bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical evaluation of platelet‐rich plasma and bioactive glass in the treatment of intra‐bony defects
Authors: Demir Becen , Şengün Dilek , Berberoğlu Atilla 
Published: July 2007

AbstractBackground: There are limited numbers of studies focused on the using of platelet‐rich plasma (PRP) combined with different types of bone substitutes in intra‐bony defects.Aim: The purpose of this study was to evaluate the effect of bioactive glass graft material (BG) with and without PRP on the clinical healing of intra‐bony defects.Materials and Methods: Twenty‐nine intra‐bony defects were randomly treated with either PRP/BG or BG alone. Clinical parameters were recorded at baseline and repeated 9 months after surgery and surgical reentries were also performed.Results: The results showed that both treatment modalities were effective. Pocket depth reduction of 3.60 ± 0.51 mm, clinical attachment gain of 3.3 ± 1.77 mm and defect fill of 3.47 ± 0.53 mm were noted in the PRP/BG group, with 3.29 ± 1.68, 2.86 ± 1.56 and 3.36 ± 0.55 mm improvements, respectively, noted for the BG group. None of the differences between the two treatment modalities were statistically significant.Conclusions: It is suggested that both PRP/BG combination and BG alone are effective in the treatment of intra‐bony defects. The results also showed that using PRP with BG has no additional benefit in the reduction of pocket depth, clinical attachment gain and defect fill.
Early oral presentation of Crohn's disease
Authors: William Thomas , Marsch Wolfgang‐Christian , Schmidt Frank , Kreft Burkhard 
Published: July 2007

SummaryInflammatory changes of the oral mucosa in children can have a variety of infectious and non‐infectious etiologies. We report on a 10‐year‐old boy with progressive cobblestone‐like changes and erosions of oral mucosa over six months, which turned out to be early oral manifestations of Crohn disease.
Macro‐micro dermatology: Erythematous papules and lentigo‐like macules – a new entity?
Authors: Shabrawi‐Caelen Laila El , Hofer Angelika , Kerl Helmut 
Published: July 2007

SummaryGalli‐Galli disease is usually characterized by reticulate hyperpigmentation of the flexures. Rare patients may present without this finding, instead having only localized erythematous papules and brown, lentigo‐like macules on the trunk and extremities. Histological changes consist of elongated and in part hyperpigmented rete ridges and areas of acantholysis.
Losartan decreases vasopressin‐mediated cAMP accumulation in the thick ascending limb of the loop of Henle in rats with congestive heart failure
Authors: Torp M. , Brønd L. , Hadrup N. , Nielsen J. B. , Prætorius J. , Nielsen S. , Christensen S. , Jonassen T. E. N. 
Published: July 2007

AbstractIntroduction:  Vasopressin (AVP) stimulates sodium reabsorption and Na,K,2Cl‐cotransporter (NKCC2) protein level in the thick ascending limb (TAL) of Henle's loop in rats. Rats with congestive heart failure (CHF) have increased protein level of NKCC2, which can be normalized by angiotensin II receptor type‐1 (AT1) blockade with losartan.Aim:  In this study, we investigated whether CHF rats displayed changes in AVP stimulated cAMP formation in the TAL and examined the role of AT1 receptor blockade on this system.Method:  CHF was induced by ligation of the left anterior descending coronary artery (LAD). SHAM‐operated rats were used as controls. Half of the rats were treated with losartan (10 mg kg day−1 i.p.).Results:  CHF rats were characterized by increased left ventricular end diastolic pressure. Measurement of cAMP in isolated outer medullary TAL showed that both basal and AVP (10−6 m) stimulated cAMP levels were significantly increased in CHF rats (25.52 ± 4.49 pmol cAMP μg−1 protein, P < 0.05) compared to Sham rats (8.13 ± 1.14 pmol cAMP μg−1 protein), P < 0.05). Losartan significantly reduced the basal level of cAMP in CHF rats (CHF: 12.56 ± 1.93 fmol μg−1 protein vs. Los‐CHF: 7.49 ± 1.08, P < 0.05), but not in Sham rats (SHAM: 4.66 ± 0.59 vs. Los‐SHAM: 4.75 ± 0.71). AVP‐mediated cAMP accumulation was absent in both groups treated with losartan (Los‐SHAM: 4.75 ± 0.71 and Los‐CHF: 7.49 ± 1.08).Conclusion:  The results indicate that the increased NKCC2 protein level in the mTAL from CHF rats is associated with increased cAMP accumulation in this segment. Furthermore, the finding that AT1 receptor blockade prevents AVP‐mediated cAMP accumulation in both SHAM and CHF rats suggests an interaction between angiotensin II and AVP in regulation of mTAL Na reabsorption.
Interindividual differences in muscle sympathetic nerve activity: a key to new insight into cardiovascular regulation?
Authors: Gunnar Wallin B. 
Published: July 2007

