Clinical Outcomes and Medical Burdens of Neonatal Arrhythmias in Children's Hospitals in China: A Protocol for Multi-Center Retrospective Cohort Study.

Neonatal arrhythmias are significant contributors to infant mortality. Timely diagnosis and treatment are essential for neonates with non-benign arrhythmias to avoid severe complications, and ongoing treatment and follow-up are sometimes needed. The main objective of this study will be to understand the incidence and demographic characteristics of arrhythmias in hospitalized neonates in China and the related factors of outcomes. A secondary objective will be to establish the first follow-up system for neonatal arrhythmias in China. The medical burdens of neonatal arrhythmias in China will also be investigated. The data from the Futang Research Center of Pediatric Development (FRCPD) database between January 2016 and December 2021 were obtained. Newborns admitted to member hospitals with a discharge diagnosis of "neonatal arrhythmia" (ICD-10 code P29.151) or "arrhythmia" (ICD-10 code I49.904) were included. The medical record information was collected and classified into two groups: heart failure and non-heart failure. The differences between the two groups and independent risk factors for neonatal arrhythmias complicated with heart failure were analyzed. In addition, a follow-up study of patients discharged from Beijing Children's Hospital was conducted to evaluate their outcomes at the age of 3 years old. Factors influencing hospitalization costs were analyzed using rank-sum tests and multiple linear regression. It is anticipated that the study findings will provide new and comprehensive data on the health needs of neonatal arrhythmias in China. The study will establish the first follow-up system for neonatal arrhythmias in China. This study will help reduce the burden of patients and their families as well as the society.

Effects of HMGB1/RAGE/cathespin B inhibitors on alleviating hippocampal injury by regulating microglial pyroptosis and caspase activation in neonatal hypoxic-ischemic brain damage.

Microglia play a crucial role in regulating neuroinflammation in the pathogenesis of neonatal hypoxic-ischemic brain damage (HIBD). Pyroptosis, an inflammatory form of programmed cell death, has been implicated in HIBD; however, its underlying mechanism remains unclear. We previously demonstrated that high-mobility group box 1 protein (HMGB1) mediates neuroinflammation and microglial damage in HIBD. In this study, we aimed to investigate the association between HMGB1 and microglial pyroptosis and elucidate the mechanism involved in rats with HIBD (both sexes were included) and in BV2 microglia subjected to oxygen-glucose deprivation. Our results showed that HMGB1 inhibition by glycyrrhizin (20 mg/kg) reduced the expression of microglial pyroptosis-related proteins, including caspase-1, the N-terminus fragment of gasdermin D (N-GSDMD), and pyroptosis-related inflammatory factors, such as interleukin (IL) -1ß and IL-18. Moreover, HMGB1 inhibition resulted in reduced neuronal damage in the hippocampus 72 h after HIBD and ultimately improved neurobehavior during adulthood, as evidenced by reduced escape latency and path length, as well as increased time and distance spent in the target quadrant during the Morris water maze test. These results revealed that HIBD-induced pyroptosis is mediated by HMGB1/receptor for advanced glycation end products (RAGE) signaling (inhibition by FPS-ZM1, 1 mg/kg) and the activation of cathespin B (cat B). Notably, cat B inhibition by CA074-Me (5 mg/kg) also reduced hippocampal neuronal damage by suppressing microglial pyroptosis, thereby ameliorating learning and memory impairments caused by HIBD. Lastly, we demonstrated that microglial pyroptosis may contribute to neuronal damage through the HMGB1/RAGE/cat B signaling pathway in vitro. In conclusion, these results suggest that HMGB1/RAGE/cat B inhibitors can alleviate hippocampal injury by regulating microglial pyroptosis and caspase activation in HIBD, thereby reducing the release of proinflammatory mediators that destroy hippocampal neurons and induce spatial memory impairments.

Immunological assessment of a patient with Omenn syndrome resulting from compound heterozygous mutations in the RAG1 gene.

