High-risk factors for early failure of high-flow nasal cannula oxygen therapy in children / 中国当代儿科杂志

OBJECTIVE@#To determine the high-risk factors for early failure of high-flow nasal cannula (HFNC) oxygen therapy in children with acute respiratory insufficiency (ARI).@*METHODS@#The clinical data of 123 children with ARI were reviewed who received HFNC oxygen therapy in the pediatric intensive care unit from January to June, 2018. The children who did not require an upgrade of respiratory support during hospitalization and were successfully weaned from HFNC were classified as HFNC success group (69 cases). Of the remaining children (54 cases) who required an upgrade of their respiratory support during hospitalization, those that needed to upgrade their respiratory support within 48 hours of receiving HFNC were classified as early HFNC failure group (46 cases). Risk factors for early failure of HFNC were determined using multivariate logistic regression analysis.@*RESULTS@#The incidence rates of shock, sepsis, intracranial hypertension syndrome, and multiple organ dysfunction syndrome were significantly higher in the early HFNC failure group than in the HFNC success group (P4.5 and PaCO/PaO ratio >0.64 were independent risk factors for early HFNC failure (OR=5.535 and 9.089 respectively; P4.5 or PaCO/PaO ratio >0.64 have relatively high risk of early HFNC failure.

Role of c-Jun N-terminal kinase-mediated FOXO3a nuclear translocation in neuronal apoptosis in neonatal rats with hypoxic-ischemic brain damage / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the mechanisms of neuroprotective effects of c-Jun N-terminal kinase (JNK)/FOXO3a transcription factor signaling pathway inhibition on hypoxic-ischemic neuronal apoptosis in neonatal rats with hypoxic-ischemic brain damage (HIBD).</p><p><b>METHODS</b>Sixty-four 7-day-old Sprague-Dawley rats were divided into four groups: hypoxia-ischemia (HI), sham-operated, JNK specific inhibitor AS601245-treated, and DMSO vehicle. Rats' cerebral cortexes were collected at 24 hours after HI. Western blot was used to detect the protein expression of JNK, p-JNK, FOXO3a, nuclear and cytoplasmic FOXO3a, Bim, and CC3. TUNEL staining was used to detect the apoptotic cells.</p><p><b>RESULTS</b>Compared with the sham-operated group, p-JNK protein increased (P<0.01), nuclear protein of FOXO3a increased (P<0.01), cytoplasmic protein decreased (P<0.01), and pro-apoptotic proteins Bim and CC3 increased 24 hours after HI (P<0.01). Compared with the HI and DMSO vehicle groups, p-JNK protein was reduced (P<0.01), nuclear protein of FOXO3a was also reduced (P<0.01), cytoplasmic protein increased (P<0.01), and Bim and CC3 proteins decreased (P<0.01) in the AS601245-treated group 24 hours after HI. TUNEL positive cells were reduced in the AS601245-treated rats compared with the HI and DMSO vehicle groups 24 hours after HI (P<0.01).</p><p><b>CONCLUSIONS</b>JNK activity increases in the neonatal rat brain with HI damage. JNK activity inhibition can inhibit FOXO3a translocation from cytoplasm to nucleus and downregulate the levels of pro-apoptotic proteins Bim and CC3, leading to the reduction of neuronal apoptosis.</p>

Effect of NF-κB on proliferation of rat pulmonary artery smooth muscle cells inhibited by simvastatin / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the effects of NF-κB on proliferation of rat pulmonary artery smooth muscle cells (PASMC) inhibited by simvastatin.</p><p><b>METHODS</b>PASMC isolated from rats and cultured in vitro were randomly divided into four groups (n=6 each): control, platelet-derived growth factor (PDGF) treatment, PDGF+simvastatin treatment, and PDGF+simvastatin+parthenolide (NF-κB inhibitor) treatment. MTT colorimetric assay and flow cytometry were performed to detect cell proliferation and cell cycle distribution. Immunohistochemistry was performed to detect the expression of NF-κB protein. Real-Time PCR was performed to detect NF-κB mRNA expression.</p><p><b>RESULTS</b>Compared with the control group, MTT values of PASMC at all time points, cell proportion at the S phase and G2+M phase, NF-κB protein and mRNA expression increased significantly in the PDGF group (P<0.05). With the intervention of simvastatin, the levels of above indexes decreased compared with the PDGF group (P<0.05). With the intervention of simvastatin and parthenolide, the levels of above indexes decreased more obviously, but were not significantly different from those in the simvastatin intervention group.</p><p><b>CONCLUSIONS</b>Simvastatin can inhibit proliferation of PASMC and cell cycle process. NF-κB may play an important role in the inhibitory effect of simvastatin on the proliferation of PASMC.</p>

Effect of nuclear transcription factor kappaB pathway on proliferation in rat pulmonary artery smooth muscle cells induced by platelet-derived growth factor / 中华实用儿科临床杂志

