bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vivo evaluation of a moisture‐activated orthodontic adhesive: a comparative clinical trial
Authors: Karamouzos A , Mavropoulos A , Athanasiou AE , Kolokithas G 
Published: March 2003

Structured Abstract
Authors –
Karamouzos A, Mavropoulos A, Athanasiou AE, Kolokithas G.
Objectives –
To evaluate and compare the clinical performance of a water‐activated, ethyl‐cyanoacrylate adhesive to a conventional composite resin. The null hypothesis tested was that there was no difference in bracket survival distribution, over a period of orthodontic treatment, for brackets bonded with either bonding agent.
Design –
Single center randomized controlled clinical study.
Setting and Sample Population – Twenty‐five consecutive patients (15 females and 10 males) were selected and treated with fixed appliances in a university postgraduate orthodontic clinic. All teeth, but the molars, were bonded with twin stainless steel brackets (n=429) using a split‐mouth technique and random allocation of the two adhesives.
Outcome Measure –
Bond failure rates during a period of 9 months were estimated for each adhesive system and the corresponding bracket survival curves were plotted using the Kaplan–Meier product‐limit estimate. Bracket survival distributions with respect to adhesive material, tooth location, investigator, and bond failure interface were then compared by means of a log‐rank test. Bond failure interface was determined using the Adhesive Remnant Index (ARI).
Results – The water‐activated bonding material recorded a significantly higher bond failure (22.4%) than the composite resin (5.1%). There were also statistically significant differences in bracket survival distributions between the two adhesives (log‐rank test: p < 0.001). Premolars exhibited higher bond failure rates than incisors and canines (p < 0001). The predominant mode of failure was within the bonding material.
Conclusion –
Further investigations focused on the improvement of the physical and mechanical properties of the water‐activated bonding system are needed to make it a reliable alternative adhesive for the direct bonding of orthodontic brackets.
The role of complement in inflammation and adaptive immunity
Authors: Barrington Robert , Zhang Ming , Fischer Michael , Carroll Michael C. 
Published: March 2003

Summary:Major advances in our understanding of the immunobiology of complement were made within the past 5 years primarily due to the development of gene‐targeting technology. New strains of mice bearing specific deficiencies in serum complement proteins or their receptors were developed using this approach. Characterization of these mice has provided new and exciting insights into the biology of the complement system. In this review, we discuss recent results on two important aspects of the complement system, i) host protection and inflammation, and ii) regulation of B lymphocytes of adaptive immunity. While these two roles appear distinct, they are linked. We discuss how natural antibody and classical pathway complement work together in host protection against bacterial infection on the one hand but, on the other, they co‐operate to induce inflammation as observed in reperfusion injury. Significantly, the lymphocytes that produce natural antibody, the B‐1 lymphocytes, are regulated in part by the complement system.We thank current and past members of the lab who contributed to the work. We especially thank Drs A. Prodeus and R. Reid. The research was supported by grants from the National Institutes of Health to M.C.C. R.B. is supported by a fellowship from the American Arthritis Foundation.
Role of the C5b‐9 complement complex in cell cycle and apoptosis
Authors: Rus Horea G. , Niculescu Florin I. , Shin Moon L. 
Published: March 2003

Summary:Assembly of C5b‐9 on cell membranes results in transmembrane channels and causes cell death. When the number of C5b‐9 molecules is limited, nucleated cells are able to escape cell death by endocytosis and by shedding of membranes bearing C5b‐9. Sublytic C5b‐9 induces proto‐oncogenes, activates the cell cycle, and enhances cell survival. In addition, C5b‐9 reverses the differentiated phenotype of post‐mitotic cells, such as oligodendrocytes and skeletal muscle cells. The signal transduction pathways responsible for cell cycle activation by C5b‐9 include Gi‐mediated activation of extracellular signal‐regulated kinase 1 and phosphatidylinositol 3‐kinase (PI3‐K). Cell survival enhanced by C5b‐9 is mediated by the PI3‐K/Akt pathway, which inhibits apoptosis through regulation of BAD. These findings indicate that complement activation and membrane assembly of sublytic C5b‐9 play an important role in inflammation by promoting cell proliferation and by rescuing apoptotic cells.This work was supported by NIH grants NS36231 and NS15662 and by multiple sclerosis pilot award PP‐696.
Ficolins and the lectin complement pathway
Authors: Matsushita Misao , Fujita Teizo 
Published: March 2003

