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Abstract Plants have evolved a complex and elaborate signaling network to respond appropriately to the pathogen invasion by regulating expression of defensive genes through certain transcription factors. The APETALA2/ethylene response factor (AP2/ERF) family members have been determined as key regulators in growth, development, and stress responses in plants. Moreover, a growing body of evidence has demonstrated the critical roles of AP2/ERFs in plant disease resistance. In this review, we describe recent advances for the function of AP2/ERFs in defense responses against microbial pathogens. We summarize that AP2/ERFs are involved in plant disease resistance by acting downstream of mitogen activated protein kinase (MAPK) cascades, and regulating expression of genes associated with hormonal signaling pathways, biosynthesis of secondary metabolites, and formation of physical barriers in an MAPK-dependent or -independent manner. The present review provides a multidimensional perspective on the functions of AP2/ERFs in plant disease resistance, which will facilitate the understanding and future investigation on the roles of AP2/ERFs in plant immunity.

Abstract Most of the information obtained by humans comes from colour images. However, salt‐and‐pepper noise (SPN) during signal acquisition, encoding, transmission, and decoding easily interferes with the quality of colour images. Most existing SPN denoising methods decompose a colour image into three independent matrices according to the colour channel and then recover each channel signal independently, ignoring the strong data correlation between channels. In addition, most existing SPN denoising methods apply only a single model‐driven or data‐driven approach and fail to take the advantages of their combination fully. Therefore, we first regard a colour image contaminated by SPN as the sum of an SPN tensor and a tensor with missing data. In this manner, we transform the denoising problem into a low‐rank tensor reconstruction problem. We then introduce a model‐driven‐based parallel matrix factorization low‐rank tensor reconstruction algorithm and a data‐driven‐based FFDNet denoising network to restore the colour image better. The proposed method not only enhances the similarity of the colour image channels but also explores the deep prior of the colour image to capture the image details. Finally, the proposed method is compared with some advanced denoising methods. The results show that the proposed method achieves a competitive denoising performance.

Background: Currently dual-energy X-ray absorptiometry (DXA) and phantom-based quantitative computed tomography (PB-QCT) have been utilized to diagnose osteoporosis widely in clinical practice. While traditional phantom-less QCT (PL-QCT) is limited by the precision of manual calibration using body tissues, such as fat and muscle. Objective: The aim of this study is to validate the accuracy and precision of one newly-developed automatic PL-QCT system to measure spinal bone mineral density (BMD) and diagnose osteoporosis. Methods: A total of 36 patients were enrolled for comparison of BMD measurement between DXA and QCT. CT images of 63 patients were analyzed by both PB-QCT and newly developed automatic PL-QCT system, then the BMD results generated by the automatic PL-QCT were utilized to diagnose osteoporosis. The diagnostic outcomes were compared with that of DXA and PB-QCT to assess the performance of the new system. Results: BMD test results showed that the automatic PL-QCT system had higher precision than previous studies performed with QCT, while maintaining similar capability to diagnose osteoporosis as DXA and PB-QCT. Area under curve (AUC) result of PL-QCT was larger than 0.8 for predicting spine DXA T-score in receiver operating characteristic (ROC) analysis. Pearson correlation analysis (r ​= ​0.99) showed strong linear correlation and Bland-Altman analysis (bias ​= ​3.0mg/cc) indicated little difference between the two methods. The precision result (CV ​= ​0.89%) represented good reproducibility of the new system. Conclusion: The traditional PL-QCT system has relatively low reproducibility due to the manual selection of the region of interest (ROI) of body tissues. Automatic selection of ROI in this new system makes the BMD testing more convenient and improves precision significantly. Compared with traditional BMD measurement methods, the automatic PL-QCT system had higher precision in accurate diagnosis of osteoporosis with great potential in translational research and wide clinical application. Translational potential statement: With high accuracy and precision, the automatic PL-QCT system could serve as an opportunistic screening tool for osteoporosis patients in the future. It could also facilitate related researches by providing more reliable data collection, both retrospectively and longitudinally.

