Park, Kap-Joo;Kim, Eun-Jung;Cho, Myung-Hwan;Lee, Jae-Seok
Food Science and Biotechnology
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제15권6호
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pp.833-837
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2006
To determine whether alcohol-treated rat liver cells can be protected by a static magnetic field (SMF), we analyzed the blood chemistry and histology of hepatic tissue removed from alcohol-exposed rats that had been exposed to a static magnetic field. The rats were exposed to a 0.3 tesla (3,000 gauss) magnetic field (MF) for 24 hr daily for 5 weeks with appropriate controls. Glutamic pyruvic transaminase activity and the triglyceride levels in animals exposed to the north (N) or south (S) pole of the MF decreased significantly (p<0.01 and p<0.05, respectively) compared with negative control animals with alcohol exposure. A histological examination of hepatic tissue revealed a moderate to severe accumulation of fat vacuoles of various sizes in the cytoplasm of the hepatocytes of animals in the negative control group throughout the study; whereas in groups exposed to the MF poles, fewer fat vacuoles were seen compared with the negative control group. Electron microscopic observations showed that exposure to the N or S pole protected organelles, including the nucleus, from damage during exposure to this toxic agent, as indicated by the fact that the nucleus and the mithochondria virtually retained their shape throughout this study. These results suggest that exposure to a SMF could be an excellent way of protecting against alcohol-induced damage to the rat liver cell.
PURPOSE: This study examined the immediate effects of Graston instrument-assisted soft-tissue mobilization (GIASTM) and self-stretching on the muscular properties of the gastrocnemius in athletes. METHODS: Thirty subjects (All in their 20 s) were distributed randomly and evenly into two groups of 15 each: GIASTM and stretching. The subjects had no history of gastrocnemius damage in the previous three months. The muscle tone, stiffness, elasticity, and mechanical stress relaxation time (MSRT) of the gastrocnemius were blind-tested. RESULTS: The GIASTM group showed significant changes in all categories, while only MSRT changed significantly in the self-stretching group after intervention. A comparison of the two groups revealed significant differences in stiffness, elasticity, and MSRT (Time required for the muscle to recover after distortion after intervention in the GIASTM group. CONCLUSION: In this study, significant decreases in muscle tone and stiffness, as well as significant increases in elasticity, were observed in the gastrocnemius of the GIASTM group. On the other hand, sSelf-stretching showed significant differences in MSRT. Therefore, GIASTM is more effective in the recovery of the gastrocnemius muscle from fatigue than self-stretching. This study suggests that GIASTM can help prevent damage to the gastrocnemius in athletes and contribute to their training and rehabilitation programs.
The effects of total dietary restriction(100% restriction of energy intake) on thiobarbituric acid reactive substance(TBARS) contents and intracellular antioxidant enzymes activities in the liver and kidney of young male Sprague Dawley rats were studied. The TBARS contents were reduced in both liver and kidney, up to 77% and 79% of the control rats, fed ad libitum, respectively at 7 days after dietary restriction . Superoxide dismutase(SOD) activities in the liver and kidney of rats were increased significantly by total dietary restriction. However, the activity of catalase in kidney was decreased 27% at 6 days after dietary restriction, but this enzyme activity did not change in liver. The changes of glutathione peroxidae(GSHPx) and catalase activities in the liver and kidney of rats with dietary restriction were not significant. These result suggested that dietary restriction reduce the free radical induced by tissue damage, as determined by TBARS content, in both the liver and kidney but the changes of activities of antioxidant enzymes may not be a contributory factor in reducing oxidative damage to tissue.
Considering the role of viscosity in the hemorheology, the characteristics of non-Newtonian fluid are important in the pulsatile blood flows. Stenosis, with an abnormal narrowing of the vessel, contributes to block blood flows to downstream tissue and lead to plaque rupture. Therefore, systematic analysis of blood flow around stenosed vessels is crucial. In this study, non-Newtonian behaviors of blood analog fluids around the micro-stenosis with 60 % severity in diameter of $500{\mu}m$ was examined by using CFX under the pulsatile flow conditions with the period of 10 s. Viscosity information of two non-Newtonian fluids were obtained by fitting the value of normal blood and highly viscous blood. As the Newtonian fluid, the water at room temperature was used. During the pulsatile phase, wall shear stress (WSS) is highly oscillated. In addition, high viscous solution gives rise to increases the variation in the WSS around the micro-stenosis. Highly oscillating WSS enhance increasing tendency of plaque instability or rupture and damage of the tissue layer. These results, related to the influence on the damage to the endothelium or stenotic lesion, may help clinicians understand relevant mechanisms.
Background Posttraumatic lymphedema (PTL) is sparsely described in the literature. The aim of this study is to propose a comprehensive approach for prevention and treatment of PTL using lymphovenous anastomosis (LVA) and lymphatic vessels free flap, reporting our experience in the management of early-stage lymphedema. Methods A retrospective observational study was performed between October 2017 and July 2022. Functional assessment with magnetic resonance lymphangiography and indocyanine green lymphography was performed. Patients with lymphedema and functional lymphatic channels were included. Cases with limited soft tissue damage were proposed for LVA, and those with acute or prior soft tissue damage needing skin reconstruction were proposed for superficial circumflex iliac artery perforator lymphatic vessels free flap (SCIP-LV) to treat or prevent lymphedema. Primary and secondary outcomes were limb volume reduction and quality of life (QoL) improvement, respectively. Follow-up was at least 1 year. Results Twenty-eight patients were operated using this approach during the study period. LVA were performed in 12 patients; mean reduction of excess volume (REV) was 58.82% and the improvement in QoL was 49.25%. SCIP-LV was performed in seven patients with no flap failure; mean REV was 58.77% and the improvement QoL was 50.9%. Nine patients with acute injury in lymphatic critical areas were reconstructed with SCIP-LV as a preventive approach and no lymphedema was detected. Conclusion Our comprehensive approach provides an organized way to treat patients with PTL, or at risk of developing it, to have satisfactory results and improve their QoL.
