bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bacteraemia due to dental flossing
Authors: Crasta Kenneth , Daly Christopher G. , Mitchell David , Curtis Brad , Stewart Douglas , Heitz‐Mayfield Lisa J. A. 
Published: March 2009

AbstractAims: The aims of this study were to (1) investigate the incidence of bacteraemia following flossing in subjects with chronic periodontitis or periodontal health; (2) identify the micro‐organisms in detected bacteraemias; and (3) identify any patient or clinical factors associated with such bacteraemia.Material and Methods: Baseline blood samples were obtained from 30 individuals with chronic periodontitis (17 M:13 F, 29–75 years) and 30 with periodontal health (17 M:13 F, 28–71 years) following a non‐invasive examination. Each subject's teeth were then flossed in a standardized manner and blood samples obtained 30 s and 10 min. after flossing cessation. Blood samples were cultured in a BACTEC™ system and positive samples subcultured for identification.Results: Forty per cent of periodontitis subjects and 41% of periodontally healthy subjects tested positive for bacteraemia following flossing. Viridans streptococci, which are commonly implicated in infective endocarditis (IE), were isolated from 19% of positive subjects and accounted for 35% of microbial isolates. Twenty per cent of subjects had a detectable bacteraemia at 10 min. post‐flossing. No patient or clinical factors were significantly associated with post‐flossing bacteraemia.Conclusions: Dental flossing can produce bacteraemia in periodontally healthy and periodontally diseased individuals at a rate comparable with that caused by some dental treatments for which antibiotic prophylaxis is given to prevent IE.
TLR4 as a risk factor for periodontal disease: a reappraisal
Authors: Ozturk Ayla , Vieira Alexandre R. 
Published: March 2009

AbstractAim: To determine whether genetic variants of the TLR4 gene are associated with either chronic or aggressive periodontitis.Methods: A systematic electronic search of literature was conducted to identify all published studies without any language restriction on the association between TLR4 and periodontal diseases, including chronic periodontitis and aggressive periodontitis. All case–control studies evaluating the TLR4 Asp299Gly and Thr399Ile polymorphisms in chronic or aggressive periodontitis were identified. A meta‐analysis of the studies that fulfilled the inclusion criteria was performed.Results: Seven studies comprising 744 chronic periodontitis cases and 855 controls and four studies consisting of a total of 295 aggressive periodontitis cases and 456 controls were included in the meta‐analysis. In the pooled analysis, the TLR4 299Gly allele (TLR4+896 A>G) appeared to be a genetic risk factor for susceptibility to chronic periodontitis with a random effects and fixed effects odds ratio (OR) of 1.43 [95% confidence interval (CI):1.04–1.97; p=0.03]. On the other hand, the TLR4 399Ile polymorphism (TLR4+1196 C>T) showed a protective effect against aggressive periodontitis with a random effects OR of 0.29 (95% CI: 0.13–0.61; p=0.001).Conclusion: Our results suggest that the alleles 299Gly and 399Ile in TLR4 can be a potential genetic marker for periodontal disease.
Essential oils in one‐stage full‐mouth disinfection: double‐blind, randomized clinical trial of long‐term clinical, microbial and salivary effects
Authors: Cortelli Sheila Cavalca , Cortelli José Roberto , Holzhausen Marinella , Franco Gilson Cesar Nobre , Rebelo Renato Zanotta , Sonagere Alan Salinas , Queiroz Celso da Silva , Costa Fernando Oliveira 
Published: March 2009

AbstractAim: This randomized clinical trial evaluated the effects of an essential oils‐containing mouthrinse for full‐mouth disinfection.Material and Methods: Fifty patients were assigned to receive full‐mouth disinfection with either essential oils or placebo. At baseline, 2 and 6 months of treatment the primary outcomes probing depth (PD), plaque index (PlI) and modified gingival index (MGI) were monitored. Additional monitoring included bacterial presence (by polymerase chain reaction) in subgingival, saliva and tongue samples; flows, pH, total protein and alkaline phosphatase salivary levels. The following statistics were used: anova, Student's t‐test, χ2 and Kruskal–Wallis (p<0.05).Results: Mean PD3.5 mm was reduced over time in both the placebo and the test groups, but there was no difference in PD reduction between groups at 2 and 6 months. At 2 and 6 months, PlI and MGI showed greater reductions in the test group than in the placebo group. Porphyromona gingivalis was not reduced in any site. At 6 months, Campylobacter rectus increased in both groups, while Tannerella forsythensis decreased subgingivally in the test group. S. sanguinis increased, except subgingivally, in the placebo group. Salivary pH and flows were not altered. Total protein reduced only in the test group. Alkaline phosphatase did not change in either group.Conclusions: Essential oils for full‐mouth disinfection showed clinical benefits, namely reducing plaque and gingival inflammation without altering basic salivary parameters.
Dose–response relationship between periodontal inflamed surface area and HbA1c in type 2 Diabetics
Authors: Nesse Willem , Linde Annemiek , Abbas Frank , Spijkervet Frederik Karst Lucien , Dijkstra Pieter Ubele , De Brabander Eric Carl , Gerstenbluth Izzy , Vissink Arjan 
Published: March 2009

