• 제목/요약/키워드: Ultrastructural changes

검색결과 333건 처리시간 0.024초

Malathion이 발생중(發生中)인 개배(鷄胚) 척수(脊髓)의 미세구조(微細構造)와 acetylcholinesterase 활성(活性)에 미치는 영향(影響) (Effects of Malathion on the Ultrastructure and the Acetylcholinesterase Activity of the Developing Spinal Cord in Chick Embryos)

  • 김완종;등영건;최임순
    • Applied Microscopy
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    • 제18권1호
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    • pp.60-76
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    • 1988
  • Chick embryos which have received a single injection of the organophosphate compound, malathion (0.1 mg/0.05 ml, 0.5 mg/0.05 ml, 1.0 mg/0.05 ml or 2.0 mg/0.05 ml) via the yolk sac at certain times (2 days, 4 days or 6 days after incubation) have been investigated. After 9 days of incubation, chick embryos were harvested to examine the effects of malathion on the ultrastructure and the acetylcholinesterase(AChE) activity of the developing spinal cord. The effects of simultaneous injection of malathion and nicotinamide were also compared. On ultrastructural findings, neurons in the ventral horn of spinal cord showed to be inhibited in their differentiation by malathion; nuclear irregularity, separation of nuclear membranes, reduction of ribosomal distribution, and cytoplasmic vacuoles were observed. In the younger embryos treated with relatively high doses of malathion, nucleus and cytoplasmic organelles of neurons were severely destroyed, and the neurons were shown to be necrotic. On cytochemical study of AChE by electron microscope, the positive reaction products of AChE were localized at the membranes of nucleus and endoplasmic reticulum of neurons. Inhibition of AChE activity was severe in groups treated with relatively low doses of malathion. Nicotinamide (5.0 mg/0.05 ml) alleviated malathion-induced morphological alterations. In conclusion, it is suggested that malathion changes the ultrastructure and reduces. AChE activity in differentiating neurons, and the severity of which is consistently dose- and age-dependent.

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Effect of the Inhibition of Platelet Activating Factor on Oxidative Lung Injury Induced by Interleukin-$1\;{\alpha}$

  • Lee, Young-Man;Park, Yoon-Yub
    • The Korean Journal of Physiology and Pharmacology
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    • 제2권4호
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    • pp.479-491
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    • 1998
  • In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

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흰쥐의 난자성숙에 있어서의 칼슘의 대사 (Metabolism of Calcium in the Oocyte Maturation of Rat)

  • 홍순갑;이준영
    • Clinical and Experimental Reproductive Medicine
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    • 제23권3호
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    • pp.357-366
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    • 1996
  • The present experiments aimed to investigate the metabolism of calcium during oocyte maturation in rat. The concentration of free calcium and calmodulin in oocytes was measured respectively by using of fluo-3/AM and FITC with microscope fluorescence spectrometer. The ultrastructural localization of calcium precipitates in oocytes was observed with the transmission electron microscope. Cumulus-free immature oocytes(GV-oocyte) were cultured in vitro through 15 hours. The free calcium concentration in GV oocyte was $55.9{\pm}3.5nM$. In calcium-containing medium, the free calcium concentration was increased in germinal vesicle breakdown(GVBD) oocyte($64.2{\pm}7.3nM$). In normal medium after calcium chelator treatment ($10{\mu}M$ BAPTA/AM), the free calcium contents were slightly lower than those in control group. In calcium-free medium, the free calcium content was drastically increased in GVBD($72.7{\pm}3.4nM$) and metaphase I - anaphase I ($88.0{\pm}3.4nM$) oocyte. In maturation rate of oocytes, GVBD rate was high in control group($82.9{\pm}6.55%$) and calcium chelator treatment group($91.2{\pm}4.4%$), but in calcium-free medium group, it was low and then the oocyte was degenerated without polar body formation. Relative content of calmodulin in oocyte was significantly(P<0.001) increased in metaphase I - anaphase I than in GV and GVBD oocyte. The calcium precipitates were observed in mitochondria and cytoplasm of GV oocyte but that were not observed in mitochondria of GVBD and metaphase I - anaphase I oocyte. And then the calcium precipitates reappeared in mitochondria of metaphase II oocyte. The above results indicate that changes in free calcium and calmodulin concentration of oocyte occur according to the maturational stages and the extracellular calcium is required during oocyte maturation. Also change of calcium localization in oocyte occurs according to the maturational stages.

