bluuebunny/crossref_metadata_2025_split huggingface dataset:
Measurement of human sensation for developing sensible textiles
Authors: Lee Myungeun , Cho Gilsoo 
Published: January 2009

AbstractHuman perceptive faculties consist of 5 senses: visual, auditory, olfactory, taste, and tactile sense. Visual is the most powerful sense for human perception followed by the auditory sense. This article attempts to find the connection between the visual and the auditory senses. In particular, the aim is to convert sound to color based on human perception. Natural sounds were selected as stimuli and analyzed by sound color and psychoacoustic factors. In addition, subjective perception was evaluated, and electroencephalogram (EEG) was measured using psychophysiological methods in 20 participants. From the factor analysis results of subjective responses, 4 factors were determined: Emotion, Action, Atmosphere, and Strength. To convert sounds to colors, a multidimensional scale analysis was performed using the results of the EEG responses. Bird sound was converted to green, wave sound to red, and rain sound to red‐purple. The results were presented by textile designs. From these results, the ability of natural sounds to convert to colors was proven, so that the transformed colors can be used to help design textiles. © 2009 Wiley Periodicals, Inc.
Development of a usability evaluation framework with quality function deployment: From customer sensibility to product design
Authors: Jin Beom Suk , Ji Yong Gu , Choi Kyeyoun , Cho Gilsoo 
Published: January 2009

AbstractThe aim of this research was to develop a usability evaluation model based on customer sensation using quality function deployment (QFD), which evaluates the relationship between consumer sensation and usability among the physical design factors of dishwashers. Four aspects of the evaluation model were analyzed with QFD: overall sensation factors, detail sensation factors, usability evaluation factors, and physical design factors of products in 3 sequential processes. The sensation evaluation factors and the usability evaluation factors were created from the results of the sensation and usability tests. Moreover, experts and manufacturers were involved in selecting the physical design factors. With the evaluation model using these 4 aspects, physical design factors influencing user sensation were generated. These factors were Label Icon, Rack Size, Shape of Knob, and LCD size. In addition, the degree of influences was tested and design guidelines derived from the final physical design factors were generated. © 2009 Wiley Periodicals, Inc.
Running wild: Neurogenesis in the hippocampus across the lifespan in wild and laboratory‐bred Norway rats
Authors: Epp Jonathan Richard , Barker Jennifer Marie , Galea Liisa Ann Margaret 
Published: January 2009

AbstractThe dogmatic view that new neurons are not produced in the adult mammalian brain has been overturned in light of mounting evidence that neurogenesis continues to occur within two neurogenic niches, the subventricular zone and the hippocampus. In mammals, new neurons are incorporated into the hippocampus throughout life and are influenced by environmental and genetic factors. Most studies use captive‐bred animals, and no previous studies have examined neurogenesis in free‐living rats despite the common use of laboratory rats. In particular, exercise upregulates neurogenesis in the hippocampus and exercise levels would certainly differ between wild and captive populations. Therefore, it is unclear whether results from captive populations can be generalized to natural populations or reflect variations from an artificial and inappropriate “baseline” level. To address this, we compared levels of cell proliferation and the number of immature neurons (using the endogenous markers Ki67 and doublecortin, respectively) in captured wild juvenile and adult Norway rats to three captive strains (Sprague‐Dawley, Long‐Evans, and Brown Norway) of the same species. Here, we show that the level of cell proliferation and young immature neuron survival in the dentate gyrus of juvenile wild rats is significantly higher than in Sprague‐Dawley rats, but not Long‐Evans or Brown Norway rats. However, cell proliferation and the number of immature neurons in the hippocampus of adult wild rats are within the normal range of captive‐bred rats at all adult ages examined. This finding is surprising given the dissimilar environments, including stressors and opportunities for exercise, encountered by each population. © 2009 Wiley‐Liss, Inc.
Hippocampus‐dependent learning is associated with adult neurogenesis in MRL/MpJ mice
Authors: Thuret Sandrine , Toni Nicolas , Aigner Stefan , Yeo Gene W. , Gage Fred H. 
Published: January 2009

