The study of phase transition of MoS2regulated by H.

The mixed-phase MoS2(1T/2H MoS2) with heterostructure exhibited high catalytic activity. The specific ratios of 1T/2H could exhibit optimal performance in various applications. Therefore, more methods need be developed for synthesizing 1T/2H mixed-phase MoS2. Herein, a viable route was studied for the phase transition of 1T/2H MoS2regulated by H+. Briefly, the commercially available bulk MoS2was used to obtain 1T/2H MoS2via chemical intercalation of Li+. Then the residual Li+around 1T/2H MoS2was replaced by H+in acidic electrolytes, owing to the extremely higher charge-to-volume ratio of H+. Thus, the thermodynamically unstable 1T phase lost the protection of residual Li+and could be re-transforming into the relatively stable 2H phase. The change of the 2H/(2H+1T) ratio was measured using novel extinction spectroscopy, which provides a rapid identification method in comparison with x-ray photoelectron spectroscopy (XPS). The experimental results revealed that the concentration of H+influenced the phase transition velocity of MoS2. In particular, the phase transition from 1T to 2H phase in the H+solution was faster at the beginning, and the higher the H+concentration in an acidic solution, the faster the increase in 2H content. For an instant, the ratio of the 2H phase was increased by 7.08% in an acidic solution (CH+= 2.00 M) after 1 h, which was several times greater than the case in the distilled water. This finding provides a promising method to easily obtain different ratios of 1T/2H MoS2, which is beneficial for further development of catalytic performance especially in energy generation and storage.

High Resolution Electrochemical Imaging for Sulfur Vacancies on 2D Molybdenum Disulfide.

Molybdenum disulfide (MoS2 ) is considered as one of the most promising non-noble-metal catalysts for hydrogen evolution reaction (HER). To achieve practical application, introducing sulfur (S) vacancies on the inert basal plane of MoS2 is a widely accepted strategy to improve its HER activity. However, probing active sites at the nanoscale and quantitatively analyzing the related electrocatalytic activity in electrolyte aqueous solution are still great challenges. In this work, utilizing high-resolution scanning electrochemical microscopy, optimized electrodes and newly designed thermal drift calibration software, the HER activity of the S vacancies on an MoS2 inert surface is in situ imaged with less than 20-nm-radius sensitivity and the HER kinetic data for S vacancies, including Tafel plot and onset potential, are quantitatively measured. Additionally, the stability of S vacancies over the wide range of pH 0-13 is investigated. This study provides a viable strategy for obtaining the catalytic kinetics of nanoscale active sites on structurally complex electrocatalysts and evaluating the stability of defects in different environments for 2D material-based catalysts.

Hsa_circ_0094606 promotes malignant progression of prostate cancer by inducing M2 polarization of macrophages through PRMT1-mediated arginine methylation of ILF3.

Circular RNA (circRNA), a type of noncoding RNAs, has been demonstrated to act vital roles in tumorigenesis and cancer deterioration. Although tumor-associated macrophages are involved in tumor malignancy, the interactions between circRNAs and tumor-associated macrophages in prostate cancer (PCa) remain unclear. In the present study, we found that hsa_circ_0094606 (subsequently named circ_0094606) could promote proliferation, epithelial-mesenchymal transition (EMT) as well as migration of PCa cells through cell viability and migration assays and the determination of EMT markers. Mass spectrometry analysis after RNA pull-down experiment identified that circ_0094606 bound to protein arginine methyltransferase 1 (PRMT1) in PCa cells, and further functional assays revealed that circ_0094606 promoted the malignant progression of PCa by binding to PRMT1. Moreover, co-immunoprecipitation (Co-IP), glutathione-S-transferase (GST) pull-down and immunofluorescence showed that PRMT1 mediated arginine methylation of ILF3 to stabilize the protein. Bioinformatics analysis combined with data from RNA-binding protein immunoprecipitation and RNA pull-down suggested that ILF3 could stabilize IL-8 mRNA, which promoted the M2 polarization in coculture study. Finally, in vivo experiments showed that circ_0094606 subserve PCa growth and promoted the M2 polarization of macrophages through the PRMT1/ILF3/IL-8 regulation pathway, supporting circ_0094606 as a potential novel effective target for PCa treatment.

