bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of pond water, sediment and sediment extract samples from new hampshire, usa on early Xenopus development and metamorphosis: comparison to native species
Authors: Fort Douglas J. , Rogers Robert L. , Paul Robbin R. , Miller Mark F. , Clark Patrick , Stover Enos L. , Yoshioko Joy , Quimby Fred , Sower Stacia A. , Reed Karen L. , Babbitt Kimberly J. , Rolland Rosalind 
Published: August 2002

AbstractIn an effort to assess potential ecological hazards to amphibian species in selected regions within New Hampshire, the traditional Frog Embryo Teratogenesis Assay—Xenopus (FETAX), a 14‐/21 day tail resorption thyroid disruption assay and >30 day limb development tests were conducted with representative surface water and sediment samples. Two separate sets of samples collected from five sites were evaluated. The primary objectives of the study were to determine if samples were capable of inducing early embryo‐larval maldevelopment, to determine if maldevelopment included limb defects, to determine if thyroxine co‐administration altered the rates of limb malformation and to evaluate the impact of the samples on growth rates, developmental progress and metamorphic climax. Results from these studies suggested that pond water and sediment extract samples, but not whole sediment samples, from B2, FW, LP and W ponds were capable of inducing abnormal early embryo‐larval development. In addition, water samples from B2 and W ponds induced significant abnormal hindlimb development. Some abnormal forelimb development was noted in the tail resorption studies, but not to the same extent as the hindlimbs. Each of the water samples induced appreciable developmental delay, including the paired reference site B1, which could be reversed by the addition of exogenous thyroxine. Copyright © 2001 John Wiley & Sons, Ltd.
Production of superoxide anion, lipid peroxidation and DNA damage in the hepatic and brain tissues of rats after subchronic exposure to mixtures of TCDD and its congeners
Authors: Hassoun Ezdihar A. , Li Feng , Abushaban Ahmed , Stohs Sidney J. 
Published: August 2002

AbstractIn this study the induction of oxidative stress in the hepatic and brain tissues of rats after subchronic exposure to various mixtures of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) and two of its congeners, namely 2,3,4,7,8‐pentachlorodibenzofuran (PeCDF) and 3,3′,4,4′,5‐pentachlorobiphenyl (PCB 126) was investigated. Four mixtures of TCDD and its congeners, corresponding to 10, 22, 46 and 100 ng of toxic equivalence (TEQ) kg−1 day−1, were administered to groups of rats for 13 weeks. The animals were sacrificed at the end of the exposure period and the biomarkers of oxidative stress, including the production of superoxide anion, lipid peroxidation and DNA single‐strand breaks (SSBs), were determined in the hepatic and brain tissues. All mixtures caused dose‐dependent increases in the production of superoxide anion, lipid peroxidation and DNA SSBs in both tissues, with significantly higher damage in the hepatic compared with the brain tissues. The 22 ng TEQ dose level (TEQ = 22) contains TCDD, PeCDF and PCB 126 at levels that correspond to 7.3, 14.5 and 73.3 ng kg−1 day−1, respectively, and it produced effects that correspond to ca. 50% of the maximal production of superoxide anion, lipid peroxidation and DNA SSBs in the hepatic and brain tissues of those animals. Relative to the doses that are required to produce 50% of the maximal production of the biomarkers of oxidative stress by the individual congeners in hepatic and brain tissues of rats, the concentrations of the congeners in TEQ = 22 did result in significant interactivity, probably in the form of additive effects in the hepatic but not in brain tissues. Copyright © 2001 John Wiley & Sons, Ltd.
Site‐specific percutaneous absorption of methyl salicylate and VX in domestic swine
Authors: Duncan E. J. Scott , Brown April , Lundy Paul , Sawyer Thomas W. , Hamilton Murray , Hill Ira , Conley John D. 
Published: August 2002

