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Rationale Infancy is a time of elevated risk of injury. Past research has focused mostly on the type of injuries, leaving many gaps in knowledge about contextual information that could aid in injury prevention planning. Methods In this longitudinal study, a participant-event recording method was used in which mothers tracked their infants’ home injuries through three motor development stages (sitting up independently, crawling, and walking). A contextual analysis elucidated where injuries occurred, their type and severity, the infant’s and parent’s behaviors at the time, if the infant had done the risk behavior before and been injured, the level of supervision, and the nature of any safety precautions parents implemented following these injuries. Results Injuries occurred as often in play as in nonplay areas and were due to physically-active nonplay activities more so than play activities; mothers were often doing chores. Bumps and bruises were the most common types of injuries. As infants became more mobile, supervision scores declined and injury severity scores increased. Infants had done the risk behavior leading to injury previously about 60% of the time, with higher scores associated with parents implementing fewer preventive actions in response to injury. When mothers did implement a safety precaution, greater injury severity was associated with more modifications to the environment and increased supervision; teaching about safety was infrequent. Conclusion Implications of these results for injury prevention messaging are discussed.

Significance: Inflammation is a normal response to injury, but uncontrolled inflammation can lead to several diseases. In recent years, research has shown endogenously synthesized hydrogen sulfide (H2S) to be a novel mediator of inflammation. This review summarizes the current understanding and recent advances of H2S role with respect to inflammation in different diseases. Recent Advances: Promising early results from clinical studies suggest an important role of H2S in human inflammatory disease. Critical Issues: Defining the precise mechanism by which H2S contributes to inflammation is a complex challenge, and there is active ongoing research that is focused on addressing this question. Most of this work has been conducted on animal models of human disease and isolated/cultured cells, and its translation to the clinic is another challenge in the area of H2S research. Future Directions: Defining the mechanism by which H2S acts as an inflammatory mediator will help us better understand different inflammatory diseases and help develop novel therapeutic approaches for these diseases.

Alcohol misuse is long established as a contributor to the pathophysiology of the lung. The intersection of multi-organ responses to alcohol-mediated tissue injury likely contributes to the modulation of lung in response to injury. Indeed, the negative impact of alcohol on susceptibility to infection and on lung barrier function is now well documented. Thus, the alcohol lung represents a very likely comorbidity for the negative consequences of both COVID-19 susceptibility and severity. In this review, we present the known alcohol misuse ramifications on the lung in the context of the current coronavirus pandemic., Highlights • COVID-19 pandemic contributes to sever lung disease. • Chronic alcohol misuse is attributed to lung disfunction. • Alcohol-associated impairment of innate lung defense and increased injury should represent a poor background for COVID-19 infection and severity.

Oligodendrocyte precursor cell differentiation into myelinating oligodendrocytes is critical for remyelination in the central nervous system after injury. In this issue of Neuron, Niu et al. (2021) detail a novel role for ring finger protein Rnf43, which is expressed in response to injury and is essential to promote remyelination in vivo.

A wound is a break in the continuity of the skin. The body’s response to injury and the restoration of the same is healing. Wound healing is a biological process that is initiated by trauma and often terminated by scar formation. In this research, guava leaf extract was used as antiseptic and its efficacy was tested to commercially available products. The result revealed that all mice which received guava leaf extract formed scar earlier as compared to povidone iodine and PNSS. Since maturation phase which also refers to remodeling phase is responsible for the new epithelium and final scar tissue formation, and as the development of these completes the complex process of wound healing, the researchers suggest that the use of guava leaf extract in comparison with povidone iodine and PNSS when it comes to wound healing is the most affordable in treatment and promoting normal and more rapid wound healing.

