BACKGROUND:Advances in neonatal intensive care have led to an increased survival of very low birth weight (VLBW, <1,500 g) and extremely low birth weight infants (ELBW, <1,000 g). Several abnormalities may occur in these children, e.g. esophageal atresia (EA), imperforate anus or abdominal wall defects. Correction of EA is often performed as a staged procedure in this group of patients.OBJECTIVES:To evaluate the feasibility of a primary correction of EA in 4 ELBW and VLBW infants.METHODS:Between 2002 and 2004, 4 infants below 1,200 g were operated on in our institution with a diagnosis of EA with lower tracheoesophageal fistula. Birth weight ranged from 780 to 1,120 g (median: 920 g), gestational age from 28 to 30 weeks. Treatment included closure of the tracheoesophageal fistula and primary anastomosis of the esophagus in a one-step procedure.RESULTS:Primary correction of EA and fistula repair was feasible in all children. Initially, all children had a normal passage of the esophagus as observed in barium swallowing. One child suffering from a leakage of the anastomosis was managed conservatively. Another infant suffered from spontaneous small bowel perforation 6 days after surgery, which was treated by laparotomy. One child developed stenosis of the esophagus and required a single dilatation 14 months after initial treatment. In the 4th child, a type II cleft syndrome was subsequently diagnosed, requiring secondary cleft repair together with semifundoplication. This child eventually died from cytomegalovirus pneumonia.CONCLUSIONS:Primary repair of EA and closure of a tracheoesophageal fistula is technically feasible and offers a good treatment option for ELBW and VLBW infants. Staged repair can be avoided. Infants with cleft syndrome are still a diagnostic and therapeutic challenge.
even reverse itself, and so fi xed stopping rules dictated by predetermined signifi cance levels for differences in outcome are increasingly discouraged [3] . Additional information such as the medical plausibility of the difference, ethical considerations both for the trial participants and for the wider target population, evidence from other relevant trials and the nature of the disease under consideration may also be important [2, 4–6] . The decision to stop a trial for harm can also be based on adverse events, although attribution of the cause of an adverse event may be diffi cult [3] . There is less guidance available on when and how trials should be stopped for futility. The 2005 DAMOCLES study [3] highlights a recognition in the literature that termination of a trial may be recommended where it is considered that there is no longer a reasonable chance of accumulating suffi cient evidence against the null hypothesis (usually due to poor recruitment or to external information becoming available [7] ). However, it is unclear whether trials should be stopped on these grounds [3, 4] . Another reason for stopping for futility is that the trial is unlikely to come to a sound conclusion [3] . This is illustrated in the trial by Thome et al. The diffi culty with this trial was that, at the time of the interim analysis, the majority of the patients randomized to the active arm (minimal ventilation to achieve higher PaCO 2 ) had not An important, often neglected element to planning a clinical trial is to consider the possibility of stopping the trial early, before either recruitment or follow-up is completed. A trial may be stopped for futility, harm or benefi t. A trial that is stopped on the grounds of benefi t is one that early on identifi es important treatment effects unlikely to be due to chance. A trial stopped for harm provides evidence that the treatment under investigation is unsafe for trial subjects. A trial stopped for futility requires a decision that the trial would not provide suffi ciently useful information to warrant continuation. Stopping a trial early is always a diffi cult decision to make and consideration must be given to who will be making these decisions and on what grounds they will be made. This issue of Biology in the Neonate publishes a trial by Thome et al. investigating the use of increased PaCO 2 targets on outcomes in extremely preterm neonates. It appears that this trial was stopped for futility on the grounds that the increased target levels of PaCO 2 were not being reached in the active arm of the trial. Guidance for stopping a trial for benefi t or harm is well documented [1] although approaches remain controversial. Statistical methods exist and may contribute to deciding whether the observed data imply that benefi t is very likely or, in the case of stopping for harm, very unlikely, or that the new treatment is harmful [2] . An early trend in the data under consideration may fl uctuate and Published online: April 19, 2006
This paper briefly reviews the systemic and pulmonary hemodynamic actions of the most frequently used vasopressor-inotropes and inotropes in the preterm and term neonate. It is important to note that very little is known about the medium- and long-term cardiovascular and neurodevelopmental benefits of the use of these medications in the neonate.
