Publications by authors named "Wen-Wen Dong"

36 Publications

Evaluation of efficacy and safety of PARP inhibitors in breast cancer: A systematic review and meta-analysis.

Breast 2021 May 27;59:44-50. Epub 2021 May 27.

Department of Breast, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, China. Electronic address:

Background: Many breast cancer clinical trials with PARPi have been completed or are currently carried out, either by monotherapy or combined with chemotherapy. We aim to assess the efficacy and safety of PARPi in breast cancer patients as compared to chemotherapy.

Methods: A comprehensive literature search of PubMed, EMBASE, CENTRAL, conference meetings and clinical trial registry was performed. The primary outcomes were progression-free survival (PFS), overall survival (OS), overall response rate (ORR). The secondary outcome was safety profile. The comparative effects were measured using hazard ratio (HR) or relative risk (RR) with 95% confidence interval. Subgroup analyses were conducted based on types of intervention and baseline characteristics of patients.

Results: Six RCTs (n = 1953) were included. Two RCTs were recognized as high risk. PARPi was associated with an improved PFS (HR, 0.65; 95% CI, 0.56-0.74), OS (HR, 0.86; 95% CI, 0.73-1.01), and a higher ORR (RR, 1.38; 95% CI, 1.05-1.82). PARPi, however, significantly increased risk of grade 3-4 thrombocytopenia (RR, 1.63; 95% CI, 1.06-2.52). Monotherapy was observed with lower risk of disease progression and higher ORR rate than combination therapy, 0.56 to 0.65 and 2.21 to 1.05, respectively. For patients without prior platinum treatment, PARPi significantly improved PFS (HR, 0.64; 95% CI, 0.52-0.79).

Conclusions: PARPi was observed with a significantly improved efficacy in aspects of PFS and ORR, but also higher risk of grade 3-4 thrombocytopenia as compared to chemotherapy. PARPi was a better choice for patients who had not received previous platinum treatment.
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http://dx.doi.org/10.1016/j.breast.2021.05.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8215282PMC
May 2021

Upregulation of Matrix Metalloproteinase-9 Protects against Sepsis-Induced Acute Lung Injury via Promoting the Release of Soluble Receptor for Advanced Glycation End Products.

Oxid Med Cell Longev 2021 10;2021:8889313. Epub 2021 Feb 10.

School of Kinesiology, The Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai 200438, China.

Dysregulation of matrix metalloproteinase- (MMP-) 9 is implicated in the pathogenesis of acute lung injury (ALI). However, it remains controversial whether MMP-9 improves or deteriorates acute lung injury of different etiologies. The receptor for advanced glycation end products (RAGE) plays a critical role in the pathogenesis of acute lung injury. MMPs are known to mediate RAGE shedding and release of soluble RAGE (sRAGE), which can act as a decoy receptor by competitively inhibiting the binding of RAGE ligands to RAGE. Therefore, this study is aimed at clarifying whether and how pulmonary knockdown of MMP-9 affected sepsis-induced acute lung injury as well as the release of sRAGE in a murine cecal ligation and puncture (CLP) model. The analysis of GEO mouse sepsis datasets GSE15379, GSE52474, and GSE60088 revealed that the mRNA expression of MMP-9 was significantly upregulated in septic mouse lung tissues. Elevation of pulmonary MMP-9 mRNA and protein expressions was confirmed in CLP-induced mouse sepsis model. Intratracheal injection of MMP-9 siRNA resulted in an approximately 60% decrease in pulmonary MMP-9 expression. It was found that pulmonary knockdown of MMP-9 significantly increased mortality of sepsis and exacerbated sepsis-associated acute lung injury. Pulmonary MMP-9 knockdown also decreased sRAGE release and enhanced sepsis-induced activation of the RAGE/nuclear factor-B (NF-B) signaling pathway, meanwhile aggravating sepsis-induced oxidative stress and inflammation in lung tissues. In addition, administration of recombinant sRAGE protein suppressed the activation of the RAGE/NF-B signaling pathway and ameliorated pulmonary oxidative stress, inflammation, and lung injury in CLP-induced septic mice. In conclusion, our data indicate that MMP-9-mediated RAGE shedding limits the severity of sepsis-associated pulmonary edema, inflammation, oxidative stress, and lung injury by suppressing the RAGE/NF-B signaling pathway via the decoy receptor activities of sRAGE. MMP-9-mediated sRAGE production may serve as a self-limiting mechanism to control and resolve excessive inflammation and oxidative stress in the lung during sepsis.
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http://dx.doi.org/10.1155/2021/8889313DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7889353PMC
February 2021

synthesis of hierarchical [email protected](OH) heterostructures for enhanced pseudocapacitor and oxygen evolution reaction performances.

Dalton Trans 2021 Mar;50(8):3060-3066

College of Materials and Chemical Engineering, Key Laboratory of Inorganic Nonmetallic Crystalline and Energy Conversion Materials, China Three Gorges University, Yichang, 443002, P. R. China.

Integrating the merits of different components to construct heterostructures for energy storage and conversion has attracted intensive attention. Herein, taking advantage of bimetallic MOFs and transition bimetal hydroxide, we have successfully used nanoflower-like Ni1-xCox(OH)2 as both the precursor and template to in situ construct three dimensional (3D) [email protected](OH)2 (denoted as [email protected]) hierarchical heterostructures. Benefiting from the optimized composition with hierarchical heterostructures assembled by ultrathin nanosheets, [email protected] possesses rich effective active sites and high electrochemical reactivity, delivering superior pseudocapacitor performance with a specific capacitance of 1855.3 F g-1 at 2 A g-1 and good rate performance. Besides, [email protected] also exhibits excellent OER activity with small overpotentials of 193 mV and 310 mV at 10 and 100 mA cm-2, respectively.
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http://dx.doi.org/10.1039/d0dt03872eDOI Listing
March 2021

Heat stress decreases egg production of laying hens by inducing apoptosis of follicular cells via activating the FasL/Fas and TNF-α systems.

Poult Sci 2020 Nov 8;99(11):6084-6093. Epub 2020 Aug 8.

Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai'an City, P. R. China. Electronic address:

Heat stress (HS) causes significant economic losses in the poultry industry every year. However, the mechanisms for the adverse effects of HS on avian follicular development are largely unknown. The aim of this study was to test whether HS induces apoptosis of follicular cells and impairs egg production by activating the FasL/Fas and tumor necrosis factor (TNF)-α systems. To this end, Hy-Line Brown laying hens, at 32 wk of age, were either exposed to HS of 35°C to 37°C or maintained at 24°C to 26°C (control) for 5 D. At the end of the HS period, follicle numbers, apoptosis, FasL/Fas and TNF-α activation, oxidative stress, and hormone secretion were examined in ovarian follicles. Egg production was observed daily during both the stressed (day S1-S5) and the poststress recovery (day R1-R15) periods. The results demonstrated that HS on hens significantly 1) decreased laying rates from day S3 to R6; 2) reduced numbers of large yellow and hierarchical follicles; 3) triggered apoptosis while increasing the expression of FasL, Fas, TNF-α, and TNF-receptor 1 in small and large yellow follicles; and 4) increased levels of oxidative stress, corticotrophin-releasing hormone, and corticosterone while decreasing the estradiol/progesterone ratio in follicular fluid in small and large yellow follicles. Taken together, the results suggested that hen HS impaired egg production by reducing the number of follicles through inducing apoptosis and that it triggered apoptosis in follicular cells by activating the FasL/Fas and TNF-α systems.
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http://dx.doi.org/10.1016/j.psj.2020.07.024DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7647730PMC
November 2020

Potential mechanism and key genes involved in mechanical ventilation and lipopolysaccharide‑induced acute lung injury.

Mol Med Rep 2020 Nov 14;22(5):4265-4277. Epub 2020 Sep 14.

Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China.

Mechanical ventilation (MV) and lipopolysaccharide (LPS) infection are common causes of acute lung injury. The aim of the present study was to identify the key genes and potential mechanisms involved in mechanical ventilation (MV) and lipopolysaccharide (LPS)‑induced acute lung injury (ALI). Gene expression data of adult C57BL/6 mice with ALI induced by inhaling LPS, MV and LPS + MV were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) associated with MV, LPS and LPS + MV were screened, followed by functional enrichment analysis, protein‑protein interaction network construction, and prediction of transcription factors and small molecule drugs. Finally, the expression of key genes was verified in vivo using reverse transcription‑quantitative PCR. A total of 63, 538 and 1,635 DEGs were associated with MV, LPS and LPS + MV, respectively. MV‑associated genes were significantly enriched in the 'purine ribonucleotide metabolic process'. LPS and LPS + MV‑associated genes were significantly enriched in 'cellular response to cytokine stimulus' and 'cell chemotaxis'. All three conditions were enriched in 'TNF signaling pathway' and 'IL‑17 signaling pathway'. Expression levels of C‑X‑C motif chemokine ligand (CXCL)2, CXCL3 and CXCL10 were upregulated in the LPS and LPS + MV groups. Adenosine A2b receptor, zinc finger and BTB domain‑containing 16 and hydroxycarboxylic acid receptor 2 were identified as DEGs in the MV group. Compared with the control group, Early growth response 1 and activating TF 3 was upregulated in all three groups. Similarities and differences were observed among the MV‑ and LPS‑induced ALI, and MV may enhance the effects of LPS on gene expression. MV may affect urine ribonucleotide metabolic‑related processes, whereas LPS may cause cell chemotaxis and cytokine stimulus responses in ALI progression. The inflammatory response was shared by MV and LPS. The results of the present study may provide insight into a theoretical basis for the study and treatment of ALI.
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http://dx.doi.org/10.3892/mmr.2020.11507DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7533521PMC
November 2020

A novel approach for the forensic diagnosis of drowning by microbiological analysis with next-generation sequencing and unweighted UniFrac-based PCoA.

Int J Legal Med 2020 Nov 2;134(6):2149-2159. Epub 2020 Jul 2.

Department of Forensic Pathology, China Medical University School of Forensic Medicine, Shenyang, China.

The diagnosis of drowning is one of the major challenges in forensic practice, especially when the corpse is in a state of decomposition. Novel indicators of drowning are desired in the field of forensic medicine. In the past decade, aquatic bacteria have attracted great attention from forensic experts because they can easily enter the blood circulation with drowning medium, and some of them can proliferate in the corpse. Recently, the advent of next-generation sequencing (NGS) has created new opportunities to efficiently analyze whole microbial communities and has catalyzed the development of forensic microbiology. We presumed that NGS could be a potential method for diagnosing drowning. In the present study, we verified this hypothesis by fundamental experiments in drowned and postmortem-submersed rat models. Our study revealed that detecting the bacterial communities with NGS and processing the data in a transparent way with unweighted UniFrac-based principal coordinates analysis (PCoA) could clearly discriminate the skin, lung, blood, and liver specimens of the drowning group and postmortem submersion group. Furthermore, the acquired information could be used to identify new cases. Taken together, these results suggest that we could build a microbial database of drowned and postmortem-submersed victims by NGS and subsequently use a bioinformatic method to diagnose drowning in future forensic practice.
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http://dx.doi.org/10.1007/s00414-020-02358-1DOI Listing
November 2020

Upregulation of sphingosine kinase 1 contributes to ventilator-associated lung injury in a two-hit model.

Int J Mol Med 2019 Dec 21;44(6):2077-2090. Epub 2019 Oct 21.

Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, P.R. China.

Ventilator‑associated lung injury (VALI) remains a significant medical problem in intensive care units. The present study aimed to investigate the role of sphingosine kinase 1 (SPHK1) in VALI using a two‑hit model and explore the potential underlying molecular mechanism. Mice were divided into five groups: i) Non‑ventilated group; ii) non‑ventilated + lipopolysaccharide (LPS) group; iii) ventilated group; iv) ventilated + LPS group; and v) ventilated + LPS + SPHK1 inhibitor group. Mice were administered LPS (1 mg/kg) via an intraperitoneal injection. After 12 h, the mice were anesthetized and connected to a ventilator (10 ml/kg at 150 breaths/min) for 4 h. SPHK1 inhibitor (50 mg/kg) was injected intraperitoneally 1 h prior to ventilation. Mouse lung vascular endothelial cells were treated with LPS and SPHK1 inhibitor, and then subjected to cyclic stretch for 4 h. The present results suggested that the expression of SPHK1 and sphingosine 1 phosphate was upregulated in the two‑hit model of VALI; SPHK1 inhibitor could attenuate VALI in the two‑hit model as observed by hematoxylin and eosin staining, and affected the cell count and the protein content levels in the bronchoalveolar lavage fluid. In addition, treatment with SPHK1 inhibitor reduced the wet‑to‑dry ratio of the lungs and suppressed Evans blue dye leakage into the lung tissue. Furthermore, SPHK1 inhibitor exhibited protective effects on the two‑hit model of VALI by inhibiting the Ras homolog family member a‑mediated phosphorylation of myosin phosphatase target subunit 1 (MYPT‑1) and endothelial hyperpermeability. Additionally, mice were divided into five additional groups: i) Non‑ventilated group; ii) non‑ventilated + LPS group; iii) ventilated group; iv) ventilated + LPS group; and v) ventilated + LPS + Rho‑associated coiled‑coil forming protein kinase (ROCK)1 inhibitor group. ROCK1 inhibitor (10 mg/kg) was injected intraperitoneally 1 h prior to ventilation. The present results suggested that ROCK1 inhibitor could attenuate mechanical stretch‑induced lung endothelial injury and the phosphorylation of MYPT‑1 in vivo and in vitro. Collectively, the present findings indicated that upregulation of SPHK1 may contribute to VALI in a two‑hit model.
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http://dx.doi.org/10.3892/ijmm.2019.4379DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6844625PMC
December 2019

Downregulation of R-Spondin1 Contributes to Mechanical Stretch-Induced Lung Injury.

