The oxygen evolution reaction on cobalt atom embedded nitrogen doped graphene electrocatalysts: a density functional theory study.

The oxygen evolution reaction (OER) is essential for the development of renewable energy conversion and storage technologies. Eight N-doped graphenes containing variable numbers of embedded cobalt atoms (Coxy-NG, x = 1-4, y = 1-3, where x represents the number of embedded Co atoms and y represents different configurations) were designed and their OER electrocatalytic activities were systematically studied through density functional theory calculations. The significant roles of the number of Co atoms and their configuration in their OER performance were discussed in detail. Co31-NG occupies the peak of the activity volcano plot with a low overpotential of 0.31 V, which is smaller than Co11-NG with only one Co atom and even superior to the widely used IrO2 (0.56 V). The electronic structure and electron density analysis reveal that the outstanding electrocatalytic performance is due to the orbital hybridization between Co and N atoms and the increased positive charge on in-plane Co due to the out-of-plane Co atoms/clusters. This work clarifies the important role of transition atoms and provides excellent examples for reducing the overpotential through embedding several transition metal atoms onto single-atom electrocatalysts.

First Report of Powdery Mildew Caused by Erysiphe polygoni on Trifolium repens in China.

White clover (Trifolium repens L.) belongs to the Fabaceae family legume and is cultivated in China for its medicinal properties and ornamental value. White clover is grown around the world for forage, turf , green manure and soil conservation purposes (Zhang el al. 2016). In October 2021, an investigation of a 1,000 m2 plant nursery in Lanzhou, China (36°06'N, 103°83'E) found that 80% of White clover plants were infected, and powdery mildew covered 95% of the leaf area. The disease had seriously destroyed the forage quality and reduced the ornamental value. Initially, thin, radial, irregular white colonies appeared on leaves and gradually spread to stems. The white colonies then expanded and thickened to cover upper surface of the leaf, and microscopic hyphae appeared on the bottom of the leaf. In severe cases, the infection resulted in dieback of the leaf. A small area of sporulating fungus was stripped off from the leaf surface with tape and mounted in sterile water for microscopic examination (Mukhtar et al. 2017). Conidiophores were cylindrical, consisting of a foot cell followed by three to four short cells, measuring 75 to 160 × 7 to 10 µm. Conidiophores had straight, cylindric foot cells ranging from 25 to 40 µm long. Singly produced conidia were hyaline and ranged in shape from oblong to cylindrical. Conidia lacked distinct fibrotic bodies and measured 30 to 45 × 15 to 25 µm in length. Long, unbranched germ tubes formed from the ends of the conidia and nipple-shaped appressoria developed on epiphytic mycelia. Based on these morphological characteristics, the pathogen was initially identified morphologically as Erysiphe polygoni (Braun and Cook 2012). To validate the identity, the internal transcribed spacer (ITS) region of the pathogen (SY77) rDNA was amplified by PCR and sequenced using the ITS1/ITS4 primers (White et al. 1990). The resulting sequences were registered to GenBank (GenBank Accession No.OM280998). The ITS sequence of the SY77 was 100% (640/640) identical to E. polygoni (LC009892) on Polygonum aviculare in the United Kingdom and 99% (638/640) identical to E. polygoni (MK685172) on Antigonon leptopus in Taiwan. MEGA 7.0 was used to conduct the neighbor-joining phylogenetic analysis using the ITS sequences from GenBank. The data indicated that the strain SY77 and E. polygoni clustered together on the same branch. Pathogenicity tests were conducted by gently pressing the infected leaves onto five healthy potted White clover plants, while five non-inoculated plants were used as controls (Michael et al. 2021). The plants were maintained in a growth chamber (25 ℃, 14 h light, and 10 h dark period, RH > 80%). After 10 days, the inoculated plants developed powdery mildew symptoms, whereas the control plants remained symptom-free. The fungus on the inoculated plants was re-isolated, re-identified, and confirmed as E. polygoni based on morphological observations and molecular identification. There is no previous report on E. polygoni causing powdery mildew on White clover in China. The powdery mildew caused by E. polygoni on Red clover has been reported in China and Bulgaria, respectively (Yuan el al.1991; Galina el al. 2017). To our knowledge, this is the first report of powdery mildew caused by E. polygoni on White clover in China. References: 1. Zheng, L., et al. 2018. Plant Dis. 102:628. 2. Mukhtar, G., et al. 2017. Plant Dis.101:1, 246. 3. Braun, U., and Cook, R. T. A. 2012. Taxonomic Manual of the Erysiphales (Powdery Mildews), CBS Biodiversity Series No.11. CBS, Utrecht. 4. Michael, R. F., et al. 2021.Plant Dis. First look.( doi.org/ 10.1094/PDIS-09-21-2060-PDN). 5. Yuan, Q. H., el al.1991. Pratacult Sci.05:59 (in Chinese). 6. Galina, N., et al, 2017. BIOTECHNOL Anim Husb.33.127.

