Search

A great amount of new S‐wave data has been combined to image the mantle structure down to lower mantle depth near the southeastern margin of Eurasia and understand the tectonics in South China since the Mesozoic. Our results reveal a large‐scale structure beneath the South China Sea, with a prominent, broad low‐velocity feature of at least 1500‐km wide in and below the mantle transition zone (MTZ) and a pronounced low‐velocity feature of nearly 500‐km wide in the lowermost mantle. Together these features may represent the head‐and‐tail of an upwelling mantle plume that has interacted with and deformed by the subducting plates in the region. The Andaman–Sumatra plate is seen subducting steeply without stagnation in the MTZ over the large‐scale low‐velocity structure, suggesting that the upwelling mantle may have exerted significant influence on the overlying plate tectonics. Our results suggest a long‐term extensional regime near the southeastern margin of Eurasia, which may help to understand the formation of the large‐scale intra‐plate magmatism and mineralization with accumulation of huge amount of rare metal elements in South China during the Mesozoic, and the continental breakup, the southeastward extrusion of Indochina, and the opening of the South China Sea during the Cenozoic. [ABSTRACT FROM AUTHOR]

Background and Purpose: Non-alcoholic hepatic fatty liver disease (NAFLD) is a manifestation of the metabolic syndrome in the liver and non-alcoholic steatohepatitis (NASH) represents its advanced stage. R17 derived from bouchardatine, shows benefits in the metabolic syndrome, but has not been tested in the liver. The present study examined the pharmacological effects of R17 in a model of NAFLD/NASH and its mode of action.Experimental Approach: The effects of R17 were examined in mice fed a high-fat (HF) diet to induce the pathological characteristics of NAFLD/NASH and in cultures of HuH7 cells. We used histological and immunohistochemical techniques along with western blotting and siRNA. Generation of ROS and apoptosis were measured.Key Results: Administration of R17 (20 mg·kg-1 , i.p. every other day) for 5 weeks reversed HF-induced hepatic triglyceride content, inflammation (inflammatory cytokines and macrophage numbers), injury (hepatocyte ballooning and apoptosis, plasma levels of alanine aminotransferase and aspartate aminotransferase), and fibrogenesis (collagen deposition and mRNA expression of fibrosis markers). In cultured cells, R17 reduced cell steatosis from both lipogenesis and fatty acid influx. The attenuated inflammation and cell injury were associated with inhibition of both endoplasmic reticulum (ER) stress and oxidative stress. Notably, R17 activated the liver kinase B1-AMP-activated protein kinase (AMPK) pathway by inhibiting activity of ATP synthase, rather than direct stimulation of AMPK.Conclusion and Implications: R17 has therapeutic potential for NAFLD/NASH. Its mode of action involves the elimination of ER and oxidative stresses, possibly via activating the LKB1-AMPK axis by inhibiting the activity of ATP synthase. [ABSTRACT FROM AUTHOR]

Review: synthesis, biological and medicinal application of nucleosides, DNA, and RNA posphonates and phosphoramidates [ABSTRACT FROM AUTHOR]

The article describes the case of a 72-year-old woman who had toxic epidermal necrolysis associated with the aromatic antiepileptic drug lamotrigine (LTG). The patient received methylprednisolone and LTG for optical neuromyelitis. She was eventually discharged after spending 21 days in the hospital and receiving intravenous immunoglobulin and methylprednisolone.

Transient receptor potential ankyrin 1 (TRPA1) plays an important role in different cardiovascular diseases. However, the role of TRPA1 in dilated cardiomyopathy (DCM) remains unclear. Here, we aimed to investigate the role of TRPA1 in DCM induced by doxorubicin (DOX) and explore its possible mechanisms. GEO data were used to explore the expression of TRPA1 in DCM patients. DOX (2.5 mg/kg/week, 6 weeks, i.p.) was used to induce DCM. Bone marrow‐derived macrophages (BMDMs) and neonatal rat cardiomyocytes (NRCMs) were isolated to explore the role of TRPA1 in macrophage polarization, cardiomyocyte apoptosis, and pyroptosis. In addition, DCM rats were treated with the TRPA1 activator, cinnamaldehyde to explore the possibility of clinical translation. TRPA1 expression was increased in left ventricular (LV) tissue in DCM patients and rats. TRPA1 deficiency aggravated the cardiac dysfunction, cardiac injury, and LV remodeling in DCM rats. In addition, TRPA1 deficiency promoted the M1 macrophage polarization, oxidative stress, cardiac apoptosis, and pyroptosis induced by DOX. RNA‐seq results showed that TRPA1 knockout promoted the expression of S100A8, an inflammatory molecule that belongs to the family of Ca2+‐binding S100 proteins, in DCM rats. Furthermore, S100A8 inhibition attenuated M1 macrophage polarization in BMDMs isolated from TRPA1 deficiency rats. Recombinant S100A8 promoted the apoptosis, pyroptosis, and oxidative stress in primary cardiomyocytes stimulated with DOX. Finally, TRPA1 activation via cinnamaldehyde alleviated the cardiac dysfunction and reduced S100A8 expression in DCM rats. Taken together, these results suggested that TRPA1 deficiency aggravates DCM by promoting S100A8 expression to induce M1 macrophage polarization and cardiac apoptosis. [ABSTRACT FROM AUTHOR]

Review: [55 refs. [ABSTRACT FROM AUTHOR]

A new and highly enantioselective method for catalytic [2 + 2] cycloadditions between unactivated alkenes and allenoates is disclosed. [ABSTRACT FROM AUTHOR]

