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The relationship among polycystic ovary syndrome (PCOS), endometrial cancer (EC), and glycometabolism remains unclear. We explored shared genes between PCOS and EC, using bioinformatics to unveil their pathogenic connection and influence on EC prognosis. Gene Expression Omnibus datasets GSE226146 (PCOS) and GSE196033 (EC) were used. A protein–protein interaction (PPI) network was constructed to identify the central genes. Candidate markers were screened using dataset GSE54250. Differences in marker expression were confirmed in mouse PCOS and human EC tissues using RT‐PCR and immunohistochemistry. The effect of PGD on EC proliferation and migration was explored using Ki‐67 and Transwell assays. PGD's impact on the glycometabolic pathway within carbon metabolism was assessed by quantifying glucose content and lactic acid production. R software identified 31 common genes in GSE226146 and GSE196033. Gene Ontology functional classification revealed enrichment in the "purine nucleoside triphosphate metabolism process," with key Kyoto Encyclopedia of Genes and Genomes pathways related to "carbon metabolism." The PPI network identified 15 hub genes. HK2, NDUFS8, PHGDH, PGD, and SMAD3 were confirmed as candidate markers. The RT‐PCR analysis validated distinct HK2 and PGD expression patterns in mouse PCOS ovarian tissue and human EC tissue, as well as in normal and EC cells. Transfection experiments with Ishikawa cells further confirmed PGD's influence on cell proliferation and migration. Suppression of PGD expression impeded glycometabolism within the carbon metabolism of EC cells, suggesting PGD as a significant PCOS risk factor impacting EC proliferation and migration through modulation of single carbon metabolism. These findings highlight PGD's pivotal role in EC onset and prognosis. [ABSTRACT FROM AUTHOR]

In this paper, we consider an explicit fully‐discrete approximation of the Cahn–Hilliard–Cook (CHC) equation with additive noise, performed by a standard finite element method in space and a kind of nonlinearity‐tamed Euler scheme in time. The main result in this paper establishes strong convergence rates of the proposed scheme. The key ingredient in the proof of our main result is to employ uniform moment bounds for the numerical approximations. To the best of our knowledge, the main contribution of this work is the first result in the literature which establishes strong convergence for an explicit fully‐discrete finite element approximation of the CHC equation. Finally, numerical results are finally reported to confirm the previous theoretical findings. [ABSTRACT FROM AUTHOR]

Brain networks extracted by independent component analysis (ICA) from magnitude‐only fMRI data are usually denoised using various amplitude‐based thresholds. By contrast, spatial source phase (SSP) or the phase information of ICA brain networks extracted from complex‐valued fMRI data, has provided a simple yet effective way to perform the denoising using a fixed phase change. In this work, we extend the approach to magnitude‐only fMRI data to avoid testing various amplitude thresholds for denoising magnitude maps extracted by ICA, as most studies do not save the complex‐valued data. The main idea is to generate a mathematical SSP map for a magnitude map using a mapping framework, and the mapping framework is built using complex‐valued fMRI data with a known SSP map. Here we leverage the fact that the phase map derived from phase fMRI data has similar phase information to the SSP map. After verifying the use of the magnitude data of complex‐valued fMRI, this framework is generalized to work with magnitude‐only data, allowing use of our approach even without the availability of the corresponding phase fMRI datasets. We test the proposed method using both simulated and experimental fMRI data including complex‐valued data from University of New Mexico and magnitude‐only data from Human Connectome Project. The results provide evidence that the mathematical SSP denoising with a fixed phase change is effective for denoising spatial maps from magnitude‐only fMRI data in terms of retaining more BOLD‐related activity and fewer unwanted voxels, compared with amplitude‐based thresholding. The proposed method provides a unified and efficient SSP approach to denoise ICA brain networks in fMRI data. [ABSTRACT FROM AUTHOR]

Background: Kidney renal clear cell carcinoma (KIRC) is a prevalent type of urological malignancy. The present study aimed to predict biomarkers for KIRC. Methods: We collected transcriptomic and clinical information for KIRC from The Cancer Genome Atlas and GSE22541 cohorts. Results: Unsupervised clustering of 35 epithelial–mesenchymal transformation (EMT)‐related differentially expressed gene profiles divided samples into two clusters with distinct immune characteristics. Six genes (IL20RB, DDC, ANKRD36BP2, F2RL1, TEK, and AMN) were found to construct a prognostic risk model using multivariate Cox regression analysis. Kaplan–Meier analysis suggested the better prognosis of the KIRC patients in the low‐risk group than that in the high‐risk group. Immune infiltration analyses was conducted using xCell and single‐sample gene set enrichment analysis, indicating that the risk score was associated with the immune microenvironment of the KIRC. Prognostic marker gene‐targeted medications with high drug sensitivity were predicted in KIRC patients. Conclusions: In summary, the present study identified IL20RB, DDC, ANKRD36BP2, F2RL1, TEK, and AMN as prognostic biomarkers, providing insight into immunotherapy and gene‐targeted drugs of KIRC. [ABSTRACT FROM AUTHOR]

The blood‐retinal barrier (BRB), homeostasis, neuronal integrity, and metabolic processes are all directly influenced by Müller cells, the most important retinal glial cells. We isolated primary Müller cells from Sprague–Dawley (SD) neonatal rats and treated them with glucose at varying doses. CCK‐8 was used to quantify cellular viability, and a TUNEL assay was performed to detect cell apoptosis. ELISA, immunofluorescence, and western blotting were used to assess cAMP/PKA/CREB signaling, Kir4.1, AQP4, GFAP, and VEGF levels, respectively. H&E staining was used to examine histopathological alterations in diabetic retinopathy (DR)‐affected retinal tissue in rats. As glucose concentration increases, gliosis of Müller cells became apparent, as evidenced by a decline in cell activity, an increase in apoptosis, downregulation of Kir4.1 level, and overexpression of GFAP, AQP4, and VEGF. Treatments with low, intermediate, and high glucose levels led to aberrant activation of cAMP/PKA/CREB signaling. Interestingly, blocking cAMP and PKA reduced high glucose‐induced Müller cell damage and gliosis by a significant amount. Further in vivo results suggested that cAMP or PKA inhibition significantly improved edema, bleeding, and retinal disorders. Our findings showed that high glucose exacerbated Müller cell damage and gliosis via a mechanism involving cAMP/PKA/CREB signaling. [ABSTRACT FROM AUTHOR]

