Insights into Adsorption Behavior and Mechanism of Br- onto Nickel-Aluminum Layered Double Hydroxides Intercalated with Different Inorganic Anions.

Layered double hydroxides (LDHs) have garnered significant attention from researchers in the field of adsorption due to their unique laminated structures and ion exchange properties. LDHs with various anion intercalation showed different adsorption effects on adsorbing ions, but the corresponding adsorption mechanisms are ambiguous. In this study, three types of NiAl-LDHs were synthesized, utilizing NO3-, CO32-, or Cl- as the interlayer anions. Batch tests were conducted to study their adsorption performances for Br-. Among them, the LDH with a NO3- intercalation layer exhibited the highest adsorption capacity for Br-, reaching up to 1.40 mmol g-1. The adsorption kinetics, mechanism, and renewability of these NiAl-LDHs were systematically compared. As a result, the type of Br- adsorption by all three materials was single molecular layer chemisorption. Moreover, the thermodynamic results of adsorption suggested that the adsorption of Br- was a spontaneous exothermic process. X-ray photoelectron spectroscopy, X-ray diffraction, and point of zero charge analysis collectively indicated that the adsorption of Br- by LDHs primarily occurred through interlayer ion exchange and electrostatic interactions. Structural characterizations of the adsorbents revealed that Br- entered the interlayers of the three LDHs, causing varying degrees of reduction in the interlayer spacing. Density functional theory calculations indicated that the interlayer binding energy of LDH with NO3- intercalation was the lowest, thereby making it more susceptible NO3- to be exchanged with Br-. Finally, the stability of the NiAl-LDHs was studied. The NiAl-LDHs retains a high removal efficiency of Br- even after 5 cycles of adsorption and desorption.

Microbial metabolites affect tumor progression, immunity and therapy prediction by reshaping the tumor microenvironment (Review).

Several studies have indicated that the gut microbiome and tumor microbiota may affect tumors. Emerging metabolomics research illustrates the need to examine the variations in microbial metabolite composition between patients with cancer and healthy individuals. Microbial metabolites can impact the progression of tumors and the immune response by influencing a number of mechanisms, including modulation of the immune system, cancer or immune­related signaling pathways, epigenetic modification of proteins and DNA damage. Microbial metabolites can also alleviate side effects and drug resistance during chemotherapy and immunotherapy, while effectively activating the immune system to exert tumor immunotherapy. Nevertheless, the impact of microbial metabolites on tumor immunity can be both beneficial and harmful, potentially influenced by the concentration of the metabolites or the specific cancer type. The present review summarizes the roles of various microbial metabolites in different solid tumors, alongside their influence on tumor immunity and treatment. Additionally, clinical trials evaluating the therapeutic effects of microbial metabolites or related microbes on patients with cancer have been listed. In summary, studying microbial metabolites, which play a crucial role in the interaction between the microbiota and tumors, could lead to the identification of new supplementary treatments for cancer. This has the potential to improve the effectiveness of cancer treatment and enhance patient prognosis.

Highly specific vaginal microbiome signature for gynecological cancers.

To investigate the vaginal microbiota signature of patients with gynecologic cancer and evaluate its diagnostic biomarker potential. We incorporated vaginal 16S rRNA-seq data from 529 women and utilized VSEARCH to analyze the raw data. α-Diversity was evaluated utilizing the Chao1, Shannon, and Simpson indices, and ß-diversity was evaluated through principal component analysis using Bray-Curtis distances. Linear discriminant analysis effect size (LEfSe) was utilized to determine species differences between groups. A bacterial co-abundance network was constructed utilizing Spearman correlation analysis. A random forest model of gynecologic tumor risk based on genus was constructed and validated to test its diagnostic efficacy. In gynecologic cancer patients, vaginal α-diversity was significantly greater than in controls, and vaginal ß-diversity was significantly separated from that of controls; there was no correlation between these characteristics and menopause status among the subject women. Women diagnosed with gynecological cancer exhibited a reduction in the abundance of vaginal Firmicutes and Lactobacillus, while an increase was observed in the proportions of Bacteroidetes, Proteobacteria, Prevotella, Streptococcus, and Anaerococcus. A random forest model constructed based on 56 genus achieved high accuracy (area under the curve = 84.96%) in gynecological cancer risk prediction. Furthermore, there were discrepancies observed in the community complexity of co-abundance networks between gynecologic cancer patients and the control group. Our study provides evidence that women with gynecologic cancer have a unique vaginal flora structure and microorganisms may be involved in the gynecologic carcinogenesis process. A gynecological cancer risk prediction model based on characteristic genera has good diagnostic value.

