Ovarian cancer classification and prognosis assessment model based on prognostic target genes in key microRNA-target gene networks.

BACKGROUND: The present study was designed to screen key microRNA (miRNA)-target gene networks for ovarian cancer (OC) and to classify and construct a risk assessment system for OC based on the target genes. METHODS: OC sample data of The Cancer Genome Atlas dataset and GSE26193, GSE30161, GSE63885 and GSE9891 datasets were retrospectively collected. Pearson correlation analysis and targeted analysis of miRNA and target gene were performed to screen key miRNA-target gene networks. Target genes associated with the prognosis of OC were screened from key miRNA-target gene networks for consensus clustering and least absolute shrinkage and selection operator-based regression machine learning analysis of OC samples. RESULTS: Twenty target genes of 2651 key miRNA-target gene pairs had significant prognostic correlation in each OC cohort, and OC was divided into three clusters. There were differences in prognostic outcome, biological pathways, immune cell abundance and susceptibility to immune checkpoint blockade (ICB) therapy and anti-tumor drugs among the three molecular clusters. S2 exhibited the least advantage in prognosis and immunotherapy response rate in the three molecular clusters, and the pathways regulating immunity, hypoxia, metabolism and promoting malignant progression of cancer, as well as infiltrating immune and stromal cell population abundance, were the highest in this cluster. An eight-target gene prognostic model was created, and the risk index obtained by using this model not only significantly distinguished the immune characteristics of the sample, but also predicted the response of the sample to ICB treatment, and helped to screen 36 potential anti-OC drugs. CONCLUSIONS: The present study provides a classification strategy for OC based on prognostic target genes in key miRNA-target gene networks, and creates a risk assessment system for predicting prognosis and response to ICB therapy in OC patients, providing molecular basis for prognosis and precise treatment of OC.

Factors associated with adverse pregnancy outcomes of maternal syphilis in Henan, China, 2016-2022.

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 analyse the association between the related factors and APOs in maternal syphilis. 7,030 pregnant women infected with syphilis in Henan Province between January 2016 and December 2022 were selected as participants. Information on their demographic and clinical characteristics, treatment status, and pregnancy outcomes was collected. Multivariate logistic regression models and chi-squared automatic interaction detector (CHAID) decision tree models were used to analyse the factors associated with APOs. The multivariate logistic regression results showed that the syphilis infection history (OR = 1.207, 95% CI, 1.035-1.409), the occurrence of abnormality during pregnancy (OR = 5.001, 95% CI, 4.203-5.951), not receiving standard treatment (OR = 1.370, 95% CI, 1.095-1.716), not receiving any treatment (OR = 1.313, 95% CI, 1.105-1.559), and a titre ≥1:8 at diagnosis (OR = 1.350, 95%CI, 1.079-1.690) and before delivery (OR = 1.985, 95%CI, 1.463-2.694) were risk factors. A total of six influencing factors of APOs in syphilis-infected women were screened using the CHAID decision tree model. Integrated prevention measures such as early screening, scientific eugenics assessment, and standard syphilis treatment are of great significance in reducing the incidence of APOs for pregnant women infected with syphilis.

[Latest Findings on the Effect of Gastrointestinal Microecology Remodeling of Tumor Microenvironment on Tumor Stemness].

Gastrointestinal microecology (GM) system is composed of normal gut microbiota and its living environment. The impact of GM on human health and many diseases has been widely studied. The impact of GM system on tumors is mainly reflected in the remodeling of the tumor microenvironment (TME). TME, a special microenvironment that tumors live in, can regulate the characteristics of tumor cells and affect the occurrence and development of tumors through intercellular contact and the secretion of cytokines. At present, cancer stem cell (CSC) model is considered an important theory that explains the origin and malignant progression of tumors. The formation and proliferation of CSC usually represent increased tumor invasion, metastasis, and chemotherapy resistance, resulting in poor clinical prognosis in patients. Therefore, it is important to study the role and mechanism through which GM system affects the acquisition of CSC characteristics through remodeling TME, thereby affecting tumor invasion, metastasis, and chemotherapy resistance. Studies on this topic are of great significance for clinical understanding of tumor malignant progression and improving tumor treatment outcomes. However, due to the low content of single bacteria in the gastrointestinal model, high heterogeneity, and difficulty in tracing distant metastasis, there are still great limitations in the previous research. Herein, we reviewed the research progress in the effect of GM remodeling of TME on the acquisition of tumor stemness, tumor invasion and metastasis, and the resistance to chemotherapy.

