bluuebunny/crossref_metadata_2025_split huggingface dataset:
Models for e‐government
Authors: Beynon‐Davies Paul 
Published: March 2007

PurposeThis paper aims to present a meta‐model for electronic government (e‐government) which takes account of the broad nature of this contemporary socio‐technical phenomenon. As such it contains within it a number of possible “business models” for the development of e‐government – strategies for e‐government focused around key business processes and information systems.Design/methodology/approachThis meta‐model is built from literature taken from the domains of informatics, business and public administration. It is also built on established academic, policy and practitioner literature from the domain of e‐government itself.FindingsThe paper demonstrates and validates the use of this meta‐model in three ways. First, it is used as an explanatory tool to help review the contemporary experience of e‐government in the UK. To help in this process we position specific case examples of e‐government against the model from this experience. Second, it is used to evaluate a number of existing models of e‐government, particularly those which provide an explicit framework of e‐government progress. A number of deficiencies in such models are identified from this evaluation. Third, the meta‐model is proposed as a framework for evaluating and potentially benchmarking e‐government. The intention is to raise the perspective of evaluation and benchmarking in this area beyond its contemporary focus on electronic service delivery.Originality/valueTo demonstrate the worth of this approach, the paper describes the application of elements of this meta‐model in two evaluation/benchmarking exercises undertaken by the author in the context of regional e‐government.
E‐inclusion as a further stage of e‐government?
Authors: Sahraoui Sofiane 
Published: March 2007

PurposeAn IT rationalist discourse predominates in the e‐government literature. Furthermore, and whenever an alternative and holistic discourse is developed, e‐government evaluation remains mechanistic. E‐inclusion is rightfully advocated as a socially inclusive strategy for e‐government planning and development but it is erroneously considered as a further stage of e‐government development, following the fourth and transactional stage. The paper aims to reconfigure e‐government and e‐inclusion as two parallel processes of government intervention to support a socially inclusive development strategy through a national IT strategy.Design/methodology/approachThis paper reviews the general discourse surrounding e‐government development and implementation, highlighting its mechanistic underpinnings and contrasting it with an inclusive approach to e‐government. The mechanistic discourse of e‐government is analyzed through key constructs that underlie the e‐government concept. Vision and objectives, e‐government evaluation, e‐government models and the enabling role of ICT will be analyzed in view of sorting out the predominance of a mechanistic theme in their elaboration. The synthesis part of this work introduces e‐inclusion based on a more organic and community‐centered approach to e‐government in light of the insufficiencies earlier identified.FindingsWhilst e‐inclusion provides a good platform to pinpoint insufficiencies of the predominant mechanistic approach to e‐government, it remains doubtful whether it could be achieved within the realm of e‐government programs alone.Practical implicationsModels, roadmaps and strategies for e‐inclusion should explicitly outline the premises for a socially inclusive e‐government and not consider e‐inclusion as a further and mechanical stage of the e‐government stage model. E‐government evaluation has to pinpoint the inclusion aspects of existing projects by going beyond mechanistic measurements.Originality/valueThis paper questions a major assumption in the e‐government literature, namely that e‐inclusion follows e‐government. By drawing from the political science literature, it identifies a niche for e‐inclusion which helps reconceptualize it as socially inclusive government rather than a further stage of e‐government.
An executive's guide to business transformation
Authors: Bititci Umit S. 
Published: March 2007

PurposeThe objective of this article is to provide executives with a practical high‐level roadmap to business transformation.Design/methodology/approachOver the past 20 years in his role as an academic, researcher and consultant, the author and his team have worked with and observed several organizations of varying sizes. This resulted in the identification of patterns associated with failed and successful transformation attempts, which in turn have been summarized into a formula for business transformation.FindingsAny successful business transformation will have to address all eight components of the business transformation model. These are: value streams, strategy, organization, people, processes, systems and resources, leadership and performance measurement. For a transformation attempt to succeed, all eight components must be addressed. Most failed transformation attempts have failed to address one or more of these components.Practical implicationsThe roadmap for business transformation provides a high‐level checklist to facilitate executives to plan their transformation journey with a certain degree of confidence. The article provides practical guidelines and tips to ensure that each component of the formula is appropriately addressed.Originality/valueThe article provides a holistic and practical look at business transformation from an executive's viewpoint.
031 IGF‐I stimulates VEGF production in endothelial cells by inhibiting poly(ADP‐Ribose)‐polymerase
Authors: Beckert S. , Scheuenstuhl H. , Farrahi F. , Aslam R. , Hunt TK. , Hussain Z. 
Published: March 2007