Crit Care Med 2019 07;47(7):e587-e596

Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Objectives: The R-spondin family attenuates tissue damage via tightening endothelium and preventing vascular leakage. This study aims to investigate whether R-spondins protect against mechanical stretch-induced endothelial dysfunction and lung injury and to reveal the underlying mechanisms.

Design: Randomized controlled study.

Setting: University research laboratory.

Subjects: Patients scheduled to undergo surgery with mechanical ventilation support. Adult male Institute of Cancer Research mice. Primary cultured mouse lung vascular endothelial cells.

Interventions: Patients underwent a surgical procedure with mechanical ventilation support of 3 hours or more. Mice were subjected to mechanical ventilation (6 or 30 mL/kg) for 0.5-4 hours. Another group of mice were intraperitoneally injected with 1 mg/kg lipopolysaccharide, and 12 hours later subjected to mechanical ventilation (10 mL/kg) for 4 hours. Mouse lung vascular endothelial cells were subjected to cyclic stretch for 4 hours.

Measurements And Main Results: R-spondin1 were downregulated in both surgical patients and experimental animals exposed to mechanical ventilation. Intratracheal instillation of R-spondin1 attenuated, whereas knockdown of pulmonary R-spondin1 exacerbated ventilator-induced lung injury and mechanical stretch-induced lung vascular endothelial cell apoptosis. The antiapoptotic effect of R-spondin1 was mediated through the leucine-rich repeat containing G-protein coupled receptor 5 in cyclic stretched mouse lung vascular endothelial cells. We identified apoptosis-stimulating protein of p53 2 as the intracellular signaling protein interacted with leucine-rich repeat containing G-protein coupled receptor 5. R-spondin1 treatment decreased the interaction of apoptosis-stimulating protein of p53 2 with p53 while increased the binding of apoptosis-stimulating protein of p53 2 to leucine-rich repeat containing G-protein coupled receptor 5, therefore resulting in inactivation of p53-mediated proapoptotic pathway in cyclic stretched mouse lung vascular endothelial cells.

Conclusions: Mechanical ventilation leads to down-regulation of R-spondin1. R-spondin1 may enhance the interaction of leucine-rich repeat containing G-protein coupled receptor 5 and apoptosis-stimulating protein of p53 2, thus inactivating p53-mediated proapoptotic pathway in cyclic stretched mouse lung vascular endothelial cells. R-spondin1 may have clinical benefit in alleviating mechanical ventilator-induced lung injury.
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http://dx.doi.org/10.1097/CCM.0000000000003767DOI Listing
July 2019

Propofol Protects Lung Endothelial Barrier Function by Suppression of High-Mobility Group Box 1 (HMGB1) Release and Mitochondrial Oxidative Damage Catalyzed by HMGB1.

Med Sci Monit 2019 May 1;25:3199-3211. Epub 2019 May 1.

Department of Anesthesiology, International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China (mainland).

BACKGROUND The processes of mechanical ventilation-induced lung injury (VILI) triggers the release of high-mobility group box 1 (HMGB1), a prominent damage-associated molecular pattern (DAMP) family member, which can cause damage to pulmonary vascular endothelial cells. We aimed to determine whether propofol protected against endothelial cell injury induced by HMGB1 in vitro and in vivo. MATERIAL AND METHODS ICR mice (male) were mechanically ventilated for 4 h after anesthetization at both low tidal volume (LVT, 6 ml/kg) and high tidal volume (HVT, 30 ml/kg). A propofol bolus (10 mg/kg) was administered to the animals prior to the onset of ventilation, followed by infusion at 5 mg/(kg·h). We obtained confluent cultures of mouse lung vascular endothelial cells (MLVECs) and then performed cyclic stretching at 20% stretch for 4 h with or without propofol. RESULTS HMGB1 reduced the expression of tight junctions between endothelial cells, including VE-cadherin and ZO-1, and increased endothelial permeability, and both were blocked by propofol. We found that MLVECs exhibited mitochondrial oxidative damage by HMGB1, which was successfully suppressed through administration of MnTBAP as well as propofol. Propofol ameliorated HVT-associated lung vascular hyperpermeability and HMGB1 production in vivo. Propofol also inhibited HMBG1 release caused by cyclic stretching in MLVECs in vitro. CONCLUSIONS Our results prove that the cyto-protective function of propofol protects against lung ventilation-induced dysfunction of the lung endothelial barrier. This function of propofol is mediated through inhibition of HMGB1 release caused by mechanical stretching and mitochondrial oxidative damage triggered by HMGB1.
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http://dx.doi.org/10.12659/MSM.915417DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6507496PMC
May 2019

Ultrafine Pt Nanoparticles and Amorphous Nickel Supported on 3D Mesoporous Carbon Derived from Cu-Metal-Organic Framework for Efficient Methanol Oxidation and Nitrophenol Reduction.

ACS Appl Mater Interfaces 2018 Apr 9;10(15):12740-12749. Epub 2018 Apr 9.

School of Materials Science and Engineering , Nanyang Technological University , Singapore 639798 , Singapore.

The development of novel strategy to produce new porous carbon materials is extremely important because these materials have wide applications in energy storage/conversion, mixture separation, and catalysis. Herein, for the first time, a novel 3D carbon substrate with hierarchical pores derived from commercially available Cu-MOF (metal-organic framework) (HKUST-1) through carbonization and chemical etching has been employed as the catalysts' support. Highly dispersed Pt nanoparticles and amorphous nickel were evenly dispersed on the surface or embedded within carbon matrix. The corresponding optimal composite catalyst exhibits a high mass-specific peak current of 1195 mA mg Pt and excellent poison resistance capacity ( I/ I = 1.58) for methanol oxidation compared to commercial Pt/C (20%). Moreover, both composite catalysts manifest outstanding properties in the reduction of nitrophenol and demonstrate diverse selectivities for 2/3/4-nitrophenol, which can be attributed to different integrated forms between active species and carbon matrix. This attractive route offers broad prospects for the usage of a large number of available MOFs in fabricating functional carbon materials as well as highly active carbon-based electrocatalysts and heterogeneous organic catalysts.
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http://dx.doi.org/10.1021/acsami.8b01970DOI Listing
April 2018

Ligand-Controlled Integration of Zn and Tb by Photoactive Terpyridyl-Functionalized Tricarboxylates as Highly Selective and Sensitive Sensors for Nitrofurans.

