The key mechanism of hypoxic-ischemic encephalopathy(HIE) is two-times energy exhaustion.Recently, electrophysiology, cell physiology and imageology are performed to figure out some new biomarkers for clinical diagnosis and prognosis. And now, there are different therapies for HIE. For Sub-low temperature therapy,selecting appropriate time of therapy window is more important, and the therapeutic effects of other therapies,hyperbaric oxygenation, neuroprotectants, neural stem cell transplantation etc, need to be validated clinically.

Neonatal jaundice is one of the common diseases in preterm neonates. But there are still some problems to be determined,for example,the clinical diagnosis criteria for neonatal jaundice,the prediction,diagnosis and therapies for hyperbilirubinemia,and diagnosis for bilirubin encephalopathy in early-stage and prevention from bilirubin encephalopathy sequelae.

The fetal inflammatory response syndrome (FIRS) is a state of activation of the innate immune system in the fetus body and is a kind of neonatal inflammation for 72 hours after birth.It is defined as the following items ＞ 2:(1) breathing too fast (＞ 60 times/min),accompanied by breathing difficulties or with oxygen desaturation; (2) temperature instability ＞ 37.9 ℃ or ＜ 36 ℃ ; (3) capillary filling time ＞ 3 s;(4) the white blood cell count ＞34 × 109/L,or ＜4 × 109/L; (5) CRP ＞ 10 mg/L; (6) IL-6 or IL-8 ＞70 g/ml;(7) gene testing of 16S rRNA for PCR is positive.FIRS can be induced by infectious and non-infectious factors.In FIRS,fetal immune system is over-activated to the external violation,which causes uncontrolled release of inflammatory mediators and cytokines.A variety of inflammatory mediators and cytokines directly or indirectly activate the coagulation system and interfere with the body's anticoagulation system,which induces the coagulation disorders.Multiple organ systems involved in the inflammatory response throughout this process.FIRS can lead to premature delivery,perinatal death,cerebral white matter damage,necrotizing enterocolitis,and affect fetal lung maturity and multi-organ damage.In order to reduce fetal injury,it is necessary for appropriate treatment and prediction of the FIRS.

Fetal inflammatory response syndrome is a sub-clinical state that cause fetal immune sys-tem could be activated and released large amounts of proinflammatory cytokines.Either caused by infection of factors such as chorioamnionitis,fetal sepsis or non-infectious factors such as asphyxia,chronic lack of oxy-gen,which are likely to cause neurological damage in preterm or full-term children .This article reviewed the progress on the mechanism of neonatal encephalopathy caused by fetal inflammatory response syndrome.

Procalcitonin (PCT) has been recognized a marker of infectious diseases for the past few years.The value of PCT is specific elevation in infectious diseases or inflammation caused by bacterial and it has an important role in the identification of bloodstream infections,bacterial and non-bacterial,rational usage of antibiotics and prediction disease prognosis.PCT is a high value diagnostic indicators.However,the PCT do not reflect a clear advantage in the diagnosis of neonatal infection.In this paper,the composition of the PCT,the source in the body of PCT,the metabolism of PCT,laboratory testing methods of PCT and its applications in neonatal infection were reviewed in order to gain a deeper understanding of the value of PCT in the neonatal diagnosis of infectious diseases.

Objective To analyze the clinical characteristics of Klebsiella pneumoniae infection in preterm infants. Methods Clinical data of 75 preterm infants infected with Klebsiella pneumoniae treated in BaYi Children's Hospital from February 6,2008 to February 10,2010 were retrospectively analyzed.The difference of auxiliary examination between early-onset and late-onset infection group were compared by two independent samples t test.Spearman correlation analysis and non-conditional Logistic regression analysis were used to analyze the high risk factors and the prognostic factors of Klebsiella pneumoniae infection in preterm infants. Results The incidence of Klebsiella pneumoniae infection was 2.8％ (75/2721) in preterm infants,and the mortality rate was 9.3％ (7/75). There were 71 cases of Klebsiella pneumoniae sepsis and 4 cases of Klebsiella pneumoniae pneumonia.Among 75 cases,63 cases were early-onset infection (onset age≤72 h) and 12 were late-onset infection (onset age＞72 h).All patients presented with poor response,heart rate during quiet sleep ＞ 160/min and low oxygen saturation.The mean corpuscular volume and mean corpuscular hemoglobin concentration in early-onset Klebsiella pneunoniae infection cases were higher than those in late-onset neonates [(128.87±24.60) fl vs (113.72±13.54) fl,t=-2.07,P＜0.05and (38.11±2.15) pg vs (36.98±1.05) pg,t=-2.76,P＜0.05].Low birth weight and caesarean section were associated with early-onset Klebsiella pneumoniae sepsis (r=0.250 and -0.240,P＜0.05). The prognosis of Klebsiella pneumoniae infection was associated with hospital stay and duration of premature rupture of membranes (r=0.368 and 0.318,P＜0.05). Conclusions There were no specific clinical manifestations for Klebsiella pneumoniae infection in preterm infants.Preterm infants with low birth weight,long duration of premature rupture of membranes,delivered by caesarean section and received invasive operation are likely to develop Klebsiella pneumoniae infection.

