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Background: Pyroptosis may affect cancer progression by regulating the tumor microenvironment (TME) and biological function of cancer cells. The relationship between pyroptosis-related genes (PRGs) and prostate adenocarcinoma (PRAD) and its TME is unclear. Method: In our study, we carried out an overall bioinformatics analysis to build a prognostic PRGs model based on TME and molecular heterogeneity and external validation, then verified the relationship between PRGs and PRAD cells through cell experiments. The relationship between PRGs and tumor-immune cells, immune pathways, immune infiltration, cell-cell communication, genomic alteration tumor mutation burden, microsatellite-instability and drug sensitivity were analyzed. Results: A total of 36 PRGs were up- or down-regulated in PRAD. Functional enrichment analysis indicated that 33 PRGs were mostly involved in Salmonella infection, apoptosis and some signaling pathways (NOD-like receptor, C-type lectin receptor, AGE-RAGE, Cytosolic DNA-sensing, TNF and p53). We identified five prognostic genes (CHMP4C, PLGG1, TP53, GSDMB and PJVK) and constructed a PRGs model to predict progression free survival (PFS) in PRAD patients with high accuracy. And, it was verified with an external database. We found that there was a marked correlation between prognostic PRGs and immune cells, immune pathway, immune cell infiltration, tumor mutation burden and microsatellite instability. Finally, we increased the level of pyroptosis by LPS and established an RNA interference cell line. It was found that the protein expression of NT-GSDMD decreased. Meanwhile, knocking out the above genes affected their promotion of the proliferation of PRAD cells. The above experiments further showed that the five genes were indeed related to pyroptosis. Conclusion: We established PRGs signatures based on immune microenvironment and molecular heterogeneity through public data and verified them through external data and cell experiments. Our results might help to better understand the impact of proptosis on the progress of PRAD, and provided a new direction for the treatment of PRAD patients.

BACKGROUND: Toll-like receptors participate in various biological mechanisms, mainly including the immune response and inflammatory response. Nevertheless, the role of TLRs in STAD remains unclear. OBJECTIVE: We aimed to explore the expression, prognosis performance of TLRs in STAD and their relationship with immune infiltration. METHODS: Student’s t-test was used to evaluate the expression of TLRs between STAD tissues and normal tissues. Kaplan-Meier method was applied to explored the prognosis value of TLRs in STAD. And qRT-PCR validated their expression and prognosis value. Spearman’s correlation analysis and Wilcoxon rank-sum test were used to assess the association between TLRs and immune infiltration in STAD. RESULTS: The mRNA level of TLR3 was downregulated in STAD. We summarized genetic mutations and CNV alteration of TLRs in STAD cohort. Prognosis analysis revealed that STAD patients with high TLR3 expression showed better prognosis in OS, FP and PPS. The result of qRT-PCR suggested that TLR3 expression was decreased in STAD tissues and STAD patients with high TLR3 mRNA level had a better OS. Univariate and multivariate cox regression analysis suggested TLR3 expression and clinical stage as independent factors affecting STAD patients’ prognosis. A positive association existed between TLR3 expression and the abundance of immune cells and the expression of various immune biomarkers. Furthermore, key targets related to TLR3 were identified in STAD, mainly including MIR-129 (GCAAAAA), PLK1, and V$IRF1_01. CONCLUSIONS: Our result demonstrated TLR3 as a prognosis marker and associated with immune infiltration in STAD.

