乙烯硫脲致畸胎鼠直肠末端Gli2基因的表达

目的　探讨乙烯硫脲致畸胎鼠直肠末端sonichedgehog(Shh)基因转录因子Gli2基因表达水平。方法　妊娠Wistar大鼠 2 4只随机分成 2组 ,实验组 (n =12 )在孕 11、13d分别给予 1%乙烯硫脲 (12 5mg/kg)胃管注入 ,对照组 (n =12 )予等量蒸馏水。孕 16d处死母鼠 ,实验组每只母鼠取 4只体质量相似的无肛畸形胎鼠 ,对照组取 4只体质量相似正常胎鼠 ,各取其直肠末端 1cm提取RNA ,采用RT PCR法检测Gli2基因表达 ,比较两组之间Gli2基因表达水平。结果　先天性无肛胎鼠直肠末端Gli2基因表达水平明显低于正常胎鼠直肠末端 (P =0 .0 0 4)。结论　Gli2基因表达水平减低与先天性无肛畸形的发生密切相关 ,乙烯硫脲致畸机制之一是影响Shh信号转导系统。     

先天性肛门直肠畸形胎鼠直肠末端NGF及受体TrkA与p75的表达

目的 观察神经生长因子(NGF)及其受体TrkA、p75在先天性肛门直肠畸形(ARM)动物模型胎鼠直肠末端的表达及分布.方法 选用成年SD孕鼠16只,实验组10只,对照组6只,实验组在孕11d及13d时分别以1％乙烯硫脲(125mg/kg)灌胃制作ARM动物模型,对照组灌入等量生理盐水,两组孕鼠在孕20 d手术取出宫内胎鼠,进行形态学观察及畸形率统计,并取胎鼠盆腔、会阴部矢状面大体标本HE染色及直肠末端石蜡包埋切片,免疫组化检测NGF及其受体TrkA、p75在正常胎鼠和ARM胎鼠直肠末端的分布情况并半定量分析.结果 正常组:胎鼠存活率100％,肛门开口正常,实验组:存活率80.7％,实验组ARM发生率98.7％、短尾畸形5.1％、无尾畸形94.8％、双足内翻6.4％、脊柱裂6.4％,盆腔会阴部矢状切面HE染色显示:ARM胎鼠肛门为一闭合盲端,无正常肛门结构,直肠盲端为增生鳞状上皮组织及增厚的肌层,未见肠腺分布,直肠末端黏膜下及肌间神经丛数量:ARM组为46.40±16.08,对照组为96.33±18.57,两组比较,差异有统计学意义(P＜0.01);免疫组化结果显示:NGF、TrkA、p75主要分布在胎鼠直肠末端黏膜下、肌间神经丛,其中NGF主要分布在细胞核,TrkA分布在细胞质,p75在细胞核、细胞质均有分布,其积分光密度(IOD值):对照组分别为731.75±232.18、262.82±101.72、134.67±67.13,ARM组分别为17.97±74.95、33.15±11.13、113.01±36.47,两组比较,差异有统计学意义(P＜0.01).结论 NGF及其受体TrkA、p75可能共同参与ARM的发生、发展过程.     

Gli2基因在胎鼠后肠发育后期的表达

目的探讨胎鼠后肠发育与sonichedgehog(Shh)基因转录因子Gli2基因表达水平的关系。方法48只妊娠Wistar大鼠随机分成2组,实验组(n=24)在孕11d按125mg/kg胃管注入1%乙烯硫脲(ethylenethiourea,ETU),对照组(n=24)给予等量蒸馏水。两组分别于孕12d、14d和16d各处死8只母鼠,每只母鼠取4只体重相似的胎鼠,取其直肠1cm提取RNA,采用半定量RT_PCR法检测Gli2基因表达。结果实验组胎鼠直肠Gli2基因表达水平明显低于对照组(P<0.05),实验组Gli2基因表达呈一低水平线,而对照组随妊娠时间呈一下降的曲线。结论Gli2基因表达水平在胎鼠后肠发育中具有重要的作用。     

