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Force‐responsive molecules that produce fluorescent moieties under stress provide a means for stress‐sensing and material damage assessment. In this work, we report a mechanophore based on Diels‐Alder adduct TAD‐An of 4,4′‐(4,4′‐diphenylmethylene)‐bis‐(1,2,4‐triazoline‐3,5‐dione) and initiator‐substituted anthracene that can undergo retro‐Diels‐Alder (rDA) reaction by pulsed ultrasonication and compressive activation in bulk materials. The influence of having C−N versus C−C bonds at the sites of bond scission is elucidated by comparing the relative mechanical strength of TAD‐An to another Diels‐Alder adduct MAL‐An obtained from maleimide and anthracene. The susceptibility to undergo rDa reaction correlates well with bond energy, such that C−N bond containing TAD‐An degrades faster C−C bond containing MAL‐An because C−N bond is weaker than C−C bond. Specifically, the results from polymer degradation kinetics under pulsed ultrasonication shows that polymer containing TAD‐An has a rate constant of 1.59×10−5 min−1, while MAL‐An (C−C bond) has a rate constant of 1.40×10−5 min−1. Incorporation of TAD‐An in a crosslinked polymer network demonstrates the feasibility to utilize TAD‐An as an alternative force‐responsive probe to visualize mechanical damage where fluorescence can be "turned‐on" due to force‐accelerated retro‐Diels‐Alder reaction. [ABSTRACT FROM AUTHOR]

In this paper, we study the low Mach and Froude number limit of global strong solutions to the fluid‐vacuum free boundary problem of the planar magnetohydrodynamic (MHD) equations with degenerate viscosity coefficients and well‐prepared initial data. Only the initial energy at the basic level is required to be small. The main difficulties are the degeneracy of the system yielded by vanishing of the density close to the free boundary, the singular terms due to the large coefficients inversely proportional to the Mach number and the Froude number, and the strong coupling of the magnetic field and the velocity. The uniform estimates of solutions with respect to the Mach number and the Froude number are established, which is the first result on the MHD equations with vacuum free boundary. At the same time, we obtain the convergence rates for the strong solutions global in time with well‐prepared initial data as the Mach number and the Froude number vanish. [ABSTRACT FROM AUTHOR]

Introduction: Patients presenting with brain metastases (BMs) from lung squamous cell carcinoma (LUSC) often encounter an extremely poor prognosis. A well‐developed prognostic model would assist physicians in patient counseling and therapeutic decision‐making. Methods: Patients with LUSC who were diagnosed with BMs between 2000 and 2018 were reviewed in the Surveillance, Epidemiology, and End Results (SEER) database. Using the multivariate Cox regression approach, significant prognostic factors were identified and integrated. Bootstrap resampling was used to internally validate the model. An evaluation of the performance of the model was conducted by analyzing the area under the curve (AUC) and calibration curve. Results: A total of 1812 eligible patients' clinical data was retrieved from the database. Patients' overall survival (OS) was significantly prognosticated by five clinical parameters. The nomogram achieved satisfactory discrimination capacity, with 3‐, 6‐, and 9‐month AUC values of 0.803, 0.779, and 0.760 in the training cohort and 0.796, 0.769, and 0.743 in the validation cohort. As measured by survival rate probabilities, the calibration curve agreed well with actual observations. There was also a substantial difference in survival curves between the different prognostic groups stratified by prognostic scores. For ease of access, the model was deployed on a web‐based server. Conclusions: In this study, a nomogram and a web‐based predictor were developed to assist physicians with personalized clinical decisions and treatment of patients who presented with BMs from LUSC. [ABSTRACT FROM AUTHOR]

Aim: Psilocin is an active metabolite form of psilocybin and exerts psychoactive effects. Recent studies suggest that psilocin may have regulatory effects on abuse drugs, but the mechanisms remain unclear. In this study, we want to explore the effects of psilocin on methamphetamine (METH)‐induced alterations of behavior in mice and its molecular mechanisms. Methods: Acute METH administration model and conditioned place preference (CPP) model were used to investigate the effects of psilocin on METH‐induced alterations of behavior. Western blot was used to detect the expression of proteins. Results: In the acute 2 mg/kg METH administration model, 1 mg/kg psilocin counteracted METH‐induced elevation of activity. In the 1 mg/kg METH‐induced CPP model, 1 mg/kg psilocin inhibited CPP formation during the acquisition phase. However, psilocin did not impact METH extinction and relapse. Molecular results showed that the regulatory effect of psilocin on METH was underscored by altered expression of dopamine 2 receptor (D2R) and phosphorylated extra‐cellular signal‐regulated kinase (p‐ERK) in the prefrontal cortex (PFC), nucleus accumbens (NAc), and ventral tegmental area (VTA). Trifluoperazine (TFP)‐2HCl is a D2R inhibitor, and SCH772984 is a selective extra‐cellular signal‐regulated kinase (ERK) inhibitor that effectively inhibits ERK1/2 phosphorylation. The results indicated that 2 mg/kg TFP‐2HCl and 10 mg/kg SCH772984 blocked METH‐induced hyperactivity and acquisition of METH‐induced CPP. Conclusion: Psilocin has regulatory effects on METH‐induced alterations of behavior in mice via D2R‐mediated signal regulation of ERK phosphorylation. [ABSTRACT FROM AUTHOR]

