瘦素/脂联素值与肥胖儿童体质量指数及糖脂代谢的关系

目的 探讨瘦素/脂联素(L/A)值与单纯性肥胖儿童体质量指数(BMI)、糖脂代谢及肥胖症发病的关系.方法 单纯性肥胖60例和57例健康儿童,采用放射免疫分析(RIA)法测定其血清瘦素水平;ELISA法测定其血清脂联素、空腹胰岛素(FINS)水平;免疫比浊法测定其血脂各成分.分析并比较血清瘦素、脂联素及L/A值与肥胖儿童BMI、糖脂代谢的相关性.结果 1.肥胖儿童血清瘦素、FINS和三酰甘油(TG)水平与健康对照组相比明显增加;脂联素水平降低,差异均有显著性(Pa＜0.05,0.01).2.单纯性肥胖儿童瘦素与BMI、FINS、TG水平均呈显著正相关(r=0.408,0.301,0.301 Pa＜0.05,＜0.01);脂联素水平与BMI、FINS、TG均呈显著负相关(r=-0.360,-0.413,-0.258 Pa＜0.01,＜0.05).3.L/A值与BMI、FINS、TG呈显著正相关(r=0.780,0.764,0.601 Pa＜0.001).结论 血清瘦素和脂联素与肥胖儿童的发病有关,可作为儿童肥胖的监控指标;L/A值较单独瘦素、脂联素更能反映肥胖症儿童的代谢状况,可为肥胖症儿童糖脂代谢提供更为有效的监测指标.     

儿童单纯性肥胖与胰岛素抵抗综合征危险因素的关系

目的 探讨儿童单纯性肥胖与胰岛素抵抗综合征危险因素的关系.方法 单纯性肥胖患儿50例为肥胖组(男23例,女27例),选取同期健康儿童30例为健康对照组(男14例,女16例).对每位对象采用同一磅秤标准方法 测量其身高、体质量,并计算其体质量指数(BMI).血压测定采用儿童标准血压测定法获得.采用发光免疫法、快速测血糖法分别对2组儿童的血糖、血胰岛素、血脂进行检测,计算稳态模型胰岛素抵抗指数(HOMA-IRI)、胰岛素敏感指数(HOMA-ISI),并应用SPSS 12.0软件进行统计学分析.结果 肥胖组儿童HOMA-IRI、舒张压与健康对照组比较均显著增高(t=3.939,3.278 P_＜0.01);收缩压、三酰甘油与健康对照组比较均显著增高(t=2.536,2.573 Pa＜0.05);HOMA-ISI、高密度脂蛋白均显著低于健康对照组(t=-4.750 P＜0.01,t=-2.982 P＜0.05).肥胖组儿童BMI与HOMA-IRI呈显著正相关(r=0.294 P＜0.05).结论 儿童单纯性肥胖与胰岛素抵抗综合征危险因素密切相关,儿童期积极开展对肥胖的干预,对预防和控制成年期诸多慢性疾病的发生有重要意义.     

肥胖儿童非酒精性脂肪肝炎54例

目的 观察不同程度肥胖儿童非酒精性脂肪肝炎(NASH)的发病状况,探讨其可能的发病机制.方法 体质量指数(BMI)≥23的7～16岁单纯性肥胖儿童123例.按BMI分为3组:BMI≥30组34例,25≤BMI＜30组57例,23≤BMI＜25组32例.分别进行肝脏B超检查,并检测血转氨酶、胆固醇、三酰甘油(TG)及空腹血糖/空腹胰岛素比值(FlGIR).将另24例仅有肥胖而无肝脂肪病变者设为对照组.结果 123例患儿中B超发现肝脂肪病变99例(80.49%),其中符合NASH诊断标准者54例(43.90%).所有患儿中,BMI≥30组脂肪肝炎及FGIR＜7的发生率均显著高于其他2组(Pa ＜0.01).相关分析表明,ALT和AST与BMI分级、血胆固醇、TG、FGIR均有相关性(r=0.413,0.290,0.379,-0.477 Pa ＜0.01;r=0.359,0.349,0.348,-0.369 Pa ＜0,01).NASH患儿与对照组血脂、FGIR、BMI比较差异均有统计学意义(X2=9.84,25.59 Pa ＜0.01;t=5.05P＜0.01).结论 BMI ≥30是肥胖儿童发生NASH的高危因素,且脂代谢紊乱和胰岛素抵抗可能与其发病有关.     