AbstractThe site specificity of the percutaneous absorption of methyl salicylate (MeS) and the organophosphate nerve agent VX (O‐ethyl S‐(2‐diisopropylaminoethyl) methylphosphonothioate) was examined in anaesthetized domestic swine that were fully instrumented for physiological endpoints. Four different anatomical sites (ear, perineum, inguinal crease and epigastrium) were exposed to the MeS and the serum levels were measured over a 6‐h time period. The dose absorbed at the ear region was 11 μg cm−2 with an initial flux of 0.063 μg cm−2min−1, whereas at the epigastrium region the dose absorbed was 3 μg cm−2 with an initial flux of 0.025 μg cm−2min−1. For this reason further studies were carried out with VX on the ear and the epigastrium only. In animals treated with agent on the epigastrium, blood cholinesterase (ChE) activity began to drop 90 min after application and continued to decline at a constant rate for the remainder of the experiment to ca. 25% of awake control activity. At this time there were negligible signs of poisoning and the medical prognosis was judged to be good. In contrast, the ChE activity in animals receiving VX on the ear decreased to 25% of awake control values within 45 min and levelled out at 5–6% by 120 min. Clinical signs of VX poisoning paralleled the ChE inhibition, progressing in severity over the duration of the exposure. It was judged that these animals would not survive. The dramatic site dependence of agent absorption leading to vastly different toxicological endpoints demonstrated in this model system has important ramifications for chemical protective suit development, threat assessment, medical countermeasures and contamination control protocols. Copyright © 2002 Crown in the right of Canada. Published by John Wiley & Sons, Ltd.
Hydroxyapatite coating on titanium by thermal substrate method in aqueous solution
Authors: Kuroda Kensuke , Ichino Ryoichi , Okido Masazumi , Takai Osamu 
Published: August 2002

AbstractA new hydrocoating method (the thermal substrate method) is proposed for coating calcium phosphates such as hydroxyapatite (HA), on titanium substrates in an aqueous solution. Several factors (e.g., the type of ion source, the heating time and temperature, and the surface roughness of the substrate) affected the characteristics of the precipitate formed by this method. The solution used included 3 mmol dm−3 Ca(H2PO4)2 and 7 mmol dm−3 CaCl2, and its pH was adjusted to 6.5. The experimental studies were conducted under the following conditions: temperature 45–160°C, heating time 10–20 min, and surface roughness of substrate #120–#2000 grid ground using energy paper. A high quality of precipitate, whose predominant component was HA, was obtained on titanium substrates by the thermal substrate method in an aqueous solution. No significant difference in the precipitates was found with the type of ion source. The amount of HA precipitate increased with increasing temperature and with increasing heating time. The features of the precipitate were different, depending on the surface roughtness of the substrate: HA regularly nucleated along the grooves of the rough surface (#120 and #400 grid), and in the case of the fine surface (#1200–#2000 grid), a uniform precipitation occurred. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 390–397, 2002
Adhesion between poly(ethylene‐co‐vinyl alcohol) (EVA) and titanium
Authors: Matsumura Kazuaki , Hyon Suong‐Hyu , Nakajima Naoki , Peng Chunyan , Iwata Hiroo , Tsutsumi Sadami 
Published: August 2002

AbstractLap shear adhesive strength between titanium and various kinds of commercial polymers was evaluated. Among them, poly(ethylene‐co‐vinyl alcohol) (EVA) showed the highest strength. The results of electron spectroscopy for chemical analysis and the contact angle to water indicated that the high adhesive strength of EVA might be due to its high hydrophilicity. Water resistance of adhesion by water immersing at 37°C was investigated. In the case of polyurethane‐titanium, the adhesive strength decreased immediately. In contrast, EVA‐titanium kept its initial adhesive strength for at least up to 1 month. It was confirmed that surface modification of titanium by hydrogen peroxide enhanced the adhesive and peeling strength. It was based on not only an increase in surface adhesive area but also an increase in the hydrophilicity of titanium by the production of Ti‐OH. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 60: 309–315, 2002; DOI 10.1002/jbm.10051
Effect of surface treatment of NiTi alloy on its corrosion behavior in Hanks’ solution
Authors: Cissé O. , Savadogo O. , Wu M. , Yahia L'H. 
Published: August 2002

