Objective To demonstrate the association between fluid intake and sodium intake during the first 10 days of life and the risk of chronic lung disease (CLD) in very low birth weight (VLBW) infants.Methods A retrospective analysis of data from VLBW infants enrolled in the Neonatal Department of our hospital; 130 infants with birth weight between 790 and 1 470 g were randomized, among which 12 infants was diagnosised CLD. The daily fluid intake and sodium intake during the first 10 days of life were compared between the infants without CLD and those who developed CLD. Demographic and clinical neonatal variables were also compared. Results 118 infants survived without CLD and 12 infants developed CLD. Analysis showed that the daily fluid intakes were higher (day 2～10) and weight loss less (day 6～9) in the group of infants who developed CLD. In addition, the daily sodium intakes were also higher (day 2～6) in infants who developed CLD. Conclusion In the VLBW infants treated during the post surfactant era, higher fluid or sodi-um intake during the first 10 days of life were associated with an increased risk of CLD. The finding suggests that careful attention to fluid balance might be an important means to reduce the incidence of CLD.

Objective To explore the influence of retinoic acid (RA) on the expressions of insulin-like growth factor (IGF)-Ⅱ,type 2 IGF receptor (IGF-2R) and IGF binding protein (IGFBP)-2 mRNA and polypeptides in lungs of hyperoxia-exposed premature rats and its possible molecular mechanism. Methods On the 2nd postnatal day, 260 Sprague-Dawley(SD)preterm rats were randomly divided into 4 groups. Group Ⅰ: air + normal saline (NS) group; Group Ⅱ: hyperoxia(85% O_2) + NS group; Group Ⅲ: air+ RA group; Group Ⅳ: hyperoxia(85% O_2) + RA group. RA was injected to group Ⅲ, Ⅳ intraperitoneally (500 ?g/kg) since the 3rd day after birth, while NS was given to group Ⅰ,Ⅱ daily at the same time as group Ⅲ and Ⅳ. On day 4, 7, 10, 14 and 21 after birth, 8 rats in each group were killed. The mortality of preterm rats was recorded and lung radical alveolar counts (RAC) were examined. The mRNA analysis (RT-PCR) and polypeptides analysis (Western Blot) of IGF-Ⅱ, IGF-2R and IGFBP-2 were performed. Results 1. On the 4～7th day of exposure, the survival rate in all groups were similar. After 7 days of 85% O_2 exposure, the survival rate in group Ⅱ, Ⅳ dropped sharply and there was a significant difference comparing to group Ⅰ, Ⅲ( P

Objective To investigate the clinical effect and safety of paracetamol in premature infants with patent ductus arteriosus(PDA). Method A protrospective comparsion study was performed onthe data of premature infants with PDA. Seventy-two premature infants with echocardiographically comfirmed PDA were randomized into the oral paracetamol group(n1=18) and the ibuprofen group(n2=54), and the rate of ductal closure, side effects and complications were compared between the two groups. Results The ductus was 66.7% (12 infants) in the paracetamol group, which was similar to 70.4% (38 cases) in the ibuprofen group, with no significant difference(χ2=0.087,P=0.768).Except for the incidence of hyperbilirubinemia in the paracetamol group was higher than that in the ibuprofen group (P<0.05), no statistical differences were found in the other index (P>0.05), including oliguria,NEC,renal impairment,the incidence of IVH3-4 and gastrointestinal bleeding. Conclusions The clinical effect of paracetamol in premature infants with PDA is similar to that of ibuprofen , withlower incidence of hyperbilirubinemia, and paracetamol is worthy of amplication in clinical practice.