Specific vaginal and gut microbiome and the anti-tumor effect of butyrate in cervical cancer women.

OBJECTIVE: To investigate the vaginal and gut microbes changes during the carcinogenesis of cervical and the auxiliary diagnostic value. To investigate the effect of microbiome-specific metabolites butyric on cervical cancer cells. METHODS: We studied 416 vaginal 16S rRNA sequencing data and 116 gut sequencing data. Reads were processed using VSEARCH. We used Shannon index, Chao1 index, Simpson diversity index, ß diversity index, Linear discriminant analysis Effect Size (LEfSe), co-abundance network and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis to explore microbiome differences between groups. We constructed random forest models based on genus and verified its discriminant effect. Finally, we used the cell counting kit-8 (CCK-8) method to detect cell proliferation capacity and flow cytometry to detect apoptosis and induction of cell cycle progression. RESULTS: Compared to the non-cancerous population, patients with cervical cancer had unique microbial community characteristics in both vaginal and gut ecological niches. Our predictive model based on genus in two ecological regions achieved high accuracy in the diagnosis of cervical cancer (vaginal model AUC=91.58 %; gut model AUC=99.95 %). Butyric inhibited cervical cancer cell proliferation in a concentration-dependent manner and promoted apoptosis of cancer cells. CONCLUSION: Significant differences were found in vaginal and gut microbes in patients with cervical cancer compared to the non-cancerous population. The prediction models constructed at the genus level in both ecological sites have good diagnostic value. Microorganisms may be involved in cervical cancer progression in a metabolite-dependent way, and targeting butyric may provide therapeutic options for cervical cancer.

Whole Exome Sequencing reveals clinically important pathogenic mutations in DNA repair genes across lung cancer patients.

Lung cancer remains a substantial health challenge, with distinct genetic factors influencing disease susceptibility and progression. This study aimed to decipher the landscape of DNA repair gene mutations in Pakistani lung cancer patients using Whole Exome Sequencing (WES) and to investigate their potential functional implications through downstream analyses. WES analysis of genomic DNA from 15 lung cancer patients identified clinically important pathogenic mutations in 6 DNA repair genes, including, BReast CAncer gene 1 (BRCA1), BReast CAncer gene 2 (BRCA2), Excision Repair Cross Complementing rodent repair deficiency, complementation group 6 (ERCC6), Checkpoint Kinase 1 (CHEK1), mutY DNA glycosylase (MUTYH), and RAD51D (RAD51 Paralog D). Kaplan-Meier (KM) analysis showed that pathogenic mutations in BRCA1, BRCA2, ERCC6, CHEK1, MUTYH, and RAD51D genes were the prognostic biomarkers of worse OS in lung cancer patients. To explore the functional impact of these mutations, we performed Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Immunohistochemistry (IHC) analyses. Our results revealed a down-regulation in the expression of the mutated genes, indicating a potential link between the identified mutations and reduced gene activity. This down-regulation could contribute to compromised DNA repair efficiency, thereby fostering genomic instability in lung cancer cells. Furthermore, targeted bisulfite sequencing analysis was employed to assess the DNA methylation status of the mutated genes. Strikingly, hypermethylation in the promoters of BRCA1, BRCA2, ERCC6, CHEK1, MUTYH, and RAD51D was observed across lung cancer samples harboring pathogenic mutations, suggesting the involvement of epigenetic mechanism underlying the altered gene expression. In conclusion, this study provides insights into the genetic landscape of DNA repair gene mutations in Pakistani lung cancer patients. The observed pathogenic mutations in BRCA1, BRCA2, ERCC6, CHEK1, MUTYH, and RAD51D, coupled with their down-regulation and hypermethylation, suggest a potential convergence of genetic and epigenetic factors driving genomic instability in lung cancer cells. These findings contribute to our understanding of lung cancer susceptibility and highlight potential avenues for targeted therapeutic interventions in Pakistani lung cancer patients.

