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Find video protocols related to scientific articles indexed in Pubmed.
Wavelength-locking-free 1.57µm differential absorption lidar for CO2 sensing.
Opt Express
PUBLISHED: 11-18-2014
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We propose a novel wavelength-locking-free differential absorption lidar system for CO2 sensing. The ON-line wavelength laser was wavelength modulated around a specific CO2 absorption line to ensure that the emission from the ON-line laser hit the atmospheric CO2 absorption line peak twice a cycle. In the meantime, the intensity of the ON-line and OFF-line wavelength lasers were sinusoidally intensity modulated to enhance the SNR of the back-scattered signal. As a consequence, the system configuration was simplified and the measurement error caused by the deviation of CO2 absorption coefficient from the long-time ON-line wavelength drifting was completely eliminated. Furthermore, a more precise calibration method was developed which could simultaneously calibrate the offset and precision of the lidar detector. This method could be applied to other differential-absorption-based lidar systems. The result showed that a measurement precision of 0.525% for the column concentration was achieved in 1 s time interval through a path of 780m. We recorded the CO2 concentration variation for 12 hours starting from mid-night, the result showed that the course of the concentration derived from the DIAL was in good agreement with that of the in situ CO2 sensor only when the status of atmosphere was stable.
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[Treatment of acute gastric mucosal lesion after pericardial devascularization of advanced schistosomiasis: a report of 15 cases].
Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi
PUBLISHED: 10-28-2014
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To discuss the therapy for acute gastric mucosal lesion (AGML) after pericardial devascularization of advanced schistosomiasis.
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Cobalt carbonate/ and cobalt oxide/graphene aerogel composite anodes for high performance li-ion batteries.
ACS Appl Mater Interfaces
PUBLISHED: 10-28-2014
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Nanocomposites consisting of ultrafine, cobalt carbonate nanoneedles and 3D porous graphene aerogel (CoCO3/GA) are in situ synthesized based on a one-step hydrothermal route followed by freeze-drying. A further heat treatment produces cobalt oxide nanoparticles embedded in the conductive GA matrix (Co3O4/GA). Both the composite anodes deliver excellent specific capacities depending on current density employed: the CoCO3/GA anode outperforms the Co3O4/GA anode at low current densities, and vice versa at current densities higher than 500 mA g(-1). Their electrochemical performances are considered among the best of similar composite anodes consisting of CoCO3 or Co3O4 active particles embedded in a graphene substrate. The stable multistep electrochemical reactions of the carbonate compound with a unique nanoneedle structure contribute to the excellent cyclic stability of the CoCO3/GA electrode, whereas the highly conductive networks along with low charge transfer resistance are responsible for the high rate performance of the Co3O4/GA electrode.
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Exploiting the kinetic interplay between GPIb?-VWF binding interfaces to regulate hemostasis and thrombosis.
Blood
PUBLISHED: 10-09-2014
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Platelet-VWF interactions must be tightly regulated in order to promote effective hemostasis and prevent occlusive thrombus formation. However, it is unclear what role the inherent properties of the bond formed between the platelet receptor GPIb? and the A1 domain of VWF play in these processes. Using VWF-A1 knock-in mice with mutations that enhance (I1309V) or disrupt (R1326H) GPIb? binding, we now demonstrate that the kinetic interplay between two distinct contact surfaces influences the site and extent to which platelets bind VWF. Incorporation of R1326H mutation into the major site shortened bond lifetime, yielding defects in hemostasis and thrombosis comparable to VWF deficient animals. Similarly, disrupting this region of contact with an allosteric inhibitor impaired human platelet accrual in damaged arterioles. In contrast, the I1309V mutation near the minor site prolonged bond lifetime, which was essential for the development of a type 2B-like VWD phenotype. However, combining the R1326H and I1309V mutations normalized both bond kinetics and the hemostatic and thrombotic properties of VWF. These findings broaden our understanding of mechanisms governing platelet-VWF interactions in health and disease, and underscore the importance of combined biophysical and genetic approaches in identifying potential therapeutic avenues for treating bleeding and thrombotic disorders.
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Advanced Oxidation Protein Products Exacerbates Lipid Accumulation and Atherosclerosis Through Downregulation of ATP-Binding Cassette Transporter A1 and G1 Expression in Apolipoprotein E Knockout Mice.
Circ. J.
PUBLISHED: 09-26-2014
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Both clinical data and basic science studies suggest that advanced oxidation protein products (AOPPs) may contribute to the progression of atherosclerosis. The aim of this study was to investigate the effects of AOPPs on ATP-binding cassette transporter (ABC) A1 and ABCG1 expression, lipid accumulation and atherosclerotic lesions in apolipoprotein E knockout (apoE-KO) mice.Methods?and?Results:Male 8-week-old apoE-KO mice were fed a high-fat/high-cholesterol diet. Mice received intraperitoneal injections of AOPPs (5 mg/kg) and/or Janus Kinase (JAK) inhibitor AG-490 (5 mg/kg) once every other day for 8 weeks. As shown in our data, AOPPs increased lipid levels of plasma, and promoted advanced lesions in the aortic regions in apoE-KO mice. The ABCA1, ABCG1 and liver X receptor alpha (LXR?) expression were downregulated in apoE-KO mice treated with AOPPs, whereas the lesions in the aortas were decreased, and the ABCA1, ABCG1 and LXR? expression were upregulated in mice treated with AOPPs plus AG-490, compared to the mice treated with AOPPs only. The ABCA1 and LXR? expressions of aortas, liver and intestine were downregulated in the AOPPs group, while the expressions were upregulated in the AOPPs-plus-AG-490 group when compared to the AOPPs group. The same results can be also observed in peritoneal macrophages.
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[Health risk assessment of heavy metals in atmospheric dust of Qingdao City].
Huan Jing Ke Xue
PUBLISHED: 09-24-2014
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Based on the 89 atmospheric dust samples and soil samples that were collected around Qingdao, we tested and analyzed the contents of Cd, Cr, Cu, Hg, Ni, Pb, Zn. Based on these analysis results, the risk of heavy metals in atmospheric dusts to human health were assessed by using the US EPA Health Risk Assessment Model. Analysis showed that the average contents of Cd, Cr, Cu, Hg, Pb, Zn in the atmospheric dust of Shinan, Shibei and Laoshan districts were the highest. Therefore, the air pollution of these districts was more serious than the districts of Licang, Chengyang and Huangdao. Comparing the average contents of heavy metals in atmospheric dust with those in soil, we found that only the content of Hg in atmospheric dust collected from the districts of Shinan, Shibei and Laoshan was lower than that in the corresponding soil. All the contents of other heavy metals in atmospheric dust were higher than those in corresponding soil. As a whole, the heavy metals in atmospheric dust of Qingdao City showed slight difference and were less harmful to human health. However, it was harmful in some samples to human health if the contents of Cr and Pb in atmospheric dusts of Shinan, Laoshan and Chengyang districts were always kept at such high densities. Besides, the accumulation of heavy metals in atmospheric dust through various approaches and categories may obviously increase the risk of damaging human health.
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[Dan'e-fukang soft extract for dysmenorrhea: a meta-analysis].
Zhejiang Da Xue Xue Bao Yi Xue Ban
PUBLISHED: 09-05-2014
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To assess the efficacy and safety of Dan'e-fukang soft extract for dysmenorrhea by meta-analysis.
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Urotensin II increases foam cell formation by repressing ABCA1 expression through the ERK/NF-?B pathway in THP-1 macrophages.
Biochem. Biophys. Res. Commun.
PUBLISHED: 09-03-2014
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Foam cell formation in the arterial wall plays a key role in the development of atherosclerosis. Recent studies showed that Urotensin II (U II) is involved in the pathogenesis of atherosclerosis. Here we examined the effects of human U II on ATP-binding cassette transporter A1 (ABCA1) expression and the underlying mechanism in THP-1 macrophages.
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[Effect of PLA/starch slow-release carbon source on biological denitrification].
Huan Jing Ke Xue
PUBLISHED: 08-28-2014
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We used polylactic acid (PLA) and starch to develop a slow-release carbon source and biofilm carrier by blending and fusing techniques for removing nitrate contamination from groundwater, investigated the changes of nitrate, nitrite concentrations and COD in denitrification process supplied by the slow-release carbon source in different mass ratios [PLA/starch (P: S) were 8:2, 7:3, 6:4, 5:5, respectively]. The experimental results demonstrated that the best mass ratio of PLA/starch was 5:5, resulting in a nitrate removal rate of more than 99%. A high denitrification performance was achieved in continuous fixed-bed reactor, the effluent nitrate concentration was below 2 mg x L(-1). These experiments provide scientific basis for the development of environmentally-friendly and controllable slow-release carbon source.
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Interleukin-27 inhibits foam cell formation by promoting macrophage ABCA1 expression through JAK2/STAT3 pathway.
Biochem. Biophys. Res. Commun.
