bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of hyaluronan on osteoblast proliferation and differentiation in rat calvarial‐derived cell cultures
Authors: Huang L. , Cheng Y. Y. , Koo P. L. , Lee K. M. , Qin L. , Cheng J. C. Y. , Kumta S. M. 
Published: August 2003

AbstractHyaluronan (or hyaluronic acid, HA) is an essential component of extracellular matrices. It interacts with other macromolecules and plays a predominant role in tissue morphogenesis, cell migration, differentiation, and adhesion. The cell signaling functions of HA are mediated through the CD‐44 receptor and are dependent upon the molecular weight of the polymer. We hypothesized that an HA of appropriate molecular weight alone in optimal concentration may induce osteoblast differentiation and bone formation. Enzyme‐digested calvarial‐derived mesenchymal cells from 2‐day‐old newborn rats were cultured with the addition of HA of three different molecular weights (2300, 900, and 60 kDa). We added, 0.5, 1.0, and 2.0 mg/mL HA for each molecular weight to the medium at the first plating of cells. After 7 to 20 days in culture, cell proliferation and differentiation were evaluated by measuring thymidine incorporation, alkaline phosphatase activity, and osteocalcin gene expression. The effects of HA on bone formation were examined by using Alizarin red staining for mineralization. The results showed that low molecular weight HA (60 kDa) significantly stimulated cell growth, increased osteocalcin mRNA expression in a dose‐dependent manner, but showed no apparent effects on alkaline phosphatase activity and bone mineralization. On the other hand, high‐weight HA (900 and 2300 kDa) significantly increased all the parameters examined, particularly alkaline phosphatase activity, in a dose‐dependent manner and stimulated cell mineralization to 126% and 119% of the controls, respectively, in the 1.0 mg/mL dose. Our findings suggest that HA has a molecular weight‐specific and dose‐specific mode of action that may enhance the osteogenic and osteoinductive properties of bone graft materials and substitutes due to its stimulatory effects on osteoblasts. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 66A: 880–884, 2003
Influence of dentinal polyelectrolytes on wet demineralized dentin, a bonding substrate
Authors: Piemjai M. , Iwasaki Y. , Nakabayashi N. 
Published: August 2003

AbstractThe objective of this study was to show the influence of dissolved dentinal polyelectrolytes on the characteristics of dentin (bonding substrate) demineralized by citric acid in the absence or presence of ferric chloride. The demineralizing agent was an aqueous mixture of 0, 1, 3, or 10% ferric chloride in 10% citric acid (10–0, 10–1, 10–3, 10–10, respectively). The hypothesis was that the concentration of dissolved dentinal noncollagenous substances, mainly polyelectrolytes soluble in water, must be decreased by their aggregation with ferric ions, which changes the characteristics of demineralized dentin, the rates of demineralization, and dehydration. Cervical bovine dentin was prepared in 3 × 2 × 2‐mm blocks, each weighing 20.0 ± 0.5 mg. The rate of demineralization was investigated by measuring the weight loss resulting from demineralization by immersion in 10 mL of conditioner at 2‐h intervals. The dehydration rate of wet demineralized dentin was determined using two methods: (1) weight loss in a desiccator under 263 Pa pressure and (2) differential scanning calorimetry (DSC). Twenty, 12, 8, and 4 h were required to complete demineralization of the blocks with the 10–0, 10–1, 10–3, and 10–10 solutions, respectively. The 10–10 wet demineralized dentin showed the highest rate of dehydration, followed in descending order by the 10–3, 10–1, and 10–0 specimens. Ferric chloride in dentin conditioners provided both a higher rate of dentin demineralization and a higher dehydration rate of wet demineralized dentin. These results suggest that in the presence of ferric chloride, a decreasing amount of dissolved polyelectrolytes aggregated with ferric ions in the substrates may increase the permeability of dentin to water and citric acid. Improvement of monomer permeability is essential to the preparation of good hybridized dentin, providing a more stable and reliable bonding and also protecting the dentin and pulp from infection. A further study of bonding substrates is required in order to understand the role of hybridized dentin in improved dental treatment. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 66A: 789–794, 2003
High‐affinity augmentation of endothelial cell attachment: Long‐term effects on focal contact and actin filament formation
Authors: Mathur Anshu B. , Chan Bernard P. , Truskey George A. , Reichert William M. 
Published: August 2003

