How Take Out The Ac Control From Hona Accord 99
Immunol Allergy Clin North Am. Writer manuscript; available in PMC 2012 Feb 1.
Published in final edited course equally:
PMCID: PMC3052954
NIHMSID: NIHMS237922
The Impact of Psychological Stress on Wound Healing: Methods and Mechanisms
Jean-Philippe Gouin
aDepartment of Psychology, The Ohio State University, USA
b Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, USA
Janice Thousand. Kiecolt-Glaser
aDepartment of Psychology, The Ohio State University, U.s.
b Constitute for Behavioral Medicine Enquiry, The Ohio Country University College of Medicine, USA
c Section of Psychiatry, The Ohio State University Higher of Medicine, United states of america
Synopsis
Converging and replicated evidence indicate that psychological stress tin can modulate wound healing processes. This article reviews the methods and findings of experimental models of wound healing. Psychological stress can have a substantial and clinically relevant bear upon on wound repair. Physiological stress responses can direct influence wound healing processes. Furthermore, psychological stress can indirectly modulate the repair procedure by promoting the adoption of health-damaging behaviors. Translational work is needed to develop innovative treatments able to attenuate stress-induced delays in wound healing.
Keywords: wound healing, stress, cytokine, cortisol, psychoneuroimmunology, oxytocin
Wound healing is a critical process involved in the recovery from injury and surgical procedures. Poor healing increases the chance for wound infections or complications, lengthens hospital stays, magnifies patient discomfort, and slows return to activities of daily living. Converging show from different research paradigms suggest that psychological stress and other behavioral factors tin can bear upon wound healing. A meta-analytic report using diverse wound healing models and outcomes institute that beyond studies at that place was an average correlation of −.42 between psychological stress and wound healing [i]. This suggests that the relationship between stress and wound repair is not only statistically significant, but too clinically relevant. This review presents information and methods from observational, experimental, and interventional studies corroborating the impact of stress on wound healing. Potential behavioral and physiological mechanisms explaining the association between stress and impaired wound healing are also discussed.
Observational studies
Prospective studies examining wound healing-related complications following surgery provide prove for the impact of stress on wound repair. Greater fearfulness or distress prior to surgery has been associated with poorer outcomes including longer hospital stays, more postoperative complications, and higher rates of rehospitalization [2,3]. For example, amid 111 patients undergoing gallstone removal surgery, those who reported more than stress on the 3rd postoperative mean solar day had a longer infirmary stay, compared to less anxious individuals[four]. Amid 309 consenting consecutive patients who underwent an elective coronary artery bypass graft surgery, patients who were more optimistic were less likely to be re-hospitalized than less optimistic individuals. Conversely, patients who experienced more depressive symptoms were more likely to require rehospitalization for infection-related complications than individuals reporting less distress [5]. This result was replicated in a written report of 72 patients undergoing coronary artery featherbed surgery. Patient who had more depressive symptoms at discharge had more infections and poorer wound healing in the following 6 weeks after surgery, compared to participants who reported less distress [6].
Psychological factors can likewise modulate healing of chronic wounds. L-3 older adults with chronic lower leg wounds were followed longitudinally to assess speed of wound repair. Patients who experienced the highest levels of depression and anxiety (based on a median carve up of the Hospital Anxiety and Low Scale) were 4 times more likely to be categorized in the delayed healing group, compared to individuals who reported less distress [vii]. Importantly, in these observational studies, distress predicted wound healing outcomes over and above differences in sociodemographic variables and medical status. Psychological distress thus appears to influence recovery from medical procedures and healing of chronic wounds in clinical settings.
Experimental studies
Brute and human studies in which standard wounds are created experimentally and healing is closely monitored over time provide the strongest evidence of the impact of stress on wound repair. Three main wounding methodologies have been used to written report the effect of stress on wound healing.
Dial biopsy model
Punch biopsies are used to create standard full-thickness dermal wounds every bit well as mucosal wounds. Daily pictures of the wound permit for a quantification of changes in wound size over time.
The get-go human experimental report examining the impact of stress on wound healing involved family dementia caregivers. Caregivers take to bargain daily with the loss of retentiveness, inappropriate emotions, and wandering and restless behavior of their loved ones. Caregiving stress has been associated with heightened anxiety and depression, allowed dysregulation, increased risk for cardiovascular disorders, and even death [viii]. Family dementia caregiving thus represents an excellent model of chronic stress in humans. A 3.5 mm punch biopsy wound was created on the nondominant forearm of 13 women caregivers and 13 sociodemographically-similar noncaregiving controls. Caregivers took 24% longer to heal the small, standardized dermal wound than matched controls, providing initial bear witness that chronic stress tin delay wound repair [ix].