PUBLISHED: 08-20-2014
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The purpose of this study is to determine whether IL-27 regulates macrophage ABCA1 expression, foam cell formation, and also explore the underlying mechanisms. Here, we revealed that IL-27 decreased lipid accumulation in THP-1 derived macrophages through markedly enhancing cholesterol efflux and increasing ABCA1 expression at both protein and mRNA levels. Our study further demonstrated that IL-27 increased ABCA1 level via activation of signal transducer and activator of transcription 3 (STAT3). Inhibition of Janus kinase 2, (JAK2)/STAT3 suppressed the stimulatory effects of IL-27 on ABCA1 expression. The present study concluded that IL-27 reduces lipid accumulation of foam cell by upregulating ABCA1 expression via JAK2/STAT3. Therefore, targeting IL-27 may offer a promising strategy to treat atherosclerotic vascular disease.
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MicroRNA-590 attenuates lipid accumulation and pro-inflammatory cytokine secretion by targeting lipoprotein lipase gene in human THP-1 macrophages.
Biochimie
PUBLISHED: 08-19-2014
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Accumulating evidence suggests that microRNA-590 (miR-590) has protective effects on cardiovascular diseases, but the mechanism is unknown. Interestingly, previous studies from our laboratory and others have shown that macrophage-derived lipoprotein lipase (LPL) might accelerate atherosclerosis by promoting lipid accumulation and inflammatory response. However, the regulation of LPL at the post-transcriptional level by microRNAs has not been fully understood. In this study, we explored whether miR-590 affects the expression of LPL and its potential subsequent effects on lipid accumulation and pro-inflammatory cytokine secretion in human THP-1 macrophages.
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Rapamycin protects kidney against ischemia reperfusion injury through recruitment of NKT cells.
J Transl Med
PUBLISHED: 08-19-2014
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NKT cells play a protective role in ischemia reperfusion (IR) injury, of which the trafficking in the body and recruitment in injured organs can be influenced by immunosuppressive therapy. Therefore, we investigated the effects of rapamycin on kidneys exposed to IR injury in early stage and on trafficking of NKT cells in a murine model.
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[Research advances on ADAM28 expression and ADAM28-mediated tumor metastasis].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
PUBLISHED: 08-19-2014
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A disintegrin-metalloproteinase 28 (ADAM28) is one of important members of ADAM family, that is involved in various biological events including cell adhesion, proteolysis, growth and metastasis of solid tumors and hematological malignancies. Studies have shown that ADAM28 is highly expressed in several human tumors, such as lung, breast and bladder cancers, and chronic lymphocytic leukemia, and its tissue expression levels correlate with cancer metastasis. ADAM28-mediated cancer cell metastasis may be related with the cleavage of von Willebrand's factor (vWF), insulin-like growth factor binding protein-3 (IGFBP-3) and connective tissue growth factor (CTGF), as well as the promoting PSGL-1/P-selectin-mediated cell adhesion. This review summarizes the basic and translational aspects of ADAM28 biology that might stimulate the interest in ADAM28 research and discovery of novel ADAM28 targets, providing potential novel therapies for metastatic cancers.
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Si/ZnO nanocomb arrays decorated with Ag nanoparticles for highly efficient surface-enhanced Raman scattering.
Opt Lett
PUBLISHED: 08-15-2014
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High-density ZnO nanocombs were first grown on a nanoporous silicon pillar array, and pre-prepared 3D Si/ZnO/Ag nanocomb arrays were employed as substrates for surface-enhanced Raman scattering (SERS). The finite-difference time-domain simulation result shows that two kinds of inter-Ag-NP nanogaps in the geometry create a large number of SERS "hot spots," which contributes to the detection limits for rhodamine-6G as low as 10?¹² M and the Raman enhancement factor as large as 10?. The linear dependence between the Raman peak intensities and the concentrations of thiram provides a new calibration method for rapid and quantitative detection of trace organic molecules.
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Antiinflammatory effects of orientin-2"-O-galactopyranoside on lipopolysaccharide-stimulated microglia.
Biol. Pharm. Bull.
PUBLISHED: 08-05-2014
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Microglia activation-mediated neuroinflammation plays an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and human immunodeficiency virus (HIV)-associated dementia. Inhibition of microglia activation may alleviate neurodegeneration under neuroinflammatory conditions. In the present study, we compared three flavone C-glycosides extracted from Trollius chinensis BUNGE using a cell-based assay to evaluate their antiinflammatory effects on microglial cells. The results showed that orientin-2"-O-galactopyranoside (OGA) significantly inhibited the production of nitric oxide and tumor necrosis factor (TNF)-? in lipopolysaccharide (LPS)-stimulated microglial cells. OGA also markedly inhibited the LPS-induced expression of TNF-?, interleukin-1?, inducible nitric oxide (NO) synthase, and cyclooxygenase-2, which was accompanied by suppression of the activation of nuclear factor (NF)-?B and the extracellular signal-regulated kinase (ERK) signal pathway. In addition, OGA decreased LPS-induced reactive oxygen species generation, which appears to be related to the activation of the NF-E2-related factor2 (NRF2)/ heme oxygenase-1 (HO-1) pathway in BV-2 microglial cells. Furthermore, OGA reduced the cytotoxicity of activated microglia toward HT-22 neuroblastoma cells in a co-culture system. Taken together, the present study demonstrated that the induction of HO-1-mediated inhibition of the NF-?B and ERK pathways contributes significantly to the antineuroinflammatory and neuroprotective effects elicited by OGA.
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[Progress and challenges of the National Schistosomiasis Control Program during the period of the 12th Five-Year Plan].
Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi
PUBLISHED: 07-29-2014
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The achievements of the national schistosomiasis control program during the period of the 12th Five-Year Plan were reviewed, in particular, the reduction of the prevalence and progress in control activities were evalucated among different regions of China. Moreover, current difficulties of schistosomiasis control and gaps to achieve the transmission interruption of the disease in China were analyzed, which provide more evidences to formulate the future efforts and work-plan to eliminate the disease in the country.
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Inhibition of smooth muscle cell proliferation by ezetimibe via the cyclin D1-MAPK pathway.
J. Pharmacol. Sci.
PUBLISHED: 07-23-2014
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Proliferation of vascular smooth muscle cells (VSMCs) contributes to the development of atherosclerosis. Ezetimibe is a new lipid lowering agent that inhibits cholesterol absorption. In the present study we attempted to investigate whether ezetimibe has any effect on VSMC proliferation and the potential mechanisms involved. Our data showed ezetimibe abrogated the proliferation and migration of primary rat VSMCs induced by Chol:M?CD. Mechanically, we found that ezetimibe was capable of abolishing cyclin D1, CDK2, phospho-Rb (p-Rb), and E2F protein expressions that were upregulated by Chol:M?CD treatment. In addition, Ezetimibe was able to reverse cell cycle progression induced by Chol:M?CD, which was further supported by its down-regulation of cyclin D1 promoter activity in the presence of Chol:M?CD. Furthermore, ezetimibe abrogated the increment of phospho-ERK1/2 (p-ERK1/2) and nuclear accumulation of ERK1/2 in VSMCs induced by Chol:M?CD. Inhibition of the MAPK pathway by using ERK1/2 inhibitor PD98059 attenuated the reduction effect of ezetimibe on the expressions of phosphor-MEK1 (p-MEK1), p-ERK1/2, and cyclin D1. Taken together our data suggest that ezetimibe inhibits Chol:M?CD-induced VSMCs proliferation and leads to cell cycle arrest at the G0/G1 phase by suppressing cyclin D1 expression via the MAPK signaling pathway. These novel findings support the potential pleiotropic effect of ezetimibe in cardiovascular disease.
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Clostridium difficile carriage in hospitalized cancer patients: a prospective investigation in eastern China.
BMC Infect. Dis.
PUBLISHED: 07-16-2014
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Clostridium difficile carriage has been considered as a potential source for the deadly infection, but its role in cancer patients is still unclear. We aimed to identify the clinical and immunological factors that are related to C. difficile carriage in Chinese cancer patients.
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[Effects of scalp acupuncture combined with auricular point sticking on cognitive behavior ability in patients with vascular dementia].
Zhongguo Zhen Jiu
PUBLISHED: 07-16-2014
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To compare the therapeutic differences among scalp acupuncture combined with auricular point sticking, body acupuncture and western medication for treatment of vascular dementia (VD).
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1-O-tigloyl-1-O-deacetyl-nimbolinin B inhibits LPS-stimulated inflammatory responses by suppressing NF-?B and JNK activation in microglia cells.
J. Pharmacol. Sci.
PUBLISHED: 07-11-2014
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Overactivation of microglia may contribute to the pathogenesis of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and HIV dementia. Thus, regulating microglial activation has been an important therapeutic strategy for treating neurodegenerative diseases. In this research, we compared three limonoids compounds extracted from Melia toosendan by a cell-based assay to investigate their anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated microglia cells. Our study indicated that 1-O-tigloyl-1-O-deacetyl-nimbolinin B (TNB) markedly suppressed the production of nitric oxide (NO) and tumor necrosis factor (TNF)-? in LPS-stimulated microglia cells. TNB also inhibited the gene expression of inducible nitric oxide synthase (iNOS), TNF-?, cyclooxygenase (COX-2), and interleukin (IL)-1?. In addition, TNB inhibited generation of intracellular reactive oxygen species (ROS). We found that TNB significantly attenuated the nuclear translocation of NF-?B, inhibiting the activation of c-jun N-terminal kinase (JNK) in LPS-stimulated BV-2 cells. Furthermore, TNB reduced cytotoxicity of activated microglia toward HT-22 hippocampal cells in a co-culture system. Taken together, our experimental results reveal, for the first time, that TNB is a potent inhibitor of microglia-mediated inflammation, and it might be a potential candidate for the treatment of neurodegenerative diseases.