Comprehensive Summary: The biochemical property and functional identification of three recombinant glycosyltransferases, including β‐1,4‐rhamnosyltransferase (Cps8R), β‐1,4‐galactosyltransferase (Cps8J) and α‐2,3‐sialyltransferase (Cps8K) involved in the biosynthesis of the tetrasaccharide repeating unit of serotype VIII capsular polysaccharide (CPS) of Group B Streptococci (GBS), were systematically investigated. Subsequently, these recombinant enzymes were employed for one‐pot three‐enzyme efficient synthesis of the tetrasaccharide repeating unit of GBS serotype VIII CPS using the chemically synthesized Glcα‐PP‐(CH2)11‐OPh as the starting substrate in a satisfying yield of 87%. [ABSTRACT FROM AUTHOR]

The Brassicaceae is an economically and scientifically important family distributed globally, including oilseed rape and the model plant, Arabidopsis thaliana. Although growing molecular data have been used in phylogenetic studies, the relationships among major clades and tribes of Brassicaceae are still controversial. Here, we investigated the core Brassicaceae phylogenetics using 222 plastomes and 235 nrDNA cistrons, including 106 plastomes and 112 nrDNA cistrons assembled from newly sequenced genome skimming data of 112 taxa. The sampling covered 73 genera from 61.5% tribes and four unassigned genera and species. Three well supported lineages LI, LII, and LIII were revealed in our plastomic analyses, with LI sister to LII + LIII. In addition, the monophyly of the newly delimitated LII was strongly supported by three different partition strategies, concatenated methods under Bayesian and Maximum Likelihood analyses. LII comprised 13 tribes, including four tribes previously unassigned to any lineage, that is Biscutelleae as the earliest diverging clade and Cochlearieae as the sister to Megacarpaeeae + Anastaticeae. Within LII, the intertribal relationships were also well resolved, except that a conflicting position of Orychophragmus was detected among different datasets. In LIII, Shehbazia was resolved as a member of Chorisproreae, but Chorisproreae, Dontostemoneae, and Euclidieae were all resolved as paraphyletic, which was also confirmed by nrDNA analyses. Moreover, the loss of the rps16 gene was detected as likely to be a synapomorphy of the tribes Arabideae and Alysseae. Overall, using genome skimming data, we resolved robust phylogenetic relationships of core Brassicaceae and shed new light on the complex evolutionary history of this family. [ABSTRACT FROM AUTHOR]

Objectives: Circular RNAs (circRNAs) are non‐coding RNAs, some of which are thought to be involved in gastric cancer development. Here, we examined the functions of circRNA hsa_circ_006100 in gastric cancer cells and an animal model of gastric cancer. Materials and Methods: The expression of hsa_circ_006100, miR‐195 and various functional genes was determined by quantitative RT‐PCR. Cell viability, clone formation, apoptosis and cell migration/invasion abilities were analysed by the CCK‐8 assay, crystal violet staining, Hoechst staining and Transwell assay, respectively. A tumour model was established by subcutaneously injecting tumour cells into nude mice. Levels of protein expression were analysed by Western blotting and immunohistochemistry. Results: A bioinformatics analysis showed that miR‐195 was negatively co‐expressed with hsa_circ_006100. Patients with a high hsa_circ_006100 level or low miR‐195 level had tumours with a high TNM stage, poor cellular differentiation and lymph node metastasis. miR‐195 was targeted and inhibited by hsa_circ_006100. Overexpression of hsa_circ_006100 enhanced cellular viability and proliferation, while miR‐195 suppressed hsa_circ_006100‐enhanced cell growth and induced apoptosis in MGC‐803 and AGS cells. Forced hsa_circ_006100 expression promoted the migration and invasion of MGC‐803 and AGS cells, while those activities were inhibited by miR‐195. Mechanistically, GPRC5A was predicted as a target of miR‐195 and was upregulated in gastric cancer. A miR‐195 inhibitor restored cell viability, proliferation, migration and invasion, and repressed apoptosis via GPRC5A. In vivo studies showed that knockdown of hsa_circ_006100 delayed tumour growth, reduced PCNA expression and upregulated miR‐195 and BCL‐2 expression which was restored by miR‐195 inhibition due to GPRC5A/EGFR signalling, and changed the EMT phenotype in vivo. Conclusions: Hsa_circ_006100 functions as an oncogene in gastric cancer and exerts its effects via miR‐195/GPRC5A signalling. [ABSTRACT FROM AUTHOR]

