bluuebunny/crossref_metadata_2025_split huggingface dataset:
Brain systems for baroreflex suppression during stress in humans
Authors: Gianaros Peter J. , Onyewuenyi Ikechukwu C. , Sheu Lei K. , Christie Israel C. , Critchley Hugo D. 
Published: May 2011

AbstractThe arterial baroreflex is a key mechanism for the homeostatic control of blood pressure (BP). In animals and humans, psychological stressors suppress the capacity of the arterial baroreflex to control short‐term fluctuations in BP, reflected by reduced baroreflex sensitivity (BRS). While animal studies have characterized the brain systems that link stressor processing to BRS suppression, comparable human studies are lacking. Here, we measured beat‐to‐beat BP and heart rate (HR) in 97 adults who performed a multisource interference task that evoked changes in spontaneous BRS, which were quantified by a validated sequence method. The same 97 participants also performed the task during functional magnetic resonance imaging (fMRI) of brain activity. Across participants, task performance (i) increased BP and HR and (ii) reduced BRS. Analyses of fMRI data further demonstrated that a greater task‐evoked reduction in BRS covaried with greater activity in brain systems important for central autonomic and cardiovascular control, particularly the cingulate cortex, insula, amygdala, and midbrain periaqueductal gray (PAG). Moreover, task performance increased the functional connectivity of a discrete area of the anterior insula with both the cingulate cortex and amygdala. In parallel, this same insula area showed increased task‐evoked functional connectivity with midbrain PAG and pons. These novel findings provide human evidence for the brain systems presumptively involved in suppressing baroreflex functionality, with relevance for understanding the neurobiological mechanisms of stressor‐related cardiovascular reactivity and associated risk for essential hypertension and atherosclerotic heart disease. Hum Brain Mapp, 2011. © 2011 Wiley‐Liss, Inc.
Chemical tags: Applications in live cell fluorescence imaging
Authors: Wombacher Richard , Cornish Virginia W. 
Published: May 2011

AbstractTechnologies to visualize cellular structures and dynamics enable cell biologists to gain insight into complex biological processes. Currently, fluorescent proteins are used routinely to investigate the behavior of proteins in live cells. Chemical biology techniques for selective labeling of proteins with fluorescent labels have become an attractive alternative to fluorescent protein labeling. In the last ten years the progress in the development of chemical tagging methods have been substantial offering a broad palette of applications for live cell fluorescent microscopy. Several methods for protein labeling have been established, using protein tags, peptide tags and enzyme mediated tagging. This review focuses on the different strategies to achieve the attachment of fluorophores to proteins in live cells and cast light on the advantages and disadvantages of each individual method. Selected experiments in which chemical tags have been successfully applied to live cell imaging will be discussed and evaluated. (© 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Diabetic retinopathy and signaling mechanism for activation of matrix metalloproteinase‐9
Authors: Mohammad Ghulam , Kowluru Renu A. 
Published: May 2011

AbstractIn the pathogenesis of diabetic retinopathy, H‐Ras (a small molecular weight G‐protein) and matrix metalloproteinase‐9 (MMP9) act as pro‐apoptotic, accelerating the apoptosis of retinal capillary cells, a phenomenon that predicts its development and the activation of MMP9 is under the control of H‐Ras. The goal of this study is to elucidate the cellular mechanism by which H‐Ras activates MMP9 culminating in the development of diabetic retinopathy. Using isolated retinal endothelial cells, the effect of regulation of H‐Ras downstream signaling cascade, Raf‐1, MEK, and ERK, was investigated on glucose‐induced activation of MMP9. In vitro results were confirmed in the retina obtained from diabetic mice manipulated for MMP9 gene, and also in the retinal microvasculature obtained from human donors with diabetic retinopathy. Regulation of Raf‐1/MEK/ERK by their specific siRNAs and pharmacologic inhibitors prevented glucose‐induced activation of MMP9 in retinal endothelial cells. In MMP9‐KO mice, diabetes had no effect on retinal MMP9 activation, and H‐Ras/Raf‐1/MEK signaling cascade remained normal. Similarly, donors with diabetic retinopathy had increased MMP9 activity in their retinal microvessels, the site of histopathology associated with diabetic retinopathy, and this was accompanied by activated H‐Ras signaling pathway (Raf‐1/ERK). Collectively, these results suggest that Ras/Raf‐1/MEK/ERK cascade has an important role in the activation of retinal MMP9 resulting in the apoptosis of its capillary cells. Understanding the upstream mechanism responsible for the activation of MMP9 should help identify novel molecular targets for future pharmacological interventions to inhibit the development/progression of diabetic retinopathy. J. Cell. Physiol. 227: 1052–1061, 2012. © 2011 Wiley Periodicals, Inc.
MicroRNAs in the midst of myeloid signal transduction
Authors: Stoffers Sara L. , Meyer Sara E. , Grimes H. Leighton 
Published: May 2011

