bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diffusion spectral imaging modules correlate with EEG LORETA neuroimaging modules
Authors: Thatcher Robert W. , North Duane M. , Biver Carl J. 
Published: May 2011

AbstractObjectives: The purpose of this study was to test the hypothesis that the highest temporal correlations between 3‐dimensional EEG current source density corresponds to anatomical Modules of high synaptic connectivity. Methods: Eyes closed and eyes open EEG was recorded from 19 scalp locations with a linked ears reference from 71 subjects age 13–42 years. LORETA was computed from 1 to 30 Hz in 2,394 cortical gray matter voxels that were grouped into six anatomical Modules corresponding to the ROIs in the Hagmann et al.'s [2008] diffusion spectral imaging (DSI) study. All possible cross‐correlations between voxels within a DSI Module were compared with the correlations between Modules. Results: The Hagmann et al. [ 2008] Module correlation structure was replicated in the correlation structure of EEG three‐dimensional current source density. Conclusions: EEG Temporal correlation between brain regions is related to synaptic density as measured by diffusion spectral imaging. Hum Brain Mapp, 2011. © 2011 Wiley‐Liss, Inc.
Optimal design for nonlinear estimation of the hemodynamic response function
Authors: Maus Bärbel , van Breukelen Gerard J. P. , Goebel Rainer , Berger Martijn P. F. 
Published: May 2011

AbstractSubject‐specific hemodynamic response functions (HRFs) have been recommended to capture variation in the form of the hemodynamic response between subjects (Aguirre et al., [1998]: Neuroimage 8:360–369). The purpose of this article is to find optimal designs for estimation of subject‐specific parameters for the double gamma HRF. As the double gamma function is a nonlinear function of its parameters, optimal design theory for nonlinear models is employed in this article. The double gamma function is linearized by a Taylor approximation and the maximin criterion is used to handle dependency of theD‐optimal design on the expansion point of the Taylor approximation. A realistic range of double gamma HRF parameters is used for the expansion point of the Taylor approximation. Furthermore, a genetic algorithm (GA) (Kao et al., [2009]: Neuroimage 44:849–856) is applied to find locally optimal designs for the different expansion points and the maximin design chosen from the locally optimal designs is compared to maximin designs obtained bym‐sequences, blocked designs, designs with constant interstimulus interval (ISI) and random event‐related designs. The maximin design obtained by the GA is most efficient. Random event‐related designs chosen from several generated designs andm‐sequences have a high efficiency, while blocked designs and designs with a constant ISI have a low efficiency compared to the maximin GA design. Hum Brain Mapp, 2011. © 2011 Wiley‐Liss, Inc.
Self‐face recognition in social context
Authors: Sugiura Motoaki , Sassa Yuko , Jeong Hyeonjeong , Wakusawa Keisuke , Horie Kaoru , Sato Shigeru , Kawashima Ryuta 
Published: May 2011

AbstractThe concept of “social self” is often described as a representation of the self‐reflected in the eyes or minds of others. Although the appearance of one's own face has substantial social significance for humans, neuroimaging studies have failed to link self‐face recognition and the likely neural substrate of the social self, the medial prefrontal cortex (MPFC). We assumed that the social self is recruited during self‐face recognition under a rich social context where multiple other faces are available for comparison of social values. Using functional magnetic resonance imaging (fMRI), we examined the modulation of neural responses to the faces of the self and of a close friend in a social context. We identified an enhanced response in the ventral MPFC and right occipitoparietal sulcus in the social context specifically for the self‐face. Neural response in the right lateral parietal and inferior temporal cortices, previously claimed as self‐face‐specific, was unaffected for the self‐face but unexpectedly enhanced for the friend's face in the social context. Self‐face‐specific activation in the pars triangularis of the inferior frontal gyrus, and self‐face‐specific reduction of activation in the left middle temporal gyrus and the right supramarginal gyrus, replicating a previous finding, were not subject to such modulation. Our results thus demonstrated the recruitment of a social self during self‐face recognition in the social context. At least three brain networks for self‐face‐specific activation may be dissociated by different patterns of response‐modulation in the social context, suggesting multiple dynamic self‐other representations in the human brain. Hum Brain Mapp, 2011. © 2011 Wiley‐Liss, Inc.
Aryl hydrocarbon receptor‐mediated impairment of chondrogenesis and fracture healing by cigarette smoke and benzo(α)pyrene
Authors: Kung Ming H. , Yukata Kiminori , O'Keefe Regis J. , Zuscik Michael J. 
Published: May 2011

