bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glucocorticoids mediate differential anti‐apoptotic effects in human fibroblasts and keratinocytes via sphingosine‐1‐phosphate formation
Authors: Hammer S. , Sauer B. , Spika I. , Schraut C. , Kleuser B. , Schäfer‐Korting M. 
Published: February 2004

AbstractGlucocorticoids are potent anti‐inflammatory and immunomodulatory drugs which also induce growth inhibition in a variety of cell types. For this reason long‐term treatment of inflammatory skin diseases may result in irreversible skin atrophy. To elucidate whether the antiproliferative action of glucocorticoids in fibroblasts is accompanied by induction of apoptosis we investigated the influence of dexamethasone (DEX) on both parameters. Interestingly, we revealed that growth inhibitory concentrations of this glucocorticoid did not induce fibroblast apoptosis. Moreover, DEX protected these cells from apoptosis induced by tumor necrosis factor α (TNFα)/actinomycin, UV‐irradiation, and cell permeable ceramides. These findings are in contrast to the lack of anti‐apoptotic effects detected in keratinocytes. Although DEX inhibited TNFα mediated nuclear factor‐kappa (NF‐κB) activity in fibroblasts, this mechanism was not involved in its cytoprotection as it was verified by specific NF‐κB inhibitors. Therefore, we looked for alternative intracellular mediators. Coincubation of fibroblasts with the sphingosine kinase inhibitor N,N‐dimethylsphingosine, which blocks formation of the sphingolipid degradation product sphingosine‐1‐phosphate (S1P), abrogated the protective glucocorticoid effect almost completely. As preincubation with S1P reduced the number of apoptotic cells after stimulation with TNFα/actinomycin and moreover DEX increased the intracellular S1P content a role of this sphingolipid in the cytoprotection by DEX is suggested. © 2004 Wiley‐Liss, Inc.
Cisplatin restores p53 function and enhances the radiosensitivity in HPV16 E6 containing SiHa cells
Authors: Huang Haimei , Huang Shian‐Yi , Chen Ting‐Ting , Chen Ja‐Chi , Chiou Chian‐Ling , Huang Ter‐Mei 
Published: February 2004

AbstractMost HPV‐positive cervical cancer cells possess wild type p53 gene, but its normal p53 functions are disrupted by expression of HPVs E6. Treatment with 0–20 μM cisplatin for 24 h in HPV16 E6 containing SiHa cells suppressed E6 mRNA, reduced E6 protein, and restored p53 expression in dose‐dependent manners. Dual‐parameter flow cytometric analysis indicated that sub‐G1 apoptotic cells, but not necrotic cells were the major species for cisplatin‐induced cytotoxicity in SiHa cells. After 0–10 μM cisplatin treatment, slightly more apoptotic cells appeared from SiHa cells than those from dominant negative p53‐transfected SiHa cells. There was no different ionizing radiation (IR)‐induced apoptosis in these two different cells. On the other hand, cisplatin enhanced more IR‐induced sub‐G1 apoptosis in SiHa than mp53‐SiHa cells. These accompanied with prolonged p53 restoration in irradiated‐SiHa cells after 24 h cisplatin treatment and thereafter. In contrast, it was not found in cells after irradiation alone. Similar results were also shown in Mdm2 expression in SiHa cells after combined treatment. Therefore, cisplatin restored p53 expression and prolonged IR‐induced p53 restoration would be possible candidates to response more sub‐G1 apoptosis in irradiated SiHa cells. These results provided another new explanation on cisplatin sensitizing radiotherapy for HPV16 E6 containing cancer cells. © 2004 Wiley‐Liss, Inc.
TAK‐778 enhances osteoblast differentiation of human bone marrow cells via an estrogen‐receptor‐dependent pathway
Authors: Rosa A.L. , Beloti M.M. 
Published: February 2004