肛门直肠畸形大鼠胚胎后期肠管Cajal间质细胞的研究

目的 研究肛门直肠畸形(ARM)胎鼠胚胎后期16 d(E16)、21d(E21)小肠、结肠和直肠Cajal间质细胞(ICC)的发育情况.方法 体重250～300 g的wistar大鼠,雌雄鼠夜间合笼交配.早晨雌鼠阴道涂片,发现精子被认为是E0.孕鼠随机分成4组,E16对照组孕鼠2只、实验组孕鼠8只,E21对照组孕鼠2只、实验组孕鼠6只.胚胎第10天实验组孕鼠经胃管注入125 mg/kg的ETU,对照组孕鼠经胃管注入等量生理盐水.E16、E21孕鼠腹腔注射10%水合氯醛6 ml/kg,剖宫取出所有胎鼠,辨认胎鼠是否存在畸形及畸形类型.选取对照组胎鼠、实验组无畸形胎鼠和ARM胎鼠,在大体显微镜下解剖整个肠管.选取距盲肠8cm处小肠,距盲肠2咖处结肠,距肛门0.5 cm处直肠各一段.使用c-kit抗体通过SABC免疫组织化学方法研究E16和E2t对照组、实验组乙烯硫脲(ETU)诱导无畸形胎鼠、实验组ETU诱导ARM胎鼠小肠、结肠和直肠c-kit抗体表达情况.结果 E16对照组小肠、结肠、直肠肌间神经从周围可见中等量c-kit抗体染色阳性细胞,肌层部分细胞c-kit抗体染色阳性.E21对照组肌间神经丛周围c-kit抗体染色阳性细胞增多,可见阳性细胞网络形成.E16、E21实验组无畸形胎鼠小肠、结肠、直肠和实验组ARM胎鼠小肠与对照组相比,阳性细胞面积百分比、平均光密度值、积分光密度值和对照组相比,P>0.05,差异无统计学意义.而实验组ARM胎鼠结肠,直肠阳性细胞面积百分比、平均光密度值和积分光密度值明显减小P<0.05,差异有统计学意义.结论 ARM胎鼠胚胎后期小肠ICC发育正常而结肠、直肠ICC发育异常,这可能影响生后肠管ICC网络的形成和功能的发挥,可能是ARM术后便秘的病因之一.     

先天性肛门直肠畸形胎鼠腰骶髓副交感神经元发育异常的研究

目的　探讨先天性肛门直肠畸形是否同时存在副交感神经支配异常以及对术后排便功能的影响。方法　 2 0只Wistar孕鼠 ,分为ETU致畸组 (15只 )和对照组 (5只 )。孕 2 0d时 ,将荧光金注射入正常胎鼠直肠壁及畸形胎鼠的直肠盲端肌层内。荧光显微镜下观察副交感神经元的数量 ,形态和分布。结果　①致畸组胎鼠手术存活率为 6 0 .0 % ,而对照组存活率为 71.4 % ;②对照组 :荧光金标记的副交感神经元位于脊髓侧角 ,分布在L6到S1脊髓节段 ,标记神经元数量为 (90 1± 4 6 )个。神经元体积较大。ETU致畸组中外观正常组、低位畸形组、高位畸形组标记神经元数量分别为 (899± 36个 )、(5 88± 10 2 )个和 (2 4 2± 92 )个 ,畸形组与正常组、外观正常组相比 ,统计学差异显著 ,而且神经元细胞体积明显减小。结论　①先天性肛门直肠畸形胎鼠骶髓副交感神经元数目减少 ,体积减小 ,呈发育不良改变。畸形位置愈高 ,神经元数量减少愈明显 ;②本研究结果提示人类先天性肛门直肠畸形术后便秘的发生可能与副交感神经元数量减少有关。     

