A survey of neonatal births in maternity departments in urban China in 2005 / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the epidemiology of births in urban China.</p><p><b>METHODS</b>A retrospective study was conducted on neonates born in 2005 in the maternity departments of 72 urban hospitals from 22 provinces in China.</p><p><b>RESULTS</b>A total of 45722 infants born between January 1, 2005 and December 31, 2005 were enrolled. The male to female sex ratio was 1.13:1. Preterm births accounted for 8.1%. The incidence of very low birth weight infants was 0.7%. A total of 99.7% of mothers delivering at term had conceived naturally and 0.3% had experienced assisted reproduction. A total of 98.4% of mothers who delivered preterm had conceived naturally and 1.6% had experienced assisted reproduction. The proportion of vaginal deliveries was 50.8% compared to 49.2% delivered by cesarean sections. Many cesarean sections (38.1%) were due to social factors. Infants with an Apgar score≤7 at 1 minute accounted for 4.8%, and 1.6% of infants had an Apgar score≤7 at 5 minutes. Of all the infants included in the study, 7.14% were admitted to neonatal units for treatment. The death rate of all included infants was 0.74%.</p><p><b>CONCLUSIONS</b>The proportion of preterm births was higher in 2005 than in 2002-2003. The proportion of cesarean section deliveries was much higher in urban China than in most other Asian countries and America.</p>

An epidemiologic investigation of newborns from obstetric departments in the central south region of China / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the birth information of newborn infants from obstetric departments in the Central South Region of China.</p><p><b>METHODS</b>A retrospective investigation was carried out in 15582 newborns from obstetric departments of 23 hospitals in the Central South Region of China between January 1 and December 31 of 2005.</p><p><b>RESULTS</b>The sex ratio (male/female) of neonates was 1.16∶1. The proportion of preterm infants was 8.11%. The very low birth weight infants accounted for 0.73%. The neonates born by spontaneous labor accounted for 57.52%. Cesarean sections accounted for 40.82% (social factor of cesarean section: 29.91%). The incidence of neonatal asphyxia was 3.78%, in which 0.75% of the cases were severe asphyxia. The mortality of newborn infants was 0.55%, in which the mortality of preterm infants was 5.56%.</p><p><b>CONCLUSIONS</b>The proportion of preterm infants and the incidence of neonatal asphyxia is high in the Central South Region of China. The proportion of births delivered by cesarean section is high, and social factors are probably responsible for the high rate.</p>

Measurement of umbilical activin A level in preterm infants / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To evaluate the clinical significance of umbilical activin A in preterm infants.</p><p><b>METHODS</b>Forty-one preterm infants (gestation 28 to 36 weeks) were enrolled. Fetal membranes, umbilical cords and blood samples from umbilical vein were obtained. Umbilical activin A level was measured using ELISA. The histological examinations of fetal membranes and umbilical cords were performed.</p><p><b>RESULTS</b>The umbilical level of activin A averaged 2069 pg/mL in the 41 preterm infants. The umbilical activin A level in the 5 infants with intrauterine infection was higher than in those without intrauterine infection (2510 pg/mL vs 1975 pg/mL; P<0.01). Umbilical activin A level at cutoff of 2490 pg/mL showed a sensitivity of 80.0% and a specificity of 90.6% as a marker of intrauterine infection. There were no significant differences in the umbilical activin A level between the infants with and without respiratory distress syndrome. Umbilical activin A level was positively correlated with the duration of postnatal oxygen therapy (r=0.326, P<0.05).</p><p><b>CONCLUSIONS</b>Umbilical activin A may serve a marker of intrauterine infection in preterm infants. The umbilical activin A level is correlated with the duration of postnatal oxygen therapy.</p>

Relationship between alveolar epithelial type II cells and pulmonary surfactant protein A levels in young rats with acute lung injury / 中国当代儿科杂志