AbstractTAK‐778, a derivative of ipriflavone, has been shown to induce bone growth in in vitro and in vivo models. However, there are no studies evaluating by which mechanism TAK‐778 exerts its effect. Considering the evidences that its precursors act via classical estrogen‐receptor (ER)‐mediated signaling, in the present study, we tested the hypothesis that TAK‐778 induces osteogenesis in human bone marrow cell culture via an ER‐dependent pathway. Cells were cultured in 24‐well culture plates at a cell density of 2 × 104 cells/well in culture medium containing: TAK‐778 (10−5 M), Tamoxifen (10−5 M), TAK‐778 (10−5 M) + Tamoxifen (10−5 M), and vehicle. During the culture period, cells were incubated at 37°C in a humidified atmosphere of 5% CO2 and 95% air. At 7, 14, and 21 days, cell proliferation, cell viability, total protein content, alkaline phosphatase (ALP) activity, and bone‐like formation were evaluated. Data were compared by two‐way ANOVA and Duncan's multiple range test. TAK‐778 did not affect cell viability. Cell number was reduced by TAK‐778. Total protein content, ALP activity, and bone‐like formation were increased by TAK‐778. In general, Tamoxifen did not have any effect on cell behavior. However, when cells were cultured in medium containing both TAK‐778 and Tamoxifen, the effect of TAK‐778 on osteoblast differentiation was inhibited. The present results show that TAK‐778 enhances osteoblast differentiation in human bone marrow cell culture, at least in part, via an ER‐dependent pathway, since its effect was inhibited by Tamoxifen, a well‐known estrogen receptor antagonist. © 2004 Wiley‐Liss, Inc.
RGA protein associates with a TRPV ion channel during biosynthesis and trafficking
Authors: Barnhill Jason C. , Stokes Alexander J. , Koblan‐Huberson Murielle , Shimoda Lori M.N. , Muraguchi Atsushi , Adra Chaker N. , Turner Helen 
Published: February 2004

AbstractTRPV ion channels transduce a range of temperature stimuli. We proposed that analysis of the protein–protein interactions made by TRPV2 might give insight into the key issues surrounding this channel. These issues include the potential functional significance of TRPV2 in non‐sensory tissues, the molecules involved in transducing its activation signal(s) and the mechanism by which its trafficking to the cell surface is regulated. Here we describe the interaction of TRPV2 channel with the RGA gene product. RGA is a four‐transmembrane domain, intracellularly localized protein. RGA associates with TRPV2 in a rat mast cell line that is a native context for both proteins. The interaction between TRPV2 and RGA is transient and occurs intracellularly. RGA does not accompany TRPV2 to the cell surface. Formation of the TRPV2/RGA complex is dependent upon a cellular glycosylation event, suggesting that RGA may play a chaperone or targeting role for TRPV2 during the maturation of the ion channel protein. These data record a novel protein–protein interaction for TRPV2 and provide a foundation for future study of the potential regulatory contribution of RGA to TRPV2 function. © 2004 Wiley‐Liss, Inc.
Latent membrane protein 1 of Epstein–Barr virus plays an important role in the serum starvation resistance of Epstein–Barr virus‐immortalized B lymphocytes
Authors: Park Chan‐Hee , Kim Hak‐Ryul , Kim Ju , Jang Sun‐Hee , Lee Kyung‐Yeol , Chung Gook‐Hyun , Jang Yong‐Suk 
Published: February 2004

AbstractWe have previously shown that SNU‐1103, which is a latency type III Epstein–Barr virus (EBV)‐transformed lymphoblastoid cell line (LCL) that was developed from a Korean cancer patient, resists serum starvation‐induced G1 arrest. In this study, we examined the role of latent membrane protein‐1 (LMP‐1) in serum starvation resistance, since LMP‐1 is known to be essential for EBV‐mediated immortalization of human B lymphocytes. The LMP‐1 gene from SNU‐1103 was introduced into the EBV‐negative BJAB cell line, and shown to be associated with resistance to G1 arrest during serum starvation. Western blot analyses of the LMP‐1‐transfected cells revealed several protein alterations as compared to vector‐transfected control cells. The expression of key cell‐cycle regulatory proteins was affected in the G1 phase: the expression of cyclin D3, CDK2, p27, and E2F‐4 was up‐regulated, and the expression of cyclin D2, CDK6, p21, and p103 was down‐regulated during serum starvation. These results imply that of the several EBV viral genes expressed in EBV‐negative B lymphoma cells, LMP‐1 mediates resistance to serum starvation‐induced G1 arrest. However, we cannot rule out the possibility that other EBV genes are also involved in the cell‐cycle progression of the EBV‐transformed LCL during serum starvation, since the altered protein expression profile of the LMP‐1 transfectants was distinct from that of the SNU‐1103 cells that expressed all of the EBV viral proteins. © 2004 Wiley‐Liss, Inc.
Internalization but not binding of thrombospondin‐1 to low density lipoprotein receptor‐related protein‐1 requires heparan sulfate proteoglycans
Authors: Wang Shuxia , Herndon Mary E. , Ranganathan Sripriya , Godyna Svetlana , Lawler Jack , Argraves W. Scott , Liau Gene 
Published: February 2004

