bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dissemination of a Sjögren's syndrome–associated extranodal marginal‐zone B cell lymphoma: Circulating lymphoma cells and invariant mutation pattern of nodal Ig heavy‐ and light‐chain variable‐region gene rearrangements
Authors: Hansen A. , Reiter K. , Pruss A. , Loddenkemper C. , Kaufmann O. , Jacobi A. M. , Scholze J. , Lipsky P. E. , Dörner T. 
Published: December 2005

AbstractObjectiveBoth the genesis and outgrowth of extranodal marginal‐zone B cell lymphomas (MZLs) of the mucosa‐associated lymphoid tissue (MALT) type are generally thought to represent antigen‐driven processes. We undertook this study to analyze lymphoma progression and dissemination outside of the MALT‐type lesions.MethodsHistopathologic and Ig heavy‐ and light‐chain variable‐region gene (VH/L) analyses were performed in sequential tissue samples from a patient with primary Sjögren's syndrome (SS) with glandular (parotid) manifestations and subsequent nodal dissemination of a low‐grade MZL.ResultsThis MZL expressed a CD20+,CD27+,sIgM/κ+,IgD−,CD5−,CD10−,Bcl‐6−,CD23−,p53−,p21−,MDM2− phenotype and mutated VH1–69/D2–21/JH4α–VκA27/Jκ2 Ig rearrangements. Notably, circulating lymphoma cells from the parotid glands occurred transiently in the patient's blood, as detected by single‐cell polymerase chain reaction. In addition, 2 minor B cell clones (clones 2 and 3, with VH3–07/D3–22/JH3b–Vλ3L/Jλ2/3 and VH3–64/D3–03/JH2–VκA19/Jκ2 rearrangements, respectively) were also detected in the parotid glands and blood, and 1 of these (clone 2) was also detected in the lymph nodes. Ig VH/L analyses revealed ongoing (antigen‐driven) mutations of the glandular lymphoma rearrangements, but an invariant mutation pattern of their nodal counterparts.ConclusionThese data indicate coexpansion and transient (re)circulation of the lymphoma clone and 2 additional glandular B cell clones in a primary SS–associated extranodal MZL. Combined histologic and molecular features of the nodal lymphoma subclone reflect a process of “follicular colonization” that eventually froze the mutation machinery after accumulation of additional (antigen‐driven) Ig VH/L mutations.
Production of lipid peroxidation products in osteoarthritic tissues: New evidence linking 4‐hydroxynonenal to cartilage degradation
Authors: Morquette Barbara , Shi Qin , Lavigne Patrick , Ranger Pierre , Fernandes Julio C. , Benderdour Mohamed 
Published: December 2005

AbstractObjectiveThe lipid peroxidation product 4‐hydroxynonenal (HNE) is prominently produced in osteoarthritic (OA) synovial cells, but its specific contribution to cartilage destruction is not understood. This study was designed to test whether HNE signaling and binding are involved in OA cartilage degradation through type II collagen (CII) and matrix metalloproteinase 13 (MMP‐13) modulation.MethodsHNE levels in synovial fluid and in isolated OA chondrocytes treated with free radical donors were determined by enzyme‐linked immunosorbent assay. The formation of the HNE/CII adducts was measured in cartilage explants by immunoprecipitation. Levels of CII and MMP‐13 messenger RNA and protein were determined by reverse transcription–polymerase chain reaction, Western blotting, and by the use of commercial kits.ResultsLevels of HNE/protein adducts were higher in OA synovial fluid compared with normal synovial fluid and were higher in OA chondrocytes treated with free radical donors compared with untreated cells. In cartilage explants, HNE induced CII cleavage, as established by the generation of neoepitopes. The level of HNE/CII adducts was increased in OA cartilage explants incubated with free radical donors. Modification of CII by HNE accelerated its degradation by active MMP‐13. In isolated OA chondrocytes, HNE inhibited the expression of CII and tissue inhibitor of metalloproteinases 1 and induced MMP‐13 mainly through activation of p38 MAPK. In vitro, HNE binding to MMP‐13 activated this enzyme at a molar ratio of 1:100 (MMP‐13 to HNE).ConclusionThe increased level of HNE in OA cartilage and the ability of HNE to induce transcriptional and posttranslational modifications of CII and MMP‐13 suggest that this aldehyde could play a role in OA.
Contribution of congestive heart failure and ischemic heart disease to excess mortality in rheumatoid arthritis
Authors: Nicola Paulo J. , Crowson Cynthia S. , Maradit‐Kremers Hilal , Ballman Karla V. , Roger Véronique L. , Jacobsen Steven J. , Gabriel Sherine E. 
Published: December 2005