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Short-term Storage and Cryopreservation of Abalone (Haliotis discus hannai) Sperm

  • 강경호;김재민;김영훈
    • 한국패류학회지
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    • 제20권1호
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    • pp.17-26
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    • 2004
  • In present study, attempts were made to preserve abalone (Haliotis discus hannai) sperm in liquid form at low temperature, to evaluate the effect of various diluents in short-term storage on sperm, and cryopreservation procedures were optimized for the cryoprotectants and freezing rates, as well as the motility, survival rate, and the ultrastructural changes of sperm after short-term storage and cryopreservation were observed. The abalone sperm reached maximum motility until about 4 min after activation. The motility was constant for about 16 min, after which it dropped gradually, and about 50 min later all motility ceased. In Hanks' balanced salt solution (HBSS, 300 and 400 mOsmol/kg) and 150, 250 and 350 mOsmol/k artificial seawater (ASW), the sperm was immotile. After 100% ASW was added, motility of those sperm, which are in 300, 400 mOsmol/kg HBSS, 250, 350 mOsmol/kg ASW, could be again restored incompletely. Sperm motility can be maintained for 20 days of cold storage only in ASW of 850 and 1200 mOsmol/kg. A high motility index of 3.5-4.5 was observed for the first 8 days in 850 and 950 mOsmol/kg ASW. In other diluents sperm motility was constant less than 10 days, and the motility index was obviously lower than that of sperm in 850 and 1200 mOsmol/kg ASW. After 20 days of cold storage, survival rates of 10.2%-20.7% were obtained in ASW and 300 mOsmol/kg HBSS, and that in 400 HBSS (65.3%) was significantly higher than others. The constant period of sperm motility stored in 850 mOsmol/kg ASW was obviously longer than that in 1200 mOsmol/kg ASW after 6 days of storage. The sperm plunged into liquid nitrogen all died except that sperm using 15% glycerol as cryoprotectant restored 10.4% of motility. The highest motility index (3.4) was obtained with 5% glycerol and freezing procedure: $-50^{\circ}C$/min from $20^{\circ}C$ to $-80^{\circ}C$.

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Selenium이 adriamycin에 의해서 유발되는 랫드 신장병변에 미치는 영향 (The effect of selenium on renal lesions induced by adriamycin in rats)

  • 박은성;이준섭
    • 대한수의학회지
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    • 제37권1호
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    • pp.41-57
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    • 1997
  • This study was carried out to investigate the effect of selenium on the adriamycininduced renal lesions in male Sprague Dawley rats. A total of 60 Sprague-Dawley male rats were divided into 2 control groups(C1: saline, C2: selenium) and 2 treatment groups(T1: adriamycin, T2: adriamycin+selenium). The rats of the C1 and T1 groups were given normal saline(0.15ml/rat), the rats of the C2 and T2 groups were given sodium selenite(0.5mg/kg) intraperitoneally three days a week for 4 weeks. The treatment groups were dosed intraperitoneally with adriamycin(2mg/kg/day) five days at the second week. Animals were sacrificed at the 1st week, 2nd week and 3rd week after dosing with adriamycin. The morphologic abnormalities of the glomeruli and tubules in the kidney of male rats were examined histopathologically and electron microscopically.The results obtained were as follows : The mean body weight of adriamycin dosed group was significantly decreased as compared with that of control group at 4th week(p<0.05). In adriamycin and selenium dosed group, the mean body weight was decreased until the end of 2nd week but gradually increased from 3rd to 4th week. The histopathological findings of the renal corpuscle in adriamycin dosed group were parietal epithelial cell proliferation, vacuolization of glomerulus, and thickened basement membrane of the parietal epithelium. Proximal convoluted tubules were significantly dilated and the lumens were filled with renal cast. These lesions were generally not very significant in the rats given adriamycin and selenium. The electron microscopical findings of the renal glomerulus in the adriamycin dosed group were focal loss and fusion of the pedicels of the podocyte, and some vacuoles in the cytoplasm of the podocytes. There were numerous cytoplasmic vacuoles in the proximal and distal convoluted tubular cells. However, these ultrastructural changes were not significantly observed in the renal tubules of the rats of adriamycin and selenium dosed group. These results suggest that selenium may act as an inhibitor of the renal lesions induced by adriamycin in male rats.

