No abstract available.

BACKGROUND: To study the prognosis of patients with lung cancer, many investigators have reported the methods to detect cell proliferation in tissues including PCNA, thymidine autoradiography, flow cytometry and Ki-67. PCNA, also known as cyclin, is a cell related nuclear protein with 36KD intranuclear polypeptide that is maximally elevated in S phase of proliferating cells. In this study, PCNA was identified by paraffin-embedding tissue using immunohistochemistry which has an advantage of simplicity and maintenance of tissue architecture. The variation of PCNA expression is known to be related with proliferating fraction, histologic type, anatomic(TNM) stage, degree of cell differentiation, S-phase fraction and survival rate. We analyzed the correlation between PCNA expression and S-phase fraction, survival. METHODS: To investigate expression of PCNA in primary lung cancer, we used immunohistochemical stain to paraffin-embedded sections of 57 resected primary non-small cell lung cancer specimen and the results were analyzed according to the cell type, cell differentiation, TNM stage, S-phase fraction and survival. RESULTS: PCNA expression was dMded into five group according to degree of staging(-, +, ++, +++,++++). Squamous cell type showed high positivity than in adenocarcinoma. Nonsignificant difference related to TNM stage was noticed. Nonsignificant difference related to degree of cell differentiation was noticed. S-phase fraction was increased wit advance of PCNA positivity, but t could not reach the statistic significance. The 2 year survival rate and median survival time were -50% 13 months, +75% 41.3 months, ++73% 33.6 months, +++67% 29.0 months, ++++25% 9 months with statistic significance (P<0.05, Kaplan-Meier, generalized Wilcox). CONCLUSION: From this study. PCNA expression was high positive n squamous cell cancer. And, there was no relationship between PCNA positivity and TNM stage, cellular differentiation or S-phase fraction. But, the patients with high positive PCNA staining showed poor survival rate than the patients with lower positive PCNA. It was concluded that PCNA immunostaining is a simple and useful method for survival prediction in paraffin embedded tissue of non-small cell lung cancer.
Adenocarcinoma ; Autoradiography ; Carcinoma, Non-Small-Cell Lung* ; Cell Differentiation ; Cell Proliferation ; Cyclins ; Flow Cytometry ; Humans ; Immunohistochemistry ; Lung Neoplasms ; Neoplasms, Squamous Cell ; Nuclear Proteins ; Paraffin ; Prognosis ; Proliferating Cell Nuclear Antigen* ; Research Personnel ; S Phase ; Survival Rate* ; Thymidine

No abstract available.
Arthroplasty* ; Hip Joint* ; Hip*

No abstract available.
Exostoses*

To determine the neuromuscular effect and its reversals of gentamicin, alone or in combination with metocurine, pharmacodynamic studies were done using a common peroneal nerve- anterior tibialis muscle preparation in 24 adult cats weighing 2.5-4.0 kg. The median effective dose of gentamicin obtained by cumulative dose-response study was 21.6+/-4.83 mg/kg. Under the pretreatment of gentamicin, the onset and duration of metocurine was 1.32+/-0.91 min and 28.8+/-10.95 min, respectively. There was no significant difference in the recovery indicies for its reversal between neostigmine and calcium. Each values of recovery indices were 1.85+/-0.65 and 2.05+/-1.00 min with neostigmine and calcium, respectively. These results suggested that gentamicin by itself had neuromuscular blocking effect. With the pretreatrnent of gentamicin, the onset of metocurine was shortened to one third and its duration was prolonged as much as seven times. Additionally, metocurine induced neuromuscular block with pretreatment of gentamicin was reversed completely.
Adult ; Animals ; Calcium* ; Cats* ; Gentamicins* ; Humans ; Neostigmine* ; Neuromuscular Agents ; Neuromuscular Blockade*