Stress tin can also impede healing of a punch biopsy wound amongst younger people who experienced less intense stress. Twenty-four healthy young men were followed for 21 days after a standard iv mm punch biopsy was performed on their forearm. In that study, wound healing was assessed using ultrasound biomicroscopy. Stress levels were measured using a cocky-report questionnaire, the Perceived Stress Scale. College perceived stress on the mean solar day of the biopsy was associated with slower wound healing [10]. A substantial correlation of −.59 was found betwixt perceived stress and healing progress betwixt the days 7 and 21 subsequently the biopsy [x].
Pain, a physical and psychological stressor, can besides influence wound healing. A 2 mm full thickness wound was placed on the back of one upper arm of obese women prior to receiving elective gastric featherbed surgery. Greater astute hurting immediately after surgery and persistent pain in the four weeks following surgery were associated with slower healing of the experimental wound [11]. Pain generates psychological distress, and, when compounded by the presence of other stressors, can put a person at increased risk for delayed wound repair [12].
Well-controlled animal studies corroborate the impact of stress on wound healing observed in humans. Mice subjected to restraint stress healed a standardized 3.five mm total-thickness punch biopsy wound on average of 27% more slowly than control mice who were non exposed to the stressor [13]. Restraint stress was likewise associated with delayed wound healing in a reptilian species, the Urosaurus ornatus (tree lizard) [14]. Social stressors can also impair wound healing. Monogamous California mice, Peromyscus californicus, healed a punch biopsy wound more than slowly when stressed by the separation from their conspecifics, compared to when they were continuously housed with their conspecifics [15].
Like cutaneous wounds, mucosal wound healing is also responsive to psychological stress, every bit demonstrated by a written report with academic examination stress. Using a within-bailiwick design, 11 dental students had a biopsy performed on their hard palate during their summer vacation and again 3 days before a major exam. Mucosal wounds placed before the examination healed on boilerplate 40% more slowly than identical wounds fabricated during summer vacation. Importantly, the differences in the rate of healing were very consistent: no student healed as rapidly during examinations as during vacation [16].
The impact of negative emotions on mucosal wound healing was replicated in a larger study. Among 193 good for you undergraduate students who received a three.5 mm wound on the hard palate, individuals reporting high levels of depressive symptoms were almost 3.6 times more likely to be classified as slow healers, compared to less dysphoric students [17].
Blister wounds model
The blister wounds model is another experimental paradigm to study the impact of psychological factors on wound healing. Blisters wounds are produced by the application of a vacuum pump on the forearm. A gentle suction creates a separation of the epidermis from the dermis over the course of one hour. One of the strengths of this method is that it allows for the drove of data on cytokine product at the wound site, as described below. In this model, wound healing is assessed via measurement of the rate of transepidermal water loss (TEWL). One of the chief functions of the peel is to limit movement of water in and out of the trunk. The permeability of the epidermis increases after the blister wound, but decreases as healing process unfolds. A computerized evaporimetry musical instrument tin can measure vapor force per unit area slope in the air layers shut to the pare surface. TEWL measurement is a noninvasive method to monitor changes in the stratum corneum barrier function of the skin that provides an splendid objective method for evaluation of wound healing.
Using a cicatrice wounds paradigm, the give-and-take of a marital disagreement, a commonplace stressor, delayed wound repair. Married couples were invited for two 24-hour admissions at a hospital research unit. During both visits, eight eight mm suction blisters were created on the participants' nondominant forearm. Wound healing was monitored for 14 days using TEWL measurements. During the first admission, couples participated in a structured social support interaction task. During the second visit, couples were asked to discuss marital disagreements during a 30-minute period. Later both interaction tasks, couples remained in the enquiry unit of measurement until the next morn to allow for cytokine measurements and to minimize external influences on wound healing [18].