Background. Liver hepatocellular carcinoma (LIHC) is a malignance with high incidence and recurrence. Pyroptosis is a programed cell death pattern which both activates the effective immune response and causes cell damage. However, their potential applications of pyroptosis-related genes (PRGs) in the prognostic evaluation and immunotherapy of LIHC are still rarely discussed. Methods. Comprehensive bioinformatics analyses based on TCGA-LIHC dataset were performed in the current study. Results. A total of 33 PRGs were selected to perform the current study. Of these 33 PRGs, 26 PRGs with upregulation or downregulation in LIHC tissues were identified. We also summarized the related genetic mutation variation landscape. GO and KEGG pathway analysis demonstrated that these 26 PRGs were primarily associated with pyroptosis, positive regulation of interleukin-1 beta production, and NOD-like receptor signaling pathway. An unfavorable OS appeared in LIHC patients with high CASP3, CASP4, CASP6, CASP8, GPX4, GSDMA, GSDME, NLRP3, NLRP7, NOD1, NOD2, PLCG1, and SCAF11 expression and low NLRP6 expression. A prognostic signature constructed by the above 14 prognostic PRGs had moderate to high accuracy to predict LIHC patients’ prognosis. And risk score was correlated with the expression of CASP6, CASP8, GPX4, GSDMA, GSDME, NLRP6, and NOD2. Of these 7 genes, CASP8 was identified as the core gene in PPI network. Moreover, lncRNA MIR17HG/hsa-miRNA-130b-3p/CASP8 regulatory axis in LIHC was also detected. Conclusions. The current study indicated the crucial role of PRGs in the prognostic evaluation of LIHC patients and their correlations with tumor microenvironment in LIHC.

A father’s lifetime experience is a major risk factor for a range of diseases in an individual. The influences of exposure can also be transmitted to offspring. Previous studies demonstrated that plasticisers can damage the male offspring reproductive system, but the link between mammalian research and human non-obstructive azoospermia remains underexplored. Here, we analysed reproduction-related genes from four publicly available single-cell RNA-Seq datasets and RNA-Seq datasets on GEO databases to investigate the correlation between human non-obstructive azoospermia and exposure to plasticisers during pregnancy. The R software was used in statistical analyses. A total of 9 co-upregulated genes and 1 co-downregulated gene were found. The Gene Ontology enrichment analyses were performed using the “clusterProfiler” package. Single-cell analyses were conducted to visualise the gene expression pattern in testis cell subgroups. Immunohistochemical images were used to evaluate the level of protein in testicular organs from The Human Protein Atlas. GSVA results provided further functional annotations. Three signature genes, i.e. COL1A1, CYP17A1 and KIF11, might serve as promising diagnostic biomarkers in non-obstructive azoospermia caused by plasticisers. Our results provided a potential new protocol to evaluate the feasibility of life or clinical intervention in patients with non-obstructive azoospermia. We believe that these observations will improve our understanding of the potential mechanisms of plasticiser contributions to human non-obstructive azoospermia and help identify potential targets for immunotherapy in the future.

A novel and highly-efficient N-heterocycle assembly methodology catalyzed by a cobalt-N,N-bidentate complex via acceptorless dehydrogenation coupling of alcohols and amines has been established.

Two cobalt oxyfluoride antiferromagnets CoMOF5(pyz)(H2O)2 (M = Nb 1, Ta 2; pyz = pyrazine) have been synthesized via conventional hydrothermal methods and characterized by thermogravimetric (TGA) analysis, FTIR spectroscopy, electron spin resonance (ESR), magnetic susceptibility, and magnetization measurements at both static low field and pulsed high field. The single-crystal X-ray diffraction indicates both compounds 1 and 2 are isostructural and crystallize in the monoclinic space group C2/m with a two-dimensional Co2+ triangular lattice in the ab plane, separated by the nonmagnetic MOF5 (M = Nb 1, Ta 2) octahedra along the c-axis with large intertriangular-lattice Co···Co distance. Because of low dimensionality together with frustrated triangular lattice, compounds 1 and 2 exhibit no long-range antiferromagnetic order until ∼3.7 K. Moreover, a spin flop transition is observed in the magnetization curves at 2 K for both compounds, which is further confirmed by ESR spectra. In addition, the ESR spectra suggest the presence of a zero-field spin gap in both compounds. The high field magnetization measured at 2 K saturates at ∼7 T with Ms = 1.55 μB for 1 and 1.71 μB for 2, respectively, after subtracting the Van Vleck paramagnetic contribution, which is usually observed for Co2+ ions with pseudospin spin of 1/2 at low temperature. Powder-averaged magnetic anisotropy of g = 3.10 for 1 (3.42 for 2) and magnetic superexchange interaction J/kB = -3.2 K for 1 (-3.6 K for 2) are obtained.

