Objective To investigate the risk factors for concurrent sepsis in neonates with necrotizing enterocolitis (NEC). Methods A retrospective analysis was performed for the clinical data of 273 neonates with NEC. The risk factors for concurrent sepsis were analyzed from the aspects of perinatal factors and treatment regimen before the diagnosis of NEC. Results The incidence rate of concurrent sepsis in NEC was 32.2% (88/273). The neonates with stage Ⅲ NEC had a significantly higher incidence rate of concurrent sepsis than those with stage Ⅱ NEC (69.0% vs 15.9%; P < 0.05). Of all neonates with sepsis, 62.5% experienced sepsis within 3 days after the diagnosis of NEC, and 37.5% experienced sepsis more than 3 days after the diagnosis. Compared with those without concurrent sepsis, the neonates with concurrent sepsis had significantly lower gestational age and birth weight (P < 0.05). The neonates who had scleredema, had stage Ⅲ NEC, needed gastrointestinal decompression after the diagnosis of NEC, and experienced a long time of gastrointestinal decompression tended to develop sepsis more easily (P < 0.05). Scleredema (OR=9.75, 95%CI:2.84-33.52, P < 0.001), stage Ⅲ NEC (OR=12.94, 95%CI:6.82-24.55, P < 0.001), and gastrointestinal decompression (OR=2.27, 95%CI:1.14-4.5, P=0.02) were independent risk factors for concurrent sepsis in NEC. Conclusions Scleredema, stage Ⅲ NEC, and gastrointestinal decompression are independent risk factors for concurrent sepsis in neonates with NEC.
Objective To investigate the neurodevelopmental outcomes of extremely low birth weight (ELBW) and very low birth weight (VLBW) infants at a corrected age (CA) of 18 months and related factors influencing the outcomes. Methods The ELBW and VLBW infants who were admitted to the neonatal intensive care unit, survived, and discharged between January 2013 June 2014 were enrolled. These infants were followed up at CAs of 40 weeks and 1, 3, 6, 12, and 18 months to evaluate the neurodevelopmental outcomes. According to the neurodevelopmental status, the infants were divided into normal and abnormal neurodevelopment groups. The differences in clinical data were compared, and the risk factors for abnormal neurodevelopment in ELBW and VLBW infants were analyzed. Results A total of 338 ELBW and VLBW infants were enrolled, and 15 died during hospitalization. At the CA of 18 months, 145 infants (44.9%) survived and had complete follow-up data, 75 (23.2%) died, and 103 (31.9%) were lost to follow-up. Of the 145 infants who survived and had complete follow-up data, 71 (49.0%) had neurodevelopmental impairment (NDI), and 3 (2.1%) had cerebral palsy. No infants experienced visual damage with blindness in one or both eyes or hearing loss with a need for hearing aid. The logistic regression analysis showed that bronchopulmonary dysplasia (BDP) (OR=3.530, P < 0.001) and sepsis (OR=2.528, P=0.035) were independent risk factors for NDI in ELBW and VLBW infants, and the incidence of NDI increased with the severity of BDP. Conclusions Sepsis and BPD, especially severe BPD, are risk factors for NDI in ELBW and VLBW infants.
Objective To investigate the factors influencing the prognosis of patent ductus arteriosus (PDA) in very low birth weight (VLBW) infants. Methods A total of 194 VLBW infants who were admitted from January 2012 to December 2014 were enrolled as study subjects. According to cardiac ultrasound findings and treatment outcome, these infants were divided into non-PDA group, spontaneous closure group, pharmaceutical closure group, and surgical closure group. Their clinical and echocardiographic characteristics were analyzed. Results The spontaneous closure rate of PDA was 58.7%. The spontaneous closure group showed significantly higher gestational age, birth weight, and proportion of small-for-gestational-age infants than the pharmaceutical and surgical closure groups (P < 0.05). The pharmaceutical and surgical closure groups had a significantly higher incidence rate of neonatal respiratory distress syndrome and a significantly higher proportion of infants who were given pulmonary surfactant (PS) than the spontaneous closure group (P < 0.05). During different periods of time, the spontaneous closure group had a significantly smaller ductus arteriosus diameter than the pharmaceutical and surgical closure groups (P < 0.05). The multivariate logistic regression analysis showed that gestational age, application of PS, and ductus arteriosus diameter at 48 hours were significantly associated with the prognosis of PDA. The major transductal flow pattern in the spontaneous closure group was closing pattern, while in the pharmaceutical and surgical closure groups, the main flow patterns were pulmonary hypertension and growing patterns within 48 hours and growing pattern on days 4 and 7. Conclusions The VLBW infants have a high spontaneous closure rate of PDA. A decreased closure rate of PDA is associated with the lower gestational age and the application of PS. PDA with a large ductus arteriosus diameter and a growing or pulsatile flow pattern cannot easily achieve spontaneous closure.