AbstractThe amino‐terminal domain of the extracellular matrix (ECM) protein thrombospondin‐1 (TSP‐1) mediates binding to cell surface heparan sulfate proteoglycans (HSPG) as well as binding to the endocytic receptor, low density lipoprotein‐related protein (LRP‐1). We previously found that recombinant TSP‐1 containing the amino‐terminal residues 1–214, retained both of these interactions (Mikhailenko et al. [1997]: J Biol Chem 272:6784–6791). Here, we examined the activity of a recombinant protein containing amino‐terminal residues 1–90 of TSP‐1 and found that this domain did not retain high‐affinity heparin‐binding. The loss of heparin‐binding correlated with decreased binding to the fibroblast cell surface. However, both ligand blotting and solid phase binding studies indicate that this truncated fragment of TSP‐1 retained high‐affinity binding to LRP‐1. Consistent with this, it also retained the ability to block the uptake and degradation of 125I‐TSP‐1. However, TSP‐11–90 itself was poorly endocytosed and this truncated amino‐terminal domain was considerably more effective than the full‐length heparin‐binding domain (HBD) of TSP‐1 in blocking the catabolism of endogenously expressed TSP‐1. These results indicate that TSP‐1 binding to LRP‐1 does not require prior or concomitant interaction with cell surface HSPG but suggest subsequent endocytosis requires high‐affinity heparin‐binding. © 2004 Wiley‐Liss, Inc.
Activity‐dependent gene regulation in conditionally‐immortalized muscle precursor cell lines
Authors: Macpherson Peter C.D. , Suhr Steven T. , Goldman Daniel 
Published: February 2004

AbstractSkeletal muscle contractile activity has been implicated in many aspects of muscle cell differentiation and maturation. Much of the research in this area has depended upon costly and labor‐intensive cultures of isolated primary muscle cells because widely available immortalized muscle cell lines often do not display a high level of either spontaneous or stimulated contractile activity. We sought to develop conditionally‐immortalized skeletal muscle cell lines that would provide a source of myofibers that exhibit robust spontaneous contractile activity similar to primary muscle cultures. Using a tetracycline‐regulated retroviral vector expressing a temperature‐sensitive T‐antigen to infect primary myoblasts, we isolated individual clonal muscle precursor cell lines that have characteristics of activated satellite cells during growth and rapidly differentiate into mature myotubes with spontaneous contractile activity after culture in non‐transformation‐permissive conditions. Comparison of these cell lines (known as rat myoblast‐like tetracycline (RMT) cell lines) to primary cell cultures revealed that they share a wide variety of morphological, physiological, and biochemical characteristics. Most importantly, the time‐course and extent of activity‐dependent gene regulation observed in primary cell culture for all genes tested, including subunits of the nicotinic acetylcholine receptor (nAChR), muscle specific kinase (MuSK), and myogenin, is reproduced in RMT lines. These immortalized cell lines are a useful alternative to primary cultures for studying muscle differentiation and molecular and physiological aspects of electrical activity in muscle fibers. © 2004 Wiley‐Liss, Inc.
Effect of LPS on basal and induced apo E secretion by 25‐OH chol and 9cRA in differentiated CaCo‐2
Authors: Ripollés Piquer B. , Nazih H. , Neunlist M. , Huvelin J.M. , Bard J.M. 
Published: February 2004

AbstractThe infection and inflammation process is associated with disturbances in lipid and lipoprotein metabolism. The apolipoprotein E (apo E) plays an important role in the lipoprotein metabolism and has been linked to inflammatory disease such as atherosclerosis and Alzheimer disease. An anti‐inflammatory effect has also been suggested. The heterodimer nuclear receptor Liver‐X‐Receptorα/Retinoid‐X‐Receptor (LXRα/RXR) is considered to be a transcription factor for apo E. The aim of this study was to determine whether lipopolysaccharide (LPS) (principal component of the outer membrane Gram‐negative bacteria) has an effect on apo E secretion by intestinal mucosa cells, using the Caco‐2 cell line. Differentiated Caco‐2 cells grown on filter inserts were incubated apically with LPS and/or 25‐hydroxycholesterol (25‐OH chol) and 9 cis retinoic acid (9cRA), ligands of LXR and RXR, respectively. The apical and basolateral media were separately collected. Apo E was detected by specific antibodies after protein separation by Two‐dimensional nondenaturing gradient gel electrophoresis and apo E secreted in the cell culture media was measured by enzyme linked immunosorbent assay (ELISA). Apo E mRNA was analyzed by reverse transcription‐polymerase chain reaction (RT‐PCR). LXRα and RXR mass was analyzed by Western Blot. We demonstrate here that CaCo‐2 cells secrete apo E, by either apical or basolateral sides, associated with a high‐density like lipoprotein, with a stoke's diameter comprised between 7.10 and 8.16 nm. We show that only apical secretion is decreased by LPS in a dose and time dependent manner. This is associated with a decrease in apo E gene expression contrasting with an increase of Il‐8, a chemokine factor. Moreover, we demonstrate that only basolateral apo E secretion by CaCo‐2 is significantly increased by 25‐OH chol and 9cRA while apical secretion remains unchanged. LPS does not decrease the 25‐OH chol and 9cRA mediated apo E secretion in basolateral compartment, while apical secretion is diminished under these circumstances. Our results provide evidence for the polarized secretion of apo E by intestinal epithelium. They also demonstrate that apo E secretion by CaCo‐2 cell line is decreased by LPS through an LXRα/RXR independent signaling pathway. © 2004 Wiley‐Liss, Inc.
Dual roles of E‐cadherin in prostate cancer invasion
Authors: Chunthapong Jirapat , Seftor Elisabeth A. , Khalkhali‐Ellis Zhila , Seftor Richard E.B. , Amir Sumaira , Lubaroff David M. , Heidger Paul M. , Hendrix Mary J.C. 
Published: February 2004