Aim To compare cardioprotection effects between carvedilol and metoprolol in canine late reperfusion of acute myocardial infarction.Methods Eighteen anesthetized dogs were randomly divided into three groups: late reperfusion group(LR,n=6),late reperfusion after metoprolol treatment group(LR+M,n=6),and late reperfusion after carvedilol treatment group(LR+C,n=6),respectively orally giving physiological saline,metoprolol(1 mg?kg~(-1)?d~(-1)),and carvedilol(1 mg?kg~(-1)?d~(-1)) for seven days,and then late reperfusion of acute myocardial infarction model was made by ligating the coronary for 6 h,followed by reperfusion for 6 h.SOD,GR activity and MDA content of infarction brim myocardium were detected by colorimetry,Fas/FasL were detected by immunohistochemistry,apoptosis index(AI) were detected by TUNEL.Results Compared with LR,Myocardial MDA content in LR+C was decreased,and SOD and GR activities were significantly higher,but LR+M did not change.The expression of Fas/FasL and apoptosis index were significantly lowered in LR+M and LR+C,especially in LR+C.Conclusion Carvedilol and metoprolol have cardioprotection on late reperfusion of acute myocardial infarction,and carvedilol is superior to metoprolol and the pharmacological effects may due to its antioxidant effect.

Objective:To analyze the clinical and gene mutation characteristics of congenital disorder of glycosylation (CDG) caused by compound heterozygous mutation of the COG6 gene ( COG6-CDG). Methods:This study retrospectively analyzed the clinical data and genetic test results of a patient with COG6-CDG in Bayi Children's Hospital, the Seventh Affiliated Medical Center of Chinese PLA General Hospital, in August 2019. Literature was retrieved with keywords including COG6, COG6-CDG, congenital disorders of glycosylation typeⅡL and congenital disorders of glycosylationⅡL in China National Knowledge Infrastructure, Wanfang Database, VIP Database, PubMed, and Web of Science Database from the establishment to July 2020, to summarize the clinical and genetic characteristics of COG6-CDG. Results:(1) Case report: The 59-day-old baby boy, with a gestational age of 27 +5 weeks and birth weight of 1 180 g, presented with multi-system involvement on admission, including unidentified progressive hepatosplenomegaly with jaundice and ascites, persistent thrombocytopenia, microcephaly, hypotonia, hypohidrosis, hyperkeratosis, and recurrent hyperthermia, infection, and hypoglycemia, as well as dysfunctions of the heart, gastrointestinal tract, lungs, kidneys, ocular fundus, and the coagulation system. Despite given ventilator-assisted ventilation, anti-infection therapy, abdominal puncture and drainage, and blood transfusion, the patient still had an aggravated condition and eventually died of multiple organ failures 192 d after birth. Genetic analysis showed that the nuclear family carried compound heterozygous mutations in the COG6 gene (NM_020751.2), including missense mutations of c.662C>T(p.T221M) in exon 7 and c.443T>C(p.I148T) in exon 5, which were both novel mutations and originated from the mother and father, respectively. (2) Literature review: Eight related papers were retrieved, including 20 cases. The main manifestations were various degrees of nervous system abnormalities and growth retardation, complicated by abnormalities of the liver, heart, gastrointestinal tract, blood, immunity, teeth, and bones. All the reported cases suffered from mental and growth retardation, and nine deaths were reported. A total of 11 COG6 gene mutations were identified, and most of them were c.1167-24A>G splicing mutations in a deep intron (seven cases), followed by c.1646G>T (four cases) and c.511C>T (three cases). Conclusions:COG6-CDG commonly manifests as multi-system and multi-organ dysfunctions with poor prognosis. Gene detection is conducive to the accurate diagnosis of COG6-CDG. Our case carries compound heterozygous mutations of c.662C>T(p.T221M) and c.443T>C(p.I148T), which are unreported novel mutations.

ObjectiveTo detect the ultrastructure of neural stem cells (NSCs) cultured in vitro .MethodsNSCs separated from the cortex of 17—19 days Wistar rat fetus were cultured and induced to differentiate in vitro. Electron microscopes were used to visualize the ultrastructure of these cells before and after differentiation.ResultsNSCs had the similar cellular size, morphology and intracellular structures pre-differentiation. Cells were able to proliferate via mitosis. The nucleus/cytoplasm ratio was very high. The nucleus was poly-morphological. Cells had very little cytoplasm and no mature organelles. After differentiation, several processes protruded out from cellular surface. Cells became flat shape, the volume of cytoplasm increased dramatically and various kinds of mature organelles appeared in the cytoplasm. Cells differentiated into two kinds of cells,neural cells and glial cells,with quite different morphology and intracellular structure. ConclusionNSC is one kind of original cells which can be induced to differentiate into mature neural cells and glial cells.

Objective To explore the effects of the stromal cell-derived factor on chemotaxis of cord blood ACl33+ cells.Methods The optimal SDF-1 concentration is detected in Transwell system.Migration was calculated from the number of cells found to have passed through an 8-um pore size polycarbonate membrane.Results The chemotactic rate of fresh cord blood AC133+ cells increases along with the concentration of SDF-1,however,it tends to be stable when the concentration of SDF-1 reaches 150 ng/ml.There is no difference in the chemotactic rate of cord blood AC133+ cells between the group with CXCR4-blocking antibody and the group without SDF-1.Conclusion Transwell Plate can simulate the phenomenon of cell crossing endothelium.The chemotactic rate of cord blood AC133+ cells increases progressively along with the concentration of SDF-1,however,the chemotactic rate tends to equability when SDF-1 reaches a certain concentration.The chemotactic rate does not have a marked change while continuing to increase the concentration of SDF-1.There is no difference in the chemotactic rate of cord blood AC133+ cells between the group using CXCR4-blocking antibody and the group without SDF-1.