GWAS Atlas: an updated knowledgebase integrating more curated associations in plants and animals.

GWAS Atlas (https://ngdc.cncb.ac.cn/gwas/) is a manually curated resource of genome-wide genotype-to-phenotype associations for a wide range of species. Here, we present an updated implementation of GWAS Atlas by curating and incorporating more high-quality associations, with significant improvements and advances over the previous version. Specifically, the current release of GWAS Atlas incorporates a total of 278,109 curated genotype-to-phenotype associations for 1,444 different traits across 15 species (10 plants and 5 animals) from 830 publications and 3,432 studies. A collection of 6,084 lead SNPs of 439 traits and 486 experiment-validated causal variants of 157 traits are newly added. Moreover, 1,056 trait ontology terms are newly defined, resulting in 1,172 and 431 terms for Plant Phenotype and Trait Ontology and Animal Phenotype and Trait Ontology, respectively. Additionally, it is equipped with four online analysis tools and a submission platform, allowing users to perform data analysis and data submission. Collectively, as a core resource in the National Genomics Data Center, GWAS Atlas provides valuable genotype-to-phenotype associations for a diversity of species and thus plays an important role in agronomic trait study and molecular breeding.

RNA methylation patterns, immune characteristics, and autophagy-related mechanisms mediated by N6-methyladenosine (m6A) regulatory factors in venous thromboembolism.

Recent studies have found a link between deep vein thrombosis and inflammatory reactions. N6-methyladenosine (m6A), a crucial element in immunological regulation, is believed to contribute to the pathophysiology of venous thromboembolism (VTE). However, how the m6A-modified immune microenvironment is involved in VTE remains unclear. In the present study, we identified a relationship between VTE and the expression of several m6A regulatory elements by analyzing peripheral blood samples from 177 patients with VTE and 88 healthy controls from public GEO databases GSE19151 and GSE48000. We used machine learning to identify essential genes and constructed a diagnostic model for VTE using multivariate logistic regression. Unsupervised cluster analysis revealed a marked difference between m6A modification patterns in terms of immune cell infiltration, inflammatory reactivity, and autophagy. We identified two m6A-related autophagy genes (i.e., CHMP2B and SIRT1) and the crucial m6A regulator YTHDF3 using bioinformatics. We also examined two potential mechanisms through which YTHDF3 may affect VTE. m6A modification, immunity, and autophagy are closely linked in VTE, offering novel mechanistic and therapeutic insights.

Advances in spatial transcriptomics and its applications in cancer research.

Malignant tumors have increasing morbidity and high mortality, and their occurrence and development is a complicate process. The development of sequencing technologies enabled us to gain a better understanding of the underlying genetic and molecular mechanisms in tumors. In recent years, the spatial transcriptomics sequencing technologies have been developed rapidly and allow the quantification and illustration of gene expression in the spatial context of tissues. Compared with the traditional transcriptomics technologies, spatial transcriptomics technologies not only detect gene expression levels in cells, but also inform the spatial location of genes within tissues, cell composition of biological tissues, and interaction between cells. Here we summarize the development of spatial transcriptomics technologies, spatial transcriptomics tools and its application in cancer research. We also discuss the limitations and challenges of current spatial transcriptomics approaches, as well as future development and prospects.

Root endophyte-mediated alteration in plant H2O2 homeostasis regulates symbiosis outcome and reshapes the rhizosphere microbiota.

Endophytic symbioses between plants and fungi are a dominant feature of many terrestrial ecosystems, yet little is known about the signaling that defines these symbiotic associations. Hydrogen peroxide (H2O2) is recognized as a key signal mediating the plant adaptive response to both biotic and abiotic stresses. However, the role of H2O2 in plant-fungal symbiosis remains elusive. Using a combination of physiological analysis, plant and fungal deletion mutants, and comparative transcriptomics, we reported that various environmental conditions differentially affect the interaction between Arabidopsis and the root endophyte Phomopsis liquidambaris, and link this process to alterations in H2O2 levels and H2O2 fluxes across root tips. We found that enhanced H2O2 efflux leading to a moderate increase in H2O2 levels at the plant-fungal interface is required for maintaining plant-fungal symbiosis. Disturbance of plant H2O2 homeostasis compromises the symbiotic ability of plant roots. Moreover, the fungus-regulated H2O2 dynamics modulate the rhizosphere microbiome by selectively enriching for the phylum Cyanobacteria, with strong antioxidant defenses. Our results demonstrated that the regulation of H2O2 dynamics at the plant-fungal interface affects the symbiotic outcome in response to external conditions and highlight the importance of the root endophyte in reshaping the rhizosphere microbiota.