Inorg Chem 2018 Apr 21;57(7):3833-3839. Epub 2018 Mar 21.

Department of Chemistry and Biochemistry , California State University, Long Beach , 1250 Bellflower Boulevard , Long Beach , California 90840 , United States.

The integration of terpyridyl and tricarboxylate functionality in a novel ligand allows concerted 3:1 stoichiometric assembly of size-and charge-complementary Zn/Tb ions into a water-stable 3D luminescent framework (CTGU-8) capable of highly selective, sensitive, and recyclable of nitrofurans.
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http://dx.doi.org/10.1021/acs.inorgchem.7b03200DOI Listing
April 2018

Efficient Gas-Sensing for Formaldehyde with 3D Hierarchical CoO Derived from Co-Based MOF Microcrystals.

Inorg Chem 2017 Nov 7;56(22):14111-14117. Epub 2017 Nov 7.

College of Materials and Chemical Engineering, Hubei Provincial Collaborative Innovation Center for New Energy Microgrid, Key Laboratory of Inorganic Nonmetallic Crystalline and Energy Conversion Materials, China Three Gorges University , Yichang, 443002, China.

Detecting formaldehyde at low operating temperature and maintaining long-term stability are of great significance. In this work, a hierarchical CoO nanostructure has been fabricated by calcining Co-based metal-organic framework (MOF) microcrystals. CoO-350 particles were used for efficient gas-sensing for the detecting of formaldehyde vapor at lower working temperature (170 °C), low detection limit of 10 ppm, and long-term stability (30 days), which not only is the optimal value among all reported pure CoO sensing materials for the detection of formaldehyde but also is superior to that of majority of CoO-based composites. Such extraordinarily efficient properties might be resulted from hierarchically structures, larger surface area and unique pore structure. This strategy is further confirmed that MOFs, especially Co-clusters MOFs, could be used as precursor to synthesize 3D nanostructure metal oxide materials with high-performance, which possess high porosity and more active sites and shorter ionic diffusion lengths.
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http://dx.doi.org/10.1021/acs.inorgchem.7b02254DOI Listing
November 2017

NLRP3 Inflammasome Activation Contributes to Mechanical Stretch-Induced Endothelial-Mesenchymal Transition and Pulmonary Fibrosis.

Crit Care Med 2018 01;46(1):e49-e58

Department of Physiology, Second Military Medical University, Shanghai, China.

Objectives: Mechanical ventilation can induce lung fibrosis. This study aimed to investigate whether ventilator-induced lung fibrosis was associated with endothelial-mesenchymal transition and to uncover the underlying mechanisms.

Design: Randomized, controlled animal study and cell culture study.

Setting: University research laboratory.

Subjects: Adult male Institute of Cancer Research, NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) knockout and wild-type mice. Primary cultured mouse lung vascular endothelial cells.

Interventions: Institute of Cancer Research, NLRP3 knockout and wild-type mice were subjected to mechanical ventilation (20 mL/kg) for 2 hours. Mouse lung vascular endothelial cells were subjected to cyclic stretch for 24 hours.

Measurements And Main Results: Mice subjected to mechanical ventilation exhibited increases in collagen deposition, hydroxyproline and type I collagen contents, and transforming growth factor-β1 in lung tissues. Ventilation-induced lung fibrosis was associated with increased expression of mesenchymal markers (α smooth muscle actin and vimentin), as well as decreased expression of endothelial markers (vascular endothelial-cadherin and CD31). Double immunofluorescence staining showed the colocalization of CD31/α smooth muscle actin, CD31/vimentin, and CD31/fibroblast-specific protein-1 in lung tissues, indicating endothelial-mesenchymal transition formation. Mechanical ventilation also induced NLRP3 inflammasome activation in lung tissues. In vitro direct mechanical stretch of primary mouse lung vascular endothelial cells resulted in similar NLRP3 activation and endothelial-mesenchymal transition formation, which were prevented by NLRP3 knockdown. Furthermore, mechanical stretch-induced endothelial-mesenchymal transition and pulmonary fibrosis were ameliorated in NLRP3-deficient mice as compared to wild-type littermates.

Conclusions: Mechanical stretch may promote endothelial-mesenchymal transition and pulmonary fibrosis through a NLRP3-dependent pathway. The inhibition of endothelial-mesenchymal transition by NLRP3 inactivation may be a viable therapeutic strategy against pulmonary fibrosis associated with mechanical ventilation.
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http://dx.doi.org/10.1097/CCM.0000000000002799DOI Listing
January 2018

Surfactant-Assisted Phase-Selective Synthesis of New Cobalt MOFs and Their Efficient Electrocatalytic Hydrogen Evolution Reaction.

Angew Chem Int Ed Engl 2017 10 18;56(42):13001-13005. Epub 2017 Aug 18.

Department of Chemistry and Biochemistry, California State University, Long Beach, 1250 Bellflower Boulevard, Long Beach, CA, 90840, USA.

Reported herein are two new polymorphic Co-MOFs (CTGU-5 and -6) that can be selectively crystallized into the pure 2D or 3D net using an anionic or neutral surfactant, respectively. Each polymorph contains a H O molecule, but differs dramatically in its bonding to the framework, which in turn affects the crystal structure and electrocatalytic performance for hydrogen evolution reaction (HER). Both experimental and computational studies find that 2D CTGU-5 which has coordinates water and more open access to the cobalt site has higher electrocatalytic activity than CTGU-6 with the lattice water. The integration with co-catalysts, such as acetylene black (AB) leads to a composite material, AB&CTGU-5 (1:4) with very efficient HER catalytic properties among reported MOFs. It exhibits superior HER properties including a very positive onset potential of 18 mV, low Tafel slope of 45 mV dec , higher exchange current density of 8.6×10  A cm , and long-term stability.
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http://dx.doi.org/10.1002/anie.201707238DOI Listing
October 2017

Protective Effects of Hydrogen-Rich Saline Against Lipopolysaccharide-Induced Alveolar Epithelial-to-Mesenchymal Transition and Pulmonary Fibrosis.

Med Sci Monit 2017 May 19;23:2357-2364. Epub 2017 May 19.

Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China (mainland).