AbstractThe hippocampus is involved in declarative memory and produces new neurons throughout adulthood. Numerous experiments have been aimed at testing the possibility that adult neurogenesis is required for learning and memory. However, progress has been encumbered by the fact that abating adult neurogenesis usually affects other biological processes, confounding the interpretation of such experiments. In an effort to circumvent this problem, we used a reverse approach to test the role of neurogenesis in hippocampus‐dependent learning, exploiting the low levels of adult neurogenesis in the MRL/MpJ strain of mice compared with other mouse strains. We observed that adult MRL/MpJ mice produce 75% fewer new neurons in the dentate gyrus than age‐matched C57BL/6 mice. Learning‐induced synaptic remodeling, spatial learning, and visual recognition learning were reduced in MRL/MpJ mice compared with C57BL/6 mice. When MRL/MpJ mice were allowed unlimited access to running wheels, neurogenesis along with spatial learning and visual recognition learning were increased to levels comparable to those in running C57BL/6 mice. Together, these results suggest that adult neurogenesis is correlated with spatial learning and visual recognition learning, possibly by modulating morphological plasticity in the dentate gyrus. © 2009 Wiley‐Liss, Inc.
Hippocampal synapsin isoform levels are linked to spatial memory enhancement by SGS742
Authors: John Julius Paul Pradeep , Sunyer Berta , Höger Harald , Pollak Arnold , Lubec Gert 
Published: January 2009

AbstractSynapsins are essential proteins for synaptic plasticity and there is no information available for their role in cognitive enhancement (CE) of spatial memory formation. It was therefore the aim of the study to link individual synapsin proteins and their isoforms to spatial memory formation enhanced by SGS742 in the mouse. Extracted hippocampal proteins from a cognitive study treating OF1 mice with the cognitive enhancer SGS742 and tested in the Morris water maze, were run on two‐dimensional gel electrophoresis. Subsequently, protein spots were unambiguously identified by qQ‐TOF mass spectrometry. Quantification of proteins from four groups (NaCl‐treated mice, SGS742‐treated mice, SGS742‐treated yoked controls, and NaCl‐treated yoked controls) was carried out according to an in‐gel stable isotope labeling method. A total of 17 protein spots representing synapsin isoforms were identified and quantified. Using quantification of individual synapsin isoforms showed that these can be clearly assigned to CE by the GABAB antagonist SGS742. Quantitative determination of individual synapsin isoform showed an increase in SGS742‐treated mice (mean ± SD) of ratios between light and heavy stable isotope labeled synapsin protein (SGS742 vs. controls: 2.19 ± 0.41 for synapsin Ia, and 1.41 ± 0.81 for synapsin IIa). Synapsins Ib and IIb were not linked to CE. The NaCl‐treated controls and the use of yoked controls that were ruling out swimming‐ and stress‐mediated changes of synapsins, unequivocally allow to propose a role for synapsins Ia and IIa in the mechanism of CE of spatial memory formation. © 2009 Wiley‐Liss, Inc.
Down‐regulation of the expression of RB18A/MED1, a cofactor of transcription, triggers strong tumorigenic phenotype of human melanoma cells
Authors: Ndong Jean de La Croix , Jean Didier , Rousselet Nathalie , Frade Raymond 
Published: January 2009