Aims To assess the efficacy and safety, primarily in relation to the haemodynamic effects, of interatrial shunting devices (ISD) for the treatment of heart failure (HF), we conducted a systematic review and a meta-analysis. Methods and results We used the MEDLINE, Cochrane Library, Embase, and PubMed databases to identify clinical studies (published to 4 August 2021) that evaluated the effect of ISD on HF. The primary endpoint was defined as changes in pulmonary capillary wedge pressure (PCWP). Secondary endpoints included (i) other haemodynamic indexes, including cardiac output (CO), right atrial pressure (RAP), and mean pulmonary artery pressure (mPAP) by right heart catheterization, and (ii) change from baseline in 6 min walk distance (6MWD). After a literature search and detailed evaluation, six trials enrolling a total of 203 individuals were included in the quantitative analysis. Pooled analyses showed that after ISD implantation, PCWP decreased by a mean 3.10 mmHg [95% confidence interval (CI) -4.56 to -1.64; I 2 = 0%; P < 0.0001]. Overall, CO increased by 0.77 L/min (95% CI 0.02 to 1.52; P = 0.04; I 2 = 82%), but there were no significant changes in RAP or mPAP. The mean 6MWD increased by 32.33 m (95% CI 10.74 to 53.92; P = 0.003; I 2 = 0) after ISD implantation. Conclusions Interatrial shunting device can effectively reduce PCWP, increase CO and 6MWD, and has no obvious adverse effects on the right heart and pulmonary pressure. Studies with larger sample size and longer follow-up time are needed for further verification. [ABSTRACT FROM AUTHOR]

Herein, we prepared Fe(II), Zn(II), hydroxylammonium, and hydrazinium pentazolates and investigated their thermal behavior, decomposition kinetics, and thermodynamic activation parameters. The thermolysis of metal and non‐metal salts featured three and two mass‐loss stages, respectively, with the decomposition of pentazolate anions occurring at 105–135 °C. Moreover, metal salts exhibited higher thermal safety than non‐metal salts under the same conditions. Iron and zinc pentazolates decomposed at lower temperatures than sodium pentazolate, i. e., Fe(II) and Zn(II) ions promoted the decomposition of pentazolate anions. The obtained results demonstrate that the prepared compounds hold great promise as energetic catalysts for solid propellant decomposition. [ABSTRACT FROM AUTHOR]

The role of hepatitis E virus (HEV) in developing hepatocellular carcinoma (HCC) is unclear. Our study aimed to investigate the role of HE infection in HCC development and the effect of hepatitis B virus (HBV) and HEV coinfection on HCC risk. A hospital‐based case‐control study was conducted. A total of 474 eligible HCC cases and 586 control patients were successfully recruited. The fasting venous blood was collected from the patients at the first visited to hospital and HBV infection and HEV infection were examined within 5 days. Crude and adjusted odd ratios (ORs) with 95% confidence interval (95% CI) were estimated by using logistic regression model. HBV infection (OR: 63.10, 95% CI: 42.02‐97.26) rather than HEV infection (OR: 1.08, 95% CI: 0.721‐1.65) was associated with an increased risk of HCC after adjustment for confounders. The association between HBV infection and HCC risk was more remarkable in male (OR: 72.61, 95% CI: 45.10‐121.38) than in female (OR: 61.89, 95% CI: 25.74‐169.26). In comparison with patients who infected with neither HEV nor HBV, those who infected with only HBV (OR: 69.62, 95% CI: 40.90‐123.52) and who coinfected with HEV and HBV (OR: 67.48, 95% CI:37.23‐128.19) were significantly associated with an increased risk after adjustment for potential confounders. The results showed that HBV infection rather than HEV infection was associated with an increased risk of HCC, and the HEV infection may alleviate the promoting impact of HBV on HCC development. What's new Chronic infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) are among the many factors associated with the risk of hepatocellular carcinoma (HCC). The role of hepatitis E virus (HEV) in the development of HCC is unclear, however. This case‐control study in a high‐risk area in China investigates the role of HEV infection in HCC development and the effect of HBV and HEV co‐infection on HCC risk. The results support the strong association between HBV infection and HCC risk. Co‐infection with HEV and HBV, but not infection with HEV alone, is significantly associated with an increased HCC risk. [ABSTRACT FROM AUTHOR]

Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases. [ABSTRACT FROM AUTHOR]

High-resolution temperature variation was examined about 40 days near the ocean bottom at 20 sites within an area of 110 × 120 km2 close to the continental margin of the northern South China Sea (depth ≈ 4,000 m). The monitoring depth (0.5 m above the bottom) was presumably within the lower part of the bottom mixed layer, compared to its median thickness of 63 m. At all sites, the bottom water had temperature variance less than 0.01°C, and it alternatively varied in the near-quiescent and internal wave states with time interval of diurnal period or even longer. Spectra of temperature variation showed that diurnal frequency dominated over the internal wave band. At different sites, the transition between internal wave band of scaling -2 and the inertial subrange turbulence of scaling -5/3 cannot easily be discriminated, attributed to the different intermittent presences of internal waves (tides). However, the resolved viscous-convective and viscous-diffusive subranges in the temperature spectrum provide the opportunity to evaluate the thermal (X) and kinetic energy (ε) dissipation rates near the ocean bottom at each site. Close to a seamount, X and ε were inferred to be about 1.2 × 10-12 °C2s-1 and 7.2 × 10-10 m2s-3, respectively, and they were strongly modulated by the diurnal internal tides. In the flat abyssal plain, X and ε were much weaker, about at 3.2 × 10-14 °C2s-1 and 1.7 × 10-11 m2s-3, respectively. The spatial distribution of the nominal thermal X, kinetic energy ε and the turbulent diffusivity Kρ indicated that they varied in the ranges [3.9 × 10-15 1.9 × 10-12] °C2s-1, [2.0 × 10-12 1.1 × 10-9] m2s-3, and [8.3 × 10-6 5.2 × 10-3] m2s-1, respectively, representing the different influences of internal waves and local topography. [ABSTRACT FROM AUTHOR]