<p><b>OBJECTIVE</b>This study examined the relationship between the ultrastructural alterations of alveolar epithelial cells type II (AEC-II) and pulmonary surfactant protein A (SP-A) levels in the lung tissue of young rats with acute lung injury (ALI) in order to explore the possible mechanism of ALI.</p><p><b>METHODS</b>Forty-eight young Sprague-Dawley rats were randomly divided into control and ALI groups. The rats in the ALI group were intraperitoneally injected with 4 mg/kg of lipopolysaccharide (LPS) in order to induce ALI. The control subjects were injected with the same volume of normal saline. Rats were sacrificed at 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of the left lung and fixed with 2.5% glutaraldehyde for transmission electron microscope examination and for Western blot test of SP-A.</p><p><b>RESULTS</b>The microvilli of AEC-II disappeared 24 hrs after LPS injection. After 24 and 48 hrs of LPS injection, lamellar body (Lb) increased in number, enlarged in size and reduced in density, and the ring-like arrangement of Lb was present. By 48 hrs after LPS injection, giant Lb with vacuole-like deformity appeared. The contents of lung SP-A in the ALI group 24 hrs (6.52+/-0.62 vs 5.02+/-0.35; P<0.01) and 48 hrs (6.65+/-0.62 vs 5.01+/-0.36; P<0.01) after LPS injection were significantly higher than those in the control group. By 72 hrs after LPS injection, Lbs ruptured and were reduced in number. The shape of the nuclei was irregular and the border was blurred. The content of lung SP-A was greatly reduced in the ALI group 72 hrs after LPS injection compared with that in the control group (3.87+/-0.50 vs 5.22+/-0.36; P<0.01).</p><p><b>CONCLUSIONS</b>The alterations of AEC-II and lung SP-A were time-dependent in young rats with ALI induced by LPS. In the early stage of ALI, the lung SP-A content showed a compensatory increase. With the increasing injury of AEC-II cells, the secretion of SP-A presented with a decompensation and the lung SP-A content decreased. This may be one possible mechanism for the development of ARD.</p>

Multicenter investigation for incidence of periventricular leukomalacia in premature infants in China / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Sponsored by the Subspecialty Group of Neonatology of Pediatric Society, China Medical Association, more than 10 large-scale hospitals participated in the near two-year multicenter investigation for brain injuries in premature infants in China. This study presented the investigation result for the incidence of periventricular leukomalacia (PVL) in premature infants from 10 Third Class A Level hospitals.</p><p><b>METHODS</b>The premature infants with a gestation age<37 weeks in the 10 hospitals were given routine cranial ultrasound scanning within seven days after birth, and then repeated every 3-7 days until discharge from January 2005 to August 2006. The severity of PVL was graded based on de Vries classification.</p><p><b>RESULTS</b>A total of 4 933 premature infants were enrolled. The total incidence of PVL and the incidence of cystic PVL were 2.3% (112/4 933) and 0.3% (16/4 933), respectively. Of the 112 PVL cases, 96 (85.7%) were with grade I, 14 (12.5%) with grade II, and 2 (1.8%) with grade III. The incidence of PVL in 4 maternal and child health care hospitals were significantly lower than that in 6 general or children's hospitals (1.4% vs 2.8%) (X2=10.284, P<0.01). Vaginal delivery and mechanical ventilation were possible high-risk factors for the development of cystic PVL.</p><p><b>CONCLUSIONS</b>The data of the multicenter investigation can basically reflect the situation about the occurrence of PVL in premature infants in major big cities of China. It is important to improve the ability to recognize the sonogram of non-cystic periventricular white matter injury.</p>

Changes of pulmonary surfactant protein A in young rats with acute lung injury induced by lipopolysaccharide / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Pulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury.</p><p><b>METHODS</b>Sprague-Dawley rats were randomly assigned to control and lung injury groups. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the lung injury group. The same amount of normal saline was given for the control group. The two groups were subdivided into 6 groups sacrificed at 6, 12, 24, 36, 48 and 72 hrs of injection (n=8 each). Western blot was employed to detect SP-A concentration in the lung tissues.</p><p><b>RESULTS</b>SP-A concentration in the lung injury group was not different from the the control group within 12 hrs after LPS injection. SP-A concentration in the lung injury group was elevated significantly during 24-48 hrs after LPS injection, peaking at 36 hrs (6.94+/-0.80 vs 5.01+/-0.36; P< 0.01), compared with the controls. However, SP-A concentration in the lung injury group was significantly reduced 72 hrs after LPS injection compared with the controls (P< 0.01).</p><p><b>CONCLUSIONS</b>The changes of lung SP-A concentration in rats following acute lung injury were time-dependent. The transient elevation of SP-A concentration in the lungs indicated a strong compensation ability of SP-A in the host defence against acute lung injury.</p>

