• Biomedical Science Letters
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• v.9 no.1
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• pp.37-42
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• 2003

The present study was conducted to determine whether administration of heat extract of Lepidii Semen has an inhibitory effect on neutrophil-derived oxidative injury following dermal scald burn in rats. Acute lung injury was induced by scald burn (15% of TBSA) in rats. To identify acute edematous lung injury, protein concentrations and numbers of polymorphonuclear leukocytes were measured in bronchoalveolar lavage (BAL) at 5 h after skin burn. In addition, the level of lung KC (neutrophil chemoattractant cytokine) and activity of lung myeloperoxidase (MPO) were measured, and histopathological changes were observed as well. Lung weight and concentration of BAL protein, the index of lung injury, were clearly increased at 5 h postburn compared with those of sham-operated group. Administration of heat extract of Lepidii Semen after scald burn inhibited the production of KC in lung tissue and decreased the activity of lung MPO related to infiltration of neutrophils. In histopathological changes in lung tissue, infiltration of inflammatory cells and pulmonary edema induced by skin burn were decreased by administration of heat extract of Lepidii Semen after scald burn. These results suggest that Lepidii Semen may be an effective medical stuff for acute lung injury induced by skin burn.

• Journal of Pharmacopuncture
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• v.12 no.3
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• pp.89-95
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• 2009

We report the case of a 65-year-old female with burn injury from scalds. She was observed with a burn injury of the right arm and leg that occurred 6 days before. She was treated with pharmacoacupuncture Soyeom, and herb medicine daily for 3 weeks. After Twenty days, burn wound size was reduced and tissue regeneration was accelerated. In conclusion, it is our belief that pharmacoacupuncture and herb medicine is effective to treat burn injury, and future studies will be required to ascertain this method on burn injury.

• Biomedical Science Letters
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• v.10 no.2
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• pp.107-113
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• 2004

This study was conducted to investigate an effect of Mori Cortex in the cardiac injury following dermal scald burn in rats. Sprague-Dawley rats were induced scald bum (15％ of total body surface area). Heart was removed at 5 h postburn and examined with biochemical assay, ultrastructural observations and stereological analysis. The activity of serum aspartate aminotransferase and creatinine was increased at 5 h postburn compared with them of control. Administration of heat extracts of Mori Cortex after scald burn inhibited the production of KC (neutrophil chemoattractant cytokine) and increased the activity of protein kinase C (PKC) in heart tissue. The activity of myeloperoxidase (MPO) in heart tissue was decreased both at 5 h postburn and in case of Mori Cortex administration after scald burn. Ultrastructurally, many contraction bands and separation of intercalated disk induced by scald burn were decreased by administration of heat extracts of Mori Cortex. In stereological analysis, administration of Mori Cortex after scald burn resulted the volume densities of myofibril and mitochondria were increased compared with them of burn control. These data suggest that Mori Cortex may be a useful stuff to the range of available treatments for cardiac injury induced by skin burn.

• Journal of Veterinary Clinics
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• v.37 no.6
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• pp.331-335
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• 2020

A 13-year-old female Poodle presented with gallbladder rupture caused by a mucocele and hypoperfusion. The animal had a thermal burn injury caused by a forced-air warming device used for hypothermia during surgery. This could be attributed to two causes. First, the forced-air warming device was used with direct hosing, without attachment to an air blanket, and the heat was concentrated in a single area. Second, perioperative peripheral hypoperfusion hampered heat dissipation and increased the susceptibility to a burn injury. These findings suggest that an air blanket should be used with a forced-air warming device according to the manufacturer's instructions. Furthermore, patients with peripheral hypoperfusion are at a higher risk of burn injuries and require close monitoring.

• Journal of the Korean Burn Society
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• v.24 no.2
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• pp.34-37
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• 2021

A 46-year-old female presented a mass on her right lower leg where she had a burn injury due to moxibustion 10 years ago. Physical examination revealed a 3 cm sized firm nodule with tenderness. Plain radiograph was performed and it revealed well-defined calcifications. According to the history of moxibustion burn injury and the result of plain radiograph, dystrophic calcinosis cutis caused by burn injury was suspected. The patient underwent excisional biopsy using pre-,intra-, and post-operative ultrasonography (USG). There was no sign of recurrence. Herein, we report a case of a 46-year-old healthy woman who presented with single hard nodule on the right lower leg. Our case is worthwhile in two respects. First, It is first case report of dystrophic calcinosis cutis due to moxibustion burn injury. In east asian culture, moxibustion is a commonly conducted procedure and it often induces burn injury. Second, USG was used pre-, intra-, and post-operatively to assess the shape, location, and depth of the calcinosis cutis and to determine the surgical margin.

