Objective The goal of nutrition of the preterm infant is to meet the growth rate of the healthy fetus of the same gestational age and to produce the same body composition of the healthy fetus in terms of organ growth, tissue components, and cell number and structure. Nutritional quantity and quality are fundamental for normal growth and development of preterm infants, including neurodevelopmental outcomes. Failure to provide the necessary amounts of all of the essential nutrients has produced not only growth failure, but also increased morbidity and less than optimal neurodevelopment. Growth velocities during the NICU hospitalization period for preterm infants exert a significant effect on neurodevelopmental and anthropometric outcomes. Despite the obvious need for optimal nutrition, growth failure is almost universal among preterm infants. There is every reason, therefore, to optimize nutrition of the preterm infant, in terms of total energy and protein, but also in terms of individual components such as amino acids, specific carbohydrates and lipids, and even oxygen. This review presents scientific rationale for nutrient requirements and practical guidelines and approaches to intravenous and enteral feeding for preterm infants. Intravenous feeding, including amino acids, should be started right after birth at rates that are appropriate for the gestational age of the infant. Enteral feeding should be started as soon as possible after birth, using mother's colostrum and milk as first choices. Enteral feeding should begin with trophic amounts and advanced as rapidly as tolerated, decreasing IV nutrition accordingly, while maintaining nutrient intakes at recommended rates. Feeding protocols are valuable for improving nutrition and related outcomes. Further research is needed to determine the optimal nutrition and rate of growth in preterm infants that will achieve optimal neurocognitive benefits while minimizing the longer-term risk of chronic diseases.
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Objective To evaluate the clinical characteristics and risk factors of clonal evolution after immunosuppressive therapy (IST) in children with severe/very severe aplastic anemia (SAA/VSAA). Methods The clinical data of 231 children with newly-diagnosed SAA/VSAA who received IST were retrospectively studied. The incidence and risk factors of clonal evolution after IST were analyzed. Results The 5-year overall survival rate of the 231 patients was 82.7%. Except for 18 cases of early deaths, 213 patients were evaluated for IST efficacy. Among the 231 patients, cytogenetic abnormalities for at least two chromosome metaphase were detectable in 14 (7.4%) patients, and PNH clones were detectable in either peripheral red blood cells or neutrophils for 95 patients. Among the 213 patients evaluated for IST efficacy, 15 patients experienced clonal evolution after IST. Five patients had PNH and trisomy 8 which were defined as favorable progressions, and ten patients experienced monosomy 7 and MDS/AML as unfavorable progressions. The 5-year accumulative incidence of favorable and unfavorable progression were (2.2±2.2)% and (4.8±3.3)%, respectively. Until the last follow-up, 100% (5/5) of patients with favorable progressions and 50% (5/10) of patients with unfavorable progressions survived. WBC > 3.5×109/L, CD3+T cell percentage > 80%, dosage of antithymocyte globulin > 3.0 mg/ (kg·d) and no response to IST were related to unfavorable progressions by univariate analysis. Cox multivariate analysis revealed that an increased CD3+T cell percentage (> 80%) and no response to IST were independent risk factors for unfavorable progressions. Conclusions The children with SAA/VSAA who have an increased CD3+T cell percentage at diagnosis or have no response to IST are in high risks of unfavorable progressions.
Objective To study the epidemiological characteristics of respiratory adenovirus (ADV) infections in children from the Suzhou area, China. Methods The clinical data of ADV-positive children out of 35 529 children with respiratory tract infections who were hospitalized in the Children's Hospital of Soochow University between January 2006 and December 2015 were retrospectively studied. Results Of the 35 529 children with respiratory tract infections, 440 (1.24%) were ADV-positive. There was no significant difference in the rate of ADV infections between boys and girls (1.18% vs 1.34%). The ADV infection rates of children at the age of < 1 year old, 1-3 years old, 3-7 years old and 7-14 years old were 0.39% (71/18 002), 1.12% (103/9 191), 3.14% (201/6 398), and 3.35% (65/1 938) respectively and the rate increased with age (P < 0.01). The ADV infection rates in spring[1.85% (60/8 658)] and summer[2.20% (189/8 606)] were significantly higher than in autumn[0.30% (27/8 952)] and winter[0.69% (64/9 313)] (P < 0.01). Conclusions The ADV infection rate is increased with age in the children from the Suzhou area, but it is not associated with gender. ADV infections are more common in spring and summer.