A series of phenanthroline-based ligands have been synthesised and their influence as bidentate nitrogen ligands in heteroleptic [Cu(P^P)(N^N)]+ photosensitisers in light-driven water reduction has been studied. In this noble-metal-free Cu-Fe-based photocatalytic water reduction system, the structural effects of the nitrogen ligands have been explored, including the steric and electronic effects of substituents at the 2,9- and 4,7-positions of phenanthroline. Ligands were prepared that led to increased hydrogen generation, with turnover numbers (TONCu) of up to 1388 being observed. All the new complexes were electrochemically and photophysically characterised. We demonstrate for the first time that the presence of fluorine in nitrogen ligands increases the efficacy of copper complexes in photocatalytic hydrogen production. [ABSTRACT FROM AUTHOR]

Four dinuclear copper( II) complexes, Cu2( L1 -4)4·( CH3OH)2( 1-4) ( HL1 = m-anisic acid, HL2 = p-anisic acid, HL3 = m-toluic acid, HL4 = p-toluic acid) were synthesized and characterized by IR spectroscopy, elemental analysis, and X-ray powder and single crystal diffraction. All of the complexes are consisting of two Cu( II) cations, four L ligands and two methanol molecules, in which the L ligands are coordinated with copper cations by bidentate bridging coordination mode. There exists hydrogen bond interaction or CH...π interaction in the complexes, forming three-dimensional network structures. Theoretical study of the complexes was carried out by density functional theory B3LYP method. [ABSTRACT FROM AUTHOR]

Background Endothelial dysfunction is an early event of cardiovascular disease in type 2 diabetes ( T2D) and can occur before albuminuria. Oxidative stress has been found to play a key role in the development of endothelial dysfunction. Therefore, we hypothesized that increases in plasma advanced oxidized protein products ( AOPPs), a family of oxidized, dityrosine-containing protein compounds generated during oxidative stress, could serve as an early marker of endothelial dysfunction in T2D patients without albuminuria. Methods We conducted a cross-sectional investigation of 147 newly diagnosed T2D patients (112 without albuminuria and 35 with albuminuria) and 49 age-matched healthy control subjects. Flow-mediated vasodilation ( FMD) was used to assess endothelium-dependent vasodilator function, and plasma soluble intercellular adhesion molecule-1 ( sICAM-1) concentrations were determined to evaluate vascular injury. Plasma AOPPs concentrations were measured using a modified spectrophotometric assay. Results Plasma AOPPs concentrations were significantly elevated in normoalbuminuric patients with T2D compared with healthy controls. Plasma AOPPs concentrations were correlated with FMD and plasma sICAM-1 concentrations in this population. Multivariate regression analysis demonstrated that increased plasma AOPPs was the strongest risk factor for impaired endothelial vasodilation and increased sICAM-1 in these patients. Similar results were observed in T2D patients with albuminuria. Conclusions Increased plasma AOPPs concentrations were an independent risk factor for endothelial dysfunction, and therefore may be an early marker of vasculopathy in individuals at an early stage of diabetes. [ABSTRACT FROM AUTHOR]

Background: In China, over 50% of lung cancer cases occur in nonsmokers. Thus, identifying high‐risk individuals for targeted lung cancer screening is crucial. Beyond age and smoking, determining other risk factors for lung cancer in the Asian population has become a focal point of research. Using 30,000 participants in the prospectively enrolled cohort at China's National Cancer Center (NCC) over the past 14 years, we categorized participants by risk, with an emphasis on nonsmoking females. Materials and Method s : Between November 2005 and December 2019, 31,431 individuals voluntarily underwent low‐dose computed tomography (LDCT) scans for lung cancer screening at the NCC. We recorded details like smoking history, exposure to hazards, and family history of malignant tumors. Using the 2019 NCCN criteria, participants were categorized into high‐, moderate‐, and low‐risk groups. Additionally, we separated non‐high‐risk groups into female never smokers (aged over 40) exposed to second‐hand smoke (SHS) and others. Any positive results from initial scans were monitored per the I‐ELCAP protocol (2006), and suspected malignancies were addressed through collaborative decisions between patients and physicians. We analyzed and compared the detection rates of positive results, confirmed lung cancers, and cancer stages across risk, age, and gender groups. Results: Out of 31,431 participants (55.9% male, 44.1% female), 3695 (11.8%) showed positive baseline LDCT scans with 197 (0.6%; 106 females, 91 males) confirmed as lung cancer cases pathologically. Malignancy rate by age was 0.1% among those aged under 40 years, 0.4% among those aged 40–49 years, 0.8% among those aged 50–59 years, and 1.2% among those aged 60 years and older. From the 25,763 participants (56.9% male, 43.1% female) who completed questionnaires, 1877 (7.3%) were categorized as high risk, 6500 (25.2%) as moderate risk, and 17,386 (67.5%) as low risk. Of the 23,886 in the non‐high‐risk category, 8041 (33.7%) were females over 40 years old exposed to SHS. The high‐risk group showed the highest lung cancer detection rate at 1.4%. However, females exposed to SHS had a notably higher detection rate than the rest of the non‐high‐risk group (1.1% vs. 0.5%; p < 0.0001). In this cohort, 84.8% of the detected lung cancers were at an early stage. Conclusions: In our study, using LDCT for lung cancer screening proved significant for high‐risk individuals. For non‐high‐risk populations, LDCT screening could be considered for nonsmoking women with exposure to SHS. [ABSTRACT FROM AUTHOR]