NanoSIMS has been widely used for in-situ sulfur isotopic analysis (32S and 34S) of micron-sized grains or complex zoning in sulfide in terrestrial and extraterrestrial samples. However, the conventional spot mode analysis is restricted by depth effects at the spatial resolution < 0.5–1 μm. Thus sufficient signal amount cannot be achieved due to limited analytical depths, resulting in low analytical precision (1.5‰). Here we report a new method that simultaneously improves spatial resolution and precision of sulfur isotopic analysis based on the NanoSIMS imaging mode. This method uses a long acquisition time (e.g., 3 h) for each analytical area to obtain sufficient signal amount, rastered with the Cs+ primary beam of ∼100 nm in diameter. Due to the high acquisition time, primary ion beam (FCP) intensity drifting and quasi-simultaneous arrival (QSA) significantly affects the sulfur isotopic measurement of secondary ion images. Therefore, the interpolation correction was used to eliminate the effect of FCP intensity variation, and the coefficients for the QSA correction were determined with sulfide isotopic standards. Then, the sulfur isotopic composition was acquired by the segmentation and calculation of the calibrated isotopic images. The optimal spatial resolution of ∼ 100 nm (Sampling volume of 5 nm × 1.5 μm2) for sulfur isotopic analysis can be implemented with an analytical precision of ∼1‰ (1SD). Our study demonstrates that imaging analysis is superior to spot-mode analysis in irregular analytical areas where relatively high spatial resolution and precision are required and may be widely applied to other isotopic analyses.

Abstract Background To identify candidate key genes and pathways related to resting mast cells in meningioma and the underlying molecular mechanisms of meningioma. Methods Gene expression profiles of the used microarray datasets were obtained from the Gene Expression Omnibus (GEO) database. GO and KEGG pathway enrichments of DEGs were analyzed using the ClusterProfiler package in R. The protein-protein interaction network (PPI), and TF-miRNA- mRNA co-expression networks were constructed. Further, the difference in immune infiltration was investigated using the CIBERSORT algorithm. Results A total of 1499 DEGs were identified between tumor and normal controls. The analysis of the immune cell infiltration landscape showed that the probability of distribution of memory B cells, regulatory T cells (Tregs), and resting mast cells in tumor samples were significantly higher than those in the controls. Moreover, through WGCNA analysis, the module related to resting mast cells contained 158 DEGs, and KEGG pathway analysis revealed that the DEGs were dominant in the TNF signaling pathway, cytokine-cytokine receptor interaction, and IL-17 signaling pathway. Survival analysis of hub genes related to resting mast cells showed that the risk model was constructed based on 9 key genes. The TF-miRNA- mRNA co-regulation network, including MYC-miR-145-5p, TNFAIP3-miR-29c-3p, and TNFAIP3-hsa-miR-335-3p, were obtained. Further, 36 nodes and 197 interactions in the PPI network were identified. Conclusion The results of this study revealed candidate key genes, miRNAs, and pathways related to resting mast cells involved in meningioma development, providing potential therapeutic targets for meningioma treatment.

Abstract Background and aims Glioblastoma (GBM) is a common and aggressive primary brain tumor, and the prognosis for GBM patients remains poor. This study aimed to identify the key genes associated with the development of GBM and provide new diagnostic and therapies for GBM. Methods Three microarray datasets (GSE111260, GSE103227, and GSE104267) were selected from Gene Expression Omnibus (GEO) database for integrated analysis. The differential expressed genes (DEGs) between GBM and normal tissues were identified. Then, prognosis-related DEGs were screened by survival analysis, followed by functional enrichment analysis. The protein–protein interaction (PPI) network was constructed to explore the hub genes associated with GBM. The mRNA and protein expression levels of hub genes were respectively validated in silico using The Cancer Genome Atlas (TCGA) and Human Protein Atlas (HPA) databases. Subsequently, the small molecule drugs of GBM were predicted by using Connectivity Map (CMAP) database. Results A total of 78 prognosis-related DEGs were identified, of which10 hub genes with higher degree were obtained by PPI analysis. The mRNA expression and protein expression levels of CETN2, MKI67, ARL13B, and SETDB1 were overexpressed in GBM tissues, while the expression levels of CALN1, ELAVL3, ADCY3, SYN2, SLC12A5, and SOD1 were down-regulated in GBM tissues. Additionally, these genes were significantly associated with the prognosis of GBM. We eventually predicted the 10 most vital small molecule drugs, which potentially imitate or reverse GBM carcinogenic status. Cycloserine and 11-deoxy-16,16-dimethylprostaglandin E2 might be considered as potential therapeutic drugs of GBM. Conclusions Our study provided 10 key genes for diagnosis, prognosis, and therapy for GBM. These findings might contribute to a better comprehension of molecular mechanisms of GBM development, and provide new perspective for further GBM research. However, specific regulatory mechanism of these genes needed further elaboration.