Kolmer cells (epiplexus macrophages) are the least studied population of phagocytic cells in the mammalian brain. In the present work, we studied the response of these cells to high blood pressure and ischemic brain injury caused by a short middle cerebral artery occlusion. We used spontaneously hypertensive SHR and normotensive WKY rats. Kolmer cells of normotensive WKY animals had a small volume of perinuclear cytoplasm with a cortical concentration of Iba-1 protein. These cells had characteristic thin, sometimes tortuous processes. Moderate activation due to high blood pressure in SHR rats was accompanied by an increase in the perinuclear cytoplasm volume and the appearance of numerous straight thin processes. Further activation caused by ischemia led to the disappearance of processes and the cells became round. The structural rearrangements were accompanied by the disappearance of the Iba-1 protein concentration gradient in the cytoplasm. Also, the intranuclear accumulation of the cytoplasmic Iba-1 protein in Kolmer cells was first discovered, independent of their activation. That indicates the polyfunctionality of this protein in the cell. The obtained results point to the involvement of Kolmer cells in the brain's response to injury.

Axon regeneration is orchestrated by many genes that are differentially expressed in response to injury. Through a comparative analysis of gene expression profiling, injury-responsive genes that are potential targets for understanding the mechanisms underlying regeneration have been revealed. As the efficiency of axon regeneration in both the peripheral and central nervous systems can be manipulated, we suggest that identifying regeneration-associated genes is a promising approach for developing therapeutic applications in vivo. Here, we review the possible roles of stem cell marker- or stemness-related genes in axon regeneration to gain a better understanding of the regeneration mechanism and to identify targets that can enhance regenerative capacity., Nerve cells: activating genetic switches to repair injury Understanding which genes are switched on/off in nerve cells in response to injury may help develop new treatments to repair nerves. Nerve cells can be cued to regenerate in both the central (brain and spinal cord) and peripheral nervous systems. Studying patterns of post-injury gene activation may allow therapeutic boosting of injury-responsive genes to cue nerve regrowth. Jinyoung Lee and Yongcheol Cho at Korea University, Seoul, South Korea have reviewed those genes identified as markers of stem cells (cells with high regenerative capacity) that are differentially regulated in nerve cells. They present several promising target genes for further study, noting that little is known of the mechanisms underlying regeneration or the interacting genetic pathways. These results point the way to identifying genetic targets to improve treatment for nerve damage.

Inflammation is a vital process in response to injury and infection. However, hyper-inflammation have been linked to the pathophysiology of diseases such as atherosclerosis, cancers, neuroinflammat...

A wound is damage to the typical anatomic structure. Wound healing is an immediate therapeutic response to injury. It is a creation of the combined response of some cell types towards injury. Wound healing takes place by a sequence of molecular events which cooperate to fix tissue integrity and cell work. In typical healthy individual under ordinary conditions, these physiological events take place smoothly. Though sometimes, these molecular events are arrested, this brings about in struggle to heal. There is an assortment of approaches for the way toward managing and controlling both acute injuries (acute wounds) and ceaseless non-mending wounds (chronic non-healing wounds). The principal objective of these two cases is to achieve better-wound healing. Ideal formulations of wound healing should not only enhance the healing process but also reduce pain, infection and loss of electrolytes, proteins and liquids from the injury. A broad scope of items typically introduced with target various parts of the wound healing process depends on numerous types of wounds and novel polymers utilised for the conveyance of medications to both acute and ceaseless injuries. These include alginate, hydrocolloids, hydrofibers, polyurethane, and hydrogels. This article gives particular importance to different novel approaches in the management of wound healing. This review draws out the data and hopes to provide understanding into traditional, current and imminent techniques and methods for wound management.

Nutrition, the process by which a body nourishes itself through the transformation of food into energy and body tissues, is the most important factor in health maintenance, response to injury or illness, short-term and long-term rehabilitation, and longevity. Most rehabilitation providers and the individuals they treat have limited training and knowledge on even the basics of nutrition. An appropriate diet for individuals who are either in a health maintenance or an active program of rehabilitation includes 1500 to 2500 calories per day delivered via a balanced range of foodstuffs, preferably in a whole-food, plant-based manner.

