bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitro dissolution of melt‐derived 45S5 and sol‐gel derived 58S bioactive glasses
Authors: Sepulveda P. , Jones J. R. , Hench L. L. 
Published: August 2002

AbstractEffects of powder type, particle size (5–20 μm; 90–300 μm; 90–710 μm), and type of dissolution medium on the dissolution behavior of bioactive glasses were investigated in vitro using melt‐derived 45S5 and sol‐gel derived 58S bioactive glass powders. Dissolution studies were performed in simulated body fluid and in α‐MEM based cell culture medium at 37°C under dynamic conditions (1 Hz) for periods of 30 min, 1, 2, 4, 8, 17, and 22 h. The concentrations of elements dissolved from the glasses were evaluated using inductively coupled plasma analysis. The reacted powders were analyzed for bioactivity using Fourier transform infrared spectrometry to observe the formation of a calcium phosphate layer on the surface. The non‐porous surfaces of melt‐derived 45S5 glass powders exhibited lower dissolution rates and rate of surface layer formation than 58S gel‐glass powders. The rates of dissolution for both types of powders were lower in culture medium, compared to simulated body fluid , and increased as the particle size decreased. Thus, particle size range, glass type, and powder volume fraction can be used as a means to control the release rate of active ions that stimulate the gene expression and cellular response for tissue proliferation and repair. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 61: 301–311, 2002
Regeneration of canine peroneal nerve with the use of a polyglycolic acid–collagen tube filled with laminin‐soaked collagen sponge: a comparative study of collagen sponge and collagen fibers as filling materials for nerve conduits
Authors: Toba Toshinari , Nakamura Tatsuo , Shimizu Yasuhiko , Matsumoto Kazuya , Ohnishi Katsunori , Fukuda Seijun , Yoshitani Makoto , Ueda Hiroki , Hori Yoshio , Endo Katsuaki 
Published: August 2002

AbstractA novel artificial nerve conduit was developed and its efficiency was evaluated on the basis of promotion of peripheral nerve regeneration across an 80‐mm gap in dogs. The nerve conduit was made of a polyglycolic acid–collagen tube filled with laminin‐soaked collagen sponge. Conduits filled with either sponge‐ or fiber‐form collagen were implanted into an 80‐mm gap of the peroneal nerve (five dogs for each form). Twelve months postoperatively nerve regeneration was superior in the sponge group both morphometrically (percentage of neural tissue: fiber: 39.7 ± 5.2, sponge: 43.0 ± 4.5, n=3) and electrophysiologically (fiber: CMAP 1.06 ± 0.077, SEP 1.32 ± 0.127 sponge: CMAP 1.04 ± 0.106, SEP 1.24 ± 0.197, n=5), although these differences were not statistically significant. The observed regeneration was complementary to successful results reported previously in the same model, in which collagen fibers exclusively were used. The results indicate a possible superiority of collagen sponge over collagen fibers as filling materials. In addition, the mass‐producibility, superior scaffolding potential, and capacity for gradual release of soluble factors of the sponge provide make it an attractive alternative to fine fibers, which are both technologically difficult and costly to produce. This newly developed nerve conduit has the potential to enhance peripheral nerve regeneration across longer gaps commonly encountered in clinical settings. © 2001 John Wiley & Sons, Inc. J Biomed Mater Res (Appl Biomater) 58: 622–630, 2001
Tobramycin‐containing bone cement and systemic cefazolin in a one‐stage revision. Treatment of infection in a rabbit model
Authors: Nijhof Marc W. , Fleer Andre , Hardus Karin , Vogely H. Charles , Schouls Leo M. , Verbout Abraham J. , Dhert Wouter J. A. 
Published: August 2002

AbstractThe efficacy of tobramycin‐containing bone cement with that of systemic cefazolin for treatment of infection in a one‐stage revision model is compared. In addition, the value of detecting bacterial DNA after antibiotic treatment was investigated. An implant was inserted into the right tibia of rabbits after inoculation with Staphylococcus aureus. At 28 days, the implant was removed. Subsequently, either plain bone cement with or without systemic administration of cefazolin, or tobramycin‐containing bone cement was injected into the medullary canal. The tibiae were cultured 14 days after revision (Day 42), and showed a significant decrease in bacterial counts for both antibiotic groups compared with the control group (p≤0.05). The rate of infection in the tobramycin‐cement group was slightly higher (2/9) than in the cefazolin group (0/8), although the difference was not significant. Persistence of bacterial DNA after antibiotic treatment may be the result of delayed clearance of DNA and not a sign of active infection. This animal model shows that in a one‐stage revision tobramycin‐containing bone cement can reduce size and rate of infection, although systemic cefazolin may be more efficacious. Therefore, the use of antibiotic‐containing bone cement combined with systemic antibiotic might provide optimal treatment. © 2001 John Wiley & Sons, Inc. J Biomed Mater Res (Appl Biomater) 58: 747–753, 2001
Evaluation of the biocompatibility of a chitosan scaffold in mice
Authors: VandeVord Pamela J. , Matthew Howard W. T. , DeSilva Stephen P. , Mayton Lois , Wu Bin , Wooley Paul H. 
Published: August 2002

