Biology of the neonate最新文献

Few studies have investigated the velocities of fetal growth. The aim of the present study was to determine the pattern of 'fetal' growth velocities in a Chinese population. The gestation-specific measurements of the body weight, body length and head circumference in a representative sample of 5,045 male and 4,484 female newborns delivered between 26 and 42 weeks of gestation at 12 hospitals in Hong Kong were obtained. Peak growth velocity occurred before 30 weeks of gestation for head circumference, at week 30 for length and at week 30 for weight. When compared with data obtained from a French population, a significant difference in the growth velocity for body weight was observed below 32 weeks between French and Chinese infants, suggesting an ethnic difference in fetal growth of this parameter.

Background: Postnatal alterations in pulmonary mechanics, energetics and functional residual capacity (FRC) describe the structural maturation of the preterm respiratory system.

Objective: To evaluate longitudinal changes in pulmonary function in infants with respiratory distress syndrome (RDS) treated with oxygen, positive pressure ventilation and synthetic surfactant (Exosurf).

Methods: Serial pulmonary function tests were performed in surfactant-treated infants [mean +/- SD birth weight (BW) = 1,112 +/- 276 g, gestational age (GA) = 29 +/- 3 weeks] at postnatal ages: <3 days, 1, 2, 3, 4 and 6-8 weeks until term postmenstrual age (PMA). Tidal volume, pulmonary compliance (C(L)), pulmonary resistance (R(T)) and flow-resistive work were analyzed following simultaneous measurements of airflow and transpulmonary pressure signals. Serial FRC measurements were made in a randomly selected group.

Results: Prior to 28 weeks' PMA, C(L) was unchanged irrespective of GA. At age 1 week the likelihood ratio (LR) for bronchopulmonary dysplasia (BPD) based on C(L), R(T) and GA was predicted to be >90% for those with BW <750 g (LR >100) as compared to <10% probability (LR = 0.3) for infants >1,500 g. Significant linear increase in C(L) to PMA was evident >28 weeks' PMA (r = 0.86, p < 0.01) at 0.17 ml/cm H2O/kg/week. By term PMA, mean C(L) was 2.60 +/- 0.07 ml/cm H2O. Improvements in FRC of preterm infants with RDS who recovered occur at a more rapid rate ( approximately 25 ml/kg) compared to those who developed BPD ( approximately 20 ml/kg).

Conclusions: Slow but incremental postnatal pulmonary improvement, minimal <28 weeks' PMA, were comparable for all infants. Along with diminished FRC, these changes reflect persistent deleterious effects of positive pressure ventilation, alveolar hyperoxia and unrecognized pulmonary overdistension.

Background: The antioxidant status of the tissue affected by ischemia-reperfusion is of great importance for the primary endogenous defense against the free-radical-induced injury.

Objective: In this study, we aimed to evaluate the relationship between the activities of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT)] in cerebrospinal fluid (CSF) and severity of hypoxic-ischemic encephalopathy (HIE) in newborns.

Methods: Thirty full-term asphyxiated infants (gestational age >37 weeks) and 11 full-term infants (none of whom showed any signs of asphyxia) were included in this study. Activities of SOD, GPX, and CAT in CSF were measured within the first 72 h of life in infants with HIE and controls.

Results: Activity of SOD in CSF was significantly higher in infants with HIE compared with controls (p<0.05). GPX and CAT activities were higher in infants with HIE than they were in controls; however, the differences were not statistically significant (p > 0.05). The activities of GPX and CAT were significantly increased in severe HIE as compared with mild HIE and controls (p < 0.05).

Conclusion: Both the duration of the hypoxic-ischemic insult and the severity of HIE modulate elevations of enzymatic activity as an adaptive response to excessive free radical production in CSF in newborn infants with HIE. The activities of antioxidant enzyme alterations in CSF correspond highly to the severity of HIE, and these patterns may be useful for diagnostic and prognostic purposes.

Our understanding of lung development in the past two decades has moved from an anatomical to a histological basis and, most recently, to a molecular basis. Tissue interactions specify tracheal and lung primordia formation, program branching morphogenesis of the airway epithelium and regulate epithelial differentiation. In addition, lung development is influenced by mechanical and humoral factors. The regulatory molecules involved in morphogenetic signaling include growth and transcription factors and extracellular matrix molecules. These morphogenetic signals are responsible for lung patterning and differentiation. We will provide a brief overview of molecular signaling during early respiratory formation, airway branching, pulmonary vascularization and epithelial differentiation. We will then review aberrant morphogenetic signaling in human lung abnormalities, such as tracheoesophageal fistula, congenital diaphragmatic hernia, pulmonary hyperplasia, alveolar capillary dysplasia, congenital cystic adenomatoid malformation and bronchopulmonary dysplasia.

