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To study risk factors for severe hand, foot and mouth disease (HFMD) complicated by heart and lung failure and treatment experience.A total of 198 children with severe HFMD between March and August in 2011 were enrolled. Univariate analysis and logistic regression model were used to analyze the risk factors severe HFMD complicated by heart and lung failure. The effects of combination therapy with immunoglobulin+dexamethasone+ribavirin were observed.Univariate analysis indicated that HFMD patients with heart and lung failure had higher proportions of consciousness, tachypnoea, abnormal hemodynamics, increased troponin and EV71 infection than HFMD patients without heart and lung failure (P0.05).Multivariate logistic regression analysis indicated that tachypnoea, abnormal hemodynamics and EV71 infection were the main risk factors for heart and lung failure. Compared with combination therapy with dexamethasone+ribavirin, combination therapy with immunoglobulin+dexamethasone+ribavirin was more effective for preventing hemodynamic changes in children with severe HFMD (P0.01). Compared with HFMD patients with heart and lung failure, the effect of the combination therapy with immunoglobulin+dexamethasone+ribavirin was better in HFMD patients without heart and lung failure (P0.01).The main risk factors for heart and lung failure in children with severe HFMD include tachypnoea, abnormal hemodynamics and EV71 infection. Early combination therapy with immunoglobulin+dexamethasone+ribavirin can reduce the incidence of heart and lung failure in children with severe HFMD.

To investigate nasal carriage of community-acquired Staphylococcus aureus and its drug sensitivities in healthy children in Chengdu.Nasal swabs were collected from healthy children from primary schools and kindergartens in Chengdu in two stages (2005-2007 and 2008-2010). All specimens were cultivated. Once S. aureus was identified, drug susceptibility tests (disk diffusion method) were performed with penicillin, erythromycin, clindamycin, ceftazidime and vancomycin.430 S. aureus were identified from 2373 specimens, with a positive rate of 18.12%. Resistant to penicillin was found in 90% of tests. The isolated S. aureus was also resistant (6.28%) to methicillin-resistant Staphylococcus aureus (MRSA). The first stage identified higher rate of MRSA than the second stage (4.28% versus 9.25%, P = 0.037). Isolates from children living in cities were more likely to be resistant to cefoxitin than isolates from children living in countryside (14.74% versus 2.56%, P = 0.006) in the second stage. We did not find vancomycin-resistant S. aureus.Nasal carriage of S. aureus among healthy children in Chengdu is common and the nasal carried S. aureus is highly resistant to commonly used antibiotics.

This study examined changes to pro-inflammatory cytokine IFN-γ and chemokine IP-10 in the arterial blood of premature infants before and after mechanical ventilation, with the aim of exploring possible mechanisms of ventilation-induced lung injury.Twenty-three neonates requiring mechanical ventilation were enrolled in this study. Arterial blood samples were collected for measuring IFN-γ and IP-10 levels using ELISA before and 4 hours after mechanical ventilation.Blood IFN-γ and IP-10 increased significantly from 59 ± 40 pg/mL and 130 ± 67 pg/mL respectively before mechanical ventilation to 105 ± 54 pg/mL and 220 ± 80 pg/mL respectively after 4 hours of mechanical ventilation (P0.01).Serum IFN-γ and IP-10 levels increase after mechanical ventilation, suggesting that both may participate in the immune-inflammatory process of ventilation-induced lung injury.

To analyze potential mutation of keration 9 gene (KRT9) in a Chinese family affected with epidermolytic palmoplantar keratoderma (EPPK) and to correlate genotype with the phenotype.Genomic DNA was extracted from peripheral blood samples of 12 patients and 13 healthy individuals from the family and 100 unrelated individuals. Polymerase chain reaction (PCR) was used to amplify exons 1 and 6 of KRT9 gene. PCR products were sequenced bidirectionally in order to identify potential mutations.A heterozygous transversional mutation, 488G→A, was identified in exon 1 of KRT9 gene in all patients, which has resulted in substitution of a glutamine residue for arginine acid at position 163 (R163Q) of the KRT9 protein. The same mutation was not found in the 13 healthy members from the family and 100 unrelated individuals.The 488G→A mutation of KRT9 gene is probably the cause of EPPK in this Chinese family.

