bluuebunny/crossref_metadata_2025_split huggingface dataset:
Titanium release from implants prepared with different surface roughness
Authors: Wennerberg Ann , Ide‐Ektessabi Ari , Hatkamata Shino , Sawase Takashi , Johansson Carina , Albrektsson Tomas , Martinelli Anna , Södervall Ulf , Odelius Hans 
Published: September 2004

AbstractObjectives: There may be a risk of greater ion release for surface‐enlarged implants than conventionally turned components. The major aim of the present paper was to investigate whether a correlation exists between ion release and a surface roughness relevant for today's commercial implants. Other aims were to compare ion release after two insertion times and concentration in bone tissue as a function of distance from the implant surface.Material and methods: Lactic acid aqueous solution (pH=2.3) and phosphate‐buffered saline were used for the in vitro investigation. For the in vivo investigation, synchrotron radiation X‐ray fluorescence (SRXRF) spectroscopy and secondary ion mass spectroscopy (SIMS) were performed 12 weeks and 1 year after implantation in rabbit tibiae.Results: The average height deviation (Sa) was 0.7, 1.27, 1.43 and 2.21 μm, respectively, for the four surfaces investigated. No difference in ion release was found in vitro. In vivo, SRXRF demonstrated slightly higher values for the roughest surface up to a distance of 400 μm from the implant surface; thereafter no difference was found. SIMS demonstrated no difference in ion release for the roughest and smoothest surfaces, but slightly more titanium in bone tissue after 1 year than after 12 weeks. Titanium rapidly decreased with distance from the implant surface.Conclusion: At a level relevant for commercial oral implants, no correlation was found between increasing roughness and ion release, neither in vitro nor in vivo.
Morphologic, functional and behavioral effects of titanium dioxide exposure on nerves
Authors: Onur Mehmet Ali , Taş Zeynep , Gürpınar Aylin , Şahin Saime , Çehreli Murat Cavit 
Published: September 2004

AbstractObjectives: The purpose of this study was to explore morphologic, functional, and behavioral effects of titanium dioxide (TiO2) on nerves.Material and methods: A total of 17 albino rats were used for nerve conduction experiments, hot‐plate tests, and histological evaluation. TiO2 was implanted unilaterally on the sciatic nerves of five rats. Ten days after surgery, test and control nerves were dissected and their signal transduction speeds were quantified by suction electrodes in a bath containing a Tyrode solution. Twelve rats were divided into three equal groups resulting in equal number of nerves (n=8) for TiO2 implantation, surgical exposure of the nerves, and for use as controls. One week after surgery, hot‐plate tests were undertaken for 10 consecutive days to determine response latencies of the nerves. At the termination of the experiments, the nerves were harvested, processed, and examined under a microscope.Results: The signal transduction speeds of TiO2‐implanted nerves was similar to control specimens (P>0.05). The avoidance responses of TiO2‐implanted, surgically exposed, and control nerves were comparable (P>0.05). At the cellular level, TiO2 did not lead to any signs of adverse reactions on nerves.Conclusions: TiO2, the main oxide surrounding endosseous titanium implants, does not alter the structure and the function of myelinated nerves.
Proteome analysis of cashmere
Authors: YOKOHAMA Michinari , MASUDA Takeshi , AMANO Takashi , HIRAYAMA Hiroki , MANABE Takashi 
Published: September 2004

ABSTRACTAs an analysis of the cashmere proteins by Type IV 2‐DE, ten kinds of components, including three components with molecular mass 42–50 kDa whose expression level increased in the winter, were separated. In analyzing nine components of these ten using a mass spectrometer, the three components of molecular mass 70–120 kDa and pI 5.3 were identified as keratin type II microfibrillar (accession no. KRSHL2), keratin 48 k type I microfibrillar component 8c‐1 (accession no. KRSHL1) and cytosolic phospholipase A2 (accession no. O77793), respectively. The three components whose expression level increased in the winter, were identified as keratin type I microfibrillar 48 kDa component 8C‐1 (accession no. P02534) and keratin type I microfibrillar 47.6 kDa (accession no. P25690) (pI 5.2/42 kDa), keratin type II microfibrillar component 7C (accession no. P15241) and keratin typeII‐sheep (accession no. S34165) (pI 5.5/45 kDa), and the keratin type II microfibrillar component 5 (accession no. P25691) (pI 5.8–6.0/45 kDa), respectively. The three components of less than 17 kDa were identified as hair keratin type II intermediate filament (accession no. CAA51836) (pI 5.2) and keratin high‐sulfur matrix protein IIIB2 (accession no. P02447) with a different isoelectric point (pI 5.4 and 5.9), respectively.
Effect of bilateral cecal ligation on use of dietary energy in growing chickens
Authors: SUGAHARA Kunio , MATSUMOTO Mako , YAMADA Motoko , YAOSHIZAWA Fumiaki , KARASAWA Yutaka 
Published: September 2004

