Academic literature on the topic 'Scar healing'

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Journal articles on the topic "Scar healing"

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Bashyam, Hema. "Scar-free healing." Journal of Experimental Medicine 205, no. 1 (January 7, 2008): 2. http://dx.doi.org/10.1084/jem.2051iti4.

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Pugliese, Eugenia, João Q. Coentro, Michael Raghunath, and Dimitrios I. Zeugolis. "Wound healing and scar wars." Advanced Drug Delivery Reviews 129 (April 2018): 1–3. http://dx.doi.org/10.1016/j.addr.2018.05.010.

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Stoica, Alexandra Elena, Alexandru Mihai Grumezescu, Anca Oana Hermenean, Ecaterina Andronescu, and Bogdan Stefan Vasile. "Scar-Free Healing: Current Concepts and Future Perspectives." Nanomaterials 10, no. 11 (October 31, 2020): 2179. http://dx.doi.org/10.3390/nano10112179.

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Every year, millions of people develop scars due to skin injuries after trauma, surgery, or skin burns. From the beginning of wound healing development, scar hyperplasia, and prolonged healing time in wound healing have been severe problems. Based on the difference between adult and fetal wound healing processes, many promising therapies have been developed to decrease scar formation in skin wounds. Currently, there is no good or reliable therapy to cure or prevent scar formation. This work briefly reviews the engineering methods of scarless wound healing, focusing on regenerative biomaterials and different cytokines, growth factors, and extracellular components in regenerative wound healing to minimize skin damage cell types, and scar formation.
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Monavarian, Mehri, Safaa Kader, Seyedsina Moeinzadeh, and Esmaiel Jabbari. "Regenerative Scar-Free Skin Wound Healing." Tissue Engineering Part B: Reviews 25, no. 4 (August 2019): 294–311. http://dx.doi.org/10.1089/ten.teb.2018.0350.

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Ud-Din, Sara, Susan W. Volk, and Ardeshir Bayat. "Regenerative healing, scar-free healing and scar formation across the species: current concepts and future perspectives." Experimental Dermatology 23, no. 9 (July 21, 2014): 615–19. http://dx.doi.org/10.1111/exd.12457.

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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of scar structure, mechanics, and ventricular function after myocardial infarction in the rat." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (January 2010): H221—H228. http://dx.doi.org/10.1152/ajpheart.00495.2009.

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The mechanical properties of the healing scar are an important determinant of heart function following myocardial infarction. Yet the relationship between scar structure, scar mechanics, and ventricular function remains poorly understood, in part because no published study has tracked all of these factors simultaneously in any animal model. We therefore studied the temporal evolution of scar structure, scar mechanics, and left ventricular (LV) function in large anterior myocardial infarcts in rats. At 1, 2, 3, and 6 wk after left anterior descending coronary ligation, we examined LV function using sonomicrometry, infarct mechanical properties using biaxial mechanical testing, infarct structure using polarized light microscopy, and scar collagen content and cross-linking using biochemical assays. Healing infarcts in the rat were structurally and mechanically isotropic at all time points. Collagen content increased with time and was the primary determinant of scar mechanical properties. The presence of healing infarcts influenced systolic LV function through a rightward shift of the end-systolic pressure-volume relationship (ESPVR) that depended on infarct size, infarct collagen content, and LV dilation. We conclude that in sharp contrast to previous reports in large animal models, healing infarcts are structurally and mechanically isotropic in the standard rat model of myocardial infarction. On the basis of the regional strain patterns we observed in healing rat infarcts in this study and in healing pig infarcts in previous studies, we hypothesize that the local pattern of stretching determines collagen alignment in healing myocardial infarct scars.
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Gorti, Goutham Krishna, and R. James Koch. "Modulation of wound healing and scar formation." Current Opinion in Otolaryngology & Head and Neck Surgery 10, no. 4 (August 2002): 287–91. http://dx.doi.org/10.1097/00020840-200208000-00009.

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Rich, L. "Dermal Wound Closure Methods Alter Scar Healing." Academic Emergency Medicine 12, Supplement 1 (May 1, 2005): 74. http://dx.doi.org/10.1197/j.aem.2005.03.205.

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DiPietro, Luisa A. "Angiogenesis and scar formation in healing wounds." Current Opinion in Rheumatology 25, no. 1 (January 2013): 87–91. http://dx.doi.org/10.1097/bor.0b013e32835b13b6.

