bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of the Sonic hedgehog pathway in squamous cell carcinoma of the skin and the mucosa of the head and neck
Authors: Schneider Sven , Thurnher Dietmar , Kloimstein Philipp , Leitner Verena , Petzelbauer Peter , Pammer Johannes , Brunner Markus , Erovic Boban M. 
Published: May 2010

AbstractBackgroundActivation of the hedgehog pathway may contribute to carcinogenesis. This study characterizes the expression pattern in squamous cell carcinoma of the skin and the head and neck.MethodsTissue microarrays were constructed with samples of squamous cell carcinoma of the skin and the head and neck. All tissue samples were immunohistochemically stained for 7 Hedgehog pathway molecules.ResultsSignificant (p < .0001) overexpression of all evaluated molecules could be observed in the tumor samples compared with healthy control tissues. Expression of Gli‐2 showed significant upregulation and that of Smoothened and Patched significant downregulation in head and neck compared with skin carcinoma. High expression of Sonic hedgehog correlates significantly (p = .001) with poor overall survival in patients with head and neck cancer.ConclusionsHedgehog signaling is differentially regulated in squamous cell carcinomas of the skin and the head and neck. Sonic hedgehog expression may serve as a prognostic factor in patients with head and neck cancer. © 2010 Wiley Periodicals, Inc. Head Neck, 2011
Intraoperative parathyroid hormone monitoring to determine long‐term success of total parathyroidectomy for secondary hyperparathyroidism
Authors: Moor James W. , Roberts Steven , Atkin Steven L. , England R. James A. 
Published: May 2010

AbstractBackgroundUse of intraoperative parathyroid hormone (ioPTH) monitoring during total parathyroidectomy for secondary hyperparathyroidism is common, although its ability to predict long‐term normoparathyroid state is not known.MethodsProspective evaluation of 57 consecutive patients undergoing total parathyroidectomy for renal hyperparathyroidism with ioPTH monitoring and follow‐up PTH assays were used to categorize the patients into 3 groups: success, adequate biochemical control, and failure.ResultsThere was no statistically significant difference in percentage reduction of ioPTH between the 3 groups (p = .07), although there was a moderate negative correlation between percentage reduction of ioPTH and percentage reduction of PTH at follow‐up (R = 0.57).ConclusionsWhen used under current guidelines, ioPTH monitoring is of no use in predicting long‐term cure for these patients because it does not predict success. Patients that undergo total parathyroidectomy are required to have long‐term calcium and PTH assay follow‐up because normoparathyroidism cannot be assumed. Using the regression equation calculated, success may be predicted for future patients. © 2010 Wiley Periodicals, Inc. Head Neck, 2010
Downregulation of Ches1 and other novel genes in oral cancer cells chronically exposed to areca nut extract
Authors: Chen Yin‐Ju , Liao Chun‐Ta , Chen Po‐Jen , Lee Li‐Yu , Li Yi‐Chen , Chen I‐How , Wang Hung‐Ming , Chang Joseph T. , Chen Li‐Ju , Yen Tzu‐Chen , Tang Chuan‐Yi , Cheng Ann‐Joy 
Published: May 2010

AbstractBackgroundThis study was undertaken to identify the genes in response to areca nut extract, a potential carcinogen of oral cancer.MethodsTwo oral cancer sublines chronically treated with areca nut extract were established. Methods such as microarray and immunohistochemistry were used to screen and validate the genes' altered expressions in areca nut extract‐sublines or in cancer tissues.ResultsA total of 35 genes were differentially expressed in both sublines. Several functional pathways were significantly altered. Six genes were confirmed over 2‐fold of changes, including Ches1. Functional analyses showed that overexpression of Ches1 suppressed cell growth and arrested cells in the G2/M phase. Consistently, this gene has reduced expression in 52% of oral cancer tissues, which was significantly correlated with the areca nut chewing habit of patients (p = .04).ConclusionWe identified 35 candidates and validated 6 genes that may be associated with areca nut‐induced oral cancer. Loss of Ches1 may be attributed to areca nut extract–induced oral carcinogenesis. © 2010 Wiley Periodicals, Inc. Head Neck, 2011
The interplay between parental beliefs about children's emotions and parental stress impacts children's attachment security
Authors: Stelter Rebecca L. , Halberstadt Amy G. 
Published: May 2010