Orsellinic acid (OA) derivatives are produced by filamentous fungi using nonreducing polyketide synthases (nrPKSs). The chain‐releasing thioesterase (TE) domains of such nrPKSs were proposed to also catalyze dimerization to yield didepsides, such as lecanoric acid. Here, we use combinatorial domain exchanges, domain dissections and reconstitutions to reveal that the TE domain of the lecanoric acid synthase Preu6 of Preussia isomera must collaborate with the starter acyl transferase (SAT) domain from the same nrPKS. We show that artificial SAT‐TE fusion proteins are highly effective catalysts and reprogram the ketide homologation chassis to form didepsides. We also demonstrate that dissected SAT and TE domains of Preu6 physically interact, and SAT and TE domains of OA‐synthesizing nrPKSs may co‐evolve. Our work highlights an unexpected domain–domain interaction in nrPKSs that must be considered for the combinatorial biosynthesis of unnatural didepsides, depsidones, and diphenyl ethers. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to characterize the topological alterations and classification performance of high‐order functional connectivity (HOFC) networks in cognitively preserved patients with Parkinson's disease (PD), relative to low‐order FC (LOFC) networks. Methods: The topological metrics of the constructed networks (LOFC and HOFC) obtained from fifty‐one cognitively normal patients with PD and 60 matched healthy control subjects were analyzed. The discriminative abilities were evaluated using machine learning approach. Results: The HOFC networks in the PD group showed decreased segregation and integration. The normalized clustering coefficient and small‐worldness in the HOFC networks were correlated to motor performance. The altered nodal centralities (distributed in the precuneus, putamen, lingual gyrus, supramarginal gyrus, motor area, postcentral gyrus and inferior occipital gyrus) and intermodular FC (frontoparietal and visual networks, sensorimotor and subcortical networks) were specific to HOFC networks. Several highly connected nodes (thalamus, paracentral lobule, calcarine fissure and precuneus) and improved classification performance were found based on HOFC profiles. Conclusion: This study identified disrupted topology of functional interactions at a high level with extensive alterations in topological properties and improved differentiation ability in patients with PD prior to clinical symptoms of cognitive impairment, providing complementary insights into complex neurodegeneration in PD. [ABSTRACT FROM AUTHOR]

Background: Following catheter ablation for atrial fibrillation (AF), there are dynamic changes in the atrial myocardium associated with damage to and necrosis of atrial tissue and other procedure related changes in rhythm and anticoagulation. Early time‐dependent changes in biomarkers of necrosis, inflammation, and coagulation have been reported. This study examines mid‐term (4–8 weeks post‐ablation) changes in biomarkers and explores their ability to predict AF recurrence at one‐year. Methods: Twenty‐seven patients (mean age 65.4 ± 9.7 years, 30% female) undergoing catheter ablation for AF had peripheral venous blood samples obtained at the time of ablation and 4–8 weeks later. All samples were processed to obtain plasma which was frozen for subsequent analysis. Coagulation studies were performed at the Northwestern Special Hemostasis Laboratory: VWF, ADAMTS13, PAI‐1, D‐dimer, and TAT complexes. A commercial lab analyzed samples for CRP, cystatin C, fibrinogen, galectin, IL‐6, MMP‐2, myoglobin, NT‐proBNP, PAI‐1, TIMP‐1, TIMP‐2, TPA, and VWF. Results: Significant changes were noted with higher levels of ADAMTS13 (p < 0.0001), fibrinogen (p = 0.004), MMP‐2 (p = 0.0002), TIMP‐2 (p = 0.003), and TPA (p = 0.001) compared to lower levels of TAT (p < 0.0001) and NT‐proBNP (p = 0.0001) at follow up post‐ablation. One year after ablation, AF had recurred in 11/26 (42%) of patients. None of the biomarker changes predicted the 1‐year outcome, and there was no significant association with the use of warfarin versus rivaroxaban. Conclusion: In patients undergoing catheter ablation for AF, there were significant changes in pre‐ vs post‐ablation levels of multiple biomarkers. However, these changes were not associated with 1‐year outcome of AF recurrence. [ABSTRACT FROM AUTHOR]

Orsellinic acid (OA) derivatives are produced by filamentous fungi using nonreducing polyketide synthases (nrPKSs). The chain‐releasing thioesterase (TE) domains of such nrPKSs were proposed to also catalyze dimerization to yield didepsides, such as lecanoric acid. Here, we use combinatorial domain exchanges, domain dissections and reconstitutions to reveal that the TE domain of the lecanoric acid synthase Preu6 of Preussia isomera must collaborate with the starter acyl transferase (SAT) domain from the same nrPKS. We show that artificial SAT‐TE fusion proteins are highly effective catalysts and reprogram the ketide homologation chassis to form didepsides. We also demonstrate that dissected SAT and TE domains of Preu6 physically interact, and SAT and TE domains of OA‐synthesizing nrPKSs may co‐evolve. Our work highlights an unexpected domain–domain interaction in nrPKSs that must be considered for the combinatorial biosynthesis of unnatural didepsides, depsidones, and diphenyl ethers. [ABSTRACT FROM AUTHOR]

Efferocytosis is defined as the clearance of apoptotic cells (ACs) in physiological and pathological states and is performed by efferocytes, such as macrophages. Efferocytosis can lead to the resolution of inflammation and restore tissue homoeostasis; however, the mechanisms of efferocytosis in determining inflammation resolution are still not completely understood, and the effects of efferocytosis on other proresolving properties need to be explored and explained. In this review, the process of efferocytosis will be summarized briefly, and then these mechanisms and effects will be thoroughly discussed. In addition, the association between mechanisms of efferocytosis in determining resolution of inflammation and cardiovascular diseases will also be reviewed, as an understanding of this association may provide information on novel treatment targets. [ABSTRACT FROM AUTHOR]

The photoinduced regio- and enantioselective coupling of naphthols and derivatives thereof is achieved in the confined chiral coordination space of a RuII metalloligand based cage. The racemic or enantiopure cages encapsulate naphthol guests, which then undergo a regiospecific 1,4-coupling, rather than the normal 1,1-coupling, to form 4-(2-hydroxy-1-naphthyl)-1,2-napthoquinones; moderate stereochemical control is achieved with homochiral cages. The photoreactions proceed under both aerobic and anaerobic conditions but through distinct pathways that nevertheless involve the same radical intermediates. This unusual dimerization constitutes a very rare example of asymmetric induction in biaryl coupling by making use of coordination cages with dual functionality-photoredox reactivity and stereoselectivity. [ABSTRACT FROM AUTHOR]