Couples' blister wounds healed more slowly following the marital disharmonize visit than after the social support visit, suggesting that the stress induced by the discussion of marital disagreements interfered with wound repair. Furthermore, the quality of the word also influenced the rate of healing. Couples who had more hostile and negative interactions beyond both the support and the conflict discussions healed wounds more slowly than couples whose interactions were less negative. The overall differences related to hostility were substantial. The blister wounds in high hostile couples healed at merely threescore% of the rate of low hostile couples [18].
In a different subset of participants from the same report, positive behaviors during the social support chore were too related to wound repair. Individuals who displayed more than cocky-disclosure, acceptance of their partner, relationship-enhancing statements, and sense of humor during the interaction task healed the blister wounds faster than participants who exhibited less positive behaviors during the marital interaction task [19].
Difficulties in managing i's anger has besides been associated with impaired wound healing. Blister wounds were created on the forearm of 98 community-dwelling participants who were followed for 14 days to monitor healing speed. Anger management styles were assessed via a self-written report questionnaire, the Spielberger Acrimony Expression Scale. Participants who had difficulty controlling the expression of their acrimony were iv.ii times more likely to be classified as slow healers than individuals who reported better anger control. Furthermore, individuals with anger management problems secreted more than cortisol in response to the blistering process. The increased glucocorticoid product was in turn related to delayed healing [20].
Tape stripping to disrupt skin barrier role
Another wound healing model consists of the repeated awarding of cellophane record to remove a layer of epidermis cells, causing a disruption of the stratum corneum barrier role of the skin. This procedure impacts epidermal permeability. Wound healing is assessed by measuring the charge per unit of recovery of the skin bulwark function using TEWL measurements.
Acute laboratory stressors can delay the recovery of peel barrier function post-obit its disruption by tape stripping. Xx-five women participated in the Trier Social Stress Test (TSST), a psychosical stressor [21]. The TSST, a standardized laboratory stressor with a mock job interview and a mental arithmetic job, induces reliable changes in centre rate, cortisol and cytokine production, and subjective anxiety responses [22,23]. Pare bulwark repair was delayed in women after the TSST, compared to a stress-free menstruation [21].
This result was replicated in a larger study of 85 healthy young men and women. Individuals who participated in the TSST had a slower recovery of skin barrier function than participants who engaged in a reading control task [24]. Furthermore, positive affect had a protective consequence on stress-induced delays in peel barrier recovery. Stressed individuals reporting more positive affect recovered faster from the tape stripping procedure than stressed participants who had low trait positive affect [25].
Academic exam stress impacts skin barrier recovery. Twenty-7 professional person and medical students underwent a tape stripping procedure at 3 occasions: right after their wintertime and spring vacations, and during their wintertime final examination calendar week. Skin barrier recovery was significantly delayed at three, vi, and 24 hours after record stripping during the exam menstruation, compared to the two holiday periods. Furthermore, students reporting the near stress during the examination period had slower recovery in peel barrier role, compared to participants who experienced less exam-induced stress [26].
The interpersonal stress associated with the dissolution of a committed marital human relationship can impede recovery of the stratum corneum barrier function of the peel. Twenty-eight women who were going through a divorce or a separation and 27 women who reported loftier levels of marital satisfaction underwent a tape stripping procedure on both facial cheeks. Socially stressed women had delayed peel barrier recovery at 3 and 24 hours following the tape stripping procedure, compared to less stressed women [27].
In animal models, different types of stressors can besides impair skin bulwark recovery. Three days of immobilization stress delayed skin barrier function recovery even for 7 days, compared to control rats not exposed to the stressor [28]. Social reorganization stress associated with cage transfer as well dumb the restoration of skin bulwark function in rats [29]. These results converge with human information indicating that psychological stress can disrupt skin barrier recovery.
Intervention studies
Intervention studies that improve healing outcomes by reducing psychological stress provide farther evidence of the touch of psychological and behavioral factors in wound repair. Meta-analyses of clinical studies show that behavioral stress management interventions earlier surgery have been associated with improved post-operative outcomes, including fewer medical complications and shorter hospital stays [xxx,31].
Written emotional disclosure interventions tin decrease psychological distress, ameliorate self-reported health, enhance aspects of cellular immunity, and decrease health care utilization [32]. Men were randomized to a written emotional disclosure intervention or a non-intervention command group, and received a punch biopsy on the nondominant forearm. Healing was assessed using ultrasound biomicropsy at iii occasions during a 21-twenty-four hours period. Men who participated in the emotional disclosure intervention had smaller wounds at 14 and 21 days, compared to control participants [33].