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Deliaert, A. E. K., E. Van den Kerckhove, S. Tuinder, S. M. J. S. Noordzij, T. S. Dormaar, and R. R. W. J. van der Hulst. "Smoking and its effect on scar healing." European Journal of Plastic Surgery 35, no. 6 (January 3, 2012): 421–24. http://dx.doi.org/10.1007/s00238-011-0661-3.

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Dissertations / Theses on the topic "Scar healing"

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Montgomery, Jade. "Building a Better Scar: Re-engineering Extracellular Matrix Structure in Dermal Scars." Diss., Virginia Tech, 2020. http://hdl.handle.net/10919/104233.

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Introduction Cutaneous scars represent a common surgical complication, yet no effective drug therapy for scar treatment currently exists despite huge patient and physician demand. A connexin 43 (Cx43) carboxyl terminus (CT) mimetic peptide, alpha Connexin Carboxy-Terminus 1 (αCT1), has demonstrated efficacy in improving long-term scar appearance in pre-clinical and clinical trials. However, current understanding of the mechanism-of-action by which αCT1 improves long-term scar appearance with early intervention treatment is not well understood. Methods In vivo: Scar biopsies from 1) human, 2) Sprague-Dawley rat, and 3) IAF Hairless guinea pig trials of αCT1 were examined for collagen matrix structure at 4 weeks (all models), and 2 and 6 weeks (rat and guinea pig models only). Collagen matrix variables examined included local disorganization of the fibers, a variable that is higher in unwounded skin compared to scar tissue, and density of the fibers, which is higher in scar tissue but can also be used as an early temporal marker of the rate of healing. In vitro: Primary murine dermal fibroblasts were isolated from the whole dermis of 3-4 week old transgenic mice expressing collagen 1(α2) GFP-tpz. Cells were sorted for expression via FACS and plated on prealigned collagen substrate for 7 days under conditions favorable to generating extracellular matrix. Results All in vivo scar biopsies demonstrated some level of altered collagen matrix structure with αCT1 treatment. Treated scars had higher local disorganization of the collagen fibers within the wound, and an increase in collagen matrix density compared to control at certain earlier timepoints that tended to decrease or disappear at later timepoints. The IAF Hairless guinea pig, a novel splinted wound healing model presented herein, was found to closely replicate the human dermal collagen profile and changes in collagen profile spurred by αCT1, significantly outperforming the traditional rat model. Primary dermal murine fibroblasts treated in vitro with αCT1 significantly increased synthesis of procollagen 1, the precursor of collagen 1 necessary for constructing the extracellular matrix, suggesting that at least part of the reason for higher collagen density at early in vivo timepoints is due to increased collagen synthesis by fibroblasts. Conclusion αCT1 treatment in the early stages of wound healing prompts individual fibroblasts to increase their output of collagen and create a more disorganized early collagen matrix. These early changes potentially spur the long-term scar appearance improvements seen in clinical trials, and provide a basis for future work to discover the cellular pathways to alter in order to improve wound healing and cutaneous scarring outcomes.
Doctor of Philosophy
Skin wounds frequently result in scars that can range from barely visible to enormous eyesores. Almost everyone will experience at least one skin wound in their lifetime leading to a scar that they wish were less visible, feeding the multi-billion dollar market for anti-scarring agents. However, many of the products on store shelves that claim to reduce scar appearance have not proven those claims. Most of the therapies that do have some degree of scientific evidence to support their claims are difficult to use properly, such as silicone sheeting, and often result in only minor improvements to scar appearance. Alpha Connexin Carboxy-Terminus 1 (αCT1), marketed in clinical trials as Granexin® gel, is a protein-based therapy that works on the cellular level to fundamentally alter the skin's initial reaction to wounding and improving long-term scar appearance. This dissertation explores the link between cellular processes altered by αCT1 and long-term clinical improvements in scar appearance by studying both the extracellular matrix present in the scar in human and animal models and the creation of that extracellular matrix by dermal fibroblasts. In both human and animal models, topical application of αCT1 had no effect on skin surface appearance at early timepoints of 2-6 weeks, correlating with previous research that found scar appearance only improved at 3+ months post-injury. However, deep within the newly constructed tissue of the scar, these studies show the collagen organizational structure of αCT1-treated scars is more similar to unwounded skin and slightly more dense at early timepoints, suggesting αCT1 marginally improved the speed of healing. These findings in humans and animals were also verified in part in cell culture experiments that found dermal fibroblasts increased collagen output in response to αCT1 treatment. A novel wound healing model in the hairless guinea pig, superior at replicating human skin than established models like the rat, is also presented and shown to have effects strongly similar to the human with αCT1 treatment. These results provide a fundamental insight into the mode-of-action by which αCT1 may improve long term scar appearance and identifies early collagen structure as a target for future therapeutics to modify, as well as a new animal model in which to test them.
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Cook, Julian. "Mathematical models for dermal wound healing : wound contraction and scar formation /." Thesis, Connect to this title online; UW restricted, 1995. http://hdl.handle.net/1773/6756.

