bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical bond failure of pre‐coated and operator‐coated orthodontic brackets
Authors: Kula K , Schreiner R , Brown J , Glaros A 
Published: March 2003

Structured Abstract
Objectives –
To test the hypothesis that there is no significant difference in clinical bracket failure between the 3M APC Mini Twin™ bracket system and the Transbond XT™ adhesive during orthodontic treatment.
Design –
A randomized, split mouth, prospective clinical trial.
Setting and Sample Population –
The Department of Orthodontics and Dentofacial Orthopedics at University of Missouri, Kansas City. Twenty‐nine subjects who were treatment planned to receive comprehensive orthodontics using 0.018 slot appliances.
Experimental Variable –
The adhesive pre‐coated brackets (APC ) system was randomly assigned to one side of the mouth and the Transbond XTTMwas assigned to the opposite side.
Outcome Measure –
The absence of any of the brackets at the time of a regular or emergency orthodontic appointment.
Results –
There was no significant difference (P > 0.05) in bracket failure between the 3M APC Mini TwinTM bracket system and the Transbond XTTM adhesive at any time period (90, 180, or 365 days). The failure rate of brackets on premolars was higher than on incisors or canines.
Conclusion –
APC Mini TwinTM bracket system and Transbond XTTMadhesive are equally effective in maintaining brackets clinically. Inexperienced operators had an overall 7.5% bond failure 12 months following bracket placement.
Tgf‐β1, Tgf‐β2, Tgf‐β3 and Msx2 expression is elevated during frontonasal suture morphogenesis and during active postnatal facial growth
Authors: Adab K , Sayne JR , Carlson DS , Opperman LA 
Published: March 2003

Structured Abstract
Authors –
Adab K, Sayne JR, Carlson DS, Opperman LA.
Objectives –
It is hypothesized that regulation of facial suture morphogenesis is similar to that of cranial sutures, with expression of similar regulatory molecules, governing suture formation and patency. The present study was designed to characterize the morphology of the frontonasal (FN) suture of the rat at different developmental stages and to investigate the presence and temporal‐spatial expression of transforming growth factor‐beta 1 (Tgf‐β1), Tgf‐β2, Tgf‐β3 and Msx2 mRNA within these structures.
Setting and sample population –
The Department of Biomedical Sciences at Texas A&M University System Health Science Center, Baylor College of Dentistry, Dallas, TX USA. Histological sections and RNA isolated from FN suture tissues of Sprague‐Dawley rats, aged embryonic day 16 through postnatal day 20.
Method –
Sections were examined after immunohistochemical staining. Gene expression was determined by densitometric analysis of RT‐PCR products run on agarose gels.
Results –
FN sutures develop slightly later than cranial sutures and show increased complexity over time when compared to cranial sutures. FN sutures were closely associated with the nasal capsular cartilage, with intervening layers of perichondrium and periosteum. The pattern of expression of Tgf‐βs within the FN suture tissues was similar to that seen in the cranial sutures. However, mRNA and protein of the Tgf‐βs were differentially expressed over time compared to cranial sutures. In FN sutures, Tgf‐β mRNA levels were elevated both during the period of suture morphogenesis and during active bone growth from the suture in the early postnatal period. Msx2 mRNA expression was elevated in both the prenatal and postnatal periods, similar to Tgf‐β mRNA expression.
Conclusion –
Tgf‐β and Msx2 are present in facial sutures similar to cranial sutures, but are differenentially expressed over time, perhaps reflecting different bone growth rates from these sutures.
Mannose‐binding lectin: targeting the microbial world for complement attack and opsonophagocytosis
Authors: Jack Dominic L. , Klein Nigel J. , Turner Malcolm W. 
Published: March 2003

