bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rheological properties of ionically crosslinked poly(propylene)‐type thermoplastic elastomers
Authors: Fujiyama Mitsuyoshi , Yamane Kazuhiro , Ayama Kazuhiko , Inata Hitoshi 
Published: October 2002

AbstractMaleic anhydride was grafted onto poly(propylene) (PP)‐type thermoplastic elastomer PER by reactive processing with a screw extruder and a maleated PER (MPER) was prepared. With the intent of ionic crosslinking, metal compounds such as aluminum stearate (AlSt), magnesium stearate (MgSt), calcium stearate (CaSt), zinc stearate (ZnSt), potassium stearate (KSt), sodium stearate (NaSt), magnesium hydroxide (MH), zinc oxide (ZnO), and zinc sulfide (ZnS) were added to the MPER and melt‐mixed with the screw extruder, and crosslinked compounds were obtained. The degree of crosslinking estimated from the gel fraction was in the order AlSt, MgSt, CaSt, ZnSt > NaSt, KSt > MH > ZnO, ZnS > MPER. The rheological properties, such as capillary flow properties and dynamic viscoelasticities, of the compounds were measured and their melt processabilities were evaluated. The viscosity increased with increasing the content of the metal compounds and the increase was higher at the lower shear rate. The increasing effect of the viscosity at low shear rates was AlSt > MgSt > ZnSt > NaSt > KSt > MH > ZnO > ZnS > MPER. Namely, the viscosity increasing effect of the metal salt of stearic acid is the higher for the larger ionic charge and the viscosity increasing effects of other compounds are lower than those of the metal salts of stearic acid. Accordingly, by changing the kind and content of the metal compounds, the viscosity can be freely controlled. Considering also other rheological characteristics, these ionically crosslinked compounds are assumed to show ideal flow processabilities except for the extrudate appearance. To improve the appearance, it is necessary to dilute the compound with unmodified PER, PP, or fillers. © 2002 Wiley Periodicals, Inc. J Appl Polym Sci 86: 2887–2897, 2002
Increased transcriptional activities of transforming growth factor β receptors in scleroderma fibroblasts
Authors: Yamane Kenichi , Ihn Hironobu , Kubo Masahide , Tamaki Kunihiko 
Published: October 2002

AbstractObjectiveTo investigate the molecular mechanism of the overexpression of transforming growth factor β receptors (TGFβRs) in dermal fibroblasts from patients with systemic sclerosis (SSc).MethodsDermal fibroblasts from 7 patients with diffuse SSc of recent onset and from 7 healthy individuals were studied. The expression of TGFβR type I (TGFβRI), TGFβRII, and type I collagen proteins in dermal fibroblasts was determined by immunoblotting. TGFβRI, TGFβRII, and α2(I) collagen messenger RNA (mRNA) were evaluated by Northern blot analysis. The transcriptional activities of the TGFβRI and TGFβRII genes were examined by luciferase assay.ResultsSSc fibroblasts expressed increased levels of TGFβRI and TGFβRII protein and mRNA, as well as increased levels of type I collagen protein and α2(I) collagen mRNA. Moreover, the half‐lives of TGFβRI and TGFβRII mRNA in SSc fibroblasts did not change compared with those in control dermal fibroblasts. The promoter activities of the TGFβRI and TGFβRII genes were both significantly increased in SSc fibroblasts compared with those in control fibroblasts. Calphostin C, a specific inhibitor of protein kinase C (PKC), inhibited TGFβRI promoter activity in SSc fibroblasts, and LY294002, an inhibitor of phosphoinositide 3‐kinase (PI 3‐kinase), inhibited TGFβRII promoter activity in SSc fibroblasts. Moreover, calphostin C and LY294002 inhibited the up‐regulation of TGFβRI and TGFβRII mRNA, respectively, in SSc fibroblasts.ConclusionThese results suggest that increased levels of TGFβRs in SSc fibroblasts play a role in excessive collagen production, and that up‐regulation of TGFβR expression might occur at the transcriptional levels. PKC and/or PI 3‐kinase might contribute to the up‐regulation of TGFβR expression in SSc fibroblasts.
Detection of nitrotyrosine in aging and osteoarthritic cartilage: Correlation of oxidative damage with the presence of interleukin‐1β and with chondrocyte resistance to insulin‐like growth factor 1
Authors: Loeser Richard F. , Carlson Cathy S. , Carlo Marcello Del , Cole Ada 
Published: October 2002