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Integrating novel chemical weapons and evolutionarily increased competitive ability in success of a tropical invader.
New Phytol.
PUBLISHED: 07-08-2014
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The evolution of increased competitive ability (EICA) hypothesis and the novel weapons hypothesis (NWH) are two non-mutually exclusive mechanisms for exotic plant invasions, but few studies have simultaneously tested these hypotheses. Here we aimed to integrate them in the context of Chromolaena odorata invasion. We conducted two common garden experiments in order to test the EICA hypothesis, and two laboratory experiments in order to test the NWH. In common conditions, C. odorata plants from the nonnative range were better competitors but not larger than plants from the native range, either with or without the experimental manipulation of consumers. Chromolaena odorata plants from the nonnative range were more poorly defended against aboveground herbivores but better defended against soil-borne enemies. Chromolaena odorata plants from the nonnative range produced more odoratin (Eupatorium) (a unique compound of C. odorata with both allelopathic and defensive activities) and elicited stronger allelopathic effects on species native to China, the nonnative range of the invader, than on natives of Mexico, the native range of the invader. Our results suggest that invasive plants may evolve increased competitive ability after being introduced by increasing the production of novel allelochemicals, potentially in response to naïve competitors and new enemy regimes.
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A micromechanical model for estimating alveolar wall strain in mechanically ventilated edematous lungs.
J. Appl. Physiol.
PUBLISHED: 06-19-2014
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To elucidate the micromechanics of pulmonary edema has been a significant medical concern, which is beneficial to better guide ventilator settings in clinical practice. In this paper, we present an adjoining two-alveoli model to quantitatively estimate strain and stress of alveolar walls in mechanically ventilated edematous lungs. The model takes into account the geometry of the alveolus, the effect of surface tension, the length-tension properties of parenchyma tissue, and the change in thickness of the alveolar wall. On the one hand, our model supports experimental findings (Perlman CE, Lederer DJ, Bhattacharya J. Am J Respir Cell Mol Biol 44: 34-39, 2011) that the presence of a liquid-filled alveolus protrudes into the neighboring air-filled alveolus with the shared septal strain amounting to a maximum value of 1.374 (corresponding to the maximum stress of 5.12 kPa) even at functional residual capacity; on the other hand, it further shows that the pattern of alveolar expansion appears heterogeneous or homogeneous, strongly depending on differences in air-liquid interface tension on alveolar segments. The proposed model is a preliminary step toward picturing a global topographical distribution of stress and strain on the scale of the lung as a whole to prevent ventilator-induced lung injury.
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Mesenchymal stem cell-derived microparticles: a promising therapeutic strategy.
Int J Mol Sci
PUBLISHED: 06-18-2014
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Mesenchymal stem cells (MSCs) are multipotent stem cells that give rise to various cell types of the mesodermal germ layer. Because of their unique ability to home in on injured and cancerous tissues, MSCs are of great potential in regenerative medicine. MSCs also contribute to reparative processes in different pathological conditions, including cardiovascular diseases and cancer. However, many studies have shown that only a small proportion of transplanted MSCs can actually survive and be incorporated into host tissues. The effects of MSCs cannot be fully explained by their number. Recent discoveries suggest that microparticles (MPs) derived from MSCs may be important for the physiological functions of their parent. Though the physiological role of MSC-MPs is currently not well understood, inspiring results indicate that, in tissue repair and anti-cancer therapy, MSC-MPs have similar pro-regenerative and protective properties as their cellular counterparts. Thus, MSC-MPs represent a promising approach that may overcome the obstacles and risks associated with the use of native or engineered MSCs.
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The reaction mechanisms and kinetics of CF3CHFOCH 3 and CHF 2CHFOCF 3 with atomic chlorine: a computational study.
J Mol Model
PUBLISHED: 06-05-2014
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Due to their lack of effect on the ozone depletion, hydrofluoroethers are considered as potential candidates for third generation refrigerants. In the present work, the mechanisms and kinetics of reaction of the Cl atom with CF(3)CHFOCH(3) and CHF(2)CHFOCF(3) were investigated theoretically using quantum chemical methods and transition state theory. Four reaction pathways for the title reaction were explored. By using conventional transition state theory with Eckart tunneling correction, the rate constants of the title reaction were obtained over the temperature range 200-300 K. Kinetic calculations demonstrate that H-abstraction from the -CH(3) group in CF(3)CHFOCH(3) and H-abstraction from the -CHF2 group in CHF(2)CHFOCF(3) are major reaction pathways, with the barrier heights of the two paths calculated to be -1.04 and 4.33 kcal mol(-1), respectively. However, the contribution of H-abstraction from the -CHFO- group for the two reactions should also be taken into account with increased temperature. At 298 K, the calculated overall rate constants of the reaction of CHF(2)CHFOCF(3) with the Cl atom are 4.27?×?10(-15) cm(3) molecule(-1) s(-1), which is consistent with the experimental value of (1.2?±?2.0)?×?10(-15) cm(3) molecule(-1) s(-1).
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ADAMTS13 and its variants promote angiogenesis via upregulation of VEGF and VEGFR2.
Cell. Mol. Life Sci.
PUBLISHED: 06-05-2014
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Severe plasma ADAMTS13 deficiency results in the clinical disorder thrombotic thrombocytopenic purpura. However, other potential pathophysiological roles of ADAMTS13 in endothelial cell biology remain unexplored. The goals of this study were to understand the angiogenic pathways ADAMTS13 activates and to identify the important structural components of ADAMTS13 that stimulate angiogenesis. Incubation of human umbilical vein endothelial cells (HUVEC) with 150 ng/mL (1 nM) of recombinant human ADAMTS13 induced VEGF expression by 53 % and increased VEGF mRNA by over sixfold, both within 10 min; the measured VEGF levels steadily decreased over 2 h, as shown by Western blot and ELISA. Phosphorylation of VEGFR2 was significantly enhanced in HUVEC after incubation with ADAMTS13 (1 nM). Structure-function analysis showed that an ADAMTS13 variant containing thrombospondin type 1 (TSP1) 2-8 repeats (TSP1 2-8), TSP1 2-8 plus CUB domains (TSP1 2-8 plus CUB), or TSP1 5-8 repeats plus CUB domains (TSP1 5-8 plus CUB) increased HUVEC proliferation by 41-54 % as compared to the EBM-2 controls. Chemotaxis assays further demonstrated that the TSP1 domains of ADAMTS13 increased HUVEC migration by 2.65-fold. Incubation of HUVEC with both ADAMTS13 variants containing TSP1 repeats and anti-VEGF IgG abrogated the enhanced effect of ADAMTS13 on proliferation, migration, and VEGFR2 phosphorylation. In conclusion, ADAMTS13-induced endothelial cell angiogenesis occurs via the upregulation of VEGF and phosphorylation of VEGFR2. This angiogenic activity depends on the C-terminal TSP1 repeats of ADAMTS13.
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The GPER agonist G-1 induces mitotic arrest and apoptosis in human vascular smooth muscle cells independent of GPER.
J. Cell. Physiol.
PUBLISHED: 05-29-2014
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The G protein-coupled estrogen receptor (GPER) has been implicated in the regulation of smooth muscle cell (SMC) proliferation. The GPER selective agonist G-1 has been a useful tool for exploring the biological roles of GPER in a variety of experimental settings, including SMC proliferation. The present study, originally designed to investigate cellular and signaling mechanisms underlying the regulatory role of GPER in vascular SMC proliferation using G-1, unexpectedly revealed off-target effects of G-1. G-1 (1-10 ?M) inhibited bromodeoxyuridine (BrdU) incorporation of human SMCs and caused G2/M cell accumulation. G-1 treatment also increased mitotic index concurrent with a decrease in phosphorylation of Cdk1 (Tyr 15) and an increase in phosphorylation of the mitotic checkpoint protein BuBR1. Furthermore, G-1 caused microtubule disruption, mitotic spindle damage, and tubulin depolymerization. G-1 induced cell apoptosis as indicated by the appearance of TUNEL-positive and annexin V-positive cells with enhanced cleavage of caspases 3 and 9. However, neither the GPER antagonist G-15 nor the MAPK kinase inhibitor PD98059 prevented these G-1 effects. Down-regulation of GPER or p44/42 MAPK with siRNA transfection also did not affect the G-1-induced apoptosis. We conclude that G-1 inhibits proliferation of SMCs through mechanisms involving mitotic arrest and apoptosis, independent of GPER and the MAPK pathway. J. Cell. Physiol. © 2014 Wiley Periodicals, Inc.
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Immuno-PCR for detection of Giardia lamblia cysts in water.
