Статті в журналах: "Wound healing Physiology"

1

Strodtbeck, Frances. "Physiology of wound healing." Newborn and Infant Nursing Reviews 1, no. 1 (March 2001): 43–52. http://dx.doi.org/10.1053/nbin.2001.23176.

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2

Rhee, John S., David Hom, and Timothy Lian. "Wound Healing and Flap Physiology." Otolaryngology–Head and Neck Surgery 143, no. 5 (November 2010): 718. http://dx.doi.org/10.1016/s0194-5998(10)02297-7.

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3

Silver, I. A. "The physiology of wound healing." Journal of Wound Care 3, no. 2 (March 2, 1994): 106–9. http://dx.doi.org/10.12968/jowc.1994.3.2.106.

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4

Flanagan, M. "The physiology of wound healing." Journal of Wound Care 9, no. 6 (June 2000): 299–300. http://dx.doi.org/10.12968/jowc.2000.9.6.25994.

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5

Rhee, John S., David Hom, and Timothy Lian. "Wound Healing and Flap Physiology." Otolaryngology - Head and Neck Surgery 143, no. 5 (November 2010): 718. http://dx.doi.org/10.1016/j.otohns.2010.09.045.

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6

Young, Alistair, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 29, no. 10 (October 2011): 475–79. http://dx.doi.org/10.1016/j.mpsur.2011.06.011.

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7

Harper, Daniel, Alistair Young, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 32, no. 9 (September 2014): 445–50. http://dx.doi.org/10.1016/j.mpsur.2014.06.010.

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8

Singh, Shailendra, Alistair Young, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 35, no. 9 (September 2017): 473–77. http://dx.doi.org/10.1016/j.mpsur.2017.06.004.

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9

Hunt, Thomas K. "The physiology of wound healing." Annals of Emergency Medicine 17, no. 12 (December 1988): 1265–73. http://dx.doi.org/10.1016/s0196-0644(88)80351-2.

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10

Norris, Susan O’Brien, Barbara Provo, and Nancy A. Stotts. "Physiology of Wound Healing and Risk Factors that Impede the Healing Process." AACN Advanced Critical Care 1, no. 3 (November 1, 1990): 545–52. http://dx.doi.org/10.4037/15597768-1990-3010.

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In the critically ill patient, wound repair can be impeded by processes inherent to the illness, its treatment, and the critical care environment. This vulnerability to wound complications increases patient morbidity and mortality as well as length of stay, resource consumption, and hospital cost. The physiology of wound healing and factors that impede wound repair are discussed. Those factors commonly seen in critical illness include advanced age, diabetes mellitus, compromised immunocompetence, inadequate perfusion, and oxygenation, infection, malnutrition, obesity, and preoperative illness. Knowledge of management of the physiologic factors that affect wound healing enables the nurse to maximize tissue repair and prevent wound complications

11

Clancy, John, Andrew McVicar, and Damian Muncaster. "The Physiology of Wound Healing and Wound Assessment." British Journal of Perioperative Nursing (United Kingdom) 11, no. 8 (August 2001): 362–70. http://dx.doi.org/10.1177/175045890101100805.

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12

Phillips, Steven J. "Physiology of Wound Healing and Surgical Wound Care." ASAIO Journal 46, no. 6 (November 2000): S2—S5. http://dx.doi.org/10.1097/00002480-200011000-00029.

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13

Lloyd-Jones, Menna. "Tissue viability: the physiology of wound healing." British Journal of Healthcare Assistants 1, no. 4 (July 2007): 181–84. http://dx.doi.org/10.12968/bjha.2007.1.4.24265.

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14

Gantwerker, Eric A., and David B. Hom. "Skin: Histology and Physiology of Wound Healing." Facial Plastic Surgery Clinics of North America 19, no. 3 (August 2011): 441–53. http://dx.doi.org/10.1016/j.fsc.2011.06.009.

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15

Honrado, Carlo P., and Craig S. Murakami. "Wound Healing and Physiology of Skin Flaps." Facial Plastic Surgery Clinics of North America 13, no. 2 (May 2005): 203–14. http://dx.doi.org/10.1016/j.fsc.2004.11.007.

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16

Gantwerker, Eric A., and David B. Hom. "Skin: Histology and Physiology of Wound Healing." Clinics in Plastic Surgery 39, no. 1 (January 2012): 85–97. http://dx.doi.org/10.1016/j.cps.2011.09.005.

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17

Childress, Beverly B., and Joyce K. Stechmiller. "Role of Nitric Oxide in Wound Healing." Biological Research For Nursing 4, no. 1 (July 2002): 5–15. http://dx.doi.org/10.1177/1099800402004001002.

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Chronic wounds mainly affect elderly individuals and persons with comorbid diseases due to a compromised immune status. An age-related decline in immune function deters proper healing of wounds in an orderly and timely manner. Thus, older adults with 1 or more concomitant illnesses are more likely to experience and suffer from a nonhealing wound, which may drastically decrease their quality of life and financial resources. Novel therapies in wound care management rely heavily on our current knowledge of wound healing physiology. It is well established that normal wound healing occurs sequentially and is strictly regulated by pro-inflammatory cytokines and growth factors. A multitude of commercial products such as growth factors are available; however, their effectiveness in healing chronic wounds has yet to be proven. Recently, investigators have implicated nitric oxide (NO) in the exertion of regulatory forces on various cellular activities of the inflammatory and proliferative phases of wound healing. Gene therapy in animal studies has shown promising results and is furthering our understanding of impaired wound healing. The purpose of this article is to review the literature on NO and its role in wound healing. A discussion of the physiology of normal healing and the pathophysiology of chronic wounds is provided.

