Impact of a nationwide training program for neonatal resuscitation in China / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Seventeen million births occur in China each year. Neonatal mortality is the leading cause of under 5-year-old child deaths, and intrapartum-related injury accounts for much of mental retardation in young children. The Chinese Ministry of Health sought to improve infant and child survival through a nationwide initiative to have at least one person trained in neonatal resuscitation at every birth. The aim of the current study was to evaluate the impact of China Neonatal Resuscitation Program (NRP) on policy and infrastructure changes and its effectiveness in decreasing the incidence of mortality among newborn infants.</p><p><b>METHODS</b>The Chinese NRP incorporated policy change, professional education, and creation of a sustainable health system infrastructure for resuscitation. Multidisciplinary teams from all 31 provinces and municipal states disseminated NRP in a train-the-trainer cascade. The intervention targeted 20 provinces with high neonatal mortality and programs to reduce maternal mortality. Program evaluation data came from 322 representative hospitals in those provinces.</p><p><b>RESULTS</b>Changes in policy permitted midwives to initiate resuscitation and required resuscitation training for licensure. From 2004 through 2009 more than 110,659 professionals received NRP training in the 20 target provinces, with 94% of delivery facilities and 99% of counties reached. Intrapartum-related deaths in the delivery room decreased from 7.5 to 3.4 per 10,000 from 2003 to 2008, and the incidence of Apgar ≤ 7 at 1 minute decreased from 6.3% to 2.9%.</p><p><b>CONCLUSIONS</b>The Chinese NRP achieved policy changes promoting resuscitation, trained large numbers of professionals, and contributed to reduction in delivery room mortality. Improved adherence to the resuscitation algorithm, extension of training to the township level, and coverage of births now occurring outside health facilities can further increase the number of lives saved.</p>

Relationship between ACE gene insertion or deletion polymorphism and left ventricular mass in newborns admitted to the neonatal intensive care unit / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the relationship between angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and left ventricular mass (LVM) in newborns admitted to the neonatal intensive care unit (NICU).</p><p><b>METHODS</b>Seventy-two newborns admitted to the NICU were enrolled. ACE genotypes were determined by genomic DNA which was isolated from heel-prick blood. Disease status of the newborns was evaluated by the Neonatal Critical Score (draft) on postnatal day 1. LVM and LVM index (LVMI) were evaluated by echocardiography on postnatal days 1-3.</p><p><b>RESULTS</b>DD genotype was identified in 11 cases, ID genotype in 31 cases, and II genotype in 30 cases. There were no significant differences in clinical characteristics, critical score and body measurements in newborns with different genotypes. The DD genotype group showed significantly lower LVMI than the group with ID+II genotypes (29±4 g/m2 vs 35±8 g/m2; P<0.05).</p><p><b>CONCLUSIONS</b>ACE gene polymorphism is associated with the LVMI in newborns admitted to the NICU. The LVMI of DD genotype carriers is significantly lower than that of ID+II genotypes carriers, which suggests that D allele may be associated with the growth and development of left ventricular.</p>

A meta-analysis of nasal intermittent positive pressure ventilation in treatment of respiratory distress syndrome in premature infants / 中华儿科杂志

<p><b>OBJECTIVE</b>To assess the efficacy of nasal intermittent positive pressure ventilation (NIPPV) in treatment of respiratory distress syndrome (RDS) in premature infants.</p><p><b>METHODS</b>According to the requirements of Cochrane systematic review, a thorough literature search was performed among PubMed (1977-2008), Embase (1989-2008), OVID, Cochrane (2008), Chinese Digital Hospital Library (www.chkd.cnki.net) and Chinese Biomedical Literature Disk Database (CBMdisc). Quality assessments of clinical trials were carried out. Randomized controlled trials (RCTs) with NIPPV and RDS were enrolled, and Revman 4.2 software was used for meta-analysis. The trials were analyzed using relative risk (RR) for dichotomous data, weighted mean difference (WMD) were used for continuous data, both kind of data were expressed by 95% confidence intervals (95% CI). For homogenous data (P> or =0.10), fixed effects model was calculated, for heterogeneity data (P<0.10), random effects model was calculated.</p><p><b>RESULTS</b>Five RCTs involving 284 premature infants diagnosed as respiratory distress syndrome (RDS) were included. Three studies comparing NIPPV with nasal continuous positive airway pressure (NCPAP) in the postextubation period, the extubation failure rate was 8.34% vs 40.79% in NIPPV group and NCPAP group, the NIPPV group had significantly lower extubation failure rates [RR 0.21 (95% CI: 0.10-0.45; P<0.001)]. Two of the above-mentioned three studies analyzed bronchopulmonary dysplasia (BPD) rates, the incidence of BPD was 39.34% vs 54.39% in NIPPV group and NCPAP group, the NIPPV group had a trend towards lower BPD rates, but this did not reach statistical significance [RR 0.73 (95% CI: 0.49-1.07; P=0.11)]. NIPPV was used as primary mode in two studies, one compared with conventional ventilation (CV), which detected that the NIPPV group had significantly lower BPD rates (10% vs. 33.33%, P=0.04); the other compared with NCPAP, which also showed that NIPPV group had significantly lower BPD rates (2.33% vs. 17.07%, P=0.03).</p><p><b>CONCLUSION</b>The primary mode NIPPV was found to be feasible as a method of ventilation in preterm infants with RDS, and was associated with a decreased incidence of BPD. In the postextubation period, NIPPV is more effective in preventing failure of extubation than NCPAP.</p>