The biomedical application of corannulene π‐bowls is historically limited by low solubility and bioavailability despite the potential in their unique electronic properties for new functional materials. Herein, the unexpected role and molecular mechanism of Corranulene π‐bowls are uncovered in biomedical applications as an effective anticancer agent for Warburg effect mediated selective tumor targeting. The corannulene triazolyl monosaccharides Cor‐sugars exhibit highly potent cytotoxicity against human cancer cells and effectively inhibit xenograft growth of hyperglycolytic tumors. Particularly, the galactose‐conjugated Cor‐gal exhibits superior in vivo anticancer efficacy in A549 tumor models with outstanding safety profile compared to doxorubicin. Moreover, the combined treatment of Cor‐gal with immune checkpoint inhibitor results in an effective synergy in treating H460 human lung carcinoma. An uptake mechanism study reveals that Cor‐sugars exploit tumor‐specific glucose transporter glucose transporter 1 (GLUT1) for targeted cell delivery and intra‐tumoral accumulation through the cancer‐specific Warburg effect. Their significant anticancer activity is attributed to multiphasic DNA‐binding and cell cycle alteration effects. This study uncovers new molecular properties of corannulene buckybowl and enabling their potential new applications in biomedical engineering. [ABSTRACT FROM AUTHOR]

Insufficient immune cell infiltration into the tumor microenvironment (TME) greatly compromises the clinical application of immune‐checkpoint inhibitors (ICIs)‐based immunotherapy. Recent findings have shown that activation of the cyclic GMP‐AMP synthase‐stimulator of interferon genes (cGAS‐STING) pathway can enhance natural immunity and increase lymphocyte infiltration into the TME, which presents a promising strategy for cancer immunotherapy. In this study, we constructed hydroxyapatite nanoparticles co‐loaded with curcumin and L‐oxaliplatin (Cur/L‐OHP@HAP NPs). We analyzed the particle‐size distribution, zeta potential, spectral characteristics (Fourier‐transform infrared spectroscopy, X‐ray photoelectron spectroscopy, ultraviolet–visible spectroscopy), and drug‐release properties of the Cur/L‐OHP@HAP NPs. The cellular uptake of the Cur/L‐OHP@HAP NPs detected by flow cytometry and confocal laser‐scanning microscopy. We comprehensively evaluated the anti‐tumor properties and immune‐activating effects of the NPs, both in vitro and in vivo. Physicochemical characterizations demonstrated that the Cur/L‐OHP@HAP NPs were successfully synthesized and were capable of pH‐dependent drug release. Notably, the Cur/L‐OHP@HAP NPs efficiently entered cancer cells, after which the released L‐OHP induced nuclear DNA (nDNA) damage to some extent. HAP promoted the release of intracellular Ca2+ stores in cancer cells, and curcumin inhibited Ca2+ efflux, resulting in intracellular Ca2+ overload and the release of mitochondrial DNA (mtDNA). Damage to both nDNA and mtDNA greatly stimulated the cGAS‐STING pathway, thereby activating natural immunity, accompanied by immune cell recruitment to the TME. In summary, the Cur/L‐OHP@HAP NPs show good prospects for improving cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Introduction: The effects of edaravone against pentylenetetrazole (PTZ)‐induced epilepsy in male albino rats were investigated. Edaravone is a well‐known commercial drug used in the treatment of strokes and amyotrophic lateral sclerosis (ALS). Antioxidant and free radical scavenging activities of edaravone have been reported in patients with ALS. Methods: In this study, the experimental groups were as follows: sham, control, 5 mg/kg edaravone, and 10 mg/kg edaravone. Behavioral assessment, determination of biochemical markers, apoptosis, nitric oxide (NO), and mRNA and protein expression of cyclooxygenase‐II (COX‐II) were carried out. Seizure incidence, including generalized tonic–clonic seizure (GTCS) and minimal clonic seizure (MCS), was directly associated with PTZ administration in rats. Results: Edaravone supplementation substantially increased MCS and GTCS latency in rats, and biochemical markers were significantly altered in the brain tissue of PTZ‐treated rats. Edaravone treatment normalized altered biochemical markers compared with the untreated control. Apoptosis and NO levels were significantly reduced by more than 50% compared to their respective controls. COX‐II mRNA was increased by 130% in PTZ‐treated rats, while edaravone supplementation reduced mRNA and protein expression of COX‐II by more than 20% and 40%, respectively. Immunohistochemistry indicated that COX‐II protein expression was reduced by 13.2% and 33.7% following supplementation with 5 and 10 mg/kg edaravone, respectively. Conclusion: Taken together, our results suggest that edaravone functions by downregulating the levels of COX‐II and NO and is a potential candidate for the treatment of PTZ‐induced epilepsy. Edaravone supplementation significantly normalized altered lipid peroxidation and antioxidant biochemical markers. Apoptosis and NO levels were reduced compared to their respective controls. mRNA and protein expression of COX‐II was substantially reduced following edaravone supplementation. Taken together, our results suggest that edaravone is a potential candidate for the treatment of PTZ‐induced epilepsy and functions by downregulating the levels of COX‐II and NO. [ABSTRACT FROM AUTHOR]

