黄芩苷预处理对实验性自身免疫性脑脊髓炎大鼠的神经保护作用及机制

目的 探讨黄芩苷(BAC)预处理对实验性自身免疫性脑脊髓炎(EAE)大鼠神经元凋亡及核因子(NF)-κB P65蛋白和mRNA表达的影响,探讨神经元凋亡的调节机制.方法 健康Wistar大鼠随机分为对照组、EAE组、地塞米松(DXM)组、BAC组.各组于EAE模型制作当日分别给予预处理,每日1次,共7 d.观察各组发病率,记录神经功能评分.分别于第7、14、21天处死大鼠,留取脊髓行NF-κB P65免疫组化染色,TUNEL法检测神经元凋亡,提取总RNA检测NF-κB P65 mRNA的表达.结果 (1)对照组大鼠无发病,DXM组和BAC组发病率分别为56.25%、50.00%,较EAE组(87.50%)明显降低,差异有非常显著性(P＜0.01).DXM组、BAC组神经功能评分分别为1.56±0.34、1.46±0.20,与EAE组(2.78±0.31)相比明显降低,差异有非常显著性(P＜0.01).(2)对照组各时间点凋亡神经元少见,EAE组3个时间点神经元凋亡指数(AI)分别为23.25±1.82、63.00±4.66和31.50±3.63,DXM组为16.75±1.28、33.88±1.46及22.00±2.45,BAC组为15.25±1.67、34.25±3.28及21.88±3.09,差异有非常显著性(P＜0.01).(3)对照组偶见NF-κB P65阳性神经元.在3个时间点,EAE组、DXM组和BAC组脊髓内神经元NF-κB P65阳性率均较EAE组明显减低,差异有显著性(P＜0.05).(4)在3个时间点,对照组脊髓内NF-κB P65 mRNA灰度比值变化不明显.DXM组和BAC组脊髓内神经元NF-κB P65 mRNA灰度比值均较EAE组明显下降,差异均有非常显著性(P＜0.01).结论 BAC预处理能明显抑制大鼠脊髓内NF-κB P65的活化,减少神经元的凋亡,起到神经保护作用.     

miRNA338调节人神经母细胞瘤细胞中CXCR4表达的研究

目的 微小RNA( microRNA,miRNA)是一类非编码小分子RNA组成的家族,能够通过降解靶mRNA或抑制其翻译过程参与调节基因表达.本研究旨在探索上调miR338水平后人神经母细胞瘤细胞系SH-SY5Y中CXCR4表达变化,进而了解miR338调节神经母细胞瘤侵袭与转移的分子机制.方法 将人工合成的成熟miR338前体(pre-mir-338)转染入SH-SY5Y细胞,而后利用实时荧光定量RT-PCR检测转染前后各组细胞miR338的表达水平.应用半定量RT-PCR及Western蛋白印迹法分别从mRNA水平、蛋白水平检测各实验组CXCR4的表达变化.结果 实时荧光定量PCR法检测对照组及各实验组细胞miR338基因含量,发现转染了pre-mir-338的10 nM,30 nM,50 nM,100 nM组miR338含量分别为空白对照组的1.32倍,1.62倍,1.90倍及1.86倍,差异具有统计学意义(P＜0.05),成功将pre-mir-338转染入细胞达到miR338过表达的目的；转染组(10 nM组、30 nM组、50nM组)CXCR4基因mRNA相对光密度值分别为0.75±0.06,0.58±0.08,0.24±0).05,依次降低,均明显低于空白对照组1.11±0.08,空载对照组1.04±0.08(P＜0.05).转染组CX-CR4蛋白0).24±0.06较未转染组0.56±0.08降低(P＜0.05).结论 miR338能够通过下调神经母细胞瘤细胞CXCR4 miRNA及蛋白的表达参与调节肿瘤的侵袭与转移,人工合成的pre-mir-338有望通过替代方式为神经母细胞瘤的治疗提供新的途径.     