Background: Prenatal exposure to magnesium sulfate, a drug that is frequently used for attempted tocolysis in preterm labor, could alter neutrophil functional activity in infants born preterm. Objectives: To determine the association between maternal tocolysis with magnesium sulfate and the cord blood neutrophil functional activity of preterm neonates. Methods: The chemotaxis, random motility, and chemiluminescence of neutrophils were compared in the cord blood of 10 preterm neonates born to mothers tocolysed with magnesium sulfate, 10 preterm infants whose mothers had not received any tocolysis, and 10 term infants. Data regarding the maternal and neonatal magnesium and calcium levels were collected and analyzed in association with the cord blood neutrophil functional activity of the preterm infants. Results: Neutrophil functional activity in the cord blood of the preterm neonates was significantly lower than in term neonates. However, the alteration of neutrophil chemotaxis, random motility and chemiluminescence was more noticeable in neonates with intrapartum exposure to magnesium sulfate as compared to preterm infants whose mothers received no tocolysis (30.9 ± 2.3 vs. 36.7 ± 2.7 µm, p < 0.01; 26.6 ± 1.9 vs. 33.1 ± 3.1 µm, p < 0.01; and 74.3 ± 6.5 vs. 89.9 ± 6.25 ×103 counts per min (cpm), p < 0.01, respectively). Furthermore, the reduction in neutrophil functional activity of preterm infants with intrapartum exposure to magnesium was directly correlated with the maternal serum magnesium levels (r = –0.90 to –0.85, p < 0.01). Conclusion: In infants born preterm, intrapartum exposure to magnesium sulfate is a risk factor contributing to the alteration in neutrophil motility and post-phagocytic bactericidal capacity.
BACKGROUND:Congenital truncation of the glucocorticoid receptor (GR) is known to lead to lethal lung immaturity in newborn mice associated with increased lung cellularity (ratio of tissue to airspace) and, as we previously showed, prolonged expression of the retinoid-responsive growth factor midkine.OBJECTIVES:We sought to determine if these changes would be reversed by transgenic expression of GR exclusively in the distal airway epithelium.METHODS:Mice were generated with expression of transgenic rat (r) GR driven by the human (h) SP-C promoter, on a background of congenital GR truncation.RESULTS:Transgenic epithelial GR expression reduced lung cellularity and midkine expression to levels comparable to wild-type littermates. Nevertheless, the newborn transgenic mice still displayed respiratory failure. Moreover, epithelial expression of the GR transgene did not alter expression of a number of important markers of lung maturation.CONCLUSIONS:Our data demonstrating normalization of the lung tissue to airspace ratio in neonatal mice expressing transgenic GR in the distal airway epithelium is consistent with the concept that normal mesenchymal cell loss is due to GR-responsive stimulation from epithelial cells. However, we could find no evidence of altered apoptotic activity between the groups of mice. We speculate that correction of the severe neonatal lung phenotype of GR-deficient mice will require expression of normal GR in non-epithelial as well as epithelial tissues.
β-Adrenergic receptor (βAR) activation has been shown to maintain heart rate during hypoxia and to rescue the fetus from the fetal lethality that occurs in the absence of norepinephrine. This study examines whether the same subtype of βAR is responsible for survival and heart rate regulation. It also investigates which βARs are located on the early fetal heart and whether they can be directly activated during hypoxia. Cultured E12.5 mouse fetuses were treated with subtype-specific βAR antagonists to pharmacologically block βARs during a hypoxic insult. Hypoxia alone reduced heart rate by 35–40% compared to prehypoxic levels. During hypoxia, heart rate was further reduced by 31% in the presence of a β1AR antagonist, CGP20712A, at 100 nM, but not with a β2 (ICI118551)- or a β3 (SR59230A)-specific antagonist at 100 nM. Survival in utero was also mediated by β1ARs. A β1 partial agonist, xamoterol, rescued 74% of catecholamine-deficient (tyrosine-hydroxylase-null) pups to birth, a survival rate equivalent to that with a nonspecific βAR agonist, isoproterenol (87%). Receptor autoradiography showed that β1ARs were only found on the mouse heart at E12.5, while β2ARs were localized to the liver and vasculature. To determine if the response to hypoxia was intrinsic to the heart, isolated fetal hearts were incubated under hypoxic conditions in the presence of a βAR agonist. Heart rate was reduced to 25–30% by hypoxia alone, but was restored to 63% of prehypoxic levels with 100 nM isoproterenol. Restoration was completely prevented if β1ARs were blocked with CGP20712A at 300 nM, a concentration that blocks β1ARs, but not β2- or β3ARs. Our results demonstrate that β1ARs are located on the heart of early fetal mice and that β1AR stimulation maintains fetal heart rate during hypoxia and mediates survival in vivo.