AbstractThe paper reviews findings in humans regarding interindividual differences in sympathetic nerve activity. Data come predominantly from microneurographic multi‐ or single fibre recordings of sympathetic nerve activity in healthy subjects. Findings relate to interindividual differences in muscle sympathetic nerve activity (MSNA) during resting conditions and in response to surprising sensory stimuli. At rest there are marked interindividual differences in the number of multiunit MSNA bursts. At the single fibre level the differences are because of more vasoconstrictor fibres being active in subjects with high than in subjects with low number of bursts. There are inverse relationships between (i) sympathetic burst incidence and cardiac output (CO) and (ii) between sympathetic burst incidence and vascular responsiveness to noradrenaline. Both findings contribute to explaining the absence of correlation between resting levels of MSNA and blood pressure. Surprising visual, somatosensory or auditory stimuli of sufficient strength cause a short lasting inhibition of MSNA in approx. 50–60% of healthy subjects. In subjects who display significant inhibition, the stimulus‐induced blood pressure increase is smaller than in subjects without inhibition. The underlying mechanism may be related to fear of blood/injury. It is concluded that analysis of interindividual differences in sympathetic activity improves the understanding of central nervous control of the circulation.
Human PathogenicBorrelia spielmaniisp. nov. Resists Complement-Mediated Killing by Direct Binding of Immune Regulators Factor H and Factor H-Like Protein 1
Authors: Herzberger Pia , Siegel Corinna , Skerka Christine , Fingerle Volker , Schulte-Spechtel Ulrike , van Dam Alje , Wilske Bettina , Brade Volker , Zipfel Peter F. , Wallich Reinhard , Kraiczy Peter 
Published: July 2007

ABSTRACTBorrelia spielmaniisp. nov. has recently been shown to be a novel human pathogenic genospecies that causes Lyme disease in Europe. In order to elucidate the immune evasion mechanisms ofB. spielmanii, we compared the abilities of isolates obtained from Lyme disease patients and tick isolate PC-Eq17 to escape from complement-mediated bacteriolysis. Using a growth inhibition assay, we show that fourB. spielmaniiisolates, including PC-Eq17, are serum resistant, whereas a single isolate, PMew, was more sensitive to complement-mediated lysis. All isolates activated complement in vitro, as demonstrated by covalent attachment of C3 fragments; however, deposition of the later activation products C6 and C5b-9 was restricted to the moderately serum-resistant isolate PMew and the serum-sensitiveB. gariniiisolate G1. Furthermore, serum adsorption experiments revealed that allB. spielmaniiisolates acquired the host alternative pathway regulators factor H and factor H-like protein (FHL-1) from human serum. Both complement regulators retained their factor I-mediated C3b inactivation activities when bound to spirochetes. In addition, two distinct factor H and FHL-1 binding proteins, BsCRASP-1 and BsCRASP-2, were identified, which we estimated to be approximately 23 to 25 kDa in mass. A further factor H binding protein, BsCRASP-3, was found exclusively in the tick isolate, PC-Eq17. This is the first report describing an immune evasion mechanism utilized byB. spielmaniisp. nov., and it demonstrates the capture of human immune regulators to resist complement-mediated killing.
Brucella suisPrevents Human Dendritic Cell Maturation and Antigen Presentation through Regulation of Tumor Necrosis Factor Alpha Secretion
Authors: Billard Elisabeth , Dornand Jacques , Gross Antoine 
Published: July 2007