An in‐depth theoretical study has been performed to investigate the mechanism of alkene dehydrogenative silylation catalyzed by the bis(imino)pyridine cobalt methyl complex (MesPDI)Co(CH3) on the singlet, triplet and open‐shell singlet potential energy surfaces as well as the corresponding minimum energy crossing points. The formation of active catalyst [(MesPDI)Co(CH3)+HSiR3→(MesPDI)Co−[Si]+CH4] follows an open‐shell singlet potential energy surface, while the active catalyst has a triplet ground state. For 1‐butene as substrate, the formation of E/Z‐allylsilanes follows the singlet surface; and the E‐allylsilane is more favored than the Z‐allylsilane kinetically, and the expected ratio agrees with the experiment. For bulky 4,4‐dimethyl‐1‐pentene as substrate, the selectivity of allylsilane and vinylsilane is thermodynamically determined and this is supported by the need of low silane/olefin ratio (1/4) in experiment. [ABSTRACT FROM AUTHOR]

Background and Aims: Liver diseases present a wide range of fibrosis, from fatty liver with no inflammation to steatohepatitis with varying degrees of fibrosis, to established cirrhosis leading to HCC. In a multivariate analysis, serum levels of spermidine were chosen as the top metabolite from 237 metabolites and its levels were drastically reduced along with progression to advanced steatohepatitis. Our previous studies that showed spermidine supplementation helps mice prevent liver fibrosis through MAP1S have prompted us to explore the possibility that spermidine can alleviate or cure already developed liver fibrosis. Methods: We collected tissue samples from patients with liver fibrosis to measure the levels of MAP1S. We treated wild‐type and MAP1S knockout mice with CCl4‐induced liver fibrosis with spermidine and isolated HSCs in culture to test the effects of spermidine on HSC activation and liver fibrosis. Results: Patients with increasing degrees of liver fibrosis had reduced levels of MAP1S. Supplementing spermidine in mice that had already developed liver fibrosis after 1 month of CCl4 induction for an additional 3 months resulted in significant reductions in levels of ECM proteins and a remarkable improvement in liver fibrosis through MAP1S. Spermidine also suppressed HSC activation by reducing ECM proteins at both the mRNA and protein levels, and increasing the number of lipid droplets in stellate cells. Conclusions: Spermidine supplementation is a potentially clinically meaningful approach to treating and curing liver fibrosis, preventing cirrhosis and HCC in patients. [ABSTRACT FROM AUTHOR]

ABSTRACT This work describes the design, fabrication, and testing of an Archimedean spiral or spiral antenna using polymer extrusion 3D printing of polycarbonate base material. The spiral antenna design was simulated using CST Microwave Studio®, and the resulting 3D printed antenna characterized in terms of return loss, directivity, and polarization. The antenna design was embedded into a 3D printed structure using a unique ultrasonic method while a ground plane was inserted through a thermal embedding process. These fabrication methods provide process flexibility , which allows multiple conductive antenna layers to be additively constructed in a single build sequence. The method described can be used to create unique electromagnetic structures such as waveguides directly in a 3D printed dielectric part. The spiral antenna was tested with three variations of microstrip feed line used to match 50Ω impedance and introduce a 180° phase shift between the two arms of the spiral. These include a Duroid balun attached to feed of the antenna after fabrication, a Duroid balun embedded into the polycarbonate during fabrication, and the same microstrip design fabricated out of copper mesh and embedded into the structure using the polycarbonate as a dielectric substrate. The results of these three approaches will be discussed. © 2016 Wiley Periodicals, Inc. Microwave Opt Technol Lett 58:1662-1666, 2016 [ABSTRACT FROM AUTHOR]

