bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chicken α‐globin switching depends on autonomous silencing of the embryonic π globin gene by epigenetics mechanisms
Authors: Rincón‐Arano Héctor , Guerrero Georgina , Valdes‐Quezada Christian , Recillas‐Targa Félix 
Published: August 2009

AbstractSwitching in hemoglobin gene expression is an informative paradigm for studying transcriptional regulation. Here we determined the patterns of chicken α‐globin gene expression during development and erythroid differentiation. Previously published data suggested that the promoter regions of α‐globin genes contain the complete information for proper developmental regulation. However, our data show a preferential trans‐activation of the embryonic α‐globin gene independent of the developmental or differentiation stage. We also found that DNA methylation and histone deacetylation play key roles in silencing the expression of the embryonic π gene in definitive erythrocytes. However, drug‐mediated reactivation of the embryonic gene during definitive erythropoiesis dramatically impaired the expression of the adult genes, suggesting gene competition or interference for enhancer elements. Our results also support a model in which the lack of open chromatin marks and localized recruitment of chicken MeCP2 contribute to autonomous gene silencing of the embryonic α‐globin gene in a developmentally specific manner. We propose that epigenetic mechanisms are necessary for in vivo chicken α‐globin gene switching through differential gene silencing of the embryonic α‐globin gene in order to allow proper activation of adult α‐globin genes. J. Cell. Biochem. 108: 675–687, 2009. © 2009 Wiley‐Liss, Inc.
Estradiol decreases xanthine dehydrogenase enzyme activity and protein expression in non‐tumorigenic and malignant human mammary epithelial cells
Authors: Taibi Gennaro , Carruba Giuseppe , Miceli Vitale , Cocciadiferro Letizia , Nicotra Concetta M.A. 
Published: August 2009

AbstractThe retinoic acid deficiency in breast tumour epithelial cells has been ascribed to an insufficient expression of either the enzyme(s) involved in its biosynthesis or the cellular retinol binding protein (CRBP) or both. In an attempt to define the mechanisms underpinning retinoic acid deficiency in these cell model systems, we have investigated the potential regulatory effect of oestrogen (17β‐estradiol) on one key player in retinoic acid biosynthesis, the xanthine dehydrogenase (XDH). This enzyme is consistently expressed and very active in non‐malignant human mammary epithelial cells (HMEC), as opposed to tumour MDA‐MB231 and MCF7 cells. In these latter two cell lines, as opposed to HMEC cells, we observe a residual ability of XDH to produce retinoic acid from retinaldehyde and the inability to use retinol, as a consequence of a deficit in CRBP. In addition, estradiol treatment of MDA‐MB231 and MCF7 cells decreases protein expression and activity of the enzyme, with no modification of the mRNA transcript levels, eventually leading to deteriorate further retinoic acid production. J. Cell. Biochem. 108: 688–692, 2009. © 2009 Wiley‐Liss, Inc.
Clonal mesenchymal stem cells derived from human bone marrow can differentiate into hepatocyte‐like cells in injured livers of SCID mice
Authors: Tao Xin‐Rong , Li Wen‐Lin , Su Juan , Jin Cai‐Xia , Wang Xin‐Min , Li Jian‐Xiu , Hu Jun‐Kai , Xiang Zhen‐Hua , Lau Joseph T.Y. , Hu Yi‐Ping 
Published: August 2009

AbstractThere is increasing evidence that human mesenchymal stem cells (hMSCs) can be a valuable, transplantable source of hepatocytes. Most of the hMSCs preparations used in these studies were likely heterogeneous cell populations, isolated by adherence to plastic surfaces or by density gradient centrifugation. Therefore, the participation of other unknown trace cell populations cannot be rigorously discounted. Here we report the isolation and establishment of a cloned human MSC line (chMSC) from human bone marrow primary culture, through which we confirmed the hepatic differentiation capability of authentic hMSCs. chMSCs expressed markers of mesenchymal cells, but not markers of hematopoietic stem cells. In vitro, chMSCs can differentiate into either mesenchymal cells or cells exhibiting hepatocyte‐like phenotypes. When transplanted intrasplentically into carbon tetrachloride‐injured livers of SCID mice, EGFP‐tagged chMSCs engrafted into the host liver parenchyma, exhibited typical hepatocyte morphology, form a three‐dimensional architecture, and differentiate into hepatocyte‐like cells expressing human albumin and α‐1‐anti‐trypsin. By confocal microscopy, ultrafine intercellular nanotubular structures were visible between adjacent transplanted and host hepatocytes. We postulate that these structures may assist in the phenotype conversion of chMSCs, possibly by exchange of cytoplasmic components between native hepatocytes and transplanted cells. Thus, a clonal pure population of hMSCs, which can be expanded in culture, may have potential as a cellular source for substitution damaged cells in hepatic injury. J. Cell. Biochem. 108: 693–704, 2009. © 2009 Wiley‐Liss, Inc.
Swiprosin‐1 is expressed in mast cells and up‐regulated through the protein kinase CβI/η pathway
Authors: Thylur Ramesh P. , Kim Young‐Dae , Kwon Min‐Sung , Oh Hyun‐Mee , Kwon Ho‐Keun , Kim Sang‐Hyun , Im Sin‐Hyeog , Chun Jang‐Soo , Park Zee‐Yong , Jun Chang‐Duk 
Published: August 2009

