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S-doped TiO2 nanoparticles were fabricated by hydrothermal process and post-calcination, and their morphology, crystalline phase and chemical composition were characterized with transmission electron microscopy, powder X-ray diffraction and selected area electron diffraction. The results showed that S was successfully doped into the TiO2. We investigated the photocatalytic reactions in a simulated environment in tandem with thermal desorption-gas chromatography-mass spectrometry determinations. The catalytic activity of S-doped TiO2 was evaluated by monitoring the photodegradation of BTEX from wood-based panels, and 95% degradation rate in 75 min demonstrated efficient visible-light catalytic performance.

The sustainable management direction of PM

Background Metallothionein 1M (MT1M) functions to regulate cell proliferation and cancer metastasis. This study assessed the effects of MT1M overexpression and mouse double minute 2 homolog (MDM2) knockdown on the regulation of non-small cell lung cancer A549 cell viability, migration, and protein expression in vitro and explored the underlying molecular events. Methods A549 cells were stably infected with lentivirus carrying MT1M cDNA or transiently transfected MDM2 siRNA and/or treated with the p53 inhibitor for the assessment of changes in cell viability, wound healing, Transwell migration, and qRT-PCR and Western blot assays. Luciferase reporter assay was performed to investigate p53 binding to the MT1M promoter. Results The data showed that MT1M overexpression inhibited A549 cell viability and migration capacity in vitro, whereas the p53 inhibitor reversed the inhibition of A549 cell viability and migration caused by MT1M overexpression as well as the expression of MMP2, MMP9, and MMP14. Furthermore, knockdown of MDM2, an upstream inhibitor of p53 activity, was able to reduce A549 cell viability, migration, and protein expression. Thus, MDM2 knockdown had synergistic effects with MT1M overexpression on the suppression of A549 cell viability, migration, and protein expression. Conclusions In conclusion, MDM2 can bind to and phosphorylate p53 protein to inactivate the protein, thereby reducing MT1M expression and leading to tumor cell proliferation and migration.

Vascular dementia (VaD) is a complex disorder caused by reduced blood flow in the brain. However, there is no effective pharmacological treatment option available until now. Here, we reported that low-dose levamlodipine besylate could reverse the cognitive impairment in VaD mice model of right unilateral common carotid arteries occlusion (rUCCAO). Oral administration of levamlodipine besylate (0.1 mg/kg) could reduce the latency to find the hidden platform in the MWM test as compared to the vehicle group. Furthermore, vehicle-treated mice revealed reduced phospho-CaMKII (Thr286) levels in the hippocampus, which can be partially restored by levamlodipine besylate (0.1 mg/kg and 0.5 mg/kg) treatment. No significant outcome on microglia and astrocytes were observed following levamlodipine besylate treatment. This data reveal novel findings of the therapeutic potential of low-dose levamlodipine besylate that could considerably enhance the cognitive function in VaD mice.

Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal-dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome-wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy-related genes, there are changes in synaptic organization pathway node genes, such as

The appearance of the intestinal mucosa during endoscopy varies among patients with primary intestinal lymphangiectasia (PIL).To classify the endoscopic features of the intestinal mucosa in PIL under endoscopy, combine the patients' imaging and pathological characteristics of the patients, and explain their causes.We retrospectively analyzed the endoscopic images of 123 patients with PIL who were treated at the hospital between January 1, 2007 and December 31, 2018. We compared and analyzed all endoscopic images, classified them into four types according to the endoscopic features of the intestinal mucosa, and analyzed the post-lymphographic computed tomography (PLCT) and pathological characteristics of each type.According to the endoscopic features of PIL in 123 patients observed during endoscopy, they were classified into four types: nodular-type, granular-type, vesicular-type, and edematous-type. PLCT showed diffuse thickening of the small intestinal wall, and no contrast agent was seen in the small intestinal wall and mesentery in the patients with nodular and granular types. Contrast agent was scattered in the small intestinal wall and mesentery in the patients with vesicular and edematous types. Analysis of the small intestinal mucosal pathology revealed that nodular-type and granular-type lymphangiectasia involved the small intestine mucosa in four layers, whereas ectasia of the vesicular- and edematous-type lymphatic vessels largely involved the lamina propria mucosae, submucosae, and muscular layers.Endoscopic classification, combined with the patients' clinical manifestations and pathological examination results, is significant and very useful to clinicians when scoping patients with suspected PIL.