AbstractObjectiveTo determine whether oxidative damage to cartilage proteins can be detected in aging and osteoarthritic (OA) cartilage, and to correlate the results with the local production of interleukin‐1β (IL‐1β) and the responsiveness of isolated chondrocytes to stimulation with insulin‐like growth factor 1 (IGF‐1).MethodsThe presence of nitrotyrosine was used as a measure of oxidative damage. Histologic sections of knee articular cartilage, obtained from young adult and old adult cynomolgus monkeys, which develop age‐related, naturally occurring OA, were evaluated. Each cartilage section was graded histologically on a scale of 0–7 for the presence of OA‐like changes, and serial sections were immunostained using antibodies to nitrotyrosine and IL‐1β. Chondrocytes isolated and cultured from cartilage adjacent to the sections used for immunostaining were tested for their response to IGF‐1 stimulation by measuring sulfate incorporation in alginate cultures. For comparison with the monkey tissues, cartilage sections from human tissue donors and from tissue removed at the time of OA‐related joint replacement surgery were also immunostained for nitrotyrosine and IL‐1β.ResultsThe presence of nitrotyrosine was associated with aging and with the development of OA in cartilage samples from both monkeys and humans. All sections that were highly positive for IL‐1β also showed staining for nitrotyrosine. However, in a few sections from older adult monkeys and humans, nitrotyrosine was present but IL‐1β was absent, suggesting that some age‐related oxidative damage is independent of IL‐1β. In chondrocytes that were isolated from monkey cartilage positive for nitrotyrosine or IL‐1β, the response to stimulation with IGF‐1 was significantly reduced. In some samples from older adult monkeys, IGF‐1 resistance was seen in cells isolated from tissue that did not stain for nitrotyrosine or IL‐1β.ConclusionOxidative damage due to the concomitant overproduction of nitric oxide and other reactive oxygen species is present in both aging and OA cartilage. This damage can contribute to the resistance of chondrocytes to IGF‐1 stimulation, but it is unlikely to be the sole cause of IGF‐1 resistance in these chondrocytes.
Fibronectin fragments and blocking antibodies to α2β1 and α5β1 integrins stimulate mitogen‐activated protein kinase signaling and increase collagenase 3 (matrix metalloproteinase 13) production by human articular chondrocytes
Authors: Forsyth Christopher B. , Pulai Judit , Loeser Richard F. 
Published: October 2002

AbstractObjectiveTo determine if integrin‐mediated signaling results in activation of chondrocyte mitogen‐activated protein (MAP) kinases that lead to increased expression of matrix metalloproteinase 13 (MMP‐13; collagenase 3), a potent mediator of cartilage matrix degradation.MethodsHuman articular chondrocytes isolated from normal ankle and knee cartilage obtained from tissue donors were cultured in monolayers. The cells were treated with a 120‐kd fibronectin fragment (FN‐f) that binds the α5β1 integrin or with antibodies to specific integrin receptors. Activation of MAP kinases was determined by immunoblotting with phosphospecific antibodies. MMP production was measured by gelatin zymography, and MMP‐13 production and activation were determined by immunoblotting and by a fluorogenic peptide assay.ResultsHuman articular chondrocytes were found to respond to the 120‐kd FN‐f and to adhesion‐blocking antibodies to the α2β1 and α5β1 integrins with increased phosphorylation of the extracellular signal–regulated kinase 1 (ERK1)/ERK2, c‐Jun N‐terminal kinase (JNK), and p38 MAP kinases. Intact FN and integrin‐blocking antibodies to α1, α3, and αVβ3 and a nonblocking α5 antibody had no effect. After MAP kinase activation, increased phosphorylation of c‐Jun and the nuclear factor κB inhibitor was noted, followed by increased pro‐ and activated MMP‐13 in the conditioned media. Inhibitors of mitogen‐activated protein kinase kinase, p38, and JNK were each able to inhibit increased MMP‐13 production, while the interleukin‐1 receptor antagonist (IL‐1Ra) protein did not. However, the IL‐1Ra partially inhibited FN‐f–induced activation of MMP‐13.ConclusionIntegrin‐mediated MAP kinase signaling stimulated by FN‐f is associated with increased production and release of pro‐ and active MMP‐13. Autocrine production of IL‐1 appears to result in additional MMP‐13 activation. These processes may play a key role in feedback loops responsible for progressive cartilage degradation in arthritis.
Predictors of infection in rheumatoid arthritis
Authors: Doran Michele F. , Crowson Cynthia S. , Pond Gregory R. , O'Fallon W. Michael , Gabriel Sherine E. 
Published: October 2002