AbstractSwiprosin‐1 exhibits the highest expression in CD8+ T cells and immature B cells and has been thought to play a role in lymphocyte physiology. Here we report that swiprosin‐1 is also expressed in mast cells and up‐regulated in both in vitro cultured mast cells by phorbol ester and in vivo model tissues of passive cutaneous anaphylaxis and atopic dermatitis. Targeted inhibition of the specific protein kinase C (PKC) isotypes by siRNA revealed that PKC‐βI/η are involved in the expression of swiprosin‐1 in the human mast cell line HMC‐1. In contrast, down‐regulation of swiprosin‐1 by A23187 or ionomycin suggests that calcium‐signaling plays a negative role. The ectopic expression of swiprosin‐1 augmented PMA/A23187‐induced NF‐κB promoter activity, and resulted in increased expression of cytokines. Moreover, knock‐down of swiprosin‐1 attenuated PMA/A23187‐induced cytokine expression. Collectively, these results suggest that swiprosin‐1 is a PKC‐βI/η‐inducible gene and it modulates mast cell activation through NF‐κB‐dependent pathway. J. Cell. Biochem. 108: 705–715, 2009. © 2009 Wiley‐Liss, Inc.
Hemoglobin induces the expression of indoleamine 2,3‐dioxygenase in dendritic cells through the activation of PI3K, PKC, and NF‐κB and the generation of reactive oxygen species
Authors: Ogasawara Nanako , Oguro Takashi , Sakabe Toshitsugu , Matsushima Miyoko , Takikawa Osamu , Isobe Ken‐ichi , Nagase Fumihiko 
Published: August 2009

AbstractIndoleamine 2,3‐dioxygenase (IDO) is the rate‐limiting enzyme in the kynurenine (Kyn) pathway of tryptophan (Trp) metabolism. IDO is immunosuppressive and is induced by inflammation in macrophages and dendritic cells (DCs). Previous studies have shown the serum Kyn/Trp levels in patients with hemolytic anemia to be notably high. In the present study, we demonstrated that hemoglobin (Hb), but not hemin or heme‐free globin (Apo Hb), induced IDO expression in bone marrow‐derived myeloid DCs (BMDCs). Hb induced the phosphorylation and degradation of IκBα. Hb‐induced IDO expression was inhibited by inhibitors of PI3‐kinase (PI3K), PKC and nuclear factor (NF)‐κB. Hb translocated both RelA and p52 from the cytosol to the nucleus and induced the intracellular generation of reactive oxygen species (ROS). Hb‐induced IDO expression was inhibited by anti‐oxidant N‐acetyl‐L‐cysteine (NAC) or mixtures of SOD and catalase, however, IDO expression was enhanced by 3‐amino‐1,2,4‐triazole, an inhibitor of catalase, suggesting that the generation of ROS such as O, H2O2, and hydroxyl radical is required for the induction of IDO expression. The generation of ROS was inhibited by a PKC inhibitor, and this action was further enhanced by addition of a PI3K inhibitor. Hb induced Akt phosphorylation, which was inhibited by a PI3K inhibitor and enhanced by a PKC inhibitor. These results suggest that the activation of NF‐κB through the PI3K‐PKC‐ROS and PI3K‐Akt pathways is required for the Hb‐induced IDO expression in BMDCs. J. Cell. Biochem. 108: 716–725, 2009. © 2009 Wiley‐Liss, Inc.
N‐glycosylation of ATF6β is essential for its proteolytic cleavage and transcriptional repressor function to ATF6α
Authors: Guan Dongyin , Wang Hao , Li Veronica E. , Xu Yingying , Yang Min , Shen Zonghou 
Published: August 2009

