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Background: Maternal syphilis not only seriously affects the quality of life of pregnant women themselves, but also may cause various adverse pregnancy outcomes (APOs). This study aimed to analysis the association between the related factors of maternal syphilis and APOs. Methods: Pregnant women infected with syphilis in Henan Province from January 2016 to December 2022 were selected as the study participants. Data collection was conducted through the Preventing Mother-to-child Transmission of HIV, Syphilis and Hepatitis B Management Information System. Information on their demographic characteristics, treatment status, and pregnancy outcomes were collected. Multivariate Logistic regression models were used to analyze the factors associated with adverse outcomes among the study participants. Results: The average age of the 7030 study participants included was 28.55 years old, and the incidence of APOs was 12.20%. For pregnant women infected with syphilis, the multivariate logistic regression results showed that the syphilis infected history (OR=1.378, 95% CI, 1.185-1.601) and the occurrence of abnormality during pregnancy (OR=4.993, 95% CI, 4.154-5.859) were risk factors. For the syphilis positive pregnant women receiving treatment, we found the syphilis infected history (OR=1.378, 95% CI, 1.185-1.601), the occurrence of abnormality during pregnancy (OR=4.993, 95% CI, 4.154-5.859), and not receiving standard treatment (OR=1.343, 95% CI, 1.133-1.592) to be risk factors. Conclusions: Standard syphilis treatment is of great significance in reducing the incidence of APOs for pregnant women infected with syphilis.

The cost-effectiveness study of syphilis screening in pregnant women has not been synthesized. The aim of this study is to synthesizes the economic evidence of the cost-effectiveness of syphilis screening in pregnant women which might contribute to make recommendations on future direction of syphilis screening approaches. We systematically search Medline, PubMed and Web of Science for relevant studies published before May 19th 2022 and identified cost-effectiveness analysis for syphilis screening in pregnant women. The methodological design quality was appraised by Consolidated Health Economic Evaluation Reporting Standards (CHEERS) 2022 checklist. Seventeen literature met the eligibility criteria for full review. Of the seventeen studies, four studies evaluated interventions using different screening methods, seven studies assessed the combination of syphilis test and treatment interventions, three studies focused on repeat screening intervention and four studies evaluated the intervention integrated syphilis and HIV test. The most cost-effective strategy appeared to be rapid syphilis tests with high treatment rate of the positive pregnant women. The cost-effectiveness of syphilis screening in pregnancy has been widely demonstrated. It is more important to improve the compliance of maternal screening and the treatment rate of positive pregnant women while implementing screening.

Resistance to chemotherapy represents a bottleneck in clinical cancer treatment and demands urgent solutions. Dysfunction of glucose metabolism including the Warburg effect is an outstanding hallmark of aberrant cancer metabolism which remarkably fosters chemoresistance. Targeting disordered mitochondrial metabolism have paved the road for enhancing chemosensitivity. Human telomerase reverse transcriptase (hTERT) is tightly associated with cancer initiation and progression. Notably, hTERT can unconventionally translocate from nucleus to mitochondria. However, the influence of mitochondrial hTERT on glucose metabolism and the subsequent contribution to chemoresistance remains largely elusive. Here, we uncovered that mitochondrial hTERT level is negatively with chemotherapy response in patients, and disclosed the undocumented role of mitochondrial hTERT in reprogramming cancer metabolism towards Warburg effect independent of RT activity which authentically promoted chemoresistance. Mitochondrial hTERT boosted Warburg effect and weakened oxidative phosphorylation (OXPHOS) specifically via suppressing Complex I activity.Interactome profiling by mass spectrometry revealed that mitochondrial hTERT physically interacted with Complex I core subunit MT-ND1 (ND1) through its matrix loop region to hinder Complex I functions. A novel TAT-Pep designed on the basis of their interacting region effectively abrogated the hTERT-ND1 interplay, which substantially rejuvenated Complex I activity and rewired cancer metabolism from Warburg effect towards OXPHOS thereby strengthening chemosensitivity in both resistant cancer lines and patient-derived xenograft (PDX) tumor models. Collectively,our study reveals the interaction between MT-ND1 and hTERT as an essential mechanism that underlies the rewiring of cellular glucose metabolism and chemoresistance. Targeting mitochondrial hTERT-governed adverse metabolic remodeling sheds light on the avenue towards better chemotherapeutics efficacy.

Gastric cancer (GC) is the fourth leading cause of cancer-related death. Its poor prognosis is attributed to unclear pathogenesis. Currently, the most widely accepted model for elucidating the mechanism of GC is the Correa cascade, which covers several histological lesions of the gastric mucosa. GC stem cells (CSCs) are crucial for oncogenesis in the Correa cascade and GC progression. As Helicobacter pylori (H. pylori) is the etiological factor in the Correa cascade, growing evidence suggests that enhancement of gastric stem cell-like properties and increase in CSCs correlate with H. pylori infection. In this paper, we review recent studies that present pathogenic mechanisms by which H. pylori induces gastric stem cell-like properties and CSCs, which may supplement the existing Correa model of GC. First, the dysfunction of developmental signaling pathways associated with H. pylori infection leads to the enhancement of gastric stemness. Second, H. pylori infection promotes alteration of the gastric mucosal microenvironment. In addition, epithelial-mesenchymal transition (EMT) may contribute to H. pylori-induced gastric stemness. Taken together, understanding these pathogeneses will provide potential therapeutic targets for the treatment of CSCs and malignant GC in H. pylori induced-Correa cascade of GC.

