Initiating PeriCBD to probe perinatal influences on neurodevelopment during 3-10 years in China.

Adverse perinatal factors can interfere with the normal development of the brain, potentially resulting in long-term effects on the comprehensive development of children. Presently, the understanding of cognitive and neurodevelopmental processes under conditions of adverse perinatal factors is substantially limited. There is a critical need for an open resource that integrates various perinatal factors with the development of the brain and mental health to facilitate a deeper understanding of these developmental trajectories. In this Data Descriptor, we introduce a multicenter database containing information on perinatal factors that can potentially influence children's brain-mind development, namely, periCBD, that combines neuroimaging and behavioural phenotypes with perinatal factors at county/region/central district hospitals. PeriCBD was designed to establish a platform for the investigation of individual differences in brain-mind development associated with perinatal factors among children aged 3-10 years. Ultimately, our goal is to help understand how different adverse perinatal factors specifically impact cognitive development and neurodevelopment. Herein, we provide a systematic overview of the data acquisition/cleaning/quality control/sharing, processes of periCBD.

SARS-CoV-2 Infection Increases High Risk Rate of Down Syndrome Screening Test by Reducing Alpha-Fetoprotein.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been a significant global health issue in recent years. Numerous studies indicate that COVID-19 during pregnancy is associated with an increased likelihood of pregnancy complications. Additionally, pregnancy itself is known to elevate the risk of severe SARS-CoV-2 infection. To explore the potential impact of SARS-CoV-2 infection on the probability of Down syndrome in fetuses, we conducted serological testing of Down syndrome markers in pregnant women who had contracted the virus. METHODS: Serological experiments were conducted utilizing a particle chemiluminescence test. The cohort of pregnant women was categorized into three groups: a control group with no infection, a group infected with SARS-CoV-2 Omicron within the first six weeks of gestation, and a group infected beyond the sixth week of gestation. RESULTS: In the group of individuals infected within 6 gestational weeks, the infection resulted in a decrease in alpha-fetoprotein (AFP) levels and a higher positive rate of Down syndrome screening tests (p ˂ 0.05). However, in this study, SARS-CoV-2 infection did not lead to an increase in the occurrence of Down syndrome in the fetus. The positive rate of women infected beyond 6 gestational weeks was slightly higher than the non-infected group (6.2% vs. 5.7%), but these differences were not statistically significant (p > 0.05). Within the group infected beyond 6 gestational weeks, there was, compared to the control group, a decrease in free beta human chorionic gonadotropin (ß-hCG) levels (p < 0.05). CONCLUSIONS: This study presents a novel investigation into the impact of SARS-CoV-2 infection on AFP and ß-hCG levels. It has been observed that pregnant women who contract SARS-CoV-2 may exhibit an increased likelihood of positive results in serum tests conducted for Down syndrome screening. However, it is important to note that the occurrence of Down syndrome in the developing fetus does not appear to be elevated. To validate these findings, additional research involving larger and diverse cohorts is necessary.

Clinical evaluation of high-intensity focused ultrasound ablation combined with mifepristone and levonorgestrel-releasing intrauterine system to treat symptomatic adenomyosis.

OBJECTIVE: To evaluate the clinical efficacy of the combination of high-intensity focused ultrasound (HIFU), mifepristone, and levonorgestrel-releasing intrauterine system (LNG-IUS) in adenomyosis treatment. METHODS: HIFU treatment was performed in 123 patients with symptomatic adenomyosis who had refused treatment with gonadotropin-releasing hormone agonist (GnRH-a) at Anyang Maternal and Child Health Care Hospital. In the control group, 34 patients were treated with HIFU alone, 29 patients with HIFU combined with mifepristone, 10 patients with HIFU combined with LNG-IUS. In the study group, 50 patients were treated with HIFU combined with mifepristone and LNG-IUS. RESULTS: Uterine volume, dysmenorrhea pain score, menstruation volume score, and serum CA125 level were significantly lower after treatment with HIFU combined with mifepristone and LNG-IUS than before treatment (p < .05). Moreover, hemoglobin level was significantly higher than that before treatment (p < .05). After 24 months, the efficacy of HIFU combined with mifepristone and LNG-IUS was significantly higher than that of HIFU alone, HIFU combined with mifepristone or HIFU with LNG-IUS (p < .05). CONCLUSIONS: Combination therapy of HIFU, mifepristone, and LNG-IUS is an effective, safe, and inexpensive treatment for patients with symptomatic adenomyosis. This combination therapy demonstrates superior efficacy to treatment with HIFU alone, HIFU combined with mifepristone, and HIFU combined with LNG-IUS.