Summary:Mannose‐binding lectin (MBL) is an important constituent of the innate immune system. This protein binds through multiple lectin domains to the repeating sugar arrays that decorate many microbial surfaces, and is then able to activate the complement system through a specific protease called MBL‐associated protease‐2. We have used flow cytometry to study both the binding of MBL to microorganisms and the subsequent activation of complement. For selected Gram‐negative organisms, such as Salmonella and Neisseria, we have examined the relative roles of lipopolysaccharide (LPS) structure and capsule in determining binding and conclude that the LPS is of major importance. Our results from studies with several clinically relevant organisms also show that MBL binding detected by flow cytometry leads to measurable activation of purified C4, suggesting that the bound lectin is capable of initiating opsonophagocytosis and/or bacterial lysis. There is an increasing literature suggesting that MBL deficiency, which mainly results from three relatively common single point mutations in exon 1 of the gene, predisposes both to infection by extracellular pathogens and to autoimmune disease. In addition, the protein also modulates disease severity, at least in part through a complex, dose‐dependent influence on cytokine production. The mechanisms and signalling pathways involved in such processes remain to be elucidated.We thank the Medical Research Council, the Wellcome Trust and Action Research for their support. Research at the Institute of Child Health and Great Ormond Street Hospital for Children NHS Trust benefits from R&D funding received from the NHS Executive. We thank David Smithson for graphic design of the figures.
The centromeric part of the human natural killer (NK) receptor complex: lectin‐like receptor genes expressed in NK, dendritic and endothelial cells
Authors: Hofer Erhard , Sobanov Yuri , Brostjan Christine , Lehrach Hans , Düchler Markus 
Published: March 2003

Summary: The human natural killer (NK) receptor complex encompasses a region of about 2 Mb on the short arm of chromosome 12. It contains at least 18 lectin‐like receptor genes, of which some are expressed in NK and NK/T cells and function as NK receptors. Close to the CD94 and NKG2 NK receptor genes in the centromeric part, a novel family of genes, expressed in myeloid, dendritic and/or endothelial cells, recently became evident. These genes encode a receptor for oxidized low density lipoprotein in endothelial cells and three other receptors potentially serving regulatory functions in dendritic cells. Although the overall structure of the human NK receptor complex is similar to the syntenic rodent regions, the centromeric part lacks the cluster of Ly49 genes. This supports the notion that recognition of MHC class Ia molecules has evolved separately in rodents and humans in the lectin‐like Ly49 and the killer immunoglobulin‐like receptors, respectively. In the telomeric part, other lectin‐like genes expressed in different hematopoietic lineages are found. The receptors of the NK receptor complex apparently serve important functions in several leukocytes and in endothelial cells, and the exact role of these receptors, their ligands, and their distinct and co‐ordinate regulation in different cell lineages warrants further investigation.()This work was supported by grants of the Austrian National Bank and the European Commission.
Rat natural killer cell receptor systems and recognition of MHC class I molecules
Authors: Rolstad Bent , Naper Christian , Løvik Guro , Vaage John Torgils , Ryan James C. , Bäckman‐Petersson Eva , Kirsch Ralf D. , Butcher Geoffrey W. 
Published: March 2003

Summary: Rat natural killer (NK) cells recognize MHC‐I molecules encoded by both the classical (RT1‐A) and non‐classical (RT1‐C/E/M) MHC class I (MHC‐I) regions. We have identified a receptor, the STOK2 antigen, which belongs to the Ly‐49 family of killer cell lectin‐like receptors, and we have localized the gene encoding it to the rat natural killer cell gene complex. We have also shown that it inhibits NK cytotoxicity when recognizing its cognate MHC‐I ligand RT1‐A1c on a target cell. This is the first inhibitory Ly‐49–MHC‐I interaction identified in the rat and highlights the great similarity between rat and mouse Ly‐49 receptors and their MHC ligands. However, the mode of rat NK‐cell recognition of target cells indicates that positive recognition of allo‐MHC determinants, especially those encoded by the RT1‐C/E/M region, is a prevalent feature. NK cells recruited to the peritoneum as a consequence of alloimmunization display positive recognition of allodeterminants. In one case, NK cells activated in this way have been shown to be specific for the immunizing, non‐classical class I molecule RT1‐Eu. These findings show that allospecific NK cells sometimes show features reminiscent of the adaptive immune response.This research was supported by grants from the Norwegian Cancer Society, the Research Council of Norway, the Anders Jahre's Fund, the UK BBSRC to RDK (PhD studentship) and GWB (Competitive Strategic Grant). EBP also acknowledges support from The Swedish Foundation for International Cooperation in Research and Higher Education, The Knut and Alice Wallenberg Foundation and the Swedish Institute.
Immunobiology of natural killer cells and bone marrow transplantation: merging of basic and preclinical studies
Authors: Murphy William J. , Koh Crystal Y. , Raziuddin Arati , Bennett Michael , Longo Dan L. 
Published: March 2003