LncRNA MONC suppresses the malignant phenotype of Endometrial Cancer Stem Cells and Endometrial Carcinoma Cells by regulating the MiR-636/GLCE axis.

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.

Urban-rural differences in catastrophic health expenditure among households with chronic non-communicable disease patients: evidence from China family panel studies.

BACKGROUND: The prevalence of chronic non-communicable diseases (NCDs) challenges the Chinese health system reform. Little is known for the differences in catastrophic health expenditure (CHE) between urban and rural households with NCD patients. This study aims to measure the differences above and quantify the contribution of each variable in explaining the urban-rural differences. METHODS: Unbalanced panel data were obtained from the China Family Panel Studies (CFPS) conducted between 2012 and 2018. The techniques of Fairlie nonlinear decomposition and Blinder-Oaxaca decomposition were employed to measure the contribution of each independent variable to the urban-rural differences. RESULTS: The CHE incidence and intensity of households with NCD patients were significantly higher in rural areas than in urban areas. The urban-rural differences in CHE incidence increased from 8.07% in 2012 to 8.18% in 2018, while the urban-rural differences in CHE intensity decreased from 2.15% in 2012 to 2.05% in 2018. From 2012 to 2018, the disparity explained by household income and self-assessed health status of household head increased to some extent. During the same period, the contribution of education attainment to the urban-rural differences in CHE incidence decreased, while the contribution of education attainment to the urban-rural differences in CHE intensity increased slightly. CONCLUSIONS: Compared with urban households with NCD patients, rural households with NCD patients had higher risk of incurring CHE and heavier economic burden of diseases. There was no substantial change in urban-rural inequality in the incidence and intensity of CHE in 2018 compared to 2012. Policy interventions should give priority to improving the household income, education attainment and health awareness of rural patients with NCDs.

BTG1 inhibits malignancy as a novel prognosis signature in endometrial carcinoma.

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.

Inequity in inpatient services utilization: a longitudinal comparative analysis of middle-aged and elderly patients with the chronic non-communicable diseases in China.

BACKGROUND: Aging and the chronic non-communicable diseases (NCDs) challenge the Chinese government in the process of providing hospitalization services fairly and reasonably. The Chinese government has developed the basic medical insurance system to solve the problem of "expensive medical cost and difficult medical services" for vulnerable groups and alleviate the unfair phenomenon. However, few studies have confirmed its effect through longitudinal comparison. This study aimed to explore the trend in the inequity of inpatient use among middle-aged and elderly individuals with NCDs in China. METHODS: This longitudinal comparative study was based on CHARLS data in 2011, 2013 and 2015. Concentration index (CI) was used to measure the variation trend of inequity of inpatient services utilization, while the decomposition method of the CI was applied to measure the factors contributing to inequity in inpatient services utilization. The effect of each factor on the change of inequity in inpatient services utilization was divided into the change of the elasticity and the change of inequality using the Oaxaca-type decomposition method. RESULTS: The affluent middle-aged and elderly patients with NCDs used more inpatient services than poor groups. The per capita household consumption expenditure (PCE) and Urban Employee Basic Medical Insurance (UEBMI) contributed to the decline in pro-rich inequality of inpatient use, while the New Rural Cooperative Medical Scheme (NRCMS) contributed to the decline in pro-poor inequality of inpatient use. CONCLUSIONS: There was a certain degree of pro-rich unfairness in the probability and frequency of inpatient services utilization for middle-aged and elderly individuals with NCDs in China. The decrease of pro-wealth contribution of PCE and UEBMI offset the decrease of pro-poor contribution of NRCMS, and improved the equity of inpatient services utilization, favoring poor people.

Influencing factors of inequity in health services utilization among the elderly in China.