Blue light has been widely used for the treatment of neonatal hyperbilirubinemia since the 1950s. Neonatal phototherapy can decrease plasma unconjugated bilirubin level, thus preventing bilirubin encephalopathy, and greatly reduces the exchange transfusion rate. Generally, it is accepted that the side effects of neonatal phototherapy are not serious and seem to be well controlled, however recent research has provided new evidence. The short-term side effects of phototherapy include interference with maternal-infant interaction, imbalance of thermal environment and water loss, electrolyte disturbance, bronze baby syndrome and circadian rhythm disorder. In addition, phototherapy may be associated with some long-term side effects such as melanocytic nevi and skin cancer, allergic diseases, patent ductus arteriosus and retinal damage. Therefore, it is necessary to develop evidence-based guidelines, new light devices and alternative agents, as well as individualized treatments, to minimize the side effects of phototherapy.

To investigate the risk factors related to post-asphyxial multiple organ dysfunction (PA-MOD) in neonates.A total of 397 neonates with birth asphyxia were enrolled from January 2009 to December 2010.The patients were divided into PA-MOD group (n=179) and non-PA-MOD group (n=218). The risk factors of PA-MOD were retrospectively studied.Multivariate logistic regression analysis showed that severe asphyxia, fetal distress, abnormal labor, and decreased amniotic fluid were the risk factors for PA-MOD among the neonates. Spearman rank correlation analysis showed that the number of the involved organs increased along with the increase of age at admission (P0.05) and with the decrease of gestational age and birth weight (P0.05).The efforts should be made to enhance perinatal care for neonates, especially for preterm infants and low-birh-weight infants, to decrease the incidence of MOD.

To investigate the effects of dimethyloxalyl glycine on hypoxic-ischemic brain damage in newborn rats.Forty eight postnatal day 10 SD rats were divided into 3 groups, including sham surgery group, hypoxic-ischemic group and DMOG treated group. The brain tissues were collected at 4, 8, 24 and 72 hours after the hypoxic-ischemic treatment. The expressions of hypoxia inducible factor-1alpha (HIF-1alfa) protein and anti apoptoticprotein cleaved caspase 3 (CC3) were detected by immunohistochemistry. The apoptotic cells were detected by TUNEL staining.The expression level of HIF-1alpha was significantly higher in DMOG treated group than in hypoxic-ischemic group. While the expression level of CC3 was lower and the number of tunel positive cells was fewer in DMOG treated group than that in hypoxic-ischemic group.Dimethyloxalyl glycine may play a neuro-protective role in hypoxic-ischemic brain damage in newborn rats by stabilizing HIF-1alpha.

To identify the risk factors for patent ductus arteriosus (PDA) in neonates.Fifty infants with PDA and 100 infants without PDA were enrolled. Chi-square test, Student's t test and the linear correlation analysis were used to study the clinical data. Logistic regression analysis was used to investigate the independent risk factors for PDA.The prevalence of PDA was negatively correlated with the gestation age (r=-0.03, P0.05) and birth weight (r=-0.04, P0.05). Oxygen inhalation was a protective factor for the development of PDA. Fetal distress, meconium-stained amniotic fluid, oligohydramnios, cord entanglement, 1 minute Apgar score8, maternal infection and hypoxic-ischemic encephalopathy were the independent risk factors for the development of PDA.The incidence of PDA can be reduced by preventing maternal infection, premature birth, low birth weight and hypoxia.

To find a better method for harvesting highly purified neurons by comparing three methods used for co-culture of neurons and astrocytes.The co-culture models of neurons and astrocytes were established by primary culture, Banker's co-culture method or Transwell cell-culture inserts. The neurons and astrocytes cultured in vitro were from neonatal rats.The highly purified neurons were not harvested by primary culture because the neurons and astrocytes grew on the same cover slip and it was difficult to control the growth velocity of astrocytes. The highly purified neurons were harvested by Banker's co-culture method or the method using Transwell cell-culture inserts, but the procedure of the former was more complicated than that of the later.The culture method using Transwell cell-culture inserts is recommended for the establishment of the co-culture system of neurons and astrocytes.