18

Giglio, James A., A. Omar Abubaker, and Robert F. Diegelmann. "PHYSIOLOGY OF WOUND HEALING OF SKIN AND MUCOSA." Oral and Maxillofacial Surgery Clinics of North America 8, no. 4 (November 1996): 457–65. http://dx.doi.org/10.1016/s1042-3699(20)30918-3.

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19

Witte, Maria B., and Adrian Barbul. "Arginine physiology and its implication for wound healing." Wound Repair and Regeneration 11, no. 6 (November 2003): 419–23. http://dx.doi.org/10.1046/j.1524-475x.2003.11605.x.

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20

DYSON, MARY. "Advances in wound healing physiology: the comparative perspective." Veterinary Dermatology 8, no. 4 (December 1997): 227–33. http://dx.doi.org/10.1111/j.1365-3164.1997.tb00268.x.

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21

Teller, Paige, and Therese K. White. "The Physiology of Wound Healing: Injury Through Maturation." Surgical Clinics of North America 89, no. 3 (June 2009): 599–610. http://dx.doi.org/10.1016/j.suc.2009.03.006.

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22

Teller, Paige, and Therese K. White. "The Physiology of Wound Healing: Injury Through Maturation." Perioperative Nursing Clinics 6, no. 2 (June 2011): 159–70. http://dx.doi.org/10.1016/j.cpen.2011.04.001.

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23

Rodrigues, Melanie, Nina Kosaric, Clark A. Bonham, and Geoffrey C. Gurtner. "Wound Healing: A Cellular Perspective." Physiological Reviews 99, no. 1 (January 1, 2019): 665–706. http://dx.doi.org/10.1152/physrev.00067.2017.

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Wound healing is one of the most complex processes in the human body. It involves the spatial and temporal synchronization of a variety of cell types with distinct roles in the phases of hemostasis, inflammation, growth, re-epithelialization, and remodeling. With the evolution of single cell technologies, it has been possible to uncover phenotypic and functional heterogeneity within several of these cell types. There have also been discoveries of rare, stem cell subsets within the skin, which are unipotent in the uninjured state, but become multipotent following skin injury. Unraveling the roles of each of these cell types and their interactions with each other is important in understanding the mechanisms of normal wound closure. Changes in the microenvironment including alterations in mechanical forces, oxygen levels, chemokines, extracellular matrix and growth factor synthesis directly impact cellular recruitment and activation, leading to impaired states of wound healing. Single cell technologies can be used to decipher these cellular alterations in diseased states such as in chronic wounds and hypertrophic scarring so that effective therapeutic solutions for healing wounds can be developed.

24

Thiruvoth, FrijiMeethale, DeviPrasad Mohapatra, DineshKumar Sivakumar, RaviKumar Chittoria, and Vijayaraghavan Nandhagopal. "Current concepts in the physiology of adult wound healing." Plastic and Aesthetic Research 2, no. 5 (2015): 250. http://dx.doi.org/10.4103/2347-9264.158851.

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25

Ascenção, A. M. S., H. V. D. Boer, T. B. Paiva, and L. M. Vianna. "P.89 Physiology of vitamin D3 on wound healing." Clinical Nutrition 17 (August 1998): 53. http://dx.doi.org/10.1016/s0261-5614(98)80245-8.

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26

Russell, Linda. "Understanding physiology of wound healing and how dressings help." British Journal of Nursing 9, no. 1 (January 13, 2000): 10–21. http://dx.doi.org/10.12968/bjon.2000.9.1.6406.

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27

Hu, Michael S., Mimi R. Borrelli, H. Peter Lorenz, Michael T. Longaker, and Derrick C. Wan. "Mesenchymal Stromal Cells and Cutaneous Wound Healing: A Comprehensive Review of the Background, Role, and Therapeutic Potential." Stem Cells International 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/6901983.

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Cutaneous wound repair is a highly coordinated cascade of cellular responses to injury which restores the epidermal integrity and its barrier functions. Even under optimal healing conditions, normal wound repair of adult human skin is imperfect and delayed healing and scarring are frequent occurrences. Dysregulated wound healing is a major concern for global healthcare, and, given the rise in diabetic and aging populations, this medicoeconomic disease burden will continue to rise. Therapies to reliably improve nonhealing wounds and reduce scarring are currently unavailable. Mesenchymal stromal cells (MSCs) have emerged as a powerful technique to improve skin wound healing. Their differentiation potential, ease of harvest, low immunogenicity, and integral role in native wound healing physiology make MSCs an attractive therapeutic remedy. MSCs promote cell migration, angiogenesis, epithelialization, and granulation tissue formation, which result in accelerated wound closure. MSCs encourage a regenerative, rather than fibrotic, wound healing microenvironment. Recent translational research efforts using modern bioengineering approaches have made progress in creating novel techniques for stromal cell delivery into healing wounds. This paper discusses experimental applications of various stromal cells to promote wound healing and discusses the novel methods used to increase MSC delivery and efficacy.

28

Auger, F. A., D. Lacroix, and L. Germain. "Skin Substitutes and Wound Healing." Skin Pharmacology and Physiology 22, no. 2 (2009): 94–102. http://dx.doi.org/10.1159/000178868.