AbstractBackground: A dose–response relationship between the amount of inflamed periodontal tissue and HbA1c level, might be indicative for a causal association between periodontitis and type 2 diabetes.Aim: To assess a dose–response relationship between the periodontal inflamed surface area (PISA), as a measure of the amount of inflamed periodontal tissue, and HbA1c levels in type 2 diabetics.Material and Methods: Forty consecutive dentate type 2 diabetics attending their general practitioner for regular check‐up, underwent full‐mouth probing pocket depth and bleeding on probing assessment. From these data PISA was calculated. HbA1c levels were retrieved from patients' medical files. The dose–response relationship between PISA and HbA1c levels was assessed using multiple linear regression analyses, controlling for factors that might influence PISA or HbA1c levels.Results: The higher the PISA of type 2 diabetics was, the higher their HbA1c levels were. On a group level, an increase of PISA with 333 mm2 was associated with a 1.0 percentage point increase of HbA1c, independent of the influence of other factors.Conclusion: On a group level, there is a dose–response relationship between PISA and HbA1c in type 2 diabetics. This might be an indication of a causal relationship between type 2 diabetes and periodontitis.
Early evolution of vertebrate photoreception: lessons from lampreys and lungfishes
Authors: COLLIN Shaun P. 
Published: March 2009

AbstractLampreys (Agnatha) and lungfish (Dipnoi) are representatives of the earliest and the intermediate stages in vertebrate evolution, respectively, and survived in the Cambrian (approximately 540 mA, lampreys) and Devonian (approximately 400 mA, lungfishes) Periods. The unique phylogenetic position of these two groups presents us with an exciting opportunity to understand life in ancient times and to begin to trace the evolution of vision and photoreception in vertebrates. Using a multidisciplinary approach employing anatomical and molecular techniques, the evolution of photoreception is explored in these extant, living fossils to predict the environmental lighting conditions to which our vertebrate ancestors were exposed. Contrary to expectations, the retinae of the southern hemisphere lamprey (Geotria australis Gray, 1851) and the Australian lungfish (Neoceratodus forsteri Krefft, 1870) are far from “primitive,” each possessing five types of photoreceptors, many with spectral filters for tuning the light. Detailed ultrastructural analysis reveals that all five receptor types in G. australis are cone‐like, whereas N. forsteri possesses four cone types and a single type of rod. Each receptor type also contains a different visual pigment (opsin gene); that is, LWS, SWS1, SWS2, RhA and RhB in G. australis and LWS, SWS1, SWS2, Rh1 and Rh2 in N. forsteri, all of which are expressed within the retina and are sensitive to different parts of the electromagnetic spectrum, providing the potential for pentachromatic and tetrachromatic color vision, respectively.
Neuroprotective Effects of Calmodulin Peptide 76‐121aa: Disruption of Calmodulin Binding to Mutant Huntingtin
Authors: Dudek Nichole L. , Dai Ying , Muma Nancy A. 
Published: March 2009

AbstractHuntington's disease (HD) is a neurodegenerative disease caused by mutant huntingtin protein containing an expanded polyglutamine tract, which may cause abnormal protein–protein interactions such as increased association with calmodulin (CaM). We previously demonstrated in HEK293 cells that a peptide containing amino acids 76‐121 of CaM (CaM‐peptide) interrupted the interaction between CaM and mutant huntingtin, reduced mutant huntingtin‐induced cytotoxicity and reduced transglutaminase (TG)‐modified mutant huntingtin. We now report that adeno‐associated virus (AAV)‐mediated expression of CaM‐peptide in differentiated neuroblastoma SH‐SY5Y cells, stably expressing an N‐terminal fragment of huntingtin containing 148 glutamine repeats, significantly decreases the amount of TG‐modified huntingtin and attenuates cytotoxicity. Importantly, the effect of the CaM‐peptide shows selectivity, such that total TG activity is not significantly altered by expression of CaM‐peptide nor is the activity of another CaM‐dependent enzyme, CaM kinase II.In vitro, recombinant exon 1 of huntingtin with 44 glutamines (htt‐exon1‐44Q) binds to CaM‐agarose; the addition of 10 µM of CaM‐peptide significantly decreases the interaction of htt‐exon1‐44Q and CaM but not the binding between CaM and calcineurin, another CaM‐binding protein. These data support the hypothesis that CaM regulates TG‐catalyzed modifications of mutant huntingtin and that specific and selective disruption of the CaM‐huntingtin interaction is potentially a new target for therapeutic intervention in HD.
Highlights from the perspectives in melanoma XII conference
Authors: Kirkwood John M. , Eggermont Alexander 
Published: March 2009