Folate metabolic profiling and expression of folate metabolism-related genes during panicle development in foxtail millet (Setaria italica (L.) P. Beauv).

BACKGROUND: Foxtail millet grain has higher folate content than other cereal crops. However, the folate metabolite content and the expression patterns of folate metabolite-related genes are unknown. RESULTS: Liquid chromatography-mass spectrometry was used to investigate 12 folate metabolites in a foxtail millet panicle. The content of total folate and derivatives gradually decreased during panicle development. Polyglutamate 5-formyl-tetrahydrofolate was the major form. Twenty-eight genes involved in the folate metabolic pathway were identified through bioinformatic analysis. These genes in Setaria italica, S. viridis and Zea mays showed genomic collinearity. Phylogenetic analysis revealed that the folate-related genes were closely related among the C4 plants compared to C3 plants. The gene expressions were then studied at three panicle development stages. The gene expression patterns were classified into two groups, namely SiADCL1 and SiGGH as two key enzymes, which are responsible for folate synthesis and degradation; their expression levels were highest at the early panicle development stage, up to 179.11- and 163.88-fold, respectively. Their expression levels had a similar downward trend during panicle development and were significantly positively correlated with the concentration of total folate and folate derivatives. However, SiSHMT3 expression levels were significantly negatively correlated with total folate concentration. CONCLUSION: Besides being the major determinants of folate and folate derivatives accumulation, SiADCL1 and SiGGH expression levels are key limiting factors in the foxtail millet panicle. Therefore, SiADCL1 and SiGGH expression levels can be targeted in genetic modification studies to improve folate content in foxtail millet seeds in the future. © 2021 Society of Chemical Industry.

Comparative transcriptomic analysis reveals the regulatory mechanism of the gibberellic acid pathway of Tartary buckwheat (Fagopyrum tataricum (L.) Gaertn.) dwarf mutants.