Objective To investigate the association of gene polymorphisms of Toll-like receptor 3 (TLR3)-1377C/T and expression of TLR3 with the susceptibility to enterovirus 71 (EV71) encephalitis in children. Methods A total of 187 children with EV71 infection (59 children in the encephalitis group and 128 in the non-encephalitis group) and 232 children who underwent physical examination were enrolled in the case-control study. Polymerase chain reaction-restriction fragment length polymorphism was used to detect the TLR3-1377C/T gene polymorphisms. ELISA was used to measure the serum level of TLR3. Results There were no significant differences in the genotype and allele frequencies of TLR3-1377C/T between the non-encephalitis group and the encephalitis group. Compared with the control group, the encephalitis group and the non-encephalitis group had significant increases in the serum level of TLR3 (P < 0.05), and the non-encephalitis group had the highest level (P < 0.05). The encephalitis group had a significantly higher EV71 viral load than the non-encephalitis group (P < 0.01). The children aged < 1 year or ≥ 1 year in the encephalitis group and the non-encephalitis group had significant increases in the serum level of TLR3 compared with their counterparts in the control group (P < 0.05), and the children aged < 1 year or ≥ 1 year in the non-encephalitis group had a significantly higher serum level of TLR3 than those in the encephalitis group (P < 0.05). In the encephalitis group, the children aged ≥ 1 year had a significantly higher TLR3 concentration than those aged < 1 year (P < 0.05), and there were no significant differences in the TLR3 concentration between the children aged ≥ 1 year and < 1 year in the non-encephalitis group and the control group. In the encephalitis group, the proportion of children aged < 1 year was significantly higher than those aged ≥ 1 year (P < 0.05). Conclusions The TLR3-1377C/T gene polymorphisms are not significantly associated with the development of EV71 encephalitis. Low expression of TLR3 might weaken the inhibitory effect on virus replication and promote the development of EV71 encephalitis. The deficiency in the expression of TLR3 in serum after EV71 infection might be an important factor for the development of encephalitis in infants.
Objective To study the clinical effect and mechanism of action of esmolol in the treatment of severe hand, foot, and mouth disease (HFMD). Methods A prospective randomized controlled trial was performed. A total of 102 children with severe HFMD were enrolled in the study and were randomly divided into conventional treatment and esmolol treatment groups (n=51 each). The children in the conventional treatment group were given conventional treatment according to the guidelines for the diagnosis and treatment of HFMD. Those in the esmolol treatment group were given esmolol in addition to the conventional treatment. The heart rate (HR), systolic blood pressure (SBP), and respiratory rate (RR) were continuously monitored for all children. Blood samples were collected from all children before treatment and 1, 3, and 5 days after treatment to measure the levels of norepinephrine (NE), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and nuclear factor-kappa B (NF-κB) p65 in mononuclear cells. Serum levels of myocardial enzymes and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured before treatment and after 5 days of treatment. Results There were no significant differences in HR, SBP, RR, NE, TNF-α, IL-6, NF-κB p65, serum myocardial enzymes, and NT-proBNP before treatment between the conventional treatment and esmolol treatment groups. Both groups had significant reductions in these parameters at each time point (P < 0.05). Compared with the conventional treatment group, the esmolol treatment group had significant improvements in the above parameters after 1 and 3 days of treatment (P < 0.05). After 5 days of treatment, the esmolol treatment group had significant improvements in serum levels of myocardial enzymes and NT-proBNP compared with the conventional treatment group (P < 0.05). Conclusions Early application of esmolol can effectively stabilize the vital signs of the children with severe HFMD. Its mechanism of action may be related to reducing serum catecholamine concentration, alleviating myocardial damage, improving cardiac function, and reducing inflammatory response.