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29

McElvain, Kelly, Joshua Klister, Alessandra Ebben, Sandeep Gopalakrishnan, and Mahsa Dabagh. "Impact of Wound Dressing on Mechanotransduction within Tissues of Chronic Wounds." Biomedicines 10, no. 12 (November 30, 2022): 3080. http://dx.doi.org/10.3390/biomedicines10123080.

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Chronic wounds are significant public health problems impacting the health-related quality of individuals’ lives (due to disability, decreased productivity, and loss of independence) and an immense economic burden to healthcare systems around the world. In this study, our main objective is to investigate how mechanotransduction can impact the healing process in chronic wounds. We have developed new three-dimensional models of wound tissue to study the distribution of forces within these tissues exerted by wound dressings with different characteristics. The roles of mechanical forces on wound healing have gained significant clinical attention; the application of mechanical forces is expected to influence the physiology of tissue surrounding a wound. We aim to investigate whether the force transmission within wound tissue is impacted by the dressing characteristics and whether this impact may differ with wound tissue’s properties. Our results show that wound dressings with lower stiffnesses promote force transmission within a wound tissue. This impact is even more significant on stiffer wound tissues. Furthermore, we show that size of wound dressing alters forces that transmit within the wound tissue where dressings with 9 cm length show higher stresses. The wound tissue stiffening has been associated with healing of a wound. Our results demonstrate that wounds with stiffer tissue experience higher stresses. Taken all together, our findings suggest that low stiffness of wound dressing and its size may be introduced as a criterion to explain parameters predisposing a chronic wound to heal. This study’s findings on the role of dressings and tissue characteristics demonstrate that precision dressings are required for wound management and understanding how a dressing impacts mechanotransduction in wound tissue will lead to design of novel dressings promoting healing in chronic wounds.

30

Branski, Ryan C. "Perioperative Voice Recovery: A Wound-Healing Perspective." Perspectives on Voice and Voice Disorders 23, no. 2 (July 2013): 42–46. http://dx.doi.org/10.1044/vvd23.2.42.

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To describe the wound healing process through an oversimplified graphic, a classic cartoon in a Dermatology Clinics textbook shows a Volkswagen Beetle, with the license plate TRAUMA that has driven through a wooden fence, leaving both a substantive hole in the fence and piles of broken wooden planks. The obvious priority would be to rebuild the fence so that it is identical to its pretrauma state. This analogy and accompanying graphic provide a framework for a unique perspective on wound healing. For the sake of simplicity, let us assume that the vocal fold is a fence, and instead of a Volkswagen Beetle, the trauma is surgical excision of a vocal fold lesion. Immediately following surgery, the human body initiates the process of rebuilding vocal fold tissue. From a physiological perspective, it would be ideal to regain the original architecture of the vocal fold to ensure minimal alteration to phonatory physiology. Unfortunately, beyond the 2nd trimester of gestation, wounds heal with subsequent scarring. In the vocal folds, this scarring can have significant deleterious effects on vocal fold pliability and lead to dysphonia. However, investigators have shown that wounds heal regeneratively (i.e., no scarring) in the fetal environment. This observation provides potential targets for therapies to direct wound healing toward a more favorable outcome. In this article, I provide a brief overview of the biochemical processes associated with wound healing. Subsequently, I outline the underlying rationale for tissue mobilization in the context of acute vocal fold injury.

31

Scott, Christopher, James Bonner, Danqing Min, Philip Boughton, Rebecca Stokes, Kuan Minn Cha, Stacey N. Walters, et al. "Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing." American Journal of Physiology-Cell Physiology 307, no. 4 (August 15, 2014): C349—C357. http://dx.doi.org/10.1152/ajpcell.00306.2013.

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Aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor that binds to partners to mediate responses to environmental signals. To investigate its role in the innate immune system, floxed ARNT mice were bred with lysozyme M-Cre recombinase animals to generate lysozyme M-ARNT (LAR) mice with reduced ARNT expression. Myeloid cells of LAR mice had altered mRNA expression and delayed wound healing. Interestingly, when the animals were rendered diabetic, the difference in wound healing between the LAR mice and their littermate controls was no longer present, suggesting that decreased myeloid cell ARNT function may be an important factor in impaired wound healing in diabetes. Deferoxamine (DFO) improves wound healing by increasing hypoxia-inducible factors, which require ARNT for function. DFO was not effective in wounds of LAR mice, again suggesting that myeloid cells are important for normal wound healing and for the full benefit of DFO. These findings suggest that myeloid ARNT is important for immune function and wound healing. Increasing ARNT and, more specifically, myeloid ARNT may be a therapeutic strategy to improve wound healing.

32

Grasso, Silvina, Julio A. Hernández, and Silvia Chifflet. "Roles of wound geometry, wound size, and extracellular matrix in the healing response of bovine corneal endothelial cells in culture." American Journal of Physiology-Cell Physiology 293, no. 4 (October 2007): C1327—C1337. http://dx.doi.org/10.1152/ajpcell.00001.2007.