Cyanobacterial blooms are often associated with an increase in abundance of small-bodied zooplankton. The hypothesis that toxic cyanobacteria lead to in the dominance of small-bodied zooplankton was tested by investigating competitive outcomes with three common cladoceran species, analysing cladoceran remains in sediments, and identifying zooplankton resting eggs., Although the large-bodied cladoceran Daphnia pulex outcompeted the medium-sized cladoceran Simocephalus vetulus when fed green algae in laboratory experiments, the presence of toxic cyanobacteria completely altered this competitive outcome. Similar shifts in competitive dominance with the presence of cyanobacteria were observed when both D. pulex and S. vetulus competed with the small-bodied cladoceran Bosmina longirostris., Sediment cores from Dianshan Lake, the largest shallow lake in Shanghai, and surface sediments from 10 random ponds and rivers in the area were collected to recover the cladoceran and total zooplankton communities. Microcystin concentrations in sediments were used as a proxy for cyanobacterial abundances in nature. Altogether, cladoceran remains representing 10 genera were recovered from the sediment samples. Microcystin concentrations in the Dianshan Lake sediment cores were positively correlated with Bosmina abundance, but negatively correlated with both Daphnia and Diaphanosoma abundance. The proportion of large-bodied cladocerans significantly declined in relation to small-bodied species with increasing microcystin concentrations in the lake sediments., Fifty-eight types of zooplankton resting eggs were recovered in sediments from Shanghai waters and identified using DNA barcoding. The abundance of both a lecanid rotifer and total rotifers significantly increased with increasing cyanobacteria in the sediment cores, whereas the dominant copepod, Sinocalanus tenellus, decreased. However, these trends were not observed in comparison of surface sediments from 10 ponds and rivers in the area., These results indicate that the presence of toxic cyanobacteria may have altered the zooplankton communities and contributed to increased dominance of small-bodied species. This study also demonstrates that cladoceran remains and zooplankton resting eggs recovered from sediment cores are convenient natural archives for evaluating zooplankton responses to cyanobacterial blooms. [ABSTRACT FROM AUTHOR]

Semaphorins (Semas), which belongs to the axonal guidance molecules, include 8 classes and could affect axon growth in the nervous system. Recently, semaphorins were found to regulate other pathophysiological processes, such as immune response, oncogenesis, tumor angiogenesis, and bone homeostasis, through binding with their plexin and neuropilin receptors. In this review, we summarized the detailed role of semaphorins and their receptors in the pathological progression of various cardiovascular diseases (CVDs), highlighting that semaphorins may be potential therapeutic targets and novel biomarkers for CVDs. [ABSTRACT FROM AUTHOR]

Cardiac apoptosis has been identified as one of the main precipitating factors of heart failure (HF) throughout the whole course of progressive disease. Limited to the lack of diagnostic markers and effective drug targets, cardiac apoptosis is still a major clinical challenge. Here, we reveal a potential novel therapeutic target for cardiac apoptosis. In the cause of the study, we found that KLHL38 was highly expressed in cardiac tissue of HF patients via GEO data‐mining, which was further verified in the heart tissue of transverse aortic constriction mice. Meanwhile, the expression of KLHL38 is negatively correlated with myocardin protein level, which is a key cardiac apoptosis regulator. The KLHL38 overexpression obviously promoted cardiomyocyte apoptosis treated with staurosporine by facilitation of myocardin's ubiquitylation and subsequent proteasomal degradation. These findings reveal a new therapeutic target, which may provide a new theoretical foundation for the treatment of myocardial apoptosis in clinical practice. [ABSTRACT FROM AUTHOR]

For the purpose of investigating the coordination behavior of sterically congested alkenes and exploring the possibility of cofacial complexation in the polycyclic aromatic system for the formation of extended polymeric networks, a new tetradentate ligand, 1,1,2,2-tetrakis[4-(1 H-1,2,4-triazol-1-yl)phenyl]ethylene (TTPE), has been designed and synthesized. By using TTPE as a building block with regard to the self-assembly with MnCl2 ⋅4 H2O, a novel two-dimensional coordination framework {[Mn(TTPE)Cl2] ⋅4 CHCl3} n ( 1) can be isolated. Anion-exchange and organic-group-functionalized aromatic guest TTPE-loaded host-guest complex experimental results indicate that coordinated Cl− anions in the 2D framework of 1 can be completely replaced with dissociative ClO4− groups in an irreversible single-crystal-to-single-crystal transformation fashion, as evidenced by the anion-exchange products of {[Mn(TTPE)(H2O)2](ClO4)2 ⋅0.5 TTPE ⋅5.25 H2O} n ( 2). Interestingly, TTPE, acting as an organic template, was encapsulated in the confined space of the 2D grid of 2. To the best of our knowledge, such large organic molecules encapsulated in the reactive organic-group-functionalized aromatic-guest-loaded host-guest complex are unprecedented up to now. Luminescence measurements illustrate that 1 and 2 represent novel examples of sensing materials based on triazole derivatives. Further, 2 has been demonstrated by tuning the fluorescence response of porous metal-organic frameworks as a function of adsorbed small analytes. [ABSTRACT FROM AUTHOR]

Direct conversion of methane into value‐added chemicals, such as methanol under mild conditions, is a promising route for industrial applications. In this work, atomically dispersed Rh on TiO2 suspended in an aqueous solution was used for the oxidation of methane to methanol. Promoted by copper cations (as co‐catalyst) in solution, the catalysts exhibited high activity and selectivity for the production of methanol using molecular oxygen with the presence of carbon monoxide at 150 °C with a reaction pressure of 31 bar. Millimole level yields of methanol were reached with the selectivity higher than 99 % using the Rh/TiO2 catalysts with the promotion of the copper cation. CO was the reductive agent to generate H2 from H2O, which led to the formation of H2O2 through the reaction of H2 and O2. Atomically dispersed Rh activated the C−H bond in CH4 and catalyzed the oxidation using H2O2. Copper cations maintained the low‐valence state of Rh. Moreover, copper acted as a scavenger for suppressing the overoxidation, thus leading to the high selectivity of methanol. [ABSTRACT FROM AUTHOR]

Direct conversion of methane into value‐added chemicals, such as methanol under mild conditions, is a promising route for industrial applications. In this work, atomically dispersed Rh on TiO2 suspended in an aqueous solution was used for the oxidation of methane to methanol. Promoted by copper cations (as co‐catalyst) in solution, the catalysts exhibited high activity and selectivity for the production of methanol using molecular oxygen with the presence of carbon monoxide at 150 °C with a reaction pressure of 31 bar. Millimole level yields of methanol were reached with the selectivity higher than 99 % using the Rh/TiO2 catalysts with the promotion of the copper cation. CO was the reductive agent to generate H2 from H2O, which led to the formation of H2O2 through the reaction of H2 and O2. Atomically dispersed Rh activated the C−H bond in CH4 and catalyzed the oxidation using H2O2. Copper cations maintained the low‐valence state of Rh. Moreover, copper acted as a scavenger for suppressing the overoxidation, thus leading to the high selectivity of methanol. [ABSTRACT FROM AUTHOR]

