细胞间黏附分子-1在急性肝内胆汁淤积性肝损伤大鼠模型中的表达

目的 探讨细胞间黏附分子-1(ICAM-1)在急性肝内胆汁淤积性肝损伤大鼠模型中的表达及其意义.方法 雄性SD大鼠α-异硫氰酸萘酯(ANIT)50 mg/kg一次灌胃,建立急性肝内胆汁淤积性肝损伤动物模型,实时荧光定量PCR检测灌胃后大鼠24、48、72 h肝组织中ICAM-1 mRNA表达量,全自动生化分析仪检测其血清总胆红素(TB)、结合胆红素(DB)、ALT、γ-谷氨酰转肽酶(GGT)水平.取大鼠肝组织行病理学检查.采用SPSS 12.0软件进行统计学分析.结果 模型组24、48、72 h肝组织ICAM-1 mRNA表达量分别为3.43±0.58、5.32±0.67、2.54±0.41,均显著高于对照组(Pa＜0.05);模型组24、48 h肝组织ICAM-1 mRNA表达量分别与同一时间点的血清TB、DB、ALT、GGT水平呈正相关(Pa＜0.05),模型组72 h肝组织ICAM-1mRNA表达量与其72 h时血清TB、DB、ALT、GGT水平无相关性(Pa＞0.05);模型组24、48、72 h肝组织ICAM-1 mRNA表达量均与同一时间点肝组织病理损伤程度分级呈正相关(Pa＜0.05).结论 ICAM-1在肝内胆汁淤积性肝损伤大鼠肝组织中基因表达增高,其参与了胆汁淤积性肝损伤的病理过程.     

转录因子ΚB和早期生长反应因子1在急性肝内胆汁淤积性肝损伤大鼠模型中的表达

目的 研究转录因子核因子KB(nuclear factor-KB,NF-KB)和早期生长反应因子1(early growth response factor-1,Egr-1)在急性肝内胆汁淤积性肝损伤大鼠模型中的表达及意义.方法 将α-异硫氰酸萘酯(ANIT)按50 ms/ks一次灌胃大鼠,建立急性肝内胆汁淤积性肝损伤的动物模型,免疫组织化学法和实时荧光定量PCR分别检测灌胃后24、48、72 h肝组织中NF-KB p65蛋白表达和Egr-1 mRNA表达量,全自动生化分析仪检测血清总胆红素(TB)、直接胆红素(DB)、丙氨酸氨基转移酶(ALT)、γ-谷氨酰转肽酶(GGT).结果 模型组24、48、72 h肝组织Egr-1 mRNA表达量分别为(12.73±3.02)×10-2、(8.19±2.29)×10-2(5.79±0.78)×10-2,24、48 h均高于对照组(P均＜0.05),72 h与对照组差异无统计学意义(P＞0.05);模型组24、48、72 h肝组织NF-KB p65核表达阳性细胞率分别为48.3%、26.5%、2.7%,其中24、48 h均高于对照组(P均＜0.05),72 h与对照组差异无统计学意义(P＞0.05).模型组24、48 h NF-KB p65核表达阳性细胞分级分别与同一时间点的血清TB、DB、ALT呈正相关(P均＜0.05);模型组24、48 h Egr-1 mRNA表达量分别与同一时间点的血清TB、DB、ALT、CA T呈正相关(P均＜0.05);模型组72 h肝组织NF-KB p65、Egr-1 mRNA表达量与72 h时血清TB、DB、ALT、GGT无相关关系(P均＞O.05);模型组24、48 h NF-KB p65核表达阳性细胞分级与同一时间点的血清GGT亦无相关关系(P均＞0.05);模型组24、48 h肝组织Egr-1 mRNA表达量及NF-KB p65核表达阳性细胞分级均与同一时间点肝组织病理损伤程度分级呈正相关(P均＜0.05);模型组72 h肝组织Egr-1 mR-NA表达量及NF-KB p65核表达阳性细胞分级均与同一时间点肝组织病理损伤程度分级无相关关系(P均＞0.05).结论 NF-KB和Egr-1在肝内胆汁淤积性肝损伤肝组织中表达增高,与肝损伤程度相关,参予了肝内胆汁淤积性肝损伤的病理过程.     

