To develop the theoretical basis for neuronal antioxidant therapy, the study employed in vitro model of oxidative stress of cortical neurons in order to examine the repair mechanisms triggered in the damaged neurons by PGC-1α/NRF1/NRF2/TFAM signal pathway. The functions of proteins in this signal pathway were examined using online STRING software, which analyzed the network of protein–protein interactions (PPI). The hub genes in PGC-1α/NRF1/NRF2/TFAM signal pathway were analyzed with Cytoscape software. In vitro, the cortical neurons were treated with 25, 50, 75, or 100 μM H2O2. The inhibition rate of neurons with various concentrations of H2O2 was assessed by CCK8, thereupon the neuronal cells were exposed to H2O2 in optimal concentration of 75 μM for 24, 48, or 72 h. The time-dependent changes in the expression of PGC-1α, NRF1, NRF2, ATP-5α, and TFAM in neurons damaged by H2O2-induced oxidative stress were analyzed by Western blotting. The ROS level in damaged neurons, the value of mitochondrial membrane potential (MMP), permeability of mitochondrial permeability transition pores (MPTP), and apoptosis of neurons were analyzed by flow cytometry. Analysis of PPI network showed that transcriptional coactivator PGC-1α is the key regulator of energy metabolism in the cortical neurons, while NRF1 and NRF2 play important roles in mitochondrial biogenesis and in the response to oxidative stress. TFAM is required for basal transcription of mitochondrial DNA, and it is a hub gene in PGC-1α/NRF1/NRF2 pathway. Western blotting and flow cytometry showed that during the development of oxidative stress, PGC-1α activated the expression of NRF1, NRF2, and TFAM and simultaneously prevents MPP loss and MPTP opening. At this, NRF1/NRF2 diminished ROS level and reduced apoptosis, while TFAM enhanced expression of ATP-5α. Therefore, PGC-1α exerts the antioxidant and antiapoptotic effects in cortical neurons exposed to oxidative stress via activation of NRF1/NRF2/TFAM signal pathway.

Gestational diabetes mellitus (GDM) significantly impacts maternal and neonatal health, yet its influence on the neonatal intestinal microbiota remains poorly characterized. This study investigated the effects of maternal GDM on offspring microbiota by analyzing meconium samples from newborns of GDM-affected mothers (n = 16) and healthy controls (n = 16). Microbiome analysis revealed distinct composition alterations in the intestinal microbiota of GDM-exposed neonates. Significant differences in microbial abundance were observed between groups: at the phylum level, the GDM group exhibited a significant increase in Bacteroidetes but significant reductions in Actinobacteria and Proteobacteria. At the genus level, opportunistic pathogens including Bacteroides and Escherichia-Shigella were significantly enriched in the GDM group. These findings demonstrate that maternal GDM perturbs the initial colonization of the neonatal intestinal microbiota. Interventions targeting maternal glycemic control during gestation may mitigate offspring microbiota dysbiosis and its potential clinical implications.

This study aims to analyze the pathways and the placental brain axis genes of gestational diabetes mellitus (GDM) affecting offspring neurodevelopment. Differentially expressed genes (DEGs) were identified through transcriptome sequencing of placental tissues. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed on DEGs. A protein-protein interaction (PPI) network was constructed and annotated using the STRING online software. The expression of neurodevelopment-related genes was analyzed by qPCR. Hubgenes were analyzed using Cytoscape 3.7.1 software. The correlation between Hubgenes and placental brain axis genes was analyzed through literatures alignment. The pathways of GDM affecting offspring neural development were predicted using the KEGG database. The placental transcriptome revealed that there were 404 DEGs between GDM and Normal groups. Among these DEGs, 125 were upregulated and 279 were downregulated. GO analysis indicated that DEGs were mainly involved in intracellular calcium activated chloride channel activity, anion channel activity, G protein-coupled peptide receptors, etc. Additionally, KEGG analysis revealed that DEGs were predominantly involved in neuroactive ligand receptor interaction pathways. STRING online software analysis revealed that the DLGAP1, NXNL2, SCG2, SLC18A2, LYNX1, GRM1, DLGAP1, BIRC7 genes were associated with neurodevelopment. PCR validation of these 8 genes was consistent with transcriptome results (P<0.05). Literatures alignment showed that DLGAP1, GRM1 and SLC18A2 are placental brain axis genes that influence offspring neurodevelopment. The placental brain axis genes DLGAP1, GRM1, SLC18A2 have been found to influence GDM offspring neurodevelopment through the regulation of the Gq/PLC/PKC pathway.