AbstractObjectiveAlthough mortality among patients with rheumatoid arthritis (RA) is higher than in the general population, the relative contribution of comorbid diseases to this mortality difference is not known. This study was undertaken to evaluate the contribution of congestive heart failure (CHF) and ischemic heart disease (IHD), including myocardial infarction, to the excess mortality in patients with RA, compared with that in individuals without RA.MethodsWe assembled a population‐based inception cohort of individuals living in Rochester, Minnesota, in whom RA (defined according to the criteria of the American College of Rheumatology [formerly, the American Rheumatism Association]) first developed between 1955 and 1995, and an age‐ and sex‐matched non‐RA cohort. All subjects were followed up until either death, migration from the county, or until 2001. Detailed information from the complete medical records was collected. Statistical analyses included the person‐years method, cumulative incidence, and Cox regression modeling. Attributable risk analysis techniques were used to estimate the number of RA deaths that would be prevented if the incidence of CHF was the same in patients with RA and non‐RA subjects.ResultsThe study population included 603 patients with RA and 603 subjects without RA. During followup, there was an excess of 123 deaths among patients with RA (345 RA deaths occurred, although only 222 such deaths were expected). The mortality rates among patients with RA and non‐RA subjects were 39.0 and 29.2 per 1,000 person‐years, respectively. There was a significantly higher cumulative incidence of CHF (but not IHD) in patients with RA compared with non‐RA subjects (37.1% versus 27.7% at 30 years of followup, respectively; P < 0.001). The risk of death associated with either CHF or IHD was not significantly different between patients with RA and non‐RA subjects. If the risk of developing CHF was the same in patients with RA and individuals without RA, the overall mortality rate difference between RA and non‐RA hypothetically would be reduced from 9.8 to 8.0 excess deaths per 1,000 person‐years; that is, 16 (13%) of the 123 excess deaths could be prevented.ConclusionCHF, rather than IHD, appears to be an important contributor to the excess overall mortality among patients with RA. CHF contributes to this excess mortality primarily through the increased incidence of CHF in RA, rather than increased mortality associated with CHF in patients with RA compared with non‐RA subjects. Eliminating the excess risk of CHF in patients with RA could significantly improve their survival.
The therapeutic effects of basic fibroblast growth factor contained in gelatin hydrogel microspheres on experimental osteoarthritis in the rabbit knee
Authors: Inoue Atsuo , Takahashi Kenji A. , Arai Yuji , Tonomura Hitoshi , Sakao Kei , Saito Masazumi , Fujioka Mikihiro , Fujiwara Hiroyoshi , Tabata Yasuhiko , Kubo Toshikazu 
Published: December 2005