AbstractChitosan scaffolds appear to be suitable for a variety of tissue engineering applications. This study addressed the biocompatibility of chitosan in a mouse implantation model. Porous chitosan scaffolds were implanted in mice, and animals were sacrificed after 1, 2, 4, 8, or 12 weeks. Macroscopic inspection of the implantation site revealed no pathological inflammatory responses. Histological assessment indicated marked neutrophil accumulation within the implant, which resolved with increasing implantation time. Gram staining and limulus assays revealed no evidence of infection or endotoxin. Collagen was observed within the chitosan pore spaces, indicating that connective tissue matrix was deposited within the implant. Angiogenic activity associated with the external implant surface was also observed. Cellular immune responses were determined by lymphocyte proliferation assays, and antibody responses were measured using ELISA techniques. These assays indicated a very low incidence of chitosan‐specific reactions. Although there was a large migration of neutrophils into the implantation area, there were minimal signs of any inflammatory reaction to the material itself. This preliminary study demonstrates that chitosan has a high degree of biocompatibility in this animal model. Overall, the findings suggest that chitosan may be suitable for the development of implantable materials. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 585–590, 2002
Electrically communicating three‐dimensional cardiac tissue mimic fabricated by layered cultured cardiomyocyte sheets
Authors: Shimizu Tatsuya , Yamato Masayuki , Akutsu Takumitsu , Shibata Takahiko , Isoi Yuki , Kikuchi Akihiko , Umezu Mitsuo , Okano Teruo 
Published: August 2002

AbstractRecent progress in stem cell biology is likely to provide implantable sources of human cardiomyocytes in the near future. This possibility has encouraged cardiac tissue engineering. To construct heart‐like tissue, we have exploited the capabilities of novel cell culture surfaces grafted with a temperature‐responsive polymer, poly(N‐isopropylacrylamide) (PIPAAm), to produce intact viable monolayer cell sheets simply by reducing culture temperature. Cultured chick embryonic cardiomyocyte sheets detached from PIPAAm‐grafted surfaces were layered into tissue‐like laminate stacks using hydrophilic support and transfer membranes. The layered cell sheets rapidly adhered to each other, establishing cell‐to‐cell connections characteristic of heart tissue, including desmosomes and intercalated disks. Bilayer cell sheets pulsed spontaneously and synchronously, altering their characteristic pulsing frequency with applied electric stimulation transmitted across the sheets. These results demonstrate that electrically communicative three‐dimensional cardiac constructs can be achieved by stacking monolayer cardiomyocyte sheets. Cardiac tissue engineering based on this technology will facilitate new in vitro heart models and may prove useful for in vivo cardiovascular tissue repair. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 60: 110–117, 2002
Chromium(VI) interaction with plant and animal mitochondrial bioenergetics: A comparative study
Authors: Fernandes M. A. S. , Santos M. S. , Alpoim M. C. , Madeira V. M. C. , Vicente J. A. F. 
Published: August 2002