ObjectiveThe aim of this study was to analyse the clinical characteristics and related risk factors of Pediatric Sepsis, construct a column-line diagram model to predict the likelihood of Pediatric Sepsis, and validate the model to facilitate primary care paediatricians to quickly and quantitatively assess the risk of Pediatric Sepsis.MethodsThis single-center retrospective study included children hospitalized for infections at Gansu Provincial Maternity and Child-Care Hospital from January 2018 to June 2024. Data on 39 variables covering baseline characteristics, vital signs, and laboratory indicators were collected. The samples were randomized into training and validation groups in a 7:3 ratio. Least Absolute Shrinkage and Selection Operator (LASSO) regression was used for initial data screening and dimensionality reduction, followed by Logistic regression to identify independent risk factors for sepsis. Predictive modeling was then performed. The performance of the column-line plots was internally validated using ROC curves, calibration curves, and decision curve analysis (DCA).ResultsThe development dataset included 834 patients with severe infections, of whom 212 (25.4%) developed sepsis. Seven predictors were identified as independent risk factors: respiratory rate, temperature, immature granulocyte percentage, platelets, procalcitonin, fibrinogen, and lactic acid. A predictive column-line diagram was created using these predictors. Internal validation showed that the column-line diagrams had good discriminatory ability, calibration, and clinical applicability.ConclusionA column-line diagram was successfully developed to predict the incidence of sepsis in children using seven commonly used clinical and laboratory indicators. The model demonstrated good performance and clinical validity through internal validation.

The Western China Birth Cohort (WCBC) is a large-scale, multi-centered, prospective birth cohort study designed to address critical gaps in maternal and child health research in Western China, a region with diverse altitudes, ethnic groups, and unique environmental exposures. WCBC had enrolled 15,093 pregnant women across eight clinical centers in five provinces (Qinghai, Gansu, Guizhou, Chongqing, and Sichuan), spanning from the high-altitude Qinghai-Tibet Plateau to lowland regions. WCBC has collected over 220,000 medical records, 80,000 questionnaires, and 12 different types of biological samples, including peripheral blood, cord blood, dried blood spots, placenta, umbilical cord, decidua, saliva, feces, throat and nasal swabs, vaginal swabs, and breast milk. By integrating advanced multi-omics measurement, including genomics, proteomics, exosome profiling, metabolomics, spatial transcriptomics, single-cell RNA sequencing, culturome, metagenomics, and virosome analysis, WCBC provides a valuable platform to explore gene-environment interplay, early-life determinants of health, and long-term disease risks in diverse populations in Western China.