AbstractCoadsorption of high‐affinity avidin with lower affinity cell adhesion protein fibronectin has been shown to significantly augment short‐term (1 h) adhesion and spreading of endothelial cells; however, the longer term persistence of avidin binding and its effect on endothelial cell adhesion have not been addressed. In this study, the presence of avidin–biotin bonds 24 h after cell adhesion to the dual ligand surfaces was verified by laser confocal microscopy of a fluorescent avidin analog, streptavidin. Total internal reflection microscopy showed that the focal contact area, focal contact density, and cell spreading all increased significantly at 24 h compared to fibronectin‐treated control surfaces. Focal contact area was identical when measured with cells that were labeled with either the fluorescent streptavidin or a carbocyanine dye incorporated in the cell membrane. Confocal images of stress fibers formed in cells adherent to dual ligand surfaces after 24 h were thicker and more numerous compared to cells adherent to fibronectin controls. The results indicate that 24 h after initial attachment avidin–biotin is localized to focal contacts on the basal surface and affects cell spreading, actin filament organization, and focal contact density. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 66A: 729–737, 2003
The profits and perils of international outsourcing
Authors: Bean LuAnn 
Published: August 2003

AbstractMore and more companies are outsourcing work abroad. This trend is transforming everything from call centers
to credit cards. But there are both benefits and dangers for your company. The author investigates how companies
are using this strategy today and gives some solid advice to help you choose the right outsourcing model for your
particular company. © 2003 Wiley Periodicals, Inc.
Key trends in Southeast Asia
Authors: Jasmon Abadan , Nordin Mohd Ridzuan 
Published: August 2003

AbstractTempted to do business in Southeast Asia (SEA)? Many SEA countries offer very attractive
incentives—in addition to a low‐cost, high‐quality labor force. They also allow 100 percent
foreign ownership, tax holidays, and capital allowances. But there are important differences compared to developed
countries. Government agencies and corporations play a different role, and business decisions may not be made in
the way you expect. What must you know to avoid potential problems? Where are the best opportunities?
© 2003 Wiley Periodicals, Inc.
An insider's guide to doing business in India
Authors: Rathinasamy R. S. , Mantripragada Krishna G. , Krishnan Rishikesha T. , Shivaswamy Melkote K. 
Published: August 2003

AbstractMany U.S. companies are searching for foreign business opportunities. And the world's largest
democracy—India—has become a favorite of U.S. multinational companies. But what is the Indian business
climate really like? What risks do you face? What pitfalls should you avoid? Where are the best
fast‐growth opportunities? Here is a comprehensive, hands‐on guide to doing business in India
that will answer those vital questions and more. © 2003 Wiley Periodicals, Inc.
How to handle the threat of catastrophe
Authors: Sánchez Carol , Goldberg Stephen R. 
Published: August 2003

AbstractOne major task CEOs face is to minimize risk and vulnerability to catastrophic events. Since 9/11, we know
that simply having insurance—and conventional emergency planning—is not enough. And in addition to
global terrorism, other catastrophes threaten—including cyber crime and new diseases like SARS. Traditional
risk management strategies dealt with two types of danger: known and unknown risk. But now we also have a third
kind: unknowable risk! So how should we handle catastrophic threats today? © 2003 Wiley
Periodicals, Inc.
Euro M&A: Dealmakers rethink their strategies
Authors: Metwalli Ali M. , Tang Roger Y.W. 
Published: August 2003

AbstractM&A (merger and acquisition) activities in the European Union expanded steadily in the 1990s,
reaching a peak in 1999 and 2000. But there was a big slowdown after that, due to a faltering global economy, the
9/11 attacks, and fears of terrorism and regulatory changes. Many firms were forced to rethink their M&A
strategies. © 2003 Wiley Periodicals, Inc.
Hedge accounting: What's the problem with IASC standards?
Authors: Hernández Francisco Gabriel Hernández 
Published: August 2003

AbstractThe International Accounting Standards Committee (IASC) requires companies use IAS 39 and IAS 32 in
accounting for financial instruments and hedging activities. But this causes problems, says the author. Instead,
he offers an alternative approach. © 2003 Wiley Periodicals, Inc.
Pro‐ethics activities: Do they really reduce fraud?
Authors: Singleton Tommie , King Brett , Messina Frank M. , Turpen Richard A. 
Published: August 2003

AbstractWe have seen a growing number of extraordinary financial frauds over the past few years. So critics call for
more focus on ethics, and more pro‐ethics activities. But do ethics programs really reduce fraud? The
results of one study may surprise you. © 2003 Wiley Periodicals, Inc.
International auditing and managing exports
Authors: Goldberg Stephen R. , Godwin Joseph H. 
Published: August 2003

AbstractO'Regan, David. 2003. International Auditing, Practical Resource Guide (New York:
John Wiley & Sons).Reynolds, Frank. 2003. Managing Exports: Navigating the Complex Rules, Controls, Barriers, and
Laws (New York: John Wiley & Sons).
How much does bad data cost your company?
Authors: Jankovsky Lynn , Grimme Julie 
Published: August 2003