Integrative Analysis of N6-methyladenosine RNA modifications related genes and their Influences on Immunoreaction or fibrosis in myocardial infarction.

Increasing studies have shown that N6-methyladenosine (m6A) modification plays an important role in cardiovascular diseases. In this study, we systematically investigated the regulatory mode of m6A genes in myocardial infarction (MI) by combining bioinformatics analysis of clinical samples with animal experiments. We utilized gene expression data of clinical samples from public databases to examine the expression of m6A genes in heart tissues and found a large difference between the healthy control group and MI group. Subsequently, we established an MI diagnosis model based on the differentially expressed m6A genes using the random forest method. Next, unsupervised clustering method was used to classify all MI samples into two clusters, and the differences in immune infiltration and gene expression between different clusters were compared. We found LRPPRC to be the predominant gene in m6A clustering, and it was negatively correlated with immunoreaction. Through GO enrichment analysis, we found that most differentially expressed genes between the two clusters were profibrotic. By means of WGCNA, we inferred that GJA4 might be a core molecule in the m6A regulatory network of MI. This study demonstrates that m6A regulators probably affects the immune-inflammatory response and fibrosis to regulate the process of MI, which provides a potential therapeutic target.

Enhanced Tensile Properties, Biostability, and Biocompatibility of Siloxane-Cross-Linked Polyurethane Containing Ordered Hard Segments for Durable Implant Application.

This work developed a series of siloxane-modified polyurethane (PU-Si) containing ordered hard segments by a facile method. The polyaddition between poly(ε-caprolactone) and excess diurethane diisocyanate was carried out to synthesize a polyurethane prepolymer with terminal isocyanate groups, which was then end-capped by 3-aminopropyl triethoxysilane to produce alkoxysilane-terminated polyurethane; the target products of PU-Si were obtained with hydrolysis and the condensation of alkoxysilane groups. The chemical structures were confirmed by FT-IR and XPS, and the effect of the siloxane content or cross-linked degree on the physicochemical properties of the PU-Si films was investigated in detail. The formation of the network structure linked by Si-O-Si bonds and interchain denser hydrogen bonds endowed PU-Si films with fine phase compatibility, low crystallinity, high thermal stability, and excellent tensile properties. Due to the high cross-linked degree and low interfacial energy, the films displayed a high surface water contact angle and low equilibrium water absorption, which resulted in slow hydrolytic degradation rates. Furthermore, the evaluation of protein adsorption and platelet adhesion on the PU-Si film surface presented high resistance to biofouling, indicating superior surface biocompatibility. Consequently, the siloxane-cross-linked polyurethane, which possessed excellent tensile properties, high biostability, and superior biocompatibility, showed great potential to be explored as biomaterials for durable implants.

Identification and development of an independent immune-related genes prognostic model for breast cancer.

