Vicinity Of Wounds Research Articles

Extracellular Matrix Mimicking Wound Microenvironment Responsive Amyloid-Heparin@TAAgNP Co-Assembled Hydrogel: An Effective Conductive Antibacterial Wound Healing Material.

Bioengineered composite hydrogel platforms made of a supramolecular coassembly have recently garnered significant attention as promising biomaterial-based healthcare therapeutics. The mechanical durability of amyloids, in conjunction with the structured charged framework rendered by biologically abundant key ECM component glycosaminoglycan, enables us to design minimalistic customized biomaterial suited for stimuli responsive therapy. In this study, by harnessing the heparin sulfate-binding aptitude of amyloid fibrils, we have constructed a pH-responsive extracellular matrix (ECM) mimicking hydrogel matrix. This effective biocompatible platform comprising heparin sulfate-amyloid coassembled hydrogel embedded with polyphenol functionalized silver nanoparticles not only provide a native skin ECM-like conductive environment but also provide wound-microenvironment responsive on-demand superior antibacterial efficacy for effective diabetic wound healing. Interestingly, both the cytocompatibility and antibacterial properties of this bioinspired matrix can be fine-tuned by controlling the mutual ratio of heparin sulfate-amyloid and incubated silver nanoparticle components, respectively. The designed biomaterial platform exhibits notable effectiveness in the treatment of chronic hyperglycemic wounds infected with multidrug-resistant bacteria, because of the integration of pH-responsive release characteristics of the incubated functionalized AgNP and the antibacterial amyloid fibrils. In addition to this, the aforementioned assemblage shows exceptional hemocompatibility with significant antibiofilm and antioxidant characteristics. Histological evidence of the incised skin tissue sections indicates that the fabricated composite hydrogel is also effective in controlling pro-inflammatory cytokines such as IL6 and TNFα expressions at the wound vicinity with significant upregulation of angiogenesis markers like CD31 and α-SMA.

Multifunctional Hydrogel Enhances Inflammatory Control, Antimicrobial Activity, and Oxygenation to Promote Healing in Infectious Wounds.

Chronic infected wounds often fail to heal through normal repair mechanisms, and the persistent response of reactive oxygen species (ROS) and inflammation is a major contributing factor to the difficulty in their healing. In this context, we developed an ROS-responsive injectable hydrogel. This hydrogel is composed of ε-polylysine grafted (EPL) with caffeic acid (CA) and hyaluronic acid (HA) grafted with phenylboronic acid (PBA). Before the gelation process, a mixture CaO2@Cur-PDA (CCP) consisting of calcium peroxide (CaO2) coated with polydopamine (PDA) and curcumin (Cur) is embedded into the hydrogel. Under the conditions of chronic refractory wound environments, the hydrogel gradually dissociates. HA mimics the function of the extracellular matrix, while the released caffeic acid-grafted ε-polylysine (CE) effectively eliminates bacteria in the wound vicinity. Additionally, released CA also clears ROS and influences macrophage polarization. Subsequently, CCP further decomposes, releasing Cur, which promotes angiogenesis. This multifunctional hydrogel accelerates the repair of diabetic skin wounds infected with Staphylococcus aureus in vivo and holds promise as a candidate dressing for the healing of chronic refractory wounds.

Exosome-mimetic vesicles derived from fibroblasts carrying matrine for wound healing.

Chronic skin wounds are a leading cause of hospital admissions and reduced life expectancy among older people and individuals with diabetes. Delayed wound healing is often attributed to a series of cellular abnormalities. Matrine, a well-studied component found in Sophora flavescens, is recognized for its anti-inflammatory effects. However, its impact on wound healing still remains uncertain. This study aims to explore the potential of matrine in promoting wound healing. In this study, we utilized gradient extrusion to produce fibroblast-derived exosome-mimetic vesicles as carriers for matrine (MHEM). MHEM were characterized using transmission electron microscopy and dynamic light scattering analysis. The therapeutic effect of MHEM in wound healing was explored in vitro and in vivo. Both matrine and MHEM enhanced the cellular activity as well as the migration of fibroblasts and keratinocytes. The potent anti-inflammatory effect of matrine diluted the inflammatory response in the vicinity of wounds. Furthermore, MHEM worked together to promote angiogenesis and the expression of transforming growth factor β and collagen I. MHEM contained growth factors of fibroblasts that regulated the functions of fibroblasts, keratinocytes and monocytes, which synergistically promoted wound healing with the anti-inflammatory effect of matrine. MHEM showed enhanced therapeutic efficacy in the inflammatory microenvironment, for new tissue formation and angiogenesis of wound healing.