The recombination activating gene 1 (RAG1) is essential for V(D)J recombination during T- and B-cell development. In this study, we presented a case study of a 41-day-old female infant who exhibited symptoms of generalized erythroderma, lymphadenopathy, hepatosplenomegaly, and recurrent infections including suppurative meningitis and septicemia. The patient showed a T+B-NK+ immunophenotype. We observed an impaired thymic output, as indicated by reduced levels of naive T cells and sjTRECs, coupled with a restricted TCR repertoire. Additionally, T-cell CFSE proliferation was impaired, indicating a suboptimal T-cell response. Notably, our data further revealed that T cells were in an activated state. Genetic analysis revealed a previously reported compound heterozygous mutation (c. 1186C > T, p. R396C; c. 1210C > T, p. R404W) in the RAG1 gene. Structural analysis of RAG1 suggested that the R396C mutation might lead to the loss of hydrogen bonds with neighboring amino acids. These findings contribute to our understanding of RAG1 deficiency and may have implications for the development of novel therapies for patients with this condition.

A fatal case of neonatal viral sepsis caused by human parainfluenza virus type 3.

BACKGROUND: Sepsis is a systemic inflammatory response syndrome caused by severe infection in children, but cases of sepsis associated with human parainfluenza virus (HPIV) have been rarely reported in newborns. CASE PRESENTATION: We report a case of HPIV-3 positive full-term newborn admitted to the Neonatal Intensive Care Unit of Beijing Children's Hospital due to hematuria, gloomy spirit, inactivity and loss of appetite for 6 h. He had septic shock when he arrived the Accident & Emergency Department requiring immediate intubation and mechanical ventilation. Intravenous antibiotics were started. He had completely negative response to all anti-shock treatments including fluid resuscitation and vasopressor supports, and died 14 h later. Viral nucleic acid detection and metagenomic next-generation sequencing (mNGS) analyses of nasopharyngeal aspirate and blood specimens verified an HPIV-3 infection, with negative bacterial culture results. The HPIV-3 strain detected in this patient was subtyped as HPIV C3a, and two unreported amino acid mutations were found in the HN protein region. CONCLUSION: The patient had a severe infection associated with HPIV-3, which was the cause of sepsis and septic shock. This study showed the diagnostic value of mNGS in etiological diagnosis, especially in severe neonatal case.

[A cross-sectional study of enterovirus nucleic acid test with throat swabs for term late neonates during coronavirus disease 2019]. / æ–°åž‹å† çŠ¶ç— æ¯’æ„ŸæŸ“æœŸé—´è¶³æœˆçš„æ™šæœŸæ–°ç”Ÿå„¿å’½æ‹­å­è‚ é“ç— æ¯’æ ¸é ¸æ£€æµ‹æ¨ªæ–­é¢ç ”ç©¶.

OBJECTIVES: To investigate the positive rate of enterovirus (EV) nucleic acid in throat swabs of term late neonates hospitalized during the coronavirus disease 2019 (COVID-19) epidemic and the clinical characteristics of the neonates. METHODS: A single-center cross-sectional study was performed on 611 term late infants who were hospitalized in the neonatal center from October 2020 to September 2021. Throat swabs were collected on admission for coxsackie A16 virus/EV71/EV universal nucleic acid testing. According to the results of EV nucleic acid test, the infants were divided into a positive EV nucleic acid group (8 infants) and a negative EV nucleic acid group (603 infants). Clinical features were compared between the two groups. RESULTS: Among the 611 neonates, 8 tested positive for EV nucleic acid, with a positive rate of 13.1‰, among whom 7 were admitted from May to October. There was a significant difference in the proportion of infants contacting family members with respiratory infection symptoms before disease onset between the positive and negative EV nucleic acid groups (75.0% vs 10.9%, P<0.001). There were no significant differences between the two groups in demographic data, clinical symptoms, and laboratory test results (P>0.05). CONCLUSIONS: There is a certain proportion of term late infants testing positive for EV nucleic acid in throat swabs during the COVID-19 epidemic, but the proportion is low. The clinical manifestations and laboratory test results of these infants are non-specific. Transmission among family members might be an important cause of neonatal EV infection.