Objective To explore the effect of nuclear transcription factor kappaB(NF-κB) pathway on proliferation of rat pulmonary artery smooth muscle cells (PASMC) induced by platelet-derived growth factor (PDGF).Methods PASMC isolated from rats and cultured in vitro were divided into 3 groups according to the randomization principle:control group(cultured by M199),PDGF treatment group(cultured by M199 and stimulated by PDGF),PDGF + parthenolide treatment group (cultured by M199 and stimulated by PDGF,and intervented by the NF-κB inhibitors parthenolide).MTT colorimetric assay and flow cytometry were performed to detect cell proliferation and cell cycle distribution.Immunohistochemistry was performed to detect the expressions of NF-κB and COX-2 protein.Fluorescence quantitative RT-PCR was performed to detect NF-κB and COX-2 mRNA expressions.One-way ANOVA was used for statistical analysis,multiple comparisons were analyzed by LSD.Results Compared with the control group,MTT value of PASMC was increased significantly when induced by PDGF at each time points(all P ＜ 0.05).MTT value decreased dramatically after the intervention of NF-κB inhibitor parthenolide(P ＜0.05).Data from flow cytometry detection showed that cell proportion of S phase and G2 + M phase increased significantly in PDGF treatment group,which had statistical difference compared with control group (all P ＜ 0.05).Compared with PDGF induced group,after the intervention of parthenolide,cell proportion of S phase and G2 + M phase ratio decreased dramatically (P ＜ 0.05).The expressions of NF-κB and COX-2 protein and mRNA were promoted in the PDGF induced group compared with the control group (all P ＜ 0.05).Compared with PDGF induced group,after the intervention of parthenolide,the expressions of NF-κB and COX-2 protein and mRNA decreased dramatically(all P ＜ 0.05).Conclusions PDGF can induce proliferation of PASMC,promote cell cycle process and enhance the expressions of NF-κB and COX-2 protein and mRNA.NF-κB pathway involves in the proliferation of PASMC induced by PDGF.

Study of enterovirus 71-induced autophagy in human malignant glioma cell line U251 / 中华实用儿科临床杂志

Objective To show evidences that autophagy is induced in human malignant glioma cell line U251 by enterovirus(EV71) and its effect on the expression of microtubule-associated protein 1 lightchain 3 (LC3) in vitro.Methods U251 cells were cultured in RPMI 1640 for 24 hours,then randomly divided into experimental group and control group.In experimental group,EV71 were added in cell culture holes at multiplicity of infection (MOI) equal to 1,and cultured continuously.After 12 hours post infection of U251 cells with EV71,autophagic vacuoles of U251 cells were marked by monodansylcadaverine staining and observed under fluorescence microscope.After 24 hours post infection,expression and intracellular distribution of LC3 protein in U251 cells were observed under fluorescence microscope by immunofluorescence.Expressions of LC3-I and LC3-Ⅱ protein were measured by Western blot and analysis of LC3-Ⅱ protein expression was performed with semi-quantitative calculation at 2,4,8,12,24 and 48 hours post infection of U251 cells with EV71,respectively.Results Autophagic vacuoles stained by MDC in U251 cells appeared as distinct dot-like structures distributed under fluorescence microscope.The number of autophagic vacuoles were increased significantly at 12 hours post infection of U251 cells with EV71 when compared with control group.The morphological features of these cells became significantly shrunken,smaller and irregular shape at 24 hours post infection of U251 cells,and the expressions of LC3 protein were significantly higher in experimental group than those in control group.Under a fluorescence microscope,LC3 protein distributed within the cytoplasm or localizing in the perinuclear regions.At 4 hours post infection of U251 cells with EV71,the expression of LC3-Ⅱ protein started to increase,and was significantly higher than that in control group (P ＜ 0.01).Conclusion These results indicate that EV71 can effectively induce autophagy of human malignant glioma cell line U251,and play its oncolytic effect.

Risk factors of heart and lung failure in children with severe hand, foot and mouth disease and treatment experience / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study risk factors for severe hand, foot and mouth disease (HFMD) complicated by heart and lung failure and treatment experience.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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 (P<0.05).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 (P<0.01). 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 (P<0.01).</p><p><b>CONCLUSIONS</b>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.</p>

Decreased mRNA expressions of T-type channel alpha1H and alpha1G in the sperm of varicocele patients and their implication / 中华男科学杂志

<p><b>OBJECTIVE</b>To study the relationship of varicocele (VC) with the expressions of T-type channel alpha1H and alpha1G in the sperm of VC patients.</p><p><b>METHODS</b>Based on the WHO criteria, we examined the semen samples by computer-aided sperm analysis (CASA), and divided the samples into groups A (normal semen from volunteers, n = 20), B (normal semen from VC patients, n = 16) and C (abnormal semen from VC patients, n = 44). We optimized the semen by discontinuous Percoll grade centrifugation, and determined the mRNA expressions of T-type channel alpha1H and alpha1G in the three groups using using reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Compared with group A, the mRNA expressions of alpha1H and alpha1G showed with no significant decrease in group B (P>0.05), but were remarkably reduced in group C (P<0.01).</p><p><b>CONCLUSION</b>The abnormal mRNA expressions of T-type channel alpha1H and alpha1G may be one of the causes of declined semen quality and consequently infertility in VC patients, which has pointed out a new direction for the studies of the causes and treatment of VC-related infertility.</p>

Effects of endogenous carbon monoxide on gene expression profiles associated with the apoptosis of pulmonary arterial smooth muscle cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To identify the gene expression profiles associated with the apoptosis of pulmonary arterial smooth muscle cells stimulated by carbon monoxide (CO).</p><p><b>METHODS</b>Primary cultured Sprague-Dawley rat pulmonary arterial smooth muscle cells (PASMC) were stimulated by platelet-derived growth factor (PDGF, 20 ng/mL) and hemin (20 μmol/L). Cells were harvested after 2 hrs and Affymetrix microarrays were used to detect the gene expression profile.</p><p><b>RESULTS</b>Some genes associated with Map2k3 (P38) signal pathway, such as CyclinD1, CyclinH, CyclinL1, MAP2K3, Kras and Nras, were upregulated, but P27 expression was downregulated after PDGF treatment. After endogenous CO treatment, some genes associated with P53 pathway, such as Gadd45α, P21 and Trp53inp1, were upregulated.</p><p><b>CONCLUSIONS</b>P53 pathway probably plays an important role in apoptosis of pulmonary arterial smooth muscle cells treated with endogenous CO.</p>