bluuebunny/crossref_metadata_2025_split huggingface dataset:
Extracorporeal shock wave treatment modulates skin fibroblast recruitment and leukocyte infiltration for enhancing extended skin‐flap survival
Authors: Kuo Yur‐Ren , Wang Chun‐Ting , Wang Feng‐Sheng , Yang Kuender D. , Chiang Yuan‐Cheng , Wang Ching‐Jen 
Published: January 2009

ABSTRACTExtracorporeal shock wave (ESW) treatment has a positive effect of rescuing ischemic skin flaps. This study assessed whether ESW treatment rescues the compromised flap tissue by suppressing the apoptosis of ischemic tissue and recruiting tissue remodeling. We used a random‐pattern extended dorsal–skin‐flap (10 × 3 cm) rodent model. Thirty‐six male Sprague–Dawley rats were divided into three groups. Group I, the control group, received no treatment. Group II received one session of ESW treatment (500 impulses at 0.15 mJ/mm2) immediately after surgery. Group III received two sessions of ESW treatment, immediately and the day after the surgery. Results indicated that the necrotic area in the flaps in group II was significantly smaller than that of the flaps in group I (p<0.01). Transferase dUTP‐nick end labeling (TUNEL) analysis revealed a significant decrease in the number of apoptotic cells in group II. Hydrogen peroxide (H2O2) expression in circulation blood was significantly decreased in group II on the day after ESW treatment. Immunohistochemical staining indicated that compared with no treatment, ESW treatment could substantially increase proliferating cell nuclear antigen (PCNA), endothelial nitric oxide synthase, and prolyl 4‐hydroxylase (rPH) expression, reduce CD45 expression, and suppress 8‐hydroxyguanosine (8‐OG) expression in the ischemic zone of the flap tissue. In conclusion, ESW treatment administered at an optimal dosage exerts a positive effect of rescuing ischemic extended skin flaps. The mechanisms of action of ESWs involve modulation of oxygen radicals, attenuation of leukocyte infiltration, decrease in tissue apoptosis, and recruitment of skin fibroblasts, which results in increased flap tissue survival.
Prostaglandin E2 differentially regulates contraction and structural reorganization of anchored collagen gels by human adult and fetal dermal fibroblasts
Authors: Parekh Aron , Sandulache Vlad C. , Singh Tripti , Cetin Selma , Sacks Michael S. , Dohar Joseph E. , Hebda Patricia A. 
Published: January 2009

ABSTRACTContraction and remodeling of granulation tissue by fibroblasts is a crucial component of dermal wound healing. Postnatal wounds heal with imperfect repair and scar formation, whereas tissue repair in fetal wounds is regenerative. Prostaglandin E2 (PGE2) modulates the behavior of fibroblasts in the wound bed. This study was designed to investigate the mechanism by which PGE2 regulates an in vitro model of granulation tissue, anchored collagen gels, by human adult and fetal dermal fibroblasts. We hypothesized that PGE2 differentially regulates contraction and remodeling of anchored collagen gels by these fibroblast phenotypes. These results indicate that once tension was generated, fetal fibroblasts exerted lower contractile forces resulting in less collagen contraction. This coincided with less prominent stress fibers, yet fetal fibroblasts were able to substantially remodel the collagen architecture. This mechanism was differentially modulated by PGE2 and was mimicked with a PGE2 receptor agonist, indicating a cyclic adenosine monophosphate (cAMP)‐dependent mechanism through the EP2 receptor. However, direct up‐regulation of cAMP led to decreases in contraction and remodeling by both fibroblast phenotypes indicating an altered signaling pathway. Therefore, targeting cAMP via the EP2 receptor could potentially decrease adult fibroblast contractile forces to the levels of the fetal fibroblast phenotype in order to decrease dermal scarring.
Emblica officinalis exerts wound healing action through up‐regulation of collagen and extracellular signal‐regulated kinases (ERK1/2)
Authors: Sumitra Miriyala , Manikandan Panchatcharam , Gayathri Vinaya Subramani , Mahendran Panchatcharam , Suguna Lonchin 
Published: January 2009

