Objective To study the neuropsychological behavior development of preterm infants and low birth weight infants,and to provide a reference to the early prevention and intervention on developmental retardations.Methods A total of 101 preterm infants and/or low birth weight infants received the infant development test of 0 ～ 6 year-old children intelligence developmental scale for neurological development and autism behavior checklist(ABC).Results 25 boys and 5 girls suffered from different psychological mental disorders.The occurrences were as follows:10 cases with mental retardation,9 cases with the language development delay,9 cases with motor retardation,1 case with cerebral palsy and 1 case with autism spectrum disorder.The incidence of intelligence problems were that language retardation (18.9％),the fine motor (16.8％),the adapative ability (12.6％),social action (9.5 ％) and the motor delay (3.2％).There were significant differences in the scores of social communication(x2=8.88,P=0.003),adaptive ability(x2=7.41,P=0.007),the fine motor(x2 =6.22,P=0.01) and total developmental quotient(x2 =5.58,P=0.02) between city children'and rural area.The behavioral problems more consisted in self-care ability and language retardation.Conclusion Preterm infants and low birth weight infants are exposed to language,fine motor,adaptive and communication ability problems,especially the children living in country.It is necessary to improve the early education and intervention for the rural preterm infants and low birth weight infants.

Objective To understand the underlying mechanism of mites-induced pediatric asthma by bioinformatic analysis on speciifc microRNA (miRNA) array and target gene screening. Methods This is a case control study of 62 pairs of dust mites-induced asthma children with age and gender matched healthy controls. Twelve pairs were randomly selected for miRNA array. The abnormal expression of miRNAs was compared between asthma and control children. The results were validated by RT-qPCR and bioinformatic analysis in remaining pairs of children. Results Six miRNAs (miRNA-151a-5p, 625-5p, 126-3p, 513a-5p, 27b-3p, 22-3p) were signiifcantly down-regulated more than two folds in dust mites-induced asthma children than those in controls. The enriched bioinformatics analysis showed that these miRNAs and their target genes CBL, PPARGC1B, ESR1, ONECUT2, EGFR, SYK, and STAT1 were related to inlfammatory cytokine signaling pathway. Conclusion It is suggested that miR-22-3p, 513a-5p, 625-5p, 27b-3p, and miRNA-target genes form a network through co-regulation to target genes to participate dust mites-induced asthma in children.

Objective To investigate the inhibitory effect and mechanism of rosiglitazone on chemokines secretion in renal tubular epithelial cells (HK-2) stimulated by lipopolysaccharide (LPS). Methods Cells were divided into four groups: control (CON), LPS (1 mg/L),rosiglitazone (10 μmol/L), rosiglitazone (10 μmol/L) +LPS (1 mg/L). MCP-1 and IL-8 expression was measured using real time PCR and ELISA. PPARγ was knockdown by RNAi to investigate whether the inhibitory effect of rosiglitazone was PPARγ-dependent or -independent. The NF-κB in nucleus was detected by Western blotting. The DNA binding activity of NF-κB was determined by electrophoretic mobility shift assay. Results Compared with CON group, the expressions of IL-8 and MCP-1 were increased by (4.30±0.45) and (4.80±1.29) times in mRNA level, (1.39±0.18)and (2.11 ±0.47) times in protein level, respectively, in LPS-stimulated HK-2 cells (P＜0.05).Application of rosiglitazone followed by LPS significantly reduced IL-8 and MCP-1 secretion compared with LPS group (decreasing by 66.37% and 71.88% in mRNA levels, while 41.68% and 47.87% in protein levels) (P＜0.05). In pcDNATM 6.2-GW/EmGFP-miPPARγ transfected cells, IL-8and MCP-1 only were decreased by 18.16% and 16.83% in mRNA level, while 11.39% and 11.86%% in protein level in rosiglitazone pretreated group, showing no significant difference compared with LPS group. Rosiglitazone did not block NF-κB nuclear translocation while significantly inhibiting the DNA binding activity of NF-κB. Conclusions Rosiglitazone inhibits the expressions of MCP-1 and IL-8 via a PPARγ-dependent mechanism in HK-2 cells, resulting from inhibition the DNA binding activity of NF-κB.

Objective To construct an expression system to produce the virus-like particles containing a part of the sequence of PSA mRNA, which are ribonuclease-resistant due to the encapsulation of the mRNA by bacteriophage MS2 coat proteins. Methods The PCR products of PSA cDNA fragments were cloned to TA vector pBS-T, then the targeted segments could be obtained when the pBS-T-PSA were digested by restriction endonuclease Hind Ⅲ and cloned to prokaryocytic expression vector pNCCL1. The recombinant plasmids named PNCCL1-PSA were transfected into E. Coli BL21-DE3 and induced to express with IPTG. Results The recombinant plasmids were successfully constructed. The bacteriophage MS2 coat protein which expressed in BL21 can self- assemble to form ribonuclease resistant virus-like particles and the PSA mRNA was encapsulated into virus-like particles. Conclusions The virus-like particle containing PSA mRNA can be expressed in prokaryocyte and it can be used as standard and control in detecting PSA mRNA. It provides a new, stable and ribonuclease-resistant RNA standard in RNA detection.