AbstractThe mechanism of Cr(VI)‐induced toxicity in plants and animals has been assessed for mitochondrial bioenergetics and membrane damage in turnip root and rat liver mitochondria. By using succinate as the respiratory substrate, ADP/O and respiratory control ratio (RCR) were depressed as a function of Cr(VI) concentration. State 3 and uncoupled respiration were also depressed by Cr(VI). Rat mitochondria revealed a higher sensitivity to Cr(VI), as compared to turnip mitochondria. Rat mitochondrial state 4 respiration rate triplicated in contrast to negligible stimulation of turnip state 4 respiration. Chromium(VI) inhibited the activity of the NADH‐ubiquinone oxidoreductase (complex I) from rat liver mitochondria and succinate‐dehydrogenases (complex II) from plant and animal mitochondria. In rat liver mitochondria, complex I was more sensitive to Cr(VI) than complex II. The activity of cytochrome c oxidase (complex IV) was not sensitive to Cr(VI). Unique for plant mitochondria, exogenous NADH uncoupled respiration was unaffected by Cr(VI), indicating that the NADH dehydrogenase of the outer leaflet of the plant inner membrane, in addition to complexes III and IV, were insensitive to Cr(VI). The ATPase activity (complex V) was stimulated in rat liver mitochondria, but inhibited in turnip root mitochondria. In both, turnip and rat mitochondria, Cr(VI) depressed mitochondrial succinate‐dependent transmembrane potential (Δψ) and phosphorylation efficiency, but it neither affected mitochondrial membrane permeabilization to protons (H+) nor induced membrane lipid peroxidation. However, Cr(VI) induced mitochondrial membrane permeabilization to K+, an effect that was more pronounced in turnip root than in rat liver mitochondria. In conclusion, Cr(VI)‐induced perturbations of mitochondrial bioenergetics compromises energy‐dependent biochemical processes and, therefore, may contribute to the basal mechanism underlying its toxic effects in plant and animal cells. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:53–63, 2002; Published online in Wiley Interscience (www.interscience.wiley.com). DOI 10.1002/jbt.10025
Four patients with both thrombotic thrombocytopenic purpura and autoimmune thrombocytopenic purpura: The concept of a mixed immune thrombocytopenia syndrome and indications for plasma exchange
Authors: Baron Beverly W. , Martin Marisa Saint , Sucharetza Brian S. , Jeon Hye‐Ran , Baron Joseph M. 
Published: August 2002

AbstractAutoimmune thrombocytopenic purpura (ATP) and thrombotic thrombocytopenic purpura (TTP) are each well recognized clinical syndromes which may appear as single episodes or may have chronic relapsing courses. We present four patients negative for human immunodeficiency virus (HIV) infection who appear to have both diagnoses with either concomitant or intermingled episodes, and we review seven additional patients reported in the literature with similar features. All four of our patients are female, two have underlying connective tissue disorders, and their ATP processes came to our attention because of incomplete response of the platelet count to plasma exchange therapy (PEX) during a TTP phase (Cases 1 and 2) or development of thrombocytopenia in the absence of microangiopathy on the background of prior typical TTP episodes (Cases 3 and 4). Recognition of the ATP diagnosis in each case resulted in discontinuation of PEX (Cases 1 and 2) or not instituting PEX (Cases 3 and 4). In each instance, a satisfactory rise in platelet count followed treatment for ATP. Based upon this experience, we conclude that some individuals may have a mixed immune thrombocytopenia syndrome; careful analysis of the mechanism of thrombocytopenia, especially in recurrent episodes and in patients who respond incompletely to PEX for TTP, is important when deciding whether to initiate or continue PEX, or to consider therapies appropriate for other mechanisms of thrombocytopenia. J. Clin. Apheresis 16:179–185, 2001. © 2001 Wiley‐Liss, Inc.
Ethanolamine is a co‐mitogenic factor for proliferation of primary hepatocytes
Authors: Ajioka Itsuki , Akaike Toshihiro , Watanabe Yoshifumi 
Published: August 2002

AbstractMature adult parenchymal hepatocytes can enter the S phase in the presence of growth factors such as HGF and EGF, but rarely proliferate in culture. We hypothesized that the cell cycle of hepatocytes in culture is restricted before G2/M phase and we attempted to identify the factor that induces cell cycle progression. We found that the conditioned medium from long‐term cultured hepatocytes contained co‐mitogenic activity with other growth factors, which was attributed to ethanolamine (Etn). Etn induced not only DNA synthesis but also cell replication of cultured hepatocytes with various other growth factors. Etn and HGF synergistically induced cyclin D1, A and B expression, however, only cyclin B but not cyclin A formed a complex with Cdc2. In addition, Etn combined with HGF enhanced PKCβII expression and translocated PKCβII to the plasma membrane, and induced filopodia formation, which was inhibited by an antisense oligonucleotide against PKCβII. In addition, blocking the cytoskeleton rearrangement with inhibitors (colchicine, cytochalasin D, or chlerythrine (a specific PKC inhibitor)) inhibited cyclin expression and cell proliferation. Although Etn enhanced the downstream product, cellular phosphatidylethanolamine (PE), PE itself did not show any Etn‐like activities on hepatocytes. Taken together, our results indicate that Etn functions as a co‐replication factor to promote the cell cycle of mature hepatocytes to G2/M phase in the presence of growth factors. The activity is thought to be mediated by PKCβII‐dependent cyclin B expression. J. Cell. Biochem. 84: 249–263, 2002. © 2001 Wiley‐Liss, Inc.
Differential maintenance and de novo methylating activity by three DNA methyltransferases in aging and immortalized fibroblasts
Authors: Lopatina Nadejda , Haskell Joyce F. , Andrews Lucy G. , Poole Joseph C. , Saldanha Sabita , Tollefsbol Trygve 
Published: August 2002