AbstractA recent project at Motorola that addressed the cost of bad data accomplished several important goals. Among
these, the project identified the cost of bad data for a certain data element and then calculated the percentage
of cost of the element in terms of total cost. This contributed to the knowledge of reducing cost by understanding
the cost drivers; it also helped managers in prioritization, resource management, and implementation of
enterprisewide systems. © 2003 Wiley Periodicals, Inc.
Effect of dexamethasone withdrawal on osteoblastic differentiation of bone marrow stromal cells
Authors: Porter Ryan M. , Huckle William R. , Goldstein Aaron S. 
Published: August 2003

AbstractDexamethasone is capable of directing osteoblastic differentiation of bone marrow stromal cells (BMSCs) in vitro, but its effects are not lineage‐specific, and sustained exposure has been shown to down‐regulate collagen synthesis and induce maturation of an adipocyte subpopulation within BMSC cultures. Such side effects might be reduced if dexamethasone is applied in a regimented manner, but the discrete steps in osteoblastic maturation that are stimulated by dexamethasone are not known. To examine this, dexamethasone was added to medium to initiate differentiation of rat BMSCs cultures and then removed after a varying number of days. Cell layers were analyzed for cell number, rate of collagen synthesis, expression of osteocalcin (OC), bone sialoprotein (BSP) and lipoprotein lipase (LpL), and matrix mineralization. Withdrawal of dexamethasone at 3 and 10 days was found to enhance cell number relative to continuous exposure, but did not affect to decrease collagen synthesis slightly. Late markers of osteoblastic differentiation, BSP expression and matrix mineralization, were also sensitive to dexamethasone and increased systematically with exposure while LpL systematically decreased. These results indicate that dexamethasone acts at both early and late stages to direct proliferative osteoprogenitor cells toward terminal maturation. J. Cell. Biochem. 90: 13–22, 2003. © 2003 Wiley‐Liss, Inc.
Immune cell proliferation is suppressed by the interferon‐γ‐induced indoleamine 2,3‐dioxygenase expression of fibroblasts populated in collagen gel (FPCG)
Authors: Sarkhosh Kourosh , Tredget Edward E. , Karami Ali , Uludag Hasan , Iwashina Takashi , Kilani Ruhangiz T. , Ghahary Aziz 
Published: August 2003

AbstractIndoleamine 2,3‐dioxygenase (IDO), a tryptophan‐catabolizing enzyme, is an intracellular enzyme possessing various immunosuppressive properties. Here, we report the possible use of this enzyme to suppress proliferation of immune cells cocultured with IDO‐expressing fibroblasts of an allogenic skin substitute. Fetal skin fibroblasts embedded within bovine collagen were treated with cytokine interferon‐γ (IFN‐γ) to induce expression of IDO mRNA and protein. Expression of IDO mRNA was evaluated by Northern analysis. IDO enzyme activity was evaluated by measurement of kynurenine and tryptophan levels in the IFN‐γ untreated and treated fibroblasts. The results of Northern analysis showed a dose‐dependent increase in expression of IDO mRNA in response to various concentrations of IFN‐γ used. The levels of kynurenine and tryptophan measured, as the bioactivity of IDO, were significantly different in the IFN‐γ treated fibroblasts, compared to those of controls (P < 0.001). In a lasting effect experiment, the expression of IDO mRNA was gradually reduced to an undetectable level within 32 h of IFN‐γ removal. The results of Western blot analysis, however, revealed a significantly longer (192 h) lasting effect of IFN‐γ on IDO protein level, relative to that of mRNA expression. To demonstrate immunosuppressive effects of IDO on proliferation of immune cells, IDO‐expressing fibroblasts were cocultured with peripheral blood mononuclear cells (PBMC) for a period of 5 days. The results of 3H‐thymidine incorporation showed a significant reduction in proliferation of PBMC when cocultured with IDO‐expressing fibroblasts, compared to those cocultured with non‐IDO‐expressing fibroblasts (P < 0.001). Furthermore, addition of IDO‐inhibitor (1‐methyl‐d‐tryptophan) reversed the suppressive effects of IDO on PBMC proliferation in a dose‐dependant fashion. To test the viability of immune cells cocultured with IDO‐expressing fibroblasts, FACS analysis of the PI stained PBMC was conducted and no significant difference was found between these cells and the controls. In another set of experiments, we showed that migration rate and subsequent proliferation of IDO‐expressing fibroblasts are also the same as those of control cells. In conclusion, IDO‐expressing allogenic fibroblasts embedded within collagen gel suppress the proliferation of allogenic immune cells, while they still remain viable in this IDO‐induced tryptophan‐deficient culture environment. J. Cell. Biochem. 90: 206–217, 2003. © 2003 Wiley‐Liss, Inc.
Fluorescence activated cell sorting reveals heterogeneous and cell non‐autonomous osteoprogenitor differentiation in fetal rat calvaria cell populations
Authors: Purpura Kelly A. , Zandstra Peter W. , Aubin Jane E. 
Published: August 2003