Coastal wetland, affected by the interaction of land and marine ecosystems, is a typical fragile and sensitive zone. Spartina alterniflora is the most successful invasive species in global coastal zone, with important impact on coastal wetland ecosystems. We systematically summarized available literature, and reviewed the effects of S. alterniflora invasion on biogeochemical cycling (soil carbon, nitrogen, phosphorus cycling, and soil heavy metal migration) and biological community (microorganisms, plants, and animals) in coastal wetlands. Then, three perspectives were proposed for the future research: 1) strengthening the mechanism of the impact of S. alterniflora invasion on ecosystem health of coastal wetlands; 2) focusing on the coupling mechanism of the interaction between S. alterniflora community and coastal wetland environment in the context of global change; 3) carrying out long-term positioning monitoring to clarify the responses of coastal wetlands at different stages of S. alterniflora invasion. This review could provide guidance for the ecological utilization and management of S. alterniflora.滨海湿地受海、陆生态系统的交互影响,是典型的生态脆弱带和敏感区。互花米草是全球海岸带最为成功的外来入侵物种,对滨海湿地生态系统已经产生了重要的影响。本文对已有相关研究进行了系统梳理,揭示了互花米草入侵对滨海湿地生态系统生物地球化学循环(碳循环、氮循环、磷循环及土壤重金属迁移)和入侵地生物群落(微生物、植物和动物)的影响。并在此基础上对今后研究的重点提出了展望: 加强互花米草入侵对滨海湿地生态系统健康影响机制研究;重点关注全球变化背景下互花米草群落与湿地环境互馈耦合;开展长时序定位监测,厘清滨海湿地生态系统对互米草不同入侵阶段的响应差异,以期对互花米草的生态利用和治理提供指导。.

Wound healing impairment is increasingly recognized to be a consequence of hyperglycemia-induced dysfunction of endothelial precursor cells (EPCs) in type 2 diabetes mellitus (T2DM). Metformin exhibits potential for the improvement of endothelial function and the wound healing process. However, the underlying mechanisms for the observed beneficial effects of metformin application remain to be completely understood. The present study assessed whether metformin, a widely used therapeutic drug for T2DM, may accelerate wound closure in T2DM db/db mice. Genetically hyperglycemic db/db mice were used as the T2DM model. Metformin (250 mg/kg/day; intragastric) was administered for two weeks prior to EPC collection and wound model creation in db/db mice. Wound healing was evaluated by alterations in the wound area and the number of platelet endothelial cell adhesion molecule-positive cells. The function of the isolated bone marrow-derived EPCs (BM-EPCs) was assessed by a tube formation assay. The number of circulating EPCs, and the levels of intracellular nitric oxide (NO) and superoxide (O2−) were detected by flow cytometry. Thrombospondin-1 (TSP-1) expression was determined by western blot analysis. It was observed that treatment with metformin accelerated wound healing, improved angiogenesis and increased the circulating EPC number in db/db mice. In vitro, treatment with metformin reversed the impaired BM-EPC function reflected by tube formation, and significantly increased NO production while decreasing O2− levels in BM-EPCs from db/db mice. In addition, TSP-1 expression was markedly attenuated by treatment with metformin in cultured BM-EPCs. Metformin contributed to wound healing and improved angiogenesis in T2DM mice, which was, in part, associated with stimulation of NO, and inhibition of O2− and TSP-1 in EPCs from db/db mice.

To locate multiple sources through time-difference-of-arrival (TDOA) measurements, existing algorithms generally require the matching relationship between measurements and the corresponding sources. In this paper, we propose a new Bayesian learning method for cases where the matching relationship is not given and off-grid error is considered. To achieve this, first we propose a new basis generator, which casts the localization problem within the Bayesian learning scheme. Then, we modify the existing sparse Bayesian inference (SBI) approaches and explore the priors on fingerprinting weights, resulting in two intermediate algorithms. On these foundations, a subspace-based robust SBI (SRSBI) algorithm is proposed as the core of this paper. SRSBI is highlighted by its ability to work free from iteration when estimating off-grid targets. What' more, SRSBI offers considerable robustness against initial guesses of hyper-parameters. Numerical simulations demonstrate the superiority of SRSBI in terms of accuracy, robustness and speed, compared to the other reported ones.

To investigate the role of SRC kinase inhibitor PP2 in drug resistance to adriamycin (ADM) in breast cancer cells and invasion, metastasis of cells.MTT assay was used to detect the inhibitory effect of ADM on MCF-7 and MCF-7/ADM cells. The 50% inhibitory concentration (ICADM inhibited the proliferation of MCF-7 more than MCF-7/ADM cells (The resistance of MCF-7 to ADM is accompanied by increased expression of SRC. SRC inhibitor PP2 can reduce the cell resistance, ability of invasion and metastasis.