BACKGROUND: Breast cancer is one of the main malignant tumors that threaten the lives of women, which has received more and more clinical attention worldwide. There are increasing evidences showing that the immune micro-environment of breast cancer (BC) seriously affects the clinical outcome. This study aims to explore the role of tumor immune genes in the prognosis of BC patients and construct an immune-related genes prognostic index. METHODS: The list of 2498 immune genes was obtained from ImmPort database. In addition, gene expression data and clinical characteristics data of BC patients were also obtained from the TCGA database. The prognostic correlation of the differential genes was analyzed through Survival package. Cox regression analysis was performed to analyze the prognostic effect of immune genes. According to the regression coefficients of prognostic immune genes in regression analysis, an immune risk scores model was established. Gene set enrichment analysis (GSEA) was performed to probe the biological correlation of immune gene scores. P < 0.05 was considered to be statistically significant. RESULTS: In total, 556 immune genes were differentially expressed between normal tissues and BC tissues (p < 0. 05). According to the univariate cox regression analysis, a total of 66 immune genes were statistically significant for survival risk, of which 30 were associated with overall survival (P < 0.05). Finally, a 15 immune genes risk scores model was established. All patients were divided into high- and low-groups. KM survival analysis revealed that high immune risk scores represented worse survival (p < 0.001). ROC curve indicated that the immune genes risk scores model had a good reliability in predicting prognosis (5-year OS, AUC = 0.752). The established risk model showed splendid AUC value in the validation dataset (3-year over survival (OS) AUC = 0.685, 5-year OS AUC = 0.717, P = 0.00048). Moreover, the immune risk signature was proved to be an independent prognostic factor for BC patients. Finally, it was found that 15 immune genes and risk scores had significant clinical correlations, and were involved in a variety of carcinogenic pathways. CONCLUSION: In conclusion, our study provides a new perspective for the expression of immune genes in BC. The constructed model has potential value for the prognostic prediction of BC patients and may provide some references for the clinical precision immunotherapy of patients.

Analysis of the role of the interleukins in colon cancer.

BACKGROUND: The role of interleukin family in colon cancer remained controversial. The purpose of this study was to investigate the association between interleukin family and colon cancer progression through bioinformatics methods and to validate such association in clinical patients. METHODS: A total of 15 differentially expressed interleukins between the colon cancer tissue and normal colon tissue were evaluated from the Cancer Genome Atlas (TCGA) database with R software and only interleukin-7 (IL-7) was significantly associated with survival. The signaling pathway associated with IL-7 was then investigated using gene enrichment analysis. In addition, subsets of TNM were analyzed in detail and univariate and multivariate COX regression analysis were conducted. Finally, we performed western blotting, immunohistochemistry, cell proliferation and cell apoptosis analysis to examine the expression of IL-7 in patients with intestinal cancer. RESULTS: The study demonstrated that IL-7 could inhibit the progression of colon cancer. In addition, IL-7 was found to be associated with overall survival (OS) and pathological stage. Further analysis of IL-7 expression with clinical data indicated that IL-7 was a key factor in inhibiting colon cancer progression. CONCLUSION: IL-7 was a key factor in inhibiting the progression of colon cancer and was closely related to overall survival.

Protective role of N-acetyl-l-tryptophan against hepatic ischemia-reperfusion injury via the RIP2/caspase-1/IL-1ß signaling pathway.

Context: Hepatic ischemia-reperfusion injury (HIRI) is a complex process observed during liver resection and transplantation. N-acetyl-l-tryptophan (l-NAT), an antagonist of neurokinin 1 receptor, has been used for the treatment of nausea and neurodegenerative diseases. Objective: This study investigates the protective effect of l-NAT against HIRI and explores the potential underlying mechanisms. Materials and methods: Adult male Sprague-Dawley (SD) rats were randomly divided into three groups: sham, I/R and I/R + l-NAT. HIRI model was generated by clamping the hepatic artery, portal vein and common bile duct with a microvascular bulldog clamp for 45 min, and then removing the clamp and allowing reperfusion for 6 h. BRL cells were exposed to 200 µM H2O2 with or without 10 µM l-NAT for 6 h. Results: After l-NAT intervention, the structure of hepatic lobules was intact, and no swelling was noted in the cells. Furthermore, cell viability was found to be significantly enhanced when compared with the controls (p < 0.05). The mRNA and protein expression levels of serine-threonine kinase 2 (RIP2) and interleukin-1ß (IL-1ß) were significantly increased in the I/R and H2O2 groups when compared with the controls; however, these levels were significantly decreased after l-NAT intervention. Similarly, IL-1ß activity and caspase-1 activity were significantly decreased in the H2O2 group when compared with the controls, after l-NAT intervention. Conclusions: Our findings indicated that l-NAT may exert a hepatoprotective role in HIRI through inhibiting RIP2/caspase-1/IL-1ß signaling pathway, which can provide evidence for l-NAT to be a potential effective drug against HIRI during clinical practice.