AbstractThe clinical literature strongly suggests that bone healing in cigarette smokers is impaired. Since cigarette smoke (CS) contains numerous polycyclic aromatic hydrocarbons (PAHs), and since dioxins impair bone formation in vivo via the Aryl Hydrocarbon Receptor (AHR), we investigated the impact of PAH/AHR signaling on chondrogenesis and on healing in a mouse tibial fracture model. We established that CS activates AHR signaling in fractures by up‐regulating the AHR target gene cytochrome p4501A1 (Cyp1A1). For in vitro studies, we employed the mouse limb bud micromass chondrogenesis model. After confirming that chondrocytes express AHR during differentiation, we treated cells with a prototypical PAH found in CS, benzo(α)pyrene (BaP), or cigarette smoke extract (CSE). Both BaP and CSE strongly inhibited chondrogenesis in mesenchymal cells generated from E11 limb buds, with BaP also accelerating chondrocyte hypertrophy in cultures generated from E12 limb buds. Detection of DNA adducts in the BaP‐treated cultures suggests that the distinct phenotypic effects of BaP may be due to the formation of reactive metabolites. Blockade of AHR signaling with the AHR antagonist MNF reverses the effects of BaP, but not CSE, suggesting that CSE inhibition of chondrogenesis is AHR‐independent. Correlating with these results, tibial fracture calluses from BaP‐treated mice were smaller and contained less mineralized tissue than vehicle controls. Overall, BaP is identified as a potent inhibitor of chondrogenesis in vitro with correlated effects on fracture healing similar to those of CS itself, suggesting a basis for PAHs as key compounds in the influence of CS on fracture repair. J. Cell. Physiol. 227: 1062–1070, 2012. © 2011 Wiley Periodicals, Inc.
Phosphorylation of the gastric tumor suppressor RUNX3 following H. pylori infection results in its localization to the cytoplasm
Authors: Cinghu Senthilkumar , Goh Yun‐Mi , Oh Byung‐Chul , Lee You‐Soub , Lee Ok‐Jun , Devaraj Halagowder , Bae Suk‐Chul 
Published: May 2011

AbstractAs H. pylori infection progresses, intestinal metaplasia (IM), a key event in gastric carcinogenesis, develops in the stomach. The mechanism by which H. pylori infection causes the trans‐differentiation of gastric cells to intestinal‐type cells remains an important question. In the current study, we found that RUNX3 is deregulated in all human IM specimens examined by either down regulation or mislocalization; Aberrant localization of a gastric tumor suppressor RUNX3 is observed in most human cases of IM with concurrent H. pylori infection, and RUNX3 is down‐regulated in most cases of IM without H. pylori‐infection. The cytoplasmic mislocalization of a RUNX3 was associated with H. pylori‐induced c‐Src activation and RUNX tyrosine phosphorylation. Moreover, gastric epithelial cells of Runx3−/− mice expressed the intestinal markers Muc2 and Li‐Cadherin, which suggests that the deregulation of Runx3 is a key event in the intestinalization of the gastric epithelium. Collectively, the results of the current study suggest that RUNX3 deregulation is associated with H. pylori‐induced pathogenesis and the development of IM. J. Cell. Physiol. 227: 1071–1080, 2012. © 2011 Wiley Periodicals, Inc.
TWEAK causes myotube atrophy through coordinated activation of ubiquitin‐proteasome system, autophagy, and caspases
Authors: Bhatnagar Shephali , Mittal Ashwani , Gupta Sanjay K. , Kumar Ashok 
Published: May 2011