Summary: Thromboxane A2 (TXA2) has been implicated in the pathogenesis of vascular complications, but the underlying mechanism remains unclear. The contraction of renal arterial rings in mice was measured by a Multi Myograph System. The intracellular calcium concentration ([Ca2+]i) in vascular smooth muscle cells (VSMCs) was obtained by using a fluo‐4/AM dye and a confocal laser scanning microscopy. The results show that the U46619‐induced vasoconstriction of renal artery was completely blocked by a TXA2 receptor antagonist GR32191, significantly inhibited by a selective phospholipase C (PI‐PLC) inhibitor U73122 at 10 μmol/L and partially inhibited by a Phosphatidylcholine ‐ specific phospholipase C (PC‐PLC) inhibitor D609 at 50 μmol/L. Moreover, the U46619‐induced vasoconstriction was inhibited by a general protein kinase C (PKC) inhibitor chelerythrine at 10 μmol/L, and a selective PKCδ inhibitor rottlerin at 10 μmol/L. In addition, the PKC‐induced vasoconstriction was partially inhibited by a Rho‐kinase inhibitor Y‐27632 at 10 μmol/L and was further completely inhibited together with a putative IP3 receptor antagonist and store‐operated Ca2+ (SOC) entry inhibitor 2‐APB at 100 μmol/L. On the other hand, U46619‐induced vasoconstriction was partially inhibited by L‐type calcium channel (Cav1.2) inhibitor nifedipine at 1 μmol/L and 2‐APB at 50 and 100 μmol/L. Last, U46619‐induced vasoconstriction was partially inhibited by a cell membrane Ca2+ activated C1− channel blocker 5‐Nitro‐2‐(3‐phenylpropylamino) benzoic acid (NPPB) at 50 and 100 μmol/L. Our results suggest that the U46619‐induced contraction of mouse intrarenal arteries is mediated by Cav1.2 and SOC channel, through the activation of thromboxane‐prostanoid receptors and its downstream signaling pathway. [ABSTRACT FROM AUTHOR]

Spatial source phase, the phase information of spatial maps extracted from functional magnetic resonance imaging (fMRI) data by data‐driven methods such as independent component analysis (ICA), has rarely been studied. While the observed phase has been shown to convey unique brain information, the role of spatial source phase in representing the intrinsic activity of the brain is yet not clear. This study explores the spatial source phase for identifying spatial differences between patients with schizophrenia (SZs) and healthy controls (HCs) using complex‐valued resting‐state fMRI data from 82 individuals. ICA is first applied to preprocess fMRI data, and post‐ICA phase de‐ambiguity and denoising are then performed. The ability of spatial source phase to characterize spatial differences is examined by the homogeneity of variance test (voxel‐wise F‐test) with false discovery rate correction. Resampling techniques are performed to ensure that the observations are significant and reliable. We focus on two components of interest widely used in analyzing SZs, including the default mode network (DMN) and auditory cortex. Results show that the spatial source phase exhibits more significant variance changes and higher sensitivity to the spatial differences between SZs and HCs in the anterior areas of DMN and the left auditory cortex, compared to the magnitude of spatial activations. Our findings show that the spatial source phase can potentially serve as a new brain imaging biomarker and provide a novel perspective on differences in SZs compared to HCs, consistent with but extending previous work showing increased variability in patient data. [ABSTRACT FROM AUTHOR]

RAD51D (RAD51L3) is a member of the RAD51 gene family which plays important roles in maintaining genomic stability and preventing DNA damage. This study is aimed to investigate the associations between RAD51D polymorphisms and the hereditary susceptibility of hepatocellular carcinoma (HCC). In this study we conducted a hospital–based case‐control study including 805 cases (HCC patients) and 846 controls (nontumor patients) in Guangxi, China. A total of two Single–nucleotide polymorphisms (SNPs) rs12947947 and rs28363292 of RAD51D were selected and genotyped. Although we did not find two SNPs individually that had any significant main effect on risk of HCC, We found that the combined genotypes with 1‐2 risk genotypes were associated with significantly increased overall risk of HCC (OR = 1.462, 95% CI = 1.050‐2.036). According to the results of further stratification analysis, GT/GG genotype of rs28363292 increased HCC risk in zhuang people (OR = 3.913, 95% CI = 1.873‐8.175) and nonhepatitis B virus (HBV) infection population (OR = 1.774, 95% CI = 1.060‐2.969), the combined 1‐2 risk genotypes increased the risk of HCC in zhuang people (OR = 2.817, 95% CI = 1.532‐5.182) and non‐HBV infected population (OR = 1.567, 95% CI = 1.042‐2.358). Our results suggest that rs12947947 and rs28363292 polymorphisms may jointly contribute to the risk of HCC. Further large studies and functional studies are required to validate our findings. [ABSTRACT FROM AUTHOR]

