'흑구슬' 포도에서 발생되는 빈가지의 발생 원인을 구명하고 눈의 기본 특성 및 괴사 유형을 구분하여 괴사 발생에 미치는 영향을 구명하고자 하였다. 1번마디부터 4번 마디에서는 결과모지에 가까울수록 눈의 크기는 작았으나 4번 마디 상부에 위치한 눈에서는 차이가 없었다. 1번 마디의 눈괴사율이 32.0%로 가장 높았으며, 4~10번 마디의 눈은 84.0~96.0%가 정상눈이었다. 시기별 눈의 크기는 7월이 6.40mm로 가장 컸으며 8월에서 10월까지는 차이를 보이지 않았다. 눈괴사와 주아괴사는 10월에 가장 많았으나 부아괴사는 7월부터 발생하여 이후에는 차이가 없었다. 가지 세력과 액아의 괴사발생간의 관계를 알아보기 위하여 상관분석을 실시한 결과, 가지 굵기 및 마디 길이는 괴사발생과 상관관계가 나타내지 않았으나 눈의 크기와 괴사 발생간에는 음의 상관관계를 나타내었으며 부아괴사와 가장 밀접하였다. 따라서 '흑구슬' 포도에서 눈의 괴사발생이 적고 충실함에도 불구하고 꽃송이 출현이 적은 것은 1번 눈의 괴사가 원인이므로 단초전정시 3마디를 남기고 전정을 할 경우 수량확보에 도움이 될것으로 생각된다.

The majority of strokes are caused by ischemia and result in brain tissue damage, leading to problems of the central nervous system including hemiparesis, dysfunction of language and consciousness, and dysfunction of perception. The purpose of this study was to investigate the effects of Poly(ADP-ribose) polymerase(PARP) on necrosis in neuronal cells that have undergone needle electrode electrical stimulation(NEES) prior to induction of ischemia. Ischemia was induced in male SD rats(body weight 300g) by occlusion of the common carotid artery for 5 min, after which the blood was reperfused. After induction of brain ischemia, NEES was applied to Zusanli(ST 36), at 12, 24 and 48 hours. Protein expression was investigated using immuno-reactive cells, which react to PARP antibodies in cerebral nerve cells, and Western blotting. The results were as follows: In the cerebral cortex, the number of PARP reactive cells after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. PARP expression after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. As a result, NEES showed the greatest effect on necrosis- related PARP immuno-reactive cells 24 hours after ischemia, indicating necrosis inhibition, blocking of neural cell death, and protection of neural cells. Based on the results of this study, NEES can be an effective method of treating dysfunction and improving function of neuronal cells in brain damage caused by ischemia.

Enterococcus faecalis, a gram-positive bacterium, has been implicated in endodontic infections, particularly in chronic apical periodontitis. Proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), are involved in the pathogenesis of these apical lesions. E. faecalis has been reported to stimulate macrophages to produce TNF-α. The present study investigated the mechanisms involved in TNF-α production by a murine macrophage cell line, RAW 264.7 in response to exposure to E. faecalis. Both live and heat-killed E. faecalis induced high levels of gene expression and protein release of TNF-α. Treatment of RAW 264.7 cells with cytochalasin D, an inhibitor of endocytosis, prevented the mRNA up-regulation of TNF-α by E. faecalis. In addition, antioxidant treatment reduced TNF-α production to baseline levels. Inhibition of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein (MAP) kinase also significantly attenuated E. faecalis-induced TNF-α expression by RAW 264.7 cells. Furthermore, activation of NF-κB and AP-1 in RAW 264.7 cells was also stimulated by E. faecalis. These results suggest that the phagocytic uptake of bacteria is necessary for the induction of TNF-α in E. faecalis-stimulated macrophages, and that the underlying intracellular signaling pathways involve reactive oxygen species, ERK, p38 MAP kinase, NF-κB, and AP-1.