For a nested L-shaped array (N-LsA) composed of two orthogonal nested subarrays, the self-difference co-array of each nested subarray is hole-free, whereas cross-difference co-arrays between subarrays have holes. Due to the existence of holes, virtual cross-correlation matrices with increased degree of freedoms (DOFs) can not be constructed from cross-difference co-arrays, which will degrade the performance of direction of arrival (DOA) estimation. To overcome this problem, a high resolution two-dimensional (2-D) DOA estimation algorithm is exploited for N-LsA in this paper. Specifically, by using oblique projection operators, filled cross-difference co-arrays can be achieved by filling the holes, and virtual cross-correlation matrix will be obtained. Then the virtual correlation matrix of the N-LsA, which consists of virtual cross-correlation matrices and virtual autocorrelation matrices given by filled self-difference co-arrays, is reconstructed for 2-D DOA estimation. Additionally, the proposed algorithm contains an automatic angle-pairing procedure and can handle underdetermined DOA estimation. The estimation error, Cramer-Rao bound and computational complexity are derived. Simulation results show that the proposed algorithm offers substantial performance improvement over the existing algorithms.

According to a component analysis of RP3 aviation kerosene and eight surrogate models′ comparative data, a surrogate model comprising n-dodecane/1,3,5-trimethylcyclohecane/n-propylbenzene (73.0%/14.7%/12.3%, mass fraction) was obtained. A detailed mechanism for the combustion of RP-3 surrogate fuel at high temperature was developed using an automatic generation software package, ReaxGen. Ignition delay times simulated using this mechanism were compared with experimental data. A detailed mechanism was reduced by adopting rate-of-production analysis and approximate trajectory optimization algorithm (ATOA) reduced methods. Finally, the sensitivity of ignition delay time was analyzed under conditions of different equivalent ratios and pressures using the reduced mechanism. Differences in key reactions contributing to the ignition delay time were identified at different equivalent ratios. The results indicate that our mechanisms can characterize the ignition delay time during combustion of RP-3 kerosene at high temperature.

SummaryAims The receptor tyrosine kinase ErbB4 is present throughout the primate brain and has a distinct functional profile. In this study, we investigate the potential role of endothelial ErbB4 receptor signaling in the brain. Results Here, we show that the endothelial cell-specific deletion of ErbB4 induces decreased exploratory behavior in adult mice. However, the water maze task for spatial memory and the memory reconsolidation test reveal no changes; additionally, we observe no impairment in CaMKII phosphorylation in Cdh5Cre;ErbB4f/f mice, which indicates that the endothelial ErbB4 deficit leads to decreased exploratory activity rather than direct memory deficits. Furthermore, decreased brain metabolism, which was measured using micro-positron emission tomography, is observed in the Cdh5Cre;ErbB4f/f mice. Consistently, the immunoblot data demonstrate the downregulation of brain Glut1, phospho-ULK1 (Ser555), and TIGAR in the endothelial ErbB4 conditional knockout mice. Collectively, our findings suggest that endothelial ErbB4 plays a critical role in regulating brain function, at least in part, through maintaining normal brain energy homeostasis. Conclusions Targeting ErbB4 or the modulation of endothelial ErbB4 signaling may represent a rational pharmacological approach to treat neurological disorders.

Refractory wound is a dreaded complication of diabetes and is highly correlated with EPC dysfunction caused by hyperglycemia. Acarbose is a widely used oral glucose-lowering drug exclusively for T2DM. Previous studies have suggested the beneficial effect of acarbose on improving endothelial dysfunction in patients with T2DM. However, no data have been reported on the beneficial efficacy of acarbose in wound healing impairment caused by diabetes. We herein investigated whether acarbose could improve wound healing in T2DMdb/dbmice and the possible mechanisms involved. Acarbose hastened wound healing and enhanced angiogenesis, accompanied by increased circulating EPC number indb/dbmice. In vitro, a reversed BM-EPC dysfunction was observed after the administration of acarbose indb/dbmice, as reflected by tube formation assay. In addition, a significantly increased NO production was also witnessed in BM-EPCs from acarbose treateddb/dbmice, with decreased O2levels. Akt inhibitor could abolish the beneficial effect of acarbose on high glucose induced EPC dysfunction in vitro, accompanied by reduced eNOS activation. Acarbose displayed potential effect in promoting wound healing and improving angiogenesis in T2DM mice, which was possibly related to the Akt/eNOS signaling pathway.

In this study, the process of electrospinning was combined with traditional spin process to fabricate twisted continuous nanofiber/cotton hybrid yarns. The morphologies and structures of the prepared polyacrylonitrile (PAN) nanofiber/cotton hybrid yarns were investigated. Results showed that the twisted hybrid yarns can withstand the abrasion in conventional textile processes such as spinning. This novel method has shown potential for the production of hybrid yarns consisting of nanofibers and cotton fibers for potential applications in the textile industry.