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It has classically been accepted that the healing of narrow wounds in epithelia occurs by the formation of a contractile actin cable, while wide wounds are resurfaced by lamellipodia-dependent migration of border cells into the denuded area. To further investigate the general validity of this idea, we performed systematic experiments of the roles of wound geometry, wound size, and extracellular matrix (ECM) in wound healing in monolayers of bovine corneal endothelial cells, a system shown here to predominantly display any of the two healing mechanisms according to the experimental conditions. We found that, in this system, it is the absence or presence of the ECM on the wound surface that determines the specific healing mode. Our observations demonstrate that, independent of their size and geometry, wounds created maintaining the ECM heal by migration of cells into the wound area, while ECM removal from the wound surface determines the predominant formation of an actin cable. While the latter mechanism is slower, the actin cable permits the maintainance of the epithelial phenotype to a larger extent during the healing process, as also confirmed by our finding of a more conserved localization of cadherin and vinculin. We also introduce a model that simulates experimental findings about the dynamics of healing mechanisms, both for the maintenance or removal of the ECM on the wound surface. The findings of this study may contribute to the understanding of physiological and pathological aspects of epithelial wound healing and to the design of therapeutic strategies.

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Potekaev, Nikolai N., Olga B. Borzykh, German V. Medvedev, Denis V. Pushkin, Marina M. Petrova, Artem V. Petrov, Diana V. Dmitrenko, Elena I. Karpova, Olga M. Demina, and Natalia A. Shnayder. "The Role of Extracellular Matrix in Skin Wound Healing." Journal of Clinical Medicine 10, no. 24 (December 18, 2021): 5947. http://dx.doi.org/10.3390/jcm10245947.

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Impaired wound healing is one of the unsolved problems of modern medicine, affecting patients’ quality of life and causing serious economic losses. Impaired wound healing can manifest itself in the form of chronic skin wounds or hypertrophic scars. Research on the biology and physiology of skin wound healing disorders is actively continuing, but, unfortunately, a single understanding has not been developed. The attention of clinicians to the biological and physiological aspects of wound healing in the skin is necessary for the search for new and effective methods of prevention and treatment of its consequences. In addition, it is important to update knowledge about genetic and non-genetic factors predisposing to impaired wound healing in order to identify risk levels and develop personalized strategies for managing such patients. Wound healing is a very complex process involving several overlapping stages and involving many factors. This thematic review focuses on the extracellular matrix of the skin, in particular its role in wound healing. The authors analyzed the results of fundamental research in recent years, finding promising potential for their transition into real clinical practice.

34

Rybinski, Brad, Janusz Franco-Barraza, and Edna Cukierman. "The wound healing, chronic fibrosis, and cancer progression triad." Physiological Genomics 46, no. 7 (April 1, 2014): 223–44. http://dx.doi.org/10.1152/physiolgenomics.00158.2013.

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For decades tumors have been recognized as “wounds that do not heal.” Besides the commonalities that tumors and wounded tissues share, the process of wound healing also portrays similar characteristics with chronic fibrosis. In this review, we suggest a tight interrelationship, which is governed as a concurrence of cellular and microenvironmental reactivity among wound healing, chronic fibrosis, and cancer development/progression (i.e., the WHFC triad). It is clear that the same cell types, as well as soluble and matrix elements that drive wound healing (including regeneration) via distinct signaling pathways, also fuel chronic fibrosis and tumor progression. Hence, here we review the relationship between fibrosis and cancer through the lens of wound healing.

35

Quirós, Miguel, and Asma Nusrat. "Contribution of Wound-Associated Cells and Mediators in Orchestrating Gastrointestinal Mucosal Wound Repair." Annual Review of Physiology 81, no. 1 (February 10, 2019): 189–209. http://dx.doi.org/10.1146/annurev-physiol-020518-114504.

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The gastrointestinal mucosa, structurally formed by the epithelium and lamina propria, serves as a selective barrier that separates luminal contents from the underlying tissues. Gastrointestinal mucosal wound repair is orchestrated by a series of spatial and temporal events that involve the epithelium, recruited immune cells, resident stromal cells, and the microbiota present in the wound bed. Upon injury, repair of the gastrointestinal barrier is mediated by collective migration, proliferation, and subsequent differentiation of epithelial cells. Epithelial repair is intimately regulated by a number of wound-associated cells that include immune cells and stromal cells in addition to mediators released by luminal microbiota. The highly regulated interaction of these cell types is perturbed in chronic inflammatory diseases that are associated with impaired wound healing. An improved understanding of prorepair mechanisms in the gastrointestinal mucosa will aid in the development of novel therapeutics that promote mucosal healing and reestablish the critical epithelial barrier function.

36

Becirovic-Agic, Mediha, Upendra Chalise, Mira Jung, Jocelyn R. Rodriguez-Paar, Shelby R. Konfrst, Elizabeth R. Flynn, Jeffrey D. Salomon, Michael E. Hall, and Merry L. Lindsey. "Faster skin wound healing predicts survival after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 322, no. 4 (April 1, 2022): H537—H548. http://dx.doi.org/10.1152/ajpheart.00612.2021.

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Faster skin wound healers had more efficient cardiac healing after myocardial infarction (MI). Two plasma proteins at D3 MI, EAF1 and A2M, predicted MI death in 66% of cases. ApoD regulated both skin and cardiac wound healing in male mice by promoting inflammation. The skin was a mirror to the heart and common pathways linked wound healing across organs.

37

Roy, Sashwati, Savita Khanna, Cameron Rink, Sabyasachi Biswas, and Chandan K. Sen. "Characterization of the acute temporal changes in excisional murine cutaneous wound inflammation by screening of the wound-edge transcriptome." Physiological Genomics 34, no. 2 (July 2008): 162–84. http://dx.doi.org/10.1152/physiolgenomics.00045.2008.