AbstractObjectiveTo investigate the therapeutic effects of basic fibroblast growth factor (bFGF) contained in gelatin hydrogel microspheres on osteoarthritis (OA) development in rabbit knee joints.Methods125I‐labeled bFGF contained in gelatin hydrogel microspheres was administered to the knee joints of normal rabbits to confirm the sustained‐release kinetics of bFGF in the knee joint. In addition, the expression of proteoglycan core protein messenger RNA was examined using real‐time polymerase chain reaction to confirm the anabolic effects on the cartilage treated with the sustained release of bFGF. The bFGF in gelatin hydrogel microspheres was administered to the knee joint once every 3 weeks (a total of twice) from 4 weeks after anterior cruciate ligament transection (ACLT). Ten weeks after ACLT, gross morphologic and histologic examinations were performed.ResultsSustained release of bFGF in the knee joint continued for >7 days and induced the anabolic effects on the cartilage. Intraarticular injections of bFGF contained in gelatin hydrogel microspheres suppressed the progression of OA in the ACLT rabbit model.ConclusionOur findings demonstrated that sustained release of bFGF into the joint had therapeutic effects on OA development in a rabbit model. Our results suggest the potential feasibility of a new conservative treatment for OA.
Projections of US prevalence of arthritis and associated activity limitations
Authors: Hootman Jennifer M. , Helmick Charles G. 
Published: December 2005

AbstractObjectiveTo update the projected prevalence of self‐reported, doctor‐diagnosed arthritis and arthritis‐attributable activity limitations among US adults ages 18 years and older from 2005 through 2030.MethodsBaseline age‐ and sex‐specific prevalence rates of arthritis and activity limitation, using the latest surveillance case definitions, were estimated from the 2003 National Health Interview Survey, which is an annual, cross‐sectional, population‐based health interview survey of ∼31,000 adults. These estimates were used to calculate projected arthritis prevalence and activity limitations for 2005–2030 using future population projections obtained from the US Census Bureau.ResultsThe prevalence of self‐reported, doctor‐diagnosed arthritis is projected to increase from 47.8 million in 2005 to nearly 67 million by 2030 (25% of the adult population). By 2030, 25 million (9.3% of the adult population) are projected to report arthritis‐attributable activity limitations. In 2030, >50% of arthritis cases will be among adults older than age 65 years. However, working‐age adults (45–64 years) will account for almost one‐third of cases.ConclusionBy 2030, the number of US adults with arthritis and its associated activity limitation is expected to increase substantially, resulting in a large impact on individuals, the health care system, and society in general. The growing epidemic of obesity may also significantly contribute to the future burden of arthritis. Improving access and availability of current clinical and public health interventions aimed at improving quality of life among persons with arthritis through lifestyle changes and disease self‐management may help lessen the long‐term impact.
A new model for an etiology of rheumatoid arthritis: Smoking may trigger HLA–DR (shared epitope)–restricted immune reactions to autoantigens modified by citrullination
Authors: Klareskog Lars , Stolt Patrik , Lundberg Karin , Källberg Henrik , Bengtsson Camilla , Grunewald Johan , Rönnelid Johan , Erlandsson Harris Helena , Ulfgren Ann‐Kristin , Rantapää‐Dahlqvist Solbritt , Eklund Anders , Padyukov Leonid , Alfredsson Lars 
Published: December 2005

AbstractObjectiveTo investigate whether smoking and HLA–DR shared epitope (SE) genes may interact in triggering immune reactions to citrulline‐modified proteins.MethodsIn a case–control study involving patients with recent‐onset rheumatoid arthritis (RA), we studied interactions between a major environmental risk factor (smoking), major susceptibility genes included in the SE of HLA–DR, and the presence of the most specific autoimmunity known for RA (i.e., antibodies to proteins modified by citrullination). Immunostaining for citrullinated proteins in cells from bronchoalveolar lavage fluid was used to investigate whether smoking is associated with citrullination in the lungs.ResultsPrevious smoking was dose‐dependently associated with occurrence of anticitrulline antibodies in RA patients. The presence of SE genes was a risk factor only for anticitrulline‐positive RA, and not for anticitrulline‐negative RA. A major gene–environment interaction between smoking and HLA–DR SE genes was evident for anticitrulline‐positive RA, but not for anticitrulline‐negative RA, and the combination of smoking history and the presence of double copies of HLA–DR SE genes increased the risk for RA 21‐fold compared with the risk among nonsmokers carrying no SE genes. Positive immunostaining for citrullinated proteins was recorded in bronchoalveolar lavage cells from smokers but not in those from nonsmokers.ConclusionWe identified an environmental factor, smoking, that in the context of HLA–DR SE genes may trigger RA‐specific immune reactions to citrullinated proteins. These data thus suggest an etiology involving a specific genotype, an environmental provocation, and the induction of specific autoimmunity, all restricted to a distinct subset of RA.
An altered immune response to Epstein‐Barr nuclear antigen 1 in pediatric systemic lupus erythematosus
Authors: McClain Micah T. , Poole Brian D. , Bruner Benjamin F. , Kaufman Kenneth M. , Harley John B. , James Judith A. 
Published: December 2005

