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1 odels including mouse deep partial-thickness burn wounds.
2 in both murine full-thickness excisional and burn wounds.
3  strategy to improve clinical care of severe burn wounds.
4 eadily formed biofilms within full-thickness burn wounds.
5  this study focused on shock wave effects in burn wounds.
6 zation and skin regeneration in third-degree burn wounds.
7 re them to combat infections in contaminated burn wounds.
8 t microbial organisms isolated from infected burn wounds.
9  pathogenesis of P. aeruginosa infections in burn wounds.
10 nt role of the soxR gene in the infection of burn wounds.
11 activity in wound fluid obtained from acute (burn) wounds.
12 nist accelerates re-epithelialization in pig burn wounds (100% re-epithelialization in antagonist-tre
13 e treatment to the superficial second-degree burn wound after debridement/topical antiseptic therapy
14  shown the abilities to prevent infection of burn wound, aid healing, and an anti-inflammatory dressi
15 luate cutaneous microbial populations on the burn wound and corresponding spared skin on days 0, 3, 7
16 s study, we utilize a panel of P. aeruginosa burn wound and cystic fibrosis (CF) lung isolates to dem
17 mited bacterial growth and spread within the burn wounds and a decrease in systemic dissemination of
18 ximize therapeutic success for patients with burn wounds and chronic wound disorders.
19 ctions of full thickness murine third-degree burn wounds and rescued mice from lethal Pseudomonas aer
20 dels, including the surgical wound, abscess, burn wound, and acute pneumonia models.
21 appeared in the dermis of skin bordering the burn wound, and further increased in response to wound i
22 slands of regenerating epithelium within the burn wound, and in the duct and proximal tubules of eccr
23 uscitation, respiratory support, care of the burn wound, and long range evacuation.
24 iety of diseases, including cystic fibrosis, burn wounds, and chronic suppurative otitis media.
25 maintain tissue perfusion, early excision of burn wounds, and rapid wound coverage.
26                                              Burn wounds are prone to infection by Pseudomonas aerugi
27  efficiently on burn wounds, suggesting that burn wounds are purine-deficient environments.
28  mouse and human skin samples identified the burn wound as a primary source of G-CSF and IL-6 secreti
29 en-activated protein kinase inhibitor to the burn wound attenuated pulmonary neutrophil infiltration
30 opolymers, can facilitate closure of massive burn wounds by increasing the availability of autologous
31 guidelines along with the standardization of burn wound care and continued provider education have re
32 g represents a breakthrough in second-degree burn wound care.
33 = 0.011) reduction in alpha diversity on the burn wound compared to spared skin throughout the sampli
34 d to provide an extended period of temporary burn wound coverage.
35 ing the use of this technology with standard burn wound coverage.
36 d December 2007 to receive standard therapy (burn wound debridement/topical antiseptic therapy) with
37   Here we demonstrate that the presence of a burn wound dramatically affects expression of both human
38             An adhesive yet easily removable burn wound dressing represents a breakthrough in second-
39                        Current second-degree burn wound dressings absorb wound exudate, reduce bacter
40  MMP-1 accumulates in the fluid phase of the burn wound environment within 2 d of injury and reaches
41  siderophores increased significantly in the burn wound environment.
42      RON protein was markedly upregulated in burn wound epidermis and accessory structures, in prolif
43       The primary endpoint, time to complete burn wound epithelialization, was determined by independ
44                               Finally, early burn wound excision and coverage with new biodegradable
45                Standard burn care with early burn wound excision and grafting.
46 eparin-binding growth factors was studied in burn wound fluid (BWF) from 45 pediatric patients who ha
47 nsepidermal water loss every 12 hours on the burn wounds for 72 hours postburn.
48             The severity of tissue injury in burn wounds from associated inflammatory and immune sequ
49                             Infection of the burn wound has always been a major factor in retardation
50 e data support a role for PDGF and HB-EGF in burn wound healing and suggest that the response to inju
51  Hydrogel treatment accelerated third-degree burn wound healing by rapid wound closure, improved re-e
52 e roles of individual cell types involved in burn wound healing following PBM treatments and noted di
53 ficacy of PBM treatments in a full-thickness burn wound healing in C57BL/6 mice.
54  temperature-monitored PBM protocol improved burn wound healing in mice with elevated TGF-B signaling
55 GF-B1(LB3/LB3) complex and failed to improve burn wound healing in these mice.
56 gar Holding, Ulaanbaatar, Mongolia) in ovine burn wound healing models.
57 ntributions of TGF-B1 signaling in these PBM-burn wound healing, we utilized a chimeric TGF-B1/B3 kno
58 ficient and effective supplement therapy for burn wound healing.
59 following PBM treatments plays a key role in burn wound healing.
60 cells (ASCs) accelerates the process of acid burn wound-healing.
61 he mechanism of EPO action on the healing of burn wounds in the skin of pigs with experimentally indu
62 xist regarding diagnostics and management of burn wounds in veterinary patients and current knowledge
63 lg not only accelerates the healing of acute burn wounds in wild-type mice, but also improves the hea
64                  Using porcine second-degree burn wounds infected with P. aeruginosa biofilm cells, w
65 cutoff values were determined for mortality, burn wound infection (at least two infections), sepsis (
66  insulin improves outcome following a lethal burn wound infection are not known, the data suggest tha
67                                Resistance to burn wound infection could also be conferred to recipien
68 hGSTA4 expression negatively correlates with burn wound infection episodes per patient.