A novel free surface electrospining via a stepped pyramid-shaped spinneret was used to prepare composite nanofibers containing microparticles. We investigate the spinnability of Polyacrylonitrile (PAN) solution containing graphite powder microparticles. The influence of microparticle on fiber diameter has been studied. This method can be used to produce composite nanofibers containing microparticles structures by electrospinning in mass scale.

This paper use 2007 and 2010 SPOT-5 images as a data source, combined with RS and GIS technology, introduced the concept of hemeroby, developed a suitable landscape classification system in Ximen Island, systematically evaluated the dynamic changes of hemeroby of Ximen Island marine Protected Areas. The results indicated that from 2007 to 2010, the ecological environment of Ximen Island has gradually improved. Completely disturbed landscape type decreased sharply in total area, while undisturbed types were increased a lot. From the perspective of total characteristics of the spatial distribution of hemeroby index, the residential , traffic land and landscape surrounding anthropogenic interference with the highest index.

The aim of this study was to investigate the protective effect of simvastatin against radiation-induced tissue injury in mice. Mice were radiated with 4 Gy or 8 Gy after 20 mg/kg/d simvastatin treatment over 2 weeks. Morphological changes were observed in the jejunum and bone marrow, and apoptotic cells were determined in both tissues. Peripheral blood cells were counted, and the superoxide dismutase (SOD) activity and the malondialdehyde (MDA) level in tissues of both thymus and spleen were measured. Compared with the radiation-only group, 20 mg/kg/d simvastatin administration significantly increased the mean villi height and decreased apoptotic cells in jejunum tissue, and stimulated regeneration and reduced apoptotic cells in bone marrow. Peripheral blood cell analysis revealed that simvastatin treatment induced a larger number of red blood cells and increased the hemoglobin level present after 4 Gy of radiation. Interestingly, it was also found that the number of peripheral endothelial progenitor cells was markedly increased following simvastatin administration. Antioxidant determination for tissues displayed that simvastatin therapy increased the SOD activity after both 4 and 8 Gy of radiation, but only decreased the MDA level after 4 Gy. Simvastatin ameliorated radiation-induced tissue damage in mice. The radioprotective effect of simvastatin was possibly related to inhibition of apoptosis and improvement of oxygen-carrying and antioxidant activities.

The low productivity of conventional single-needle electrospinning inhibits the application of nanofibers to a commercial level. In order to improve the productivity of the electrospinning technique, a terraced spinneret has been designed based on the finite element analysis in this paper. The electric field distribution was modeled with the use of Ansoft Maxwell software. The experiment results demonstrated this special design spinneret has the potential to produce smooth nanofibers on a large scale.

In this paper, we presented a novel system of electrospinning to directly prepare fibrous meshes with micro/nanoparticles. Acetate cellulose (CA) as the material of micro/nanoparticles was dissolved in the mixture of acetone and dichloromethane as well as polyvinyl alcohol (PVA) was dissolved into deionized water, respectively. We successfully fabricated CA microspheres by an oil-in-water (O/W) emulsion/solvent evaporation technique, instilling CA solution into the stirring PVA aqueous solution. Then the hybrid solution was fabricated into a fibrous mat through electrospinning. CA micro/nanoparticles were wrapped in PVA fibers which indicated that the hybrid system of electrospinning had great potential in biomedicine when combing biodegradable microspheres with drugs.

Suaeda salsa is the characteristics vegetation in the wetlands of Northern China. By acquiring Suaeda Salsa biomass, building spectral reflectance curve, probing into the relationship between the vegetation indices and the biomass, and finally achieving Suaeda Salsa’s biomass remote sensing monitor in the ShuangTai river estuary, Conclusions are as follows: 1). Correlation coefficient between the biomass and the vegetation indices (RVI and NDVI) is low, and Linear regression equation (R2) is 0.342 and 0.316, and the Logarithmic regression equation (R2) is 0.319 and 0.21, and the Quadratic equation (R2) is 0.589 and 0.568. Correlation coefficient between the biomass and the vegetation indices (PVI, SAVI and MSAVI) is high, and the linear regression equation is 0.626、0.698 and 0.679, respectively. The logarithmic regression equation is 0.592、0.706 and 0.683 respectively and the quadratic equation is 0.688、0.711 and 0.683. 2). Suaeda salsa’s biomass is consistent with the distribution area in the Shuangtai river estuary. Total biomass maintained at 2.9 × 107- 4.2 × 108kg in 1990, and dropped to 3.4 × 106 ~ 3.5 × 107kg in 1995. In 2000, the quadratic function of vegetation version biomass rebounded, but linear function continues to fall. Biomass increased rapidly, reaching 1.46 ~ 2.4 × 108kg in 2005.