BACKGROUND: Tartary buckwheat is an important minor crop species with high nutritional and medicinal value and is widely planted worldwide. Cultivated Tartary buckwheat plants are tall and have hollow stems that lodge easily, which severely affects their yield and hinders the development of the Tartary buckwheat industry. METHODS: Heifeng No. 1 seeds were treated with ethylmethanesulfonate (EMS) to generate a mutant library. The dwarf mutant ftdm was selected from the mutagenized population, and the agronomic characteristics giving rise to the dwarf phenotype were evaluated. Ultra-fast liquid chromatography-electrospray ionization tandem mass spectrometry (UFLC-ESI-MS/MS) was performed to determine the factors underlying the different phenotypes between the wild-type (WT) and ftdm plants. In addition, RNA sequencing (RNA-seq) was performed via the HiSeq 2000 platform, and the resulting transcriptomic data were analysed to identify differentially expressed genes (DEGs). Single-nucleotide polymorphism (SNP) variant analysis revealed possible sites associated with dwarfism. The expression levels of the potential DEGs between the WT and ftdm mutant were then measured via qRT-PCR and fragments per kilobase of transcript per million mapped reads (FPKM). RESULT: The plant height (PH) of the ftdm mutant decreased to 42% of that of the WT, and compared with the WT, the mutant and had a higher breaking force (BF) and lower lodging index (LI). Lower GA4 and GA7 contents and higher contents of jasmonic acid (JA), salicylic acid (SA) and brassinolactone (BR) were detected in the stems of the ftdm mutant compared with the WT. Exogenous application of GAs could not revert the dwarfism of the ftdm mutant. On the basis of the transcriptomic analysis, 146 homozygous SNP loci were identified. In total, 12 DEGs with nonsynonymous mutations were ultimately identified, which were considered potential candidate genes related to the dwarf trait. When the sequences of eight genes whose expression was downregulated and four genes whose expression was upregulated were compared, SKIP14, an F-box protein whose sequence is 85% homologous to that of SLY1 in Arabidopsis, presented an amino acid change (from Ser to Asn) and was expressed at a lower level in the stems of the ftdm mutant compared with the WT. Hence, we speculated that this amino acid change in SKIP14 resulted in a disruption in GA signal transduction, indirectly decreasing the GA content and downregulating the expression of genes involved in GA biosynthesis or the GA response. Further studies are needed to determine the molecular basis underlying the dwarf phenotype of the ftdm mutant. CONCLUSION: We report a Tartary buckwheat EMS dwarf mutant, ftdm, suitable for high-density planting and commercial farming. A significant decrease in GA4 and GA7 levels was detected in the ftdm mutant, and 12 DEGs expressed in the stems of the ftdm mutant were selected as candidates of the dwarfing gene. One nonsynonymous mutation was detected in the SKIP14 gene in the ftdm mutant, and this gene had a lower transcript level compared with that in the WT.

DLX5 gene regulates the Notch signaling pathway to promote glomerulosclerosis and interstitial fibrosis in uremic rats.

Uremia largely results from the accumulation of organic waste products normally cleared by the kidneys, which commonly accompanies kidney failure and chronic kidney disease. However, genetic investigations in a uremia remain largely unclear. This study aimed to determine the expression patterns of distal-less homeobox 5 (DLX5) in uremia rat model and further to study its effects on glomerulosclerosis and interstitial fibrosis. Uremic expression chip was applied to screen differentially expressed genes in uremia. Next, we used small interfering RNA-mediated RNA interference to specifically silence DLX5 in experimental uremic rats to understand the regulatory mechanism of DLX5. To understand effect of Notch1 signaling pathway in uremia, we also treated experimental uremic rats with γ-secretase inhibitor (GSI), an inhibitor of Notch1 signaling pathway. The expression of fibronectin (FN), laminin (LN), transforming growth factor-ß1 (TGF-ß1), Hes1, Hes5, and Jagged2 was determined. The semiquantitative assessment was applied to verify the effects of DLX5 on glomerulosclerosis. In the uremic expression chip, we found that DLX5 was upregulated in uremia samples, and considered to regulate the Notch signaling pathway. We found that small interfering RNA-mediated DLX5 inhibition or Notch1 signaling pathway inhibitory treatment relieved and delayed the kidney injury and glomerulosclerosis in uremia. Meanwhile, inhibition of DLX5 or Nothch1 signaling pathway reduced expression of FN, LN, Nothch1, TGF-ß1, Hes1, Hes5, and Jagged2. Intriguingly, we discovered that Notch1 signaling pathway was inhibited after silencing DLX5. In conclusion, these findings highlight that DLX5 regulates Notch signaling, which may, in turn, promote complications of uremia such as kidney fibrosis, providing a novel therapeutic target for treating uremia.

Gastrin-releasing peptide receptor gene silencing inhibits the development of the epithelial-mesenchymal transition and formation of a calcium oxalate crystal in renal tubular epithelial cells in mice with kidney stones via the PI3K/Akt signaling pathway.

