• The Korean Journal of Malacology
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• v.27 no.3
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• pp.213-221
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• 2011

Equilateral venus, Gomphina veneriformis exposed to tribultyltin chloride (TBTCl) for 36 weeks was showed ultrastructural changes of the mantle. The fine mantle had 4-folds and its epidermal layer consisted of simple columnar epithelial cells and ciliated cells and secretory cells. Inner and outer epidermal layer covered connective tissue. The mantle exposed to TBTCl at 12 weeks was decreased cilia in the inner epidermal layer, and observed extension of the hemolymph sinus and destruction of the septum. At 20 weeks, it revealed vacuole formation and pycnosis in the cytoplasm, and scattered muscular fiber. After 28 weeks of exposure, the mantle revealed partially degenerative changes in the epidermal layer. In the ciliated cells, basal body was isolated from the cilia and rootlet complex and basal foot were scattered. The sarcolemma had debris fiber. At 36 weeks, it observed degenerative cells that it revealed disappearance of the cilia, atrophic nucleus, poorly membrane and destruction of the cresternae in the mitochondria, and increasing heterophagosome. The outer epithelial cell had necrotic nuclus, numeous lysosome and disappearance of the microvilli. Therefore, results of this study suggested that chronical TBTCl exposure in the Gomphina veneriformis induced the disorders of shell growth and physiological function with histopathological changes of the mantle.

• The Journal of Korean Academy of Prosthodontics
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• v.28 no.2
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• pp.1-28
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• 1990

The severe atrophic edentulism with poor neuromuscular control militates against successful conventional denture therapy. To such situation, a prescribing of dental implant treatment has been considered with some probability. Implant materials used as a trial for dental implants includes metals, plastic polymers and ceramics. The purpose of this study was to observe histologic response in osseointegration process at titanium implant-tissue interface based on biocompatibility at specific period of sequential natures which were divided into a half month, one, month, two months, three months and immediate as a base line. In this study, unilateral lower left premolar and molar teeth were extraced in three dogs. After allowing to heal for 6 months, three kinds of osseointegrated implant, $Br{\aa}nemark$, Corevent and kimplant(a prototype of SNU implant study)were inserted in each dog respectively according to the above sequence from front to back. The specimens were taken from those dogs at the same time since implant were inserted quite reverse order of the specified periods, and decalcified and processed for histologic examination for the light microscopy and the electron microscopy. The microscopic histologic findings at the interface between titanium implants and tissue were interpretated as follows : A. Light microscopic findings : a. Immediate : Implant were surrounded by compact bone and spongy bone. Microcrak was observed in the superficial bone tissue. Osteocytes were disappeared and bone lacunae were observed as a vacant space in some parts. In the contacting with the spongy bone, bone trabeculae and bone marrow were in contact with the implant. b. A half Month : Osteoblasts exist as a monolayer in th inner bone trabeculae and do bone additiocn. Osteoblasts&inflammatory cells were observed in some parts. c. One Month : The presence of osteoclasts decreased. Osteoblasts did active bone fromation, and bone marrow was in contact with the implant in the many places. d. Two Months : Bone formation was advanced in comparison with the b and c. The presence of osteoclsts was not observed. e. Three Months : The superficial bone tissue contacted with the implants was entirely composed by the compact bone. B. Electron microscopic findings : a. A half month and one month group : In the parts of the active bone formation, osteoblasts with the well developed endoplasmic reticulum and Golgi apparatus were arranged in the monolayer. In the parts of the bone resorption, ruffled border was well developed and many osteoclasts with the well-developed golgi apparatus, mitochondria, vacuole, vesicle and lysosome were existed. b. Three months group : No osteoblasts were observed in the superficial bone tissue. Bone matrix with collaen fiber was observed. c. No significant dirrerence in the histologic findings was observed in $Br{\aa}nemark$, Core-vent and kimplant.

• Tuberculosis and Respiratory Diseases
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• v.75 no.1
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• pp.9-17
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• 2013