Dong Chul Lee;Kyung Jin Lee;Hohyung Lee;Sung Hoon Koh;Jin Soo Kim;Si Young Roh
Archives of Plastic Surgery
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제51권1호
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pp.110-117
/
2024
Percutaneous first annular pulley (A1 pulley) release, which has been increasingly used to treat trigger fingers, has been widely established as a safe and simple procedure. Multiple studies have reported positive results of percutaneous A1 pulley release. In this study, however, we report cases of patients who developed complications after undergoing percutaneous A1 pulley release at local clinics. A total of six patients visited our hospital for infectious complications after percutaneous A1 pulley release. Various sequelae such as damage to normal structures, insufficient procedure, and tissue necrosis were observed during the exploration. A retrospective study was conducted to identify the cause and trend of the observed complications by instruments (HAKI knife or needle). In the HAKI knife group, there was a tendency for damage to normal structures, while in the needle group, an insufficient release or serious soft tissue necrosis was observed. Based on these cases, our findings confirm the existence and characteristics of infectious complications following the percutaneous A1 pulley release. We further identify that the type of instrument used predicts the nature of complications. Thus, reliable and skilled performance of the procedure by experts is essential for safe treatment.
The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.
Objectives : Polygalae Radix (POL) has an ameliorating effect on learning and memory impairment caused by cerebral hypoperfusion. In regard to POL's action mechanism, this study was carried out to investigate the effects of POL on oxidative damage and neuronal apoptosis induced by cerebral hypoperfusion in rats.Methods : The cerebral hypoperfusion was induced by permanent bilateral common carotid artery occlusion (pBCAO) in Sprague-Dawley rats. POL was administered orally once a day (130 mg/kg of water-extract) for 28 days starting at 4 weeks after the pBCAO. Superoxide dismutase (SOD) activities and malondialdehyde (MDA) levels in the brain tissue were measured using ELISA method. Expressions of 4-hydroxynonenal (4HNE) and 8-hydroxy-2'- deoxyguanosine (8-OHdG) were observed using immunohistochemistry. In addition, neuronal apoptosis was evaluated with Cresyl violet staining, TUNEL labeling, and immunohistochemistry against Bax and caspase-3.Results : POL treatment significantly increased SOD activities and significantly reduced MDA levels in the cerebral cortex. The up-regulations of 4HNE and 8-OHdG expression caused by pBCAO in the CA1 of hippocampus were significantly attenuated by POL treatment. POL treatment also restored the reduction of CA1 thickness and CA1 neurons caused by pBCAO and significantly attenuated the apoptotic markers including TUNEL-positive cells, Bax, and caspase-3 expression in the CA1 of hippocampus.Conclusions : The results show that POL attenuated the oxidative damage in brain tissue and neuronal apoptosis in the hippocampus caused by the cerebral hypoperfusion. It suggests that POL can be a beneficial medicinal herb to treat the brain diseases related to cerebral hypoperfusion.
Objectives: This study evaluated the effects of Ssanghwa-tang (SHT) on lung injury and muscle loss in a COPD mouse model. Methods: C57BL/6 mice were challenged with cigarette smoke extract and lipopolysaccharide, and then treated with two concentrations of SHT (250 and 500 mg/kg). After sacrifice, the bronchoalveolar lavage fluid (BALF) or lung tissue was analyzed by cytospin, ELISA, real-time PCR, flow cytometry analysis, and H&E and Masson's trichrome staining. The grip strength of COPD mice was measured using a grip strength meter. The running time of COPD mice was measured by a treadmill test. Muscle tissue of the quadriceps was stained with H&E and Masson's trichrome staining. Results: SHT significantly inhibited the increase in neutrophil numbers in BALF and significantly decreased immune cell activity in BALF and lung tissue. It also significantly inhibited the increase in TNF-α, IL-17, and MIP2 in BALF. Real-time PCR analysis revealed that the mRNA expression of TNF-α, IL-17, MIP2, and TRPV1 in lung tissue showed a significant decrease compared with the control group. Lung tissue damage was significantly reduced in the histological analysis. The grip strength and running time of the COPD mice showed a significant decrease compared with the control group. In histological staining, SHT was found to reduce the damage to muscle tissue. Conclusions: This study indicates that SHT can be used as a therapeutic agent for COPD patients by inhibiting lung injury and muscle loss.
Kim, Nam-Keun;Lee, Sook-Hwan;Ko, Jung-Jae;Roy, Rabindra;Lee, Hey-Kyung;Kwak, In-Pyung;Cha, Kwang-Yul
Journal of Genetic Medicine
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제2권1호
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pp.31-34
/
1998
The N-methylpurine-DNA glycosylase (MPG), a ubiquitous DNA repair enzyme, removes N-methylpurine and other damaged purines induced in DNA. Tissue-specific mRNA levels of the N-methylpurine-DNA glycosylase (MPG) were investigated in Balb/c mice of four different growing stages; newborn, 1, 4 and 8-weeks postpartum. MPG expressions in the newborn and the 8-week-old mice were the highest in thymus and testis, respectively. The tested tissues of the newborn mice had consistently higher MPG mRNA level than 8-week-old adults except in testis and thymus. The MPG mRNA level in testis was the lowest in the newborn mice, but it attained the highest in the 8-week-old mice. The levels of MPG mRNA among the different tissues in the newborn and the 8-week-old mice were more than 9.0 and 19.0-fold respectively. These results suggest that the of MPG expression was dependent on the growing stage and had tissue-specificity.
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