AbstractThis study investigated how parental beliefs about children's emotions and parental stress relate to children's feelings of security in the parent–child relationship. Models predicting direct effects of parental beliefs and parental stress, and moderating effects of parental stress on the relationship between parental beliefs and children's feelings of security were tested. Participants were 85 African American, European American, and Lumbee American Indian 4th and 5th grade children and one of their parents. Children reported their feelings of security in the parent–child relationship; parents independently reported on their beliefs and their stress. Parental stress moderated relationships between three of the four parental beliefs about the value of children's emotions and children's attachment security. When parent stress was low, parental beliefs accepting and valuing children's emotions were not related to children's feelings of security; when parent stress was high, however, parental beliefs accepting and valuing children's emotions were related to children's feelings of security. These findings highlight the importance of examining parental beliefs and stress together for children's attachment security. Copyright © 2010 John Wiley & Sons, Ltd.
VEGF receptor binding peptide‐linked high mobility box group‐1 box A as a targeting gene carrier for hypoxic endothelial cells
Authors: Han Jee Seung , Kim Hyun Ah , Lee Sanghyun , Lee Minhyung 
Published: May 2010

AbstractHigh mobility group box‐1 (HMGB‐1) is a nuclear protein that can bind to and condense plasmid DNA. In this study, we developed a recombinant VEGF receptor binding peptide (VRBP) linked to HMGB‐1 box A (VRBP‐HMGB1A) as a targeting gene carrier to hypoxic endothelial cells. Hypoxic endothelial cells in ischemic tissues of solid tumors are important targets for gene therapy. A recombinant VRBP‐HMGB1A expression vector, pET21a‐VRBP‐HMGB1A was constructed. VRBP‐HMGB1A was over‐expressed in BL21 strain and purified by nickel‐chelate affinity chromatography. Complex formation between VRBP‐HMGB1A and pCMV‐Luc was confirmed by gel retardation assay. pCMV‐Luc was retarded completely at a 2/1 weight ratio (peptide/plasmid). For transfection assays, calf pulmonary artery endothelial (CPAE) cells were incubated under hypoxia for 24 h, prior to transfection to induce the VEGF receptors on the cells. VRBP‐HMGB1A/pCMV‐Luc complexes were transfected to hypoxic CPAE cells. The highest transfection efficiency was at a 30/1 weight ratio (peptide/plasmid). In addition, VRBP‐HMGB1A had higher efficiency than poly‐L‐lysine (PLL) specifically in hypoxic CPAE cells, However, VRBP‐HMGB1A had lower efficiency than PLL in 293, H9C2, and normoxic CPAE cells. In MTT assay, VRBP‐HMGB1A was less toxic than PLL to cells. In conclusion, VRBP‐HMGB1A is a potential gene carrier for targeting hypoxic endothelial cells and thus, may be useful for cancer gene therapy. J. Cell. Biochem. 110: 1094–1100, 2010. Published 2010 Wiley‐Liss, Inc.
Transcriptional suppression of mir‐29b‐1/mir‐29a promoter by c‐Myc, hedgehog, and NF‐kappaB
Authors: Mott Justin L. , Kurita Satoshi , Cazanave Sophie C. , Bronk Steven F. , Werneburg Nathan W. , Fernandez‐Zapico Martin E. 
Published: May 2010