AbstractThe role(s) of E‐cadherin in tumor progression, invasion, and metastasis remains somewhat enigmatic. In order to investigate various aspects of E‐cadherin biological activity, particularly in prostate cancer progression, our laboratory cloned unique subpopulations of the heterogeneous DU145 human prostatic carcinoma cell line and characterized their distinct biological functions. The data revealed that the highly invasive, fibroblastic‐like subpopulation of DU145 cells (designated DU145‐F) expressed less than 0.1‐fold of E‐cadherin protein when compared to the parental DU145 or the poorly invasive DU145 cells (designated DU145‐E). Experimental disruption of E‐cadherin function stimulated migration and invasion of DU145‐E and other E‐cadherin‐positive prostate cancer cell lines, but did not affect the fibroblastic‐like DU145‐F subpopulation. Within the medium of parental DU145 cells, the presence of an 80 kDa E‐cadherin fragment was detected. Subsequent functional analyses revealed the stimulatory effect of this fragment on the migratory and invasive capability of E‐cadherin‐positive cells. These results suggest that E‐cadherin plays an important role in regulating the invasive potential of prostate cancer cells through an unique paracrine mechanism. © 2004 Wiley‐Liss, Inc.
Sonographic and computed tomographic demonstration of hydatid cysts communicating with the biliary tree
Authors: Valle‐Sanz Yolanda del , Lorente‐Ramos Rosa M. 
Published: February 2004

AbstractHepatic hydatid disease is usually silent and discovered incidentally. Rupture of a hydatid cyst into the biliary tree is a serious complication and produces a clinical picture of biliary obstruction. We present the cases of 2 patients who had only nonspecific symptoms and laboratory test results indicative of biliary tract obstruction. The results of sonographic examinations of both patients strongly suggested the presence of hepatic hydatid cysts communicating with the biliary tree. CT examination provided additional information in 1 patient but only confirmed the sonographic findings in the other. Both cases were surgically confirmed. Demonstration of the cyst and intrabiliary hydatid contents should form the basis for the diagnosis of a hydatid cyst's rupture into the biliary tree; detecting the point of communication further supports the diagnosis. An accurate preoperative diagnosis of this disease is essential for its prompt surgical management. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:144–148, 2004
Evaluation of preoperative sonography in acute cholecystitis to predict technical difficulties during laparoscopic cholecystectomy
Authors: Cho Kyung Soo , Baek Seung Yon , Kang Byung Chul , Choi Hye‐Young , Han Ho‐Seong 
Published: February 2004