Background and Purpose: Non‐alcoholic steatohepatitis (NASH) is the more severe form of metabolic associated fatty liver disease (MAFLD) and no pharmacological treatment as yet been approved. Identification of novel therapeutic targets and their agents is critical to overcome the current inadequacy of drug treatment for NASH. Experimental Approach The correlation between heat shock factor 1 (HSF1) levels and the development of NASH and the target genes of HSF1 in hepatocyte were investigated by chromatin‐immunoprecipitation sequencing. The effects and mechanisms of SYSU‐3d in alleviating NASH were examined in relevant cell models and mouse models (the Ob/Ob mice, high‐fat and high‐cholesterol diet and the methionine‐choline deficient diet‐fed mice). The actions of SYSU‐3d in vivo were evaluated. Key Results: HSF1 is progressively reduced with mitochondrial dysfunction in NASH pathogenesis and activation of this transcription factor by its newly identified activator SYSU‐3d effectively inhibited all manifestations of NASH in mice. When activated, the phosphorylated HSF1 (Ser326) translocated to nucleus and bound to the promoter of PPARγ coactivator‐1α (PGC‐1α) to induce mitochondrial biogenesis. Thus, increasing mitochondrial adaptive oxidation and inhibiting oxidative stress. The deletion of HSF1 and PGC‐1α or recovery of HSF1 in HSF1‐deficiency cells showed the HSF1/PGC‐1α pathway was mainly responsible for the anti‐NASH effects of SYSU‐3d independent of AMP‐activated protein kinase (AMPK). Conclusion and Implications: Activation of HSF1 is a practical therapeutic approach for NASH treatment via the HSF1/PGC‐1α/mitochondrial pathway and SYSU‐3d can be considered as a potential candidate for the treatment of NASH. [ABSTRACT FROM AUTHOR]

Objective: Based on a large public cohort, we aimed to investigate the prevalence of distant metastases in patients with osteosarcoma, to evaluate the survival of patients with different metastases and to reveal the related risk and prognostic factors for distant metastases. Methods: The information of osteosarcoma patients with or without distant metastases was retrospectively extracted from the Surveillance, Epidemiology, and End Result database from January 2010 to December 2015. Patients were excluded if they were diagnosed at autopsy or via death certification. The Kaplan–Meier method was used to calculate the overall survival in the entire cohort and across patients with metastases to different organs. The related prognostic factors were investigated by univariate and multivariate Cox proportional hazard regression analysis. The logistic regression method was used to reveal the risk factors for the development of different metastases. The effects of different variables on the survival and prevalence of distant metastases were compared using subgroup analysis. Variables with P < 0.05 in the univariate regression analysis were further examined using multivariate regression analysis. Results: In total, 1470 osteosarcoma patients (mean age 30 ± 22 years) were included, among which 278 patients (18.9%) were initially diagnosed with distant metastasis. The median follow‐up duration was 33.0 (30.2–35.8) months. The lung was the most common metastatic site (83.8%), followed by the bone (21.9%), liver (2.9%), and brain (2.2%). A total of 232 patients (83.5%) presented only one distant metastatic site, while the other 46 patients showed two or more metastatic sites. A lower proportion of metastasis was observed in patients aged from 25 to 59 years [odds ratio (OR) = 0.59; 95% confidence interval (CI): 0.37–0.95]. More metastases were noted in patients with T2/T1 (OR = 1.91; 95% CI: 1.28–2.84), T3/T1 (OR = 4.48; 95% CI: 1.78–11.30) and N1/N0 stages (OR = 6.66; 95% CI: 2.68–16.56). The 1‐, 3‐, and 5‐year overall survival rates for metastatic patients were 57.3% (95% CI: 50.8%–63.8%), 25.3% (95% CI: 18.8%–31.9%), and 18.1% (95% CI: 10.2%–26.0%), respectively. Metastatic patients older than 25 years were prone to have poor survival and a relatively better prognosis (hazard ratio = 0.41; 95% CI: 0.25–0.69) was noticed among those who underwent surgery on the primary site. Different metastatic organs have homogeneous and heterogeneous risk and prognostic factors. Conclusion: The high incidence of initial distant metastasis in osteosarcoma and the inconsistent predictive factors should be given more attention in the clinical management of patients with osteosarcoma. [ABSTRACT FROM AUTHOR]

Abstract . Two aliphatic dicarboxy1ic acid ligands, iminodiacetic acid (H2L1) and 3,3-thiodipropionic acid (H2L2), were used to construct two novel lead(II) frameworks, namely, [Pb(μ4-L1)Br] n ( 1) and [Pb3(μ9-L2)(μ2-Br)2Br2] n ( 2), under hydrothermal conditions. It has to be noted that for 1 the central PbII ions are bridged by L2- ligands resulting in infinite right- and left-handed helical Pb-(O-C-O)-Pb linkage. Compound 2 represents a novel 3D hybrid luminescent lead(II) framework with I3O0 type connectivity. For 2 infinite 2D Pb-O-Pb inorganic layers and trinuclear Pb3Br4 clusters are inter-linked forming a 3D inorganic connectivity. In 1 the five-coordinate central PbII ions adopt a hemi-directed coordination arrangement, whereas in 2 six-coordinate Pb1, six-coordinate Pb2, and four-coordinate Pb3 atoms adopt hemi-directed coordination arrangements. The variable lead(II) coordination environment and flexible coordination modes of carboxy1ic acid ligands such as H2L1 and H2L2 also reveal great potential for constructing novel inorganic-organic hybrid materials. Furthermore TGA, FT-IR, PXRD, elemental analysis, and photo-luminescent properties of 1 and 2 were investigated. [ABSTRACT FROM AUTHOR]