AbstractThe following meeting highlights are from the Perspectives in Melanoma XII conference, held in Scheveningen/The Hague, the Netherlands, on October 2–4, 2008. Selected reviews are included but further discussions of these and other presentations are posted at http://www.MelanomaCare.org.
Preoperative topical cyclopentolate can be omitted when using intracameral lidocaine in phacoemulsification surgery
Authors: Lundberg Björn , Behndig Anders 
Published: March 2009

Abstract.Purpose:  To evaluate the mydriatic effect of topical cyclopentolate 1% when combined with topical phenylephrine 10% and intracameral lidocaine 1% in phacoemulsification cataract surgery.Methods:  We performed a prospective, double‐masked, randomized trial including 20 patients with age‐related cataract, who were scheduled for unilateral phacoemulsification and intraocular lens (IOL) implantation. Patients were given either two drops of phenylephrine 10% at 30 mins and 15 mins prior to surgery (group 1), or two drops each of cyclopentolate 1% and phenylephrine 10% at the same time points (group 2). All patients were also given lidocaine 1% intracamerally at the beginning of the procedure. Intraoperative pupil sizes were assessed from video‐recordings.Results:  Initially, pupil sizes were significantly smaller in group 1 (4.8 ± 1.2 mm versus 6.5 ± 1.4 mm; p = 0.0098), but the lidocaine injection increased the pupil sizes in group 1 significantly, so that pupil sizes in both groups were equalized throughout the surgical procedure.Conclusions:  Preoperative topical cyclopentolate does not enhance mydriasis in phacoemulsification surgery when using intracameral lidocaine and can be omitted when intracameral lidocaine is used.
Trastuzumab-Induced HER Reprogramming in “Resistant” Breast Carcinoma Cells
Authors: Narayan Murli , Wilken Jason A. , Harris Lyndsay N. , Baron Andre T. , Kimbler Kimberly D. , Maihle Nita J. 
Published: March 2009

Abstract
Although trastuzumab (Herceptin) is an important advance in the treatment of breast cancer, a significant proportion of patients do not respond to trastuzumab either alone or in combination with chemotherapy. In this study, we observe that epidermal growth factor receptor (EGFR) and HER3 expression is substantially increased after long-term trastuzumab exposure of HER2-positive breast carcinoma–derived cell lines that show primary resistance to trastuzumab. Furthermore, long-term trastuzumab exposure of trastuzumab-resistant cell lines induces de novo sensitivity to the EGFR-targeted agents gefitinib or cetuximab in two of three cell lines accompanied by increased EGFR expression. Together, these results indicate that primary trastuzumab resistance is not synonymous with lack of responsiveness to trastuzumab and, importantly, suggest that trastuzumab priming may sensitize trastuzumab-resistant tumors to other HER family-directed therapeutics. [Cancer Res 2009;69(6):2191–4]
Endothelin-1 Stimulates Lymphatic Endothelial Cells and Lymphatic Vessels to Grow and Invade
Authors: Spinella Francesca , Garrafa Emirena , Di Castro Valeriana , Rosanò Laura , Nicotra Maria Rita , Caruso Arnaldo , Natali Pier Giorgio , Bagnato Anna 
Published: March 2009