Summary: Natural killer (NK) cells mediate acute rejection of bone marrow, but not solid tissue, allografts in lethally irradiated mice. Precisely how and why this rejection occurs is still unclear. In allogeneic bone marrow transplantation (BMT), a spectrum of results is possible; one result can be marrow graft failure due to host rejection of the graft by NK and T cells and, at the opposite spectrum, the occurrence of graft‐versus‐host disease (GVHD). Donor NK cells, however, appear capable of improving donor engraftment without giving rise to GVHD and thus may be of use as an immunotherapy following BMT. As NK‐cell inhibitory receptors play a role in bone marrow cell rejection, these same inhibitory receptors may also affect NK responses towards tumor cells. It has been demonstrated that blocking the interaction of inhibitory receptors with MHC determinants on tumor cells can result in greater antitumor effects. Thus, NK cells are capable of mediating both positive and negative effects during BMT depending on whether they are of host versus donor origin and their state of activation. Understanding their role in BMT provides insights as to their physiological roles and points the way to potential clinical uses.The authors are grateful for the excellent secretarial assistance by Ms Laura Knott. The authors thank Dr Lisbeth Welniak for critically reviewing the manuscript. WJM is particularly grateful to the members of his laboratory for contributing to the projects over the years and to his two mentors, MB and DLL, for their training and guidance, which allowed him to develop his studies on the basic and preclinical aspects of NK cells in BMT in his laboratory. This project has been funded in whole or in part with Federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. N01‐CO‐56000, and by NIH grants CA36922, CA70134, and AI38938. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government.
The role of STAT6 in mast cell IL‐4 production
Authors: Sherman Melanie A. 
Published: March 2003

Summary: Interleukin (IL)‐4 has an important role in regulating antibody production and inflammation. The major IL‐4 producers are CD4+ T cells, but the development of an IL‐4‐producing phenotype in these cells requires IL‐4 signaling through the STAT6 pathway during differentiation. The cellular source of this early IL‐4 is not known, but mast cells are a possible candidate due to their immediate and indiscriminate release of IL‐4 upon activation. In this review we summarize the evidence that STAT6 signaling is not required for mast cell IL‐4 production, which is consistent with their possible role as a link between the innate immune response and T‐cell activation. We also describe an isoform of STAT6 that is expressed in mast cells and that appears to act as a repressor of IL‐4 transcription. This STAT6 signaling pathway may be part of a feedback mechanism to protect surrounding tissues from IL‐4‐mediated inflammation during an infection.The author would like to thank Dr. Melissa Brown for her generous support, helpful discussions and critical review of the manuscript and Dr. Virginia Secor for her collaboration with this project. Drs. Andrew Neish, Jeremy Boss and S. Wright Caughman provided helpful comments. M.A.S. was a fellow of the Cancer Research Institute and this project is currently supported by the National Institutes of Health (KO1 AR 02157‐01).
Ribosomes and secretory granules in human mast cells: close associations demonstrated by staining with a chelating agent
Authors: Dvorak Ann M. , Morgan Ellen S. 
Published: March 2003

Summary: The distribution of ribosomes was investigated in mature human mast cells with a chelation‐based staining protocol known to bleach DNA‐rich structures, leaving RNA‐rich structures unbleached. With this method, electron‐dense ribosomes were adjacent to, attached to, and within secretory granules, which were also bleached with the chelation method that we used. The finding of these ribosome–secretory granule relationships suggests that secretory granules in mature human mast cells may participate in RNA metabolism.This work was supported by a grant (AI 33372) from the National Institutes of Health. We thank Peter K. Gardner for editorial assistance in the preparation of the manuscript and Patricia Fox for printing the electron micrographs.
Eosinophil trafficking to sites of allergic inflammation
Authors: Broide David , Sriramarao P. 
Published: March 2003