ABSTRACTIn order to determine the role of the cecum on energy use in growing chickens, metabolizability of the dietary energy and energy expenditure were examined in the week following bilateral ligation and washing out of the cecum. Apparent metabolizable energy (AME) values were 14.30 and 13.69 kJ/g air‐dry matter for sham‐operated and cecally ligated chickens, respectively. These values were found to be significantly different (P < 0.05). Although AME intake and fasting heat production were decreased by cecal ligation, the distribution of AME (measured as fasting and feeding heat production, as well as heat increment and energy retention, as a proportion of AME intake) was not affected. These results suggest that the cecum helps chickens extract AME from corn‐soybean type diets with little, if any, effect on AME use, based on the present study of growing chickens in the week following cecal ligation.
Functional indispensability of fibronectin associated on the mesenchymal cell surface during the early period of feather development in the chick embryo in vitro
Authors: KOBAYASHI Ken , FUKUNAGA Shigeharu , TAKENOUCHI Kazuaki , NAKAMURA Fumio 
Published: September 2004

ABSTRACTTo clarify the role of fibronectin (FN) during the early period of feather development, reconstituted skin consisting of intact epithelium and isolated mesenchymal cells from embryonal chick skin was used. In early feather development, FN was localized around mesenchymal cells of the dermal condensation. Isolated mesenchymal cells had associated with FN on their surfaces. FN on the cell surface dissociated following EDTA treatment, and EDTA‐treated cells re‐associated with exogenous FN. The intact epithelium also bound to exogenous FN at the placode. When FN‐associated or FN‐reassociated mesenchymal cells were used, the reconstituted skin formed feather rudiments only at the positions where the epithelial placode existed originally, and the locality of tenascin transferred from the placode to the mesenchyme during the period of feather bud formation. However, in reconstituted skin using FN‐dissociated mesenchymal cells, feather rudiments did not form. Additionally, the epithelial placodes disappeared, and tenascin was distributed uniformly on the surface of the epithelium and not localized in the mesenchyme. These findings suggest that FN associated on the surfaces of mesenchymal cells maintains the functions of mesenchymal cells as dermal condensation and mediates epithelial‐mesenchymal interactions during the early period of feather development. The results also suggest that reconstituted skin is a useful tool for functional studies on the extracellular matrix.
Function of opioids in the enteric nervous system
Authors: Wood J. D. , Galligan J. J. 
Published: September 2004

AbstractAlterations in gastrointestinal motility and secretion underlie the constipating action of therapeutically administered opiates. The prototype opiate is morphine, which acts to delay gastric emptying and intestinal transit, to suppress intestinal secretion of water and electrolytes and to suppress transport of bile into the duodenum. The effects of opiates, synthetic opioids and endogenously released opioid peptides on these organ‐level gastrointestinal functions reflect actions on electrical and synaptic behaviour of neurones in the enteric nervous system. Adverse effects and positive therapeutic effects of administration of opioid‐receptor‐blocking drugs on the digestive tract must be understood in the context of the neurophysiology of the enteric nervous system and mechanisms of neural control of gastrointestinal smooth muscle, secretory glands and blood–lymphatic vasculature. We review here the integrated systems of physiology and cellular neurobiology that are basic to understanding the actions of opioid agonists and antagonists in the digestive tract.
Salmonella: a continuing problem
Authors: Hardy A 
Published: September 2004

AbstractSalmonella was the archetypal food poisoning organism of the 20th century. It achieved a high public profile following the salmonella-in-eggs crisis of 1988–89, but by then had been the subject of public health concern and scientific interest for over a century. Early associated with animal foods, the advent of phage typing in the 1940s began to reveal the complexity of its environmental associations. This paper explores the story of salmonella as a continuing problem in epidemiology, microbiology and public health, in the food chain, and in the kitchen.
Thrombotic thrombocytopenic purpura associated with statin treatment
Authors: Sundram F , Roberts P , Kennedy B , Pavord S 
Published: September 2004