AbstractProinflammatory cytokine TWEAK has now emerged as a key mediator of skeletal muscle‐wasting in many catabolic conditions. However, the mechanisms by which TWEAK induces muscle proteolysis remain poorly understood. Here, we have investigated the role of ubiquitin‐proteasome system, autophagy, and caspases in TWEAK‐induced muscle wasting. Addition of TWEAK to C2C12 myotubes stimulated the ubiquitination of myosin heavy chain (MyHC) and augmented the expression of E3 ubiquitin ligase MuRF1. Pretreatment of myotubes with proteasome inhibitors MG132 or lactacystin or knockdown of MuRF1 by RNAi blocked the TWEAK‐induced degradation of MyHC and myotube atrophy. TWEAK increased the expression of several autophagy‐related molecules. Moreover, the inhibitors of autophagy improved the levels of MyHC in TWEAK‐treated myotubes. TWEAK also increased activity of caspases in C2C12 myotubes. Pan‐caspase or caspase 3 inhibitory peptide inhibited the TWEAK‐induced loss of MyHC and myotube diameter. Our study demonstrates that nuclear factor‐kappa B (NF‐κB) transcription factor is essential for TWEAK‐induced expression of MuRF1 and Beclin1. Furthermore, our results suggest that caspases contribute, at least in part, to the activation of NF‐κB in response to TWEAK treatment. Collectively, the present study provides novel insight into the mechanisms of action of TWEAK in skeletal muscle. J. Cell. Physiol. 227: 1042–1051, 2012. © 2011 Wiley Periodicals, Inc.
Induction of Paneth cell degranulation by orally administered Toll‐like receptor ligands
Authors: Rumio Cristiano , Sommariva Michele , Sfondrini Lucia , Palazzo Marco , Morelli Daniele , Viganò Laura , De Cecco Loris , Tagliabue Elda , Balsari Andrea 
Published: May 2011

AbstractThe secretory activity of Paneth cells is related to the bacterial milieu in the small intestine; however, the molecules involved in inducing Paneth cell secretion of enzymes and antimicrobial peptides are not well‐defined. Mice treated orally with CpG‐oligodeoxynucleotide (ODN), an agonist of Toll‐like receptor (TLR) 9, showed rapid and massive Paneth cell degranulation. CpG‐ODN‐induced degranulation was not observed in TLR9−/− mice or in chimeric TLR9−/− mice reconstituted with wild‐type (WT) bone marrow, but was observed in WT mice reconstituted with TLR9−/− bone marrow, indicating a role for TLR9‐expressing gastrointestinal cells in CpG recognition. The TLR3 agonist polyinosinic‐polycytidylic acid also induced rapid degranulation, whereas the TLR4 and TLR5 agonists LPS and flagellin, respectively, induced late degranulation mediated by TNF‐α. Our evidence that TLR9 and TLR3 agonists induce Paneth cell degranulation points to the need for further studies of the mechanisms underlying Paneth cell function as an avenue toward preventing infection and treating inflammatory bowel diseases. J. Cell. Physiol. 227: 1107–1113, 2012. © 2011 Wiley Periodicals, Inc.
Latexin regulates the abundance of multiple cellular proteins in hematopoietic stem cells
Authors: Mitsunaga Kanae , Kikuchi Jiro , Wada Taeko , Furukawa Yusuke 
Published: May 2011