We hypothesized that enriching surfactant with hyaluronan would restore lung function when tested in a premature animal model. Newborn piglets (85% gestation, term 112–114 days) were delivered by cesarean section, subjected to mechanical ventilation (tidal volume 6– 8 ml/kg) and randomly assigned to treatment with 50 or 100 mg/kg Curosurf (C50 and C100), 50 or 100 mg/kg Curosurf mixed with 2.5% HA (w/w, CH50 and CH100). A ventilated and not treated group (Cont) and a not treated and not ventilated group (Non) were included as controls. Six hours after treatment the lungs were removed and biochemical, biophysical, cytological and histological analyses were carried out. The CH100, CH50, C100 and C50 groups had variable but significantly improved alveolar phospholipid content, minimal surface tension, alveolar aeration and wet/dry lung weight ratios, but little histological evidence of lung injury. CH100, CH50 and C100 groups had the best effects in terms of oxygenation, lung compliance and histology and evidence of decreased inflammation (IL-8 and TNF-α mRNA expression). We conclude that HA added to 50 mg/kg Curosurf or use of 100 mg/kg Curosurf with or without HA provides the best effects in terms of lung function and reduction of inflammation.
Background: Doxapram is a respiratory stimulant widely used for the treatment of idiopathic apnea of prematurity, although it has been demonstrated that it can induce a transient decrease of cerebral blood flow and that isolated mental delay in infants weighing <1,250 g is associated with the total dosage and duration of doxapram therapy. Objectives: To evaluate the effects of doxapram on cerebral hemodynamics in preterm infants using cerebral Doppler ultrasonography and near-infrared spectroscopy. Methods: Preterm infants who required treatment with doxapram for apnea of prematurity unresponsive to caffeine were treated with doxapram at an hourly dose of 0.5 mg·kg–1·h–1, followed by 1.5 and 2.5 mg·kg–1·h–1. Results: 20 preterm infants were studied. Doxapram induced a significant decrease of oxygenated hemoglobin (O2Hb) and cerebral intravascular oxygenation (HbD = O2Hb – HHb) and an increase of HHb and CtOx concentrations, while cerebral blood volume and cerebral blood flow velocity did not change. Conclusions: Doxapram infusion induces the increase of cerebral oxygen consumption and requirement and the contemporary decrease of oxygen delivery probably mediated by a decrease of cerebral blood flow. Caution must be recommended in prescribing this drug for apnea of prematurity.
Objective: To prospectively investigate the longitudinal changes of amplitude-integrated electroencephalographic (aEEG) activity in preterm infants <30 weeks gestational age (GA). Methods: Infants (GA <30 weeks) without evidence of neurological abnormalities had weekly aEEG recordings performed. The relative duration of the three aEEG patterns (discontinuous low voltage, discontinuous high voltage and continuous) was determined and the influence of GA and postnatal age (PNA) on the occurrence of each pattern was assessed. Results: Ninety-eight infants (median GA 26 weeks; range 23–29 weeks) were studied. With higher GA (OR 1.68, 95% CI 1.33–2.13) and PNA (OR 1.91, 95% CI 1.53–2.38), the likelihood for the occurrence of continuous activity increased. The discontinuous low-voltage pattern was less likely to occur with increasing GA (OR 0.68, 95% CI 0.55–0.83) and PNA (OR 0.70, 95% CI 0.61–0.81). Conclusion: Maturation of aEEG activity in preterm infants is influenced by both GA and PNA.