Abstract Background This study was intended to investigate the genomic landscape of the immune microenvironments of brain metastases in breast cancer. Methods Three gene expression profile datasets (GSE76714, GSE125989 and GSE43837) of breast cancer with brain metastases were downloaded from Gene Expression Omnibus (GEO) database. After differential expression analysis, the tumor immune microenvironment and immune cell infiltration were analyzed. Then immune-related genes were identified, followed by function analysis, transcription factor (TF)-miRNA–mRNA co-regulatory network analysis, and survival analysis of metastatic recurrence. Results The present results showed that the tumor immune microenvironment in brain metastases was immunosuppressed compared with primary caner. Compared with primary cancer samples, the infiltration ratio of plasma cells in brain metastases samples was significantly higher, while the infiltration ratio of macrophages M2 cells in brain metastases samples was significantly lower. Total 42 immune-related genes were identified, such as THY1 and NEU2. CD1B, THY1 and DOCK2 were found to be implicated in the metastatic recurrence of breast cancer. Conclusions Targeting macrophages or plasma cells may be new strategies for immunotherapy of breast cancer with brain metastases. THY1 and NEU2 may be potential therapeutic targets for breast cancer with brain metastases, and THY1, CD1B and DOCK2 may serve as potential prognostic markers for improvement of brain metastases survival.

Polymetallic complexes with covalently bridged metal centers that interact magnetically are important in the molecular magnetism field, with binuclear compounds receiving special attention because they represent the simplest type of multinuclear species with covalently bridged metal centers. Herein, we report the synthesis and properties of two new binuclear FeII complexes, namely, {[Fe(abpt-TPE)(NCS)2]2(bpym)}·2MeOH·2MeCN (1) and {[Fe(abpt-TPE)(NCS)2]2(bpym)}·2CH2Cl2 (2) (bpym = 2,2′-bipyrimidine). The crystal structure is analyzed at different temperatures, and its properties are analyzed by variable-temperature magnetic susceptibility and variable-temperature fluorescence emission spectroscopy tests. Variable-temperature magnetic susceptibility measurements of two binuclear compounds show different types of magnetic behavior. Complex 1 exhibits two-step spin transition behavior with an intermediate state near 150 K (Tc1 = 191 K, Tc2 = 111 K); 1 undergoes an [LS–LS] ↔ [LS–HS] ↔ [HS–HS] spin transition during thermal induction. On the other hand, complex 2 exhibits intramolecular antiferromagnetic coupling, with J = −0.47 cm−1. The analysis of correlations between the structural characteristics and different types of magnetic behaviors for two binuclear complexes, revealed that the different magnetic behaviors shown by the two complexes are attributable to different degrees of [FeN6] octahedral distortion caused by different lattice solvents, ligand strain and crystal stacking.

To eliminate the influence of spacesuits’ joint resistant torque on the operation of astronauts, an active spacesuit scheme based on the joint-assisted exoskeleton technology is proposed. Firstly, we develop a prototype of the upper limb exoskeleton robot and theoretically analyse the prototype to match astronauts’ motion behavior. Then, the Jiles-Atherton model is adopted to describe the hysteretic characteristic of joint resistant torque. Considering the parameter identification effects in the Jiles-Atherton model and the local optimum problem of the basic PSO (particle swarm optimization) algorithm, a SA- (simulated annealing-) PSO algorithm is proposed to identify the Jiles-Atherton model parameters. Compared with the modified PSO algorithm, the convergence rate of the designed SA-PSO algorithm is advanced by 6.25% and 20.29%, and the fitting accuracy is improved by 14.45% and 46.5% for upper limb joint model. Simulation results show that the identified J-A model can show good agreements with the measured experimental data and well predict the unknown joint resistance torque.