The enzymatic activity and function of a new α‐1,3‐glucosyltransferase, Cps18CU, derived from Streptococcus pneumoniae serotype 18C was identified for the first time using the enzymatically synthetic disaccharide Rhaβ1,4‐Glcα‐PP‐O(CH2)11‐OPh as the acceptor substrate. Further investigation on substrate specificity revealed that Cps18CU exhibited broad toleration toward various NDP‐Glc donors and also accepted such disaccharide acceptor containing Rhaβ1,4‐Glc moiety in structure. Finally, Cps18CU was employed into a one‐pot two‐enzyme reaction system, furnishing trisaccharide Glcα1,3‐Rhaβ1,4‐Glcα‐PP‐O(CH2)11‐OPh in an 81 % yield. [ABSTRACT FROM AUTHOR]

Zooxanthellae are very important for the coral reef ecosystem. The diversity of coral hosts is high in the South China Sea, but the diversity of zooxanthellae has not yet been investigated. We chose the Zhubi Coral Reef of the Nansha Islands as the region to be surveyed in the present study because it represents a typical tropical coral reef of the South China Sea and we investigated zooxanthellae diversity in 10 host scleractinian coral species using polymerase chain reaction (PCR) of the large subunit rRNA and restriction fragment length polymorphism (RFLP) patterns. Pocillopora verrucosa, Acropora pelifera, Acropora millepora, Fungia fungites, Galaxea fascicularis, and Acropora pruinosa harbor Clade C, Goniastrea aspera harbors Clade D, and Acropora formosa harbors Clades D and C. Therefore, the Clade C is the dominant type in the Zhubi Coral Reef of the Nansha Islands. Furthermore, the results of the present also disprove what has been widely accepted, namely that one coral host harbors only one algal symbiont. The coral-algal symbiosis is flexible, which may be an important mechanism for surviving coral bleaching. Meanwhile, on the basis of the results of the present study, we think that Symbiodinium Clade D may be more tolerant to stress than Symbiodinium Clade C. (Managing editor: Ya-Qin Han) [ABSTRACT FROM AUTHOR]

Periodontitis is a chronic inflammatory disease that results in the destruction of periodontal soft tissue and the resorption of alveolar bone. Evidence indicates that in diabetic patients, hyperglycemia suppresses periodontal ligament stem cell (PDLSC) functions and leads to difficulties in periodontal repair. The present study aimed to explore the mechanisms by which high‐glucose concentrations aggravate cell viability reduction in human CD146‐positive PDLCs (CD146+PDLCs) under tumor necrosis factor‐alpha (TNF‐alpha) induction. CD146+PDLCs were isolated from periodontal ligament tissues and treated in the absence or presence of 10 ng/ml of TNF‐alpha and 30 mM glucose. Cell viability was detected using Cell Counting Kit‐8 assays and Luminescent Cell Viability Assays. Western blotting and real‐time polymerase chain reaction were performed to determine tumor necrosis factor‐alpha receptor‐1 (TNFR‐1) protein and messenger RNA expression. Bisulfite and MassArray methylation analyses were used to analyze the methylation status of the TNFR‐1 gene. Our results indicated that cell viability was reduced after treatment with a combination of both high‐glucose concentration and TNF‐alpha. Treatment with 30 mM glucose suppressed DNA methyltransferase (DNMT) activities and DNMT1 protein expression, and this was accompanied by the upregulation of TNFR‐1. Additionally, we found that the CpG island located within the TNFR‐1 gene was hypomethylated under 30 mM glucose conditions. S‐adenosylmethionine, an established methyl donor, reversed TNFR‐1 upregulation and restored cell viability against high‐glucose concentration and TNF‐alpha. In conclusion, the present findings suggest that high‐glucose‐induced CpG island hypomethylation within the TNFR‐1 gene plays an essential role in TNFR‐1 upregulation, and this further enhances the cell viability reduction of CD146+PDLCs caused by TNF‐alpha. [ABSTRACT FROM AUTHOR]

The aim of this study was to explore the effects of platelet‐rich plasma on gingipain‐caused changes in cell morphology and apoptosis of osteoblasts. Mouse osteoblasts MC3T3‐E1 cells were treated with gingipain extracts from Porphyromonas gingivalis in the presence or absence of platelet‐rich plasma. Apoptosis was detected with terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling staining. F‐actin was determined by phalloidin‐fluorescent staining and observed under confocal microscopy. Western blot analysis was used to detect integrin β1, F‐actin, and G‐actin protein expressions. A knocking down approach was used to determine the role of integrin β1. The platelet‐rich plasma protected osteoblasts from gingipain‐induced apoptosis in a dose‐dependent manner, accompanied by upregulation of integrin β1. Platelet‐rich plasma reversed the loss of F‐actin integrity and decrease of F‐actin/G‐actin ratio in osteoblasts in the presence of gingipains. By contrast, the effects of platelet‐rich plasma were abrogated by knockdown of integrin β1. The platelet‐rich plasma failed to reduce cell apoptosis and reorganize the cytoskeleton after knockdown of integrin β1. In conclusion, platelet‐rich plasma inhibits gingipain‐induced osteoblast apoptosis and actin cytoskeleton disruption by upregulating integrin β1 expression. [ABSTRACT FROM AUTHOR]