AbstractObjectivePatients with rheumatoid arthritis (RA) have been shown to have an increased susceptibility to the development of infections. The exact causes of this increased risk are unknown, but may relate to immunologic disturbances associated with the disease or to the immunosuppressive effects of agents used in its treatment. This study was undertaken to identify predictors of serious infections among patients with RA. Identification of such factors is the necessary first step in reducing the excess risk of infection in RA.MethodsMembers of a population‐based incidence cohort of Rochester, Minnesota residents ages ≥18 years, who had been diagnosed with RA between 1955 and 1994, were followed up longitudinally through their complete medical records until January 1, 2000. We examined potential risk factors for the development of all objectively confirmed (by microbiology or radiology) infections and for infections requiring hospitalization. Potential risk factors included RA severity measures (rheumatoid factor positivity, elevated erythrocyte sedimentation rate, extraarticular manifestations of RA, and functional status), comorbidities (diabetes mellitus, alcoholism, and chronic lung disease), and other risk factors for infection (presence of leukopenia, smoking). Predictors were identified using multivariate time‐dependent Cox proportional hazards modeling.ResultsThe 609 RA patients in the cohort had a total followup time of 7,729.7 person‐years (mean 12.7 years per patient). A total of 389 patients (64%) had at least 1 infection with objective confirmation, and 290 (48%) had at least 1 infection requiring hospitalization. Increasing age, presence of extraarticular manifestations of RA, leukopenia, and comorbidities (chronic lung disease, alcoholism, organic brain disease, and diabetes mellitus), as well as use of corticosteroids, were strong predictors of infection (P < 0.004) in both univariate and multivariate analyses. Notably, use of disease‐modifying antirheumatic drugs was not associated with increased risk of infection in multivariate analyses, after adjustment for demographic characteristics, comorbidities, and disease‐related variables.ConclusionWe identified a number of strong predictors of infections in a population‐based cohort of patients with RA. These results can be used to prospectively identify high‐risk patients, who may benefit from closer followup and implementation of preventive strategies.
Mice lacking endogenous major histocompatibility complex class II develop arthritis resembling psoriatic arthritis at an advanced age
Authors: Bárdos Tamás , Zhang Jian , Mikecz Katalin , David Chella S. , Glant Tibor T. 
Published: October 2002

AbstractObjectiveTo describe and characterize a novel inflammatory toe disease with severe bone destruction that developed spontaneously in “humanized” (HLA transgenic) mice lacking their own major histocompatibility complex (MHC).MethodsWe studied 5 different HLA transgenic mouse lines (HLA–DR2.Ab0, DR3.Ab0, DR4.Ab0, DQ6.Ab0, and DQ8.Ab0) in similar genetic background for an extended period of time (>14 months). Clinical, radiologic, and histologic abnormalities were monitored, and the MHC‐related major immunologic parameters in affected and resistant mice were compared.ResultsAnimals of 4 transgenic lines (HLA–DR2.Ab0, DR4.Ab0, DQ6.Ab0, and DQ8.Ab0) developed severe toe inflammation accompanied by progressive bone resorption, hyperkeratosis, alopecia, loss of nails, and shortening and thickening of the distal phalanges. HLA–DR3.Ab0 transgenic mice were resistant to inflammation. The disease manifested only at advanced ages (6 months or older) and affected 70–100% of the mice, with a female preponderance. The clinical signs and the radiographic and histopathologic features of the affected toes were not similar to those of any disease previously described in mice but did resemble those described for human psoriatic arthritis (PsA). Mice from the 4 susceptible lines expressed lower levels of the HLA transgene and exhibited significantly fewer CD4+ cells in the peripheral blood and reduced natural killer cell activity compared with mice from the resistant HLA–DR3.Ab0 line.ConclusionThis novel, spontaneously developing PsA‐like toe disease in MHC‐manipulated mice seems to be related to the absence of endogenous MHC class II. Replacement with HLA transgene expression that is insufficient (or no replacement at all) may result in imbalanced MHC class I and class II functions and lead to development of the disease.
Long‐term followup of children with neonatal lupus and their unaffected siblings
Authors: Martin Victor , Lee Lela A. , Askanase Anca D. , Katholi Margaret , Buyon Jill P. 
Published: October 2002

