• Title/Summary/Keyword: Fatty Degeneration

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Effects of an Extract from A. gmelini Weber on Hepatotoxicity Induced by $CCl_4$in Rats - II. Some Dosage Effects of an Extract from A. gmelini on Hepatotoxicity Induced by $CCl_4$in Rats (흰쥐에서 사염화 탄소로 유도된 간독성에 미치는 더위지기 추출물의 영향-II. 더위지기 추출물의 투여용량이 사염화 탄소 독성에 미치는 효과)

  • 권진욱;이규승
    • Environmental Analysis Health and Toxicology
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    • v.17 no.2
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    • pp.175-185
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    • 2002
  • To investigate effects of A. gmelini on the 14-day CCl$_4$induced hepatotoxicity, extracts were prepared in 3 ml saline at the dose of 50, 500, 5,000 mg/kg b.w. to administer orally everyday and same concentration (1 : 9, CCl$_4$: olive oil v/v) of CCl$_4$administered intraperitoneally with 2.5 ml/kg b.w. On the 7th day, hemanalysis showed following recovery values; AST 9.9∼64.6%, ALT 36.9∼71.9%, ALP 75.3∼93.7%, BUN 53.8∼59.7%, TBIL 60.4∼100.0< %, TCHO 77.7∼100.0< %, and TG 60.4∼100.0< %. Even if, 14-day CCl$_4$induced hepatotoxicity recovery was found to depend on doses of extract, and recovery values of each treatment were AST 13.8∼56.4%, ALT 15.7∼68.0%, ALP 53.4∼84.4%, BUN 76.9∼100.0< %, TBIL 60.4 ∼ 100.0< %, TCHO 82.6∼99.3< %, and TG 56.7∼99.7%. By histological examination of liver, hydropic degeneration, fatty change, lipid accumulation and necrosis were also recovered.

Effects of an Extract from A. gmelini Weber on Hepatotoxicity Induced by $CCl_4$in Rats - I. Effects of an Extract from A. gmelini on Hepatotoxicity Induced by Different Levels of $CCl_4$ (흰쥐에서 사염화 탄소로 유도된 간독성에 미치는 더위지기 추출물의 영향- I. 사염화탄소 독성유발 심화 수준에 대한 더위지기 추출물의 회복효과)

  • 권진욱;이규승
    • Environmental Analysis Health and Toxicology
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    • v.17 no.2
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    • pp.161-174
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    • 2002
  • To investigate effects of A. gmelini on the 14-day CCl$_4$induced hepatotoxicity, extracts were prepared in 3 ml saline at the dose of 5,000 mg/kg b.w. to administer orally once daily. Each concentration (5:5, 2:5 : 7.5, 1:9, CCl$_4$: olive oil v/v) of CCl$_4$was orally administered with 2.5 ml/kg b.w., During the experiment, halves of the rats were sacrificed every 7 day and hemanalysis was done. On the 7th day, hemanalysis showed following recovery values; AST 52.6∼61.4%, ALT 55.9∼86.1%, ALP 46.0∼70.9%, BUN 75.7∼100.0< %, TBIL 55.2∼96.1%, TCHO 38.0∼63.7%, and TG 55.2∼96.0%. On the 14th day, recovery values of each treatment were GOT 37.7∼43.1%, GPT 19.8∼45.9%, ALP 58.1∼95.9%, BUN 57.6∼100.0< %, TBIL 78.6∼100.0< %, TCHO 56.9∼100.0< %, and TG 10.0∼5l.2%. By histological examination of liver, hydropic degeneration, fatty change, lipid accumulation and necrosis were also recovered by administration of A. gmelini extract.

A Study on the Histopathological Changes of Experimental Bite-marks with the Progress of Time (실험교흔조직의 수상 후 경과시간에 따른 병리조직학적 변화에 관한 연구)

  • 윤창륙;김종열
    • Journal of Oral Medicine and Pain
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    • v.10 no.1
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    • pp.41-52
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    • 1985
  • In order to observe the histopathological changes with the progress of time after formation of bite-mark, experimental bite-marks were made in female rats and histopathological examinations were performed in the given sites immediately, 5 minutes, 10 minutes, 30 minutes, I hr., 4 hrs., 8 hrs., 12 hrs., 24 hrs., and 48 hrs, after injury. Results and Summary 1. Subcutaneous loose connective tissues and fatty layers were compressed immediately after formation of bite-marks, injured epithelia showed hydropic degeneration 5 minutes later. 2. Inflammatory cells emigrated into tissues with hemorrhages in the tissues after 10 minutes, and more increased centered around the blood vessels.- These distributed most densely in the tissues, after 12 hrs., thereafter, were decreased and distributed in various groups of crowdy appearances, after 48 hrs. 3. After 10 minutes, neutrophils emigrated into tissues and disappeared gradually with an appearance of monocytes. These disappeared completely, after 24 hrs. Lymphocytes and plasma cells were see n at 48 hrs. later. 4. Adherence of mast cells to injured sites occurred immediately, and which adhered to blood vessel walls of injured sites, after 10 minutes. 8 hrs. later, degranulation in emigrated inflammatory cells showed, and these degranulation disappeared gradually with a progress of time.