BACKGROUND: With the rise of the aging population, it is particularly important for health services to be used fairly and reasonably in the elderly. This study aimed to assess the present inequality and horizontal inequity for health service use among the elderly in China and to identify the main determinants associated with the disparity. METHODS: This cross-sectional study was based on the sample of the survey of the China Health and Retirement Longitudinal Study (CHARLS) for 2015. The elderly was defined as individuals aged 60 and above, with a total of 7836 participants. We used the concentration index (CI) and the horizontal inequity (HI) to measure the inequity of the utilization of health services. The method of concentration index decomposition was utilized to measure the contribution of various influential factors to the overall unfairness. RESULTS: The CI for the probability and the frequency of outpatient use were 0.1102 and 0.1015, respectively, and the corresponding values of inpatient use were 0.2777 and 0.2980, respectively. The household consumption expenditure disparity was the greatest inequality factor favoring the better-off. The Urban Employee Basic Medical Insurance made a pro-wealth contribution to inequality in frequency of health services utilization (17.58% for outpatient and 13.40% for inpatient). The contributions of New Rural Cooperative Medical Scheme on reducing unfairness in inpatient use were limited (- 2.23% for probability of inpatient use and - 5.89% for frequency of inpatient use). CONCLUSIONS: There was a strong pro-rich inequality in both the probability and the frequency of use for health services among the elderly in China. The medical insurance was not enough to address this inequity, and different medical insurance schemes had different effects on the unfairness of health service utilization.

Accessing Early Differentiation of Virus-Specific Follicular Helper CD4+ T Cell in Acute LCMV-Infected Mice.

Follicular Helper T (TFH) cells are perceived as an independent CD4+ T cell lineage that assists cognate B cells in producing high-affinity antibodies, thus establishing long-term humoral immunity. During acute viral infection, the fate commitment of virus-specific TFH cells is determined in the early infection phase, and investigations of the early-differentiated TFH cells are crucial in understanding T cell-dependent humoral immunity and optimizing vaccine design. In the study, using a mouse model of acute lymphocytic choriomeningitis virus (LCMV) infection and the TCR-transgenic SMARTA (SM) mouse with CD4+ T cells specifically recognizing LCMV glycoprotein epitope I-AbGP66-77, we described procedures to access the early fate commitment of virus-specific TFH cells based on flow cytometry stainings. Furthermore, by exploiting retroviral transduction of SM CD4+ T cells, methods to manipulate gene expression in early-differentiated virus-specific TFH cells are also provided. Hence, these methods will help in studies exploring the mechanism(s) underlying the early commitment of virus-specific TFH cells.

LIN28B induced PCAT5 promotes endometrial cancer progression and glycolysis via IGF2BP3 deubiquitination.

Endometrial cancer (EC) cells exhibit abnormal glucose metabolism, characterized by increased aerobic glycolysis and decreased oxidative phosphorylation. Targeting cellular glucose metabolism in these cells could be an effective therapeutic approach for EC. This study aimed to assess the roles of LIN28B, PCAT5, and IGF2BP3 in the glucose metabolism, proliferation, migration, and invasion of EC cells. LIN28B highly expressed in EC, binds and stabilizes PCAT5. PCAT5, overexpressed in EC, and its 1485-2288nt region can bind to the KH1-2 domain of IGF2BP3 to prevent MKRN2 from binding to the K294 ubiquitination site of IGF2BP3, thus stabilizing IGF2BP3. Finally, IGF2BP3 promotes the aerobic glycolysis, proliferation, migration and invasion of EC cells by stabilizing the key enzymes of glucose metabolism HK2 and PKM2. Taken together, our data reveal that the LIN28B/PCAT5/IGF2BP3 axis is critical for glucose reprogramming and malignant biological behavior in EC cells. Therefore, targeting this axis may contribute to the development of a novel therapeutic strategy for EC metabolism.

The cost-effectiveness of syphilis screening in pregnant women: a systematic literature review.

Introduction: The cost-effectiveness study of syphilis screening in pregnant women has not been synthesized. This study aimed to synthesize the economic evidence on the cost-effectiveness of syphilis screening in pregnant women that might contribute to making recommendations on the future direction of syphilis screening approaches. Methods: We systematically searched MEDLINE, PubMed, and Web of Science databases for relevant studies published before 19 January 2023 and identified the cost-effectiveness analyses for syphilis screening in pregnant women. The methodological design quality was appraised by the Consolidated Health Economic Evaluation Reporting Standards (CHEERS) 2022 checklist. Results: In total, 17 literature met the eligibility criteria for a full review. Of the 17 studies, four evaluated interventions using different screening methods, seven assessed a combination of syphilis testing and treatment interventions, three focused on repeat screening intervention, and four evaluated the interventions that integrated syphilis and HIV testing. The most cost-effective strategy appeared to be rapid syphilis testing with high treatment rates in pregnant women who were positive. Discussion: The cost-effectiveness of syphilis screening for pregnancy has been widely demonstrated. It is very essential to improve the compliance with maternal screening and the treatment rates for positive pregnant women while implementing screening.