AbstractThe effect of surface modification of NiTi shape memory alloy on its corrosion behavior in Hanks’ solution was determined. The near‐equi‐atomic super elastic NiTi (Ni 55.8 wt %) alloy used for this study was provided by Memry USA. The surfaces of heat‐treated samples were modified by mechanical polishing (MP), electropolishing (EP), and electropolishing followed by chemical passivation (CP). As‐heat‐treated samples with straw‐colored oxide finishes (SCO) and blue‐colored oxide finishes (BO) also were included in the study. Surface analysis was performed using auger electron spectroscopy (AES), atomic force microscopy (AFM), and contact angle measurements (CAM). It was shown that surface roughness increased in the order CP < EP < SCO < BO < MP. The nickel release within the five groups of NiTi samples, as determined by atomic absorption spectrophotometry, reduced in time over the measured period. The level of Ni ions released over a 25‐day immersion period was highest in the SCO sample (0.002 μg/day). This Ni level is negligible compared with the daily intake of Ni in an ordinary diet. The auger electron spectroscopy (AES) analyses indicated that before immersion in Hanks’ physiologic solution, the main surface composition of all the samples was titanium and nickel, with a small amount of oxygen, carbon, and sulphur as contaminants. And the surface oxide thickness of the different samples increased in the order CP < EP < MP < BO < SCO. On the other hand, for the electrodes treated under the same conditions, the mean breakdown potential value decreased in the order BO > MP > CP > EP > SCO while the corrosion current density and rate increased in the order CP < SCO < EP < BO < MP. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 61: 339–345, 2002
Application of frog (Rana tigerina Daudin) skin collagen as a novel substrate in cell culture
Authors: Kumar K. V. Sathya Sai , Sai K. Purna , Babu M. 
Published: August 2002

AbstractCollagen and collagen‐based materials have extensive application in biomedical devices and tissue engineering. The current paper pertains to the application of frog (Rana tigerina Daudin) skin collagen as a novel substrate in cell culture. The study deals with the behavior, morphology, and physiology of keratinocytes and fibroblasts over dry and reconstituted collagen substratum, which are the key cells involved in wound repair. The advantage of using frog skin collagen as a substratum lies in the ease with which the reconstituted gel can be formed. Further, frog skin collagen is highly hydrophilic, which may be attributed to the fact that amphibians, as the first vertebrates connecting water and land, must have evolved certain physiologic specializations. These studies also contribute to the hypothesis that part of the healing efficacy of frog skin may be due to the collagen since proliferation, migration, and differentiation of epithelial cells are prime requisites for a normal healing mechanism. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 61: 197–202, 2002
Ultimate tensile strength of dentin: Evidence for a damage mechanics approach to dentin failure
Authors: Staninec Michal , Marshall Grayson W. , Hilton Joan F. , Pashley David H. , Gansky Stuart A. , Marshall Sally J. , Kinney John H. 
Published: August 2002

AbstractDentin structure and properties are known to vary with orientation and location. The present study explored the variation in the ultimate tensile strength (UTS) of dentin with location in the tooth. Hourglass specimens were prepared from dentin located in the center, under cusps, and in the cervical regions of human molar teeth. These were tested in tension at various distances from the pulp. Median tensile strengths ranged from 44.4 MPa in the inner dentin near the pulp, to 97.8 MPa near the dentino–enamel junction (DEJ). This increase in the median UTS with distance from the pulp to the DEJ was statistically significant (P <.001). Of particular importance was the observation that the UTS measurements followed a Weibull probability distribution, with a Weibull modulus of about 4.5. The Weibull behavior of the UTS data strongly suggests that the large variances in fracture strength data result from a distribution of preexisting defects in the dentin. These findings justify a damage‐mechanics approach to studies of dentin failure. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res (Appl Biomater) 63: 342–345, 2002
Transforming growth factor β released from natural coral implant enhances bone growth at calvarium of mature rat
Authors: Vuola Jyrki , Böhling Tom , Göransson Harry , Puolakkainen Pauli 
Published: August 2002

AbstractEarlier studies have shown that transforming growth factor β (TGF‐β) has the capability of enhancing bone formation after a single application to an orthotopic site. We investigated whether 1, 5, or 25 μg of recombinant human TGF‐β1 added to porous natural coral (NC) blocks could promote bone ingrowth in a critical size defect (CSD) model in nongrowing rats. A 6‐mm CSD in the parietal bone of Wistar rats was filled with NC disks, which were retrieved at 3 and 8 weeks. We prepared undecalcified sections for microscopy and histomorphometry to study bone formation in the implants. The differences in the means of the measured variables were compared with a one‐way analysis of variance and Tukey's Student range test, and p values smaller than 0.05 were considered statistically significant. Bone formation was enhanced in all the TGF‐β1‐treated implants at 8 weeks in comparison with the controls, but none of the implants showed complete bridging across the defect. The number of macrophages and giant cells was reduced in the TGF‐β1 implants, which showed less resorption and more intact structure than the coral controls. Void areas without any fibrous tissue ingrowth were found only in the TGF‐β1‐treated implants, which may partly explain the reduced resorption. The data suggested that TGF‐β1 induced enhanced but limited bone formation in mature rats and prevented resorption of the coral calcium carbonate matrix, possibly by hindering reactive cell formation and fibrous tissue ingrowth. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 152–159, 2002
Mutagenicity evaluation of forty‐one metal salts by the umu test
Authors: Yamamoto Akiko , Kohyama Yuko , Hanawa Takao 
Published: August 2002