Summary: The Povarov reaction, a formal [4 + 2] cycloaddition between N-aryl imines and electron-rich dienophiles, has been defined as an efficient method to approach tetrahydroquinolines and has been well established in the past decades. In general, electron-rich heterosubstituted alkenes have served as the most popular dienophiles to achieve the exclusive regioselectivity. However, the use of Lewis acids and Brønsted acids as catalysts is required in these transformations, and, to our knowledge, the Povarov reaction of electron-rich heterosubstituted alkynes has not been reported. Here, we disclose a catalyst-free Povarov reaction of formyl-ynamides with anilines for the rapid and practical synthesis of a diverse range of valuable quindolines, which not only represents the first Povarov reaction of ynamides to the best of our knowledge but also constitutes a very rare example of a catalyst-free ynamide cyclization reaction. This formal [1 + 2 + 3] annulation shows a reversed regioselectivity compared with the previous protocols.

Objective: This study aimed to investigate the molecular mechanism of tumor necrosis factor (TNF) superfamily-related genes and potential therapeutic drugs for glioblastoma multiforme (GBM) patients based on transcriptome and epigenome.Methods: Gene expression data, corresponding clinical data, and methylation data of GBM samples and normal samples in the TCGA-GBM and GTEx datasets were downloaded. The TNF-related genes were obtained, respectively, from two groups in the TCGA dataset. Then, the TNF-related differentially expressed genes (DEGs) were investigated between two groups, followed by enrichment analysis. Moreover, TNF superfamily-related gene expression and upstream methylation regulation were investigated to explore candidate genes and the prognostic model. Finally, the protein expression level of candidate genes was performed, followed by drug prediction analysis.Results: A total of 41 DEGs including 4 ligands, 18 receptors, and 19 downstream signaling molecules were revealed between two groups. These DEGs were mainly enriched in pathways like TNF signaling and functions like response to TNF. A total of 5 methylation site-regulated prognosis-related genes including TNF Receptor Superfamily Member (TNFRSF) 12A, TNFRSF11B, and CD40 were explored. The prognosis model constructed by 5 genes showed a well-prediction effect on the current dataset and verification dataset. Finally, drug prediction analysis showed that zoledronic acid (ZA)-TNFRSF11B was the unique drug–gene relation in both two databases.Conclusion: Methylation-driven gene TNFRSF12A might participate in the development of GBM via response to the TNF biological process and TNF signaling pathway and significantly associated with prognosis. ZA that targets TNFRSF11B expression might be a potential effective drug for clinical treatment of GBM.

Aims: We evaluated the synergistic effect of lipoprotein-associated phospholipase A2 (Lp-PLA2) in association with classical risk factors in predicting coronary heart disease (CHD) and demonstrated the diagnostic value of Lp-PLA2 for predicting coronary stenotic lesions in subjects with CHD. Methods: Blood samples were acquired from 911 consecutive adult subjects (662 males and 249 females) from 11 ethnic groups. Lp-PLA2 plasma levels were detected using a commercially available turbidimetric immunoassay (TIA). CHD in patients was confirmed using coronary angiography, and the severity of coronary atherosclerosis was assessed using the Gensini scoring system. Results: A binary logistic regression was performed to analyse the relationships between Lp-PLA2 and other risk factors. A multivariate logistic regression analysis revealed that Lp-PLA2 levels were significantly associated with CHD (OR, 1.882; 95% CI, 1.369-2.587, p=0.000).The area under the receiver operating characteristic curve for Lp-PLA2 was 0.589 (95%CI, 0.549-0.629, p=0.000).The synergism between Lp-PLA2 and other risk factors was also investigated. The proportion of CHD attributable to the interaction between Lp-PLA2 and age was as high as 64%. Conclusions: Lp-PLA2 levels in human plasma were positively associated with the severity of CHD, and there was a clear positive interaction between Lp-PLA2 and classical risk factors in predicting CHD.