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신연 골형성술에 있어서의 분자생물학적 최신 지견 (CURRENT REVIEW OF MOLECULAR BIOLOGY IN DISTRACTION OSTEOGENESIS)

  • 지유진;송현철;김여갑;김진;김창현
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제28권6호
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    • pp.456-463
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    • 2002
  • Distraction osteogenesis is a well-established clinical treatment for limb length discrepancy and skeletal deformities. Appropriate mechanical tension-stress is believed not to break the callus but rather to stimulate osteogenesis. In contrast to fracture healing, the mode of bone formation in distraction osteogenesis is primarily intramembranous ossification. Although the biomechanical, histological, and ultrastructural changes associated with distraction osteogenesis have been widely described, the basic biology of the process is still not well known. Moreover, the molecular mechanisms in distraction osteogenesis remain largely unclear. Recent studies have implicated the growth factor cascade is likely to play an important role in distraction. And current reserch suggested that mechanical tension-stress modulates cell shape and phenotype, and stimulates the expression of the mRNA for bone matrix proteins. This article presents the hypotheses and current research that have furthered knowledge of the molecular biology that govern distraction osteogenesis. The gene regulation of growth factors and extracellular matrix proteins during distraction osteogenesis are discussed in this article. It is believed that understanding the biomolecular mechanisms that mediate distraction osteogenesis may guide the development of targeted strategies designed to improve distraction osteogenesis and accelerate bone healing.

신생혈관 억제제 KJ3, Betulinic acid, Fumagillin의 혈관형성억제 및 신경모세포종에 대한 치료효과 (Inhibition of Tumor Growth and Angiogenesis by KJ3, Betulinic Acid, and Fumagillin in Mouse Neuroblastoma)

  • 최승훈;이정희;황의호
    • Advances in pediatric surgery
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    • 제8권2호
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    • pp.101-106
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    • 2002
  • The antiangiogenic effects of novel agent KJ3, Betulinic acid, and Fumagillin on the neovascularization were studied by examining ultrastructural alterations in the vasculature of synthetic gelform and mouse neuroblastoma C1300. Small pieces of gelform with 0.4% agar were introduced subcutaneously (s.c.) in 7 week old male CH3/HeJ mice. After the $LD_{50}s$ were determined by FACS analysis, a third of $LD_{50}$ of three drugs were injected either locally or intraperitoneally every other day for 14 days. A/J mice were inoculated s.c. with the C1300 neuroblastoma cell line, then either saline or three drugs were injected in the same manner. The antiangiogenic effects of three drugs were studied by measuring the histologic changes in tumors, and immunostaining for CD34, VIII/vWF, CD105, and thymidine phosphorylase. In the drug treated groups, the number of vessels in gelform experiments and C1300 neuroblastoma experiments were lower than the corresponding values in the control. The histologic findings were significantly different in drug treated groups on day 7, but these were not significant on day 14. These results imply that antiangiogenic agents were effective when the tumor burden is minimal.

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Cobalt-60 방사선조사가 백서의 타액선에 미치는 영향에 관한 전자현미경적 연구 (AN ELECTRON MICROSCOPIC STUDY ON THE COBALT-60 IRRADIATION EFFECTS ON THE SALIVARY GLAND OF THE WHITE RAT)