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Magnetic Resonance Imaging as a Biomarker for Duchenne Muscular Dystrophy

  • Lim, Woo-taek
    • Physical Therapy Korea
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    • v.22 no.3
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    • pp.98-105
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    • 2015
  • Muscular dystrophy is a hereditary musculoskeletal disorder caused by a mutation in the dystrophin gene. Duchenne muscular dystrophy (DMD) is one of the most common, and progresses relatively faster than other muscular dystrophies. It is characterized by progressive myofiber degeneration, muscle weakness and ultimately ambulatory loss. Since it is an X-linked recessive inheritance, DMD is mostly expressed in males and rarely expressed or less severe in females. The most effective measurement tool for DMD is magnetic resonance imaging (MRI), which allows non-invasive examination of longitudinal measurement. It can detect progressive decline of skeletal muscle size by measuring a maximal cross-sectional area of skeletal muscle. Additionally, other techniques in MRI, like $T_2$-weighted imaging, assess muscle damage, including inflammation, by detecting changes in $T_2$ relaxation time. Current MRI techniques even allow quantification of metabolic differences between affected and non-affected muscles in DMD. There is no current cure, but physical therapist can improve their quality of life by maintaining muscle strength and function, especially if treatment (and other forms of medical intervention) begins in the early stages of the disease.

Cryptogenic Temporal Hollowing

  • Park, Ie Hyon;Kwon, Heeyeon;Kim, Sang Wha
    • Archives of Craniofacial Surgery
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    • v.17 no.4
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    • pp.218-221
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    • 2016
  • Temporal hollowing is a common complication that occurs after coronal approach surgeries. However, temporal hollowing without previous nerve damage or trauma history is rare. Herein, we present a patient with cryptogenic temporal hollowing. A 22-year-old man without any history of craniofacial interventions or trauma presented with temporal hallowing. Magnetic resonance imaging revealed fatty degeneration of the left temporalis muscle. Electromyography and nerve conduction study showed no signs of neurologic abnormalities. The patient received autologous fat injection of 30 mL harvested from the left thigh using the modified Coleman technique. Temporal hollowing is commonly caused by atrophy of the superficial temporal fat pad. Its incidence is reported to be as high as 6% after coronal approach operation. Augmentation using porous hydroxyapatite or titanium mesh is a treatment option. Autologous fat graft can also be an option for mild to moderate temporal hollowing. In this case, a patient with no history of trauma, surgery, or myogenic disease developed temporal hollowing. Further study of the little-known cryptogenic form of temporal hollowing is warranted.

Study on Antihyperlipidemic Effect of Kamiondamtang (가미온담탕(加味溫膽湯)의 항고지혈 작용에 대한 연구)

  • Kim, Kyung-Soo;Jeun, Sang-Yoon;Ann, Jeung-Jo;Hong, Seok;Jeung, Su-Mi
    • Herbal Formula Science
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    • v.13 no.1
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    • pp.85-101
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    • 2005
  • Kamiondamtang(KODT) has been used in oriental medicine as stress by many medical practitioner for the study of KODT, we had fed mice divided to three groups(basal diet, hyperlipidemic diet, hyperlipidemic diet + KODT), and observed the change of weight, total cholesterol, triglyceride, SGOT, SGPT, HDL-cholesterol, LDL-cholesterol on the serum per every 7days for 6weeks. To help comparison with the results above, we had tested endothelial cells and liver. The results of this Study were obtained as fallows ; 1. Total cholesterol, triglyceride and LDL-cholesterol were decreased significantly by KODT. 2. HDL-cholesterol was increasd significantly by KODT. 3. SGOT was intended to decrease by KODT, 4. %W was decreased significantly by KODT. 5. In case of supplying KODT, WBC attatched on endothelial cells and vacuoles in muscular layer were not observed. 6. In case of supplying KODT, fatty degeneration was not observed in liver portal area.

