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1 mortality caused by sepsis is high following thermal injury.
2  mechanical hyperalgesia generated by a mild thermal injury.
3 ed therapeutic options, but without inducing thermal injury.
4 ed in the process of cytoprotection from the thermal injury.
5 ing insulin receptor signaling in rats after thermal injury.
6 responsible for the insulin resistance after thermal injury.
7  ambient temperature on metabolic rate after thermal injury.
8 of morbidity and mortality in patients after thermal injury.
9  numbers in the lungs following induction of thermal injury.
10 rafish to understand neutrophil responses to thermal injury.
11 ial for maintaining homeostasis and avoiding thermal injury.
12 potentially reducing the risk for esophageal thermal injury.
13 on in primarily cultured retinal cells after thermal injury.
14  identifying new immune targets for treating thermal injury.
15 ophy, Stevens-Johnson syndrome, and chemical/thermal injury.
16 al role of DAMPs as an immune consequence of thermal injury.
17  and also transfer the heat created to avoid thermal injury.
18 e perineurium and epineurium consistent with thermal injury.
19 ut potentially lethal complication of severe thermal injury.
20 tive agent against damage after experimental thermal injury.
21  significant levels between 7 and 24 h after thermal injury.
22 ute to observed cerebral edema in peripheral thermal injury.
23 up was quantified at 3, 7, 24, and 72 h post thermal injury.
24 eg muscle for up to 24 months after a severe thermal injury.
25 10, p < 0.03) and attenuated the sequelae of thermal injury.
26 lycan present on many host cells involved in thermal injury.
27 of morbidity and mortality in the setting of thermal injury.
28 n baby syndrome, and pediatric nonaccidental thermal injury.
29 y be triggered by MCP-1 produced early after thermal injury.
30 ss acute bacterial models of sepsis or after thermal injury.
31 P-1 into their culture fluids 12 hours after thermal injury.
32 th a mechanism similar to that reported with thermal injury.
33  especially in patients with major trauma or thermal injuries.
34  these difficult cases of severe periorbital thermal injuries.
35 ty to infection in individuals with severely thermal injuries.
36 observed in animals and patients with severe thermal injuries.
37 irless mice were subjected to full-thickness thermal injury (30% of total body surface area), cold st
38 l exudates of mice 2 days after third-degree thermal injuries affecting 15% total body surface area.
39    Propranolol treatment for 12 months after thermal injury, ameliorates the hyperdynamic, hypermetab
40                          In a mouse model of thermal injury, an increase in burn size produced a decr
41                                              Thermal injuries and endotoxemia have been shown to indu
42 eratopathy occurred after severe periorbital thermal injuries and followed a predictable course of sc
43 surface for patients with severe periorbital thermal injuries and resultant exposure keratopathy.
44 nduit harvesting subsequent to mechanical or thermal injury and during conduit storage prior to graft
45 c ischemia and reperfusion injury induced by thermal injury and endotoxemia by improving mesenteric b
46 o, showed 6-fold and 12-fold increases after thermal injury and LPS, respectively.
47 tio, showed a 7- and 10-fold elevation after thermal injury and LPS, respectively.
48 attenuates the hypermetabolic response after thermal injury and may improve the clinical outcome.
49                   This produced irreversible thermal injury and necrosis.
50 motic stress and helps protect cells against thermal injury and oxygen radicals.
51 resent important modifiable risk factors for thermal injury and poisoning but not fractures in presch
52 the premise that enhanced monocytopoiesis in thermal injury and sepsis results from an imbalance in m
53 pmental hierarchy of bone marrow cells after thermal injury and sepsis was determined by assessing th
54  by norepinephrine and the milieu created by thermal injury and sepsis.
55 e pathogenesis of P. aeruginosa infection of thermal injury and that syndecan 1-neutralizing agents m
56 at MCP-1 is produced in mice within 1 day of thermal injury, and the subsequent development of burn-a
57                                              Thermal injury at the camera trocar incision was lower i
58  the mechanical sensitivity caused by a mild thermal injury by both GBP and IBG.
59 he liver plays an important role in a severe thermal injury by modulating immune function, inflammato
60  medically recorded injury, comprising 3,649 thermal injury cases, 4,050 fracture cases and 2,193 poi
61 ing revealed an immediate tissue response to thermal injury characterized by the rapid Arp2/3-depende
62 ignificantly increased as early as 3 h after thermal injury compared to controls, remained at 7 h (p<
63 nic effect on hepatocytes 1 and 2 days after thermal injury compared with controls (p<.05).
64  an experiment to verify our hypothesis that thermal injury could be induced by the high temperature
65                    We previously showed that thermal injury depletes plasma vitamin E in pediatric bu
66             The primary outcome variable was thermal injury determined by histology from skin biopsie
67      Temperature measurements indicated that thermal injury did not contribute to tumor response.
68  cells from burned mice (6 h to 3 days after thermal injury) did not produce significant amounts of M
69                                        While thermal injury disrupts collagen fibers initially, heali
70 s (16 eyes) who sustained severe periorbital thermal injuries during combat missions in Iraq and Afgh
71 s sheath insertion, apparatus malfunction or thermal injuries during laser lithotripsy might cause in
72 oiding this complication, which is caused by thermal injury during ablation.