Summary:Ficolins, found in various tissues, are a group of proteins containing both a collagen‐like and a fibrinogen‐like domain. Recently, it was shown that ficolins present in serum are lectins with a common binding specificity for N‐acetylglucosamine (GlcNAc). The fibrinogen‐like domain is responsible for the carbohydrate binding. Mannose‐binding lectin (MBL) is also a collagenous lectin in serum that is specific for GlcNAc and mannose binding. Its domain organization is similar to that of ficolins, except that MBL has a carbohydrate‐recognition domain instead of a fibrinogen‐like domain. MBL plays a role in innate immunity by acting as an opsonin and activating complement in association with MBL‐associated serine protease (MASP) via the lectin pathway. Investigations of two types of human serum ficolins, ficolin/P35 and Hakata antigen, revealed that they are associated with MASPs and sMAP, a truncated protein of MASP‐2, and that they activate complement. These findings indicate that serum ficolins are structurally and functionally similar to MBL and have the capacity to activate the lectin pathway and thus have a role in innate immunity.This work was supported by Grants‐in‐Aid for Scientific Research (12470079 and 11670328) from the Ministry of Education, Science, Sports and Culture of Japan.
CR1 and CR1‐like: the primate immune adherence receptors
Authors: Birmingham Daniel J. , Hebert Lee A. 
Published: March 2003

Summary:Immune adherence describes the phenomenon in which complement‐opsonized substrates, such as immune complexes (IC), viruses, or bacteria, are bound by primate erythrocytes via erythrocyte complement receptors. In vivo studies have shown that this binding allows the erythrocyte to act as an inert shuttle, targeting IC to the monocyte phagocytic system and away from vulnerable tissue. Thus, immune adherence appears to play an integral role in the primate in promoting the safe clearance of circulating IC and preventing IC‐mediated pathologies. The complement receptors that mediate immune adherence comprise two unique but closely related gene products, either the type one complement receptor (CR1) in humans or CR1‐like in non‐human primates. This review focuses on the structure, function, and physiological role of the primate immune adherence receptors.
Activating and inhibitory nature of the murine paired immunoglobulin‐like receptor family
Authors: Takai Toshiyuki , Ono Masao 
Published: March 2003

Summary: Clones for murine paired immunoglobulin‐like receptors (PIR) were first isolated as those coding for type I transmembrane glycoproteins with six immunoglobulin‐like domains homologous to human FcαR, bovine Fcγ2R, and other related receptors. However, they turned out to bind neither IgA nor other immunoglobulins in the case of the ectopic expression on COS‐1 fibroblastic cells. PIR‐A and B are expressed on a wide variety of cells in the murine immune system, such as in B cells, mast cells, macrophages, and dendritic cells, mostly in a pairwise fashion. PIR‐A requires homodimeric Fc receptor common γ chain, which harbors an immunoreceptor tyrosine‐based activation motif, for its efficient cell surface expression and for the delivery of activation signaling. In contrast, PIR‐B contains immunoreceptor tyrosine‐based inhibitory motifs (ITIMs) in its cytoplasmic portion and inhibits receptor‐mediated activation signaling in vitro upon engagement with other activating‐type receptors such as the antigen receptor on B cells and the high affinity Fc receptor for IgE on mast cells. ITIMs of PIR‐B on macrophages and B cells have been shown to be constitutively phosphorylated in their tyrosine residues. Although the ligand for PIR still remains unknown, the transgenics and the gene‐targeted mice will provide us with valuable information on their physiological roles in the immune regulation.We thank Hiromi Kubagawa for discussion. This work is supported by CREST Program of JST, Virtual Research Institute of Aging funded by Boehringer Ingelheim, and by research grants from the Ministry of Education, Science, Sports and Culture of Japan to T. Takai.
Variable expression of activation‐linked surface antigens on human mast cells in health and disease
Authors: Valent P. , Schernthaner G.‐H. , Sperr W. R. , Fritsch G. , Agis H. , Willheim M. , Bühring H.‐J. , Orfao A. , Escribano L. 
Published: March 2003