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Effect of Cheunggansoyosan-gamibang on Hyperlipidemic mice (청간소요산가미방(淸肝逍遙散加味方)이 생쥐의 고지혈증에 미치는 영향)

  • Baek, Yong-Ju;Yang, Seung-Jung;Park, Hye-Sun;Kim, Kyoung-Su;Hong, Seok;Jeon, Sang-Yoon
    • Herbal Formula Science
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    • v.14 no.1
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    • pp.120-132
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    • 2006
  • Hyperlipidemia is one of dangerous factors causing the arteriosclerosis. For the study of Cheunggansoyosan-gamibang( CGSYS) on antihyperlipidemic effect, we had fed mice divided to three groups (basal diet, hyperlipidemic diet, hyperlipidemic diet + CGSYS), and observed the change of weight, total cholesterol. triglyceride, HDL-cholesterol. LDL-cholesterol. sGOT, sGPT on the serum per every 7days for 6weeks. Also to compensate for the results above, we had tested rat liver. The results of this Study were obtained as fallows ; 1. Cholesterol change on blood was decreased by CGSYS. 2. Total cholesterol. triglyceride and LDL-cholesterol were significantly decreased by CGSYS. 3. HDL-cholesterol was significantly increasd by CGSYS. 4. sGPT was significantly decreased by CGSYS. 5. sGOT was not changed by CGSYS. 6. In case of supplying CGSYS. fatty degeneration was not observed in liver portal area. This study suggests that Cheunggansoyosan-gamibang was significant effect with hyperlipidemia.

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Phospholipase A2, reactive oxygen species, and lipid peroxidation in CNS pathologies

  • Adibhatla, Rao Muralikrishna;Hatcher, J.F.
    • BMB Reports
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    • v.41 no.8
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    • pp.560-567
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    • 2008
  • The importance of lipids in cell signaling and tissue physiology is demonstrated by the many CNS pathologies involving deregulated lipid metabolism. One such critical metabolic event is the activation of phospholipase $A_2$ ($PLA_2$), which results in the hydrolysis of membrane phospholipids and the release of free fatty acids, including arachidonic acid, a precursor for essential cell-signaling eicosanoids. Reactive oxygen species (ROS, a product of arachidonic acid metabolism) react with cellular lipids to generate lipid peroxides, which are degraded to reactive aldehydes (oxidized phospholipid, 4-hydroxynonenal, and acrolein) that bind covalently to proteins, thereby altering their function and inducing cellular damage. Dissecting the contribution of $PLA_2$ to lipid peroxidation in CNS injury and disorders is a challenging proposition due to the multiple forms of $PLA_2$, the diverse sources of ROS, and the lack of specific $PLA_2$ inhibitors. In this review, we summarize the role of $PLA_2$ in CNS pathologies, including stroke, spinal cord injury, Alzheimer's, Parkinson's, Multiple sclerosis-Experimental autoimmune encephalomyelitis and Wallerian degeneration.

Dystrophin Degradation in Skeletal Muscles with Lipid Enrichment in Cattle (지방 침착률이 높은 식용소에서 나타난 골격근의 디스트로핀 소실)

  • Jeon, Sung-Hwan;Kim, Ah-Young;Lee, Eun-Mi;Lee, Eun-Joo;Hong, Il-Hwa;Hwang, Ok-Kyung;Jeong, Kyu-Shik
    • Journal of Life Science
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    • v.26 no.5
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    • pp.592-602
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    • 2016
  • This study investigated the muscular dystrophin levels in freely moving Australian cattle mainly fed grass, freely moving Korean cattle fed mainly a grain diet, and Korean cattle fed a grain diet but housed in a relatively limited space of a cow house. The total skeletal muscle specimens of 244 cattle were collected and immediately fixed in 10% neutral formalin. The same area was biopsied from the cattle in both countries. The findings showed that fatty infiltration is highly correlated with membrane-associated protein degradation in skeletal muscle, and that among several membrane-associated proteins, dystrophin showed the most significant reduction in expression in the cattle with fatty infiltration. Similarly, CD36 was more highly expressed in the cattle with fatty infiltration of skeletal muscle. Various breeding factors, such as oxidative stress; the presence of oxidized lipids in the diet; and environmental factors such as exercise, temperature and amount of time spent, may have critical effects on the degradation of normal cytoskeleton proteins, which are required for maintaining normal skeletal muscle architecture. Among the sarcolemma membrane-associated proteins, dystrophin is the most sensitive membrane protein that is involved muscular dystrophy and muscular degeneration. Thus, the present findings may be useful for studies on muscular dystrophy in humans or the pathogenesis of muscular diseases in animal models.