BACKGROUND Fibrotic change is one of the important reasons for the poor prognosis of patients with acute respiratory distress syndrome (ARDS). The present study investigated the effects of hydrogen-rich saline, a selective hydroxyl radical scavenger, on lipopolysaccharide (LPS)-induced pulmonary fibrosis. MATERIAL AND METHODS Male ICR mice were divided randomly into 5 groups: Control, LPS-treated plus vehicle treatment, and LPS-treated plus hydrogen-rich saline (2.5, 5, or 10 ml/kg) treatment. Twenty-eight days later, fibrosis was assessed by determination of collagen deposition, hydroxyproline, and type I collagen levels. Development of epithelial-to-mesenchymal transition (EMT) was identified by examining protein expressions of E-cadherin and α-smooth muscle actin (α-SMA). Transforming growth factor (TGF)-β1 content, total antioxidant capacity (T-AOC), malondialdehyde (MDA) content, catalase (CAT), and superoxide dismutase (SOD) activity were determined. RESULTS Mice exhibited increases in collagen deposition, hydroxyproline, type I collagen contents, and TGF-β1 production in lung tissues after LPS treatment. LPS-induced lung fibrosis was associated with increased expression of α-SMA, as well as decreased expression of E-cadherin. In addition, LPS treatment increased MDA levels but decreased T-AOC, CAT, and SOD activities in lung tissues, indicating that LPS induced pulmonary oxidative stress. Hydrogen-rich saline treatment at doses of 2.5, 5, or 10 ml/kg significantly attenuated LPS-induced pulmonary fibrosis. LPS-induced loss of E-cadherin in lung tissues was largely reversed, whereas the acquisition of α-SMA was dramatically decreased by hydrogen-rich saline treatment. In addition, hydrogen-rich saline treatment significantly attenuated LPS-induced oxidative stress. CONCLUSIONS Hydrogen-rich saline may protect against LPS-induced EMT and pulmonary fibrosis through suppressing oxidative stress.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5445901PMC
http://dx.doi.org/10.12659/msm.900452DOI Listing
May 2017

A Multifunctional Tb-MOF for Highly Discriminative Sensing of Eu /Dy and as a Catalyst Support of Ag Nanoparticles.

Small 2017 06 18;13(22). Epub 2017 Apr 18.

School of Materials Science and Engineering, Nanyang Technological University, Singapore, 639798, Singapore.

Exploring novel multifunctional rare earth materials is very important because these materials have fundamental interests, such as new structural facts and connecting modes, as well as potential technological applications, including optics, magnetic properties, sorption, and catalytic behaviors. Especially, employing these nanomaterials for sensing or catalytic reactions is still very challenging. Herein, a new superstable, anionic terbium-metal-organic-framework, [H N(CH ) ][Tb(cppa) (H O) ], (China Three Gorges University (CTGU-1), H cppa = 5-(4-carboxyphenyl)picolinic acid), is successfully prepared, which can be used as a turn-on, highly-sensitive fluorescent sensor to detect Eu and Dy , with a detection limitation of 5 × 10 and 1 × 10 m in dimethylformamide, respectively. This result represents the first example of lanthanide-metal-organic-frameworks (Ln-MOF) that can be employed as a discriminative fluorescent probe to recognize Eu and Dy . In addition, through ion exchanging at room temperature, Ag(I) can be readily reduced in situ and embedded in the anionic framework, which leads to the formation of [email protected] composite with uniform size and distribution. The as-prepared [email protected] shows remarkable catalytic performance to reduce 4-nitrophenol, with a reduction rate constant κ as large as 2.57 × 10 s ; almost the highest value among all reported [email protected] composites.
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http://dx.doi.org/10.1002/smll.201602996DOI Listing
June 2017

Ag-NPs embedded in two novel Zn/Zn-cluster-based metal-organic frameworks for catalytic reduction of 2/3/4-nitrophenol.

Dalton Trans 2017 Feb;46(8):2430-2438

Department of Chemistry and Biochemistry, California State University, Long Beach, 1250 Bellflower Boulevard, Long Beach, CA 90840, USA.

By utilizing symmetrical pentacarboxylate ligands, 3,5-di(2',5'-dicarboxylphenyl)benzoic acid (HL1) and 3,5-di(2',4'-dicarboxylphenyl)benzoic acid (HL2), two novel porous Zn-MOFs, [Zn(μ-HO)(L1)]·3DMA·4HO (CTGU-3) and [Zn(μ-OH)L2(HO)]·HO (CTGU-4) have been synthesized under solvothermal conditions. CTGU-3 and CTGU-4 exhibit 3D microporous frameworks with flu and dia topologies and possess unique secondary building units [Zn(μ-HO)(RCO)] and [Zn(μ-OH)(RCO)], respectively. Such porous systems create a unique space or surface to accommodate Ag nanoparticles (Ag NPs), which could efficiently prevent Ag NPs from aggregation and leaching. In this work, two new [email protected] composites, denoted as [email protected], have been successfully fabricated through solution infiltration, for the reduction of nitrophenol. Compared with CTGU-4, CTGU-3 shows enhanced catalytic efficiency toward the reaction when it is used as a catalyst support of Ag NPs. Moreover, gas sorption and luminescence properties of two compounds were also investigated.
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http://dx.doi.org/10.1039/c7dt00024cDOI Listing
February 2017

Anionic Lanthanide MOFs as a Platform for Iron-Selective Sensing, Systematic Color Tuning, and Efficient Nanoparticle Catalysis.

Inorg Chem 2017 Feb 10;56(3):1402-1411. Epub 2017 Jan 10.

Department of Chemistry and Biochemistry, California State University, Long Beach , 1250 Bellflower Boulevard, Long Beach, California 90840, United States.

New porous anionic Ln-MOFs, namely, [MeNH][Ln(CPA)(HO)] (Ln = Eu, Gd), have been prepared through the self-assembly of 5-(4-carboxy phenyl)picolinic acid (HCPA) and lanthanide ions. They feature open anionic frameworks with 1-D hydrophilic channels and exchangeable dimethylamine ions. The Eu phase could detect Fe ions with high selectivity and sensitivity in either aqueous solution or biological condition. The ratios of lanthanide ions on this structure platform could be rationally tuned to not only achieve dichromatic emission colors with linear correlation but also attain three primary colors (RGB) and even white light with favorable correlated color temperature. Furthermore, the Ag(I)-exchanged phases can be readily reduced to afford Ag nanoparticles. The as-prepared [email protected] composite shows highly efficient catalytic performance for the reduction of 4-nitrophenol.
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http://dx.doi.org/10.1021/acs.inorgchem.6b02476DOI Listing
February 2017

A multi-responsive luminescent sensor based on a super-stable sandwich-type terbium(iii)-organic framework.

Dalton Trans 2016 Oct;45(39):15492-15499

College of Chemistry and Chemical Engineering, and Henan Key Laboratory of Function-Oriented Porous Materials, Luoyang Normal University, Luoyang 471934, P. R. China.