Targeting PRKDC activates the efficacy of antitumor immunity while sensitizing to chemotherapy and targeted therapy in liver hepatocellular carcinoma.

BACKGROUND: Liver hepatocellular carcinoma (LIHC) ranks among the malignancies with the highest mortality rates, primarily due to chemoresistance culminating in treatment failure. Despite its impact, predictive models addressing disease progression, tumor microenvironment, and drug sensitivity remain elusive for LIHC patients. Recognizing the significant influence of various programmed cell death (PCD) modes on tumor evolution, this study investigates PCD genes to elucidate their implications on the prognosis and immune landscape of LIHC. METHODS: To develop the classification and model, we employed a total of 17 genes associated with PCD patterns. To collect data, we acquired gene expression profiles, somatic mutation information, copy number variation data, and corresponding clinical data from the TCGA database, specifically from LIHC patients. Moreover, we obtained spatial transcriptome data and additional bulk datasets from the Gene Expression Omnibus (GEO) database to conduct further analysis. Various experiments were conducted to validate the role of the PCD gene PRKDC in proliferation, migration, invasion, EMT, cell cycle, therapeutic sensitivity, and antitumor immunity. RESULTS: A novel LIHC classification based on these genes divided patients into two clusters, C1 and C2. The C2 cluster exhibited characteristics indicative of poor prognosis and an immune-activated microenvironment. This group showed greater response potential to immune checkpoint inhibitors, displaying higher levels of certain immune signatures and receptors. A programmed cell death index (PCDI) was constructed using 17 selected PCD genes. This index could effectively predict patient prognosis, with higher PCDI indicating poorer survival rates and a more pro-tumor microenvironment. Immune landscapes revealed varying interactions with PCDI, suggesting therapeutic targets and insights into treatment resistance. Moreover, experiments results suggested that PRKDC can augment the invasive nature and growth of malignant cells and it can serve as a potential target for therapy, offering hope for ameliorating the prognosis of LIHC patients. CONCLUSIONS: The study uncovers the insights of programmed cell death in the prognosis and potential therapeutic interventions. And we found that PRKDC can serve as a target for enhancing the efficacy of antitumor immunity while sensitizing chemotherapy and targeted therapy in liver hepatocellular carcinoma.

Depletion of protective microbiota promotes the incidence of fruit disease.

Plant-associated microbiomes play important roles in plant health and productivity. However, despite fruits being directly linked to plant productivity, little is known about the microbiomes of fruits and their potential association with fruit health. Here, by integrating 16S rRNA gene, ITS high-throughput sequencing data, and microbiological culturable approaches, we reported that roots and fruits (pods) of peanut, a typical plant that bears fruits underground, recruit different bacterial and fungal communities independently of cropping conditions and that the incidence of pod disease under monocropping conditions is attributed to the depletion of Bacillus genus and enrichment of Aspergillus genus in geocarposphere. On this basis, we constructed a synthetic community (SynCom) consisting of three Bacillus strains from geocarposphere soil under rotation conditions with high culturable abundance. Comparative transcriptome, microbiome profiling, and plant phytohormone signaling analysis reveal that the SynCom exhibited more effective Aspergillus growth inhibition and pod disease control than individual strain, which was underpinned by a combination of molecular mechanisms related to fungal cell proliferation interference, mycotoxins biosynthesis impairment, and jasmonic acid-mediated plant immunity activation. Overall, our results reveal the filter effect of plant organs on the microbiome and that depletion of key protective microbial community promotes the fruit disease incidence.

Revealing the factors resulting in incomplete recovery of perfluoroalkyl acids (PFAAs) when implementing the adsorbable and extractable organic fluorine methods.