To investigate role of Notch1 - 3 in hyperoxia-induced lung injury in newborn rat exposed to 85% O2, SD rat litters born on the 22th day were randomly divided into two groups: room air group and hyperoxia group. The animals were sacrificed 1, 4, 7, 10, 14 and 21 days after continued exposure to oxygen (n = 40, oxygen > 0.85) or room air (n = 40). 6 rats each group were used to assess lung histological changes by HE staining and expression of Notch in lungs by immunohistochemistry. Total RNA was extracted by Trizol reagent from frozen lung tissues. Notch mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). Our results showed that 7, 14 and 21 days after O2 exposure, hyperoxia group showed lung injury characterized by pulmonary edema, hemorrhage and lung development arrest. Positive staining for Notch1, Notch 2 in hyperoxia group was much lower than those in room air group at all time points (P < 0. 01, P < 0.05), but compared with the controls, the hyperoxia group showed higher expression of Notch3 (P > 0.05). Immunostained cells were typically airways epithelia, alveolar epithelial and inflammatory cells, and fibroblasts in hyperoxia group (P < 0.01). Notch mRNA levels showed similar change as protein level (P < 0.01). It is concluded that the prolonged exposure to 85% O2 resulted in abnormal expression of Notch receptors, which might contribute to the pathogenesis of hyperoxia-induced lung injury in newborn rats. The decreased inhibition of Notch1 might be one of the protective reaction and major mechanisms for proliferation/differentiation of type II alveolar epithelial cells. The up-regulation of Notch3 activity might result in the lung development arrest of the newborn rats.
Aerobiosis ; Animals, Newborn ; Lung/*pathology ; Lung Diseases/etiology ; Lung Diseases/*metabolism ; Lung Diseases/pathology ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Random Allocation ; Rats, Sprague-Dawley ; Receptors, Notch/*biosynthesis ; Receptors, Notch/genetics

0.85) or room air ( n =40) respectively, six rats of each group were used to assess lung histologic changes with HE staining and expression of Notch in lungs with immunohistochemistry. Total RNA was extracted by Trizol reagent from the frozen lung tissues. mRNA levels of Notch were measured by reverse transcription polymerase chain reaction (RT PCR). Results 1. Hyperoxia group showed lung injury characterized by subacute alveolitis and inhibition of lung development at 7,14 and 21 days after birth from the lung histology exam. 2 Positive staining for Notch 1, Notch 2 and Jagged in hyperoxia group was much lower than control at every time point ( P0.05 ). Notch was strongly expressed in airways epithelial, alveolar epithelial and inflammatory cells, and fibroblast in hyperoxia group ( P

Objective To discuss the imaging appearances and causes of hepatic pseudolesions around the falciform ligament.Methods 40 patients (23 cases of A-type,17 cases of B-type) of hepatic pseudolesion around the falciform ligament examined by CT were collected.Combined with pathology of 2 cases,follow-up of 6 cases,MRI findings in 5 cases,and with the relevant literature reviewes,the density change of CT plain and enhanced scan and the causes of hepatic pseudolesion around the falciform ligament were analyzed retrospectively.Results There were low density in 25 cases,isodensity in 13 cases,high density in 2 cases in arterial phase,density lower than that of liver in 40 cases in portal phase,low or slightly low density in 27 cases and isodensity in 13 case of A-type in delayed phase.Of 40 cases,there were isointense in 2 cases of A-type in any sequence,and no sigal changes on out-phase images;there were intensity decline on out-phase images comparing to in-phase images in 3 cases of B type.Of 6 CT follow-up cases,there were no changes in 2 cases of A-type and shrinked or disappear in 4 cases of B-type;and there were more shrinked in 1 B-type case of MRI follow-up again after one month.Conclusion Hepatic pseudolesion of A-type can be resulted from focal fatty infiltration,and that of B-type can be caused by special blood-supply.They have characteristics in locations,and characteristic imaging appearances on CT and MRI images,and they can be clearly diagnosed generally.