Abstract
Thrombotic thrombocytopenic purpura (TTP) is a rare condition but associated with 90% mortality if left untreated. The diagnosis is usually made when there is thrombocytopenia and microangiopathic haemolytic anaemia, although the full pentad also includes fever, renal impairment, and neurological dysfunction. A variety of underlying causes have been implicated in acquired TTP including bacterial and viral infections, bone marrow and organ transplantation, pregnancy, immune disorders, and certain drugs. To date there is just one case report of TTP associated with statin treatment. The clinical course of a patient who presented with TTP after being started on simvastatin, a HMG-CoA inhibitor, is described.
SUPERGRAVITY DESCRIPTION OF FIELD THEORIES ON CURVED MANIFOLDS AND A NO GO THEOREM
Authors: MALDACENA JUAN , NUÑEZ CARLOS 
Published: September 2004

In the first part of this paper we find supergravity solutions corresponding to branes on worldvolumes of the form Rd×Σ where Σ is a Riemann surface. These theories arise when we wrap branes on holomorphic Riemann surfaces inside K3 or CY manifolds. In some cases the theory at low energies is a conformal field theory with two less dimensions. We find some non-singular supersymmetric compactifications of M-theory down to AdS5. We also propose a criterion for permissible singularities in supergravity solutions. In the second part of this paper, which can be read independently of the first, we show that there are no non-singular Randall-Sundrum or de-Sitter compactifications for large class of gravity theories.
Isoforms of the Major Peanut Allergen Ara h 2: IgE Binding in Children with Peanut Allergy
Authors: Hales Belinda J. , Bosco Anthony , Mills Kristina L. , Hazell Lee A. , Loh Richard , Holt Patrick G. , Thomas Wayne R. 
Published: September 2004

<i>Background:</i> The major peanut allergen Ara h 2 consists of two isoforms, namely Ara h 2.0101 and Ara h 2.0201. The recently identified Ara h 2.0201 isoform contains an extra 12 amino acids including an extra copy of the reported immunodominant epitope DPYSPS. This study aimed to evaluate the IgE binding of the two Ara h 2 isoforms. <i>Methods:</i> Ten clones of Ara h 2 were sequenced to assess the relative frequency of the Ara h 2 isoforms and to identify whether there was further variation in the Ara h 2 sequence. IgE binding to Ara h 2.0101 and Ara h 2.0201 was measured for 70 peanut-allergic children using an IgE DELFIA<sup>TM</sup> assay to quantitate specific IgE binding. A competition assay was used to measure whether Ara h 2.0201 contained IgE epitopes other than those found for Ara h 2.0101. <i>Results:</i> The original Ara h 2.0101 sequence was found for 6/10 clones and Ara h 2.0201 was found for 2/10 clones. Ara h 2.0201 had the expected insertion of 12 amino acids as well as substitutions at positions 40 (40G) and 142 (142E). Two new isoforms were identified as different polymorphisms of position 142. One Ara h 2.01 clone (Ara h 2.0102) contained 142E and one Ara h 2.02 clone (Ara h 2.0202) contained 142D. A polymorphism that was previously identified by other investigators at position 77 (77Q or 77R) was not found for any of the 10 sequences. Although the level of IgE binding to Ara h 2.0201 of individual patients was frequently higher than the binding to Ara h 2.0101 (p < 0.01), there was a strong correlation in binding to both isoforms (r = 0.987, p < 0.0001) and when analyzed as a group the means were similar. Ara h 2.0101 was not as efficient at blocking reactivity to Ara h 2.0201 indicating there is an additional IgE specificity for the Ara h 2.0201 isoform. <i>Conclusions:</i> Ara h 2.0201 has similar but higher IgE binding than the originally sequenced Ara h 2.0101 isoform and contains other IgE specificities.
Regulation of the single-chain urokinase–urokinase receptor complex activity by plasminogen and fibrin: novel mechanism of fibrin specificity
Authors: Higazi Abd Al-Roof , Ajawi Feras , Akkawi Sa'ed , Hess Edna , Kuo Alice , Cines Douglas B. 
Published: September 2004