Diagnostic Value of Serum Procalcitonin in Appendicitis in Infants and Young Children: Retrospective Cohort Study.

BACKGROUND: An increasing number of studies have indicated that uncomplicated acute appendicitis can be cured with antibiotics alone. Reducing the hazards of appendicitis in infants and young children is a priority problem. It is necessary to search for potential biomarkers for early diagnosis of appendicitis in infants and young children. METHODS: A retrospective cohort study, including 366 infants and young children treated in the pediatric surgery department, was conducted. Complete blood count, C-reactive protein, and procalcitonin were measured at admission and 24 hours after operation. RESULTS: The median of PCT, CRP, and WBC in the acute appendicitis group and other diseases group were 1.20, 0.11 - 4.06; 16.50, 0.81 - 76.21; 13.51, 7.53 - 26.30 and 0.03, 0.01 - 0.13; 3.35, 0.92 - 6.33; 14.34, 8.84 - 17.23 at the admission, respectively. PCT and CRP were found higher in the acute appendicitis group than that in other abdominal pain diseases group (p < 0.05). WBC is not a specific indicator for identifying acute appendicitis and other abdominal pain diseases (p > 0.05). In different acute appendicitis cases, PCT and CRP significantly increased in complicated appendicitis (p < 0.05). Data showed that WBC mildly increased in complicated appendicitis compared to acute simple appendicitis (p < 0.05). ROC curves showed that PCT was a specific indicator for identifying acute appendicitis and other abdominal pain diseases, AUCPCT = 1.000 (95% CI, 0.999 - 1.000). The median of antibiotic treatment is 4.0 d (95% CI 3.0 - 5.0) in acute appendicitis with PCT results versus 7.0 d (95% CI 5.0 - 9.0) in acute appendicitis without PCT result. CONCLUSIONS: PCT shows a high diagnostic ability for appendicitis in infants and young children at admission and assists pediatricians in management of pediatric appendicitis. The combination of these biomarkers is highly recommended. Further studies are needed to confirm our findings.

miR-101-3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5.

Lung adenocarcinoma (LUAD) has been considered as the most common cause of cancer-associated mortality. Radiotherapy resistance is one of the main reasons for LUAD treatment failure. The microRNA (miR)-101-3p has been previously reported to function as a tumor suppressor in several types of cancer, including LUAD. The present study aimed to explore the role and mechanism of miR-101-3p on radioresistance of lung adenocarcinoma cells through bioinformatics analysis and biological experiments. Based on the analysis of Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) data, it was demonstrated that the expression of miR-101-3p was low in LUAD tissues compared with normal lung tissues and was associated with poor prognosis of patients with LUAD. The results of the CCK-8 assay, colony formation assay, immunofluorescence staining, caspase-3 activity assay and western blotting demonstrated that miR-101-3p overexpression sensitized LUAD cells to ionizing radiation by decreasing the abilities of LUAD cell proliferation, colony formation, DNA damage repair and increasing caspase-3 activity and apoptosis of LUAD cells following ionizing radiation. Furthermore, according to bioinformatics analysis and luciferase assay, baculoviral IAP repeat containing 5 (BIRC5) was identified as a direct target of miR-101-3p. Increased BIRC5 expression reversed the miR-101-3p-mediated increase in LUAD cell radiotherapy sensitivity. Taken together, the results of the present study demonstrated that miR-101-3p may be considered as a potential target that can enhance LUAD cell sensitivity to radiotherapy, which may provide a new strategy to improve therapy in patients with LUAD.

Exploring the Molecular Mechanism and Biomarker of Recurrent Spontaneous Abortion Based on RNA Sequencing Analysis.