AbstractObjectiveNew examples support the concept that host immune responses to pathogenic organisms can act as the nidus for autoimmunity. Two such examples implicate the Epstein‐Barr virus (EBV) in systemic lupus erythematosus (SLE), i.e., data consistent with SLE anti‐Sm and anti–60‐kd Ro autoantibodies emerging from distinct humoral immune responses to Epstein‐Barr nuclear antigen 1 (EBNA‐1). We undertook this study to further test whether the humoral immune response to EBNA‐1 is a risk factor for pediatric SLE.MethodsSera from pediatric lupus patients and healthy matched controls were tested for anti–EBNA‐1 by Western blotting and enzyme‐linked immunosorbent assay (ELISA). To define the fine specificity of their anti–EBNA‐1 humoral immune response, fragments of EBNA‐1 and the maximally overlapping unique octapeptides of EBNA‐1 were tested by modified ELISAs.ResultsAll 36 pediatric SLE patient sera tested recognized EBNA‐1, while sera from only 25 of 36 matched EBV‐positive controls targeted EBNA‐1 (P < 0.005). Epitope mapping revealed that the humoral anti–EBNA‐1 response in pediatric SLE was distinct from and less restricted than that in matched normal individuals. Meanwhile, no significant differences between SLE patient sera and control sera were observed in the responses to other herpesviruses or in binding to sequential epitopes from cytomegalovirus immediate‐early antigen or EBNA‐2.ConclusionAnti–EBNA‐1 antibodies are associated with pediatric‐onset SLE. Furthermore, an altered humoral immune response to EBNA‐1, characteristic of SLE, has been found and may be an important SLE susceptibility factor.
Teilfertigdecken nach DIN 1045‐1. Wichtige Punkte der Bemessung und Konstruktion
Authors: Land Hartmut 
Published: December 2005

AbstractMit der Anwendung von DIN 1045‐1, Ausgabe Juli 2001 sind eingreifende Änderungen bei der Bemessung und Konstruktion von Teilfertigdecken verbunden. Das betrifft insbesondere den Nachweis der Schubkraftaufnahme in der Fuge Fertigplatte/Ortbeton. Für diesen aufwendigen Nachweis werden die Grundlagen zusammengestellt und ein Beispiel gegeben. Detailliert werden Regelungen für die Anordnung von Gitterträgern als Verbund‐/Querkraftbewehrung sowie für die Betondeckungen aufgeführt. Auflagerausbildungen sind zukünftig einfacher ausführbar.
Bauphysik‐Preis 2005
Authors: Ozimek Claudia 
Published: December 2005

AbstractZum zweiten Mal verlieh der Verlag Ernst & Sohn in diesem Jahr den Bauphysik‐Preis, um eine besondere, innovative Planungsleistung auf einem oder mehreren Teilgebieten der Bauphysik – Wärme, Feuchte, Schall, Brand, Licht – unter Berücksichtigung der funktionalen, wirtschaftlichen und gestalterischen Rahmenbedingungen des Bauwerkes auszuzeichnen.
Die Kraftwagenhalle der Kohlengroßhandlung Einmal in Aachen
Authors: Schmidt Hartwig 
Published: December 2005