73 rial posterior wall predisposes esophagus to thermal injury during catheter ablation for atrial fibri
74 technique to protect intercostal nerves from thermal injury during cryoablation of peripheral lung tu
75 hnique to protect intercostal nerves against thermal injury during image-guided percutaneous cryoabla
76 sue may serve to insulate the esophagus from thermal injury, explaining why atrioesophageal fistulas
77 (THIN) database to identify risk factors for thermal injury, fractures and poisoning in pre-school ch
78 ord from the active electrode cord decreases thermal injury from antenna coupling at the camera troca
79 e due to a combination of factors, including thermal injury (from hot tea), exposure to polycyclic ar
80                  During the initial phase of thermal injury gene expression profiles in the liver may
81 horda tympani section > trigeminal section > thermal injury = glossopharyngeal section > greater supe
82 n (1 to 16 years of age) sustaining a severe thermal injury (&gt; or =40% TBSA) were included into the s
83 Recent research in the metabolic response to thermal injury has identified many potentially beneficia
84                                            A thermal injury, however, causes hepatic damage by induci
85 on with increased matrix remodeling in acute thermal injuries in calves.
86 agogastroduodenoscopy revealed minor mucosal thermal injury in 2 of 36 RF/PF and 0 of 24 PF/PF patien
87 were increased between 36 and 48 hours after thermal injury in platelet-deficient mice compared with
88  of granule contents occurred by 2 min after thermal injury in wild-type (WT) C57BL/6 mice and in the
89 ed with increased BBB permeability following thermal injury, indicates that MMP-9 may contribute to o
90                           Both infection and thermal injury induced a macrophage population with a mo
91                                              Thermal injury induces a hypermetabolic state, which is
92                                       Severe thermal injury is associated with extreme and prolonged
93  suggest that the hypermetabolic response to thermal injury is maximal in burns as small as 20% total
94                                              Thermal injury is often associated with a proinflammator
95 despite adequate nutritional support, severe thermal injury leads to decreased anabolic hormones over
96         A variety of chemical, physical, and thermal injuries may involve the gingiva.
97             Mortality after serious systemic thermal injury may be linked to significant increases in
98 ously established a mast cell (MC)-dependent thermal injury model in mice with ulceration and scar fo
99 sruption of microvascular integrity in a rat thermal injury model is associated with gelatinase expre
100                Previous findings using a rat thermal injury model suggested that re-epithelialization
101 e active electrode/camera cords would reduce thermal injury occurring at the camera trocar incision i
102 sophageal fistula can develop as a result of thermal injury of the esophagus during ablation along th
103  of this study was to evaluate the effect of thermal injury on novel haematological parameters and to
104 sed the mechanical hyperalgesia induced by a thermal injury or the TRPV4-selective agonist 4alpha-PDD
105 city of the drugs used in protocols to treat thermal injury patients.
106 hologic findings consistent with athermal or thermal injury, respectively, such as axonal swelling, a
107 used in the treatment of acne scarring, with thermal injury resulting in collagen synthesis and remod
108                                              Thermal injury results in a number of physiologic altera
109         Here we show for the first time that thermal injury results in shedding of syndecan 1 from ho
110  exhibited RF-induced coagulation columns of thermal injury, separately generated around each microne
111 view, we outline DAMPs and their function in thermal injury, shedding light on the mechanism of steri
112 one (rhGH), given to children after a severe thermal injury, successfully improved lean muscle mass,
113                                     However, thermal injury suppresses many of these factors, and the
114 nt modifiable risk factor for poisonings and thermal injuries (tests for trend p </= 0.001) as were h
115  on blood samples acquired on the day of the thermal injury to 12 months post-injury in 39 patients (
116 well as safety concerns related to potential thermal injury to adjacent tissues may preclude the use
117 group, there was significantly less (P <.05) thermal injury to biliary epithelium in the chilled sali
118  this study, we utilized the murine model of thermal injury to examine the contribution of hepP to th
119                                    Selective thermal injury to follicles was observed histologically,
120   Tissue transplantation for conditions from thermal injury to Parkinson disease is being investigate
121 ser pulses, microscopy revealed preferential thermal injury to sebaceous follicles and glands, consis
122 n additional group was studied that received thermal injury to the anteroventral tongue.
123                     Studies have reported on thermal injury to the cornea during phacmoemulsification
124                Following severe traumatic or thermal injury to the dermis, hypertrophic scars (HTSs)
125                Following severe traumatic or thermal injury to the dermis, hypertrophic scars (HTSs)
126 hological evaluation revealed no evidence of thermal injury to the myocardium.
127                 Paradoxically, we found that thermal injury to the skin induced a robust time-depende
128 eloperfusion as a protective measure against thermal injury to the ureter.
129                  Previously we reported that thermal injury triggers distinct early tissue responses
130 activity found in PMNs from individuals with thermal injury was associated with a specific, quantitat
131 but leaflets of residual tissue remained and thermal injury was noted in all samples.
132 f heat-shock proteins can protect cells from thermal injury, we tested whether the proteasome inhibit
133 y type; compared with children under 1 year, thermal injuries were highest in those age 1-2 (OR = 2.4
134 of apoptosis and accidental cell death after thermal injury were evaluated in normal human epidermal
135   Alterations in gene expression unique to a thermal injury were identified.
136        No histologic changes consistent with thermal injury were observed in blood vessels or collage
137  esophageal temperature rises nor esophageal thermal injury were observed.
138  15 years with LSCD secondary to chemical or thermal injury who underwent CLET from April 1, 2001, th
139                C57/Bl6 mice received hepatic thermal injury with MW, RF, or cautery to create a super
140                                           In thermal injury with superimposed sepsis, neutropenia and
141  failure and improve clinical outcomes after thermal injury without any detectable adverse side effec

 
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