AbstractMicroRNAs regulate pathways contributing to oncogenesis, and thus the mechanisms causing dysregulation of microRNA expression in cancer are of significant interest. Mature mir‐29b levels are decreased in malignant cells, and this alteration promotes the malignant phenotype, including apoptosis resistance. However, the mechanism responsible for mir‐29b suppression is unknown. Here, we examined mir‐29 expression from chromosome 7q32 using cholangiocarcinoma cells as a model for mir‐29b downregulation. Using 5′ rapid amplification of cDNA ends, the transcriptional start site was identified for this microRNA locus. Computational analysis revealed the presence of two putative E‐box (Myc‐binding) sites, a Gli‐binding site, and four NF‐κB‐binding sites in the region flanking the transcriptional start site. Promoter activity in cholangiocarcinoma cells was repressed by transfection with c‐Myc, consistent with reports in other cell types. Treatment with the hedgehog inhibitor cyclopamine, which blocks smoothened signaling, increased the activity of the promoter and expression of mature mir‐29b. Mutagenesis analysis and gel shift data are consistent with a direct binding of Gli to the mir‐29 promoter. Finally, activation of NF‐κB signaling, via ligation of Toll‐like receptors, also repressed mir‐29b expression and promoter function. Of note, activation of hedgehog, Toll‐like receptor, and c‐Myc signaling protected cholangiocytes from TRAIL‐induced apoptosis. Thus, in addition to c‐Myc, mir‐29 expression can be suppressed by hedgehog signaling and inflammatory pathways, both commonly activated in the genesis of human malignancies. J. Cell. Biochem. 110: 1155–1164, 2010. Published 2010 Wiley‐Liss, Inc.
ERp57 is up‐regulated in free fatty acids‐induced steatotic L‐02 cells and human nonalcoholic fatty livers
Authors: Wang Hui , Chan Ping‐Kei , Pan Si‐Yuan , Kwon Kwok‐Ho , Ye Yan , Chu Jian‐Hong , Fong Wang‐Fun , Tsui Wilson M.S. , Yu Zhi‐Ling 
Published: May 2010

AbstractPathogenesis of nonalcoholic fatty liver disease (NAFLD) is not clear. In this study we aimed to identify proteins involved in NAFLD development in free fatty acids (FFA)‐induced hepatosteatotic cells and in human liver biopsies. Steatosis was induced by incubating a normal human hepatocyte‐derived cell line L‐02 with FFA. Differentially expressed proteins in the steatotic cells were analyzed by two‐dimensional gel electrophoresis‐based proteomics. Involvement of one of the up‐regulated proteins in steatosis was characterized using the RNA interference approach with the steatotic cells. Protein expression levels in liver biopsies of patients with NAFLD were assessed by immunohistochemistry. Proteomic analysis of L‐02 steatotic cells revealed the up‐regulation of ERp57, a condition not previously implicated in NAFLD. Knockdown of ERp57 expression with siRNA significantly reduced fat accumulation in the steatotic cells. ERp57 expression was detected in 16 out of 17 patient biopsies and correlated with inflammation grades or fibrosis stages, while in 5 normal biopsies ERp57 expression was not detectable in hepatocytes. In conclusion, ERp57 was up‐regulated in FFA‐induced steatotic hepatic cells and in NAFLD patient livers and demonstrated steatotic properties in cultured cells. Further investigations are warranted to verify the involvement of ERp57 in NAFLD development. J. Cell. Biochem. 110: 1447–1456, 2010. © 2010 Wiley‐Liss, Inc.
Differential effect of ionizing radiation exposure on multipotent and differentiation‐restricted bone marrow mesenchymal stem cells
Authors: Mussano Federico , Lee Kenneth J. , Zuk Patricia , Tran Lisa , Cacalano Nicholas A. , Jewett Anahid , Carossa Stefano , Nishimura Ichiro 
Published: May 2010