Objective To study the association of the risk factors during maternal pregnancy and the neonatal period with childhood bronchial asthma. Methods A total of 306 children with asthma (asthma group) and 250 healthy children (control group) were enrolled. Their clinical data during the neonatal period and the maternal data during pregnancy were retrospectively studied. Results The univariate analysis showed that there were significant differences in the rates of maternal use of antibiotics during pregnancy, use of antibiotics and probiotics during the neonatal period, preterm birth, cesarean section, low birth weight, and breast feeding (> 6 months) between the asthma and control groups (P < 0.05). The multivariate logistic regression analysis showed that use of antibiotics during pregnancy (OR=3.908, 95%CI: 1.277-11.962), use of antibiotics during neonatal period (OR=24.154, 95%CI: 7.864-74.183), preterm birth (OR=8.535, 95%CI: 2.733-26.652), and cesarean section (OR=4.588, 95%CI: 2.887-7.291) were independent risk factors for childhood asthma. The use of probiotics during the neonatal period (OR=0.014, 95%CI: 0.004-0.046) and breast feeding (> 6 months) (OR=0.161, 95%CI: 0.103-0.253) were protective factors for childhood asthma. Conclusions The early prevention of childhood asthma can be improved by reducing the use of antibiotics during pregnancy, reducing cesarean section, avoiding abuse of antibiotics during the neonatal period, trying breast feeding and taking probiotics in early stage.
Objective To explore the high-risk factors and analyze the clinical characteristics of massive pulmonary hemorrhage (MPH) in infants with extremely low birth weight (ELBW). Methods Two hundred and eleven ELBW infants were included in this study. Thirty-five ELBW infants who were diagnosed with MPH were labelled as the MPH group, and 176 ELBW infants without pulmonary hemorrhage were labelled as the control group. The differences in clinical characteristics, mortality rate, and incidence of complications between the two groups were analysed. The high-risk factors for MPH were identified by multiple logistic regression analysis. Results The MPH group had significantly lower gestational age, birth weight, and 5-minute Apgar score than the control group (P < 0.05). The MPH group had significantly higher rates of neonatal respiratory distress syndrome, patent ductus arteriosus (PDA), early-onset sepsis (EOS), intracranial hemorrhage, pulmonary surfactant utilization, and death compared with the control group (P < 0.01). The multiple logistic regression analysis showed that 5-minute Apgar score was a protective factor for MPH (OR=0.666, P < 0.05), and that PDA and EOS were risk factors for MPH (OR=3.717, 3.276 respectively; P < 0.01). In the infants who were discharged normally, the MPH group had a longer duration of auxiliary ventilation and a higher incidence rate of ventilator-associated pneumonia (VAP) compared with the control group (P < 0.05). Conclusions A higher 5-minute Apgar score is associated a decreased risk for MPH, and the prensence of PDA or EOS is associated an increased risk for MPH in ELBW infants. ELBW infants with MPH have a prolonged mechanical ventilation, a higher mortality, and higher incidence rates of VAP and intracranial hemorrhage compared with those without pulmonary hemorrhage.
Objective To investigate the characteristics of DUOXA2 gene mutation and the genotype-phenotype relationship in children with congenital hypothyroidism (CH) in Guangzhou, China. Methods A total of 20 CH patients with suspected thyroid dyshormonogenesis who had no DUOX2 gene mutation were enrolled. These patients who were born between 2011 and 2012 were screened and diagnosed with CH in the Guangzhou Newborn Screening Center. PCR and direct sequencing were used to analyze DUOXA2 gene mutation. Results Among the 20 patients, 2 had p.Y246X/p.Y246X homozygous mutation; 4 had monoallelic heterozygous mutation, among whom 2 carried the known pathogenic mutation c.413-414insA, 1 carried p.Y246X, and 1 carried a novel mutation, p.G79R. Reevaluation was performed at the age of 2-3 years, and the results showed that the two patients with p.Y246X/p.Y246X homozygous mutation were manifested as transient and mild permanent CH, respectively. Among the four patients with monoallelic heterozygous mutation, the one who carried p.Y246X mutation was manifested as typical permanent CH, and the other three were manifested as transient CH. Conclusions DUOXA2 gene mutation is a common molecular pathogenic basis for CH children with suspected thyroid dyshormonogenesis in Guangzhou, and most of them are manifested as transient CH. There is no association between DUOXA2 genotypes and phenotypes. The novel mutation p.G79R is probably a pathogenic mutation.