ABSTRACTBrucellais a facultative intracellular pathogen and the etiological agent of brucellosis. In some cases, human brucellosis results in a persistent infection that may reactivate years after the initial exposure. The mechanisms by which the parasite evades clearance by the immune response to chronically infect its host are unknown. We recently demonstrated that dendritic cells (DCs), which are critical components of adaptive immunity, are highly susceptible toBrucellainfection and are a preferential niche for the development of the bacteria. Here, we report that in contrast to several intracellular bacteria,Brucellaprevented the infected DCs from engaging in their maturation process and impaired their capacities to present antigen to naïve T cells and to secrete interleukin-12. Moreover,Brucella-infected DCs failed to release tumor necrosis factor alpha (TNF-α), a defect involving the bacterial protein Omp25. Exogenous TNF-α addition toBrucella-infected DCs restored cell maturation and allowed them to present antigens. Two avirulent mutants ofB. suis,B. suis bvrRandB. suis omp25mutants, which do not express the Omp25 protein, triggered TNF-α production upon DC invasion. Cells infected with these mutants subsequently matured and acquired the ability to present antigens, two properties which were dramatically impaired by addition of anti-TNF-α antibodies. In light of these data, we propose a model in which virulentBrucellaalters the maturation and functions of DCs through Omp25-dependent control of TNF-α production. This model defines a specific evasion strategy of the bacteria by which they can escape the immune response to chronically infect their host.
Proteomics-Based Identification of Proteins Secreted in Apical Surface Fluid of Squamous Metaplastic Human Tracheobronchial Epithelial Cells Cultured by Three-Dimensional Organotypic Air-Liquid Interface Method
Authors: Kim Seung-Wook , Cheon Kyounga , Kim Chang-Hoon , Yoon Joo-Heon , Hawke David H. , Kobayashi Ryuji , Prudkin Ludmila , Wistuba Ignacio I. , Lotan Reuben , Hong Waun Ki , Koo Ja Seok 
Published: July 2007

Abstract
Squamous cell carcinoma in the lung originates from bronchial epithelial cells that acquire increasingly abnormal phenotypes. Currently, no known biomarkers are clinically efficient for the early detection of premalignant lesions and lung cancer. We sought to identify secreted molecules produced from squamous bronchial epithelial cells cultured with organotypic culture methods. We analyzed protein expression patterns in the apical surface fluid (ASF) from aberrantly differentiated squamous metaplastic normal human tracheobronchial epithelial (NHTBE) and mucous NHTBE cells. Comparative two-dimensional PAGE analysis revealed 174 unique proteins in the ASF of squamous NHTBE cells compared with normal mucociliary differentiated NHTBE cells. Among them, 64 well-separated protein spots were identified by liquid chromatography-tandem mass spectrometry, revealing 22 different proteins in the ASF from squamous NHTBE cells. Expression of six of these proteins [SCC antigen 1 (SCCA1), SCC antigen 2 (SCCA2), S100A8, S100A9, Annexin I, and Annexin II] in the squamous NHTBE cells was further confirmed with immunoblot analysis. Notably, SCCA1 and SCCA2 were verified as being expressed in squamous metaplastic NHTBE cells but not in normal mucous NHTBE or normal bronchial epithelium. Moreover, SCCA1 and SCCA2 expression increased in in vitro lung carcinogenesis model cell lines with increasing malignancy. In summary, we identified proteins that are uniquely secreted from squamous metaplastic primary human bronchial epithelial cells cultured by the organotypic air-liquid interface method. These ASF proteins may be used to detect abnormal lesions in the lung without collecting invasive biopsy specimens. [Cancer Res 2007;67(14):6565–73]
Cancer Cells and Normal Cells Differ in Their Requirements for Thoc1
Authors: Li Yanping , Lin Athena W. , Zhang Xiaojing , Wang Yanqing , Wang Xiaoling , Goodrich David W. 
Published: July 2007

Abstract
The evolutionarily conserved TREX (Transcription/Export) complex physically couples transcription, messenger ribonucleoprotein particle biogenesis, RNA processing, and RNA export for a subset of genes. HPR1 encodes an essential component of the S. cerevisiae TREX complex. HPR1 loss compromises transcriptional elongation, nuclear RNA export, and genome stability. Yet, HPR1 is not required for yeast viability. Thoc1 is the recently discovered human functional orthologue of HPR1. Thoc1 is expressed at higher levels in breast cancer than in normal epithelia, and expression levels correlate with tumor size and metastatic potential. Depletion of Thoc1 protein (pThoc1) in human cancer cell lines compromises cell proliferation. It is currently unclear whether Thoc1 is essential for all mammalian cells or whether cancer cells may differ from normal cells in their dependence on Thoc1. To address this issue, we have compared the requirements for Thoc1 in the proliferation and survival of isogenic normal and oncogene-transformed cells. Neoplastic cells rapidly lose viability via apoptotic cell death on depletion of pThoc1. Induction of apoptotic cell death is coincident with increased DNA damage as indicated by the appearance of phosphorylated histone H2AX. In contrast, the viability of normal cells is largely unaffected by pThoc1 loss. Normal cells lacking Thoc1 cannot be transformed by forced expression of E1A and Ha-ras, suggesting that Thoc1 may be important for neoplastic transformation. In sum, our data are consistent with the hypothesis that cancer cells require higher levels of pThoc1 for survival than normal cells. If true, pThoc1 may provide a novel molecular target for cancer therapy. [Cancer Res 2007;67(14):6657–64]
CytochromeP450 Epoxygenase Promotes Human Cancer Metastasis
Authors: Jiang Jian-Gang , Ning Yao-Gui , Chen Chen , Ma Ding , Liu Zhen-Jun , Yang Shilin , Zhou Jianfeng , Xiao Xiao , Zhang Xin A. , Edin Matthew L. , Card Jeffrey W. , Wang Jianing , Zeldin Darryl C. , Wang Dao Wen 
Published: July 2007