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This work represents a maiden effort to systematically screen the transcriptome of the healing wound-edge tissue temporally using high-density GeneChips. Changes during the acute inflammatory phase of murine excisional wounds were characterized histologically. Sets of genes that significantly changed in expression during healing could be segregated into the following five sets: up-early (6–24 h; cytokine-cytokine receptor interaction pathway), up-intermediary (12–96 h; leukocyte-endothelial interaction pathway), up-late (48–96 h; cell-cycle pathway), down-early (6–12 h; purine metabolism) and down-intermediary (12–96 h; oxidative phosphorylation pathway). Results from microarray and real-time PCR analyses were consistent. Results listing all genes that were significantly changed at any specific time point were further mined for cell-type (neutrophils, macrophages, endothelial, fibroblasts, and pluripotent stem cells) specificity. Candidate genes were also clustered on the basis of their functional annotation, linking them to inflammation, angiogenesis, reactive oxygen species (ROS), or extracellular matrix (ECM) categories. Rapid induction of genes encoding NADPH oxidase subunits and downregulation of catalase in response to wounding is consistent with the fact that low levels of endogenous H2O2is required for wound healing. Angiogenic genes, previously not connected to cutaneous wound healing, that were induced in the healing wound-edge included adiponectin, epiregulin, angiomotin, Nogo, and VEGF-B. This study provides a digested database that may serve as a valuable reference tool to develop novel hypotheses aiming to elucidate the biology of cutaneous wound healing comprehensively.

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Chen, Jing, Yu Chen, Yajie Chen, Zicheng Yang, Bo You, Ye Chun Ruan та Yizhi Peng. "Epidermal CFTR Suppresses MAPK/NF-κB to Promote Cutaneous Wound Healing". Cellular Physiology and Biochemistry 39, № 6 (2016): 2262–74. http://dx.doi.org/10.1159/000447919.

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Background: CFTR is implicated in cutaneous wound healing although the underlying mechanisms are not fully understood. In other cell types, CFTR is reported to regulate MAPK/ NF-κB signaling. We undertook the present study to explore a possible role of CFTR in regulating MAPK/NF-κB during cutaneous wound healing. Methods& Results: The splint-excisional and incisional wound healing models were used in CFTR mutant (DF508) mice. The cell-scratch model was used in a human keratinocyte line, HaCaT, in conjunction with CFTR knockdown or overexpression. The epidermal inflammation, keratinocyte proliferation and differentiation, as well as MAPK/NF-κB signaling were examined. Inhibitors of MAPK/NF-κB were also used. Results: Both DF508 mice and HaCaT cells with CFTR knockdown exhibited delayed cutaneous wound healing with exuberant inflammation, increased proliferation and aberrant differentiation. Knockdown of CFTR in HaCaT cells resulted in phosphorylation of ERK, p38 and IκBα. The disturbance of inflammation, proliferation and differentiation in HaCaT cells were reversed by CFTR overexpression or inhibition of MAPK or NF-κB. Conclusion: CFTR plays a role in suppressing MAPK/NF-κB to relieve inflammation, reduce proliferation and promote differentiation of keratinocytes, and thus promotes cutaneous wound healing.

39

Guo, Jianming, Haidi Hu, Jolanta Gorecka, Hualong Bai, Hao He, Roland Assi, Toshihiko Isaji, et al. "Adipose-derived mesenchymal stem cells accelerate diabetic wound healing in a similar fashion as bone marrow-derived cells." American Journal of Physiology-Cell Physiology 315, no. 6 (December 1, 2018): C885—C896. http://dx.doi.org/10.1152/ajpcell.00120.2018.

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We have previously shown that bone marrow-derived mesenchymal stem cells (BMSC) accelerate wound healing in a diabetic mouse model. In this study, we hypothesized that adipose tissue-derived stem cells (ADSC), cells of greater translational potential to human therapy, improve diabetic wound healing to a similar extent as BMSC. In vitro, the characterization and function of murine ADSC and BMSC as well as human diabetic and nondiabetic ADSC were evaluated by flow cytometry, cell viability, and VEGF expression. In vivo, biomimetic collagen scaffolds containing murine ADSC or BMSC were used to treat splinted full-thickness excisional back wounds on diabetic C57BL/6 mice, and human healthy and diabetic ADSC were used to treat back wounds on nude mice. Wound healing was evaluated by wound area, local VEGF-A expression, and count of CD31-positive cells. Delivery of murine ADSC or BMSC accelerated wound healing in diabetic mice to a similar extent, compared with acellular controls ( P < 0.0001). Histological analysis showed similarly increased cellular proliferation ( P < 0.0001), VEGF-A expression ( P = 0.0002), endothelial cell density ( P < 0.0001), numbers of macrophages ( P < 0.0001), and smooth muscle cells ( P < 0.0001) with ADSC and BMSC treatment, compared with controls. Cell survival and migration of ADSC and BMSC within the scaffolds were similar ( P = 0.781). Notch signaling was upregulated to a similar degree by both ADSC and BMSC. Diabetic and nondiabetic human ADSC expressed similar levels of VEGF-A ( P = 0.836) in vitro, as well as in scaffolds ( P = 1.000). Delivery of human diabetic and nondiabetic ADSC enhanced wound healing to a similar extent in a nude mouse wound model. Murine ADSC and BMSC delivered in a biomimetic-collagen scaffold are equivalent at enhancing diabetic wound healing. Human diabetic ADSC are not inferior to nondiabetic ADSC at accelerating wound healing in a nude mouse model. This data suggests that ADSC are a reasonable choice to evaluate for translational therapy in the treatment of human diabetic wounds.