Dieulafoys lesion consists of abnormally large gastric submucosal artery which ruptures into the stomach causing massive or recurrent intragikstric bleeding. The lesion is very small and easily overlooked even at laparatomy and aan only be correctly diagnosed by endoscopy or arteriography if the patient is actively bleeding. Three patients who were admitted with bleeding of upper gastrointestinal tract and eventually diagnosed as having Dieulafoys lesions were analysed. All were men with age range of 44 to 55 years. All patient were asymptomatic before presenting with hematemesis. Two of the three patients had had history of upper Gl bleeding. One patient used analgesics daily for ureteral colic and two patient drank alcohol excessively. Gastroscopy was performed during the bleeding episode in all three patients. Dieulafoy's lesion was seen in all three cases and in the second case, there was concomittent diffuse petechia in the whole stomach. The lesion was situated on the posterior wall of upper body in one, on anterior wall of upper body in another, lesser curvature side of gastric fundus in the other case. All three patient underwent laparotomy for persistent bleeding and the lesion was suture ligated only in two patients while in one patient vagotomy and pyloroplasty was added. Resection biopsy was performed in two cases and both revealed only normal gastric mucosa. All patients discharged after complete recover.
Analgesics ; Angiography ; Arteries ; Biopsy ; Endoscopy ; Gastric Fundus ; Gastric Mucosa ; Gastroscopy ; Hematemesis ; Hemorrhage ; Humans ; Laparotomy ; Male ; Renal Colic ; Rupture ; Stomach ; Sutures ; Upper Gastrointestinal Tract ; Vagotomy

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAID) are useful in chemoprevention of colorectal cancers. Continuous NSAID administation causes 40% to 50% reduction in relative risk for colorectal cancer. Sulindac possesses an antiproliferative effect and induces apoptosis and tumor regression on colon cancer and other types of cancers. We intended to analyze the effects of sulindac in three non-small cell lung cancer cell lines. MATERIALS AND METHODS: The human lung cancer cell lines, A549, NCI-H157 and NCI-H460 were used for this study. Viability was tested by MTT assay, and cell death rate was measured by lactate dehydrogenase(LDH) release. Apoptosis was estimated by flow cytometric analysis and nuclear staining. RESULTS: Sulindac was able to decrease the viability of non-small cell lung cancer cells in a dose- and time- dependent manner. In a parallel effect of sulindac on cell death rate, LDH release was increased in sulindac-treated lung cancer cells. Sulindac significantly increased apoptosis characterized by an increase of sub-G0/G1 fraction and morphological change of nuclei. The rate of apoptotic cells after sulindac treatment in lung cancer cells increased in a time- and dose- dependent manner in flow cytometric analysis. Apoptotic cells were defined as nuclear shrinkage, chromatin condensation and nuclear fragmentation of cells. CONCLUSION: Sulindac decreases viability and induces the apoptosis of lung cancer cells. Further studies will be needed to elucidate the potential mechanism of sulindac-induced apoptosis in lung cancer cells.
Apoptosis* ; Carcinoma, Non-Small-Cell Lung ; Cell Death ; Cell Line ; Chemoprevention ; Chromatin ; Colonic Neoplasms ; Colorectal Neoplasms ; Humans* ; Lactic Acid ; Lung Neoplasms* ; Lung* ; Sulindac*

Arsenic trioxide(As2O3) was introduced into the treatment of refractory or relapsed acute promyelocytic leukemia. Some investigators have reported that arsenic trioxide had induced apoptosis in a variety of solid human tumor cell lines, including non-small cell lung cancer. Non-steroidal anti-inflammatory drugs(NSAIDs) are powerful chemopreventive agents for gastrointestinal cancers and the growth of established tumors are reduced by inducing apoptosis. It's also reported that NSAIDs enhanced tumor response to chemotherapeutic drugs or radiation. In this study, we aimed to determine whether combination of arsenic trioxide with sulindac augmented its apoptotic potential in NCI-H157 human lung cancer cells. The human lung cancer cell line NCI-H157 was treated with arsenic trioxide and sulindac. Cell viability was measured by the MTT assay. Apoptosis was measured by nuclear staining and flow cytometric analysis. The catalytic activity of the caspase families were measured by the fluorogenic cleavage of biosubstrates. The western blotting were also performed to define the mechanical basis of apoptosis. Combination treatment of arsenic trioxide and sulindac decreased the viability of NCI-H157 human lung cancer cells in a dose-dependent manner. The catalytic activity of caspase-3, 8 and 9 proteases were increased after combination treatment. Consistently PARP was cleaved from 116kDa to 85kDa fragments, and the expression of ICAD was decreased by time-dependent manner. Also combination treatment increased the expression of Fas and Fas/L. Combination therapy of arsenic trioxide with sulindac augments cell death and induces apoptosis via the activation of caspase cascade in NCI-H157 human lung carcinoma cells.
Anti-Inflammatory Agents, Non-Steroidal ; Apoptosis* ; Arsenic* ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung ; Caspase 3 ; Cell Death ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Gastrointestinal Neoplasms ; Humans* ; Leukemia, Promyelocytic, Acute ; Lung Neoplasms ; Lung* ; Peptide Hydrolases ; Research Personnel ; Sulindac*