AbstractCytochrome P450 (CYP) epoxygenases convert arachidonic acid to four regioisomeric epoxyeicosatrienoic acids (EET), which exert diverse biological activities in a variety of systems. We previously reported that the CYP2J2 epoxygenase is overexpressed in human cancer tissues and cancer cell lines and that EETs enhance tumor growth, increase carcinoma cell proliferation, and prevent apoptosis of cancer cells. Herein, we report that CYP epoxygenase overexpression or EET treatment promotes tumor metastasis independent of effects on tumor growth. In four different human cancer cell lines in vitro, overexpression of CYP2J2 or CYP102 F87V with an associated increase in EET production or addition of synthetic EETs significantly induced Transwell migration (4.5- to 5.5-fold), invasion of cells (3- to 3.5-fold), cell adhesion to fibronectin, and colony formation in soft agar. In contrast, the epoxygenase inhibitor 17-ODYA or infection with the antisense recombinant adeno-associated viral vector (rAAV)-CYP2J2 vector inhibited cell migration, invasion, and adhesion with an associated reduction in EET production. CYP overexpression also enhanced metastatic potential in vivo in that rAAV-CYP2J2–infected MDA-MB-231 human breast carcinoma cells showed 60% more lung metastases in athymic BALB/c mice and enhanced angiogenesis in and around primary tumors compared with control cells. Lung metastasis was abolished by infection with the antisense rAAV-CYP2J2 vector. CYP epoxygenase overexpression or EET treatment up-regulated the prometastatic matrix metalloproteinases and CD44 and down-regulated the antimetastatic genes CD82 and nm-23. Together, these data suggest that CYP epoxygenase inhibition may represent a novel approach to prevent metastasis of human cancers. [Cancer Res 2007;67(14):6665–74]
A Polyepitope DNA Vaccine Targeted to Her-2/ErbB-2 Elicits a Broad Range of Human and Murine CTL Effectors to Protect against Tumor Challenge
Authors: Scardino Antonio , Alimandi Maurizio , Correale Pierpaolo , Smith Steven G. , Bei Roberto , Firat Hüseyin , Cusi Maria Grazia , Faure Olivier , Graf-Dubois Stephanie , Cencioni Giulia , Marrocco Jordan , Chouaib Salem , Lemonnier François A. , Jackson Andrew Michael , Kosmatopoulos Kostas 
Published: July 2007

AbstractA cDNA vaccine (pVax1/pet-neu) was designed to encode 12 different Her-2/ErbB-2–derived, HLA-A*0201–restricted dominant and high-affinity heteroclitic cryptic epitopes. Vaccination with pVax1/pet-neu triggered multiple and ErbB-2–specific CTL responses in HLA-A*0201 transgenic HHD mice and in HLA-A*0201 healthy donors in vitro. Human and murine CTL specific for each one of the 12 ErbB-2 peptides recognized in vitro both human and murine tumor cells overexpressing endogenous ErbB-2. Furthermore, vaccination of HHD mice with pVax1/pet-neu significantly delayed the in vivo growth of challenged ErbB-2–expressing tumor (EL4/HHD/neu murine thymoma) more actively when compared with vaccination with the empty vector (pVax1) or vehicle alone. These data indicate that the pVax1/pet-neu cDNA vaccine coding for a poly-ErbB-2 epitope is able to generate simultaneous ErbB-2–specific antitumor responses against dominant and cryptic multiple epitopes. [Cancer Res 2007;67(14):7028–36]
EWS/FLI1 Regulates Tumor Angiogenesis in Ewing's Sarcoma via Suppression of Thrombospondins
Authors: Potikyan Gary , Savene Rupert O.V. , Gaulden Julie M. , France Kelly A. , Zhou Zhichao , Kleinerman Eugenie S. , Lessnick Stephen L. , Denny Christopher T. 
Published: July 2007