Introduction: Vascular Endothelial Growth Factor (VEGF) mediated angiogenesis plays a key role in wound healing. Insulin‐like Growth Factor I (IGF‐I) has been reported to be angiogenic. However, the mechanism is not known. Recently, a link between transcriptional activity and inhibition of poly(ADP‐Ribose)polymerase (PARP) has been reported. We investigated whether IGF‐I increases VEGF expression and whether this effect is regulated by the inhibition of PARP. Material and methods: Subconfluent monolayers of human umbilical vein cells were cultured and serum starved. Cultures were treated with Long‐R3‐IGF‐I for 20 h. VEGF in the supernatant was measured by ELISA and lactate by a lactate analyser. PARP activity was assessed by measuring the incorporation of 14C‐radiolabeled NAD+. All experiments were performed in triplicate. Results are given as percent change compared to control ± SD; p < 0.05 calculated by Student‘s t‐test was considered significant. Results: IGF‐I increased both VEGF (20 ± 10%, 50 ± 16%(p = 0.01) and 79 ± 13%(p = 0.0003)) and lactate production (12 ± 11%, 20 ± 12% and 48 ± 16%(p = 0.01)) in a dose dependent manner (25, 50 and 100 ng/ml). Blocking glucose utilization by 2‐desoxyglucose, decreased lactate by 70 ± 11%(p = 0.0001), but not VEGF expression. Inhibitors of MAP‐kinase (PD 98059) and Proteinkinase C (Staurosporine) reduced the IGF‐I effect on VEGF expression by 40 ± 6%(p = 0.0003) and 30 ± 7%(p = 0.01). 3‐Aminobenzamide and nicotinamide alone, inhibitors of PARP, stimulated VEGF production by 66 ± 5%(p = 0.0003) and 32 ± 8%(p = 0.002), respectively. IGF‐I inhibited PARP by 44 ± 3%(p = 0.01). Conclusion: IGF‐I enhances VEGF protein expression in endothelial cells. This is mediated through signal transduction and by inhibition of PARP.
034 Light‐Emitting Diode Therapy Increases VEGF and no Production in Raw 264.7 Cells
Authors: Leong M. , Zhao J. , Gould L.J. 
Published: March 2007

Introduction: Low‐energy laser photostimuation has been reported to affect the proliferative phase of wound healing and stimulate macrophages. Light‐emitting diodes (LED) are an efficient, inexpensive source of low energy photons. We propose that LED therapy will stimulate macrophage production of VEGF and NO. Methods: Serum‐starved RAW 264.7 cells (5 × 105cells/ml) were treated with or without LPS (10 ng/ml) and IFN‐gamma (100 Units/ml) for 24 hours. Cells were divided into groups: 1) control – no LED, 2) 670 nm, 3) 730 nm, 4) 880 nm, and 5) combination (880 nm/730 nm/670 nm) at 4 J/cm2 per wavelength. Twenty‐four hours post‐LED, conditioned media was analyzed for VEGF (ELISA) and nitrites (Greiss assay). Proliferation was assessed using BrDU incorporation. Data were analyzed using one‐way ANOVA with Tukey post‐test. Results: In serum‐starved cells, proliferation was unchanged by LED. VEGF and nitrite levels were increased in groups 4 (VEGF = 1057.1 +/− 100.3 pg/ml; nitrites = 11.13 +/− 0.79 uM) and 5 (VEGF = 1148.9 +/− 88.5 pg/ml; nitrites = 10.72 +/− 1.03 uM) compared to control (VEGF = 812.2 +/− 94.8 pg/ml; nitrites = 7.32 +/− 1.92 uM). LPS/IFN decreased proliferation 25 percent at all wavelengths compared to control + LPS/IFN (p < 0.01). Nitrite and VEGF levels were markedly elevated in all five LPS/IFN‐treated groups with no appreciable intergroup differences. Conclusions: LPS/IFN stimulation resulted in maximally elevated levels of nitrites and VEGF, possibly masking the effects of LED. Serum‐starved RAW 264.7 cells responded to LED treatment at 880 nm and combined wavelengths with increased VEGF and NO production. These results suggest that LED treatment at 880 nm and 880 nm/730 nm/670 nm may upregulate the production of pro‐angiogenic factors by macrophages in the wound bed.
035 Leptin Plays a Key Role in the Modulation of Wound Angiogenesis
Authors: Nath A.K. , Murad A. , Cha S.T. , Sierra‐Honigmann M.R. 
Published: March 2007