AbstractGenomic methylation, which influences many cellular processes such as gene expression and chromatin organization, generally declines with cellular senescence although some genes undergo paradoxical hypermethylation during cellular aging and immortalization. To explore potential mechanisms for this process, we analyzed the methylating activity of three DNA methyltransferases (Dnmts) in aging and immortalized WI‐38 fibroblasts. Overall maintenance methylating activity by the Dnmts greatly decreased during cellular senescence. In immortalized WI‐38 cells, maintenance methylating activity was similar to that of normal young cells. Combined de novo methylation activity of the Dnmts initially decreased but later increased as WI‐38 cells aged and was strikingly elevated in immortalized cells. To further elucidate the mechanisms for changes in DNA methylation in aging and immortalized cells, the individual Dnmts were separated and individually assessed for maintenance and de novo methylating activity. We resolved three Dnmt fractions, one of which was the major maintenance methyltransferase, Dnmt1, which declined steadily in activity with cellular senescence and immortalization. However, a more basic Dnmt, which has significant de novo methylating activity, increased markedly in activity in aging and immortalized cells. We have identified this methyltransferase as Dnmt3b which has an important role in neoplastic transformation but its role in cellular senescence and immortalization has not previously been reported. An acidic Dnmt we isolated also had increased de novo methylating activity in senescent and immortalized WI‐38 cells. These studies indicate that reduced genome‐wide methylation in aging cells may be attributed to attenuated Dnmt1 activity but that regional or gene‐localized hypermethylation in aging and immortalized cells may be linked to increased de novo methylation by Dnmts other than the maintenance methyltransferase. J. Cell. Biochem. 84: 324–334, 2002. © 2001 Wiley‐Liss, Inc.
Functional receptor for platelet‐derived growth factor in rat embryonic heart‐derived myocytes: Role of sequestered Ca2+ stores in receptor signaling and antagonism by arginine vasopressin
Authors: Brostrom Margaret A. , Meiners Sally , Brostrom Charles O. 
Published: August 2002

AbstractPlatelet‐derived growth factor (PDGF) is established to function importantly in the growth, development, and function of most cardiovascular tissues. However, evidence that the factor participates directly in the growth and development of the mammalian myocardium is lacking. H9c2 rat embryonic ventricular myocytes were found to respond to PDGF‐BB with a rapid mobilization of cell‐associated Ca2+ and increased rates of protein synthesis, followed by markedly increased rates of DNA synthesis. PDGF acted as a full mitogen for these myocytes. Evidence is provided that documents the expression of classical PDGF‐β, but not PDGF‐α, receptors in H9c2 cells. Scatchard analysis revealed the presence of 44,000 β‐receptors per myocyte. Cell shortening and clustering of plasmalemmal β‐receptors occurred within 30 min of exposure to PDGF‐BB. Treatment was also associated with a transient increase in the rate of synthesis of GRP78/BiP, consistent with a transitory release of Ca2+ from the sarcoplasmic/endoplasmic reticulum [S(E)R]. Increased rates of protein synthesis at early times of PDGF treatment were additive with those occurring in response to arginine vasopressin, indicating different mechanisms of translational upregulation by these agents. The mitogenic effects of PDGF were delayed by vasopressin, which causes H9c2 myocytes to undergo hypertrophy while promoting the persistent depletion of S(E)R Ca2+ stores. In the presence of PDGF, vasopressin did not induce hypertrophy. As compared to untreated myocytes, DNA synthesis in PDGF‐treated myocytes was optimized at lower extracellular Ca2+ concentrations and was significantly less sensitive to inhibition by ionomycin. H9c2 cells appear to provide a useful embryonic cardiomyocyte model in which to examine both PDGF‐activated proliferative and vasopressin‐activated hypertrophic events and the importance of transient vs. sustained Ca2+ release in these events. J. Cell. Biochem. 84: 736–749, 2002. © 2002 Wiley‐Liss, Inc.
Nuclear localization and DNA interaction of protein disulfide isomerase ERp57 in mammalian cells
Authors: Coppari Sabina , Altieri Fabio , Ferraro Anna , Chichiarelli Silvia , Eufemi Margherita , Turano Carlo 
Published: August 2002