Background: Elevated serum concentrations of S-100B, a 21-kDa protein expressed in astroglial cells, has been used to assess cerebral damage after head trauma, infection, ischemia, and perinatal asphyxia. Objective: As S-100B is eliminated by the kidneys, we investigated the feasibility of measuring S-100B in urine of newborns with severe perinatal asphyxia, and in very low birth weight (VLBW) preterm infants at risk for neurodevelopmental impairment. Methods: We first analyzed urine samples of 8 term or near-term newborns without major medical problems, followed by urine samples of 2 term newborns with severe birth asphyxia, and finally urine samples of 8 VLBW (gestational age 24–28 weeks) infants collected every 4 h for up to 10 days. Results: Urinary S-100B concentrations in 8 term or near-term newborns without major medical problems were consistently <1 µg/l. In 2 term newborns with severe asphyxia (Apgar 0/0/0 and 0/2/4) who subsequently had widespread cerebral damage on magnetic resonance imaging, peak urinary S-100B concentrations on the first day of life were 28.1 and 28.4 µg/l, respectively. In 5/8 VLBW infants, urinary S-100B was >1 µg/l in samples obtained on the first day of life (range 1.2–44.9 µg/l, median 6.8 µg/l). Peak S-100B in urine samples collected during the first 12 h of life were negatively related to gestational age (Rs = –0.882, p = 0.009). Three of the 8 preterm infants had peak urinary concentrations >10 µg/l but neither ultrasound signs of brain damage nor neurodevelopmental delay at 1 year corrected age. Conclusions: The determination of urinary S-100B concentrations might be helpful in term infants with severe asphyxia, while high urinary S-100B concentrations in preterm infants are to be attributed to immaturity.
Background: Previous studies indicate that there may be infant gender differences in cytokine expression associated with differences in neonatal morbidity. Objective: We tested the hypothesis that umbilical cord interleukin-1 receptor antagonist (IL-1ra) correlates with infant gender and neonatal outcome in preterm infants. Study Design: IL-1ra was measured in cord blood taken from 58 preterm infants (33 males, 25 females) with gestational age less than 32 weeks. Receiver operating characteristics (ROC) curve were used for identifying IL-1ra values with high sensitivity and specificity for neonatal morbidity and adverse outcome, i.e., death or survival with severe intraventricular hemorrhage or periventricular leukomalacia. Results: In the female infants, but not the male infants, cord IL-1ra values correlated with postnatal depression, expressed as Apgar scores at 1 min (correlation coefficient, rs; p value: –0.542; 0.005), 5 min (–0.571; 0.018), and 10 min (–0.442; 0.035); and postnatal age at intubation (–0.799; 0.001). The ROC area under the curve (AUC) was 0.735 for adverse outcome (p = 0.013), and 0.683 for bronchopulmonary dysplasia (p = 0.021) when all infants were included. However, there was a significant gender difference in the ROC curve for adverse outcome (p = 0.026), with AUC 0.640 (p = 0.240) in males and AUC 0.929 (p = 0.008) in females. Above a chosen cutoff at 13,500 ng/l for IL-1ra cord the sensitivity and specificity for predicting adverse outcome was 100 and 81%, respectively in females versus 50 and 84% in males. Conclusion: Increased levels of cord IL-1ra levels are associated with neonatal morbidity and adverse outcome in preterm infants. Comparable levels of IL-1ra have different predictive value depending on infant gender.
Background: Allopregnanolone is a neurosteroid produced in the brain that can alter the excitability of the CNS. Neurosteroids have neuroprotective properties, and their elevation in response to stress may protect the newborn brain following infection or hypoxia. Infection, particularly of the respiratory tract, may lead to episodes of hypoxia. Infection and hypoxia have been identified as factors contributing to neonatal morbidity and mortality. Objectives: To determine the effect of acute episodes of hypoxia alone or in combination with lipopolysaccharide (LPS) exposure on plasma and brain allopregnanolone concentrations in lambs 10–21 days old. Also, to examine plasma levels of cortisol and the cytokines, tumour necrosis factor-α and interleutkin-6 after these challenges. Results: Allopregnanolone concentrations in the brain were markedly increased after hypoxia. Hypoxia following prior LPS treatment resulted in greater increases in brain allopregnanolone concentrations compared to either the LPS or hypoxia treatment alone. Importantly, brain regions unaffected by LPS or hypoxia alone (thalamus/hypothalamus, cerebellum) showed significant increases of allopregnanolone content following the combined LPS and hypoxia treatments. Plasma tumour necrosis factor-α and interleukin-6 concentrations were increased after LPS treatment with and without hypoxia, but not by hypoxia alone. In contrast, plasma cortisol concentrations were increased after both stressors. Conclusions: These results show that the brain of young lambs readily responds to physiological stress by increased production of allopregnanolone. This response may protect the developing brain from the cytotoxicity following hypoxic and infectious episodes.