The osteogenic potential of mesenchymal stromal cells (MSCs) varies among different tissue sources. Strontium enhances the osteogenic differentiation of bone marrow-derived MSCs (BM-MSCs), but whether it exerts similar effects on placental decidual basalis-derived MSCs (PDB-MSCs) remains unknown. Here, we compared the influence of strontium on the proliferation and osteogenic differentiation of human PDB- and BM-MSCs in vitro. We found that 1 mM and 10 mM strontium, but not 0.1 mM strontium, evidently promoted the proliferation of human PDB- and BM-MSCs. These doses of strontium showed a comparable alkaline phosphatase activity in both cell types, but their osteogenic gene expressions were promoted in a dose-dependent manner. Strontium at doses of 0.1 mM and 1 mM elevated several osteogenic gene expressions of PDB-MSCs, but not those of BM-MSCs at an early stage. Nevertheless, they failed to enhance the mineralization of either cell type. By contrast, 10 mM strontium facilitated the osteogenic gene expression as well as the mineralization of human PDB- and BM-MSCs. Collectively, this study demonstrated that human PDB- and BM-MSCs shared a great similarity in response to strontium, which promoted their proliferation and osteogenic differentiation in a dose-dependent manner.

Background Treatments that target cancer stem cells play an important role in the controlling and eliminating of tumor initiation as well as in development, progression, and chemotherapy/radiotherapy resistance. In our previous study, we cultured and harvested human laryngeal cancer stem cells (CSCs) and applied microRNA biochips to screen differentially expressed miRNAs that were related to radiation tolerance in irradiated human laryngeal CSCs. According to the predicted genes and pathways of differential miRNAs target, down-regulated expression of hsa-miR-138-2-3p under radiation was thought to play a key role in enhancing the radio-sensitivity in human laryngeal squamous cancer stem cells. Method To investigate the radiational enhancement of hsa-miR-138-2-3p, we transfected hsa-miR-138-2-3p mimics that were synthesized based on the sequences of hsa-miR-138-2-3p in vitrointo human laryngeal CSCs (Hep-2, M2e, and TU212 cell lines) to make hsa-miR-138-2-3p overexpressed, and the tumorous specialities of CSCs, like cell proliferation, invasion, apoptosis, cell cycle arrest, and DNA damage were evaluated by CCK-8 assay, clone formation assay, invasion assay, flow cytometry, and comet assay. Furthermore, we explored the signal transduction pathways that regulated the cancer stem cell initiation, development, invasion, apoptosis and cell cycle arrest, which were controlled by hsa-miR-138-2-3p. Result Overexpressed hsa-miR-138-2-3p played a key role in many anti-cancer biological processes in human laryngeal CSCs: (1) it decreased laryngeal CSCs proliferation and invasion in response to radiotherapy; (2) it increased the proportion of early and late apoptosis in laryngeal CSCs after radiation, raised G1 phase arrest in laryngeal CSCs after radiation, and decreased the proportion of S stage cells of cell cycle that were related to radio-resistance in laryngeal CSCs; (3) it down-regulated the expression of β-catenin in Wnt signal pathway that was related to the tolerance of laryngeal CSCs to radiotherapy; (4) it down-regulated the expression of YAP1 in Hippo signal pathway that regulated cell proliferation, invasion and apoptosis; (5) it up-regulated the expression of p38 and JNK1 in MAPK signal pathway that was concerned to radio-sensitivity. Conclusion In the present study, it was found that hsa-miR-138-2-3p regulated the Wnt/β-catenin pathways, the Hippo/YAP1 pathways, and the MAPK/p38/JNK1 pathways that were involved in cell proliferation, invasion, apoptosis, cell cycle arrest, radio-resistance and radio-sensitivity in laryngeal CSCs. These results will be useful for a better understanding of the cell biology of hsa-miR-138-2-3p in laryngeal CSCs, and for serving hsa-miR-138-2-3p as a promising biomarker and as a target for diagnosis and for novel anti-cancer therapies for laryngeal cancers.