A super-stable multifunctional terbium(iii)-organic framework, namely {[Tb(TATAB) (HO)]·NMP·HO} (Tb-MOF, HTATAB = 4,4',4''-s-triazine-1,3,5-triyltri-m-aminobenzoic acid, NMP = N-methyl-2-pyrrolidone) was synthesized. Tb-MOF exhibits a 2D sql structure with binuclear [Tb(COO)(HO)] units as 4-connected nodes, and free water and NMP molecules are inserted between 2D layers through hydrogen-bonding interactions, forming a sandwich-type architecture. Observably, such a framework remains intact in a remarkable variety of environments such as common solvents and aqueous solutions with metal cations and inorganic anions, as well as with a pH ranging from 1 to 13. In particular, Tb-MOF can not only detect small organic molecules, metal cations and inorganic anions with high sensitivity and high selectivity, but also can accurately detect explosive 2-nitrophenol, 3-nitrophenol, 4-nitrophenol and 2,4,6-trinitrophenol in water. Its luminescence quenching response to Fe and CrO ions can be explained in terms of the competitive absorption mechanism. In addition, the luminescence intensity of Tb-MOF is strongly correlated with the pH value in a pH range from 1 to 13. Thus, this material can be potentially used as a multi-responsive luminescent sensor.
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http://dx.doi.org/10.1039/c6dt03057bDOI Listing
October 2016

An Ultrastable Europium(III)-Organic Framework with the Capacity of Discriminating Fe/Fe Ions in Various Solutions.

Inorg Chem 2016 Oct 5;55(20):10114-10117. Epub 2016 Oct 5.

State Key Laboratory of Structural Chemistry, Fujian Institute of Research on the Structure of Matter, Chinese Academy of Sciences , Fuzhou, Fujian 350002, P. R. China.

An ultrastable luminescent europium-organic framework, {[Eu(L)(HO)]·NMP·HO} (CTGU-2; NMP = N-methyl-2-pyrrolidone), can first detect Fe/Fe cations in different medium systems with high selectivity and sensitivity, and it also exhibits high sensitivity for CrO anion and acetone with a wide linear range and a low detection limit.
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http://dx.doi.org/10.1021/acs.inorgchem.6b01876DOI Listing
October 2016

Pharmacological activation of cannabinoid 2 receptor attenuates inflammation, fibrogenesis, and promotes re-epithelialization during skin wound healing.

Eur J Pharmacol 2016 Sep 3;786:128-136. Epub 2016 Jun 3.

Department of Forensic Pathology, China Medical University School of Forensic Medicine, Shenyang, China. Electronic address:

Previous studies showed that cannabinoid 2 (CB2) receptor is expressed in multiple effector cells during skin wound healing. Meanwhile, its functional involvement in inflammation, fibrosis, and cell proliferation in other organs and skin diseases implied CB2 receptor might also regulate skin wound healing. To verify this hypothesis, mice excisional wounds were created and treated with highly selective CB2 receptor agonist GP1a (1-(2,4-dichlorophenyl)-6-methyl- N-piperidin-1-yl-4H-indeno[1,2-c]pyrazole-3-carboxamide) and antagonist AM630 ([6-iodo-2- methyl-1-(2-morpholin-4-ylethyl)indol-3-yl]-(4-methoxyphenyl)methanone) respectively. The inflammatory infiltration, cytokine expression, fibrogenesis, and wound re-epithelialization were analyzed. After CB2 receptor activation, neutrophil and macrophage infiltrations were reduced, and expressions of monocyte chemotactic protein (MCP)-1, stromal cell-derived factor (SDF)-1, Interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1 and vascular endothelial growth factor (VEGF)-A were decreased. Keratinocyte proliferation and migration were enhanced. Wound re-epithelialization was accelerated. Fibroblast accumulation and fibroblast-to-myofibroblast transformation were attenuated, and expression of pro-collagen I was decreased. Furthermore, HaCaT cells in vitro were treated with GP1a or AM630, which revealed that CB2 receptor activation promoted keratinocyte migration by inducing the epithelial to mesenchymal transition. These results, taken together, indicate that activating CB2 receptor could ameliorate wound healing by reducing inflammation, accelerating re-epithelialization, and attenuating scar formation. Thus, CB2 receptor agonist might be a novel perspective for skin wound therapy.
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http://dx.doi.org/10.1016/j.ejphar.2016.06.006DOI Listing
September 2016

A Robust Luminescent Tb(III)-MOF with Lewis Basic Pyridyl Sites for the Highly Sensitive Detection of Metal Ions and Small Molecules.

Inorg Chem 2016 Apr 11;55(7):3265-71. Epub 2016 Mar 11.

School of Materials Science and Engineering and Division of Chemistry and Biological Chemistry, School of Physical and Mathematical Sciences, Nanyang Technological University , Singapore 639798, Singapore.

A new luminescent terbium-metal-organic framework [Tb3(L)2(HCOO)(H2O)5]·DMF·4H2O (1) (H4L = 4,4'-(pyridine-3,5-diyl)diisophthalic acid) has been successfully assembled by Tb(3+) ions and an undeveloped pyridyl-tetracarboxylate. Compound 1 exhibits a 3D porous (3,8)-connected (4.5(2))2(4(2).5(12).6(6).7(5).8(3)) topological framework with fascinating 1D open hydrophilic channels decorated by uncoordinated Lewis basic pyridyl nitrogen atoms. In particular, the Tb-MOF (1) can detect Cu(2+) ions with high selectivity and sensitivity, and its luminescence is nearly entirely quenched in N,N-dimethylformamide (DMF) solution and biological system. In addition, 1 still has high detection for the trace content of nitromethane with 70 ppm, which suggests that 1 is a promising example of dual functional materials with sensing copper ions and nitromethane.
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http://dx.doi.org/10.1021/acs.inorgchem.5b02294DOI Listing
April 2016

Lung endothelial barrier protection by resveratrol involves inhibition of HMGB1 release and HMGB1-induced mitochondrial oxidative damage via an Nrf2-dependent mechanism.

Free Radic Biol Med 2015 Nov 13;88(Pt B):404-416. Epub 2015 May 13.

Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, Peoples׳ Republic of China. Electronic address:

High-mobility group box 1 (HMGB1) contributes to lung vascular hyperpermeability during ventilator-induced lung injury. We aimed to determine whether the natural antioxidant resveratrol protected against HMGB1-induced endothelial hyperpermeability both in vitro and in vivo. We found that HMGB1 decreased vascular endothelial (VE)-cadherin expression and increased endothelial permeability, leading to mitochondrial oxidative damage in primary cultured mouse lung vascular endothelial cells (MLVECs). Both the mitochondrial superoxide dismutase 2 mimetic MnTBAP and resveratrol blocked HMGB1-induced mitochondrial oxidative damage, VE-cadherin downregulation, and endothelial hyperpermeability. In in vivo studies, anesthetized male ICR mice were ventilated for 4h using low tidal volume (6 ml/kg) or high tidal volume (HVT; 30 ml/kg) ventilation. The mice were injected intraperitoneally with resveratrol immediately before the onset of ventilation. We found that resveratrol attenuated HVT-associated lung vascular hyperpermeability and HMGB1 production. HVT caused a significant increase in nuclear factor-erythroid 2-related factor 2 (Nrf2) nuclear translocation and Nrf2 target gene expression in lung tissues, which was further enhanced by resveratrol treatment. HMGB1 had no effect on Nrf2 activation, whereas resveratrol treatment activated the Nrf2 signaling pathway in HMGB1-treated MLVECs. Moreover, Nrf2 knockdown reversed the inhibitory effects of resveratrol on HMGB1-induced mitochondrial oxidative damage and endothelial hyperpermeability. The inhibitory effect of resveratrol on cyclic stretch-induced HMGB1 mRNA expression in primary cultured MLVECs was also abolished by Nrf2 knockdown. In summary, this study demonstrates that resveratrol protects against lung endothelial barrier dysfunction initiated by HVT. Lung endothelial barrier protection by resveratrol involves inhibition of mechanical stretch-induced HMGB1 release and HMGB1-induced mitochondrial oxidative damage. These protective effects of resveratrol might be mediated through an Nrf2-dependent mechanism.
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http://dx.doi.org/10.1016/j.freeradbiomed.2015.05.004DOI Listing
November 2015