Summary: Mast cells (MC) are multipotent effector cells of the immune system. They contain an array of biologically active mediator substances in their granules. MC also express a number of functionally important cell surface antigens, including stem cell factor receptor (SCFR=kit=CD117), high affinity IgER (FcεRI), or C5aR (CD88). Respective ligands can induce or promote degranulation, migration, or cytokine production. Other integral surface molecules can mediate adhesion or cell aggregation. Recent data suggest that a number of critical molecules are variably expressed on the surface of human MC. In fact, depending on the environment (organ), stage of cell maturation, type of disease, and other factors, MC express variable amounts of activation‐linked antigens (CD25, CD63, CD69, CD88), cell recognition molecules (CD2, CD11, CD18, CD50, CD54), or cytokine receptors. At present, however, little is known about the mechanisms and regulation of expression of such antigens. The present article gives an overview of MC phenotypes in health and disease, and attempts to provide explanations for the phenotypic variability of MC.This study was supported by Fonds zur Förderung der Wissenschaftlichen Forschung in Österreich – FWF grants # P12517 and # P14031, Fondo de Investigaciones Sanitarias de la Seguridad Social (FIS 98/1345), and Fundación Oftalmológica J. Cortés.
Role of human FcεRI+ cells in HIV‐1 infection
Authors: Marone Gianni , Florio Giovanni , Petraroli Angelica , Triggiani Massimo , De Paulis Amato 
Published: March 2003

Summary: Enhanced serum IgE levels in adults and children with HIV‐1 infection could be a marker of poor prognosis. HIV‐1 infection is believed to involve a switch toward a “TH2‐like” cytokine pattern. HIV‐1 gp120 from different clades is a potent stimulus for histamine release from human basophils and mast cells. Gp120 also induces IL‐4 and IL‐13 synthesis from basophils. It functions as a viral superantigen by interacting with the VH3 region of IgE to induce mediator release from human FcεRI+ cells. The chemokine receptor CCR3, which binds the chemokines eotaxin and RANTES, is expressed by basophils and lung mast cells. By interacting with the CCR3 receptor on FcεRI+ cells, HIV‐1 Tat protein is a potent chemoattractant for basophils and lung mast cells. Tat protein also induces IL‐4 and IL‐13 release from basophils. Incubation of basophils with Tat protein upregulates the surface expression of the CCR3 receptor, a co‐receptor of HIV‐1 infection. Extracellular Tat affects the directional migration of human FcεRI+ cells, CCR3 expression and TH2 cytokines release. We have shown that HIV‐1 proteins gp120 and Tat trigger the release of cytokines critical for TH2 polarization from FcεRI+ cells through two distinct mechanisms. In addition, Tat upregulates the β‐chemokine receptor CCR3, making FcεRI+ cells more susceptible to infection with CCR3 tropic HIV‐1 isolates.This paper is dedicated to Rita Levi‐Montalcini who first suggested an involvement of FcεRI+ cells in HIV‐1 infection. This work was supported by a grant from the Istituto Superiore Sanità (AIDS project 40B.64 and 40A.67), CNR (Target project Biotechnology No. 99.00216.PF31 and No. 99.00401. PF49) and MURST (Rome, Italy).
Endotoxin and its binding proteins in chronic liver disease: the effect of transjugular intrahepatic portosystemic shunting
Authors: Kaser Arthur , Ludwiczek Othmar , Waldenberger Peter , Jaschke Werner , Vogel Wolfgang , Tilg Herbert 
Published: March 2003

Abstract: Background: Gut‐derived endotoxin is insufficiently cleared by the diseased liver, and thus, is elevated in plasma of patients with chronic liver disease (CLD). Endotoxin action might be modified by binding to soluble CD14 (sCD14) and lipopolysaccharide‐binding protein (LBP), both of which have not yet been sufficiently studied in CLD.Methods: Endotoxin, sCD14 and LBP have been determined in peripheral blood of 72 patients and 39 control subjects, and in portal and hepatic venous blood of 12 patients during transjugular intrahepatic portosystemic shunt (TIPS) implantation.Results: Peripheral endotoxin (average 3‐fold increased compared to controls), LBP, and sCD14 plasma levels were elevated in chronic liver disease irrespective of Child stage m, preserve/absence of cirrhosis or aetiology. LBP, and sCD14. Furthermore, endotoxin levels in the portal vein (38.1 ± 6.1 pg/ml) were only slightly elevated compared to the hepatic vein (29.2 ± 4.4 pg/ml), and peripheral endotoxin levels did not increase after TIPS.Conclusions: Decreased hepatocellular function rather than hepatic blood shunting might be responsible for endotoxemia. The elevation in LBP and sCD14 levels may be a consequence of endotoxemia.
Histopathological and immunohistochemical analysis of calcifying odontogenic cysts
Authors: Yoshida Mitsuhide , Kumamoto Hiroyuki , Ooya Kiyoshi , Mayanagi Hideaki 
Published: March 2003