Comparison of four neonatal transport scoring methods in the prediction of mortality risk in full-term, out-born infants: a single-center retrospective cohort study.

Neonatal transport scoring systems can assess severity before and after transport, improve transport efficiency, and predict the occurrence of critical illness. The aim of this study was to compare four neonatal transport scoring methods to predict mortality risk and clinical utility within the first week after transportation. This was a single-center retrospective cohort study. All patients were full-term, out-born neonates. Each patient was assessed by the Transport Risk Index of Physiologic Stability (TRIPS), Mortality Index for Neonatal Transportation (MINT), Transport-Related Mortality Score (TREMS), and Neonatal Critical Illness Score (NCIS) scoring methods. Receiver operating characteristic (ROC) curves and decision curve analysis (DCA) for each method were compared for their utility in predicting mortality risk within the 1st week after admission. In total, 368 full-term infants were included (368/770, 47.8% of all transported infants). Within the 1st week after admission, five infants (1.36%, 5/368) died while receiving advanced life support and full treatment, and 24 infants (6.52%, 24/368) died soon after they were discharged against medical advice. The areas under the curve (AUCs) for the MINT, TRIPS, TREMS, and NCIS for the prediction of mortality were 0.822, 0.827, 0.643, and 0.731, respectively (all p < 0.05). However, the clinical net benefits for the MINT and TRIPS were far superior than those for the NCIS and TREMS. CONCLUSION: It was concluded that the TRIPS and MINT might be more suitable for the prediction of mortality in full-term, out-born neonates in the neonatal intensive care unit (NICU) within the 1st week after transportation. WHAT IS KNOWN: • Neonatal transport scores can assess not only the mortality risk during transportation but also the mortality risk of critically ill newborns after admission to the NICU. • The effectiveness of neonatal transport scores in predicting mortality risk is different. WHAT IS NEW: • Our data indicate that the diagnostic efficacy of the MINT, TRIPS, and NCIS in the prediction of full-term infant mortality was high. • The TRIPS and MINT scores had better clinical utility and could be used to predict mortality within the 1st week after transportation in full-term out-born neonates.

High-mobility Group Box 1 Contributes to Hypoxic-Ischemic Brain Damage by Facilitating Imbalance of Microglial Polarization through RAGE-PI3K/Akt Pathway in Neonatal Rats.

High mobility group box 1 (HMGB1) is a damage-associated molecular pattern integral for hypoxic-ischemic brain damage (HIBD) in neonatal rats since it regulates the phenotypic polarization of microglia, as depicted in our previous studies. Since this mechanism is not clear, this study establishes an oxygen-glucose deprivation (OGD) model of highly aggressively proliferating immortalized microglia while modulating the expression of HMGB1 by plasmid transfection. The M1/M2 microglial phenotype and receptor for advanced glycation end products-phosphoinositide 3-kinase/Akt (RAGE-PI3K/Akt) activation were evaluated, showing that HMGB1 promoted the polarization of microglia to the M1 phenotype under OGD conditions. Meanwhile, RAGE, which is the main receptor of HMGB1, was activated, and phosphorylation of PI3K/Akt was upregulated. However, knockdown or inhibition of HMGB1 can weaken the activation of RAGE and phosphorylation of PI3K/Akt. The inhibition of HMGB1 or RAGE-PI3K/Akt attenuated microglial polarization to the M1 phenotype and promoted M2 microglial polarization instead, reducing the release of pro-inflammatory factors. In the neonatal HIBD rat model, the RAGE-PI3K/Akt pathway was activated seven days after hypoxic-ischemic (HI) exposure, and the activation was partly inhibited after pretreatment with the HMGB1 inhibitor. Concurrently, inhibition of the HMGB1-RAGE-PI3K/Akt pathway alleviated neuronal damage in the hippocampus. These findings verified that HMGB1 could lead to an imbalance in M1/M2 microglial polarization through activation of the RAGE-PI3K/Akt signaling pathway under OGD conditions. Obstructing this pathway may attenuate the imbalanced polarization of microglia, enabling its utilization as a therapeutic strategy against brain injury in HIBD.