The role of microbiota in the development and treatment of gastric cancer.

The stomach was once considered a sterile organ until the discovery of Helicobacter pylori (HP). With the application of high-throughput sequencing technology and macrogenomics, researchers have identified fungi and fivemajor bacterial phyla within the stomachs of healthy individuals. These microbial communities exert regulatory influence over various physiological functions, including energy metabolism and immune responses. HP is a well-recognized risk factor for gastric cancer, significantly altering the stomach's native microecology. Currently, numerous studies are centered on the mechanisms by which HP contributes to gastric cancer development, primarily involving the CagA oncoprotein. However, aside from exogenous infections such as HP and EBV, certain endogenous dysbiosis can also lead to gastric cancer through multiple mechanisms. Additionally, gut microbiota and its metabolites significantly impact the development of gastric cancer. The role of microbial therapies, including diet, phages, probiotics and fecal microbiota transplantation, in treating gastric cancer should not be underestimated. This review aims to study the mechanisms involved in the roles of exogenous pathogen infection and endogenous microbiota dysbiosis in the development of gastric cancer. Also, we describe the application of microbiota therapy in the treatment and prognosis of gastric cancer.

Identification of microbial markers associated with lung cancer based on multi-cohort 16 s rRNA analyses: A systematic review and meta-analysis.

BACKGROUND: The relationship between commensal microbiota and lung cancer (LC) has been studied extensively. However, developing replicable microbiological markers for early LC diagnosis across multiple populations has remained challenging. Current studies are limited to a single region, single LC subtype, and small sample size. Therefore, we aimed to perform the first large-scale meta-analysis for identifying micro biomarkers for LC screening by integrating gut and respiratory samples from multiple studies and building a machine-learning classifier. METHODS: In total, 712 gut and 393 respiratory samples were assessed via 16 s rRNA amplicon sequencing. After identifying the taxa of differential biomarkers, we established random forest models to distinguish between LC populations and normal controls. We validated the robustness and specificity of the model using external cohorts. Moreover, we also used the KEGG database for the predictive analysis of colony-related functions. RESULTS: The α and ß diversity indices indicated that LC patients' gut microbiota (GM) and lung microbiota (LM) differed significantly from those of the healthy population. Linear discriminant analysis (LDA) of effect size (LEfSe) helped us identify the top-ranked biomarkers, Enterococcus, Lactobacillus, and Escherichia, in two microbial niches. The area under the curve values of the diagnostic model for the two sites were 0.81 and 0.90, respectively. KEGG enrichment analysis also revealed significant differences in microbiota-associated functions between cancer-affected and healthy individuals that were primarily associated with metabolic disturbances. CONCLUSIONS: GM and LM profiles were significantly altered in LC patients, compared to healthy individuals. We identified the taxa of biomarkers at the two loci and constructed accurate diagnostic models. This study demonstrates the effectiveness of LC-specific microbiological markers in multiple populations and contributes to the early diagnosis and screening of LC.

Effects of early PCSK9 inhibitor application on inflammation levels and microcirculatory function after PCI in patients with NSTE-ACS.