Cardiac fibrosis is mediated by the activation of resident cardiac fibroblasts, which differentiate into myofibroblasts in response to injury or stress. Although myofibroblast formation is a physiological response to acute injury, such as myocardial infarction, myofibroblast persistence, as occurs in heart failure, contributes to maladaptive remodeling and progressive functional decline. Although traditional pathways of activation, such as TGFβ (transforming growth factor β) and AngII (angiotensin II), have been well characterized, less understood are the alterations in mitochondrial function and cellular metabolism that are necessary to initiate and sustain myofibroblast formation and function. In this review, we highlight recent reports detailing the mitochondrial and metabolic mechanisms that contribute to myofibroblast differentiation, persistence, and function with the hope of identifying novel therapeutic targets to treat, and potentially reverse, tissue organ fibrosis.

Astrocytes are dynamic cells residing in the central nervous system exhibiting many diverse functions. Astrocytes quickly change and present unique phenotypes in response to injury or disease. Here, we briefly summarize recent information regarding astrocyte morphology and function and provide brief insight into their phenotypic changes following injury or disease. We also present the utility of in vitro astrocyte cultures and present recent advances in biomaterial development that enable better recapitulation of their in vivo behavior and morphology.

To facilitate rational experimental design and fulfill the NIH requirement of including sex as a biologic variable, we examined the influences of genetic background and sex on responses to intervertebral disc (IVD) injury in the mouse tail. The goal of this study was to compare gene expression and histologic changes in response to a tail IVD injury (needle puncture) in male and female mice on the DBA and C57BL/6 (B6) backgrounds. We hypothesized that extracellular matrix gene expression in response to IVD injury differs between mice of different genetic backgrounds and sex. Consistent changes were detected in gene expression and histologic features after IVD injury in mice on both genetic backgrounds and sexes. In particular, expression of col1a1 and adam8 was higher in the injured IVD of DBA mice than B6 mice. Conversely, col2a1 expression was higher in B6 mice than DBA mice. Sex-associated differences were significant only in B6 mice, in which col2a1 expression was greater in male mice than in female. Histologic differences in response to injury were not apparent between DBA and B6 mice or between males and females. In conclusion, mouse tail IVD showed sex- and strain-related changes in gene expression and histology after needle puncture. The magnitude of change in gene expression differed with regard to genetic background and, to a lesser degree, sex.

Plants display extraordinary ability to revive tissues and organs lost or damaged in injury. This is evident from the root tip restoration and classical experiments in stem demonstrating re-establishment of vascular continuity. While recent studies have begun to unravel the mechanistic understanding of tissue restoration in response to injury in underground plant organs, the molecular mechanisms of the same in aerial organs remain to be ventured deeper. Here, we discuss the possibility of unearthing the regulatory mechanism that can confer universal regeneration potential to plant body and further provide a comprehensive understanding of how tissue and organ regeneration gets triggered in response to mechanical injury and later gets terminated after re-patterning and regaining the appropriate size.

Although much attention has been directed at regenerating orthopedic tissues, functional integration—be it of the graft with host tissue or for reestablishing connectivity between soft and hard tissues—remains a frontier challenge in the field. Healing at these interfaces is often undermined by the body’s own inadequate response to injury, generally resulting in the formation of disorganized, fibrous scar tissue. Broadly speaking, the interfaces in the body can be classified as either heterotypic, i.e., between two different tissue types, or homotypic, i.e., between the same tissue types. This chapter focuses on the biology of several heterotypic and homotypic interfaces, such as ligament-to-bone, tendon-to-bone, and cartilage-graft-to-cartilage, and highlights current and emerging strategies used to enhance regeneration at the interface. Recapitulating the complex structure and organization at these junctions is crucial to enabling integration and ensuring the clinical translation of tissue engineered grafts.

Acute kidney injury (AKI) remains highly prevalent, yet no optimal therapy is available to prevent it or promote recovery after initial insult. Experimental studies have demonstrated that both innate and adaptive immune responses play a central role during AKI. In response to injury, myeloid cells are first recruited and activated based on specific signals from the damaged microenvironment. The subsequent recruitment and activation state of the immune cells depends on the stage of injury and recovery, reflecting a dynamic and diverse spectrum of immunophenotypes. In this review, we highlight our current understanding of the mechanisms by which myeloid cells contribute to injury, repair, and fibrosis after AKI.