Family Integrated Care for Preterm Infants in China: A Cluster Randomized Controlled Trial.

OBJECTIVE: To explore whether family integrated care (FICare) is feasible and improves the outcomes of preterm infants in China. STUDY DESIGN: This was a multicenter prospective cluster-randomized controlled trial comparing FICare and standard care. The primary outcome was length of stay (LOS). Secondary outcomes were nosocomial infections, duration of supplemental oxygen, breastfeeding, and weight gain. Outcomes were compared using univariate and multivariable analyses adjusted for potential confounders and clustering. RESULTS: We enrolled 601 preterm infants from 11 neonatal intensive care units (FICare, n = 298; control, n = 303). The unadjusted LOS was 30.81 vs 30.26 days (mean ratio, 1.02; 95% CI, 0.85-1.22; P = .85). After adjustment, outcomes in the FICare group were improved compared with the control group, including LOS (28.26 vs 35.04 days; mean ratio, 0.81; 95% CI, 0.72-0.91), total medical expenditures (mean ratio, 0.69; 95% CI, 0.53-0.90), weight gain velocity (15.73 vs 10.30 g/day; mean difference, 5.43; 95% CI, 3.65-7.21), duration of supplemental oxygen (13.11 vs 21.42 days; mean difference, 0.71; 95% CI, 0.50-1.00), nosocomial infection rates (4.13 vs 5.84/1000 hospital days; mean ratio, 0.67; 95% CI, 0.47-0.96), antibiotic exposure (38.63 vs 57.32/100 hospital days; mean ratio, 0.67; 95% CI, 0.47-0.96), breastfeeding rates (87.25% vs 55.78%; OR, 5.42; 95% CI, 3.25-9.05), and rehospitalization rates (3.65% vs 7.48%; OR, 0.47; 95% CI, 0.28-0.77). At follow-up to 18 months, breastfeeding rates and weight were significantly (P < .05) higher over time in the FICare group. CONCLUSIONS: FICare was feasible in Chinese neonatal intensive care units and was associated with reduced hospital LOS, medical expenditures, and rates of adverse outcomes.

[Research advances in the role of ferroptosis in neonatal hypoxic-ischemic brain damage].

Neonatal hypoxic-ischemic brain damage (HIBD) remains an important cause of neonatal death and disability in infants and young children, but it has a complex mechanism and lacks specific treatment methods. As a new type of programmed cell death, ferroptosis has gradually attracted more and more attention as a new therapeutic target. This article reviews the research advances in abnormal iron metabolism, glutamate antiporter dysfunction, and abnormal lipid peroxide regulation which are closely associated with ferroptosis and HIBD.

[Effect of muscle relaxants on the prognosis of neonates with congenital esophageal atresia-tracheoesophageal fistula after surgery].

OBJECTIVE: To summarize the experience in the application of muscle relaxants in the perioperative period in neonates with congenital esophageal atresia-tracheoesophageal fistula (EA-TEF). METHODS: A retrospective analysis was performed on the medical data of 58 previously untreated neonates with EA-TEF who were treated in the Neonatal Center of Beijing Children's Hospital, Capital Medical University from 2017 to 2019. The incidence rate of anastomotic leak was compared between the neonates receiving muscle relaxants for different durations after surgery (≤ 5 days and > 5 days). The correlation between the duration of postoperative use of muscle relaxants and the duration of mechanical ventilation was evaluated. RESULTS: Among the 58 neonates with EA-TEF, 44 underwent surgery, among whom 35 with type III EA-TEF underwent thoracoscopic surgery. Among these 35 neonates, 30 (86%) received muscle relaxants after surgery, with a median duration of 4.75 days, and 6 (18%) experienced anastomotic leak. There was no significant difference in the incidence rate of anastomosis leak between the ≤ 5 days and > 5 days groups (P > 0.05). The duration of postoperative invasive mechanical ventilation was positively correlated with the duration of the use of muscle relaxants (rs=0.548, P < 0.05). CONCLUSIONS: Prolonged use of muscle relaxants after surgery cannot significantly reduce the incidence of anastomotic leak, but can prolong the duration of invasive mechanical ventilation in neonates with EA-TEF. Therefore, prolonged use of muscle relaxants is not recommended after surgery.