Objective: The purpose of this study was to investigate the influence of weather on the occurrence of acute ST-elevation myocardial infarction in Chinese subjects. Methods: Weather and climate data, as well as the occurrence of STEMI, were monitored at 2 am, 8 am, 2 pm, and 8 pm between 2003 and 2010. Generalized additive Poisson models were utilized to plot the numbers of patients with STEMI within 6 hour intervals against climatological variations, after accounting for the effects of the hour and season. Results: The inclusion of meteorological conditions, including observed atmospheric pressure (hPa, hectopascal) variations during the previous three hours and temperature (°C, degrees Celsius), significantly affected the occurrence of STEMI, as measured every six hours. Compared with the 50th percentile of atmospheric pressure variations, the RRs (95% CI) for the first percentile, 10th percentile, 25th percentile, 75th percentile, 90th percentile, and 99th percentile of atmospheric pressure variation over lag 0 were 1.66 (1.36∼2.03), 1.47 (1.30∼1.67), 1.22 (1.12∼1.33), 1.16 (1.07∼1.25), 1.27 (1.13∼1.43), and 1.16 (0.92∼1.46), respectively. Compared to the 50th percentile of temperature, the RRs (95% CI) for the first percentile, 10th percentile, 25th percentile, 75th percentile, 90th percentile, and 99th percentile of temperature over lag 0 were 0.58 (0.40∼0.83), 0.60 (0.46∼0.78), 0.69 (0.57∼0.83), 1.33 (1.14∼1.56), 1.39 (1.13∼1.71), and 1.17 (0.84∼1.63), respectively. Conclusions: Based on the eight-year, single-center study, significant relationships were observed among the occurrence of STEMI and atmospheric pressure variations during the previous three hours and temperature after account for long-term time trends.

Objective: To develop a risk score by incorporating Hemoglobin A1c(HbA1c) with traditional risk factors for the prediction of coronary artery disease (CAD) in Chinese subjects. Methods: A total of 196 consecutive subjects (131 males and 65 females) aged 38-89 years who underwent coronary angiography were enrolled in this study. HbA1c risk score sheets for the prediction of CAD were developed using age, gender and HbA1c. A receiver-operating characteristic curve analysis was used to determine the optimum cut-off levels of the HbA1c risk score for predicting CAD. Results: In the ROC curve analysis, the optimal cut-off value of the HbA1c score for predicting CAD was 5.1, with a sensitivity of 72.0% and a specificity of 75.5% (area under the curve 0.781, 95% confidence interval 0.709 to 0.854, p=0.000). Conclusions: The HbA1c score system is a simple and feasible method that can be used for the prediction of CAD. Large-scale studies are needed to further substantiate these results.

Fank1 is exclusively expressed in the testis from the meiosis phase to the haploid phase of spermatogenesis. In this study, we examined the function of Fank1 by establishing a Fank1-knockdown transgenic mouse model. The apoptotic statuses of the testes of the transgenic mice were tested using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. The FANK1 consensus DNA-binding sequence was identified using cyclic amplification of sequence target (CAST) analysis. Differentially expressed genes were examined using microarray analysis. A reduction in sperm number and an increase in apoptotic spermatocytes were observed in Fank1-knockdown mice, and the apoptotic cells were found to be primarily spermatogonia and spermatocytes. The CAST results demonstrated that the consensus DNA-binding sequence was AAAAAG, in which the percentage occurrence of each base at each position ranged from 55 to 86%. This sequence was present in the promoter regions of 10 differentially expressed genes that were examined using microarray analysis. In total, 17 genes were differentially expressed with changes in their expression levels greater than twofold. The abnormal expression of Fank1 target genes that were regulated directly or indirectly by Fank1 reduced the number of sperm in the knockdown mice. Thus, FANK1 may play a pivotal role in spermatogenesis as a transcription factor.