AbstractDebilitating effects of bone marrow from ionizing radiation exposure has been well established for hematopoietic stem cells; however, radiation toxicity of mesenchymal stem cells (MSCs) has been controversial. The present study addressed if ionizing radiation exposure differently affected bone marrow MSCs with various differentiation commitments. Mouse bone‐marrow‐derived MSCs, D1 cells of early passages (≤5 passages; p5) maintained the complete characteristics of multipotent MSCs, whereas, after ≥45 passages (p45) the differentiation capability of D1 cells became partially restricted. Both p5 and p45 D1 cells were subjected to single dose irradiation by radioactive isotope 137Cs. Radiation treatment impaired cell renewal and differentiation activities of p5 D1 cells; however, p45 D1 cells were less affected. Radiation treatment upregulated both pro‐ and anti‐apoptotic genes of p5 D1 cells in a dose‐dependent manner, potentially resulting in the various apoptosis thresholds. It was found that constitutive as well as radiation‐induced phosphorylation levels of histone H2AX was significantly higher in p45 D1 cells than in p5 D1 cells. The increased repair activity of DNA double‐strand breakage may play a role for p45 D1 cells to exhibit the relative radioresistance. In conclusion, the radiation toxicity predominantly affecting multipotent MSCs may occur at unexpectedly low doses, which may, in part, contribute to the catabolic pathology of bone tissue. J. Cell. Biochem. 111: 322–332, 2010. © 2010 Wiley‐Liss, Inc.
Temporal and spatial expression of osteoactivin during fracture repair
Authors: Abdelmagid Samir M. , Barbe Mary F. , Hadjiargyrou Michael , Owen Thomas A. , Razmpour Roshanak , Rehman Saqib , Popoff Steven N. , Safadi Fayez F. 
Published: May 2010

AbstractWe previously identified osteoactivin (OA) as a novel secreted osteogenic factor with high expression in developing long bones and calvaria, and that stimulates osteoblast differentiation and matrix mineralization in vitro. In this study, we report on OA mRNA and protein expression in intact long bone and growth plate, and in fracture calluses collected at several time points up to 21 days post‐fracture (PF). OA mRNA and protein were highly expressed in osteoblasts localized in the metaphysis of intact tibia, and in hypertrophic chondrocytes localized in growth plate, findings assessed by in situ hybridization and immunohistochemistry, respectively. Using a rat fracture model, Northern blot analysis showed that expression of OA mRNA was significantly higher in day‐3 and day‐10 PF calluses than in intact rat femurs. Using in situ hybridization, we examined OA mRNA expression during fracture healing and found that OA was temporally regulated, with positive signals seen as early as day‐3 PF, reaching a maximal intensity at day‐10 PF, and finally declining at day‐21 PF. At day‐5 PF, which correlates with chondrogenesis, OA mRNA levels were significantly higher in the soft callus than in intact femurs. Similarly, we detected high OA protein immunoexpression throughout the reparative phase of the hard callus compared to intact femurs. Interestingly, the secreted OA protein was also detected within the newly made cartilage matrix and osteoid tissue. Taken together, these results suggest the possibility that OA plays an important role in bone formation and serves as a positive regulator of fracture healing. J. Cell. Biochem. 111: 295–309, 2010. © 2010 Wiley‐Liss, Inc.
Anti‐invasion effect of rosmarinic acid via the extracellular signal‐regulated kinase and oxidation–reduction pathway in Ls174‐T cells
Authors: Xu Yichun , Xu Guanglin , Liu Li , Xu Desheng , Liu Jianwen 
Published: May 2010