Fenvalerate (FEN), a mainstream pyrethroid pesticide, was initially recommended as a low-toxicity agent for controlling agricultural and domestic pests. Despite the widespread use of FEN worldwide, little data are available on FEN-induced hepatic lesions and molecular mechanisms. In the present study, we first performed an occupational cross-sectional study on FEN factory workers and found that the levels of serum alanine aminotransferase (ALT) and total antioxidant capacity increased, whereas malondialdehyde decreased in laborers in the working areas where the levels of airborne FEN were much higher compared with the office area. The results were then confirmed by animal experiments that abnormal hepatic histology, increased ALT level, and compromised hepatic oxidative capability were observed in rats exposed to a high concentration of FEN. Furthermore, the bioinformatics analysis of gene microarray in rat liver tissue showed that FEN significantly changed the expressions of genes related to the regulation of intracellular calcium ion homeostasis and the calcium signal pathway. Finally, the functional experiments in Buffalo rat liver (BRL) cells demonstrated that FEN first activated ERK MAPK, followed by IKK and NF-κB, which triggered the transcription of genes responsible for accelerating an overload of intracellular calcium ions, prompted reactive oxygen species generation in the mitochondria, and finally, induced hepatic cellular apoptosis. The calcium signaling pathway and in particular, an overload of intracellular calcium play a critical role in this pathophysiological process via the ERK/IKK/NF-κB pathway. Our study furthers the understanding of the mechanism of FEN-induced hepatic injuries and may have implications in the prevention and control of liver diseases induced by environmental pesticides. [ABSTRACT FROM AUTHOR]

Catechol, nitrite, and dissolved metals are ubiquitous in source drinking water. Catechol and nitrite have been identified as precursors for halonitromethanes (HNMs), but the effect of metal ions on HNM formation during chlorination remains unclear. The main objective of this study was to investigate the effect of metal ions (Fe3+, Ti4+, Al3+) on the formation of trichloronitromethane (TCNM) (the most representative HNM species in disinfected water) on chlorinating catechol and nitrite. Trichloronitromethane was extracted by methyl tert-butyl ether and detected by gas chromatography. The results show that metal ions promoted the formation of TCNM and that the enhancement efficiency followed the order of Fe3+ > Ti4+ > Al3+. Trichloronitromethane formation increased greatly within 2 h, and a basic condition (pH 8-9) favored TCNM formation more than acidic or neutral conditions. The conjoint effect of the metal-ion mixtures was shown to be similar to that of the single metal ion having the highest promoting effect on TCNM formation. Our results strongly suggest that metal ions play a significant role in enhancing TCNM formation. [ABSTRACT FROM AUTHOR]

A one-pot synthesis of new oxindole-fused polycyclic scaffolds is reported. The process involves a three-component [3+2] cycloaddition followed by cyclization through an intramolecular Michael addition. The reaction gives easy access to oxindole-fused spirotetrahydrofurochromans in moderate to good yields with high regio- and diastereoselectivity. These compounds could be useful for for drug discovery. Further modification was achieved by reduction of the nitro group, and intramolecular amide formation to give the corresponding lactams. The resulting heterocyclic products show good inhibitory activity against the enzyme PTP1B in vitro. [ABSTRACT FROM AUTHOR]

Cyclins/retinoblastoma protein (pRb) pathway participates in cardiomyocyte hypertrophy. Micro RNAs (mi RNAs), the endogenous small non-coding RNAs, were recognized to play significant roles in cardiac hypertrophy. But, it remains unknown whether cyclin/Rb pathway is modulated by mi RNAs during cardiac hypertrophy. This study investigates the potential role of micro RNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy. An animal model of hypertrophy was established in a rat with abdominal aortic constriction ( AAC), and in a mouse with transverse aortic constriction ( TAC) and in a mouse with subcutaneous injection of phenylephrine ( PE) respectively. In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte and based on Ang-II-induced neonatal mouse ventricular cardiomyocyte respectively. We demonstrated that miR-16 expression was markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats and mice. Overexpression of miR-16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes, and inhibition of miR-16 induced a hypertrophic phenotype in cardiomyocytes. Expressions of cyclins D1, D2 and E1, and the phosphorylated pRb were increased in hypertrophic myocardium and hypertrophic cardiomyocytes, but could be reversed by enforced expression of miR-16. Cyclins D1, D2 and E1, not pRb, were further validated to be modulated post-transcriptionally by miR-16. In addition, the signal transducer and activator of transcription-3 and c-Myc were activated during myocardial hypertrophy, and inhibitions of them prevented miR-16 attenuation. Therefore, attenuation of miR-16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2 and E1, and activating cyclin/Rb pathway, revealing that miR-16 might be a target to manage cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

Despite the fact that tissue engineered heart valves (TEHV) hold great promise for heart valve disease treatment, one of the challenges is to find suitable seeding cells. Bone marrow derived mesenchymal stem cells (MSCs) were considered to be one of the best seed cell sources. In this study we propose a novel approach to promote stem cell differentiation into the seed cells of TEHV, valvular interstitial cells (VICs). Newly induced MSCs (iMSCs) were created from a co-culture niche in which healthy human donor derived MSCs were co-cultured with cardiac fibroblasts (H9C2 cell line). Then iMSCs were transfected with either a mock vector (iMSCsmock) as controls or with a vector that overexpresses thefibroblast inducible factor 14 (Fn14) gene (iMSCsFn14). Immunofluorescence staining was performed to assay VIC differentiation. Western blot analysis was performed to analyze the involved signaling pathway. The results demonstrate that the expression of α-smooth muscle actin (SMA) was significantly higher in iMSCsFn14 as compared with iMSCmock, and MSC, and also had higher co-alignment of α-actinin and stress fiber (F-actin) in bundles. Additionally, increased biosynthesis of extracellular matrix (ECM) proteins including collagen I, collagen III, and fibronection were observed in iMSCsFn14 in comparison with iMSCsmock. These data observed in iMSCsFn14 were in accordance with VIC phenotype from normal heart valves. In addition, the PI3K/Akt signaling pathway was activated in iMSCsFn14 which allowed higher Akt phosphorylation (p-Akt) levels and SMA levels, whereas, it was attenuated by LY294002 (PI3K/Akt inhibitor). These new findings of the effect of Fn14 on VIC-like cell differentiation may provide a novel therapeutic strategy for heart valve disease treatment. J. Cell. Physiol. 229: 580-587, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

