Objective::To analyze fetal renal abnormality genetic features and the prenatal characteristics of the 17q12 microdeletion syndrome.Methods::This prospective cohort study examined prenatal ultrasound findings of renal abnormalities in pregnant women who underwent single nucleotide polymorphism (SNP) array or copy number variation sequencing (CNV-seq) testing on amniotic fluid or fetal tissue at Tianjin Central Obstetrics and Gynecology Hospital between January 2016 and August 2022. The study cohort comprised women with advanced maternal age, fetal ultrasound anomalies, high-risk non-invasive prenatal testing results, or suspected 17q12 microdeletion syndrome. Comprehensive clinical data, including maternal age, detailed ultrasound findings, and pregnancy outcomes, were systematically collected. SNP-array analysis was conducted using an Affymetrix CytoScan 750 K Array Chip to identify CNVs and loss of heterozygosity, while CNV-seq was performed on the Illumina HiSeq 2000 platform. Detected variants were classified according to the American College of Medical Genetics and Genomics guidelines. Statistical analyses were performed using SPSS version 27.0.Results::Abnormal renal development was identified in 141 patients, among whom 26 exhibited hyperechogenic kidneys (HCK). Of these, 12 cases were associated with 17q12 microdeletion syndrome, while the remaining 14 were linked to other chromosomal abnormalities. When excluding patients with HCK, those diagnosed with polycystic kidney disease demonstrated a higher prevalence of chromosomal abnormalities compared to those with multicystic dysplastic kidney and renal dysplasia. Although isolated conditions such as horseshoe kidney, hydronephrosis, ectopic kidney, and unilateral kidney typically presented with normal chromosomal findings, the incidence of chromosomal abnormalities increased when these conditions coexisted with other anomalies. A detailed analysis of the correlation between 17q12 microdeletion syndrome and HCK revealed that 12 out of the 14 patients diagnosed with 17q12 microdeletion syndrome exhibited HCK. Genetic testing confirmed the syndrome in seven patients, with five cases attributed to novel mutations and two cases resulting from inherited mutations.Conclusion::Fetal HCK was closely associated with the 17q12 microdeletion syndrome, and polycystic kidney disease showed a higher rate of chromosomal abnormalities. Chromosome test results were mostly normal in patients with other renal abnormalities, such as kidney dysplasia, horseshoe kidneys, hydronephrosis, kidney deficiency, and ectopic kidneys. Prenatal diagnosis is recommended, especially in cases of non-isolated fetal renal abnormalities. This study provides strong evidence supporting a link between fetal renal abnormalities and genetic syndromes.

Objective::To analyze fetal renal abnormality genetic features and the prenatal characteristics of the 17q12 microdeletion syndrome.Methods::This prospective cohort study examined prenatal ultrasound findings of renal abnormalities in pregnant women who underwent single nucleotide polymorphism (SNP) array or copy number variation sequencing (CNV-seq) testing on amniotic fluid or fetal tissue at Tianjin Central Obstetrics and Gynecology Hospital between January 2016 and August 2022. The study cohort comprised women with advanced maternal age, fetal ultrasound anomalies, high-risk non-invasive prenatal testing results, or suspected 17q12 microdeletion syndrome. Comprehensive clinical data, including maternal age, detailed ultrasound findings, and pregnancy outcomes, were systematically collected. SNP-array analysis was conducted using an Affymetrix CytoScan 750 K Array Chip to identify CNVs and loss of heterozygosity, while CNV-seq was performed on the Illumina HiSeq 2000 platform. Detected variants were classified according to the American College of Medical Genetics and Genomics guidelines. Statistical analyses were performed using SPSS version 27.0.Results::Abnormal renal development was identified in 141 patients, among whom 26 exhibited hyperechogenic kidneys (HCK). Of these, 12 cases were associated with 17q12 microdeletion syndrome, while the remaining 14 were linked to other chromosomal abnormalities. When excluding patients with HCK, those diagnosed with polycystic kidney disease demonstrated a higher prevalence of chromosomal abnormalities compared to those with multicystic dysplastic kidney and renal dysplasia. Although isolated conditions such as horseshoe kidney, hydronephrosis, ectopic kidney, and unilateral kidney typically presented with normal chromosomal findings, the incidence of chromosomal abnormalities increased when these conditions coexisted with other anomalies. A detailed analysis of the correlation between 17q12 microdeletion syndrome and HCK revealed that 12 out of the 14 patients diagnosed with 17q12 microdeletion syndrome exhibited HCK. Genetic testing confirmed the syndrome in seven patients, with five cases attributed to novel mutations and two cases resulting from inherited mutations.Conclusion::Fetal HCK was closely associated with the 17q12 microdeletion syndrome, and polycystic kidney disease showed a higher rate of chromosomal abnormalities. Chromosome test results were mostly normal in patients with other renal abnormalities, such as kidney dysplasia, horseshoe kidneys, hydronephrosis, kidney deficiency, and ectopic kidneys. Prenatal diagnosis is recommended, especially in cases of non-isolated fetal renal abnormalities. This study provides strong evidence supporting a link between fetal renal abnormalities and genetic syndromes.

