is known concerning the interactions of the species associated with the chilli anthracnose although several Colletotrichum species have been reported as causal agents of chilli anthracnose disease worldwide. The ambiguous taxonomic status of Colletotrichum species has resulted in inaccurate identification which may cause practical problems in plant breeding and disease management. Although the management and control of anthracnose disease are still being extensively researched, commercial cultivars of Capsicum annuum that are resistant to the pathogens that cause chilli anthracnose have not yet been developed. This paper reviews the causal agents of chilli anthracnose, the disease cycle, conventional methods in identification of the pathogen and molecular approaches that have been used for the identification of Colletotrichum species. Pathogenetic variation and population structure of the causal agents of chilli anthracnose along with the current taxonomic status of Colletotrichum species are discussed. Future developments leading to the disease management strategies are suggested.     

中国美利奴羊新疆军垦型皮肤结构的研究

本文采用2—3岁的成年母羊10只,自肩后活体取约一平方厘米的皮肤、切片。用常规组织学方法对皮肤各层、毛囊、毛根、汗腺进行观察。测量了皮肤各层的厚度,毛、毛囊群、汗腺及皮脂腺的直径,皮脂腺、汗脉及毛囊在每平方毫米内的数量。明确了新疆军垦细毛羊皮肤结构的特点。     

中华鳖气单孢菌类疾病研究

对气单孢菌性鳖病做了大量的研究,取得了如下几方面的进展：（1）国内最先发现并报道了鳖白点病,水泡病;（2）澄清了鳖烂甲病,肿脖子病,白底板病,腹水病的病原及其关系;（3）揭示了嗜水气单孢菌在组织的分布和疾病的发生机制;（4）拟定出对各种鳖病的防治方法,多年的临床实践资料显示,在中等管理水平下,本成果的技术方法可控制“白点病”发病率在2％以下,烂甲病和肿脖子病发病率在1．5％以下,使烂甲病,肿脖子病治愈率达到85－93％,腹水病轻,中度病鳖转归率在97．7％以上。     

Two calcium-binding proteins in infiltrate macrophages of rheumatoid arthritis

The aetiology and cellular mechanism of chronic inflammatory processes are poorly understood. Macrophages act prominently in the inflammatory response and we report here that they express two calcium-binding proteins. The expression of these proteins, referred to as MRP-8 and MRP-14, is specific for cells of myeloid origin, namely granulocytes, monocytes and macrophages, and is observed in blood granulocytes and monocytes but not in normal tissue macrophages. In acutely inflamed tissues, macrophages can express MRP-14 but not MRP-8, and in chronic inflammations, such as primary chronic polyarthritis, infiltrate macrophages express both MRP-8 and MRP-14. Characterization of MRP-8 and MRP-14 could therefore be useful to the understanding of cellular processes induced in chronic inflammation.     

成年大鼠急性脊髓全横断损伤后差异表达蛋白的蛋白组学研究

为进一步阐明脊髓损伤(SCI)的修复机制,对SD成年大鼠进行急性全横断损伤,将损伤前后的大鼠脊髓总蛋白质进行固相pH梯度双向凝胶电泳(2D-PAGE),经考马斯亮蓝染色后,借助PDQuest软件从中找出差异表达蛋白质点.应用基质辅助激光解吸电离串联质谱对差异表达的蛋白质点进行鉴定,成功鉴定出38种蛋白质.其中表达上调的蛋白质有电压依赖的阴离子选择通道蛋白1,α-烯醇酶、硫氧还蛋白依赖的过氧化物还原酶3、生长因子受体结合蛋白2等,表达下调的蛋白质有谷氨酰胺合成酶、14-3-3 epsilon、磷脂酰乙醇胺结合蛋白1、血红蛋白β-1等.鉴定出的差异蛋白多数涉及到神经细胞的增殖、凋亡、应激反应等过程.     

恙虫病所致肺部损害106例临床分析

目的：加深对恙虫病所致肺部损害的认识。方法：通过症状、体征和X线胸片等对106例恙虫病进行回顾性分析，总结其肺部损害的临床特征。结果：有肺部损害占恙虫病患的53．8％(57／106)，其中咳嗽占78．9％(4．5／57)、咳痰占56．1％(32／57)、肺部哕音占45．6％(26／57)，大部分症状轻微。X线胸片显示：双肺间质炎症改变占63．2％(36／57)，肺炎改变占36．8％(21／57)，其中6例合并胸膜病变。除1例因合并中毒性心肌炎死亡外，其余病例经氯霉素或强力霉素治疗均痊愈。结论：恙虫病所致呼吸系统损害较常见，应予以重视，以免误诊。     

神经退行性疾病相关蛋白的翻译后修饰

特定靶蛋白的翻译后修饰对其执行细胞功能有重要作用,是细胞对生长、分化和应激等信号刺激所产生的调节功能的一种反应.翻译后修饰包括磷酸化修饰、乙酰化、甲基化、泛素化、类泛素化等不同的修饰.在神经退行性疾病的研究中,翻译后修饰对疾病的发生和病理影响日益受到人们的重视,我们对磷酸化、泛素化和类泛素化(SUMO化)修饰与神经退行疾病的关系及本实验室的工作进行介绍.     

试论钧瓷命名的理念和方法

钧瓷在世界陶瓷史上享有独特而崇高的地位,体现着中国人＂天人合一＂的精神理念。钧瓷命名是以中国传统文化为依据,以艺术审美为手段,以哲学的、宗教的、艺术的语言为载体,将其文化内涵恰当地表示出来,这既是钧瓷营销之必需,又有引领人们发现美、享受美的作用。在多元化的社会背景下,钧瓷的命名不但要求造成产品之间的区别,而且还要凸显其亮点,产生＂画龙点睛＂、＂点石成金＂之功效,使人们产生美好的联想,寄予微妙的情趣,获得审美的愉悦。钧瓷命名的理念、方法和技巧体现在钧瓷企业、品牌及产品的命名上。