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1.  A Phosphorus Burn 
Eplasty  2015;15:ic15.
PMCID: PMC4364261  PMID: 25834695
phosphorus; burn; injury; management; grenade
2.  Cement Burn 
Eplasty  2015;15:ic13.
PMCID: PMC4347359  PMID: 25848446
cement; burn; alkaline; chemical injury; treatment
3.  “Under Pressure”, Hair Braids in the Critically Ill 
Eplasty  2014;14:ic36.
PMCID: PMC4182963  PMID: 25328581
pressure sore; hair braids; hair weave; burn; critically ill
4.  Painful Finger 
Eplasty  2014;14:ic32.
PMCID: PMC4164618  PMID: 25328577
pain; nerve; neuroma; burn; amputation
5.  Pulmonary Injury Secondary to Feeding Tube Misplacement 
Eplasty  2014;14:ic24.
PMCID: PMC4128277  PMID: 25210575
CO2 monitoring; pulmonary injury; pneumothorax; intensive care; feeding tube
6.  Making Contact 
Eplasty  2014;14:ic13.
PMCID: PMC4034567  PMID: 24917898
electrical burn; high-voltage; hand; fasciotomy; burn
7.  Toxic Epidermal Necrolysis 
Eplasty  2014;14:ic6.
PMCID: PMC3962031  PMID: 24741389
toxic epidermal necrolysis; Lyell's syndrome; stevens-johnson syndrome; TEN; drug reaction
8.  A Fungal Burn Infection 
Eplasty  2014;14:ic5.
PMCID: PMC3938088  PMID: 24741388
Aspergillus; burn; fungus; mold; pulse lavage
9.  Tracheostomy Complication in a Burn Patient 
Eplasty  2014;14:ic1.
PMCID: PMC3889687  PMID: 24501621
tracheocutaneous fistula; persistent tracheostomy stoma; airway; trachea; burn
12.  Urban Blisters 
Eplasty  2013;13:ic37.
PMCID: PMC3601455  PMID: 23573343
14.  Pigmented Urine 
Eplasty  2013;13:ic16.
PMCID: PMC3558850  PMID: 23409207
16.  Hypoxia and Hypoxia-Inducible Factor in the Burn Wound 
The importance of hypoxia-inducible factor (HIF) in promoting angiogenesis and vasculogenesis during wound healing has been demonstrated. It is widely accepted that HIF activity can be promoted by many factors, including hypoxia in the wound or cytokines from inflammatory cells infiltrating the wound. However, there has not been a systematic exploration of the relationship between HIF activity and hypoxia in the burn wound. The location of the hypoxic tissue has not been clearly delineated. The time course of the appearance of hypoxia and the increased activity of HIF and appearance of HIF’s downstream transcription products has not been described. The aim of this study was to utilize pimonidazole, a specific tissue hypoxia marker, to characterize the spatial and temporal course of hypoxia in a murine burn model and correlate this with the appearance of HIF-1α and its important angiogenic and vasculogenic transcription products VEGF and SDF-1. Hypoxia was found in the healing margin of burn wounds beginning at 48 hours after burn and peaking at day 3 after burn. On sequential sections of the same tissue block, positive staining of HIF-1α, SDF-1, and VEGF all occurred at the leading margin of the healing area and peaked at day 3, as did hypoxia. Immunohistochemical analysis was used to explore the characteristics of the hypoxic region of the wound. The localization of hypoxia was found to be related to cell growth and migration, but not to proliferation or inflammatory infiltration.
PMCID: PMC3075089  PMID: 21362088
ypoxia; Hypoxia-inducible factor -10α; Burn; Wound Healing; Ki67 Cell Proliferation; Keratin17
17.  Chemical Burn to the Eyes 
Eplasty  2011;11:ic16.
PMCID: PMC3230139  PMID: 22148080
18.  A Shot in the Face 
Eplasty  2011;11:ic13.
PMCID: PMC3230138  PMID: 22148079
19.  Alterations in Content and Localization of Defensins in Rat Ileum and Jejunum Following Ischemia-Reperfusion. Specific Peptides, in Specific Places, for Specific Jobs? 
Eplasty  2011;11:e8.