Genetic polymorphism of surfactant protein A in neonatal respiratory distress syndrome / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the characteristics of gene expression of surfactant protein A in Chinese premature infants and the association between surfactant protein A and the risk of neonatal respiratory distress syndrome (RDS).</p><p><b>METHODS</b>Vein-blood samples (2 mL) from 18 Chinese premature infants with RDS and 28 controls were assayed for SP-A genotypes 6A2, 6A3, 1A0 and 1A1 by SSCP.</p><p><b>RESULTS</b>The frequency of allele distribution of SP-A1 allele 6A2 and 6A3 was 0.50 and 0.056 respectively in the RDS group and was 0.214 and 0.107 in the control group. Compared with the controls, SP-A1 allele 6A2 was over-represented in the RDS group (P<0.05). In contrast, SP-A1 allele 6A3 tended to be under-represented in the RDS group but there was no statistical difference when compared with the controls. The frequency of allele distribution of SP-A2 allele 1A0 and 1A1 was 0.722 and 0.667 respectively in the RDS group and was 0.679 and 0.821 respectively in the control group. There were no significant differences in the distribution frequency of SP-A2 allele 1A0 and 1A1 between the two groups. In the infants born at gestation >32 weeks, SP-A1 allele 6A2 was over-represented in the RDS group compared with the control group (frequency: 0.56 vs 0.15; P<0.05).</p><p><b>CONCLUSIONS</b>The frequency of SP-A1 allele 6A2 and 6A3 was low, in contrast, the frequency of SP-A2 allele 1A0 and 1A1 was high in normal Chinese premature infants. SP-A1 allele 6A2 may be a susceptible gene for RDS.</p>

Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced by lipopolysaccharide / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Pulmonary surfactant protein-D (SP-D) is regarded as a valuable biomarker in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This study was to explore the changes of SP-D content in lung tissue following ALI and the effect of dexamethasone (Dex) on the SP-D content in young rats.</p><p><b>METHODS</b>One hundred and forty-four 21-day-old Sprague-Dawley rats were randomly assigned into control, ALI and Dex-treated groups. ALI was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the rats from the ALI and Dex-treated groups. Normal saline was given for the control group. Dex (5 mg/kg) was administered 1 hr after LPS injection in the Dex-treated group. At each time interval of 6, 12, 24, 36, 48 and 72 hrs after LPS injection, eight rats of each group were randomly chosen and sacrificed. Western blot was employed to detect the content of SP-D in lung tissues.</p><p><b>RESULTS</b>The pulmonary SP-D content decreased significantly at 36, 48 and 72 hrs after LPS administration in the ALI group, and reduced to a nadir (0.92 +/-0.11 vs 3.27 +/- 0.52) at 48 hrs compared with that of the control group (P < 0.01). The SP-D content in the Dex-treated group increased significantly at 36,48 and 72 hrs after LPS administration when compared with the ALI group (P < 0.01). A significant difference in the SP-D content between the Dex-treated and the control group was noted only at 72 hrs after LPS administration (P < 0.05).</p><p><b>CONCLUSIONS</b>The SP-D content in lung tissue was reduced following ALI in young rats at the early stage. Early administration of Dex can significantly increase the pulmonary SP-D content.</p>

Effects of dexamethasone on the ultrastructure of alveolar type II cells in young rats with lipopolysaccharide-induced acute lung injury / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Alveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats.</p><p><b>METHODS</b>Seventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1 hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination.</p><p><b>RESULTS</b>Microvilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared.</p><p><b>CONCLUSIONS</b>Ultrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury.</p>

Differential response of developing human fetal lung explants to hyperoxia and the effects of dexamethasone on hyperoxia-exposed lungs / 中国当代儿科杂志

