Effect of PR-957 on the formation of A1 reactive astrocytes / 中国当代儿科杂志

OBJECTIVE@#To study the effect of PR-957 on the formation of A1 reactive astrocytes.@*METHODS@#The cerebral cortices of 1-day-old female rats were obtained and cultured for primary astrocytes. These cells were divided into 3 groups: control, lipopolysaccharide (LPS), and LPS+PR-957. The LPS group was treated with LPS (at a concentration of 5 μmol/L) for 48 hours; the LPS+PR-957 group was treated with PR-957 (at a final concentration of 200 nmol/L) for 1 hour and then LPS for 48 hours. Enzyme-linked immunosorbent assay was used to determine the expression of complement 3 (C3, a marker for A1 reactive astrocytes) and tumor necrosis factor alpha (TNF-α). Quantitative real-time PCR was used to determine the relative mRNA expression of glypican-6 (GPC6), SPARC-like 1 (SPARCL1), and lipocalin-2 (LCN2). All the above experiments were repeated three times independently.@*RESULTS@#C3 expression was almost not observed in the control group, but was observed in both the LPS group and the LPS+PR-957 group, with significantly lower expression observed in the LPS+PR-957 group (P<0.05). The expression of TNF-α was consistent with that of C3. Compared with the control group, the LPS and the PS+PR-957 groups had significantly reduced mRNA expression levels of GPC6 and SPARCL1 but significantly increased mRNA expression level of LCN2 (P<0.001). Compared with the LPS group, the LPS+PR-957 group had significantly increased mRNA expression levels of GPC6 and SPARCL1 but significantly reduced mRNA expression level of LCN2 (P<0.001).@*CONCLUSIONS@#LPS can induce the transformation from astrocytes to A1 reactive astrocytes, and PR-957 can inhibit the formation of LPS-induced A1 reactive astrocytes.

A review on the prevention and treatment of congenital cytomegalovirus infection in mothers and infants / 中国当代儿科杂志

Human cytomegalovirus (HCMV) has a high infection rate worldwide, and 85%-90% of congenital cytomegalovirus (CMV) infections are asymptomatic at birth, with the clinical manifestations of hearing loss, psychomotor retardation, and learning disabilities, while 10%-15% are symptomatic infections. Some preterm infants develop CMV infection after birth, which can cause sepsis-like syndrome, thrombocytopenia, neutropenia, liver injury, and lung injury. However at present, women of childbearing age have a lack of awareness of CMV. CMV education and hygiene precautions for pregnant women can prevent CMV infections in themselves and congenital CMV infections in their infants. No definite results have been obtained from the studies on the effect of CMV vaccine and high-titer immunoglobulin in preventing congenital CMV infection in fetuses. Recent studies have confirmed that the specificity and sensitivity of urinary or salivary CMV-DNA detection have reached more than 98%, which contributes to the early diagnosis of congenital CMV infection. In addition to short-term treatment with ganciclovir, long-term treatment with oral valganciclovir is safe for symptomatic congenital CMV infection and appears to have a better clinical effect than the short-term treatment. In the future, it is necessary to strengthen the health education for pregnant women, enhance the mother-to-child management of CMV infection, conduct the research on CMV vaccine, and further standardize treatment regimens.

Vitamin A level and diseases of premature infants / 中国当代儿科杂志

Vitamin A is a fat-soluble vitamin, and it is not only necessary for the normal growth and development of epithelial cells, but also plays a very important role in the normal growth and development of the retina, lungs, gastrointestinal tract, brain, and immune system. Studies have confirmed that the low level of vitamin A in premature infants at birth can last through the entire infancy. Recently, there have been particular concerns about the level of vitamin A and development of diseases in premature infants, with major focuses on the related mechanisms of action of vitamin A in respiratory distress syndrome, chronic lung disease, retinopathy of prematurity, necrotizing enterocolitis, patent ductus arteriosus, and infections in premature infants, which still awaits further investigation.This paper summarizes and analyzes the current status of research on vitamin A level and diseases of premature infants at home and abroad. In addition, although enough evidence suggests that vitamin A supplementation is beneficial to preterm infants, evidence is still lacking for recommended methods for supplementation and dose of vitamin A, and further studies are needed.