To investigate the predictive value of the hepatic steatosis index (HSI) in the first trimester for gestational diabetes mellitus (GDM), and explore the association between HSI and the risk of developing GDM. A total of 2795 pregnant women were included in this cohort study. Maternal baseline data and basic laboratory data, including alanine aminotransferase, aspartate aminotransferase, fasting plasma glucose (FPG), and others were collected during 8-13 weeks of gestation. The 75-g oral glucose tolerance test was conducted at 24-28 weeks of gestation, and according to the criteria of American Diabetes Association, the participant would be diagnosed as GDM if one of the thresholds was met: fasting blood glucose ≥ 5.1 mmol/L, 1-h blood glucose ≥ 10.0 mmol/L, or 2-h blood glucose ≥ 8.5 mmol/L. The relationship between first-trimester HSI and GDM outcomes was analyzed by using Logistic Regression, Restricted Cubic Spline and Subgroup Analyses. The nomogram model including HSI, FPG and other factors was established, and diagnostic efficacies of the nomogram model, FPG, HSI, and white blood cell count (WBC) were analysed by using the receiver operating characteristic curve. 212 pregnant women were diagnosed with GDM among 2,795.After adjusting for the covariates, compared to women in the lowest quartile (Q1), those in the highest quartile group (Q4) of first-trimester HSI had a 2.328-fold risk of developing GDM (95% CI 1.262-4.295, p < 0.05). There was a positive nonlinear dose-response relationship between the first-trimester HSI and GDM (p for overall < 0.001; p for nonlinear = 0.010). Subgroup analyses found that HSI didn't interact with covariates such as age, gravidity, parity, etc. (p > 0.05). The diagnose efficacies of the nomogram model, HSI, FPG and WBC were 0.737 (95% CI 0.702-0.773), 0.696 (95% CI 0.658-0.734), 0.631 (95% CI 0.593-0.670), and 0.569 (95% CI 0.526-0.611), respectively. First-trimester HSI, FPG, WBC, and age may jointly predict the occurrence of GDM.

Intractable pneumothorax secondary to bronchopulmonary fistula is a rare complication in neonates. We present the first report of a newborn with spontaneous pneumothorax and bronchopleural fistula treated with extracorporeal membrane oxygenation (ECMO). Positive pressure mechanical ventilation resulted in persistent air leakage from the bronchopleural fistula. When ECMO was initiated, a “total lung rest” ventilation strategy was used to facilitate the healing of bronchopleural fistula and the absorption of the pneumothorax. ECMO is an effective supportive therapy for neonate pneumothorax and bronchopulmonary fistula when conventional ventilation management fails.

Background Congenital heart disease (CHDs) is the major cause of mortality from birth defects, affecting up to 1% of live births worldwide. However, the relationship between aluminum (Al) and iron (Fe) levels and the risk of CHDs has yielded inconsistent results. Methods We conducted a pair-matched case–control study that included 97 CHDs and 194 non-CHDs to investigate the association and interaction between Al/Fe exposure and the risk of CHDs in a birth cohort study in Lanzhou, China. Results Higher concentrations of cord blood Al were associated with a greater risk of total CHDs (aOR = 2.826, 95% CI [1.009–7.266]) and isolated CHDs (aOR = 10.713, 95% CI [1.017–112.851]) compared to the lowest Al level. Both in maternal blood and cord blood, a significant dose-effect was observed between Al level and total CHDs (Ptrend < 0.05), but a similar pattern was not observed for Fe. High Al in addition to high Fe appeared to elicit a stronger association with CHDs than both lowest tertile of Al and Fe level in umbilical cord blood, particularly for multiple CHDs, septal defects and patent ductus arteriosus. Conclusions Our study suggests that exposure to Al during pregnancy (≥2,408 μg/L) is significantly associated with an increased risk of CHDs in offspring, especially septal defects, and that high levels of Al and Fe are strongly correlated with fetal heart development. Further research is needed to understand the underlying mechanisms.

缺氧缺血性脑损伤严重危害新生儿生命健康，目前仍缺乏有效治疗手段。神经干细胞能够修复神经系统损伤，本文对神经干细胞的生物学特性、新生儿缺氧缺血性脑病的病理生理过程、神经干细胞治疗缺氧缺血性脑损伤的机制、移植方式、疗效及临床应用展开综述，为神经干细胞治疗新生儿缺氧缺血性脑病提供借鉴。