High mobility group box 1 protein (HMGB1) as biomarker in hypoxia-induced persistent pulmonary hypertension of the newborn: a clinical and in vivo pilot study.

Background: Inflammation plays an important role in neonatal hypoxia-induced organ damage. Newborns with perinatal asphyxia often develop persistent pulmonary hypertension of the newborn (PPHN). The objective of this study was to explore changes in the pro-inflammatory high mobility group box-l (HMGB1) protein during hypoxia-induced PPHN clinically and in vivo. Methods: Serum samples were collected from full-term newborns at PPHN onset and remission. As controls, blood serum samples were collected from the umbilical arteries of healthy full-term newborns born in our hospital during the same period. Clinical data for neonates were collected and serum levels of HMGB1, IL-6, and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA). An animal study compared a PPHN Sprague-Dawley rat model to healthy newborn control rats. Histopathology was used to evaluate changes in the pulmonary artery wall. ELISA and western blot analyses were used to examine HMGB1 levels in the serum and lungs. Results: Serum HMGB1 levels were significantly elevated in newborns with PPHN, compared to those in healthy controls, and decreased dramatically after PPHN resolution. HMGB1 changes were positively correlated with serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels. Histopathological analysis demonstrated that the median wall thickness of pulmonary arterioles accounting for the percentage of pulmonary arteriole diameter (MT%) was not significantly different between PPHN and control groups 3 d after PPHN, although thickness of the small pulmonary arterial wall middle membrane and stenosis of the small pulmonary arteries. ELISA and western blot analyses showed similar trends between serum HMGB1 levels and HMGB1 protein expression in the lungs. Serum and lung HMGB1 levels were significantly elevated soon after PPHN onset, peaked after 24 h, and then decreased after 3 d, although they remained elevated compared to those in the control group. Conclusions: This study indicates that HMGB1 is related to hypoxia-induced PPHN pathogenesis. HMGB1 changes might thus be used as an early indicator to diagnose hypoxia-induced PPHN and evaluate its improvement. We also provide important evidence for the involvement of inflammation in the progression of hypoxia-induced PPHN.

Clinical and genetic study of 20 patients from China with Cornelia de Lange syndrome.

BACKGROUND: Cornelia de Lange syndrome (CdLS) is a rare congenital syndrome with no racial difference. The objective of this study is to report the clinical characteristics and genetic study of 20 CdLS cases from China. METHODS: This is an observational study. Suspected patients were referred for further confirmation, clinical treatment, and genetic testing under voluntary condition. Demographic data and family history, data of clinical manifestations including facial dysmorphism and developmental delay of each patient were collected. Chromosomal analysis and NIPBL/SMC1A/SMC3 gene mutational analysis were carried out by PCR, reverse transcription PCR direct sequencing in the probands, and SNP array to detect the genome-wide copy number variations. RESULTS: Twenty CdLS cases from China were included in this study. Facial dysmorphisms, feeding difficulties, and developmental delay were the major clinical manifestations. Seven patients underwent gene mutation tests. Both the SMC1A and SMC3 gene mutation tests were negative in all. A heterozygous mutation in exon 20 of the NIPBL gene in proband 2, and a heterozygous mutation in intron 38 of the NIPBL gene in proband 3 were found in 1 patient, and RT-PCR revealed a splicing mutation in exon 38, generating both normal transcript and an aberrant alternatively spliced transcript with exon 38 deletion. CONCLUSIONS: Clinical manifestations of CdLS patients from China are similar to those in the other countries. Heterozygous mutations of NIPBL gene were found.