TrkA、p75NTR mRNA在肛门直肠畸形胎鼠直肠末端的表达

目的通过检测肛门直肠畸形(ARM)胎鼠直肠末端神经生长因子受体TrkA、p75NTR mRNA的表达水平,探讨ARM直肠末端肠神经系统发育情况。方法成年SD孕鼠16只。其中实验组10只,对照组6只。实验组孕鼠在孕11 d、13 d 2次给予10 g.L-1乙烯硫脲(125 mg.kg-1)灌胃,制作先天性ARM动物模型;对照组灌胃注入等量9 g.L-1盐水。2组孕鼠在孕20 d时行剖宫手术取出胎鼠,取其直肠末端并保存于-80℃冰箱;采用反转录/实时定量PCR(RT-PCR)方法检测正常胎鼠和ARM胎鼠直肠末端TrkA、p75NTR mRNA表达情况。结果 TrkA、p75NTR mRNA在正常胎鼠直肠末端的相对表达量分别是162.221±104.675,129.778±51.976,在ARM胎鼠直肠末端中表达分别是78.937±33.425,87.145±25.812,两组比较差异均有统计学意义(Pa<0.05);琼脂糖凝胶电泳显示TrkA、p75NTR基因扩增后产物cDNA片段与引物设计的扩增片段完全吻合,TrkA、p75NTR基因条带亮度对照组均高于实验组。结论 TrkA、p75NTR mRNA在ARM胎鼠直肠末端的表达异常,提示神经生长因子及受体TrkA、p75NTR可能参与ARM肠神经系统的发育。     

叶酸缺乏孕鼠子代血细胞形态学改变及脑额区皮层超微结构表现

探讨叶酸缺乏对胎鼠宫内脑发育的影响、研究叶酸缺乏孕鼠子代胎鼠脑组织超微结构的改变及为叶酸缺乏造成脑发育障碍提供细胞水平的依据 ,及采用雌性SD大鼠实验组 30只、对照组 2 0只 ,分别饲以不含叶酸和含 2mg叶酸 kg的纯合饲料 ,两周后与雄鼠交配 ,于怀孕第 2 0天对孕鼠剖腹取胎 ,对模型进行评价并观察叶酸缺乏对胎鼠发育的影响 ,应用透射电镜观察胎鼠额区皮层超微结构的改变。结果显示 :1 .实验组孕鼠交配前及妊娠晚期末血清叶酸均明显低于对照组 ,外周血出现多分叶核粒细胞。实验组胎鼠血清叶酸也明显低于对照组 ,出现巨幼红细胞 ,RBC和HB均低于对照组 ,且伴有宫内生长限制。 2 .实验组胎鼠额区皮层超微结构观察示 :神经元出现核切迹、局灶性核周腔扩张、异染色质减少、胞质内细胞器肿胀、核糖体减少 ;某些胶质细胞亦见类似改变 ;神经毡膜性结构不完整。结论 :1 .交配前两周开始限食叶酸直至妊娠期结束 ,所建立的叶酸缺乏孕鼠动物模型处于叶酸缺乏第三阶段 ,其胎鼠宫内生长限制 ,红细胞出现巨幼变 ,但没有产生神经管闭合的异常。这是较理想的妊娠中晚期叶酸缺乏的孕鼠动物模型。 2 .母体叶酸缺乏能造成胎鼠皮层脑组织超微结构的改变 ,可能导致神经元功能的紊乱和丧失 ,以致防碍脑结构和脑功能的正?     

肛门直肠畸形胎鼠直肠末端Gli2、BMP4基因的表达

目的探讨乙烯硫脲（ETU）致畸胎鼠直肠末端Gli2、BMP4基因在胎鼠直肠肛门及其畸形发生过程中的表达和作用。方法取妊娠SD大鼠30只,按受孕时间配对分成2组,实验组（n=15）于孕10d灌胃注入10g／LETU （125mg／kg）,对照组n=15）予等量蒸馏水。两组分别于孕13d、14d、15d、16d和17d剖宫取胎鼠直肠末端1cm提取RNA,采用RT—PCR和RealtimePCR法检测Gli2、BMP4基因在直肠肛门发育不同时期的表达情况。结果采用RT-PCR法检测Gli2、BMP4基冈在直肠肛门发育不同时期的表达情况．发现在胎鼠第13～17天,实验组直肠末端Gli2、BMP4mRNA的表达水平均明显低于正常胎鼠直肠末端（P〈0．05）。而Realtime PCR检测Gli2、BMP4mRNA表达时,发现实验组Gli2的表达在胚胎第13天、第14天、第15天分别为（0．73＋0．07、0．60＋0．09、0．81＋0．06）,勺对照组相比显著降低（P〈0．05）,而在孕第16天、第17天实验组Gli2表达比对照组虽有下降,但无统计学意义;实验组BMP4的表达在孕第3～17天均较对照组下降,差异有统计学意义。结论直肠肛门的正常发育需要Shh信号通路的正常表达,Shh信号通路中转录因子Gli2和靶基囚BMP4的异常表达在肛门直肠畸形发生过程中起重要作用,ETU可能影响Shh信号转导通路和肛门直肠畸形发生。     