Morphologic, Hemostasiologic and Hemostatic Aspects of Systemic Application of Exogenous Fibrin Monomer in Model of Posttraumatic Bleeding with Underlying Intake of Warfarin

INTRODUCTION: Earlier, an ability of exogenous fibrin monomer (FM) introduced at low doses to considerably limit posttraumatic blood loss was established by us on an experimental model of warfarin coagulopathy in vivo. However, the morphologic peculiarities of fibrin formation in the wound area were not considered.
 AIM: To compare morphologic, hemostasiologic and hemostatic data based on the results of systemic application of exogenous FM to interpret their effects in the model of posttraumatic bleeding with the underlying intake of warfarin.
 MATERIALS AND METHODS: In the work, Chinchilla male rabbits were used. A comparative analysis of hemostasiologic effects and of morphologic picture of the surface of the liver in the wound area was conducted after a dosed trauma, with a preliminary systemic introduction of FM (0.25 mg/kg intravenously) or a concentrate of prothrombin complex factors (40 IU/kg intravenously) with the underlying intake of warfarin by animals (0.40.5 mg/kg/day per os for 2 weeks).
 RESULTS: Introduction of FM in warfarinised animals in the conditions of a dosed experimental liver injury promoted a hemostatic effect comparable with that of a concentrate of prothrombin complex factors. Both hemostatic drugs led to intense fibrin formation that reduced posttraumatic blood loss. The use of FM was associated with increase in the thickness of thrombotic deposits and fibrin fibers in the wound surface in comparison with placebo by 4.0 and 1.6 times, respectively (р 0.000001). This process actively involved platelets, which led to 1.7 times reduction of their quantity in the lumen of the blood vessels in the wound vicinity (р 0.0002). No effect of FM on systemic hemostatic reactions in venous blood was found, in contrast to concentrate of prothrombin complex factors.
 CONCLUSION: Exogenous FM can produce a local hemostatic effect in the conditions of dosed experimental trauma and coagulopathy induced by warfarin intake. The hemostatic effect was mediated by intense thrombosis on the wound surface with the active recruitment of platelets in the process. The peculiarities of the demonstrated effects of FM may be mediated though the mechanisms of its action that have not yet been identified, which necessitates continuation of the research in this direction.

Prediction of Concrete Compressive Strength Using a Back-Propagation Neural Network Optimized by a Genetic Algorithm and Response Surface Analysis Considering the Appearance of Aggregates and Curing Conditions

In the present research, the authors have attempted to examine the compressive strength of conventional concrete, which is made using different aggregate sizes and geometries considering various curing temperatures. To this end, different aggregate geometries (rounded and angular) were utilized in various aggregate sizes (10, 20, and 30 mm) to prepare 108 rectangular cubic specimens. Then, the curing process was carried out in the vicinity of wind at different temperatures (5 °C < T < 30 °C). Next, the static compression experiments were performed on 28-day concrete specimens. Additionally, each test was repeated three times to check the repeatability of the results. Finally, the mean results were reported as the strength of concrete specimens. Response Surface Analysis (RSA) was utilized to determine the interaction effects of different parameters including the appearance of aggregates (shape and size) and curing temperature on the concrete strength. Afterwards, the optimum values of parameters were reported based on the RSA results to achieve maximum compressive strength. Moreover, to estimate concrete strength, a back-propagation neural network (OBPNN) optimized by a genetic algorithm (GA) was used. The findings of this study indicated that the developed neural network approach is greatly consistent with the experimental ones. Additionally, the compressive strength of concrete can be significantly increased (about 30%) by controlling the curing temperature in the range of 5–15 °C.