69 ort a fatal case of S. erythrospora invasive burn wound infection in a 26-year-old male injured durin
70 se the resistance of mice to a P. aeruginosa burn wound infection through both stimulation of dendrit
71 tion to increase the resistance of mice to a burn wound infection with Pseudomonas aeruginosa, a comm
72 cial role in the pathogenesis of PA14 during burn wound infection, most likely by contributing to PA1
73 h bacterial infection in an in vivo model of burn wound infection.
74  to the pathogenesis of P. aeruginosa during burn wound infection.
75 acteria in a model of Pseudomonas aeruginosa burn wound infection.
76  of neutrophils in FL-mediated resistance to burn wound infection.
77 critical role in FL-mediated resistance to a burn wound infection.
78  the outcome of rats in response to a lethal burn wound infection.
79  and in mouse models of abdominal sepsis and burn wound infection.
80 nontreated mice did not confer resistance to burn wound infection.
81 icantly increased survival upon a subsequent burn wound infection.
82  determine the effect of fluid group on AKI, burn wound infections (BWIs), and pneumonia.
83 useful tool in studying the pathogenicity of burn wound infections and in evaluating the efficacy of
84 d (FL) significantly increases resistance to burn wound infections in a DC-dependent manner that is c
85   Severe burn injury predisposes patients to burn wound infections that can disseminate, lead to unco
86 flexible choice for passive immunotherapy in burn wound infections.
87 ual involvement in nosocomial and especially burn wound infections.
88  in the treatment of antimicrobial resistant burn wound infections.
89 al p38 MAPK inhibition significantly reduced burn wound inflammatory signaling and subsequent systemi
90  We hypothesized that topical attenuation of burn wound inflammatory signaling will control the derma
91 m infections developed in the full-thickness burn wounds inoculated with 1 x 10(4) CFU of P. aerugino
92               We propose that the depth of a burn wound is a sum of the thermal energy applied and of
93          A primary goal in the management of burn wounds is early wound closure.
94                               This region in burn wounds is likely the focus of dysregulated inflamma
95 es of severely burned patients with infected burn wounds is not known.
96                   Failure to close a massive burn wound leads to sepsis and multiple system organ fai
97 ease in functional LDH activity in sub-acute burn wounds linked to cellular infiltration.
98 sight into the local effects of Flt3L at the burn wound, localization of Langerhans cells was examine
99                 Full-thickness paravertebral burn wounds measuring 36 cm2 were created on 11 farm swi
100 n limited because of their susceptibility to burn wound microorganisms as a result of their lack of a
101 his waveform was further evaluated through a burn wound model.
102 terial infection in an in vivo second-degree burn wound model.
103 of a 53-year-old male patient with a thermal burn wound on the upper eyelid and sclera following phac
104      We first developed a procedure to treat burn wounds on mice with dextran hydrogels.
105                                              Burn wound progression is an important determinant of pa
106 ical inhibition of inflammatory signaling in burn wounds reduced systemic inflammatory response and b
107  optimal treatment course for a dermatologic burn wound requires knowledge of the wound's severity, a
108 ation-rich tool for precise interrogation of burn wound severity and healing potential in both resear
109 uginosa is extremely efficient at colonizing burn wounds, spreading systemically, and causing sepsis,
110 inosa was unable to replicate efficiently on burn wounds, suggesting that burn wounds are purine-defi
111 on of the ptrA during the infection of mouse burn wound suggests that P. aeruginosa has evolved tight
112                                   By day 21, burn wounds treated with hydrogel developed a mature epi
113 wo decades of dermal progenitor cell use for burn wound treatment and Good Manufacturing Practice-com
114  opportunities to simplify the management of burn wound treatment.
115 g opportunities to improve the management of burn wound treatment.
116  Approaches to optimise healing potential of burn wounds use targeted wound care and surgery to minim
117         Murine models of acute pneumonia and burn wounds, using both standard and nosocomial strains,
118 sed the brass comb contact burn to determine burn wound vertical injury progression with a focus on b
119                                 Edema in the burn wound was not affected by treatment, while hyperton
120 ithelialization of partial thickness porcine burn wounds was blocked following treatment with EGFR in
121          HB-EGF in the surface epithelium of burn wounds was uniformally distributed, whereas it was
122 ten used as a disinfectant and treatment for burn wounds, we present here an important fitness factor
123                                              Burn wounds were sampled at 0, 30 min, 1, 2, 4, and 24 h
124                                              Burn wounds were topically inoculated with a lethal dose
125                                Following the burn, wounds were surface-inoculated with P. aeruginosa
126                                        Adult burn wounds, which lack hyaluronan (HA), often undergo e
127               Inflammatory source control in burn wounds with topical p38 mitogen-activated protein k
128         Therefore, adding a HA derivative to burn wounds would better mimic the fetal extracellular m

 
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