Objective To investigate the status of dietary nutrition in kindergartens of Chongqing, China. Methods A total of 295 kindergartens (47 first-class ones, 88 second-class ones, and 160 third-class ones) from the 11 districts or counties of Chongqing by stratified cluster random sampling were investigated. The dietary nutrition in each kindergarten was evaluated by weighing. The dietary qualification rates were compared between the three classes of kindergartens. Results The qualification rates of energy, proteins, most vitamins, minerals, and quality proteins supply were over 60% in all three classes of kindergartens, while the qualification rates of vitamin A, ascorbic acid, calcium, and zinc supply were less than 60%. The energy supply rates at breakfast, lunch, supper and snack met the standards in less than 40% in all kindergartens. There were significant differences in the qualification rates of some nutrient parameters between different classes of kindergartens, highest in the first-class kindergartens. Conclusions The dietary nutrition is good in the first-, second-, and third-class kindergartens of Chongqing, but there is still nutrient imbalance. It is necessary to strengthen the dietary guidance in kindergartens, especially second-, and third-class kindergartens.
Objective Aromatic L-amino acid decarboxylase (AADC) deficiency is a rare autosomal recessive hereditary disease and is a congenital metabolic disorder of neurotransmitter biosynthesis. It is mainly manifested as hypotonia, oculogyric crisis, autonomic dysfunction, and developmental delay. This article reports a boy manifested as delayed motor development, hypotonia, and oculogyric crisis. Gene screening for metabolic disorders revealed new compound heterozygous mutations, c.1063dupA (p.I355fs) and c.250A > C (p.S84R), in the exon of DDC gene. The boy had a significant increase in 3-O-methyldopa as measured by dried blood spot. Therefore, he was diagnosed with AADC deficiency. After treatment with the dopamine receptor agonist pramipexole dihydrochloride, the catechol-O-methyltransferase inhibitor entacapone, and vitamin B6, the boy showed mild improvements in hypotonia, blepharoptosis, and oculogyric crisis. Clinical physicians should enhance their ability for identifying AADC deficiency, so as to facilitate early diagnosis and treatment of this disorder. Genetic counseling for birth health and prenatal diagnosis should be performed for parents in need.
The study reports a girl with pyridoxine-dependent epilepsy. The girl was admitted at the age of 2 years because of intermittent convulsions for 1.5 years and psychomotor retardation. She had a history of "hypoxia" in the neonatal period. At the age of 5 months recurrent epileptic seizures occurred. The child was resistant to antiepileptic drugs, and had many more seizures when she got cold or fever. She also had a lot of convulsive status epilepticus. No discharges were found during several video-EEG monitorings. Cerebral MRI examinations showed normal results. So Dravet syndrome was clinically suspected. ALDH7N1 gene mutation analysis revealed two heterozygote mutations, and pyridoxine-dependent epilepsy was thus confirmed. Seizures were generally controlled after pyridoxine supplementation.
Objective A two-year-old girl was admitted due to repeated yellowing of the skin and sclera for 2 years and had no other specific symptoms or signs. The use of phenobarbital could relieve the symptoms of jaundice. Multiple examinations showed increased indirect bilirubin levels, and the results of aminotransferases and liver imaging were normal. There was no evidence of hemolysis. The analysis of UGT1A1 gene in her family found that this child had double homozygous mutation of c.211G > A (G71R) and c.1456T > G (Y486D), which had been reported as the pathogenic mutation for Gilbert syndrome. Her parents carried double heterozygous mutation of G71R and Y486D and had no symptom of jaundice. The child was diagnosed as having Gilbert syndrome. It is concluded that as for patients with unconjugated hyperbilirubinemia which cannot be explained by liver damage and hemolysis, their family history should be investigated in detail and gene analysis should be performed as early as possible, in order to identify congenital bilirubin metabolic disorders.