Aims: To investigate the association of baseline serum uric acid (UA) with new‐onset diabetes, and to explore the possible effect modifiers in Chinese adults with hypertension. Materials and methods: A total of 14 943 hypertensive patients with available UA measurements and without diabetes at baseline were included from the China Stroke Primary Prevention Trial (CSPPT). Participants were randomly assigned to a double‐blind daily treatment with 10 mg enalapril and 0.8 mg folic acid or 10 mg enalapril alone. The primary outcome was new‐onset diabetes, defined as physician‐diagnosed diabetes or use of glucose‐lowering drugs during follow‐up, or fasting glucose ≥7.0 mmol/L at the exit visit. Results: Over a median follow‐up of 4.5 years, 1623 participants (10.9%) developed diabetes. Overall, there was a positive association between baseline UA and new‐onset diabetes in women (per SD increment; adjusted odds ratio [OR] 1.14, 95% confidence interval [CI] 1.07, 1.23), but not in men (adjusted OR 1.01, 95% CI 0.92, 1.10). Moreover, a stronger positive association between baseline UA and new‐onset diabetes was found among women with lower time‐averaged on‐treatment systolic blood pressure during the treatment period (<140 vs. ≥140 mmHg; P‐interaction = 0.024), higher baseline body mass index (<24 vs. ≥24 kg/m2; P‐interaction = 0.012), or higher baseline waist circumference (<80 vs. ≥80 cm; P‐interaction = 0.032). Conclusions: Our study suggested that higher baseline UA was significantly associated with increased risk of new‐onset diabetes in hypertensive Chinese women, but not in men. Further prospective studies are required to validate the differential association by sex. [ABSTRACT FROM AUTHOR]

Introduction: Although mutations in the human beta‐globin gene cluster are essentially point mutations, several large deletions have been described in recent years. Methods: We have identified a novel 223 kb deletion in a Chinese patient by multiplex ligation‐dependent probe amplification and characterized it by next‐generation sequencing, Gap‐PCR, and DNA sequence analysis. Results: The deletion extends from the 3′UTR of the δ globin gene (HBD) to 215 kb downstream of the HBB. Compound heterozygous with the typical β‐thalassemia—CD41‐42(‐CTTT) mutation, the proband presented with microcytosis and hypochromic red cells, and required regulate transfusion. The patient was clinically diagnosed with thalassemia major. Conclusion: Our study widens the mutation spectrum of β‐thalassemia. In addition, this case may spark future studies of the regulatory regions of the beta‐globin gene cluster. [ABSTRACT FROM AUTHOR]

Abstract: The discovery of highly efficient photocatalysts for water splitting remains a challenge of high importance. Here, we report a series of novel organic conjugated polymers (OCPs) that contain complexed non‐noble metals for photocatalytic hydrogen evolution. The conjugated chromophore polymers were synthesized by a Heck coupling between ferrocene and phenantholine derivatives, which absorb broadly, even up to the near‐IR region. The photocatalyst performances were investigated for hydrogen evolution by using Fe3(CO)12 as a water reduction catalyst. H2 evolution rates up to 212.4 μmol h−1, with an apparent quantum yield of 10.3 % at 380 nm, were obtained with a photocatalyst polymer based on alternating ferrocene and 4,7‐bisphenyl‐1,10‐phenanthroline units. The high activity is likely due to favorable electron transfer and coordination of Fe3(CO)12 with phenanthroline in the supramolecular OCPs. [ABSTRACT FROM AUTHOR]

In situ generated iron-based Knölker complexes were found to be efficient catalysts in a fully non-noble metal Cu-Fe photocatalytic water reduction system. These mononuclear iron catalysts were able to generate hydrogen up to 15 times faster than previously reported [Fe3(CO)12]. A reductive quenching mechanism was shown to operate by fluorescence experiments. [ABSTRACT FROM AUTHOR]