Between 1% and 15% of people are globally affected by kidney stones, and this disease has become more common since the 1970s. Therefore, this study aims to investigate the effects of gastrin-releasing peptide receptor (GRPR) gene silencing via the PI3K/Akt signaling pathway on the development of the epithelial-mesenchymal transition (EMT) and formation of a calcium oxalate crystal in renal tubular epithelial cells (TECs) of kidney stones. A total of 70 clean and healthy C57BL/6J mice were assigned into the normal ( n = 10) and kidney stones groups ( n = 60). The underlying regulatory mechanisms of GRPR were analyzed in concert with the treatment of shGRPR-1, LY294002, and shGRPR-1 + LY294002 in TECs isolated from mice with kidney stones. A series of experiments were conducted for the measurement of urinary oxalate and urinary calcium, the renal calcium salt deposition, the positive rate of GRPR, the expressions of renal TECs related genes and calcium oxalate regulation related genes, and the growth of calcium crystals induced by cells. After treatment of shGRPR-1 and shGRPR-1 + LY294002, levels of urinary oxalate and urinary calcium in the serum, as well as positive rate of GRPR, became relatively low, levels of E-cadherin enhanced, whereas levels of Akt, PI3K, GRPR, extents of PI3K and Akt phosphorylation, α-SMA, Vimentin and FSP-1, OPN, MCP-1, and CD44 decreased and a number of crystals reduced. Taken together, we conclude that GRPR gene silencing suppresses the development of the EMT and formation of the calcium oxalate crystal in renal TECs of kidney stones through the inactivation of the PI3K/Akt signaling pathway.

Effects of microRNA-370 on mesangial cell proliferation and extracellular matrix accumulation by binding to canopy 1 in a rat model of diabetic nephropathy.

As one major diabetic complication, diabetic nephropathy (DN) has been reported to be associated with various kinds of microRNA (miRNA). Thus, we conducted this study to explore the potential of miR-370 in a rat model of DN through investigation of mesangial cell proliferation and extracellular matrix (ECM). A total of 40 healthy adult male Sprague-Dawley rats were enrolled and assigned into normal (n = 10) and DN ( n = 30, DN rat model) groups. Dual-luciferase reporter assay was performed for the targeting relationship between miR-370 and canopy 1 (CNPY1). Mesangial cells were collected and transfected with prepared mimic, inhibitor or small interfering RNA (siRNA) for analyzing the effect of miR-370 on DN mice with the help of expression and cell biological processes detection. CNPY1 was confirmed as a target gene of miR-370. DN mice had increased expression of miR-370, fibronectin, type I collagen (Col I), type IV collagen (Col IV), and plasminogen activator inhibitor-1 (PAI-1) but reduced CNPY1 expression. Cells transfected with miR-370 mimic and siRNA-CNPY1 had increased expression of fibronectin, Col I, Col IV, and PAI-1 but decreased CNPY1 expression. The miR-370 mimic and siRNA-CNPY1 groups showed increased cell proliferation, as well as elevated ECM accumulation and declined cell apoptosis rate as compared with the blank and negative control groups, with reverse trends observed in the miR-370 inhibitor group. Our study concludes that overexpression of miR-370 promotes mesangial cell proliferation and ECM accumulation by suppressing CNPY1 in a rat model of DN.

Genome-wide association study of four yield-related traits at the R6 stage in soybean.

BACKGROUND: The 100-pod fresh weight (PFW), 100-seed fresh weight (SFW), 100-seed dry weight (SDW) and moisture content of fresh seeds (MCFS) at the R6 stage are crucial factors for vegetable soybean yield. However, the genetic basis of yield at the R6 stage remains largely ambiguous in soybean. RESULTS: To better understand the molecular mechanism underlying yield, we investigated four yield-related traits of 133 soybean landraces in two consecutive years and conducted a genome-wide association study (GWAS) using 82,187 single nucleotide polymorphisms (SNPs). The GWAS results revealed a total of 14, 15, 63 and 48 SNPs for PFW, SFW, SDW and MCFS, respectively. Among these markers, 35 SNPs were repeatedly identified in all evaluated environments (2015, 2016, and the average across the two years), and most co-localized with yield-related QTLs identified in previous studies. AX-90496773 and AX-90460290 were large-effect markers for PFW and MCFS, respectively. The two markers were stably identified in all environments and tagged to linkage disequilibrium (LD) blocks. Six potential candidate genes were predicted in LD blocks; five of them showed significantly different expression levels between the extreme materials with large PFW or MCFS variation at the seed development stage. Therefore, the five genes Glyma.16g018200, Glyma.16g018300, Glyma.05g243400, Glyma.05g244100 and Glyma.05g245300 were regarded as candidate genes associated with PFW and MCFS. CONCLUSION: These results provide useful information for the development of functional markers and exploration of candidate genes in vegetable soybean high-yield breeding programs.