Eosinophils play a prominent pro‐inflammatory role in allergic inflammation. Studies utilizing flow chambers, intravital videomicroscopy, and cytokine and adhesion molecule‐deficient mice have provided important insight into the mechanisms of eosinophil trafficking in inflamed blood vessels and into tissues in vivo. While the bone marrow generation of eosinophils is finely regulated by interleukin (IL)‐5, the trafficking of eosinophils into tissues is regulated by several cytokines, chemokines, and adhesion molecules with overlapping functions. Prospects for therapeutically inhibiting eosinophilic inflammation by inhibiting eosinophil adhesion to endothelium are dependent on an improved understanding of the relative importance of individual cytokines and adhesion molecules in regulating eosinophil adhesion to endothelium. Alternative strategies to inhibit eosinophilic inflammation include the use of immunostimulatory DNA sequences containing a CpG motif to act as a Th1 adjuvant to prevent Th2 responses associated with IL‐5 and eosinophilia. Immunostimulatory DNA sequences do not induce eosinophil apoptosis, but function at the level of the bone marrow to inhibit the IL‐5‐induced bone marrow generation and release of eosinophils.This research was supported by NIH grants AI 38425 and AI 33977 (DHB) and AI 35796 to (PS).
Quantitative versus morphological assessment of liver fibrosis: semi‐quantitative scores are more robust than digital image fibrosis area estimation
Authors: Wright Mark , Thursz Mark , Pullen Rebecca , Thomas Howard , Goldin Robert 
Published: March 2003

Abstract: Background/Aim: Digital image analysis (DIA) allows quantitative assessment of fibrosis on liver biopsy. Accurate determination of a threshold greyscale level representing fibrous tissue is critical. This method has not been fully evaluated in clinical practice.Methods: Digital images of stained liver biopsy sections were captured by microscopy and converted to greyscale. A novel method of determining the threshold greyscale value at which to measure fibrosis area was developed (peak proportion area change (PPAC)). Reproducibility was tested in comparison with standard interactive thresholding and with semi‐quantitative scoring using the Histological activity index (HAI) system by a histopathologist. Fibrosis areas for different sections from the same biopsy core were also compared by each method.Results: Comparison between PPAC and interactive thresholding method demonstrated superior reproducibility of the PPAC method: r > 0.7, P < 0.001 compared with r = 0.19–0.64 (not all reaching significance). On a single section, reproducibility was similar for PPAC and the modified HAI system. When different sections from the same core were compared, the HAI system was more robust.Conclusions: The PPAC method is superior to standard interactive thresholding. However, variability in DIA scores between sections invalidates the technique for clinical use and semi‐quantitative scoring systems remain the gold standard for fibrosis assessment.
Urinary steroids, FSH and CG measurements for monitoring the ovarian cycle and pregnancy in the chimpanzee
Authors: Shimizu Keiko , Douke Chisato , Fujita Shiho , Matsuzawa Tetsuro , Tomonaga Masaki , Tanaka Masayuki , Matsubayashi Kiyoaki , Hayashi Motoharu 
Published: March 2003

Abstract:Non‐invasive methods for monitoring reproductive status of chimpanzee based on the measurement of urinary steroids and gonadotropins were examined. A typical pre‐ovulatory urinary estrone conjugate (E1C) surge and post‐ovulatory increase in pregnandiol glucuronide (PdG) were seen during the menstrual cycle. Urinary follicle stimulating hormone (FSH) showed two peaks over the infertile menstrual cycle. The earliest changes indicating pregnancy were a coincident rise in E1C and chorionic gonadotropin (CG) levels and a concomitant fall in FSH levels. Urinary PdG levels showed a prolonged rise. Urinary E1C in the pregnant chimpanzee was higher than during the menstrual cycle and increased with advancing gestation, with maximum levels occurring near term. In the case of stillbirth, E1C and CG levels from mid‐ through late‐pregnancy were low and the prepartum progressive increase in E1C was not shown. The data presented here are of great practical value in captive breeding management of chimpanzees.
Does variation in patch use among butterfly species contribute to nestedness at fine spatial scales?
Authors: Summerville Keith S. , Veech Joseph A. , Crist Thomas O. 
Published: March 2003

A nested pattern occurs whenever the species observed in depauperate habitat patches are a subset of those found in more species‐rich patches. Ecologists have documented many instances of nestedness caused by population‐level processes such as colonization and extinction at biogeographic scales. However, few researchers have examined whether nestedness may exist at fine scales due to the ways in which individual organisms discriminate among potential habitat patches. In 1999, we experimentally fragmented an old‐field habitat into patches of varying size to test whether nestedness could exist on a fine spatial scale. Five treatments of differing patch size were replicated five times in a Latin square design by selectively mowing 15×15 m2 plots within an old‐field (patch areas: 225, 180, 135, 90, and 45 m2). Specifically, we tested whether butterflies foraging within a network of patches differing in area conformed to a nested subset structure. We also classified species according to (1) their flight height while foraging (high or low), and (2) their adult habitat breadth (ubiquitous, general, or restricted) to determine whether nestedness could be explained by difference in species’ tendency to discriminate among patches differing in area.