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Hallen, Michael Ryan. "Commercialization of a Novel Wound Therapy and Scar Prevention Product." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1378942204.

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Dardenne, Adrienne. "High Mobility Group Box-1 (HMGB-1) Induces Scar Formation in Early Fetal Wounds." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1336692891.

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Vigor, Charlotte Jayne. "Switching off the fibro-proliferative phase of wound healing : an investigation of the normal mechanisms and pathological scar-related defects." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446439/.

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Using in vitro models that mimic various aspects/stages of wound healing, this thesis attempted to define the events that lead to the culmination of the fibro-proliferative phase of wound healing, i.e. apoptosis and any potential defects exhibited by keloid scars. Normal scar-derived fibroblasts were found to undergo apoptosis in contractile collagen gels, whereas keloid fibroblasts did not. Investigation of the mechanisms involved indicated that this form of apoptosis required both the three-dimensional and collagenous nature of the gel and was not simply caused by removal of tension, but required biochemical cues. Collagen-contraction-induced apoptosis was found to require matrix metalloproteinase (MMP) and autocrine transforming growth factor-P (TGF-p) activity. Indeed contraction was accompanied by significantly increased expression and activation of MMPs along with indications of increased matrix breakdown. Furthermore, pure products of matrix breakdown significantly induced apoptosis of normal scar cell monolayers. The defect exhibited by keloid fibroblasts was found to be specific to that induced during collagen contraction since they were equivalent to normal scar cells in their sensitivity to other forms of apoptosis induction and demonstrated normotrophic p53 stabilisation and activation of PARP (Poly(ADP-ribose)polymerase) and caspase-3. During collagen contraction, keloid fibroblasts failed to produce biochemical cues of apoptosis and although they exhibited normal levels of MMP gene expression and activation, they failed to breakdown collagen gels. However, these cells did undergo apoptosis in response to the biochemical cues produced on normal scar cell contraction of collagen gels, but surprisingly could not respond to pure forms of matrix breakdown products. Unlike normal scar cells, keloid fibroblasts failed to differentiate into myofibroblasts in collagen gels. The addition of exogenous TGF-pl was found to restore differentiation and furthermore allowed the cells to undergo apoptosis in collagen gels. Surprisingly, TGF-pl also restored the ability of keloid cells to undergo apoptosis in response to matrix breakdown products.
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Bertheim, Ulf. "Impaired reparative processes in particular related to hyaluronan in various cutaneous disorders : a structural analysis." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-276.

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Hiwatashi, Nao. "The efficacy of a novel collagen-gelatin scaffold with basic fibroblast growth factor for the treatment of vocal fold scar." Kyoto University, 2016. http://hdl.handle.net/2433/215428.

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Final publication is available at http://onlinelibrary.wiley.com/doi/10.1002/term.2060/abstract;jsessionid=F0849D98381EEF9E83401A02B9042F4D.f04t02
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第19602号
医博第4109号
新制||医||1014(附属図書館)
32638
京都大学大学院医学研究科医学専攻
(主査)教授 別所 和久, 教授 伊佐 正, 教授 川口 義弥
学位規則第4条第1項該当
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Konz, Maximilian. "Räumlich-zeitliche Dynamik der laserinduzierten Hsp70-Expression in einem humanen Hautexplantatmodell." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-213660.