AbstractPurposeThe aim of this study was to evaluate the role of preoperative sonography in predicting technical difficulties during laparoscopic cholecystectomy in patients with acute cholecystitis.MethodsSonographic assessment of 14 parameters was performed in 55 patients during a 9‐month period: volume of gallbladder (GB), thickness of GB wall, pattern of GB wall thickening, size of largest gallstone, gallstone mobility, adhesion of GB to its bed, fat plane between GB and hepatoduodenal ligament, free fluid in GB fossa, common bile duct (CBD) dilatation, CBD stone(s), color and power Doppler signals in GB wall, and increased color and power Doppler signals in adjacent liver. Each of the 5 operative steps of laparoscopic cholecystectomy was scored as being difficult (1) or not (0). The scores for each step were added to obtain the overall difficulty score (0–5). We evaluated prospectively whether there were significant associations among the preoperative sonographic findings and the overall difficulty score, scores for each of the 5 operative steps, and operation time.ResultsThe overall difficulty score was significantly associated with a GB volume of 50 cm3 or more, GB wall thickness of 3 mm or more, and presence of color Doppler signals in the GB wall. Increased GB volume also made dissection of adhesions from the GB and dissection of Calot's triangle more difficult. Extraction of the GB from the abdomen was more difficult with a thickened GB wall or adhesion of the GB to its bed. The presence of a CBD stone, dilatation of the CBD (≥ 8 mm), color Doppler signals in the GB wall, and increased power Doppler signals in the adjacent liver were significantly associated with increased operation time.ConclusionsBased on our experience, preoperative determination of GB volume, GB wall thickness, and presence of color Doppler signals in the GB wall in patients with acute cholecystitis helps predict technical difficulties during laparoscopic cholecystectomy. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:115–122, 2004
Angiotensin‐converting enzyme gene polymorphism, carotid intima‐media thickness, and left ventricular mass index in adolescent hypertension
Authors: Páll Dénes , Settakis Georgios , Katona Éva , Zatik János , Kollár József , Limburg Martien , Fülesdi Béla 
Published: February 2004

AbstractPurposeThe aim of this study was to determine whether a positive correlation exists between the DD genotype of angiotensin‐converting enzyme (ACE) and the carotid intima‐media thickness (IMT) or left ventricular mass index (LVMI) in adolescents with hypertension.MethodsWe studied 120 hypertensive and 58 normotensive (control) adolescents. ACE gene polymorphism was determined by a standardized method. The IMT was measured in the common carotid arteries, and the LVMI was calculated on transthoracic echocardiography. The severity of hypertension was graded according to the results of ambulatory blood pressure monitoring as white coat, borderline, or proven hypertension. The association between ACE gene polymorphism and the obtained parameters was analyzed using analysis of variance and chi‐square testing.ResultsBoth the IMT and LVMI were higher in hypertensive than in control adolescents. In hypertensive subjects, no relationship was found between the different ACE genotypes and the IMT: the mean (± standard deviation) IMT in patients with the DD genotype was 0.57 ± 0.11 mm; in those with the DI genotype, 0.53 ± 0.01 mm; and in those with the II genotype, 0.55 ± 0.01 mm. The LVMI was also similar in all 3 ACE genotypes: DD, 106.7 ± 32.3 g/m2; DI, 102.2 ± 38.1 g/m2; and II, 103.2 ± 26.3 g/m2. The severity of hypertension as assessed by ambulatory blood pressure monitoring was independent of the ACE genotype.ConclusionsTarget‐organ damage (left ventricular hypertrophy and carotid atherosclerosis) is detectable in adolescents with hypertension and, in those subjects, ACE genotype polymorphism is not correlated with the severity of target‐organ damage as measured by IMT and LVMI. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:129–135, 2004
Imaging findings in a case of epidermal inclusion cyst arising within the breast parenchyma
Authors: Kwak Jin Young , Park Hai‐Lin , Kim Ji‐Young , Kim Eun‐Kyung , Chung Sun Yang , Kwon Tae‐Hee , Hong Hae‐Sook , Oh Ki Keun 
Published: February 2004

AbstractEpidermal inclusion cysts rarely occur in the breast, but when they do, the consequences can be severe. Here, we report the case of a 23‐year‐old woman who presented with a palpable mass in the right breast. The mass had persisted for 4 years and had been causing pain for 1 month at the time of the patient's presentation. We examined the mass by means of mammography and sonography. Sonographic examination revealed a well‐circumscribed solid, avascular mass suggestive of an epidermal inclusion cyst. Excision was performed at the patient's request. Histopathologic examination of the mass after excision confirmed the diagnosis of epidermal inclusion cyst and its localization within the breast parenchyma. To our knowledge, reports on epidermal inclusion cysts within the breast parenchyma are rare. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:141–143, 2004
Sonographic correlate of stationary waves
Authors: Kröger Knut , Massalha Khalid 
Published: February 2004

AbstractStationary waves are a rare and inconsistent angiographic finding that has been attributed to various causes, including angiographic artifact. We present 2 cases of patients with arterial occlusion in whom sonographic examination revealed a correlate of stationary waves that was present on angiography. This report is, to our knowledge, the first to document the phenomenon of stationary waves using an imaging modality other than angiography. If the sonographic findings presented here are accepted as a correlate of stationary waves, the phenomenon of stationary waves can no longer be considered a specific angiographic finding, and theories attributing the phenomenon to an angiographic artifact must be rejected. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:158–161, 2004