Efficacy of different hemodialysis methods on dendritic cell marker CD40 and CD80 and platelet activation marker CD62P and P10 in patients with chronic renal failure.

BACKGROUND: Chronic renal failure (CRF) has become a major public health concern, which increases the risk of stroke and systemic thromboembolism. Therefore, therapeutic strategies are in urgent requirement. This study was conducted for investigating efficacy of hemodialysis (HD), hemodiafiltration (HDF), and hemoperfusion (HP) in patients with CRF and the correlation with the presence of complications following HD therapy. METHODS: The therapeutic effect, living quality, biochemical indicators, and dry weight were detected before and after the treatment regimens. Flow cytometry was conducted to detect expressions of dendritic cell markers (CD40 and CD80) and platelet activation markers (CD62P and P10), and the relationship between their expression and therapeutic effect as well as the association of these expressions with complications was analyzed. RESULTS: After HD therapy, patients presented with decreased serum creatinine, serum phosphorus, triglyceride, parathyroid hormone, and ß2 -MG expression; increased hemoglobin, plasma albumin expressions, and dry weight; and enhanced therapeutic effect and living quality. CD62P and P10 expressions decreased, while CD40 and CD80 expressions increased following HD therapy. The therapeutic effect improved in patients with low expressions of CD40 and CD80 and high expressions of CD62P and P10 following HP treatment and complications were lower after treatment of HDF and HP. CONCLUSION: The aforementioned results indicated that CRF patients treated with HP exhibited higher expression of CD40 and CD80 and lower expression of CD62P and P10, suggesting that HP is conferred to have better efficacy than HDF and HD. Therefore, HP may be a promising clinical regimen for treatment of CRF patients.

Beraprost Sodium, a Stable Analogue of PGI2, Inhibits the Renin-Angiotensin System in the Renal Tissues of Rats with Chronic Renal Failure.

BACKGROUND/AIMS: Chronic renal failure (CRF) is a prolonged kidney condition characterized by decreased kidney function that can eventually develop into total kidney failure. The renin-angiotensin system (RAS) helps to regulate the balance between human bodily fluids and electrolytes. The aim of the present study was to investigate the effects of a prostacyclin analogue (beraprost sodium [BPS]) on the expression of key factors associated with local RAS activities in the renal tissues of rats with CRF. METHODS: After a CRF rat model was successfully established, the levels of BUN, SCr, phosphorus, and calcium were detected by an automatic biochemistry analyzer. Furthermore, the activities of malondialdehyde (MDA) and superoxide dismutase (SOD) in rat renal tissues were measured using a colorimetric method, while the activity of angiotensin-converting enzyme (ACE) was determined by ultraviolet (UV) spectrophotometry. In situ hybridization was employed to determine the expression of angiotensin II type 1 receptor (AT). Finally, the positive expression rates of cells expressing important apoptotic proteins (Bax and Bcl-2) were determined, and the protein and mRNA levels of phosphatidylinositol 3-kinase (AKT) and key factors involved in the RAS (AT1, AT2, angiotensin ACE and angiotensinogen [AGT]) were evaluated by RT-qPCR and western blot analysis. RESULTS: Initial observations revealed that treatment with BPS decreased the levels of BUN, SCr and phosphorus but increased calcium levels in the renal tissues of CRF rats. Additionally, BPS reduced the levels of MDA while increasing the levels of SOD, ACE activity, and AT1 expression in the renal tissues of CRF rats. BPS inhibited glomerular hypertension and hyperfiltration; increased the mRNA and protein levels of AKT and AT2; and decreased the mRNA and protein levels of AT1, AGT, and ACE in the renal tissues of CRF rats. CONCLUSION: The results of this study demonstrate that BPS, a PGI2 analogue, inhibits the expression of key factors involved in the local RAS, resulting in a delay in the occurrence and development of CRF. The key findings of the present study ultimately highlight the potential of this PGI2 analogue as a promising therapeutic strategy for treating CRF.