A family of energetic salts with high thermal stability and low impact sensitivity based on an oxygen-containing cation, 2,4-diamino-1,3,5-triazine-6-one, were synthesized and fully characterized by IR and multinuclear (1H, 13C) NMR spectroscopy, elemental analysis, and differential scanning calorimetry. Insights into their sensitivities towards impact, friction, and electrostatics were gained by submitting the materials to standard tests. The structures of 2,4-diamino-1,3,5-triazine-6-one nitrate, 2,4-diamino-1,3,5-triazine-6-one sulfate, 2,4-diamino-1,3,5-triazine-6-one perchlorate, 2,4-diamino-1,3,5-triazine-6-one 5-nitrotetrazolate were determined by single-crystal X-ray diffraction; their densities are 1.691, 1.776, 1.854, and 1.636 g cm−3, respectively. Most of the salts decompose at temperatures over 180 °C; in particular, the salts 2,4-diamino-1,3,5-triazine-6-one nitrate and 2,4-diamino-1,3,5-triazine-6-one perchlorate, which decompose at 303.3 and 336.4 °C, respectively, are fairly stable. Furthermore, most of the salts exhibit excellent impact sensitivities (>40 J), friction sensitivities (>360 N), and are insensitive to electrostatics. The measured densities of these energetic salts range from 1.64 to 2.01 g cm−3. The detonation pressure values calculated for these salts range from 14.6 to 29.2 GPa, and the detonation velocities range from 6536 to 8275 m s−1; these values make the salts potential candidates for thermally stable and insensitive energetic materials. [ABSTRACT FROM AUTHOR]

Pu-erh tea has shown anti-obesity effects but little is known about its effect on proliferation and differentiation of preadipocytes. This study investigated the effects of the aqueous extracts of raw pu-erh tea and ripened pu-erh tea on proliferation and differentiation of murine 3T3-L1 preadiopocytes. We examined dose and time effects of both aqueous extracts on proliferation of 3T3-L1 preadipocytes. The contents of triglycerides in cytoplasm and the mRNA expression of critical transcriptional factors involved in differentiation were determined. Cytotoxicity and apoptosis rate of preadipocytes by pu-erh tea extracts treatment were test for toxic and pro-apoptotic effects. Both aqueous extracts of pu-erh tea inhibited the proliferation of 3T3-L1 preadipocytes at the selected time points. At lower concentration of raw pu-erh tea extracts (less than 300 µg/ml) and ripened pu-erh tea extracts (less than 350 µg/ml), no significant cytotoxic and pro-apoptotic were observed. Ripened pu-erh tea was more effective with lower IC50 than raw pu-erh tea. Both extracts suppressed the differentiation and down-regulated the gene expression of peroxisome proliferator-activated receptor-γ and CCAAT/enhancer binding proteins-α. Therefore, these results indicate that both aqueous extracts of pu-erh tea can inhibit proliferation and differentiation with ripened pu-erh tea more potent. Polyphenol rich in both extracts may play a role in the inhibition of proliferation and differentiation of 3T3-L1 preadipocytes. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

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1. An in situ enclosure experiment was conducted in a deep reservoir of southern China to examine (i) the effects of a low biomass (4 g wet weight m−3) of silver carp ( Hypophthalmichthys molitrix) and nutrients on the plankton community and (ii) the response of Daphnia to eutrophication. 2. In the absence of fish, Daphnia galeata dominated the zooplankton community, whereas calanoids were dominant in the fish treatments, followed by D. galeata. Silver carp stocking significantly reduced total zooplankton biomass, and that of D. galeata and Leptodora richardi, but markedly increased the biomass of smaller cladocerans, copepod nauplii and rotifers. In contrast, nutrient enrichment had no significant effect on the plankton community except for cyclopoids. 3. Chlorophyta, Cryptophyta and Bacillariophyta were dominant phytoplankton groups during the experiment. Chlorophyta with high growth rates (mainly Chlorella vulgaris in the fish enclosures and Ankyra sp. in the fishless enclosures) eventually dominated the phytoplankton community. Total phytoplankton biomass and the biomass of edible phytoplankton [greatest axial linear dimension (GALD) < 30 μm], Chlorophyta, Cryptophyta, Bacillariophyta and Cyanobacteria showed positive responses to fish stocking, while inedible phytoplankton (GALD ≥ 30 μm) was significantly reduced in the fish enclosures. However, there was no significant effect on the plankton community from the interaction of fish and nutrients. 4. Overall, the impact of fish on the plankton community was much greater than that of nutrients. High total phosphorus concentrations in the control treatment and relatively low temperatures may reduce the importance of nutrient enrichment. These results suggest it is not appropriate to use a low biomass of silver carp to control phytoplankton biomass in warmer, eutrophic fresh waters containing large herbivorous cladocerans. [ABSTRACT FROM AUTHOR]

The present study investigated the neuroprotective effects of aucubin on hydrogen peroxide (H2O2)-induced apoptosis in PC12 cells. Exposure of PC12 cells to 0.25 m m H2O2 induced a leakage of lactate dehydrogenase and decreased cell viability, as shown by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. In a dose over 0.1 m m, aucubin increased PC12 cellular viability and markedly attenuated H2O2-induced apoptotic cell death. Quantitation of apoptosis by flow cytometry indicated that aucubin inhibited H2O2-induced apoptosis in PC12 cells. Nuclear damage was alleviated by aucubin, as shown by Hoechst staining. In addition, the levels of malondialdehyde were reduced and the activity of superoxide dismutase, catalase and glutathione peroxidase was augmented in these cells. These results indicated that aucubin inhibited H2O2-induced apoptosis in PC12 cells through regulation of the endogenous oxidant-antioxidant balance. Our results suggest that aucubin is a potential protective agent for the treatment of oxidative-stress-induced neurodegenerative disease. Copyright © 2011 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