We found significant evidence that a community of foraging Lepidoptera conformed to a nested subset structure based on the difference between the observed nestedness within the butterfly community and the nestedness obtained from randomly generated species presence/absence matrices. Poisson regression analyses demonstrated that high‐flying, habitat‐restricted species avoided the smallest patches (90 and 45 m2) in favor of larger remnants, whereas low‐flying, habitat generalists used all patch sizes. Thus, our study is one of the first to demonstrate that nestedness among species subsets can be observed at fine spatial scales (within a single 1.5 hectare field) and may be maintained by species behavioral differences: discriminating species (i.e. high‐flying, habitat restricted) avoided the smallest patches, and less discriminating species (i.e. low‐flying, ubiquitous) were distributed throughout the field without regard to patch size. Our results also suggest that nestedness should be viewed as yet another scalar pattern in ecology, generated by variation in patch use by individuals at fine‐scales as well as the more traditionally invoked processes of extinction and colonization of species at broad‐scales.
Precancerous foci in pleomorphic adenoma of the salivary gland: recognition of focal carcinoma and atypical tumor cells by P53 immunohistochemistry
Authors: Ohtaké Sachiko , Cheng Jun , Ida Hiroko , Suzuki Makoto , Ohshiro Kazufumi , Zhang Weiguo , Saku Takashi 
Published: March 2003

AbstractBackground:  It is still controversial if atypical tumor cells scattered in salivary pleomorphic adenomas are precancerous and how carcinoma arises in pleomorphic adenomas.Methods:  We studied clinicopathologically the frequency and variation of cellular atypia among tumor cells and examined the expression status of p53 gene products as well as proliferating cell nuclear antigen (PCNA) in 101 surgical materials of pleomorphic adenomas.Results:  Histopathologically, atypical tumor cells were found in 51% of the cases examined. Their mode of distribution was classified into three groups: focal (six cases, 6%) which could be identified as focal carcinoma, measuring less than 1 mm in diameter; sporadic (15 cases, 15%) and singular (30 cases, 30%). These atypical cells were located mainly within sheet‐like nests of tumor cells but not in chondroid or fibro‐hyaline foci. Immunohistochemically, most of the atypical cells were positive for p53 gene products and PCNA.Conclusion:  The results indicated that atypical cells with p53 protein accumulation in their nuclei could be regarded as cells in a precancerous state not yet forming an apparent carcinomatous nest. Some cell population with these atypical cells are likely to form focal carcinomas and then to an apparent form of carcinoma in pleomorphic adenoma.
Oral lichen planus: immunohistology of mucosal lesions
Authors: Dorrego Mariana Villarroel , Correnti María , Delgado Rafael , Tapia Felix J. 
Published: March 2003

AbstractBackground:  Current evidence suggests that immunological mechanisms are involved in oral lichen planus (OLP) pathogenesis. The events implicate activated epithelia that comprise antigen‐presenting Langerhans cells, immunocompetent keratinocytes and subepithelial inflammatory infiltrate. Also, the presence of a high density of leucocyte cells may occur for the expression of a variety of adhesion molecules. The aim of this study was to analyse the immunoexpression of some adhesion molecules as well as lymphocytic markers in order to determine the disease pathogenesis in a Venezuelan population.Methods:  The 18 OLP and 10 normal oral mucosa biopsies were immunostained for CD4, CD8, CD1a, LFA‐1, VCAM‐1 and ICAM‐1.Results:  The results showed an increased number of CD4+, CD8+, CD1a+ cells in OLP. Serial sections showed CD4+ and CD8+ cells also expressed LFA‐1. The expression of ICAM‐1 and VCAM‐1 were significantly higher in OLP.Conclusions:  The immunological reaction begins with Langerhans cells activation, which presents an antigen to CD4+ lymphocytes. Those cells through ICAM‐1 and LFA‐1 promote epithelial destruction. Afterwards, cytokine production, ICAM‐1 and VCAM‐1 expression can activate CD8+ lymphocytes leading to the chronic form of the disease.