OBJECTIVE: To investigate inflammation levels and microcirculatory function following the early application of proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitor after percutaneous coronary intervention (PCI) in patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS). METHODS: This is a retrospective study. Between December 2019 and December 2021, 120 patients with NSTE-ACS admitted to the People's Hospital of Henan University of Traditional Chinese Medicine for PCI were randomized via a web-based randomization system into a control group (60 cases) treated with atorvastatin or a PCSK9 inhibitor group (60 cases) treated with atorvastatin + evolocumab. After 6 months of treatment, between-group differences were assessed for the following measures: triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), lipoprotein(a) [Lp(a)], high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), index of microcirculatory resistance (IMR), Thrombosis in Myocardial Infarction myocardial perfusion grading (TMPG), major adverse cardiovascular events (MACEs), and adverse reactions. RESULTS: After 6 months of treatment, TG (P=0.037), TC (P<0.001), LDL-C (P<0.001), Lp(a) (P<0.001), hs-CRP (P<0.001), TNF-α (P<0.001), and IL-6 (P<0.001) levels and IMR values (P<0.001) were significantly lower in the PCSK9 inhibitor group than in the control group. TMPG grade 3 (P=0.04) was noted to occur significantly more frequently in the PCSK9 inhibitor group than in the control group. No significant between-group differences in MACEs (P>0.05) or adverse reactions (P>0.05) were observed. CONCLUSIONS: Compared with statins alone, a PCSK9 inhibitor combined with statins improves inflammation levels and microcirculatory function after PCI in patients with NSTE-ACS, and this strategy deserves clinical attention.

Vaginal and tumor microbiomes in gynecological cancer (Review).

Cervical, ovarian and endometrial cancer are the three most common types of gynecologic cancer. As a hub, the vagina connects the site of gynecological cancer with the external environment. Lactobacilli participate in the formation of a healthy vaginal microenvironment as the first line of defense against pathogen invasion; a dysbiotic vaginal microenvironment loses its original protective function and is associated with the onset, metastasis, poor efficacy and poor prognosis of gynecological cancer. The early diagnosis of cancer is the key to improve the survival time of patients with cancer. The screening of Porphyromonas, Sneathia and Atopobium vaginae, and other microbial markers, can assist the diagnosis of gynecological cancer, and screen out the high-risk population as early as possible. With the in-depth study of the microbes in tumor tissues, reasearchers have analyzed the immunological associations of microorganisms in tumor tissues. Due to the structural-functional interconnection between the organ of gynecological tumorigenesis and the vagina, the present study aims to review the relationship between vaginal and tumor microorganisms and gynecological cancer in terms of occurrence, screening, treatment and prognosis.

[Correlation between the mRNA levels of BCRP and LUNX genes and pathological types and stages of patients with non-small cell lung cancer].

OBJECTIVE: To analyze the correlation between the mRNA levels of breast cancer resistance protein (BCRP) and lung-specific X protein (LUNX) genes with pathological types and stages of patients with non-small cell lung cancer (NSCLC) and their significance for prognosis. METHODS: Eighty nine patients with NSCLC admitted to Huaihe Hospital of Henan University between June 2015 and June 2018 were recruited, with 55 patients with benign lung lesions admitted during the same period of time selected as the control group. The mRNA levels of BCRP and LUNX genes were detected in the peripheral blood samples from the two groups, and their correlation with the clinicopathological characteristics and prognosis of the patients was analyzed. RESULTS: The expression rates of BCRP and LUNX mRNA in the NSCLC group were significantly higher compared with the control group (P < 0.05). The level of BCRP mRNA of the NSCLC patients has correlated with the degree of differentiation and TNM staging (P < 0.05), but not with gender, age, smoking, pathological types and lymph node metastasis (P > 0.05). The level of LUNX mRNA of them has correlated with the degree of differentiation, TNM staging and lymph node metastasis (P < 0.05), but not with gender, age, smoking, and pathological types (P > 0.05). Compared with those with no expression, the overall survival rate of patients with BCRP and LUNX expression was significantly lower (P < 0.05). The degree of differentiation, TNM staging, lymph node metastasis, and expression of the BCRP and LUNX mRNA may all affect the prognosis of the patients. CONCLUSION: The levels of BCRP and LUNX mRNA in the peripheral blood of patients with NSCLC are significantly increased. The expression of BCRP mRNA is correlated with the degree of differentiation and TNM staging, whilst the expression of LUNX mRNA is correlated with the differentiation degree, TNM staging and lymph node metastasis. Both may be used as independent predictors for the prognosis of patients with NSCLC.