Risk factors for hearing impairment induced by cytomegalovirus infection / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the risk factors for hearing impairment induced by cytomegalovirus (CMV) infection in children.</p><p><b>METHODS</b>One hundred and fifty-eight children diagnosed with CMV infection were enrolled as subjects. Based on the results of the brainstem auditory evoked potential (BAEP) test, patients were classified into normal hearing group (n=117; BAEP≤35) and abnormal hearing group (n=41; BAEP>35). A retrospective analysis was performed on the general information, routine blood indices, liver function, copy number of CMV-DNA in urine and breast milk. The receiver operating characteristic (ROC) curve was used to predict the copy number of CMV-DNA resulting in abnormal BAEP. The Spearman rank correlation analysis was used to test the correlations of the copy number of CMV-DNA in urine with the degree of hearing impairment and platelet count.</p><p><b>RESULTS</b>The incidence rates of platelet abnormality and abnormal liver function and the copy number of CMV-DNA in urine were significantly higher in the abnormal hearing group than in the normal hearing group (P<0.01). According to the ROC curve, the copy number of CMV-DNA in urine had a sensitivity of 46.3% and a specificity of 93.2% in predicting hearing impairment when it reached 1.415×10(6) per mL. The results of correlation analysis showed that the degree of hearing impairment was positively correlated with the copy number of CMV-DNA (r=0.382, P<0.01); the platelet count was negatively correlated with the copy number of CMV-DNA in urine (r=-0.233, P=0.003).</p><p><b>CONCLUSIONS</b>An increased copy number of CMV-DNA in urine might be a risk factor for hearing impairment induced by CMV infection. Children are likely to have hearing impairment when the copy number of CMV-DNA reaches 1.415×10(6) per mL. The monitoring of hearing should be strengthened in CMV-infected children with a decreased platelet count.</p>

Risk factors and outcomes for retinopathy of prematurity in neonatal infants with a birth weight of 1,501-2,000 g in a Chinese Neonatal Unit

To determine the risk factors and outcomes of retinopathy of prematurity [rop] in infants with a birth weight of 1,501-2,000 g. Materials and methods: clinical characteristics and risk factors were compared and nonconditional logistic regression analysis was performed to determine independent predictors for rop. There were 54 [9.8%] cases of rop in 553 patients with a birth weight of 1,501-2,000 g. The most common classification of rop was in stage 1 [50/54, 92.6%; stages 2 and 3 rop: 2 infants each]. By logistic regression analysis, the following factors independently predicted rop: gestational age at birth

Experimental study on cerebral white matter damage in neonatal rat after intrauterine Escherichia coli infection / 中华儿科杂志

<p><b>OBJECTIVE</b>To investigate the expression of glial fibrillary acidic protein (GFAP), GFAP mRNA and interleukin-1beta mRNA (IL-1beta mRNA), tumor necrosis factor-alpha mRNA (TNF-alpha mRNA) in neonatal rat brain after intrauterine infection.</p><p><b>METHODS</b>Escherichia coli (E. coli) was inoculated into both uterine horns of pregnant rats when gestation was 70% complete (15 days). The control group was treated with normal saline. The pups were killed on the postnatal day 1 (P1), P3 and P7, respectively. The cerebral white matter damage of the neonatal rats was determined by HE staining. Immunohistochemistry was used for evaluation of GFAP expression in neonatal rat brains and RT-PCR to analyze GFAP mRNA, IL-1beta mRNA and TNF-alpha mRNA expression at P1, P3 and P7.</p><p><b>RESULTS</b>The major histopathological changes in neonatal cerebral white matter at P7 after intrauterine infections were: weak staining of cerebral white matter and focal rarefaction. GFAP-positive cells were observed in both the control and the E. coli-treated groups. The numbers of GFAP-positive cells of the E. coli-treated group pups were markedly increased in periventricular white matter and hippocampus at P7 compared with those of the control group (periventricular white matter: 9.73 +/- 3.55 vs 5.67 +/- 1.90, P < 0.05 and hippocampus: 7.81 +/- 3.61 vs 2.16 +/- 1.11, P < 0.05, respectively). No significantly different levels of GFAP expression in corpus callosum were found between two groups (P > 0.05). The expression of GFAP mRNA in brain of the E. coli-treated neonatal rat was higher than the control at P1, P3 (P1: 0.25 +/- 0.07 vs 0.15 +/- 0.08, P < 0.05 and P3: 0.50 +/- 0.09 vs 0.39 +/- 0.08, P < 0.05, respectively), but the expression of GFAP mRNA in brain of the neonatal rat at P7 had no significant difference between two groups (P > 0.05). The expression of IL-1beta mRNA and TNF-alpha mRNA in brain of the E. coli-treated neonatal rat were higher than of the control at P1 (IL-1beta mRNA: 0.83 +/- 0.19 vs 0.50 +/- 0.30, P < 0.05 and TNF-alpha mRNA: 0.74 +/- 0.30 vs 0.30 +/- 0.20, P < 0.05, respectively), but the expression of IL-1beta mRNA and TNF-alpha mRNA in brain of the neonatal rat at P3 and P7 had no significant difference between two groups (P > 0.05).</p><p><b>CONCLUSIONS</b>The intrauterine infection could cause neonatal white matter damage and IL-1beta, TNF-alpha may be a mechanism mediating between the two events.</p>