scholarly journals Deep Tissue Injury in Development of Pressure Ulcers: A Decrease of Inflammasome Activation and Changes in Human Skin Morphology in Response to Aging and Mechanical Load

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e69223 ◽  
Author(s):  
Olivera Stojadinovic ◽  
Julia Minkiewicz ◽  
Andrew Sawaya ◽  
Jonathan W. Bourne ◽  
Peter Torzilli ◽  
...  
2007 ◽  
Vol 102 (5) ◽  
pp. 1992-2001 ◽  
Author(s):  
Leandro R. Solis ◽  
Daniel P. Hallihan ◽  
Richard R. E. Uwiera ◽  
Richard B. Thompson ◽  
Enid D. Pehowich ◽  
...  

Pressure ulcers develop due to morphological and biochemical changes triggered by the combined effects of mechanical deformation, ischemia, and reperfusion that occur during extended periods of immobility. The goal of this study was to test the effectiveness of a novel electrical stimulation technique in the prevention of deep tissue injury (DTI). We propose that contractions elicited by intermittent electrical stimulation (IES) in muscles subjected to constant pressure would induce periodic relief in internal pressure; additionally, each contraction would also restore blood flow to the tissue. The application of constant pressure to the quadriceps muscles of rats generated a DTI that affected 60 ± 15% of the compressed muscle as assessed by magnetic resonance imaging. In contrast, in the groups of rats that received IES at 10- and 5-min intervals, DTI of the muscle was limited to 16 ± 16 and 25 ± 13%, respectively. Injury to the muscle was corroborated by histology. In an experiment with a human volunteer, compression of the buttocks reduced the oxygenation level of the muscles by ∼4%; after IES, oxygenation levels increased by ∼6% beyond baseline. Concurrently, the surface pressure profiles of the loaded muscles were redistributed and the high-pressure points were reduced during each IES-induced contraction. The results of this study indicate that IES significantly reduces the amount of DTI by increasing the oxygen available to the tissue and by modifying the pressure profiles of the loaded muscles. This presents a promising technique for the prevention of pressure ulcers in immobilized and/or insensate individuals.


2016 ◽  
Vol 29 (4) ◽  
pp. 178-190 ◽  
Author(s):  
Hyochol Ahn ◽  
Linda Cowan ◽  
Cynthia Garvan ◽  
Debra Lyon ◽  
Joyce Stechmiller

2009 ◽  
Vol 124 (2) ◽  
pp. 540-550 ◽  
Author(s):  
Noriyuki Aoi ◽  
Kotaro Yoshimura ◽  
Takafumi Kadono ◽  
Gojiro Nakagami ◽  
Shinji Iizuka ◽  
...  

2020 ◽  
Vol 18 ◽  
Author(s):  
Zirui Zhang ◽  
Shangcong Han ◽  
Panpan Liu ◽  
Xu Yang ◽  
Jing Han ◽  
...  

Background: Chronic inflammation and lack of angiogenesis are the important pathological mechanisms in deep tissue injury (DTI). Curcumin is a well-known anti-inflammatory and antioxidant agent. However, curcumin is unstable under acidic and alkaline conditions, and can be rapidly metabolized and excreted in the bile, which shortens its bioactivity and efficacy. Objective: This study aimed to prepare curcumin-loaded poly (lactic-co-glycolic acid) nanoparticles (CPNPs) and to elucidate the protective effects and underlying mechanisms of wound healing in DTI models. Methods: CPNPs were evaluated for particle size, biocompatibility, in vitro drug release and their effect on in vivo wound healing. Results : The results of in vivo wound closure analysis revealed that CPNP treatments significantly improved wound contraction rates (p<0.01) at a faster rate than other three treatment groups. H&E staining revealed that CPNP treatments resulted in complete epithelialization and thick granulation tissue formation, whereas control groups resulted in a lack of compact epithelialization and persistence of inflammatory cells within the wound sites. Quantitative real-time PCR analysis showed that treatment with CPNPs suppressed IL-6 and TNF-α mRNA expression, and up-regulated TGF-β, VEGF-A and IL-10 mRNA expression. Western blot analysis showed up-regulated protein expression of TGF-β, VEGF-A and phosphorylatedSTAT3. Conclusion: Our results showed that CPNPs enhanced wound healing in DTI models, through modulation of the JAK2/STAT3 signalling pathway and subsequent upregulation of pro-healing factors.


2010 ◽  
Vol 43 (3) ◽  
pp. 570-575 ◽  
Author(s):  
Bastiaan J. van Nierop ◽  
Anke Stekelenburg ◽  
Sandra Loerakker ◽  
Cees W. Oomens ◽  
Dan Bader ◽  
...  

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