Per- and polyfluoroalkyl substances (PFASs) are environmental contaminants of concern. Techniques that quantify total organic fluorine (TOF) such as the adsorbable organic fluorine (AOF) and extractable organic fluorine (EOF) methods are important for PFAS risk assessments. The objective of this study was to systematically evaluate each step of the AOF (loading, washing, combustion) and EOF (loading, washing, elution, combustion) methods for the recovery of ten ultrashort-, short-, and long-chain unsubstituted perfluoroalkyl acids (PFAAs). We measured the overall recovery of fluoride for each method for each PFAA, and the recovery of each PFAA around the loading, washing, and elution steps. We also measured the combustion efficiency of each PFAA by direct combustion. The overall AOF and EOF recovery ranged from 9.3%-103.3% to 21.0%-108.1%, respectively, with higher recoveries measured for PFAAs with increasing chain length in both methods. The three ultrashort-chain PFAAs (trifluoroacetic acid, perfluoropropionic acid, and perfluoropropanesulfonic acid) exhibited the lowest overall recoveries from 9.3-25.2% for AOF and 21.0-51.5% for EOF. We found that decreases in the overall recovery are the result of losses of ultrashort- and short-chain PFAAs during the washing step and the incomplete mineralization of perfluoroalkyl sulfonic acids during combustion for AOF and incomplete elution of short- and long-chain PFAAs and the loss of ultrashort-chain PFAAs during the washing step for EOF. Our data suggest that the EOF method is more appropriate than the AOF method for measuring TOF in samples containing ultrashort- and short-chain PFAAs and that methodological improvements are possible with a focus on the washing, elution, and combustion steps.

Screening of microalgae species and evaluation of algal-lipid stimulation strategies for biodiesel production.

Microalgae is considered an alternative source for biodiesel production producing renewable, sustainable and carbon-neutral energy. Microalgae property changes among species, which determines the efficiency of biodiesel production. Besides the lipid content evaluation, multi-principles (including high lipid productivity, high biomass yield, pollution resistance and desired fatty acid, etc.) for superior oil-producing species screening was proposed in this review and three microalgae species (Chlorella vulgaris, Scenedesmus obliquus and Mychonastes afer) with high bio-lipid producing prospect were screened out based on big data digging and analysis. The multilateral strategies for algal-lipid stimulating were also compared, among which, nutrient restriction, temperature control, heterotrophy and chemicals addition showed high potential in enhancing lipid accumulation; while electromagnetic field showed little effect. Interestingly, it was found that the lipid accumulation was more sensitive to nitrogen (N)-limitation other than phosphorus (P). Nutrient restriction, salinity stress etc. enhanced lipid accumulation by creating a stressed environment. Hence, optimum conditions (e.g. N:15-35 mg/L and P:4-16 mg/L) should be set to balance the lipid accumulation and biomass growth, and further guarantee the algal-lipid productivity. Otherwise, two-step cultivation could be applied during all the stressed stimulation. Different from lab study, effectiveness, operability and economy should be all considered for stimulation strategy selection. Nutrient restriction, temperature control and heterotrophy were highly feasible after the multidimensional evaluation.

Hyphosphere microorganisms facilitate hyphal spreading and root colonization of plant symbiotic fungus in ammonium-enriched soil.

Anthropogenic nitrogen inputs lead to a high ammonium (NH4+)/nitrate (NO3-) ratio in the soil, which restricts hyphal spreading of soil fungi. Access of symbiotic fungi to roots is a prerequisite for plant-fungal interactions. Hyphosphere bacteria protect fungi from environmental stress, yet the impact of hyphosphere bacteria on adaptation of host fungi to NH4+-enriched conditions remains unclear. By developing soil microcosm assays, we report that a plant-symbiotic fungus, Phomopsis liquidambaris, harbors specific hyphosphere bacteria that facilitate hyphal spreading and assist in the root colonization in NH4+-enriched soil. Genetic manipulation, 16S rRNA gene analysis and coinoculation assays revealed that the genus Enterobacter was enriched in the hyphosphere of NH4+-sensitive wild-type compared to NH4+-preferring nitrite reductase-deficient strain. The representative Enterobacter sp. SZ2-promoted hyphal spreading is only evident in nonsterilized soil. We further identified an increased abundance and diversity of ammonia-oxidizing archaea (AOA) and a synchronously decreased NH4+:NO3- ratio following SZ2 inoculation. Microbial supplementation and inhibitor assays showed that AOA-mediated reduction in NH4+:NO3- ratio is responsible for SZ2-enhanced fungal adaptation to NH4+-enriched conditions. The Ph. liquidambaris-Enterobacter-AOA triple interaction promoted rice growth in NH4+-enriched soil. Our study reveals the essential role of hyphosphere microorganism-based hyphal spreading in plant-fungal symbiosis establishment within nitrogen-affected agroecosystems.