Objective To investigate the pulmonary function after treatment in neonates with respiratory distress syndrome (RDS) at varying disease severity levels and different gestational ages. Methods A total of 107 neonates with RDS were divided into <34 weeks group (65 neonates), late preterm group (21 neonates), full-term group (21 neonates). Another 121 non-RDS children were enrolled as the control group. According to the severity of RDS, the RDS neonates were divided into mild RDS group (grades 1 and 2; 76 neonates), and severe RDS (grades 3 and 4; 21 neonates). The tidal breathing pulmonary function was measured at a corrected gestational age of 44weeks. Results The pulmonary function parameters showed no significant differences across the groups of RDS neonates of different gestational ages; the tidal volume per kilogram of body weight (VT/kg) showed no significant difference between the RDS and non-RDS groups, while the RDS group had significantly higher ratio of time to peak tidal expiratory flow to total expiratory time (tPTEF/tE) and ratio of volume to peak tidal expiratory flow to total expiratory volume (vPTEF/vE) than the non-RDS group of the same gestational age (P < 0.05). At a corrected gestational age of 44 weeks, the two groups of neonates with varying severity levels of RDS had significantly lower tPTEF/tE and vPTEF/vE than the control group (P < 0.05), and tPTEF/tE and vPTEF/vE tended to decrease with the increasing severity level of RDS. Conclusions Neonates with RDS have significantly decreased pulmonary function than those without RDS. At a corrected gestational age of 44 weeks, the tidal breathing pulmonary function in neonates with RDS is not associated with gestational age, but is associated with the severity of RDS.
Objective To investigate the incidence of congenital adrenal hyperplasia (CAH) and treatment outcomes in neonates in Ningxia, China. Methods The clinical data of CAH screening for 160 046 neonates who were born in midwifery institutions in Ningxia from July 2014 to March 2016 were analyzed. Results Among the 160 046 neonates who underwent CAH screening, 70 (0.044%) obtained a positive result and 11 were diagnosed with CAH; the incidence rate of CAH was 1/14 550 (0.069‰). Among the 11 neonates diagnosed with CAH, 9 had the salt wasting type (2 died) and 2 had simple virilization. The 9 neonates were given glucocorticoids immediately once diagnosed and all of them achieved good growth and development. Conclusions The incidence of neonatal CAH in Ningxia is 1/14 550. It is very necessary to carry out CAH screening in Ningxia, and active treatment can improve the prognosis of neonates with CAH.
Objective To investigate the factors influencing the quality of life (QOL) of children with phenylketonuria (PKU) in Anhui Province, China. Methods A total of 104 PKU children who were diagnosed and treated in three major maternal and child health hospitals in Anhui Province were enrolled as study subjects. The PedsQLTM 4.0 Generic Core Scales were used to evaluate the quality of life of these children. The multivariate logistic regression analysis was used to evaluate the factors influencing the QOL. Results The 104 PKU children had significantly lower overall QOL score and scores on the subscales of physiological functioning, emotional functioning, and social functioning than the general school-age children (P < 0.01). They also had a significantly lower score on the physiological domain consisting of emotional functioning, social functioning, and role functioning than the general school-age children (P < 0.01). The multivariate logistic regression analysis showed that an older age (≥ 4 years) of PKU children was the risk factor for poor QOL (OR=8.569, P < 0.01), and guardians' engagement at enterprises or institutions was the protective factor for QOL (OR=0.206, P < 0.05). Conclusions PKU children have a low level of QOL, and age and guardians' occupation are factors influencing the QOL.