AbstractThe RB18A/MED1 human gene, also named TRAP220, DRIP205 and PBP, encodes for a single 205 kDa component, which interacts with nuclear receptors and transcription factors. RB18A/MED1 chromosome localization on locus 17q12‐q21.1 suggests its involvement in human cancers. We herein analyzed RB18A/MED1 expression in human melanoma cell lines. We found that RB18A/MED1 is either highly or weakly expressed in melanoma cells, depending on their respectively non or highly‐tumorigenic phenotype. We therefore investigated the possible existence of a relationship between the RB18A/MED1 expression level and melanoma cell phenotype. For this purpose, we down‐regulated RB18A/MED1 expression by transfecting melanoma cells with a RB18A/MED1 small interfering RNA (siRNA), specific to the 3′‐untranslated region of native RB18A/MED1 RNA, already demonstrated to inhibit specifically RB18A/MED1 protein expression. A nonspecific (scrambled) siRNA was used as control. This RB18A/MED1 siRNA did not modify the expression of cathepsin L forms or lamin A/C, nor the secretion of procathepsin L and MMP2 in transfected cells. Analysis using a microarray membrane with 113 cancer‐related genes, western blot and specific tests, demonstrated that RB18A/MED1 knockdown significantly inhibits tissue inhibitor of metalloproteinase‐3 expression, and increases uPAR expression, two genes well known to be involved in melanoma cell invasion, through modifications of the tumor microenvironment. Indeed, RB18A/MED1 knockdown in melanoma cells in vitro increased their invasive properties, without modification of cell proliferation. Furthermore, RB18A/MED1 knockdown in vivo switched melanoma phenotype from non to strongly‐tumorigenic in nude mice. Our data thus demonstrated for the first time that a decrease of RB18A/MED1 expression in human melanoma cells increases their tumorigenic phenotype. © 2009 Wiley‐Liss, Inc.
Molecular markers predict outcome in squamous cell carcinoma of the head and neck after concomitant cisplatin‐based chemoradiation
Authors: van den Broek Guido B. , Wildeman Maarten , Rasch Coen R.N. , Armstrong Nicola , Schuuring Ed , Begg Adrian C. , Looijenga Leendert H.J. , Scheper Rik , van der Wal Jacqueline E. , Menkema Lorian , van Diest Paul J. , Balm Alfons J.M. , van Velthuysen Marie‐Louise F. , van den Brekel Michiel W.M. 
Published: January 2009

AbstractNot all patients with squamous cell carcinomas of the head and neck (HNSCC) benefit from concurrent cisplatin‐based chemoradiation, but reliable predictive markers for outcome after chemoradiation are scarce. We have investigated potential prognostic biomarkers for outcome in a large group of patients. Ninety‐one tumor biopsies taken from consecutive HNSCC patients were evaluated for protein expression on a tissue microarray. Using immunohistochemistry, 18 biomarkers, involved in various cellular pathways were investigated. Univariable and multivariable proportional hazard analyses were performed to investigate associations between each individual marker and outcome. In addition, the global test was used to test all variables simultaneously and selected combinations of markers for an overall association with local control. Univariable analysis showed statistically significant increased relative risks of RB, P16 and MRP2 for local control and MDR1 and HIF‐1α for overall survival. MRP2, MDR1 and P16 levels were positively associated with outcome whereas RB and HIF‐1α had a negative relationship. Using Goeman's global testing no combination of markers was identified that was associated with local control. Grouping the markers according to their function revealed an association between a combination of 3 markers (P16, P21 and P27) and outcome (p= 0.05) was found. In the multivariable analysis, MRP2 and RB remained significant independent predictive markers for local control. This study describes the prognostic value of biomarkers for the outcome in patients uniformly treated with concurrent chemoradiation. MRP2 and RB were found to be associated with outcome in patients treated with concurrent chemoradiation. © 2009 Wiley‐Liss, Inc.
Retracted: Overexpression of Aurora A by loss of CHFR gene expression increases the growth and survival of HTLV‐1‐infected T cells through enhanced NF‐κB activity
Authors: Tomita Mariko , Toyota Minoru , Ishikawa Chie , Nakazato Tetsuro , Okudaira Taeko , Matsuda Takehiro , Uchihara Jun‐Nosuke , Taira Naoya , Ohshiro Kazuiku , Senba Masachika , Tanaka Yuetsu , Ohshima Koichi , Saya Hideyuki , Tokino Takashi , Mori Naoki 
Published: January 2009