J AOAC Int
PUBLISHED: 05-17-2014
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Giardia lamblia cysts at low concentrations were detected in water samples using a highly sensitive immunological-PCR (IPCR) method. Magnetic gold particles were precoated with monoclonal anti-Giardia antibodies, and Giardia lamblia cysts ranging from 1 to 100 cysts were diluted in 500 microL of water. A biotinylated detection antibody bound to the G. lamblia cysts was then linked by a streptavidin bridge to biotinylated Giardia-reporter DNA. After extensive washing, reporter DNA was released by denaturation, transferred to PCR tubes, amplified, electrophoresed, and visualized. An optimized immuno-PCR method detected as little as five G. lamblia cysts. To further evaluate the specificity and the clinical application of this IPCR assay for G. lamblia cysts, Entamoeba histolytica and Cryptosporidium parvum were also collected and detected by IPCR. The data demonstrated that this monoclonal antibody-based IPCR method is particularly useful for analysis of environmental water samples in which the densities of G. lamblia cysts is very low, and provides a platform capable of rapid screening of samples from drinking water, wells, rivers, lakes, and recreational swimming pools for trace levels of G. lamblia cysts.
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Hydrogen sulfide as a potent cardiovascular protective agent.
Clin. Chim. Acta
PUBLISHED: 05-03-2014
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Hydrogen sulfide (H2S) is a well-known toxic gas with the characteristic smell of rotten eggs. It is synthesized endogenously in mammals from the sulfur-containing amino acid l-cysteine by the action of several distinct enzymes: cystathionine-?-lyase (CSE), cystathionine-ß-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) along with cysteine aminotransferase (CAT). In particular, CSE is considered to be the major H2S-producing enzyme in the cardiovascular system. As the third gasotransmitter next to nitric oxide (NO) and carbon monoxide (CO), H2S plays an important role in the regulation of vasodilation, angiogenesis, inflammation, oxidative stress and apoptosis. Growing evidence has demonstrated that this gas exerts a significant protective effect against the progression of cardiovascular diseases by a number of mechanisms such as vasorelaxation, inhibition of cardiovascular remodeling and resistance to form foam cells. The aim of this review is to provide an overview of the physiological functions of H2S and its protection against several major cardiovascular diseases, and to explore its potential health and therapeutic benefits. A better understanding will help develop novel H2S-based therapeutic interventions for these diseases.
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The novel role and underlying mechanism of Wnt5a in regulating cellular cholesterol accumulation.
Clin. Exp. Pharmacol. Physiol.
PUBLISHED: 05-02-2014
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Cholesterol accumulation is a critical step during the development and progression of atherosclerosis. Recently, Wnt5a expression has been found to be markedly upregulated in both murine and human atherosclerotic lesions. However, the effect and mechanism of Wnt5a in atherosclerosis is poorly understood. In the present study, we investigated the effects and potential mechanisms of Wnt5a on cholesterol accumulation during atherosclerosis. We used RAW264.7 and vascular smooth muscle cells (VSMC) treated with oxidized low-density lipoprotein (oxLDL) as lipid-loaded cell models. We found that expression of Wnt5a protein was increased in a concentration (25, 50, 75 and 100 ?g/mL)- and time (24, 48 and 72 h)-dependent manner by oxLDL treatment. To explore the underlying mechanism, we used Wnt5a short interference (si) RNA to knockdown Wnt5a expression in both RAW264.7 cells and VSMC, or applied recombinant Wnt5a (rWnt5a) to stimulate Wnt5a signalling. After Wnt5a knockdown, total cholesterol (TC) and free cholesterol (FC) content in both cell types increased significantly (P < 0.05) upon exposure to oxLDL. Conversely, the TC and FC content decreased markedly (P < 0.05) after treatment of cells with rWnt5a. More importantly, both protein and mRNA expression of Caveolin-1 and ATP-binding cassette transporter A1 (ABCA1) was significantly reduced after exposure of wnt5a siRNA-treated cells to oxLDL, whereas rWnt5a treatment of cells resulted in increased Caveolin-1 and ABCA1 protein expression after exposure of cells to oxLDL. Together, these findings demonstrate, for the first time, that Wnt5a reduces the accumulation of cholesterol in lipid-loaded cells by regulating the mRNA expression of Caveolin-1 and ABCA1, which are involved in reverse cholesterol transport. This may present a novel mechanism of Wnt5a-mediated cholesterol transportation in macrophages and VSMC. Therefore, targeting the Wnt5a signalling pathway may have clinical implications in atherosclerosis.
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Baicalin ameliorates H2O2 induced cytotoxicity in HK-2 cells through the inhibition of ER stress and the activation of Nrf2 signaling.
Int J Mol Sci
PUBLISHED: 04-16-2014
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Renal ischemia-reperfusion injury plays a key role in renal transplantation and greatly affects the outcome of allograft. Our previous study proved that Baicalin, a flavonoid glycoside isolated from Scutellaria baicalensis, protects kidney from ischemia-reperfusion injury. This study aimed to study the underlying mechanism in vitro. Human renal proximal tubular epithelial cell line HK-2 cells were stimulated by H2O2 with and without Baicalin pretreatment. The cell viability, apoptosis and oxidative stress level were measured. The expression of endoplasmic reticulum (ER) stress hallmarks, such as binding immunoglobulin protein (BiP) and C/EBP homologous protein (CHOP), were analyzed by western blot and real-time PCR. NF-E2-related factor 2 (Nrf2) expression was also measured. In the H2O2 group, cell viability decreased and cell apoptosis increased. Reactive Oxygen Species (ROS) and Glutathione/Oxidized Glutathione (GSH/GSSG) analysis revealed increased oxidative stress. ER stress and Nrf2 signaling also increased. Baicalin pretreatment ameliorated H2O2-induced cytotoxicity, reduced oxidative stress and ER stress and further activated the anti-oxidative Nrf2 signaling pathway. The inducer of ER stress and the inhibitor of Nrf2 abrogated the protective effects, while the inhibitor of ER stress and the inducer of Nrf2 did not improve the outcome. This study revealed that Baicalin pretreatment serves a protective role against H2O2-induced cytotoxicity in HK-2 cells, where the inhibition of ER stress and the activation of downstream Nrf2 signaling are involved.
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Adaptation of muscles of the lumbar spine to sudden imbalance in patients with lower back pain caused by military training.
J Spinal Cord Med
PUBLISHED: 03-14-2014
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Objective This study aims to investigate the effects of sudden load changes (expected and unexpected imbalance) on the activity of muscles of the lumbar spine and their central motor control strategy in military personnel with or without chronic low back pain (LBP). Design Bilateral sudden imbalance was examined (2 × 2 factorial design). Setting The 117th PLA Hospital, Hangzhou, China Participants Twenty-one male subjects with lower back pain and 21 male healthy control subjects were active members of the Nanjing Military Region land forces. Outcome measures Independent variables: LBP vs. healthy controls and imbalance anticipation (expected and unexpected imbalance).
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Ezetimibe-Mediated Protection of Vascular Smooth Muscle Cells from Cholesterol Accumulation through the Regulation of Lipid Metabolism-Related Gene Expression.
Pharmacology
PUBLISHED: 03-03-2014
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Background: Ezetimibe is a potent inhibitor of Niemann-Pick type C1-Like 1 and has been approved for the treatment of hypercholesterolemia. Our preliminary study showed that ezetimibe promotes cholesterol ef?ux from vascular smooth muscle cells (VSMCs). Our aim was to investigate the cellular mechanisms underlying the ezetimibe actions. Methods and Results: Rat VSMCs were converted to foam cells by incubation with cholesterol:methyl-?-cyclodextrin. The intracellular free cholesterol, total cholesterol, and the ratio of cholesteryl ester to total cholesterol were decreased after the incubation of VSMCs with different concentrations of ezetimibe (3, 10, 30, and 30 ?mol/l) or treated with 30 ?mol/l of ezetimibe for different time periods (6, 12, 24, and 48 h). Our results also showed that the expression of caveolin-1, liver X receptor ?, and ATP-binding cassette transporter ABCA1 was enhanced, but the expression of nSREBP-1c was decreased in a concentration- and time-dependent manner. RNA interference was used to determine the roles of caveolin-1 and SREBP-1 in the lipid-lowering effect of ezetimibe. The results showed that caveolin-1 was involved in the regulation of intracellular cholesterol content, and the expression of caveolin-1 was repressed by SREBP-1. Conclusion: The present study indicates that ezetimibe protects VSMCs from cholesterol accumulation by regulating the expression of lipid metabolism-related genes. © 2014 S. Karger AG, Basel.
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The effect of thick fibers and large pores of electrospun poly(?-caprolactone) vascular grafts on macrophage polarization and arterial regeneration.
Biomaterials
PUBLISHED: 03-01-2014
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The vascular grafts prepared by electrospinning often have relatively small pores, which limit cell infiltration into the grafts and hinder the regeneration and remodeling of the grafts into neoarteries. To overcome this problem, macroporous electrospun polycaprolactone (PCL) scaffolds with thicker fibers (5-6 ?m) and larger pores (?30 ?m) were fabricated in the present study. In vitro cell culture indicated that macrophages cultured on thicker-fiber scaffolds tended to polarize into the immunomodulatory and tissue remodeling (M2) phenotype, while those cultured on thinner-fiber scaffolds expressed proinflammatory (M1) phenotype. In vivo implantation by replacing rat abdominal aorta was performed and followed up for 7, 14, 28 and 100 d. The results demonstrated that the macroporous grafts markedly enhanced cell infiltration and extracellular matrix (ECM) secretion. All grafts showed satisfactory patency for up to 100 days. At day 100, the endothelium coverage was complete, and the regenerated smooth muscle layer was correctly organized with abundant ECM similar to those in the native arteries. More importantly, the regenerated arteries demonstrated contractile response to adrenaline and acetylcholine-induced relaxation. Analysis of the cellularization process revealed that the thicker-fiber scaffolds induced a large number of M2 macrophages to infiltrate into the graft wall. These macrophages further promoted cellular infiltration and vascularization. In conclusion, the present study confirmed that the scaffold structure can regulate macrophage phenotype. Our thicker-fiber electrospun PCL vascular grafts could enhance the vascular regeneration and remodeling process by mediating macrophage polarization into M2 phenotype, suggesting that our constructs may be a promising cell-free vascular graft candidate and are worthy for further in vivo evaluation.