目的 比较子痫前期(PE)孕妇与健康孕妇孕早中期(孕11～20周)体成分差异,探讨体成分与PE发病的关系.方法 整群抽样选取2021年2月至2022年2月于甘肃省妇幼保健院围产医学中心门诊产检且在该院住院分娩的孕妇,将确诊为PE的孕妇作为病例组(n=200),以年龄为匹配条件,1:1匹配健康孕妇作为对照组(n=200),开展病例对照研究.收集孕妇一般状况及临床资料,回顾性调查孕早中期体成分检测结果[包括孕早中期体重指数(BMI0)、体脂率(PBF)、体脂重(FM)、体脂重指数(FMI)、去脂体重(FFM)、去脂体重指数(FFMI)、孕期增重(GWG)、分娩时体重指数(BMI1)等],采用logistic回归分析探讨孕早中期体成分与PE发病风险的关系.绘制受试者工作特征(ROC)曲线,并计算ROC曲线下面积(AUC),分析体成分指标预测PE的效能.结果 两组孕妇BMI0、PBF、FM、FMI、FFM、FFMI、GWG及BMI1分布均有明显差异(P＜0.05).多因素 logistic 回归分析显示,PBF≥38.4％[OR=5.104,95％CI(1.149～22.680)]、FMI≥9.67 kg/m2[OR=9.113,95％CI(1.875～44.290)]是PE发病的独立危险因素.绘制PBF、FMI单项指标预测PE的 ROC 曲线,PBF 的 AUC 及 95％CI 为 0.728(0.678～0.777),FMI 的 AUC 及 95％CI 为 0.729(0.680～0.779).结论 孕早中期体脂过重预示孕期PE的发病风险增加,应注意控制孕前及孕早中期体脂重以降低PE发病率.

目的:探讨综合护理干预基础上的菟丝子杜仲膏穴位贴敷辅助治疗复发性流产的临床效果.方法:将68例同种免疫型复发性流产患者随机分为观察组和对照组各34例.两组患者均给予主动免疫治疗,对照组给予常规护理干预,观察组在对照组基础上给予菟丝子杜仲膏穴位贴敷辅助治疗和综合护理干预.分析两组患者用药及治疗依从性、护理满意度、保胎疗效.结果:观察组用药及治疗依从性为88.24%(30/34),优于对照组的55.88%(19/34)(P＜0.05);观察组护理满意度为94.12%(32/34),优于对照组的70.59%(24/34)(P＜0.05);观察组保胎有效率为94.44%(32/34),高于对照组的73.53%(25/34)(P＜0.05).结论:应用菟丝子杜仲膏穴位贴敷辅助治疗,并实施综合护理有利于提高复发性流产患者用药及治疗依从性、护理满意度、临床效果.

This study aimed to assess cardiovascular risk factors in the offspring of preeclampsia (PE) pregnancies. PubMed, Web of Science, Ovid, and other foreign language databases, as well as SinoMed, China National Knowledge Infrastructure, Wanfang, and China Science and Technology Journal Databases, were searched. The case-control studies on cardiovascular risk factors in the offspring of PE pregnancies from 1 January 2010 to 31 December 2019 were collected. A random-effects model or a fixed-effects model was used, and RevMan 5.3 software was used for meta-analysis to determine the OR value and 95%CI of each cardiovascular risk factor. A total of 16 documents were included in this research, all of which were case-control studies, with a total of 4046 cases in the experimental group and 31,505 in the control group. The meta-analysis that was conducted demonstrated that SBP [MD = 1.51, 95%CI (1.15, 1.88)] and DBP [MD = 1.90, 95%CI (1.69, 2.10)] values in the PE pregnancy offspring group presented an elevation relative to the non-PE pregnancy offspring group. The total cholesterol value in the PE pregnancy offspring group presented an elevation relative to the non-PE pregnancy offspring group [MD = 0.11, 95%CI (0.08, 0.13)]. The low-density lipoprotein cholesterol value in the PE pregnancy offspring group was comparable to that in the non-PE pregnancy offspring group [MD = 0.01, 95%CI (-0.02, 0.05)]. The high-density lipoprotein cholesterol value in the PE pregnancy offspring group presented an elevation relative to the non-PE pregnancy offspring group [MD = 0.02, 95%CI (0.01, 0.03)]. The non-HDL cholesterol value in the PE pregnancy offspring group presented an elevation relative to the non-PE pregnancy offspring group [MD = 0.16, 95%CI (0.13, 0.19)]. The triglycerides [MD = -0.02, 95%CI (-0.03, -0.01)] and glucose [MD = -0.08, 95%CI (-0.09, -0.07)] values in the PE pregnancy offspring group presented a depletion relative to the non-PE pregnancy group. The insulin value in the PE pregnancy offspring group presented a depletion relative to the non-PE pregnancy offspring group [MD = -0.21, 95%CI (-0.32, -0.09)]. The BMI value in the PE pregnancy offspring group presented an elevation relative to the non-PE pregnancy offspring group [MD = 0.42, 95%CI (0.27, 0.57)]. In conclusion, dyslipidemia, elevated blood pressure, and increased BMI occur postpartum with PE, all of which are risk factors for cardiovascular diseases.

