Fast Dipstick Dye Immunoassay for Detection of Immunoglobulin G (IgG) and IgM Antibodies of Human Toxoplasmosis

A dipstick dye immunoassay (DDIA) was developed to detect immunoglobulin G (IgG) or IgM antibodies of toxoplasmosis infection in humans. The assays employ a blue colloidal dye particles (D-1) conjugated to sheep anti-human IgG and rabbit anti-human IgM as the visualizing agents and a soluble antigen of tachyzoites of Toxoplasma gondii strain RH (TSA) as the detective antigen. The mixture of dye-labeled anti-human antibody-special human antibody was captured by TSA onto a nitrocellulose membrane dipstick by means of immunochromatography. The assays are rapid (the whole test can be completed within 15 min), simple, and cheap, and they don't require any equipment. They are sensitive and specific for the detection of anti-Toxoplasma IgG or IgM antibodies and generally agree closely with the results from the enzyme-linked immunosorbent assay. The assays are especially suitable for field applications.     

改良电休克治疗中呼吸机的应用

目的 比较改良电休克治疗中呼吸机和简易呼吸器的应用.方法 应用心电监护仪监测患者的血氧饱和度、心率,观察患者的意识和呼吸恢复时间;应用"作业疲劳症状自评量表"(WRFFQ)评价工作人员的疲劳程度.结果 在改良电休克治疗中应用呼吸机能够快速提高患者的血氧饱和度,作业疲劳症状自评量表显示应用呼吸机和简易呼吸器科室工作人员的疲劳程度有明显的不同.结论 改良电休克治疗中应用呼吸机代替简易呼吸器能够使改良电休克治疗更加安全有效,减轻工作人员的劳动强度.     

Regulation of the TSC pathway by LKB1: evidence of a molecular link between tuberous sclerosis complex and Peutz-Jeghers syndrome

Tuberous sclerosis complex (TSC) and Peutz-Jeghers syndrome (PJS) are dominantly inherited benign tumor syndromes that share striking histopathological similarities. Here we show that LKB1, the gene mutated in PJS, acts as a tumor suppressor by activating TSC2, the gene mutated in TSC. Like TSC2, LKB1 inhibits the phosphorylation of the key translational regulators S6K and 4EBP1. Furthermore, we show that LKB1 activates TSC2 through the AMP-dependent protein kinase (AMPK), indicating that LKB1 plays a role in cell growth regulation in response to cellular energy levels. Our results suggest that PJS and other benign tumor syndromes could be caused by dysregulation of the TSC2/mTOR pathway.     

肾综合征出血热病毒特异性双价纯化免疫血清F（ab）2的制备和临床治疗应用

１９８８年至１９９１年对收治的发病５日以内的肾综合征出血热（ＨＦＲＳ）病人应用姬鼠型ＨＦＲＳＶ陈株及家鼠型ＨＦＲＳＶＲ２２株，免疫猪所制备的特异性双价纯化免疫血清Ｆ（ａｂ）２（称Ｆ（ａｂ）２血清），治疗ＨＦＲＳ病人６５例作为研究组，以４４例作为对照组。治疗结果表明：①球结膜水肿渗出减轻，２４小时出血减轻；②白细胞病毒抗原消失迅速；③研究组出院平均早９．１天；④在洽疗后２、４日，对照组的特异性免疫荧光ＩｇＭ抗体明显高于研究组的。⑤其他实验室检测指标都以研究组为优。提纯后的免疫血清Ｆ（ａｂ）２无抗体－介导反应，无副作用及过敏反应。它含有特异性中和抗体及其他免疫因子，可中和清除体内的病毒抗原，减轻病毒血症及毛细血管壁的损伤，阻断病情发展，促进病情恢复。     

Variable MHC class I engagement by Ly49 natural killer cell receptors demonstrated by the crystal structure of Ly49C bound to H-2K(b)

The Ly49 family of natural killer (NK) receptors regulates NK cell function by sensing major histocompatibility complex (MHC) class I. Ly49 receptors show complex patterns of MHC class I cross-reactivity and, in certain cases, peptide selectivity. To investigate whether specificity differences result from topological differences in MHC class I engagement, we determined the structure of the peptide-selective receptor Ly49C in complex with H-2K(b). The Ly49C homodimer binds two MHC class I molecules in symmetrical way, a mode distinct from that of Ly49A, which binds MHC class I asymmetrically. Ly49C does not directly contact the MHC-bound peptide. In addition, MHC crosslinking by Ly49C was demonstrated in solution. We propose a dynamic model for Ly49-MHC class I interactions involving conformational changes in the receptor, whereby variations in Ly49 dimerization mediate different MHC-binding modes.     