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Die Narbenbildung des Hautorgans stellt für die gegenwärtige Medizin weiterhin eine schwierige Aufgabe dar. Die frühzeitige Beeinflussung des Wundheilungspro- zesses hin zu einer verminderten oder narbenlosen Heilung scheint von entschei- dender Bedeutung. Ein vielversprechender Ansatz ist die präoperative Laserthe- rapie und dadurch erzeugte Hitzeschockantwort. Auf molekulare Ebene kommt es u.a. zur Expression von Hitzeschockproteine. Die vorliegende in-vitro Studie beschäftigte sich mit der laserinduzierten Hochregulation des Hitzeschockproteins 70 in den epidermalen Schichten. Hierfür wurden drei nicht ablative Lasersysteme mit insgesamt 12 verschiedenen Parametereinstellungen verwendet (1.540-nm Er:Glass- , 755-nm Alexandrit-, 1.064-nm Nd:YAG-Laser). Mithilfe eines humanen Hautexplantatmodells sollte unter gleichbleibenden Bedingungen Zeitpunkt und Konzentration der maximal induzierten Hsp70-Expression sowie epidermale Schä- digungen dargestellt werden. In der verfügbaren Literatur waren hierzu nur begrenzt Daten vorhanden. Alle drei Lasersysteme zeigten signifikante Hsp70-Expressionen. Der Zeitpunkt der maximalen Hsp70-Expression konnte zwischen Tag 1 und 3 festgehalten werden. Dabei zeigten die Lasersysteme unterschiedliche Hsp70- Maxima und unterschiedliche Epidermisschädigungen. Die Ergebnisse ließen schlussfolgern, dass eine potenzielle präoperative Narbenprävention tendeziell ein Tag vor dem chirurgischen Eingriff und mit den stärkeren Parametereinstellungen des 1.064-nm Nd:YAG Lasers durchgeführt werden sollte.
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Cruz, Luiz Gustavo Balaguer. "Comparação entre o efeito do uso de diclofenaco de sódio e o laser de baixa potência (830nm) no processo de cicatrização em pele de ratos: aspectos biomecânicos e histológicos." Universidade Nove de Julho, 2014. http://bibliotecadigital.uninove.br/handle/tede/1314.

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Made available in DSpace on 2016-05-19T15:30:42Z (GMT). No. of bitstreams: 1 Luiz Gustavo Balaguer.pdf: 2319004 bytes, checksum: 8ae6797553f9db1485a7a79e6cfa0616 (MD5) Previous issue date: 2014-12-16
The skin is a coating tissue which undergoes permanent environmental action, often in aggressive forms, causing damage to this tissue. Generally, in the repair process structural changes occur which progress to the development of a scar. In this case the tissue may present morphological changes that interfere with its mechanical properties and this repair process produces a tissue with different properties than of the original tissue. Therefore, the use of therapies that favor this repair is important to seek a better scar quality. Low-level laser therapy appears as a resource used in the modulation of the inflammatory process helping the skin repair process. The objective of this study was evaluate the effect of low level laser (830nm) with 100 mW of potency us ing 1J or 3J of energy comparing to the effect of the topical sodium diclofenac on the repair process of the rat´s skin after induction of injury, analyzing the biomechanical behavior and histological changes of skin, 28 days after the harmful process. Male Wistar rats between 150g to 200g, 3 months old were used. The animals were anesthetized with association of xylazine hydrochloride and ketamine (90mg / kg and 10mg / kg, respectively, intraperitoneal injection). Once anesthetizd, 2 lesions were performed using a surgical scalpel at the dorsal area of the animal. The animals were divided into 5 groups of 7 animals: control (CTL), untreated scar (NT), scar + anti-inflammatory (DIC), scar + 1J laser (L1J) and scar + 3J laser (L3J). The pharmacological treatment and laser therapy were performed immediately after lesion induction and maintained daily irradiation until day 7. After 28 days, the animals were euthanized with an overdose of the same anesthetic and the tissue was immediately removed for histological analysis and traction trials. Results: Both the NT and group DIC showed a reduction of mechanical properties and alterations in histology analysis. L1J group showed significant improvement in mechanical properties and histological organization. We conclude that laser therapy improves certain mechanical properties of skin in this lesion model. However, more studies should be conducted to understand the proportion and organization of collagen fibers I and III biochemicaly. Either the study can be longer and evaluate the scars after the remodeling process.
A pele é um tecido de revestimento que sofre permanente ação do ambiente, muitas vezes de forma agressiva, levando a lesão deste tecido. Geralmente em seu processo de reparo ocorrem alterações estruturais que evoluem para o desenvolvimento de uma cicatriz. Neste caso o tecido pode apresentar alterações morfológicas que interferem em suas propriedades mecânicas e este processo de reparo produz um tecido com propriedades diferentes do tecido original. Dessa forma, a utilização de terapias que favoreçam esta reparação é importante para buscar uma qualidade melhor da cicatriz. A terapia com laser de baixa potência aparece como um recurso utilizado na modulação do processo inflamatório auxiliando no processo de reparo da pele. O Objetivo deste trabalho foi avaliar o efeito da terapia com laser de baixa potência de 830nm, com 100mW de potência nas energias de um 1J e 3J comparativamente ao efeito do diclofenaco de sódio tópico no processo de reparo da pele de ratos, após a indução de uma lesão controlada, observando aspectos histológicos e biomecânicos. Foram utilizados ratos wistar, entre 150g à 200g, com 3 meses de idade. Os animais foram anestesiados com associação de cloridrato de quetamina e xilazina (90mg/Kg e 10mg/Kg respectivamente, injeção intraperitoneal). Depois de anestesiados, foram realizadas 2 lesões cortantes utilizando um bisturi cirúrgico, no dorso do animal. Os animais foram divididos em 5 grupos de 5 animais: Controle (CTL), Cicatriz sem tratamento (NT), Cicatriz + Diclofenaco de sódio tópico (DIC), cicatriz + laser 1J (L1J) e cicatriz + laser 3J (L3J). O tratamento farmacológico e a terapia laser foram realizados imediatamente após a indução da lesão e mantida a irradiação diária até o sétimo dia. Após 28 dias, os animais foram eutanasiados com hiperdosagem do mesmo anestésico e o tecido foi imediatamente retirado para análises histológicas e de ensaios de tração. Resultados: Tanto o grupo NT quanto o grupo DIC apresentaram redução das propriedades mecânicas e alterações nas análises histológicas. O grupo tratado L1J e o grupo L3J apresentaram significativa melhora das propriedades mecânicas e na organização histológica. O grupo L1J apresentou resultados histológicos e biomecânicos próximos ao tecido saudável do grupo CTL. Conclusão: Concluímos que a utilização do diclofenaco de sódio tópico não conseguiu melhorar as características histológicas e biomecânicas da pele após a indução da lesão. A terapia com laser de baixa potência foi eficaz na melhora destas propriedades, sugerindo um melhor reparo tecidual. Porém, mais estudos devem ser realizados visando entender a proporção e organização das fibras de colágeno ou mesmo o estudo de tempos de reparo superiores ao utilizados neste estudo.
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Luna, Ana Luiza Alves Pinto. "Fita de silicone-gel versus fita adesiva microporosa na cicatrização de feridas operatórias ensaio clínico randomizado /." Botucatu, 2017. http://hdl.handle.net/11449/151711.

