• Molecular & Cellular Toxicology
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• v.4 no.2
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• pp.93-99
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• 2008

Human cyclin D3 gene (CCND3) located on 6p21.1 is important for the regulation of the G1-S phase transition of the cell cycle by modulating the activity of the cyclin-dependent kinases Cdk4 and Cdk6. Because little is known about the effect of cyclin D3 in various human cancers, we evaluated the intricate relationship between expression of cyclin D3 and the process of HCC development using immunohis tochemistry and TUNEL assay on 43 paraffin embedded tissues. Cyclin D3 immunoreactivity was more frequently observed in the tumors with high histologic grade and the tumors with metastasis, and more frequently expressed in HCCs with cirrhotic background and gain of 6p21.1 when compared with those with non-neoplastic tissue. Apoptotic cells were more common in tumor with cirrhotic background, amplification of 6p21.1 and expression of cyclin D3 when compared with HCCs with lower level of cyclin D3 expression. Also, we observed that some of the cyclin D3 positive cell and apoptotic cell were co-localized. From these results, it is suggested that over-expression of cyclin D3 may contribute to more rapid cell turn-over in the background of HCC, and balance between proliferation and apoptosis is a role in the progression of HCC with cirrhotic background.

• Journal of Chest Surgery
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• v.28 no.8
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• pp.731-741
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• 1995

Cardiac valve allografts have been used as replacements for diseased valves and right ventricular outflow tract reconstruction, the long term follow-up of which has been reported satisfactory. For a good long-term result, it is essential that the allograft be viable at implantation. In this study, we aimed at preparing the cardiac valve allografts aseptically, preserving them at cold- and cryo-conditions, and testing the viability of the allografts after preservation by four methods. We tested the viability of the cardiac valve allografts preserved in cold refrigerated state[4$^{\circ}$C in nutrient media & in liquid nitrogen tank[cryopreservation under -149$^{\circ}$C for pre-planned time periods. The testing methods were 1 glucose utility test 2 tissue culture 3 thymidine uptake test and 4 histologic evidence by light microscopy. We observed no differences in the viability between cold- & cryo-groups and similar results among the methods for testing the viability. In conclusion, there was no difference in the viability between cold- and cryopreserved-allografts at least for 14 days of preservation. And glucose utility test and thymidine uptake test were satisfactory in the evaluation of the allograft viability, since they were easy and rapid with relatively quantitative results.

• 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.

• Biomedical Science Letters
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• v.14 no.3
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• pp.167-172
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• 2008

We compared the clinical efficacy of LED therapy using 880 nm and 630 nm LED to test collagen accumulations in subcutaneous tissue of mouse after LED irradiation by measuring the quantity of collagen. 880 nm and 630 nm LED was irradiated on the back of ICR mouse given at $10.8J/cm^2$ followed for 30 minutes everyday for 5 weeks. Histological observation was performed by Hematoxylin & Eosin staining and Masson's Trichrome collagen staining. We also used Sircol soluble collagen assay kit for measuring the amounts of collagen in the mouse skin tissue after 1, 3, and 5 weeks post LED irradiation, respectively. Collagen generation was found at subcutaneous tissue, and the quantity of collagen in 880 nm LED group had grown more than that of 630 nm LED group at 5 weeks follow-up later. About 75% more efficacies for collagen generation were found in the group of 5th week of 880nm LED irradiation. The efficacy of 880nm LED could be more useful than 630 nm LED for synthesizing collagens in mouse subcutaneous tissue as time followed.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.1
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• pp.73-79
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• 2000

This study investigated whether propofol, an intravenous, non-barbiturate anesthetic, could reduce brain damage following global forebrain ischemia. Transient global ischemia was induced in gerbils by occlusion of bilateral carotid arteries for 3 min. Propofol (50 mg/kg) was administered intraperitoneally 30 min before, immediately after, and at 1 h, 2 h, 6 h after occlusion. Thereafter, propofol was administered twice daily for three days. Treated animals were processed in parallel with ischemic animals receiving 10% intralipid as a vehicle or with sham-operated controls. In histologic findings, counts of viable neurons were made in the pyramidal cell layer of the hippocampal CA1 area 4 days after ischemia. The number of viable neurons in the pyramidal cell layer of CA1 area was similar in animals treated with a vehicle or a subanesthetic dose of propofol. In terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, semiquantitative analysis of dark-brown neuronal cells was made in the hippocampal CA1 area. There was no significant difference in the degree of TUNEL staining in the hippocampal CA1 area between vehicle-treated and propofol-treated animals. These results show that subanesthetic dose of propofol does not reduce delayed neuronal cell death following transient global ischemia in Mongolian gerbils.

• Archives of Plastic Surgery
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• v.36 no.2
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• pp.127-134
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• 2009

Purpose: Adipose tissue injection as a free graft for the correction of soft - tissue deficiency or depression deformity is a widespread procedure in plastic surgery. This study is to analyze the changes and viability of cryopreserved adipose tissue and to find out efficient long - term storage period. Methods: After centrifugation of aspirated abdominal tissues, $10m{\ell}$ of packed Adipose tissue were freezed at $-20^{\circ}C$. For 2, 4, 6, 8 months, each frozen samples were taken and injected into scalp of SCID mice. After 15 weeks, injected Adipose tissue were sampled and analyzed at 2 months interval. We compared and analyzed each group about the weight of the injected fat, histologic impressions, activity of mitochondria, size of a fat cell and rate of survival. Results: Significant weight changes were observed in cryopreservation for 2 months(p<0.05). Histologic changes were observed, independent of the freezing period with H - E stain. Among cryopreservations for 2, 4, 6 months, no significant change were observed. The reduction of mitochondrial enzymatic activity was observed independent of time interval but activity of mitochondrial dehydrogenase was reduced less than 50% in MTT assay. Conclusion: Freezing in $-20^{\circ}C$ for 6 months has no adverse effect to Adipose tissue, but fragile adipocytes, damaged cell membrane during harvesting procedure, were disrupted within 1 - 2 month and the maximum volume reduction were followed less than 2 months. These results demonstrate that tissue preparation cells without membrane damage have the greatest viability level and cryopreservation less than 2 months has great volume effect and cryopreservation for 6 months has stable volume effect.