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Abnormal mitosis induced by wheat-rye 1R monosomic addition lines.
Genome
PUBLISHED: 02-26-2014
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Octoploid triticale were derived from common wheat (Triticum aestivum L. 'Mianyang11') × rye (Secale cereale L. 'Kustro'), and some progeny were obtained by the backcrossing of triticale with 'Mianyang11' followed by self-fertilization. In situ hybridization using rye genomic DNA and repetitive sequences pAs1 and pSc119.2 as probes was used to analyze the mitotic chromosomes of these progeny. Three wheat-rye 1R monosomic addition lines and a wheat line (12FT-1685) containing a 1R and a 1BL.1RS translocation chromosome were identified. Abnormal mitosis was observed in the two lines. During mitosis of a 1R monosomic addition line (3-8-20-1R-2), lagging chromosomes, micronuclei, chromosomal bridges, and the one pole segregation of 1R chromosome were observed. Abnormal mitotic behaviour of chromosomes was also observed in some of the self-progeny plants of lines 12FT-1685 and 3-8-20-1R-2. These progeny contained 1R chromosome or 1R chromosome arm. In addition, 4B chromosomes were absent from one of the progeny of 3-8-20-1R-2. This abnormal mitotic behaviour of chromosomes was not observed in two other 1R monosomic addition lines. These results indicate that a single 1R chromosome added to wheat might cause abnormal mitotic behaviour of both wheat and rye chromosomes and different genetic variations might occurr among the sibling 1R monosomic addition lines.
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Anti-inflammatory activity of ezetimibe by regulating NF-?B/MAPK pathway in THP-1 macrophages.
Pharmacology
PUBLISHED: 02-15-2014
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Inflammation plays a crucial role in atherosclerosis. Monocytes/macrophages are involved in the inflammatory process during atherogenesis. Here, we performed daily gavage of ezetimibe in apolipoprotein E-deficient mice fed with a high-fat diet and found that ezetimibe administration decreased the level of C-reactive protein significantly. To investigate the potential molecular mechanism, we employed microarray analysis on the cultured macrophages treated with Chol:M?CD in the presence or absence of ezetimibe. We found that ezetimibe dramatically down-regulated the expression of the tumor necrosis factor-? (TNF-?) gene. Consistent with the microarray results, TNF-? protein levels were inhibited by ezetimibe. Moreover, ezetimibe suppressed the promoter activity of TNF-? but not TNF-? lacking the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B) binding domain in THP-1 cells treated with phorbol myristate acetate and Chol:M?CD. Furthermore, treatment of THP-1 macrophages with ezetimibe resulted in the degradation of I?B and subsequently inhibited nuclear translocation of NF-?B and its transcriptional activity. Inhibition of the mitogen-activated protein kinase (MAPK) pathway using PD98059 attenuated the reduction effect of ezetimibe on the expression of NF-?B. Collectively, our results demonstrated that the anti-inflammatory properties of ezetimibe in THP-1 macrophages are, at least in part, through suppression of NF-?B activation via the MAPK pathway. These data provide direct evidence for the potential application of ezetimibe in the prevention and treatment of inflammatory diseases.
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Chlamydia pneumoniae negatively regulates ABCA1 expression via TLR2-Nuclear factor-kappa B and miR-33 pathways in THP-1 macrophage-derived foam cells.
Atherosclerosis
PUBLISHED: 01-30-2014
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ATP-binding cassette transporter A1 (ABCA1) is critical in exporting cholesterol from macrophages and plays a protective role in the development of atherosclerosis. This study was to determine the effects and potential mechanisms of Chlamydia pneumoniae (C. pneumoniae) on ABCA1 expression and cellular cholesterol efflux in THP-1 macrophage-derived foam cells.
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Tumor necrosis factor-alpha 308G>A polymorphism and risk of rheumatic heart disease: a meta-analysis.
Sci Rep
PUBLISHED: 01-27-2014
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Rheumatic heart disease (RHD) remains a serious cardiovascular disorder across the world. Tumor necrosis factor alpha (TNF-?) codifies a potent immunomodulator and pro-inflammatory cytokine that mediates diverse pathological processes. A promoter 308G>A polymorphism in TNF-? has been implicated in RHD risk. However, the results remain controversial. Therefore, to evaluate more precise estimations of the relationship, a meta-analysis was performed. A total of 7 studies including 735 RHD cases and 926 controls were involved in this meta-analysis. Overall, our results revealed that there was a significant association with RHD risk in three genetic models (homozygous model: OR = 3.06, 95%CI = 1.22-10.60, P = 0.020; dominant model, OR = 2.03, 95%CI = 1.01-4.07, P = 0.048; and recessive model, OR = 4.26, 95%CI = 2.41-7.55, P < 0.001). Further ethnic population analysis found a significantly increased risk of RHD among Asians and Europeans. Interestingly, similar results were found among hospital-based studies. Begg's funnel plot and Egger's test did not reveal any publication bias. Taken together, this meta-analysis demonstrates that the TNF-? 308G>A polymorphism is associated with RHD susceptibility, and it contributes to the increased risk of RHD. However, additional well-designed studies with larger samples are warranted to confirm these findings.
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Synthesis of 5?-cholestan-6-one derivatives and their inhibitory activities of NO production in activated microglia: discovery of a novel neuroinflammation inhibitor.
Bioorg. Med. Chem. Lett.
PUBLISHED: 01-25-2014
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Glial activation-mediated neuroinflammation plays a pivotal role in the process of several neuroinflammatory diseases including stroke, Alzheimer's diseases, Parkinson's diseases, multiple sclerosis and ischemia. Inhibition of microglial activation may ameliorate neuronal degeneration under the inflammatory conditions. In the present study, a number of 5?-cholestan-6-one derivatives were prepared and the anti-inflammatory effects of these compounds were evaluated in LPS-stimulated BV-2 microglia cells. Those derivatives were synthesized from readily available hyodeoxycholic acid (1). Among the tested compounds, several analogs (16-18, 25, 35, 38) exhibited potent inhibitory activities on nitric oxide production with no or weak cell toxicity. Compound 16 also significantly suppressed the expression of TNF-?, interleukin (IL)-1?, cyclooxygenase (COX-2) as well as inducible nitric oxide synthase (iNOS) in LPS-stimulated BV-2 microglia cells. In addition, compound 16 markedly reduced infarction volume in a focal ischemic mice model.
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MicroRNA-19b promotes macrophage cholesterol accumulation and aortic atherosclerosis by targeting ATP-binding cassette transporter A1.
Atherosclerosis
PUBLISHED: 01-19-2014
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Macrophage accumulation of cholesterol leads to foam cell formation which is a major pathological event of atherosclerosis. Recent studies have shown that microRNA (miR)-19b might play an important role in cholesterol metabolism and atherosclerotic diseases. Here, we have identified miR-19b binding to the 3'UTR of ATP-binding cassette transporter A1 (ABCA1) transporters, and further determined the potential roles of this novel interaction in atherogenesis.
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MicroRNA-27a/b regulates cellular cholesterol efflux, influx and esterification/hydrolysis in THP-1 macrophages.
Atherosclerosis
PUBLISHED: 01-19-2014
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Macrophage cholesterol homeostasis maintenance is the result of a balance between influx, endogenous synthesis, esterification/hydrolysis and efflux. Excessive accumulation of cholesterol leads to foam cell formation, which is the major pathology of atherosclerosis. Previous studies have shown that miR-27 (miR-27a and miR-27b) may play a key role in the progression of atherosclerosis.
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Endogenous endothelial progenitor cells participate in neovascularization via CXCR4/SDF-1 axis and improve outcome after stroke.
CNS Neurosci Ther
PUBLISHED: 01-17-2014
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To study whether endogenous endothelial progenitor cells (EPCs) are involved in neovascularization after stroke.
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Growth differentiation factor-15 induces expression of ATP-binding cassette transporter A1 through PI3-K/PKC?/SP1 pathway in THP-1 macrophages.
Biochem. Biophys. Res. Commun.
PUBLISHED: 01-14-2014
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The aim of this study was to determine whether ATP-binding cassette transporter A1 (ABCA1) was up-regulated by growth differentiation factor-15 (GDF-15) via the phosphoinositide 3-kinase (PI3K)/protein kinase C? (PKC?)/specificity protein 1 (SP1) pathway in THP-1 macrophages.
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Interleukin-17A in lipid metabolism and atherosclerosis.