Serum gastrin levels and clinical conditions in response to early minimal feeding in premature infants / 中华儿科杂志

<p><b>OBJECTIVE</b>To study serum gastrin levels in response to early minimal feeding in premature infants and evaluate the clinical effect of early minimal feeding.</p><p><b>METHODS</b>Premature infants with critical score < or = 90 were randomly assigned into two groups: early minimal feeding group (n = 48), non-early minimal feeding group (n = 47). Other premature infants (n = 30) without any complications (critical score > 90) were assigned as normal control group. The premature infants in normal control group were fed with water at 6 h after birth, 1 - 2 ml/kg every time, after once or twice, they were fed with formula, increasing in the amount of formula gradually, until adequate. The premature infants in early minimal feeding group were fed with formula within 72 h after birth, 0.5 - 1 ml/kg, once every 3 h, the amount of formula was increased gradually, until adequate. The premature infants without early minimal feeding were not fed with formula until the illness was stable, the amount of formula was increased gradually until adequate. Situation of gastrointestinal feeding tolerance, growth and development, and clinical symptoms were observed and recorded for the three groups. Serum gastrin levels were monitored at 1, 3, 7 day after birth by radioimmunoassay.</p><p><b>RESULTS</b>Serum gastrin concentrations in the three groups elevated from 1 to 7 days. In early minimal feeding group [(82.4 +/- 24.5) ng/L] and non-early minimal feeding group [(87.0 +/- 40.2) ng/L], the concentrations were significantly higher than those in normal control group [(66.4 +/- 19.7) ng/L] at day 1 (F = 3.36, P < 0.05). At day 3 and 7, the concentrations in early minimal feeding group [(96.3 +/- 14.6) ng/L, (113.0 +/- 16.5) ng/L] were significantly higher than those in non-early minimal feeding group [(73.9 +/- 13.5) ng/L, (92.4 +/- 12.2) ng/L] (P < 0.05). There were significant differences among the three groups in infants with feeding intolerance (2/30, 5/48, 14/47), the period reached full enteral feeding [(20.6 +/- 5.7) d, (27.8 +/- 6.1) d, (39.5 +/- 4.7) d], and in number of hospital day [(29.0 +/- 4.6) d, (39.0 +/- 4.8) d, (48.0 +/- 5.6) d] (P < 0.05). There were significant differences between early minimal feeding group and non-early minimal feeding group in the weight gain three and four weeks after birth [(19.1 +/- 2.4) g/d, (11.9 +/- 3.3) g/d], the period reached birthweight [(19.8 +/- 4.2) d, (25.2 +/- 5.1) d] (P < 0.05). There were no significant difference among the three groups in the weight gain in one and two weeks after birth [(5.9 +/- 2.9) g/d vs. (5.0 +/- 2.1) g/d], the numbers of premature infants with infection, anemia, apnea, or hypoglycemia.</p><p><b>CONCLUSION</b>Early minimal feeding in premature infants leads to secretion of gastrin, promotes the development of gastrointestine and may not be associated with occurrence of complications.</p>

Influence of angiotensin converting enzyme gene insertion/deletion polymorphism and beta3-adrenergic receptor gene Trp64Arg polymorphism on fetal growth and neonatal insulin sensitivity / 中华儿科杂志