ABSTRACTDuring wound healing, the wound site is rich in oxidants, such as hydrogen peroxide, mostly contributed by neutrophils and macrophages. Ascorbic acid and tannins of low molecular weight, namely emblicanin A (2,3‐di‐O‐galloyl‐4,6‐(S)‐hexahydroxydiphenoyl‐2‐keto‐glucono‐δ‐lactone) and emblicanin B (2,3,4,6‐bis‐(S)‐hexahydroxydiphenoyl‐2‐keto‐glucono‐δ‐lactone) present in Emblica officinalis (emblica), have been shown to exhibit a very strong antioxidant action. We proposed that addition of these antioxidants to the wound microenvironment would support the repair process. The present investigation was undertaken to determine the efficacy of emblica on dermal wound healing in vivo. Full‐thickness excision wounds were made on the back of the rat and topical application of emblica accelerated wound contraction and closure. Emblica increased cellular proliferation and cross‐linking of collagen at the wound site, as evidenced by an increase in the activity of extracellular signal‐regulated kinase 1/2, along with an increase in DNA, type III collagen, acid‐soluble collagen, aldehyde content, shrinkage temperature and tensile strength. Higher levels of tissue ascorbic acid, α‐tocopherol, reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase support the fact that emblica application promotes antioxidant activity at the wound site. In summary, this study provides firm evidence to support that topical application of emblica represents a feasible and productive approach to support dermal wound healing.
Impaired cutaneous wound healing in mice lacking tetranectin
Authors: Iba Kousuke , Hatakeyama Naoko , Kojima Takashi , Murata Masaki , Matsumura Tadaki , Wewer Ulla M. , Wada Takuro , Sawada Norimasa , Yamashita Toshihiko 
Published: January 2009

ABSTRACTTetranectin was originally purified from human serum on the basis of plasminogen kringle 4‐binding properties. Tetranectin enhances plasminogen activation by a tissue‐type plasminogen activator so that it has been suggested to play a role in tissue remodeling. We have generated mice with a targeted disruption of the tetranectin gene to elucidate the biological function of tetranectin. In this study, we showed that wound healing was markedly delayed in tetranectin‐null mice compared with wild‐type mice. A single full‐thickness incision was made in the dorsal skin. By 14 days after the incision, the wounds fully healed in all wild‐type mice based on the macroscopic closure; in contrast, the progress of wound healing in the tetranectin null mice appeared to be impaired. In histological analysis, wounds of wild‐type mice showed complete reepithelialization and healed by 14 days after the incision. However, those of tetranectin‐null mice never showed complete reepithelialization at 14 days. At 21 days after the injury, the wound healed and was covered with an epidermis. These results supported the fact that tetranectin may play a role in the wound healing process.
Depth of penetration of negative pressure wound therapy into underlying tissues
Authors: Murphey Gary C. , Macias Brandon R. , Hargens Alan R. 
Published: January 2009

ABSTRACTNegative pressure wound therapy has become ubiquitous in orthopedic surgery and it is therefore important to understand the physiologic conditions of this therapy. The purpose of this study was to determine the magnitude and depth of negative pressure transmission into underlying muscle tissue in a wound model. We hypothesized that the negative pressure is not transmitted beyond 2 mm into underlying muscle tissue. Using both an isolated muscle and a live animal wound model, we applied open cell foam dressing to the tissue. Using a series of vacuum‐assisted closure negative pressure settings (0, −75, −125, −200 mmHg) interstitial fluid pressure was measured in the underlying tissue with a solid‐state pressure transducer catheter at 1/10 mm depth intervals. In the ex vivo isolated‐muscle model, the effect of negative pressure wound therapy on interstitial fluid pressure was extinguished and not significantly different than controls at a depth <2 mm. In the live animal wound model, the magnitude of interstitial fluid pressures corresponded directly with negative pressure settings (p<0.01) and inversely with depth into muscle (p<0.01). Interstitial fluid pressures were significantly (p<0.05) less than control interstitial fluid pressures (0 mmHg setting) at depths of 0.5, 0.4, and 0.9 mm below the foam/muscle interface when the applied pressures were −75, −125, and −200 mmHg, respectively. Negative pressure wound therapy penetrates no more than 1 mm into rabbit wound tissue at the highest negative pressure setting (−200 mmHg) when using open‐cell foam dressing.
FGF‐10 and specific structural elements of dermatan sulfate size and sulfation promote maximal keratinocyte migration and cellular proliferation
Authors: Radek Katherine A. , Taylor Kristen R. , Gallo Richard L. 
Published: January 2009

