Peritraumatic dissociation is one of the most critical acute responses to a traumatic experience, partly because it predicts subsequent posttraumatic stress disorder. Despite this, there is little understanding about the factors that influence peritraumatic dissociation. This study investigated the extent to which peritraumatic dissociation is predicted by the amount of perceived warning that participants had of the impact of the trauma.
Inositol kinase and its product accelerate wound healing by modulating calcium levels, Rho GTPases, and F-actin assembly
- Proceedings of the National Academy of Sciences of the United States of America
- Published over 6 years ago
Wound healing is essential for survival. We took advantage of the Xenopus embryo, which exhibits remarkable capacities to repair wounds quickly and efficiently, to investigate the mechanisms responsible for wound healing. Previous work has shown that injury triggers a rapid calcium response, followed by the activation of Ras homolog (Rho) family guanosine triphosphatases (GTPases), which regulate the formation and contraction of an F-actin purse string around the wound margin. How these processes are coordinated following wounding remained unclear. Here we show that inositol-trisphosphate 3-kinase B (Itpkb) via its enzymatic product inositol 1,3,4,5-tetrakisphosphate (InsP4) plays an essential role during wound healing by modulating the activity of Rho family GTPases and F-actin ring assembly. Furthermore, we show that Itpkb and InsP4 modulate the speed of the calcium wave, which propagates from the site of injury into neighboring uninjured cells. Strikingly, both overexpression of itpkb and exogenous application of InsP4 accelerate the speed of wound closure, a finding that has potential implications in our quest to find treatments that improve wound healing in patients with acute or chronic wounds.
Adipocytes have many functions in various tissues beyond energy storage, including regulating metabolism, growth, and immunity. However, little is known about their role in wound healing. Here we use live imaging of fat body cells, the equivalent of vertebrate adipocytes in Drosophila, to investigate their potential behaviors and functions following skin wounding. We find that pupal fat body cells are not immotile, as previously presumed, but actively migrate to wounds using an unusual adhesion-independent, actomyosin-driven, peristaltic mode of motility. Once at the wound, fat body cells collaborate with hemocytes, Drosophila macrophages, to clear the wound of cell debris; they also tightly seal the epithelial wound gap and locally release antimicrobial peptides to fight wound infection. Thus, fat body cells are motile cells, enabling them to migrate to wounds to undertake several local functions needed to drive wound repair and prevent infections.
Angiogenesis is critical for wound healing. Insufficient angiogenesis can result in impaired wound healing and chronic wound formation. Electrical stimulation (ES) has been shown to enhance angiogenesis. We previously showed that ES enhanced angiogenesis in acute wounds at one time point (day 14). The aim of this study was to further evaluate the role of ES in affecting angiogenesis during the acute phase of cutaneous wound healing over multiple time points. We compared the angiogenic response to wounding in 40 healthy volunteers (divided into two groups and randomised), treated with ES (post-ES) and compared them to secondary intention wound healing (control). Biopsy time points monitored were days 0, 3, 7, 10, 14. Objective non-invasive measures and H&E analysis were performed in addition to immunohistochemistry (IHC) and Western blotting (WB). Wound volume was significantly reduced on D7, 10 and 14 post-ES (p = 0.003, p = 0.002, p<0.001 respectively), surface area was reduced on days 10 (p = 0.001) and 14 (p<0.001) and wound diameter reduced on days 10 (p = 0.009) and 14 (p = 0.002). Blood flow increased significantly post-ES on D10 (p = 0.002) and 14 (p = 0.001). Angiogenic markers were up-regulated following ES application; protein analysis by IHC showed an increase (p<0.05) in VEGF-A expression by ES treatment on days 7, 10 and 14 (39%, 27% and 35% respectively) and PLGF expression on days 3 and 7 (40% on both days), compared to normal healing. Similarly, WB demonstrated an increase (p<0.05) in PLGF on days 7 and 14 (51% and 35% respectively). WB studies showed a significant increase of 30% (p>0.05) on day 14 in VEGF-A expression post-ES compared to controls. Furthermore, organisation of granulation tissue was improved on day 14 post-ES. This randomised controlled trial has shown that ES enhanced wound healing by reduced wound dimensions and increased VEGF-A and PLGF expression in acute cutaneous wounds, which further substantiates the role of ES in up-regulating angiogenesis as observed over multiple time points. This therapeutic approach may have potential application for clinical management of delayed and chronic wounds.
Cognitive models of post-traumatic stress disorder (PTSD) posit that negative cognitions regarding the self and the world underlie the disorder. In contrast, scarring models - which postulate that distress brings about an elevation in vulnerability - predict the inverse relationship. Both models were tested amongst 156 Israeli trauma victims. Participants were assessed for PTSD symptoms and trauma-related cognitions (negative thoughts regarding self and world) over 2 weeks (T1), 4 weeks (T2), and 12 weeks (T3) following the traumatic event. A cross-lagged structural equation modeling analysis yielded evidence for both cognitive vulnerability and scarring. Baseline PTSD was prospectively associated with an increase in negative cognitions regarding both the self and the world during the T1-T2 period. Negative cognitions regarding the self were prospectively associated with an increase in PTSD symptoms during both T1-T2 and T2-T3 periods. PTSD symptoms and negative cognitions regarding the self thus appear to form a vicious cognitive-symptomatic cycle which might impede recovery.