Na~+-牛磺酸转运体基因在急性肝内胆汁淤积大鼠肝组织的表达及意义

目的 通过研究α-异硫氰酸萘酯(ANIT)所致的急性肝内胆汁淤积大鼠肝组织Na+-牛磺酸转运体基因(ntcp)表达的变化,以进一步探讨急性肝内胆汁淤积发生的分子机制.方法 选用40只幼年雄性SD大鼠为实验对象,随机分为正常对照组(8只)、中毒组(32只).中毒组幼鼠按100 mg/kg一次性灌服ANIT诱导急性肝内胆汁淤积病变.观察各组在灌服ANIT后24、48、72和96 h血清总胆红素(TB)、丙氨酸转氨酶(ALT)的浓度,同时用RT-PCR测定肝组织中ntcp-mRNA的表达,并在光学显微镜下观察肝脏的形态学改变.实验结果采用SPSS软件包分析.结果 灌服ANIT后,中毒组大鼠血清ALT、TB逐渐升高,24 h增加明显,48 h达高峰,72 h逐渐下降,96 h已显著下降,差异有统计学意义(P<0.05).中毒组大鼠肝组织ntcp-mRNA表达水平低于正常对照组,48 h表达最低,72 h逐渐恢复.差异有统计学意义(P<0.05).结论 ANIT所致的急性肝内胆汁淤积使肝脏功能受损,导致血清酶学改变.急性胆汁淤积肝组织基底膜ntcp基因转录水平明显下降为机体的一种负反馈机制,可减轻胆汁淤积程度,保护肝细胞.     

大黄素预处理对幼龄大鼠肝内胆汁淤积的保护作用

目的探讨大黄素对肝内胆汁淤积幼龄大鼠的保护作用。方法将120只Sprague Dawley(SD)大鼠随机分为对照组、模型组及大黄素高、中、低剂量组,每组24只,对照组和模型组采用羧甲基纤维素钠溶液灌胃,其余组以不同剂量大黄素溶液灌胃。实验第5天各组(对照组除外)采用α-萘异硫氰酸酯(ANIT,50 mg/kg)一次性灌胃建立肝内胆汁淤积模型。ANIT灌胃后24、48、72 h各组分别处死8只大鼠,比色法检测各组血清总胆红素(TBIL)、直接胆红素(DBIL),总胆汁酸(TBA)、碱性磷酸酶(ALP)、γ谷氨酰转移酶(GGT)、谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,采用苏木精-伊红染色于光镜下观察各组不同时间点肝脏形态学改变。结果 24、48、72 h模型组较对照组血清TBIL、DBIL、TBA、ALP、GGT、ALT、AST水平均显著升高(P0.01)。模型组造模后48 h较24 h及72 h时血清TBIL、DBIL、TBA、ALT、AST水平均有不同程度升高(P0.05)。24、48、72 h大黄素各剂量组较模型组TBIL、TBA水平有不同程度降低(P0.05)。24、48、72 h大黄素高、低剂量组较中剂量组血清TBA水平明显升高(P0.05)。模型组大鼠48 h病理改变最重;大黄素各剂量组各时间点肝脏病理较模型组减轻,其中大黄素中剂量组较大黄素高、低剂量组比较改善更明显。结论大黄素可以改善ANIT诱导幼龄大鼠肝内胆汁淤积,中剂量组效果最好。     