Evaluation of Carotid Plaque Neovascularization in Patients With Coronary Heart Disease on Contrast-Enhanced Ultrasonography.

OBJECTIVES: To examine the repeatability of quantitative time-intensity curve analysis of neovascularization within carotid plaques with contrast-enhanced ultrasonography (US) and to investigate carotid plaque neovascularization in patients with coronary heart disease using contrast-enhanced US and the correlation between risk factors and acute coronary syndrome (ACS). METHODS: Sixty patients with ACS and 60 with stable coronary artery disease (CAD) underwent conventional carotid and contrast-enhanced US, and plaque enhancement was observed and analyzed quantitatively. Carotid contrast-enhanced US was performed within 1 month of ACS occurrence. Interobserver and intraobserver variability of the measurements was assessed. The peak signal intensity was the maximum number of contrast microbubbles that local tissues could accumulate, reflecting the local microvascular density and representing the capillary volume. RESULTS: The ACS group had higher low-density lipoprotein cholesterol (mean ± SD, 3.21 ± 0.75 versus 2.53 ± 0.71 mmol/L; P < .01) and high-sensitivity C-reactive protein (CRP; 3.76 ± 0.19 versus 2. 93 ± 0.15 mg/L; P < .01) levels than the stable CAD group. The proportion of soft plaques in the ACS group (81%) was higher than in the stable CAD group (53%). The proportion of plaque enhancement, peak signal intensity, and plaque-to-carotid lumen enhancement intensity ratio were higher in the ACS group than the stable CAD group. The peak signal intensity was correlated with the high-sensitivity CRP value. Logistic regression analyses indicated that age (65-74 years), high-sensitivity CRP, and enhancement intensity were correlated with the occurrence of ACS. The sensitivity and specificity of the peak signal intensity in carotid plaques were 80.0% and 88.3%, respectively (cutoff value, 9.97 dB; area under the receiver operating characteristic curve, 0.865). The time-intensity curve measurements had good repeatability. CONCLUSIONS: Carotid plaque enhancement is a potential independent risk factor for ACS occurrence. These results illustrate the correlation of carotid plaque vulnerability with the coronary artery symptomatic state according to the common pathogenetic mechanism of atherosclerosis.

Impaired right and left ventricular function in asymptomatic children with repaired tetralogy of Fallot by two-dimensional speckle tracking echocardiography study.

BACKGROUND: Early detection of right ventricular (RV) and left ventricular (LV) dysfunction in patients with repaired tetralogy of Fallot (TOF) is essential because dysfunction is correlated with a poor clinical outcome. The aim of this study was to assess RV and LV function in asymptomatic children with repaired TOF by two-dimensional ultrasound speckle tracking echocardiography (STE). METHODS: Fifty-six asymptomatic children with a preserved biventricular ejection fraction (EF) after repair of TOF and 35 healthy control subjects were studied. RV and LV strain and strain rate were measured by STE. RVEF and pulmonary regurgitation (PR) were assessed using cardiac magnetic resonance imaging. RESULTS: Compared with the control subjects, RV regional longitudinal strain and strain rate and global longitudinal strain (GLS) and strain rate (GLSR) were impaired in children with repaired TOF. Likewise, LV circumferential and radial strain and strain rate were reduced in patients with TOF. In contrast, longitudinal strain and strain rate did not differ between the groups. RV and LV GLSR were correlated with postoperative follow-up period (r1 = -0.44; r2 = -0.48). RV GLS and GLSR were associated with RVEF (r1 = 0.64; r2 = 0.60) and PR (r1 = -0.48; r2 = -0.49). LV circumferential strain rate was related to PR (r = -0.45). CONCLUSIONS: STE can identify abnormalities that may represent early impairment of RV and LV systolic function in postoperative TOF patients with a preserved EF. PR is associated with decreased biventricular performance in repaired patients. STE-derived strain and strain rate may be useful indices for detecting the early deterioration of biventricular performance in patients with TOF.