Objective To investigate the protective effect of histone acetylation against hypoxic-ischemic cortical injury in neonatal rats. Methods A total of 90 neonatal rats aged 3 days were divided into three groups: sham-operation, cortical injury model, and sodium butyrate (a histone deacetylase inhibitor) treatment. The rats in the model and the sodium butyrate treatment groups were intraperitoneally injected with lipopolysaccharide (0.05 mg/kg), and then right common carotid artery ligation was performed 2 hours later and the rats were put in a hypoxic chamber (oxygen concentration 6.5%) for 90 minutes. The rats in the sham-operation group were intraperitoneally injected with normal saline and the right common carotid artery was only separated and exposed without ligation or hypoxic treatment. The rats in the sodium butyrate treatment group were intraperitoneally injected with sodium butyrate (300 mg/kg) immediately after establishment of the cortical injury model once a day for 7 days. Those in the sham-operation and the model groups were injected with the same volume of normal saline. At 7 days after establishment of the model, Western blot was used to measure the protein expression of histone H3 (HH3), acetylated histone H3 (AH3), B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (BAX), cleaved caspase-3 (CC3), and brain-derived neurotrophic factor (BDNF). Immunofluorescence assay was used to measure the expression of 5-bromo-2'-deoxyuridine (BrdU) as the cortex cell proliferation index. Results The sodium butyrate treatment group had a significantly lower HH3/AH3 ratio than the model group (P < 0.05), which suggested that the sodium butyrate treatment group had increased acetylation of HH3. Compared with the model group, the sodium butyrate treatment group had a significant increase in Bcl-2/Bax ratio, a significant reduction in CC3 expression, and a significant increase in BDNF expression (P < 0.05). The sodium butyrate treatment group had a significant increase in the number of BrdU-positive cells in the cortex compared with the model group (P < 0.05), and BrdU was mainly expressed in the neurons. Conclusions Increased histone acetylation may protect neonatal rats against cortical injury by reducing apoptosis and promoting regeneration of neurons. The mechanism may be associated with increased expression of BDNF.
Objective To investigate the protective effect of heat shock protein 70 (HSP70) against hypoxic pulmonary hypertension (HPH) in neonatal rats. Methods A total of 128 neonatal rats were randomly divided into blank control group, HPH model group, empty virus group, and HSP70 group, with 32 rats in each group. Before the establishment of an HPH model, the rats in the blank control group and HPH model group were given caudal vein injection of 5 μL sterile saline, those in the empty virus group were given caudal vein injection of 5 μL Ad-GFP (1 010 PFU/mL), and those in the HSP70 group were given caudal vein injection of 5 μL Ad-HSP70 (1 010 PFU/mL). HPH model was prepared in the HPH model, empty virus, and HSP70 groups after transfection. At 3, 7, 10, and 14 days after model establishment, a multi-channel physiological recorder was used to record mean pulmonary arterial pressure (mPAP), optical and electron microscopes were used to observe the structure and remodeling parameters of pulmonary vessels, and Western blot was used to measure the protein expression of HSP70, hypoxia-inducible factor-1α (HIF-1α), endothelin-1 (ET-1), and inducible nitric oxide synthase (iNOS) in lung tissues. Results At 3, 7, 10, and 14 days after model establishment, the HPH model group and the empty virus group had a significantly higher mPAP than the blank control group (P < 0.05). On days 7 and 10 of hypoxia, the blank control group and the HSP70 group had significantly lower MA% and MT% than the HPH model group and the empty virus group (P < 0.01); on day 14 of hypoxia, the HPH model group, empty virus group, and HSP70 group had similar MA% and MT% (P > 0.05), but had significantly higher MA% and MT% than the blank control group (P < 0.01). On days 3, 7 and 10 of hypoxia, the HSP70 group had significantly higher protein expression of HSP70 than the HPH model group, empty virus group, and blank control group (P < 0.01); the HSP70 group had significantly lower expression of HIF-1α, ET-1, and iNOS than the HPH model group and the empty virus group (P < 0.05) and similar expression of HIF-1α, ET-1, and iNOS as the blank control group (P > 0.05). Conclusions In neonatal rats with HPH, HSP70 transfection can increase the expression of HSP70 in lung tissues, downregulate the expression of HIF-1α, ET-1, and iNOS, alleviate pulmonary vascular remodeling, and reduce pulmonary artery pressure; therefore, it may become a new strategy for the treatment of HPH in neonates.
