• Medical Lasers
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• v.9 no.1
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• pp.51-57
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• 2020

Background and Objectives For experiments on simulated burn, the preparation of an animal model is a very important step. The purpose of the current experiment is to design a simple and controllable method for the preparation of third-degree scald in a mouse model using the boiling water method. Materials and Methods A total of 18 Swiss mice were used. After the anesthetization, the mice were scalded by boiling water (100℃) using a mold with a 1 cm² circle area on the dorsum at contact times of 3s, 5s, and 8s. After confirming that 8 seconds of scald can cause a third-degree scald, the skin samples were collected at day 2, 4, 6, 8, 10, and 12, and analyzed by histopathological examinations. The wound retraction index (WRI) was also measured. Results Third-degree scald involving full-thickness skin was observed in the 8-second scald group, while a 3-second scald caused a superficial second-degree scald and a 5-second scald caused a deep second-degree scald. After third-degree scald, the burn wound continued to contract until day 14. Conclusion The scalding model of mice can be successfully established by the boiling water method. This method is easy to operate, it has a low cost, and it can control the scald depth by controlling the scald time. This is adequate to study skin thermal injury in the future. The scald model established by this method can last for 14 days.

• 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.

• Biomedical Science Letters
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• v.11 no.2
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• pp.243-248
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• 2005

The present study was conducted to determine whether skin spread of Myrrha and Tending Diancibo Pu (TDP) irradiation have a remarkable effect on the cell regeneration as well as wound healing following dermal scald burn injury. Burn injury was induced on dorsal surface $(TBSA\;15\~20\%)$ by scald burn in rats. Postburn concentration of serum protein was significantly decreased compared with sham-treated, double treatment with Myrrha and TDP was significantly increased the protein concentration compared with that of burn control. The content of keratinocyte growth factor (KGF) at 48 h is higher than that of at 24 h, and double treatment with Myrrha and TDP was the most effective to increase the production of KGF in all experimental groups. Morphologically, epithelial regeneration and dermal collagen synthesis by fibroblasts were accelerated in Myrrha and TDP treated group compared with bum control at same time postburn. At 48 h after burn, all dermal connective tissues are recovered to new collagen fibers in case of Myrrha and TDP double treated group. The data suggest that double treatment with skin spread of Myrrha and TDP radiation have a remarkable effect of to accelerate cell regeneration and wound healing in case of scald burn skin.

• Journal of the Korean Home Economics Association
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• v.9 no.2
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• pp.34-39
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• 1971

By analyzing the relationships between the cookery methods and the loss of Ascorbic acid included in fresh vegetables, t he best cookery method to minimize the loss of it has been studied. For being scald and parch, those scald only in the water and those parch the salad oil had fained the least loss of it, while those parch had gotten generally the less loss than those scald. And when the cooked vegetables were left alone in the air. Ascorbic acid included in those were decayed exponentially, and its half time was about two hours.

• The Plant Pathology Journal
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• v.26 no.3
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• pp.260-263
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• 2010

Scald, caused by Rhynchosporium secalis has been the major yield-reducing factor for barley production during the last decade. In this study, pathogenic groups of R. secalis were identified to obtain a global picture of the assembly of isolates involved in Syrian populations which is essential for the development of scald-resistant barley cultivars. To identify a number of pathogenic groups, 49 isolates collected over ten years from major barley growing areas in Syria were evaluated on five differential barley genotypes. Genotypes presented a continuous range of response from highly susceptible to moderately resistant, but none were immune to the disease. A cluster analysis placed isolates in six distinct differential pathogenic groups. Mean disease rating of 39.24% was the separation point between avirulent and virulent reactions. Isolate Rs46 exhibited distinct differential virulence patterns associated with high frequency across all genotypes. Hence, the data presented here provides crucial information for future selection of isolates to develop durable barley scald resistance.

• Biomedical Science Letters
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• v.7 no.3
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• pp.145-149
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• 2001

The present study was conducted to determine whether local production of neutrophil chemoattractant cytokines preceded the influx of neutrophils 1311owing dermal scald burn injury. In order to inhibit the influx of neutrophils, we induced scald burn injury on dorsal skin of rats (TBSA 15%) and spread Rhubarb (R. undulatum L.) and complex (Rhubarb+Olibanum+Myrrha) on scald skin in rats. 1. Levels of dermal KC, the indicator of skin iuflammation, caused by burn gradually increased 5 hours, 24 hours (p<0.001) and 72 hours (p<0.001) after the burn occurred. After 24 hours it occurs, KC in skin was decreased by both skin spread of Rhubarb (p<0.05) and complex (p<0.05) compared to scald bum group. After 72 hours, KC by skin sp.end of Rhubarb and complex was significantly decreased (p<0.01), and the inhibition effect of KC production by complex is higher than by Rhubarb. 2. KC content in serum was increased (p<0.01) at 24 hours after burn injury and comes down back to the normal level after 72 hours. At 24 hours postbunt both Rhubarb (p<0.05) and complex (p<0.01) skin spread decreased KC in serum. The inhibition effect of KC production by complex skin spread group is higher than by Rhubarb skin spread group. The data suggest that the KC production effects by Rhubarb skin spread group and complex skin spread group are high. Especially the endurance of the effect by complex skin spread group was longer than by Rhubarb skin spread group. The inhibition effect of KC production by complex skin spread group increases more than by Rhubarb skin spread group as time passes.

• Biomedical Science Letters
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• v.7 no.3
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• pp.139-143
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• 2001

The present study was conducted to determine whether skin spread of Myrrha has an effect on the cell regeneration as well as wound healing following dermal scald burn injury, keratinocyte growth factor (KGF) level was analyzed immunologically in conjunction with the histological changes occurred in skin tissue. The KGF contents in Myrrha skin spread group, which shows cell regeneration ability in skin tissue after burn, increased after 5 hours. After 24 hours, 'the content of Myrrha skin spread group is noticeably higher than at 5 hours postburn. After 72 hours, KGF was decreased compared to at 24 hours postburn. Acceleration effect of KGF production in Myrrha skin spread group was high. Together with the result of histological changes, skin spread of Myrrha reduced protein degeneration and edema in dermis, and induced proliferation of epithelial cells. The data suggest that Myrrha has accelerate cell regeneration and wound healing in case of scald burn skin by spreading of paste.

• 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.

• The Journal of Korean Physical Therapy
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• v.11 no.3
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• pp.115-121
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• 1999

The effects of scald bum Injury ($40-45\%$ of total body surface area), there were not inhalation and secondary infection, on the histological changes and the levels of oxygen free radical generating and scavenging enzymes have been determined in liver tissue of rat models. It was found that dermal epithelium was left out with edema of dermis layer and hydorpic swelling of hepatocytes, Burn injury increased liver weight (L.W./B.W.) and serum aspartate aminotransferase content (pThe data of this study suggest that liver damage Induced by scald burn injury leads to dysbalance of oxygen free radical generating and scavenging enzymes.

• 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.