ABSTRACTFibroblast growth factor‐10 (FGF‐10) is essential for epithelial development, while other members of this family, such as FGF‐7, are not. FGF‐10 is abundantly released into wounds following injury, and likely an essential growth factor required for this process. To evaluate how activation of this growth factor is controlled, multiple glycosaminoglycans were combined with FGF‐10 assayed by measurement of the proliferation of cell lines expressing FGF receptor‐2‐IIIb, or keratinocyte migration in an in vitro wound repair assay. Dermatan sulfate (DS) exhibited greater potency than heparan sulfate or other chondroitin sulfates found in wounds. Structural variants of DS between 10 and 20 disaccharides containing iduronic acid showed maximal capacity to enable FGF‐10 receptor stimulation. Furthermore, FGF‐10 and DS markedly enhanced migration of keratinocytes in an in vitro wound scratch assay, while FGF‐7 or other glycosaminoglycans did not. These data strongly suggest that FGF‐10 activity is uniquely important in wound repair and that specific DS structural properties are necessary to promote FGF‐10 function. These observations identify a novel interplay between DS and FGF‐10 in mediating wound repair.
A novel cell‐adhesive scaffold material for delivering keratinocytes reduces granulation tissue in dermal wounds
Authors: Masuda Ryuji , Mochizuki Mayumi , Hozumi Kentaro , Takeda Akira , Uchinuma Eiju , Yamashina Shohei , Nomizu Motoyoshi , Kadoya Yuichi 
Published: January 2009

ABSTRACTNovel peptide‐conjugated chitosan membranes were fabricated and used to deliver keratinocytes to dermal wounds in mice. Three active peptides of 12 or 13 amino acids each, RLVSYNGIIFFLK (A5G27), ASKAIQVFLLAG (A5G33), and AGTFALRGDNPQG (A99) were selected from a cell‐adhesive peptide library of laminin, a major constituent of basement membrane. The peptides were synthesized and coupled to chitosan membranes, and the resulting peptide–chitosan membranes were tested for keratinocyte attachment. Two of the peptides that bind to cell surface heparin‐like receptors (A5G27 and A5G33) were found to promote strong keratinocyte attachment, whereas the one that binds to integrin (A99) was inactive. Subsequently, A5G27– and A5G33–chitosan membranes were tested as vehicles for keratinocyte delivery in a wound model. We found that keratinocytes were delivered into the full‐thickness wound with either membrane. Using the A5G33–chitosan membrane, we further evaluated the activity of the delivered keratinocytes in wound healing. Immunohistochemistry for granulation tissue markers, including tenascin and α‐smooth muscle actin, showed that keratinocyte delivery by the present peptide–chitosan membranes in the wound bed provided a favorable condition for keratinocyte migration along the wound surface and reduced granulation tissue formation.
Tissue engineering a model for the human ear: Assessment of size, shape, morphology, and gene expression following seeding of different chondrocytes
Authors: Kusuhara Hirohisa , Isogai Noritaka , Enjo Mitushiro , Otani Hitoshi , Ikada Yoshito , Jacquet Robin , Lowder Elizabeth , Landis William J. 
Published: January 2009

ABSTRACTThis study examines the tissue engineering of a human ear model through use of bovine chondrocytes isolated from four different cartilaginous sites (nasoseptal, articular, costal, and auricular) and seeded onto biodegradable poly(l‐lactic acid) and poly(l‐lactide‐ɛ‐caprolactone) (50 : 50) polymer ear‐shaped scaffolds. After implantation in athymic mice for up to 40 weeks, cell/scaffold constructs were harvested and analyzed in terms of size, shape, histology, and gene expression. Gross morphology revealed that all the tissue‐engineered cartilages retained the initial human auricular shape through 40 weeks of implantation. Scaffolds alone lost significant size and shape over the same period. Quantitative reverse transcription‐polymerase chain reaction demonstrated that the engineered chondrocyte/scaffolds yielded unique expression patterns for type II collagen, aggrecan, and bone sialoprotein mRNA. Histological analysis showed type II collagen and proteoglycan to be the predominant extracellular matrix components of the various constructs sampled at different implantation times. Elastin was also present but it was found only in constructs seeded with auricular chondrocytes. By 40 weeks of implantation, tissue‐engineered cartilage of costal origin became calcified, marked by a notably high relative gene expression level of bone sialoprotein and the presence of rigid, nodular protrusions formed by mineralizing rudimentary cartilaginous growth plates. The collective data suggest that nasoseptal, articular, and auricular cartilages represent harvest sites suitable for development of tissue‐engineered human ear models with retention over time of three‐dimensional construct architecture, gene expression, and extracellular matrix composition comparable to normal, nonmineralizing cartilages. Calcification of constructs of costal chondrocyte origin clearly shows that chondrocytes from different tissue sources are not identical and retain distinct characteristics and that these specific cells are inappropriate for use in engineering a flexible ear model.
Lumbar Stimulation Belt for Therapy of Low‐Back Pain
Authors: Popović Dejan B. , Bijelić Goran , Miler Vera , Došen Strahinja , Popović Mirjana B. , Schwirtlich Laszlo 
Published: January 2009