The iodate anion group has been widely used for design and synthesis of functional materials including nonlinear optical materials but rarely for magnetic materials. Particularly, none of magnetic iodate fluorides has been reported yet. In this work, first, two novel magnetic iodate fluorides MIO

Background: Long noncoding RNAs regulate various biological effects in the progression of cancers. We found that the expression of SNHG1 was significantly up-regulated in bladder cancer after analyzing data obtained from TCGA and GEO. However, the potential role of SNHG1 remains to be investigated in bladder cancer. It was validated that SNHG1 was overexpressed in bladder cancer tissues detected by qRT-PCR and FISH, which was also associated with poor clinical outcome. Additionally, SNHG1 was verified to facilitate tumor proliferation and repress apoptosis in vitro and in vivo. Results: SNHG1 could act as a competitive endogenous RNA and decrease the expression of murine double minute 2 (MDM2) by sponging microRNA-9-3p. Furthermore, MDM2 induced ubiquitination and degradation of PPARγ that contributed to the development of bladder cancer. Conclusions: the study elucidated that SNHG1 played an important role in bladder cancer and provided a potential therapeutic target for bladder cancer.

Background The feasibility and safety of laparoscopic major hepatectomy (LMH) are still uncertain. The purpose of the present study is to compare the short- and long-term outcomes of LMH with those of open major hepatectomy (OMH) for hepatocellular carcinoma (HCC). Method Between January 2012 and December 2018, a total of 26 patients received laparoscopic major hepatectomy in our center. To minimize any confounding factors, a 1:3 case-matched analysis was conducted based on the demographics and extent of liver resection. Data of demographics, perioperative outcomes, and long-term oncologic outcomes were reviewed. Results Intraoperative blood loss (P = 0.007) was significantly lower in the LMH group. In addition, the LMH group exhibited a lower overall complication rate (P = 0.039) and shorter postoperative hospital stay (P = 0.024). However, no statistically significant difference was found between LMH and OMH regarding operation time (P = 0.215) and operative cost (P = 0.860). Two laparoscopic cases were converted to open liver resection. In regard to long-term outcomes, there was no significant difference between LMH and OMH regarding disease-free survival (DFS) (P = 0.079) and overall survival (OS) (P = 0.172). Conclusion LMH can be an effective and safe alternative to OMH for selected patients with liver cancer in short- and long-term outcomes.

Background As a rate‐limiting enzyme of glycolysis, pyruvate kinase muscle isozyme M2 (PKM2) participates in tumor metabolism and growth. The regulatory network of PKM2 in cancer is complex and has not been fully studied in bladder cancer. The 5‐methylcytidine (m5C) modification in PKM2 mRNA might participate in the pathogenesis of bladder cancer and need to be further clarified. This study aimed to investigate the biological function and regulatory mechanism of PKM2 in bladder cancer. Methods The expression of PKM2 and Aly/REF export factor (ALYREF) was measured by Western blotting, qRT‐PCR, and immunohistochemistry. The bioprocesses of bladder cancer cells were demonstrated by a series of experiments in vitro and in vivo. RNA immunoprecipitation, RNA‐sequencing, and dual‐luciferase reporter assays were conducted to explore the potential regulatory mechanisms of PKM2 in bladder cancer. Results In bladder cancer, we first demonstrated that ALYREF stabilized PKM2 mRNA and bound to its m5C sites in 3′‐untranslated regions. Overexpression of ALYREF promoted bladder cancer cell proliferation by PKM2‐mediated glycolysis. Furthermore, high expression of PKM2 and ALYREF predicted poor survival in bladder cancer patients. Finally, we found that hypoxia‐inducible factor‐1alpha (HIF‐1α) indirectly up‐regulated the expression of PKM2 by activating ALYREF in addition to activating its transcription directly. Conclusions The m5C modification in PKM2 mRNA in the HIF‐1α/ALYREF/PKM2 axis may promote the glucose metabolism of bladder cancer, providing a new promising therapeutic target for bladder cancer., Our data suggested that m5C may play a critical role in hypoxia/glycolysis network and targeting HIF‐1α/ALYREF/PKM2 signaling may be a promising therapeutic strategy to treat bladder cancer.