单纯性肥胖儿童胰岛素抵抗与肿瘤坏死因子-α的关系

目的探讨单纯性肥胖儿童胰岛素抵抗与肿瘤坏死因子-α(TNF-α)的关系。方法单纯性肥胖患儿50例作为观察组(男23例,女27例);选取同期健康儿童30例为对照组(男14例,女16例)。采用发光免疫法、放射免疫法、快速测血糖法分别对两组儿童的血糖、血胰岛素、血脂和TNF-α进行检测。并作对比分析。结果观察组稳态模型胰岛素抵抗指数(HOMA-IR)、TNF-α及舒张血压(DBP),与对照组比较均明显升高(t=3.939,4.938,3.278 P均<0.01);收缩血压(SBP)、空腹三酰甘油(TC)与对照组比较均明显升高(t=2.536,2.573 P均<0.05);胰岛素敏感指数(HOMA-ISI)观察组明显低于对照组(t=-4.75 P<0.01)。观察组TNF-α与体质量指数(BMI)、TC、HOMA-IR均呈显著正相关(r=0.284,0.328,0.361 P均<0.05)。TNF-α与HOMA-ISI呈显著负相关(r=-0.36 P<0.01)。BMI与HOMA-IR呈显著正相关性(r=0.294 P<0.05)。结论单纯性肥胖儿童存在胰岛素抵抗,血清TNF-α与肥胖儿童的BMI、TC、BP、胰岛素抵抗密切相关,TNF-α可能参与胰岛素抵抗病理生理机制。     

血清25羟-维生素D3水平与儿童肥胖之间的关系

目的 探讨儿童血清25羟-维生素D3[25-(OH)D3]水平与体质量、肥胖程度、体质量指数(BMI)、血脂的关系,以及他们在肥胖儿童中可能的发生机制.方法 以2011年7月至2013年2月在无锡市妇幼保健院儿童营养门诊就诊的儿童为研究对象,共244例.调查所有受试者每日服用维生素D情况,测量身高、体质量、BMI及25-(OH)D3水平和微量元素,其中38例3岁以上肥胖儿童测定脂代谢水平.结果 1.肥胖儿童的血清25-(OH)D3水平为(68.31 ±23.06) nmol/L,其中36个月龄以上组肥胖儿童最低,为(55.03±15.18) nmol/L.2.肥胖组和超重组儿童血清25-(OH) D3水平远低于正常体质量组儿童水平(F=4.739,P＜0.05).3.重度肥胖儿童25-(OH) D3水平显著低于轻、中度肥胖儿童(F=9.711,P＜0.05).4.儿童体质量、身高/体质量百分比及BMI与25-(OH) D3水平呈负相关(r=-0.365、-0.237、-0.175,P均＜0.001).5.3岁以上肥胖儿童体质量、三酰甘油水平与25-(OH) D3均呈负相关(r=-0.476、-0.324,P均＜0.05).结论 血清25-(OH)D3水平降低与肥胖有关.其原因可能是肥胖者脂肪组织增多,维生素D滞留在脂肪细胞中,导致血清维生素D水平减低.肥胖儿童体内维生素D的消耗高于正常儿童,需要补充更多的维生素D才能达到正常25-(OH)D3水平.     

肥胖儿童血浆内源性硫化氢水平变化的研究

目的 探讨肥胖儿童血浆硫化氢(H2S)水平及其影响因素.方法 2007年3月至6月选取北京大学第一医院儿科常规体检肥胖儿童36例(肥胖组),超重儿童40例(超重组),正常儿童40名(对照组).测量身高、体重,得出体重指数(BMI);常规测量血压;对其家族史进行调查.测量其血浆总胆固醇、三酰甘油(甘油三酯)、低密度脂蛋白和高密度脂蛋白水平;测定血浆H2S水平.结果 肥胖、超重组儿童体内H2S含量较对照组下降,差异有统计学意义(P<0.05).肥胖组、超重组三酰甘油高于对照组,高密度脂蛋白较对照组显著降低,差异有统计学意义(P<0.05).肥胖组收缩压较对照组升高,差异有统计学意义(P<0.05).结论 肥胖、超重儿童血浆H2S水平降低,提示肥胖儿童体内存在舍硫氨基酸体系代谢失衡.     