AbstractWe developed the STIMBELT, an electrical stimulation system that comprises a lumbar belt with up to eight pairs of embedded electrodes and an eight‐channel electronic stimulator. The STIMBELT is an assistive system for the treatment of low‐back pain (LBP). We describe here technical details of the system and summarize the results of its application in individuals with subacute and chronic LBP. The direct goals of the treatment were to relieve pain, reduce muscle spasms, increase strength and range of motion, and educate individuals with LBP in reducing the chances of its reoccurrence. The outcome measures include: a Visual Analogue Scale (VAS), the Oswestry LBP Disability Questionnaire, the Short Form (SF)‐12 health survey, and the Manual Muscle Test. The results indicate significant benefits for individuals who use the STIMBELT in addition to the conventional therapy as opposed to only the conventional therapy.
The Relationship Between Leptin Level and Oxidative Status Parameters in Hemodialysis Patients
Authors: Horoz Mehmet , Aslan Mehmet , Koylu Ahmet O. , Bolukbas Cengiz , Bolukbas Filiz F. , Selek Sahbettin , Erel Ozcan 
Published: January 2009

AbstractBoth serum leptin level and oxidative stress are increased in hemodialysis (HD) patients. In the present study, we aimed to investigate whether there is association between oxidative status and leptin level in HD patients. Thirty‐five HD patients and 25 healthy controls were enrolled in the present study. Serum leptin level, total peroxide (TP) level, total antioxidant capacity (TAC), and oxidative stress index (OSI) were determined. Serum leptin level, TP level, and OSI were significantly higher in HD patients than controls (all P < 0.001) while TAC was lower (P < 0.001). In HD patients, serum leptin level was significantly correlated with TP level and OSI (r = 0.372, P <  0.001 and r = 0.409, P < 0.001, respectively). The correlation of serum leptin level with TP level and OSI remained statistically significant after adjusting for age, gender, and body‐fat percentage (r = 0.446, P < 0.001 and r = 0.463, P < 0.001, respectively). Hyperleptinemia seems to be associated with increased oxidative stress in HD patients, and this association may provide better understanding about the disorders related to either elevated serum leptin levels and/or increased oxidative stress in HD patients.
Contribution of NADH Increases to Ethanol’s Inhibition of Retinol Oxidation by Human ADH Isoforms
Authors: Chase Jennifer R. , Poolman Mark G. , Fell David A. 
Published: January 2009

Background:  A decrease in retinoic acid levels due to alcohol consumption has been proposed as a contributor to such conditions as fetal alcohol spectrum diseases and ethanol‐induced cancers. One molecular mechanism, competitive inhibition by ethanol of the catalytic activity of human alcohol dehydrogenase (EC 1.1.1.1) (ADH) on all‐trans‐retinol oxidation has been shown for the ADH7 isoform. Ethanol metabolism also causes an increase in the free reduced nicotinamide adenine dinucleotide (NADH) in cells, which might reasonably be expected to decrease the retinol oxidation rate by product inhibition of ADH isoforms.Methods:  To understand the relative importance of these two mechanisms by which ethanol decreases the retinol oxidation in vivo we need to assess them quantitatively. We have built a model system of 4 reactions: (1) ADH oxidation of ethanol and NAD+, (2) ADH oxidation of retinol and NAD+, (3) oxidation of ethanol by a generalized Ethanoloxidase that uses NAD+, (4) NADHoxidase which carries out NADH turnover.Results:  Using the metabolic modeling package ScrumPy, we have shown that the ethanol‐induced increase in NADH contributes from 0% to 90% of the inhibition by ethanol, depending on (ethanol) and ADH isoform. Furthermore, while the majority of flux control of retinaldehyde production is exerted by ADH, Ethanoloxidase and the NADHoxidase contribute as well.Conclusions:  Our results show that the ethanol‐induced increase in NADH makes a contribution of comparable importance to the ethanol competitive inhibition throughout the range of conditions likely to occur in vivo, and must be considered in the assessment of the in vivo mechanism of ethanol interference with fetal development and other diseases.
The Conners' 10‐item scale: findings in a total population of Swedish 10–11‐year‐old children
Authors: Westerlund Joakim , Ek Ulla , Holmberg Kirsten , Näswall Katharina , Fernell Elisabeth 
Published: January 2009