Peripherally inserted central catheter (PICC) is widely used to provide a long-term access for the administration of total parenteral nutrition and medications. Catheter-related infections (CRI) are common complications of PICC. The purpose of this retrospective study was to investigate the role of low-dose heparin added to the total nutrient admixture (CTNA) in the prevention of CRI.Eighty-three neonates who underwent PICC received TNA with (heparin group, n=43) or without heparin (0.5 U/mL) (control group, n=40). The incidence of CRI was compared between the two groups.The incidences of catheter obstruction (5% vs 20%) and the catheter-tip colonization (2% vs 18%) in the heparin group were significantly lower than those in the control group (p0.05). None of the neonates in the heparin group had clinical evidence of catheter-related bloodstream infection, but 5 cases in the control group (p0.05).The administration of low-dose heparin in TNA may decrease the incidences of catheter obstruction and CRI.

To investigate the relationship between the expression of glucose transporter protein 1 and the apoptosis of neuron during hypoxic-ischemia brain damage in neonatal rats.Total 120 10-day old SD rats were divided into normal group, sham control group and hypoxic-ischemia (HI) group. In HI group, hypoxic-ischemia brain damage (HIBD) were generated according to Rice-Vannucci method, brain tissues were harvested at 2, 8, 24, 48 and 72 h after HI. The brain samples were also collected at the same time points in normal group and sham control group. The pathological changes was observed by hematoxylin-eosin (HE) staining, the mRNA expression of glucose transporter 1 (GLUT1) was detected by reverse transcriptase-polymerase chain reaction (RT-PCR), the protein expressions of GLUT1 and cleaved caspase-3 (CC3) were detected by immunohistochemistry, the apoptosis of neuron was measured by TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining.HE staining showed that the degree of brain cell damage increased with time after HI, the loss of neuronal cells peaked at 48 h, while the cells in control group apperanted in an orderly and normal morphology. The mRNA and protein expressions of GLUT1 were increased after HI, which began to increase at 2 h, and reach the peak at 24 h. and the expression levels at each time points were statistically higher (P0.01) than those in control group. CC3 protein expression also began to increase at 2 h, peaked at 48 h after HI, which was higher than that of control group (P0.01). The number of positive cells was significantly increased after HI,with a peak at 48 h.The mRNA and protein expression of GLUT1 in brain tissue increased significantly after hypoxic-ischemia, and the peak time was earlier than that of CC3 protein and cellular apoptosis. This suggests that GLUT1 expression upregulation may be a certain degree of inhibition on neuronal apoptosis.

Pharmacological intervention is an important means for the treatment of hypoxic-ischemic encephalopathy (HIE). As meta-analyses and randomized controlled clinical trials based on evidence-based medicine are able to provide the most reliable evidence for clinical practice, this study searched several databases in order to find the clinical evidence for the pharmacological treatment of neonatal HIE.Meta-analyses and randomized (or quasi-randomized) controlled trials (RCT) for pharmacological therapy of HIE in term or late preterm newborn infants were searched from the databases of MEDLINE, EMBASE, Oxford Neonatal Group and Cochrane Library. The relevant literatures were statistically analyzed.Four Meta-analyses and thirteen RCTs were found to be involved in barbiturate, allopurinol, magnesium sulfate, mannitol, naloxone and dopamine therapy. None of the drugs could significantly decrease the mortality and the incidence of seizure or severe neurodevelopmental disabilities in newborn infants with HIE.Current clinical evidence indicates that no individual drug could decrease mortality and improve the neurodevelopmental outcomes in infants with HIE. Problems such as small scale in sampling and discrepancy in the identification of drug efficacy which exist in the clinical trials might lead to the uncertain effect of the drugs, and large sized and collaborative clinical trials are needed in the future.