Background Neuropathic pain (NP) is a frequent finding in patients diagnosed with spinal cord injuries (SCIs). We aimed to investigate the effects of voluntary exercise on NP after SCI and to elucidate its potential mechanisms. MethodsA rat model of post-SCI NP induced by compression of the posterior or lateral cervical spinal cord was used to evaluate the effects of voluntary exercise by measuring the bilateral withdrawal of the hind paws using the Von Frey filament and Hargreaves tests. The place escape/avoid paradigm was used to evaluate supraspinal pain processing and somatosensory evoked potentials (SEPs) were used to examine disturbances in proprioception. Locomotor function was evaluated using Basso, Beattie, and Bresnahan (BBB) scoring. Pathologic findings in hematoxylin and eosin-stained tissue and magnetic resonance imaging were used to evaluate the morphological changes after SCI. The lesion size within the cervical spinal cord was evaluated by staining with Eriochrome cyanine R. Quantitative polymerase chain reaction and immunohistochemistry were used to assess the expression of calcitonin gene-related peptide (CGRP) and ionized calcium-binding adapter molecule 1 (Iba-1) in the lumbar dorsal horns. ResultsAll injured rats developed mechanical hypersensitivity, hyposensitivity, and thermal hyperalgesia in the contralateral hind paws at one week post-injury. Rats that underwent lateral compression injury developed NP in the ipsilateral hind paws one week later than rats with a posterior compression injury. Our findings revealed that voluntary exercise ameliorated mechanical allodynia and thermal hyperalgesia, and significantly improved proprioception as measured by SEP, but had no impact on mechanical hypoalgesia or motor recovery and provided no significant neuroprotection after recovery from an acute SCI. SCI-induced NP was accompanied by increased expression of CGRP and Iba-1 in the lumbar dorsal horn. These responses were reduced in rats that underwent voluntary exercise. ConclusionsVoluntary exercise ameliorates NP that develops in rats after compression injury. Increased expression of CGRP and Iba-1 in the lumbar dorsal horns of rats exhibiting symptoms of NP suggests that microglial activation might play a crucial role in its development. Collectively, voluntary exercise may be a promising therapeutic modality to treat NP that develops clinically in response to SCI.

Single cell biology has the potential to elucidate many critical biological processes and diseases, from development and regeneration to cancer. Single cell analyses are uncovering the molecular diversity of cells, revealing a clearer picture of the variation among and between different cell types. New techniques are beginning to unravel how differences in cell state-transcriptional, epigenetic, and other characteristics-can lead to different cell fates among genetically identical cells, which underlies complex processes such as embryonic development, drug resistance, response to injury, and cellular reprogramming. Single cell technologies also pose significant challenges relating to processing and analyzing vast amounts of data collected. To realize the potential of single cell technologies, new computational approaches are needed. On March 17-19, 2021, experts in single cell biology met virtually for the Keystone eSymposium "Single Cell Biology" to discuss advances both in single cell applications and technologies.

Vascular remodeling is a prominent feature of pulmonary hypertension. This process involves increased muscularization of already muscularized vessels as well as neo-muscularization of non-muscularized vessels. The cell-of-origin of the newly formed vascular smooth muscle cells has been a subject of intense debate in recent years. Identifying these cells may have important clinical implications since it opens the door for attempts to therapeutically target the progenitor cells and/or reverse the differentiation of their progeny. In this context, the dominant model is that these cells derive from pre-existing smooth muscle cells that are activated in response to injury. In this mini review, we present the evidence that is in favor of this model and, at the same time, highlight other studies indicating that there are alternative cellular sources of vascular smooth muscle cells in pulmonary vascular remodeling.

The enhanced permeability retention (EPR) effect based nanomedicine has been widely used for tumor targeting during the past decades. Here we unexpectedly observed the similar “EPR effect” at the site of injury. We found that the temporary dilated and leaky blood vessels caused by the potent vasodilator histamine in response to injury allowed the injected nanoparticles to pass through the vasculature and reached the injured tissue. Our finding shows the potential underline mechanism of “EPR effect” at the injured site. By loading with antibiotics, we further demonstrated a new strategy for prevention of infection at the site of injury.