Wounding-induced changes in cellular pressure and localized auxin signalling spatially coordinate restorative divisions in roots

Wound healing in plant tissues, consisting of rigid cell wall-encapsulated cells, represents a considerable challenge and occurs through largely unknown mechanisms distinct from those in animals. Owing to their inability to migrate, plant cells rely on targeted cell division and expansion to regenerate wounds. Strict coordination of these wound-induced responses is essential to ensure efficient, spatially restricted wound healing. Single-cell tracking by live imaging allowed us to gain mechanistic insight into the wound perception and coordination of wound responses after laser-based wounding in Arabidopsis root. We revealed a crucial contribution of the collapse of damaged cells in wound perception and detected an auxin increase specific to cells immediately adjacent to the wound. This localized auxin increase balances wound-induced cell expansion and restorative division rates in a dose-dependent manner, leading to tumorous overproliferation when the canonical TIR1 auxin signaling is disrupted. Auxin and wound-induced turgor pressure changes together also spatially define the activation of key components of regeneration, such as the transcription regulator ERF115. Our observations suggest that the wound signaling involves the sensing of collapse of damaged cells and a local auxin signaling activation to coordinate the downstream transcriptional responses in the immediate wound vicinity.

Experimental and numerical study of platelets rolling on a von Willebrand factor-coated surface

Blood platelets circulate in the blood and adhere to wounded vessels to initiate coagulation and healing. The first step of this process is the capture of flowing platelets by adhesive molecules located at the wounded vessel wall. In this article, we study the transport of fixed blood platelets in a microfluidic channel coated with von Willebrand factor (vWF), a large multimeric protein expressed by endothelial cells in the vicinity of wounds. We measure the number of platelets adsorbed at the channel surface as a function of both time and space. Experimental results are compared with a new transport model. We show that transverse diffusion is an important feature of our model, while the rolling behaviour of the bounded platelets can be neglected.

Influences of low-frequency and other noises produced by wind turbines: An epidemiological literature review.

Objectives Due to its' environment-friendly and clean energy characteristics, wind power has been increasingly used globally, particularly in advanced countries. However, concerns about health hazards, especially due to low-frequency and other noises generated from wind turbines, have been reported repeatedly. In order to manage adverse health effects appropriately, regulatory standards or guidelines that consider the health of residents need to be developed. To provide a scientific basis for the development of such regulatory standards and guidelines, this paper conducted a literature review to analyze epidemiological studies involving residents living in the vicinity of wind farms.Methods Using the PubMED database, epidemiological papers that examined the health effects of noises produced by wind turbines were searched and collected. Additional papers were collected from the abstracts presented at relevant international academic conferences such as the Inter-Noise 2013 and Wind Turbine Noise 2015. An evidence table comprising the study design, subjects, exposure assessment, outcomes, confounders, and research results of each selected study was created.Results A total of 11 papers were collected (2 of which were abstracts from the international academic conferences). These studies reported outcomes such as perception of noises, annoyance caused by the noises, and the association of the noises with stress and sleeplessness. Significant associations between the noises or annoyance produced by wind turbines and subjective adverse health effects were reported repeatedly. Two studies reported an odds ratio of 1.1 for an increase of 1 dB in the A-weighted sound pressure level as a factor representing the influence level. For other factors, it was not possible to compare the magnitude of the impact among the collected studies. Individual attitudes toward wind power and landscapes, economic benefits of wind farms, visibility of wind turbines, sensitivity to sounds, and concerns over health hazards were reported as confounders.Conclusion Significant associations between the noises or annoyance produced by wind turbines and subjective adverse health effects were reported repeatedly. However, there was insufficient evidence to conclude whether the annoyance was caused by the psychological response to the construction of wind farms or by the actual exposure to noises generated by wind farms.

