• Korean Journal of Veterinary Research
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• v.39 no.3
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• pp.635-644
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• 1999

The effect of isoprothiolane(di-isopropyl-1,3-dithiolan-2-ylidenemalonate) aganist fat necrosis in Hanwoo(Korean Cattle) sire was evaluated. The 10 heads of Hanwoo sire suffering from fat necrosis were given 50mg/kg body weight of isoprothiolane(0.2g/kg of Fujix, Japan) orally once a day for 8 weeks. In 30% of these, the size of the necrotic fat masses had decreased significantly 7 months after the adminstration. Isoprothiolane did not affect on live body weight and semen characteristics. However the sire affected with fat necrosis had higher MCHC(Mean corpuscular hemoglobin concentration) than normal sire in hematologic values 10 weeks after administration. Number of RBC(red blood cell) and PCV(packed cell volume) 10 weeks after administration had been increased than those before administration(p < 0.05). The serum concentrations of creatinine, triglyceride, and total cholesterol 10 weeks after administration were higher than those before administration while the concentration of glucose was vice versa. The isoprothiolane may reduce the oxidation of glucose, increase the glucose transfer to lipids, and increase blood supply to necrotic masses. These results indicate that isoprothiolane may be useful as the therapeutic agent aganist fat necrosis.

• Archives of Craniofacial Surgery
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• v.18 no.3
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• pp.162-165
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• 2017

Background: It is controversial issue that heparin decreases thrombosis for microsurgical anastomosis, and its effective role is under discussion. This study is for proving whether low-dose heparin is preventing thrombosis in free flap reconstruction. Methods: Through chart reviews of 134 patients, using low-dose heparin for free tissue transfer from 2011 to 2016, retrospective analysis was performed. 33 patients received low-dose heparin therapy after surgery. And 101 patients received no-heparin therapy. Complications included flap necrosis, hematoma formation, dehiscence and infection. Results: In no-heparin therapy group, comparing the flap necrosis revealed 16 cases (15.84%). And, flap necrosis was 6 cases (18.18%) in low-dose heparin therapy group. The statistical analysis of flap necrosis rate showed no significant difference (p=0.75). The results showed that there was no significant difference of flap necrosis rate between two groups. Conclusion: In this study, patients in the low-dose heparin group had no significantly lower rates of flap failure compared with no-heparin group. This suggests that low-dose heparin may not prevent thrombosis and subsequent flap failure to a significant extent.

• Horticultural Science & Technology
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• v.33 no.1
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• pp.18-23
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• 2015

Time-specific responses of flower bud differentiation were investigated in 'Shinko' (Pyrus pyrifolia Nakai) pear grown at different altitudes from July through December 2013 to determine their suitability as scions in a top-grafting system. Flower bud initiation and bud necrosis were monitored on each of three sections of one-year-old shoots: terminal, middle, and basal. Flower bud differentiation s tarted in September in the highlands of the Lishan area, and in J uly in the lowlands of the Zhoulan area. In Lishan, flower bud differentiation was higher in the middle and basal segments; during leaf fall, however, flower bud differentiation occurred rapidly in the terminal segment. In Zhoulan, flower buds began to differentiate from the terminal section of the shoot, and severe flower bud necrosis was noted. In July, flower buds developed normally; however, in early August, some of the buds at the basal segment showed browning. During leaf fall, some flower buds showed symptoms of necrosis with rapid and complete browning. Flower bud necrosis began at the basal segment and progressed rapidly towards middle and terminal sections. Before leaf fall, flower buds fell off when scales swelled. The terminal and middle parts of the current-year shoots, with some flower buds, collected in October or later from the Lishan area could be used as scions for top-grafting of 'Shinko' pear. Each grafting scion was a 3-5 cm shoot with one flower bud. These results suggest that scions from the terminal and middle segments of stems of 'Shinko' pear from the Lishan area can be used as scions whereas those from Zhoulan area show necrosis and might not be suitable as scions.