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Roy, Sashwati, and Chandan K. Sen. "MiRNA in innate immune responses: novel players in wound inflammation." Physiological Genomics 43, no. 10 (May 2011): 557–65. http://dx.doi.org/10.1152/physiolgenomics.00160.2010.

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Chronic wounds represent a major and rising socioeconomic threat affecting over 6.5 million people in the United States costing in excess of US $25 billion annually. Wound healing is a physiological response to injury that is conserved across tissue systems. In humans, wounding is followed by instant response aimed at hemostasis, which in turn provides the foundation for inflammatory processes that closely follow. Inflammation is helpful and a prerequisite for healing as long as it is mounted and resolved in a timely manner. Chronic inflammation derails the healing cascade resulting in impaired wound closure. Disruption of Dicer, the RNase III enzyme that generates functional miRNAs, has a major impact on the overall immune system. Emerging studies indicate that miRNAs, especially miR-21, miR-146a/b, and miR-155, play a key role in regulating several hubs that orchestrate the inflammatory process. Direct evidence from studies addressing wound inflammation being limited, the current work represents a digest of the relevant literature that is aimed at unveiling the potential significance of miRNAs in the regulation of wound inflammation. Such treatment would help establish new paradigms highlighting a central role of miRs in the understanding and management of dysregulated inflammation as noted in conjunction with chronic wounds.

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Wietecha, Mateusz S., Lin Chen, Matthew J. Ranzer, Kimberly Anderson, Chunyi Ying, Tarun B. Patel, and Luisa A. DiPietro. "Sprouty2 downregulates angiogenesis during mouse skin wound healing." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 2 (February 2011): H459—H467. http://dx.doi.org/10.1152/ajpheart.00244.2010.

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Angiogenesis is regulated by signals received by receptor tyrosine kinases such as vascular endothelial growth factor receptors. Mammalian Sprouty (Spry) proteins are known to function by specifically antagonizing the activation of the mitogen-activated protein kinase signaling pathway by receptor tyrosine kinases, a pathway known to promote angiogenesis. To examine the role of Spry2 in the regulation of angiogenesis during wound repair, we used a model of murine dermal wound healing. Full-thickness excisional wounds (3 mm) were made on the dorsum of anesthetized adult female FVB mice. Samples were harvested at multiple time points postwounding and analyzed using real-time RT-PCR, Western blot analysis, and immunofluorescent histochemistry. Spry2 mRNA and protein levels in the wound bed increased significantly during the resolving phases of healing, coincident with the onset of vascular regression in this wound model. In another experiment, intracellular levels of Spry2 or its dominant-negative mutant (Y55F) were elevated by a topical application to the wounds of controlled-release gel containing cell permeable, transactivator of transcription-tagged Spry2, Spry2Y55F, or green fluorescent protein (as control). Wound samples were analyzed for vascularity using CD31 immunofluorescent histochemistry as well as for total and phospho-Erk1/2 protein content. The treatment of wounds with Spry2 resulted in a significant decrease in vascularity and a reduced abundance of phospho-Erk1/2 compared with wounds treated with the green fluorescent protein control. In contrast, the wounds treated with the dominant-negative Spry2Y55Fexhibited a moderate increase in vascularity and elevated phospho-Erk1/2 content. These results indicate that endogenous Spry2 functions to downregulate angiogenesis in the healing murine skin wound, potentially by inhibiting the mitogen-activated protein kinase signaling pathway.

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Yang, J., L. W. Tyler, R. B. Donoff, B. Song, A. J. Torio, G. T. Gallagher, T. Tsuji, et al. "Salivary EGF regulates eosinophil-derived TGF-alpha expression in hamster oral wounds." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 1 (January 1, 1996): G191—G202. http://dx.doi.org/10.1152/ajpgi.1996.270.1.g191.

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Using hamster as an oral wound healing model, we examined eosinophils and their expression of transforming growth factor-alpha (TGF-alpha) and transforming growth factor-beta 1 (TGF-beta 1). Oral wounds healed approximately two times faster than their cutaneous counterparts. Eosinophils infiltrated prominently into oral wounds; however, unlike the dual expression of TGF-alpha and TGF-beta 1 in skin wounds, oral wound-associated eosinophils expressed TGF-beta 1, but not TGF-alpha. Because saliva is present in oral environments and contains epidermal growth factor (EGF) and TGF-alpha, sialoadenectomy was performed in this model to determine whether the lack of TGF-alpha expression by eosinophils in oral wounds is due to the presence of salivary EGF and/or TGF-alpha. We found that eosinophils in sialoadenectomized hamsters did express TGF-alpha during oral wound healing but that such expression was suppressed when EGF was added to their drinking water. Taken together, our findings suggest that eosinophil-derived TGF-alpha and salivary TGF-alpha/ EGF may have complementary roles in contributing to TGF-alpha in oral wound healing.

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Nouvong, Aksone, Aaron M. Ambrus, Ellen R. Zhang, Lucas Hultman, and Hilary A. Coller. "Reactive oxygen species and bacterial biofilms in diabetic wound healing." Physiological Genomics 48, no. 12 (December 1, 2016): 889–96. http://dx.doi.org/10.1152/physiolgenomics.00066.2016.