AbstractProtein disulfide isomerase ERp57 is localized predominantly in the endoplasmic reticulum, but is also present in the cytosol and, according to preliminary evidence, in the nucleus of avian cells. Conclusive evidence of its nuclear localization and of its interaction with DNA in vivo in mammalian cells is provided here on the basis of DNA–protein cross‐linking experiments performed with two different cross‐linking agents on viable HeLa and 3T3 cells. Nuclear ERp57 could also be detected by immunofluorescence in HeLa cells, where it showed an intracellular distribution clearly different from that of an homologous protein, located exclusively in the endoplasmic reticulum. Mammalian ERp57 resembles the avian protein in its recognition of S/MAR‐like DNA sequences and in its association with the nuclear matrix. It can be hypothesized that ERp57, which is known to associate with other proteins, in particular STAT3 and calreticulin, may contribute to their nuclear import, DNA binding, or other functions that they fulfil inside the nucleus. J. Cell. Biochem. 85: 325–333, 2002. © 2002 Wiley‐Liss, Inc.
Mapping of intrinsic bent DNA sites in the upstream region of DNA puff BhC4‐1 amplified gene
Authors: Fiorini Adriana , Basso Luiz Roberto , Paçó‐Larson Maria Luisa , Fernandez Maria Aparecida 
Published: August 2002

AbstractWe have identified bent DNA sites in the distal and proximal DNA puff BhC4‐1 amplified gene promoter region of Bradysia hygida. The 2D modeling of the 3D DNA path and the ENDS ratio values calculated in this promoter region resulted in the identification of ten pronounced bent sites named BhC4B − 9 to + 1. The 1847 bp fragment (− 3697 to − 1850) in relation to the transcription start site shows multiple bending sites, BhC4B − 9 to BhC4B − 4, with periodicity ∼300 bp. The analysis of the other identified bent region, starting at position − 957, reveals that the BhC4B + 1 bent site colocalizes with the putative BhC4‐1 minimal promoter. The sequence analysis of bent site BhC4B − 4 shows a distribution of dA•dT at ∼10 bp intervals between the middle of each tract, but intervals with more than one turn, ∼20 bp, two helix turns, were detected in the other bent sites described here. The bent sites BhC4B − 6 and BhC4B − 4, contain two consensus sequences, with 60 bp each. The apparent molecular weight of fragments in the BhC4‐1 promoter region were estimated in agarose gels and compared with the data obtained in polyacrylamide gels without and with ethidium bromide. The mobility reduction ratios (R‐values) were determined, and a high R‐value, 1.80, for a 1215 bp fragment in the distal promoter region and a 1.23 significant R‐value for a 662 bp fragment in the proximal segment were found. To further analyze the predicted bent DNA sites in these fragments, the 2D trajectories of the 3D DNA path and other parameters, AT percentage, roll angle, ENDS ratio and ΔG, were determined. The role of these bent sites in the BhC4‐1 transcription regulation is discussed. © 2001 Wiley‐Liss, Inc.
Protein tyrosine phosphatase SHP‐1 specifically recognizes C‐terminal residues of its substrates via helix α0
Authors: Yang Jian , Cheng Zhiliang , Niu Tianqi , Liang Xiaoshan , Zhao Zhizhuang Joe , Zhou G. Wayne 
Published: August 2002

AbstractThe catalytic domain of protein tyrosine phosphatase SHP‐1 possesses distinct substrate specificity. It recognizes the P‐3 to P‐5 residues of its substrates via the β5‐loop‐β6 region. To study the substrate specificity further, we determined the structure of the catalytic domain of SHP‐1 (C455S) complexed with a less‐favorable‐substrate peptide originated from SIRPα. The complex has disordered N‐terminal peptide structure and reduced interactions between the N‐terminal peptide and the β5‐loop‐β6 region. This could be the basis for the lower affinity of peptide pY427 for the catalytic domain of SHP‐1. In addition, by comparing the SHP‐1/less‐favorable peptide complex structure with the SHP‐1/substrate complex structures, we identified a novel substrate‐recognition site in the catalytic domain of SHP‐1. This site was formed by helix α0 and the α5‐loop‐α6 motif of SHP‐1, and specifically bound residues at the P + 4 and further C‐terminal positions of peptide substrates. © 2001 Wiley‐Liss, Inc.