AbstractMetallic biomaterials implanted in a human body may corrode and wear, releasing metal ions and debris which may induce adverse reactions such as inflammation, allergy, neoplastic formation, developmental malformation, etc. Mutagenicity is a very fundamental and important toxicity related to carcinogenicity and reproductive/developmental toxicity because the damages to genes or DNA can be a cause of carcinogenesis and developmental abnormalities. However, available mutagenic data on metallic ions and compounds are restricted to the number of elements. Therefore, to obtain the systematic data necessary for metal ion mutagenicity, 41 metal salts encompassing 36 metals and 5 metallic elements tested with different valences, were evaluated on their mutagenicity by a microbial test, the umu test. As a result, K2Cr2O7, RhCl3, IrCl4, and MgCl2 are positive without metabolic activation. Concentrations having the maximum mutagenic effect (Cmax) are 9.65 × 10−5, 1.00 × 10−4, 3.11 × 10−3, 4.12 × 10−3 mol · L−1, respectively. CuCl2, VCl3, CuCl, RhCl3, K2Cr2O7, and IrCl4 are positive with metabolic activation by S‐9 mix with Cmax of 1.60 × 10−5, 3.91 × 10−5, 1.57 × 10−4, 2.00 × 10−4, 3.86 × 10−4, 1.56 × 10−2 mol · L−1, respectively. Thirty‐five metal salts were negative for tests performed both with and without metabolic activation, whereas it was impossible to evaluate the mutagenicity of MoCl5 and ZrCl4 by the umu test because of their colorimetric reaction to testing reagents. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 176–183, 2002
Probe of specific interaction between a simplified synthetic glycopolymer and erythrocytes as mediated by a glucose transporter (GLUT) on a cell membrane
Authors: Park Keun‐Hong , Na Kun , Akaike Toshihiro , Lee Kang Choon 
Published: August 2002

AbstractIn order to develop a biomimetic polymer for cell recognition, we synthesized poly [3‐O‐(4′‐vinylbenzyl)‐D‐glucose] (PVG), a polystyrene derivative with reduced glucose moiety, and studied the specific interaction of this PVG with erythrocytes, carried by a glucose transporter (GLUT‐1), on a cell membrane. To clarify the specific interaction between the PVG and the erythrocytes, fluorescence isothiocyanate‐ (FITC) labeled polymer was used to prove and visualize the specific interaction. We found that labeled polymer strongly binds to erythrocytes, probably due to the specific interaction mediated by the presence of GLUT‐1 on the cell membrane. The fluorescence intensity of PVG on erythrocytes was time and dose dependent. To verify the specific interaction between the PVG and the erythrocytes, cells were pretreated with phloretin, an inhibitor of GLUT‐1, before adding the FITC‐labeled PVG polymer to the cell‐culture medium. This treatment suppressed the interaction of PVG with erythrocytes. A confocal laser microscopic study further confirmed this interaction. The results from this study provide evidence that a biomimetic polymer of PVG interacts with erythrocytes mediated by GLUT‐1 on cell membranes. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 591–594, 2002
Effects of quercetin on antioxidant defense in streptozotocin‐induced diabetic rats
Authors: Sanders Ruth A. , Rauscher Frederick M. , Watkins John B. 
Published: August 2002