益生菌对异硫氰酸萘酯诱导淤疸幼鼠胃肠激素的影响及其干预胆汁淤积的机制

目的 通过观察益生菌制剂双歧三联活菌片对异硫氰酸萘酯(ANIT)诱导的急性肝内胆汁淤积幼鼠胃肠激素的影响,探讨其干预胆汁淤积的可能机制.方法 SD幼鼠72只随机分为对照组(8只)、中毒组(32只)、干预组(32只).适应性喂养3 d后,中毒及干预组大鼠一次性灌服ANIT(200 mg/kg)诱导急性肝内胆汁淤积;干预组于ANIT灌胃前2 d,每天灌服双歧三联活菌片[4.2×108个活菌/(kg·d)].观察各组在灌服ANIT后48、96、144、192 h各时间点胆汁流量、血总胆红素(TB)、ALT及胃动素(MTL)、血管活性肠肽(VIP)的变化.应用SPSS 12.0软件对资料进行统计学分析.结果 1.灌服ANIT后48 h中毒及干预组胆流中断,血清TB和ALT水平明显升高,但干预组较中毒组程度轻.48 h后胆汁流量、TB和ALT逐渐恢复,干预组在144 h恢复正常,中毒组192 h基本恢复.2.ANIT灌胃后48 h,中毒、干预组血浆MTL水平较对照组明显降低, VIP较对照组明显升高,但干预组较中毒组程度轻;48 h后,MTL、VIP逐渐恢复,但干预组较中毒组恢复快.另外,在192 h干预组MTL较对照组升高,VIP较对照组降低.结论 双歧三联活菌片能够通过其中的双歧杆菌、乳酸杆菌调节胃肠激素的分泌,从而促进肠道运动,有助于胆汁淤积的恢复.     

急性肝内胆汁淤积大鼠小肠上皮紧密连接蛋白ZO-1和Occludin表达的变化

目的 研究急性肝内胆汁淤积大鼠小肠上皮细胞紧密连接蛋白ZO-1和Occludin表达的变化及其发病机制.方法　雄性21日龄SD大鼠40只随机分为空白对照组(10只)和模型组(30只).模型组大鼠采用α-异硫氰酸萘酯50 mg·kg-1一次性灌胃,建立急性肝内胆汁淤积动物模型.空白对照组只灌服等量蓖麻油.于灌胃后24 h、48 h、72 h采用免疫组织化学和Western blot法检测其末端回肠黏膜紧密连接蛋白ZO-1和Occludin的分布和表达,并利用检测分析系统对Western blot图像结果进行定量分析.结果　ZO-1蛋白和Occludin蛋白主要沿大鼠小肠黏膜上皮细胞膜的顶端呈线状分布.模型组大鼠24 h时ZO-1蛋白和Occludin蛋白的阳性染色较空白对照组减少,48 h减少最为明显,72 h阳性染色有所恢复.Western blot结果与免疫组织化学结果一致,模型组24 h已开始下降(ZO-1:0.129 4±0.048 1,Occludin:0.195 0±0.044 1),48 h最低(ZO-1:0.039 5±0.009 5,Occludin:0.013 7±0.009 2),72 h开始恢复(ZO-1:0.202 4±0.049 8,Occludin:0.149 4±0.035 5),模型组各时间点ZO-1与Dccludin与空白对照组(ZO-1:0.288 7±0.023 7,Occludin:0.426 6±0.067 0)比较差异均有统计学意义(Pa＜0.01).结论　急性肝内胆汁淤积大鼠小肠黏膜上皮存在紧密连接蛋白分布异常及数量改变,影响肠黏膜上皮屏障的完整性,破坏小肠黏膜屏障.     

抗氧自由基药物对急性肝功能衰竭大鼠血清IL-18的影响

目的了解IL-18与急性肝功能衰竭(AHF)的关系,探讨不同剂量还原型谷胱甘肽(GSH)治疗AHF的疗效。方法 Wister雄性大鼠42只随机分组,造模。空白对照(N)组(n=6)不予任何处理;模型对照(MG)组(n=12)每日静脉注射生理盐水,共5 d;大剂量治疗(GSH1)组(n=12)、小剂量(GSH2)组(n=12)每日分别静脉注射GSH 600 mg/kg、200 mg/kg,共5 d。于造模后24 h、48 h、72 h、7 d各组测定血清ALT、AST及IL-18值。结果各组大鼠造模后,24 h血清ALT、AST明显升高,48 h血清ALT、AST达到最高水平,以后各组存活大鼠血清ALT、AST逐渐下降,7 d时与N组相比差异仍有统计学意义(P0.05),GSH1组血清AST与N组相比差异无统计学意义(P0.05),而GSH1组、GSH2组与MG组相比24 h、48 h有统计学意义(P0.05),72 h、7 d差异无统计学意义(P0.05)。GSH1组和GSH2组相比,ALT 24 h、48 h有统计学意义(P0.05),AST 48 h有统计学意义(P0.05),两者其余时点差异无统计学意义(P0.05)。各组大鼠造模后,24 h血清IL-18明显升高,48 h达最高水平,以后各组存活大鼠血清IL-18逐渐下降,7 d时仍高于N组(P0.05)。GSH1组、GSH2组与MG组相比,48 h、72 h、7 d差异有统计学意义(P0.05),24 h差异无统计学意义(P0.05),GSH1组与GSH2组相比48 h差异有统计学意义(P0.05),其余时点差异均无统计学意义(P0.05)。结论 IL-18与AHF关系密切,IL-18可作为AHF的监测指标之一;早期应用大剂量抗氧自由基药物GSH能明显改善AHF大鼠的肝功能,促进受损肝细胞修复、再生。     