Two new compounds from Ganoderma lucidum.

Two pairs of new enantiomers, lucidulactones A and B (1 and 2), and two known compounds were isolated from Ganoderma lucidum. Their structures were determined by means of spectroscopic methods. The chiral HPLC was used to separate the ( - )- and (+)-antipodes of the new compounds.

Early effect of essential hypertension on the left ventricular twist-displacement loop by two-dimensional ultrasound speckle tracking imaging.

OBJECTIVE: To investigate two-dimensional (2D) ultrasound speckle tracking imaging (STI) in the evaluation of the early changes in the left ventricular (LV) twist-displacement loop in patients with hypertension (EH). METHODS: Sixty-five EH patients with left ventricular normal geometry (LVN) - including 33 cases with non-left atrial enlargement (NLAE) and 32 cases with left atrial enlargement (LAE) - along with 45 healthy individuals were enrolled in this study. Basal and apical 2D LV short-axis images were acquired and analyzed to obtain the LV rotation (LVrot) and LV radial displacement. Once the LV twist and LV radial displacement were calculated, an LV twist-displacement loop was constructed. Group comparisons between peak twist (Ptw), twist at mitral valve opening (MVOtw), untwisting rate (Utw R), systolic radial displacement (SD), systolic slope (SS), isovolumic relaxation radial displacement (IVRD) and isovolumic relaxation slope (IVRS) were performed. RESULTS: (1) The Ptw and MVOTw were greater in the NLAE and LAE groups when compared to the normal group while the UTw R was lower in likewise comparison. (2) The LV twist was correlated to the radial displacement in systole and in the isovolumic relaxation period. The SS and IVRS were greater in the NLAE and LAE groups when compared to the normal group. CONCLUSIONS: The LV twist-displacement loop can be reconstructed noninvasively by 2D ultrasound STI. EH affects the systolic and early diastolic component of the twist-displacement loop by increasing the LV twist and decreasing the LV untwisting respectively impairing LV relaxation. The assessment of the LV twist-displacement loop may be useful in the evaluation of early features of LV dysfunction in EH patients.

Combined fabrication of zeolitic imidazolate framework-8 and lanthanide towards coordination polymers: A dual-signal fluorescent probe for sensing Cu2+ based on synergistic effect of aggregation-induced emission and antenna effect.

Copper ion (Cu2+) detection remains an important task for monitoring water quality because of its specific toxicity. Herein, a new dual-signal fluorescent probe was developed by combining zeolitic imidazolate framework-8 (ZIF-8) and lanthanide for the detection of Cu2+ for the first time. The lanthanide coordination polymer (guanosine monophosphate and Eu3+, GMP/Eu) was initially incorporated into ZIF-8 to yield ZIF-8/GMP/Eu nanomaterials with extremely weak single emission fluorescence at 618 nm. It was found that the resulted nanomaterials could display a dual emission fluorescence at 515 nm and 618 nm after the introduction of tetracycline (TC) due to the synergistic effect of aggregation-induced emission effect (AIE, TC induced by ZIF-8) and antenna effect (AE, between TC and GMP/Eu). Interestingly, in the presence of Cu2+, the AIE of TC was destroyed because of the interaction of Cu2+ with ZIF-8 and TC. The AE between TC and GMP/Eu disappeared due to the formation of complex between TC and Cu2+. A dual-signal fluorescent probe of ZIF-8/GMP/Eu/TC was thereby established for sensing Cu2+ in the range of 0.5-100 µM. Such a dual-signal response strategy that intelligently utilized the "ON"/"OFF" of AIE and AE can not only eliminate the background interference, but also ensure the improved selectivity of Cu2+ sensing. Subsequently, the dual-signal fluorimetric strategy was applied for the detection of Cu2+ in environmental water samples, indicating the potential feasibility of applications for water quality monitoring.