Objective To investigate the changes in the expression levels of peripheral blood T helper 9 (Th9) cells and cytokine interleukin-9 (IL-9) in children in the acute stage of Kawasaki disease (KD) and their clinical significance. Methods A total of 45 children in the acute stage of KD who were treated from April 2014 to July 2015 were enrolled, and the children were followed up in the recovery stage. Another 45 healthy children who underwent physical examination were enrolled as the control group. Flow cytometry was used to measure the percentage of peripheral blood Th9 cells, and ELISA was used to measure the serum level of IL-9. Results The children in the acute stage of KD showed a significantly higher percentage of Th9 cells and a significantly higher serum level of IL-9 compared with those in the recovery stage and the control group (P < 0.05). The percentage of Th9 cells and serum level of IL-9 showed no significant differences between the children in the recovery stage and those in the control group (P > 0.05). In the acute stage, the percentage of Th9 cells was positively correlated with the levels of IL-9, C-reactive protein (CRP), procalcitonin (PCT), erythrocyte sedimentation rate (ESR), platelet count (PLT), and globulin (r=0.624, 0.324, 0.402, 0.382, 0.467, and 0.386 respectively, all P < 0.05), but negatively correlated with serum albumin (r=-0.306, P < 0.05). The serum level of IL-9 was positively correlated with the levels of CRP, PCT, ESR, PLT, and globulin (r=0.365, 0.456, 0.403, 0.423, and 0.453 respectively, all P < 0.05), but negatively correlated with serum albumin (r=-0.343, P < 0.05). Conclusions The children in the acute stage of KD show significant increases in the percentage of peripheral Th9 cells and serum cytokine IL-9 level, which return to normal in the recovery stage. In the acute stage of KD, the expression levels of Th9 and IL-9 are closely correlated with laboratory markers. The results suggest that Th9 cells and IL-9 play important roles in the pathogenesis and outcome of KD.
Objective To establish a food allergy model in Brown Norway (BN) rats by gavage of ovalbumin (OVA) without any adjuvant, and to evaluate this model. Methods A total of 20 male BN rats aged 3 weeks were randomly divided into allergy group and control group (n=10 each). BN rats in the allergy group were given OVA 1 mg per day by gavage, and all the rats were treated for 41 days continuously. On day 42, the rats in the allergy group were given OVA 100 mg by gavage for challenge. The rats in the control group were given normal saline of the same volume by gavage. Differences in body length, body weight, and food intake were compared between the two groups on days 7, 14, 21, 28, 35, and 42. ELISA was used to measure the serum OVA-IgE level and plasma histamine level after challenge on day 42, and the changes in rats' appearance and fecal properties were observed. The model of food allergy was considered successful when the serum OVA-IgE level in the allergy group was no less than the mean serum OVA-IgE level + 3 standard deviation in the control group. Results There were no significant differences in body length, body weight or food intake between the allergy and control groups at all time points (P > 0.05). On day 21, the control group had a significantly higher food intake than the allergy group (P < 0.05). On day 42 after challenge, the allergy group showed significantly higher serum OVA-IgE and plasma histamine levels than the control group (P < 0.05). The sensitization rate (rate of successful modeling) was 90%. The fecal properties showed no significant differences between the two groups. Conclusions OVA by gavage without any adjuvant can successfully establish the model of food allergy in BN rats and has a high success rate. Food allergy induced by OVA may reduce food intake within a short period of time, but no influence on rats' body length or body weight has been observed.
Objective To investigate the influence of lead exposure in rats during the developmental stage on the expression of leptin in plasma, cerebrospinal fluid, and hippocampus, as well as investigating whether leptin is associated with the mechanism of cognitive impairment induced by lead exposure. Methods The rat model of cognitive impairment after chronic lead exposure was established by adding lead acetate into drinking water. According to the concentration of lead acetate in drinking water, the rats were divided into control (0 ppm), low-lead (50 ppm), medium-lead (200 ppm), and high-lead groups (1000 ppm), with 16 rats in each group. Atomic absorption spectrometry was used to measure the content of lead in the plasma, cerebrospinal fluid and hippocampus. ELISA was used to measure the level of leptin in the plasma and cerebrospinal fluid. Immunohistochemistry was used to observe the distribution of leptin protein in the hippocampus. Western blot was used for relative quantification of leptin proteins in the hippocampus. Results Compared with the control group, the lead exposure groups showed significant increases in the content of lead in blood, cerebrospinal fluid, and hippocampus (P < 0.01), as well as significant reductions in the levels of leptin in plasma and cerebrospinal fluid (P < 0.05). The results of immunohistochemical staining showed that leptin was mainly distributed in the cytoplasm of pyramidal neurons in the hippocampal CA region. The results of Western blot showed that compared with the control group, the three lead exposure groups showed a slight increase in the protein expression of leptin in the hippocampus (P > 0.05). Conclusions Lead exposure can reduce the levels of leptin in plasma and cerebrospinal fluid in rats, which may be associated with the mechanism of cognitive impairment induced by lead exposure.