AbstractObjectiveTo determine in a longitudinal cohort study whether children with varied manifestations of neonatal lupus or their unaffected siblings later develop autoantibodies and/or rheumatic diseases.MethodsTo obtain information on the health of children ages ≥8 years who had manifestations of neonatal lupus (affected group) and their unaffected siblings (unaffected group), questionnaires were sent to mothers (with anti‐SSA/Ro and/or anti‐SSB/La antibodies) who were enrolled in the National Institute of Arthritis and Musculoskeletal and Skin Diseases/Hospital for Joint Diseases Research Registry for Neonatal Lupus. Children of healthy mothers referred by the Registry enrollees comprised the control group. Further data were provided by review of medical records.ResultsFifty‐five mothers enrolled in the Registry returned questionnaires on 49 children with neonatal lupus and their 45 unaffected siblings. Six children with definite rheumatic/autoimmune diseases were identified: 2 with juvenile rheumatoid arthritis, 1 with Hashimoto thyroiditis, 1 with psoriasis and iritis, 1 with diabetes mellitus and psoriasis, and 1 with congenital hypothyroidism and nephrotic syndrome. All had neonatal lupus, and their mothers had manifestations of autoimmune diseases (Sjögren's syndrome in 4, systemic lupus erythematosus/Sjögren's syndrome in 1, and undifferentiated autoimmune disease in 1). Antinuclear antibodies were present in 4 of 55 sera tested (2 of 33 affected children and 2 of 22 unaffected children). No serum contained antibodies reactive with SSA/Ro or SSB/La antigens.ConclusionThese data suggest that children with neonatal lupus require continued followup, especially prior to adolescence and if the mother herself has an autoimmune disease. While there was no apparent increased risk of systemic lupus erythematosus, the development of some form of autoimmune disease (systemic or organ‐specific) in early childhood may be of concern. During adolescence and young adulthood, individuals with neonatal lupus and their unaffected siblings do not appear to have an increased risk of developing systemic rheumatic diseases.
Prospect theory analysis of guessing in multiple choice tests
Authors: Bereby‐Meyer Yoella , Meyer Joachim , Flascher Oded M. 
Published: October 2002

AbstractThe guessing of answers in multiple choice tests adds random error to the variance of the test scores, lowering their reliability. Formula scoring rules that penalize for wrong guesses are frequently used to solve this problem. This paper uses prospect theory to analyze scoring rules from a decision‐making perspective and focuses on the effects of framing on the tendency to guess. In three experiments participants were presented with hypothetical test situations and were asked to indicate the degree of certainty that they thought was required for them to answer a question. In accordance with the framing hypothesis, participants tended to guess more when they anticipated a low grade and therefore considered themselves to be in the loss domain, or when the scoring rule caused the situation to be framed as entailing potential losses. The last experiment replicated these results with a task that resembles an actual test. Copyright © 2002 John Wiley & Sons, Ltd.
Family of the green fluorescent protein: Journey to the end of the rainbow
Authors: Matz Mikhail V. , Lukyanov Konstantin A. , Lukyanov Sergey A. 
Published: October 2002

AbstractMembers of the family of the Green Fluorescent Protein (GFP) are the only known type of natural pigments that are essentially encoded by a single gene, since both the substrate for pigment biosynthesis and the necessary catalytic moieties are provided within a single polypeptide chain. In sharp contrast to the state of knowledge just three years ago when GFP was the only known protein of its kind, a whole family of related proteins, exhibiting striking diversity of features have now been identified. This provides new possibilities for a variety of studies ranging from applied biotechnology to evolutionary ecology. BioEssays 24:953–959, 2002. © 2002 Wiley Periodicals, Inc.
Lighting up gap junction channels in a flash
Authors: Evans W. Howard , Martin Patricia E.M. 
Published: October 2002