<p><b>OBJECTIVE</b>This study aimed to explore the effects of hyperoxia on the development of fetal lung by investigating the changes of morphological and cell proliferation induced by hyperoxia in cultured fetal lungs as well as the effects of dexamethasone on hyperoxia-exposed lungs.</p><p><b>METHODS</b>Human fetal lung explants at the pseudoglandular stage of development were cultured randomly either in normoxia (21% O2/5% CO2) or hyperoxia (95% O2/5% CO2) for 72 hrs. Dexamethasone was added into the feeding medium at the concentration of 10(-6)M. Harvested tissues were stained for pancytokeratin to identify epithelial cells, with Ki-67 as a marker of proliferation. The effects of lung morphometry were analyzed using computer assisted image analysis. The mean airway thickness, the proportion of the surface area occupied by airways, the mean airway surface area and the index of the epithelium proliferation were measured.</p><p><b>RESULTS</b>The lung architectures remained unchanged after 72 hrs normoxia culture, whereas hyperoxia culture resulted in significant dilation of airways and thinning of epithelium, with the surface area of airways of 6662 microm(2) vs 2728 microm(2) and the thickness of airways of 7.8 microm vs 8.1 microm (P < 0.05). Hyperoxia culture also resulted in an increase in the proportion of the surface area occupied by airways than normoxia culture (35.2% vs 23.4%; P < 0.05). The surface area of airways (3174 microm(2)) and the proportion of the surface area occupied by airways (23.9%) decreased significantly in hyperoxia-cultured lungs after dexamethasone administration (P < 0.05). The epithelium proliferation index in hyperoxia-cultured lungs (21.8%) was higher than that in normoxia-cultured lungs (5.1%) and dexamethasone-treated hyperoxia-cultured lungs (7.4%) (P < 0.05).</p><p><b>CONCLUSIONS</b>The exposure of pseudoglandular lungs to hyperoxia modulates the lung architecture to resemble saccular lungs with higher epithelium proliferation index. Dexamethasone may inhibit the effects induced by hyperoxia.</p>

Reconstructing Renal Injury Model Induced by Intrauterine Asphyxia in Newborn Rats / 实用儿科临床杂志

Objective To establish a newborn animal model of renal injury caused by intrauterine asphyxia and explore the mechanism of renal injury in neonate after asphyxia.Methods After two-horn uterus and vessels supplying uterus and ovary were exposed in 21-day-pregnant Wistar rats,arterial clamp occluded one side of vessels.The occluding time were 10 and 30 minutes.Then arterial clamp was taken off,and reperfusion for 30 minutes,2,6,12 and 24 hours respectively.Reaching prescribed time uterus horn was opened rapidly and pups were removed.The pups sacrificed by decapitation.Kidneys were taken out and studied by HE staining and electron microscope.Results Kidney of fetal rats in 21 gestational age was developmental and mature degree of tubules dropped behind that of glomerule.Changes of proximal tubules were early and serious compared with distal tubules during ischemia and reperfusion stages.Conclusion Ischemia and reperfusion to graded pregnant rat can supply an ideal model to study injury of kidney and other organs(intraute)-rously.

Change of neurokinin A plasma level in asthmatic children / 中华儿科杂志

<p><b>OBJECTIVE</b>Chronic inflammation of airway in bronchial asthma is caused by many complicated elements. Recently, a close attention has been paid to the neurogenic inflammation in airway which is mediated by sensory neuropeptides secreted by sensory nerve in the lung. Neurokinin A (NKA) is an important sensory neuropeptide leading to neurogenic inflammation in airway. Experimental studies showed that NKA has a close relation to asthma. The purpose of the present study was to investigate the changes of NKA in plasma of asthmatic children and possible relationship between sensory neuropeptides and asthma in children.</p><p><b>METHODS</b>Thirty-five children with bronchial asthma were studied; 16 of the cases were < 3 yrs and 19 were >or= 3 yrs. Eighteen of the cases had severe asthma and 16 had mild asthma. None of the subjects was treated with glucocorticoid within 3 days before the study started; 15 healthy children without history of asthma or family history of asthma were enrolled as control subjects. Plasma was collected from each case during acute attack of asthma and their clinical remission of the asthmatic children. After purifying with SEP-pak C(18), NKA content was detect by enzyme-linked immunosorbent assay (ELISA) as instructed by the manufacturer of the NKA Kit (NKA unit: ng/L).</p><p><b>RESULTS</b>(1) The content of plasma NKA of asthmatic children was significantly higher at the asthma attack (256 +/- 153) than that at their clinical remission stage (70 +/- 66; q = 9.497, P < 0.01) and than that of the normal control group (38 +/- 6; q = 8.599, P < 0.01); no significant difference in plasma NKA was found between the clinical remission stage and the normal control group (q = 1.245, P > 0.05). (2) There was a significant positive correlation between the asthmatic clinical state and the levels of plasma NKA; the contents of plasma NKA at the stage of acute attack in severe asthma (296 +/- 170) were significantly higher than those of the mild asthmatic children (190 +/- 99; q = 3.77, P < 0.05).</p><p><b>CONCLUSIONS</b>The contents of plasma NKA were significantly higher during the asthma attack stage of children, and the higher was the level of NKA, the more severe the attack.; with asthma remission, the contents of plasma NKA decreased to normal; the contents of plasma NKA has a close relation to the asthmatic children.</p>