bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytoplasmic accumulation of connexin32 protein enhances motility and metastatic ability of human hepatoma cells in vitro and in vivo
Authors: Li Qingchang , Omori Yasufumi , Nishikawa Yuji , Yoshioka Toshiaki , Yamamoto Youhei , Enomoto Katsuhiko 
Published: March 2007

AbstractConnexins have long been believed to suppress tumour development during carcinogenesis by exerting gap junctional intercellular communication (GJIC). Although GJIC is abrogated in hepatocellular carcinoma (HCC), connexin32 (Cx32) protein tends to remain expressed in cytoplasm, but not in cell–cell contact areas; thus, it is incapable of forming gap junctions. Hypothesising that cytoplasmic Cx32 protein that has accumulated in HCC should have its proper functions, which are independent of GJIC, we established an inducible expression system of Cx32 in human HuH7 HCC cells, which were unable to support the formation of Cx32‐mediated gap junctions, so that Cx32 protein could be overexpressed by doxycycline (Dox) withdrawal. Although the established clone HuH7 Tet‐off Cx32 cells exhibited a 4‐fold increase in Cx32 expression after Dox withdrawal, none of them were dye‐coupled, and Cx32 protein was retained in the Golgi apparatus. However, the proliferation rate of the HuH7 Tet‐off Cx32 cells was significantly higher in the Dox‐free medium than in the Dox‐supplemented one. Transwell assays also revealed that Dox withdrawal enhanced serum‐stimulated motility and invasiveness into Matrigel of the HuH7 Tet‐off Cx32 cells. Furthermore, when HuH7 Tet‐off Cx32 cells were xenografted into the liver of SCID mice, only the mice to which no Dox was administered developed metastatic lesions, indicating that overexpression of cytoplasmic Cx32 protein induced metastasis of HuH7 cells. Our results suggest that, while Cx32‐mediated GJIC suppresses the development of HCCs, cytoplasmic Cx32 protein exerts effects favourable for HCC progression, such as invasion and metastasis, once the cells have acquired a malignant phenotype. © 2007 Wiley‐Liss, Inc.
Stock option backdating bedlam
Authors: Ciesielski Jack T. , Weirich Thomas R. 
Published: March 2007

AbstractNow that the dust has settled a bit, we take a closer‐look at the recent stock option backdating scandal. Stock option plans have usually been justified by saying they aligned management's interests with those of shareholders. But the authors point out that by backdating stock options, the board of directors weakens the bond between top management and shareholders.What caused this latest financial scandal? Was it one more example of unbridled executive greed? Or was it mostly sloppy recordkeeping? This article examines the issues, and the future implications for companies. © 2007 Wiley Periodicals, Inc.
Rebalancing the accounting profession
Authors: Sharman Paul A. 
Published: March 2007

AbstractAn alarming shift of balance has occurred in the accounting profession—a shift from a focus on work that facilitates business and economic development toward an emphasis on satisfying regulatory requirements. One result is that accountants are increasingly being trained to satisfy these regulatory requirements instead of being provided with the skills they need to become financial professionals who contribute as performance advisors and strategic business partners. This article presents steps needed to rebalance the accounting profession. © 2007 Wiley Periodicals, Inc.
Effects of prolyl hydroxylase inhibitors on adipogenesis and hypoxia inducible factor 1 alpha levels under normoxic conditions
Authors: Floyd Z. Elizabeth , Kilroy Gail , Wu Xiying , Gimble Jeffrey M. 
Published: March 2007