AbstractMicroRNA (miRNA) play important roles in the development and physiological function of hematopoietic stem/progenitor and mature cell lineages. In addition, deregulated miRNA expression and subsequent gene expression changes are associated with hematologic diseases including myelodysplastic syndromes and acute myeloid leukemia. This review focuses on myelopoiesis as a model to highlight the involvement of miRNA in the regulation of normal and malignant cellular signaling pathways. By incorporating miRNA regulation into well‐established myeloid signal transduction pathways, we hope to shed light on targetable factors both upstream and downstream of miRNA signaling. These pathway‐specific miRNA functions suggest scenarios wherein miRNA‐based therapeutics may be beneficial either alone or in combination with current therapies. J. Cell. Physiol. 227: 525–533, 2012. © 2011 Wiley Periodicals, Inc.
HIV‐1 Nef perturbs the function, structure, and signaling of the Golgi through the Src Kinase Hck
Authors: Hiyoshi Masateru , Takahashi‐Makise Naoko , Yoshidomi Yuka , Chutiwitoonchai Nopporn , Chihara Takashi , Okada Masato , Nakamura Nobuhiro , Okada Seiji , Suzu Shinya 
Published: May 2011

AbstractThe interaction between HIV‐1 Nef and the Src kinase Hck in macrophages has been shown to accelerate the progression to AIDS. We previously showed that Nef disturbed the N‐glycosylation/trafficking of Fms, a cytokine receptor essential for maintaining macrophages in an anti‐inflammatory state, in an Hck‐dependent manner. Here, we show the underlying molecular mechanism of this effect. Using various Hck isoforms and their mutants and Golgi‐targeting Hck mutants, we confirmed that Hck activation at the Golgi causes the Nef‐induced Fms N‐glycosylation defect. Importantly, we found that both the co‐expression of Nef and Hck and the expression of a Golgi‐targeted active Hck mutant caused alterations in the distribution of GM130, a Golgi protein that was shown to be required for efficient protein glycosylation. Moreover, the activation of Hck at the Golgi caused strong serine phosphorylation of the GM130‐interacting Golgi structural protein GRASP65, which is known to induce Golgi cisternal unstacking. Using pharmacological inhibitors, we also found that the activation of Hck at the Golgi followed by the activation of the MAP kinase ERK‐GRASP65 cascade is involved in the Fms N‐glycosylation defect. These results suggest that Nef perturbs the structure and signaling of the Golgi by activating Hck at the Golgi, and thereby, induces the N‐glycosylation/trafficking defect of Fms, which is in line with the idea that Src family kinases are crucial Golgi regulators. J. Cell. Physiol. 227: 1090–1097, 2012. © 2011 Wiley Periodicals, Inc.
Stromal cell‐derived factor‐1/CXC receptor 4 and β1 integrin interaction regulates urokinase‐type plasminogen activator expression in human colorectal cancer cells
Authors: Huang Wen‐Shih , Chin Chih‐Chien , Chen Cheng‐Nan , Kuo Yi‐Hung , Chen Te‐Chuan , Yu Hong‐Ren , Tung Shui‐Yi , Shen Chien‐Heng , Hsieh Yung‐Yu , Guo Su‐Er , Shi Chung‐Sheng , Liu Ta‐Ju , Kuo Hsing‐Chun 
Published: May 2011