Leptin is a pleiotropic cytokine constitutively expressed in adipose tissue and upregulated by hypoxia in sites of tissue injury and in the placenta. Leptin has been demonstrated to play a role in normal and pathological wound healing and it is gene is acutely expressed in experimental wounds. Angiogenesis is among the most salient and well‐documented biological actions of leptin. Therefore it was hypothesized that leptin may play in the modulation of wound neovascularization. Using a murine model of experimental wounds the modulation of wound angiogenesis was investigated by treatment of the wounds to either recombinant leptin or a neutralizing anti‐leptin antibody. The parameters measured were: a)woundblood flow using laser Doppler imaging; b)vesseldensity by counting the number of CD‐31 positive vessels in wound sections; c)angiogenic transcriptionalprofiling using quantitative real‐time RT‐PCR; and d)validation of transcriptionalprofiling by immunohistochemistry and immunoblotting. The treatment of wounds with leptin had a marked effect in wound blood flow that was most significant at 24hours post‐wounding with average increase of 55% with respect to the controls. The effect diminished significantly by 72 hours (24%) and became negligible thereafter. Leptin also accelerate wound neovascularization by 24 hours where the number of small caliber vessels averaged 30/mm2 in leptin treated vessels and 13/mm2 in the controls (n = 10; P < 0.005). However, the number of vessels measured by 72 hours not significantly different between controls and leptin‐treated wounds. In addition transcriptional profiling reveled changes in gene expression of molecules related to angiogenesis such as VEGF, PlGF, Tie‐1, Tie‐2, Flt‐1, Flk‐1, FGF‐2 and endothelial markers like CD‐31, endoglin and eNOS. Overall, time course analysis throughout the healing process showed that leptin treatment induced an early shift in the expression of many of the analyzed transcripts. The most salient changes could be observed as early as 6 hours post‐wounding and included: TSP‐1 (+8.7); FLK‐1(+9); Ang‐2 (+18); CD31(+5.3); endoglin (+7.6); eNOS (+4.2); FGF‐2 (+4.3); etc. Leptin mRNA was also significantly increased (+10) as well as the long‐form of its receptor ObR‐b (+9). Conversely, when wounds were exposed to anti‐leptin antibodies, healing progression was impaired and changes in the transcriptional profile showed diminished expression of several genes related to wound neovascularization. Some examples by 24 hours: Endoglin(−2.5); Flk‐1(−2.8); eNOS (−5.1); Ang‐2 (−5.1); CD31(−3); VEGF‐A (−3.6). In conclusion, leptin had and early and significant effect in modulating wound neovascularization. The effect of treatment of wounds with exogenous leptin did not elicit hypervascularization of the wound and appeared to only accelerate what appeared to be a self‐limited process of wound angiogenesis.Funded by a Cedars‐Sinai grant from the Skirball‐Kenis Center for Plastic and Reconstructive Surgery.
045 Adenoviral HTERT Transfection Results in Altered Phospho‐erk Activity in Human Dermal Fibroblasts
Authors: Lu Leonard , Rosenberg David S. , Mogford Jon E. , Mustoe Thomas A. 
Published: March 2007