Aims: The aim of the present study was to evaluate the cicatricial repair of a corneal artificial perforation in rats with 10-0 nylon suture, N-butyl-2-cyanoacrylate (NBCA) adhesive, or NBCA + methacryloxysulfolane (NBCA-MS) adhesive through microscopic and histological assays. Methods: Twenty Wistar rats were randomly divided into 4 groups each containing 5 rats: (1) control group (corneal trauma without suturing and tissue adhesives), (2) suture group, (3) NBCA group and (4) NBCA-MS group. A central full-thickness 2-mm laceration was performed in the left eyes of the studied rats in all 4 groups. The presence of corneal edema, corneal neovascularization and tissue adhesive/suture were evaluated. On the 21st day, the rats were sacrificed and histological examination was performed to determine irregularity of corneal layers, superficial epithelization, polymorphonuclear leucocytes and neovascularization. Results: Tissue adhesives were as effective as suturing in closing full-thickness corneal wounds and no difference in postoperative healing was observed clinically. As for the histological results, suture-treated eyes had persistent corneal irregularity that can limit visual acuity and may also lead to astigmatism. Conclusions: The use of tissue adhesives constitutes a viable alternative clinical procedure to conventional sutures. Possible influences on astigmatism are hypothetical, as no objective measure of astigmatism was performed in the test animals.
With the growing demand for the specialized care of wounds, there is an ever expanding abundance of wound care modalities available. It is difficult to identify which products or devices enhance wound healing and thus a critical and continual look at new advances is necessary. The goal of any wound regimen should be to optimize wound healing by combining basic wound care modalities including debridement, off-loading, and infection control with the addition of advanced therapies when necessary. This review takes a closer look at current uses of negative pressure wound therapy, bioengineered alternative tissues, and amniotic membrane products. While robust literature may be lacking, current wound care advances are showing great promise in wound healing. This article is protected by copyright. All rights reserved.
Lacerations, abrasions, burns, and puncture wounds are common in the outpatient setting. Because wounds can quickly become infected, the most important aspect of treating a minor wound is irrigation and cleaning. There is no evidence that antiseptic irrigation is superior to sterile saline or tap water. Occlusion of the wound is key to preventing contamination. Suturing, if required, can be completed up to 24 hours after the trauma occurs, depending on the wound site. Tissue adhesives are equally effective for low-tension wounds with linear edges that can be evenly approximated. Although patients are often instructed to keep their wounds covered and dry after suturing, they can get wet within the first 24 to 48 hours without increasing the risk of infection. There is no evidence that prophylactic antibiotics improve outcomes for most simple wounds. Tetanus toxoid should be administered as soon as possible to patients who have not received a booster in the past 10 years. Superficial mild wound infections can be treated with topical agents, whereas deeper mild and moderate infections should be treated with oral antibiotics. Most severe infections, and moderate infections in high-risk patients, require initial parenteral antibiotics. Severe burns and wounds that cover large areas of the body or involve the face, joints, bone, tendons, or nerves should generally be referred to wound care specialists.
Low-level laser therapy (LLLT) has been extensively employed to improve epithelial wound healing, though the exact response of epithelium maturation and stratification after LLLT is unknown. Thus, this study aimed to assess the in vitro growth and differentiation of keratinocytes (KCs) and in vivo wound healing response when treated with LLLT. Human KCs (HaCaT cells) showed an enhanced proliferation with all the employed laser energy densities (3, 6 and 12 J/cm(2) , 660 nm, 100 mW), together with an increased expression of Cyclin D1. Moreover, the immunoexpression of proteins related to epithelial proliferation and maturation (p63, CK10, CK14) all indicated a faster maturation of the migrating KCs in the LLLT-treated wounds. In that way, an improved epithelial healing was promoted by LLLT with the employed parameters; this improvement was confirmed by changes in the expression of several proteins related to epithelial proliferation and maturation. Immunofluorescent expression of cytokeratin 10 (red) and Cyclin D1 (green) in (A) Control keratinocytes and (B) Low-level laser irradiated cells. Blue color illustrates the nuclei of the cells (DAPI staining).
Insufficient angiogenesis in severe wounds delays wound repair because of a lack of blood supply to the wound site. Therefore, pro-angiogenic therapeutics may enhance wound repair. Many studies have investigated various physical and biochemical cues to improve angiogenesis, such as biocompatible materials, surface modifications, angiogenic factors and coculture systems using various cell types. However, the present capability to mimic the micro- and nanostructure of the natural microenvironment, particularly its porous, fibrous features, is limited. Nanotopography may represent a promising tool to overcome these limitations. Here, we discuss various approaches to the use of nanotopography to enhance angiogenesis and consider the combination of coculture systems with nanotopography to mimic the native environment for promotion of angiogenesis in wound healing and repair.