Physical exercise can reduce psychological distress in addition to improving cardiovascular function [34]. Older adults were randomized to an exercise intervention (one-hr aerobic practise session, three times per calendar week) or a not-intervention command grouping. One calendar month after the beginning of the intervention, participants received a iii.5 mm punch biopsy on the back of their nondominant upper arm. Older adults who exercised healed their wounds faster than those in the control group [35]. In accord with these human data, older mice randomized to a 30-infinitesimal daily exercise period during 8 days healed a punch biopsy wound faster than sedentary command mice [36].
Social support is associated with better wellness outcomes [37]. In fauna studies, monogamous rodents who were housed in pairs healed a standard punch biopsy wound faster than rodents housed alone [38]. Pair housing as well buffered the affect of restraint stress on wound healing. Immobilization stress dumb cutaneous wound healing in Siberian hamsters housed alone, but not in hamsters housed in pairs [39]. These data betoken that the presence of a familial conspecific improves wound healing outcomes in monogamous rodents.
A pharmacological agent commonly used in the treatment of mood and anxiety disorders, fluoxetine [40]. In a study using alternating isolation and crowding stress, stressed Wistar rats who received fluoxetine healed at a similar pace as their non-stress counterparts, and faster than stressed animals who received simply a vehicle injection [41]. These results indicate that pharmacological stress reduction may also amend wound healing.
In summary, a wide array of astute and chronic stressors tin can disrupt the healing process. Furthermore, the impact of stress on wound repair has been observed across different methodologies and with different healing outcomes and nearly results have replicated in at least two independent laboratories. Collectively, results from observation, experimental, and intervention studies provide potent evidence that psychological stress can influence wound healing.
Biology of wound healing
A brief review of the biology of wound healing is presented to highlight the pathways by which psychological stress can impede the repair procedure. Wound healing progresses through several overlapping stages [42]. In the initial inflammatory stage, vasoconstriction and blood coagulation are followed by platelet activation and the release of platelet-derived growth factors (PDGFs) as well as chemoattractant factors released by injured parenchymal cells. Cytokines and chemokines, such as IL-1α, IL-1β, transforming growth factor-β (TGF-β), vascular endothelial growth cistron (VEGF), tumor necrosis cistron alpha (TNF-α), and IL-8 play important roles in the early on phase of wound healing. These factors human activity equally chemoattractants for the migration of phagocytes and other cells to the site, starting the proliferative phase which involves the recruitment and replication of cells necessary for tissue regeneration and capillary regrowth. The final step, wound remodeling, may go along for weeks or months. Thus, the healing procedure is a cascade, and success in the later stages of wound repair is highly dependent on initial events [43].
Inflammation plays a central role early in this cascade, and proinflammatory cytokines are essential to this endeavor; they aid to protect confronting infection and gear up injured tissue for repair by enhancing the recruitment and activation of phagocytes [44]. Furthermore, cytokines released by recruited cells regulate the ability of fibroblasts and epithelial cells to remodel the damaged tissue [44]. IL-1 produced early later tissue injury can regulate the production, release, and activation of metalloproteinases that are important in the destruction and remodeling of the wound; IL-1 also regulates fibroblast chemotaxis and the production of collagen [44]. Moreover, IL-1 stimulates the product of other cytokines that are important for wound healing, including IL-2, IL-6, and IL-8 [44]. Confirming the importance of proinflammatory cytokines in the healing process, IL-6 knock-out mice healed a standard wound 3 times more slowly than wild-type mice [45]. Accordingly, deficits early in the wound repair cascade tin have agin downstream consequences.
Physiological pathways of the stress-induced wound healing impairment
Psychological stress leads to the activation of the hypothalamic-pituitary-adrenal and the sympathetic-adrenal-medullary axes [46]. Enhanced glucocorticoids and catecholamines production tin direct influence several components of the healing process. Substantial show from animate being and humans studies betoken that physiological stress responses can retard the initial inflammatory phase of wound healing [47]. Figure 1 presents a schematic representation of the behavioral and physiological pathways linking stress and wound healing.
Behavioral and physiological pathways linking psychological stress and wound healing.