Objective: To determine alterations in quantities and distributions of natural antimicrobials following ischemia-reperfusion injury. We hypothesized that these compounds would be upregulated in areas of small intestine where changes in permeability and cellular disruption were likely and where protective mechanisms would be initiated. Methods: Rats with ischemia-reperfusion underwent superior mesenteric artery clamping and reperfusion. Shams were subjected to laparotomy but no clamping. Ileum and jejunum were harvested and sectioned, and subjected to fluorescence deconvolution microscopy for determinations of content and localization of rat beta defensins, 1, 2, 3; rat neutrophil protein-1; and cathelicidin LL-37. Modeling was performed to determine cellular location of antimicrobials. Results: Ischemia-reperfusion increased neutrophil defensin alpha (RNP-1) in jejunum; rat beta defensin 1 was increased 2-fold in ileal mucosa and slightly reduced in jejunal mucosa; rat beta defensin 2 was reduced by ischemia-reperfusion in ileum, but slightly increased in jejunum; rat beta defensin 3 was concentrated in the muscularis externa and myenteric plexus of the jejunum; ischemia-reperfusion did not alter cathelicidin LL-37 content in the small intestine, although a greater concentration was seen in jejunum compared with ileum. Conclusion: Ischemia-reperfusion injury caused changes in antimicrobial content in defined areas, and these different regulations might reflect the specific roles of jejunum versus ileum.
PMCID: PMC3044598  PMID: 21369366
20.  Upregulation of Defensins in Burn Sheep Small Intestine 
Eplasty  2009;10:e6.
Objective: The aim of this study was to visualize and localize the sheep antimicrobials, β-defensins 1, 2, and 3, (SBD-1, SBD-2, SBD-3), sheep neutrophil defensin alpha (SNP-1), and the cathelicidin LL-37 in sheep small intestine after burn injury, our hypothesis being that these compounds would be upregulated in an effort to overcome a compromised endothelial lining. Response to burn injury includes the release of proinflammatory cytokines and systemic immune suppression that, if untreated, can progress to multiple organ failure and death, so protective mechanisms have to be initiated and implemented. Methods: Tissue sections were probed with antibodies to the antimicrobials and then visualized with fluorescently labeled secondary antibodies and subjected to fluorescence deconvolution microscopy and image reconstruction. Results: In both the sham and burn samples, all the aforementioned antimicrobials were seen in each of the layers of small intestine, the highest concentration being localized to the epithelium. SBD-2, SBD-3, and SNP-1 were upregulated in both enterocytes and Paneth cells, while SNP-1 and LL-37 showed increases in both the inner circular and outer longitudinal muscle layers of the muscularis externa following burn injury. Each of the defensins, except SBD-1, was also seen in between the muscle layers of the externa and while burn caused slight increases of SBD-2, SBD-3, and SNP-1 in this location, LL-37 content was significantly decreased. Conclusion: That while each of these human antimicrobials is present in multiple layers of sheep small intestine, SBD-2, SBD-3, SNP-1, and LL-37 are upregulated in the specific layers of the small intestine.
PMCID: PMC2803769  PMID: 20076788
21.  Nuclear Localization of HBD-1 in Human Keratinocytes 
Objective: Human defensins and cathelicidins are a family of cationic antimicrobial peptides (AMPs), which play multiple roles in both innate and adaptive immune systems. They have direct antimicrobial activity against several microorganisms including burn pathogens. The majority of components of innate and adaptive immunity either express naturally occurring defensins or are otherwise chemoattracted or functionally affected by them. They also enhance adaptive immunity and wound healing and alter antibody production. All mechanisms to explain multiple functions of AMPs are not clearly understood. Prior studies to localize defensins in normal and burned skin using deconvolution fluorescence scanning microscopy indicate localization of defensins in the nucleus, perinuclear regions, and cytoplasm. The objective of this study is to further confirm the identification of HBD-1 in the nucleus by deconvolution microscopic studies involving image reconstruction and wire frame modeling. Results: Our study demonstrated the presence of intranuclear HBD-1 in keratinocytes throughout the stratum spinosum by costaining with the nuclear probe DAPI. In addition, HBD-1 sequence does show some homology with known cationic nuclear localization signal sequences. Conclusion: To our knowledge, this is the first report to localize HBD-1 in the nuclear region, suggesting a role for this peptide in gene expression and providing new data that may help determine mechanisms of defensin functions.