[Risk factors for neonatal pulmonary hemorrhage in the neonatal intensive care unit of a municipal hospital].

OBJECTIVE: To investigate the risk factors for neonatal pulmonary hemorrhage (NPH) in the neonatal intensive care unit (NICU) of a municipal hospital, and to provide a basis for the early identification and treatment of NPH. METHODS: A total of 112 neonates who were admitted to the NICU of Shaoyang Central Hospital of Hunan Province and diagnosed with NPH were enrolled as the case group. A nested case-control method was used to select, as a control group (n=224), the neonates who underwent the treatment with an assisted mechanical ventilator and did not experience pulmonary hemorrhage. Univariate analysis and unconditional logistic regression analysis were used to identify the high risk factors for NPH. RESULTS: The univariate analysis showed that compared with the control group, the case group had significantly higher incidence rates of gestational diabetes and cholestasis in mothers, cesarean delivery, gestational age <34 weeks, 5-minute Apgar score ≤5, birth weight <2 500 g, heart failure and disseminated intravascular coagulation (DIC) before the development of NPH, partial pressure of oxygen/fraction of inspired oxygen (oxygenation index, OI) ≤100, and a reduction in mean platelet volume. The multivariate logistic regression analysis showed that DIC, heart failure, and OI ≤100 were independent risk factors for NPH (OR=33.975, 3.975, 1.818 respectively; P<0.05). CONCLUSIONS: Heart failure, OI ≤100, and DIC are risk factors for the development of NPH in the NICU of the municipal hospital.

5-aminolevulinic acid combined with sodium ferrous citrate ameliorates H2O2-induced cardiomyocyte hypertrophy via activation of the MAPK/Nrf2/HO-1 pathway.

Hydrogen peroxide (H2O2) causes cell damage via oxidative stress. Heme oxygenase-1 (HO-1) is an antioxidant enzyme that can protect cardiomyocytes against oxidative stress. In this study, we investigated whether the heme precursor 5-aminolevulinic acid (5-ALA) with sodium ferrous citrate (SFC) could protect cardiomyocytes from H2O2-induced hypertrophy via modulation of HO-1 expression. HL-1 cells pretreated with/without 5-ALA and SFC were exposed to H2O2 to induce a cardiomyocyte hypertrophy model. Hypertrophy was evaluated by planar morphometry, (3)H-leucine incorporation, and RT-PCR analysis of hypertrophy-related gene expressions. Reactive oxygen species (ROS) production was assessed by 5/6-chloromethyl-2',7'-ichlorodihydrofluorescein diacetate acetylester. HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf2) protein expressions were analyzed by Western blot. In our experiments, HL-1 cells were transfected with Nrf2 siRNA or treated with a signal pathway inhibitor. We found several results. 1) ROS production, cell surface area, protein synthesis, and expressions of hypertrophic marker genes, including atrial natriuretic peptide, brain natriuretic peptide, atrial natriuretic factor, and ß-myosin heavy chain, were decreased in HL-1 cells pretreated with 5-ALA and SFC. 2) 5-ALA and SFC increased HO-1 expression in a dose- and time-dependent manner, associated with upregulation of Nrf2. Notably, Nrf2 siRNA dramatically reduced HO-1 expression in HL-1 cells. 3) ERK1/2, p38, and SAPK/JNK signaling pathways were activated and modulate 5-ALA- and SFC-enhanced HO-1 expression. SB203580 (p38 kinase), PD98059 (ERK), or SP600125 (JNK) inhibitors significantly reduced this effect. In conclusion, our data suggest that 5-ALA and SFC protect HL-1 cells from H2O2-induced cardiac hypertrophy via activation of the MAPK/Nrf2/HO-1 signaling pathway.