内质网应激相关因子CCAAT/增强子结合蛋白同源蛋白及Caspase-12在癫(癎)性脑损伤大鼠中的表达及促红细胞生成素对其影响

目的 在建立氯化锂-毛果芸香碱癫(痫)持续状态模型的基础上,观察内质网应激相关因子CCAAT/增强子结合蛋白同源蛋白(CHOP)和Caspase-12的表达变化,探讨促红细胞生成素(EPO)产生脑保护作用的可能机制.方法 21 ～30 d SD大鼠96只随机分为对照组(n=32)、氯化锂-毛果芸香碱癫(癎)组(n=32)及EPO干预组(n=32),每组按6h、24 h、48 h、72 h时间点又分为4个亚组,每亚组8只.观察各组大鼠的行为学变化,用免疫组织化学法检测各时间点各组大鼠CHOP及Caspase-12的表达水平.结果 氯化锂-毛果芸香碱癫(痫)组大鼠海马区CHOP的表达水平明显增加,6h开始增加,24h达到高峰,后逐渐下降,至72 h仍高于对照组,与对照组同一时间点比较差异均有统计学意义(Pa＜0.05);氯化锂-毛果芸香碱癫(痫)组大鼠海马区Caspase-12的表达水平在6h开始增加,48 h达到高峰,72 h开始下降,但仍高于对照组,与对照组同一时间点比较差异均有统计学意义(Pa＜0.05).EPO干预组海马区CHOP及Caspase-12的表达较同一时间点氯化锂-毛果芸香碱癫(癎)组均下降,差异有统计学意义(Pa＜0.05).结论 CHOP和Capase - 12在癫(癎)发作后表达明显增加,提示内质网应激机制在癫(癎)性脑损伤的发生发展中具有重要作用;EPO可能通过内质网应激机制产生脑保护作用.     

组蛋白乙酰化/去乙酰化失衡对平面细胞极性途径关键基因影响的研究

目的观察组蛋白乙酰化/去乙酰化失衡对胎鼠心脏的致畸作用及对H9C2心肌细胞平面细胞极性(PCP)途径关键基因Vangl2、Scrib、Rac1表达的影响。方法将40只C57/B6孕小鼠随机分为空白对照组(n=10)、溶剂对照组(n=10)和丙戊酸(VPA)组(n=20);应用组蛋白去乙酰化酶(HDAC)抑制剂VPA单次剂量700 mg/kg腹腔注射妊娠第10.5天(E10.5 d)VPA组孕鼠,溶剂对照组孕鼠腹腔注射等量生理盐水,空白对照组不做任何处理。于E15.5 d处死孕鼠,统计死胎率;取活胎鼠心脏行苏木精-伊红(HE)染色,观察VPA对胎鼠心脏的致畸作用。培养H9C2心肌细胞并将其分为空白对照组、溶剂对照组和VPA组,VPA组以不同浓度(2.0、4.0、8.0 mmol/L)作用于H9C2心肌细胞,溶剂对照组加入等量生理盐水,空白对照组不进行任何处理。实时荧光定量PCR和Western blot检测HDAC1~3及Vangl2、Scrib、Rac1基因在VPA干预后24、48、72 h mRNA及其蛋白表达水平;比色法测定总HDAC活性变化。结果 VPA组胎鼠死亡率为31.7%,心脏畸形发生率显著高于两对照组(P0.05)。与两对照组相比,不同浓度VPA干预后各时间点,HDAC1 mRNA表达水平均显著升高(P0.05),而蛋白表达水平于48 h及72 h显著降低(P0.05);不同浓度VPA干预后,HDAC2 mRNA仅在24 h表达显著下降(P0.05),而蛋白表达水平在各时间点均显著下调(P0.05);HDAC3 mRNA在VPA(4.0 mmol/L、8.0 mmol/L)干预的各时间点均表达增高(P0.05),而蛋白表达水平在不同浓度VPA干预后各时间点均下调(P0.05)。与两对照组相比,不同浓度VPA干预后,Vangl2、Scrib mRNA及其蛋白表达水平在48 h、72 h均显著下降(P0.05),Vangl2蛋白表达仅在72 h降低(P0.05)。与两对照组相比,VPA(4.0及8.0 mmol/L)干预后24 h,总HDAC活性显著降低(P0.05);干预后48 h、72 h,不同浓度VPA组总HDAC活性均明显降低(P0.05)。结论 VPA可能通过直接抑制HDAC1~3蛋白表达水平及总HDAC活性致乙酰化/去乙酰化失衡,从而导致PCP途径关键分子Vangl2、Scrib mRNA及蛋白表达水平下调,这可能是先天性心脏病发生的机制之一。     