Abstract
The lymphatic vasculature is essential for tissue fluid homeostasis and cancer metastasis, although the molecular mechanisms involved remain poorly characterized. Endothelin-1 (ET-1) axis plays a crucial role in angiogenesis and tumorigenesis. Here, we first report that ET-1 acts as a lymphangiogenic mediator. We performed in vitro and in vivo studies and show that lymphatic endothelial cells produce ET-1, ET-3, and express the endothelin B receptor (ETBR). In these cells, ET-1 promotes proliferation, invasiveness, vascular-like structures formation, and phosphorylation of AKT and p42/44 mitogen-activated protein kinase through ETBR. In normoxic conditions, ET-1 is also able to up-regulate the expression of vascular endothelial growth factor (VEGF)-C, VEGF receptor-3, and VEGF-A, and to stimulate hypoxia-inducible factor (HIF)-1α expression similarly to hypoxia. Moreover, HIF-1α silencing by siRNA desensitizes VEGF-C and VEGF-A production in response to ET-1 or hypoxia, implicating HIF-1α/VEGF as downstream signaling molecules of ET-1 axis. Double immunofluorescence analysis of human lymph nodes reveals that lymphatic vessels express ETBR together with the lymphatic marker podoplanin. Furthermore, a Matrigel plug assay shows that ET-1 promotes the outgrowth of lymphatic vessels in vivo. ETBR blockade with the specific antagonist, BQ788, inhibits in vitro and in vivo ET-1–induced effects, demonstrating that ET-1 through ETBR directly regulates lymphatic vessel formation and by interacting with the HIF-1α–dependent machinery can amplify the VEGF-mediated lymphatic vascularization. Our results suggest that ET-1 axis is indeed a new player in lymphangiogenesis and that targeting pharmacologically ETBR and related signaling cascade may be therapeutically exploited in a variety of diseases including cancer. [Cancer Res 2009;69(6):2669–76]
Identification of Ligand-Induced Proteolytic Cleavage and Ectodomain Shedding of VEGFR-1/FLT1 in Leukemic Cancer Cells
Authors: Rahimi Nader , Golde Todd E. , Meyer Rosana D. 
Published: March 2009

Abstract
Vascular endothelial growth factor receptor-1/fms-related tyrosine kinase 1 (VEGFR-1/FLT1) is expressed as a membrane-bound receptor tyrosine kinase and as an alternatively spliced soluble protein (sVEGFR-1) containing the 1-6 IgG-like domain of its ectodomain. sVEGFR-1 is known as a naturally occurring inhibitor of angiogenesis and as a surrogate marker for cancer progression; it is also linked to pregnancy-induced hypertension called preeclampsia and to avascularity of normal cornea. It remains an open question whether alternative mRNA splicing is the only mechanism by which sVEGFR-1 is generated. In this study, we show that in leukemic cancer cells, PlGF and VEGF-A both induce tyrosine phosphorylation of VEGFR-1 and render it susceptible to ectodomain shedding, resulting in the generation of sVEGFR-1 and an intracellular cytoplasmic fragment. Activation of protein kinase C and tumor necrosis factor-α–converting enzyme family metalloproteases are critically required for the occurrence of sVEGFR-1. Following the removal of the ectodomain, the remnant of VEGFR-1 remains attached to the membrane, and the activity of γ-secretase/presenilin is required for its release from the cell membrane. We propose that sVEGFR-1 produced via ectodomain shedding plays a prominent role in the VEGF receptor system by antagonizing VEGF receptor signaling by acting as a dominant-negative form and/or forming a nonsignaling dimerizing complex with VEGF receptors. [Cancer Res 2009;69(6):2607–14]
Epigenetic Regulation of c-ROS Receptor Tyrosine Kinase Expression in Malignant Gliomas
Authors: Jun Hyun Jung , Woolfenden Steve , Coven Shanie , Lane Keara , Bronson Roderick , Housman David , Charest Alan 
Published: March 2009

Abstract
The proto-oncogene tyrosine kinase c-ROS is an orphan receptor whose normal expression pattern is tightly spatio-temporally restricted during development. In glioma, c-ROS mRNA expression is frequently ectopically up-regulated. In this study, we determined by immunohistochemical means that c-ROS receptor protein is present in 25% of low-grade and 30% of malignant glioma tumor samples from tissue microarrays. We then explored the molecular basis for the up-regulation of c-ROS expression in these tumors. We identified and characterized the c-ROS gene promoter region and report that the ectopic expression of c-ROS in tumors is tied to hypomethylation of a CpG island in the c-ROS promoter. Bisulfite sequencing analysis in glioma tumor samples revealed that demethylation of the CpG island (−384 to −132 bp) correlated with c-ROS expression. Moreover, c-ROS expression could be activated by treatment of c-ROS–negative cells with the demethylating agent 5-aza-2′-deoxycytidine. These results establish a strong link between c-ROS promoter demethylation and gain of c-ROS expression and function in glioma. Our data suggest that epigenetic activation of c-ROS represents an important oncogenic mechanism for glioma initiation and progression and suggest that cautionary measures in the clinical use of 5-aza-dC for the treatment of glioma be taken into consideration. [Cancer Res 2009;69(6):2180–4]
Identification of CD20 C-Terminal Deletion Mutations Associated with Loss of CD20 Expression in Non-Hodgkin's Lymphoma
Authors: Terui Yasuhito , Mishima Yuji , Sugimura Natsuhiko , Kojima Kiyotsugu , Sakurai Takuma , Mishima Yuko , Kuniyoshi Ryoko , Taniyama Akiko , Yokoyama Masahiro , Sakajiri Sakura , Takeuchi Kengo , Watanabe Chie , Takahashi Shunji , Ito Yoshinori , Hatake Kiyohiko 
Published: March 2009