In the title compound, C12H6N2O2·C2H5OH, the molecule of the 1,10-phenanthroline-5,6-dione is approximately planar, with a maximum deviation of 0.051 (1) Å. In the crystal, molecules are linked by O—H...N and weak C—H...O hydrogen bonds, forming supramolecular chains propagating along [110]. π–π stacking interactions are observed between the pyridine rings of neighbouring chains, the centroid–centroid separations being 3.6226 (11) and 3.7543 (11) Å.

In the title complex, [Fe(NCS)2(C18H18N4)], the FeII cation is chelated by a tris(2-pyridylmethyl)amine ligand and coordinated by two thiocyanate anions in a distorted N6 octahedral geometry. In the crystal, weak C—H...S hydrogen bonds and π–π stacking interactions between parallel pyridine rings of adjacent molecules [centroid–centroid distance = 3.653 (3) Å] link the molecules into a two-dimensional supramolecular architecture. The structure contains voids of 124 (9) Å3, which are free of solvent molecules.

OBJECTIVE: to explore the impact of admission serum creatinine concentration on the in-hospital mortality and its interaction with age and gender in patients with acute ST-segment elevation myocardial infarction (STEMI) in China. METHODS: 1424 acute STEMI patients were enrolled in the study. Anthropometric and laboratory measurements were collected from every patient. A Cox proportional hazards regression model was used to determine the relationships between the admission serum creatinine level (Cr level), age, sex and the in-hospital mortality. A crossover analysis and a stratified analysis were used to determine the combined impact of Cr levels with age and gender. RESULTS: Female (HR 1.687, 95%CI 1.051 ∼ 2.708), elevated Cr level (HR 5.922, 95%CI 3.780 ∼ 9,279) and old age (1.692, 95%CI 1.402 ∼ 2.403) were associated with a high risk of death respectively. After adjusting for other confounders, the renal dysfunction was still independently associated with a higher risk of death (HR 2.48, 95% CI 1.32 ∼ 4.63), while female gender (HR 1.19, 95%CI 0.62 ∼ 2.29) and old age (HR 1.77, 95%CI 0.92 ∼ 3.37) was not. In addition, crossover analysis revealed synergistic effects between elevated Cr level and female gender (SI = 3.01, SIM = 2.10, AP = 0.55). Stratified analysis showed that the impact of renal dysfunction on in-hospital mortality was more pronounced in patients

In the title centrosymmetric dinuclear EuIII complex, [Eu2(CH3COO)6(C12H8N2)2], each EuIII cation is coordinated by seven O atoms from five acetate anions and two N atoms from one phenanthroline ligand in a distorted tricapped trigonal-prismatic geometry. Four acetate anions bridge two EuIII cations to form the dinuclear complex, with an Eu...Eu distance of 3.9409 (8) Å. Weak intermolecular C—H...O hydrogen bonding is present in the crystal structure.

In the the title compound, C19H18BrNO3, the furanone ring is almost planar [maximum atomic deviation = 0.019 (3) Å] and is nearly perpendicular to the two phenyl rings, making dihedral angles of 88.96 (17) and 87.71 (17)°. Intermolecular C—H...O hydrogen bonding is present in the crystal structure.

In the title compound, {[AgSm(C6H4NO2)2(C2O4)]·H2O}n, the asymmetric unit contains one SmIII ion, one AgI ion, two unique isonicotinate (ina) ligands, two half oxalate (ox) ligands (one on an inversion centre, the other on a twofold axis) and one uncoordinated water molecule. The central SmIII ion is nine-coordinated by four O-donor atoms from separate bidentate bridging ox ligands and five O-donor atoms from the two ina ligands (both bidentate) and a symmetry-related ina ligand [Sm—O = 2.389 (4)–2.791 (4) Å], giving a distorted monocapped square antiprismatic geometry. The AgI ion is three-coordinated in a T-shaped geometry involving two ina N-donor atoms [Ag—N = 2.181 (6) and 2.185 (5) Å] and a bridging oxalate O-donor atom [Ag—O = 2.620 (4) Å]. The three-dimensional heterometallic Sm—Ag coordination polymer, having a unique (3,4,6)-connected five-nodal net topology, is constructed from two-dimensional samarium–oxalate layers and pillared Ag(ina)2 subunits. Intermolecular water–carboxylate O—H...O hydrogen-bonding interactions are also present.