Recently, in high-performance sports, there has been a significant increase in the volume and intensity of training loads, an increase in the duration of the competition period and its intensity, significant psychoemotional loads that affect the health status and quality of life of professional athletes, determine the incidence rate and a higher risk of injury in highly qualified athletes. Trauma and disease are considered as a polyetiological variant of the systemic inflammatory response syndrome, associated with the formation of «pathological» systems and their further dynamic change. One of the most striking manifestations of the systemic inflammatory reaction syndrome is pronounced metabolic disorders with a shift in metabolic processes towards hypermetabolism-hypercatabolism. The catabolic type of metabolic processes is characterized by the development of a pronounced protein-energy deficiency, a violation of nutrition and the inability to provide the body with the necessary nutrients in a natural way.

Adult stem cells are rare, undifferentiated cells found in all tissues of the body. Although normally kept in a quiescent, nondividing state, these cells can proliferate and differentiate to replace naturally dying cells within their tissue and to repair its wounds in response to injury. Due to their proliferative nature and ability to regenerate tissue, adult stem cells have the potential to treat a variety of degenerative diseases as well as aging. In addition, since stem cells are often thought to be the source of malignant tumors, understanding the mechanisms that keep their proliferative abilities in check can pave the way for new cancer therapies. While adult stem cells have had limited practical and clinical applications to date, several clinical trials of stem cell-based therapies are underway. This report details recent research presented at the New York Academy of Sciences on March 14, 2019 on understanding the factors that regulate stem cell activity and differentiation, with the hope of translating these findings into the clinic.

Objectives The purpose of the current study was to compare injury and running history among current and former runners who consider themselves either injured or uninjured. Design Cross-sectional survey. Setting Online survey, available to any individuals over the age of 18 who currently run (runners) or who once ran regularly but are no longer running (former runners). Participants 312 participants (age 38 ± 12 years, 219 males, 89 females, 4 did not disclose) completed the survey. Main outcome measures This study assessed injury incidence, consequences of injury such as time off, and reported injury diagnoses and treatments. Chi-square and frequency analyses were calculated to describe running status, injury counts, and response to injury. Results Most participants (80%) reported 1 + running injury. 775 total injuries were reported. The four most common injuries were iliotibial band syndrome (34%), plantar fasciitis (30%), strained thigh/hip muscle (25%), and medial tibial stress syndrome (22%). About 40% of participants continued to run with these injuries. Conclusions Injury frequencies (80%) agreed with those reported in the literature. The results of this study also support the notion that running injuries exist on a continuum of severity and that the individual response to injury is complex and determined by various factors.

Missed fractures are common in pediatric trauma patients. Pediatric bone differs from adult bone in its composition and response to injury, leading to fracture patterns that may be subtle, radiographically unfamiliar, and challenging to distinguish from normal variation. Familiarity with the unique fracture types of the pediatric skeleton and site-specific injury patterns is critical, because prompt diagnosis can significantly alter clinical management and outcome. This article examines the unique features of pediatric bone contributing to missed fractures, the incidence of missed fractures, common injury types of the pediatric skeleton, and frequently missed site-specific fracture patterns, highlighting problem-solving techniques for challenging cases.

Understanding the basic properties of how axons respond to injury in the mammalian central nervous system (CNS) is of fundamental value for developing strategies to promote neural repair. Axons possess complex morphologies with stereotypical branching patterns. However, current knowledge of the axonal response to injury gives little consideration to axonal branches, nor do strategies to promote axon regeneration. This article reviews evidence from in vivo spinal cord imaging that axonal branches markedly impact the degenerative and regenerative responses to injury. At a major bifurcation point, depending on whether one or both axonal branches are injured, neurons may choose either a more self-preservative response or a more dynamic response. The stabilizing effect of the spared branch may underlie a well-known divergence in neuronal responses to injury, and illustrates an example where in vivo spinal cord imaging reveals insights that are difficult to elucidate with conventional histological methods.