人体内和体表的微生物构成了微生物的群组,各菌群之间在某种程度上保持相对的平衡[1].人的肠道建立始于生命最初1 000 d[2],肠道健康始于子宫[3],而婴儿期称为"肠道微生物发展的最好窗口期",是建立肠道正常微生态的"关键时期".

目的 研究常量金属元素钙、镁、钾和钠在正常孕妇静脉血及胎儿脐血中的分布规律,评价各元素胎盘传输效能(PTE,某元素脐血浓度/母血浓度)及影响因素.方法 随机选取200对来源于兰州地区出生队列样本库的生物样本入组,检测分娩前母血和新生儿脐血中钙、镁、钾和钠元素浓度并进行相关性分析,分析各元素的PTE及其影响因素.结果 母全血与脐血血钙、镁、钠、钾元素中值浓度分别为9.93和9.59 mg/L、29.44和30.35 mg/L、441.92和429.51 mg/L、686.02和896.35 mg/L;钙元素和镁元素、钾元素和镁元素显著正相关;血钾元素PTE高(PTE＞1),而血钙、镁、钠元素母胎界面PTE无明显差异;胎膜早破对钾元素PTE会产生影响(P＜0.05),分娩方式、产时使用缩宫素和生理盐水对钠元素的PET也有影响(P＜0.05);而其余因素对血钙、镁、钠、钾元素PTE的影响均差异无统计学意义(P＞0.05).结论 产时个体间血钙、镁、钾和钠元素PTE离散度大,钾元素PTE高,谨防输注过量问题;胎膜早破、分娩方式及产时药物输注对PTE会造成影响.

目的 检测健康孕妇外周全血及其脐血中必需微量金属元素锌、硒、铜、钼、铬、钴和铁含量,分析各微量元素胎盘传输效能及影响因素.方法 研究样本来源于甘肃省妇幼保健院2012—2014年建立的兰州地区出生队列生物样本库,随机抽样选取健康产妇分娩前外周静脉全血和新生儿脐血深低温冻存生物样本,通过电感耦合等离子质谱法检测血锌、铁、铜、硒、钼、铬和钴元素水平,计算各元素的胎盘传输效能(PT E,指某元素脐血浓度/母血浓度),分析母血和脐血中各元素PT E及影响因素.结果 共计194对健康孕产妇母外周全血和脐血样本接受检测.母血的血锌、铜、铁浓度分别为(4809.27±2097.27)μg/L、(1063.45±404.13)μg/L、(317811.07±128063.82)μg/L,脐血的血锌、铜浓度分别为(1713.27±622.36)μg/L、(535.69±191.59)μg/L、(436418.33±141689.29)μg/L;母血的血硒、铬中值浓度分别为56.47μg/L、78.18μg/L,脐血的血硒、铬中值浓度分别为85.27μg/L、115.31μg/L.母血的血锌、铜浓度高于脐血(t值分别为80.30、66.64),母血血硒、铬的中值浓度均低于脐血(Z值分别为-5.44、-4.66),差异均有统计学意义(P<0.05).不同个体血中必需金属微量元素PTE差异大,血锌、铜PTE较低(PTE<1),而血铁、硒、铬元素PTE较高(PTE>1);仅发现胎膜早破与血硒PTE有关(Z=-3.12,P<0.05).结论 血铁、硒、铬元素PT E较高,要谨防摄入过量;孕妇一般状况、产前及产时因素对PT E未见明显影响.