AbstractRetraction: The following article has been retracted through agreement between the first author and several coauthors, the journal Editor‐in‐Chief, Peter Lichter, and John Wiley & Sons, Ltd.: Tomita M, Toyota M, Ishikawa C, Nakazato T, Okudaira T, Matsuda T, Uchihara JN, Taira N, Ohshiro K, Senba M, Tanaka Y, Ohshima K, Saya H, Tokino T, Mori N. (2009). Overexpression of Aurora A by loss of CHFR gene expression increases the growth and survival of HTLV‐1‐infected T cells through enhanced NF‐kappaB activity. Int J Cancer; 124 (June (11)): 2607‐2615, published online on 12 JAN 2009 in Wiley Online Library (www.onlinelibrary.wiley.com). After an investigation the retraction has been agreed due to inappropriate duplication of images and overlap with other published work.
The prognostic value of cytology and fluorescence in situ hybridization in the follow‐up of nonmuscle‐invasive bladder cancer after intravesical Bacillus Calmette‐Guérin therapy
Authors: Savic Spasenija , Zlobec Inti , Thalmann George N. , Engeler Daniel , Schmauss Martina , Lehmann Kurt , Mattarelli Gianfranco , Eichenberger Tobias , Dalquen Peter , Spieler Peter , Schoenegg René , Gasser Thomas C. , Sulser Tullio , Forster Thomas , Zellweger Tobias , Casella Roberto , Bubendorf Lukas 
Published: January 2009

AbstractMolecular markers reliably predicting failure or success of Bacillus Calmette‐Guérin (BCG) in the treatment of nonmuscle‐invasive urothelial bladder cancer (NMIBC) are lacking. The aim of our study was to evaluate the value of cytology and chromosomal aberrations detected by fluorescence in situ hybridization (FISH) in predicting failure to BCG therapy. Sixty‐eight patients with NMIBC were prospectively recruited. Bladder washings collected before and after BCG instillation were analyzed by conventional cytology and by multitarget FISH assay (UroVysion®, Abbott/Vysis, Des Plaines, IL) for aberrations of chromosomes 3, 7, 17 and 9p21. Persistent and recurrent bladder cancers were defined as positive events during follow‐up. Twenty‐six of 68 (38%) NMIBC failed to BCG. Both positive post‐BCG cytology and positive post‐BCG FISH were significantly associated with failure of BCG (hazard ratio (HR)= 5.1 and HR= 5.6, respectively; p < 0.001 each) when compared to those with negative results. In the subgroup of nondefinitive cytology (all except those with unequivocally positive cytology), FISH was superior to cytology as a marker of relapse (HR= 6.2 and 1.4, respectively). Cytology and FISH in post‐BCG bladder washings are highly interrelated and a positive result predicts failure to BCG therapy in patients with NMIBC equally well. FISH is most useful in the diagnostically less certain cytology categories but does not provide additional information in clearly malignant cytology. © 2009 UICC
Ascochlorin activates p53 in a manner distinct from DNA damaging agents
Authors: Jeong Ji‐Hak , Nakajima Hiroo , Magae Junji , Furukawa Chiharu , Taki Keiko , Otsuka Kensuke , Tomita Masanori , Lee In‐Seon , Kim Cheorl‐Ho , Chang Hyeun‐Wook , Min Kwan‐Sik , Park Kwang‐Kyun , Park Kwan‐Kyu , Chang Young‐Chae 
Published: January 2009