AbstractLatexin is the only known carboxypeptidase A inhibitor in mammals and shares structural similarity with cystatin C, suggesting that latexin regulates the abundance of as yet unidentified target proteins. A forward genetic approach revealed that latexin is involved in homeostasis of hematopoietic stem cells (HSCs) in mice; however, little is known about the mechanisms by which latexin negatively affects the numbers of HSCs. In this study, we found that latexin is preferentially expressed in hematopoietic stem/progenitor cells, and is co‐localized with the molecules responsible for the interaction of HSCs with a bone marrow niche, such as N‐cadherin, Tie2, and Roundabout 4. Latexin‐knockout young female mice showed an increase in the numbers of KSL (c‐Kit+/Sca‐1+/linegae marker‐negative) cells, which may be attributable to enhanced self‐renewal because latexin‐deficient KSL cells formed more colonies than their wild‐type counterparts in methylcellulose culture. Proteomic analysis of Sca‐1+ bone marrow cells demonstrated that latexin ablation reduced the abundance of multiple cellular proteins, including N‐cadherin, Tie2, and Roundabout 4. Finally, we found that latexin expression was lost or greatly reduced in approximately 50% of human leukemia/lymphoma cell lines. These results imply that latexin inhibits the self‐renewal of HSCs by facilitating the lodgment of HSCs within a bone marrow niche to maintain HSC homeostasis. J. Cell. Physiol. 227: 1138–1147, 2012. © 2011 Wiley Periodicals, Inc.
Characterization of a p‐nitrophenol‐degrading mixed culture with an improved methodology of fluorescence in situ hybridization and confocal laser scanning microscopy
Authors: Suárez‐Ojeda María Eugenia , Montón Helena , Roldán Mónica , Martín‐Hernández Mariángel , Pérez Julio , Carrera Julián 
Published: May 2011

AbstractBACKGROUND: Confocal laser scanning microscopy (CLSM) provides critical information of the presence of autofluorescence signals inherent to the samples under study, which may interfere with probe fluorescence. Therefore, it is important to determine the emission spectrum of the biomass autofluorescence under study in order to avoid, as much as possible, this wavelength range when selecting specific probe emissions and to modify, if necessary, the original fluorescence in situ hybridization (FISH) protocol in order to enhance probes signals.RESULTS: Microbial characterization of a p‐nitrophenol‐degrading activated sludge through a conventional FISH protocol was not possible because the fluorescence signal of the unlabelled cells was similar to or even higher than the signal emitted by hybridized cells, impeding the separation of the two signals and therefore, preventing biomass characterization. An optimized but simple FISH approach was developed in order to ease observation of the p‐nitrophenol‐degrading bacteria studied in this work. The final results allowed identification of Arthrobacter sp. (Micrococcaceae family) and genus Acinetobacter (Moraxellaceae family) in the p‐nitrophenol‐degrading activated sludge, whereas no hybridization was found for Pseudomonas spp.CONCLUSIONS: The hypothesis of a mixed culture following, at the same time, different degradation pathways has been confirmed through the microbial characterization of enriched p‐nitrophenol‐degrading activated sludge. Copyright © 2011 Society of Chemical Industry
Particle size distribution based evaluation of biodegradation and treatability for leachate from organic waste
Authors: Doǧruel Serdar , Köktuna Merve , Çokgör Emine Ubay , Sözen Seval , Orhon Derin 
Published: May 2011