Resveratrol ameliorates lipopolysaccharide-induced epithelial mesenchymal transition and pulmonary fibrosis through suppression of oxidative stress and transforming growth factor-β1 signaling.

Clin Nutr 2015 Aug 6;34(4):752-60. Epub 2014 Sep 6.

Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, PR China. Electronic address:

Background & Aims: Fibrotic changes seem to be responsible for the high mortality rate observed in patients with acute respiratory distress syndrome (ARDS). The present study aimed to determine whether resveratrol, a natural antioxidant polyphenol, had anti-fibrotic effects in the murine model of lipopolysaccharide (LPS)-induced pulmonary fibrosis.

Methods: Fibrosis was assessed by determination of collagen deposition, hydroxyproline and type I collagen levels in lung tissues. Development of epithelial-mesenchymal transition (EMT) was identified by the loss of E-cadherin accompanying by the acquisition of α-smooth muscle actin (α-SMA). Transforming growth factor (TGF)-β1 content, levels of phosphorylated Smad2/Smad3 and Smad4, malondialdehyde (MDA) content, total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity, and catalase (CAT) activity in lung tissues were determined.

Results: LPS increased collagen deposition, hydroxyproline and type I collagen contents, and meanwhile induced EMT process, stimulated TGF-β1 production and Smad activation in lung tissues on day 21 to day 28 after LPS administration. In addition, LPS treatment resulted in a rapid induction of oxidative stress as evidenced by increase of MDA and decreases of T-AOC, CAT and SOD activities as early as 7 days after LPS treatment, which was persistent for at least 4 weeks. In contrast, resveratrol treatment attenuated LPS-induced EMT and pulmonary fibrosis, meanwhile it suppressed LPS-induced oxidative stress, TGF-β1 production and activation of Smad signaling pathway.

Conclusions: Resveratrol may ameliorate LPS-induced EMT and pulmonary fibrosis through suppression of oxidative stress and TGF-β1/Smad signaling pathway. Application of antioxidants may represent a useful adjuvant pharmacologic approach to reduce ARDS-associated pulmonary fibrosis.
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http://dx.doi.org/10.1016/j.clnu.2014.08.014DOI Listing
August 2015

Three novel lanthanide metal-organic frameworks (Ln-MOFs) constructed by unsymmetrical aromatic dicarboxylatic tectonics: synthesis, crystal structures and luminescent properties.

Molecules 2014 Sep 11;19(9):14352-65. Epub 2014 Sep 11.

College of Materils & Chemical Engineering, Collaborative Innovation Center for Microgrid of New Energy of Hubei Province, China Three Gorges University, Yichang 443002, China.

Three novel Ln(III)-based coordination polymers, {[Ln2 (2,4-bpda)3 (H2O)x]·yH2O}n (Ln = La (III) (1), x = 2, y = 0, Ce (III) (2), Pr (III) (3), x = 4, y = 1) (2,4-H2bpda = benzophenone-2,4-dicarboxylic acid) have been prepared via a solvothermal method and characterized by elemental analysis, IR, and single-crystal X-ray diffraction techniques. Complex 1 exhibits a 3D complicated framework with a new 2-nodal (3,7)-connected (42·5) (44·51·66·8) topology. Complexes 2 and 3 are isomorphous, and feature a 3D 4-connected (65·8)-CdSO4 network. Moreover, solid-state properties such as thermal stabilities and luminescent properties of 1 and 2 were also investigated. Complex 1 crystallized in a monoclinic space group P21/c with a = 14.800 (3), b = 14.500 (3), c = 18.800 (4) Å, β = 91.00 (3), V = 4033.9 (14) Å3 and Z = 4. Complex 2 crystallized in a monoclinic space group Cc with a = 13.5432 (4), b = 12.9981 (4), c = 25.7567 (11) Å, β = 104.028 (4), V = 1374.16 (7) Å3 and Z = 4.
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http://dx.doi.org/10.3390/molecules190914352DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6271744PMC
September 2014

Di-aqua-bis-[5-(pyrazin-2-yl-κN (1))-3-(pyridin-3-yl)-1,2,4-triazolido-κN (1)]zinc.

Acta Crystallogr Sect E Struct Rep Online 2014 Apr 5;70(Pt 4):m116. Epub 2014 Mar 5.

College of Materials & Chemical Engineering, China Three Gorges University, Yichang 443002, People's Republic of China.

In the title compound, [Zn(C11H7N6)2(H2O)2], the Zn(II) cation, located on an inversion center, is N,N'-chelated by two 5-(pyrazin-2-yl)-3-(pyridin-3-yl)-1,2,4-triazolide anions and is further coordinated by two water mol-ecules in a distorted N4O2 octa-hedral geometry. In the anionic ligand, the pyrazine and pyridine rings are twisted with respect to the central triazole ring by 5.77 (10) and 11.54 (10)°, respectively. In the crystal, classical O-H⋯N and weak C-H⋯O hydrogen bonds and π-π stacking inter-actions between aromatic rings [the centroid-centroid distances between triazole and pyrazine rings, and between triazole and pyridine rings are 3.623 (2) and 3.852 (2) Å, respectively] connect the mol-ecules into a three-dimensional supra-molecular architecture.
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http://dx.doi.org/10.1107/S1600536814004176DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998535PMC
April 2014

Identification of wild soybean miRNAs and their target genes responsive to aluminum stress.

BMC Plant Biol 2012 Oct 5;12:182. Epub 2012 Oct 5.

State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Agriculture, South China Agricultural University, Guangzhou, 510642, China.

Background: MicroRNAs (miRNAs) play important regulatory roles in development and stress response in plants. Wild soybean (Glycine soja) has undergone long-term natural selection and may have evolved special mechanisms to survive stress conditions as a result. However, little information about miRNAs especially miRNAs responsive to aluminum (Al) stress is available in wild soybean.