Background: In cancer cells, autophagy is generally induced as a pro-survival mechanism in response to treatment-associated genotoxic and metabolic stress. Thus, concurrent autophagy inhibition can be expected to have a synergistic effect with chemotherapy on cancer cell death. Monensin, a polyether antibiotic, is known as an autophagy inhibitor, which interferes with the fusion of autophagosome and lysosome. There have been a few reports of its effect in combination with anticancer drugs. We performed this study to investigate whether erlotinib, an epidermal growth factor receptor inhibitor, or rapamycin, an mammalian target of rapamycin (mTOR) inhibitor, is effective in combination therapy with monensin in non-small cell lung cancer cells. Methods: NCI-H1299 cells were treated with rapamycin or erlotinib, with or without monensin pretreatment, and then subjected to growth inhibition assay, apoptosis analysis by flow cytometry, and cell cycle analysis on the basis of the DNA contents histogram. Finally, a Western blot analysis was done to examine the changes of proteins related to apoptosis and cell cycle control. Results: Monensin synergistically increases growth inhibition and apoptosis induced by rapamycin or erlotinib. The number of cells in the sub-$G_1$ phase increases noticeably after the combination treatment. Increase of proapoptotic proteins, including bax, cleaved caspase 3, and cleaved poly(ADP-ribose) polymerase, and decrease of anti-apoptotic proteins, bcl-2 and bcl-xL, are augmented by the combination treatment with monensin. The promoters of cell cycle progression, notch3 and skp2, decrease and p21, a cyclin-dependent kinase inhibitor, accumulates within the cell during this process. Conclusion: Our findings suggest that concurrent autophagy inhibition could have a role in lung cancer treatment.

• Applied Microscopy
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• v.25 no.3
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• pp.51-62
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• 1995

It has been well known that ischemia and reperfusion injury to skeletal muscle following an acute arterial occlusion causes significant morbidity and mortality. The skeletal muscle, which contains high energy phosphate compounds, has ischemic tolerance. During the ischemia, the ATP is catalyzed to hypoxanthine anaerobically and hypoxanthine dehydrogenase is converted to xanthine oxidase. During reperfusion, the hypoxanthine is catalyzed to xanthine by xanthine oxidase under $O_2$, presence and that results in production of cytotoxic oxygen free radicals. These cytotoxic free radicals, $O_2^-,\;H_{2}O_2,\;OH^-$, are toxic and make lesions in skeletal muscle during reperfusion. The authors perform the present study to investigate the effects of allopurinol, the inhibitor of xanthine oxidase, on reperfused ischemic skeletal muscles by observing the ultrastructural changes of the muscle fibers. A total of 48 healthy Sprague-Dawley rats weighing from 200 g to 250 g were used as experimental animals. Under urethane(3.0mg/kg., IP) anesthesia, lower abdominal incision was done and the left common iliac artery were ligated by using vascular clamp for 1, 2 and 6 hours. The left rectus femoris muscles were obtained at 6 hours after the removal of vascular clamp. In the allopurinol pretreated group, 50mg/kg of allopurinol was administered once a day for 2 days and before 2 hours of ischemia. The specimens were sliced into $1mm^3$ and prepared by routine methods for electron microscopic observations. All preparations were stained with uranyl acetate and lead citrate, and then observed with Hitachi -600 transmission electron microscope. The results were as follows: 1. In 1 hour ischemia/6 hours reperfused rectus femoris muscles of rats, decreased glycogen particles and electron density of mitochondrial matrix and dilated terminal cisternae are seen. In 2 hours ischemia/6 hours repersed rectus femoris muscles of rats, mitochondria with electron lucent matrix, irregularly dilated triad and spheromembranous bodies are observed. In 6 hours ischemia/6 hours reperfused rectus femoris muscles of rats, irregularly arranged myofibrils, and many spheromembranous bodies, fat droplets and lysosome are seen. 2. In 1 hour ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol, decreased glycogen particle and dilated cisternae of sarcoplasmic reticulum and triad are observed. In 2 hours ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol decreased electron density of mitochondrial matrix and spheromembranous bodies are seen. In 6 hours ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol, mitochondria with electron lucent matrix, spheromembranous bodies and dilated cisternae of sarcoplasmic reticulum and terminal cistern are observed. The results suggest that the allopurinol attenuates the damages of the skeletal muscles of rats during ischemia and reperfusion.

• Korean Journal of Clinical Laboratory Science
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• v.52 no.3
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• pp.245-252
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• 2020

Macrophage cell death contributes to the formation of plaque, leading to the development of atherosclerosis. The accumulation of triglyceride (TG) is also associated with the pathogenesis of atherosclerosis. A previous study reported that TG induces the cell death of macrophages. This study examined whether the cytoplasmic release of cathepsin B from lysosome is associated with the TG-induced cell death of macrophage. The release of cathepsin B was increased in the TG-treated THP-1 macrophages, but the TG treatment did not affect cathepsin B expression. Furthermore, the inhibition of cathepsin B by its inhibitor, CA-074 Me, partially inhibited the TG-induced cell death of macrophage. TG-triggered macrophage cell death is mediated by the activation of caspase-1, -2, and apoptotic caspases. Therefore, this study investigated whether cathepsin B is implicated in the activation of these caspases. The inhibition of cathepsin B blocked the activation of caspase-7, -8, and -1 but did not affect the activity of caspase-3, -9, and -2. Overall, these results suggest that TG-induced cytoplasmic cathepsin B causes THP-1 macrophage cell death by activating caspase-1, leading to subsequent activation of the extrinsic apoptotic pathway.