Purpose of Review Cardiac fibroblast activation contributes to fibrosis, maladaptive remodeling and heart failure progression. This review summarizes the latest findings on cardiac fibroblast activation dynamics derived from single-cell transcriptomic analyses and discusses how this information may aid the development of new multispecific medicines. Recent Findings Advances in single-cell gene expression technologies have led to the discovery of distinct fibroblast subsets, some of which are more prevalent in diseased tissue and exhibit temporal changes in response to injury. In parallel to the rapid development of single-cell platforms, the advent of multispecific therapeutics is beginning to transform the biopharmaceutical landscape, paving the way for the selective targeting of diseased fibroblast subpopulations. Summary Insights gained from single-cell technologies reveal critical cardiac fibroblast subsets that play a pathogenic role in the progression of heart failure. Combined with the development of multispecific therapeutic agents that have enabled access to previously “undruggable” targets, we are entering a new era of precision medicine.

Leukocyte recruitment to the site of injury is a crucial event in the regulation of an inflammatory response. Tight regulation of interactions between the endothelium and circulating leukocytes is necessary to ensure a protective response to injury does not result in inflammatory disease. Rising interest in the broad immunoregulatory roles displayed by members of the glycan-binding galectin family suggests that these proteins could be an attractive target for therapeutic intervention, since their expression is significantly altered in disease. The focus of this review is to summarize current knowledge on the role of galectins in leukocyte trafficking during inflammation and the clinical approaches being taken to target these interactions for treatment of inflammatory disease.

Despite the high incidence of brain injuries in children, we have yet to fully understand the unique vulnerability of a young brain to an injury and key determinants of long-term recovery. Here we consider how early life stress may influence recovery after an early age brain injury. Studies of early life stress alone reveal persistent structural and functional impairments at adulthood. We consider the interacting pathologies imposed by early life stress and subsequent brain injuries during early brain development as well as at adulthood. This review outlines how early life stress primes the immune cells of the brain and periphery to elicit a heightened response to injury. While the focus of this review is on early age traumatic brain injuries, there is also a consideration of preclinical models of neonatal hypoxia and stroke, as each further speaks to the vulnerability of the brain and reinforces those characteristics that are common across each of these injuries. Lastly, we identify a common mechanistic trend; namely, early life stress worsens outcomes independent of its temporal proximity to a brain injury.

Introduction: After ischemic stroke (IS), peripheral leukocytes infiltrate the damaged region and modulate the response to injury. We previously showed that peripheral blood cells display different gene expression profiles after IS and these transcriptional programs reflect the changes in immune processes in response to IS. Dissecting the temporal dynamics of gene expression after IS improves our understanding of the changes of molecular and cellular pathways involved in acute brain injury. Methods: We analyzed the transcriptomic profiles of 33 IS patients in isolated monocytes, neutrophils and whole blood. RNA-sequencing was performed on all the stroke samples as well as 12 controls with vascular risk factors (diabetes and/or hypertension and/or hypercholesterolemia). To identify differentially expressed genes, subjects were split into time points (TPs) from stroke onset (TP1= 0-24 h; TP2= 24-48 h; and TP3= > 48 h), and controls were assigned TP0. A linear regression model including time and the interaction of diagnosis x TP with cutoff of p|1.2| was used. Time dependent changes were analyzed using artificial neural networks to identify clusters of genes that behave in a similar way across TPs. Results: Unique patterns of temporal expression were distinguished for the three sample types. These include genes not expressed in TP0 that peak only within the first 24 h, others that peak or decrease in TP2 and TP3, and more complex patterns. Genes that peak at TP1 in monocytes and neutrophils are related to cell adhesion and leukocyte differentiation/migration, respectively. Early peaks in whole blood occur in genes related to transcriptional regulation. In monocytes, interleukin pathways are enriched across all TPs, whereas there is a trend of suppression after 24 h in neutrophils. The inflammasome pathway is enriched in the earlier TPs in neutrophils, while not enriched in monocytes until over 48 hours. Conclusion: Our analyses on gene expression dynamics and cluster patterns allow identification of key genes and pathways at different time points following ischemic injury that are valuable as IS biomarkers and may be possible treatment targets.