AbstractNach dem Vorbild der 1911–13 in Breslau errichteten “Jahrhunderthalle” entstand 1924 in Aachen die Kraftwagenhalle der Firma Einmal als Stahlbetonrippenkuppel – eine ungewöhnliche Halle aus Fertigteilen und Ortbeton für den Fuhrpark einer Kohlengroßhandlung.
An Efficient Enzymatic Synthesis of Benzocispentacin and Its New Six‐ and Seven‐Membered Homologues
Authors: Forró Enikő , Fülöp Ferenc 
Published: December 2005

AbstractA very efficient enzymatic method was developed for the synthesis of new enantiomeric benzocispentacin and its six‐ and seven‐membered homologues through the Lipolase (lipase B from Candida antarctica) catalyzed enantioselective (E>200) ring opening of 3,4‐benzo‐6‐azabicyclo[3.2.0]heptan‐7‐one, 4,5‐benzo‐7‐azabicyclo[4.2.0]octan‐8‐one, and 5,6‐benzo‐8‐azabicyclo[5.2.0]nonan‐9‐one with H2O in iPr2O at 60 °C. The (1R,2R)‐β‐amino acids (ee≥96 %, yields≥40 %) and (1S,6S)‐, (1S,7S)‐, and (1S,8S)‐β‐lactams (ee>99 %, yields≥44 %) produced could be easily separated. The ring opening of racemic and enantiomeric β‐lactams with 18 % HCl afforded the corresponding β‐amino acid hydrochlorides.
Non‐centrosomal microtubule‐organising centres in cold‐treated cultured Drosophila cells
Authors: Cottam Deborah M. , Tucker John B. , Rogers‐Bald Margaret M. , Mackie John B. , Macintyre John , Scarborough Julie A. , Ohkura Hiroyuki , Milner Martin J. 
Published: December 2005

AbstractIn this paper we describe a new type of non‐centrosomal microtubule‐organising centre (MTOC), which is induced by cold treatment of certain cultured Drosophila cells and allows rapid reassembly of microtubule (MT) arrays. Prolonged cooling of two types of cultured Drosophila cells, muscle cells in primary culture and a wing imaginal disc cell line Cl.8+ results in disassembly of MT arrays and induces the formation of clusters of short MTs that have not been described before. Upon rewarming, the clusters are lost and the MT array is re‐established within 1 h. In Cl.8+ cells, γ‐tubulin‐containing centrosomes are detected, both in cell extensions and in the expected juxtanuclear position, and γ‐tubulin co‐localises with the cold‐induced MT clusters. The MT plus‐end‐binding protein, Drosophila EB1, decorates growing tips of MTs extending from clusters. We conclude that the cold‐induced MT clusters represent acentrosomal MTOCs, allowing rapid reassembly of MT arrays following exposure to cold. Cell Motil. Cytoskeleton 63, 2006. © 2005 Wiley‐Liss, Inc.
Aroyl‐Pyrrolyl Hydroxyamides: Influence of Pyrrole C4‐Phenylacetyl Substitution on Histone Deacetylase Inhibition
Authors: Mai Antonello , Massa Silvio , Valente Sergio , Simeoni Silvia , Ragno Rino , Bottoni Patrizia , Scatena Roberto , Brosch Gerald 
Published: December 2005

AbstractThe novel aroyl‐pyrrolyl hydroxyamides 4 a–a′ are analogues of the lead compound 3‐(1‐methyl‐4‐phenylacetyl‐1H‐pyrrol‐2‐yl)‐N‐hydroxy‐2‐propenamide (2) and are active as HDAC inhibitors. The benzene ring of 2 was substituted with a wide range of electron‐donating and electron‐withdrawing groups, and the effect was evaluated on three HDACs from maize, namely HD2, HD1‐B (a class I HDAC), and HD1‐A (a class II HDAC). Inhibition studies show that the benzene 3′ and, to a lesser extent, 4′ positions of 2 were the most suitable for the introduction of substituents, with the 3′‐chloro (in 4 b) and the 3′‐methyl (in 4 k) derivatives being the most potent compounds, reaching the same activity as SAHA. Inhibition data for 4 b,k against mouse HDAC1 were consistent with those observed in the maize enzyme. The substituent insertion on the benzene ring of 2 (compounds 4 a–a′) abated the slight (3‐fold) selectivity for class II HDACs displayed by 2. Compound 4 b showed interesting, dose‐dependent antiproliferative and cytodifferentiation properties against human acute promyelocytic leukemia HL‐60 cells.
Group IIA phospholipase A2 is coexpressed with SNAP‐25 in mature taste receptor cells of rat circumvallate papillae
Authors: Oike Hideaki , Matsumoto Ichiro , Abe Keiko 
Published: December 2005