To investigate the protective effect of retinoic acid (RA) on hyperoxic lung injury and the role of RA as a modulator on mitogen-activated protein kinases (MAPKs), gastation 21 d Sprague-Dawley (SD) fetuses (term = 22 d) were delivered by hysterotomy. Within 12-24 h of birth, premature rat pups were randomly divided into 4 groups (n=12 each): air-exposed control group (group I); hyperoxia-exposed group (group II), air-exposed plus RA group (group III), hyperoxia-exposed plus RA group (group IV). Group I, III were kept in room air, and group II, IV were placed in 85 % oxygen. The pups in groups III and IV were intraperitoneally injected with RA (500 microg/kg every day). All lung tissues of premature rat pups were collected at the 4th day after birth. Terminal transferase d-UTP nick end labeling (TUNEL) staining was used for the detection of cell apoptosis. The expression of PCNA was immunohistochemically detected. Western blot analysis was employed for the determination of phosphorylated and total nonphosphorylated ERKs, JNKs or p38. Our results showed that lungs from the pups exposed to hyperoxia for 4 d exhibited TUNEL-positive nuclei increased markedly throughout the parenchyma (P<0.01), and decreased significantly after RA treatment (P<0.01). The index of PCNA-positive cells was significantly decreased (P<0.01), and was significantly increased by RA treatment (P<0.01). The air-space size was significantly enlarged, secondary crests were markedly decreased in hyperoxia-exposed animals. RA treatment improved lung air spaces and secondary crests in air-exposed pups, but had no effect on hyperoxia-exposure pups. Western blotting showed that the amounts of JNK, p38 and ERK proteins in hyperoxia-exposure or RA-treated lung tissues were same as those in untreated lung tissues (P>0.05), whereas activation of these MAPKs was markedly altered by hyperoxia and RA. After hyperoxia exposure, p-ERK1/2, p-JNK1/2 and p-p38 were dramatically increased (P<0.01), whereas p-JNK1/2 and p-p38 were markedly declined and p-ERK1/2 was further elevated by RA treatment (P<0.01). It is concluded that RA could decrease cell apoptosis and stimulate cell proliferation under hyperoxic condition. The protection of RA on hyperoxia-induced lung injury was related to the regulation of MAP kinase activation.

Despite many advances in perinatology,especially in neonatology,bronchopulmonary dysplasia remains one of the most common complications among extremely premature infants (gestational age ＜ 28 weeks).Infants with bronchopulmonary dysplasia are prone to extrauterine growth retardation due to increased energy consumption of respiratory system,chronic stress,inflammation,drug use and fluid restriction.Adequate nutrition is essential for alveolus development,functional maturation of the lung,lung injury repair and prevention of infection.This review describes active nutritional strategy for extremely premature infants with bronchopulmonary dysplasia,including parenteral and enteral nutrition supplement,periodic nutritional assessment and nutrition adjustment in the event of extrauterine growth retardation.

Currently,the brain death guidelines of neonates and infants have not been generally accepted and used in clinical practice by the pediatric critical care team in China.This article reviewed and discussed when to withdrawal resuscitation,the update recommendations regarding appropriate examination criteria,definition and diagnose of brain death in neonates,infants and children in United States in 2011.

To investigate role of Notch1-3 in hyperoxia-induced lung injury in newborn rat exposed to 85% O2, SD rat litters born on the 22th day were randomly divided into two groups: room air group and hyperoxia group. The animals were sacrificed 1, 4, 7, 10, 14 and 21 days after continued exposure to oxygen (n=40, oxygen＞0.85) or room air (n=40). 6 rats each group were used to assess lung histological changes by HE staining and expression of Notch in lungs by immunohistochemistry. Total RNA was extracted by Trizol reagent from frozen lung tissues. Notch mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). Our results showed that 7, 14 and 21 days after O2 exposure, hyperoxia group showed lung injury characterized by pulmonary edema, hemorrhage and lung development arrest. Positive staining for Notch1,Notch 2 in hyperoxia group was much lower than those in room air group at all time points (P＜0.01, P＜0.05), but compared with the controls, the hyperoxia group showed higher expression of Notch3 (P＞0.05). Immunostained cells were typically airways epithelia, alveolar epithelial and inflammatory cells, and fibroblasts in hyperoxia group (P＜0.01). Notch mRNA levels showed similar change as protein level (P＜ 0.01). It is concluded that the prolonged exposure to 85 % O2 resulted in abnormal expression of Notch receptors, which might contribute to the pathogenesis of hyperoxia-induced lung injury in newborn rats. The decreased inhibition of Notch1 might be one of the protective reaction and major mechanisms for proliferation/differentiation of type Ⅱ alveolar epithelial cells. The up-regulation of Notch3 activity might result in the lung development arrest of the newborn rats.