AbstractThe stromal cell‐derived factor‐1 (SDF‐1)/CXC receptor 4 (CXCR4) axis has been shown to play a role in colorectal cancer progression. In addition, the protease urokinase‐type plasminogen activator (uPA) is an important factor in tumor cell invasion and metastasis. However, the mechanism by which SDF‐1 mediates uPA expression in human colorectal cancer cells remains unknown. We investigated the molecular mechanism governing the interaction between SDF‐1 stimulation and uPA expression in three human colon cancer cell lines (DLD‐1, SW48, and COLO 205). We found that SDF‐1 stimulation led to an increase in the expression and secretion of uPA in these cells. Experiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitogen‐activated protein kinase (MAPK) and phosphatidylinositol 3‐kinase (PI3K)/Akt pathways are critical for SDF‐1‐induced uPA expression. Analysis of transcription factor binding using ELISA and chromatin immunoprecipitation assays revealed that SDF‐1 increased Sp1‐ and AP‐1‐DNA‐binding activities in DLD‐1 cells. Inhibition of Sp1 and AP‐1 activation blocked the SDF‐1‐induced expression and activity of the uPA promoter. The effect of SDF‐1 on DLD‐1 signaling and uPA expression was mediated by the CXCR4/β1 integrin axis. In summary, our findings elucidate the mechanisms of SDF‐1/CXCR4 downstream signaling and provide insights into the function of SDF‐1 in colon cancer cells. J. Cell. Physiol. 227: 1114–1122, 2012. © 2011 Wiley Periodicals, Inc.
Role of lipoxin A4 in the cell‐to‐cell interaction between all‐trans retinoic acid‐treated acute promyelocytic leukemic cells and alveolar macrophages
Authors: Tsai Wen‐Hui , Shih Chung‐Hung , Wu Hung‐Yi , Chien Hong‐Yu , Chiang Yee‐Chen , Lai Shu‐Lien , Hsu Shau‐Chieh , Kou Yu Ru , Hsu Hui‐Chi 
Published: May 2011

AbstractDifferentiation therapy with all‐trans retinoic acid (ATRA) has been used successfully to treat acute promyelocytic leukemia (APL), but such treatment also causes differentiation syndrome (DS) by inducing APL cell infiltration into alveolar spaces. The mechanism underlying the clearance of infiltrated APL cells has not been investigated in detail. Lipoxin A4 (LXA4) is an important anti‐inflammatory mediator during the resolution of inflammation. In this study, the role of LXA4 in the cell–cell interaction between alveolar macrophages (AMϕ; NR8383 cells) and APL NB4 cells was investigated and found that conditioned medium (CM) harvested from ATRA‐treated NR8383 (ATRA‐NR8383) cells was able to induce the transmigration of ATRA‐NB4 cells. However, the pro‐migratory activity of CM was attenuated progressively when ATRA‐NR8383 cells were co‐cultured with increased cell dosages of apoptotic NB4 cells. A significantly higher amount of LXA4 was released into the CM by ATRA‐NR8383 cells when they were co‐cultured with apoptotic ATRA‐NB4 cells. Expression of a receptor for LXA4 (ALX/FPR2) was enhanced in both ATRA‐NB4 cells and ATRA‐NR8383 cells. Exogenous LXA4 treatment was able to inhibit the transmigration of ATRA‐NB4 cells and induce the phagocytic clearance of apoptotic cells by ATRA‐NR8383 cells. The anti‐migratory activity of exogenous LXA4 was attenuated by pre‐treating ATRA‐NB4 cells with an ALX/FPR2 inhibitor. We conclude that AMϕ‐derived LXA4 plays an important role in the interaction between AMϕ and APL cells and that this contributes to clearance of apoptotic APL cells. J. Cell. Physiol. 227: 1123–1129, 2012. © 2011 Wiley Periodicals, Inc.
Free fatty acids induce transglutaminase 2‐dependent apoptosis in hepatocytes via ER stress‐stimulated PERK pathways
Authors: Kuo Ting‐Fang , Tatsukawa Hideki , Matsuura Tomokazu , Nagatsuma Keisuke , Hirose Shigehisa , Kojima Soichi 
Published: May 2011

AbstractNon‐alcoholic steatohepatitis (NASH), a progressive form of fatty liver, shares histological similarities with alcoholic steatohepatitis (ASH), including accumulated fat, hepatic apoptosis, and fibrous tissues in the liver, but the molecular mechanisms responsible for hepatic apoptosis remain unclear. We previously reported that transglutaminase 2 (TG2), induced in the nuclei of ethanol‐treated hepatocytes, crosslinks and inactivates the transcription factor Sp1, leading to hepatic apoptosis. In this study, we investigated whether a similar change is involved in NASH, and if so, how TG2 and crosslinked Sp1 (CLSp1) are induced. Elevated nuclear TG2 and CLSp1 formation was demonstrated in NASH patients, as well as increased activation of apoptosis inducing factor (AIF) and release of cytochrome c. In Hc human normal hepatocytes treated with free fatty acids (FFAs), biochemical analyses revealed that ethanol and FFAs provoked fat accumulation, endoplasmic reticulum (ER) stress, increased nuclear factor kappa B (NFκB), and nuclear TG2. Salubrinal, a selective inhibitor of the ER stress‐induced pancreatic ER kinase (PERK) signaling pathway, inhibited NFκB activation, nuclear TG2 expression, and apoptosis only if it was induced by FFAs, but not by ethanol. These results suggest that FFAs could increase ER stress and lead to nuclear NFκB activation and TG2 induction through PERK‐dependent pathways, resulting in TG2‐mediated apoptosis accompanying crosslinking and inactivation of Sp1, activation of AIF, and release of cytochrome c. J. Cell. Physiol. 227: 1130–1137, 2012. © 2011 Wiley Periodicals, Inc.
Role of senescent fibroblasts on alkali‐induced corneal neovascularization
Authors: Zhou Qingjun , Yang Lingling , Qu Mingli , Wang Yao , Chen Peng , Wang Yiqiang , Shi Weiyun 
Published: May 2011

