胃癌组织p16基因蛋白表达的意义

目的　检测 p1 6基因蛋白在胃癌组织、癌旁组织中的表达及其分布特点 ,分析其与胃癌临床病理学特征及预后的关系 .方法　采用 S- P免疫组织化学法对 53例胃癌组织及 35例癌旁组织进行 p1 6蛋白的定位观察 .结果　各病理类型胃癌组织、癌旁组织均有 p1 6基因蛋白表达 .阳性率分别为 62 .3% (33/53)和 88.6% (31 /35) ,阳性细胞的棕黄色颗粒主要位于细胞核 .胃癌 p1 6基因蛋白表达与性别、年龄、肿瘤部位在统计学上无差异 (P>0 .0 5) ;而与组织学类型、病理分级、淋巴结转移、临床病理分期在统计学上有差异 (P<0 .0 5) .p1 6蛋白阳性者 5年生存率 51 .0 %高于 p1 6蛋白阴性者 2 0 .0 % (P<0 .0 5) .结论　 p1 6基因缺失和表达水平的改变与胃癌发生、发展密切相关 ,检测 p1 6基因蛋白表达可作为辅助临床判断胃癌的生物学行为及推测预后的指标     

消化道狭窄应用内支架治疗的现状与展望

文章主要分析消化道支架的种类、特征和内支架在消化道狭窄治疗中的应用现状,探讨支架材料应用的发展趋势.     

Central metabotropic glutamate receptors differentially participate in interleukin-1beta-induced mechanical allodynia in the orofacial area of conscious rats.

The present study investigated the role of central metabotropic glutamate receptors (mGluRs) in interleukin-1beta (IL-1beta)-induced mechanical allodynia and mirror-image mechanical allodynia in the orofacial area. Experiments were carried out on male Sprague-Dawley rats weighing 230 to 280 g. After administration of 0.01, 0.1, 1, or 10 pg of IL-1beta into a subcutaneous area of the vibrissa pad, we examined the withdrawal behavioral responses produced by 10 successive trials of an air-puff ramp pressure applied ipsilaterally or contralaterally to the IL-1beta injection site. Subcutaneous injection of IL-1beta produced mechanical allodynia and mirror-image mechanical allodynia in the orofacial area. Intracisternal administration of CPCCOEt, a mGluR1 antagonist, or MPEP, a mGluR5 antagonist, reduced IL-1beta-induced mechanical allodynia and mirror-image mechanical allodynia. Intracisternal administration of APDC, a group II mGluR agonist, or L-AP4, a group III mGluR agonist, reduced both IL-1beta-induced mechanical allodynia and mirror-image mechanical allodynia. The antiallodynic effect, induced by APDC or L-AP4, was blocked by intracisternal pretreatment with LY341495, a group II mGluR antagonist, or CPPG, a group III mGluR antagonist. These results suggest that groups I, II, and III mGluRs differentially modulated IL-1beta-induced mechanical allodynia, as well as mirror-image mechanical allodynia, in the orofacial area. PERSPECTIVE: Central group I mGluR antagonists and groups II and III mGluR agonists modulate IL-1beta-induced mechanical allodynia and mirror-image mechanical allodynia in the orofacial area. Therefore, the central application of group I mGluR antagonists or groups II and III mGluR agonists might be of therapeutic value in treating pain disorder.     

纯氧和空气复苏患儿24个月随访观察

目的 探讨纯氧和空气复苏对新生儿发育的影响,为新生儿复苏用氧选择提供依据.方法 对2005年1月-2007年1月在保定市妇幼保健院进行窒息复苏的30例患儿在24个月时进行随访,依据复苏用氧浓度分为纯氧复苏组(20例)和空气复苏组(10例),内容包括出生时胎龄、出生体重、身长、头围、阿氏评分(1 min,5 min)、心率(1 min,5 min)、随访时体重、身长、头围及运动发育标志(坐、爬、站、走时间).结果 出生时患儿身体数据差异无统计学意义,24个月随访,患儿身高、体重、头围及运动发育标志差异均无统计学意义(P>0.05).结论 空气复苏对新生儿窒息患者是安全有效的.     