AbstractAdipocyte function is highly regulated in response to changing oxygen levels and physiological regulation of adipocyte formation involves factors originally identified as hypoxia‐responsive proteins. Inhibition of adipogenesis at low oxygen tension is associated with activation of hypoxia inducible factor‐1 alpha (HIF‐1α), a transcription factor essential for cellular responses to decreased oxygen levels whose activity is regulated by prolyl hydroxylase (PHD) enzymes. However, HIF‐1α RNA expression has been detected during the initial stages of adipocyte formation under aerobic conditions, suggesting a physiological role for HIF‐1α during adipogenesis under a range of oxygen levels. Here we investigated the expression of HIF‐1α during adipogenesis using the murine 3T3‐L1 adipocyte model. Our results indicate the tissue‐specific form of HIF‐1α is upregulated during adipogenesis with maximal levels obtained within the first 24 h after induction. The increase in HIF‐1α l.1 gene expression corresponds to increased nuclear HIF‐1α protein, which gradually declines throughout adipogenesis under aerobic conditions. Each of the three HIF prolyl hydroxylases involved in regulating HIF‐1α stability is expressed during adipogenesis. The prolyl hydroxylase domain 1 (PHD1) isoform of the HIF prolyl hydroxylases is expressed in early adipogenesis and the PHD2 and PHD3 isoforms are expressed during late adipogenesis. Pharmacological inhibition of PHD activity during the initial stages of adipogenesis abrogates the formation of adipocytes and inhibits gene expression of each of the PHD. However, inhibition of PHD activity does not consistently regulate HIF‐1α l.1 expression or HIF‐1α protein levels, suggesting that hydroxylation‐independent mechanisms are involved in regulating HIF‐1α expression in adipocytes under aerobic conditions. J. Cell. Biochem. 101: 1545–1557, 2007. © 2007 Wiley‐Liss, Inc.
Alteration of the insulin‐like growth factor axis during in vitro differentiation of the human osteosarcoma cell line HOS 58
Authors: Viereck Volker , Siggelkow Heide , Pannem Rajeswararao , Braulke Thomas , Scharf Jens‐Gerd , Kübler Bernd 
Published: March 2007

AbstractThe insulin‐like growth factors I and II (IGF‐I, IGF‐II), their receptors, and high affinity binding proteins (IGFBPs) represent a family of cellular modulators that play essential roles in the development and differentiation of cells and tissues including the skeleton. Recently, the human osteosarcoma cell line HOS 58 cells were used as an in vitro model of osteoblast differentiation characterized by (i) a rapid proliferation rate in low‐density cells that decreased continuously with time of culture and (ii) an increasing secretion of matrix proteins during their in vitro differentiation. In the present paper, HOS 58 cells with low cell density at early time points of the in vitro differentiation (i) displayed a low expression of IGF‐I and ‐II; (ii) synthesized low levels of IGFBP‐2, ‐3, ‐4, and ‐5, but (iii) showed high expression levels of both the type I and II IGF receptors. During the in vitro differentiation of HOS 58 cells, IGF‐I and ‐II expressions increased continuously in parallel with an upregulation of IGFBP‐2, ‐3, ‐4, and ‐5 whereas the IGF‐I receptor and IGF‐II/M6P receptor mRNA were downregulated. In conclusion, the high proliferative activity in low cell density HOS 58 cells was associated with high mRNA levels of the IGF‐IR, but low concentrations of IGFBP‐2. The rate of proliferation of HOS 58 cells continuously decreased during cultivation in parallel with a decline in IGF‐IR expression, but increase of mitoinhibitory IGFBP‐2. These data are indicative for a role of the IGF axis during the in vitro differentiation of HOS 58 cells. J. Cell. Biochem. 102: 28–40, 2007. © 2007 Wiley‐Liss, Inc.
An ROS generator, antimycin A, inhibits the growth of HeLa cells via apoptosis
Authors: Park Woo Hyun , Han Yong Whan , Kim Suhn Hee , Kim Sung Zoo 
Published: March 2007

AbstractAntimycin A (AMA), an inhibitor of electron transport in mitochondria, has been used as a reactive oxygen species (ROS) generator in biological systems. Here, we investigated the in vitro effect of AMA on apoptosis in HeLa cells. AMA inhibited the growth of HeLa cells with an IC50 of about 50 µM. AMA efficiently induced apoptosis, as evidenced by flow cytometric detection of sub‐G1 DNA content, annexin V binding assay, and DAPI staining. This apoptotic process was accompanied by the loss of mitochondrial membrane potential (ΔΨm), Bcl‐2 down‐regulation, Bax up‐regulation, and PARP degradation. All caspase inhibitors used in this experiment, especially pan‐caspase inhibitor (Z‐VAD), could rescue some HeLa cells from AMA‐induced cell death. When we examined the changes of the ROS, H2O2 or O, in AMA‐treated cells, H2O2 and O were markedly increased. In addition, we detected the depletion of GSH content in AMA‐treated cells. Pan‐caspase inhibitor showing the efficient anti‐apoptotic effect significantly reduced GSH depletion by AMA. Superoxide dismutase (SOD) and catalase did not reduce intracellular ROS, but these could strongly rescue the cells from apoptosis. However, these anti‐apoptotic effects were not accompanied by the recovery of GSH depletion. Interestingly, catalase significantly decreased the CMF negative (GSH depletion) and propidium iodide (PI) positive cells, indicating that catalase strongly maintained the integrity of the cell membrane in CMF negative cells. Taken together, these results demonstrate that AMA potently generates ROS, induces the depletion of GSH content in HeLa cells, and strongly inhibits the growth of HeLa cells throughout apoptosis. J. Cell. Biochem. 102: 98–109, 2007. © 2007 Wiley‐Liss, Inc.
Akt2, but not Akt1 or Akt3 mediates pressure‐stimulated serum‐opsonized latex bead phagocytosis through activating mTOR and p70 S6 kinase
Authors: Shiratsuchi Hiroe , Basson Marc D. 
Published: March 2007