AbstractCellular senescence acts as a potent regulator of tumor suppression and fibrosis limitation; however, its contribution and crosstalk with neovascularization during normal wound healing has not been examined. Here, we explored the role of senescent fibroblasts on neovascularization with a mouse model of alkali‐induced corneal wound healing. Senescent cells accumulated in corneal stroma from day 7 to 27 after alkali burn and peaked on day 14, which was consistent with the development of corneal neovascularization (CNV). In vitro and in vivo assays confirmed that the senescent cells were derived primarily from activated corneal fibroblasts. Furthermore, senescent corneal fibroblasts exhibited enhanced synthesis and secretion of extracellular matrix‐degrading enzymes (matrix metalloproteinases 2, 3, and 14 and tissue‐ and urokinase‐type plasminogen activators) and angiogenic factors (vascular endothelial growth factor) and decreased expression of anti‐angiogenic factors (pigment epithelium‐derived factor and thrombospondins), which supported the proliferation, migration, and promotion of tube formation of vascular endothelial cells. Intrastromal injection of premature senescent fibroblasts induced CNV earlier than that of normal fibroblasts, while matrix metalloproteinase inhibitors blocked the early onset of senescent cell‐induced CNV. Therefore, senescent fibroblasts promoted the alkali‐induced CNV partially via the enhanced secretion of matrix metalloproteases. J. Cell. Physiol. 227: 1148–1156, 2012. © 2011 Wiley Periodicals, Inc.
Human nuclear clusterin mediates apoptosis by interacting with Bcl‐XL through C‐terminal coiled coil domain
Authors: Kim Nayoung , Yoo Jae Cheal , Han Jae Yoon , Hwang Eun Mi , Kim Yoon Sook , Jeong Eun Young , Sun Choong‐Hyun , Yi Gwan‐Su , Roh Gu Seob , Kim Hyun Joon , Kang Sang Soo , Cho Gyeong Jae , Park Jae‐Yong , Choi Wan Sung 
Published: May 2011

AbstractClusterin (CLU), a glycoprotein, is involved in apoptosis, producing two alternatively spliced isoforms in various cell types. The pro‐apoptotic CLU appears to be a nuclear isoform (nuclear clusterin; nCLU), and the secretory CLU (sCLU) is thought to be anti‐apoptotic. The detailed molecular mechanism of nCLU as a pro‐apoptotic molecule has not yet been clear. In the current study, overexpressed nCLU induced apoptosis in human kidney cells. Biochemical studies revealed that nCLU sequestered Bcl‐XL via a putative BH3 motif in the C‐terminal coiled coil (CC2) domain, releasing Bax, and promoted apoptosis accompanied by activation of caspase‐3 and cytochrome c release. These results suggest a novel mechanism of apoptosis mediated by nCLU as a pro‐apoptotic molecule. J. Cell. Physiol. 227: 1157–1167, 2012. © 2011 Wiley Periodicals, Inc.
Sorptive sequestration of 2‐chlorophenol by zeolitic materials derived from bagasse fly ash
Authors: Shah Bhavna , Tailor Ritesh , Shah Ajay 
Published: May 2011

AbstractBACKGROUND: Water pollution by toxic organic compounds is of great concern and increasingly there are demands for effective sorbents to remove them. Bagasse fly ash, a sugar industry solid waste with disposal problems, was utilized as a source for the synthesis of zeolitic material. The efficiency of virgin and synthesized material was examined for the sorption of 2‐chlorophenol.RESULTS: Zeolitic materials have been synthesized by alkaline hydrothermal and fusion methods. Zeolite P and Analcime were the major components of the zeolitic material. These materials were characterized by XRF, PXRD, FTIR and SEM and were found to have improved morphology with new crystalline phases. Batch sorption experiments for the removal of 2‐chlorophenol by virgin and zeolitic materials were carried out to evaluate isotherm capacities and kinetics of sorption processes. The Langmuir isotherm better fits the equilibrium data which concur with physical sorption. Kinetic studies showed better correlation coefficients for pseudo‐second‐order and intraparticle diffusion model, confirming that the sorption rate was controlled by film diffusion followed by pore diffusion. Desorption studies were performed to regenerate the activity of the spent sorbents. The practical utility of sorbents was tested by column study.CONCLUSION: Bagasse fly ash, readily available at very low cost was successfully converted into zeolitic material. The synthesized zeolitic material showed enhanced capacities for the sorption of 2‐chlorophenol and can be utilized as a low cost sorbent for treatment of phenolic waste‐water. Copyright © 2011 Society of Chemical Industry
Electrochemical synthesis of dimethyl carbonate from methanol, CO2 and propylene oxide in an ionic liquid
Authors: Yan Cuihong , Lu Bin , Wang Xiaoguang , Zhao Jingxiang , Cai Qinghai 
Published: May 2011