Distinct immune microenvironment of lung adenocarcinoma in never-smokers from smokers.

Lung cancer in never-smokers (LCINS) presents clinicopathological and molecular features distinct from that in smokers. Tumor microenvironment (TME) plays important roles in cancer progression and therapeutic response. To decipher the difference in TME between never-smoker and smoker lung cancers, we conduct single-cell RNA sequencing on 165,753 cells from 22 treatment-naive lung adenocarcinoma (LUAD) patients. We find that the dysfunction of alveolar cells induced by cigarette smoking contributes more to the aggressiveness of smoker LUADs, while the immunosuppressive microenvironment exerts more effects on never-smoker LUADs' aggressiveness. Moreover, the SPP1hi pro macrophage is identified to be another independent source of monocyte-derived macrophage. Importantly, higher expression of immune checkpoint CD47 and lower expression of major histocompatibility complex (MHC)-I in cancer cells of never-smoker LUADs imply that CD47 may be a better immunotherapy target for LCINS. Therefore, this study reveals the difference of tumorigenesis between never-smoker and smoker LUADs and provides a potential immunotherapy strategy for LCINS.

T-Cell Mineralocorticoid Receptor Deficiency Attenuates Pathologic Ventricular Remodelling After Myocardial Infarction.

BACKGROUND: Mineralocorticoid receptor (MR) antagonists have been widely used to treat heart failure (HF). Studies have shown that MR in T cells plays important roles in hypertension and myocardial hypertrophy. However, the function of T-cell MR in myocardial infarction (MI) has not been elucidated. METHODS: In this study, we used T-cell MR knockout (TMRKO) mouse to investigate the effects of T-cell MR deficiency on MI and to explore the underlying mechanisms. Echocardiography and tissue staining were used to assess cardiac function, fibrosis, and myocardial apoptosis after MI. Flow cytometry and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect immune cell infiltration and inflammation. RESULTS: T-cell MR deficiency significantly improved cardiac function, promoted myocardial repair, and inhibited myocardial apoptosis, fibrosis, and inflammation after MI. Luminex assays revealed that TMRKO mice had significantly lower levels of interferon-gamma (IFN-γ) and interleukin-6 (IL-6) in serum and infarcted myocardium than littermate control mice. In cultured splenic T cells, MR deficiency suppressed IL-6 expression, whereas MR overexpression enhanced IL-6 expression. Chromatin immunoprecipitation (ChIP) assay demonstrated that MR bound to the MR response element on the promoter of IL-6 gene. Finally, T-cell MR deficiency significantly suppressed accumulation of macrophages in infarcted myocardium and differentiation of proinflammatory macrophages, thereby alleviating the consequences of MI. CONCLUSIONS: T-cell MR deficiency improved pathologic ventricular remodelling after MI, likely through inhibition of accumulation and differentiation of proinflammatory macrophages. At the molecular level, MR may work through IFN-γ and IL-6 in T cells to exert functions in MI.

Aging-related features predict prognosis and immunotherapy efficacy in hepatocellular carcinoma.

The aging microenvironment serves important roles in cancers. However, most studies focus on circumscribed hot spots such as immunity and metabolism. Thus, it is well ignored that the aging microenvironment contributes to the proliferation of tumor. Herein, we established three prognosis-distinctive aging microenvironment subtypes, including AME1, AME2, and AME3, based on aging-related genes and characterized them with "Immune Exclusion," "Immune Infiltration," and "Immune Intermediate" features separately. AME2-subtype tumors were characterized by specific activation of immune cells and were most likely to be sensitive to immunotherapy. AME1-subtype tumors were characterized by inhibition of immune cells with high proportion of Catenin Beta 1 (CTNNB1) mutation, which was more likely to be insensitive to immunotherapy. Furthermore, we found that CTNNB1 may inhibit the expression of C-C Motif Chemokine Ligand 19 (CCL19), thus restraining immune cells and attenuating the sensitivity to immunotherapy. Finally, we also established a robust aging prognostic model to predict the prognosis of patients with hepatocellular carcinoma. Overall, this research promotes a comprehensive understanding about the aging microenvironment and immunity in hepatocellular carcinoma and may provide potential therapeutic targets for immunotherapy.