Insulin-like growth factor-1 (IGF-1) is a brain-specific multifunctional protein involved in neuronal polarity and axonal guidance. Mature IGF-1 triggers three enzymes, mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K), and phosphoinositide phospholipase C-γ (PLC-γ), which are its predominant downstream regulators. The PI3K-AKT signaling pathway is upstream of the mammalian target of rapamycin (mTOR), which is of great importance in the induction of autophagy. However, whether the neuroprotective effect of IGF-1 against excitotoxicity is mediated by autophagy through the PI3K/AKT/mTOR pathway remains to be elucidated. The induction of autophagy following NMDA treatment was determined by microtubule-associated protein light chain 3 (LC3) conversion and the result of this autophagy was assessed by monitoring the cleavage of caspase 3 in cultured hippocampal neurons. Cell viability was determined using MTT and LDH assay, and PI-staining was used to estimate the fate of autophagy and the protective effect of IGF-1. In addition, IGF-1 was found to decrease autophagy induced by NMDA using transmission electron microscopy and MDC staining. The protective effect of IGF-1 against autophagy was accompanied with up-regulation of phospho-AKT (p-AKT) and phospho-mTOR (p-mTOR), which was blocked by the inhibitor of PI3K. At the same time, the activation of NR2B resulting in the down-regulation of p-AKT and p-mTOR was blocked by IGF-1. Together, these data suggest that NMDA induces the autophagy, followed by apoptosis in cultured hippocampal neurons, and that IGF-1 can block this effect via inhibition of NR2B receptors and activation of the PI3K-AKT-mTOR pathway. J. Cell. Physiol. 229: 1618-1629, 2014. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

ABSTRACT: Aim: Whether the burden of advanced oxidation protein products (AOPP) accumulation, a marker of oxidative stress, is affected by dialysis modality remains unclear. We compared the serum levels of AOPP in patients on haemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) and tested the hypothesis that an accumulation of AOPP was an independent risk factor for cardiovascular disease. Methods: This was a cross-section study. A total of 2095 patients (1539 HD, 556 CAPD) were recruited from the nine largest dialysis centres in China. Persons in medical centres for disease screening were selected as controls. Patients maintained on HD were dialyzed twice or thrice weekly. CAPD patients used lactate-buffered, glucose-containing solutions. The patients' data were abstracted from the medical record. The serum levels of AOPP were determined by spectrophotometric detection. Results: The levels of AOPP were significantly elevated in both HD and CAPD patients compared to healthy controls. Accumulation of AOPP was more significant in HD compared to CAPD population. Meanwhile, AOPP accumulation was associated with the presence of ischaemic heart disease (IHD) only in HD, but not CAPD patients. A higher proportion of IHD was found in the HD population among those with higher levels of AOPP in each category of age and irrespective of the presence or absence of high triglyceride. Multivariate regression analysis indicated that accumulation of AOPP was an independent risk factor for IHD in HD population. Conclusion: Accumulation of AOPP was more significant in HD compared to CAPD patients. The level of AOPP was independently associated with IHD only in HD patients. [ABSTRACT FROM AUTHOR]

This study investigated whether proteinuria not only could serve as a marker of renal outcome but also could monitor the renoprotection of renin–angiotensin system (RAS) inhibitor treatment in patients with nondiabetic chronic kidney disease (CKD). Data from the Renoprotection of Optimal Antiproteinuric Doses (ROAD) trial were used to examine the contribution of the antiproteinuric effect of benazepril and losartan on renal outcome (the primary composite end point of doubling of serum creatinine and end-stage renal disease or death) in 339 Chinese nondiabetic CKD patients with overt proteinuria and renal insufficiency. The degree of proteinuria at month 6 of treatment (residual proteinuria) and during follow-up (time-average proteinuria) showed a close relationship with renal end points. Lowering of proteinuria reduced the risk of renal progression in patients with high, as well as low, proteinuria at baseline. After adjustment for baseline risk markers, therapy-induced change in these variables at month 6 and during follow-up—high residual proteinuria and time-average proteinuria (≥1.0 g/d)—remained the independent predictors for renal end points. Therefore, minimization of proteinuria at least to less than 1.0 g/d should be a therapeutic goal in the management of nondiabetic patients with heavy proteinuria and renal insufficiency. [ABSTRACT FROM PUBLISHER]

Abstract: To clarify the characteristics of TCR αβ T cells in the peripheral blood of patients with chronic hepatitis B (CHB), we investigated the patterns of Complementarity Determining Region3 (CDR3) length distribution for all 24 TCR BV gene families and 32 TCR AV gene family in the peripheral blood lymphocytes of two patients with CHB and two healthy controls by immunoscope spectratyping technique. We found that the profiles of CDR3 length distribution for all TCR AV and TCR BV family showed Gaussian distribution (the polyclonal TCR αβ T cells) in healthy controls, however, the restricted usage of TCR BV and TCR AV family (the oligoclonal TCR αβ T cells) has been monitored in two CHB patients, furthermore, the oligoclonal TCR αβ T cells showed the different CDR3 sequences and length, it might be correlated to the different epitope of hepatitis B virus (HBV) or the different HLA type of the patients. Detailed analysis of the CDR3 length of TCR αβ T cells might be interesting to light on the further study of the individualized immunotherapy of CHB and the further research of the new T lymphocyte epitope vaccine of HBV. [Copyright &y& Elsevier]