Extracellular matrix (ECM) remodeling is crucial in the regulation of gastric cancer (GC) progression. This work aims to reveal novel posttranslational modifications and their relevant mechanisms in GC. In 3D matrix culture and animal models, it is found that fibrillin 1 (FBN1) expression is increased in advanced GC and has succinylation modification. The succinylation modification of FBN1 blocks its degradation by matrix metalloproteinases (MMPs). The long-term accumulation and deposition of FBN1 enhance tumor progression by activating TGF-β1 and intracellular PI3K/Akt pathway. The FBN1 succinylation site monoclonal antibody can effectively intervene the effect of succinylation modification and inhibit GC progression. FBN1 is specifically upregulated in the progression of GC compared with other tumors. In conclusion, FBN1 is widely present in the form of K672-succinylated modifications in GC. Besides, the succinyl group of FBN1 blocks its binding to MMP2, inhibits its degradation by MMP2, and leads to the accumulation of FBN1, which poses a long-term risk to the poor prognosis of GC.

Background Circular RNAs (circRNAs) have received considerable attention in human cancer research. However, many circRNAs remain to be detected. In our study, we determined novel circRNAs and investigated their effects on bladder cancer (BCa). Methods Microarray dataset GSE92675 was downloaded from Gene Expression Omnibus (GEO). Then, we combined computational biology with quantitative real-time polymerase chain reaction (qRT-PCR) to select related circRNAs in BCa. The selected circRNA–microRNA (miRNA)–messenger RNA (mRNA) regulatory subnetwork was determined by Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Results The regulatory network constructed from the microarray dataset (GSE92675) contained 49 differentially expressed circRNAs (DECs). GO and KEGG analyses showed that the MAPK and PI3K–AKT signaling pathways were statistically significant. On the basis of qRT-PCR and the degree value calculated by the cytoHubba plugin of Cytoscape, hsa_circ_0011385 was finally confirmed. The subnetwork around hsa_circ_0011385 was constructed. In addition, we created a protein–protein interaction (PPI) network composed of 67 nodes and 274 edges after removing independent nodes. GO and KEGG analyses showed that hubgenes were involved in cell cycle activities. Moreover, they could be regulated by miRNAs and play an eventful role in BCa pathogenesis. Conclusions We proposed a novel circRNA–miRNA–mRNA network related to BCa pathogenesis. This network might be a new molecular biomarker and could be used to develop potential treatment strategies for BCa.

Background. Colon adenocarcinoma (COAD) is a malignancy with a high incidence and is associated with poor quality of life. Dysfunction of circadian clock genes and disruption of normal rhythms are associated with the occurrence and progression of many cancer types. However, studies that systematically describe the prognostic value and immune-related functions of circadian clock genes in COAD are lacking. Methods. Genomic data obtained from The Cancer Genome Atlas (TCGA) database was analyzed for expression level, mutation status, potential biological functions, and prognostic performance of core circadian clock genes in COAD. Their correlations with immune infiltration and TMB/MSI score were analyzed by Spearman’s correlation analysis. Pearson’s correlation analysis was performed to analyze their associations with drug sensitivity. Lasso Cox regression analysis was performed to construct a prognosis signature. Moreover, an mRNA-miRNA-lncRNA regulatory axis was also detected by ceRNA network. Results. In COAD tissues, the mRNA levels of CLOCK, CRY1, and NR1D1 were increased, while the mRNA levels of ARNTL, CRY2, PER1, PER3, and RORA were decreased. We also summarized the relative genetic mutation variation landscape. GO and KEGG pathway analyses demonstrated that these circadian clock genes were primarily correlated with the regulation of circadian rhythms and glucocorticoid receptor signaling pathways. COAD patients with high CRY2, NR1D1, and PER2 expression had worse prognosis. A prognostic model constructed based on the 9 core circadian clock genes predicted the COAD patients’ overall survival with medium to high accuracy. A significant association between prognostic circadian clock genes and immune cell infiltration was found. Moreover, the lncRNA KCNQ1OT1/hsa-miRNA-32-5p/PER2/CRY2 regulatory axis in COAD was also detected through a mRNA-miRNA-lncRNA network. Conclusion. Our results identified CRY2, NR1D1, and PER2 as potential prognostic biomarkers for COAD patients and correlated their expression with immune cell infiltration. The lncRNA KCNQ1OT1/hsa-miRNA-32-5p/PER2/CRY2 regulatory axis was detected in COAD and might play a vital role in the occurrence and progression of COAD.