• Journal of Korean Foot and Ankle Society
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• v.24 no.4
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• pp.148-155
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• 2020

Purpose: Minor foot amputations are performed for recurrent or infected ulcers or osteomyelitis of the diabetic feet. Patients may require a large amount of bone resection for wound closure. On the other hand, this results in more foot dysfunction and a longer time to heal. The authors describe fillet flap coverage to avoid more massive resection in selected cases. This study shows the results of fillet flap coverage for the closure of diabetic foot minor amputation. Materials and Methods: This was a retrospective case series of patients who underwent forefoot and midfoot amputation and fillet flap for osteomyelitis or nonhealing ulcers between March 2013 to November 2017. In addition, the patient comorbidities, hospital days, complications, and duration to complete healing were evaluated. Results: Fourteen fillet flap procedures were performed on 12 patients. Of those, two had toe necrosis, nine had forefoot necrosis, and three had midfoot necrosis. Eleven forefoot amputations and three midfoot amputations were performed. Among forefoot necrosis after a fillet flap, three patients had revision surgery for partial necrosis of the flap, and two patients had an additional amputation. Two patients had additional amputations among those with midfoot necrosis. By the fillet flap, the amputation size was reduced as much as possible. The mean initial healing days, complete healing days, and hospital stay was 70.6 days, 129.0 days, and 60.0 days, respectively. Conclusion: The fillet flap facilitates restoration of the normal foot contour and allows salvage of the metatarsal or toe.

• Journal of fish pathology
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• v.34 no.1
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• pp.63-70
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• 2021

As a part of research to elucidate the pathogenesis of so called Soft Tunic Syndrome(STS), that caused mass mortalities in the cultured sea squirts, Halocynthia roretzi, the epidemiological and pathological analysis were done to both clinically normal and diseased groups of the farms of Tongyoung and Geoje coastal areas in southeast sea from February to July, 2008. In the histological finding of the tunic, most of individuals showed tunic softness syndromes that included the disarrangement and destruction of tunic fiber with the simultaneous presence of flagellates-like cells, recently suspected as main agents of tunic softness syndromes. Simultaneously, the intensive degenerative changes of the skeletal muscle of diseased sea squirts were recognized. The changes were characterized with the hyalinization and condensation of muscle fibril and hemocytic infiltration in the muscle fibers. Those were thought to be a kind of typical Zenker's necrosis as in the skeletal muscle of higher vertebrates. Besides of the diseased sea squirts, Zenker's necrosis of skeletal muscles were seen in the normal ones. Epidemiological inquiry for diseased groups revealed that the higher incidences of tunic softness syndrome were recorded in the fast growing groups and in the sites presuming the organic pollution. And Higher malondialadehyde(MDA) and glutathione peroxidase(GPx) activity were detected in the groups showing STS. Those results suggested that Zenker's necrosis of body muscles was a kind of"nutritional myopathy" by oxidative stress. Conclusively, it was considered that Zenker's necrosis of body muscles gives an important clue for elucidating pathogenesis of STS of cultured squirts. And it seems that the necrosis were caused by the oxidative stress to body muscle during abnormal rapid growth of sea squirts.

• Korean Journal of Radiology
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• v.22 no.8
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• pp.1279-1288
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• 2021