Glucocorticoids
Stress-induced glucocorticoid product has been associated with delayed wound healing. In humans, greater awakening cortisol secretion the day following a punch biopsy was associated with greater perceived stress and delayed wound healing [x]. In animal studies, restraint stress led to a 4-fold elevation in corticosterone levels [thirteen]. Blocking glucocorticoid function with a glucocorticoid receptor antagonist, RU40555, eliminated the stress-induced delay in wound healing in stressed animals [13,39]. Preventing glucocorticoid product via adrenalectomy also reduced the effects of restraint stress on wound healing [39]. Furthermore, exogenous administration of glucocorticoid slowed wound healing, compared to a vehicle injection [13].
Catecholamines
Increased catecholamine production likewise appears to play a office in stress-induced impairment in wound healing. Administration of an α-adrenergic receptor adversary adulterate the restraint stress-induced harm of wound healing in mice [48]. In a study using a rotation stress model, administration of a β-adrenergic receptor adversary, propanolol hydrochloride, attenuated the stress-induced impairment in wound healing in mice [49]. In a burn wound model, mice injected with a β-adrenergic receptor antagonist exhibited improved re-epitheliazation of burn down wounds, compared to mice who received a vehicle injection [50]. Furthermore, injection of norepinephrenine can reduce keratinocyte motility and migration in vitro [fifty]. These data provide evidence of a role for catecholamines in stress-induced impairment in wound repair.
Oxytocin and Vasopressin
The two hypothalamic peptides, oxytocin and vasopressin, modulated physiological stress responses and social bonding processes in animal and man work. In a couples study using the blister wounds model, individuals who had more positive interactions with their partner during a social back up task had higher plasma oxytocin levels. College circulating oxytocin levels were in turn associated with faster healing of the standard cicatrice wounds. Furthermore, in women, merely non in men, greater plasma vasopressin levels were related to faster healing [nineteen].
Well-controlled animal studies approve the office of oxytocin in mediating the beneficial effects of social relationships on wound healing. Exogenous oxytocin administration adulterate the stress-induced corticosterone production and impairment in wound healing [39,51]. Furthermore, assistants of an oxytocin receptor antagonist eliminated the beneficial bear on of pair housing on wound healing [39]. Collectively, these results suggest that in addition to modulating stress responses, oxytocin may have a directly influence on the healing process.
Local Cytokine Production
Diminished expression of proinflammatory cytokines at the wound site is another pathway by which stress can delay the initial stage of wound healing. The suction blister model provides a method to monitor in vivo cytokine expression at the wound site in humans. After raising several blisters and removing their roofs (the epidermis), plastic templates with wells containing a salt solution and autologous serum are placed over the lesions to monitor poly peptide expression at the wound site. The autologous serum-buffer solution is aspirated from the wells with a syringe at different time intervals, allowing for jail cell phenotyping and cytokine measurement equally the local immune response evolves.
Using this arroyo, women who reported more perceived stress produced significantly lower IL-1α and IL-8 levels at the wound site, five and 24 hours subsequently the baking procedure [52]. Marital disagreement also influenced local cytokine production [18]. Product of 3 proinflammatory cytokines at the wound site, IL-1β, IL-6, and TNF-α, were lower after the discussion of a marital disagreement than after a social support discussion, paralleling the impact of marital conflict on wound healing [18]. In these two studies, local cytokine product was not significantly associated with serum levels of the same cytokines, underscoring the different biological significance of local and systemic product of these molecules.
In a clinical written report, patients undergoing an hernia removal surgery who reported greater preoperative stress had a lower concentration of IL-1β in the wound drain fluid, 20 hours after the operation, compared to patients who experienced less preoperative distress [53]. Furthermore, two stressors that can impair cutaneous and mucosal wound healing, family dementia caregiving and academic examinations, were also associated with poorer stimulated product of IL-1β after treatment with lipopolysaccharide [9,16]. Corroborating human data, mice subjected to restraint stress had lower levels of IL-β mRNA at the wound site, compared to control mice [54,55].
Stress-induced glucocorticoid production might effectively decrease cytokine product at the wound site. Exogenous assistants of glucocorticoid diminished IL-1α, IL-1β, and TNF-α expression at the site after wounding in mice [42]. Similarly, animate being and human being studies accept also demonstrated that stress-induced elevations in glucocorticoids can transiently suppress IL-1β, TNF-α, and PDGF product [52,55] . Accordingly, dysregulation of glucocorticoid secretion provides one obvious neuroendocrine pathway through which stress alters the initial inflammatory stage of wound healing.