AbstractBACKGROUND: The study evaluated the relationship between particle size distribution (PSD) of chemical oxygen demand (COD) and treatability of leachate generated by organic waste. PSD determinations were performed together with physico‐chemical and biological treatability studies. Leachate biodegradation was also evaluated by means of oxygen uptake rate (OUR) profiles and experimental results were used for calibration of the adopted mathematical model.RESULTS: The leachate was characterized by a COD content of 80 000 mg L−1 in summer. PSD analysis showed a bimodal distribution with around 60% of the COD below 2 nm and 25% above 1600 nm. Chemical treatment by lime and alum provided limited COD removal (30‐35%). The extent of COD removal was higher than the particulate COD fraction above 1600 nm, it also occurred in the soluble range below 2 nm through adsorption. A modeling study indicated three major COD fractions that could be correlated with PSD analysis: readily biodegradable COD and slowly biodegradable COD in the soluble range and hydrolyzable COD fraction in the particulate range.CONCLUSION: PSD‐based COD fractionation adequately explained limitations of chemical treatment efficiency; it was also a reliable complement to the currently used respirometric tests for biodegradation, providing insight to the fate of different COD fractions included in the soluble range (<2 nm) and yielding concrete supporting information on the generation of soluble residual microbial products. Copyright © 2011 Society of Chemical Industry
Programmed neuronal cell death induced by HIV‐1 tat and methamphetamine
Authors: Qi Li , Gang Lu , Hang Kwong Wing , Ling Choi Heung , Xiaofeng Zeng , Zhen Li , David Wai YEW , Sang Poon Wai 
Published: May 2011

AbstractApoptosis and autophagy are the two major types of programmed cell death (PCD) in neurons. Homeostatic autophagy often precedes apoptosis, and when apoptosis is blocked, the failure to keep homeostasis will lead to necrosis instead. It has been reported that human immunodeficiency virus (HIV) infected methamphetamine (Meth) abusers represent greater neuropathological abnormalities than Meth abusers or HIV‐positive non‐Meth users. Recent publications suggest that Tat and Meth when administered together result in greater neuronal damage than when administered separately. However, the cellular events of the combined Tat‐Meth effect have not yet been fully characterized. Therefore, we investigated the effects of Tat and/or Meth on apoptosis and autophagy to elucidate whether PCD was involved in Tat and/or Meth‐induced neuronal damage. Annexin‐V‐FITC/PI staining assay was used to detect cellular apoptosis using a neuroblastoma cell line SH‐SY5Y. Cellular ultrastructural changes were observed under transmission electron microscopy (TEM). Flow‐cytometric data showed apoptosis following Meth treatment, and more extensive apoptosis with Tat + Meth treatment. The most important finding was that the autophagosome and/or multilamellar bodies (MLBs) were most pronounced with Tat + Meth treatment, were less so with Meth treatment, and infrequent with Tat treatment. This suggests the involvement of autophagy and apoptosis in Tat with Meth‐elicited cell damage. However, the relation between apoptosis and autophagy remains unknown in this experiment. Further research is needed to analyze the relation among related molecules. A thorough understanding of this multifaceted relationship will be critical for the assessment of therapeutic modalities for patients with HIV with drug abuse. Microsc. Res. Tech., 2011. © 2011 Wiley Periodicals, Inc.
Zinc as an essential trace element in the acceleration of matrix vesicles‐mediated mineral deposition
Authors: Kawakubo Atsushi , Matsunaga Tsunenori , Ishizaki Hidetaka , Yamada Shizuka , Hayashi Yoshihiko 
Published: May 2011

AbstractBACKGROUND: Zinc (Zn) has a potent stimulatory effect on osteoblastic bone formation and an inhibitory effect on osteoclastic bone resorption. PURPOSE: The effect of Zn on the function of matrix vesicles (MVs) remains controversial. The purpose of this study was to investigate the effect of Zn on alkaline phosphatase (ALP) activity of osteoblasts and in the initial biological MVs‐mediated mineral deposition. STUDY DESIGN: Osteoblasts were treated with varying concentrations of Zn dissolved in culture medium. After three, five, and seven days of culture, ALP activity was assayed. For the detection of a low level of calcium concentration in MVs, X‐ray fluorescence (XRF) analyses were applied. The effect of Zn for the transformation of calcium phosphate was analyzed using a scanning electron microscope fitted with an energy dispersive X‐ray microanalysis (EDX) system. RESULTS: The ALP activity of osteoblasts in culture medium supplemented with 1 × 10−5M of Zn was significantly increased at both five and seven days. XRF data demonstrated higher levels of calcium concentration over time in the Zn‐supplemented group. EDX data showed that mineral deposits beginning on day 3 were transformed from whitlockite to calcium phosphate near hydroxyapatite, and that Zn accelerated this transformation. CONCLUSIONS: The proper concentration of Zn increased the ALP activity of osteoblasts after five and seven days of incubation. The present XRF and EDX data suggest that the increase of mineral deposition with Zn exposure for one to five days might be mediated by the activation of ALP and calcium‐binding proteins. Microsc. Res. Tech., 2011. © 2011 Wiley Periodicals, Inc.
WHY DO FIRMS PAY BRIBES? FIRM‐LEVEL EVIDENCE FROM THE CAMBODIAN GARMENT INDUSTRY
Authors: Kasuga Hidefumi 
Published: May 2011