Objective To investigate the role of miRNA-210 in hypoxic-ischemic brain edema in neonatal rats. Methods A total of 80 neonatal rats were randomly divided into control group, normal saline group, miRNA-210 expression inhibition group, and miRNA-210 overexpression group, with 20 rats in each group. Each group was randomly divided into sham-operation group and hypoxia-ischemia (HI) group, with 10 rats in each group. The neonatal rats in the HI group were treated with ligation of the left common carotid artery and then put in a hypoxia cabin with mixed gas of 8% O2 and 92% N2 for 2 hours; those in the sham-operation group were treated with isolation of the left common carotid artery only, without ligation or hypoxia treatment. After HI or sham-operation, the rats in the normal saline group, miRNA-210 expression inhibition group, and miRNA-210 overexpression group were intracranially injected with normal saline (2.5 mg/kg), miRNA-210 inhibitor (2.5 mg/kg), and miRNA-210 mimic (2.5 mg/kg) respectively. No treatment was given to the rats in the control group. The rats were sacrificed three days later, and the left brain tissue was harvested. Fluorescent quantitative PCR was used to measure the expression of miRNA-210; the dry-wet weight method was used to measure the water content of brain tissue; hematoxylin and eosin staining was used to observe the histomorphological changes in the brain. Results The HI groups showed significant reductions in the expression of miRNA-210 and significant increases in the water content of brain tissue compared with the corresponding sham-operation groups (P < 0.05). Compared with the normal saline HI group, the miRNA-210 expression inhibition HI group showed a significant reduction in the expression of miRNA-210 and a significant increase in the water content of brain tissue (P < 0.05), and the miRNA-210 overexpression HI group showed a significant increase in the expression of miRNA-210 and a significant reduction in the water content of brain tissue (P < 0.05). The results of hematoxylin and eosin staining suggested that the miRNA-210 expression inhibition HI group showed marked edema, and the miRNA-210 overexpression HI group showed a significant improvement in edema. Conclusions Neonatal rats show down-regulated expression of miRNA-210 after HI, suggesting that miRNA-210 may be involved in the development and progression of hypoxic-ischemic brain edema in neonatal rats.
Objective To investigate the effect of phosphoinositide 4-phosphate (PI4P) on human glioma U87 cells and the mechanism of action of PI4P in the development of human glioma through the overexpression or silencing of PI4P in human glioma U87 cells, and to provide a new target for basic research and clinical treatment of glioma. Methods LV-Helper1, LV-Helper2, pWPXLd-PI4P, and pLL3.7-shPI4P were used to package pWPXLd-PI4P and pLL3.7-shPI4P lentiviruses. The U87-GFP (PI4P-overexpression control group), U87-GFP-PI4P (PI4P-overexpression experimental group), U87-Scramble (PI4P-silencing control group), and U87-shPI4P (PI4P-silencing experimental group) cell lines were established. Wound-healing assay and Transwell assay were used to evaluate cell migration and invasion, and Western blot was used to measure the expression of PI4P in each group. Results Western blot detected the expression of exogenous PI4P in the U87-GFP-PI4P cell line, and the U87-shPI4P cell line showed reduced expression of PI4P compared with the U87-Scramble cell line in the control group. The U87-GFP-PI4P cell line with PI4P overexpression had a significantly stronger ability of migration than the U87-GFP cell line in the control group (P < 0.01); the U87-shPI4P cell line with PI4P silencing had a reduced ability of migration than the U87-Scramble cell line in the control group (P < 0.01). The U87 cell line with PI4P overexpression had a significantly stronger invasion ability than the control group (P < 0.05); after PI4P silencing, the experimental group showed a significant reduction in invasion ability compared with the control group (P < 0.05). Conclusions In human glioma U87 cells, PI4P can promote the invasion and migration of glioma cells and may become a new target in the basic research and clinical treatment of glioma.
As a kind of mitochondrial membrane protein with protein kinase activity, phosphatase and tensin homolog deleted on chromosome ten induced kinase 1 (PINK1) is involved in many biological metabolic processes. Since PINK1 had been found to be associated with Parkinson's disease, researchers have been exploring its biological function. PINK1 localizes in the outer mitochondrial membrane and regulates cell function through phosphorylating proteins. PINK1 is involved in mitochondrial function, mitochondrial morphology and mitochondrial autophagy, but the regulatory pathway is not yet clear. PINK1 is expressed widely in many tissues with a variety of biological activity, especially in tissues with high energy consumption. It may therefore be involved in the development and regulation of many diseases. Mutations in PINK1 were originally discovered to cause autosomal recessive Parkinson's disease. Recently some research has revealed that PINK1 is related to the development of neonatal hypoxic-ischemic encephalopathy, cancer, diabetes and other diseases. Studying and exploring the biological functions of PINK1 will facilitate the identification of the targets for therapeutic intervention for its related diseases. This review article mainly focuses on recent studies about the biological function and related diseases of PINK1.