心脉隆对窒息新生鼠心肌缺氧诱导因子-1α的影响

目的：心脉隆是从昆虫类美洲大蠊中提取和制备的化合物,主要用于心血管疾病的治疗。该文研究心脉隆对窒息新生鼠心肌缺氧诱导因子-1α(HIF-1α)与血浆内皮素1（ET-1）的影响,探讨心脉隆对心肌缺氧缺血性损伤的保护机制。方法：新生7日龄Sprague-Dawley大鼠随机分为假手术组(n=30)、窒息组(n=30)、心脉隆组(n=30)。每组再分6 h,24 h,72 h 3个时间点,每个时间点各10只,心脉隆组在进行窒息前5 min给予心脉隆注射液5 mg/kg腹腔注射。检测新生鼠心肌的HIF-1α,ET-1,心肌酶CK及心肌组织病理学。结果：窒息组4只鼠死亡,心脉隆组1只鼠死亡。窒息组心肌HIF-1α的表达与血浆ET-1水平于6 h升高,24 h达到高峰,72 h下降,均高于假手术组(P＜0.01);3个时间点均可见心肌缺血,24 h还可见细胞坏死;HIF-1α的表达与血浆ET-1水平呈正相关(r=0.876,P＜0.01)。与窒息组同时间点比较,心脉隆组心肌酶CK、血浆ET-1的水平和心肌HIF-1α的表达均显著减低(P＜0.01),且可见心肌缺血改善,未见细胞坏死。结论：窒息时心肌HIF-1α表达和血浆ET-1,CK水平升高;心脉隆可降低HIF-1α表达,降低血浆ET-1的水平,减轻心肌缺氧缺血性损伤。［中国当代儿科杂志,2009,11（8）：683-686］     

Allergic factors associated with the development of asthma and the influence of cetirizine in a double-blind, randomised, placebo-controlled trial: First results of ETA®

There is a common progression known as the allergic march from atopic dermatitis to allergic asthma. Cetirizine has several antiallergic properties that suggest a potential effect on the development of airway inflammation and asthma in infants with atopic dermatitis. Methods. Over a two year period, 817 infants aged one to two years who suffered from atopic dermatitis and with a history of atopic disease in a parent or sibling were included in the ETAC^® (Early Treatment of the Atopic Child) trial, a multi-country, double-blind, randomised, placebo-controlled trial. The infants were treated for 18 months with either cetirizine (0.25mg/ kg b.i.d.) or placebo. The number of infants who developed asthma was compared between the two groups. Clinical and biological assessments including analysis of total and specific IgE antibodies were performed. Results. In the placebo group, the relative risk (RR) for developing asthma was elevated in patients with a raised level of total IgE (≥ 30 kU/I) or specific IgE (≥ 0.35 kUA/I) for grass pollen, house dust mite or cat dander (RR between 1.4 and 1.7). Compared to placebo, cetirizine significantly reduced the incidence of asthma for patients sensitised to grass pollen (RR = 0.5) or to house dust mite (RR = 0.6). However, in the population that included all infants with normal and elevated total or specific IgE (intention-to-treat - ITT), there was no difference between the numbers of infants developing asthma while receiving cetirizine or placebo. The adverse events profile was similar in the two treatment groups. Discussion. Raised total IgE level and raised specific IgE levels to grass pollen, house dust mite or cat dander were predictive of subsequent asthma. Cetirizine halved the number of patients developing asthma in the subgroups sensitised to grass pollen or house dust mite (i.e. 20% of the study population). In view of the proven safety of the drug, we propose this treatment as a primary pharmacological intervention strategy to prevent the development of asthma in specifically sensitised infants with atopic dermatitis.     