BACKGROUND: Recurrent spontaneous abortion (RSA) is defined as the failure of two or more consecutive clinical pregnancies before 20 weeks of gestation. It is a hot issue in contemporary obstetrics. The etiology of RSA is complicated. Exploring the molecular mechanisms of RSA will be helpful for the prevention and precise therapy at the molecular level. This study aimed to provide novel insights into the biological characteristics and related pathways of differentially expressed genes (DEGs) in RSA. METHODS: The data set GSE121950 was obtained from GEO data sets. We identified the DEGs using the affy pack-age in R programming software. Gene set enrichment analysis (GESA) and GenePattern tools were performed to examine the gene expression differences between RSA and control group. Protein-protein interaction (PPI) analysis was performed using STRING online tool (https://string-db.org/). qRT-PCR was carried out to validate the expression levels of DEGs in 16 villus tissue samples from patients with induced abortion and 16 villus tissue samples from RSA patients. RESULTS: A total of 628 DEGs with adjPval < 0.05 and |logFC| > 1 were obtained, including 155 up-regulated genes and 473 down-regulated genes. Ten gene ontology (GO) terms and 10 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were screened out by comparing the genome-wide gene set expression patterns of normal and RSA tissues. Eight genes involved in RSA were identified from the hippo signaling pathway, cytokine-cytokine receptor interaction pathway, and allograft rejection pathway. CONCLUSIONS: Present findings demonstrated that several cytokine regulation processes have a deep impact on RSA. A number of genes involved in the hippo signaling pathway, cytokine-cytokine receptor interaction pathway, and allograft rejection pathway may be critical mediators or participators in the pathogenesis of RSA. Although further in vivo and in vitro validations are required, our data may provide an important theoretical basis to elucidate the pathogenesis of RSA.

NUPR1 maintains autolysosomal efflux by activating SNAP25 transcription in cancer cells.

In the advanced stages of cancer, autophagy is thought to promote tumor progression through its ability to mitigate various cellular stresses. However, the details of how autophagy is homeostatically regulated in such tumors are unknown. Here, we report that NUPR1 (nuclear protein 1, transcriptional regulator), a transcriptional coregulator, is aberrantly expressed in a subset of cancer cells and predicts low overall survival rates for lung cancer patients. NUPR1 regulates the late stages of autolysosome processing through the induction of the SNARE protein SNAP25, which forms a complex with the lysosomal SNARE-associated protein VAMP8. NUPR1 depletion deregulates autophagic flux and impairs autolysosomal clearance, inducing massive cytoplasmic vacuolization and premature senescence in vitro and tumor suppression in vivo. Collectively, our data show that NUPR1 is a potent regulator of autolysosomal dynamics and is required for the progression of some epithelial cancers.

Rs2853677 modulates Snail1 binding to the TERT enhancer and affects lung adenocarcinoma susceptibility.

Genome wide association studies (GWAS) have shown that SNPs in non-coding regions are associated with inherited susceptibility to cancer. The effect of one single SNP, however, is weak. To identify potential co-factors of SNPs, we investigated the underlying mechanism by which SNPs affect lung cancer susceptibility. We found that rs2853677 is located within the Snail1 binding site in a TERT enhancer. This enhancer increases TERT transcription when juxtaposed to the TERT promoter. The binding of Snail1 to the enhancer disrupts enhancer-promoter colocalization and silences TERT transcription. The high risk variant of rs2853677 disrupts the Snail1 binding site and derepresses TERT expression in response to Snail1 upregulation, thus increasing lung adenocarcinoma susceptibility. Our data suggest that Snail1 may be a co-factor of rs2853677 for predicting lung adenocarcinoma susceptibility and prognosis.

Ectopic Ikaros expression positively correlates with lung cancer progression.

Ikaros, encoded by the IKZF1 gene, is a pivotal transcription factor whose expression and utilization is dynamically altered during hematopoietic development. However, the molecular mechanisms controlling the transcription of the IKZF1 gene are unclear in lung cancer cell lines. Here we show the role of Ikaros in a cohort of grade IIIA lung cancer patients, with particular emphasis on its relationship with clinical outcomes and expression levels. The expression levels of Ikaros were positively correlated with the prognosis in the lung cancer patients. We also demonstrated that Ikaros expression is ectopically activated in a panel of lung cancer cell lines primarily through demethylation of its promoter. Moreover, gain-of-function experiments revealed that Ikaros inhibits migration and invasion of lung cancer cells in vitro. Our results thus shed light on how Ikaros can act as a lineage competency factor to facilitate lung cancer progression.