• Nutrition Research and Practice
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• v.16 no.5
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• pp.589-603
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• 2022

BACKGROUND/OBJECTIVES: Previous studies have reported that protein supplementation contributes to the attenuation of inflammation. Serious trauma such as burn injury usually results in the excessive release of inflammatory factors and organs dysfunction. However, a few reports continued to focus on the function of protein ingestion in regulating burn-induced inflammation and organ dysfunction. MATERIALS/METHODS: This study established the rat model of 30% total body surface area burn injury, and evaluated the function of blended protein (mixture of whey and soybean proteins). Blood routine examination, inflammatory factors, blood biochemistry, and immunohistochemical assays were employed to analyze the samples from different treatment groups. RESULTS: Our results indicated a decrease in the numbers of white blood cells, monocytes, and neutrophils in the burn injury group administered with the blended protein nutritional support (Burn+BP), as compared to the burn injury group administered normal saline supplementation (Burn+S). Expressions of the pro-inflammatory factors (tumor necrosis factor-α and interleukin-6 [IL-6]) and chemokines (macrophage chemoattractant protein-1, regulated upon activation normal T cell expressed and secreted factor, and C-C motif chemokine 11) were dramatically decreased, whereas anti-inflammatory factors (IL-4, IL-10, and IL-13) were significantly increased in the Burn+BP group. Kidney function related markers blood urea nitrogen and serum creatinine, and the liver function related markers alanine transaminase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase were remarkably reduced, whereas albumin levels were elevated in the Burn+BP group as compared to levels obtained in the Burn+S group. Furthermore, inflammatory cells infiltration of the kidney and liver was also attenuated after burn injury administered with blended protein supplementation. CONCLUSIONS: In summary, nutritional support with blended proteins dramatically attenuates the burn-induced inflammatory reaction and protects organ functions. We believe this is a new insight into a potential therapeutic strategy for nutritional support of burn patients.

• BMB Reports
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• v.46 no.1
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• pp.47-52
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• 2013

Intestinal epithelial cell (IEC) apoptosis induced by hypoxia compromise intestinal epithelium barrier function. Both Akt and Hsp90 have cytoprotective function. However, the specific role of Akt and $Hsp90{\beta}$ in IEC apoptosis induced by hypoxia has not been explored. We confirmed that hypoxia-induced apoptosis was reduced by $Hsp90{\beta}$ overexpression but enhanced by decreasing $Hsp90{\beta}$ expression. $Hsp90{\beta}$ overexpression enhanced BAD phosphorylation and thus reduced mitochondrial release of cytochrome C. Reducing $Hsp90{\beta}$ expression had opposite effects. The protective effect of $Hsp90{\beta}$ against apoptosis was negated by LY294002, an Akt inhibitor. Further study showed that Akt phosphorylation was enhanced by $Hsp90{\beta}$, which was not due to the activation of upstream PI3K and PDK1 but because of stabilization of pAkt via direct interaction between $Hsp90{\beta}$ and pAkt. These results demonstrate that $Hsp90{\beta}$ may play a significant role in protecting IECs from hypoxia-induced apoptosis via stabilizing pAkt to phosphorylate BAD and reduce cytochrome C release.

• Journal of Korean Physical Therapy Science
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• v.8 no.1
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• pp.923-934
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• 2001

In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total body surface area 30%) except for inhalated injury. At 5 and 24 h after scald bum, biochemical assay and morphological changes in skin tissue, serum and liver tissue were examined. The effects of bum injury on the levels of glutathione, lipid peroxide and on the activities of oxygen free radical generating and scavenging enzymes have been determined in association with observing of histologic and ultrastructural changes, measuring the protein concentration in plasma, and counting the number of intravascular polymorphonuclear leukocytes. The activity of xanthine oxidase, an enzyme of oxygen free radical generating system. was elevated (p<0.01) in serum, but not in skin and in liver tissue. Futhermore, thermal injury decreased not only the protein concentration in plasma but also the number of leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.

• Korean Journal of Biological Psychiatry
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• v.12 no.2
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• pp.159-164
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• 2005

Objective:The aim of this study was to evaluate the temperament and character profiles of the patients with posttraumatic stress disorder(PTSD) after burn injury. Methods:The study subjects consisted of 23 PTSD patients after burn injury, 24 patients not being diagnosed as PTSD after burn injury(non-PTSD) and 53 healthy controls. The assessment of PTSD was performed using clinician administered PTSD scale. All participants were instructed to complete the Temperament and Character Inventory(TCI), the Beck Depression Inventory and the State and Trait Anxiety Inventory of Spielberger. Results:The PTSD group after burn injury, compared with the non-PTSD group and the normal controls, had the higher novelty seeking and harm avoidance scores. But there were no differences in other dimensions in the TCI among the three groups. Conclusion:The results of this study suggest that the PTSD group after burn injury showed the specific properties of temperament and character compared with the non-PTSD group and the normal group.

• Applied Microscopy
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• v.31 no.1
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• pp.37-47
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• 2001

In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total burn surface area $20\sim25\%$) except for inhalated injury. At 5 and 24 h after scald burn, biochemical assay and morphological changes in serum and liver tissue were examined. Skin burn increased liver weight (% of body weight, p<0.05) and the activity of serum aniline amino-transferase (ALT, p<0.05), in addition, the activity of xanthine oxidase (XO), an enzyme of oxygen free radical generating system, was elevated (p<0.01) in serum, but not in skin and in liver. Postburn treatment of allopurinol intraperitoneally decreased liver weight, serum ALT activity and serum XO activity. Scald burn induced ultrastructurally swelling of endoplasmic reticulum, ribosome detachment, accumulation of lipid, dilatation of bile canaliculi and intercellular space, neutrophil infiltration, activation of Kupffer's cells and degeneration of hepatocytic microvilli. Futhermore , thermal injury decreased not only the protein concentration in plasma but also the number of intravascular leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. However allopurinol injection after burn inhibited post burn ultrastructural changes. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.