• Title/Summary/Keyword: Necrosis Cell

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Calcium in Infectious Hematopoietic Necrosis Virus (IHNV) Infected Fish Cell Lines (Calcium in Infectious Hematopoietic Necrosis Virus (IHNV) Infected Fish Cell Lines)

  • Kim, Nam Sik;Heo, Gang Jun;Lee, Chan Hui
    • Journal of Microbiology
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    • v.34 no.3
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    • pp.263-263
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    • 1996
  • Infection of fish cells with IHNV resulted in gradual increase in cytosolic free $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in CHSE, gradual decrease in $[Ca^{2+}]_i$ in FHM, and no significant change in RTG cells. The degree of $[Ca^{2+}]_i$ increase or decrease was dependent on the amount of infectious virus, and these $[Ca^{2+}]_i$ variations were maximal at 16 hours after virus infection (p. i.) in both cell lines. When the fish cells were infected with inactivated IHNV, evident variation in $[Ca^{2+}]_i$ was not observed. Thus, infectivity of IHNV appears to correlate with changes in $[Ca^{2+}]_i$ in virus-infected cells. These IHNV-induced $[Ca^{2+}]_i$ changes were partially blocked by cycloheximide, but not affected by cordycepin. It seems to be that virus-induced $Ca^{2+}$ variations were more related with protein synthesis than RNA synthesis. Various $Ca^{2+}$ related drugs were used in search for the mechanisms of the $[Ca^{2+}]_i$, changes following IHNV infection of CHSE cells. Decreasing extracellular $Ca^{2+}$ concentration or blocking $Ca^{2+}$ influx from extracellular media inhibited the IHNV-induced increase in $[Ca^{2+}]_i$, in CHSE cells. Similar results were obtained with intracellular $Ca^{2+}$ blockers. Thus it is suggested that both the extracellular and the intracellular $Ca^{2+}$ sources are important in IHNV-induced $[Ca^{2+}]_i$ increase in CHSE cells.

Background Cytologic Features of Metastatic Carcinomas in the Liver in Fine Needle Aspiration Cytology - Analysis of 20 Cases - (간의 전이성 상피암 20예의 세침 천자 흡인시 배경 병변의 세포학적 소견)

  • Myong, Na-Hye;Koh, Jae-Soo;Ha, Chang-Won;Cho, Kyung-Ja;Jang, Ja-June
    • The Korean Journal of Cytopathology
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    • v.2 no.2
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    • pp.90-97
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    • 1991
  • Liver is generally known as an organ which is most commonly involved by the metastic tumors. According to the tendency of using fine needle aspiration in the diagnosis of hepatic tumors, the differentital diagnosis between hepatocellular carcinoma and metastatic carcinoma frequently has been a main issue in the poorly differentitated cases, especially to the pathologists of Korea, an endemic area of hepatocellular carcinoma. Until now the problem has been usually solved by the comparison of cytologic characteristics of their tumor cells but not by background cytologic features which rarely have been studied. We observed the background cytologic features helpful for the differential diagnosis through the analysis of 20 cases who had confirmed primary cancer and were diagnosed as metastatic carcinomas in the liver by fine needle aspiration cytology. Twenty cases included 9 adenocarcinomas, 7 spuamous cell carcinomas, 1 small cell carcinoma, 1 carcinoid, 1 adenoid cystic carcinoma, and 1 renal cell cacinoma. Analysis of background cytologic features revealed that 77% of adenocacinoma cases showed benign mesenchymal components and hepatocytes and spuamous cell carcinoma cases disclosed benign mesenchymal tissue (71%) and necrosis (57%), Remaining cases showed variable combinations of benign mesenchymal component, necrosis, hepatocytes, and bile duct epithelial cells. No case revealed atypical hepatocytic naked nuclei, a useful cytologic finding of hepatocellular carcinoma. In summary, the background cytologic features more commonly observed in metastatic carcinomas than in the hepatocellular carcinoma were benign mesenchymal components, hepatocytes, necrosis, and bile duct epithelium. The endothelial cells and hepatocytic naked nuclei, two relatively specific findings of hepatocellular carcinoma were not observed except for renal ceil carcinoma. Above background cytologic features are thought to be helpful for the differential diagnosis between the hepatocellular carcinoma and various metastatic carcinomas in the poorly differentiated cases.