Human telomerase reverse transcriptase (hTERT) is a rate-limiting enzyme which dictates the activity of human telomerase and thus decides the life span of cells. The aim of this study was to explore the expression of hTERT in bone marrow from children with beta-thalassemia major and the relationship between the expression of hTERT and hemoglobin levels.Multiple allele specific polymerase chain reaction (MASPCR) was used for targeted DNA amplification and gene mutation analysis of beta-thalassemia. hTERT mRNA expression in bone marrow was examined using real-time reverse transcription polymerase chain reaction (RT-PCR) analysis in 29 children with beta-thalassemia major, in 10 children with agranulocytosis and in K562 cell line. The hemoglobin levels in peripheral blood were measured. The relationship between hTERT expression and hemoglobin levels was evaluated by the Spearman test in the beta-thalassemia major group.hTERT mRNA expression significantly increased in bone marrow from children with beta-thalassemia major compared with that from children with agranulocytosis (0.2928+/- 0.0838 vs 0.0993+/- 0.0336; P0.01), but was significantly lower than that in K562 cell line (0.8291+/- 0.0908) (P0.01). A significantly inverse correlation was found between hTERT mRNA expression and hemoglobin levels (r=-0.841, P0.01).A low hemoglobin concentration might contribute to the up-regulation of marrow hTERT expression in children with beta-thalassemia major.

To investigate the relationship between HIF-1alpha expression and neuron apoptosis in hypoxia/hypoxia ischemia brain injury and elucidate the role of HIF-1alpha in regulating neuron apoptosis.Postnatal day 10 SD rats were divided into three groups: the hypoxia ischemia group (HI), the hypoxia group and sham controls. Rat brains were collected at 4 h, 8 h and 24 h after hypoxia from each group. Immunohistochemistry was used to detect the protein expression of HIF-1alpha and active caspase-3. Apoptosis positive cells were determined by TUNEL staining. HE staining was used to detect histopathological damage.The expression of HIF-1alpha protein was significantly upregulated at 4 h, peaked at 8 h, and decreased at 24 h after hypoxia/HI. The expression level of HIF-1alpha protein in hypoxia/HI group was much higher than that in sham controls (P0.01). The expression of activated caspase-3 protein was increased at 4 h and 8 h after hypoxia/HI and significantly upregulated at 24 h, but in sham controls the activated caspase-3 protein remains at a very low level (P0.01). TUNEL staining showed that positive cells significantly increased at 24 h after hypoxia/HI. HE staining showed that neuronal degeneration and edema became prominent at 24 h after hypoxia/HI. The expression of HIF-1alpha protein was higher in hypoxia groups than that in hypoxia ischemia groups at the same time points (P0.05). However, the expression of activated caspase-3, the number of TUNEL positive cells and the degree of histopathological damage were lower in hypoxia groups than that in hypoxia ischemia groups at the same time points (P0.05).The variation tendency of HIF-1alpha and activated caspase-3 expression was opposite, and the expression of HIF-1alpha protein and histopathological damage degree was inverse correlation in HIBD. Therefore, it suggested that HIF-1alpha may play a protective role in neuron after hypoxia/HI.

To evaluate the feasibility and safety of the peripherally inserted central catheters (PICC) as a venous access for newborns who need a long-term venous transfusion.Sixty-five newborns receiving PICC and 80 newborns receiving peripheral intravenous catheters (PIV) from April 2006 to February 2008 were included in this study. A retrospective cohort study was used to compare the indwelling time of catheters, catheter-related mechanical complications, the incidence of sepsis, and the mortality between the two groups.The indwelling time of catheters in the PICC and the PIV groups was 18.75+/-7.62 days (range:7-62 days) and 1.49+/-0.57 days (range: 30 minutes to 4 days) respectively. The indwelling time of catheters in the PICC group was significantly longer than that in the PIV group (0.01). The incidence of catheter-related mechanical complications in the PICC group was significantly lower than that in the PIV group (27.7% vs 63.8%;0.01). There were no significant differences in the incidence of sepsis and the mortality between the two groups.The application of PICC can cause a decrease in the number of venous puncture. PICC is a safe and effective venous access in newborns.