Abstract:Method and Results: Calcifying odontogenic cysts (COCs) were examined histopathologically and immunohistochemically to characterize the histological and cytological properties of these lesions. Histopathologically, COCs showed thin or thick lining epithelium with ghost cells. COCs were classified according to proliferative type or nonproliferative type lining epithelium, the presence or absence of ameloblastomatous appearance, and the presence or absence of odontoma in the cyst walls. Immunohistochemically, amelogenin protein was expressed chiefly in ghost cells, whereas cytokeratin 19 (CK19) and bcl‐2 proteins were expressed chiefly in lining epithelial cells. The proportion of cases positive for bcl‐2 protein was slightly higher in COCs with odontoma than in those without odontoma. Lining epithelial cells sporadically showed positive reactions for Ki‐67 antigen. Mean Ki‐67 labeling index was slightly greater in COCs with proliferative type lining epithelium, COCs with ameloblastomatous appearance of the cyst walls, and COCs with odontoma of the cyst walls than in COCs without these histological features. Our results suggest that ghost cells or lining epithelial cells show ameloblastic cytodifferentiation or odontogenic epithelial characteristics, that bcl‐2 protein is associated with survival of lining epithelial cells in COCs, and that high proliferation potential is associated with ameloblastomatous proliferation or combined odontoma. COCs exhibited various histological features with several transitional forms, and immunohistochemical examinations revealed little or no difference in cytodifferentiation and cellular activity among COCs.Conclusion: We conclude that COCs with various histological features have neoplastic potential and may not be separate entities within the same histological spectrum.
Altered expression of collagen XVII in ameloblastomas and basal cell carcinomas
Authors: Parikka Mataleena , Kainulainen Tiina , Tasanen Kaisa , Bruckner‐Tuderman Leena , Salo Tuula 
Published: March 2003

Abstract:Background: Collagen XVII (BP180) is an epithelial transmembrane protein, which presumably plays a role in cell migration and differentiation under both physiological and pathological conditions. Ameloblastoma, the most common odontogenic neoplasm, and basal cell carcinoma (BCC) of the skin exhibit similar growth patterns and share histological features.Methods: Here, we examined the distribution and expression of collagen XVII in ameloblastomas and BCCs using immunohistochemistry and non‐radioactive in situ hybridization. In both tumors, the distribution of collagen XVII varied in different parts of the lesions.Results: In ameloblastomas, immunostaining for collagen XVII was usually localized in the basal and suprabasal cells of the tumor nests, although in some tumors, a diffuse intracellular staining was detected in the central cells of the neoplastic islands. In BCCs, collagen XVII was mostly seen as diffuse cytoplasmic staining in some central and peripheral cells of the tumor islands and also at the cell membranes in the basal keratinocytes of the epidermis overlying the tumor nests. Double immunostaining with antibody against γ2 chain of laminin‐5 showed that these two components of the keratinocyte adhesion complex are usually co‐localized in ameloblastomas and BCCs. In both tumors, collagen XVII mRNA was found in the basal epithelial cells and in some central and peripheral cells of the tumor islands, while the stromal cells were negative.Conclusions: These findings indicate that the expression of collagen XVII may be differentially regulated in various parts of the tumor. Diffuse intracellular distribution of collagen XVII and a consequent loss of critical cellular attachments may contribute to the infiltrative and progressive growing potential of tumors.
The treatment of oral aphthous ulceration or erosive lichen planus with topical clobetasol propionate in three preparations: a clinical and pilot study on 54 patients
Authors: Muzio Lorenzo Lo , Della Valle Antonio , Mignogna Michele D. , Pannone Giuseppe , Bucci Paolo , Bucci Eduardo , Sciubba James 
Published: March 2003