OBJECTIVETo investigate the effect of Inonotus obliquus polysaccharides on testicular injury induced by exposure to high power microwave (HPM) in rats.

METHODSA total of 30 male Wistar rats were randomly divided into 5 groups, i.e., the normal control group, the microwave radiation model group, the treatment group, the new microwave radiation model group, and the prevention group, 6 in each group. All rats, except those in the normal control group, were exposed to microwave at an average power density of 200 mW/cm2 for 6 min. Rats in the control group and the model group were administered with normal saline by gastrogavage, once a day. Rats in the treatment group and the prevention group were given with Inonotus obliquus polysaccharides by gastrogavage, 2 mL each time (400 mg/kg body weight), once a day. All rats were sacrificed on the 11th day.The sperm density and the rate of sperm deformity were determined. Pathological changes of testis were observed by light microscope and transmission electron microscope.

RESULTSShort-term HPM irradiation could significantly reduce the sperm density and increase the sperm deformity rate (P < 0.05). Meanwhile, obvious pathological changes of testes occurred. Compared with the two model groups, the sperm density increased and the sperm deformity rate decreased in the treatment group and the prevention group (P < 0.05). Under the light microscope, injuries of spermatogenic cells and stromal cells, as well as vascular dilatation and congestion were obviously alleviated in the treatment group and the prevention group. Mitochondrial swelling and endoplasmic reticulum expansion shown by ultrastructural observation were also significantly alleviated. Of them, injuries of spermatogenic cells and inflammation response were milder in the treatment group than in the prevention group.

CONCLUSIONSInonotus obliquus polysaccharides had significant protective effect on microwave radiation induced testicular injury. Better effect was obtained by therapeutic medication than preventive medication.

Animals ; Basidiomycota ; chemistry ; Male ; Microwaves ; adverse effects ; Polysaccharides ; pharmacology ; Radiation Injuries, Experimental ; prevention & control ; Radiation-Protective Agents ; pharmacology ; Rats ; Rats, Wistar ; Testis ; drug effects ; pathology ; radiation effects

OBJECTIVENeonatal unconjugated hyperbilirubinemia is one of the most common conditions encountered by the practicing pediatricians. Although it is usually self-limited and benign, the condition is of importance because of the rare instances in which severe hyperbilirubinemia can lead to bilirubin encephalopathy or kernicterus. The uridine diphosphate-glucuronosyl transferase 1A1 (UGT 1A1) gene controls bilirubin conjugation by determining the structure of the enzyme glucuronosyltransferase, which is synthesized in the hepatocyte. In the recent years much has been learned about the relationship between UGT 1A1 gene mutation and neonatal hyperbilirubinemia. This study aimed to investigate the roles of UGT 1A1 gene mutation in the development of neonatal hyperbilirubinemia in Guangxi.

METHODSA total of 73 cases with hyperbilirubinemia and 31 healthy neonates were enrolled. UGT 1A1 G71R genotypes were identified by the (amplification refractory mutation system, ARMS) and direct sequencing method in all the neonates. To analyze the incidence of bilirubin encephalopathy, the peak (total serum bilirubin, TSB) concentration after 72 hours of age, and the possibility of TSB > 20 mg/dl of each group.

RESULTS(1) The frequencies of allele G71R were 0.1915 in this study, 0.2329 in hyperbilirubinemia group vs. 0.097 in healthy groups. The allele gene frequency of G71R in neonatal hyperbilirubinemia was higher than that in the normal group (P < 0.05). (2) Homozygous neonates had higher possibility to develop bilirubin encephalopathy and higher TSB concentration 72 hours after birth (28.57%, 23.12 ± 4.58) than the normal group (0%, 17.68 ± 2.69). The difference between the former two was significant (P < 0.001). (3) The TSB of the 5 neonates was > 20 mg/dl in G71R homozygous type, the odds ratio and 95%CI were 7.955 (1.349, 46.899).

CONCLUSION(1) G71R mutation gene was associated with neonatal jaundice in Guangxi region. (2) The possibility of TSB > 20 mg/dl in G71R homozygous was higher than those of the wild-type. (3) The incidence of bilirubin encephalopathy and TSB concentration after 72 hours of age for neonates who were homozygous to G71R gene were higher than the wild-type.

Case-Control Studies ; China ; epidemiology ; Genotype ; Glucuronosyltransferase ; genetics ; Humans ; Hyperbilirubinemia, Neonatal ; epidemiology ; genetics ; Infant, Newborn ; Mutation

OBJECTIVETo study the correlation between glucose-6-phosphate dehydrogenase (G-6-PD) activities and three common mutations of G-6-PD gene G1388A, G1376T and A95G and investigate the effects of G-6-PD gene mutations on neonatal jaundice in Nanning, Guangxi.