• Journal of the korean academy of Pediatric Dentistry
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• v.39 no.4
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• pp.412-417
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• 2012

Mucopolysaccharidosis (MPS) is a disorder which is caused by the defect of the lysosomal enzyme that is essentially needed for resolution of glycosaminoglycans (GAGs). Metabolite of GAGs will accumulate in the lysosome of cells and will result in the dysfunction of cells, tissues, and organs. Eventually, patients will manifest both mental retardation and physical disorders. In worst cases, mucopolysaccharidosis can cause premature death. The current clinical types have been classified as MPS from type I to type IX according to the defect of certain enzyme. The dental complications have been reported as delay of eruption, enamel hypoplasia, microdontia, malocclusion, condylar defects, gingival hyperplasia and dentigerous cystlike follicle. This clinical report presents the case of a boy with MPS type II, Hunter Syndrome which has various dental complications.

• Proceedings of the KSMRM Conference
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• 1999.11a
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• pp.69-71
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• 1999

최근 한국 의학의 발전은 전체 한국의 선진화를 선도하다고 보기에는 힘드리만 최소한 국제무대에의 진출은 괄목할만한 발전을 보이고 있다. 최근에 들어 국내 방사선영상과련 학회의 발전은 날로 비약적인 추세를 보이고 있다. 일례로 대한방사선의학회는 본 저자가 전공의 하던 1980년도 초기만 해도 호텔의 큰 홀 한 개만 빌려서 하루만 해도 넉넉하게 진행되었다. 그러나 최근의 학회사정은 대형호텔 1개층 통째로 빌리고 3일간 진행해도 여유가 없을 정도이며 더욱이 추계학회는 지방에서 유치할만한 공간이 부족하여 이제는 없어져야할 지경에 이러렀다. 그뿐 아니라 대한 자기공명의과학회를 포함한 각종 학회가 이제 그 규모를 더해가고 있어. 대한민국에 있어서 진단 방사선영역의 의학은 급속히 발전하여 RSNA, ISMRM등에서도 세계 발표순위가 4-5위권을 다투게 되었다. 이러한 발전은 양적인 발전이 우세하여 주로 임상연구에 기반을 두고 있는데 이 자체로는 장기적인 발전에 한계점이 있으므로 앞으로는 기초과학연구에 기초한 질적 발전을 같이 추구하여야만 균형있는 성장을 기대할 수 있겠다. 이러한 기존의 구성에 최근 급격한 변화를 주도하는 학문이 MRI부분이 되며 이 분야를 연구하는 PhD 들의 역할이 크게 대두되고 있다. 현재 국내에도 초기 단계이지만 MRI를 생산하고 있으며 PhD들의 활동이 성장단계에 접어들었다고 할수 있다. 과거 우리의 NRI역사에서는 금성사 MR기계처럼 육성되기 전에 시들며 노력하던 기술진이 흩어져야 했던 어두운 기억이 있다. 이러한 시점에서 우리의 힘들었던 과거를 돌이켜보며 또 하나의 기초부분이 육성되 수 있도록 서로가 격려하며 협조하여야 될 것으로 생각되어 다음과 같이 요약을 하였다. 소기관으로는 세포 막, 미토콘드리아 (mitochondria), endoplasmic reticulum, Golgi 체, lysosome, peroxisome 그리고 세포질등이 있으며, 이들중에서 lysosomes, peroxisomes, 그리고 미토콘드리아가 특정한 유전성 백질질환에 중요한 역할을 하는 것이 밝혀졌다. 이러한 질환들은 최소한 각 소기관에 의한 질환군으로 분류될 수 있다.SXR이 ER의 transactivation 효과를 약간 촉진한 반면 MDA-MB-231세포는 SXR을 제외한 CAR와 PPAR${\gamma}$에 의해 ER의 transactivation 효과가 약간 증가되는 경향을 보였다. 이러한 결과는 유방암세포에서는 CAR, SXR, PPAR${\gamma}$과 같은 xenobiotic nuclear receptor에 의한 ER transactivation 효과가 간암세포와는 다르게 나타나며, 유방암의 종류에 따라서 endogenous CAR, SXR, PPAR${\gamma}$수용체가 다르게 발현됨으로써 이들에 대한 반응이 서로 상이한 특징을 나타낼 수 있을 것으로 사료된다. 따라서 estrogen receptor에 의해 매개되는 estrogn의 전사활성조절기전이 표적세포에 따라 다른 경로를 포함 할 수 있음을 시사한다.서 흡착 능력이 우수하게 나타났으며, 황화수소는 펄라이트, 왕겨, 소나무수피에서 상대적으로 우수한 것으로 나타났으며, 혼합충전재는 암모니아의 경우 코코넛과 펄라이트의 비율이 7：3인 혼합 재료 3번과 소나무수피와 펄라이트의 비율이 7：3인 혼합 재료 6번에서 다른 혼합 재료에 비하여 우수한 것으