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Orientador: Aristides Augusto Palhares Neto
Resumo: Introdução: A cicatriz desempenha um importante papel no resultado final de uma cirurgia. Muitos fatores são implicados no processo de cicatrização patológica, e diversos produtos e curativos foram desenvolvidos para prevenção de cicatriz hipertrófica e quelóide, porém poucos tem evidências que o suportem. Objetivos: Comparar o resultado da cicatriz cirúrgica após utilização da fita de silicone e da fita microporosa. Métodos: Realizamos um ensaio clínico controlado, cego e randomizado, onde um lado da incisão foi randomizado para receber a fita de silicone e o outro lado recebeu o tratamento controle (fita adesiva microporosa). Foram selecionadas pacientes submetidas a abdominoplastia ou mastoplastia de aumento com implantes de silicone no período de maio a outubro de 2016. A Escala de Cicatrização de Vancouver foi utilizada para avaliar as cicatrizes. Resultados: Foram selecionadas para o estudo 17 pacientes. A idade média das pacientes foi de 31,4 ± 6,7, sendo a mínima de 20 e a máxima de 45 anos. Vemos na comparação dos tipos de curativo que os valores de p foram próximos a 5%, sugerindo uma associação do uso da fita de silicone com melhores resultados estéticos e funcionais da cicatriz em relação à fita microporosa. Notamos também que os dois tipos de curativo tiveram uma redução significativa em seus escores do primeiro para o terceiro mês (traduzindo uma melhora no aspecto da cicatriz), porém a fita de silicone teve uma redução superior à fita microporosa (45,6% e 39,2%... (Resumo completo, clicar acesso eletrônico abaixo)
Mestre
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Books on the topic "Scar healing"

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Chamberlain, Janet. The manipulation of scar formation in adult dermal wound healing. Manchester: University of Manchester, 1993.

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Okun, James D. Erasing scars: Herpes and healing. [United States: J.D. Okun], 1997.

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Healing the scars of emotional abuse. Grand Rapids, Mich: F.H. Revell, 1995.

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Jantz, Gregory L. Healing the scars of emotional abuse. Grand Rapids: Revell, 2009.

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Healing the scars: Derelict land in Wales. [Swansea]: University College of Swansea, 1988.

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Olson, Gail A. Scars and stripes: Healing the wounds of war. Bradenton, Fla: Human Services Institute, 1992.

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B, Silverstein Virginia, and Nunn Laura Silverstein, eds. Cuts, scrapes, scabs, and scars. New York: Franklin Watts, 1999.

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Is this a Daddy Sunday?: Healing the scars of divorce. Crowborough: Monarch, 1994.