Objective: To assess the diagnostic performance of the Liver Imaging Reporting and Data System (LI-RADS) version 2018 treatment response algorithm (TRA) for the evaluation of hepatocellular carcinoma (HCC) treated with transarterial radioembolization. Materials and Methods: This retrospective study included patients who underwent transarterial radioembolization for HCC followed by hepatic surgery between January 2011 and December 2019. The resected lesions were determined to have either complete (100%) or incomplete (< 100%) necrosis based on histopathology. Three radiologists independently reviewed the CT or MR images of pre- and post-treatment lesions and assigned categories based on the LI-RADS version 2018 and the TRA, respectively. Diagnostic performances of LI-RADS treatment response (LR-TR) viable and nonviable categories were assessed for each reader, using histopathology from hepatic surgeries as a reference standard. Inter-reader agreements were evaluated using Fleiss κ. Results: A total of 27 patients (mean age ± standard deviation, 55.9 ± 9.1 years; 24 male) with 34 lesions (15 with complete necrosis and 19 with incomplete necrosis on histopathology) were included. To predict complete necrosis, the LR-TR nonviable category had a sensitivity of 73.3-80.0% and a specificity of 78.9-89.5%. For predicting incomplete necrosis, the LR-TR viable category had a sensitivity of 73.7-79.0% and a specificity of 93.3-100%. Five (14.7%) of 34 treated lesions were categorized as LR-TR equivocal by consensus, with two of the five lesions demonstrating incomplete necrosis. Interreader agreement for the LR-TR category was 0.81 (95% confidence interval: 0.66-0.96). Conclusion: The LI-RADS version 2018 TRA can be used to predict the histopathologic viability of HCCs treated with transarterial radioembolization.

• Journal of Microbiology and Biotechnology
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• v.26 no.4
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• pp.790-798
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• 2016

Chlamydiae, obligate intracellular bacteria, are associated with a variety of human diseases. The chlamydial life cycle undergoes a biphasic development: replicative reticulate bodies (RBs) phase and infectious elementary bodies (EBs) phase. At the end of the chlamydial intracellular life cycle, EBs have to be released to the surrounded cells. Therefore, the interactions between Chlamydiae and cell death pathways could greatly influence the outcomes of Chlamydia infection. However, the underlying molecular mechanisms remain elusive. Here, we investigated host cell death after Chlamydia infection in vitro, in L929 cells, and showed that Chlamydia infection induces cell necrosis, as detected by the propidium iodide (PI)-Annexin V double-staining flow-cytometric assay and Lactate dehydrogenase (LDH) release assay. The production of reactive oxygen species (ROS), an important factor in induction of necrosis, was increased after Chlamydia infection, and inhibition of ROS with specific pharmacological inhibitors, diphenylene iodonium (DPI) or butylated hydroxyanisole (BHA), led to significant suppression of necrosis. Interestingly, live-cell imaging revealed that Chlamydia infection induced lysosome membrane permeabilization (LMP). When an inhibitor upstream of LMP, CA-074-Me, was added to cells, the production of ROS was reduced with concomitant inhibition of necrosis. Taken together, our results indicate that Chlamydia infection elicits the production of ROS, which is dependent on LMP at least partially, followed by induction of host-cell necrosis. To our best knowledge, this is the first live-cell-imaging observation of LMP post Chlamydia infection and report on the link of LMP to ROS to necrosis during Chlamydia infection.

• Korean Journal of Medicinal Crop Science
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• v.25 no.5
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• pp.322-327
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• 2017

Background: Cynaroside is a flavone, a flavonoid-like compound, known by different names (luteoloside and cinaroside). It is commonly found in Lonicera japonica Thunb., Chrysanthemum moriflium, and Angelica keiskei. The process of cell death has been classified as necrosis and apoptosis. Necrosis refers to unregulated cell death induced by a chemotherapeutic agent. Doxorubicin is an anthracycline anti-cancer drug used to treat acute leukemia, cancer, and lymphoma. However, it induces nephrotoxicity including tubular damage. Therefore, we investigated the protective effect of cynaroside against doxorubicin-induced necrosis in HK-2 cells. Methods and Results: To confirm the beneficial effect of cynaroside on doxorubicin-induced necrosis, HK-2 cells, a human proximal tubule epithelial cell line were treated with $10{\mu}M$ doxorubicin and $80{\mu}M$ cynaroside. Doxorubicin treatment resulted in increased DNA fragmentation, caspase-3 activity and mitochondria hyperactivation during cell necrosis. However, pretreatment with $80{\mu}M$ cynaroside attenuated DNA fragmentation, caspase-3 activity and mitochondria hyperactivation induced by $10{\mu}M$ doxorubicin in HK-2 cells. Conclusions: These results indicated that pretreatment with cynaroside ameliorated doxorubicin-induced necrosis in HK-2 cells. Therefore, cynaroside be used as a therapeutic agent for improving doxorubicin-induced nephrotoxicity. However, further studies are required to evaluated the toxicity of cynaroside treatment in animals and to determine its protective effect against doxorubicin-induced nephrotoxicity in an animal model.