Identification of novel molecules and pathways associated with fascin actin­bundling protein 1 in laryngeal squamous cell carcinoma through comprehensive transcriptome analysis.

Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor with a poor prognosis. Fascin actin­bundling protein 1 (FSCN1) has been reported to play a crucial role in the development and progression of LSCC; however, the underlying molecular mechanisms remain unknown. Herein, a whole transcriptome microarray analysis was performed to screen for differentially expressed genes (DEGs) in cells in which FSCN1 was knocked down. A total of 462 up and 601 downregulated mRNA transcripts were identified. Functional annotation analysis revealed that these DEGs were involved in multiple biological functions, such as transcriptional regulation, response to radiation, focal adhesion, extracellular matrix­receptor interaction, steroid biosynthesis and others. Through co­expression and protein­protein interaction analysis, FSCN1 was linked to novel functions, including defense response to virus and steroid biosynthesis. Furthermore, crosstalk analysis with FSCN1­interacting proteins revealed seven DEGs, identified as FSCN1­interacting partners, in LSCC cells, three of which were selected for further validation. Co­immunoprecipitation validation confirmed that FSCN1 interacted with prostaglandin reductase 1 and 24­dehydrocholesterol reductase (DHCR24). Of note, DHCR24 is a key enzyme involved in cholesterol biosynthesis, and its overexpression promotes the proliferation and migration of LSCC cells. These findings suggest that DHCR24 is a novel molecule associated with FSCN1 in LSCC, and that the FSCN1­DHCR24 interaction may promote LSCC progression by regulating cholesterol metabolism­related signaling pathways.

Clinical outcomes and predictive factors of stent grafts treatment for symptomatic central venous obstruction in end stage kidney disease patients with arteriovenous access.

To assess the efficacy of stent grafts (SGs) in managing central venous obstruction disease (CVOD) in hemodialysis (HD) patients with arteriovenous (AV) access, and to identify predictive factors influencing the SG treatment outcomes. HD subjects with CVOD who underwent SGs placement at our center between August 2018 and June 2022 were enrolled. Survival curve analysis using the Kaplan-Meier method and log-rank test was performed. Cox proportional hazards regression analysis was employed to identify predictive factors associated with outcomes. A total of 59 SG implantation procedures for CVOD were analyzed, comprising 30 cases of stenosis and 29 cases of occlusion. The access circuit primary patency (ACPP) at 6, 12, and 24 months post-SG placement were 80.9%, 53.8%, and 31.4%, respectively, while, the target lesion primary patency (TLPP) were 91.3%, 67.6%, and 44.5%, respectively. Subgroup analysis revealed higher TLPP in the stenosis group compared to the occlusion group, although the difference was not statistically significant (P = 0.165). The TLPP was significantly improved by SG placement in those who had antecedent balloon dilations (P < 0.001). Cox proportional hazards regression identified target lesion length ≥ 30 mm and procedure defects as independent predictors of lower TLPP after SG treatment for CVOD in HD patients. SG placement demonstrates safety and efficacy in managing CVOD among HD patients, leading to improved TLPP of endovascular therapy (EVT) for CVOD. Notably, long target lesions (≥ 30 mm) and procedure defects emerged as predictive factors influencing TLPP.

Emerging roles and potential clinical applications of translatable circular RNAs in cancer and other human diseases.

Circular RNAs (circRNAs) are a special class of single-stranded RNA molecules with covalently closed loops widely expressed in eukaryotic organisms. CircRNAs have long been considered to play important roles in various physiological and pathological processes as non-coding RNAs. However, circRNAs have recently garnered considerable attention due to their ability to be translated into peptides/proteins via internal ribosome entry site- or N6-methyladenosine-mediated pathways or rolling translation mechanisms. Furthermore, dysregulation of translatable circRNAs and their encoded proteins has been associated with developing and progressing diseases such as cancer. This review aims to summarize the driving mechanisms of circRNA translation and the available strategies in circRNA translation research. The main focus is on the emerging biological functions of translatable circRNAs, their regulatory mechanisms, and potential clinical applications in human diseases to provide new perspectives on disease diagnosis, prognosis, and targeted therapy.