  • 박창서
    • 치과방사선
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    • 제15권1호
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    • pp.27-40
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    • 1985
  • This study was undertaken to observe the histopathologic changes in salivary gland of the white rats when exposed to megavoltage fractionated dose of cobalt-60 irradiation and 78 female white rats, weighing approximately 180gm, were divided into control and 3 experimental groups. Irradiation on experimental groups was delivered by using 6000 curies MeV ALCYON cobalt-60 teletherapy unit with exposure rate 183 rads per minute, in source skin distance 80cm, 600 rads every 3 days. In experimental groups, Group Ⅰwas irradiated of total dose 1200 rads for a period of 6 days, Group Ⅱ was irradiated of total dose 2400 rads for a period of 12 days and Group Ⅲ was irradiated of total dose of 4800 rads for a period of 24 days. The animals were sacrificed serially at 3 hours, 6 hours, 10 hours, 1st day, 4th day, 7th day after each completion of irradiation exposure. At sacrifice, salivary glands were excised and examined microscopically and electromicroscopically. The results were as follows: 1. The acinar cells of parotid and submaxillary gland showed damage varied with dose, 1200 rads resulted in very mild injury while 4800 rads caused most extensive injury. 2. The acinar cells of parotid and submandibular gland showed similar ultrastructural alterations, appeared as pleomorphic nucleus, decreased numbers and pleomorphism of secretory granules, distention of rough endplasmic reticulum, expansion and pallor appearance of mitochondria, and hypertrophy of Golgi complex. 3. Parotid serous cells were the most sensitive components, displaying morphological alterations of radiation damage as early as 3 hours, followed by submandibular seromucinous cells and secretory tubular cells. 4. The mucous cells of sublingual gland, as well as the whole ductal lining cells of each salivary gland, displayed no significant alterations. No evidence of microvascular injury through whole experimental groups indicated that microvascular impairment does not contribute to early salivary gland injury.

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탈색된 머리카락의 미세구조적 변화 (Ultrastructural Changes of Hair Treated with Bleaching Agent)

  • 장병수;이귀영
    • Applied Microscopy
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    • 제36권1호
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    • pp.25-33
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    • 2006
  • 정상성인 여성의 머리카락에 미용실에서 일반적으로 시술하는 탈색제를 사용한 다음 탈색직후, 탈색 후 10일, 20일이 경과한 머리카락을 채취하여 머리카락의 손상정도를 고배율의 투과 및 주사전자현미경으로 관찰하였다. 탈색직후 머리카락의 표면은 정상 머리카락과 비슷한 상태로 관찰되었으며 비늘이 분리되거나 손상됨 없이 나타났다. 탈색 후 10일 경과된 머리카락은 비늘이 분리되어 있고 일부 큐티클세포의 세포질은 조각이 나 있거나 떨어져 나갔다. 이 시기에 머리카락은 비늘이 떨어져 나가면서 표면에 세포부스러기들이 그대로 부착되어 있고, 비늘의 모양은 끝 쪽이 날카로운 모양을 하고 있었다. 탈색 후 20일이 경과된 머리카락은 표면 전체가 비늘의 분리에 의해서 거칠게 나타났다.

Oxygen/Glucose Deprivation and Reperfusion Cause Modifications of Postsynaptic Morphology and Activity in the CA3 Area of Organotypic Hippocampal Slice Cultures

  • Jung, Yeon Joo;Suh, Eun Cheng;Lee, Kyung Eun
    • The Korean Journal of Physiology and Pharmacology
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    • 제16권6호
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    • pp.423-429
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    • 2012
  • Brain ischemia leads to overstimulation of N-methyl-D-aspartate (NMDA) receptors, referred as excitotoxicity, which mediates neuronal cell death. However, less attention has been paid to changes in synaptic activity and morphology that could have an important impact on cell function and survival following ischemic insult. In this study, we investigated the effects of reperfusion after oxygen/glucose deprivation (OGD) not only upon neuronal cell death, but also on ultrastructural and biochemical characteristics of postsynaptic density (PSD) protein, in the stratum lucidum of the CA3 area in organotypic hippocampal slice cultures. After OGD/reperfusion, neurons were found to be damaged; the organelles such as mitochondria, endoplasmic reticulum, dendrites, and synaptic terminals were swollen; and the PSD became thicker and irregular. Ethanolic phosphotungstic acid staining showed that the density of PSD was significantly decreased, and the thickness and length of the PSD were significantly increased in the OGD/reperfusion group compared to the control. The levels of PSD proteins, including PSD-95, NMDA receptor 1, NMDA receptor 2B, and calcium/calmodulin-dependent protein kinase II, were significantly decreased following OGD/reperfusion. These results suggest that OGD/reperfusion induces significant modifications to PSDs in the CA3 area of organotypic hippocampal slice cultures, both morphologically and biochemically, and this may contribute to neuronal cell death and synaptic dysfunction after OGD/reperfusion.