Clin. Chim. Acta
PUBLISHED: 01-07-2014
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Interleukin-17 (IL-17) A, the most important cytokine of the IL-17 family predominantly secreted by T helper 17 (Th17) cells, plays a critical role in the development of inflammatory diseases. Its receptor is an obligate heterodimer composed of IL-17 receptor (IL-17R) A and C, the main members of the IL-17R family. Binding of IL-17A to the IL-17RA/C complex can activate a variety of downstream signaling pathways such as nuclear factor kappa-B (NF-?B), activator protein 1 (AP1) and CCAAT/enhancer-binding protein (C/EBP) to induce the expression of proinflammatory cytokines and chemokines. IL-17A also promotes mRNA stability. Growing evidence shows that IL-17A is involved in lipid metabolism and the pathogenesis of atherosclerosis, a chronic inflammatory arterial disease driven by both innate and adaptive immune responses to modified lipoproteins. In the current review, we describe recent progress on regulation and signaling of IL-17A, and highlight its impacts on lipid metabolism and atherosclerosis.
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Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux.
PLoS ONE
PUBLISHED: 01-01-2014
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Epigallocatechin gallate (EGCG) is a major polyphenol in green tea with beneficial effects on the impairment in learning and memory. Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and whether its protective effect involves improvement of autophagic flux. As expected, our results showed that CUMS significantly impaired memory performance and inhibited autophagic flux as indicated by elevated LC3-II and p62 protein levels. At the same time, we observed an increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling in the CA1 regions. Interestingly, chronic treatment with EGCG (25 mg/kg, i.p.) significantly improved those behavioral alterations, attenuated histopathological abnormalities in hippocampal CA1 regions, reduced amyloid beta1-42 (A?1-42) levels, and restored autophagic flux. However, blocking autophagic flux with chloroquine, an inhibitor of autophagic flux, reversed these effects of EGCG. Taken together, these findings suggest that the impaired autophagy in CA1 regions of CUMS rats may contribute to learning and memory impairment. Therefore, we conclude that EGCG attenuation of CUMS-induced learning and memory impairment may be through rescuing autophagic flux.
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Dual Regulation of Myocardin Expression by Tumor Necrosis Factor-? in Vascular Smooth Muscle Cells.
PLoS ONE
PUBLISHED: 01-01-2014
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De-differentiation of vascular smooth muscle cells (VSMCs) plays a critical role in the development of atherosclerosis, a chronic inflammatory disease involving various cytokines such as tumor necrosis factor-? (TNF?). Myocardin is a co-factor of serum response factor (SRF) and is considered to be the master regulator of VSMC differentiation. It binds to SRF and regulates the expression of contractile proteins in VSMCs. Myocardin is also known to inhibit VSMC proliferation by inhibiting the NF-?B pathway, whereas TNF? is known to activate the NF-?B pathway in VSMCs. NF-?B activation has also been shown to inhibit myocardin expression and smooth muscle contractile marker genes. However, it is not definitively known whether TNF? regulates the expression and activity of myocardin in VSMCs. The current study aimed to investigate the role of TNF? in regulating myocardin and VSMC function. Our studies showed that TNF? down-regulated myocardin expression and activity in cultured VSMCs by activating the NF-?B pathway, resulting in decreased VSMC contractility and increased VSMC proliferation. Surprisingly, we also found that TNF? prevented myocardin mRNA degradation, and resulted in a further significant increase in myocardin expression and activity in differentiated VSMCs. Both the NF-?B and p44/42 MAPK pathways were involved in TNF? regulation of myocardin, which further increased the contractility of VSMCs. These differential effects of TNF? on myocardin seemingly depended on whether VSMCs were in a differentiated or de-differentiated state. Taken together, our results demonstrate that TNF? differentially regulates myocardin expression and activity, which may play a key role in regulating VSMC functions.
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[Study on the FTIR spectra of OH in olivines from mengyin kimberlite].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 12-28-2013
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The results of FTIR spectra study of OH in olivines from Mengyin kimberlite show that there are more than 60 OH absorption peaks in the range of 3800-3000 cm(-1). We identified four major spectral features in the OH absorption bands of kimberlitic olivines. One is with nuOH in the range of 3800-3700 cm(-1), which is caused by the vapour of the room circumstance, and can not be regarded as intrinsic or non-intrinsic nuOH of the olivines. Another one is with nuOH in the range of 3710-3620 cm(-1), which belongs to three "water"-bearing minerals including serpentine, talc and Mg-bearing amphiboles, which is the non-intrinsic nuOH of the olivines. There is the possibility that H in hydrous minerals mainly entered into olivines during post-emplacement processes of the kimberlite magma. The third one is with nuOH in the range of 3620-3425 cm(-1), which originated from H occupying the Si-defect in the olivine structure, forming humite-like defects, and/or the defects that H occupies (Mg,Fe)-depletion, which is certainly attributed to the intrinsic nuOH of the olivines. In this case, H possibly entered into olivines following its immersion in the high temperature and rich fluid kimberlite magma in the mantle circumstance. The last one is with nuOH in the range of 3425-3000 cm(-1). In this area, nuOH is assigned to fluid inclusions of the olivines, and is the non-intrinsic nuOH of olivines. Fluid inclusions can enter into the olivines either during post-emplacement processes of the kimberlite magma or during the periods that olivines were formed in the mantle.
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[Effect of ladder ring suture of esophageal mucosa vascular combined with Nissen s fundoplication on prevention from rebleeding of patients with advanced schistosomiasis].
Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi
PUBLISHED: 12-24-2013
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To evaluate the effectiveness of the ladder ring suture of the esophageal mucosa vascular combined with Nissens fundoplication on provention from rebleeding of patients with advaced schistosomiasis
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[Relationship between corneal thickness and postmortem interval in rabbit].
Fa Yi Xue Za Zhi
PUBLISHED: 12-20-2013
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To explore the relationship between corneal thickness and postmortem interval (PMI) in rabbit.
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Carboxyl Terminus of ADAMTS13 Directly Inhibits Platelet Aggregation and Ultra Large von Willebrand Factor String Formation Under Flow in a Free-Thiol-Dependent Manner.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 12-19-2013
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ADAMTS13 (A Disintegrin And Metalloprotease with Thrombospondin type 1 repeats, 13) cleaves von Willebrand factor (VWF), thereby inhibiting thrombus formation. Proteolytic cleavage relies on the amino-terminal (MDTCS) domains, but the role of the more distal carboxyl-terminal domains of ADAMTS13 is not fully understood. A previous study demonstrated the presence of multiple surface-exposed free sulfhydryls on ADAMTS13 that seemed to interact with those on VWF under shear. Here, we determined the physiological relevance of such an interaction in antithrombotic responses under flow.
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The effects of miR-467b on lipoprotein lipase (LPL) expression, pro-inflammatory cytokine, lipid levels and atherosclerotic lesions in apolipoprotein E knockout mice.
Biochem. Biophys. Res. Commun.
PUBLISHED: 11-18-2013
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Atherosclerosis is a lipid disorder disease characterized by chronic blood vessel wall inflammation driven by the subendothelial accumulation of macrophages. Studies have shown that lipoprotein lipase (LPL) participates in lipid metabolism, but it is not yet known whether post-transcriptional regulation of LPL gene expression by microRNAs (miRNAs) occurs in vivo. Here, we tested that miR-467b provides protection against atherosclerosis by regulating the target gene LPL which leads to reductions in LPL expression, lipid accumulation, progression of atherosclerosis and production of inflammatory cytokines in apolipoprotein E knockout (apoE(-/-)) mice. Treatment of apoE(-/-) mice with intra-peritoneal injection of miR-467b agomir led to decreased blood plasma levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), tumor necrosis factor-alpha (TNF-?), interleukin-6 (IL-6), IL-1? and monocyte chemotactic protein-1 (MCP-1). Using Western blots and real time PCR, we determined that LPL expression in aorta and abdominal cavity macrophages were significantly down-regulated in the miR-467b agomir group. Furthermore, systemic treatment with miR-467b antagomir accelerated the progression of atherosclerosis in the aorta of apoE(-/-) mice. The present study showed that miR-467b protects apoE(-/-) mice from atherosclerosis by reducing lipid accumulation and inflammatory cytokine secretion via downregulation of LPL expression. Therefore, targeting miR-467b may offer a promising strategy to treat atherosclerotic vascular disease.
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Biochemistry and physiological functions of ADAMTS7 metalloprotease.
Adv Biochem
PUBLISHED: 11-14-2013
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Here, we provide a comprehensive review of current findings concerning the biochemistry and physiological functions of ADAMTS7, a metalloprotease that is known to interact with cartilage oligomeric matrix protein, progranulin, and alpha2-macroglobulin. Such broad substrate specificity and potentially diverse physiological functions make ADAMTS7 an interesting enzyme to study. ADAMTS7 has been shown to play a role in the pathogenesis of arthritis and disc disorders. More recently, the ADAMTS7 locus is identified to have a strong association with coronary atherosclerotic disease. However, the role of ADAMTS7 in the development of atherosclerosis is yet to be determined. The development of an easy and high throughput assay for ADAMTS7 activity and appropriate animal models will allow us to uncover the novel mechanisms of coronary arterial disease.
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Myocardin and Smooth Muscle Differentiation.