Objective To investigate the changes in the mRNA and protein expression of high-mobility group box 1 (HMGB1), Toll-like receptor 4 (TLR4), and nuclear factor-kappa B (NF-κB) in lung tissues of asthmatic mice and the interventional effect of vitamin D. Methods A total of 48 BALB/c mice were randomly divided into control group, asthma group, and 1,25-(OH)2D3 intervention group, with 16 mice in each group. An animal model of asthma was established, and lung tissue samples were taken in each group at weeks 1 and 2 of ovalbumin challenging. Conventional hematoxylin-eosin staining was used to measure airway wall thickness. Immunohistochemical staining was used to observe the expression of HMGB1, TLR4, and NF-κB in lung tissues. Quantitative real-time PCR and Western blot were used to investigate the changes in the mRNA and protein expression of HMGB1, TLR4, and NF-κB. Results At weeks 1 and 2 of ovalbumin challenging, compared with the control group, the asthma group had a significant increase in airway wall thickness and the intervention group had a significant reduction compared with the asthma group (P < 0.05). The asthma group had significantly higher mRNA expression of HMGB1, TLR4, and NF-κB in lung tissues than the control group, and the intervention group had significantly lower mRNA expression of TLR4 and NF-κB than the asthma group (P < 0.05). At week 1 of ovalbumin challenging, there was no significant difference in the mRNA expression of HMGB1 between the intervention group and the asthma group (P > 0.05). At week 2, the intervention group had a significant reduction in the mRNA expression of HMGB1 compared with the asthma group (P < 0.05). At weeks 1 and 2 of ovalbumin challenging, the asthma group had significantly higher protein expression of HMGB1, TLR4, and NF-κB in lung tissues than the control group, and the intervention group had significantly lower expression than the asthma group (P < 0.05). Airway wall thickness was positively correlated with the mRNA expression of HMGB1, TLR4, and NF-κB in lung tissues (r=0.804, 0.895, and 0.834; P < 0.05). Conclusions The HMGB1/TLR4/NF-κB signaling pathway plays an important role in the pathogenesis of asthma, and an appropriate amount of 1,25-(OH)2D3 has a regulatory effect on this pathway and may prevent the progression of asthma. Therefore, 1,25-(OH)2D3 is expected to become a new choice for the treatment of asthma.
Objective To study the expression and significance of the mammalian target of rapamycin (mTOR)/eukaryote initiating factor 4E binding protein 1 (4EBP1)/hypoxia inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway in asthmatic mice. Methods Forty SPF level 6-8 week-old female Balb/C mice were randomly divided into control, asthma, budesonide and mTOR inhibitor (rapamycin) intervention groups (n=10 each). The asthmatic mouse model was prepared via OVA induction and challenge test. The intervention groups were administered with rapamycin at the dosage of 3 mg/kg by an intraperitoneal injection or budesonide suspension at the dosage of l mg by aerosol inhalation respectively 30 minutes before the OVA challenge. The control and asthma groups were treated with normal saline instead. The concentrations of HIF-1α and VEGF in bronchoalveolar lavage fluid (BALF) were examined using ELISA 24 hours after the last challenge. The pathological changes of lung tissue were observed by hematoxylin-eosin (HE) staining. The p-mTOR and p-4EBP1 from the lung tissues were detected by immunohistochemistry and Western blot. Pearson analysis was used to study the correlation between p-mTOR, p-4EBP1, HIF-1α, and VEGF expression. Results Compared with the control group, inflammatory cell infiltration and secretions in the trachea increased in the asthma group. The levels of HIF-1α and VEGF in BALF and p-mTOR and p-4EBP1 expression in lung tissues also increased (P < 0.01). Compared with the asthma group, inflammatory cell infiltration and secretions in the trachea were reduced in the two intervention groups, and the levels of HIF-1α and VEGF in BALF and p-mTOR and p-4EBP1 expression in lung tissues were also reduced (P < 0.01). There were no significant differences in the above changes between the two intervention groups and control group (P > 0.05). In the asthma group, there was a pairwise positive correlation between lung p-mTOR and p-4EBP1 expression and HIF-1α and VEGF levels in BALF (P < 0.05). However, there were no correlations in the above indexes in the intervention groups and control group. Conclusions p-mTOR, p-4EBP1, HIF-1α and VEGF together are involved in the pathogenesis of asthma. Rapamycin treatment can block this signaling pathway, suggesting that this pathway can be used as a novel target for asthma treatment.