Background Endothelial dysfunction has been suggested as a possible causal link between hyperglycemia and microvascular complications in diabetes mellitus. The effect of metformin on endothelial progenitor cells (EPCs) is still unclear. This study was designed to test the hypothesis that metformin could accelerate wound healing by improving the impaired EPC functions in streptozotocin-induced diabetic mice. Methods Streptozotocin (STZ, 60 mg/kg/d × 5 d, i.p.) was injected to induce type 1 diabetes in male C57BL/6 mice. Mice were treated with metformin (250 mg/kg/d, i.g.) for consecutive 14 days. Wound closure was evaluated by wound area and number of CD31 stained capillaries. Functions of bone marrow-endothelial progenitor cells (BM-EPCs) were assessed by tube formation and migration assays, and expression of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) was determined by western blot analysis. Results Metformin accelerated wound closure and stimulated angiogenesis in diabetic mice. The number of circulating EPCs was increased significantly in metformin treated diabetic mice. Abilities of tube formation and migration of BM-EPCs were impaired in diabetic mice, which were improved by metformin. Expression of both phosphorylated-AMPK and phosphorylated-eNOS was significantly increased, and nitric oxide (NO) production was enhanced by metformin in BM-EPCs of diabetic mice. In vitro, metformin improved impaired BM-EPC functions, and increased phosphorylated-eNOS expression and NO production in cultured BM-EPCs caused by high glucose, which was prevented by the AMPK inhibitor compound C. Conclusions Our results suggest that metformin could improve BM-EPC functions in STZ-induced diabetic mice, which was possibly dependent on the AMPK/eNOS pathway. Electronic supplementary material The online version of this article (doi:10.1186/s12933-016-0408-3) contains supplementary material, which is available to authorized users.

Endothelial cell dysfunction is the primary cause of microvascular complications in diabetes. Diazoxide enables beta cells to rest by reversibly suppressing glucose-induced insulin secretion by opening ATP-sensitive K+ channels in the beta cells. This study investigated the role of diazoxide in wound healing in mice with streptozotocin (STZ)-induced diabetes and explored the possible mechanisms of its effect. Compared to the controls, mice with STZ-induced diabetes exhibited significantly impaired wound healing. Diazoxide treatment (30 mg/kg/d, intragastrically) for 28 days accelerated wound closure and stimulated angiogenesis in the diabetic mice. Circulating endothelial progenitor cells (EPCs) increased significantly in the diazoxide-treated diabetic mice. The adhesion, migration, and tube formation abilities of bone marrow (BM)-EPCs were impaired by diabetes, and these impairments were improved by diazoxide treatment. The expression of both p53 and TSP-1 increased in diabetic mice compared to that in the controls, and these increases were inhibited significantly by diazoxide treatment. In vitro, diazoxide treatment improved the impaired BM-EPC function and diminished the increased expression of p53 and TSP-1 in cultured BM-EPCs caused by high glucose levels. We conclude that diazoxide improved BM-EPC function in mice with STZ-induced diabetes, possibly via a p53- and TSP-1-dependent pathway.

A modified lattice hydrodynamic model of traffic flow is proposed by introducing the density difference between the leading and the following lattice. The stability condition of the modified model is obtained through the linear stability analysis. The results show that considering the density difference leads to the stabilization of the system. The Burgers equation and mKdV equation are derived to describe the density waves in the stable and unstable regions respectively. Numerical simulations show that considering the density difference not only could stabilize traffic flow but also makes the lattice hydrodynamic model more realistic.