To investigate the mechanism of potassium channel in brain edema caused by hypoxia-ischemia (HI).Astrocytes were obtained from 3-day-old SD rats, cultured, and randomly divided into 2 groups: normoxia group, cultured under normoxic condition, and hypoxic-ischemic group, cultured under hypoxic-ischemic condition. The cell volume was measured by radiologic method. Patch-clamp technique was used to observe the electric physiological properties of the voltage-gated potassium channels (Kv) in a whole cell configuration, and the change of voltage-gated potassium channel current (IKv) was recorded in cultured neonatal rat astrocyte during HI. Aquaporin 4 (AQP4) expression vector was constructed from pSUPER vector and transfected into the astrocytes (AQP4 RNAi) to construct AQP4 knockdown (AQP4-/-) cells. cellular volume was determined using [3H]-3-O-methyl-D-glucose uptake in both AQP4-/- and AQP4+/+ cells under the condition of HI. Real time PCR and Western blotting were used to detect the mRNA and protein expression of AQP4.The percentages of the AQP4+/+ and AQP4-/- astrocyte volumes in the condition of HI for 0.5, 1, 2, and 4 h were 104+/-7, 109+/-6, 126+/-12, and 152+/-9 times, and 97+/-7, 105+/-9, 109+/-7, and 132+/-6 times as those of their corresponding control groups (all P0.05), thus showing that the cellular volume of both AQP4+/+ and AQP4-/- astrocytes significantly increased during HI and the degrees of edema mediated by AQP4 knockdown at different time points were all significantly milder (all P0.05). The current density values at the time points 0.5, 1, 2, and 4 h of the HI group were 107+/-9, 91+/-10, 76+/-6, 37+/-11, respectively, compared to that of the control group of 116+/-8, showing a tendency of time-dependent decreasing manner (all P0.05).During HI, the downregulation of outward potassium (K+) conductance may prevent the emission of intracellularly accumulated K+ ions, thus resulting in osmotically derived water influx into astrocytes via aquaporin-4 and then cell swelling.

To examine the changes of JAKs-STATs pathway in the subventricular zone and choroid plexus of neonatal rats with PVL.A PVL model was established by right common carotid artery ligation followed by 4 h 6% oxygen exposure in 2-day-rat, the neonatal rats performed a sham operation, without hypoxia-ischemia were used as the control grobp. The rats were sacrificed at 0 h, 3 h, 6 h, 12 h, 1 d, 3 d. 7 d of HI, and the brain tissues were collected, immunohistochemistry was applied to detect the expression of P-JAK2 and P-STAT3.The expression levels of P-JAK2 and P-STAT3 increased significantly after HI, peaked at 1 d, and remained at a higher level than control until 7 days of HI, the difference was significant (P0.01).HI resulted in the activation of JAKs-STATs pathway in the subventricular zone and choroid plexus, and this pathway might participated in the pathophysiological process of PVL.

To explore the effect of HIF-1alpha on the proliferation and apoptosis of SiHa cells in hypoxia, as well as the role of HIF-1alpha in the development of uterine cervix cancer.The eukaryotic expression vector containing full length HIF-1alpha (pcDNA3. 1-full length HIF-1alpha) was transfected into SiHa cell, the mock plasmid (pcDNA3. 1) was also transfected into SiHa cell as the negative control. The expression of HIF-1alpha and VEGF were detected by Western Blotting and immunocytochemistry. Cell proliferation was detected by MTT colorimetric assay after the treatment of varied concentration of CoCl2, and cell apoptosis was detected by TUNEL.The level of HIF-1alpha and VEGF expression in the cells transfected with full length HIF-1alpha was higher than that in the untransfected group and pcDNA3. 1 group (P0.05), the survival ability of the cells in HIF-1alpha group was also higher than that of other two groups no matter in anoxia or in hypoxia (P0.05), the ratio of apoptosis was less than untransfected group and pcDNA3. 1 group (P0.05).HIF-1alpha inhibited cell apoptosis in CoCl2 induced hypoxia and stimulated cell proliferation. These results suggest that HIF-1alpha may play an important role in the development of uterine cervix cancer.