This study was performed to investigate the effects of Needle Electrode Electrical Stimulation(NEES) on ischemia-induced cere˗ brovascular accidents. After obstruction and reperfusion of arteries in white mice, the amounts of necrosis and inflammation related sub˗ stances Bax, IL-6, Caspase-3, and COX-2 were measured in neurons of the fore-brain. The following results were obtained. This study used 21 male specific pathogen free(SPF) SD rats, 8 weeks of age and approximately 300g in weight. Each exposed artery was completely occluded with non-absorbent suture thread and kept in that state for 5 minutes. The sutures were then removed to allow reperfusion of blood. Test group is control group(common carotid artery occlusion models), a GI(underwent common carotid artery occlusion), and NEES(underwent NEES after artery occlusion). The GI and NEES groups were given 12, 24, or 48 hours of reperfusion before NEES. NEES device(PG6, ITO, Japan, 9V, current, 2Hz) was used to stimulate the bilateral acupoint ST36 of the SD rats for 30 minutes while they were sedated with 3% isoflurane. An immuno-his˗ tochemistry test was done on the forebrains of the GI induced rats. Both Bax and Caspase-3 immuno-reactive cells, related to apoptosis, were greater in the GI than the NEES group. Cox-2 and IL-6 immuno-reactive cells, related to inflammation, were greater in the GI and NEES groups than the control group. We can expect that applying NEES after ischemic CVA is effective for preventing brain cells from being destroyed. And we can conclude NEES should be applyed on early stage of ischemic CVA.

Nitric oxide(NO) is a labile, uncharged, reactive radical that functions as a sensitive mediator of intercellular communication in diverse tissues. It has been reported that NO is produced by osteoblast and these results may suggest that NO is integrally involved in the regulation of osteoclast formation and osteoclast resorption activity by osteoblastic cells. We examined the effect of cytokines on NO release by mouse bone marrow cell. We also examined the effects of cytokines and sodium nitroprusside(SNP) on the formation of osteoclast-like cell from mouse bone marrow cells in culture. Cytokines stimulated NO production of mouse bone marrow cells, and N-nitro-L-arginine methyl ester, a specific inhibitor of NO synthase, suppressed the cytokine-induced NO production. SNP showed dual action in the generation of osteoclasts. The addition of (30μM)SNP inhibited the formation of tartrate resistant acid phosphatase(TRAP)(+) multinucleated cell, whereas lower concentration(30μM) of SNP enhanced it. Although the precise action of NO remains to be elucidated in detail, the action of NO in osteoclast generation in our studies seems to be associated, at least in part, with bone metabolism and bone pathophysiology.

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is a well-known inducer of apoptotic cell death in many tumor cells. 1RAIL is expressed in human placenta, and cytotrophoblast cells express 1RAIL receptors. However, the role of TRAIL in human placentas and cytotrophoblast cells is not. well understood. In this study a trophoblast cell line, JEG-3, was used as a model system to examine the effect of TRAIL. on key intracellular signaling pathways involved in the control of trophoblastic cell apoptosis and survival JEG-3 cells expressed receptors for 1RAIL, death receptor (DR) 4, DR5, decoy receptor (OcR) 1 and DeR2. Recombinant human TRAIL (rhTRAIL) did not have a cytotoxic effect determined by MIT assay and did not induce apoptotic cell death determined by poly-(ADP-ribose) polymerase cleavage assay. rhTRAIL induced a rapid and transient nuclear translocation of nuclear factor-kB(NF-kB) determined by immunoblotting using nuclear protein extracts. rhTRAIL rapidly activated extracellular signal-regulated protein kinase (ERK) 1/2 as determined by immnoblotting for phospho-ERK1/2. However, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38MAPK) and Akt (protein kinase B) were not activated by rhTRAIL. The ability of 1RAIL to induce NF-kB and ERK1/2 suggests that interaction between TRAIL and its receptors may play an important role in trophoblast cell function during pregnancy.