AbstractAscochlorin, a prenylphenol antitumor antibiotic, profoundly increases the expression of endogenous p53 by increasing protein stability in the human osteosarcoma cells and human colon cancer cells. Ascochlorin also increases DNA binding activity to the p53 consensus sequence in nuclear extract and enhances transcription of p53 downstream targets. Ascochlorin specifically induces p53 phosphorylation at ser 392 without affecting ser 15 or 20, whereas DNA damaging agents typically phosphorylate these serines. Moreover, ascochlorin does not induce phosphorylation of ATM and CHK1, an established substrate of ATR that is activated by genotoxins, nor does it increase DNA strand break, as confirmed by comet assay. The structure‐activity relationship suggests that p53 activation by ascochlorin is related to inhibition of mitochondrial respiration, which is further supported by the observation that respiratory inhibitors activate p53 in a manner similar to ascochlorin. These results suggest that ascochlorin, through the inhibition of mitochondrial respiration, activates p53 through a mechanism distinct from genotoxins. © 2009 UICC
A cohort study of cancer among sarcoidosis patients
Authors: Boffetta Paolo , Rabkin Charles S. , Gridley Gloria 
Published: January 2009

AbstractSarcoidosis is a chronic inflammatory condition that may increase the risk of cancer, but limited information is available on occurrence of cancer in these patients. We compared the incidence of cancer among 2,013 White and 3,755 Black male patients admitted to Veterans hospitals in the United States during 1969–1996 with a diagnosis of sarcoidosis, with that of 2,792,503 White and 662,204 Black nonsarcoidosis patients admitted to the same hospitals. Patients suffering from pulmonary and autoimmune diseases were excluded from the study, as was the first year of follow‐up after first admission for sarcoidosis. A total of 241 malignant neoplasms were diagnosed in sarcoidosis patients [relative risk 0.99, 95% confidence interval (CI) 0.87–1.13]. The risks of rectal cancer (relative risk 2.12; 95% CI 1.27–3.52), colon cancer (relative risk 1.55; 95% CI 0.99–2.43) and kidney cancer (relative risk 1.84; 95% CI 1.02–3.33) were increased in sarcoidosis patients when compared with other Veterans hospital patients, whereas the risk of lung cancer was decreased (relative risk 0.60; 95% CI 0.42–0.85). The risk of kidney cancer remained elevated 10 years after first admission. Results were generally consistent among ethnic groups, although the increased risk of colon and kidney cancer was observed only in White patients. These results provide further evidence for an increased risk of specific cancers in patients with sarcoidosis, but do not support any additional increase in overall cancer risk. © 2009 Wiley‐Liss, Inc.
Modulation of pentose phosphate pathway during cell cycle progression in human colon adenocarcinoma cell line HT29
Authors: Vizán Pedro , Alcarraz‐Vizán Gema , Díaz‐Moralli Santiago , Solovjeva Olga N. , Frederiks Wilma M. , Cascante Marta 
Published: January 2009

AbstractCell cycle regulation is dependent on multiple cellular and molecular events. Cell proliferation requires metabolic sources for the duplication of DNA and cell size. However, nucleotide reservoirs are not sufficient to support cell duplication and, therefore, biosynthetic pathways should be upregulated during cell cycle. Here, we reveal that glucose‐6‐phosphate dehydrogenase (G6PDH) and transketolase (TKT), the 2 key enzymes of oxidative and nonoxidative branches of the pentose phosphate pathway (PPP), respectively, which is necessary for nucleotide synthesis, are enhanced during cell cycle progression of the human colon cancer cell line HT29. These enhanced enzyme activities coincide with an increased ratio of pentose monophosphate to hexose monophosphate pool during late G1 and S phase, suggesting a potential role for pentose phosphates in proliferating signaling. Isotopomeric analysis distribution of nucleotide ribose synthesized from 1,2‐13C2‐glucose confirms the activation of the PPP during late G1 and S phase and reveals specific upregulation of the oxidative branch. Our data sustain the idea of a critical oxidative and nonoxidative balance in cancer cells, which is consistent with a late G1 metabolic check point. The distinctive modulation of these enzymes during cell cycle progression may represent a new strategy to inhibit proliferation in anticancer treatments. © 2009 UICC
Transforming growth factor‐β induces CD44 cleavage that promotes migration of MDA‐MB‐435s cells through the up‐regulation of membrane type 1‐matrix metalloproteinase
Authors: Kuo Yi‐Chih , Su Cheng‐Hsi , Liu Chin‐Yi , Chen Tien‐Hua , Chen Chie‐Pein , Wang Hwai‐Shi 
Published: January 2009