AbstractMonocytes and macrophages play critical roles in innate host defense and are sensitive to mechanical stimuli. Tissue pressure is often altered in association with inflammation or infection. Low pressure (20 mmHg), equivalent to normal tissue pressure, increases phagocytosis by primary monocytes and PMA‐differentiated THP‐1 macrophages, in part by FAK and ERK inhibition and p38 activation. PI‐3K is required for macrophage phagocytosis, but whether PI‐3K mediates pressure‐stimulated phagocytosis is not known. Furthermore, little is known about the role played by the PI‐3K downstream Kinases, Akt, and p70 S6 kinase (p70S6K) in modulating macrophage phagocytosis. Thus, we studied the contribution of PI‐3K, Akt, and p70S6K to pressure‐increased serum‐opsonized bead phagocytosis. Pressure‐induced p85 PI‐3K translocation from cytosolic to membrane fractions and increased Akt activation by 36.1 ± 12.0% in THP‐1 macrophages. LY294002 or Akt inhibitor IV abrogated pressure‐stimulated but not basal phagocytosis. Basal Akt activation was inhibited 90% by LY294002 and 70% by Akt inhibitor IV. Each inhibitor prevented Akt activation by pressure. SiRNA targeted to Akt1, Akt2, or Akt3 reduced Akt1, Akt2, and Akt3 expression by 50%, 45%, and 40%, respectively. However, only Akt2SiRNA abrogated the pressure‐stimulated phagocytosis without affecting basal. Pressure also activated mTOR and p70S6K. mTORSiRNA and p70S6K inhibition by rapamycin or p70S6KSiRNA blocked pressure‐induced, but not basal, phagocytosis. Changes in tissue pressure during inflammation may regulate macrophage phagocytosis by activation of PI‐3K, which activates Akt2, mTOR, and p70S6K. J. Cell. Biochem. 102: 353–367, 2007. © 2007 Wiley‐Liss, Inc.
Androgen receptor stimulates bone sialoprotein (BSP) gene transcription via cAMP response element and activator protein 1/glucocorticoid response elements
Authors: Takai Hideki , Nakayama Youhei , Kim Dong‐Soon , Arai Masato , Araki Shouta , Mezawa Masaru , Nakajima Yu , Kato Naoko , Masunaga Hiroshi , Ogata Yorimasa 
Published: March 2007

AbstractBone sialoprotein (BSP) is an early marker of osteoblast differentiation. Androgens are steroid hormones that are essential for skeletal development. The androgen receptor (AR) is a transcription factor and a member of the steroid receptor superfamily that plays an important role in male sexual differentiation and prostate cell proliferation. To determine the molecular mechanism involved in the stimulation of bone formation, we have analyzed the effects of androgens and AR effects on BSP gene transcription. AR protein levels were increased after AR overexpression in ROS17/2.8 cells. BSP mRNA levels were increased by AR overexpression. However, the endogenous and overexpressed BSP mRNA levels were not changed by DHT (10−8 M, 24 h). Whereas luciferase (LUC) activities in all constructs, including a short construct (nts −116 to +60), were increased by AR overexpression, the basal and LUC activities enhanced by AR overexpression were not induced by DHT (10−8M, 24 h). The effect of AR overexpression was abrogated by 2 bp mutations in either the cAMP response element (CRE) or activator protein 1 (AP1)/glucocorticoid response element (GRE). Gel shift analyses showed that AR overexpression increased binding to the CRE and AP1/GRE elements. Notably, the CRE‐protein complexes were supershifted by phospho‐CREB antibody, and CREB, c‐Fos, c‐Jun, and AR antibodies disrupted the complexes formation. The AP1/GRE‐protein complexes were supershifted by c‐Fos antibody and c‐Jun, and AR antibodies disrupted the complexes formation. These studies demonstrate that AR stimulates BSP gene transcription by targeting the CRE and AP1/GRE elements in the promoter of the rat BSP gene. J. Cell. Biochem. 102: 240–251, 2007. © 2007 Wiley‐Liss, Inc.
Quantitative MR imaging of children with sickle cell disease: Striking T1 elevation in the thalamus
Authors: Steen R. Grant , Langston James W. , Reddick Wilburn E. , Ogg Robert , Chen Gang , Wang Winfred C. 
Published: March 2007