Arch. Biochem. Biophys.
PUBLISHED: 10-15-2013
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Myocardin (MYOCD), a co-transcriptional activator of serum response factor (SRF), stimulates the expression of smooth muscle (SM) genes and inhibits the cell cycle. In addition to its roles in the development, MYOCD may be critically involved in the pathogenesis of proliferative vascular diseases. This review mainly focuses on how MYOCD activity is regulated and how it inhibits cell proliferation.
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NPC1, intracellular cholesterol trafficking and atherosclerosis.
Clin. Chim. Acta
PUBLISHED: 09-27-2013
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Post-lysosomal cholesterol trafficking is an important, but poorly understood process that is essential to maintain lipid homeostasis. Niemann-Pick type C1 (NPC1), an integral membrane protein on the limiting membrane of late endosome/lysosome (LE/LY), is known to accept cholesterol from NPC2 and then mediate cholesterol transport from LE/LY to endoplasmic reticulum (ER) and plasma membrane in a vesicle- or oxysterol-binding protein (OSBP)-related protein 5 (ORP5)-dependent manner. Mutations in the NPC1 gene can be found in the majority of NPC patients, who accumulate massive amounts of cholesterol and other lipids in the LE/LY due to a defect in intracellular lipid trafficking. Liver X receptor (LXR) is the major positive regulator of NPC1 expression. Atherosclerosis is the pathological basis of coronary heart disease, one of the major causes of death worldwide. NPC1 has been shown to play a critical role in the atherosclerotic progression. In this review, we have summarized the role of NPC1 in regulating intracellular cholesterol trafficking and atherosclerosis.
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ABCG5/ABCG8 in cholesterol excretion and atherosclerosis.
Clin. Chim. Acta
PUBLISHED: 09-19-2013
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Cholesterol is essential for the growth and function of all mammalian cells, but abnormally increased blood cholesterol is a major risk factor for atherosclerotic cardiovascular disease. ATP-binding cassette (ABC) transporters G5 (ABCG5) and G8 (ABCG8) form an obligate heterodimer that limits intestinal absorption and facilitates biliary secretion of cholesterol and phytosterols. Consistent with their function, ABCG5 and ABCG8 are located on the apical membrane of enterocytes and hepatocytes. Liver X receptor is the major positive regulator of ABCG5 and ABCG8 expression. Mutations in either of the two genes cause sitosterolemia, a condition in which cholesterol and plant sterols accumulate in the circulation leading to premature cardiovascular disease. Overexpression of ABCG5 and ABCG8 in mice retards diet-induced atherosclerosis because of reduced circulating and hepatic cholesterol. In the current review, we summarize recent developments and propose a future framework that provides new perspectives on the regulation of cholesterol metabolism and treatment of atherosclerotic cardiovascular disease.
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Treatment of polycystic liver disease: a hypothesis, patient characteristics, short and long-term results.
Ann Hepatol
PUBLISHED: 09-11-2013
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Non-total liver resecting invasive treatment of polycystic liver disease has different recurrence rates. The aim of this study is to illustrate why the recurrence rates are different. We established a hypothesis that the cyst number is a constant in polycystic liver disease in a patients lifetime.
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Cd2+ as a Ca2+ surrogate in protein-membrane interactions: isostructural but not isofunctional.
J. Am. Chem. Soc.
PUBLISHED: 08-21-2013
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Due to its favorable spectroscopic properties, Cd(2+) is frequently used as a probe of Ca(2+) sites in proteins. We investigate the ability of Cd(2+) to act as a structural and functional surrogate of Ca(2+) in protein-membrane interactions. C2 domain from protein kinase C? (C2?) was chosen as a paradigm for the Ca(2+)-dependent phosphatidylserine-binding peripheral membrane domains. We identified the Cd(2+)-binding sites of C2? using NMR spectroscopy, determined the 1.6 Å crystal structure of Cd(2+)-bound C2?, and characterized metal-ion-dependent interactions between C2? and phospholipid membranes using fluorescence spectroscopy and ultracentrifugation experiments. We show that Cd(2+) forms a tight complex with the membrane-binding loops of C2? but is unable to support its membrane-binding function. This is in sharp contrast with Pb(2+), which is almost as effective as Ca(2+) in driving the C2?-membrane association process. Our results provide the first direct evidence for the specific role of divalent metal ions in mediating protein-membrane interactions, have important implications for metal substitution studies in proteins, and illustrate the potential diversity of functional responses caused by toxic metal ions.
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Arsenic trioxide induces apoptosis in B-cell chronic lymphocytic leukemic cells through down-regulation of survivin via the p53-dependent signaling pathway.
Leuk. Res.
PUBLISHED: 07-25-2013
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Arsenic trioxide (As2O3) can induce apoptosis in many tumors. However, the associated mechanisms are not clearly understood. We found that As2O3 significantly inhibited the proliferation of WSU-CLL cells and induced apoptosis in dose- and time-dependent manners. WSU-CLL cells treated with 2?M As2O3 showed survivin down-regulation and p53 up-regulation. Survivin siRNA combined with As2O3 further inhibited the proliferation of WSU-CLL cells. p53 inhibition by siRNA prevented the down-regulation of survivin by As2O3 and prevented the As2O3-induced cytotoxicity of WSU-CLL cells. These results suggest that As2O3 may be of therapeutic value for chronic lymphocytic leukemia.
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Ag@SiO2 core-shell nanoparticles on silicon nanowire arrays as ultrasensitive and ultrastable substrates for surface-enhanced Raman scattering.
Nanotechnology
PUBLISHED: 07-23-2013
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Ag nanoparticles (NPs) coated with silica nanolayers were decorated onto a large-scale and uniform silicon nanowire array (SiNWA) by simple chemical etching and metal reduction processes. The three-dimensional Ag/SiNWAs thus formed are employed as a substrate for surface-enhanced Raman scattering (SERS), and a detection limit for rhodamine 6G as low as 10(-16) M and a Raman enhancement factor as large as 10(14) were obtained. Simulation results show that two kinds of inter-Ag-NP nanogaps in three-dimensional geometry create a huge number of SERS hot spots where electromagnetic fields are substantially amplified, contributing to the higher SERS sensitivity and lower detection limit. The excellent SERS stability of Ag/SiNWAs is attributed to the presence of the SiO2 nanolayer around Ag NPs that prevented the Ag NP surface from being oxidized. The calibration of the Raman peak intensities of rhodamine 6G and thiram allowed their quantitative detection. Our finding is a significant advance in developing SERS substrates for the fast and quantitative detection of trace organic molecules.
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Estrogen metabolite 2-methoxyestradiol prevents hypertension in deoxycorticosterone acetate-salt rats.
Cardiovasc Drugs Ther
PUBLISHED: 07-06-2013
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Our early work showed that the estrogen metabolite 2-methoxyestradiol (2ME) inhibits proliferation of vascular smooth muscle cells (SMCs) and vascular contractility through an endothelium-dependent mechanism. The aim of this study was to examine whether 2ME prevents the development of hypertension in rats.
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Uric Acid Levels in Obstructive Sleep Apnea Patients with Atrial Fibrillation.
Arch. Med. Res.
PUBLISHED: 06-27-2013
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The objective of this observational study was to determine whether there is an association between atrial fibrillation (AF) and uric acid and to identify the risk markers for AF in obstructive sleep apnea (OSA).
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Variations of morphology and photosynthetic performances of Ulva prolifera during the whole green tide blooming process in the Yellow Sea.
Mar. Environ. Res.
PUBLISHED: 06-14-2013
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Since 2007, the worlds largest macroalgal blooms have occurred along the coastal area of the Yellow Sea for 6 consecutive years. In 2012, shipboard surveying and satellite remote sensing were used to monitor the whole blooming process. The blooms originated in Rudong sea area of the South Yellow Sea where bloom patches were of dark green and filamentous thalli were the dominant morphology. The scale of the blooms reached its peak size in Rizhao sea area of the North Yellow Sea, and decreased promptly and became insignificant in Qingdao coast where the blooms turned yellow, mostly with air sac blades. Meanwhile, vegetative cells of the green tide algae changed into cytocysts gradually from which germ cells were released as the blooms drifted northward. Additionally, chlorophyll contents and fluorescence activity of free-floating thalli in the North Yellow Sea were both significantly lower than that in the South Yellow Sea. Those studies presented here contributed to increasing our understanding about how the green tide declined gradually in the North Yellow Sea.
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[Sequences analysis of jlFABP2 and the correlation between polymorphisms and body weight gain in Cyprinus carpio var. jian].