AbstractActivation of plasminogen by urokinase plasminogen activator (uPA) plays important roles in several physiologic and pathologic conditions. Cells secrete uPA as a single-chain molecule (scuPA). scuPA can be activated by proteolytic cleavage to a 2-chain enzyme (tcuPA). scuPA is also activated when it binds to its receptor (uPAR). The mechanism by which the enzymatic activity of the scuPA/suPAR complex is regulated is only partially understood. We now report that the plasminogen activator activity of the scuPA/suPAR complex is inhibited by Glu- and Lys-plasminogen, but not by mini-plasminogen. In contrast, neither Glunor Lys-plasminogen inhibits the activation of plasminogen by 2-chain uPA. Inhibition of scuPA/suPAR activity was evident at a Glu-plasminogen concentration of approximately 100 nM, and at physiologic plasma concentrations inhibition was nearly complete. A plasminogen fragment containing kringles 1-3 inhibited the enzymatic activity of scuPA/suPAR with an inhibition constant (Ki) equal to 1.9 μM, increased the Michaelis constant (Km) of scuPA/suPAR from 18 nM to 49 nM, and decreased the catalytic constant (Kcat) approximately 3-fold from 0.035 sec—1 to 0.011 sec—1. Inhibition of scuPA/suPAR by plasminogen was completely abolished in the presence of fibrin clots. These studies provide insight into the regulation of uPA-mediated plasminogen activation and identify a novel mechanism for its fibrin specificity.
Dendritic cell-derived IL-2 production is regulated by IL-15 in humans and in mice
Authors: Feau Sonia , Facchinetti Valeria , Granucci Francesca , Citterio Stefania , Jarrossay David , Seresini Samantha , Protti Maria Pia , Lanzavecchia Antonio , Ricciardi-Castagnoli Paola 
Published: September 2004

AbstractDendritic cells (DCs) are involved in the initiation and regulation of innate and adaptive immune responses. Several molecular mechanisms regulate these diverse DC functions, and we have previously reported that mouse dendritic cells (mDCs) can produce interleukin-2 (IL-2) in vitro and in vivo, in response to microbial activation and T-cell-mediated stimuli. This property is shared by different DC subtypes, including Langerhans cells. Here we show that, on appropriate stimulation, human DCs, both plasmacytoid and myeloid subtypes, also express IL-2. Interestingly, the production of IL-2 by myeloid DCs is induced by T-cell-mediated stimuli and depends on the presence of IL-15. The key role of this cytokine in regulating IL-2 production was also confirmed in the mouse system. In particular, we could show that DCs from IL-15-deficient mice were strongly impaired in the ability to produce IL-2 after interactions with different microbial stimuli. Our results indicate that DC-produced IL-2 is tightly coregulated with the expression of IL-15.
The CD28 family: a T-cell rheostat for therapeutic control of T-cell activation
Authors: Riley James L. , June Carl H. 
Published: September 2004

AbstractThe CD28 family of receptors (CD28, cytotoxic T-lymphocyte–associated antigen 4 [CTLA-4], inducible costimulator [ICOS], program death-1 [PD-1], and B- and T-lymphocyte attenuator [BTLA]) plays a critical role in controlling the adaptive arm of the immune response. While considerable information is available regarding CD28 and CTLA-4, the function of the more recently discovered members of the CD28 family is less well understood. This review will highlight recent findings regarding the CD28 family with special emphasis on effects the CD28 family has on immunopathology, the discovery of costimulatory antibodies with superagonist function, and the status of clinical trials using various strategies to augment or block T-cell costimulation.
High factor VIII levels in venous thromboembolism show linkage to imprinted loci on chromosomes 5 and 11
Authors: Berger Mario , Mattheisen Manuel , Kulle Bettina , Schmidt Henriette , Oldenburg Johannes , Bickeböller Heike , Walter Ulrich , Lindner Tom H. , Strauch Konstantin , Schambeck Christian M. 
Published: September 2004