AbstractActivating transcription factor 6 (ATF6), a member of the ATF/CREB family of transcription factors, has two isoforms of 90‐kDa (p90ATF6α) and 110‐kDa (p110 ATF6β) as endoplasmic reticulum (ER) transmembrane glycoprotein. ATF6β contains five evolutionarily conserved N‐linked glycosylation sites and is a key transcriptional repressor of ATF6α, which contribute to regulating the strength and duration of ATF6‐dependent ER stress response (ERSR) gene induction. Although it is well established that p110ATF6β can be cleaved and generate a nuclear form of 60‐kDa (p60ATF6β) that inhibits ATF6α‐mediated ERSR genes activation, the functional significance of p110 ATF6β N‐linked glycosylation is unknown. Herein, we found that the fully unglycosylated ATF6β cannot be proteolytic cleaved, be detectable in nucleus after dithiothreitol treatment, and repress the transcriptional activity of ATF6α. These results provide the first evidence that unglycosylated ATF6β may directly facilitate the expression of ERSR genes by losing its repressor function to ATF6α. J. Cell. Biochem. 108: 825–831, 2009. © 2009 Wiley‐Liss, Inc.
Involvement of the JNK activation in terbinafine‐induced p21 up‐regulation and DNA synthesis inhibition in human vascular endothelial cells
Authors: Hsu Sung‐Po , Ho Pei‐Yin , Liang Yu‐Chih , Ho Yuan‐Soon , Lee Wen‐Sen 
Published: August 2009

AbstractPreviously, we demonstrated that the extracellular signal‐regulated kinase (ERK)‐mediated pathway contributes to the terbinafine (TB)‐induced increases of p21 and p53 protein level as well as decrease of DNA synthesis in human umbilical venous endothelial cells (HUVEC). The aim of this study is to examine the involvement of c‐Jun NH2‐terminal kinase (JNK) in the TB‐induced increase of p21 protein level and DNA synthesis inhibition. Western blot analysis and kinase assay demonstrated that TB treatment increased both the protein level and the kinase activity of JNK1/2 in HUVEC. Transfection of HUVEC with JNK1 dominant negative (DN‐JNK1) prevented the TB‐induced increases of p21 and p53 protein level and decrease of DNA synthesis, suggesting that JNK1/2 activation is involved in the TB‐induced cell cycle arrest in HUVEC. Moreover, over‐expression of mitogen‐activated protein kinase (MEK)‐1 prevented the TB‐induced increase of JNK1/2 protein levels, suggesting that MEK‐1 is an upstream inhibitor of JNK. Transfection of HUVEC with DN‐JNK1 prevented the TB‐induced inhibition of ERK phosphorylation, suggesting that JNK1/2 might serve as a negative regulator of ERK. Taken together, our results suggest that JNK activation is involved in the TB‐induced inhibition of ERK phosphorylation, p53 and p21 up‐regulation and DNA synthesis inhibition in HUVEC. J. Cell. Biochem. 108: 860–866, 2009. © 2009 Wiley‐Liss, Inc.
Reliability and validity of the youth outcome questionnaire self‐report
Authors: Ridge Nathanael W. , Warren Jared S. , Burlingame Gary M. , Wells M. Gawain , Tumblin Katherine M. 
Published: August 2009

AbstractThe psychometric properties of an adolescent mental health outcome instrument (Youth Outcome Questionnaire Self‐Report version [Y‐OQ‐SR]) were examined. Participants were 206 adolescents (ages 12–18; mean age=15). The Y‐OQ‐SR was evaluated in terms of its internal consistency, test‐retest reliability, and concurrent validity. Criterion measures included the Behavior Assessment System for Children, Self‐Report of Personality—Adolescent Version (SRP), and the Child Behavior Checklist Youth Self Report (YSR). Analyses revealed very good internal consistency and test‐retest reliability of the Y‐OQ‐SR total score and subscales, and moderate to good concurrent validity with the SRP and YSR. The Y‐OQ‐SR appears to be a valid and reliable self‐report measure of psychosocial distress that warrants further study in youth psychotherapy research. © 2009 Wiley Periodicals, Inc. J Clin Psychol 65:1–12, 2009.
An efficient method for synthesis of pyrano[3,2‐c]pyridine derivatives under microwave irradiation
Authors: Wang Shu‐Liang , Han Zheng‐Guo , Tu Shu‐Jiang , Zhang Xiao‐Hong , Yan Shu , Hao Wen‐Juan , Shi Feng , Cao Xu‐Dong , Wu Shan‐Shan 
Published: August 2009