Unambiguous characterization of 5-substituted-4-thiopyrimidine nucleosides (ribonucleosides and 2'-deoxynucleosides) was performed using NMR spectroscopy. Assignments of all proton and carbon signals of 5-bromo-4-thiouridine and related nucleosides were systematically carried out and firmly established by COSY and HMQC techniques. The NMR data of various 4-thiopyrimidine nucleosides are compared, and the key contributing factors discussed. The approach presented here is applicable to other modified nucleosides and nucleotides, as well as nucleobases. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Non‐noble metal photocatalysts have received widespread attention with the popularity of photocatalytic hydrogen evolution. Here, a brand‐new series of ZnFe2O4/Al‐MCM‐41 photocatalysts were synthesized with a simple hydrothermal strategy and analyzed through various characterizations. The results revealed that 40 % loading of Zinc ferrite (ZnFe2O4) showed the most remarkable hydrogen evolution effect without noble metal decorated. It has a maximum photocatalytic hydrogen evolution of 4525.4 μmol g−1 in 3 h, which is about 5.4 times higher than that of pure ZnFe2O4. These results are mainly owing to the loading of Al‐MCM‐41, which can provide more surface reaction sites and delay the recombination of charges and holes. Moreover, the composite shows good cyclability and stability, with a high hydrogen evolution after three repeated cycles. [ABSTRACT FROM AUTHOR]

Protein regulator of cytokinesis 1 (PRC1) is a microtubule bundling protein that is involved in the regulation of the central spindle bundle and spindle orientation during mitosis. However, the functions of PRC1 during meiosis have rarely been studied. In this study, we explored the roles of PRC1 during meiosis using an oocyte model. Our results found that PRC1 was expressed at all stages of mouse oocyte meiosis, and PRC1 accumulated in the midzone/midbody during anaphase/telophase I. Moreover, depleting PRC1 caused defects in polar body extrusion during mouse oocyte maturation. Further analysis found that PRC1 knockdown did not affect meiotic spindle formation or chromosome segregation; however, deleting PRC1 prevented formation of the midzone and midbody at the anaphase/telophase stage of meiosis I, which caused cytokinesis defects and further induced the formation of two spindles in the oocytes. PRC1 knockdown increased the level of tubulin acetylation, indicating that microtubule stability was affected. Furthermore, KIF4A and PRC1 showed similar localization in the midzone/midbody of oocytes at anaphase/telophase I, while the depletion of KIF4A affected the expression and localization of PRC1. The PRC1 mRNA injection rescued the defects caused by PRC1 knockdown in oocytes. In summary, our results suggest that PRC1 is critical for midzone/midbody formation and cytokinesis under regulation of KIF4A in mouse oocytes. [ABSTRACT FROM AUTHOR]

To research the impact of autophagy on alveolar epithelial cell inflammation and its possible mechanism in the early stages of hypoxia, we established a cell hypoxia–reoxygenation model and orthotopic left lung ischemia–reperfusion model. Rat alveolar epithelial cells stably expressing GFP‐LC3 were treated with an autophagy inhibitor (3‐MA) or an autophagy promoter (rapamycin), followed by hypoxia–reoxygenation treatment for 2, 4, and 6 hr in vitro. In vivo, 20 male Sprague Dawley rats were randomly divided into four groups (model group: No blocking of the hilum in the left lung; control group: Blocking of the hilum in the left lung for 1 hr with dimethyl sulfoxide lavage; 3‐MA group: Blocking of the hilum in the left lung for 1 hr with 100 ml/kg of 3‐MA (5 μmol/L) solution lavage; and rapamycin group: Blocking of the hilum in the left lung for 1 hr with 100 ml/kg of rapamycin (250 nmol/L) solution lavage) to establish an orthotopic left lung ischemia model. This study demonstrated that rapamycin significantly suppressed the nuclear factor kappa B signaling pathway and limited the expression of proinflammatory factors. A contrary result was found after the 3‐MA pretreatment. These findings indicate that autophagy reduces ischemia–reperfusion injury by repressing inflammatory signaling pathways in the early stages of hypoxia in vitro and in vivo. Autophagy could be a new protective method for application in lung ischemia–reperfusion injury. [ABSTRACT FROM AUTHOR]

The article discusses research which analyzed the gravity and magnetic evidence for the geological setting of major mineral systems of the main metallogenic belts in South China. Topics covered include the metallogenic factors of the deposits, the difference in the type and metal association of the deposits, and the distribution of termination sites of different mineral systems in the area which provide indications for future ore-prospecting exploration in South China.

Objectives: DNA damage and errors of accurate chromosome segregation lead to aneuploidy and foetal defects. DNA repair and the spindle assembly checkpoint (SAC) are the mechanisms developed to protect from these defects. Checkpoint kinase 1 (CHK1) is reported to be an important DNA damage response protein in multiple models, but its functions remain unclear in early mouse embryos. Materials and Methods: Immunofluorescence staining, immunoblotting and real‐time reverse transcription polymerase chain reaction were used to perform the analyses. Reactive oxygen species levels and Annexin‐V were also detected. Results: Loss of CHK1 activity accelerated progress of the cell cycle at the first cleavage; however, it disturbed the development of early embryos to the morula/blastocyst stages. Further analysis indicated that CHK1 participated in spindle assembly and chromosome alignment, possibly due to its regulation of kinetochore‐microtubule attachment and recruitment of BubR1 and p‐Aurora B to the kinetochores, indicating its role in SAC activity. Loss of CHK1 activity led to embryonic DNA damage and oxidative stress, which further induced early apoptosis and autophagy, indicating that CHK1 is responsible for interphase DNA damage repair. Conclusions: Our results indicate that CHK1 is a key regulator of the SAC and DNA damage repair during early embryonic development in mice. [ABSTRACT FROM AUTHOR]

Objective: In this study, the clinical effect of negative pressure drainage‐assisted irrigation (NPDI) technique was evaluated in treating maxillofacial space infection (MSI) by comparing with traditional technique. Method: A prospective study was conducted in 58 patients with MSI. The patients were randomly divided into two groups based on different treatment techniques. Thirty patients receiving NPDI were included in NPDI group, and 28 patients receiving traditional technique were included in traditional group. Case data (gender, age, etiology, concurrent illness, diabetes, involved spaces, preoperative white cell count, airway control method) and clinical effect (postoperative hospital stay, total cost of admission) for the two groups were analyzed. Results: Patients in both groups were cured clinically. There were no significant differences in gender, age, etiology, concurrent illness, diabetes, involved spaces, preoperative white cell count, and airway control method in NPDI group and traditional group (p >.05). The postoperative hospital stay and the total cost of admission in the NPDI group were significantly lower than the traditional group (p <.001). Conclusion: Negative pressure drainage‐assisted irrigation used in the treatment of MSI can shorten the postoperative hospital stay, reduce the total cost of admission, and show favorably clinical effect. It is a clinically recommended method for MSI. [ABSTRACT FROM AUTHOR]