AbstractThe taste buds are composed of heterogeneous cell populations with diverse properties and at different stages of maturity. It is important to define the relationships between cell properties and cell maturity to understand the molecular events involved in intracellular taste signaling. In the present study, in situ hybridization analysis indicated that group IIA phospholipase A2 (PLA2‐IIA) is expressed in a subset of taste bud cells. Immunohistochemical studies showed that PLA2‐IIA was expressed in a subset of cells expressing phospholipase Cβ2, a molecule essential for taste signaling in taste receptor cells, and also that some PLA2‐IIA‐positive cells expressed gustducin (Ggust), a bitter‐taste‐signaling molecule. Although PLA2‐IIA and Ggust were expressed at similar frequencies in taste buds, bromodeoxyuridine (BrdU) chase experiments indicated that the expression of Ggust began 2 days after BrdU injection, whereas the expression of PLA2‐IIA commenced after 4 days. In addition, PLA2‐IIA was coexpressed with SNAP‐25, a synaptosomal‐associated protein. These results indicated that PLA2‐IIA is expressed in mature taste receptor cells that possess exocytotic machinery. J. Comp. Neurol. 494:876–886, 2006. © 2005 Wiley‐Liss, Inc.
Kainic acid‐induced recurrent mossy fiber innervation of dentate gyrus inhibitory interneurons: Possible anatomical substrate of granule cell hyperinhibition in chronically epileptic rats
Authors: Sloviter Robert S. , Zappone Colin A. , Harvey Brian D. , Frotscher Michael 
Published: December 2005

AbstractKainic acid‐induced neuron loss in the hippocampal dentate gyrus may cause epileptogenic hyperexcitability by triggering the formation of recurrent excitatory connections among normally unconnected granule cells. We tested this hypothesis by assessing granule cell excitability repeatedly within the same awake rats at different stages of the synaptic reorganization process initiated by kainate‐induced status epilepticus (SE). Granule cells were maximally hyperexcitable to afferent stimulation immediately after SE and became gradually less excitable during the first month post‐SE. The chronic epileptic state was characterized by granule cell hyperinhibition, i.e., abnormally increased paired‐pulse suppression and an abnormally high resistance to generating epileptiform discharges in response to afferent stimulation. Focal application of the γ‐aminobutyric acid type A (GABAA) receptor antagonist bicuculline methiodide within the dentate gyrus abolished the abnormally increased paired‐pulse suppression recorded in chronically hyperinhibited rats. Combined Timm staining and parvalbumin immunocytochemistry revealed dense innervation of dentate inhibitory interneurons by newly formed, Timm‐positive, mossy fiber terminals. Ultrastructural analysis by conventional and postembedding GABA immunocytochemical electron microscopy confirmed that abnormal mossy fiber terminals of the dentate inner molecular layer formed frequent asymmetrical synapses with inhibitory interneurons and with GABA‐immunopositive dendrites as well as with GABA‐immunonegative dendrites of presumed granule cells. These results in chronically epileptic rats demonstrate that dentate granule cells are maximally hyperexcitable immediately after SE, prior to mossy fiber sprouting, and that synaptic reorganization following kainate‐induced injury is temporally associated with GABAA receptor‐dependent granule cell hyperinhibition rather than a hypothesized progressive hyperexcitability. The anatomical data provide evidence of a possible anatomical substrate for the chronically hyperinhibited state. J. Comp. Neurol. 494:944–960, 2006. © 2005 Wiley‐Liss, Inc.