Background. Liver hepatocellular carcinoma (LIHC) ranks the sixth in global cancer incidence with poor prognosis. Necroptosis is a kind of regulated cell death and has been proved to be of significance in cancer occurrence and progression. However, few studies comprehensively discuss the potential applications of necroptosis-related genes (NRGs) in the prognostic evaluation and immunotherapy of LIHC. Methods. The prognostic signature in the present study was built up using LASSO Cox regression analysis. Integrated bioinformatics tools were utilized to explore the potential mRNA-miRNA-lncRNA regulatory axis in LIHC. Furthermore, qRT-PCR method was used to verify the EZH2 expression in LIHC tissues. Furthermore, prognostic performance of EZH2 in LIHC was assessed by Kaplan-Meier method. Results. A total of 14 NRGs were differentially expressed in LIHC tissues. The overall genetic mutation status of these NRGs in LIHC was also shown. NRGs were significantly correlated with programmed necrotic cell death, as well as Toll-like receptor signaling pathway in GO and KEGG pathway analysis. Kaplan-Meier analysis revealed that ALDH2, EZH2, NDRG2, PGAM5, RIPK1, and TRAF2 were related to the prognosis. A prognostic signature was constructed by these six genes and showed medium to high accuracy in the prediction of LIHC patients’ prognosis. Further analysis revealed that NRGs were correlated with pathological stage, immune infiltration, and drug resistance in LIHC. Moreover, we identified a potential lncRNA TUG1/miR-26b-5p/EZH2 regulatory axis in LIHC, which might affect the progression of LIHC. qRT-PCR suggested a higher mRNA level of EZH2 in LIHC tissues. And a poor overall survival rate was detected in LIHC patients with high EZH2 expression. Moreover, EZH2 expression and cancer stage were identified as the independent risk factors affecting LIHC patients’ prognosis. Conclusion. In the present study, we conducted comprehensive bioinformatic analyses and built up a necroptosis-related prognostic signature containing four genes (ALDH2, EZH2, NDRG2, and PGAM5) for patients with LIHC, and this prognostic signature showed a medium to high predictive accuracy. And our study also identified a lncRNA TUG1/miR-26b-5p/EZH2 regulatory axis, which might be of great significance in LIHC progression. In addition, based on the data from our center, the result of qRT-PCR and survival analysis showed a higher mRNA level of EZH2 in LIHC tissues and an unfavorable prognosis in high EZH2 expression group, respectively.

Background This meta-analysis was performed to elucidate the association between the expression of lactate dehydrogenase (LDH) and the prognosis of various malignant neoplasms. Materials and Methods Qualified studies were systematically identified from relevant databases, including PubMed, Cochrane Library, Embase, WanFang, and HowNet. A total of 17 eligible studies with 4,176 patients that complied with the inclusion criteria were enrolled in this meta-analysis. The 17 articles were published from 2011 to 2018. The hazard ratio (HR) and 95% confidence interval (95%CI) were obtained from the selected studies. Results The analysis that included all LDH-related studies showed a significant association with the overall survival (OS) outcome (HR = 1.74, P = 0.001) but exhibited an insignificant association with the disease-free survival (DFS) or recurrence-free survival (RFS) outcome (HR = 1.40, P = 0.072). High lactate dehydrogenase A (LDHA) expression was significantly relevant to inferior OS (HR = 1.88, 95%CI: 1.37-2.59) and DFS or RFS (HR = 1.56, 95%CI: 1.29-1.89). Conclusions High LDH expression and the prognostic outcome of various cancer patients are significantly correlated. High LDHA expression is a promising biomarker for forecasting the survival of patients and the recurrence of different cancers in these patients. Further associative studies are required due to the complex role of LDH genes.