IL4I1 and tryptophan metabolites enhance AHR signals to facilitate colorectal cancer progression and immunosuppression.

OBJECTIVE: The molecular mechanisms underlying tumor progression and drug resistance in colorectal cancer remain to be fully understood. Recent studies have reported a pro-tumorigenic role of an amino acid oxidase named interleukin-4-induced-1 (IL4I1). Here, we investigate the role and molecular mechanism of IL4I1 in colorectal cancer. METHODS: We employed bioinformatics analysis and experimental validation by using clinical samples and a variety of cell-based assays, including western blot, Transwell assay, patient-derived organoid culture, Immunofluorescence assay, T cell cytotoxicity assay, and flow cytometry. RESULTS: Bioinformatics analysis showed a higher IL4I1 expression in colorectal cancer tissues than in normal tissues. In vitro overexpression of IL4I1 enhanced the proliferation, migration, and invasion of colorectal cancer cells. In addition, deprivation of Tryptophan (Trp) in cultural medium diminished the oncogenic effect of IL4I1. Furthermore, we observed a positive correlation of IL4I1 and AHR expression in the TCGA database of colorectal cancer. We also detected an enhanced cytoplasmic expression and nuclear translocation of Aryl hydrocarbon receptor (AHR). Moreover, IL4I1 overexpression suppressed the cytolytic killing of tumor cells and enhanced T cell exhaustion. Finally, in the organoid culture model, we found that immunotherapy and SR-1 combination treatment could induce higher level of apoptosis than did the immunotherapy or SR-1 treatment alone. CONCLUSION: we demonstrated that IL4I1 facilitated colorectal cancer progression and immunosuppression through tryptophan metabolism dependent on AHR activation.

Identifying distinctive tissue and fecal microbial signatures and the tumor-promoting effects of deoxycholic acid on breast cancer.

Introduction: A growing body of evidence indicates that the dysbiosis of both mammary and intestinal microbiota is associated with the initiation and progression of breast tumors. However, the microbial characteristics of patients with breast tumors vary widely across studies, and replicable biomarkers for early-stage breast tumor diagnosis remain elusive. Methods: We demonstrate a machine learning-based method for the analysis of breast tissue and gut microbial differences among patients with benign breast disease, patients with breast cancer (BC), and healthy individuals using 16S rRNA sequence data retrieved from eight studies. QIIME 2.0 and R software (version 3.6.1) were used for consistent processing. A naive Bayes classifier was trained on the RDP v16 reference database to assign taxonomy using the Vsearch software. Results: After re-analyzing with a total of 768 breast tissue samples and 1,311 fecal samples, we confirmed that Halomonas and Shewanella were the most representative genera of BC tissue. Bacteroides are frequently and significantly enriched in the intestines of patients with breast tumor. The areas under the curve (AUCs) of random forest models were 74.27% and 68.08% for breast carcinoma tissues and stool samples, respectively. The model was validated for effectiveness via cohort-to-cohort transfer (average AUC =0.65) and leave-one-cohort-out (average AUC = 0.66). The same BC-associated biomarker Clostridium_XlVa exists in the tissues and the gut. The results of the in-vitro experiments showed that the Clostridium-specific-related metabolite deoxycholic acid (DCA) promotes the proliferation of HER2-positive BC cells and stimulates G0/G1 phase cells to enter the S phase, which may be related to the activation of peptide-O-fucosyltransferase activity functions and the neuroactive ligand-receptor interaction pathway. Discussion: The results of this study will improve our understanding of the microbial profile of breast tumors. Changes in the microbial population may be present in both the tissues and the gut of patients with BC, and specific markers could aid in the early diagnosis of BC. The findings from in-vitro experiments confirmed that Clostridium-specific metabolite DCA promotes the proliferation of BC cells. We propose the use of stool-based biomarkers in clinical application as a non-invasive and convenient diagnostic method.