BACKGROUND: Matrix metalloproteinases (MMPs) are a large family of proteolytic enzymes, which are in volved in the degradation of many different components of the extracellular matrix. There is increasing evidence indicating that individual MMPs have important roles in tumor invasion and metastasis. A tissue inhibitor of metalloproteinase(TIMPs) has been reported to inhibit tumor invasion by inactivating the MMPs. In this study, the correlation between MMPs and TIMPs expression, and the clinical outcome was investigated. METHODS: Immunohistochemical staining of MMP-2,9 and TIMP-1,2 were performed on paraffin-embedded tumor sections from 74 resected primary non-small cell lung cancers. RESULTS: In 74 patients, MMP-2, MMP-9, TIMP-1, and TIMP-2 immunoreactivity was demonstrated in 24 (34%), 19(26%), 27(36%) and 32(43%) of the paraffin-embedded tumors, respectively. The median survival of the MMP-2 positive cases was significantly shorter than that of the negative cases(20 vs 34 months). The median survival of the TIMP-2 positive cases was also was significantly longer than that of negative case (34 vs 18 months). The MMP-2, and MMP-9 expression level had a positively correlation with a more advanced stage and lymph node metastasis. There was inverse correlation between TIMP-2 expression and tumor invasion. The median survival of the MMP-2 negative/TIMP-2 positive cases was higher than that of the other cases. CONCLUSION: These results suggest that tumor invasion and lymph node metastasis are closely related to MMP-2 and MMP-9 expression. There was an inverse correlation between TIMP-2 MMP-9 expression, and tumor invasion.
Carcinoma, Non-Small-Cell Lung* ; Extracellular Matrix ; Humans ; Lung Neoplasms ; Lymph Nodes ; Matrix Metalloproteinases ; Neoplasm Metastasis ; Peptide Hydrolases ; Tissue Inhibitor of Metalloproteinase-1 ; Tissue Inhibitor of Metalloproteinase-2

BACKGROUND: Arsenic trioxide (As2O3) has been used to treat acute promyelocytic leukemia, and it induces apoptosis in a variety of solid tumor cell lines including non-small cell lung cancer cells. However, nonsteroidal anti- inflammatory drugs (NSAID) can enhance tumor response to chemotherapeutic drugs or radiation. It was previously demonstrated that a combination treatment with As2O3 and sulindac induces the apoptosis of NCI-H157 human lung carcinoma cells by activating the caspase cascade. This study aimed to determine if a combination treatment augmented its apoptotic potential through other pathways except for the activation of the caspase cascade. MATERIAL AND METHODS: The NCI-H157 cells were treated with As2O3, sulindac and antioxidants such as glutathione (GSH) and N-acetylcysteine (NAC). The cell viability was measured by a MTT assay, and the level of intracellular hydrogen peroxide (H2O2) generation was monitored fluorimetrically using a scopoletin-horse radish peroxidase (HRP) assay. Western blotting and mitochondrial membrane potential transition analysis were performed in order to define the mechanical basis of apoptosis. RESULTS: The viability of the cells was decreased by a combination treatment of As2O3 and sulindac, and the cells were protected using antioxidants in a dose-dependent manner. The increased H2O2 generation by the combination treatment was inhibited by antioxidants. The combination treatment induced changes in the mitochondrial tran-smembrane potential as well as the expression of the Bcl-2 family proteins, and increased cytochrome c release into the cytosol. However, the antioxidants inhibited the effects of the combination treatment. CONCLUSION: Combination treatment with As2O3 and sulindac induces apoptosis in NCI-H157 human lung carcinoma cells via ROS generation with a mitochondrial dysfunction.
Acetylcysteine ; Antioxidants ; Apoptosis* ; Arsenic* ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung ; Cell Line, Tumor ; Cell Survival ; Cytochromes c ; Cytosol ; Glutathione ; Humans* ; Hydrogen Peroxide ; Leukemia, Promyelocytic, Acute ; Lung* ; Membrane Potential, Mitochondrial ; Peroxidase ; Raphanus ; Sulindac*