AbstractAim: To present normative data for the Swedish version of the Conners' 10‐item scale, to validate the scale by comparing children with and without attention deficit/hyperactivity disorder (ADHD), to explore the factor structure of this scale and to investigate behavioural characteristics and gender differences among 10‐ to 11‐year‐old children, as rated by parents and teachers respectively.Methods: Parents and teachers rated 509 10‐ to 11‐year‐old children (261 boys and 248 girls) from a population‐based cohort in a Swedish municipality.Results: The Conners' 10‐item scale discriminated very well between children with and without ADHD. Confirmatory factor analyses confirmed a two‐dimensional structure of the scale with items measuring restless/impulsive behaviour in one factor and items measuring emotional lability in another. An ANOVA revealed that parents and teachers reported different behavioural characteristics in boys as compared to girls.Conclusion: The Conners' 10‐item scale is a valid screening instrument for identification of ADHD. The two subscales can be used separately, in addition to the total score, to get a more detailed picture of the child's behaviour. Parents and teachers pay attention to different aspects of problem behaviour in boys and girls. The less disruptive behaviour of girls needs to be highlighted.
Development and Testing of the Context Assessment Index (CAI)
Authors: McCormack Brendan , McCarthy Geraldine , Wright Jayne , Coffey Alice 
Published: January 2009

ABSTRACT Aim: To test the psychometric properties of the Context Assessment Index (CAI). Background: We used the Promoting Action on Research Implementation in Health Services Framework (PARIHS) as the theoretical framework for the study. The framework shows the successful implementation of evidence in practice as dependent on the inter‐relationship of the nature of the evidence, the quality of the context, and expert facilitation. However, a comprehensive method of assessing context has not yet been available. Methods: A five‐stage instrument development and testing methodology was used. Principal components analysis, exploratory factor analysis, and expert panel feedback were used to develop and refine the CAI model. The model was further tested for psychometric properties of internal consistency and test–retest scores. Telephone interviews were conducted with expert nurses to gauge the usability of the instrument. These stages of development and testing resulted in a final 37‐item, five‐factor CAI model. Findings: This 37‐item model was accepted as a reasonable explanation of the data. The measures of homogeneity were calculated for each of the five factors to measure internal reliability. The Cronbach's alpha score for the complete questionnaire was estimated at 0.93. All five factors achieved a satisfactory estimated level of internal consistency in scoring, ranging from 0.78 to 0.91. Test–retest scores indicate reliability of the findings, and the feedback from focus group participants suggests that the instrument has practical utility. Conclusions: The CAI provides clinicians with the means to assess and understand the context in which they work and the effect this has on using evidence in practice.
Identification and Expression of Floral Organ Homeotic Genes from Alpinia oblongifolia (Zingiberaceae)
Authors: Xia Yong‐Mei , Gao Xue‐Mei , Li Qing‐Jun 
Published: January 2009

Abstract Current understanding of the classical ABC model of floral development has provided a new set of characters to evaluate floral evolution. However, what is still lacking is a clear assessment of this genetic program across monocots. Here, to investigate the evolution of members of class A and B genes in monocots, we report the sequence characteristic and transcript expression of three new MADS‐box genes in Alpinia oblongifolia Hayata. Sequence and phylogenetic analysis reveals that these genes are FUL‐like and AP3‐like. Therefore, they were termed AoFL1, AoFL2 and AoAP3. AoFL1 contains the FUL motif, but AoFL2 lacks this motif. Their expression revealed by in situ hybridization may reflect the ancestral function of FUL‐like genes in the specification of inflorescence and floral meristems. The AoAP3 gene contains two conserved motifs, the PI‐derived and paleoAP3 motifs. The AoAP3 transcripts located to the corolla and stamen, and hybridization signals were detected in the central whorl. These expression patterns suggest that the functions of homologous organ identity genes are diversified in A. oblongifolia. The implications of these findings on the conservation of homologous gene function are discussed.