根据WHO新分类对493例非霍奇金淋巴瘤的临床病理分析

目的探讨非霍奇金淋巴瘤(NHL)的临床病理特点,评价世界卫生组织(WHO)2001淋巴瘤新分类标准的实用性.方法复查1992-2003年500例既往经病理诊断为NHL的病例,观察其形态学、免疫学及临床特点,按WHO新分类标准进行重新定性和分类,对其中156例有随访的病例进行生存率分析.结果 500例中,493例NHL,其中B细胞肿瘤69.0%,T和NK细胞肿瘤29.8%;前六位最常见类型为弥漫大B细胞淋巴瘤(DLBCL)、滤泡性淋巴瘤(FL)、非特殊型周围T细胞淋巴瘤(PT-un)、T淋巴母细胞淋巴瘤(T-LBL)、MALT型结外边缘区B细胞淋巴瘤(MALT)及B-小淋巴细胞性淋巴瘤(B-SLL);青少年中最常见为LBL、DLBCL及Burkitt淋巴瘤.在本组病例中,LBL在所有患者尤其是青少年患者中的比例均明显高于国外报道,FL的比例明显高于国内报道.不同类型NHL的生存情况在总体上差异有统计学意义(P<0.001),其中边缘区B细胞淋巴瘤(MZL)与SLL的预后最佳,LBL与PT-un的预后最差,DLBCL与FL介于前两组之间.按WHO推荐的两种方法划分的FL不同级别之间,生存情况差异无统计学意义(P>0.05).结论淋巴瘤WHO2001新分类实用性强、便于掌握,各亚型的形态学、免疫学指标可靠,结合临床能较好应用于淋巴瘤的诊断和预后.但是,建议国内同行对FL的判断及分级标准进一步审定.     

CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer.

Intestinal metaplasia is a key event in multistep gastric carcinogenesis. CDX2, a master regulator of intestinal phenotype, was shown to play a tumor-suppressive role in colon cancer. However, it was reported to be expressed in nearly all gastric intestinal metaplasia and many gastric cancers. As CDX2 is differentially expressed in normal stomach and intestine, we sought to relate the CDX2 expression to gastrointestinal differentiation along gastric carcinogenesis. The expression of CDX2 protein in gastric intestinal metaplasia, dysplasia and cancer was examined and related to their gastrointestinal differentiation. CDX2 expression was significantly decreased in incomplete intestinal metaplasia, which expresses both gastric mucins (MUC5AC and MUC6) and intestinal mucin (MUC2), compared with complete intestinal metaplasia, which expresses intestinal mucin (MUC2) only. Although incomplete intestinal metaplasia morphologically resembles colon, its CDX2 expression was apparently lower than that in the normal colon. Moreover, CDX2 expression was progressively reduced in gastric dysplasia and cancer. The CDX2 expression in gastric cancer was also inversely correlated with the expression of gastric mucins. As incomplete intestinal metaplasia is associated with higher risk of gastric cancer, its lower CDX2 expression compared with that in complete intestinal metaplasia and normal colon epithelium resolved the current contradiction between the tumor-suppressive role of CDX2 in the colon and the high prevalence of CDX2 in intestinal metaplasia. Further decrease of CDX2 expression in gastric dysplasia and cancer suggests that CDX2 plays a similar anticarcinogenic role in intestinal metaplasia as it does in colon. Intestinal metaplasia or dysplasia with low expression of CDX2 may serve as predictive markers for gastric cancer.     

Arthrobacter scleromae sp. nov. isolated from human clinical specimens

A gram-positive, coryneform bacterium was isolated from swollen scleromata of a dermatosis patient. An analysis of its phenotypic, chemotaxonomic, and genotypic characteristics showed that this bacterium is closely associated with Arthrobacter oxydans and Arthrobacter polychromogenes but that it belongs to a distinct species, for which the name Arthrobacter scleromae sp. nov. is proposed.     

Correlation of AIB1 overexpression with advanced clinical stage of human colorectal carcinoma

AIB1, a member of the steroid receptor coactivator 1 family, has been cloned on 20q12 and is a candidate oncogene in human breast cancer. It is commonly amplified and overexpressed in several types of human cancers. In this study, we examined the expression of AIB1, as related to clinicopathologic features, in 85 human colorectal cancers (CRCs). The status of the number of AIB1 copies, p53 expression, and DNA ploidy was also analyzed. The overexpression of AIB1 was detected in 35% of CRCs. Amplification of AIB1 was observed in 10% of CRCs. In addition, the overexpression of AIB1 was observed more frequently in CRCs in later clinical stages (T3 N1 M0/T3 N0 2M1), compared with that in T3 N0 M0 stage (P < .05). These results suggest that overexpression of AIB1 might provide a selective advantage for the developmental growth and/or progression of subsets of CRCs. In addition, a significant correlation (P < .05) of overexpression of AIB1 with p53 overexpression as well as with aneuploid DNA content was observed in these CRCs. The overexpression of p53 was also correlated significantly with CRC DNA ploidy (P < .05). Furthermore, there was a substantial population of CRCs showing overexpression of both AIB1 and p53 protein and all had aneuploid DNA content; most of these were in the later clinical stage. These findings suggest a possible convergence of AIB1 with a pathway involving p53, which might induce chromosomal instability and affect the clinical phenotype of a subset of CRCs.