Introduction: Telomeres are nucleoprotein structures at the ends of each chromosome. Due to the inability of DNA polymerase to replicate the full length of the chromosome, up to 50–200 base pairs of the telomere are lost during each successive round of cell division. In adult human somatic cells, telomerase is not active resulting in progressive loss of telomere length and entry into replicative senescence as observed in cell culture. hTERT is the catalytic subunit of telomerase, an enzyme which maintains telomere length. Transfection of human dermal fibroblasts (HDFs) by hTERT has been shown to reverse the senescent phenotype seen in aging HDFs in vitro. ERK (p44/42) is a MAP kinase which functions as a critical intermediary in the determination of cell growth and differentiation. Activation of ERK occurs through phosphorylation of threonine and tyrosine residues.  Methods: In order to delineate some of the cellular mechanisms by which hTERT functions, we treated adenoviral hTERT (Ad‐hTERT) transfected HDFs with TGFB1, and assayed phosphorylated ERK activity by Western blotting. Results: Ad‐hTERT treated HDFs demonstrated a 2–3 fold increase in phospho‐ERK activity. In addition, our preliminary findings show that Ad‐hTERT transfected HDFs have increased TGFB1, TGFB1‐Receptor I and II, and COL1A1 gene expression by real‐time rtPCR.  Conclusions: Increased phosphor‐ERK activity as well as increased TGFB1, TGFB1‐Receptor I and II, and COL1A1 gene expression is seen in hTERT transfected HDF’s. Further studies will focus on defining other intermediary changes resulting from Ad‐hTERT tranfection.Funding source: Geron Corporation
055 The Effect of an Oxygen Emulsion on Collagen Deposition in Second‐Degree Burn Wound Repair
Authors: Li J. , Zhang Y.P. , Zhu L. , Mertz P.M. , Cazzaniga A.L. , Ricotti C. , Zalesky P.J. , Hsu L.C. , Creech J. , Eaglstein W.H. , Davis S.C. 
Published: March 2007

A porcine model of second‐degree burn wound was used to evaluate the effect of a newly developed topical oxygen emulsion (TOE) on collagen deposition during wound repair. A total of 6 pigs were used for the study. The burn wounds were treated with air exposure (no treatment), vehicle control or TOE, which contains super‐saturated oxygen and releases oxygen in sustained high level when applied topically. Skin wound samples were collected at days 0, 1, 4, 7, 10, 14 and 21 after wounding. Semi‐quantitative Reverse Transcription and Polymerase Chain Reactions (RT‐PCR) were used to examine the mRNA expressions for type I and type III collagens and matrix metalloprotease‐1 (MMP‐1). RT‐PCR products were run on ethidium bromide gel and analyzed under UV light with Bio‐Rad Gel Document 2000 system. The expression intensity was recorded as the mean gray value. One‐way analysis of variance was used for statistical analysis. The results showed: 1). Higher mRNA expressions of collagen III and MMP‐1 were observed in TOE treatment group compared with air exposure and vehicle control groups. 2). MMP‐1 expression increased shortly after wounding with peak at days 4 and 7. 3). Collagen III expression increased earlier with peak at day 10 and day 14. 4). Collagen I expression level increased later than that of collagen III. Significant increase was seen after day 10 with the highest at day 21. However, there was no significant difference between vehicle control and TOE treatment groups. The data suggests that sustained high level of oxygen release by TOE may promote wound repair through the mechanism of increased expressions of type I and type III collagens. The TOE also increased the expression of MMP‐1, which might accelerate clearing damaged collagens in the earlier phase of wound healing and promote collagen remodeling in the later phase.This study was supported by grants from DOD/DARPA and the Dermatology Foundation of South Florida.
063 The Human Forearm Biopsy Model for Acute Wound Healing
Authors: Serena T. , Li V. W. , Li W. W. 
Published: March 2007

Background: The study of wound biology and effects of advanced modalities would benefit from a reliable human model for normal healing. Eaglstein et al. previously suggested that the forearm biopsy may be useful in acute wound healing studies (J Am Acad Dermatol 45:857, 2001). The Wound Healing Cooperative Group (WHCG) here validates this model in healthy individuals treated with topical growth factor therapy. Methods: In our randomized, double‐blinded study design, 20 normal healthy volunteers underwent four 6 mm biopsies of the flexor surface of both forearms. Biopsy sites were randomly assigned to a control arm (daily bacitracin) or to one of three treatment arms: i) rhPDGF‐BB 0.01% gel (Q.D.), ii) rhPDGF‐BB (Q.O.D.), iii) rhPDGF‐BB (Q.D. × 7 days followed by bacitracin alone daily). The wounds were examined, measured and photographed daily until complete healing was achieved. Adverse events were monitored. Rates of healing and time‐to‐complete closure were measured. Repeat biopsies of a subset of healing wounds were performed for gene microarray analysis. Results: The forearm biopsy model allowed direct quantitative and qualitative comparisons of acute wound healing outcomes achieved by rhPDGF‐BB regimens versus standard care alone. There were no infectious complications. Subject compliance was excellent with < 3% of visits missed. Conclusion: The forearm biopsy model has several advantages in the study of acute wounds: it allows for comparison of topical agents in a controlled fashion; studies can be conducted easily with good patient compliance; and the forearm allows for repeat imaging and tissue harvesting for gene profiling during healing. Acknowledgements: Funding from The Angiogenesis Foundation.
067 Reversal of ε(γ‐Glutamyl) Lysine Cross‐Linking and Down‐Regulation of Fibronectin and Tissue Transglutaminase (tTGase) Activity in Hypertrophic Scars Following Treatment with 0.8% 1,4 DAB 2HCL
Authors: Hardas B. , Dolynchuk K. , Jacob C. , Griffin M. , Panchal C. 
Published: March 2007