Abstract
Suppression of the expression of antiangiogenic factors has been closely associated with multiple malignancies. Thrombospondins 1 and 2 are members of a family of angiogenic inhibitors that are regulated by several oncogenes. In this study, we investigate the role of thrombospondins in Ewing's sarcoma and their regulation by EWS/ETS fusion oncoproteins. We show that the EWS/FLI1 fusion suppresses the expression of thrombospondins in both NIH3T3 fibroblasts and Ewing's sarcoma tumor–derived cell lines. This regulation depends on an intact EWS/FLI1 DNA-binding domain and may involve direct interactions between EWS/FLI1 and thrombospondin promoter regions. Forced expression of thrombospondins in Ewing's sarcoma cell lines inhibited the rate of tumor formation in vivo and markedly decreased the number of microvessels present in the tumors. These findings suggest that thrombospondins play a biologically significant role in tumor vascularization in Ewing's sarcoma and suggest potential therapeutic strategies for future therapeutic intervention. [Cancer Res 2007;67(14):6675–84]
HER4 D-Box Sequences Regulate Mitotic Progression and Degradation of the Nuclear HER4 Cleavage Product s80HER4
Authors: Strunk Karen E. , Husted Carty , Miraglia Leah C. , Sandahl Melissa , Rearick William A. , Hunter Debra M. , Earp H. Shelton , Muraoka-Cook Rebecca S. 
Published: July 2007

Abstract
Heregulin-mediated activation of HER4 initiates receptor cleavage (releasing an 80-kDa HER4 intracellular domain, s80HER4, containing nuclear localization sequences) and results in G2-M delay by unknown signaling mechanisms. We report herein that s80HER4 contains a functional cyclin B–like sequence known as a D-box, which targets proteins for degradation by anaphase-promoting complex (APC)/cyclosome, a multisubunit ubiquitin ligase. s80HER4 ubiquitination and proteasomal degradation occurred during mitosis but not during S phase. Inhibition of an APC subunit (APC2) using short interfering RNA knockdown impaired s80HER4 degradation. Mutation of the s80HER4 D-box sequence stabilized s80HER4 during mitosis, and s80HER4-dependent growth inhibition via G2-M delay was significantly greater with the D-box mutant. Polyomavirus middle T antigen–transformed HC11 cells expressing s80HER4 resulted in smaller, less proliferative, more differentiated tumors in vivo than those expressing kinase-dead s80HER4 or the empty vector. Cells expressing s80HER4 with a disrupted D-box did not form tumors, instead forming differentiated ductal structures. These results suggest that cell cycle–dependent degradation of s80HER4 limits its growth-inhibitory action, and stabilization of s80HER4 enhances tumor suppression, thus providing a link between HER4-mediated growth inhibition and cell cycle control. [Cancer Res 2007;67(14):6582–90]
BCR-Tyrosine 177 Plays an Essential Role in Ras and Akt Activation and in Human Hematopoietic Progenitor Transformation in Chronic Myelogenous Leukemia
Authors: Chu Su , Li Liang , Singh Harjeet , Bhatia Ravi 
Published: July 2007

Abstract
Chronic myelogenous leukemia (CML) results from the transformation of a primitive hematopoietic cell by the BCR/ABL gene. BCR/ABL signaling has been studied in cell lines and murine models, but the transforming effects of BCR/ABL are highly dependent on cellular context, and mechanisms responsible for the transformation of primitive human hematopoietic cells remain poorly understood. Current targeted therapies fail to eliminate malignant CML progenitors, and improved understanding of crucial molecular mechanisms of progenitor transformation may facilitate the development of improved therapeutic approaches. We investigated the role of BCR/ABL tyrosine 177 (BCR/ABL-Y177) in CML progenitor transformation by comparing the effects of expression of Y177-mutated BCR/ABL, wild-type BCR/ABL, or green fluorescent protein alone on normal CD34+ cells. We show that BCR/ABL-Y177 plays a critical role in CML progenitor expansion, proliferation, and survival. BCR/ABL expression results in enhanced Ras and Akt activity but reduced mitogen-activated protein kinase activity in human hematopoietic cells, which is reversed by BCR/ABL-Y177 mutation. Blocking BCR/ABL-Y177–mediated signaling enhances targeting of CML progenitors by imatinib mesylate. Our studies indicate that BCR/ABL-Y177 plays an essential role in Ras and Akt activation and in human hematopoietic progenitor transformation in CML. [Cancer Res 2007;67(14):7045–53]