[miR-181c promotes the migration and angiogenesis of human A549 cells via targeting inhibition of reversion-inducing cysteine-rich protein with Kazal motifs (RECK)].

Objective To investigate the impact of miR-181c on migration and angiogenesis of lung cancer cells. Methods The Oncomine platform, UALCAN was used to analyze the differential expression of miR-181c and reversion-inducing cysteine-rich protein with Kazal motifs (RECK) in lung cancer obtained from the Cancer Genome Atlas (TCGA) database. The targeting relationship between miR-181c on RECK gene was predicted using Targetscan software. miR-181c mimic, inhibitor and negative control were introduced into A549 cells respectively. After transfection, the real-time quantitative PCR was used to detect the relative expressions of miR-181c and RECK mRNA, and Western blot analysis was used to detect the expression levels of RECK, matrix metalloproteinase 2 (MMP2) and MMP9 proteins. TranswellTM assay was performed to analyze the cell migration ability. The secretion of vascular endothelial growth factor (VEGF)-A in the cell culture supernatant was analyzed by using ELISA. Human umbilical vein endothelial cells (HUVECs) were treated with the culture supernatant, then in vitro tubule formation assay was carried out to evaluate the angiogenesis ability. The targeting correlation between miR-181c and RECK was validated by double luciferase reporter gene assay. Results UALCAN analysis displayed that the expression of miR-181c was significantly higher and RECK expression was significantly lower in lung cancer tissues compared to that in normal tissues. Targetscan prediction showed that there was a miR-181c binding site in the 3'-untranslated region (3' UTR) of RECK gene. miR-181c could downregulate the expression of RECK, increase the expressions of MMP2 and MMP9, and promote the A549 cell migration. ELISA and tubule formation assay showed that miR-181c could induce the secretion of VEGF-A in A549 cells and enhance the ability of HUVECs differentiae into tubules. The double luciferase reporter gene assay confirmed that RECK was the direct regulation target of miR-181c. Conclusion miR-181c promotes the migration and angiogenesis of human A549 cells by directly targeting RECK.

[Association of GSTP1 and PLCE1 gene polymorphisms with primary esophageal cancer].

OBJECTIVE: To assess the association of polymorphisms of glutathione S-transferase P1 (GSTP1) and phospholipase C epsilon-1 (PLCE1) genes with the susceptibility of primary esophageal cancer and their interaction with environmental factors. METHODS: 162 patients with primary esophageal cancer and 162 healthy controls were recruited in this cross-sectional study. Basic information such as gender, age, history of smoking and alcohol consumption and family history of esophageal cancer were collected. Single nucleotide polymorphisms at A105G locus of GSTP1 gene and rs3765524, rs2274223 and rs3781264 loci of PLCE1 gene were detected. A logistic regression model was established to analyze the risk factors of esophageal cancer and the interaction among the factors. RESULTS: The proportions of individuals with smoking history, family history of esophageal cancer and hot diet in esophageal cancer group were higher than those in the control group (P<0.05). Conditional Logistic regression analysis showed that smoking, family history of esophageal cancer and GG genotype at the rs2274223 locus of PLCE1 gene were the risk factors for esophageal cancer (P<0.05), and AG/GG genotypes at the A105G locus of GSTP1 gene were the protective factors for esophageal cancer (P<0.05). In the two-factor interaction model, both AA genotype at A105G locus of GSTP1 gene and GG genotype at rs2274223 locus of PLCE1 gene had an interaction with smoking, and the risk of esophageal cancer has increased by 83.6% and 85.7%, respectively (P<0.05). AA genotype at A105G locus of GSTP1 gene, GG genotype at rs2274223 locus of PLCE1 gene and smoking constituted the best three-factor interaction model, and the risk of esophageal cancer has increased by 244.0% (P<0.05). Four-factor interaction model analysis showed that the risk of esophageal cancer among individuals with AA genotype at A105G locus of GSTP1 gene, GG genotype at rs2274223 locus of PLCE1 gene, smoking and family history of esophageal cancer has increased by 264.4% (P<0.05). CONCLUSION: The AG and GG genotypes at the A105G locus of GSTP1 gene are protective factors for esophageal cancer, and the GG genotype at rs2274223 locus of PLCE1 gene is a risk factor, both of them may interact with smoking and affect the susceptibility to esophageal cancer.