Increased inflammation is the key mechanism that mediates sepsis induced cardiac injury. Resolvin D1 (RvD1), a bioactive lipid mediator synthesized from docosahexaenoic acid, can attenuate the severity of many inflammation‐related diseases through anti‐inflammatory and pro‐resolving properties. However, the protective role of RvD1 in sepsis induced cardiac injury remains unclear. Mice were randomly divided into three groups: the control group, LPS group and RvD1 + LPS group. LPS (10 mg/kg, i.p.) was used to establish a sepsis‐induced cardiac injury model. RvD1 (5 ug/kg, i.p.) was injected 30 min before LPS injection. RvD1 treatment significantly attenuated the deteriorated cardiac function and cardiac injury induced by LPS, as evidenced by the improved left ventricular ejection fraction, serum levels of cardiac injury markers and severity of cardiomyocyte apoptosis. In addition, RvD1 treatment significantly attenuated the infiltration of pro‐inflammatory M1 macrophages and expression of inflammatory cytokines in the heart. Mechanistically, the attenuated activation of NK‐κB and MAPK signaling mediated the anti‐inflammatory and antiapoptotic effects of RvD1. In addition, LPS‐induced infiltration of neutrophils and M1 macrophages in the spleen was significantly attenuated by the RvD1 treatment. Results of the present study suggest that RvD1 protects the heart against LPS‐induced injuries by attenuating the local and systemic inflammatory response, highlighting the therapeutic effects of RvD1 in sepsis‐induced cardiac injury. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSCs) have multilineage differentiation potential and can transform into neuron cells under an appropriate environment. Retinoic acid (RA) facilitates the neuronal differentiation of MSCs. We found that RXRα, a RA receptor, was significantly upregulated in RA‐induced process. Here, we show that RXRα collaborated with myocardin‐related transcription factor‐A (MRTF‐A) to strongly promote the RA‐induced process as evidenced by the increase in NF‐H expression and NF‐H promoter transcription activity. Our studies reveal that RXRα and MRTF‐A exhibit protein interactions and synergistically inhibit the MSCs apoptosis by enhancing the P21 expression. Furthermore, RXRα and MRTF‐A can activate P21 transcription by affecting the formation of the MRTF‐A/RXRα/RARE complex. These findings reveal the important roles of RXRα and MRTF‐A signaling in RA‐induced neural‐like differentiation of MSCs and describe a new mechanism underlying the synergistic interaction of RXRα and MRTF‐A. [ABSTRACT FROM AUTHOR]

Background: Kawasaki disease (KD) is an acute, self‐limited vasculitis. Coronary artery aneurysm (CAA) serves as a major contributor to the long‐term prognosis of KD. In addition, acute KD usually also leads to several kinds of noncoronary cardiac abnormalities (NCA) involving the pericardium, myocardium and endocardium. Materials and methods: A total of 142 Chinese children with KD were recruited from July 2015 to April 2018. Blood samples were collected at 24 hours pre‐intravenous immunoglobulin (IVIG) therapy. Several inflammatory mediators and biomarkers for acute myocardial infarction were detected. Echocardiography and electrocardiography (ECG) were performed. Results: Plasma white blood cell counts (WBC) were significantly increased in patients with IVIG‐nonresponsive KD when compared with their IVIG‐responsive counterparts. A total of 106 children (74.65%) suffered from NCA, including 8 patients (5.63%) with pericardial effusion, 23 patients (16.20%) with acute myocarditis, 101 patients (71.13%) with valvular regurgitation and 8 patients (5.63%) with abnormal ECG. No significant differences were observed in the distribution of clinical classification and the response to IVIG therapy regardless of NCA exhibited or not. Conclusions: Noncoronary cardiac abnormalities is almost universal in acute KD and mainly manifests as valvular regurgitation. However, it has no influence on clinical classification and the response to IVIG therapy. [ABSTRACT FROM AUTHOR]

Introduction: Forty‐one consensus review rules are presented to a large number of hematology laboratories worldwide, as suggested by the International Consensus Group for Hematology Review. Research on the review criteria has mainly focused on adjusting the threshold of each parameter to establish optimized criteria with better efficiency based on the consensus group criteria. This study aimed to optimize the review criteria by combining hematologic parameters on a Sysmex XE‐5000 hematology analyzer (XE‐5000). Material and methods: A total of 662 nucleated red blood cell (NRBC) and 406 atypical lymphocyte cell (AL) flagged samples were used to establish hematologic parameters associated with NRBC and AL, respectively. Another set of 1423 optimization samples were used to validate the optimized criteria of NRBC and AL by combining associative hematologic parameters. The efficiency of each set of criteria was compared and optimized to obtain better efficiency, an acceptable slide review rate, and a low false‐negative rate. Results: In the optimization NRBC set combining triple parameters, compared with the default setting (P <.001), the slide review rate declined from 30.26% to 14.42%, and the efficiency increased from 75.65% to 91.02%. In the optimization AL set combining triple parameters, compared with the default setting (P <.001), the slide review rate declined from 40.60% to 11.80%, and the efficiency increased from 64.02% to 93.00%. Conclusions: Based on the adjustment of Q‐flag values combining associative hematologic parameters, the optimal criteria with a low false‐negative rate not only might have a higher efficiency but also may significantly reduce the slide review rate. [ABSTRACT FROM AUTHOR]

Intellectual disability (ID) describes a wide range of serious human diseases caused by defects in central nervous system development and function. Some mutant genes have been found to be associated with these diseases, but not all cases can be explained, thus suggesting that other disease‐causing genes have not yet been discovered. Sialic acid is involved in a number of key biological processes, including embryo formation, nerve cell growth, and cancer cell metastasis, and very recently it has been suggested that N‐acetylneuraminic acid synthase‐mediated synthesis of sialic acid is required for brain and skeletal development. CMP‐sialic acid synthetase (CMAS) is one of four enzymes involved in NeuNAc metabolism, as it catalyzes the formation of CMP‐NeuNAc. Before the present study, no links between mutations in CMAS and incidences of human ID had been reported. In the current study, we recruited a recessive nonsyndromic ID pedigree with consanguineous marriage in which all patients have typical clinical manifestations of ID. We identified the NM_018686.3:c.563G > A (p.Arg188His) substitution in CMAS as being responsible for the disease in this family. Conservation analysis, structural prediction, and enzyme activity experiments demonstrated that (p.Arg188His) influences protein dimerization and alters CMAS enzyme activity. Our results offer a new orientation for future research and clinical diagnosis. [ABSTRACT FROM AUTHOR]

The article presents a case study of 10-year-old girl complaining of upper abdominal pain and vomiting. It notes the vital signs of axillary temperature, respiratory rate in physical examination, routine stool and urine tests showing weak positive faecal occult blood without erythrocytes, and normal ultrasonography.