Pathological Studies on the Experimentally Induced Rodenticide Poisoning in Ruminant (반추수(反芻獸)의 살서제중독(殺鼠劑中毒)에 관한 병리학적(病理學的) 연구(硏究))

  • Lee, Cha-Soo;Park, Cheong-Kyu;Cho, Yong-Joon;Kwak, Soo-Dong
    • Korean Journal of Veterinary Research
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    • v.22 no.2
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    • pp.221-232
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    • 1982
  • This paper dealt with the pathological and clinical findings on the experimentally induced rodenticide (fluoroacetate, zinc phosphide, thallium sulfate, coumarin) and NaCN poisoning of ruminants (Holstein cattle and/or Korean native goat) for the purpose of the diagnosis in the accidental rodenticide poisoning of cattle. The results observed are summarized as follows: Fluoroacetate poisoning (cattle and goat): in the clinical signs, there were depression, convulsion, dyspnea, groan, grinding of the teeth, vomiting, opisthotonus and post-mortem tympany. In the macroscopical findings, the blood was more or less poor coagulative and dark red, bloody fluid with foam in the trachea, hyperemia and hemorrhage of tracheal mucosa and lung, cloudy swelling and hyperemia of kidney, epicardial hemorrhage(cattle), and hyperemia of abomasum, intestine and brain were observed. In the microscopical findings, there were pulmonary edema and hemorrhage, necrosis of convoluted tubular epithelium and interstitial hemorrhage of kidney, focal coagulative necrosis of myocardium, hemorrhage of pancreas and spleen, dilatation of Virchow-Robin space and hyperemia of brain, and necrosis with desquamation of mucosal epithelia of abomasum and upper small intestine. In the histological lesions of the liver, lobular peripheral hyperemia, centrilobular necrosis and cytoplasmic inclusion bodies of the hetatic cells were observed. The cytoplasmic inclusion body of the hepatic cells was not seen in the affected goat, but hydropic degeneration of the hepatic cells was marked. Zinc phosphide poisoning (cattle and goat): clinically, the affected animals died in recumbent position after ataxia, dyspnea and convulsion. In the macroscopical findings, hyperemia and hemorrhage of lung, cloudy swelling and hyperemia of liver and kidney, hemorrhage of spleen (cattle), and catarrh of abomasum and small intestine were observed. In the microscopical findings, necrosis of the convoluted tubular epithelium and hyperemia of kidney, hemorrhage of spleen, hyperemia of lung, hyperemia or hemorrhage of heart, cloudy. swelling and fatty changes of hepatic cells, dilatation of hepatic central vein, hyperemia of brain, and catarrh of abomasal and small intestinal mucosae were observed. Thallium sulfate poisoning (cattle): in the macroscopical findings dark red color of blood, hyperemia and hemorrhage of lung, bloody fluid with foam in the tracheal mucosa, petechiae of tracheal mucosa, cloudy swelling and hemorrhage of liver, necrotic lesions and hemorrhage of renal cortex and epicardial hemorrhage were observed. In the microscopical findings, severe hemorrhages of the lung, cloudy swelling and necrosis of hepatic cells, hyperemia and hemorrhage of liver, focal coagulative necrosis of mycordium, necrosis of the convoluted tubular epithelium and hyperemia of kidney, hyperemia and hemorrhage of spleen and dilatation of Virchow-Robin apace in brain were observed. Coumarin poisoning (goat): the poisoned animals died in the state of groan and depression. In the macroscopical findings, poor coagulation of blood, hemorrhage of lung, cloudy swelling and severe hemorrhages of liver, cloudy swelling and hemorrhage of kidney, abomasal hemorrhage, catarrh of small intestine, and hyperemia and hemorrhage of the other organs were observed, In the microscopical findings, hyperemia and hemorrhage of lung and kidney, cloudy swelling of the convoluted tubular epithelium of kidney, severe hepatic hyperemia, cloudy swelling and hydropic degeneration of heptatic cell, and hyperemia and hemorrhage of brain and spleen were observed. NaCN poisoning (cattle and goat): clinically, there were convulsion, severe dyspnea, paresis of hind limb, depression and then rigor of four limbs. In the macroscopical findings, bright red color of blood, hyperemia and bright and red tinge of lung cloudy swelling of kidney and liver, and hyperemia of abomasum were observed. In the microscopical findings, cloudy swelling and hydropic degeneration of hepatic cell, hyperemia and edema of lung, necrosis and degeneration of the convoluted tubular epithelium and hemorrhage in kidney, dilatation of Virchow-Robin space of brain and hemorrhage of spleen were observed.

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