<p><b>OBJECTIVE</b>To understand the influence of angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and beta3-adrenergic receptor (beta3-AR) gene Trp64Arg polymorphism on fetal growth and neonatal insulin sensitivity.</p><p><b>METHODS</b>Totally 296 newborn infants were selected into our study and divided into 2 groups according to gestational age and birth weight: adequate-for-gestational-age (AGA) group (222 cases) and small-for-gestational-age (SGA) group (74 case). Serum glucose and insulin were examined in the morning of the 3rd day before milk. Insulin sensitivity was evaluated by homeostasis model assessment (HOMA) equation. beta3-AR gene Trp64Arg polymorphism and ACE gene I/D polymorphism (202 cases) were analysed using polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP) technique. Gestational age, birth weight, birth weight percentage, serum glucose, insulin and HOMA-IR were compared among different genotype groups. Statistical analysis was performed with the SPSS 10.0 software.</p><p><b>RESULTS</b>No significant difference was found between the serum glucose level of SGA group (4.03 +/- 1.05 mmol/L) and AGA group (4.05 +/- 1.14 mmol/L), P = 0.008. The serum insulin level (converted into Ln) of SGA group (2.262 +/- 0.746) was significantly higher than that of AGA group (1.757 +/- 0.805), P < 0.001. The HOMA-IR (also converted into Ln) level of SGA group (0.217 +/- 0.367) was also significantly higher than that of AGA group (0.001 +/- 0.378), P < 0.001. In the SGA group beta3-AR gene Arg64 allele carriers had higher serum insulin and HOMA-IR level (both changed to Ln, 2.654 +/- 0.701, 0.371 +/- 0.338) compared with noncarriers (2.074 +/- 0.698, 0.143 +/- 0.360), P < 0.05. The ACE gene DD genotype carriers had higher serum insulin and HOMA-IR level (both were converted into Ln, 2.19 +/- 0.91, 0.51 +/- 1.01) compared with II (1.77 +/- 0.85, 0.02 +/- 0.93) and ID genotype group (1.77 +/- 0.83, 0.05 +/- 0.91), P < 0.05. The ACE gene DD carriers had lower birth weight percentage compared with II and ID genotype group, P < 0.05. When both genes' polymorphisms were taken into account, the newborns who had both DD genotype and Arg64 allele had obviously higher serum insulin level (Ln, 2.560 +/- 1.160) than the neonates who had only one of the polymorphisms mentioned above (1.970 +/- 0.821, 1.992 +/- 0.706) and the neonates who had neither of the two polymorphisms (1.683 +/- 0.832), P < 0.05. The newborns who had both DD genotype and Arg64 allele also had significantly higher HOMA-IR level (Ln, 1.042 +/- 1.315) than the neonates who had only one of the polymorphisms mentioned above (0.247 +/- 0.710, 0.230 +/- 0.890) and the neonates who had neither of the two polymorphisms (-0.053 +/- 0.924), P < 0.05.</p><p><b>CONCLUSION</b>Newborns SGA had impaired insulin sensitivity. beta3-AR gene Trp64Arg polymorphism and ACE gene I/D polymorphism are important factors that may connect IUGR with insulin resistance syndrome in adulthood.</p>

Relationship of the disease severity with ACE gene polymorphism and serum ACE activity in preterm infants / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the relationship of disease severity with angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and serum ACE activity in preterm infants during the first 7 days of life.</p><p><b>METHODS</b>ACE genotypes were determined in 85 preterm infants admitted to the neonatal intensive care unit (NICU). Serum ACE activity was measured and disease severity was evaluated by the Neonatal Critical Score (draft) 1, 3 and 7 days after birth.</p><p><b>RESULTS</b>Of the 85 preterm infants, DD genotype was found in 19 cases, ID genotype in 34 cases and II genotype in 32 cases. On the 1st day of life, serum ACE activity in the DD genotype (33.42+/-7.93 U/L) and the ID genotype groups (31.53+/-7.56 U/L) were significantly higher than that in the II genotype group (25.53+/-7.56 U/L) (P<0.01). After 3 and 7 days of life, serum ACE activity decreased in the three groups, but the DD genotype group remained the highest ACE activity, followed by the ID genotype and the II genotype groups. On the 1st day of life, the critical score of the DD genotype group (87.37+/-8.30) was lower than the ID genotype (95.82+/-5.85) and the II genotype groups (95.88+/-6.85) (P<0.01). On the 3rd day, the critical score of the DD genotype group was still lower than the ID genotype group (92.95+/-7.10 vs 96.94+/-5.85) (P<0.05).</p><p><b>CONCLUSIONS</b>ACE gene I/D polymorphism may be associated with the disease severity in preterm infants. The DD genotype carriers present more severe disease status, with higher serum ACE activity. Although the disease status can influence serum ACE activity, serum ACE activity is determined by the ACE genotype.</p>

Expression of caspase-3 mRNA in the hippocampus of seven-day-old hypoxic-ischemic rats and the mechanism of neural protection with magnesium sulfate / 中华儿科杂志