AbstractNineteen patients with sickle cell disease (SCD) were examined with conventional MR imaging (cMRI), including T1‐ and T2‐weighted sequences and MR angiography (MRA). qMRI mapping of T1 was also done using a precise and accurate inversion‐recovery (PAIR) technique optimized and validated previously. In addition, 21 healthy African‐American control subjects had the qMRI examination. Nonparametric Kruskal‐Wallis analysis of variance of control subjects, of SCD patients without stroke, and of SCD patients with stroke showed that T1 increased with disease severity in the thalamus, frontal white matter, genu, and occipital white matter. T1 was significantly longer in SCD patients without stroke (n=13) than in control subjects (n=21) in the thalamus and frontal white matter. In addition, T1 values were significantly longer in SCD patients with stroke than in patients without stroke in the genu and frontal white matter. Abnormality of the thalamus was identified by qMRI in a substantial fraction of patients read as normal by both cMRI and MRA, suggesting that it may be possible to use T1 elevation to identify a subset of patients with SCD who are at elevated risk for stroke.
Statistical error mapping for reliable quantitative T1 imaging
Authors: Reddick Wilburn E. , Ogg Robert J. , Steen R. Grant , Taylor June S. 
Published: March 2007

AbstractWe developed a statistically based error image for rapid appreciation of unreliable regions in quantitative water proton T1 images. The chi‐squared error and coefficient of variation of the fitted parameter were used to estimate uncertainties in the goodness‐of‐fit to monoexponential T1 relaxation and the reliability of the calculated T1, respectively, for each pixel. Errors exceeding a statistical threshold based on a .1 acceptance criterion were displayed as a color‐coded overlay on the T1 image. Error maps of quantitative T1 images from 31 healthy volunteers showed a characteristic error structure; few pixels within the parenchyma had excessive errors. Clinical cases with stroke and sickle cell disease showed deviations from the normal pattern in the spatial distribution and magnitude of chisquared errors. Disease states may deviate from monoexponential T1 relaxation more than normal brain does. The color‐coded error map is a valuable tool for investigators using quantitative MR imaging to determine tissue relaxation parameters.
Prospective comparison of helical CT and MR imaging in clinically suspected acute pulmonary embolism
Authors: Sostman H. Dirk , Layish Daniel T. , Tapson Victor F. , Spritzer Charles E. , Delong David M. , Trotter Priscilla , Macfall James R. , Patz Edward F. , Goodman Philip C. , Woodard Pamela K. , Foo Thomas K. F. , Farber Joshua L. 
Published: March 2007

AbstractThe purpose of this study is to compare sensitivity and specificity of helical CT and MR imaging for detecting acute pulmonary embolism (PE). Patients who were suspected clinically of having PE were randomly assigned to undergo either helical contrast‐enhanced CT or gradient‐echo MR (if one modality was contraindicated, the patient was assigned to the other). Patients were considered to have PE if they had: (1) high‐probability V‐Q scan and high clinical probability of PE; or (2) pulmonary angiogram positive for PE. Patients were considered not to have PE if they had either: (1) normal V‐Q scan; (2) low probability V‐Q scan and low clinical probability of PE; or (3) pulmonary angiogram negative for PE. The CT and MR images were read randomly and independently by five radiologists with varying levels of CT and MR experience. Twenty eight patients underwent CT and 25 MR. A total of 21 patients underwent pulmonary angiography (6 had PE, 15 did not have PE). Of the other 32 patients, 15 had high probability scan/high clinical probability and 17 had low probability scan/low clinical probability. For the five observers, the average sensitivity of CT was 75% and of MR 46%; the average specificity of CT was 89% and of MR 90%. Experience with vascular MR and enhanced CT influenced diagnostic accuracy. For the two vascular MR experts, average sensitivity and specificity of MR were 71% and 97%, and of CT 73% and 97%. In this pilot study, when CT and MR were interpreted with comparable expertise, they had similar accuracy for detecting pulmonary embolism.
Malignant lesions of the liver with high signal intensity on T1‐Weighted MR images
Authors: Kelekis Nikolaos L. , Semelka Richard C. , Woosley John T. 
Published: March 2007