BackgroundZinc is a trace element essential for normal fetal heart development, and excess zinc can be toxic. The relationship between maternal and fetal zinc levels and the development of congenital heart disease (CHD) in the offspring is unclear.ObjectiveTo study the effects of maternal and neonatal zinc exposure levels on the risk of developing CHD in the offspring.MethodsThe data and biological samples of the study subjects were derived from the birth cohort established by Gansu Provincial Maternity and Child Care Hospital in Lanzhou from 2010 to 2012. Questionnaire surveys were conducted at baseline in the first trimester and at follow-up visits in the second trimester, the third trimester, and 42 d after delivery. Maternal venous blood during the third trimester and neonatal umbilical venous blood at delivery were collected, and information on their birth outcomes was extracted from medical records. Ninety-seven children with CHD diagnosed by echocardiography at birth and confirmed at the follow-up after 42 d were selected as the case group, and 194 healthy full-term infants were selected as the control group, 1∶2 matched for maternal age and geographical location from the database. The zinc concentrations in whole blood of pregnant mothers and umbilical cord blood of fetuses in both groups were measured by inductively coupled plasma mass spectrometry. According to the quartiles P25 and P75 of zinc levels in the whole blood of pregnant mothers and neonatal cord blood in the control group, zinc exposure was divided into three groups: low, medium, and high. After adjusting for maternal vaginal bleeding in early pregnancy, pre-pregnancy folic acid and vitamin supplementation, birth weight, and umbilical cerclage confounders, a multiple conditional logistic regression model was applied to analyze the associations between maternal whole blood and fetal umbilical cord blood zinc levels and the risk of CHD in the offspring, and a further subgroup analysis was performed by disease classification.ResultsThe medians (P25, P75) of maternal whole blood zinc levels in the case group and the control group were 5.034 (3.456, 6.644) and 4.693 (3.411, 5.646) mg·L−1, respectively, with significant differences between the two groups (P=0.029). The medians (P25, P75) of neonatal cord blood zinc level was 2.153 (1.479, 2.405) mg·L−1 in the case group and 1.636 (1.304, 1.979) mg·L−1 in the control group, with significant differences between the two groups (P<0.001). The zinc levels of maternal whole blood and neonatal cord blood in the simple CHD group were significantly higher than those in the control group (P<0.05). The multiple conditional logistic regression model showed that compared with the maternal medium zinc exposure level group (3.41-5.65 mg·L−1), the risk of offspring CHD was 2.225 times of the high exposure level group (>5.65 mg·L−1) (OR=2.225, 95%CI: 1.017-4.868). Compared with the neonatal medium zinc exposure level group (1.30-1.98 mg·L−1), the neonatal high exposure level group (>1.98 mg·L−1) also had an increased risk of CHD (OR=4.132, 95%CI: 1.801-9.480). The subgroup analysis results showed that compared with corresponding medium exposure level groups, the risk of simple CHD in the offspring of the maternal high zinc exposure level group was increased (OR=4.081, 95%CI: 1.427-11.669), and the risks of simple CHD (OR=7.122, 95%CI: 2.126-23.854) and complex CHD (OR=5.165, 95%CI: 1.859-14.346) of neonates of the neonatal high zinc exposure level group were increased.ConclusionUnder the exposure levels of the study population, high concentrations of zinc exposure in pregnant mothers and neonates may be associated with the incidence of CHD.