Results: Two small RNA libraries and two degradome libraries were constructed from the roots of Al-treated and Al-free G. soja seedlings. For miRNA identification, a total of 7,287,655 and 7,035,914 clean reads in Al-treated and Al-free small RNAs libraries, respectively, were generated, and 97 known miRNAs and 31 novel miRNAs were identified. In addition, 49 p3 or p5 strands of known miRNAs were found. Among all the identified miRNAs, the expressions of 30 miRNAs were responsive to Al stress. Through degradome sequencing, 86 genes were identified as targets of the known miRNAs and five genes were found to be the targets of the novel miRNAs obtained in this study. Gene ontology (GO) annotations of target transcripts indicated that 52 target genes cleaved by conserved miRNA families might play roles in the regulation of transcription. Additionally, some genes, such as those for the auxin response factor (ARF), domain-containing disease resistance protein (NB-ARC), leucine-rich repeat and toll/interleukin-1 receptor-like protein (LRR-TIR) domain protein, cation transporting ATPase, Myb transcription factors, and the no apical meristem (NAM) protein, that are known to be responsive to stress, were found to be cleaved under Al stress conditions.

Conclusions: A number of miRNAs and their targets were detected in wild soybean. Some of them that were responsive to biotic and abiotic stresses were regulated by Al stress. These findings provide valuable information to understand the function of miRNAs in Al tolerance.
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http://dx.doi.org/10.1186/1471-2229-12-182DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519564PMC
October 2012

[Study of attentional bias in neglect patients by grey discriminant test].

Zhonghua Yi Xue Za Zhi 2012 Mar;92(9):612-5

Department of Neurology, First Affiliated Hospital, Anhui Medical University, Hefei 230022, China.

Objective: To explore the attentional bias in unilateral spatial neglect (USN) patients.

Methods: The grey discriminant test was conducted on 12 right-brain-damaged patients with USN (USN+), 12 right-brain-damaged patients with no evidence of USN (USN-) and 20 health controls (HC). They were matched for age, years of education, mini-mental state examination (MMSE) scores and handedness. And all patients were recruited from First Affiliated Hospital of Anhui Medical University. The attentional deviation scores were compared between three groups.

Results: The differences in scores of neglect tests for the USN+, USN- and HC groups were significant (Albert test: USN+ group -0.56 ± 0.39, USN- group 0.00 ± 0.00, HC group 0.00 ± 0.00, F((2, 41)) = 33.708, P < 0.001; line bisection test: USN+ group 0.28 ± 0.29, USN- group 0.03 ± 0.04, HC group -0.02 ± 0.04, F((2, 41)) = 14.527, P < 0.001; clock drawing by memory: USN+ group 3.58 ± 4.03, USN- group 0.08 ± 0.29, HC group 0.00 ± 0.00, F((2, 41)) = 12.558, P < 0.001; daisy copying: USN+ group 0.83 ± 0.65, USN- group 0.13 ± 0.23, HC group 0.00 ± 0.00, F((2, 41)) = 21.621, P < 0.001). The comparative results of lesion locations showed that USN+ patients were predominantly related to lesions in temporal-parietal junction. The attentional deviation scores for the USN+, USN- and HC groups were 0.92 ± 0.11, 0.41 ± 0.12 and -0.28 ± 0.15 respectively. The difference was significant (F((2, 41)) = 334.324, P < 0.001). There was with a small leftward bias in the HC group and a rightward bias in the USN+ and USN- groups. LSD test revealed that the USN+ group displayed a rightward bias much strongly than the USN- group (P < 0.001). And the results of grey discriminant test were consistent with the neglect symptoms.

Conclusions: The USN patients show a marked attentional bias toward the right side of space. And it may be attributed to the dysfunction of temporal-parietal junction.
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March 2012

Necrostatin-1 suppresses autophagy and apoptosis in mice traumatic brain injury model.

Neurochem Res 2012 Sep 27;37(9):1849-58. Epub 2012 Jun 27.

Department of Forensic Science and Laboratory of Neural Injury, Medical College of Soochow University, Suzhou 215123, Jiangsu, People's Republic of China.

Traumatic brain injury (TBI) results in neuronal apoptosis, autophagic cell death and necroptosis. Necroptosis is a newly discovered caspases-independent programmed necrosis pathway which can be triggered by activation of death receptor. Previous works identified that necrostatin-1 (NEC-1), a specific necroptosis inhibitor, could reduce tissue damage and functional impairment through inhibiting of necroptosis process following TBI. However, the role of NEC-1 on apoptosis and autophagy after TBI is still not very clear. In this study, the amount of TBI-induced neural cell deaths were counted by PI labeling method as previously described. The expression of autophagic pathway associated proteins (Beclin-1, LC3-II, and P62) and apoptotic pathway associated proteins (Bcl-2 and caspase-3) were also respectively assessed by immunoblotting. The data showed that mice pretreated with NEC-1 reduced the amount of PI-positive cells from 12 to 48 h after TBI. Immunoblotting results showed that NEC-1 suppressed TBI-induced Beclin-1 and LC3-II activation which maintained p62 at high level. NEC-1 pretreatment also reversed TBI-induced Bcl-2 expression and caspase-3 activation, as well as the ratio of Beclin-1/Bcl-2. Both 3-MA and NEC-1 suppressed TBI-induced caspase-3 activation and LC3-II formation, Z-VAD only inhibited caspase-3 activation but increased LC3-II expression at 24 h post-TBI. All these results revealed that multiple cell death pathways participated in the development of TBI, and NEC-1 inhibited apoptosis and autophagy simultaneously. These coactions may further explain how can NEC-1 reduce TBI-induced tissue damage and functional deficits and reflect the interrelationship among necrosis, apoptosis and autophagy.
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http://dx.doi.org/10.1007/s11064-012-0791-4DOI Listing
September 2012

Unique 3D self-penetrating Co(II) and Ni(II) coordination frameworks with a new (4(4).6(10).8) network topology.

Dalton Trans 2010 Dec 9;39(48):11522-5. Epub 2010 Nov 9.

College of Mechanical & Material Engineering, Hubei Key Laboratory of Natural Products Research and Development, China Three Gorges University, Yichang, 443002, China.

Two unique six-connected self-penetrating coordination polymers with a new (4(4).6(10).8) network topology, derived from the cross-linking of two 6(6)-dia subnets, were constructed from Ni(II) or Co(II) and two types of V-shaped tectons. The Ni(II) complex 1 shows an antiferromagnetic coupling via μ-carboxylate and μ-H(2)O pathways, whereas the Co(II) complex 2 exhibits the single-ion behavior in 300-34 K and then a ferromagnetic coupling at lower temperatures.
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http://dx.doi.org/10.1039/c0dt00900hDOI Listing
December 2010
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