• Archives of Plastic Surgery
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• v.43 no.6
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• pp.491-497
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• 2016

Background Hypertrophic scarring is a pathological condition that occurs after trauma or surgery. Angiogenesis occurs more often with hypertrophic scarring than with normotrophic scarring. The regulation of angiogenesis is one of the key factors in hypertrophic scar management. Vascular endothelial growth factor (VEGF) is an essential factor in the angiogenetic response. This study investigated whether decreasing the level of VEGF is effective for treating hypertrophic scarring. Methods Ten 8-week-old female New Zealand white rabbits were included. Four defects were created on each ear by using a 6-mm punch. Bevacizumab (Avastin, Roche Pharma, Basel, Switzerland) was administered in one ear and normal saline was administered in the other ear. Treatment was administered starting on day 2, every 2 days, until day 14. The levels of VEGF were measured using enzyme-linked immunosorbent assay on day 10 and histologic results were analyzed on day 40. Results Bevacizumab induced-defects showed less hypertrophic scarring when compared with the control group as measured by the scar elevation index (SEI) and loose collagen arrangement. The SEI in the experimental group was $1.89{\pm}0.13$, compared to $1.99{\pm}0.13$ in the control group (n=30, P=0.005). Additionally, the VEGF level was lower ($38.72{\pm}11.03pg$ vs. $82.50{\pm}21.64pg$, n=10, P=0.001) and fewer vessels existed ($8.58{\pm}0.76$ vs. $7.2{\pm}1.20$, n=10, P=0.007). Conclusions Preventing excessive angiogenesis is effective for preventing scar formation, especially with hypertrophic scarring. Although it is not an approach that is sufficient alone for the management of scarring, it may be one of several important strategies for scar treatment.

• The Journal of Korean Physical Therapy
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• v.14 no.1
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• pp.63-73
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• 2002

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 burn, biochemical assay in skin tissue, serum and liver tissue were examined. The effects of burn injury on the levels of glutathione, lipid peroxide and on the activities of oxygen of histologic and ultrasound changes, measuring. the protein concentration in plasma, and counting the number of intravascular polymorphonuclear leukocytes. Post burn 24 h, the content of glutathione was decreased (47.50%), whereas that of lipid peroxide was increased (37.01%), and the activity of superoxide dismutase was diminished (p<0.001). Thus decreasing the capacity of oxygen free radical scavenging enzymes led to oxidative injury in skin tissue. In liver tissue, at 24 h after scald burn, both the content of glutathione and the activity of catalase were markedly decreased (p<0.01, p<0.05), thus the imbalance between free radical generating and scavenging capacities has been induced.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.18 no.2
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• pp.138-143
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• 2015

Glycogen storage disease type IX (GSD IX) is caused by a defect in phosphorylase b kinase (PhK) that results from mutations in the PHKA2, PHKB, and PHKG2 genes. Patients usually manifest recurrent ketotic hypoglycemia with growth delay, but some may present simple hepatomegaly. Although GSD IX is one of the most common causes of GSDs, its biochemical and genetic diagnosis has been problematic due to its rarity, phenotypic overlap with other types of GSDs, and genetic heterogeneities. In our report, a 22-month-old boy with GSD IX is described. No other manifestations were evident except for hepatomegaly. His growth and development also have been proceeding normally. Diagnosed was made by histologic examination, an enzyme assay, and genetic testing with known c.3210_3212del (p.Arg1070del) mutation in PHKA2 gene.

• The Journal of Internal Korean Medicine
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• v.38 no.6
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• pp.891-901
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• 2017

Objectives: The aim of the study was to evaluate the anti-asthmatic effect of alismatis rhizoma and alisol acetate B combination therapy in a murine asthma model. Methods: C57BL/6 mice were sensitized to and challenged with a mixture of ragweed, dust mite, and aspergillus to induce an asthma animal model. Alismatis rhizoma extract and alisol acetate B combination therapy was co-administered only in the experimental group. To evaluate the anti-asthmatic effect of the combination therapy, inflammatory cell counts in bronchoalveolar lavage (BAL) fluid were determined, and tissue was examined histologically with hematoxylin and eosin (H & E) and periodic acid-Schiff (PAS) stains, by enzyme-linked immunosorbent assay (ELISA) of IgE, IL-4, and IL-5, and with reverse transcription polymerase chain reaction (RT-PCR) of IL-5, IL-33, MUC5AC. Results: Alismatis rhizoma and alisol acetate B combination therapy reduced the number of inflammatory cells, alleviated histologic features, and down-regulated all the investigated asthma mediators, IgE, IL-4, IL-5, IL-33, and MUC5AC. Conclusions: According to the above results, alismatis rhizoma and alisol acetate B combination therapy may have therapeutic potential for asthma.