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Chronic wounds are a common and debilitating complication for the diabetic population. It is challenging to study the development of chronic wounds in human patients; by the time it is clear that a wound is chronic, the early phases of wound healing have passed and can no longer be studied. Because of this limitation, mouse models have been employed to better understand the early phases of chronic wound formation. In the past few years, a series of reports have highlighted the importance of reactive oxygen species and bacterial biofilms in the development of chronic wounds in diabetics. We review these recent findings and discuss mouse models that are being utilized to enhance our understanding of these potentially important contributors to chronic wound formation in diabetic patients.

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Radek, Katherine A., Lisa A. Baer, Jennifer Eckhardt, Luisa A. DiPietro, and Charles E. Wade. "Mechanical unloading impairs keratinocyte migration and angiogenesis during cutaneous wound healing." Journal of Applied Physiology 104, no. 5 (May 2008): 1295–303. http://dx.doi.org/10.1152/japplphysiol.00977.2007.

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Although initially thought to improve an individual's ability to heal, mechanical unloading promoted by extended periods of bed rest has emerged as a contributing factor to delayed or aberrant tissue repair. Using a rat hindlimb unloading (HLU) model of hypogravity, we mimicked some aspects of physical inactivity by removing weight-bearing loads from the hindlimbs and producing a systemic cephalic fluid shift. This model simulates bed rest in that the animal undergoes physiological adaptations, resulting in a reduction in exercise capability, increased frequency of orthostatic intolerance, and a reduction in plasma volume. To investigate whether changes associated with prior prolonged bed rest correlate with impaired cutaneous wound healing, we examined wound closure, angiogenesis, and collagen content in day 2 to day 21 wounds from rats exposed to HLU 2 wk before excisional wounding. Wound closure was delayed in day 2 wounds from HLU rats compared with ambulatory controls. Although the levels of proangiogenic growth factors, fibroblast growth factor-2 (FGF-2), and vascular endothelial growth factor (VEGF) were similar between the two groups, wound vascularity was significantly reduced in day 7 wounds from HLU animals. To further examine this disparity, total collagen content was assessed but found to be similar between the two groups. Taken together, these results suggest that keratinocyte and endothelial cell function may be impaired during the wound healing process under periods of prolonged inactivity or bed rest.

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Fox, Miriam D. "Wound Care in the Neonatal Intensive Care Unit." Neonatal Network 30, no. 5 (2011): 291–303. http://dx.doi.org/10.1891/0730-0832.30.5.291.

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The skin is a vital organ with key protective functions. Infants in the NICU are at risk for skin injury because of developmental immaturity and intensive care treatments. When skin injury occurs, the neonatal nurse is challenged to provide wound care to optimize functional and cosmetic healing. Optimal wound care requires basic knowledge of the mechanisms of injury, physiology of wound healing, host factors affecting wound healing, and wound assessment. This knowledge provides the basis for determining appropriate wound treatment, including dressing selection. Attention to pain issues associated with wound care is difficult because of the infant’s developmental stage, but is essential because of the potentially negative life-long impact of pain. The premature infant’s propensity for skin stripping limits the selection of appropriate dressing, as does the paucity of research examining wound care products in this population.

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Grzesik, Wojciech J., and A. S. Narayanan. "Cementum and Periodontal Wound Healing and Regeneration." Critical Reviews in Oral Biology & Medicine 13, no. 6 (November 2002): 474–84. http://dx.doi.org/10.1177/154411130201300605.

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The extracellular matrix (ECM) of cementum resembles other mineralized tissues in composition; however, its physiology is unique, and it contains molecules that have not been detected in other tissues. Cementum components influence the activities of periodontal cells, and they manifest selectivity toward some periodontal cell types over others. In light of emerging evidence that the ECM determines how cells respond to environmental stimuli, we hypothesize that the local environment of the cementum matrix plays a pivotal role in maintaining the homeostasis of cementum under healthy conditions. The structural integrity and biochemical composition of the cementum matrix are severely compromised in periodontal disease, and the provisional matrix generated during periodontal healing is different from that of cementum. We propose that, for new cementum and attachment formation during periodontal regeneration, the local environment must be conducive for the recruitment and function of cementum-forming cells, and that the wound matrix is favorable for repair rather than regeneration. How cementum components may regulate and participate in cementum regeneration, possible new regenerative therapies using these principles, and models of cementoblastic cells are discussed.

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Mroz, Magdalena S., Natalia K. Lajczak, Bridie J. Goggins, Simon Keely, and Stephen J. Keely. "The bile acids, deoxycholic acid and ursodeoxycholic acid, regulate colonic epithelial wound healing." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 3 (March 1, 2018): G378—G387. http://dx.doi.org/10.1152/ajpgi.00435.2016.