In odontogenic osteolytic lesions, the mechanism involved in inflammation 때d osteolysis is still under debate. We investigated the role 。OL-l ~ -1 ß, -4, -6, -8, TNF- a in the expansion of the odontogenic cysts, by using 50 cases of excised odontogenic cysts. The degrees of inflammation were graded into 2 groups and immunohistochernical stainings were performed, The cytoplasrnic reaction in squamous epithelial cells, stromal cells and infIitrating inflammatory cells was examined. The relationship between the expressions of IL-1 q -1 ß, -4, -6, -8, π-JF- aand the degree of inflammation and the correlation among them were analyzed. 까1e 비Stilαγtic expressions of IL-l ~ IL-l ß and TNF-awere 66.6%, 66.6% and 4O.00Al respeαively and the epithelial exp~않sions of IL-4, -6, -8 were 32.00Al, 38.00Al and 24.00Al respeαively. IL-4, -6 and 용 were positively stained in plasma cells in 38.00Al, endothelial cells in 40.00/0 and neutrophils in 24. 00Al respectively. The expresssion rate of IL-4 in plasma cells and IL-8 in epithelium and neutrophils were inα얹sed in ca않s with marked inflammation. 까1e exp!1않sion rate of IL-1 ßin 피해ocytes and IL-4 in plasma cells were positively correlated with the expæssion of TNF-1 ain histiocytes. π1e expression rate of anti-inflammatory cytokine IL-4 in the epithelium were correlated with the expression of IL-6 in the epithelium and endothelial cells. A1though statistically insi.맑표ìcant， the expression rate of IL-6 were decreased in cases with marked inflammation and nega디vely correlated with IL-8, the proinflammatory cytokine, and the expressions of IL-4 and IL-6 in the epithelium can be considered as inhibiting the inflammatory reaction. These results suggest that the expressions of IL-4 and IL-6 suppress and IL-8 stimulates the inflammatory reaction in Odontogenic Cysts.

Doxorubicin is a anti-cancer drugs that interferes with the growth and spread of cancer cells in human body. Doxorubicin is used to treat different types of cancers that affect the ovary, thyoid and lungs, but induced side effect such as nephrotoxicity and cardiotoxicity. Thus, we investigated that the effect of iridin on doxorubicin-induced necrosis in HK-2 cells, a human proximal tubule cell. To confirm effect of iridin on doxorubicin-induced necrosis, HK-2 cells are treated with 10 μM doxorubicin and 80 μM iridin. 80 μM iridin reduced 10 μM doxorubicin-induced necrosis, the mitochondrial over activation and caspase-3 activation. However, iridin reduces anti-cancer effect of doxorubicin such as PARP1 and caspase-3 activation, checkpoint proteins (CDK4 and CDK6) in NCI-H1129 cells (Human non-small cell lung cancer cell). In HCT-116 cells (Human colorectan cancer cell), iridin do not increased protein expression of CDK4 and CDK6 decreased by doxorubicin. Results indicate that treatment of iridin was diminished doxorubicin-induced necrosis in HK-2 cells. However, iridin was decreased anti-cancer effect of doxorubicin on NCI-H1229, but not HCT-116. Thus, further experiment are required to iridin treatment on various cancer cells and animal models because effect of iridin different cell type.

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 μM doxorubicin and 80 μM cynaroside. Doxorubicin treatment resulted in increased DNA fragmentation, caspase-3 activity and mitochondria hyperactivation during cell necrosis. However, pretreatment with 80 μM cynaroside attenuated DNA fragmentation, caspase-3 activity and mitochondria hyperactivation induced by 10 μM 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 doxorubicininduced nephrotoxicity in an animal model.

급성전골수구성 백혈병(Acute promyelocytic leukemia, APL)은 혈액암의 일종으로 치료의 성적이 좋지 않 을 뿐 아니라 항암요법과 병행 하였을 경우 큰 효과를 보이는 것으로 알려져 있는 방사선 치료를 병행함에 도 불구하고 정상세포에도 작용하여 부작용을 초래한다. 본 연구에서는 이러한 부작용을 감소시키기 위하 여 감마선을 TNF-α와 같이 처리하였을 경우 정상세포와 암세포의 세포 죽음에 어떠한 영향을 미치는지 확 인하였다. HL-60 세포는 APL 세포주로서 사용하였고 DMSO를 처리하여 분화시킨 HL-60 세포는 정상과립 구의 성질을 나타내어 정상대조군으로 이용하였다. 그 결과 TNF-α와 함께 감마선을 처리한 HL-60 세포에 서만 세포독성효과를 나타내었고 세포자멸사를 유도하여 세포가 죽음에 이르게 하였다. 결론적으로 TNF-α 는 항암치료의 부작용을 없애기 위해 저농도 감마선 치료 시 함께 사용하여 암 세포의 제거를 증가시켜 암 의 치료효율을 높일 수 있는 유효물질로 사료된다.