This study attempted to use collagen-Matrigel as extracellular matrix (ECM) to supply cells with three-dimensional (3D) culture condition and employ alginate-poly- l-lysine-alginate (APA) microcapsules to control the formation of alveolus-like structure in vitro. We tested mice foetal pulmonary cells (FPCs) by immunohistochemistry after 2D culture. The alveolus-like structure was reconstructed by seeding FPCs in collagen-Matrigel mixed with APA microcapsules 1.5 ml. A self-made mould was used to keep the structure from contraction. Meanwhile, it provided static stretch to the structure. After 7, 14 and 21 days of culture, the alveolus-like structure was analysed histologically and immunohistochemically, or by scanning transmission electron microscopy (TEM). We also observed these structures under inverted phase contrast microscope. The expression of pro-surfactant protein C (SpC) was detected by reverse transcription-polymerase chain reaction (RT-PCR). We obtained fibroblasts, epithelial cells and alveolar type II (AE2) cells in FPCs. In the reconstructed structure, seeding cells surrounding the APA microcapsules constructed alveolus-like structures, the size of them ranges from 200 to 300 μm. In each reconstructed lung tissue sheet, microcapsules had integrity. Pan-cytokeratin, vimentin and SpC positive cells were observed in 7- and 14-day cultured structures. TEM showed lamellar bodies of AE2 cells in the reconstructed tissues whereas RT-PCR expressed SpC gene. Primary mice FPCs could form alveolus-like structures in collagen-Matrigel/APA microcapsules engineered scaffolds, which could maintain a differentiated state of AE2 cells. [ABSTRACT FROM AUTHOR]

1. It has been reported that allitridi, an active compound extracted from garlic, has many cardiovascular effects. However, it remains unknown whether allitridi affects major repolarization currents, such as the transient outward K current ( I), ultrarapid delayed rectifier K current ( I) and the L-type Cacurrent ( I), in human atrial myocytes. 2. In the present study, we investigated the effects of allitridi on I, I, I and the action potential in human isolated atrial myocytes using the whole-cell patch recording technique. 3. Allitridi reversibly inhibited I, but not I and I, in human atrial myocytes. These effects of allitridi on I were concentration dependent (IC = 44.9 μmol/L). Inactivation of I was accelerated and the voltage-dependent inactivation potential was shifted towards the negative direction. Allitridi (30 μmol/L) significantly prolonged action potential duration in human atrial myocytes. 4. The results of the present study indicate that allitridi inhibits I, but not I and I, and prolongs the action potential duration in human atrial myocytes. [ABSTRACT FROM AUTHOR]

1. It is known that high glucose can induce cardiomyocyte apoptosis and that macrophage migration inhibitory factor (MIF) may be involved in the development of diabetes. However, the relationship between high glucose and MIF in diabetic cardiomyopathy remains unclear. 2. In the present study, AC16 human cardiomyocytes were cultured in the presence of 25 mmol/L glucose for 20, 30 and 60 min before being subjected to western blot analyses to determine MIF expression and c-Jun N-terminal kinase (JNK) activation. In addition, AC16 cells were pretreated with 2.5 μmol/L SP600125 (a JNK inhibitor), 40 μmol/L ()-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1; an MIF antagonist) or 0.1% dimethylsulphoxide (DMSO; vehicle) for 1 h prior to exposure to 25 mmol/L glucose and culture for 72 h, followed by annexin V-fluorescein isothiocyanate/propidium iodide staining and flow cytometry analysis. Caspase 3 activity and phosphorylation of JNK were also analysed by western blotting. 3. The high concentration of glucose increased expression of endogenous MIF and JNK phosphorylation in AC16 cardiomyocytes. Pretreatment of cells with SP600125 and ISO-1 reduced glucose-induced apoptosis and caspase 3 activity. Furthermore, JNK phosphorylation was attenuated by inhibition of endogenous MIF. 4. In conclusion, myocardial cell apoptosis induced by high glucose involves the overexpression of MIF and activation of the JNK signalling pathway. The identification of a high glucose-MIF-JNK pathway will help determine potential new targets in the treatment of diabetic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Abstract: Hsp60 is an important component of defense mechanisms against diabetic myocardial injury; however, the cause of Hsp60 reduction in the diabetic myocardium remains unknown. After stimulation of cardiomyocytes with high glucose in vivo and in vitro, significant up-regulation of miR-1/miR-206 and post-transcriptional modulation of Hsp 60 were observed. Serum response factor (SRF) and the MEK1/2 pathway were involved in miR-1 and miR-206 expression in cardiomyocytes. miR-1 and miR-206 regulated Hsp60 expression post-transcriptionally and accelerated cardiomyocyte apoptosis through Hsp60. These results revealed that miR-1 and miR-206 regulate Hsp60 expression, contributing to high glucose-mediated apoptosis in cardiomyocytes. [ABSTRACT FROM AUTHOR]

Independent component analysis (ICA) utilizing prior information, also called semiblind ICA, has demonstrated considerable promise in the analysis of functional magnetic resonance imaging (fMRI). So far, temporal information about fMRI has been used in temporal ICA or spatial ICA as additional constraints to improve estimation of task-related components. Considering that prior information about spatial patterns is also available, a semiblind spatial ICA algorithm utilizing the spatial information was proposed within the framework of constrained ICA with fixed-point learning. The proposed approach was first tested with synthetic fMRI-like data, and then was applied to real fMRI data from 11 subjects performing a visuomotor task. Three components of interest including two task-related components and the 'default mode' component were automatically extracted, and atlas-defined masks were used as the spatial constraints. The default mode network, a set of regions that appear correlated in particular in the absence of tasks or external stimuli and is of increasing interest in fMRI studies, was found to be greatly improved when incorporating spatial prior information. Results from simulation and real fMRI data demonstrate that the proposed algorithm can improve ICA performance compared to a different semiblind ICA algorithm and a standard blind ICA algorithm. Hum Brain Mapp, 2010. © 2009 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