Salivary microbiome in chronic kidney disease: what is its connection to diabetes, hypertension, and immunity?

BACKGROUND: The association between oral dysbiosis and chronic kidney disease (CKD) has gained increasing attention in recent years. Diabetes and hypertension are the most common conditions in CKD. However, a case-control study with matched confounding variables on the salivary microbiome in CKD and the influence of diabetes and hypertension on the microbiome has never been reported. METHODS: In our study, we compared the salivary microbiome profile between patients with CKD and healthy controls (HC) using 16S ribosomal DNA sequencing and examine its association with diabetes, hypertension, and immunity. RESULTS: We observed that the bacterial community was skewed in the saliva of CKD, with increased Lautropia and Pseudomonas, and decreased Actinomyces, Prevotella, Prevotella 7, and Trichococcus. No difference in the bacterial community between the CKD patients complicated with and without diabetes, and between those with and without hypertension. Prevotella 7 declined in CKD patients with/without hypertension with respect to HC, while Pseudomonas increased in CKD patients with/without hypertension. Pseudomonas was negatively associated with immunoglobin G in CKD patients. Both CKD patients with positive and negative antistreptolysin O had declined Prevotella 7 and Trichococcus compared to HC, whereas increased Pseudomonas. CONCLUSIONS: Our study identifies a distinct bacterial saliva microbiome in CKD patients characterized by alteration in composition. We unravel here that the co-occurrence diseases of diabetes and hypertension are not associated with specific bacterial alterations, suggesting that bacterial dysbiosis in saliva plays a role in renal damage regardless of the occurrence of diabetes and hypertension.

The Bladder Microbiome, Metabolome, Cytokines, and Phenotypes in Patients with Systemic Lupus Erythematosus.

Emerging studies reveal unique bacterial communities in the human bladder, with alteration of composition associated to disease states. Systemic lupus erythematosus (SLE) is a complex autoimmune disease that is characterized by frequent impairment of the kidney. Here, we explored the bladder microbiome, metabolome, and cytokine profiles in SLE patients, as well as correlations between microbiome and metabolome, cytokines, and disease profiles. We recruited a group of 50 SLE patients and 50 individually matched asymptomatic controls. We used transurethral catheterization to collect urine samples, 16S rRNA gene sequencing to profile bladder microbiomes, and liquid chromatography-tandem mass spectrometry to perform untargeted metabolomic profiling. Compared to controls, SLE patients possessed unique bladder microbial communities and increased alpha diversity. These differences were accompanied by differences in urinary metabolomes, cytokines, and patients' disease profiles. The SLE-enriched genera, including Bacteroides, were positively correlated with several SLE-enriched metabolites, including olopatadine. The SLE-depleted genera, such as Pseudomonas, were negatively correlated to SLE-depleted cytokines, including interleukin-8. Alteration of the bladder microbiome was associated with disease profile. For example, the genera Megamonas and Phocaeicola were negatively correlated with serum complement component 3, and Streptococcus was positively correlated with IgG. Our present study reveals associations between the bladder microbiome and the urinary metabolome, cytokines, and disease phenotypes. Our results could help identify biomarkers for SLE. IMPORTANCE Contrary to dogma, the human urinary bladder possesses its own unique bacterial community with alteration of composition associated with disease states. Systemic lupus erythematosus (SLE) is a complex autoimmune disease often characterized by kidney impairment. Here, we explored the bladder microbiome, metabolome, and cytokine profiles in SLE patients, as well as correlations between the microbiome and metabolome, cytokines, and disease profiles. Compared to controls, SLE patients possessed a unique bladder microbial community and elevated alpha diversity. These differences were accompanied by differences in bladder metabolomes, cytokines, and patients' disease profiles. SLE-enriched genera were positively correlated with several SLE-enriched metabolites. SLE-depleted genera were negatively correlated to SLE-depleted cytokines. Alteration of the bladder microbiome was associated with disease profile. Thus, our study reveals associations between the bladder microbiome and the bladder metabolome, cytokines, and disease phenotypes. These results could help identify biomarkers for SLE.