Background: Various cytokines are reportedly associated with many neonatal diseases. Asphyxia is considered to result in ischemia-reperfusion injuries and induces abnormal inflammatory responses involving excessive cytokine production. Objectives: To evaluate alteration in sera levels of various cytokines/chemokines in case of perinatal asphyxia at birth. Methods: In orderto determine the concentrations of various cytokines/chemokines in sera, we used a highly sensitive fluorescence microsphere method. We measured the concentration of 8 types of cytokines/chemokines in sera obtained from 17 cases of asphyxia, 10 normal neonates, and 6 healthy adults. Results: The concentrations of IL-6, IL-8, and IL-10 in the sera of asphyxiated neonates were higher than those in the normal neonates. Irrespective of the presence or absence of asphyxia, sera concentrations of IL-2, IL-4, IFN-γ, and TNF-α were higher in the neonates than those in the adults. The concentration of IFN-γ in the asphyxiated neonates was lower than that in the normal neonates. Sera levels of IL-10 were higher in the asphyxiated cases than those in the normal neonates. The sera levels of IL-6, IL-8, and IL-10 in asphyxiated neonates with either a poor outcome or death were higher than those without poor outcomes. Conclusions: The concentrations of various types of cytokines/chemokines were different in neonatal sera and some of them increased drastically during asphyxia. The concentration of an anti-inflammatory cytokine IL-10 was elevated in asphyxiated neonates immediately after birth, thereby suggesting that IL-10 might be associated with neuroprotective functions.
Retinopathy of prematurity (ROP) is a multifactorial vasoproliferative retinal disorder that increases in incidence with decreasing gestational age. Recently, an association between hyperglycemia and severe ROP was found in extremely low birth weight infants (ELBWI). The purpose of this study was to evaluate the possible relation between hyperglycemia and ROP at any stage in very low birth weight infants (VLBWI). We analyzed the data of 201 VLBWI. The incidence of ROP and hyperglycemia was detected and the chi2 test was applied to investigate the association between the two variables. The Clinical Risk Index for Babies (CRIB) score was attributed as a marker of illness severity. The incidence of ROP and hyperglycemia in VLBWI was 35.3 and 19.4%, respectively. ROP developed more frequently in hyperglycemic infants (p < 0.001). The gestational age, birth weight, and Apgar scores were significantly lower, the CRIB score was higher in ROP patients. In hyperglycemic ROP patients the CRIB score was significantly higher compared to euglycemic ROP patients (mean (SD) 8.1 (4.2) vs. 5.5 (3.3); p < 0.01). A logistic regression model revealed that gestational age (OR 0.59; 95% CI 0.46-0.76; p < 0.001) and hyperglycemia (OR 3.15; 95% CI 1.12-8.84; p < 0.05) are independent risk factors in ROP development. When ELBWI were analyzed separately, gestational age (OR 0.38; 95% CI 0.20-0.72; p < 0.01) and CRIB score (OR 1.58; 95% CI 1.02-2.45; p < 0.05) were found as significant contributors. Further studies are needed to elucidate the pathophysiological role of hyperglycemia in the development of vasoproliferative retinal disorder.