In this study, we demonstrated with mechanistic evidence that parthenolide, a sesquiterpene lactone, could antagonize paclitaxel-mediated NF-κB nuclear translocation and activation by selectively targeting I-κB kinase (IKK) activity. We also found that parthenolide could target IKK activity and then inhibit NF-κB; this promoted cytochrome c release and activation of caspases 3 and 9. Inhibition of caspase activity blocked the activation of caspase cascade, implying that the observed synergy was related to caspases 3 and 9 activation of parthenolide. In contrast, paclitaxel individually induced apoptosis via a pathway independent of the mitochondrial cytochrome c cascade. Finally, exposure to parthenolide resulted in the inhibition of several NF-κB transcript anti-apoptotic proteins such as c-IAP1 and Bcl-xl. These data strengthen the rationale for using parthenolide to decrease the apoptotic threshold via caspase-dependent processes for treatment of non-small cell lung cancer with paclitaxel chemoresistance. [ABSTRACT FROM AUTHOR]

1. Ketamine is widely used for the induction of anaesthesia in high-risk patients with cardiovascular instability or severe hypovolaemia. However, the ionic mechanisms involved in the effects of ketamine at therapeutically relevant concentrations in human cardiac myocytes are unclear. The present study was designed to investigate the effects of ketamine on L-type Ca2+ (ICa), transient outward K+ (Ito), ultra-rapid delayed rectifier K+ (IKur) and inward rectifier potassium (IK1) currents, as well as on action potentials, in human isolated atrial myocytes. 2. Atrial myocytes were isolated enzymatically from specimens of human atrial appendage obtained from patients undergoing coronary artery bypass grafting. The action potential and membrane currents were recorded in both current- and voltage-clamp modes using the patch-clamp technique. 3. Ketamine inhibited ICa with an IC50 of 1.8 µmol/L. In addition, 10 µmol/L ketamine decreased the ICa peak current at +10 mV from 5.1 ± 0.3 to 2.1 ± 0.4 pA/pF ( P < 0.01), but did not change the threshold potential, peak current potential and reverse potential. 4. Ketamine had no effect on Ito, IKur or IK1, but it reversibly shortened the duration of the action potential in human atrial myocytes. 5. In conclusion, ketamine, at a clinically relevant concentration, shortens the action potential duration of the human atrial myocytes, probably by inhibiting ICa. [ABSTRACT FROM AUTHOR]

A rapid and sensitive quantitative assay method was developed for determining ribavirin pharmacokinetic in human plasma. The chromatographic separation was achieved within 4.5 min using a SinoChrom ODS-BP column (4.6 × 150 mm, 5 µm) with acetonitrile-water (1 mmol/L ammonium acetate buffer, 0.1% formic acid; 15:85, v/v) at a constant flow rate of 0.8 mL/min. The MRM pairs were m/z 245.2 → m/z 113.1 for ribavirin and m/z 226.1 → m/z 152.1 for acyclovir (internal standard), respectively, with dwell times of 200 ms for each transition. The results showed calibration curve for ribavirin was linear over a concentration range of 1-1000 ng/mL. The lower limit of quantification (LLOQ) was 1 ng/mL ribavirin. Twenty healthy volunteers received a 300 mg oral dose of ribavirin. Blood samples were then collected up to 120 h postdosing. All plasma data were comodeled for ribavirin by using noncompartmental modeling. The single dose of ribavirin was well tolerated and no serious adverse effects occurred. The mean time to maximum concentration was about 1.25 h. The mean maximum concentration of drug in plasma for oral ribavirin was 250 ng/mL. The mean elimination half-life was 43.6 h. The present study describes a simple, specific, sensitive HPLC-MS/MS method for measuring plasma drug concentration and analyzing human pharmacokinetics of ribavirin. Copyright © 2008 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Excess production of reactive oxygen species by macrophages has been implicated in many inflammatory diseases. The present study investigated the inhibitory effect of the stem bark extract of Acanthopanax senticosus on the production of superoxide anion and hydrogen peroxide in mouse peritoneal macrophages in vitro and in vivo. Exposure of mouse peritoneal macrophages to A. senticosus extract significantly suppressed superoxide anion production induced by zymosan in a dose-dependent manner. Similarly, exposure of mouse peritoneal macrophages to A. senticosus extract significantly inhibited hydrogen peroxide production induced by phorbol 12-myristate 13-acetate (PMA) in a dose-dependent manner. Intraperitoneal administration of A. senticosus extract to KM mice reduced the ex vivo production of zymosan induced-superoxide anion and PMA-induced hydrogen peroxide by their peritoneal macrophages. Exposure to A. senticosus extract did not affect the cell viability or systemic toxicity. A. senticosus inhibited reactive oxygen species production by mouse peritoneal macrophages in vitro and in vivo and may be partly responsible for the antiinflammatory function. Copyright © 2008 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