Gut Microbes in Gynecologic Cancers: Causes or Biomarkers and Therapeutic Potential.

The human intestine is home to a variety of microorganisms. In healthy populations, the intestinal flora shares a degree of similarity and stability, and they have a role in the metabolism, immunological response, and physiological function of key organs. With the rapid advent of high-throughput sequencing in recent years, several researchers have found that dysbiosis of the human gut microflora potentially cause physical problems and gynecological malignancies among postmenopausal women. Besides, dysbiosis hinders tumor treatment. Nonetheless, the importance of maintaining homeostatic gut microbiota and the effective use of probiotics in the treatment of gynecological malignancies should not be disregarded. Moreover, intestinal flora regulation and the involvement of probiotics as well as associated biologically active substances in gynecological malignancies could be an adjuvant treatment modality related to surgery and chemoradiotherapy in the future. Herein, this article aims to review the potential relationship between gut microorganisms and postmenopausal status as well as gynecologic malignancies; then the relationship between gut microbes and early screening as well as therapeutic aspects. Also, we describe the role of probiotics in the prevention, treatment, and prognosis of gynecologic malignancies.

Cadherin-dependent adhesion modulated 3D cell-assembly.

The emergence of synthetic biology has opened new avenues in constructing cell-assembly biosystems with specific gene expression and function. The phenomena of cell spreading and detachment during tissue development and cancer metastasis are caused by surface tension, which in turn results from differences in cell-cell adhesion mediated by the dimerization of cadherin expressed on the cell surface. In this study, E- and P-cadherin plasmids were first constructed based on the differential adhesion hypothesis, then they were electroporated into K562 cells and HEK293T cells, respectively, to explore the process of cell migration and assembly regulated by cadherins. Using this approach, some special 3D cell functional components with a phase separation structure were fabricated successfully. Our work will be of potential application in the construction of self-assembling synthetic tissues and organoids.

Selective and sensitive detection of miRNA-198 using single polymeric microfiber waveguide platform with heterogeneous CHA amplification strategy.

Pancreatic cancer (PC), which has a high fatality rate, is a kind of cancer with poor diagnosis and poor prognosis. Development of selective and sensitive detection platform to diagnose and prognostic of PC has attracted considerable attention. The miRNA-198 has been reported a potential prognostic and early diagnostic marker signature of PC. Herein, we report a novel sensitive detection of miRNA-198 in buffer and serum based on one dimensional chitosan/fluorescein isothiocyanate (CS/FITC) fluorescent microfiber waveguide system combined with the catalytic hairpin assembly amplification strategy. By combination with condensing enrichment effect, the proposed detection platform exhibited high specificity and sensitivity to miRNA-198 target, giving a detection limit as low as 2 fM. More importantly, the proposed detection platform can be applied directly to distinguish the expression of miRNA-198 in clinical serum, affording the ability to distinguish pancreatic cancer patients from those of healthy human beings, and quantify the expression variation of miRNA-198 for the pancreatic cancer patients before and after resection, which may pave the way to develop novel clinical diagnostic equipment for cancer diagnosis and therapeutic evaluation.

A Comparative Study of the Clinical Efficacy and Safety of Pneumatic Trabeculoplasty and Selective Laser Trabeculoplasty for Patients with Primary Open-Angle Glaucoma or Ocular Hypertension.