AbstractIdentification of osteoblast progenitors, with defined developmental capacity, would facilitate studies on a variety of parameters of bone development. We used expression of alkaline phosphatase (ALP) and the parathyroid hormone/parathyroid hormone‐related protein receptor (PTH1R) as osteoblast markers in dual‐color fluorescence activated cell sorting (FACS) to fractionate rat calvaria (RC) cells into ALP−PTH1R−, ALP+PTH1R−, ALP−PTH1R+, and ALP+PTH1R+ populations. These fractionated populations were seeded clonally (n = 96) or over a range of cell densities (∼150–8,500 cell/cm2; n = 3). Our results indicate that colony forming unit‐osteoblast (CFU‐O)/bone nodule‐forming cells are found in all fractions, but the frequency of CFU‐O and total mineralized area is different across fractions. Analysis of these differences suggests that ALP−PTH1R−, ALP−PTH1R+, ALP+PTH1R−, and ALP+PTH1R+ cell populations are separated in order of increasing bone formation capacity. Dexamethasone (dex) differentially increased the CFU‐O number in the four fractions, with the largest stimulation in the ALP− cell populations. However, there was no significant difference in the number or size distribution of CFU‐F (fibroblast) colonies that formed in vehicle versus dex. Finally, both cell autonomous and cell non‐autonomous (i.e., inhibitory/stimulatory effects of cell neighbors) differentiation of osteoprogenitors was seen. Only the ALP−PTH1R− population was capable of forming nodules at the clonal level, at approximately 3‐ or 12‐times the predicted frequency of unfractionated populations in dex or vehicle, respectively. These data suggest that osteoprogenitors can be significantly enriched by fractionation of RC populations, that assay conditions modify the osteoprogenitor frequencies observed and that fractionation of osteogenic populations is useful for interrogation of their developmental status and osteogenic capacity. J. Cell. Biochem. 90: 109–120, 2003. © 2003 Wiley‐Liss, Inc.
How is Type I procollagen synthesis regulated at the gene level during tissue fibrosis
Authors: Cutroneo Kenneth R. 
Published: August 2003

AbstractIn response to tissue injury connective tissue synthesis occurs either normally or abnormally, which is mediated by transforming growth factor‐β (TGF‐β) and other growth factors. This article will be primarily concerned with the response of injured tissues at the gene level of Type I procollagen synthesis in response to TGF‐β. This leads to provisional repair, which in turn may lead to involution, remodeling, regeneration, and ultimately repair. Alternately, continuation of provisional repair may lead to fibrosis and ultimately scarring. Scarring of internal organs such as the liver and the lung leads to loss of function and ultimately death. In the case of scarring of skin, this is a cosmetic problem and can be rectified by surgery. Type I procollagen is synthesized by two genes, proα1 (Type I) and proα2 (Type I) collagen genes. This article will focus on DNA binding sites on these two genes, which regulate the transcription of the specific gene. This article will also define specific cell signaling pathways for the turning on of the proα1 and proα2 (Type I) collagen genes. This article will address several questions. First, what is the major cytokine acting extracellularly which stimulates the transcription of the proα1 and proα2 (Type I) collagen genes during tissue fibrosis? Secondly, how are the signals transmitted by the extracellular profibrotic cytokine TGF‐β from the cellular membrane to the nucleus for transcription of the proα1 (Type I) and proα2 (Type I) collagen genes? Thirdly, what signaling pathways cross‐talk with the signaling pathways resulting in the expression of the Type I collagen genes? Fourthly, how does TGF‐β affect extracellular matrix homeostasis? Fifthly, what are the nuclear factors corresponding to the DNA elements required for the promotion of the proα1 (Type I) and proα2 (Type I) collagen genes? Finally, how are the proα1 (Type I) and proα2 (Type I) collagen genes coordinately regulated? Strategies will also be presented for reducing fibrosis, which is the result of overexpression of TGF‐β. J. Cell. Biochem. 90: 1–5, 2003. © 2003 Wiley‐Liss, Inc.
Modulation of VE‐cadherin and PECAM‐1 mediated cell–cell adhesions by mitogen‐activated protein kinases
Authors: Wu Jianqiang , Sheibani Nader 
Published: August 2003