In 2019, preterm births (PTB) accounted for approximately 0.66 million deaths globally. PTB is also associated with a significantly higher risk of mortality and long-term complications for newborns. Long-term studies associated several factors, including disruption of immune tolerance and inflammation, with PTB. However, the pathogenesis of PTB remains unclear. Gonadal steroid hormones are critical for pregnancy maintenance and regulation of immune and inflammatory responses. However, it is not clear how unbalanced gonadal steroid hormones, such as imbalanced estrogen/androgen or estrogen/progesterone contribute to PTB. In this review, we discuss how gonadal steroid hormones mediate dysfunction in immune tolerance and inflammatory responses, which are known to promote the occurrence of PTB, and provide insight into PTB prediction.

Steroid hormones, including progestagens, estrogens, androgens, corticosteroids, and their precursor cholesterol, perform essential functions in the successful establishment and maintenance of pregnancy and normal fetal development. As the core endocrine organ at the prenatal stage, the human placenta is involved in the biosynthesis, metabolism, and delivery of steroid hormones. Steroidogenic pathways are tightly regulated by placenta-intrinsic cytochrome P450 and hydroxysteroid dehydrogenase. However, the relationship between placental steroidogenic enzyme expression and adverse pregnancy outcomes is controversial. In this review, we summarize the possible upstream regulatory mechanisms of placental steroidogenic enzymes in physiologic and pathophysiologic states. We also describe the human placental barrier model and examine the potential of single-cell sequencing for evaluating the primary functions and cellular origin of steroidogenic enzymes. Finally, we examine the existing evidence for the association between placental steroidogenic enzyme dysregulation and adverse pregnancy outcomes.

In 2019, preterm births (PTB) accounted for approximately 0.66 million deaths globally. PTB is also associated with a significantly higher risk of mortality and long-term complications for newborns. Long-term studies associated several factors, including disruption of immune tolerance and inflammation, with PTB. However, the pathogenesis of PTB remains unclear. Gonadal steroid hormones are critical for pregnancy maintenance and regulation of immune and inflammatory responses. However, it is not clear how unbalanced gonadal steroid hormones, such as imbalanced estrogen/androgen or estrogen/progesterone contribute to PTB. In this review, we discuss how gonadal steroid hormones mediate dysfunction in immune tolerance and inflammatory responses, which are known to promote the occurrence of PTB, and provide insight into PTB prediction.

Steroid hormones, including progestagens, estrogens, androgens, corticosteroids, and their precursor cholesterol, perform essential functions in the successful establishment and maintenance of pregnancy and normal fetal development. As the core endocrine organ at the prenatal stage, the human placenta is involved in the biosynthesis, metabolism, and delivery of steroid hormones. Steroidogenic pathways are tightly regulated by placenta-intrinsic cytochrome P450 and hydroxysteroid dehydrogenase. However, the relationship between placental steroidogenic enzyme expression and adverse pregnancy outcomes is controversial. In this review, we summarize the possible upstream regulatory mechanisms of placental steroidogenic enzymes in physiologic and pathophysiologic states. We also describe the human placental barrier model and examine the potential of single-cell sequencing for evaluating the primary functions and cellular origin of steroidogenic enzymes. Finally, we examine the existing evidence for the association between placental steroidogenic enzyme dysregulation and adverse pregnancy outcomes.

Microplastics refer to plastic fibers, particles, or films with a particle size less than 5 mm, and microplastics pollution has become one of the major global environmental problems. Microplastics can be exposed to the human body through ingestion, inhalation and skin contact, affecting maternal and fetal health through mechanisms such as cytotoxicity and signal transduction, energy homeostasis and metabolic disorders, immune dysfunction, and as carriers of microorganisms or toxic chemicals. The purpose of this paper is to review the physical and chemical properties of microplastics, human exposure pathways, maternal-fetal effects, and its mechanisms.

Objective To investigate the therapeutic mechanism of Shengjiang Powder(SP)on acute lung injury.Methods Forty healthy SD male rats were divided into 3 groups randomly: normal group,model group,and SP group.After administration for 6 days,acute lung injury rat models were established by injecting lipopolysaccharide(LPS)into sublingual vein.Lung histological sections were prepared for the detection of NF-?B expression by immmunohistochemistry.The images of the lung histological sections were captured and the average gray values of nucleus of endothelial cells in lung micrangium were measured.Results Compared with the model group,SP could depress the expression of NF-?B in the nucleus of lung microvascular endothelial cells,and statistical difference existed between the two groups(P

[Objective] To investigate the influence of injection of substance P (SP) and its antagonist into locus ceruleus on electroacupuncture of Neiguan for acute myocardial ischemia (AMI). [Methods] Rabbit model of AMI was set up by ligating left ventricular branch of coronary artery. Forty-nine rabbits were allocated to five groups: Group A (the control group), Group B (electroacupuncture of Neiguan), Group C (injection of SP), Group D (electroacupuncture of Neiguan and injection of SP) and Group E (electroacupuncture of Neiguan and injection of SP antagonist) . Locus ceruleus was located by cerebral stereotaxic apparatus. Dynamic changes of ST segment of electrocardiogram and morphological feature of myocardium were observed. [ Results ] Injection of SP promoted the recovery of AMI and enhance the effect of electroacupuncture of Neiguan for AMI. However, the above effects were counteracted by the injection of SP antagonist. [Conclusion] SP plays an important role in reducing the damage of AMI on electroacupuncture of Neiguan and may serve as an important mediator for the connection of Neiguan and the heart.