Background Emerging evidence shows that abnormal expression of long non-coding RNA is involved in the occurrence and development of various tumors. LncRNA MONC is abnormally expressed in head and neck squamous cell carcinoma, lung cancer, colorectal cancer, and acute megakaryocytic leukemia, but the biological function and potential regulatory mechanism of MONC in endometrial cancer stem cells (ECSCs) and endometrial cancer cells (ECCs) have not been studied. In this study, we aimed to explore the tumor suppressive effect and mechanism of MONC in regulating ECSCs and ECCs. Methods We used qRT-PCR to detect the expression of MONC, miR-636 and GLCE in normal human endometrial tissues and endometrial carcinoma (EC) tissues. Luciferase assay was used to verify the binding sites between MONC and miR-636 and between miR-636 and GLCE. Double fluorescence in situ hybridization was used to locate MONC and miR-636 in cells. ECSCs were obtained by flow cytometry sorting assay. Sphere formation assay, CCK-8 assay, transwell invasion assay, cell cycle analysis and apoptosis assay were used to detect the effects of MONC/miR-636/GLCE axis on the malignant biological behavior of ECSCs and ECCs. The effect of MONC on the epithelial-to-mesenchymal transition (EMT) process was detected using western blot. Finally, we conducted in vivo verification through Tumor xenografts in BALB/C nude mice. Results In this study, we found MONC is low expression in endometrial carcinoma (EC) and patients in the MONC high-expression group had a better prognosis. MONC and miR-636 are relatively co-localized in the cytoplasm. MONC directly inhibits the malignant biological behavior of ECSCs and ECCs by directly inhibiting miR-636. Simultaneously, miR-636 may indirectly reduce the expression of MONC. Down-regulation of miR-636 may promote GLCE expression by targeting the 3′-untranslated region (UTR) of the downstream gene GLCE, thereby inhibiting the progression of ECSCs. MONC combined with miR-636 inhibited tumor epithelial-to-mesenchymal transition (EMT) process. In addition, we verified the tumor suppressive effect of MONC in nude mice, miR-636 can rescue the tumor suppressive effect of overexpressing MONC. Conclusions In conclusion, this study showed that MONC inhibits the malignant phenotypes of ECSCs and ECCs by regulating the miR-636/GLCE axis. Thus the MONC/miR-636/GLCE axis may provide novel treatment avenues for human EC.

This study aims to investigate the role of circCBFB in hepatocellular carcinoma (HCC) cell proliferation and autophagy. qRT-PCR and Western blotting analyses quantified the expression levels of circCBFB, miR-424-5p, and ATG14 in HCC tissues and/or HCC cell lines. After transfection with pcDNA3.1-CircCBFB, sh-CircCBFB, miR-424-5p mimic, miR-424-5p inhibitor, pcDNA3.1-ATG14, sh-ATG14, sh-CircCBFB + miR-424-5p inhibitor, pcDNA3.1-CircCBFB + miR-424-5p mimic, sh-CircCBFB + pcDNA3.1-ATG14, or pcDNA3.1-CircCBFB + sh-ATG14, the proliferation, cell cycle, and apoptosis of Huh-7 and HCCLM3 cells were detected, respectively, through MTT assay and flow cytometry. Western blotting measured the expression levels of ATG14 and autophagy-related proteins (LC3-ΙΙ/LC3-Ι, Beclin1, and p62). The interactions among circCBFB, miR-424-5p, and ATG14 were identified through RNA fluorescence in situ hybridization and RNA immunoprecipitation. In HCC tissues, circCBFB and ATG14 were highly expressed, and miR-424-5p expression was downregulated. Transfection of pcDNA3.1-CircCBFB, miR-424-5p inhibitor, or pcDNA3.1-ATG14 into HCC cells facilitated HCC cell proliferation and autophagy, while suppressing cell apoptosis, evidenced by elevated cell viability, increased protein levels of autophagosome markers (LC3-ΙΙ/LC3-Ι and Beclin1), repressed apoptosis rate, and suppressed protein level of autophagy receptor p62. miR-424-5p was a target gene of circCBFB, and miR-424-5p negatively mediated ATG14. CircCBFB inhibits miR-424-5p and upregulates ATG14, thus promoting HCC cell proliferation and autophagy.