A Wearable Electrochemical Sensor to Monitor Progression of Wound Healing

An enzymatic electrochemical biosensor comprising the enzyme, urate oxidase (uricase, UOx), has been investigated for detection of real-time changes in uric acid. Uric acid is a key biomarker for monitoring severity of wounds, a complex process initiated to restore tissue damage.1 Although, tracking wound healing continues to be a challenge in healthcare; it is equally demanding. In existing technology, the time taken from the appearance of a wound to the commencement of an effective wound management plan can be lengthy, as laboratory tests can take days to complete. With its presence in different bio-fluids2, this work explores the continuous monitoring of systemic uric acid in human sweat. Electrochemical techniques like cyclic voltammetry and differential pulse voltammetry have been investigated for evaluating the success of the sensor on a wearable platform as a surrogate for wound healing. On this biosensor, hydrolysis of UA was monitored to detect the oxidation of its byproduct, H2O2. Results show that the use of a redox electron shuttle such as ferrocene carboxylic acid (FCA) or metal nano-particles enable electron transfer between the active site of the enzyme and the electrode. This work explores the possibilities of embedding the biosensor in wound dressing-gauze materials as substrates and investigates the effect and role of metal nano-particles on detection. It can measure very low volumes (0.5uL) of sweat showing that such low volumes are sufficient for systemic detection of uric acid at the wound vicinity. This non-invasive approach holds promise for tracking wound chronicity and can be beneficial towards shorter hospitalization time, costs and reduced outcomes of trauma, surgery, and amputations.3 The developed biosensor could facilitate treatment with an improved, comprehensive understanding of the recovery processes associated with healing.

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing

Cell–cell fusion is widely observed during development and disease, and imposes a dramatic change on participating cells. Cell fusion should be tightly controlled, but the underlying mechanism is poorly understood. Here, we found that the JAK/STAT pathway suppressed cell fusion during wound healing in the Drosophila larval epidermis, restricting cell fusion to the vicinity of the wound. In the absence of JAK/STAT signaling, a large syncytium containing a 3-fold higher number of nuclei than observed in wild-type tissue formed in wounded epidermis. The JAK/STAT ligand-encoding genes upd2 and upd3 were transcriptionally induced by wounding, and were required for suppressing excess cell fusion. JNK (also known as Basket in flies) was activated in the wound vicinity and activity peaked at ∼8 h after injury, whereas JAK/STAT signaling was activated in an adjoining concentric ring and activity peaked at a later stage. Cell fusion occurred primarily in the wound vicinity, where JAK/STAT activation was suppressed by fusion-inducing JNK signaling. JAK/STAT signaling was both necessary and sufficient for the induction of βPS integrin (also known as Myospheroid) expression, suggesting that the suppression of cell fusion was mediated at least in part by integrin protein.

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing.

Cell-cell fusion is widely observed during development and disease, and imposes a dramatic change on participating cells. Cell fusion should be tightly controlled, but the underlying mechanism is poorly understood. Here, we found that the JAK/STAT pathway suppressed cell fusion during wound healing in the Drosophila larval epidermis, restricting cell fusion to the vicinity of the wound. In the absence of JAK/STAT signaling, a large syncytium containing a 3-fold higher number of nuclei than observed in wild-type tissue formed in wounded epidermis. The JAK/STAT ligand-encoding genes upd2 and upd3 were transcriptionally induced by wounding, and were required for suppressing excess cell fusion. JNK (also known as Basket in flies) was activated in the wound vicinity and activity peaked at ∼8 h after injury, whereas JAK/STAT signaling was activated in an adjoining concentric ring and activity peaked at a later stage. Cell fusion occurred primarily in the wound vicinity, where JAK/STAT activation was suppressed by fusion-inducing JNK signaling. JAK/STAT signaling was both necessary and sufficient for the induction of βPS integrin (also known as Myospheroid) expression, suggesting that the suppression of cell fusion was mediated at least in part by integrin protein.