Clinical trials with partial liquid ventilation demonstrate improvement in oxygenation, as well as some adverse side effects linked to the application of liquid perfluorocarbons (PFCs) during liquid ventilation. Thus, we examined the effects of systemic administration of PFC on acute lung injury (ALI) induced by lipopolysaccharide (LPS) and its effects on heme oxygenase-1 (HO-1), a compound that provides potent cytoprotection against lung injury. Rats were assigned to one of six groups (n = 8). Thirty minutes after they were challenged with LPS aerosol inhalation, perfluorohexane was given intraperitoneally every two hours. Ten hours after LPS inhalation, bronchoalveolar lavage fluid (BALF) and lung tissue were obtained for enzyme linked immunosorbent assay, histologic, and Western-blot analyses. The results showed that perfluorohexane significantly decreased the wet to dry weight ratio, malondialdehyde (MDA) production, and myeloperoxidase (MPO) activity in the lung tissue. Also, perfluorohexane reduced the total protein content and levels of tumor necrosis factor-alpha (TNF-alpha) but increased the levels of the anti-inflammatory cytokine interleukin-10 (IL-10) in the BALF, resulting in decreased pulmonary edema and the infiltration of neutrophils into the lung tissues of LPS-treated rats. Furthermore, perfluorohexane increased HO-1 protein production and stimulated HO-1 activity in the lung tissue. Pre-treatment with Zinc protoporphyrin IX, an inhibitor of HO-1, decreased the protective effects of perfluorohexane in rats. In summary, systemic perfluorohexane alleviates LPS-induced lung injury in rats, and HO-1 may be involved in the mechanism of this reduction.

To investigate the effect of baicalein on the gap junction intercellular communication (GJIC) in the TM4 Sertoli cells of the mouse testis and its related mechanism.We measured the cytotoxicity of different concentrations of baicalein on the TM4 Sertoli cells in the mouse testis by MTT, detected the fluorescence transfer of the TM4 Sertoli cells by parachute assay, and determined the expression of the protein connexin 43 ( Cx43) in the baicalein-treated cells by Western blot and immunofluorescence assay.Baicalein produced no obvious cytotoxicity on the TM4 Sertoli cells at the concentration below 60 µmol/L but significantly increased their GJIC at 0-20 µmol/L (P0.01). Western blot and immunofluorescence assay showed that 0-20 µmol/L baicalein remarkably elevated the expression of Cx43 in the TM4 cells (P0.01) and on the membrane of the TM4 cells.Baicalein at the concentration of 0-20 µmol/L can significantly enhance GJIC in mouse TM4 Sertoli cells by increasing the expression of the Cx43 protein.

Cardio-cerebral-vascular diseases, including myocardial infarction, atherosclerosis, hypertension, and stroke etc, are the major reasons for morbidity and mortality all over the world. Recent studies showed that inflammation exerts an important impact on the pathogenesis and development of cardio-cerebral-vascular diseases. "The cholinergic anti-inflammatory pathway", mainly modulated through α7 nicotinic acetylcholine receptor (α7nAChR), has attracted much attention.The purpose of this review was to discuss the role of α7nAChR during the pathological processes in myocardial infarction, atherosclerosis, hypertension and stroke.Most of the existing literatures involved in studying on myocardial infarction, atherosclerosis, hypertension and stroke showed that activation of α7nAChR might be a potential strategy for the prevention and treatment of these diseases.Targeting α7nAChR to combat inflammation might be a novel therapy in cardiocerebral- vascular diseases.

The hemeroby type classification system of Ximen Island wetland of Zhejiang Province was established based on the multiple datasets: SOPT-5 image data with a spatial resolution of 5 m in 2007 and 2010, its wetland land cover and land use status, the National Land Use Classification (on trail), and sea area use classification of marine industry standards as well as remote sensing data features. Meanwhile, the dynamic relationship between the landscape pattern and the degree of hemeroby in Ximen Island was investigated with the landscape indices and hemeroby index (HI) derived from the landscape pattern index and GIS spatial analysis. The results showed that the wetland landscape spatial heterogeneity, fragmentation and dominance index dropped, and the landscape shape index complexity was low. The human disturbance center developed from a dispersion type to a concentration type. The landscape type of the disturbance center was bare land and settlement. The HI rose up from the sea to the land. Settlement, wharf and traffic land had the highest HI. The HI of the mudflat cultivation, mudflats and raft-cultivation dramatically changed. Marine-terrestrial interlaced zone showed a low total HI with unstable characteristics. The number of patches declined of undisturbed, partially disturbed and completely disturbed landscapes. Mean patch areas of partially disturbed and completely disturbed landscapes increased, and that of the undisturbed decreased. Mean shape index of the undisturbed landscape decreased, while the partially disturbed and completely disturbed landscapes showed a trend of shape complication.

To investigate the effect of sodium valproate, a histone deacetylase inhibitor, on the cytotoxicity of doxorubicin in breast cancer cells.Western blotting was used to assess Cx43 protein expression in breast cancer Hs578T cells exposed to doxorubicin and sodium valproate. MTT assay was used to determine the cytotoxicity of doxorubicin; annexin V/PI double staining and Hochest 33258 fluorescence staining were employed to detect doxorubicin-induced early and late apoptosis, respectively.Western blotting showed that sodium valproate significantly increased Cx43 protein expression in Hs578T cells (P/0.01). The cells exposed to both sodium valproate and doxorubicin showed significantly lowered cell viability compared with the cells exposed to doxorubicin alone (P/0.01). Exposure to both sodium valproate and doxorubicin resulted in significantly increased early and late cell apoptosis rate compared with doxorubicin treatment alone (P/0.01).sodium valproate can significantly enhance the cytotoxicity of doxorubicin and increase doxorubicin-induced apoptosis in breast cancer cells in vitro possibly by enhancing the gap junction function.