Gut Mycobiome in Patients With Chronic Kidney Disease Was Altered and Associated With Immunological Profiles.

Objectives: Mounting evidence suggests that bacterial dysbiosis and immunity disorder are associated with patients with chronic kidney disease (CKD), but the mycobiome is beginning to gain recognition as a fundamental part of our microbiome. We aim to characterize the profile of the mycobiome in the gut of CKD patients and its correlation to serum immunological profiles. Methods and materials: Ninety-two CKD patients and sex-age-body mass index (BMI)-matched healthy controls (HCs) were recruited. Fresh samples were collected using sterile containers. ITS transcribed spacer ribosomal RNA gene sequencing was performed on the samples. An immunoturbidimetric test was used to assess the serum levels of immunological features. Results: The CKD cohort displayed a different microbial community from that in the HC cohort according to principal coordinate analysis (PCoA). (P=0.001). The comparison of the two cohorts showed that the CKD cohort had significantly higher gut microbial richness and diversity (P<0.05). The CKD cohort had lower abundances of Candida, Bjerkandera, Rhodotorula, and Ganoderma compared to the HC cohort, while it had higher Saccharomyces (P<0.05). However, the microbial community alteration was inconsistent with the severity of kidney damage in patients, as only patients in CKD stage 1~3 had differed microbial community concerning for HCs based on PCoA (P<0.05). The serum concentration of the kappa light chain in CKD patients was positively associated with Saccharomyces, whereas the it was negatively associated with Ganoderma (P<0.05). Conclusions: Not only was gut mycobiome dysbiosis observed in CKD patients, but the dysbiosis was also associated with the immunological disorder. These findings suggest that therapeutic strategies targeting gut mycobiome might be effective.

Alteration of Skin Microbiome in CKD Patients Is Associated With Pruritus and Renal Function.

Dysbiotic gut microbiome in chronic kidney disease (CKD) patients has been extensively explored in recent years. Skin microbiome plays a crucial role in patients with skin diseases or even systemic disorders. Pruritus is caused by the retention of uremic solutes in the skin. Until now, no studies have investigated the role of skin microbiome in CKD and its association with pruritus. Here, we aim to examine the bacterial profile of skin microbiome in CKD and whether it is correlated to pruritus. A total of 105 CKD patients and 38 healthy controls (HC) were recruited. Skin swab was used to collect skin samples at the antecubital fossa of participants. Bacterial 16S rRNA genes V3-V4 region was sequenced on NovaSeq platform. On the day of skin sample collection, renal function was assessed, and numeric rating scale was used to measure pruritus severity. Principal coordinate analysis (PCoA) revealed a significant difference in bacterial composition between the groups of CKD and HC. A depletion of bacterial diversity was observed in CKD patients. Akkermansia, Albimonas, Escherichia-Shigella, etc. showed significant higher abundance in CKD patients, whereas Flavobacterium, Blastomonas, Lautropia, etc. significantly declined in patients. Escherichia-Shigella achieved an acceptable diagnostic biomarker with area under the curve (AUC) value of 0.784 in the receiver operating characteristics (ROC) curve. In addition, CKD patients with pruritus (P-CKD) had a different bacterial community comparing to those without pruritus (non-P-CKD) and HC group. Several bacterial genera showing significant difference between P-CKD and non-P-CKD/HC, such as Oribacterium, significantly declined in P-CKD patients than that in the HC group, and Methylophaga significantly increased in P-CKD patients compared to that in HC subjects. Escherichia-Shigella was positively associated with the levels of pruritus severity, blood urea nitrogen (BUN), uric acid, and urine protein; Oribacterium was negatively associated with pruritus severity, whereas it was positively associated with estimated glomerular filtration rate (eGFR) and 24-h urine volume. The dysbiotic of skin microbiome in CKD patients and its association with pruritus and renal function shed a light on skin probiotics.