• Korean Journal of Microbiology
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• v.50 no.1
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• pp.27-32
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• 2014

Autophagy is one of the lysosomal degradation pathways to maintain cellular homeostasis. The damaged proteins or organelles are uptaken through extra- and intra-cellular stress, starvation and infected pathogens, subsequently, autophagosomes are fused with lysosomes to break down the molecules. Salmonella enterica serovar Typhimurium (S. Typhimurium), intracellular bacteria, cause acute gastroenteritis and food poisoning. Given that autophagy induced by S. Typhimurium plays an important role in the cells to control the infection, we identify whether the induction of autophagy with rapamycin, chemical inducer of autophagy, before infection regulates S. Typhimurium infection. After treatment of rapamycin or 3-methyladenine (3-MA), autophagy inhibitor, RAW264.7 cells were infected with S. Typhimurium. Pretretment of rapamycin decreased the growth rate of S. Typhimurium in the cells; otherwise, pretreatment of 3-MA increased the growth rate of S. Typhimurium. The expression of autophagy-related genes was significantly increased in the S. Typhimurium-infected cells pretreated with rapamycin. To examine whether induced autophagy by rapamycin control the infection with increase the production of reactive oxygen species (ROS) and nitric oxide (NO), antibacterial radical substrates were measured in infected cells followed by the treatment with either rapamycin or 3-MA. NO production increased in RAW264.7 cells; otherwise, ROS production remained unchanged during the infection. These findings suggest that inducing autophagy with rapamycin reveals antimicrobial activity as producing NO against S. Typhimurium infection in mouse macrophages.

• Journal of Life Science
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• v.25 no.1
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• pp.1-7
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• 2015

Cyclin D is a member of the cyclin protein family, which plays a critical role as a core member of the mammalian cell cycle machinery. D-type cyclins (D1, D2, and D3) bind to and activate the cyclin-dependent kinases 4 and 6, which can then phosphorylate the retinoblastoma tumor suppressor gene products. This phosphorylation in turn leads to release or derepression of E2F transcription factors that promote progression from the G1 to S phase of the cell cycle. Among the D-type cyclins, cyclin D3 encoded by the CCND3 gene is one of the least well studied. In the present study, we have investigated the biochemistry of the proteolytic mechanism that leads to loss of cyclin D3 protein. Treatment of human prostate carcinoma PC-3-M cells with lovastatin and actinomycin D resulted in a loss of cyclin D3 protein that was completely reversible by the peptide aldehyde calpain inhibitor, LLnL. Additionally, using inhibitors for various proteolytic systems, we show that degradation of cyclin D3 protein involves the $Ca^{2+}$-activated neutral protease calpain. Moreover, the half-life of cyclin D3 protein half-life increased by at least 10-fold in PC-3M cells in response to the calpain inhibitor. We have also demonstrated that the transient expression of the calpain inhibitor calpastatin increased cyclin D3 protein in serum-starved NIH 3T3 cells. These data suggested that the function of cyclin D3 is regulated by $Ca^{2+}$-dependent protease calpain.

• Journal of Life Science
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• v.19 no.8
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• pp.1159-1163
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• 2009

It has been postulated that endoplasmic (ER) stress is involved in the development of several diseases. However, the detailed molecular mechanisms have not been fully understood. Therefore, we characterized a genetic network of genes induced by ER stress using cDNA microarray and gene set expression coherence analysis (GSECA), and identified gene function as well as several transcription regulators associated with ER stress. We analyzed time-dependent gene expression profiles in thapsigargin-treated Sk-Hep1 using an oligonucleotide expression chip, and then selected functional gene sets with significantly high expression coherence which was processed into functional clusters according to the expression similarities. The functions related to sugar binding, lysosome, ribosomal protein, ER lumen, and ER to golgi transport increased, whereas the functions with mRNA processing, DNA replication, DNA repair, cell cycle, electron transport chain and helicase activity decreased. Furthermore, functional clusters were investigated for the enrichment of regulatory motifs using GSECA, and several transcriptional regulators associated with regulation of ER-induced gene expression were found.