Current standard therapy forpersistent pulmonary hypertension of the newborn (PPHN) consists of optimal lung inflation, hemodynamic support and selective vasodilation with inhaled nitric oxide (iNO). However, not all infants will respond. Milrinone, a phosphodiesterase (PDE) III inhibitor, is routinely used in pediatric cardiac intensive care units to improve inotropy and reduce afterload. Although its use in post-operative cardiac failure has been proven in a randomized trial, it has not been reported to be beneficial in PPHN. We report four cases with severe PPHN treated with a combination of iNO and Milrinone. All four cases were unresponsive to therapy including iNO, with a mean oxygenation index (OI) of 40 (standard deviation (SD) 12)) before Milrinone. Substantial improvement in OI (mean of 28; SD 16) was followed by extubation and survival. However, of 4 patients, 2 developed serious intraventricular hemorrhages (IVHs), and 1 had a small IVH. To clarify the risk benefit ratio, of death versus survival with impairment, a randomized controlled trial is needed.
Background: Clinically, it appears that phosphodiesterase 3 (PDE 3) inhibitors, which are used for acute cardiac failure in premature infants, dilate the ductus arteriosus (DA). Objectives: To clarify the ductus-dilating effects of PDE 3 inhibitors in near-term rat pups and their differential effects in near-term and preterm fetal rats, in in vivo studies. Methods: The in vivo ductal diameter of rat pups and fetuses was measured using a rapid whole-body freezing method, by cutting on a freezing microtome and measuring with a microscope and micrometer. Eight to twenty pups and fetuses were studied in each group. Milrinone and amrinone (specific inhibitors of PDE 3) were injected into 1-hour-old pups and the DA was studied 0.5 and 1 h later. The differential effects of these PDE 3 inhibitors on the near-term and preterm ductus were studied by injecting indomethacin (10 mg/kg) and PDE 3 inhibitors into 21D (21st day of pregnancy: term-21.5 days) and 19D dams and studying the fetal ductus 4 and 8 h later. Results: Milrinone and amrinone dilated the postnatal ductus dose-dependently. Large doses of these drugs dilated it completely, and clinically equivalent doses dilated it minimally. Milrinone and amrinone prevented constriction of the fetal ductus by indomethacin. Their ductus-dilating effects were more potent in the preterm than in the near-term fetuses, and clinically equivalent doses of these PDE 3 inhibitors dilated preterm ductus completely. Conclusion: In rats, PDE 3 inhibitors reopen the constricted postnatal DA slightly. PDE 3 inhibitors dilate the fetal DA constricted with indomethacin effectively and more sensitively in preterm than in near-term fetuses.
Background: Red blood cell (RBC) transfusions are associated with the development of retinopathy of prematurity (ROP). During the period of retinal neovascularization a rise of insulin-like growth factor 1 (IGF-1) may trigger rapid growth of new blood vessels. Objectives: To study endocrine factors in RBC transfusions that might be of importance for ROP. Methods: IGF-1, IGF-2 and their binding proteins 1–3 (IGFBP-1–3) were determined by radioimmunoassays in 7 very-low-birthweight (VLBW) infants with ROP ≧ stage 2 receiving a RBC transfusion, in 10 controls (VLBW infants with ROP ≤ stage 1, no transfusion), in supernatants of 7 RBCs and of 5 washed RBCs (WRBC). Results: IGF-1 (mean ± SD) in infants with ROP was 20.0 ± 4.2 µg/l, in controls 35.9 ± 15.2 µg/l (Mann-Whitney U test, p = 0.030). IGF-1 in RBC was 12.88 ± 5.03 µg/l and in WRBC 0.45 ± 0.74 µg/l (average of the three-course washing procedure). IGF-2 in infants with ROP was 485.67 ± 158.73 µg/l, in controls 389.9 ± 102.8 µg/l (not significant), in RBC 109.50 ± 117.89 µg/l, in WRBC 61.07 ± 30.0 µg/l. Except for IGFBP-3 other IGFBPs were barely or not detectable in RBC or WRBC. Conclusions: Considering lower IGF-1 concentrations in preterm infants than in adults (factor 20), the IGF-1 in RBC transfusions is equivalent to a single dose of 1 µg/kg IGF-1 (5–10% of the adult dose with proved metabolic responses). Endocrinological relationships between the donor’s load and the acceptor’s individual features are a new aspect of potential side effects of RBC transfusions. Further research is necessary to clarify the share of the described IGF administration on the development of ROP.