An oncolytic virus delivering tumor-irrelevant bystander T cell epitopes induces anti-tumor immunity and potentiates cancer immunotherapy.

Tumor-specific T cells are crucial in anti-tumor immunity and act as targets for cancer immunotherapies. However, these cells are numerically scarce and functionally exhausted in the tumor microenvironment (TME), leading to inefficacious immunotherapies in most patients with cancer. By contrast, emerging evidence suggested that tumor-irrelevant bystander T (TBYS) cells are abundant and preserve functional memory properties in the TME. To leverage TBYS cells in the TME to eliminate tumor cells, we engineered oncolytic virus (OV) encoding TBYS epitopes (OV-BYTE) to redirect the antigen specificity of tumor cells to pre-existing TBYS cells, leading to effective tumor inhibition in multiple preclinical models. Mechanistically, OV-BYTE induced epitope spreading of tumor antigens to elicit more diverse tumor-specific T cell responses. Remarkably, the OV-BYTE strategy targeting human severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific T cell memory efficiently inhibited tumor progression in a human tumor cell-derived xenograft model, providing important insights into the improvement of cancer immunotherapies in a large population with a history of SARS-CoV-2 infection or coronavirus disease 2019 (COVID-19) vaccination.

Trends, influencing factors and prediction analysis of under-five and maternal mortality rates in China from 1991 to 2020.

Introduction: Under-five mortality rate (U5MR) and maternal mortality rate (MMR) are important indicators for evaluating the quality of perinatal health and child health services in a country or region, and are research priorities for promoting maternal and infant safety and maternal and child health. This paper aimed to analysis and predict the trends of U5MR and MMR in China, to explore the impact of social health services and economic factors on U5MR and MMR, and to provide a basis for relevant departments to formulate relevant policies and measures. Methods: The JoinPoint regression model was established to conduct time trend analysis and describe the trend of neonatal mortality rate (NMR), infant mortality rate (IMR), U5MR and MMR in China from 1991 to 2020. The linear mixed effect model was used to assess the fixed effects of maternal health care services and socioeconomic factors on U5MR and MMR were explored, with year as a random effect to minimize the effect of collinearity. Auto regressive integrated moving average models (ARIMA) were built to predict U5MR and MMR from 2021 to 2025. Results: The NMR, IMR, U5MR and MMR from 1991 to 2020 in China among national, urban and rural areas showed continuous downward trends. The NMR, IMR, U5MR and MMR were significantly negatively correlated with gross domestic product (GDP), the proportion of the total health expenditure (THE) to GDP, system management rate, prenatal care rate, post-natal visit rate and hospital delivery rate. The predicted values of national U5MR from 2021 to 2025 were 7.3 ‰, 7.2 ‰, 7.1 ‰, 7.1 ‰ and 7.2 ‰ and the predicted values of national MMR were 13.8/100000, 12.1/100000, 10.6/100000, 9.6/100000 and 8.3/100000. Conclusion: China has made great achievements in reducing the U5MR and MMR. It is necessary for achieving the goals of Healthy China 2030 by promoting the equalization of basic public health services and further optimizing the allocation of government health resources. China's experience in reducing U5MR and MMR can be used as a reference for developing countries to realize the SDGs.

PD-1/PD-L1 blockade restores tumor-induced COVID-19 vaccine bluntness.