AbstractPurpose: Rituximab is commonly incorporated into CD20-positive B-cell lymphoma therapy to improve response and prognosis. With increasing use, resistance to rituximab is a continuing concern, but CD20 mutation as a cause of resistance has not previously been reported.Experimental Design: Freshly collected lymphoma cells from 50 patients with previously untreated or relapsed/resistant non-Hodgkin's B-cell lymphomas (diffuse large B cell, n = 22; follicular, n = 7; mucosa associated lymphoid tissue, n = 16; chronic lymphocytic leukemia, n = 2; small lymphocytic lymphoma, n = 1; lymphoplasmacytic, n = 1; mantle cell lymphoma, n = 1) were assessed for CD20 expression by flow cytometry, and CD20 gene sequencing was done on extracted DNA.Results: CD20 mutations were found in 11 (22.0%) of 50 patients and could be grouped as C-terminal deletion (8.0%), early termination (10.0%), and extracellular domain (2.0%) or transmembrane domain (2.0%) mutations. The mean fluorescence intensity of CD20 on fresh lymphoma cells was significantly lower for the C-terminal deletion mutation [3.26; 95% confidence interval (95% CI), 0.09-6.89] compared with wild type (30.8; 95% CI, 22.4-39.2; P &lt; 0.05). In contrast, early termination mutations did not show significant differences in CD20 expression compared with wild type (19.5; 95% CI, 10.7-28.4; P &gt; 0.05).Conclusions: It is possible that C-terminal deletion mutations of CD20 may be related to relapse/resistance after rituximab therapy. These mutations should be examined in patients showing progression of disease after partial remission.
Heterogeneity of the MYCN Oncogene in Neuroblastoma
Authors: Theissen Jessica , Boensch Marc , Spitz Ruediger , Betts David , Stegmaier Sabine , Christiansen Holger , Niggli Felix , Schilling Freimut , Schwab Manfred , Simon Thorsten , Westermann Frank , Berthold Frank , Hero Barbara 
Published: March 2009

Abstract
Purpose: MYCN amplification is an important therapy-stratifying marker in neuroblastoma. Fluorescence in situ hybridization with signal detection on the single-cell level allows a critical judgement of MYCN intratumoral heterogeneity.
Experimental Design: The MYCN status was investigated by fluorescence in situ hybridization at diagnosis and relapse. Heterogeneity was defined as the simultaneous presence of amplified cells (≥5 cells per slide) and nonamplified cells within one tumor or sequential change of the amplification status during the course of the disease. Likewise, heterogeneity can be detected between primary tumor and metastasis.
Results: From 1,341 patients analyzed, 1,071 showed no amplification, 250 showed homogeneous amplification, and 20 patients showed MYCN heterogeneity. Of the patients with heterogeneity, 12 of 20 had clusters of MYCN amplifications, 3 of 20 had amplified single cells, 3 of 20 showed MYCN amplifications in the bone marrow but not in the primary tumor, and 2 of 20 acquired MYCN amplification during the course of the disease. All stage 4 patients were treated according to high-risk protocols; 7 of 8 later progressed. Four patients with localized disease were treated according to high-risk protocol because of MYCN-amplified clusters; 1 of 4 later progressed. One patient treated with mild chemotherapy experienced progression. Seven patients with localized/4S disease underwent no chemotherapy: 4 of 5 patients with MYCN heterogeneity at diagnosis remained disease-free, and 1 of 5 experienced local progression. Two patients had normal MYCN status at diagnosis but acquired MYCN amplification during the course of the disease.
Conclusion: MYCN heterogeneity is rare. Our results suggest that small amounts of MYCN-amplified cells are not correlated to adverse outcomes. More patients with heterogeneity are warranted to clarify the role of MYCN heterogeneity for risk classification.