Objective. MicroRNA-124 (miR-124) was revealed to be an attractive prognostic tumour biomarker in recent studies. However, the results remain inconclusive. Hence, this meta-analysis was carried out to clarify the precise predictive value of miR-124. Materials and Methods. Relevant studies were searched in PubMed, EMBASE, Web of Science, and the Cochrane Library up to October 2018. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were extracted from the selected studies. Results. A total of 29 articles investigating the correlation between miR-124 expression and prognosis were initially identified. The pooled HR for overall survival (OS) of high miR-124 expression in multiple cancers was 0.55 (95%CI=0.50–0.61). Disease-free survival (DFS)/progression-free survival (HR=0.48, 95%CI=0.38–0.61) revealed a protective role of increased miR-124 expression. Epigenetic hypermethylation of miR-124 mediated the silencing of its expression, which is correlated significantly with unfavourable survival (OS: HR=2.06, 95%CI=1.68–2.53; DFS/recurrence-free survival: HR=2.77, 95%CI=1.85–4.16). Conclusions. Taken together, our results suggest that miR-124 plays an antioncogenic role in various tumors, such as lung cancer and colorectal cancer. If methylation of miR-124 could be prevented, progression and metastasis would be improved; thus, miR-124 may be a promising biomarker and novel therapeutic target. Further large-scale studies are needed to confirm this possible effect.

Background Liver tumours between the root angle of the middle and right hepatic veins are a special type of liver segment VIII tumour. In this study, we designed a modified median hepatic fissure approach to remove these tumours. The safety and effectiveness of the approach were evaluated. Materials and methods From April 2015 to November 2019, 11 patients with liver tumours between the angle of the middle and right hepatic veins underwent this modified median hepatic fissure approach. We retrospectively analysed data from the perioperative periods of these 11 patients, including general condition, operation time, intraoperative bleeding, and postoperative complications. Disease-free survival and overall survival were assessed. Results Of the 11 patients, 9 patients had primary hepatocellular carcinoma and 2 had colorectal liver metastases. The average intraoperative blood loss was 285 mL (150–450 mL). Two patients developed postoperative bile leakage, but there were no significant serious complications, such as intraabdominal bleeding and liver failure, in any of the patients. The liver function returned to the normal range on the 5th day after surgery. Of the 11 patients, 5 have survived for more than 3 years (45.5%), and 4 have been disease-free for more than 3 years (36.3%). Conclusions For liver tumours between the root angle of the middle and right hepatic veins, the modified median hepatic fissure approach is a safe and feasible method.

Two cobalt oxyfluoride antiferromagnets CoMOF

A new one-dimensional (1D) antiferromagnetic transition metal hybrid fluoride CoF2(H2O)2(pyz) (pyz = pyrazine) together with two new isostructural MF2(H2O)2(pyz) (M = Ni2+, Zn2+) have been successfully synthesized by the hydrothermal method. Their structures were determined by single crystal X-ray diffraction and they all crystallize in the same space group of C2/m. The magnetic property of CoF2(H2O)2(pyz) 1 was measured and discussed. The Weiss constant of -20.6 K indicates dominant antiferromagnetic interaction and the effective magnetic moment of about 5.66 μB suggests large unquenched orbital contribution and anisotropy in 1. The quantum fluctuations in the quasi-1D antiferromagnet of 1 prevent the appearance of long range magnetic order until 2.9 K, suggesting good 1D magnetism.

Circular RNAs (circRNAs) have recently emerged as essential regulators in carcinogenesis and cancer progression. Previous studies have shown that Cdr1as functions as a microRNA (miRNA) sponge in various cancer types. However, the role of Cdr1as in cisplatin chemosensitivity in bladder cancer remains unclear. Here, we used real‐time PCR to examine miRNA and gene expression in bladder cancer tissues and cell lines. The abilities of Cdr1as and its downstream regulatory molecules to induce apoptosis and promote cisplatin‐induced chemosensitivity of bladder cancer cells were determined by flow cytometry and cell counting kit. Bioinformatic analysis was utilized to predict potential miRNA target sites, and biotin‐coupled miRNA capture, biotin‐coupled probe pull‐down assay, and RNA fluorescent in situ hybridization were used to study the interaction between Cdr1as and target miRNAs. Dual‐luciferase reporter assay was also used to validate the target genes of miRNAs. The expression level of apoptotic protease‐activating factor 1 (APAF1) in bladder cancer cells was identified via western blot. Finally, the sensitivity of Cdr1as to cisplatin chemotherapy in nude mice xenografts was evaluated in terms of the size, volume of tumors, and the survival of mice. We report that Cdr1as induced the apoptosis and enhanced the cisplatin chemosensitivity of bladder cancer cells both in vitro and in vivo. Silencing of APAF1 reduced the sensitivity of bladder cancer cells to cisplatin chemotherapy. Furthermore, Cdr1as could directly sponge miR‐1270 and abolish its effect on APAF1. Our study verified that Cdr1as exerts a cisplatin‐chemosensitization effect on bladder cancer cells through the Cdr1as/miR‐1270/APAF1 axis. This newly identified axis may be a potential therapeutic target for bladder cancer patients.