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Osborn, Susan Titus. Wounded by words: Healing the invisible scars of emotional abuse. Birmingham, Ala: New Hope Publishers, 2008.

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Woodward, Mary Ann. Scars of the soul: Holistic healing in the Edgar Cayce readings. Columbus, Ohio: Brinadella Books, 1985.

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Book chapters on the topic "Scar healing"

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Panayi, Adriana C., Chanan Reitblat, and Dennis P. Orgill. "Wound Healing and Scarring." In Total Scar Management, 3–16. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9791-3_1.

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Ulrich, Magda M. W. "Fetal Wound Healing." In Textbook on Scar Management, 3–9. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_1.

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AbstractFirst- and second-trimester fetal skin wounds are known to heal without scarring.Research has excluded factors like the sterile uterine environment as the cause of scarless repair, and it is believed that scarless healing is an intrinsic property of early fetal skin. However, increasing wound size and induction of the inflammatory reaction can evoke a scar response in the fetus.For decades, research is performed to elucidate the mechanisms responsible for scarless healing in fetuses. Much research has been performed in animal studies, and several mechanisms have been proposed to be involved such as the microenvironment and the extracellular matrix, a reduced inflammatory response, differences in growth factor profile, and differences in fibroblast phenotype.It is clear that the wound healing process leading to scarless healing cannot be attributed to just one factor or mechanism but will be the result of a complex of interconnected processes.This chapter describes some of the possible mechanisms which may play a role in scarless healing.
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Téot, Luc, Claude Roques, Sami Otman, Antonio Brancati, and Rainer Mittermayr. "Managing Scars: Measurements to Improve Scar Management." In Measurements in Wound Healing, 291–312. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2987-5_15.

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Yenikomshian, Haig A., and Nicole S. Gibran. "Burn Wound Healing and Scarring Pathophysiology." In Total Scar Management, 17–23. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9791-3_2.

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Ogawa, Rei. "Mechanobiology of Cutaneous Scarring." In Textbook on Scar Management, 11–18. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_2.

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AbstractThe last phase of cutaneous wound healing produces the scar. Under normal circumstances, the immature scar then undergoes the scar maturation process over several months. This process involves tissue remodeling, which associates with a natural decrease in the inflammation and the numbers of blood vessels, collagen fibers, and fibroblasts. However, sometimes the scar maturation process is not properly engaged because inflammation continues in the scar. Consequently, the immature scar stage is prolonged. This results in the pathological scars called hypertrophic scars and keloids. Many factors that prolong the inflammatory stage have been identified. However, multiple lines of evidence acquired in recent years suggest that mechanical force can be an important cause of pathological scar development.
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Wood, Fiona M. "Scar Resurfacing." In Textbook on Scar Management, 311–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_36.

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AbstractScar resurfacing is focused on the improvement in the quality of a scar by disruption of the skin surface and reducing the bulk of the scar by control of the secondary healing process. The prerequisite is knowledge of the wound healing and scarring process such that the intervention can be designed to reduce the risk of increasing the scarring.The clinical examination and assessment of the scar will guide the selection of the technique addressing the specific aspects of the scar, such as the pigment restoration and volume reduction, with the aim of blending the scar with the surrounding uninjured skin.Understanding the natural history of the scar, the impact it has on the patient, and the techniques available for improvement provides the clinical decision-making matrix to drive an improved scar outcome. Resurfacing is one opportunity for scar modulation which needs to be taken into context relative to the range of conservative and surgical therapeutic opportunities explored within the chapters of the book.
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Moortgat, Peter, Mieke Anthonissen, Ulrike Van Daele, Jill Meirte, Tine Vanhullebusch, and Koen Maertens. "Shock Wave Therapy for Wound Healing and Scar Treatment." In Textbook on Scar Management, 485–90. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_55.