Background & AimsMetformin is currently the most widely used first-line hypoglycemic agent for diabetes mellitus. Besides glucose-lowering action, there is increasingly interest in the potential anti-inflammatory action of this drug. In the present study, we investigated the actions of metformin on experimental insulitis using STZ-induced diabetic mice.MethodsMice with acute diabetes induced by STZ were administered metformin by gavage. Changes of blood glucose and body weight, and the daily amount of food and water intake were measured. Pancreatic tissues were collected for histologic analyses. Pathological assessment and immunohistochemistry analysis were used to determine the effect of metformin on insulitis. Inflammatory cytokines in the pancreas and insulin levels were measured through ELISA analysis.ResultsMetformin significantly reduced blood glucose levels and improved aberrant water intake behavior in experimental diabetic mice. No significant differences were observed in terms of body weight and food intake behavior in metformin-treated animals. In the STZ-induced model of diabetes, we found the appearance of pronounced insulitis. However, metformin administration reduced the severity of insulitis assessed by blind pathological scoring. In addition, metformin treatment improved insulin levels in experimental diabetic mice. ELISA assay revealed decreased levels of inflammatory response marker IL-1βand TNF-αin the pancreatic tissues following metformin treatment.ConclusionMetformin attenuated insulitis in the STZ-induced mice model of diabetes. This islet-protective effect might be partly correlated with the anti-inflammatory action of metformin.

Background and Purpose— In our current food supply, sugar substitutes are widely used in beverages and other food products. However, there is limited information about the link between dietary consumption of sugar substitutes and stroke to date. This study sought to determine the effect of various sugar substitutes on the cerebral ischemic injury and endothelial progenitor cells, which have been implicated to play an important role in vascular repair and revascularization in ischemic brain tissues, in mice. Methods— After treatment with sucrose and various sugar substitutes (the doses are in the range of corresponding acceptable daily intake levels) and vehicle for 6 weeks, mice were subjected to permanent left middle cerebral artery occlusion, and the infarct volumes, angiogenesis, and neurobehavioral outcomes were determined. In addition, the number and function of endothelial progenitor cells were also examined. Results— After long-term treatment with fructose, erythritol (sugar alcohols), acesulfame K (artificial sweeteners), or rebaudioside A (rare sugars), the cerebral ischemic injury (both infarct volumes and neurobehavioral outcomes) was significantly aggravated, angiogenesis in ischemic brain was reduced, and endothelial progenitor cell function was impaired in mice compared with control. However, the similar impairments were not found in sucrose (with the same dose as fructose’s)-treated mice. Conclusions— Long-term consumption of sugar substitutes aggravated cerebral ischemic injury in mice, which might be partly attributed to the impairment of endothelial progenitor cells and the reduction of angiogenesis in ischemic brain. This result implies that dietary intake of sugar substitutes warrants further attention in daily life.

Background Sepsis is a common disease that continues to increase in incidence in the world. Diseases, such as diabetes mellitus, may make the situation worse. Diabetic patients are at increased risk for common infections. This study was designed to investigate the role of glibenclamide on myocardial injury by lipopolysaccharides (LPS) in streptozotocin induced diabetic mice (STZ-mice). Methods LPS was used to induce endotoxemia in STZ-mice. Heart rate and mean arterial pressure were measured by MPA-HBBS. Serum epinephrine level was measured by enzyme-linked immunosorbent assays (ELISA). Myocardial injury was examined by light and transmission electron microscope and TUNEL staining. Macrophage infiltration was measured by immunohistochemistry. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) levels in myocardial tissue and serum in STZ-mice, and in conditional medium of primary cultured peritoneal macrophages were determined by ELISA. Nalp3 and Caspase-1 protein levels were measured by Western blotting analysis. Results STZ administration decreased body weight and increased blood glucose in C57BL/6 mice. LPS injection caused decreases of heart rate and mean arterial pressure, and elevated serum epinephrine level in C57BL/6 mice. Compared with control mice without STZ treatment, LPS induced more severe myocardial injury and macrophage infiltration in STZ-mice, which was attenuated by pretreatment of glibenclamide. LPS stimulation enhanced the levels of IL-1β and TNF-α in both cardiac tissue and serum. Glibenclamide pretreatment significantly inhibited the serum levels of pro-inflammatory cytokines. Either high glucose or LPS increased the levels of IL-1β and TNF-α in the conditional medium of peritoneal macrophages. Glibenclamide treatment suppressed the increase of IL-1β level induced by high glucose and LPS. Furthermore, Nalp3 and Caspase-1 levels were markedly increased by high glucose plus LPS, and both proteins were significantly inhibited by glibenclamide treatment. Conclusions We conclude that glibenclamide could attenuate myocardial injury induced by LPS challenge in STZ-mice, which was possibly related to inhibiting inflammation through Nalp3 inflammasomes. Electronic supplementary material The online version of this article (doi:10.1186/s12933-014-0106-y) contains supplementary material, which is available to authorized users.