Outcomes for symmetrical and asymmetrical small for gestational age preterm infants in Canadian tertiary NICUs.

OBJECTIVE: This study aimed to compare the outcomes for symmetrical (sSGA) versus asymmetrical (aSGA) small for gestational age (SGA) < 32 weeks preterm infants. STUDY DESIGN: A total of 12,179 eligible infants admitted to the Canadian tertiary neonatal intensive care units (NICUs) over a 7-year-period in the Canadian Neonatal Network database were subcategorized as aSGA (n = 536), sSGA (n = 732), or appropriate for GA (AGA, n = 10,911). Baseline demographics, mortality, and major morbidities were compared using multivariable analysis to calculate adjusted odds ratios (AOR) and 95% confidence interval (CI). RESULTS: sSGA had higher GA (p < 0.01) and more antenatal tobacco exposure (p = 0.03). Although both the SGA groups had worse outcomes than AGA controls, aSGA versus sSGA comparison revealed lower odds (AOR [CI]) for mortality and chronic lung disease (CLD) for aSGA in the entire cohort (0.45 [0.27, 0.75] and 0.61 [0.44, 0.84], respectively) as well as for infants < 28 weeks GA (0.50 [0.27, 0.92] and 0.47 [0.29, 0.77], respectively). aSGA infants < 28 weeks GA had comparable outcomes to AGA except higher odds for CLD (1.61 [1.13, 2.27]). sSGA infants needed longer hospital stay and had higher use of oxygen and continuous positive airway pressure than aSGA. CONCLUSION: Among SGA infants < 32 weeks GA, significant intragroup differences exist in the neonatal outcomes and hospital resource utilization depending upon the presence or absence of relative "head sparing."

[Environment and congenital urinary malformations].

The development of the kidneys and other organs of the urinary tract follows the natural rule of gene-environment-lifestyle interaction. Both intrinsic and extrinsic factors may be associated with the etiology of various kinds of urinary malformations, but the environmental factor is an extrinsic factor. Related literatures were reviewed in this paper, which focuses on the association of congenital urinary malformations with possible environmental factors. It is concluded that urinary malformation is associated with low birth weight, maternal disease, placental insufficiency, maternal drug exposure, and maternal exposure to environmental pesticides. Living environment and socioeconomic factors may also influence the incidence of urinary malformation.

[Effect of IGF-1 on long-term anxiety-like behavior in rats after hypoxic-ischemic brain damage].

OBJECTIVE: To observe the changes in anxiety-like behavior among rats in the recovery stage after hypoxic-ischemic brain damage (HIBD) during the perinatal period and to investigate the effect of insulin-like growth factor 1 (IGF-1) on the long-term anxiety-like behavior and its action mechanism among rats with HIBD. METHODS: Ninety neonatal rats (7 days old) were randomly and equally divided into normal control, HIBD, and HIBD+IGF-1 groups. A neonatal rat model of HIBD was established by Rice method in the HIBD and HIBD+IGF-1 groups. The rats in the HIBD+IGF-1 group were intraperitoneally injected with IGF-1 (0.2 mg/kg) immediately after HIBD, and the other two groups were intraperitoneally injected with an equal volume of normal saline. The anxiety-like behavior was evaluated by elevated plus-maze test on postnatal days 21 and 28. The expression of tyrosine hydroxylase (TH) in the substantia nigra was measured by immunohistochemistry on postnatal days 14, 21, and 28. RESULTS: On postnatal days 21 and 28, the open-arm time (OAT) and percentage of OAT for the HIBD and HIBD+IGF-1 groups were significantly lower than those for the normal control group (P<0.05), but there were no significant differences between the HIBD and HIBD+IGF-1 groups (P>0.05); the percentage of open arm entry showed no significant difference between the three groups (P>0.05). On postnatal day 14, there were no significant differences in percentage of TH immunostaining-positive area between the three groups (P>0.05). On postnatal days 21 and 28, the HIBD and HIBD+IGF-1 groups had significantly lower percentages of TH immunostaining-positive area than the normal control group (P<0.05), but there was no significant difference between the HIBD and HIBD+IGF-1 groups (P>0.05). CONCLUSIONS: HIBD in the perinatal period may cause the changes in anxiety-like behavior in adolescent rats, which may be related to decreased expression of TH in the substantia nigra. Neonatally given IGF-1 cannot improve the long-term anxiety-like behavior in rats after HIBD, and it does not affect TH expression in the substantia nigra. IGF-1 may not regulate the changes in long-term anxiety-like behavior in adolescent rats.