Matrix Metalloproteinase
Matrix metalloproteinase (MMP) enzymes are involved in the deposition of collagen and other extracellular matrix molecules. Deposition of the basement membrane of the wound promotes cellular invasion and migration, an essential component of the early phase of wound healing. Among patients undergoing inguinal hernia surgery, those who reported greater worry about the operation had lower levels of MMP-9 in the wound drain fluid xx hours afterwards the surgery [53]. In a human report using the blister wounds model, at that place was a negative correlation between plasma cortisol levels and MMP-2 poly peptide levels at the wound site [56]. Furthermore, in an animal written report using a rotation stress model, mice subjected to the stressor had fewer activated MMP-ii and MMP-9 seven days after wounding, compared to control mice [49]. These information signal that stress can down-regulate MMP production at the wound site.
Wound cellularity
Psychological stress may reduce cell infiltration at the wound site. In a study using a restraint stress paradigm, cellularity of the wound and wound margin areas were analyzed in cross-sections of dermal and epidermal layers. Mice subjected to restraint stress had less leukocyte infiltration to the wound sites at ane and iii days after wounding, compared to command mice [13].
Increased susceptibility to infection
Stress can also increase susceptibility to wound infection. Mice exposed to restraint stress had a ii-5 log increment in opportunistic bacteria such as Staphylococcus aureus, compared to control mice not exposed to the stressor. Furthermore, seven days after wounding, 85.iv% of restraint-stress mice had bacterial counts predictive of infection, vs. 27.4 of controls [57].
The increased susceptibility to infection appears to be mediated in part by a decreased epidermal antimicrobial peptides production. Mice exposed to indisposition and crowding stress had lower epidermis levels of cathelin-related antimicrobial peptides and exhibited more severe infection following an intradermal injection of grouping A Streptococcus pyogenes [58]. This effect appears to be glucocorticoid dependent; assistants of a glucocorticoid receptor antagonist, eliminated the impact of stress on epidermis antimicrobial peptide production and administration of exogenous glucocorticoid mimicked the effects of stress on antimicrobial production [58].
Wound hypoxia
Oxygen homeostasis is critical to all phases of wound healing. Damage created to blood vessels during wounding decreases oxygen availability. Simultaneously, neutrophils' oxidative burst increases oxygen demand at the wound site. Restraint stress can farther promote wound hypoxia [59]. Compared to controls, restraint stressed mice had higher levels of inducible nitric oxide synthase levels, an indicator of wound hypoxia at the wound site [59]. Furthermore, hyperbaric oxygen therapy normalized inducible nitric oxide synthase levels and attenuated stress-induced impairments in wound healing [59].
Behavioral mechanisms linking stress and wound healing
In addition to directly modulating physiological responses to skin harm, stress can also indirectly influence wound repair by promoting the adoption of health-dissentious behaviors. Individuals who experience greater levels of stress are more likely to increase their alcohol and tobacco utilize, decrease their participation in concrete action, experience sleep disturbances, and make poorer diet choices, compared to individuals reporting less distress [sixty,61]. These negative health behavior practices tin then chemical compound the detrimental impact of stress on physiological healing processes [2].
Heavy alcohol apply has been associated with delays in prison cell migration and collagen deposition at the wound site, which in turn can impede the healing process [62]. Smoking has also been related to slowed healing of naturally occurring and surgery wounds [63]. Slumber disruption delays skin barrier recovery after record stripping and diminishes growth hormone production [21,64]. Lack of regular physical action can slow wound healing rate [36]. Furthermore, deficient intake of glucose, polyunsaturated, proteins, and certain vitamins can impede the healing process [65-67].
Conclusion
The goal of this review was to present clinical and experimental models of the bear on of stress on wound repair. Converging and replicated evidence from experimental and clinical models of wound healing indicate that psychological stress leads to clinically relevant delays in wound healing. New mechanistic information suggest ways to elucidate the multiple physiological pathways by which stress alters wound repair processes. Translational work should focus on identifying weather in which behavioral and pharmacological treatments are the about effective and on developing new treatments able to attenuate stress-induced delays in wound healing.
Acknowledgments
Work on this chapter was supported past a doctoral research training award from the Fonds de la Recherche en Santé du Québec and NIH grants AG029562, CA126857, CA131029, AT003912, Ohio State Comprehensive Cancer Center Cadre Grant CA16058, and NCRR Grant UL1RR025755.
Footnotes
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