The COVID-19 vaccinations are crucial in protecting against the global pandemic. However, accumulating studies revealed the severely blunted COVID-19 vaccine effectiveness in cancer patients. The PD-1/PD-L1 immune checkpoint blockade (ICB) therapy leads to durable therapeutic responses in a subset of cancer patients and has been approved to treat a wide spectrum of cancers in the clinic. In this regard, it is pivotal to explore the potential impact of PD-1/PD-L1 ICB therapy on COVID-19 vaccine effectiveness during ongoing malignancy. In this study, using preclinical models, we found that the tumor-suppressed COVID-19 vaccine responses are largely reverted in the setting of PD-1/PD-L1 ICB therapy. We also identified that the PD-1/PD-L1 blockade-directed restoration of COVID-19 vaccine effectiveness is irrelevant to anti-tumor therapeutic outcomes. Mechanistically, the restored COVID-19 vaccine effectiveness is entwined with the PD-1/PD-L1 blockade-driven preponderance of follicular helper T cell and germinal center responses during ongoing malignancy. Thus, our findings indicate that PD-1/PD-L1 blockade will greatly normalize the responses of cancer patients to COVID-19 vaccination, while regardless of its anti-tumor efficacies on these patients.

CircCBFB is a mediator of hepatocellular carcinoma cell autophagy and proliferation through miR-424-5p/ATG14 axis.

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.

Common Multiple Primary Cancers Associated With Breast and Gynecologic Cancers and Their Risk Factors, Pathogenesis, Treatment and Prognosis: A Review.

The mammary gland is closely related to the female reproductive system in many aspects, affecting the whole gynecological system. Breast cancer (BC) is the most common malignancy in women and associated with considerable negative effects. Due to various factors including co-pathogenic genetic mutations, environment factors, lifestyle, behavioral factors, treatment regimens and in-creased survival of patients with BC, there is an increased probability of developing additional primary gynecologic cancers such as ovarian cancer (OC), endometrial cancer (EC), and cervical cancer (CC). More and more studies have been conducted in recent years. Multiple primary cancers (MPCs), also known as multiple primary malignancies, refers to two or more different primary cancers in the same patient occurring in the same or different organs or tissues. The pathogenesis of multiple primary cancers is complex and has a negative effect on the prognosis and survival of patients. This review discusses the common types of BC-associated MPCs, namely, BC associated with OC, BC associated with EC and BC associated with CC, as well as risk factors, pathogenesis, treatment, and prognosis of MPCs associated with breast and gynecologic cancers. It provides new intervention and treatment ideas for patients with BC-associated MPCs to improve quality of life and prognosis.

Helicobacter pylori infection induces stem cell-like properties in Correa cascade of gastric cancer.

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.

Helicobacter pylori and unignorable extragastric diseases: Mechanism and implications.

Considered as the most popular pathogen worldwide, Helicobacter pylori is intensively associated with diverse gastric diseases, including gastric ulcers, chronic progressive gastritis, and gastric cancer. Aside from its pathogenic effect on gastric diseases, growing evidences reveal that H. pylori may be related to numerous extragastric diseases. In this article, we reviewed recent studies and systematically elucidated that H. pylori may interfere with many biological processes outside the stomach and influence the occurrence of various extragastric diseases. Many epidemiological studies have indicated that H. pylori plays a pathogenic role in COVID-19, atherosclerosis, hyperemesis gravidarum and several other extragastric diseases, while the effect of H. pylori is currently under investigation in gastroesophageal reflux disease, asthma, and inflammatory bowel disease. Moreover, we also summarized the possible pathogenic mechanisms of H. pylori that may be related to chronic systemic inflammation and molecular mimicker. Taken together, this review provides a new perspective on the role of H. pylori in extragastric diseases and explores the possible mechanisms, which may help guide clinical treatment.

Interaction Between LncRNA and UPF1 in Tumors.

Long non-coding RNAs (LncRNAs) can bind to other proteins or RNAs to regulate gene expression, and its role in tumors has been extensively studied. A common RNA binding protein, UPF1, is also a key factor in a variety of RNA decay pathways. RNA decay pathways serve to control levels of particular RNA molecules. The expression of UPF1 is often dysregulated in tumors, an observation which suggests that UPF1 contributes to development of a variety of tumors. Herein, we review evidence from studies of fourteen lncRNAs interact with UPF1. The interaction between lncRNA and UPFI provide fundamental basis for cell transformation and tumorigenic growth.

Low Temperature Bonding by Infiltrating Sn3.5Ag Solder into Porous Ag Sheet for High Temperature Die Attachment in Power Device Packaging.

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.