[Impact of dopamine receptor modulation on reduced anxiety-like behavior in neonatal rats after hypoxic-ischemic brain damage].

OBJECTIVE: To observe the long-term changes in anxiety-like behavior and tyrosine hydroxylase (TH) expression in the substantia nigra (SN) after hypoxic-ischemic brain damage (HIBD) in a neonatal rat model and to further explore the relationship between dopamine (DA) level and long-term anxiety-like behavior using the DA receptor (DAR) antagonist. METHODS: Seven-day-old (P7) neonatal Sprague-Dawley (SD) rats were randomized into normal control, sham-operated, HIBD and HIBD+DAR antagonist groups. HIBD model was prepared by ligating the right common carotid artery and 8% hypoxia exposure. The rats in the sham-operated group were sham-operated and were not subjected to right common carotid artery ligation and hypoxia exposure. The DAR antagonist was injected intraperitoneally before and after inducing HIBD. The same amount of normal saline was given to the other three groups as a control. Anxiety-like behavior was evaluated by elevated plus maze test, and TH expression in the SN was measured by immunohistochemistry on P14, P21, and P28. RESULTS: On P21 and P28, the time spent in the open arms and the percentage of open arms entries in the HIBD group were significantly increased compared with those in the normal control, sham-operated and HIBD+DAR antagonist groups (P<0.05); in addition, the HIBD+DAR antagonist group showed a significantly longer time spent in the open arms than the normal control group (P<0.05). On P14, P21, and P28, TH expression in the HIBD and HIBD+DAR antagonist groups was significantly lower than that in the normal control and sham-operated groups, and TH level in the HIBD group was significantly lower than that in the HIBD+DAR antagonist group (P<0.05). CONCLUSIONS: DAR antagonist allows the restoration of anxiety-like behavior and alleviates the damage to dopaminergic neurons in SD rats after HIBD.

External anatomical landmarks for urethral catheter positioning in male newborns: A prospective observational study.

BACKGROUND: Improper urethral catheterization may lead to complications such as urethral injury, catheter entanglement and urinary tract infection. Most of the related literature has focused on aseptic surgical technique, but there are no guidelines on the optimal insertion length for neonatal urinary catheterization. OBJECTIVE: To explore the external anatomical landmarks for urethral catheter positioning in male newborns. METHODS: This research is based on an observational study in Beijing Children's Hospital, China. Hospitalized male neonates who required Foley balloon catheters were prospectively enrolled in this study. The actual insertion length of the urethral catheter for male neonates and the anticipated insertion length based on anatomical landmarks were measured and compared. RESULTS: A total of 67 male neonates were enrolled. The mean body length was 50.66 ±â€¯2.93 cm, and the mean body weight was 3.33 ±â€¯0.70 kg. The mean actual insertion length of catheter was 8.77 ±â€¯0.94 cm, while the anticipated length was 10.89 ±â€¯0.95 cm. All the anticipated lengths exceeded the actual insertion length by 0.5-4.6 cm, which was deemed suitable for the procedure. CONCLUSIONS: Estimating the insertion length of urethral catheters based on external anatomical landmarks is clinically feasible. Selecting an anatomical landmark is a safe method for nurses or doctors to ensure the correct positioning of a urethral catheter. TWEETABLE ABSTRACT: The data of 67 male neonates shows that external anatomical landmarks for urethral catheter positioning in male newborns are possible.