Previous studies on the antioxidant activity of sedatives have predominantly been in vitro investigations that are lacking clinical data, resulting in conclusion without cogency. The aim of the present prospective, randomized study was to use single sedative drugs for anesthesia induction to compare their antioxidant properties. The effects on the antioxidant system of midazolam, propofol and dexmedetomidine were assessed using oxidative stress indicators and micronuclei (MN). Forty-nine patients undergoing esophageal cancer radical prostatectomy were selected. Midazolam, propofol and dexmedetomidine were used to induce anesthesia. Venous blood samples were obtained prior to and at 2 and at 24 h after surgery, and oxidative stress indicators were detected using the appropriate kits. The cytokinesis-block micronucleus cytome assay was executed and the frequencies of MN, nucleoplasmic bridges and nuclear buds were examined. It was found that the use of the three sedatives, respectively, led to a marked increase in the levels of free radical indicators at 2 h after surgery, which then decreased at 24 h after surgery. Furthermore, lower levels of oxidative stress were found following the use of propofol and dexmedetomidine compared with those following midazolam administration, and similar results were obtained regarding the level of MN. It is suggested that propofol and dexmedetomidine exhibit a superior antioxidant function to midazolam.

The aim of the present study was to investigate whether the JWA gene regulates the proliferation, migration and invasion of human esophageal squamous cell carcinoma (ESCC) and normal human esophageal cell lines through mitogen-activated protein kinase (MAPK) signal transduction pathways. The role of JWA in proliferation, migration, invasion and apoptosis was investigated in the Eca109 human ESCC and HET-1A normal human esophageal cell lines via transfection with JWA-small interfering (si)RNA. Western blot analysis was conducted to observe the effect of JWA on apoptosis and the regulatory effect of JWA on proliferation was determined using a thiazolyl blue tetrazolium bromide (MTT) assay. Cellular migration and invasion were analyzed via a Transwell assay. In addition, the expression levels of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 MAPK following JWA-siRNA transfection were detected by western blot analysis and compared with those of untreated cells. The downregulation of JWA protein decreased apoptosis and increased the proliferation, migration and invasion of the Eca109 and HET-1A cell lines. In the Eca109 cell line, the expression levels of phosphorylated (p)-ERK1/2 and p-JNK, but not those of p-p38, decreased significantly in the JWA siRNA group compared with those in the control groups. However, in the HET-1A cell line, JWA-siRNA transfection significantly inhibited the expression of p-p38 and demonstrated no effect on the expression levels of p-ERK1/2 and p-JNK. In conclusion, the JWA gene may regulate the ESCC and human esophageal cell lines through MAPK signaling pathways via different regulatory mechanisms.

To observe the influence of Cx26/Cx32 gap junction channel on the antineoplastic effect of etoposide in Hela cervical cancer cells.Fluorescence trace was used to assay the gap junction intercellular communication mediated by Cx26/Cx32 in Hela cells and its functional modulation by the pharmacological agents (oleamide, retinoid acid). A standard colony-forming assay was applied to determine the cell growth-inhibiting effect of etoposide in Hela cells with functional modulation of the gap junction. Hoechst 33258 staining was used to assess the changes in etoposide-induced apoptosis of Hela cells with altered gap junction functions.Oleamide markedly decreased while retinoid acid obviously increased the gap junction function in Hela cells. Standard colony-forming assay showed that etoposide produced a lowered antiproliferative effect in Hela cells with reduced gap junction and an increased antiproliferative effect in cells with enhanced gap junction function. In cells with a reduced gap junction function, etoposide induced a lowered apoptosis rate, which increased obviously in cells with an enhanced gap junction function.The antineoplastic effect of etoposide is reduced in Hela cells with a decreased gap junction intercellular communication mediated by Cx26/Cx32 and is enhanced in cells with an increased gap junction intercellular communication.