AbstractCD44, a transmembrane receptor for hyaluronic acid, is implicated in various adhesion‐dependent cellular processes, including cell migration, tumor cell metastasis and invasion. Recent studies demonstrated that CD44 expressed in cancer cells can be proteolytically cleaved at the ectodomain by membrane type 1‐matrix metalloproteinase (MT1‐MMP) to form soluble CD44 and that CD44 cleavage plays a critical role in cancer cell migration. Here, we show that transforming growth factor‐β (TGF‐β), a multifunctional cytokine involved in cell proliferation, differentiation, migration and pathological processes, induces MT1‐MMP expression in MDA‐MB‐435s cells. TGF‐β‐induced MT1‐MMP expression was blocked by the specific extracellular regulated kinase‐1/2 (ERK1/2) inhibitor PD98059 and the specific phosphoinositide 3‐OH kinase (PI3K) inhibitor LY294002. In addition, treatment with SP600125, an inhibitor for c‐Jun NH2‐terminal kinase (JNK), resulted in a significant inhibition of MT1‐MMP production. These data suggest that ERK1/2, PI3K, and JNK likely play a role in TGF‐β‐induced MT1‐MMP expression. Interestingly, treatment of MDA‐MB‐435s cells with TGF‐β resulted in a colocalization of MT1‐MMP and CD44 in the cell membrane and in an increased level of soluble CD44. Using an electric cell‐substrate impedance sensing cell‐electrode system, we demonstrated that TGF‐β treatment promotes MDA‐MB‐435s cell migration, involving MT1‐MMP‐mediated CD44 cleavage. MT1‐MMP siRNA transfection‐inhibited TGF‐β‐induced cancer cell transendothelial migration. Thus, this study contributes to our understanding of molecular mechanisms that play a critical role in tumor cell invasion and metastasis. © 2009 Wiley‐Liss, Inc.
The SAAP force field: Development of the single amino acid potentials for 20 proteinogenic amino acids and Monte Carlo molecular simulation for short peptides
Authors: Iwaoka Michio , Kimura Naoki , Yosida Daisuke , Minezaki Toshiya 
Published: January 2009

AbstractMolecular simulation by using force field parameters has been widely applied in the fields of peptide and protein research for various purposes. We recently proposed a new all‐atom protein force field, called the SAAP force field, which utilizes single amino acid potentials (SAAPs) as the fundamental elements. In this article, whole sets of the SAAP force field parameters in vacuo, in ether, and in water have been developed by ab initio calculation for all 20 proteinogenic amino acids and applied to Monte Carlo molecular simulation for two short peptides. The side‐chain separation approximation method was employed to obtain the SAAP parameters for the amino acids with a long side chain. Monte Carlo simulation for Met‐enkephalin (CHO‐Tyr‐Gly‐Gly‐Phe‐Met‐NH2) by using the SAAP force field revealed that the conformation in vacuo is mainly controlled by strong electrostatic interactions between the amino acid residues, while the SAAPs and the interamino acid Lennard‐Jones potentials are predominant in water. In ether, the conformation would be determined by the combination of the three components. On the other hand, the SAAP simulation for chignolin (H‐Gly‐Tyr‐Asp‐Pro‐Glu‐Thr‐Gly‐Thr‐Trp‐Gly‐OH) reasonably reproduced a native‐like β‐hairpin structure in water although the C‐terminal and side‐chain conformations were different from the native ones. It was suggested that the SAAP force field is a useful tool for analyzing conformations of polypeptides in terms of intrinsic conformational propensities of the single amino acid units. © 2009 Wiley Periodicals, Inc. J Comput Chem, 2009