肥胖伴黑棘皮病儿童代谢综合征的高危因素

目的 探讨肥胖伴黑棘皮病儿童代谢综合征(MS)的高危因素.方法 2006年11月-2007年9月在本院儿科就诊25例肥胖伴黑棘皮病儿童(病例组).男15例,女10例;年龄8.4～16.0岁,平均10.6岁;体质量(72.11±17.66)kg;身高(155±14)cm.32例身高别体质量正常的健康儿童为健康对照组.男18例,女14例;年龄7.6～15.8岁,平均9.8岁.比较二组儿童体质量指数(BMI)、胆固醇(12HO)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、血压、空腹和葡萄糖耐量试验(OGTT)2 h血糖、胰岛素和稳态模型评估法胰岛素抵抗指数(HOMA-IR)的差异,并对所有儿童进行肝脏超声波检查.采用SPSS 12.0软件进行统计学分析.结果 病例组儿童BMI、TG、LDL-C、收缩压和舒张压均显著高于健康对照组(Pa<0.01);空腹和OGTT 2h血糖、OGTT 2h胰岛素和HOMA-IR均显著高于健康对照组(Pa<0.01);BMI与收缩压、舒张压、CHO、TG、LDL-C、空腹血糖(FBG)、空腹胰岛素(FINS)以及HOMA-IR均无相关性(Pa>0.05).病例组患儿中超声诊断脂肪肝发生率为84%,健康对照组儿童肝脏B超检查均未见异常.结论 肥胖伴黑棘皮病儿童BMI增加、胰岛素抵抗、血脂紊乱和血压增高是MS的危险因素,密切随访监测此类患儿有助于早期发现MS.积极治疗肥胖症,阻断儿童血糖、血脂代谢紊乱的发生,有助于减少儿童2型糖尿病和心血管疾病的危险性.     

单纯性肥胖儿童血浆卡尼汀、游离脂肪酸水平与胰岛素抵抗的相关性

目的了解单纯性肥胖儿童血浆卡尼汀(CT)、游离脂肪酸(FFA)水平与胰岛素抵抗相关参数的关系。方法选择56例确诊为单纯性肥胖的儿童作为研究对象(肥胖组),36例健康体检儿童为健康对照组。采用放射免疫法(RIA)测定二组血浆胰岛素,高效液相色谱法(HPLC)测定血浆CT水平,酶比色法测定血浆FFA及三酰甘油(TG)。计算体质量指数(BMI)及腰臀比(WHR),按稳态模式胰岛素(HOMA-IR)计算其胰岛素抵抗指数(InRI)和胰岛素敏感指数(InSI),应用SPSS13.0软件进行统计学分析。结果肥胖组血浆CT水平为(43.67±12.75)μmol/L,健康对照组为(58.31±21.25)μmol/L,二组比较差异有统计学意义(t=2.566P<0.05)。肥胖组血浆FFA水平为(785.32±284.91)μmol/L,健康对照组为(604.87±136.52)μmol/L,二组比较差异有统计学意义(t=2.143P<0.05)。肥胖组WHR、TG、胰岛素(Ins)水平、InRI与健康对照组比较差异均有统计学意义(Pa<0.05)。血浆FFA与BMI、WHR、TG均呈正相关(r=0.403,0.320,0.406Pa<0.05),与InSI呈负相关(r=-0.364P<0.01);血浆CT与空腹胰岛素(FINS)、InSI呈正相关(r=0.365,0.364Pa<0.01),与WHR呈负相关(r=-0.614P<0.01);肥胖组血浆CT水平与FFA水平呈负相关(r=-0.592P<0.01)。结论肥胖患儿存在明显的脂肪代谢紊乱,血浆FFA及CT水平的变化与胰岛素抵抗密切相关,这些变化可能参与肥胖及肥胖相关并发症的发生。     