Serine Proteolytic Pathway Activation Reveals an Expanded Ensemble of Wound Response Genes in Drosophila

After injury to the animal epidermis, a variety of genes are transcriptionally activated in nearby cells to regenerate the missing cells and facilitate barrier repair. The range and types of diffusible wound signals that are produced by damaged epidermis and function to activate repair genes during epidermal regeneration remains a subject of very active study in many animals. In Drosophila embryos, we have discovered that serine protease function is locally activated around wound sites, and is also required for localized activation of epidermal repair genes. The serine protease trypsin is sufficient to induce a striking global epidermal wound response without inflicting cell death or compromising the integrity of the epithelial barrier. We developed a trypsin wounding treatment as an amplification tool to more fully understand the changes in the Drosophila transcriptome that occur after epidermal injury. By comparing our array results with similar results on mammalian skin wounding we can see which evolutionarily conserved pathways are activated after epidermal wounding in very diverse animals. Our innovative serine protease-mediated wounding protocol allowed us to identify 8 additional genes that are activated in epidermal cells in the immediate vicinity of puncture wounds, and the functions of many of these genes suggest novel genetic pathways that may control epidermal wound repair. Additionally, our data augments the evidence that clean puncture wounding can mount a powerful innate immune transcriptional response, with different innate immune genes being activated in an interesting variety of ways. These include puncture-induced activation only in epidermal cells in the immediate vicinity of wounds, or in all epidermal cells, or specifically in the fat body, or in multiple tissues.

Epithelial cell spreading induced by hepatocyte growth factor influences paxillin protein synthesis and posttranslational modification

Superficial wounds in the gastrointestinal tract rapidly reseal by coordinated epithelial cell migration facilitated by cytokines such as hepatocyte growth factor (HGF)/scatter factor released in the wound vicinity. However, the mechanisms by which HGF promotes physiological and pathophysiologic epithelial migration are incompletely understood. Using in vitro models of polarized T84 and Caco-2 intestinal epithelia, we report that HGF promoted epithelial spreading and RhoA GTPase activation in a time-dependent manner. Inducible expression of enhanced green fluorescent protein-tagged dominant-negative RhoA significantly attenuated HGF-induced spreading. HGF expanded a zone of partially flattened cells behind the wound edge containing basal F-actin fibers aligned in the direction of spreading. Concomitantly, plaques positive for the focal adhesion protein paxillin were enhanced. HGF induced an increase in the translation of paxillin and, to a lesser extent, beta1-integrin. This was independent of cell-matrix adhesion through beta1-integrin. Subcellular fractionation revealed increased cosedimentation of paxillin with plasma membrane-containing fractions following HGF stimulation, without corresponding enhancements in paxillin coassociation with beta1 integrin or actin. Tyrosine phosphorylation of paxillin was reduced by HGF and was sensitive to the Src kinase inhibitor PP2. With these taken together, we propose that HGF upregulates a free cytosolic pool of paxillin that is unaffiliated with either the cytoskeleton or focal cell-matrix contacts. Thus early spreading responses to HGF may partly relate to increased paxillin availability for incorporation into, and turnover within, dynamic cytoskeletal/membrane complexes whose rapid and transient adhesion to the matrix drives migration.

Surgical Pearl: Hemostasis assisted with two skin hooks

H emostasis is an essential but sometimes tedious and time-consuming aspect of cutaneous surgery. The importance of achieving hemostasis is stressed in numerous textbooks on cutaneous surgery, but details on efficient attainment of that goal are not.1-5 We describe an efficient technique that requires minimal investment in instrumentation and provides a clear division of labor between surgeon and assistant. The surgical assistant uses 2 skin hooks in unison to provide broad visualization of the wound bed and undermined skin flap, which is reflected for complete exposure (Fig 1). Intraoperative bleeding is focally controlled with tension tamponade achieved by the assistant exerting tension (stretch) on the skin flap (Fig 1) and digital pressure to bleeding vessels observed in the immediate wound vicinity (Fig 2). Once the skin hooks are engaged into the skin edge, they may be rotated 90° to 180° toward the wound and away from the assistant’s digit for added safety. With excellent exposure, the surgeon is free to efficiently visualize and target vessels with direct pressure using a sterile cotton-tipped applicator and to pinpoint electrodesiccation while the assistant provides tension and pressure control of hemorrhage. Because the surgeon individually targets, blots, and electrodesiccates the chosen vessel, the often awkward coordination and mistiming that may occur when these tasks are shared with the assistant are eliminated.