Abstract
magnified imageA series of pyrano[3,2‐c]pyridine derivatives were synthesized via reactions of 3,5‐dibenzylidene‐piperidin‐4‐one and malononitrile in N,N‐dimethylformamide under microwave irradiation. It is a simple, efficient, and promising synthetic method to construct pyrano[3,2‐c]pyridine skeleton. J. Heterocyclic Chem., (2009).
Homology modeling and molecular dynamics simulations of Dengue virus NS2B/NS3 protease: insight into molecular interaction
Authors: Wichapong Kanin , Pianwanit Somsak , Sippl Wolfgang , Kokpol Sirirat 
Published: August 2009

AbstractThe pathogenic West Nile virus (WNV) and Dengue virus (DV) are growing global threats for which there are no specific treatments. Both viruses possess a two component NS2B/NS3 protease which cleaves viral precursor proteins. Whereas for the WNV protease two crystal structures in complex with an inhibitor have been solved recently, no such information is available for the DV protease. Here, we report the generation of a homology model of DV NS2B/NS3 protease. Since it is known from the related WNV protease that it adopts a distinct conformation in free and in inhibitor‐complexed form, a special emphasis was given to the analysis of the protease flexibility. Therefore, several models of DV NS2B/NS3 protease complexed with the peptidic inhibitor (Bz‐Nle(P4)‐Lys(P3)‐Arg(P2)‐Arg(P1)‐H) were generated. The first DV protease model (DV‐1) was constructed using the available crystal structure of the apo DV NS2B/NS3 protease. The second model (DV‐2) was built taking the WNV NS3/NS2B protease in the inhibitor‐complexed form as the template structure. Molecular dynamics simulations which were carried out for the WNV crystal structures as well as for the DV models provided an understanding of the role of NS2B for maintaining the protease in the active conformation. It was also demonstrated that NS2B is not only important for maintaining NS3 in the active form, but is also essential for establishing the interaction between residues from the S2 pocket and the peptidic inhibitor. The DV NS2B/NS3 model in the productive conformation can now be used for structure‐based design purposes. Copyright © 2009 John Wiley & Sons, Ltd.
A loop in the N‐lobe of human serum transferrin is critical for binding to the transferrin receptor as revealed by mutagenesis, isothermal titration calorimetry, and epitope mapping
Authors: Mason Anne B. , Byrne Shaina L. , Everse Stephen J. , Roberts Samantha E. , Chasteen N. Dennis , Smith Valerie C. , MacGillivray Ross T. A. , Kandemir Banu , Bou‐Abdallah Fadi 
Published: August 2009

AbstractTransferrin (TF) is a bilobal transport protein that acquires ferric iron from the diet and holds it tightly within the cleft of each lobe (thereby preventing its hydrolysis). The iron is delivered to actively dividing cells by receptor mediated endocytosis in which diferric TF preferentially binds to TF receptors (TFRs) on the cell surface and the entire complex is taken into an acidic endosome. A combination of lower pH, a chelator, inorganic anions, and the TFR leads to the efficient release of iron from each lobe. Identification of residues/regions within both TF and TFR required for high affinity binding has been an ongoing goal in the field. In the current study, we created human TF (hTF) mutants to identify a region critical to the interaction with the TFR which also constitutes part of an overlapping epitope for two monoclonal antibodies (mAbs) to the N‐lobe, one of which was previously shown to block binding of hTF to the TFR. Four single point mutants, P142A, R143A, K144A, and P145A in the N‐lobe, were placed into diferric hTF. Isothermal titration calorimetry (ITC) revealed that three of the four residues (Pro142, Lys144, and Pro145) in this loop are essential to TFR binding. Additionally, Lys144 is common to the recognition of both mAbs which show different sensitivities to the three other residues. Taken together these studies prove that this loop is required for binding of the N‐lobe of hTF to the TFR, provide a more precise description of the role of each residue in the loop in the interaction with the TFR, and confirm that the N‐lobe is essential to high affinity binding of diferric hTF to TFR. Copyright © 2009 John Wiley & Sons, Ltd.
Raman spectroscopy of conducting poly (methyl methacrylate)/polyaniline dodecylbenzenesulfonate blends
Authors: Shakoor Abdul , Rizvi Tasneem Zahra 
Published: August 2009