Objective: To evaluate the clinical significance of permanent 125I prostate brachytherapy in patients with castration‐resistant prostate cancer. Methods: A retrospective study of 45 patients with castration‐resistant prostate cancer from the Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu, China was carried out. Patients were divided into two groups according to different treatments: 21 patients received endocrine therapy alone (control group), and 24 patients underwent brachytherapy combined with endocrine therapy (treatment group). Prostate‐specific antigen progression‐free survival, cancer‐specific survival, overall survival and quality of life of the two groups were compared. Results: The median prostate‐specific antigen progression‐free survival and cancer‐specific survival of the treatment group were 29 months (interquartile range 25–37 months) and 37 months (interquartile range 30–50 months), respectively. These were significantly longer than those of the control group (both P < 0.05). Prostate‐specific antigen (before androgen deprivation therapy and before brachytherapy), prostate volume, Gleason score, clinical stage and brachytherapy were associated with prostate‐specific antigen progression‐free survival and cancer‐specific survival on univariate analysis. For the quality of life after treatment, urinary symptoms/problems at 1 month after brachytherapy compared with the control group had a statistically significant difference and clinically relevant deterioration, but after 6 months there were no statistically significant differences and clinically relevant deterioration. Compared with the control group, the physical functioning, social functioning, global health and general physical discomfort of the treatment group were significantly improved. Conclusions: Brachytherapy with 125I seed implantation can effectively prolong survival of patients with castration‐resistant prostate cancer and, to a certain extent, improve patients' quality of life. [ABSTRACT FROM AUTHOR]

Alveolar macrophages play vital roles in acute lung injury, and macrophage response to hypoxia play relevant roles to disease mechanisms. There is growing evidence that cell death pathways play crucial roles in physiological and pathological settings and that the ubiquitin‐proteasome system is involved in the regulation of these processes. However, the functional role of proteasome in alveolar macrophages exposed to hypoxia‐reoxygenation (H/R) injury is unknown. We aimed to investigate the function of proteasome on alveolar macrophages exposed to H/R and the underlying mechanisms. NR8383 cells were pretreated with proteasome activator sulforaphane (SFN) or inhibitor MG‐132 for 1 hr, and then submitted to 2/6 hr, 4/6 hr, and 6/6 hr H/R treatment. Cell viability was assessed with MTT assay. Autophagy was monitored using electron transmission microscope and flow cytometry and western blotting. The endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways were equally analyzed by western blotting. Cell apoptosis was detected by immunohistochemistry, caspase3/7 activity, and western blotting. The viability of NR8383 cells exposed to H/R was affected by proteasome activity and proteasome inhibition significantly inhibited cell death. Treatment with MG‐132 led to autophagy activation and induced the survival of NR8383 cells exposed to H/R. Pretreatment with SFN significantly decreased cell autophagy and induced cell death. ER stress was activated in H/R‐treated NR8383 cells, and SFN further promoted ER stress whereas proteasome inhibition led to contrary results. Proteasome inhibtion hindered cell apoptosis as demonstrated by decreased caspase‐3/7 activity, immunolabelling, and western blot results. Proteasome inhibition might be a promising approach for treating H/R injury‐related lung diseases. [ABSTRACT FROM AUTHOR]

Abstract: 6‐Thioguanine (1a) is considered to be photochemotherapeutic due to its specific characteristics of photosensitivity to UVA light and singlet molecular oxygen generation. To extend its phototherapeutic ability, two related thioguanines, 8‐thioguanine (2a) and 6,8‐dithioguanine (3a), have been designed and explored. Since the solubility of these thioguanines in dehydrated organic solvents is too poor to study, their triacetyl‐protected ribonucleosides, that is, 2′,3′,5′‐tri‐O‐acetyl‐6‐thioguanosine (1c), 2′,3′,5′‐tri‐O‐acetyl‐8‐thioguanosine (2c) and 2′,3′,5′‐tri‐O‐acetyl‐6,8‐dithioguanosine (3c) were prepared and investigated. The absorption maxima of 1c, 2c and 3c in acetonitrile were found at longer wavelengths than that of unthiolated guanosine (4c). Especially, 3c has the longest wavelength for absorption maximum and the highest value in terms of molar absorption coefficient among all thionucleobases and thionucleosides reported. These absorption properties were also well reproduced by quantum chemical calculations. Quantum yields of singlet oxygen generation of 2c and 3c were determined by near‐infrared emission measurements to be as large as that of 1c. These results suggest that the newly synthesized thioguanosines, in particular 3c, can be further developed as a potential photosensitive agent for light‐induced therapies. [ABSTRACT FROM AUTHOR]

The fast development of the design, construction, and application of metal-organic materials including infinite metal-organic frameworks (MOFs) and discrete metal-organic cages (MOCs) has not only propelled the advance of modern supramolecular syntheses to an unprecedented level, but also burgeoned various kinds of detection and characterization technologies. Herein, complementary techniques, including di-versified NMR and ESI-MS spectrometry, solid-state crystallography, and theoretical simulation are exploited to elucidate the structural evolution of a dynamic supramolecular coordination system involving PdII-MOCs of different compositions. The combination of various kinds of modern techniques verifies the anion template effect, which leads to the preferred formation and further conversion of Pd2L4 and Pd3L6 cages. [ABSTRACT FROM AUTHOR]