METHODSOne hundred and twenty-four neonates from Nanning, Guangxi, with hyperbilirubinemia were enrolled. The ARMS-PCR and PCR/REA methods were used to determine G-6-PD gene mutations. G-6-PD activities were measured using the NBT method. The incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth were compared between the neonates with different genotypes and between the G-6-PD mutation and normal groups. The risk of blood serum bilirubin >340 mumol/L was evaluated by logistic regression analysis.

RESULTSOf the 124 cases, gene mutations were found in 37 cases, including G1388A (n=20), G1376T (n=14), A95G (n=4) and G1388A+A95G (n=1). Five cases (25%) showed normal G-6-PD activities in the G1388A gene mutation group and 4 (29%) had normal G-6-PD activities in the G1376T G1388A gene mutation group. All of 4 cases of A95G G1388A gene mutation showed a deficiency of G-6-PD activities. There were no significant differences in the incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth between the G1388A and G1376T G1388A gene mutation groups. The incidence of acute bilirubin encephalopathy, the peak bilirubin concentration 72 hrs after birth and the risk of serum bilirubin >340 micromol/L in the G-6-PD mutation group were not different from the normal group.

CONCLUSIONSG1388A, G1376T and A95G are common G-6-PD gene mutations in Nanning, Guangxi. The false negative results may be received when the NBT method is used for diagnosis of G-6-PD deficiency. There are similar effects on the incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth between different gene mutation groups. G-6-PD gene mutations alone may not contribute to the development of acute bilirubin encephalopathy and the changes of peak bilirubin concentration 72 hrs after birth and the risk of serum bilirubin >340 micromol/L.

Bilirubin ; blood ; Encephalitis ; etiology ; Female ; Genotype ; Glucosephosphate Dehydrogenase ; genetics ; metabolism ; Glucosephosphate Dehydrogenase Deficiency ; genetics ; Humans ; Infant, Newborn ; Jaundice, Neonatal ; blood ; genetics ; Male ; Mutation

Cell Adhesion Molecules ; physiology ; Chemokines ; physiology ; Cytokines ; physiology ; Genetic Predisposition to Disease ; Humans ; Lectins, C-Type ; physiology ; Peptidyl-Dipeptidase A ; physiology ; Receptors, Cell Surface ; physiology ; Severe Acute Respiratory Syndrome ; etiology ; genetics ; immunology

RNA, Messenger ; biosynthesis ; genetics ; RNA, Viral ; chemistry ; genetics ; Ribonucleases ; biosynthesis ; genetics ; Virion ; chemistry ; genetics ; alpha-Fetoproteins ; biosynthesis ; genetics

OBJECTIVETo investigate the intervention effect of thalidomide on paraquat-induced acute lung injury in mice and its mechanism.

METHODSMale ICR mice were randomly allocated to negative control group (n = 30), thalidomide control group (n = 30), paraquat poisoning group (n = 30), 50 mg/kg thalidomide treatment group (n = 30), 100 mg/kg thalidomide treatment group (n = 30), and 150 mg/kg thalidomide treatment group (n = 30). The negative control group was intraperitoneally injected with the same volume of saline; the thalidomide control group was intraperitoneally injected with thalidomide (150 mg/kg); the paraquat poisoning group was intraperitoneally injected with diluted paraquat solution (22 mg/kg); each thalidomide treatment group was intraperitoneally injected with the same volume of paraquat solution (22 mg/kg) and was injected with thalidomide (50, 100, or 150 mg/kg) 1 h later. All mice were anesthetized and sacrificed at 1, 3, or 7 d after paraquat poisoning, and their lung tissue was collected. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in lung tissue were measured by double-antibody sandwich ELISA; the mRNA expression of nuclear factor-kappa B (NF-κB) was measured by RT-PCR; the protein expression of nuclear NF-kgr;B p65 was measured by Western blot. The pathological changes of lung tissue were observed under light microscope; the wet/dry ratio of the lung was calculated.

RESULTSCompared with the negative control group, the paraquat poisoning group had significantly increased levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65 and wet/dry ratio of the lung (P < 0.05). Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65 and wet/dry ratios of the lung (P < 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65. The observation of pathological changes showed that the paraquat poisoning group had the most marked lung tissue damage at 3 d after poisoning, and the lung tissue damage was lessened in the thalidomide treatment groups.

CONCLUSIONThalidomide can reduce paraquat-induced acute lung injury and lung edema. The mechanism may include inhibition of NF-κB activation and expression and downregulation of TNF-α, IL-1β, and IL-6.

Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Cytokines ; metabolism ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred ICR ; NF-kappa B p50 Subunit ; metabolism ; Paraquat ; poisoning ; Thalidomide ; pharmacology ; Transcription Factor RelA ; metabolism