Blood Glucose Meter Buying Behavior of Diabetic Patients: Factors Influencing Purchase.

Objective: To understand the blood glucose meter buying behavior of type 2 diabetic patients with poor glycemic control (two or more HbA1c ≥ 8% during visits in one year) and identify factors influencing it. Methods: A survey was conducted among 585 diabetic patients with poor glycemic control who were treated in the outpatient or inpatient clinics of the Department of Endocrinology, Taizhou Hospital, Zhejiang Province from June 2020 to May 2021. The questionnaire collected general information and clinical data, and assessed blood glucose meter buying behavior. Chi-square test was used to compare the essential characteristics and clinical data between buyers and non-buyers of blood glucose meters. Additionally, stepwise logistic regression was used to analyze the factors influencing purchase. Results: Of the 585 questionnaires distributed, 527 (90.09%) valid questionnaires were collected. Of the 527 respondents, 285 (54.08%) had purchased blood glucose meters. Not receiving insulin therapy (OR: 1.77, 95% CI: 1.13-2.77) and unawareness of self-monitoring of blood glucose (OR: 19.46, 95% CI: 12.51-30.26) were risk factors for non-purchase. Conclusion: There is a need to actively increase the purchase of glucose meters among diabetic patients, by educating them about the importance of self-monitoring of blood glucose.

Simultaneously enhanced removal of PAHs and nitrogen driven by Fe2+/Fe3+ cycle in constructed wetland through automatic tidal operation.

The lack of dissolved oxygen and weak substrate removal capacity in constructed wetlands (CW) leads to terrible removal of nitrogen and polycyclic aromatic hydrocarbons (PAHs). In this study, automatic tidal flow CW microcosms were constructed by improving the oxygen environment (siphon and air-duct) and substrate (magnetite) to enhance purification performance and the mechanism was explored. The results showed that the addition of air-duct could improve the oxygen collection and thus improved the NH4+ removal efficiency. Additionally, nitrogen removal was improved greatly due to the simultaneous nitrification and denitrification in aerobic layer with the addition of magnetite. Mass balance indicated the microbial degradation dominated (32-62%) the removal of PAHs. Metagenomic analysis proved the existence of magnetite enhanced the number of PAHs-degrading bacteria, functional groups and metabolic pathways and thus greatly improved the microbial degradation of PAHs. Furthermore, Fe2+/Fe3+ cycle played an important role in promoting the anaerobic degradation of PAHs, which might be served as an electron conduit to establish the direct interspecies electron transfer between iron-reducing bacteria (e.g. Deltaproteobacteria bacterium) and Anaerolineae bacterium to degrade PAHs efficiently. This study provided better understanding of the simultaneous removal of PAHs and nitrogen in tidal flow CWs.

Protective Effect of Anthocyanins on Radiation-induced Hippocampal Injury through Activation of SIRT3.

BACKGROUND: Neuronal cell apoptosis is associated with radiation exposure. It is urgent to study the radiation protection of hippocampal neurons. OBJECTIVE: The purpose of this study was to investigate the protective effect of anthocyanins on radiation and its potential mechanism. MATERIALS AND METHODS: The irradiation was carried out at room temperature with 4-Gy dose. Anthocyanins were intraperitoneally administered to rats prior to radiation exposure. The immunohistology and survival of neurons within the hippocampi, neuroprotective effects of anthocyanin, mean ROS accumulation and SIRT3 expression by Western Blot and qRTPCR were performed. RESULTS: Anthocyanins inhibit radiation-induced apoptosis by activating SIRT3. SIRT3 mRNA increased 24 hours after anthocyanin performed, accompanied by an increase in SIRT3 protein and activity. CONCLUSION: Anthocyanin can effectively resist radiation-induced oxidation and support its role in scavenging cellular reactive oxygen species. The results showed that anthocyanin protected hippocampal neurons from apoptosis through the activity of SIRT3 after irradiation.