AbstractRosmarinic acid is a major phenylpropanoid isolated fromPrunella vulgarisL., which is a composition of herbal tea for centuries in China. However, the anti‐invasion activity on Ls174‐T human colon carcinoma cells has not been studied. In this study, we investigated the anti‐metastasis functions according to wound healing assay, adhesion assay, and Transwell assay and found that rosmarinic acid could inhibit migration, adhesion, and invasion dose‐dependently. Rosmarinic acid also could decrease the level of reactive oxygen species by enhancing the level of reduced glutathione hormone. In addition, rosmarinic acid repressed the activity and expression of matrix metalloproteinase‐2,9. According to Western blot and quantitative real‐time PCR assay, rosmarinic acid may inhibit metastasis from colorectal carcinoma mainly via the pathway of extracellular signal‐regulated kinase. In animal experiment, intraperitoneal administration of 2 mg of rosmarinic acid reduced weight of tumors and the number of lung nodules significantly compared with those of control group. Therefore, these results demonstrated that rosmarinic acid can effectively inhibit tumor metastasis in vitro and in vivo. J. Cell. Biochem. 111: 370–379, 2010. © 2010 Wiley‐Liss, Inc.
Identification of phospholipase C gamma1 as a protein tyrosine phosphatase mu substrate that regulates cell migration
Authors: Phillips‐Mason Polly J. , Kaur Harpreet , Burden‐Gulley Susan M. , Craig Sonya E.L. , Brady‐Kalnay Susann M. 
Published: May 2010

AbstractThe receptor protein tyrosine phosphatase PTPµ has a cell‐adhesion molecule‐like extracellular segment and a catalytically active intracellular segment. This structure gives PTPµ the ability to transduce signals in response to cell–cell adhesion. Full‐length PTPµ is down‐regulated in glioma cells by proteolysis which is linked to increased migration of these cells in the brain. To gain insight into the substrates PTPµ may be dephosphorylating to suppress glioma cell migration, we used a substrate trapping method to identify PTPµ substrates in tumor cell lines. We identified both PKCδ and PLCγ1 as PTPµ substrates. As PLCγ1 activation is linked to increased invasion of cancer cells, we set out to determine whether PTPµ may be upstream of PLCγ1 in regulating glioma cell migration. We conducted brain slice assays using U87‐MG human glioma cells in which PTPµ expression was reduced by shRNA to induce migration. Treatment of the same cells with PTPµ shRNA and a PLCγ1 inhibitor prevented migration of the cells within the brain slice. These data suggest that PLCγ1 is downstream of PTPµ and that dephosphorylation of PLCγ1 is likely to be a major pathway through which PTPµ suppresses glioma cell migration. J. Cell. Biochem. 112: 39–48, 2011. © 2010 Wiley‐Liss, Inc.
Cytokine Stimulation Promotes Increased Glucose Uptake Via Translocation at the Plasma Membrane of GLUT1 in HEK293 Cells
Authors: Zambrano Angara , Jara Evelyn , Murgas Paola , Jara Clara , Castro Maite A. , Angulo Constanza , Concha Ilona I. 
Published: May 2010

AbstractInterleukin‐3 (IL‐3) and granulocyte/macrophage colony‐stimulating factor (GM‐CSF) are two of the best‐characterized cell survival factors in hematopoietic cells; these factors induce an increase in Akt activity in multiple cell lines, a process thought to be involved in cellular survival. It is known that growth factors require sustained glucose metabolism to promote cell survival. It has been determined that IL‐3 and GM‐CSF signal for increased glucose uptake in hematopoietic cells. Interestingly, receptors for IL‐3 and GM‐CSF are present in several non‐hematopoietic cell types but their roles in these cells have been poorly described. In this study, we demonstrated the expression of IL‐3 and GM‐CSF receptors in HEK293 cells and analyzed their effect on glucose uptake. In these cells, both IL‐3 and GM‐CSF, increased glucose uptake. The results indicated that this increase involves the subcellular redistribution of GLUT1, affecting glucose transporter levels at the cell surface in HEK293 cells. Also the data directly demonstrates that the PI 3‐kinase/Akt pathway is an important mediator of this process. Altogether these results show a role for non‐insulin growth factors in the regulation of GLUT1 trafficking that has not yet been directly determined in non‐hematopoietic cells. J. Cell. Biochem. 110: 1471–1480, 2010. © 2010 Wiley‐Liss, Inc.
DNA‐backbone radio resistivity induced by spin blockade effect
Authors: Abolfath Ramin M. , Brabec Thomas 
Published: May 2010