We have identified six new 4d4 and 4d5 compounds with isolated RuCl6 octahedra, with formulas (HMA)4RuCl6·Cl (1; MA = methylamine), (HGly)4RuCl6·Cl (2; gly = glycine), (HGly)3RuCl6·2H2O (3), (NH4)2RuCl6 (4), (HPy)2RuCl6 (5; py = pyridine), and H2(4,4'-bpy)RuCl6 (6; 4,4'-bpy = 4,4'-bipyridine). We find that the temperature-dependent magnetization is well described by single-ion physics in the presence of spin-orbit coupling and negligible superexchange interactions. Further, we find that many compounds in the literature are also well described by single-ion physics, and our results demonstrate the importance of considering single-ion physics when evaluating candidate geometric frustrated magnets in the presence of spin-orbit coupling.

Background: Stomach adenocarcinoma (STAD) is one of the most prevalent malignances and ranks fifth in incidence and third in cancer-related death among all malignances. The prognosis of STAD is poor. The circadian clock is regulated by interlocked transcriptional-translational feedback loops that orchestrate circadian rhythms in some biological processes, including the immune response and metabolism. However, the association between core circadian clock genes and STAD patient prognosis is unclear. Materials and Methods: In our study, bioinformatics methods were performed to explore the expression and prognostic value of core circadian clock genes in STAD and their association with immune infiltration. Results: The mRNA levels of CLOCK, CRY1 and NR1D1 were upregulated, while the mRNA levels of CRY2, PER1, PER3 and RORA were downregulated in STAD tissues compared with normal tissues. Core circadian clock genes exert promoting or inhibiting effects on certain cancer-related hallmark pathways, including the DNA damage response, cell cycle, apoptosis and RAS/MAPK pathways. Moreover, core circadian clock genes were linked to drug sensitivity or drug resistance. Prognosis analysis revealed that high expression of PER1 and NR1D1 was associated with poor overall survival, progression-free survival, and disease-free survival rates in STAD patients. Validation analysis further confirmed our result. Immune infiltration analysis demonstrated that the expression of ICOSLG and CD70 was significantly correlated with immune cells, immune biomarkers, chemokines and their receptors. Conclusions: Our results suggest that NR1D1 and PER1 are prognostic biomarkers and are associated with immune infiltration in STAD.