Hypertrophic scar formation is an unfavorable condition which is difficult to predict, prevent or treat. Although much research has been done on understanding hypertrophic scar formation, the exact underlying molecular mechanism has not been fully elucidated.Hypertrophic scars younger than 6 months are known to over‐express tTGase. It has been shown that treatment of hypertrophic scars with topical 1, 4 DAB 2HCl inhibited ε(γ‐glutamyl) lysine cross‐linking4.In the current study, 12 paired scar biopsies, either treated or untreated with 1, 4 DAB 2HCl were examined for the presence of ε(γ‐glutamyl) lysine cross‐linking by fluorescence immunohistochemistry. In situ tTGase enzyme activity, expression of latent tissue TGF‐β binding protein‐1 (LTBP‐1) and fibronectin were also examined. Scars showed a marked reduction of ε(γ‐glutamyl) lysine cross‐linking following treatment with 1, 4 DAB 2HCl. Although the treated samples did not show any change in expression of tTGase, its in situ activity was noticeably reduced. Treated samples also demonstrated down‐regulation of fibronectin and LTBP‐1. Results suggest that topical treatment of hypertrophic scars with 1,4 DAB 2HCl not only reduced ε(γ‐glutamyl) lysine cross‐linking but also reduced tTGase activity, expression of fibronectin and LTBP‐15 which are known to play a role in extracellular matrix storage of transforming grown factor‐β(TGF‐β), responsible for wound healing and scar formation. 4Dolynchuk KN. Wound Rep Reg 1996; 4(1): 16–20. 5Verderio E, Gaudry C et al. J. Histochem 1999; 47(11): 1417–1432.
077 Human Mesenchymal Stem Cells Interact with Keratinocytes and Succesfully Accelerate Wound Healing
Authors: Akita Sadanori , Nakagawa Hiroshi , Fukui Masashi , Akino Kozo 
Published: March 2007

Human mesenchymal stem cells (hMSCs) obtained from a single donor from an iliac crest, were investigated with cutaneous wound healing models using nude rat, eliminating T cell‐mediated immune reaction to the grafted stem cell of human origin. Co‐culture of the human keratinocytes and the hMSCs revealed tight basal membranous interaction by electron microscopy.1.5 × 1.5 cm2 dorsal full‐thickness defects including panniculus carnosus of F344/NJCl‐rnu nude rats were covered by bi‐layered porcine‐derived collagen sponge artificial skin substitutes, Pelnac®, Johnson & Johnson, Tokyo, Japan, impregnated with 5 × 106 hMSCs grated to along with 0, 1, 10, or 100 μg of recombinant human basic fibroblast growth factor (bFGF). The tissues were harvested at 3, 7 42 days after grafting. The defects were remarkably epithelialized by 7 days after coverage with artificial skin substitutes and 10 μg of bFGF, while artificial substitutes with no hMSCs or artificial skin substitutes with hMSCs alone did not demonstrate such healing. The architectures of the artificial skin substitutes were integrated by day 42 in hMSCs‐treated groups. The artificial skin substitute at least plays a role in as a template or scaffold of the grafted hMSCs. Up to day 3, the mesenchymal stem cell surface markers such as CD 29 and CD 44 were remained immunopositive in the groups with hMSCs‐treated groups over the reconstructed dermis‐like tissue. By 42 days after grafting, artificial skin substitutes with hMSCs and 10 μg of bFGF demonstrated the total epithelization and the keratinocytes by this treatment exhibited the pan‐cytokeratin of human origin by immunohistochemical expressions. Thus, the hMSCs with bFGF treatment using an artificial skin substitute as a successfully heal. These results suggest that the human mesenchymal stem cells may be utilized for wound coverage together with bFGF and artificial skin substitutes.