AbstractGap junction intercellular communication channels permit the exchange of small regulatory molecules and ions between neighbouring cells and coordinate cellular activity in diverse tissue and organ systems. These channels have short half‐lives and complex assembly and degradation pathways. Much of the recent work elucidating gap junction biogenesis has featured the use of connexins (Cx), the constituent proteins of gap junctions, tagged with reporter proteins such as Green Fluorescent Protein (GFP) and has illuminated the dynamics of channel assembly in live cells by high‐resolution time‐lapse microscopy. With some studies, however, there are potential short‐comings associated with the GFP chimeric protein technologies. A recent report by Gaietta et al., has highlighted the use of recombinant proteins with tetracysteine tags attached to the carboxyl terminus of Cx43, which differentially labels ‘old’ and ‘new’ connexins thus opening up new avenues for studying temporal and spatial localisation of proteins and in situ trafficking events.1 BioEssays 24:876–880, 2002. © 2002 Wiley Periodicals, Inc.
Do different branching epithelia use a conserved developmental mechanism?
Authors: Davies Jamie A. 
Published: October 2002

AbstractFormation of branching epithelial trees from unbranched precursors is a common process in animal organogenesis. In humans, for example, this process gives rise to the airways of the lungs, the urine‐collecting ducts of the kidneys and the excretory epithelia of the mammary, prostate and salivary glands. Branching in these different organs, and in different animal classes and phyla, is morphologically similar enough to suggest that they might use a conserved developmental programme, while being dissimilar enough not to make it obviously certain that they do. In this article, I review recent discoveries about the molecular regulation of branching morphogenesis in the best‐studied systems, and present evidence for and against the idea of there being a highly conserved mechanism. Overall, I come to the tentative conclusion that key mechanisms are highly conserved, at least within vertebrates, but acknowledge that more work needs to be done before the case is proved beyond reasonable doubt. BioEssays 24:937–948, 2002. © 2002 Wiley Periodicals, Inc.
Centrosomal TACCtics
Authors: Gergely Fanni 
Published: October 2002

AbstractAlthough the centrosome was first described over 100 years ago, we still know relatively little of the molecular mechanisms responsible for its functions. Recently, members of a novel family of centrosomal proteins have been identified in a wide variety of organisms. The transforming acidic coiled‐coil‐containing (TACC) proteins all appear to play important roles in cell division and cellular organisation in both embryonic and somatic systems. These closely related molecules have been implicated in microtubule stabilisation, acentrosomal spindle assembly, translational regulation, haematopoietic development and cancer progression. In this review, I summarise what we already know of this protein family and will use the TACC proteins to illustrate the many facets that centrosomes have developed during the course of evolution. BioEssays 24:915–925, 2002. © 2002 Wiley Periodicals, Inc.
RWPV bioreactor mass transport: Earth‐based and in microgravity
Authors: Begley Cynthia M. , Kleis Stanley J. 
Published: October 2002

AbstractMass transport and mixing of perfused scalar quantities in the NASA Rotating Wall Perfused Vessel bioreactor are studied using numerical models of the flow field and scalar concentration field. Operating conditions typical of both microgravity and ground‐based cell cultures are studied to determine the expected vessel performance for both flight and ground‐based control experiments. Results are presented for the transport of oxygen with cell densities and consumption rates typical of colon cancer cells cultured in the RWPV. The transport and mixing characteristics are first investigated with a step change in the perfusion inlet concentration by computing the time histories of the time to exceed 10% inlet concentration. The effects of a uniform cell utilization rate are then investigated with time histories of the outlet concentration, volume average concentration, and volume fraction starved. It is found that the operating conditions used in microgravity produce results that are quite different then those for ground‐based conditions. Mixing times for microgravity conditions are significantly shorter than those for ground‐based operation. Increasing the differential rotation rates (microgravity) increases the mixing and transport, while increasing the mean rotation rate (ground‐based) suppresses both. Increasing perfusion rates enhances mass transport for both microgravity and ground‐based cases, however, for the present range of operating conditions, above 5–10 cc/min there are diminishing returns as much of the inlet fluid is transported directly to the perfusion exit. The results show that exit concentration is not a good indicator of the concentration distributions in the vessel. In microgravity conditions, the NASA RWPV bioreactor with the viscous pump has been shown to provide an environment that is well mixed. Even when operated near the theoretical minimum perfusion rates, only a small fraction of the volume provides less than the required oxygen levels. @ 2002 Wiley Periodicals, Inc. Biotechnol Bioeng 80: 465–476, 2002.