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The Effects of Bee Venom on Tumor Necrosis Factor (TNF)-${\alpha}$ Induced Inflammatory Human HaCaT Keratinocytes (Tumor Necrosis Factor (TNF)-${\alpha}$로 유도된 피부각질형성세포의 염증성 반응에서 봉독의 효과)

  • Lee, Woo-Ram;Kim, Kyung-Hyun;An, Hyun-Jin;Kim, Jung-Yeon;Han, Sang-Mi;Lee, Kwang-Gill;Park, Kwan-Kyu
    • Korean Journal of Pharmacognosy
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    • v.45 no.3
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    • pp.256-261
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    • 2014
  • Bee venom (BV) therapy has been used as a traditional medicine to treat a variety of conditions, such as arthritis, back pain, cancerous tumors, and skin diseases. However, regulatory effects of BV on tumor necrosis factor (TNF)-${\alpha}$-induced HaCaT cell migration or anti-inflammatory have not been explored. In the present study, we investigated the effects of BV on HaCaT cell migration and anti-inflammation. HaCaT cell migration was evaluated by wound-healing assay. The pro-inflammatory cytokines such as TNF-${\alpha}$, interleukin (IL)-$1{\beta}$, and IL-8 were examined by ELISA or Western blotting. BV treatment led to an increase in migration of HaCaT cells for 24 and 48 h. Especially, 10 ng/ml of BV were significantly increased HaCaT cell migration. Also, BV suppressed the secretion of TNF-${\alpha}$, IL-$1{\beta}$, and IL-8 in culture medium with HaCaT cells. In addition, Western blot results demonstrate that BV suppressed the expression of TNF-${\alpha}$ and IL-$1{\beta}$, in HaCaT cells. Especially, 1 or 10 ng/ml of BV markedly decreased the expression of pro-inflammatory cytokines. These results demonstrate the potential of BV for the prevention of skin inflammation induced by TNF-${\alpha}$.

Hepatic and renal toxicity study of rainbow trout, Oncorhynchus mykiss, caused by intraperitoneal administration of thioacetamide (TAA) (티오아세트아미드(thioacetamide) 복강투여로 인한 무지개송어, Oncorhynchus mykiss의 간장 및 신장 독성 반응 연구)

  • Min Do Huh;Da Hye Jeong
    • Journal of fish pathology
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    • v.36 no.2
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    • pp.415-422
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    • 2023
  • In veterinary medicine for mammals, studies are being conducted to confirm the effects of antioxidants using pathological toxicity model studies, and are also used to confirm the effect of mitigating liver or kidney toxicity of specific substances. It was considered necessary to study such a toxicity model for domestic farmed fish, so thioacetamide (TAA), a toxic substance that causes tissue damage by mitochondrial dysfunction, was injected into rainbow trout (Oncorhynchus mykiss), a major farmed freshwater fish species in Korea. The experiment was conducted with 40 rainbow trout (Oncorhynchus mykiss) weighting 53 ± 0.6 g divided into two groups. Thioacetamide(TAA) 300mg/kg of body weight was intraperitoneally injected into rainbow trout and samples were taken 1, 3, 5, 7 days after peritoneal injection. As a result, in serum biochemical analysis, AST levels related to liver function decreased 3 and 5 days after intraperitoneal injection and increased after 7 days, and ALT levels also increased after 7 days. In addition, creatinine related to renal malfunction increased 3 and 5 days after TAA injection. In histopathological analysis, pericholangitis and local lymphocyte infiltration were observed in the liver from 1 day after intraperitoneal injection of TAA, and hepatic parenchymal cell necrosis was also observed from 3 days after intraperitoneal injection. Hyaline droplet in renal tubular epithelial cell was observed from 1 day after TAA injection, and acute tubular damage such as tubular epithelial cell necrosis appeared from 3 days after TAA injection. Accordingly, it is thought that it will be able to contribute to studies that require a toxicity model.