BACKGROUND We aimed to evaluate the efficacy and safety of pneumatic trabeculoplasty (PNT) and selective laser trabeculoplasty (SLT) in the treatment of primary open-angle glaucoma (POAG) and ocular hypertension (OHT). MATERIAL AND METHODS We randomly divided 120 cases (120 eyes) of POAG or OHT into 2 groups: PNT and SLT. The changes in anterior chamber angle, intraocular pressure (IOP), treatment effect, macular retinal ganglion cell complex (GCC) thickness, visual field, adverse reactions, and complications were observed before and 3 months after treatment. RESULTS In the PNT group, the opening range of anterior chamber angle at 1 week, 2 weeks, 1 month, and 3 months after surgery was significantly larger than that before surgery. In the SLT group, the open range of anterior chamber angle was significantly less than that before surgery at 1 week and 2 weeks after surgery. The open range of anterior chamber angle in the PNT group was significantly larger than that in the SLT group at 1 week, 2 weeks, 1 month, and 3 months after surgery. The mean IOP of the 2 groups decreased significantly after surgery. The postoperative mean IOP of the SLT group was significantly higher than that of the PNT group, and the decrease of IOP in the PNT group was significantly greater than that of the SLT group. The effective rate of the PNT group was higher than that of the SLT group. CONCLUSIONS Both PNT and SLT can reduce the IOP of patients with POAG and OHT. PNT appears to have better short-term treatment efficiency than SLT.

Hollow waxberry-like cobalt-nickel oxide/S,N-codoped carbon nanospheres as a trifunctional electrocatalyst for OER, ORR, and HER.

With the aggravation of the energy crisis, increasing attention has been paid to electrocatalytic technology for renewable energy devices. In particular, the research on catalysts towards the oxygen evolution reaction (OER), oxygen reduction reaction (ORR), and hydrogen evolution reaction (HER) has become more urgent, and the development of multifunctional electrocatalysts has become a research trend. Here we report the synthesis of waxberry-like cobalt-nickel oxide/S,N-codoped carbon hollow nanocomposites as trifunctional catalysts. Uniform cobalt-nickel glycerate solid spheres are first synthesized as the precursor and subsequently chemically transformed into cobalt-nickel oxide/S,N-codoped carbon hollow nanospheres. Benefiting from the synergistic coupling of cobalt-nickel oxide and S,N-codoped carbon nanocomposites, hierarchical porosity and hollow structure, the cobalt-nickel oxide/S,N-codoped carbon nanohybrids exhibit superior trifunctional electrocatalytic activity and durability towards OER, ORR, and HER in alkaline media.

NRAS Contributes to Retinoblastoma Progression Through SNHG16/miR-183-5p/NRAS Regulatory Network.

PURPOSE: The oncogene of wild type neuroblastoma RAS viral oncogene homolog (NRAS) has been found to involve in the tumorigenesis of cancers. However, the role of NRAS in retinoblastoma (RB) progression remains largely unknown. METHODS: The expression levels of NRAS, miR-183-5p and small nucleolar RNA host gene 16 (SNHG16) were measured using quantitative real-time polymerase chain reaction assay or Western blot assay, respectively. Cell proliferation and apoptosis were analyzed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay or flow cytometry, respectively. Transwell assay was used to determine cell migration and invasion abilities. The interaction between miR-183-5p and NRAS or SNHG16 was analyzed using bioinformatics analysis and dual-luciferase reporter assay. RESULTS: NRAS was elevated in RB tissues and cell lines, knockdown of NRAS could inhibit proliferation, migration and invasion but induced apoptosis in vitro and suppressed tumor growth in vivo. NRAS was confirmed to be a target of miR-183-5p and was negatively regulated by miR-183-5p in RB cells. Moreover, overexpressed NRAS reversed miR-183-5p mediated inhibition on RB cell progression. Besides that, SNHG16 directly interacted with miR-183-5p and reduced miR-183-5p expression in RB cells. The suppression of RB cell progression induced by SNHG16 silencing could be partially attenuated by the inhibition of miR-183-5p. Besides that, SNHG16 could regulate NRAS expression through competitively binding to miR-183-5p in RB cells. CONCLUSION: NRAS functioned as an oncogene to contribute to RB progression by SNHG16/miR-183-5p/NRAS regulatory network, indicating a novel and promising therapeutic target for RB.