Introduction and objectives: Omenn syndrome (OS) is a very rare type of severe combined immunodeficiencies manifested with erythroderma, eosinophilia, hepatosplenomegaly, lymphadenopathy, and elevated level of serum IgE. OS is inherited with an autosomal recessive mode of inheritance. Germline mutations in the human RAG1 gene cause OS. Materials and methods: In this study, we investigated a 2-month-old boy with cough, mild anaemia, pneumonia, immunodeficiency, repeated infection, feeding difficulties, hepatomegaly, growth retardation, and heart failure. Parents of the proband were phenotypically normal. Results: Karyotype analysis and chromosomal microarray analysis found no chromosomal struc-tural abnormalities (46, XY) and no pathogenic copy number variations (CNVs) in the proband. Whole-exome sequencing identified a novel homozygous single nucleotide deletion (c.2662delC) in exon 2 of the RAG1 gene in the proband. Sanger sequencing confirmed that both the proband parents were carrying this variant in a heterozygous state. This variant was not identified in two elder sisters and one elder brother of the proband and in the 100 ethnically matched normal healthy individuals. This novel homozygous deletion (c.2662delC) leads to the frameshift, which finally results in the formation of the truncated protein (p.Leu888Phefs*3) V(D)J recombination-activating protein 1 with 890 amino acids compared with the wildtype V(D)J recombination-activating protein 1 of 1043 amino acids. Hence, it is a loss-of-function variant. Conclusions: Our present study expands the mutational spectrum of the RAG1 gene associated with OS. We also strongly suggested the importance of whole-exome sequencing for the genetic screening of patients with OS.

Abstract Congenital heart disease (CHDs) is the leading cause of mortality from birth defects, affecting up to 1% of live births. However, there have been inconsistent results of the relationship between aluminum (Al) /iron (Fe) level and risk of CHDs. We performed a pair-matched case–control study and included 97 cases and 194 controls to investigate the association and interaction between Al/Fe exposure and the risk of CHDs in a birth cohort study conducted in Lanzhou, China. Compared to < 25th percentile of Al in CB, risk differences were significantly detected in > 75th percentile of Al in total CHDs (aOR = 2.826, 95% CI: 1.009–7.266) and isolated CHDs (aOR = 10.713, 95% CI: 1.017–112.851). Although a similar pattern was not detected in MB of Al and Fe in both MB and CB, a significant dose-effect was observed between the Al level and total CHDs in both MB and CB (Ptrend < 0.05). Compared to both lowest tertile of Al and Fe level in umbilical cord blood, the highest tertile was associated with an increased risk of CHDs, especially for multiple CHDs, septal defects and patent ductus arteriosus. Overall, our study suggests a significant association between pregnancy Al exposure (≥ 2.408 mg/L) and risk of CHDs, especially for septal defects, and high Al and Fe elicited a strong correlation on fetal heart development. Future studies are needed to elucidate the underlying mechanism.

目的 对比分析早产与正常产产妇的孕早、中、晚期血脂水平变化差异,探讨全孕程血脂变化与早产结局关联.方法 整群抽样选取2018年6月—2020年6月在甘肃省妇幼保健院产科住院的无基础代谢及妊娠合并症疾病史的早产单胎产妇作为病例组,以体质指数(BMI)作为匹配条件,按照1:2匹配正常分娩健康单胎孕妇作为正常对照组开展病例对照研究,收集分娩结局信息资料,回顾性调查并记录两组孕产妇孕早、中、晚期血脂指标,包括三酰甘油、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇及总胆固醇等,通过单因素及多因素分析孕期血脂水平变化对早产结局的影响.结果 研究共纳入268例早产病例及525例正常对照开展研究,多因素逻辑回归结果发现,居住于乡村(OR=2.651,95％CI:1.755～4.004)、孕晚期三酰甘油高水平(OR=0.023,95％CI:1.170～7.812)和孕晚期胆固醇低水平(OR=3.130,95％CI:1.410～6.946)是早产的危险因素;孕中期胆固醇高水平(OR=0.116,95％CI:0.031～0.436)是早产的保护性因素.结论 孕晚期三酰甘油和胆固醇高水平会增加早产发病风险,应加强孕期血脂水平监测,及时实施饮食、运动等干预手段降低血脂,预防早产发生,促进母婴安全.