Even though the diagnostic and prognostic value of circulating tumor cells (CTCs) has been demonstrated, their clinical utility and widespread adoption have been limited. Herein, we describe a new device, size-dictated immunocapture chip (SDI-Chip), for efficient, sensitive, and spatially resolved capture and detection of CTCs. SDI-Chip enables selective, frequent, and extended interaction of CTCs with hydrodynamically optimized immunocoated micropillar surfaces. CTCs with different antigen expression levels can be efficiently captured and spatially resolved around the micropillars. Capture efficiency greater than 92 % with a purity of 82 % was achieved with blood samples. CTCs were detected in non-metastasis colorectal (CRC) patients, while none was detected from healthy volunteers. We believe that SDI-Chip will facilitate the transition of tumor diagnosis from anatomical pathology to molecular pathology in localized CRC patients. [ABSTRACT FROM AUTHOR]

Even though the diagnostic and prognostic value of circulating tumor cells (CTCs) has been demonstrated, their clinical utility and widespread adoption have been limited. Herein, we describe a new device, size-dictated immunocapture chip (SDI-Chip), for efficient, sensitive, and spatially resolved capture and detection of CTCs. SDI-Chip enables selective, frequent, and extended interaction of CTCs with hydrodynamically optimized immunocoated micropillar surfaces. CTCs with different antigen expression levels can be efficiently captured and spatially resolved around the micropillars. Capture efficiency greater than 92 % with a purity of 82 % was achieved with blood samples. CTCs were detected in non-metastasis colorectal (CRC) patients, while none was detected from healthy volunteers. We believe that SDI-Chip will facilitate the transition of tumor diagnosis from anatomical pathology to molecular pathology in localized CRC patients. [ABSTRACT FROM AUTHOR]

Objective The purpose of this study was to present the surgical technique and clinical results of percutaneous compression plate ( PCCP) for the treatment of femoral neck fractures. Methods Between December 2010 and April 2013, 74 consecutive patients with 74 femoral neck fractures were treated by closed reduction and PCCP implants in our university hospital. Their mean age was 51.3 years (range, 15-83 years); 38 (51.4%) were male and 46 (62.2%) of the fractures were on the left. The patients' clinical and radiographic data were analyzed retrospectively. Results There were 45 undisplaced (60.8%) and 29 displaced fractures (39.2%). Eight patients (10.8%) were lost to follow-up. The mean duration of follow-up was 18.8 months for the remaining 66 patients. At the last follow-up, mean Harris hip score was 92.9 (range, 75-100), and 65 patients (98.5%) had excellent and good outcomes. Sixty-five patients (98.5%) were able to walk independently and one (1.5%) with walking-sticks. The mean time to clinical fracture healing was 3.9 months. There were no cases of nonunion. Two patients (3.0%) had delayed union and two (3.0%) developed avascular necrosis, one of 29 (3.7%) with a displaced fracture and one of 45 (2.6%) with an undisplaced fracture. There were no other complications or prosthetic replacement. Conclusions PCCP is a stable internal fixation device that resists axial and rotational stresses. Our PCCP procedure has a low incidence of nonunion and avascular necrosis. [ABSTRACT FROM AUTHOR]

Sodium carbonate (Na2CO3) presents a huge challenge to plants by the combined damaging effects of Na+, high pH, and CO32-. Little is known about the cellular responses to Na2CO3 stress. In this study, the transcriptome of maize ( Zea mays L. cv. B73) roots exposed to Na2CO3 stress for 5 h was compared with those of NaCl and NaOH stresses. The expression of 8,319 genes, representing over a quarter of the total number of genes in the maize genome, was altered by Na2CO3 stress, and the downregulated genes (5,232) outnumbered the upregulated genes (3,087). The effects of Na2CO3 differed from those of NaCl and NaOH, primarily by downregulating different categories of genes. Pathways commonly altered by Na2CO3, NaCl, and NaOH were enriched in phenylpropanoid biosynthesis, oxidation of unsaturated fatty acids, ATP-binding cassette (ABC) transporters, as well as the metabolism of secondary metabolites. Genes for brassinosteroid biosynthesis were specifically upregulated by Na2CO3, while genes involved in ascorbate and aldarate metabolism, protein processing in the endoplasmic reticulum and by N-glycosylation, fatty acid biosynthesis, and the circadian rhythm were downregulated. This work provides the first holistic picture of early transcriptomic adaptation to Na2CO3 stress, and highlights potential molecular pathways that could be manipulated to improve tolerance in maize. [ABSTRACT FROM AUTHOR]

Octadecahedral α-Fe2O3 nanoparticles were hydrothermally synthesized in the presence of formamide. These octadecahedral α-Fe2O3 nanoparticles have a threefold axis and are enclosed by twelve dominant {112} facets and six {104} facets. In comparison with the {104} facets, the sterically less hindered {112} facets induced the selective adsorption of formamide more easily, which resulted in the gradual increase in the amount of {112} facets by decreasing the amount of {104} facets with increasing formamide. The coercivity ( Hc) of these octadecahedral particles increased successively as the aspect ratio ( c/ a) increased. The sensing capability of these particles toward H2O2 was investigated, and the response currents of the particles dominated by {112} facets showed a linear relationship with a concentration of H2O2 in the range from 40 μ M to 6.66 m M in different stages. [ABSTRACT FROM AUTHOR]

Several reports demonstrated that mesenchymal stem cells (MSCs) might differentiate into smooth muscle cells (SMCs) in vitro and in vivo. It has been shown that myocardin protein is a strong inducer of smooth muscle genes and MSCs can differentiate into SMCs in response to transforming growth factor-β (TGF-β). However, the relationship or link between myocardin and TGF-β3-induced MSC differentiation has not been fully elucidated. Here, we demonstrated that both myocardin and TGF-β3 were able to induce differentiation of rat bone marrow-derived MSCs toward smooth-muscle-like cell types, as evidenced by increasing expression of SMC-specific genes. Of note, myocardin cooperated with Smad2 to synergistically activate SM22α promoter and significantly enhance the expression of SM22α. Report assays with site-direct mutation analysis of SM22α promoter demonstrated that myocardin and Smad2 coactivated SM22α promoter mainly depending on CArG box and less on smad binding elements (SBE) sites as well. These findings reveal the cooperation of myocardin and Smad2 in process of MSC differentiation into SMCs. © 2012 IUBMB Life, 64(4): 331-339, 2012 [ABSTRACT FROM AUTHOR]

New chiral ligands (Ia,b) are prepared and successfully applied to the title reaction. [ABSTRACT FROM AUTHOR]