β-catenin与wisp-1在结肠癌中的表达及意义

目的：探讨β-catenin与wisp-1 在原发性结肠癌中表达及临床意义。方法：分别用免疫组化Envision法和实时荧光定量PCR法检测β-catenin、wisp-1 蛋白和基因在53例结肠癌及53例配对正常结肠中的表达。分析两因子表达与临床病理的关系。结果：β-catenin、wisp-1蛋白在结肠癌的异常表达率均高于正常结肠中异常表达率（P〈0.05）。结肠癌中β-catenin蛋白异常表达与淋巴结转移、Duke分期和部位有关（P〈0.05）。wisp-1蛋白异常表达与淋巴结转移、Duke分期有关。β-catenin基因在结肠癌中平均表达是其在正常结肠中的3.237倍（P〈0.05），其异常表达与肿瘤部位及淋巴结转移有关（P〈0.05）。wisp-1基因在结肠癌中平均表达是其在正常结肠中的2.908倍（P〈0.05），其异常表达与肿瘤类型有关（P〈0.05）。结论：β-catenin与wisp-1异常表达特点提示两者与结肠癌的发生发展有密切关系。     

AFP和AFU联合检测对原发性肝癌诊断的意义

利用甲胎蛋白（ＡＦＰ）和ａ－Ｌ－岩藻糖苷酶（ＡＦＵ）联合检测各种肝病及肝脏外恶性肿瘤患者１３５例，正常人３００例；对６例肝癌患者术前、术后ＡＦＰ和ＡＦＵ进行动态观察。结果显示原发性肝癌（ＰＨＣ）术前、术后ＡＦＰ和ＡＦＵ水平的变化对肝癌手术切除彻底性的明确，治疗效果的评价及预后判断有一定意义。ＡＦＰ和ＡＦＵ检测在除ＰＨＣ外的其它肝脏疾病中也有少部分呈阳性表达。正常人ＡＦＰ呈用性。ＡＰＵ在ＰＨＣ与其它肝病有显著性差别。提示ＡＦＰ和ＡＦＵ联合检测能提高ＰＨＣ的检出率和早期肝癌的发现，有着评价ＰＨＣ术后疗效、判断预后的价值。     

Possible horizontal transmission of crimean-congo hemorrhagic Fever virus from a mother to her child

The case of a child with Crimean-Congo hemorrhagic fever (CCHF) presumably infected with CCHF virus from her 27-year-old mother is described. The mother with CCHF was treated with ribavirin and did not present with any symptoms of obvious hemorrhage. The child developed fever on the 5th day after the mother's onset. The partial virus genome was amplified by RT-PCR, and nested PCR from the child and the genome sequence were identical to that from the mother, indicating possible transmission of the virus from mother to child. This case indicates the importance of preventive measures for in-house outbreaks of CCHF.     

七氟醚对新生小鼠fractalkine/CX3CR1表达及学习记忆功能的影响

目的探讨七氟醚对新生小鼠fractalkine/CX3CR1表达及学习记忆功能的影响。方法取健康6日龄C57BL/6新生小鼠36只,分为对照组(C组)、七氟醚1组(S1组)、七氟醚2组(S2组),每组12只。C组小鼠出生后第6、7和8天每天接受1次2 h的60%氧浓度的吸入;S1组小鼠出生后第6、7和8天每天接受1次2 h的2%七氟醚麻醉,吸入氧浓度为60%;S2组小鼠出生后第6、7和8天每天接受1次2 h的3%七氟醚麻醉,吸入氧浓度为60%。三组分别于出生后第9天(T_1)及出生后第34天(T_2)时各处死6只小鼠,取脑组织,采用Western blot法检测海马脑片fractakine和CX3CR1蛋白含量;real-time PCR检测海马脑片fractalkine和CX3CR1 mRNA的表达量。三组剩余6只小鼠用药3周后即出生第29天时行为期5 d的mirror水迷宫实验进行学习记忆能力测试并记录。记录出生后第29～32天小鼠的逃避潜伏期和游泳速度、原平台穿越次数。结果与C组比较,S1组和S2组学习记忆功能降低且海马脑片fractalkine和CX3CR1蛋白含量和mRNA表达量明显降低(P0.05);与S1组比较,S2组学习记忆功能降低且海马脑片fractalkine和CX3CR1蛋白含量和mRNA表达量明显降低(P0.05)。结论 6日龄小鼠连续吸入七氟醚3 d,3周后出现七氟醚麻醉浓度递增的学习记忆能力障碍。小鼠吸入七氟醚可致幼龄小鼠海马脑片fractalkine、CX3CR1蛋白含量和mRNA表达量降低。     

A Novel Mechanism of BAM8-22 Inhibiting Microglia Activation: Represses CX3CR1 Expression via Upregulating miR-184

Bone cancer pain (BCP) is the most common type of pain in cancer patients, during which microglia cells were activated. A previous study showed BAM8-22 had the ability to alleviate BCP via inhibiting microglia activation while the mechanism was not clear. This study aims to investigate the specific mechanism of BAM8-22 inhibiting microglia activation. This study was mainly investigated in BCP mice or LPS-treated microglia BV-2 cells. The behavior tests of mice were performed at 0, 1, 2, 12, and 24 h after BAM8-22 treatment. The expression of miR-184 and CX3CR1 mRNAs was detected by quantitative RT-PCR. The expression of CX3CR1 protein and microglia activation marker, Iba-1, was measured by western blot analysis. The levels of TNF-α and IL-1β were detected by ELISA. Dual-luciferase assay was performed to verify the combination between miR-184 and CX3CR1. After BAM8-22 treatment, increased miR-184 level was observed in both BCP mice and LPS-treated BV-2 cells, with the downregulated expression of Iba-1 and inflammatory cytokines, namely the inhibition of microglia activation. The inhibition of miR-184 reversed the inhibitory effect of BAM8-22 on microglia activation. Further, in vitro studies showed that miR-184 bound to the 3′UTR of CX3CR1 and inhibited microglia activation via repressing CX3CR1 expression. What’s more, the suppression of CX3CR1 expression eliminated the reversal effect of the miR-184 inhibitor on BAM8-22-induced microglia activation and decreased Iba-1 expression and pro-inflammatory cytokine secretion. In BCP models, miR-184 was upregulated by BAM8-22 and the elevated level of miR-184 bound to the 3′UTR region of CX3CR1 and repressed CX3CR1 expression, thus inhibiting the microglia activation, suggesting the potential application of miR-184/CX3CR1 for BCP treatment.