• Journal of Korean Neurosurgical Society
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• v.60 no.2
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• pp.181-188
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• 2017

Objective : The objective of this study was to analyze the correlation between further compression and necrotic area in osteoporotic vertebral fracture (OVF) patients with contrast-enhanced magnetic resonance imaging (CEMRI). In addition, we investigated the radiological and clinical outcome according to the range of the necrotic area. Methods : Between 2012 and 2014, the study subjects were 82 OVF patients who did not undergo vertebroplasty or surgical treatment. The fracture areas examined on CEMRI at admission were defined as edematous if enhancement was seen and as necrotic if no enhancement was seen. The correlation between further compression and the necrotic and edematous areas of CEMRI, age, and bone mineral density was examined. Also, necrotic areas were classified into those with less than 25% (non-necrosis group) and those with more than 25% (necrosis group) according to the percentages of the entire vertebral body. For both groups, further compression and the changes in wedge and kyphotic angles were examined at admission and at 1 week, 3 months, and 6 months after admission, while the clinical outcomes were compared using the visual analog scale (VAS) and Eastern Cooperative Oncology Group (ECOG) performance status grade. Results : Further compression was $14.78{\pm}11.11%$ at 1 month and $21.75{\pm}14.43%$ at 6 months. There was a very strong correlation between the necrotic lesion of CEMRI and further compression (r=0.690, p<0.001). The compression of the necrosis group was $33.52{\pm}12.96%$, which was higher than that of the non-necrosis group, $14.96{\pm}10.34%$ (p<0.005). Also, there was a statistically significantly higher number of intervertebral cleft development and surgical treatments being performed in the necrosis group than in the non-necrosis group (p<0.005). Moreover, there was a statistical difference in the decrease in the height of the vertebral body, and an increase was observed in the kyphotic change of wedge angle progression. There was also a difference in the VAS and ECOG performance scales. Conclusion : The necrotic area of CEMRI in OVF had a strong correlation with further compression over time. In addition, with increasing necrosis, intervertebral clefts occurred more frequently, which induced kyphotic changes and resulted in poor clinical outcomes. Therefore, identifying necrotic areas by performing CEMRI on OVF patients would be helpful in determining their prognosis and treatment course.

• Molecules and Cells
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• v.28 no.3
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• pp.139-148
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• 2009

Cell death has been traditionally classified in apoptosis and necrosis. Apoptosis, known as programmed cell death, is an active form of cell death mechanism that is tightly regulated by multiple cellular signaling pathways and requires ATP for its appropriate process. Apoptotic death plays essential roles for successful development and maintenance of normal cellular homeostasis in mammalian. In contrast to apoptosis, necrosis is classically considered as a passive cell death process that occurs rather by accident in disastrous conditions, is not required for energy and eventually induces inflammation. Regardless of different characteristics between apoptosis and necrosis, it has been well defined that both are responsible for a wide range of human diseases. Glycogen storage disease type I (GSD-I) is a kind of human genetic disorders and is caused by the deficiency of a microsomal protein, glucose-6-phosphatase-${\alpha}$ ($G6Pase-{\alpha}$) or glucose-6-phosphate transporter (G6PT) responsible for glucose homeostasis, leading to GSD-Ia or GSD-Ib, respectively. This review summarizes cell deaths in GSD-I and mostly focuses on current knowledge of the neutrophil apoptosis in GSD-Ib based upon ER stress and redox signaling.