化学中毒与急性缺氧的双因素联合效应的实验研究

目的 研究化学中毒与急性缺氧两因素的联合效应。方法 建立常压常氧、常压缺氧和低压缺氧3种模型，以梭曼(Soman)、氰化钠(NaCN)和4-DMAP(4-dimethylaminophenol)为代表，测定大鼠、小鼠、家猫、PC12细胞、兔血红细胞等在3种模型条件下对毒物药物的行为、生化和生理指标变化。结果梭曼单独作用可导致动物协调运动下降、脑等组织含水率增加、脑组织AChE活性降低、MR下调、NE和cAMP含量增加。急性缺氧单独作用也可引起动物协调运动及自主活动的降低、脑等组织含水率的增加、外周血和脑组织AChE活性升高、MR受体上调、NE和cAMP含量增加、4-DMAP药效升高。化学中毒与急性缺氧同时作用，上述变化更加复杂。结论 化学中毒与急性缺氧两种因素同时作用于机体，对机体产生广泛而复杂的损伤作用。此种作用为两因素的联合效应。缺氧引起的机体功能下降对联合效应的增加部分贡献较大。急性缺氧既可使重要的组织成分发生质或量的变化，也会影响某些抗毒剂的作用强度。     

糖皮质激素在川崎病治疗中作用的循证医学研究

目的 通过循证医学方法研究肾上腺皮质激素在川崎病治疗中的作用.方法 采用循证医学方法,检索国内外5种大型专业数据库,筛选出随机或半随机对照研究的文献,再人工筛查确定适宜文献.通过Meta分析,比较激素与丙种球蛋白治疗川崎病在退热时间和冠状动脉病变发生率方面的差异.结果 初筛得到443篇文献.经过人工检索,8篇文献符合要求而被纳入标准.其中,3篇文献共有49例川崎病患儿接受甲基强的松龙治疗,5篇文献共有406例患儿接受强的松治疗.对照组共有33例接受静脉丙种球蛋白治疗,435例接受阿司匹林治疗.各组间患儿性别、年龄、病程差异无显著意义.①甲基强的松龙组(3篇文献):24例发生冠状动脉病变,对照组18例发生,两组病变发生率差异无显著意义.在退热方面,1篇文献显示甲基强的松龙组发热时间明显较丙种球蛋白组缩短,差异有显著意义;2篇文献显示差异无显著意义.②强的松组(8篇文献):28例发生冠状动脉瘤,阿司匹林对照组11例发生,3篇文献提示强的松组冠状动脉瘤发生率明显高于对照组.强的松组76例发生冠状动脉扩张,对照组75例发生,3篇文献提示强的松组冠状动脉扩张发生率明显高于对照组,2篇文献提示强的松组冠状动脉扩张发生率略低于对照组,但差异无显著意义.结论 目前的研究资料显示,激素治疗与丙种球蛋白治疗川崎病在冠状动脉病变发生率方面尚无差异或增高.在缩短热程上两者差异也不显著.尚可进一步通过更大数量病例的随机对照研究来证实本结果.目前治疗川崎病不主张单独应用激素.     

Blockade of LTB4-induced chemotaxis by bioactive molecules interfering with the BLT2-Gαi interaction

BLT2, a low-affinity leukotriene B₄ (LTB₄) receptor, is a member of the G-protein coupled receptor (GPCR) family and is involved in the pathogenesis of inflammatory diseases such as asthma. Despite its clinical implications, however, no pharmacological inhibitors are available. In the present study, we screened for small molecules that interfere with the interaction between the third intracellular loop region of BLT2 (BLT2_iL3) and the Gα_i3 protein subunit (Gα_i3), using a high-throughput screening (HTS) assay with a library of 1040 FDA-approved drugs and bioactive compounds. We identified two small molecules—purpurin [1,2,4-trihydroxy-9,10-anthraquinone; IC₅₀ = 1.6 μM for BLT2] and chloranil [tetrachloro-1,4-benzoquinone; IC₅₀ = 0.42 μM for BLT2]—as specific BLT2-blocking agents. We found that blockade of the BLT2_iL3-Gα_i3 interaction by these small molecules inhibited the BLT2-downstream signaling cascade. For example, BLT2-signaling to phosphoinositide-3 kinase (PI3K)/Akt phosphorylation was completely abolished by these molecules. Furthermore, we observed that these small molecules blocked LTB₄-induced chemotaxis by inhibiting the BLT2-PI3K/Akt-downstream, Rac1-reactive oxygen species-dependent pathway. Taken together, our results show that purpurin and chloranil interfere with the interaction between BLT2_iL3 and Gα_i3 and thus block the biological functions of BLT2 (e.g., chemotaxis). The present findings suggest a potential application of purpurin and chloranil as pharmacological therapeutic agents against BLT2-associated inflammatory human diseases.