To explore the effect of dominant negative HIF-1alpha (dn HIF-1alpha) on biological characteristics of uterine cervix cancer cell SiHa and elucidate the related mechanism.pcDNA3. 1-dn HIF-1alpha was transfected into SiHa cells. The expression of HIF-1alpha and VEGF protein were detected by immunocytochemical method and Western Blotting. The growth proliferation of cells was surveyed by the MTT assay and cell apoptosis was detected through TUNEL after treated with CoCl2, meanwhile the results were compared with the group transfected with mock plasmid and untransfected group.After successfully transfected with relevant plasmid, there's no obvious difference of expression of HIF-1alpha among dn HIF-1alpha group, pcDNA3. 1 group, and untransfected group, however the expression of VEGF of dn HIF-1alpha group was significantly lower than that of the others (P0. 05). The proliferation ability of dn HIF-1alpha group was obviously lower than that of the other two (P0.05), whether it was under normoxia or chemical hypoxia induced by CoCl2. The characteristic apoptotic morphology was most significantly apparent in dn HIF-1alpha group among these three (P0.05).Domain negative HIF-1alpha can inhibit the proliferation of uterine cervix cancer cell and accelerate its apoptosis under hypoxia induced by CoCl2, as well as decrease the expression of VEGF protein. The implications of all this were that the domain negative HIF-1alpha may play an important role in the therapy of uterine cervix cancer.

To investigate whether Aurora A is involved in prostate cancer carcinogenesis.The expressions of Aurora A mRNA and protein in prostate cancer tissue and cell line were measured using RT-PCR, immunohistochemistry and Western blot analyses. Meanwhile, A DNAzyme targeting at Aurora A mRNA was performed to detect the inhibition effect of Aurora A in regulating the growth of prostate cancer cell line PC3.Aurora A expression was up-regulated in 91% prostate cancer tissue as well as in prostate cancer cell lines such as PC3, LNCaP and Du145. Furthermore, Aurora A expression suppressed by cell transduction of a DNAzyme targeting at Aurora A mRNA made the PC3 cells both arrest the cell cycle in G2/M phase and increase the cell apoptosis.These findings suggest that Aurora A up-regulation may be involved in carcinogenesis of prostate cancer, and that aurora A gene may be a valuable target for treatment of prostate cancer.

To examine the effect of Aurora A on the biological phenotypes of prostate cancer cells and the role of Aurora A in the carcinogenesis of prostate cancer.Full length Aurora A gene was cloned and transfected into the prostate cancer cell line LNCaP to construct a positive cell clone with high expression of Aurora A. The growth and proliferation of the cells was detected by MTT. The mobility of the cells was examined by transwell cell layer infiltration assay. The growth and motility of LNCaP-Aurora A cells were compared with those of the LNCaP-pcDNA3. 1/LNCaP cells.Compared to the LNCaP-pcDNA3. 1/ LNCaP cells, the cells with high expression of Aurora A had faster proliferation and stronger invasive ability. Three days after cultivation, more LNCaP-Aurora A cells had grown than the LNCaP-pcDNA3. 1/LNCaP cells (P0.05).The increased expression of Aurora A is closely associated with the malignant phenotypes of prostate cancer. Aurora A may play a very important role in the carcinogenesis of prostate cancer.

To explore the relationship between Aurora A expression and cell sensitivity to taxol, and elucidate the effect of Aurora A on the treatment efficacy of taxol for prostate cancer.A cell clone highly expressing Aurora A was constructed through transfected with full length Aurora A gene, and then termed as Du145-Aurora A. Cells were treated with different dose taxols. The growth inhibition rates of cells were detected by MTT assay, and the cell apoptosis rates were detected through flow cytometry. The growth inhibition and apoptosis rates of Du145-Aurora A and Du145 cells were compared for Aurora A up-regulated expression. Simultaneously, cells Du145-Aurora A were treated with DNAzymes for down-regulating the Aurora A expression, and then the variations of cell growth inhibited rate and apoptosis rate were detected.Up-regulation of Aurora A expression reduced the cell inhibition and apoptosis rates when treated by taxol, but the down-regulation of Aurora A expression after DNAzymes applied increased the cell inhibition and apoptosis rates when treated by taxol.There is a positive relationship between Aurora A expression and treatment efficacy of taxol for prostate cancer, and inhibiting Aurora A expression will enhance the treatment efficacy of taxol for prostate cancer.