Role of Autophagy in the Control of Cell Death and Inflammation

  • Lee, Myung-Shik
    • IMMUNE NETWORK
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    • v.9 no.1
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    • pp.8-11
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    • 2009
  • There is mounting evidence that autophagy is involved in diverse physiological and pathological processes that have immense relevance in human development, diseases and aging. Immunity and inflammation are not exceptions. Here, the role of autophagy in the control of immune processes particularly that related to cell death and inflammation is discussed.

Isolation of infectious pancreatic necrosis virus from rainbow trout in Korea (국내(國內) 무지개 송어(松魚)에서의 IPN 바이러스의 분리(分離))

  • Lyoo, Young-soo;Chang, Chung-ho;Jean, Young-hwa;Lee, Jong-oh;Rhee, Je-chin
    • Korean Journal of Veterinary Research
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    • v.31 no.2
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    • pp.195-199
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    • 1991
  • Infectious pancreatic necrosis(IPN) virus was known as a causative agent of newly recognized viral disease of young rainbow trout characterized by highly contagious, high mortality and necrosis of pancreas. Several strains of IPN viruses were recovered from young rainbow trout that have been shown a typical cinical sign of infectious pancreatic necrosis disease. The field isolate produced cytopathic effect, and multiplied up to $10^{6.0}$ to $10^{6.5}$ $TCID_{50}/0.1ml$ in BT cell culture. In the indirect immunofluorescent assay with trout anti-IPN virus IgG and goat anti-trout IgG FITC conjugate, these isolates were proved to be a IPN virus that were closely related with VR277 strain of IPN virus antigenically.

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An abattoir survey and pathologic study of abdominal fat necrosis on Korean indigenous cattle (도축 한우의 복강내 지방괴사증 발생과 병리조직학적 연구)

  • 이성효;김추철;최길성;임채웅;서문정;최인열;채효석
    • Korean Journal of Veterinary Service
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    • v.21 no.1
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    • pp.67-77
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    • 1998
  • The bovine fat necrosis is often seen as an incidental lesion in the adipose tissues of the abdominal cavity. Most of affected animals, however, have been detected at the slaughter house or routine necropsy. The purpose of this study was to examine the occurrence and distribution of abdominal fat necrosis in Korean native cattle, and its pathologic features. Postmortem inspection at an Chonju abattoir during a three-month period in 1997 detected at necrosis lesions in 67(6.6%) of the 1,012 animals received for slaughter. The occurrence was mainly in alimentary tracts and perirenal. Both sexes were affected, but the lesion were predominantly occurred in female. Gross lesions were white or yellowish in color and formed hard lumps irregular in shape ranging from small nodules to large solid masses. On the cut surface, lesions were occasionally seen chalky calcified granules and some of the lesions contained oil-like fluid. The surface of irregular shaped masses constricted kidneys and intestinal loops. Microscopically, the masses were encapsulated by thickened fibrous tissue, which infiltrated deeply and divided them into many irregular lobules. Initial lesions presented mild inflammatory cell and fibrous proliferation. It became fibroplasia in progressive lesions and resembled chronic lesion, eventhough no grossly apparent inflammatory reaction. The hard consistency of masses, due to fibroplasia, can compress the intestines, urinary organs, and reproductive organs.