Background: Neonatal hearts are less susceptible to developing myocardial dysfunction after hypoxia and/or ischemia than adult hearts. Differences in intracellular calcium homeostasis may be responsible for reduced calcium overload of the immature myocardium leading to the observed protection against ischemia. Objective: To assess differences in baseline and post-ischemic gene expression of calcium handling proteins after ischemia in neonatal and adult rabbit hearts. Methods: We used isolated antegrade perfused rabbit hearts (age 2 days, 28 days, n = 32), which were exposed to ischemia and hypothermia simulating myocardial stunning comparable to neonatal asphyxia. Gene and protein expression of the sodium–calcium exchanger (NCX), the sarco-endoplasmatic reticulum Ca2+-ATPase 2a (SERCA) and calsequestrin (CSQ) were measured using quantitative real-time PCR and Western blotting. Results: After ischemia and reperfusion in neonatal and adult hearts, a significant decrease in myocardial performance was recorded. At the mRNA level, significant differences in the baseline expression of NCX, SERCA and CSQ between neonatal and adult hearts were observed. In neonatal post-ischemic hearts, NCX and CSQ expression were significantly higher at the mRNA level than in controls. In contrast, SERCA expression remained unchanged in neonatal hearts and decreased in adult hearts compared to the non-ischemic controls. Conclusion: These findings suggest that changes in gene expression of calcium handling proteins may be involved in the different susceptibility of neonatal compared to adult hearts to developing myocardial dysfunction after ischemia.
Background: Macrosomic fetuses represent a continuing challenge in obstetrics. Objectives: We studied maternal risk factors of fetal macrosomia and maternal and infant outcome in such cases. Methods: A retrospective cohort study was carried out with a total of 26,961 singleton pregnancies between 1989 and 2001. Records of 886 mothers who gave birth to live born infants weighing ≧4,500 g were compared to those of 26,075 mothers with normal weight (<4,500 g) infants. Multiple regression analysis was used to identify independent reproductive risk factors. Perinatal complications were also assessed. Results: The incidence of fetal macrosomia was 3.4%. Diabetes, previous macrosomic birth, postdatism (>42 weeks of gestation), obesity (BMI > 25 before pregnancy), male infant, gestational diabetes mellitus, and non-smoking were independent risk factors of fetal macrosomia, with adjusted risks of 4.6, 3.1, 3.1, 2.0, 1.9, 1.6, 1.4, respectively. In the macrosomic group, birth and maternal traumas occurred significantly more often than in the control group. However, records of subsequent pregnancies (n = 250) after the study period showed that a previous uncomplicated birth appeared to decrease complication risks. Conclusions: Most cases of fetal macrosomia occur in low-risk pregnancies and evaluation of maternal risks cannot accurately predict which women will eventually give birth to an overweight newborn. After an uncomplicated birth of a macrosomic infant, vaginal delivery may be a safe option for the infant and mother.
AIM:To compare the efficiency of turquoise light with that of TL52 blue in treatment of preterm infants with jaundice at the same level of body irradiance.METHODS:Infants with gestational age 28-37 weeks and non-haemolytic hyperbilirubinemia were treated for 24 h with either turquoise light (OSRAM L18W/860 fluorescent lamps) or blue light (Philips TL20W/52 fluorescent lamps). The concentrations of serum total bilirubin and bilirubin isomers were measured by the Vitros routine method and by HPLC, respectively.RESULTS:The decrease in serum concentrations of total bilirubin, total bilirubin isomers and the toxic Z,Z-bilirubin was greatest for infants treated with turquoise light. Further, the increase in Z,E-bilirubin was smaller and there was a trend towards a higher rise in E,Z-bilirubin.CONCLUSIONS:Turquoise light has a greater bilirubin reducing effect than TL52 blue light with equal irradiance, expressed both by serum total bilirubin, total bilirubin isomers and Z,Z-bilirubin, i.e. the turquoise spectral range is more efficient than the blue. This is in accordance with deeper penetration into the skin, lower production of the Z,E-bilirubin and greater production of E,Z-bilirubin and lumirubin, in infants under turquoise light. This suggests, given equal irradiances, that light in the turquoise spectral range is preferable to the TL52 blue in treatment of newborn jaundiced infants.