孕鼠叶酸缺乏对子鼠胰岛素样生长因子系统甲基化的影响

目的观察孕期叶酸缺乏对胎鼠生长发育及胰岛素样生长因子(IGF)系统甲基化的影响。方法将22只Sprague-Dawley雌鼠随机分为叶酸缺乏组(n=12)和正常对照组(n=10),分别喂养叶酸缺乏饲料和普通饲料,2周后与雄鼠交配,两组各8只雌鼠成功受孕,于怀孕第20天对孕鼠剖腹取胎,每组取32只胎鼠测量其头尾长、体重。两组分别另取8只胎鼠,采用ELISA法对其脑、肝脏组织中的叶酸、IGF-1、胰岛素样生长因子结合蛋白(IGFBP)-3水平进行检测。两组分别另取3只胎鼠,使用全基因组甲基化测序方法检测其脑、肝脏组织IGF系统的甲基化情况。同时采用ELISA法对两组孕鼠血清IGF-1、IGFBP-3水平进行检测。结果叶酸缺乏组胎鼠头尾长、体重较正常对照组降低(P0.05);叶酸缺乏组孕鼠血清IGF-1、IGFBP-3与胎鼠脑、肝脏组织中的叶酸、IGFBP-3水平均低于正常对照组(P0.05);叶酸缺乏组胎鼠脑组织中IGF-1R、IGF-2R、IGFBP-2、IGFBP-5、IGFBP-6、IGFBP-7的甲基化水平均高于正常对照组(P0.05);而在肝脏组织中,相比于正常对照组,叶酸缺乏组胎鼠IGF-1R、IGF-2R、IGFBP-3、IGFBP-5甲基化水平增加,IGF-2甲基化水平则下降(P0.05)。结论孕鼠叶酸缺乏会影响胎鼠宫内的生长发育,其机制可能与胰岛素生长因子系统的甲基化异常有关。     

孕期维生素A缺乏导致胎鼠肛门直肠发育畸形的实验研究

目的 观察维生素A缺乏(vitamin A,VA)对胎鼠肛门直肠畸形(anorectal malforma-tions,ARM)的发生和末端直肠肠壁内神经系统(enteric nervous system,ENS)发育的影响.方法 SD成年雌性大鼠60只,随机分为三组(于孕前2周开始每组喂以不同剂量的VA饮食至孕期结束):①VAD组(n:20只):喂以VA缺乏饲料;②正常对照组(作为阴性对照组,n=20只):喂以普通饲料;③ETU组(即乙烯硫脲组,作为阳性对照组,n=20只):喂以普通饲料.于妊娠第10天,ETU组经胃管注入1%的乙烯硫脲(ethylenethiourea,ETU)(125 mg/kg);于妊娠第20天,所有孕鼠行剖宫术取胎鼠.观察活胎鼠ARM发生率以及用免疫组织化学方法检测胎鼠末端直肠PGP 9.5和S-100蛋白的表达水平.结果 (1)血清VA水平:经VA缺乏饲料喂养2周后VAD组的血清VA浓度明显低于正常对照组(P=0.0310)和ETU组(P=0.0401);(2)ARM发生率:VAD组和ETU组的胎鼠ARM发生率分别为64.5%(20/31)、45.9%(61/133),两组之间差异无统计学意义(P>0.05);正常对照组未发现ARM;(3)免疫组织化学结果:①在有肛门胎鼠末端直肠中,PGP 9.5和S-100在VAD组中的表达明显低于ETU组(PGP 9.5的P值=0.0156、S-100的P值=0.0105)和正常对照组(PGP9.5的P值=0.0091、S-100的P值=0.0024), 而ETU组和正常对照组两组之间表达差异无统计学意义(P>0.05);②在无肛畸形胎鼠末端直肠中,PGP9.5和S-100在VAD组中的表达明显低于ETU组(P<0.0001);VAD组和ETU组的无肛胎鼠末端直肠中的表达均显著低于各自的有肛门胎鼠组(VAD组:PGP9.5和S-100的P值均<0.0001;ETU组:PGP 9.5的P值=0.0203、S-100的P值=0.0122).结论 孕期VA缺乏会导致胎鼠ARM的形成,胎鼠末端直肠ENS发育程度与其ARM有关.     

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.