The title compound, C19H30BrNO5, was obtained via a tandem asymmetric Michael addition–elimination reaction of 3,4-dibromo-5-[(S)-l-menthyloxy]furan-2(5H)-one and l-valine in the presence of potassium hydroxide. The molecular structure contains an approximately planar (r.m.s. deviation = 0.0204 Å) five-membered furanone ring and a six-membered menthyloxy ring adopting a chair conformation. The crystal packing is stabilized by intermolecular O—H...O and N—H...O hydrogen bonding.

The title compound, C19H30ClNO5, was obtained by the tandem asymmetric Michael addition–elimination reaction of (5S)-3,4-dichloro-5-(l-menthyloxy)furan-2(5H)-one and l-valine in the presence of potassium hydroxide. The furanone unit is approximately planar (r.m.s. deviation = 0.0204 Å) and the six-membered cyclohexane ring adopts a chair conformation. The crystal structure is stabilized by a network of O—H...O and N—H...O hydrogen bonds.

The three-dimensional polymeric title compound, {[Zn(C9H4N2O4)]·H2O}n, contains one crystallographically independent ZnII atom, one fully deprotonated 1H-benzimidazole-5,6-dicarboxylate (bdc) ligand and one uncoordinated water molecule. The ZnII atom is four-coordinated by three O atoms and one N atom from the bdc ligands, giving a distorted tetrahedral coordination geometry. The uncoordinated water molecule is bound to the main structure through a strong bdc–water N—H...O hydrogen bond, and two much weaker water–bdc O—H...O interactions.

The title compound, C17H26ClNO5, was prepared via a tandem asymmetric Michael addition–elimination reaction of (5S)-3,4-dichloro-5-(l-menthyloxy)furan-2(5H)-one and l-alanine in the presence of potassium hydroxide. The five-membered furanone ring is approximately planar while the six-membered menthyloxy ring adopts a chair conformation. The crystal packing is stabilized by intermolecular O—H...O and N—H...O hydrogen bonds.

In the title compound, C11H12ClN5O, the triazolone and pyrimidine rings are almost coplanar [dihedral angle = 2.98 (14)°]. The total puckering amplitude QT of the seven-membered lactam ring is 0.706 (3) Å.

Heat shock protein 20 (Hsp20) is a small molecule heat shock protein that plays an important role in plant growth, development, and stress resistance. Little is known about the function of Hsp20 family genes in apple (Malus domestica). Here, we performed a genome-wide analysis of the apple Hsp20 gene family, and a total of 49 Hsp20s genes were identified from the apple genome. Phylogenetic analysis revealed that the 49 genes were divided into 11 subfamilies, and MdHsp18.2b, a member located in the CI branch, was selected as a representative member for functional characterization. Treatment with NaCl and Botryosphaeria dothidea (B. dothidea), the causal agent of apple ring rot disease, significantly induced MdHsp18.2b transcription level. Further analysis revealed that overexpressing MdHsp18.2b reduced the resistance to salt stress but enhanced the resistance to B. dothidea infection in apple calli. Moreover, MdHsp18.2b positively regulated anthocyanin accumulation in apple calli. Physiology assays revealed that MdHsp18.2b promoted H2O2 production, even in the absence of stress factors, which might contribute to its functions in response to NaCl and B. dothidea infection. Hsps usually function as homo- or heterooligomers, and we found that MdHsp18.2b could form a heterodimer with MdHsp17.9a and MdHsp17.5, two members from the same branch withMdHsp18.2b in the phylogenetic tree. Therefore, we identified 49 Hsp20s genes from the apple genome and found that MdHsp18.2b was involved in regulating plant resistance to salt stress and B. dothidea infection, as well as in regulating anthocyanin accumulation in apple calli. [ABSTRACT FROM AUTHOR]