Background: In spite of advances in development and application of immunosuppressive agents, the long-term survival of grafts still needs to be advanced caused by antibody-mediated rejection (ABMR). Many researchers have paid attention to this area. However, little was known about the role of genes and immune cells in the development of ABMR. Methods: In total, 2533 biopsy cases from four different cohorts were collected. Three Gene Expression Omnibus (GEO) datasets (GSE36059, GSE98320 and GSE12403) were used as the training set, and one GEO dataset and twenty biopsy samples from our center were used for validation. The potential diagnostic prediction value of the signature and immune profiles were also explored. Findings: The LASSO regression model and PPI network were performed to search candidate biomarkers. LAPTM5, GBP2, CCL5 and KLRD1 were obtained as diagnostic biomarkers (AUC = 0·934, 95% CI 0·923-0·943). Immune cell infiltration analysis revealed that γδ T cells which could secrete IL-17A were most related with four biomarkers. The infiltration of γδ T cells and IL-17A were significantly higher in ABMR group than that in ST group. Interpretation: We have identified and established a diagnostic model containing four transcripts as diagnostic biomarkers of ABMR following kidney transplantation. Several types of immune cells were inferred to be involved in the process of ABMR. Among these, γδ T cells were most related with four biomarkers, which may promote ABMR by producing IL-17A. Funding: This work was supported by the National Natural Science Foundation of China [grant numbers 82070769, 81900684, 81870512, 81770751, 81570676, 81470981, 81100532], Project of Jiangsu Province for Important Medical Talent [grant number ZDRCA2016025], the “333 High Level Talents Project” in Jiangsu Province [grant numbers BRA2017532, BRA2016514, BRA2015469], the Standardized Diagnosis and Treatment Research Program of Key Diseases in Jiangsu Province [grant number BE2016791], the Open Project Program of Health Department of Jiangsu Province [grant number JSY-2-2016-099], Jiangsu Province Natural Science Foundation Program [grant number BK20191063]. Declaration of Interest: None to declare. Ethical Approval: This study was approved by the local ethics committee of the First Affiliated Hospital of Nanjing Medical University (2016-SR-029).

A layered iron selenite fluoride CsFe3(SeO3)2F6 1 was hydrothermally synthesized. Single-crystal X-ray diffraction studies show that 1 has a trigonal (P3m1) lattice, where [Fe3(SeO3)2F6]− blocks o...

We hydrothermally synthesized a layered PbFePO4F2 (P21/n). Fe3+ cations (S = 5/2) within the layer are connected via F− and (PO4)3– anions to give a novel (distorted) 1/6th bond depleted triangular lattice. The χ(T) suggests strong antiferromagnetic interactions with a Weiss constant of −125 K, but geometrical frustration and low dimensionality appear to prohibit a long-range order down to 23 K.

Reducing the Schottky barrier height (SBH) of metal-MoS2 interface with no deteriorating the intrinsic properties of MoS2 channel layer is crucial to realize the high-performance MoS2 nanodevice. To realize this expectation, a promising approach is present in this study by doping the boron nitride (BN) buffer layer between metal electrode and MoS2 channel layer. Results demonstrate that no matter the types of concentrations and dopants the intrinsic electronic structure, low electron effective mass of MoS2 channel layer, and the weak Fermi level pinning effects of metal/BN-MoS2 interfaces are preserved and not deteriorated. More importantly, the n- and p-type SBHs of metal/BN-MoS2 interfaces are significantly reduced by the electron-poor and -rich dopants, respectively, when the doped BN buffer layer spreads all over the nanodevice, which is in contrast to the traditional doping rule. Moreover, both the n- and p-type SBHs are further decreased and even eliminated when the concentrations of dopants increase. The n-type SBH of doped Au/BxN-MoS2 interface and the p-type SBH of doped Pt/BNx-MoS2 interface can be reduced to -0.21 and -0.61 eV by doping with high concentrations of Li and O, respectively. This theoretical work provides an effective and promising method to realize high-performance MoS2 nanodevices with negligible SBHs.

A diamond spin chain system, one of the one-dimensional frustrated lattices, is known to exhibit novel properties, but experimental studies have been exclusively confined to materials with a single spin component. Here, we report on the synthesis, structure, and magnetic properties of a new diamond chain compound Cu2FePO4F4(H2O)4 1 composed of mixed-spins of Cu2+ (S = 1/2 × 2) and Fe3+ (S = 5/2). Compound 1 crystallizes in the space group C2/c of the monoclinic crystal system with a = 7.7546(4) A, b = 12.1290(6) A, c = 9.9209(6) A, β = 105.29(1)°, and Z = 4. DC magnetization, Mossbauer spectroscopy, and heat capacity measurements revealed an antiferromagnetic order at 11.3 K with a small ferromagnetic component. It is suggested that ferrimagnetic diamond chains are arranged in an antiferromagnetic fashion (i.e., [...Fe(↑)-2Cu(↓↓)-Fe(↑)...] and [...Fe(↓)-2Cu(↑↑)-Fe(↓)...]) within the ab plane to cancel net magnetization, and the spin orientation of the diamond chains changes alternately along the c axis du...