A high-performance liquid chromatography method with fluorescence detection (HPLC-FLD) for the determination of levofloxacin in human plasma is described. Neutralized with phosphate buffer (pH 7.0), the sample (0.1 mL) was extracted with dichlormethane (1 mL). After voltex-mixing and centrifuged at 3000 g for 6 min at 4°C, the upper aqueous layer was aspirated using a micro vacuum pump and the organic layer was directly transferred to a clean test tube without pipetting. The organic solvent was evaporated and the residues were reconstituted with the mobile phase. Levofloxacin and terazosin (internal standard, IS) were chromatographically separated on a C18 column with a mobile phase containing phosphate buffer (pH 3.0, 10 m m), acetonitrile and triethylamine (76:24:0.076, v/v/v) at a flow rate of 1 mL/min. The analytes were detected using fluorescence detection at an excitation and emission wavelength of 295 and 440 nm, respectively. The linear range of the calibration curves was 0.0521-5.213 µg/mL for levofloxacin with a lower limit of quantitation (0.0521 µg/mL). The retention times of levofloxacin and terazosin were 2.5 and 3.1 min, respectively. Within- and between-run precision was less than 12 and 11%, respectively. Accuracy ranged from −6.3 to 4.5%. The recovery ranged from 86 to 89% at the concentrations of 0.0521, 0.5213 and 5.213 µg/mL. The present HPLC-FLD method is sensitive, efficient and reliable. The method described herein has been successfully used for the pharmacokinetic and bioequivalence studies of a levofloxacin formulation product after oral administration to healthy Chinese volunteers. Copyright © 2007 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Excess nitric oxide (NO) production has been implicated in inflammatory diseases. The present study investigated the inhibitory effect of the stem bark extract of Acanthopanax senticosus (A. senticosus) on NO production in murine macrophages in vitro and in vivo. In vitro exposure of RAW264.7 cells to 1, 10, 50, 100, 250, 500 and 1000 µg/mL of A. senticosus extract significantly suppressed NO production induced by lipopolysaccharide (LPS) and interferon gamma (IFN- γ) in a dose-dependent manner. In vitro exposure of mouse resident peritoneal macrophages to 1, 10, 100 and 1000 µg/mL of A. senticosus extract significantly suppressed NO production induced by LPS and IFN- γ in a dose-dependent manner. In vivo administration of A. senticosus extract (50, 100 and 200 mg/kg) to KM mice dose-dependently inhibited LPS and IFN- γ induced production of NO in isolated mouse peritoneal macrophages ex vivo. Exposure to A. senticosus extract had no effect on cell viability and systemic toxicity. The results demonstrated that the stem bark extract of A. senticosus extract inhibits NO production in murine macrophages in vitro and in vivo. Copyright © 2007 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Excessive nitric oxide (NO) production after cerebral hypoxia-ischaemia (HI) may induce cellular injury in various ways, including reaction with superoxide to form the highly reactive peroxynitrite. We characterized the spatial and temporal formation of peroxynitrite through immunohistochemical detection of nitrosylated proteins. Nitrotyrosine immunoreactivity peaked around 3 h post-HI and was detected in areas of injury, as judged by the loss of microtubule-associated protein-2 (MAP-2) staining, in neurones, glia and endothelial cells. Nitrotyrosine staining co-localized with three other cellular markers of injury, active caspase-3, nuclear translocation of apoptosis-inducing factor (AIF) and an oligonucleotide hairpin probe detecting specific DNA strand breaks. The number of nitrotyrosine-positive cells at early time points outnumbered the cells positive for the other three markers of injury, indicating that nitrosylation preceded caspase-3 activation. Pharmacological inhibition of neuronal and inducible nitric oxide synthase (nNOS and iNOS) using 2-iminobiotin, which has been demonstrated earlier to be neuroprotective, significantly reduced nitrotyrosine formation and caspase-3 activation, but not nuclear translocation of AIF, in cortex and striatum of the ipsilatral hemisphere. In summary, nitrotyrosine is an early marker of cellular injury and inhibition of nNOS and iNOS is a promising strategy for neuroprotection after perinatal HI. [ABSTRACT FROM AUTHOR]

In the title clathrate complex, {[Sn2(CH3)6(C2N2S3)(C10H8N2)]·C10H8N2} n, two independent Sn atoms are five-coordinated in a distorted trigonal–bipyramidal geometry. The asymmetric unit contains two independent 4,4′-bipyridine systems, one of which bridges two independent Sn atoms [Sn—N = 2.588 (7) and 2.591 (7) Å], leading to the formation a one-dimensional polymeric zigzag chain. [ABSTRACT FROM AUTHOR]

In the title compound, C14H12O2, the dihedral angle between the two aromatic rings is 60.02 (4)°. The crystal structure is stabilized by intramolecular O—H...O and intermolecular C—H...O hydrogen bonds. [ABSTRACT FROM AUTHOR]

The title compound, [Sn4(CH3)8(C7HF4O2)4O2], was obtained from the reaction of the ligand 2,3,4,5-tetrafluorobenzoic acid and dimethyltin(IV) oxide. The Sn atom is five-coordinate and displays trigonal–bipyramidal geometry. The molecule is centrosymmetric about the Me4Sn2O2 core and molecules are linked by C—H...O and C—H...F intermolecular interactions. [ABSTRACT FROM AUTHOR]

In the crystal structure, the title compound, C16H16O5, forms an intra­molecular O—H⋯O hydrogen bond and two short inter­molecular C—H⋯O contacts. [ABSTRACT FROM AUTHOR]

In the binuclear title complex, [Ag2(C9H5O6)2(C12H9N3)2], the two AgI atoms are in a trigonal planar environment formed by two N atoms from two 2-(3-pyridyl)benzimidazole ligands and one O atom from a 3,5-dicarboxybenzoate ligand, forming a centrosymmetric cyclic dimer. Intermolecular N—H⋯O and O—H⋯O hydrogen bonding interactions aggregate the binuclear units into a three-dimensional framework. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To test the hypothesis that locally directed gene transfer of human vascular endothelial growth factor 165 (hVEGF165 ) is able to passivate hepatic venous metallic stents by accelerating endo­thelialization and augmenting the biocompatibility of endovascular stents. METHODS: Complexes of pAdtrackCMV-hVEGF165 and lipofectamine were smeared homogeneously on the surface of the stents coated with poly-L-lysine. Bare stents were used as controls. All stents were implanted into the right hepatic vein by transjugular intrahepatic venous stent deployment. RESULTS: At the end of the first week after implantation, green fluorescence and the expression of the hVEGF165 gene were detected in the transferred stent vessels of the treated group, but were not detected in the control group. Scanning electron microscopy revealed that the endothelialization of stents was more pronounced in the treated group than that in the control group. At the end of the eighth week after implantation, quantitative angiography analysis showed the internal diameter of the stent was significantly greater in the treated group than in the control group. The de novo intima, their mean areas and percentage cross-sectional area narrowing in the treated group were significantly less than those in the control group. Immunohistochemical analysis indicated that the proliferation of vascular smooth muscle cells was more active in the control group than that in the treated group. CONCLUSION: Local gene transfer of hVEGF165 can passivate endovascular stents by accelerating stent endothelialization and enhancing their biocompatibility in the hepatic vein, resulting in a reduction of thrombus formation and attenuation of intimal hyperplasia. [ABSTRACT FROM AUTHOR]