AbstractThis paper investigates the causes and effects of bribe payments using data from garment‐producing firms in Cambodia. We uncover the reasons why firms pay bribes and describe what they receive in return. We test the hypothesis that bribe payments reduce bureaucratic delays and find that bribery can improve productivity by reducing bureaucratic delays. The evidence suggests that, if the government improves administrative services, firms can reduce unofficial payments because unavoidable bureaucratic delays compel them to pay bribes. Our evidence also suggests that foreign ownership can explain why firms are not harassed heavily in this industry. Copyright © 2011 John Wiley & Sons, Ltd.
Effect of antiviral therapy on the immunohistochemical expression of bcl‐xL and bax protein in patients with HBeAg‐negative chronic hepatitis B
Authors: Cholongitas Evangelos , Papatheodoridis George V. , Manesis Emanuel K. , Petraki Kaliopi , Tiniakos Dina , Hadziyannis Stephanos J. 
Published: May 2011

AbstractThe effect of antiviral treatment on apoptosis in chronic hepatitis B (CHB) has not been clarified. We evaluated the hepatic immunohistochemical expression of the pro‐apoptotic bax and the antiapoptotic bcl‐xL protein in HBeAg‐negative CHB patients before and after treatment. In our study we included 72 paired biopsies from 36 HBeAg‐negative CHB patients: 29 treated (interferon‐alfa: 17, adefovir: 12) and 7 untreated. Changes in expression of apoptotic proteins (D‐bax, D‐bcl‐xL), necroinflammation and fibrosis (D‐grade/D‐stage) (Ishak classification) were evaluated. We found that Bax‐positive compared to bax‐negative biopsies had worse necroinflammation (8.2 vs. 6.7, P = 0.05) and fibrosis score (3.9 vs. 3, P = 0.036). bcl‐xL‐positive compared to bcl‐xL‐negative biopsies had lower intralobular inflammation (1.6 vs. 2.2, P = 0.03). Decreased compared to stable/increased D‐bax was associated with greater improvement in necroinflammation only in treated patients (D‐grade: −4.6 vs. −1.6, P = 0.05) and greater fibrosis improvement in interferon treated patients (D‐stage: −0.4 vs. 0.55, P = 0.05). Increased compared to stable/decreased total apoptotic trend [D‐apoptosis: (D‐bax)‐(D‐bcl‐xL)], was associated with worsening fibrosis, particularly in adefovir treated patients (D‐stage: 2.3 vs. 0, P = 0.004). In the 11 patients without significant changes from 1st to 2nd biopsy, increased apoptosis was more frequent in treated than untreated cases (P = 0.046). In multivariate analysis, bax change was independently associated with change of grade (P = 0.038) and antiviral therapy (P = 0.015). In conclusions, in HBeAg‐negative CHB, histological improvement after treatment is associated with decreased hepatocyte apoptosis. In patients without substantial histological changes, treatment seems to increase the apoptosis of hepatocytes, thus having a possible protective effect on hepatocarcinogenesis. J. Med. Virol. 83:1165–1171, 2011. © 2011 Wiley‐Liss, Inc.