Acute tubular necrosis (ATN) is a syndrome of intrinsic renal injury secondary to ischemic or toxic causes without parenchymal damages and usually non-oliguria. A 20-year old man presented with acute renal failure preceded by 2 days of watery diarrhea. He had been anuria for 48hr with intravenous fluid therapy. Oliguria persisted for 10 days and he required hemodialysis support for 6 days before renal recovery. He denied the use of any regular medication and any intravenous drug use. Renal biopsy revealed severe ATN. Histopathologic findings were marked desquamation of proximal tubular epithelial cells with intact distal tubules and normal glomeruli. We report an unusual case of ATN with anuria and clinically severe features.

Hepatocellular carcinoma (HCC) is the fifth most common cancer and the third leading cause of cancer-related deaths worldwide. The radiologic findings of liver abscess, HCC, and metastatic tumor to the liver may be quite similar, and a specific diagnosis cannot be made using procedures such as serum tumor marker assay, computerized tomography, and ultrasonography of the liver. We report on a case of HCC successfully diagnosed and treated by surgery which was misconceived as a liver abscess.

To search for immunoactive natural products exerting anti-inflammatory activity, we have evaluated the effects on the water extracts of Artemisia princeps Pampanini (APP) on lipopolysaccharide-induced nitric oxide (NO), tumor necrosis factor-α (TNF-α), and prostaglandin E2 (PGE2) production by RAW 264.7 macrophage cell line. Our data indicate that this extract is a potent inhibitor of NO production and it also significantly decreased PGE2 and TNF-α production. Consistent with these results, the protein and mRNA expression level of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) was inhibited by water extracts of APP in a dose-dependent manner. These results suggest that APP may exert anti-inflammatory and analgesic effects possibly by suppressing the inducible NO synthase and COX-2 expressions.

To search for immunoactive natural products exerting anti-inflammatory activity, we have evaluated the effects of the ethanol extracts of Rubus coreanus Miq. (ERC) on lipopolysaccharide-induced nitric oxide (NO), tumor necrosis factor-α (TNF-α), and Interferon-γ (IFN-γ) production by RAW 264.7 macrophage cell line. Our data indicate that this extract is a potent inhibitor of NO production and it also significantly decreased IFN-γ and TNF-α production. Consistent with these results, the protein level of inducible Nitric Oxide Synthase (iNOS) and cyclooxygenase-2 (COX-2) was inhibited by ethanol extracts of ERC in a dose-dependent manner. These results suggest that ERC may exert anti-inflammatory and analgesic effects possibly by suppressing the inducible NO synthase and COX-2 expressions.

Naturally occurring substances are important biomedical resources with low toxicity and ethnopharmacology-based efficacy. Four out of 45 extracts (Celastrus orbiculatus, Cercis chinensis, Stephanadra incisa, and Weigela subsessilis) prepared from the bark of Korea Forest plants exhibited more than 50% of inhibition on TNF-α production in lipopolysaccharide (LPS)-activated RAW264.7 cells at 100 μg/ml. In particular, potential inhibitory components of 4 extracts showed more than 50% inhibition seemed to be concentrated in methylene chloride (MC) fraction from C. orbiculatus, in ethyl acetate (EtOAc) fraction from C. chinensis and in hexane (Hx) fraction from S. incisa, whereas inhibitory activities of W. subssilis were broadly seen in non-polar solvent fractions such as Hx, MC and EtOAc. Therefore, our results suggest that extracts from C. orbiculatus, C. chinensis, S. incisa and W. subsessilis may be developed as a therapeutic remedy against TNF-α-mediated diseases such as rheumatoid arthritis or further fractionated to isolate active components having antiTNF-α inhibitory activity.