AbstractBACKGROUND: Dimethyl carbonate (DMC) can be used effectively as an environmentally benign substitute for highly toxic phosgene and dimethyl sulfate in carbonylation and methylation, as well as a promising octane booster owing to its high oxygen content. Two‐step transesterification from epoxide, methanol, and CO2 is widely used in the bulk production of DMC. However, major disadvantages of this process are high energy consumption, and high investment and production costs. A one pot synthesis of DMC from carbon dioxide, methanol, and epoxide was, therefore, developed. But the yields of DMC are below 70% due to the thermodynamic limitation.RESULTS: Electrochemical synthesis of DMC was conducted with platinum electrodes from methanol, CO2 and propylene oxide in an ionic liquid was conducted. The bmimBr (1‐butyl‐3‐methylimidazolium bromide)‐methanol‐propylene oxide system with CO2 bubbling allows DMC to be effectively synthesized and a high yield (75.5%) was achieved.CONCLUSION: In this electrolysis, redox reactions of substrates, CO2, methanol, and propylene oxide, on Pt electrodes were carried out, producing the activated particles, CH3O−, CH3OH+, CO2− and PO−, resulting in the effective synthesis of DMC with a 75.5% yield in an ionic liquid (bmimBr). Finally, a mechanism for this synthesis reaction was proposed, which is very different from those reported in the literature. Copyright © 2011 Society of Chemical Industry
Recovery of nickel from spent catalysts using ultrasonication‐assisted leaching
Authors: Oza Rachit , Shah Nikhil , Patel Sanjay 
Published: May 2011

AbstractBACKGROUND: Solid catalysts containing metals or metal oxides play a key role in the chemical process industries to produce valuable products and fuels and consequently are left as solid wastes after a certain period of use. Disposal of these spent catalysts requires compliance with stringent environmental regulations because of their hazardous nature and content of toxic chemicals. Therefore recovery of the metals by various methods has been explored. In the present study recovery of nickel from spent nickel catalysts using ultrasonication‐assisted leaching has been investigated.RESULT: The effect on nickel recovery of acid concentration, temperature, solid to liquid (S:L) ratio, and time of digestion were studied in detail and optimized for the ultrasonication route. The results obtained are compared with the chelation route and conventional acid leaching technique. Using ultrasonication‐assisted leaching 95% extraction of nickel was achieved at 90 °C, 40% nitric acid concentration and S:L ratio 1:10 (g:mL) in 50 min from the spent nickel–alumina catalysts.CONCLUSION: Using an ultrasonication technique 95% recovery of nickel was significantly faster (50 min) than the chelation route (7 h), while with conventional acid leaching a maximum of 93% nickel recovery was obtained in 9 h. Compared with conventional acid leaching the purity of leached nickel salts was good and they could be recycled for the preparation of fresh catalysts after removing Al impurities. Copyright © 2011 Society of Chemical Industry
Digital image inpainting and microscopy imaging
Authors: Stanciu Stefan G. , Hristu Radu , Stanciu George A. 
Published: May 2011

AbstractA considerable amount of image processing techniques known as inpainting techniques have been recently developed aiming to provide solutions for filling in missing or damaged regions in a digital image. Typical such techniques reconstruct a defined area by using information from its neighborhood, for example, by completing inside the missing region the isophote lines arriving at its boundaries. In this article, we show that inpainting techniques have considerable potential usefulness in microscopy imaging, even though experimenting and using them in this domain has been almost entirely neglected up until now. In this purpose, we experiment the “curvature‐preserving” partial differential equations as a solution to inpainting regions in images collected by several optical and scanning probe microscopy techniques. The results achieved are presented along with a discussion on typical problematic scenarios of microscopy imaging for which this type of techniques can provide a viable solution. Microsc. Res. Tech., 2011. © 2011 Wiley Periodicals, Inc.