AbstractEndothelial cell transition from a differentiated, quiescent phenotype to a migratory, proliferative phenotype is essential during angiogenesis. This transition is dependent on alterations in the balanced production of stimulatory and inhibitory factors, which normally keep angiogenesis in check. Activation of MAPK/ERKs is essential for endothelial cell migration and proliferation. However, its role in regulation of endothelial cell adhesive mechanisms requires further delineation. Here, we show that sustained activation of MAPK/ERKs results in disruption of cadherin‐mediated cell–cell adhesion, down‐regulation of PECAM‐1 expression, and enhanced cell migration in microvascular endothelial cells. Expression of a constitutively active MEK‐1 in mouse brain endothelial (bEND) cells resulted in down‐regulation of VE‐cadherin and catenins expression concomitant with down‐regulation of PECAM‐1 expression. In contrast, inhibition of MEK‐1 restored parental morphology, cadherin/catenins expression and localization. These data are further supported by our observation that sustained activation of MAPK/ERKs in phorbol myristate acetate incubated HUVEC lead to disruption of cadherin‐mediate cell–cell interactions and enhanced capillary formation on Matrigel. Thus, sustained activation of MAPK/ERKs plays an important role in disruption of cell–cell adhesion and migration of endothelial cells. J. Cell. Biochem. 90: 121–137, 2003. © 2003 Wiley‐Liss, Inc.
Skeletal muscle metabolism in physiology and in cancer disease
Authors: Giordano Anna , Calvani Menotti , Petillo Orsolina , Carteni' Maria , Melone Maria Rosa A.B. , Peluso Gianfranco 
Published: August 2003

AbstractSkeletal muscle is a tissue of high demand and it accounts for most of daily energy consumption. The classical concept of energy metabolism in skeletal muscle has been profoundly modified on the basis of studies showing the influence of additional factors (i.e., uncoupling proteins (UCPs) and peroxisome proliferator activated receptors (PPARs)) controlling parameters, such as substrate availability, cellular enzymes, carrier proteins, and proton leak, able to affect glycolysis, nutrient oxidation, and protein degradation. This extremely balanced system is greatly altered by cancer disease that can induce muscle cachexia with significant deleterious consequences and results in muscle wasting and weakness, delaying or preventing ambulation, and rehabilitation in catabolic patients. J. Cell. Biochem. 90: 170–186, 2003. © 2003 Wiley‐Liss, Inc.
Pitavastatin alters the expression of thrombotic and fibrinolytic proteins in human vascular cells
Authors: Markle Ronald A. , Han Jihong , Summers Barbara D. , Yokoyama Toru , Hajjar Katherine A. , Hajjar David P. , Gotto Antonio M. , Nicholson Andrew C. 
Published: August 2003

AbstractIn addition to lowering blood lipids, clinical benefits of 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG Co‐A; EC 1.1.1.34) reductase inhibitors may derive from altered vascular function favoring fibrinolysis over thrombosis. We examined effects of pitavastatin (NK‐104), a relatively novel and long acting statin, on expression of tissue factor (TF) in human monocytes (U‐937), plasminogen activator inhibitor‐1 (PAI‐1), and tissue‐type plasminogen activator (t‐PA) in human aortic smooth muscle cells (SMC) and human umbilical vein endothelial cells (HUVEC). In monocytes, pitavastatin reduced expression of TF protein induced by lipopolysaccharide (LPS) and oxidized low‐density lipoprotein (OxLDL). Similarly, pitavastatin also reduced expression of TF mRNA induced by LPS. Pitavastatin reduced PAI‐1 antigen released from HUVEC under basal, OxLDL‐, or tumor necrosis factor‐alpha (TNF‐α)‐stimulated conditions. Reductions of PAI‐1 mRNA expression correlated with decreased PAI‐1 antigen secretion and PAI‐1 activity as assessed by fibrin–agarose zymography. In addition, pitavastatin decreased PAI‐1 antigen released from OxLDL‐treated and untreated SMC. Conversely, pitavastatin enhanced t‐PA mRNA expression and t‐PA antigen secretion in untreated OxLDL‐, and TNF‐α‐treated HUVEC and untreated SMC. Finally, pitavastatin increased t‐PA activity as assessed by fibrin–agarose zymography. Our findings demonstrate that pitavastatin may alter arterial homeostasis favoring fibrinolysis over thrombosis, thereby reducing risk for thrombi at sites of unstable plaques. J. Cell. Biochem. 90: 23–32, 2003. © 2003 Wiley‐Liss, Inc.