AbstractHigh factor VIII (FVIII) levels are known to be a risk factor for deep venous thrombosis, but the mechanisms responsible for high FVIII levels remain unclear. Here, a new phenotype “FVIII level residuum” (FVIII-R) was defined in order to eliminate the impact of common determinants on FVIII levels. We studied 13 families of patients with thrombosis and reproducibly high FVIII levels of unknown origin. Since familial clustering was evident, we looked for a possible genetic basis. A genome scan was performed with 402 evenly spaced microsatellite markers. A quantitative linkage analysis using variance component methods showed suggestive evidence for linkage of FVIII-R with a locus on chromosome 8 (logarithm of odds [LOD] = 2.1). In addition, we performed parametric exploratory linkage analysis of dichotomized FVIII-R, taking a parent-of-origin effect into account. Single-trait-locus MOD-score analysis showed suggestive evidence for linkage under an imprinting model at chromosomes 5 and 11. Furthermore, a 2-trait-locus analysis under a multiplicative model for the loci of chromosomes 5 and 11 yielded a remarkable LOD of 4.44. It confirmed the finding of paternal imprinting, obtained by single-trait-locus analysis, at both loci. Our results suggest that high FVIII levels in venous thromboembolism represent a complex trait caused by several genetic factors.
Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia
Authors: Druhan Lawrence J. , Ai Jing , Massullo Pam , Kindwall-Keller Tamila , Ranalli Mark A. , Avalos Belinda R. 
Published: September 2004

AbstractSevere congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a myeloid maturation arrest in the bone marrow, ineffective neutrophil production, and recurrent infections. Most patients respond to treatment with granulocyte colony-stimulating factor (G-CSF), and the majority harbor mutations in the neutrophil elastase gene. In the subset of patients with SCN transforming to acute myeloid leukemia (AML), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected. Here, we report a novel mutation in the extracellular portion of the G-CSFR within the WSXWS motif in a patient with SCN without AML who was refractory to G-CSF treatment. The mutation affected a single allele and introduced a premature stop codon that deletes the distal extracellular region and the entire transmembrane and cytoplasmic portions of the G-CSFR. Expression of the mutant receptor in either myeloid or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it. WT/mutant G-CSFR heterodimers appeared to be retained in the endoplasmic reticulum and/or Golgi and accumulate intracellularly. These findings together with 2 previous case reports of extracellular mutations in the G-CSFR in patients with SCN unresponsive to G-CSF suggest a common mechanism underlying G-CSF refractoriness.
Graft calcifications and dysfunction following liver transplantation
Authors: Tzimas George N , Afshar Mohammad , Chevet Eric , Emadali Anouk , Vali Hojatollah , Metrakos Peter P 
Published: September 2004

Abstract
Background
The molecular events, following ischemia and reperfusion (I/R) of the liver during transplantation are largely unknown. There is evidence that apoptotic and necrotic events may take place, and occasionally result in primary graft dysfunction. We herein report two cases, where significant I/R injury correlated with the development of liver calcification and primary liver dysfunction.

Case Presentation
Both patients with clinical and biochemical evidence of primary graft dysfunction demonstrated calcification at light and electron microscopy levels. In addition, one patient had macroscopic evidence of calcification on cross-sectional imaging. Both patients died secondary to the sequelae of the graft dysfunction.

Conclusions
Severe I/R-induced injury to the liver, clinically leads to graft dysfunction. This is due to advanced apoptotic and/or necrotic events at the hepatocyte level that may, on the most severe form, lead to calcification. The study of microcalcification at the early posttransplant period could provide insight in the events taking place following significant ischemia/reperfusion-induced injury to the graft.
Lead editorial: The need for greater perspective and innovation in epidemiology
Authors: Phillips Carl V , Goodman Karen J , Poole Charles ,   the editors of Epidemiologic Perspectives & Innovations
Published: September 2004

AbstractThis editorial introduces the new online, open-access, peer-reviewed journal, Epidemiologic Perspectives & Innovations. Epidemiology (which we define broadly, to include clinical research and various approaches to studying the health of populations) is a critically important field in informing decisions about the health of individuals and populations. But the desire for new information means that the health science literature is overwhelmingly devoted to reporting new findings, leaving little opportunity to improve the quality of the science. By creating a journal dedicated to all topics of and about epidemiology, except standard research reports, we hope to encourage authors to write more on the neglected aspects of the field. The journal will publish articles that analyze policy implications of health research, present new research methods and better communicate existing methods, reassess previous results and dogma, and provide other innovations in and perspectives on the field. Online publishing will permit articles of whatever length is required for the work, speed the time to publication and allow free access to the full content.