Yi Chuan
PUBLISHED: 06-05-2013
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Two replicate intestine fatty acid binding protein genes (jlFABP2a and jlFABP2b) were cloned from Cyprinus carpio var. jian using PCR. Both ORFs were 399 bp in length sharing 92.2% similarity with each other, and 88.0% and 90.5% with their counterpart in zebrafish, respectively. The gene structure of jlFABP2s was same as other FABPs, which contained four exons and three introns. Sequences and lengths of introns between 2a and 2b. were obviously different Phylogenetic tree displayed that two jlFABP2s corresponded to one zebrafish FABP2 which matches the fact that the chromosome number of common carp was twice of zebrafish. Real time-PCR showed that jlFABP2 genes mainly expressed in intestine and the expression level was very significantly higher than other tissues such as brain, liver, muscle, kidney, and gonad (P<0.01). The expression level of jlFABP2a was significantly (male, P<0.05) or very significantly (females, P<0.01) higher than 2b in intestine; and 2b was expressed slightly higher than 2a in other tissues. It seemed that 2a expressed specifically in intestine, while 2b expressed ubiquitously. Twelve and four SNP loci were found at jlFABP2a and 2b introns through comparison sequences from 8 individuals, respectively. Genotypes of I1-A15G, I1-A99G, I2-C487T, and I3-A27T on jlFABP2a were detected using PCR-RFLP in selection population of C. carpio var. jian. The SNP genotypes and individual weight gain correlation indicated that four SNPs were significantly (P<0.05 or P<0.01) associated with adult weight gain. Diplotype analysis displayed that individuals with genotype AGGGCCXX or AGGGXXAT grew faster than other individuals by 15%. The individuals with these two genotypes only occupied 9% in total selection populations, indicating the presence of large selection space. The 4 SNPs detected in this experiment can be used in C. carpio var. Jian growth selection breeding plan.
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Theoretical Studies on Gas-Phase Reactions of Sulfuric Acid Catalyzed Hydrolysis of Formaldehyde and Formaldehyde with Sulfuric Acid and H2SO4···H2O Complex.
J Phys Chem A
PUBLISHED: 06-05-2013
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The gas-phase reactions of sulfuric acid catalyzed hydrolysis of formaldehyde and formaldehyde with sulfuric acid and H2SO4···H2O complex are investigated employing the high-level quantum chemical calculations with M06-2X and CCSD(T) theoretical methods and the conventional transition state theory (CTST) with Eckart tunneling correction. The calculated results show that the energy barrier of hydrolysis of formaldehyde in gas phase is lowered to 6.09 kcal/mol from 38.04 kcal/mol, when the sulfuric acid is acted as a catalyst at the CCSD(T)/aug-cc-pv(T+d)z//M06-2X/6-311++G(3df,3pd) level of theory. Furthermore, the rate constant of the sulfuric acid catalyzed hydrolysis of formaldehyde combined with the concentrations of the species in the atmosphere demonstrates that the gas-phase hydrolysis of formaldehyde of sulfuric acid catalyst is feasible and could be of great importance for the sink of formaldehyde, which is in previously forbidden hydrolysis reaction. However, it is shown that the gas-phase reactions of formaldehyde with sulfuric acid and H2SO4···H2O complex lead to the formation of H2C(OH)OSO3H, which is of minor importance in the atmosphere.
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Evolutionary increases in defense during a biological invasion.
Oecologia
PUBLISHED: 05-07-2013
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Invasive plants generally escape from specialist herbivores of their native ranges but may experience serious damage from generalists. As a result, invasive plants may evolve increased resistance to generalists and tolerance to damage. To test these hypotheses, we carried out a common garden experiment comparing 15 invasive populations with 13 native populations of Chromolaena odorata, including putative source populations identified with molecular methods and binary choice feeding experiments using three generalist herbivores. Plants from invasive populations of C. odorata had both higher resistance to three generalists and higher tolerance to simulated herbivory (shoot removal) than plants from native populations. The higher resistance of plants from invasive populations was associated with higher leaf C content and densities of leaf trichomes and glandular scales, and lower leaf N and water contents. Growth costs were detected for tolerance but not for resistance, and plants from invasive populations of C. odorata showed lower growth costs of tolerance. Our results suggest that invasive plants may evolve to increase both resistance to generalists and tolerance to damage in introduced ranges, especially when the defense traits have low or no fitness costs. Greater defenses in invasive populations may facilitate invasion by C. odorata by reducing generalist impacts and increasing compensatory growth after damage has occurred.
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An Experimental Study Addressing the Promotion of Mandibular Defect Repair Through the Intermittent Subcutaneous Injection of Parathyroid Hormone.
J. Oral Maxillofac. Surg.
PUBLISHED: 05-02-2013
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Parathyroid hormone (PTH) is a major regulator of bone metabolism. Various animal studies and clinical trials have addressed the treatment of osteoporosis and fracture healing with the intermittent administration of PTH, whereas few studies have investigated the effects of PTH on mandibular defect repair. This study sought to examine the feasibility of using recombinant human PTH (rhPTH) to promote the repair of mandibular defects and to provide a preliminary investigation of the underlying mechanisms of this phenomenon.
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Modulation of multifunctional N,O,P ligands for enantioselective copper-catalyzed conjugate addition of diethylzinc and trapping of the zinc enolate.
Chem Asian J
PUBLISHED: 04-19-2013
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In this work, we have successfully synthesized a new family of chiral Schiff base–phosphine ligands derived from chiral binaphthol (BINOL) and chiral primary amine. The controllable synthesis of a novel hexadentate and tetradentate N,O,P ligand that contains both axial and sp3-central chirality from axial BINOL and sp3-central primary amine led to the establishment of an efficient multifunctional N,O,P ligand for copper-catalyzed conjugate addition of an organozinc reagent. In the asymmetric conjugate reaction of organozinc reagents to enones, the polymer-like bimetallic multinuclear Cu-Zn complex constructed in situ was found to be substrate-selective and a highly excellent catalyst for diethylzinc reagents in terms of enantioselectivity (up to >99?%?ee). More importantly, the chirality matching between different chiral sources, C2-axial binaphthol and sp3-central chiral phosphine, was crucial to the enantioselective induction in this reaction. The experimental results indicated that our chiral ligand (R,S,S)-L1- and (R,S)-L4-based bimetallic complex catalyst system exhibited the highest catalytic performance to date in terms of enantioselectivity and conversion even in the presence of 0.005?mol?% of catalyst (S/C = 20?000, turnover number (TON) = 17,600). We also studied the tandem silylation or acylation of enantiomerically enriched zinc enolates that formed in situ from copper-L4-complex-catalyzed conjugate addition, which resulted in the high-yield synthesis of chiral silyl enol ethers and enoacetates, respectively. Furthermore, the specialized structure of the present multifunctional N,O,P ligand L1 or L4, and the corresponding mechanistic study of the copper catalyst system were investigated by 31P?NMR spectroscopy, circular dichroism (CD), and UV/Vis absorption.
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[The heating effect of the Er3+/Yb3+ doped Y2O3 nanometer powder by 980 nm laser diode pumping].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 04-17-2013
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The Er3+ and Yb3+ doped Y2O3 Nano powder was prepared by sol-gel method. Based on 2H11/2 --> 4I15/2 and 4S3/2 --> 4I15/2 green conversion luminescence intensity rate of Er3+, the sample surface temperature changes caused by the increase in 980 nm diode laser pump power were studied. The results show that with pump power increasing, the sample surface temperature substantially rises. And the surface temperature reached to 820 K when the pump power was 1 000 mW. The phenomenon plays an important role in the analysis of upconversion process, especially with saturation power. And this feature has a potential application prospect in the biomedicine, soft tissue hole burning as well as the field of temperature sensing materials.
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Identification and differential expression of human carcinoma-associated antigens in hepatocellular carcinoma tissues.
Exp. Biol. Med. (Maywood)
PUBLISHED: 04-12-2013
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This study was designed to identify and verify hepatocellular carcinoma (HCC)-associated human carcinoma antigens (HCAs) that may be useful as tumor markers for HCC. We found that BCE075 and BCD021 anti-HCA antibodies were immunostained in the liver tissue samples and showed specific staining. Their expression was increased in HCC compared with normal liver tissues (P = 0.008). Immunoprecipitation and mass spectrometry analyses of the proteins precipitated by these two antibodies were identified to be cytoskeleton-associated protein 4 (CLIMP63) and brain-type glycogen phosphorylase (PYGB). This study demonstrated that HCC tissues expressed specific HCA glycoproteins, suggesting that our mouse monoclonal anti-HCA antibodies could be useful for immunohistochemical analysis of HCA expression as potential biomarkers for HCC diagnosis.
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AAV-mediated expression of an ADAMTS13 variant prevents shigatoxin-induced thrombotic thrombocytopenic purpura.
Blood
PUBLISHED: 03-20-2013
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Severe deficiency of plasma ADAMTS13 activity causes thrombotic thrombocytopenic purpura (TTP), a life-threatening syndrome for which plasma is the only effective therapy currently available. As much as 5% of TTP cases are hereditary, resulting from mutations of the ADAMTS13 gene. Here, we report the efficacy and safety of recombinant adeno-associated virus serotype 8 (AAV8)-mediated expression of a murine ADAMTS13 variant (MDTCS), truncated after the spacer domain, in a murine model of TTP. Administration of AAV8-hAAT-mdtcs at doses greater than 2.6 × 10(11) vg/kg body weight resulted in sustained expression of plasma ADAMTS13 activity at therapeutic levels. Expression of the truncated ADAMTS13 variant eliminated circulating ultralarge von Willebrand factor multimers, prevented severe thrombocytopenia, and reduced mortality in Adamts13(-/-) disease-prone mice triggered by shigatoxin-2. These data support AAV vector-mediated expression of a comparable truncated ADAMTS13 variant as a novel therapeutic approach for hereditary TTP in humans.
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