Abstract:Background: This study evaluated the clinical use of a corticosteroid in three preparations (topical clobetasol propionate ointment, clobetasol propionate in an oral analgesic base, and clobetasol propionate in an adhesive denture paste).Methods: Fifty‐four patients (34 males and 20 females) with a history of vesiculo‐ulcero‐erosive oral lesions were selected: 24 with oral erosive lichen planus and 30 with aphthae. The subjects enrolled were randomly divided into three groups, each of 18 patients (10 with aphthae and 8 with lichen planus): the first was treated with topical clobetasol propionate ointment (0.05%) directly on the lesion(s) three times a day; the second with clobetasol propionate in an adhesive denture paste in equal amounts (1:1) two times a day; the third with clobetasol propionate in an oral analgesic base (Orabase‐B) in equal amounts (1:1) two times a day. Each subject scored his or her symptoms daily from most severe (7) to none (0) by verbal assessments using a categorical scale.Results: In all cases, the administration of the corticosteroid was effective in producing remission of symptoms in each group of patients. Significant differences (P<0.05) between groups were determined by the Kruskal–Wallis test. The Dunn test was used in order to detect which group differs from the others; clobetasol and adhesive denture paste correlated with an early remission of pain in lichen and apthous lesions.Conclusion: The results suggest that topical application of clobetasol in an adhesive denture paste is an effective drug for symptomatic oral vesiculo‐erosive and/or ulcerative lesions.
Betel quid‐associated oral lesions and oral Candida species in a female Cambodian cohort
Authors: Reichart P. A. , Schmidtberg W. , Samaranayake L. P. , Scheifele C. 
Published: March 2003

AbstractBackground:  Betel quid chewing (BQC) is still prevalent among elderly Cambodian women and is associated with a wide variety of oral mucosal lesions. BQC has also been associated with a reduced rate of dental caries and changes in the oral microbiological flora.Methods:  Since no studies were available on the impact of BQC on the oral carriage of Candida species, in this study oral swabs (Fungiquick®, Hain Diagnostika, Germany) were taken from the tongue and palate of 48 Cambodian women with BQC habit (study group) and 13 control subjects without BQC habit (control group) to determine the spectrum of Candida species in these two groups. In addition, we investigated lesions of the oral mucosa likely to be associated with BQC habit in both study and control groups.Results:  The median duration of BQC was 10 years (range 10 months−30 years). The following oral lesions were found in the study group: betel chewer's mucosa (85.4%), oral leukoplakia (8.3%), leukoedema (37.5%) and oral lichen planus (4.2%). Oral candidiasis was seen neither in BQ‐chewers nor in controls. Candida spp. were found in 70.8% of the cases (controls 69.2%). Whilst C. albicans was isolated from 27.1% of the study cohort, C. tropicalis was the second most common isolate. One control case was colonised by C. dubliniensis – the first report of this organism from a Cambodian population. There was no significant difference in the candidal carriage rate or the Candida species isolated between the study and the control group.Conclusions:  Mycological findings from the present study do not indicate that BQC has a significant effect on oral colonisation by Candida species.
Analysis of the Ki‐67 antigen at the invasive tumour front of human oral squamous cell carcinoma
Authors: Tumuluri V. , Thomas G. A. , Fraser I. S. 
Published: March 2003

AbstractBackground:  It is hypothesised that cell proliferation, as measured by the Ki‐67 labelling index (LI) at the invasive tumour front (ITF) was directly related to the histological grade in human oral squamous cell carcinomas (SCCs).Methods:  Tissues from 42 human oral SCCs were collected and stained with an antibody directed against the Ki‐67 antigen using an advanced polymer staining system. Quantitation of the immunopositive cells was performed on two parallel sections at the invasive tumour front (ITF), using an image analyser. The Ki‐67 LI was expressed as the number of positive nuclei/mm2 of epithelium. The control tissue used was normal epithelium at the excision margin.Results:  The mean Ki‐67 LI for oral SCCs at the ITF was significantly greater than that for the excision margin tissue (P < 0.0001). There was a positive association between increasing Ki‐67 LI and increasing Broders' grade (P < 0.05), with a well‐differentiated tumour having the lowest mean Ki‐67 LI (1549 ± 806) and a poorly differentiated tumour having the highest value (2232 ± 771). A similar trend was observed between the mean Ki‐67 LI and Bryne's multifactorial grading system.Conclusions:  It was concluded from this study that cell proliferation (as measured by the Ki‐67 antigen) at the ITF had a strong positive relationship with histological grading in human oral SCC.
Sparganosis: a rare case of the oral cavity
Authors:   Anak Iamaroon,   Kom Sukontason, Sukontason Kabkaew 
Published: March 2003

AbstractSparganosis is a rare parasitic disease. We here reported an extremely rare case of intraoral sparganosis in a 21‐year‐old Thai female. Clinically, the lesion presented as an asymptomatic nodule 1 cm × 1 cm in the left upper labial mucosa. An excisional biopsy was performed and the pathological examinations revealed a larva of a sparganum surrounded by a fibrous capsule heavily infiltrated with eosinophils. Excision of the lesion was curative. The possible route of infection of the patient might be due to drinking water, contaminated with Cyclops containing procercoid larvae.