Objective To investigate the host-defense role of short palate, lung, and nasal epithelium clone 1 (SPLUNC1) in Streptococcus pneumoniae (SP) infection and the effect of resveratrol (Res) on SPLUNC1 expression, and to provide new thoughts for the treatment of diseases caused by SP infection. Methods According to the multiplicity of infection (MOI), BEAS-2B cells with SP infection were divided into control group, MOI20 SP group, and MOI50 SP group. According to the different concentrations of Res, the BEAS-2B cells with MOI20 SP infection pretreated by Res were divided into 12.5Res+SP group, 25Res+SP group, and 50Res+SP group (the final concentrations of Res were 12.5, 25, and 50 μmol/L, respectively). Cell Counting Kit-8 was used to measure cell activity and determine the optimal concentration and action time of SP and Res. In the formal experiment, the cells were divided into control group, Res group, SP group, and Res+SP group. Real-time PCR and ELISA were used to measure the mRNA and protein expression of SPLUNC1. Results Over the time of SP infection, cell activity tended to decrease. Compared with the control group and the MOI20 SP group, the MOI50 SP group had a reduction in cell activity. Compared with the MOI20 SP group, the 25Res+SP group had increased cell activity and the 50Res+SP group had reduced cell activity (P < 0.05). MOI20 SP bacterial suspension and 25 μmol/L Res were used for the formal experiment. Over the time of SP infection, the mRNA expression of SPLUNC1 in BEAS-2B cells firstly increased and then decreased in the SP group and the Res+SP group (P < 0.05). Compared with the SP group, the Res+SP group had significant increases in the mRNA and protein expression of SPLUNC1 at all time points (P < 0.05). Compared with the control group, the Res group had no significant changes in the mRNA and protein expression of SPLUNC1 (P > 0.05). Conclusions SP infection can induce SPLUNC1 expression and the host-defense role of SPLUNC1. Res can upregulate SPLUNC1 expression during the development of infection and enhance cell protection in a concentration- and time-dependent manner.
With the development of treatment, the survival rate of premature infants has significantly increased, especially extremely premature infants and very low birth weight infants. This has led to an increase in incidence of bronchopulmonary dysplasia (BPD) year by year. BPD has been one of the most common respiratory system diseases in premature infants, especially the small premature infants. Arrested alveolar development is an important cause of BPD. Therefore, the mechanism of arrested alveolar development and the intervention measures for promoting alveolar development are the focuses of research on BPD. Selecting the appropriate animal model of BPD is the key to obtaining meaningful results in the basic research on BPD. Based on above, several common methods for establishing an animal model of BPD and the corresponding changes in pathophysiology are summarized and evaluated in order to provide a reference for selecting the appropriate animal model in studies on the pathogenesis, pathophysiology, and prevention and control strategies of BPD.
The time phase of epileptic seizures has attracted more and more attention. Epileptic seizures have their own circadian rhythm. The same type of epilepsy has different seizure frequencies in different time periods and states (such as sleeping/awakening state and natural day/night cycle). The circadian rhythm of epileptic seizures has complex molecular and endocrine mechanisms, and currently there are several hypotheses. Clarification of the circadian rhythm of epileptic seizures and prevention and administration according to such circadian rhythm can effectively control seizures and reduce the adverse effects of drugs. The research on the circadian rhythm of epileptic seizures provides a new idea for the treatment of epilepsy.