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AbstractShock Wave Therapy (SWT) meets all the requirements for the ideal non-invasive scar treatment. It is safe, well tolerated by patients, cost-effective, easy to apply, has low complication rates, and can be used in an outpatient setting. The overall effect of SWT is an improvement of tissue homeostasis, accompanied by an improvement of the tissue self-healing abilities, and it seems to focus on inducing tissue regeneration and matrix remodeling in vivo by means of mechanotransduction.SWT has a beneficial effect on wound healing and is characterized by an upregulation of the angio-active factors as nitric oxide (NO) and vascular endothelial growth factor (VEGF) leading to induced angiogenesis. A downregulation of alpha-SMA expression, myofibroblast phenotype, TGF-β1 expression, fibronectin, and collagen type I are measured after SWT on scars, leading to improvement of several relevant scar parameters like height, pliability, vascularity, and pigmentation, and thus ameliorating function.For a full treatment outline, the energy flux density (EFD), the number of pulses, the pulse frequency, and the number and interval of treatments are the most relevant parameters. The EFD for soft tissue indications is typically in the range of 0.08–0.25 mJ/mm2, while scars and fibrosis are treated with an EFD ranging between 0.15 and 0.33 mJ/mm2. These settings seem to be ideal to induce the optimal cell responses for each indication.All the presented findings are fundamental knowledge for further investigation of SWT to reduce the fibrous component in regenerating and remodeling tissues. However, the full potential of SWT in wound healing and scar treatment needs further unraveling.
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Le Touze, Anne. "Scars in Pediatric Patients." In Textbook on Scar Management, 397–404. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_46.

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AbstractPhysiological healing process is not much different in children, but the resulting scar is very rich in collagen and very dense. Therefore, when dealing with children, it is necessary to be aware of these particularities and to “guide” the scaring process to avoid disgracious and disabling scars.
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Myers, Simon R., and Ali M. Ghanem. "Wound healing and scar formation." In Plastic and reconstructive surgery, 1–11. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118655412.ch1.

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Poetschke, Julian, and Gerd G. Gauglitz. "Onion Extract." In Textbook on Scar Management, 209–13. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_24.

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AbstractMultiple studies on hypertrophic scar and keloid formation have led to a plethora of therapeutic strategies in order to prevent or attenuate keloid and hypertrophic scar formation. To date, preventing pathologic scarring remains undoubtedly more effective than treating it. Next to specific surgical techniques and an appropriate general aftercare of fresh wounds, a multitude of scar gels, creams, patches, and ointments are available and are being promoted for scarless wound healing. Next to silicone-based products, onion extract or cepalin has been highlighted as one potential anti-scarring agent over recent years. Based on several studies, onion extract alone or in combination with allantoin and heparin seems to alleviate the wound-healing process and appears beneficial for preventional application in fresh scars. The study data available, however, remains overall relatively poor and clearly objective data regarding this approach is widely missing.
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Conference papers on the topic "Scar healing"

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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Collagen Fiber Structure Correlates With Mechanical Environment in Healing Myocardial Infarcts." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206767.

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Mechanics of healing myocardial infarcts are an important determinant of ventricular function. Large collagen fibers are the major contributors to the mechanical properties of healing scar. It has been suggested that an anisotropic structure, as observed in healing pig scars, may help preserve ventricular function, and that the alignment of collagen fibers could be guided by the regional mechanical environment in the infarct — in pig scars the alignment of collagen fibers was in the direction of greatest stretch [1]. By contrast, in the standard rat model of infarction we found that scars are structurally and mechanically isotropic at all time points in healing [2].
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Gossé, Alban, Gwen Iarmarcovai, Alexandre Capon, Alain Cornil, and Serge Mordon. "Scar prevention by laser-assisted scar healing (LASH) using thermal post-conditioning." In SPIE BiOS: Biomedical Optics, edited by Steven L. Jacques, E. Duco Jansen, and William P. Roach. SPIE, 2009. http://dx.doi.org/10.1117/12.807807.

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Gundiah, Namrata, Debby Chang, Peng Zhang, Mark Ratcliffe, and Lisa Pruitt. "Structural and Mechanical Characteristics of Healing Myocardial Scar Tissue." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59998.

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An anteroapical transmural myocardial infarction was created in Dorset sheep and resulting scar tissues were excised two (Group A, n=5, 10.6 ± 1.2 weeks) and eight months (Group B, n=6, 36.8 ± 1.4 weeks) post infarction [1]. Samples were oriented in longitudinal and circumferential directions in a biaxial stretcher, preconditioned and tested in displacement control at room temperature in BDM solution. Stress-strain plots were obtained for samples. Histology was performed by cryo-sectioning specimens into 8 μm slices and staining using Hematoxylin & Eosin. Stress-strain analyses show that circumsferential direction was stiffer than longitudinal for Group A. Group B samples show a reverse trend and are stiffer than Group A. Stained sections show more collagen in the endocardial surface for Group B samples while Group A samples have added collagen in the epicardial side. A high density of fat cells was seen in Group B samples that may affect stiffness trends.
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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of Scar Mechanical Properties During Myocardial Infarct Healing in Rat." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176422.