Inhibition of superficial scald in apples by wounding: changes in lipids and phenolics

Abstract `Granny Smith' apples (Malus domestica Borkh) were wounded with a hypodermic needle or not prior to cold storage for 7 months at 0°C. Wounded apples did not develop superficial scald adjacent to the wounded areas while non-wounded tissue developed scald on greater than 60% of the apple surface. Changes in conjugated trienes (CT) and membrane lipids that occurred as a result of scald formation were measured by examination of non-scalded tissue (achieved via wounding), scalded tissue on the same apple, and/or scalded tissue on the control fruit. Scald development was associated with an increase in CT and total glycolipid (GL) content, and a decrease in the proportion of linolenic acid (18:3) of the GL fraction and the GL unsaturation index (UI). These changes indicate that the chloroplast membrane is most affected by scald formation, possibly by the oxidative effect of CT. The reason for scald inhibition in the wound vicinity remains unknown. The increase in cinnamic acid derivatives in the wound area suggests an antioxidant activity.

Immunocytochemical expression of the blood-brain barrier glucose transporter (GLUT-1) in neural transplants and brain wounds.

The present study examined the immunocytochemical expression of the blood-brain barrier glucose transporter (GLUT-1) in a series of fetal neocortical transplants, autonomic tissue transplants, and stab wounds to the rat brain. GLUT-1 is one of a family of different glucose transporters and is found exclusively on barrier-type endothelial cells. In the brain it is responsible for the regulated facilitative diffusion of glucose across the blood-brain barrier. This investigation is the first to determine if this important molecule is altered during the process of angiogenesis that occurs following neural transplantation procedures or direct brain injury. Beginning in late fetal brain, e.g., E18 and continuing into maturity, GLUT-1 was strongly and exclusively expressed on normal cerebral vessels. In solid fetal central nervous system (CNS) transplants up to around 3 weeks postoperative, GLUT-1 was only weakly expressed, particularly as exemplified by colloidal gold immunostaining when compared with the host. At later times examined, up to 15 months postoperative, GLUT-1 immunoexpression was comparable with the normal adjacent brain. In autonomic tissue transplants, where the vessels do not have a blood-brain barrier, as expected, GLUT-1 was not expressed. In stab wounds, at 1 week there was extensive gliosis, and the injured vessels appeared fragmented and collapsed but still expressed GLUT-1, although to a somewhat lesser extent than normal brain. Between 3 and 6 weeks, GLUT-1 was expressed on tortuous vessels and in apparently fibrillar processes in the wound vicinity with a similar pattern to astrocyte (GFAP) reactivity. These results suggest the occurrence of a down-regulation of GLUT-1 in early transplants, perhaps related to reduced glycolytic activity or transient ischemia, or possibly due to the utilization of alternative energy sources. That GLUT-1 expression was not entirely lost in stab wounds to the mature brain suggests that the protein may be more labile in fetal or perinatal brain than in the adult and may not be affected by direct injury. Coupled with previous transplantation studies that have shown reduced neuronal glycolysis and potential barrier alterations, the reduction of GLUT-1 activity within nearly the identical time frame could indicate a relatively early critical period in cellular metabolism following transplantation of CNS tissue.

Intrinsic electric fields promote epithelization of wounds in the newt, Notophthalmus viridescens

The lateral electric fields (LFs) in the vicinity of small wounds made in hindlimb digit tip skin of Notophthalmus viridescens have been measured and manipulated. Healing of these wounds was assessed by crystal violet staining and by histology. Paired experiments were conducted on the animals: the healing of one digit's wound was compared with healing of the contralateral digit's wound whose LF was changed from that of its contralateral wound. When currents were passed through the animal (into one wound and out of the contralateral wound) so that the LF of one wound was zero while the contralateral wound had an enhanced LF, the wounds with the enhanced LF healed more rapidly than the wounds with the zero LF. When digits on one side were treated with 30 μ M benzamil in an artificial pond water so that their wound LFs were reduced to approximately zero, and the contralateral wounds were kept in artificial pond water without benzamil so that they had normal wound LFs, there was significantly less epithelization of the benzamil-treated wounds than of the control wounds. This effect on wound healing was reversed by adding currents that restored the normal wound LFs, but not by adding currents that reversed the wound LFs to the opposite polarity. When currents were added to reverse the wound LFs on one side of the animal, leaving the contralateral wounds free of added currents, the wounds with the reversed LFs healed more poorly than the contralateral wounds with normal LFs. These results are consistent with the hypothesis that the intrinsic LFs in the vicinity of wounds promote epithelization of these wounds.