AbstractIn light of evidence that some complications of diabetes mellitus may be caused or exacerbated by oxidative damage, we investigated the effects of subacute treatment with the antioxidant quercetin on tissue antioxidant defense systems in streptozotocin‐induced diabetic Sprague‐Dawley rats (30 days after streptozotocin induction). Quercetin, 2‐(3,4‐dihydroxyphenyl)‐3,5,7‐trihydroxy‐4H‐1‐benzopyran‐4‐one, was administered at a dose of 10mg/kg/day, ip for 14 days, after which liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione content, and activities of the free‐radical detoxifying enzymes catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. Treatment of normal rats with quercetin increased serum AST and increased hepatic concentration of oxidized glutathione. All tissues from diabetic animals exhibited disturbances in antioxidant defense when compared with normal controls. Quercetin treatment of diabetic rats reversed only the diabetic effects on brain oxidized glutathione concentration and on hepatic glutathione peroxidase activity. By contrast, a 20% increase in hepatic lipid peroxidation, a 40% decline in hepatic glutathione concentration, an increase in renal (23%) and cardiac (40%) glutathione peroxidase activities, and a 65% increase in cardiac catalase activity reflect intensified diabetic effects after treatment with quercetin. These results call into question the ability of therapy with the antioxidant quercetin to reverse diabetic oxidative stress in an overall sense. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:143–149, 2001
26S proteasome inhibition induces apoptosis and limits growth of human pancreatic cancer
Authors: Shah Shimul A. , Potter Michael W. , McDade Theodore P. , Ricciardi Rocco , Perugini Richard A. , Elliott Peter J. , Adams Julian , Callery Mark P. 
Published: August 2002

AbstractThe 26S proteasome degrades proteins that regulate transcription factor activation, cell cycle progression, and apoptosis. In cancer, this may allow for uncontrolled cell division, promoting tumor growth, and spread. We examined whether selective inhibition of the 26S proteasome with PS‐341, a dipeptide boronic acid analogue, would block proliferation and induce apoptosis in human pancreatic cancer. Proteasome inhibition significantly blocked mitogen (FCS) induced proliferation of BxPC3 human pancreatic cancer cells in vitro, while arresting cell cycle progression and inducing apoptosis by 24 h. Accumulation of p21Cip1‐Waf‐1, a cyclin dependent kinase (CDK) inhibitor normally degraded by the 26S proteasome, occurred by 3 h and correlated with cell cycle arrest. When BxPC3 pancreatic cancer xenografts were established in athymic nu/nu mice, weekly administration of 1 mg/kg PS‐341 significantly inhibited tumor growth. Both cellular apoptosis and p21Cip1‐Waf‐1 protein levels were increased in PS‐341 treated xenografts. Inhibition of tumor xenograft growth was greatest (89%) when PS‐341 was combined with the tumoricidal agent CPT‐11. Combined CPT‐11/PS‐341 therapy, but not single agent therapy, yielded highly apoptotic tumors, significantly inhibited tumor cell proliferation, and blocked NF‐κB activation indicating this systemic therapy was effective at the cancer cell level. 26S proteasome inhibition may represent a new therapeutic approach against this highly resistant and lethal malignancy. J. Cell. Biochem. 82: 110–122, 2001. © 2001 Wiley‐Liss, Inc.
Possible involvement of protein kinase C in the induction of adipose differentiation‐related protein by Sterol ester in RAW 264.7 macrophages
Authors: Chen Jin‐Shan , Greenberg Andrew S. , Tseng Yung‐Zu , Wang Seu‐Mei 
Published: August 2002

AbstractThe accumulation of lipid droplets in macrophages contributes to the formation of foam cells, an early event in atherosclerosis. It is, therefore, important to elucidate the mechanisms by which lipid droplets accumulate and are utilized. Sterol ester (SE)‐laden RAW 264.7 macrophages accumulated lipid droplets in a time‐dependent manner up to 16 h, which was enhanced by cotreatment with 0.1 μM phorbol 12‐myristate 13‐acetate (PMA). Inhibition of protein kinase C (PKC) activity by cotreatment with 0.3 μM calphostin C CAL for 16 h resulted in coalescence of small lipid droplets into large ones and increased accumulation of lipid droplets, although to a lesser extent than after PMA cotreatment. Immunostaining for adipose differentiation‐related protein (ADRP) revealed a fluorescent rim at the surface of each medium to large lipid droplet. ADRP appearance correlated with lipid droplet accumulation and was regulated by PMA in a time‐dependent manner. Induction of ADRP expression by PMA or CAL required SE, since ADRP levels in PMA‐ or CAL‐treated non‐SE‐laden macrophages were comparable to those in untreated cells. Removal of SE from the incubation medium resulted in the concomitant dissolution of lipid droplets and down‐regulation of ADRP. In conclusion, the above results suggest that ADRP may be an important protein in the regulation of lipid droplet metabolism in lipid‐laden macrophages and that this regulation may be mediated by PKC activity. J. Cell. Biochem. 83: 187–199, 2001. © 2001 Wiley‐Liss, Inc.