Schwann cell precursors (SCPs) are a transient population in the embryo, closely associated with nerves along which they migrate into the periphery of the body. Long considered to be progenitors that only form Schwann cells—the myelinating cells of nerves, current evidence suggests that SCPs have much broader developmental potential. Indeed, different cell marking techniques employed over the past 20 years have identified multiple novel SCP derivatives throughout the body. It is now clear that SCPs represent a multipotent progenitor population, which also display a level of plasticity in response to injury. Moreover, they originate from multiple origins in the embryo and may reflect several distinct subpopulations in terms of molecular identity and fate. Here we review SCP origins, derivatives and plasticity in development, growth and repair.

Background Musculoskeletal disorders in emergency nurses result in physical, psychological and financial strain. Contributing factors include: environmental, organisational, patient-related, medical emergencies, nurse’s knowledge and health status. Stress and moral distress impact on nurses changing manual handling practices. Methods Part of a cross-sectional survey of Australian emergency nurses, this study used content analysis to identify occurrence of change to practice and enablers to reporting injury. Secondary interpretive analysis using moral distress theory informed an alternative understanding of why nurses may not change their practice in response to injury. Results Most respondents made practice changes and reported pain/injury; 23% did not change, and 45.7% did not report. Respondents considered change impossible due to high demands and lack of resources; a position where nurses may have felt pressured to carry out unsafe manual handling practices. When conflicted between reporting a perceived insignificant injury, with feelings of guilt, nurses can feel devalued. Moral distress can occur when nurses and managers are conflicted between providing care and caring for self. Conclusions A culture of trust, respect and open communication decreases stress/moral distress, enables safer manual handling and reporting of pain/injury. Moral distress is an invisible workplace challenge that needs to be met for staff wellbeing.

Reactive astrocytes are astrocytes undergoing morphological, molecular, and functional remodeling in response to injury, disease, or infection of the CNS. Although this remodeling was first described over a century ago, uncertainties and controversies remain regarding the contribution of reactive astrocytes to CNS diseases, repair, and aging. It is also unclear whether fixed categories of reactive astrocytes exist and, if so, how to identify them. We point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic-vs-neuroprotective or A1-vs-A2. We advocate, instead, that research on reactive astrocytes include assessment of multiple molecular and functional parameters—preferably in vivo—plus multivariate statistics and determination of impact on pathological hallmarks in relevant models. These guidelines may spur the discovery of astrocyte-based biomarkers as well as astrocyte-targeting therapies that abrogate detrimental actions of reactive astrocytes, potentiate their neuro- and glioprotective actions, and restore or augment their homeostatic, modulatory, and defensive functions., Funding: CNRS, CEA, ANR, and France Alzheimer to CE.; MCINN (PID2019-107633RB-I00) and Generalitat de Catalunya (2017-SGR547, Grup de demències Sant Pau) to E.G. US Centers for Disease Control and Prevention to J. P.O. Alzheimer’s Association (AACF-17-524184) and NIH-NIA (K08AG064039) to A.S.-P. DFG (SPP1757, STE 552/5, STE 552/4), EU (H2020-MSCA-ITN project 722053 EU-GliaPhD) and BMBF (16GW0182 CONNEXIN) to C.S. Swiss National Science Foundation grant 31003A 173124/1; SNSF NCCR ‘Transcure’ (51NF40-160620); Synapsis Foundation Heidi Seiler-Stiftung 2018-PI01 to A.Volterra. NIH-NINDS (NS084030), Dr. Miriam and Sheldon G. Adelson Medical Foundation and Wings for Life to M.V.S. The authors thank T. Yohannan of Alpha Language Services, Barcelona, for expert copy editing.