Background Endometrial carcinoma (EC) is one of the three major malignant tumors of the female reproductive system. In recent years, the incidence and mortality rate of EC have increased. B-cell translocation gene 1 (BTG1) is an anti-proliferation gene that regulates the occurrence and development of a variety of tumors, but there is no research regarding this gene in EC. Methods Based on The Cancer Genome Atlas (TCGA) database, we used a variety of bioinformatics tools and databases to explore the expression and prognosis of BTG1. We verified expression and prognosis of BTG1 in EC using qRT-PCR and analyzed the relevant clinicopathological parameters. We functionally enriched BTG1 and related genes in EC patients through the bioinformatics website and analyzed miRNA targets of BTG1 and interacting protein networks. Cell proliferation, wound healing, transwell invasion, and cell apoptosis assays were used to detect the effects of BTG1 on the malignant biological behavior of endometrial carcinoma cells (ECCs). The effect of BTG1 on the epithelial-to-mesenchymal transition (EMT) process was detected using western blot. Results We analyzed the expression and prognosis of BTG1 based on TCGA and found that low expression of BTG1 was associated with poor EC prognosis. The qRT-PCR suggested that BTG1 had low expression in EC. BTG1 expression was significantly correlated with overall survival (OS) shortening. Clinicopathological analysis suggested that expression of BTG1 was related to invasion depth and the International Federation of Gynecology and Obstetrics (FIGO) stage. EC pathological tissue type, fertility history, lymphatic metastasis, menopause, estrogen receptor (ER), progesterone receptor (PR), and age of diagnosis were not related. Functional enrichment analysis showed that BTG1 plays an important role in regulating embryonic development, tumorigenesis, apoptosis, and cell cycle. Biological behavior experiments suggest that BTG1 inhibits proliferation, migration, and invasion of ECCs, and promotes apoptosis of ECCs. Western blot indicated that BTG1 inhibited the EMT process of ECCs. Conclusions BTG1, as a tumor suppressor gene, plays an important role in the occurrence and development of EC. We believe that BTG1 can be used as a potential prognostic biomarker for EC.

Background: Endometrial carcinoma is one of the three major malignant tumors in gynecology. ABO blood type is associated with the prognosis of a variety of malignancies. This study assessed the relationship between ABO blood type and prognosis of endometrial carcinoma.Methods: We retrospectively analyzed the relationship between ABO blood type and endometrial carcinoma prognosis in patients with primary endometrial carcinoma who underwent surgery from Shengjing Hospital affiliated to China Medical University from January 2012 to February 2017. Univariate analysis, multivariate analysis, and stratified analysis were performed.Results: In the multivariate analysis, 2009 FIGO stage (HR=2.806, 95% CI=1.289, 6.109), Pathological tissue type (HR=0.199, 95% CI=0.079, 0.503) was an independent and important risk factor for OS. We divided the ABO blood type into A and non-A groups, B and non-B groups, O and non-O groups, AB and non-AB groups, and failed to measure the significant results of OS. After we excluded 9 patients who had recurrence, metastasis, or death within 1 year of enrollment, the OS-significant results were similar to those described above.Conclusions: Our study suggest that there is no association between ABO blood type and EC prognosis, and additional cohort studies are needed for validation.

Additional file 1: Table S1. Primer Sequences.

Additional file 8: Table S6. The miRNAs binding to BTG1 in miRDB.

Additional file 5: Table S3. Significantly enriched GO annotations (Cellular Components) of BTG1 in endometrial carcinoma in Metascape.

Additional file 2: Table S2. Sequences of plasmid.

Additional file 7: Table S5. Significantly enriched GO annotations (Molecular Functions) of BTG1 in endometrial carcinoma in Metascape.

Additional file 6: Table S4. Significantly enriched GO annotations (Biological Processes) of BTG1 in endometrial carcinoma in Metascape.

We have proposed a high temperature die attach method with porous Ag sheet as an interlayer for power device packaging. Sn-3.5Ag solder paste can infiltrate into the porous Ag sheet through capillary forces and Sn can react with the porous Ag sheet and Ag metallizations at the interfaces to form Ag3Sn after reflow at 260 °C for 10 min. The large specific surface area and the high diffusion rates between Ag and Sn accelerate the Sn consumption in the porous Ag structure, thus significantly reducing the processing time. The difference of the melting points of the die attach material before and after reflow could be expanded as large as 259 °C. The bondlines show good electrical and thermal conductivities. Furthermore, the average shear strength of the bondlines at 300 °C is higher than 20 MPa. The porous Ag skeleton remained in the bondline would contribute greatly to the heat dissipation and the electrical signal transmission in power devices.

Table S1. The comparison of demographic characteristics between the elderly using outpatient services and those not using outpatient services, China, 2015. Table S2. The comparison of demographic characteristics between the elderly using inpatient services and those not using inpatient services, China, 2015. Table S3. Contribution to inequalities in the probability of outpatient service utilization, China, 2015. Table S4. Contribution to inequalities in the frequency of outpatient service utilization, China, 2015. Table S5. Contribution to inequalities in the probability of inpatient service utilization, China, 2015. Table S6. Contribution to inequalities in the frequency of inpatient service utilization, China, 2015. (DOCX 54 kb)