AbstractCoherent control of OH‐free radicals interacting with the spin‐triplet state of a DNA molecule is investigated. A model Hamiltonian for molecular spin singlet‐triplet resonance is developed. We illustrate that the spin‐triplet state in DNA molecules can be efficiently populated, as the spin‐injection rate can be tuned to be orders of magnitudes greater than the decay rate due to small spin‐orbit coupling in organic molecules. Owing to the nano‐second life‐time of OH free radicals, a non‐equilibrium free energy barrier induced by the injected spin triplet state that lasts approximately longer than one‐micro second in room temperature can efficiently block the initial Hydrogen abstraction and DNA damage. For a direct demonstration of the spin‐blockade effect, a molecular simulation based on an ab‐initio Car‐Parrinello molecular dynamics is deployed. © 2010 Wiley Periodicals, Inc. J Comput Chem 2010
Computing ensembles of transitions from stable states: Dynamic importance sampling
Authors: Perilla Juan R. , Beckstein Oliver , Denning Elizabeth J. , Woolf Thomas B. 
Published: May 2010

AbstractThere is an increasing dataset of solved biomolecular structures in more than one conformation and increasing evidence that large‐scale conformational change is critical for biomolecular function. In this article, we present our implementation of a dynamic importance sampling (DIMS) algorithm that is directed toward improving our understanding of important intermediate states between experimentally defined starting and ending points. This complements traditional molecular dynamics methods where most of the sampling time is spent in the stable free energy wells defined by these initial and final points. As such, the algorithm creates a candidate set of transitions that provide insights for the much slower and probably most important, functionally relevant degrees of freedom. The method is implemented in the program CHARMM and is tested on six systems of growing size and complexity. These systems, the folding of Protein A and of Protein G, the conformational changes in the calcium sensor S100A6, the glucose–galactose‐binding protein, maltodextrin, and lactoferrin, are also compared against other approaches that have been suggested in the literature. The results suggest good sampling on a diverse set of intermediates for all six systems with an ability to control the bias and thus to sample distributions of trajectories for the analysis of intermediate states. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2011
Expression of GFAT1 and OGT in podocytes: Transport of glucosamine and the implications for glucose uptake into these cells
Authors: Rogacka Dorota , Piwkowska Agnieszka , Jankowski Maciej , Kocbuch Katarzyna , Dominiczak Marek H. , Stępiński Jan K. , Angielski Stefan 
Published: May 2010

AbstractGlutamine:fructose‐6‐phosphate amidotransferase (GFAT) and N‐acetylglucosaminyltransferase (OGT) participate in glucosamine (GlcN) production and its utilization in O‐glycosylation, one of key post‐translational modifications of nuclear and cytoplasmic proteins. For this purpose, cells require a high rate of intracellular production of GlcN and/or significant GlcN delivery. We studied the expression of GFAT1 and OGT and measured uptake of glucose and GlcN in cultured rat podocytes, the main cellular component of glomerular filtration barrier. RT‐PCR revealed the presence of both GFAT1 and OGT mRNA. Immunofluorescence of GFAT1 has shown staining signal diffused within the cytoplasm of the cell body and processes. However, OGT was distinctly visible around the nucleus and, in diffuse form, within the cytoplasm of cell bodies and processes. Glucose was transported (1.3 ± 0.2 nmol/min/mg protein) mainly by facilitative transporter systems whilst GlcN uptake (1.1 ± 0.2 nmol/min/mg protein) in a significant part, involved a sodium‐dependent transporter. There was interplay between glucose and GlcN uptake. In the presence of GlcN (50 µM), the rate of glucose uptake decreased by about 50%. The rate of GlcN uptake decreased by 28% in the presence of 5.6 mM glucose. Our results suggest that cultured podocytes possess limited ability to synthesize GlcN internally and therefore may need to receive GlcN from the extracellular environment. J. Cell. Physiol. 225: 577–584, 2010. © 2010 Wiley‐Liss, Inc.