The first successful trial of surfactant treatment for respiratory distress syndrome (RDS) was reported in 1980. Since then there have been numerous randomised trials demonstrating first, the efficacy of surfactant treatment in reducing pulmonary air leaks and increasing survival and second, assessing various other aspects of therapy. These studies show that multiple doses may be needed if surfactant is used to treat established RDS but early or prophylactic treatment is superior for infants with gestational ages less than 30 weeks. Natural surfactants (containing proteins) are more effective than synthetic products (protein free), the latter now being infrequently used. Natural surfactants vary and should not be considered to be equivalent in their effects. A porcine surfactant (poractant alfa) acts more rapidly than a bovine preparation (beractant) in infants with moderate to severe RDS. A meta-analysis of 5 comparative studies suggests that a dose of 200 mg/kg of poractant alfa is associated with lower mortality compared with 100 mg/kg of beractant. Chronic lung disease remains a problem but it is hoped that early treatment with surfactant combined with extubation to continuous positive airway pressure will reduce this complication of prematurity. The newer synthetic surfactants, containing analogues of surfactant protein B or C, have undergone some trials for treatment of RDS but comparative studies which have just been published do not show that they are superior to existing natural surfactants. However, as they are more resistant to inactivation they may have a role in treatment of adult or acute RDS. The last 25 years have seen a large increase in basic science research on surfactants with determination of the structure and function of the four surfactant proteins probably being the most important advances. Future studies will focus on widening the indications for surfactant treatment, developing non-invasive means of administration and assessing the role of the newer synthetic surfactants.

Background: As screening for retinopathy of prematurity (ROP) is costly, time-consuming for the ophthalmologist and discomforting for the neonate, the minimum number of infants should be screened for ROP, without missing infants with severe ROP, at risk for threshold ROP.

Objectives: To develop a diagnostic screening guideline for ROP that would safely reduce the number of ROP screening funduscopies in our department.

Methods: Data of 275 infants admitted between 1996 and 2000 and screened for ROP according to our Dutch National guideline were studied. Significant risk factors for ROP were calculated, using logistic regression analysis and used to develop a guideline. The discriminative power of the guideline was evaluated using the area under the curve for the receiver operating characteristic curve.

Results: Significant risk factors for ROP were: gestational age, birth weight and number of erythrocyte transfusions within the first 4 weeks of life. The combination of these 3 factors resulted in the highest area under the curve: 0.793. Using these 3 factors, a diagnostic screening guideline for ROP was developed: if birth weight + 2 x (gestational age - 20) - 6 x erythrocyte transfusion value within the first 4 weeks of life >or=34, no screening for ROP is necessary. Using this guideline, 22.2% of the infants of the study group could have been excluded from screening; 3.8% of the infants with ROP stages 1-2 would have been missed.

Conclusion: In our department, ROP screening can be safely reduced using our diagnostic screening guideline.

Heterotaxy results from failure of the developing embryo to establish normal left-right asymmetry. Typical manifestations include abnormal symmetry and malposition of the thoraco-abdominal organs and vessels, complex congenital heart disease and extracardiac defects involving midline-associated structures. The spleen is almost always affected, and there is syndromic clustering of the malformations corresponding to the type of splenic abnormality present. This review outlines the embryologic and genetic background of the heterotaxy syndrome as well as the characteristic anatomic features, clinical manifestations, and diagnostic clues of its two main presentations with asplenia or polysplenia.

This is a brief review of neonatal chronic lung disease, sometimes called the 'new bronchopulmonary dysplasia (BPD)'. The clinical, radiographic and pathological features of this condition have changed considerably in recent years because of major advances in perinatal care, including widespread use of antenatal glucocorticoid therapy, postnatal surfactant replacement and improved respiratory and nutritional support. Authentic animal models, featuring lengthy mechanical ventilation of surfactant-treated, premature neonatal baboons and lambs, have provided important insights on the pathophysiology and treatment of this disease. Lung histopathology after 2-4 weeks of positive-pressure ventilation with oxygen-rich gas results in failed formation of alveoli and lung capillaries, excess disordered elastin accumulation, smooth muscle overgrowth in small pulmonary arteries and airways, chronic inflammation and interstitial edema. Treatment interventions that have been tested in these animal models include nasal application of continuous positive airway pressure, high-frequency mechanical ventilation, inhaled nitric oxide and retinol. The challenge now is to improve understanding of the molecular mechanisms that regulate normal lung growth and development, and to clarify the dysregulation of lung structure and function that occurs with injury and subsequent repair so that effective treatment or prevention strategies can be devised and implemented.