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The intestinal epithelium constitutes an innate barrier which, upon injury, undergoes self-repair processes known as restitution. Although bile acids are known as important regulators of epithelial function in health and disease, their effects on wound healing processes are not yet clear. Here we set out to investigate the effects of the colonic bile acids, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA), on epithelial restitution. Wound healing in T84 cell monolayers grown on transparent, permeable supports was assessed over 48 h with or without bile acids. Cell migration was measured in Boyden chambers. mRNA and protein expression were measured by RT-PCR and Western blotting. DCA (50–150 µM) significantly inhibited wound closure in cultured epithelial monolayers and attenuated cell migration in Boyden chamber assays. DCA also induced nuclear accumulation of the farnesoid X receptor (FXR), whereas an FXR agonist, GW4064 (10 µM), inhibited wound closure. Both DCA and GW4064 attenuated the expression of CFTR Cl− channels, whereas inhibition of CFTR activity with either CFTR-inh-172 (10 µM) or GlyH-101 (25 µM) also prevented wound healing. Promoter/reporter assays revealed that FXR-induced downregulation of CFTR is mediated at the transcriptional level. In contrast, UDCA (50–150 µM) enhanced wound healing in vitro and prevented the effects of DCA. Finally, DCA inhibited and UDCA promoted mucosal healing in an in vivo mouse model. In conclusion, these studies suggest bile acids are important regulators of epithelial wound healing and are therefore good targets for development of new drugs to modulate intestinal barrier function in disease treatment. NEW & NOTEWORTHY The secondary bile acid, deoxycholic acid, inhibits colonic epithelial wound healing, an effect which appears to be mediated by activation of the nuclear bile acid receptor, FXR, with subsequent downregulation of CFTR expression and activity. In contrast, ursodeoxycholic acid promotes wound healing, suggesting it may provide an alternative approach to prevent the losses of barrier function that are associated with mucosal inflammation in IBD patients.

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Mirastschijski, Ursula, Dongsheng Jiang, and Yuval Rinkevich. "Genital Wound Repair and Scarring." Medical Sciences 10, no. 2 (April 18, 2022): 23. http://dx.doi.org/10.3390/medsci10020023.

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Skin wound repair has been the central focus of clinicians and scientists for almost a century. Insights into acute and chronic wound healing as well as scarring have influenced and ameliorated wound treatment. Our knowledge of normal skin notwithstanding, little is known of acute and chronic wound repair of genital skin. In contrast to extra-genital skin, hypertrophic scarring is uncommon in genital tissue. Chronic wound healing disorders of the genitals are mostly confined to mucosal tissue diseases. This article will provide insights into the differences between extra-genital and genital skin with regard to anatomy, physiology and aberrant wound repair. In light of fundamental differences between genital and normal skin, it is recommended that reconstructive and esthetic surgery should exclusively be performed by specialists with profound expertise in genital wound repair.

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Zhou, Xiangjun, Wei Zhang, Qisheng Yao, Hao Zhang, Guie Dong, Ming Zhang, Yutao Liu, Jian-Kang Chen, and Zheng Dong. "Exosome production and its regulation of EGFR during wound healing in renal tubular cells." American Journal of Physiology-Renal Physiology 312, no. 6 (June 1, 2017): F963—F970. http://dx.doi.org/10.1152/ajprenal.00078.2017.

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Kidney repair following injury involves the reconstitution of a structurally and functionally intact tubular epithelium. Growth factors and their receptors, such as EGFR, are important in the repair of renal tubules. Exosomes are cell-produced small (~100 nm in diameter) vesicles that contain and transfer proteins, lipids, RNAs, and DNAs between cells. In this study, we examined the relationship between exosome production and EGFR activation and the potential role of exosome in wound healing. EGFR activation occurred shortly after scratch wounding in renal tubular cells. Wound repair after scratching was significantly promoted by EGF and suppressed by EGFR inhibitor gefitinib. Interestingly, scratch wounding induced a significant increase of exosome production. The exosome production was decreased by EGF and increased by gefitinib, suggesting a suppressive role of EGFR signaling in exosome production. Conversely, inhibition of exosome release by GW4869 and manumycin A markedly increased EGFR activation and promoted wound healing. Moreover, exosomes derived from scratch-wounding cells could inhibit wound healing. Collectively, the results indicate that wound healing in renal tubular cells is associated with EGFR activation and exosome production. Although EGFR activation promotes wound healing, released exosomes may antagonize EGFR activation and wound healing.

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Kung, Hsiu-Ni, Mei-Jun Yang, Chi-Fen Chang, Yat-Pang Chau та Kuo-Shyan Lu. "In vitro and in vivo wound healing-promoting activities of β-lapachone". American Journal of Physiology-Cell Physiology 295, № 4 (жовтень 2008): C931—C943. http://dx.doi.org/10.1152/ajpcell.00266.2008.

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Impaired wound healing is a serious problem for diabetic patients. Wound healing is a complex process that requires the cooperation of many cell types, including keratinocytes, fibroblasts, endothelial cells, and macrophages. β-Lapachone, a natural compound extracted from the bark of the lapacho tree ( Tabebuia avellanedae), is well known for its antitumor, antiinflammatory, and antineoplastic effects at different concentrations and conditions, but its effects on wound healing have not been studied. The purpose of the present study was to investigate the effects of β-lapachone on wound healing and its underlying mechanism. In the present study, we demonstrated that a low dose of β-lapachone enhanced the proliferation in several cells, facilitated the migration of mouse 3T3 fibroblasts and human endothelial EAhy926 cells through different MAPK signaling pathways, and accelerated scrape-wound healing in vitro. Application of ointment with or without β-lapachone to a punched wound in normal and diabetic ( db/ db) mice showed that the healing process was faster in β-lapachone-treated animals than in those treated with vehicle only. In addition, β-lapachone induced macrophages to release VEGF and EGF, which are beneficial for growth of many cells. Our results showed that β-lapachone can increase cell proliferation, including keratinocytes, fibroblasts, and endothelial cells, and migration of fibroblasts and endothelial cells and thus accelerate wound healing. Therefore, we suggest that β-lapachone may have potential for therapeutic use for wound healing.

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