儿童肥胖与代谢综合征的相关性

目的 探讨儿童肥胖与代谢综合征(MS)各指标的关系.方法 选择60例肥胖患儿作为肥胖组,60例正常体质量儿童作为健康对照组,比较2组体质量指数(BMI)、腰围与身高比(WHtR)、平均动脉压(MAP)、三酰甘油(TG)、空腹胰岛素(FIS)、血尿酸(UA)、脂蛋白(LP)及胰岛素敏感指数(ISI)和抵抗指数(IRI)等MS指标,并进行统计学处理.结果 肥胖组BMI、WHtR、MAP、TG、FIS、UA、LP及ISI、IRI均显著高于健康对照组,差异均有统计学意义(Pa<0.05).结论 肥胖儿童存在胰岛素抵抗及脂血谢紊乱,并有血压、血UA升高.对处于生长发育期的儿童,应控制和预防肥胖发展,以降低MS及成年时糖尿病、冠心病的发生.     

肥胖症儿童血清抵抗素水平与胰岛素抵抗关系的研究

目的探讨肥胖症儿童血清抵抗素水平与高胰岛素血症和(或)胰岛素抵抗的关系。方法采用酶联免疫法测定34例肥胖儿童,31例正常对照的血清抵抗素水平。分析血清抵抗素与体重指数、体脂百分比、腰臀比及空腹血糖、空腹胰岛素水平、胰岛素抵抗指数、胰岛β细胞功能指数的相关关系。结果(1)肥胖组及对照组抵抗素浓度(对数转换值3.1±0.5)高于对照组(对数转换值2.7±0.8)(P<0.05)。(2)抵抗素与性别、年龄、收缩压、舒张压无相关关系;与体重指数、体脂百分比、腰臀比呈正相关(相关系数分别为r=0.299、0.304、0.322,P<0.01);与空腹血糖及空腹胰岛素水平呈正相关(相关系数为r=0.299和r=0.303,P<0.05);与胰岛素抵抗指数呈正相关(r=0.324,P<0.01),与胰岛β细胞功能指数无相关关系。(3)多元逐步回归分析表明,胰岛素抵抗指数为影响抵抗素最为显著的因素(R2=0.105);标准化偏回归系数0.279(P<0.01)。结论肥胖症儿童血清抵抗素水平较正常儿童增高,并与肥胖程度,脂肪分布密切相关。抵抗素可能与肥胖症儿童发生高胰岛素血症和(或)胰岛素抵抗有关。     

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.     

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.     

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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.     

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.     

alpha -SMOOTH MUSCLE ACTIN DISTRIBUTION IN THE PULMONARY VASCULATURE COMPARING HYPOPLASTIC AND NORMAL FETAL LUNGS

We investigated the intra-acinar pulmonary vascular muscularization in the developing human fetal lung between the 17th and 24th gestational weeks, that is, during the canalicular phase of lung development. Fifteen hypoplastic and 25 normal developed lungs were included in this study using monoclonal alpha -smooth muscle (sm) actin antibodies for smooth muscle detection. Computer-aided image analysis was performed for morphometrical measurements and statistical evaluation. Alphasm-actin-immunoreactive intra-acinar vessels down to a luminal diameter of less than 10 mu m were detected in hypoplastic as well as in normally developed lungs. Crucial differences presented as follows: significantly higher density of intra-acinar vessels, especially due to alpha -sm-actin-negative vessels less than 30 mu m in luminal diameter, in the control group; significantly higher alpha -sm-actin immunoreactivity per section unit as well as per vessel in the hypoplastic lung group. As suggested by others, alpha-sm-actin-positive cells of the intra-acinar vessel wall in the developing human lung were demonstrated to be smooth muscle cells, their immediate precursors, and pericytes. We conclude that the increased alpha -sm-actin immunoreactivity represents muscularization of the vessel wall in functional terms and may be regarded as one structural cause among others for the establishment of persistent fetal circulation in hypoplastic lungs.     

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.