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孤独症谱系障碍(autistic-spectrum disorders,ASDs)近年来患病率逐年攀升至1%左右,其症状往往伴随终生,成为严重威胁儿童健康和发展的神经发育性疾患;注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是儿童期最常见的精神障碍,国内报道患病率为4.13%～5.83%,其症状可延续至青少年期,甚至到成年期[1]。这两类精神障碍在成年期的临床表现、共患病、治疗策略和预后与儿童期有哪些不同呢?本文通过回顾相     

Infiltrations of Epstein-Barr virus-carrying cells in granular lymphocyte-proliferative disorders corresponding to chronic active Epstein-Barr virus infection

A 21-year-old man with granular lymphocyte-proliferative disorders (GLPD) associated with chronic active Epstein-Barr virus (EBV) infection is described. Chromosomal analyses revealed several clonal abnormalities and two of them were mainly repetitious. High copy numbers of monoclonal EBV genome were also detected in the proliferative large granular lymphocytes (LGLs), indicating the monoclonal expansion of EBV-infected LGLs. The patient had an indolent course for several years, and there was no evidence of infiltrations of his bone marrow until the end stage. At autopsy, microscopic studies revealed marked infiltrations of LGL in the liver and spleen, and the infiltrating cells were NK-cell immunophenotype. The infiltrated LGLs showed latency I.     

LUTEINIZING HORMONE RECEPTOR MUTATIONS IN DISORDERS OF SEXUAL DEVELOPMENT AND CANCER

Human male sexual development is regulated by chorionic gonadotropin (CG) and luteinizing hormone (LH). Aberrant sexual development caused by both activating and inactivating mutations of the human luteinizing hormone receptor (LHR) have been described. All known activating mutations of the LHR are missense mutations caused by single base substitution. The most common activating mutation is the replacement of Asp-578 by Gly due to the substitution of A by G at nucleotide position 1733. All activating mutations are present in exon 11 which encodes the transmembrane domain of the receptor. Constitutive activity of the LHR causes LH releasing hormone-independent precocious puberty in boys and the autosomal dominant disorder familial male-limited precocious puberty (FMPP). Both germline and somatic activating mutations of the LHR have been found in patients with testicular tumors. Activating mutations have no effect on females. The molecular genetics of the inactivating mutations of the LHR are more variable and include single base substitution, partial gene deletion, and insertion. These mutations are not localized and are present in both the extracellular and transmembrane domain of the receptor. Inactivation of the LHR gives rise to the autosomal recessive disorder Leydig cell hypoplasia (LCH) and male hypogonadism or male pseudohermaphroditism. Severity of the clinical phenotype in LCH patients correlates with the amount of residual activity of the mutated receptor. Females are less affected by inactivating mutation of the LHR. Symptoms caused by homozygous inactivating mutation of the LHR include polycystic ovaries and primary amenorrhea.     

EXCITING NEW TREATMENT APPROACHES FOR PATHYPHYSIOLOGIC MECHANISMS OF SICKLE CELL DISEASE

During the past several decades, our understanding of the complex pathophysiology of vasoocclusion associated with sickle cell disease has improved greatly. Interaction of genes, hemoglobin molecules, red cell membrane and metabolic changes, cell-cell interactions and cell-plasma interactions, red cell adhesion to vascular endothelium, activation of coagulation, and vascular reactivity play a role in vaso occlusion. Penicillin prophylaxis of pneumococcal infections and appropriate use of blood transfusions and other supportive measures improved survival of sickle cell patients. Hydroxyurea made a major impact on sickle cell therapy when it was shown to decrease acute painful episodes, acute chest syndrome, and the need for blood transfusion in adults. Significant experience in the use of hydroxyurea has been accumulated in older children. The benefits and risks of hydroxyurea for younger children and long-term risks in all patients will be evaluated in future investigations. Other promising therapies include butyrate compounds, clotrimazole, magnesium supplementation, poloxamer 188, antiadhesion agents, anticoagulant approaches, and nitric oxide. Hemopoietic transplantation remains the only curative therapy. However, several transgenic mouse models are available for studies of gene therapy or other treatment approaches on biochemical, cellular, and pathologic effects of mutant genes.     