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The mechanics of healing myocardial infarcts are an important determinant of post-infarction left ventricular (LV) function and remodeling. Large animal infarct models are well studied; healing infarct scars have been shown to be mechanically and structurally anisotropic [1], and this anisotropy may help preserve LV function during some stages of healing [2]. At the same time, it has been suggested that the rat model of myocardial infarction is more similar to humans in the range of infarct sizes and observed LV dysfunction [3]. However, in the rat model, infarct mechanics and their effect on the overall LV function have not been described so far.
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Шадрин, Валериан Сергеевич, Петр Михайлович Кожин, Олеся Олеговна Шошина, and Александр Леонидович Русанов. "IN VITRO MODEL OF A HYPERTROPHIC SCAR." In Наука. Исследования. Практика: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Июнь 2020). Crossref, 2020. http://dx.doi.org/10.37539/srp291.2020.39.77.014.

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Изучение нарушения ранозаживления, приводящего к развитию гиперпластических процессов, является актуальной задачей мирового здравоохранения. Для более детального изучения данной проблематики предложена новая in vitro модель, которая является более удобной для применения и при этом отражает признаки, характерные для гипертрофического рубцевания. The study of wound healing disorders leading to the development of hyperplastic processes is an actual problem of world health. A new in vitro model is proposed for a more detailed study of this problem. This model is more convenient for use and at the same time reflects the signs characteristic of hypertrophic scarring.
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Gurkan, Umut Atakan, Alexandra Dubikovsky, Lynetta J. Freeman, Paul W. Snyder, Russell D. Meldrum, and Ozan Akkus. "In Vivo Actuation System for Mechanostimulation of Large Wound Healing." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53183.

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The incidence of large open wounds in the US is estimated to be about 5–7 million per year which results in a cost of greater than $20 billion for wound management [1]. Large open wounds occur due to burns, trauma, and secondary to surgical interventions, ulcers or pressure sores. The current clinical practice is to treat large open wounds by delayed primary closure where skin is stretched under constant tension to approximate wound edges by relying on the extensibility of the neighboring skin, by skin grafting or by managing the wound to heal by second intention. Delayed primary closure is inapplicable when the strength of the skin is compromised (e.g. age, diabetes). Furthermore, delayed primary closure usually leads to excessive wound tension which introduces hypertrophic scars [2] and ischemia [3] to the skin and the underlying muscles. Skin autografts may result in morbidity of the donor site. Therefore, there is the need for noninvasive methods which will enable large wound closure in a reasonable time frame with minimal scar formation while alleviating or reducing the need for skin graft harvest.
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Riemann, Iris, Alexander Ehlers, Ronan LeHarzic, Sven Martin, Annette Reif, and Karsten König. "In vivo multiphoton tomography of skin during wound healing and scar formation." In Biomedical Optics (BiOS) 2007, edited by Ammasi Periasamy and Peter T. C. So. SPIE, 2007. http://dx.doi.org/10.1117/12.702407.

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Thomopoulos, S., R. Das, H. M. Kim, D. Zeltser, K. Kousari, and L. Galatz. "The Role of the Loading Environment on the Developing Tendon-to-Bone Insertion." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206837.

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A transition zone forms at the attachment of tendon to bone during post-natal development [1]. We previously showed that this transitional tissue reduces stress concentrations at the insertion and hence reduces the risk for failure [2]. During tendon-to-bone healing, on the other hand, a transition zone does not develop at the interface [3]. Unlike development, inferior scar tissue fills the repair site and the repair is prone to rupture at the attachment. Understanding the development of the insertion will allow us to develop solutions to augment tendon-to-bone healing.
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Hanifi-Moghaddam, Pejman, and Amrollah Mostafazadeh. "Substances Secreted by Starved Human Dermal Fibroblasts Enhancing the Wound Healing Process in Rat without Scar: A Potential Acellular System for Wound Healing." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2772.

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Elkhalil, H., J. C. Bischof, and V. H. Barocas. "Cryoinjury of a Contractile Tissue-Equivalent: In Vitro Experiments." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192819.

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Cryosurgery, the minimally-invasive destruction of undesirable tissues by freezing, is an attractive technique for treating diseases where tight control over lesion size and minimal scar tissues are crucial, such as cancer and dermatologic disorders (1, 2). Unlike hyperthermic (high temperature) treatments, cryosurgery maintains the integrity of the extracellular matrix (ECM) while destroying the cells of the tissue. The undamaged ECM results in a unique wound healing process, which, compared to most injuries, leads to a better tissue recovery. Thus, cryosurgery has been of great interest in many clinical fields and has been studied extensively. However, numerous questions remain.
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