重组人促红细胞生成素对新生大鼠高体积分数氧肺损伤的防治效果

目的 探讨重组人促红细胞生成素(rhEPO)对新生大鼠高体积分数氧(高氧)肺损伤的防治作用.方法 新生SD大鼠96只随机分为:空气加9 g/L盐水组(Ⅰ组),空气加rhEPO组(Ⅱ组),高氧加9 g/L盐水组(Ⅲ组),高氧加rhEPO组(Ⅳ组).Ⅲ、Ⅳ组新生大鼠暴露于950 mL/L氧气中,Ⅱ、Ⅳ组新生大鼠于暴露第2、4、6天予rhEPO 800 U/kg腹部皮下注射.在暴露第3、7、14天,各组分别取8只处死,HE染色观察其肺组织结构变化,双抗体夹心法测定其肺组织IL-8.Western blot检测其核因子-κB(NF-κB)p65蛋白水平.结果 与Ⅰ组比较,随高氧暴露时间延长,Ⅲ组第3天出现肺泡炎性反应渗出,第7天更为明显,第14天肺泡数量减少,大小不均,肺大泡形成;Ⅳ组病理改变减轻,炎性反应细胞浸润减少.Ⅳ组第7、14天肺组织核因子-κB(NF-κB)p65水平较Ⅲ组显著减少[(0.28±0.07)%vs(0.35±0.07)%,(0.27±0.05)%vs(0.33±0.06)% Pa<0.05],其肺组织匀浆中IL-8水平较Ⅲ组有所减少[(112.38±32.08)ng/L vs (158.0±37.33)ng/L,(98.78±29.66)ns/L vs (170.88±42.26)ng/L Pa<0.05].结论 rhEPO对新生大鼠高氧肺损伤有保护作用,机制可能与抑制NF-κB活化、减少IL-8分泌有关.     

胆红素对大鼠星形胶质细胞和神经元核因子-κB／IκBα表达的影响

目的探讨胆红素是否影响大鼠星形胶质细胞和神经元核因子(NF)-κB的活化。方法 100μmol／L胆红素分别作用于原代培养大鼠星形胶质细胞和神经元,于0、30、60及120min收集标本,免疫细胞化学染色检测NF-κB亚基P65核移位、western Blot检测NF-κB抑制因子IκBα蛋白表达。结果胆红素干预星形胶质细胞30 min时,出现P65大量核移位(91.0±5.9)％,至60 min核移位率显著下降(50.03±9.69)％,120 min时核移位恢复至干预前水平。30 min时IκBα蛋白表达消失,至30 min、60 min均有蛋白明显表达；神经元各组间P65核移位和IκBα蛋白表达差异均无显著性。结论胆红素可诱导星形胶质细胞NF-κB活化。     

核因子-κB活性变化在早产儿脑室周围白质软化中的作用

目的 探讨核因子-κB(NF-κB)在早产儿脑室周围白质软化(INL)发病机制中的作用,为早产儿PVL的预防和治疗提供依据.方法 经头颅B超诊断为PVL的早产儿25例,并根据PVL病变程度分为Ⅰ、Ⅱ级PVL组17例(男9例,女8例),Ⅲ、Ⅳ级PVL组8例(男5例,女3例);对照组23例为同期住院未并PVL的早产儿,男12例,女11例.二组分别取脐血或出生6 h内静脉血2 mL,应用ELISA测定其血单核细胞NF-κB活性.结果 1.Ⅰ、Ⅱ级PVL组早产儿外周血单核细胞NF-κB活性(0.951±0.325)与对照组(0.694±0.281)比较,有显著性差异(P<0.05);2.Ⅰ、Ⅱ级PVL组早产儿外周血单核细胞NF-κB活性与Ⅲ、Ⅳ级PVL组(1.372±0.330)比较,亦有显著性差异(P<0.01).结论 PVL早产儿外周血NF-κB活性增高,且PVL病变越重,NF-κB活性越高,提示NF-κB作为多种炎性反应信号转导途径的汇聚点,在早产儿PVL损伤过程中可能发挥着重要作用.     