Bibliometric data: a disaster for many non-American biomedical journals

Bibliometric data published by the Institute of Scientific Information in Philadelphia (ISI), and which was previously discussed in Acta Paediatrica , has increasingly been used despite all the relevant and severe criticism that has been raised against this method of evaluating individual research results and grading scientific journals. It is obvious that the present trend regarding the use of bibliometric data as a basis for priorities and funding of research and for the promotion of individual scientists favours American-oriented research projects at the expense of those that are based on concepts of predominantly European relevance.

Conclusion: For the future of non-American research, it is important that no single super-power, i.e. the USA, should dominate scientific priorities. The condition for efficient European competition is that European Centres with high levels of competence for creative research and training of scientists from all over the world are established. In addition, it is important that the results of European research are published in prestigious European journals, as was the situation before World War II.     

Personality profiles and heart rate variability (vagal tone) in children with recurrent abdominal pain

The aim of the study was to explore psychological factors and autonomic activity in children with recurrent abdominal pain and to compare them with those in a control group of healthy children. The Personality Inventory for Children was used for assessment of developmental, emotional and psychosocial factors in 25 children with recurrent abdominal pain (age, 7-15 y). Parasympathetic and sympathetic functions in these children and in 23 healthy control subjects (age, 7-13 y) were also investigated, non-invasively using a computerized polygraph. Vagal tone (parasympathetic function) was indexed by calculation of respiratory sinus arrhythmia in beats/min. Skin conductance (sympathetic function) was recorded by the constant current method. On the Personality Inventory for Children, 16 patients had high scores on somatic concern. Several patients had scores in the clinical range for depression, withdrawal and anxiety, but the mean scores for these personality profile scales were well within the normal range of healthy children. Interestingly, there was a spike on the L (Lie)-scale for most of the patients and 15 patients had scores above or close to the clinical cut-off value. As compared with the scores in healthy children, vagal tone and sympathetic tone were normal. Conclusion: Many children with recurrent abdominal pain have scores in the clinical range for depression, withdrawal, anxiety and L-scale indicating coping problems, denial and a trend towards somatic concern that may contribute to the evolution of abdominal pain. Autonomic nerve activity was not disturbed in these children.     

Understanding infant formula

The World Health organisation recommends breast feeding infants for the first six months of life. When this breast feeding does not occur either through parental choice or medical need, infant formulas will be required. There is a bewildering array of formulas on the UK market for many different requirements. When faced with an unsettled infant many parents (and healthcare professionals) will experiment with the infant formula available and then attend the paediatric clinic looking for help and advice. It is therefore essential that paediatricians understand what milks are available and what the key differences between different products are. This review attempts to provide a simple guide through many of the formulations currently available in the UK; and offers advice for the dietary management of the child with extra calorie requirements, infants with cow's milk protein allergy, gastro oesophageal reflux disease, apparent unresolved hunger and infantile colic. Whatever the underlying condition, there is likely to be an infant formula that is suitable in this generation of ever expanding formulations.     

Overcoming surfactant inhibition with polymers

Inhibition of the function of pulmonary surfactant in the alveolar space is an important element of the pathophysiology of many lung diseases, including meconium aspiration syndrome, pneumonia and acute respiratory distress syndrome. The known mechanisms by which surfactant dysfunction occurs are (a) competitive inhibition of phospholipid entry into the surface monolayer (e.g. by plasma proteins), and (b) infiltration and destabilization of the surface film by extraneous lipids (e.g. meconium-derived free fatty acids). Recent data suggest that addition of non-ionic polymers such as dextran and polyethylene glycol to surfactant mixtures may significantly improve resistance to inhibition. Polymers have been found to neutralize the effects of several different inhibitors, and can produce near-complete restoration of surfactant function. The anti-inhibitory properties of polymers, and their possible role as an adjunct to surfactant therapy, deserve further exploration.