Electric fields and wound healing

There are many points of view from which one may consider the healing of wounded skin, several of which are dealt with in earlier chapters. We would like to focus on one aspect of wound healing that has received only scant attention: the possible role of electric fields in the migration of epithelial cells that must occur in order to heal wounded skin. This cell migration is one of the earliest signs of epithelial repair of epidermal wounds, both in mammals and in amphibians. 1 One important reason for the lack of attention to electrical aspects of skin healing can be attributed to the paucity of information, useful to an understanding of wound healing, about the mammalian skin's ability to generate electrical currents. The bulk of the literature on the electrical properties of mammalian skin is concerned with psychophysiology. 2 4 There is some information about electrical properties of skin that may be relevant to wound healing. Some years ago, Herlitzka 5 confirmed DuBois-Reymond's 1860 observation 6 that about 1 microampere of current leaves small epidermal wounds made in human fingers when the wounds are immersed in saline. Much more recently. Illingworth and Barker 7 have found currents with densities ranging from 10 to 30 μA/cm 2 leaving the stumps of accidentally amputated children's fingertips when the stumps are immersed in saline. We, working with Barker, have added to this information 8 by studying the current-generating capacity of the glabrous epidermis of the cavy, and, particularly, the gradients of electrical potential that exist in the vicinity of wounds made in such skin. Subsequently, we have begun study of wound healing in a simpler system, larval Xenopus skin. We here will review this information, present some previously unpublished observations, and speculate on the possible relevance of this information to wound healing.

Eutypa armeniacae . [Descriptions of Fungi and Bacteria

Abstract A description is provided for Eutypa armeniacae . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: As a pathogen on apricot ( Prunus armeniaca ) and Ceanothus spp. As a saprophyte on apricot ( Prunus armeniaca ), almond ( Prunus amygdalus [Prunus dulcis] ), apple ( Malus sylvestris , walnut ( Juglans regia ), grapevine ( Vitis vinifera ), tamarisk ( Tamarix sp.), Ceanothus spp. and Berberis darwinii . DISEASE: 'Gummosis' or 'dieback' of apricots in Australia (Adam et al. , 1952). ' Cytosporina dieback' of apricots in California (42, 474). A contributing factor to the syndrome known as 'apricot apoplexy' in various European countries (Carter, private communications). Dieback of Ceanothus spp. in Australia and California (Moller et al. , 1971). The dieback disease of apricots is also known to be associated with this pathogen in New Zealand (40, 88) and South Africa (Price, 1973). On apricot, the classical symptoms occur on trees of all ages: cankering, sometimes associated with exudation of gum, in the vicinity of wounds which expose the sapwood, most commonly those made by pruning instruments. Ultimately the leaves on the part of the branch distal to the canker wither and die, usually in mid- to late summer, typically remaining attached for many months because no abscission layer has formed. Internally, the sapwood is discoloured light brown to dark brown, with a dffluse margin. Pycnidia may appear, usually in winter, on wood and bark nearby advanced infections. The pycnidiospores have never been seen to germinate and appear to have no role in transmission of the pathogen. Perithecia are immersed in a stroma which may develop two or more years after death of a branch. The stroma may remain productive for at least six years, producing one generation of perithecia annually, maturing in early spring. In California and in South Africa, external canker symptoms were for many years confused with those caused by bacteria or the genus Pseudomonas , but the internal symptoms are usually quite distinctive and the presence of E. armeniacae has been confirmed by culturing and by serology. GEOGRAPHICAL DISTRIBUTION: Australia, New Zealand, North America (California), Europe (France, Spain, Switzerland), South Africa. Absent from Chile in a disease survey conducted by English et al. (1967). Absence of records from the Asian continent are attributed to lack of information. TRANSMISSION: Entirely by air-borne ascospores; secondary dispersal from the tree surfaces is by water-splash and run during rainfall, carrying ascospores to the vessels exposed at wounds (45, 511).