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A Review of Rat Models of Avascular Necrosis of the Femoral Head Treated with Natural Extracts

  • Go-Woon, Kim;Hyoung-Yong, Park;Yeon-Cheol, Park
    • Journal of Acupuncture Research
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    • v.39 no.4
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    • pp.239-248
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    • 2022
  • To determine the effect of Korean medicine treatment of avascular necrosis of the femoral head (ANFH) this study reviewed both single ingredients and bioactive compounds in the treatment of ANFH in a rat model. Literature was retrieved from PubMed and Google Scholar using the keywords "femur head necrosis," "natural extract," and "rat." The data from studies analyzed included: rats' characteristics, development methods of ANFH, natural extracts administration, observation methods, and outcome indicators. Two independent researchers screened all articles retrieved and 26 studies were chosen. The most used rat species was the Sprague Dawley rat (76.9%). To induce ANFH, steroid injections (46.2%), and oral gavage (53.8%) were typically used. Studies focused mainly on factors affecting bone formation (65.3%), and apoptosis (53.8%). Research on ANFH focused on using traditional natural substances mentioned in classical literature to confirm its effectiveness against anti-inflammation, osteogenesis, and cell death. ANFH has a diverse etiology, therefore research models such as genetic analysis of human-derived samples from ANFH patients may shed more light on the condition. Moreover, research into herbal medicines and pharmacoacupuncture treatment of ANFH should precede.

Connections Between Various Trigger Factors and the RIP1/RIP3 Signaling Pathway Involved in Necroptosis

  • Zhang, Yuan-Yuan;Liu, Hao
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.12
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    • pp.7069-7074
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    • 2013
  • Programmed cell death is a basic cellular process that is critical to maintaining tissue homeostasis. In contrast to apoptosis, necrosis was previously regarded as an unregulated and uncontrollable process. However, as research has progressed, necrosis, also known as necroptosis or programmed necrosis, is drawing increasing attention, not least becasu of its possible impications for cancer research. Necroptosis exhibits a unique signaling pathway that requires the involvement of receptor interaction protein kinases 1 and 3 (RIP1 and RIP3), mixed lineage kinase domain-like (MLKL), and phosphoglycerate mutase 5 (PGAM5) and can be specifically inhibited by necrostatins. Not only does necroptosis serve as a backup cell death program when apoptosis is inhibited, but it is now recognized to play a pivotal role in regulating various physiological processes and the pathogenesis of a variety of human diseases such as ischemic brain injury, immune system disorders and cancer. The control of necroptosis by various defined trigger factors and signaling pathways now offers the opportunity to target this cellular process for therapeutic purposes. The purpose of this paper is to review current findings concerning the connections between various trigger factors and the RIP1/RIP3 signaling pathway as it relates to necroptosis.

Involvement of macrophages in germ cell death in the rattestis with acute experimental testicular torsion

  • Moon, Changjong;Shin, Taekyun
    • Korean Journal of Veterinary Research
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    • v.44 no.3
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    • pp.329-334
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    • 2004
  • Ischemia/reperfusion(I/R) injury of the rat testis causes germ cell death and infiltration of inflammatory cells. To investigate the mechanism of germ cell death in torsion of the rat testis, apoptosis and macrophage activation were studied using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling(TUNEL) method and immunohistochemistry in the testes of Sprague-Dawley rats subjected to 1.5 h of ischemia, followed by 0, 1, 3, 6, 12, 24, 48 and 96 h of reperfusion. Apoptotic, TUNEL-positive cells were found at the base of the seminiferous epithelia after I/R. TUNEL-positive cells were significantly increased 6 h after repair of the torsion, and there was a significant peak in apoptosis 24 h after reperfusion, as compared with normal or sham-operated controls. In contrast, histological evidence of germ cell necrosis in the seminiferous tubules was first visible 24 h after reperfusion. In the testis of sham-operated rats, ED2-positive resident macrophages were found diffusely in the interstitial space, while ED1-positive monocyte-like macrophages were rarely found. After I/R, ED1-positive cells were significantly increased beginning 12 h after reperfusion, while ED2-positive immunoreactivity did not change during the experimental period. Together, the results of this study confirmed that increased numbers of ED1-positive macrophages, but not resident ED2-positive macrophages, infiltrated the interstitial space surrounding damaged tubules and induced germcell death.