Construction of circRNA-based ceRNA network and its prognosis-associated subnet of clear cell renal cell carcinoma.

Circular RNAs (circRNAs) are novel biomarkers of various cancers. CircRNAs can sponge miRNAs and regulate target mRNAs, which was called competing endogenous RNAs (ceRNA). This study was designed to identify circRNAs related to patients with clear cell renal cell carcinoma (ccRCC) and the first to select three independent Gene Expression Omnibus microarrays covering circRNAs, miRNAs, and mRNAs for multiple analyses. The data of clinical cases applied in our study were obtained from The Cancer Genome Atlas. We successfully conducted a circRNA/miRNA/mRNA ceRNA network related to ccRCC patients via R software and Cytoscape including 8 circRNAs, 6 miRNAs, and 49 mRNAs. The prognosis-associated subnet covered 8 circRNAs, 6 miRNAs, and 22 mRNAs. Quantitative real-time PCR was applied to measure our prediction in three renal cell lines and 23 pairs of tissues. Small interfering RNA targeting the back-splice region of hsa_circ_0001167 was further implied to confirm the regulation. Ultimately, hsa_circ_0001167/hsa-miR-595/CCDC8 regulatory axis was identified in this study, which may serve as prognostic indicators. Lower levels of hsa_circ_0001167 and CCDC8 were potentially correlated with worse patient survival.

Theabrownin inhibits the cytoskeleton­dependent cell cycle, migration and invasion of human osteosarcoma cells through NF­κB pathway­related mechanisms.

Considering the high metastatic potential of osteosarcoma, not only pro­apoptosis, but also anti­metastasis is important for anti­osteosarcoma therapy. Previously, the authors reported the pro­apoptotic and tumor­inhibitory effects of theabrownin (TB) on osteosarcoma cells; however, its effects on the metastasis­related migration and invasion of osteosarcoma cells remain unknown. The present study conducted RNA sequencing (RNA­seq) on xenograft zebrafish samples and performed in vitro experiments, including RT­qPCR, cell viability analysis, clone formation assay, cell cycle analysis, immunofluorescence, cell migration assay, cell invasion assay, wound healing assay and western blot (WB) analysis to evaluate the anti­metastatic effects and mechanism of TB against osteosarcoma cells. The RNA­seq data revealed that TB significantly downregulated the expression of genes involved in the microtubule bundle formation of U2OS cells, which was verified by RT­qPCR. The cell viability and clone formation data indicated that TB significantly inhibited U2OS cell viability and colony numbers. The results of cell cycle analysis revealed the blocked cell cycle progression of U2OS by TB. The immunofluorescent data revealed an evident cytoskeleton­inhibitory effect of TB against the microfilament and microtubule formation of U2OS cells. The results of cell migration and invasion demonstrated that TB significantly inhibited U2OS cell migration and invasion. The results of WB analysis revealed that TB significantly regulated key molecules of epithelial­mesenchymal transition [EMT; e.g., E­cadherin, vimentin, Snail­1, Slug and zinc finger E­box­binding homeobox 1 (ZEB­1)] and those of the nuclear factor (NF)­κB pathway (e.g., NF­κB, phospho­IKKα and phospho­IKKß), indicating that NF­κB pathway­related EMT suppression may mediate the mechanisms underlying the anti­migratory and anti­invasive effects of TB against osteosarcoma. To the best of our knowledge, this is the first study on the inhibitory effects and mechanisms of TB on the cytoskeleton­dependent cell cycle, migration and invasion of human osteosarcoma cells. The findings presented herein suggest that TB may be a promising anti­metastatic candidate for anti­osteosarcoma therapy.