RNA干扰趋化因子受体4基因表达对神经母细胞瘤体外侵袭能力的影响

目的 构建趋化因子受体4(CXCR4)小分子干扰RNA(siRNA)表达载体,研究其对体外神经母细胞瘤侵袭能力的影响.方法 选择CXCR4高表达的神经母细胞瘤SH-SY5Y细胞系,设计合成人CXCR4基因不同靶点的能编码siRNA的3条双链DNA序列,克隆到真核表达载体pSilencerTMneo中构建siRNA表达载体,体外脂质体介导转染SH-SY5Y细胞,用半定量RT-PCR分析CXCR4基因mRNA的变化,用免疫组织化学和Western blot分析CXCR4蛋白表达,Transwell小室检测细胞的侵袭能力.结果 成功构建了CXCR4-siRNA表达载体,转染后半定量RT-PCR检测神经母细胞瘤细胞CXCR4 mRNA丰度分别为siR1转染组0.32±0.09、siR2转染组0.35±0.13和siR3转染组0.33±0.11,相对于对照组0.58±0.13表达下降(P＜0.05);转染后免疫组化检测神经母细胞瘤细胞CXCR4的蛋白表达分别为siR1转染组75.98±4.81、siR2转染组75.52±3.95和siR3转染组76.35±6.51,相对于对照组92.196±3.89表达下降(P＜0.01);转染后Western b1ot检测神经母细胞瘤细胞CXCR4的蛋白表达分别为siR1转染组0.1103±0.0023、siR2转染组0.1203±0.015和siR3转染组0.1308±0.0018,相对于对照组0.4832±0.0012表达下降(P＜0.01);且转染后神经母细胞瘤细胞侵袭能力较对照组53.11±3.72降低(P＜0.05),siR1转染组为25.48±2.81、siR2转染组为30.89±2.77、siR3转染组为18.83±1.79.结论 CXCR4-siRNA表达载体通过降低CXCR4基因的蛋白表达能显著抑制神经母细胞瘤细胞的体外侵袭能力,有望为神经母细胞瘤的基因治疗开辟新途径.

Abstract：

Objective To explore the effect of silencing chemokine receptor type 4 (CXCR4) by siRNA on the invasion capability of neuroblastoma cell line SH-SY5Y in vitro. Methods Three siRNAs targeting CXCR4 were chemically synthesized and transfected into SH-SY5Y cells. The transfection efficiency was observed under fluorescence microscope. CXCR4 expression at mRNA and protein levels were detected by semi-quantitative RT-PCR and Western blotting. The invasion capability of the cells was evaluated by Boyden Chamber in vitro. Results Compared with control groups, after the SH-SY5Y cells being transfeeted with the three CXCR4 targeting siRNAs, CXCR4 mRNA in transfected cells significantly decreased (0. 32 ± 0. 09, 0. 35 ± 0. 13 and 0. 33 ± 0. 11 vs 0. 58 ± 0. 13, P＜0. 05 ), CXCR4 protein detected by immunohistochemistry was decreased (75. 98 ± 4. 81, 75. 52 ± 3. 95and 76. 35 ± 6. 51 vs 92. 196 ± 3. 89, P＜0. 01 ), CXCR4 protein detected by Western blotting was also decreased (0. 1103 ± 0. 0023, 0. 1203 ± 0. 0015 and 0. 1308 ± 0. 0018 vs 0. 4832 ± 0. 0012, P＜0. 01 ).The invasion capability of the SH-SY5Y cells was decreased 48 hours after the cells were transfected (25.48±2.81, 30.89±2.77 and 18.83± 1.79 vs 53. 11 ±3.72, P＜0.05). Conclusions Silencing CXCR4 by siRNA decreases the invasion capability of SH-SY5Y cells.     

NF-κB经典信号通路介导铁过载对沙鼠心肌细胞线粒体的损伤

目的通过检测铁过载沙鼠心肌细胞内NF-κB经典信号通路关键物质的水平及电镜观察线粒体损伤程度,探索NF-κB经典信号通路是否介导了铁过载损伤心肌细胞线粒体的过程。方法将24只蒙古沙鼠随机分为4组,分别为对照组(不进行任何干预)、溶剂对照组(腹腔注射生理盐水)、铁过载组(腹腔注射右旋糖酐铁16周)及铁过载+PDTC组(腹腔注射右旋糖酐铁,同时注射PDTC 16周)。Western blot方法检测心肌细胞中NF-κB经典信号通路的关键物质IκB-α、p-IκB-α、胞浆p65及胞核p65的水平;电镜观察各组心肌细胞线粒体形态学改变并行Flameng评分。结果 (1)与其它3组比较,铁过载组p-IκB-α、胞浆p65水平降低,胞核p65水平明显增高,差异有显著性(P0.05);(2)铁过载组线粒体Flameng评分高于其它3组,差异有显著性(P0.05);铁过载+PDTC组线粒体Flameng评分高于对照组和溶剂对照组,但低于铁过载组,差异有显著性(P0.05)。结论铁过载能够激活沙鼠心肌细胞NF-κB经典信号通路,从而损伤心肌细胞线粒体。     