<p><b>OBJECTIVE</b>There was consanguineous relationship between caspase-3 and early damage after hypoxia and ischemia. Caspase-3 plays a key role in the process of apoptosis in neuron. Magnesium sulfate could protect neuron from injuries, but the mechanism was not clear. The study was to investigate the expression of caspase-3 mRNA in the hippocampus of seven-day-old hypoxic-ischemic rats and the possible mechanism of neural protection with magnesium sulfate.</p><p><b>METHODS</b>The model of seven-day-old hypoxia-ischemia rats was established. The rats were divided randomly into 6 groups as follows: (1) normal control (n = 4); (2) sham surgery control (n = 4); (3) hypoxia-ischemia (n = 4); (4) sodium chloride injection with hypoxia-ischemia (n = 4); (5) magnesium sulfate pre-injection with hypoxia-ischemia (n = 4); (6)magnesium sulfate post-injection with hypoxia-ischemia (n = 4). The therapy groups received a bolus injection of 500 mg/kg magnesium sulfate intraperitoneally 0.5 hour before or after hypoxia-ischemia. Semi-quantitative RT-PCR was used to measure caspase-3 mRNA expression in the hippocampus 24 hours after hypoxia-ischemia.</p><p><b>RESULTS</b>The expression of caspase-3 mRNA was significantly increased in the hippocampus of the hypoxia-ischemia pups (1.88 +/- 0.36 vs 0.97 +/- 0.46, P < 0.05). The expression of caspase-3 mRNA in rats with magnesium sulfate pre-injection and post-injection decreased significantly (1.54 +/- 0.49, 1.65 +/- 0.48 vs 1.88 +/- 0.36, P < 0.05).</p><p><b>CONCLUSION</b>Caspase-3 was activated in the hippocampus of the seven-day-old rats 24 hours after hypoxia-ischemia. The suppression of the expression of caspase-3 mRNA in the hippocampus was probably related to the protective effect of magnesium sulfate on the brain injury of hypoxia-ischemia.</p>

Effects of recombinant human erythropoietin on the immune function of premature rats / 中华儿科杂志

<p><b>OBJECTIVE</b>To observe the effect of recombinant human erythropoietin (rHuEPO) on immune function of premature rats.</p><p><b>METHODS</b>RHuEPO of 250 IU/(kg.t) or 500 IU/(kg.t) was administered to premature rats every other day for nineteen days. The control premature rats were received normal saline. The changes of hemoglobin (Hb), serum erythropoietin (EPO), red blood cell (RBC) immune function, T lymphocyte proliferative responsiveness, and production of tumor necrosis factor alpha (TNF-alpha) were observed.</p><p><b>RESULTS</b>Premature rats showed lower levels on Hb, RBC immune function, T cell responsiveness and production of TNF-alpha compared with mature rats at birth. The postnatal declines of Hb and RBC immune function were lessened in the treated groups of premature rats, the higher dosage group of 500 IU/(kg.t) was more significant than the lower dosage group of 250 IU/(kg.t). When experiments were over, Hb of control premature rats was (7.72 +/- 0.89) g/dl, Hb of premature rats received 500 IU/(kg.t) was (10.08 +/- 0.90) g/dl (P < 0.01). C3b-R% of control premature rats was (11.00 +/- 0.95)%, C3b-R% of premature rats received 500 IU/(kg.t) was (17.75 +/- 1.04)% (P < 0.01). IC-R% in control premature rats was (12.83 +/- 1.33)%, IC-R% of premature rats received 500 IU/(kg.t) was (10.50 +/- 1.67)% (P < 0.01). The postnatal rise of T cell responsiveness and the production of TNF-alpha in premature rats increased in the treated groups, which was more significant in the higher dosage group of 500 IU/(kg.t) than in the lower dosage group of 250 IU/(kg.t). The OD index of control premature rats was 0.159 +/- 0.014, the OD index of premature rats received 500 IU/(kg.t) was 0.354 +/- 0.050 (P < 0.01). TNF-alpha in control premature rats was (0.270 +/- 0.014) ng/ml, TNF-alpha of premature rats received 500 IU/(kg.t) was (0.415 +/- 0.010) ng/ml (P < 0.01).</p><p><b>CONCLUSIONS</b>(1) Premature rats had lower RBC immune function and T cell responsiveness and underproduction of TNF-alpha at birth. (2) Premature rats had an improvement with the RBC immune function after rHuEPO administration. (3) Premature rats had improvements with T cell responsiveness and TNF-alpha after rHuEPO administration, and there was a positive correction between the RBC immune function and T cell responsiveness with the production of TNF-alpha.</p>