AbstractPolyaniline soluble in organic solvents was prepared using dodecylbenzenesulphonic acid (DBSA) as functional dopant. The solubility parameter was calculated and the most suitable solvent chloroform was checked for the solubility and the most compatible polymer PMMA was selected for blending. Miscibility was maximized with 1% by weight of hydroquinone. Blending of doped polyaniline with dodecylbenzenesulphonic acid (PAni.DBSA) in poly (methyl methacrylate) (PMMA) was explained by a change in the conformation of the polymeric chains leading to an increase in the conductivity. The electrical conductivity increased as the weight percent of PAni.DBSA increased, showing a percolation threshold as low as 3.0% by weight and the highest conductivity was achieved at 20% by wt of PAni.DBSA. Scanning electron micrographs showed lowest level of phase separation. Raman spectroscopy is used to characterize the blending process of two polymers aiming to understand the transformations in different types of charged segments. Raman results give complementary data about the blending process showing that together with the structural change of the polymeric chains, there is also a chemical transformation of these polymers. Analysis of Raman spectra was done investigating the relative intensities of the bands at 574 cm−1 and 607 cm−1. A relationship between conductivity and Raman was also proposed. Copyright © 2009 John Wiley & Sons, Ltd.
Research on the Raman spectral character and diagnostic value of squamous cell carcinoma of oral mucosa
Authors: Li Yi , Wen Zhi‐Ning , Li Long‐Jiang , Li Meng‐Long , Gao Ning , Guo Yan‐Zhi 
Published: August 2009

AbstractEarly diagnosis of oral carcinomas is essential for successful treatment. The purpose of the present study is to apply near‐infrared Raman spectroscopy to detect oral squamous cell carcinoma (SCC) and leukoplakia (OLK), in order to establish the diagnostic model of the Raman spectra of oral diseases. We collected Raman spectra of normal, OLK and SCC by near‐infrared Fourier transform Raman spectroscopy. The biochemical variations between different lesions were analyzed by the characteristic bands in the subtracted mean spectra. Gaussian radial basis function support vector machines (SVM) were used to classify spectra and establish the diagnostic models. Major differences were observed in the range between 800 and 1800 cm−1. Compared with normal mucosa, high contents of protein, DNA and lipid in SCC and OLK were observed, but the difference between OLK and normal tissue was not as much as that between normal and SCC. SVM displayed a powerful ability in the classifying of normal and SCC, and the specificity, sensitivity and accuracy were 100, 97.56 and 98.75%, respectively. In discriminating between the OLK and normal groups, the three parameters were 85, 68 and 72.5%. The algorithm showed good ability in grouping and modeling of OLK and SCC, and the three parameters were 95, 97.43 and 96.25%. Combined with SVM, near‐infrared Raman spectroscopy can detect biochemical variations in oral normal mucosa, OLK and SCC, and establish diagnostic models accurately. Copyright © 2009 John Wiley & Sons, Ltd.
Cochlear implantation following treatment for medulloblastoma
Authors: Roland J. Thomas , Cosetti Maura , Liebman Tracey , Waltzman Susan , Allen Jeffrey C. 
Published: August 2009

AbstractObjectives/Hypothesis:Medulloblastoma is the most common pediatric malignant tumor of the central nervous system in children. Treatment includes surgical excision, external beam radiation, and multiagent chemotherapy. Otologic sequelae are common and may result from radiation and/or chemotherapy. Profound sensorineural hearing loss (SNHL) is a known complication of neuro‐oncologic treatment and may render these patients eligible for cochlear implantation (CI). Issues of CI in this population, including diagnosis, treatment of preoperative middle ear disease, operative and postoperative course, performance data, and long‐term tumor surveillance are highlighted and reviewed.Study Design:Retrospective chart review.Methods:Three patients treated for pediatric medulloblastoma with surgical resection, postoperative hyperfractioned craniospinal radiotherapy, and multiagent adjuvant chemotherapy who underwent cochlear implantation were identified. Details of neuro‐oncologic treatment and associated otologic complications are presented and analyzed. Primary outcome assessment includes treatment of middle ear pathology, perioperative cochlear implant course, and postimplantation performance data.Results:Each patient required surgical treatment of chronic ear disease 4 to 16 years after chemoradiation. All progressed to profound SNHL and were implanted 8 to 17 years post–neuro‐oncologic treatment. There were no intraoperative complications, and full insertion of the cochlear implant electrode array was achieved in each patient. One patient developed postoperative wound dehiscence requiring operative closure. Postimplantation performance data support significant benefit in all patients.Conclusions:Patients treated for pediatric medulloblastoma develop otologic sequelae, including profound SNHL, and may require cochlear implantation. Successful management of middle ear and mastoid pathology involves consideration of potential future cochlear implantation. Postoperative performance data supports cochlear implantation in this population. Laryngoscope, 2010