靶向小干扰RNA抑制人神经母细胞瘤裸鼠荷瘤生长及转移的实验研究

目的 探讨靶向CXCR4的小干扰RNA(siRNA)对人神经母细胞瘤QDDQ-NM细胞裸鼠肿瘤的生长及转移的抑制作用.方法 采用本实验室已成功建立QDDQ-NM裸鼠荷瘤模型,以CXCR4为靶基因,设计合成siRNA序列及对照序列HK.通过瘤体局部多位点注射,将CXCR4-siRNA转染到裸鼠皮下荷瘤内.A组(阳性治疗组),B组(阴性治疗组),同时设立空载体对照组(C组)和空白对照组(D组).观察肿瘤的转移及治疗前后体积变化,并用RT-PCR方法及免疫组化方法检测CXCR4的基因转录及蛋白表达情况,来评价CXCR4-siRNA对肿瘤的作用.结果 A组转移率为25％明显小于其余3组对照组(75％,58％,75％),其肿瘤体积也显著低于其余3组,利用RT-PCR检测CXCR4基因在转录水平的表达,A组为1.0451±0.0778,B、C、D组分别为1.4286±0.0655、1.3839±0.0037、1.3882±0.0733(P＜0.05),A组CXCR4蛋白表达水平也显著低于B、C、D组(P＜0.05).结论脂质体介导的CXCR4-siRNA对神经母细胞瘤的生长及转移有明显抑制作用,可为下一步肿瘤治疗提供基础.     

姜黄素对哮喘小鼠体内NF-κB、IκB及p-IκB含量的影响

目的 了解姜黄素对哮喘小鼠核因子(NF)-κB、IκB、p-IκB的含量的影响.方法 对30只Balb/c小鼠随机分组,分为正常对照组、哮喘组及姜黄素干预哮喘小鼠.应用卵清蛋白溶液建立哮喘小鼠模型;对各组小鼠进行肺功能的检测;检测各组肺组织中的NF-κB、IκB及p-IκB的含量.结果 哮喘组胞浆内NF-κB较对照组减少(P＜0.01),而姜黄素干预组胞浆内NF-κB含量较哮喘组明显增加,具有统计学意义(P＜0.05).哮喘组胞核内NF-κB较对照组明显增加(P＜0.01),而姜黄素干预组胞核内NF-κB较哮喘组明显减少,差异具有统计学意义(P＜0.05).哮喘组胞浆内的p-IκB含量显著高于对照组(P＜0.01),而姜黄素干预组胞浆内的p-IκB含量显著低于哮喘组,差异具有统计学意义(P＜0.01).哮喘组胞浆内的IκB含量显著低于对照组(P＜0.01),而姜黄素干预组IκB含量较哮喘组显著增高,差异具有统计学意义(P＜0.01).结论 姜黄素通过减轻IκB的磷酸化抑制NF-κB转录入核内,从而减轻哮喘小鼠的气道高反应性.     

胆红素对大鼠星形胶质细胞和神经元核因子-κB/IκBα表达的影响

目的探讨胆红素是否影响大鼠星形胶质细胞和神经元核因子(NF)-κB的活化.方法 100μmol/L胆红素分别作用于原代培养大鼠星形胶质细胞和神经元,于0、30、60及120min收集标本,免疫细胞化学染色检测NF-κB亚基P65核移位、Western Blot检测NF-κB抑制因子IκBα蛋白表达.结果胆红素干预星形胶质细胞30 min时,出现P65大量核移位(91.0±5.9)%,至60 min核移位率显著下降(50.03±9.69)%,120 min时核移位恢复至干预前水平.30 min时IκBα蛋白表达消失,至30 min、60 min均有蛋白明显表达;神经元各组间P65核移位和IκBα蛋白表达差异均无显著性.结论胆红素可诱导星形胶质细胞NF-κB活化.     

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.     

�¶�֢��ϵ�ϰ���ע��ȱ�ݶද�ϰ������ڵ�ת��

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.