AbstractOur purpose was to identify the histologic types of malignant liver lesions with high signal intensity (SI) on T1‐weighted images and to describe the MR imaging features. Thirteen patients with malignant liver lesions high in SI on T1‐weighted images were studied with a 1.5‐T MR imager using pre‐ and serial postcontrast spoiled gradient‐echo (SGE) sequences (all patients), T2‐weighted fat‐suppressed spin‐echo sequences (all patients), precontrast T1‐weighted fat‐suppressed spin‐echo sequences (five studies in five patients), and precontrast out‐of‐phase SGE sequences (seven studies in six patients). Images were reviewed retrospectively to determine number of lesions; lesion size; SI of lesions on T1‐weighted, T2‐weighted, and fat‐attenuated T1‐weighted images; distribution of high SI in lesions on T1‐weighted images; and tumor enhancement pattern. Seven patients had multiple tumors high in SI on T1‐weighted images and six patients had solitary tumors. Seventy‐two lesions were less than 1.5 cm in diameter and 35 lesions were more than 1.5 cm in diameter. Nine patients had solid malignant lesions and four patients had cystic malignant lesions. All tumors more than 1.5 cm in diameter were heterogeneously high in SI on T1‐weighted images, and all tumors less than 1.5 cm were completely homogeneous or homogeneous with a small central hypointense focus. All tumors were more conspicuous on T1‐weighted fat‐attenuated images, both on excitation spoiled fat‐suppressed spin‐echo or on out‐of‐phase SGE images with the exception of one fat‐containing hepatocellular carcinoma (HCC). In one patient with melanoma metastases and one patient with multiple myeloma nodules, appreciably more lesions were detected on out‐of‐phase SGE images. Causes of hyperintensity were considered to be either fat, melanin, central hemorrhage, or high protein content, all of which may be seen in a variety of tumors. Fat‐attenuation techniques are helpful in the detection of these lesions.
Evaluation of the effects of intravascular MR contrast media (gadolinium dendrimer) on 3D time of flight magnetic resonance angiography of the body
Authors: Bourne Michael W. , Margerun Larry , Hylton Nola , Campion Brian , Lai Jan‐Ji , Derugin Nikita , Higgins Charles B. 
Published: March 2007

AbstractThe aims of this preliminary study were to establish the efficacy and minimum effective dose of TG5(FdDO3A)52 gadolinium dendrimer for contrast‐enhanced, three‐dimensional (3D) time of flight (TOF) magnetic resonance angiography (MRA) of the body. In a dose ranging study in eight rabbits (Group A), each of two animals received 0.03; 0.02; 0.01; or 0.005 mmol/kg of the agent for 3D‐TOF MRA of the pelvic circulation in the axial and coronal planes. An additional nine animals (Group B) received a dose of 0.02 mmol/kg for 3D‐TOF MRA of the mediastinum, abdomen or of the lower limbs. Quantitative and qualitative analyses of the images from Group A demonstrated a dose‐related reduction in saturation effects and improved visualization of vascular structures, with maximal augmentation of the contrast‐to‐noise ratio (CNR) at 0.03 mmol/kg. The dose of 0.02 mmol/kg was found to be the minimal effective dose at the three vascular regions.
Gamekeeper thumb: Diagnosis of ulnar collateral ligament injury using magnetic resonance imaging, magnetic resonance arthrography and stress radiography
Authors: Harper Michael T. , Chandnani Vijay P. , Spaeth Joseph , Santangelo James R. , Providence Bertram C. , Bagg Mark A. 
Published: March 2007

AbstractUlnar collateral ligament (UCL) tears may be nondisplaced or displaced relative to the adductor pollicis aponeurosis. Nondisplaced tears typically heal with immobilization whereas displaced tears require surgery. Nineteen patients with UCL injuries were evaluated using MR imaging (MRI), MR arthrography, and stress radiography (SR) to determine the efficacy of these techniques in differentiating nondisplaced from displaced UCL tears. Nineteen patients with UCL injuries were evaluated. MRI was utilized in 5 patients, and MR arthrography in 14, with 12 of these 14 undergoing SR. They were followed until resolution of symptoms; those without relief, and those with suspected displaced UCL tears were surgically explored. Surgery and imaging was correlated. Eight patients underwent surgical repair. SR was abnormal in six patients treated surgically, but was negative in four of six conservatively treated patients with MR findings of nondisplaced tears. All patients with MR or MR arthrographic findings interpreted as being normal or as having a nondisplaced tear improved after conservative treatment. Based on surgical findings and clinical follow‐up, MR arthrography accurately diagnosed 13 of 14 UCL injuries, with one false‐positive interpretation. SR is often falsely negative. MR imaging with or without intra‐articular contrast injection proved to be accurate in a small series of patients with UCL injuries.