Efficient vascularization of skin tissue supports wound healing in response to injury. This includes elevated blood circulation, tissue oxygenation, and perfusion. Cold physical plasma promotes wound healing in animal models and humans. Physical plasmas are multicomponent systems that generate several physicochemical effectors, such as ions, electrons, reactive oxygen and nitrogen species, and UV radiation. However, the consequences of plasma treatment on wound oxygenation and perfusion, vital processes to promote tissue regeneration, are largely unexplored. We used a novel hyperspectral imaging (HSI) system and a murine dermal full-thickness wound model in combination with kINPen argon plasma jet treatment to address this question. Plasma treatment promoted tissue oxygenation in superficial as well as deep (6 mm) layers of wound tissue. In addition to perfusion changes, we found a wound healing stage-dependent shift of tissue hemoglobin and tissue water index during reactive species-driven wound healing. Contactless, fast monitoring of medical parameters in real-time using HSI revealed a plasma-supporting effect in wound healing together with precise information about biological surface-specific features.

This chapter presents an overview of immunologic aspects of both immediate and delayed hypersensitivity in the skin, and emphasizes delayed contact hypersensitivity reactions, or allergic contact dermatitis (ACD). Dermal hypersensitivity reactions are inflammatory reactions of the skin that either defend the host against pathologic agents or damage host tissue and cause disease. The inflammatory process is a general response to injury and, as such, it is not usually reflective of the various types of dermal hypersensitivity when examined by histopathology alone. Noneczematous dermal lesions can occasionally dominate eczema, especially in sensitized elderly persons who also tend to have more persistent and intractable cases of ACD. UV radiation produces some of the more profound effects on dermal hypersensitivity when compared to other physical agents. The incorporation of monoclonal antibodies into enzyme and fluorescent immunoassays has produced new diagnostic and research tools that are sensitive and specific for molecules involved in dermal hypersensitivity reactions.

Derangement of fibrinolysis has been an interest of surgical scientists for over 200 years. Appreciation of the spectrum of fibrinolysis following severe injury confirms the long-perceived notion that pathology occurs at the extremes of any protease system. Trauma can provoke overactivation of fibrinolysis resulting in uncontrolled bleeding or inhibition resulting in fibrinolysis shutdown resulting in organ dysfunction. While the CRASH II trial demonstrated a modest benefit in survival using antifibrinolytic medication in trauma patients, there are likely superior resuscitation strategies to improve survival in patients with abnormal fibrinolytic activity. This chapter is intended to refresh the reader’s historic appreciation of trauma-induced fibrinolysis and emphasize the physiologic role of the fibrinolytic system in response to injury.

Research into potential targets for cardiac repair encompasses recognition of tissue-resident cells with intrinsic regenerative properties. The adult vertebrate heart is covered by mesothelium, named the epicardium, which becomes active in response to injury and contributes to repair, albeit suboptimally. Motivation to manipulate the epicardium for treatment of myocardial infarction is deeply rooted in its central role in cardiac formation and vasculogenesis during development. Moreover, the epicardium is vital to cardiac muscle regeneration in lower vertebrate and neonatal mammalian-injured hearts. In this review, we discuss our current understanding of the biology of the mammalian epicardium in development and injury. Considering present challenges in the field, we further contemplate prospects for reinstating full embryonic potential in the adult epicardium to facilitate cardiac regeneration.

Complex tissue regeneration is extremely rare among adult mammals. An exception, however, is the superior tissue healing of multiple organs in spiny mice (Acomys). While Acomys species exhibit the remarkable ability to heal complex tissue with minimal scarring, little is known about their cardiac structure and response to cardiac injury. In this study, we first examined baseline Acomys cardiac anatomy and function in comparison with commonly used inbred and outbred laboratory Mus strains (C57BL6 and CFW). While our results demonstrated comparable cardiac anatomy and function between Acomys and Mus, Acomys exhibited a higher percentage of cardiomyocytes displaying distinct characteristics. In response to myocardial infarction, all animals experienced a comparable level of initial cardiac damage. However, Acomys demonstrated superior ischemic tolerance and cytoprotection in response to injury as evidenced by cardiac functional stabilization, higher survival rate, and smaller scar size 50 days after injury compared to the inbred and outbred mouse strains. This phenomenon correlated with enhanced endothelial cell proliferation, increased angiogenesis, and medium vessel maturation in the peri-infarct and infarct regions. Overall, these findings demonstrate augmented myocardial preservation in spiny mice post-MI and establish Acomys as a new adult mammalian model for cardiac research.