PMCID: PMC2064969  PMID: 18091980
22.  Liver Disease in Burn Injury 
Objective: To assess mortality risk and extent of increased length of hospital stay in patients with burn injury with preexisting liver disease. Methods: Records of 31,338 adults who were admitted with burns to 70 burn centers were reviewed from the American Burn Association National Burn Repository. Demographics, percentage burn, and medical characteristics of 180 patients with liver disease were compared with all patients without liver disease and to a propensity score–matched sample of 180 patients without liver disease. Risk of mortality as well as lengths of both intensive care and total stay were compared after matching for demographics, burn injury, and preexisting medical conditions. Results: Patients with liver disease were significantly more likely to have a history of a number of medical comorbidities, including alcohol abuse, drug abuse, a psychiatric diagnosis, chronic pulmonary disease, hypertension, and diabetes. Patients with liver disease were significantly more likely to die in the hospital (27.2% vs 6.9%, odds ratio = 5.0, 95% confidence interval = 3.6–7.0, P < .01), and this held even when compared with a propensity score–matched group of patients without liver disease, but with similar demographics, burn injury, and medical profiles. Lengths of both intensive care and total hospital stay were 122.5% (P < .01) and 86.7% (P < .01) longer, respectively, among patients with liver disease than among all other patients. In a matched sample, lengths of both intensive care and total stays were longer, albeit not significantly so (41.6%, P = .12; 35.5%, P = .07). Conclusions: Liver impairment worsens the prognosis in patients with thermal injury.
PMCID: PMC1892842  PMID: 17625613
23.  Editorial 
PMCID: PMC2255572  PMID: 17091132
24.  Modulation of the Complement System by Human β-Defensin 2 
Objective: Human β-defensin (HBD) and the complement system are two important innate immune mechanisms active against a broad range of burn and wound pathogens. However, excessive or uncontrolled complement activation, following thermal injury, contributes to tissue damage. Previous studies from our laboratory suggested a decreased expression of HBD-2 in burn wounds and its absence in burn blister fluid. Prior studies have demonstrated that human neutrophil peptide can bind to the C1q component of the complement system and prevent complement activation. The objective of this study was to determine whether HBD-1 and HBD-2 can also bind to the C1q component and modulate complement activity. Methods: The binding efficiency of HBD-1 and HBD-2 to the C1q component was determined by utilizing dot blot hybridization. The effect of HBD-2 on the activation of the complement system by the classical and alternative pathways was determined by CH50 and AP50 assays. In addition, the ability of HBD-1 and HBD-2 to inhibit C1q activity was predicted by a comparison with known C1q inhibitor peptide 2J in a DNAStar computer modeling study. Results: C1q binding to HBD-2 was strong, whereas C1q binding to HBD-1 was weak. HBD-2 inhibits the classical pathway significantly without affecting the alternative pathway. In addition, a computer modeling study also revealed structural homology of HBD-2 with known C1q inhibitory sequences of HBD-2. Conclusion: HBD-2 inhibits the classical pathway. The replacement of missing defensin, a natural inhibitor of the complement system, may have a dual protective role not only as an antimicrobial agent but also in providing protection against uncontrolled activation of the complement system.
PMCID: PMC1769518  PMID: 17235375
25.  Wound Healing of Cutaneous Sulfur Mustard Injuries 
Sulfur mustard is an alkylating chemical warfare agent that primarily affects the eyes, skin, and airways. Sulfur mustard injuries can take several months to heal, necessitate lengthy hospitalizations, and result in significant cosmetic and/or functional deficits. Historically, blister aspiration and/or deroofing (epidermal removal), physical debridement, irrigation, topical antibiotics, and sterile dressings have been the main courses of action in the medical management of cutaneous sulfur mustard injuries. Current treatment strategy consists of symptomatic management and is designed to relieve symptoms, prevent infections, and promote healing. There are currently no standardized or optimized methods of casualty management that prevent or minimize deficits and provide for speedy wound healing. Several laboratories are actively searching for improved therapies for cutaneous vesicant injury, with the aim of returning damaged skin to optimal appearance and normal function in the shortest time. Improved treatment will result in a better cosmetic and functional outcome for the patient, and will enable the casualty to return to normal activities sooner. This editorial gives brief overviews of sulfur mustard use, its toxicity, concepts for medical countermeasures, current treatments, and strategies for the development of improved therapies.
PMCID: PMC1501116  PMID: 16921406

Results 1-25 (25)